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Adaptive immune system is classified into two types: Humoral which is mediated by {{c1::B cells}}<div>Cell-mediated which is mediated by {{c1::T cells}}<br><div><br></div></div>
Subtypes of T cells &amp; function<div>T helper cell ---&gt; {{c1::Activate T / B cells &amp; macrophages, mediate inflammation}}</div><div>Cytotoxic T lymphocyte (CTL)&nbsp;<span>&nbsp;</span><span>---&gt;&nbsp;</span>{{c1::Killing infected cells}}<span>&nbsp;</span></div><div>T regulator cell<span>&nbsp;</span><span>---&gt;&nbsp;</span>{{c1::suppression of other T cells}}<span>&nbsp;</span></div><div><br></div>"<img src=""paste-b08420b0f7a09e0ffcae01ae14ea6b3360347c6a.jpg"">"
T cell activation needs three steps to polarize into a specific subset (Th1/2/17):&nbsp;<div>{{c1::Induction}} --&gt; {{c1::Commitment}} --&gt; {{c1::Amplification}}</div><div><br></div>"Induction promotes the differentiation of naive cd4 T cells by producing cytokines for each subset<div>Commitment is when progressive activation leads to stable changes in expressed genes</div><div>Amplification is when there are cytokines which promote the production of only one subset, and suppress all the others.&nbsp;</div><div><img src=""paste-88f47a7c68492953e580f4af3be9c680f696a00b.jpg""><br></div><div><br></div>"
Polarization of one naive CD4 T cell to a specific subset depends on the {{c1::cytokine environment}}
Th1 is activated in the case of {{c1::intracellular microbal}} infection<div>Th2 is activated in the case of {{c1::Helminith }} infections</div><div>Th17 is activated in the case of {{c1::extracellular bacteria or fungi&nbsp;}} infection</div>
"Th1 cells<div>Activated by the signals: {{c1::IL-12 made by macrophages and IFN-g by NK cells}}</div><div>Transcription factors expressed: {{c1::T-bet}}, {{c1::STAT1}}, {{c1::STAT4}}</div><div>Th1 cells are activated in the case of: {{c1::Intracellular microbes}}</div><div>How will Th1 cells fight the infection? {{c1::stimulates inflammation // produces IFN-g which stimulates production of cytokines // induces macrophages to kill microbes // stimulates B cells to produce IgG antibodies</div><div><img src=""paste-91f779a45bcf60db9093838a684f6cb9dad05b12.jpg""><span>}}&nbsp;</span></div><div><br></div>"
Th2 cells<div>Activated by the signal: {{c1::IL-4}}</div><div>Transcription factors expressed: {{c1::GATA-3}} &amp; {{c1::STAT6}}</div><div>Th2 cells are activated in the case of: {{c1::Helminith infections}}</div><div>Th2 will secrete IL4/5/13.</div><div>Role of IL-4? {{c1::Autocrine growth and promotes B cell production of IgE}}</div><div>Role of IL-5? {{c1::activates eosinophils}}</div><div>Role of IL-13? {{c1::Mucosal secretions}}</div>"<div><img src=""paste-6bec1d13b8a5e894f670b327f601ffaf492b6a8b.jpg""><br></div>IgE will activate mast cells and coat helminiths.&nbsp;<div>IL4&amp;13 will activate M2 macrophages which promote fibrosis&nbsp;</div>"
Th17 cells<div>Activated by the signals: {{c1::IL-1 &amp;IL-6 by APC, &amp; TGF-beta}}</div><div>Transcription factors expressed: {{c1::STAT3}} &amp; {{c1::RORgt}}</div><div>Th17 cells are activated in the case of: {{c1::extracellular bacterial or fungal infections}}</div><div>Role of Th17 cells in the immune system? {{c1::Recruit neutrophils and produce antimicrobial peptides}}</div><div>Role of IL-23? {{c1::stabilizes Th17 cells.}}</div><div>Role of IL-21? {{c1::Amplifies the response}}</div>"<img src=""paste-bb33f6a538ea196d89dbae6658c618d012bb494d.jpg"">"
Cytotoxic T lymphocytes express the cell marker {{c1::CD8}}<div>They are activated by {{c1::cells expressing MHC I due to intracellular pathogen (Viruses)}}</div><div>CTL induce apoptosis by releasing: {{c1::Perforins, granzymes and granulysin&nbsp;}}</div>
Regulatory T cells (Treg) are generated by self antigen recognition in the {{c1::thymus}} &amp; {{c1::peripheral lymphoid tissue}}<div>Survival of Treg is done by the expression of the TF {{c1::FoxP3}}</div><div>Role of Tregs is to {{c1::suppress activation of other self-reactive and pathogenic lymphocytes}}</div><div>&nbsp;<br><div><br></div></div>"<img src=""paste-b9cba0ae562ba307bc91f1741cc7a99db992582e.jpg"">"
Normal individuals dont respond to food antigens due to {{c1::induced tolerance via Treg cells}}in allergic patients food antigens promote Th2 activation and IgE production
HLA class I includes: {{c1::HLA-A // B // C}}<div>HLA class II includes: {{c1::HLA-DR // DQ // DP}}</div>
"Which MHC class is the picture seen below and which T cell binds to it?<div><img src=""paste-294cc26f0fa33fa60e05f72015252db1f745e2b2.jpg""><br></div><div>{{c1::MHC Class I, Cd8 Cytotoxic T lymphocyte}}</div><div><img src=""paste-78796925af2484890e60773544d9e6fceb1a46a7.jpg""><br></div><div>{{c1::MHC Class II CD4 T helper cell}}</div>"
"The HLA genes show polymorphism and polygeny. In the end how many genes will be expressed in one individual? {{c1::6 genes co-dominantly expressed<div><img src=""paste-f6384110bc7e25ddb451bb61d200e7ba19de2468.jpg""><br></div>}}"Three genes are passed down from the paternal, and another three from the maternal side. in total 6 are expressed
The {{c1::MHC class I and II}} are the most immunogenic antigens recognized during rejection of a transplant
The most immunogenic MHC antigens in order are {{c1::HLA-DR}}, {{c1::HLA-B}}, {{c1::HLA-A}}
Which peptide binding groove is bigger, MHC I or MHC II?<div>{{c1::MHC II}}</div>
"How come only 6 HLA genes are needed to be recognized and bind to a HUGE number of of different T cell receptors?<div>{{c1::because of the presence of a conserved pattern of amino acids (MOTIF)&nbsp;</div><div><img src=""paste-4b4b9a312e341d51bc3e605d2108e0e63bd196d9.jpg"">}}</div>""Anchor residues are located in the lower portion of the peptinde and will bind in the groove of the MHC molecule, and the outer portion will be recognized by T cells<div><img src=""paste-fa7032d38fc7cd7c5169d6a94524c5dddaad7e48.jpg""></div>"
Variation in the MHC alleles in terms of binding affects {{c1::binding variability within the groove}}<div><br></div>"<div>In class I variation in alpha1&amp;2. class II variation in only beta1</div><img src=""paste-784bdbb7206d67307dce708f7415238b5240783e.jpg"">"
Homogeneity of the HLA alleles is {{c1::disadvantageous since it promotes pathogens to mutate and resist:: Advantageous or disadvantageous? }}<div>Heterogeneity is {{c1::advantageous since it allows more antigen binding and therefore a higher T cell response.&nbsp;}}</div>Polymorphism allows the survival of the population, not necessarily the individual&nbsp;
Functional features of cytokines:<div>{{c1::Pleitropic: one cytokine can act on different cells}}</div><div>{{c1::Redundant: Multiple cytokines can have the same functional effect}}</div><div>{{c1::Synergistic: two cytokines may produce additive or synergistic effects}}</div><div>{{c1::Antagonistic: Effect of cytokines opposite of another&nbsp;}}</div>"<img src=""paste-269e996caf948970f8e9299b8f77ca254768f6c9.jpg"">"
Type I cytokine receptor (hematopoietin receptor family) is divided into three subgroups based on a common component in each subgroup.&nbsp;<div>Common component in group 1: {{c1::Gamma chain}}</div><div>Common component in group 2: {{c1::Beta chain}}<br></div><div>Common component in group 3: {{c1::gp130 signaling component}}<br></div>"<img src=""paste-2605d0aa9664a2ac11f4c5e0e7e4ffef6780f6ca.jpg"">"
SCID is a condition affecting {{c1:: T and B }}cells<div>Knockout of the {{c1::GammaC }}&nbsp;<span>subunit of the type 1 cytokine receptors</span><span>&nbsp;will cause SCID</span></div><div>Interleukins and function which are affected by this:</div><div><div><br></div> <div>IL-2 {{c1::is essential for proliferation of activated T cells (T cell growth factor)}}</div> <div>IL-4 {{c1::is important for the differentiation to Th2 cells}}</div><div>IL-7 {{c1::is a very essential in driving early proliferation of progenitor T cells.}}<br></div> <div>IL-15 {{c1::is usually secreted following viral infection}}</div></div>"<img src=""paste-3a0626dd20d02127bee87bcc7d9a3971cdadb8d8.jpg"">"
{{c1::Chemokines}} are cytokines which regulate the migration of leukocytes to the site of interest&nbsp;
{{c1::Interferons}} are produced by virus-infected cells to protect neighboring cells from the infection
{{c1::Macrophages}} are the main cytokine producers of the innate immune cells<div>{{c1::Antigen specific T cells}} are the main cytokine producers in the adaptive immune system</div>
Local and systemic effect of inflammatory cytokines TNF-alpha, IL-1, IL-6:<div>{{c1::Increased capillary permeability}}&nbsp;</div><div>{{c1::Infiltration of immune cells}}&nbsp;</div><div>{{c1::Blood clotting to prevent spreading}}&nbsp;</div><div><br></div>good in local infections but bad if systemic bc it causes&nbsp;<div>systemic edema--&gt; decreased blood volume--&gt;collapsed vessels</div><div>Hypoproteinemia</div><div>neutropenia followed by neutrophilia</div><div>DIC</div>
T cell differentiation depends on:<div>{{c1::Antigen presented by APCs}}&nbsp;</div><div>{{c1::Cytokines available}}&nbsp;&nbsp;</div>
cytokine action regulated by:<div>{{c1::Their transient production}}&nbsp;</div><div>{{c1::Only produced in presence of antigen or potent inflammatoy stimulus}}&nbsp;</div><div>{{c1::restricted to cells expressing receptors}}&nbsp;&nbsp;</div><div>{{c1::inhibitory cytokines like IL-10 and TGF-beta present to tone it down&nbsp;}}</div>
"Let's say you see a patient infected with mycobacterium leprae. this pathogen will hide within the phagosome of macrophages and prevent binding to lysosomes.&nbsp;<div>Two different immune responses are possible, which response correlates with which picture? explain yourself&nbsp;</div><div><img src=""paste-2c52c5d45a611c6c968412ffac77692180fbf0ba.jpg""><br></div><div><span>{{c1::</span>TH1 response: Mild form tuberculoid leprosy. forms granulomas which contains the infection, induces hypoxia and kills it.&nbsp;</div><div>}}</div><div><img src=""paste-40e633c20b9dcc8bab8c8249a7e0d44ba61681fb.jpg""><br></div><div><span>{{c1::</span>TH2 response: Severe form lepromatous leptosy. forms IL-4 &amp; IL-5 which produce antibodies. this is useless since the pathogen is within phagosomes where antibodies cannot reach</div><div>}}</div>"
How do some invaders interfere with cytokine activity?<div>{{c1::Either by making cytokine antagonists (IFN-gamma or IL-1 are pro-inflammatory, so decreasing them decreases inflammation)&nbsp;}}</div><div>Or</div><div>{{c1::cytokine agonists (IL-10 is anti-inflammatory)}}</div>
Cytokines used in therapy:<div>Anti IL-2 in {{c1::kidney transplantation}}</div><div>Anti IL-4 in {{c1::asthma}}<br></div><div>Anti IL-6 in {{c1::rheumatoid arthritis and crohns disease}}<br></div><div>Anti TNF-alpha in {{c1::theumatoid arthritis}}<br></div><div>Side effect of blocking cytokines? {{c1::You block inflammation}}</div>
Naive T cells encounter their unique antigen by circulating though peripheral lymphoid organs<div>They are activated by two independent signals:&nbsp;</div><div>-{{c1::MHC molecule recognition}}</div><div>-{{c1::Co-stimulatory factors B7 on APC and CD28 on T cell}}</div>"<img src=""paste-af69fe54826a092b23e22ec7a585704e0fa1d4da.jpg"">"
<div>Th1 cells will release the following cytokines with a specific functionL</div>IL-2 produced by TH1 induces {{c1::T cell proliferation}}<div>IL-3 and GM-CSF stimulates {{c1::macrophage production}}<div>MCP-1 function is {{c1::recruiting new macrophages}}</div></div><div>IFN-g and CD40 ligand will induce {{c1::macrophages to destroy intracellular microbes}}</div><div>Fas ligand or TNF-beta will {{c1::kill old macrophages}}</div><div>TNF alpha and beta produces {{c1::endothelial receptors for macrophage exit from BVs}}</div>
Do T helper cells stimulate the differentiation of CD8 T cells? If yes, how?<div>{{c1::Yes, but indirectly. Activated T helper express CD40L, which binds to CD40 on APCs. This will increase the expression of co-stimulatory molecules on APCs making it more efficient in stimulating CD8 cells}}</div>"<img src=""paste-16397efc484ad633556da1990a2a89648adfc6dc.jpg"">"
What are cells which use antibody dependent cell-mediated cytotoxicity (ADCC)<div>{{c1::NK cells}}, {{c1::macrophages}} &amp; {{c1::eosinophils&nbsp;}}</div>antibodies coat the pathogen which allows recognition and killing&nbsp;
"A male patient comes with a burning feeling in the urethra and a purulent exudate. he suspects that the underlying cause was unprotected sexual intercourse. After a blood culture and a gram smear you visualize gram negative diplococci within PMNs.&nbsp;<div><img src=""paste-4aa7dc61db19a05bd0b87a27f56908de12322c72.jpg""><br></div><div>most likely diagnosis? {{c1::Neisseria gonorrheae}}</div><div>Treatment? {{c1::Ceftriaxon and azithromycin}}</div>"
"A young patient presents in pediatrics with a stiff neck and petechia which do not go away with glass pressing. CSF was turbid and h<span>is culture shows gram negative diplococci inside PMNs.&nbsp;</span><div><img src=""paste-d69a6e8e0aaa91631881ac466df5f7ec07ecf92d.jpg""><br></div><div><img src=""paste-517e7c25e89a83b2b1ee2a403cfa83ad019b734e.jpg""><br></div><div>Diagnosis? {{c1::N. meningitidis}}<span>&nbsp;</span></div><div><span>Treatment: {{c1::ceftriaxone}}</span></div>"
Neisseria gonorrhoeae infects {{c1::non-ciliated columnar}} epithelial cells&nbsp;<div>Bacteria then adheres and commits parasite-directed endocytosis and will stay in the {{c1::subepithelial}} region</div><div>{{c1::LOS}} from the bacteria will induce strong inflammatory response</div><div>{{c1::TNF-alpha}} will damage the mucosa&nbsp;</div><div>The bacteria will get phagocytized but will survive within {{c1::PMNs}} because of the presence of porin</div><div>It needs iron which it gets from {{c1::hemoglobin}}, {{c1::lactoferrin}}, and {{c1::transferrin}}</div><div>susceptible patients are those with an {{c1::inborn compliment deficiency, or those with a serum resistant strain}}&nbsp;</div><div>LOS will bind to host sialic acid and {{c1::increase serum resistance}}<br></div>
N.&nbsp;gonorrhea will infect the following organs:<div>-{{c1::Cervix}}</div><div>-{{c1::Vagina in prepubertals}}&nbsp;</div><div>-{{c1::Urethra in males}}</div><div>-{{c1::Conjunctiva of newborns}}&nbsp;</div><div>-{{c1::Proctitis}}&nbsp;</div><div><br></div><div>Disseminated infections:&nbsp;</div><div>Local spread--&gt; {{c1::from cervix can move up all the way to peritoneum (Pelvic inflammatory disease&nbsp;}}</div><div>Via blood stream --&gt; {{c1::arthritis usually unilateral&nbsp;}}</div><div><br></div>
How to take samples of N.&nbsp;gonorrhea in:<div>Males: {{c1::urethral swab}}</div><div>Females: {{c1::endocervical swab}}</div><div>PCR can be done to confirm the diagnosis of N.&nbsp;gonorrhea and chlamydia together, since if you have one you probably have the other too</div>
N.&nbsp;Gonorrhea is {{c1::extremely drug-resistant:: susceptible or drug resistant?}}.&nbsp;<div>Is there a vaccine? {{c1::No vaccines.}}</div><div>Prevention? {{c1::condoms}}</div>
Main phenotypic difference between N. gonorrhea and N. meningitidis is that&nbsp;<span>meningitidis is {{c1::capsulated}}</span><div>N. meningitidis can be found in the {{c1::nasopharynx}}</div><div>Most N.meningitidis is by subtype capsule {{c1::A}}</div>Capsule B has sialic acid homopolymer which is a similar antigen to our own body. it is difficult for the body to recognize it.&nbsp;
Pathogenesis pathway of N. meningitidis:<div>{{c1::Nasopharynx}} --&gt; {{c1::blood circulation}} --&gt; {{c1::meninges&nbsp;}}</div>
Explain the waterhouse friderchisen syndrome in N.Meningitidis<div>{{c1::Causes necrosis of the adrenal cortex --&gt; endocrine homeostasis collapse}}</div>
Physical examination of N. meningitidis?&nbsp;<div>-{{c1::patients feel discomfort when you lift a bent leg (increases internal pressure)}}</div><div>-{{c1::when you lift their head it will be&nbsp;<span>compensated by bending the knees</span><span>}}</span><span>&nbsp;</span></div><div>-{{c1::bulging fontanelle}}</div><div>&nbsp;&nbsp;</div>"<img src=""paste-5211a08e7f56cb866fd07afa6fa59f17e2b43a41.jpg"">"
Diagnosis of N. meningitidis:&nbsp;<div>-{{c1::Not chilled CSF}}</div><div>-{{c1::Blood cuture}}</div><div>-{{c1::PCR}}</div><div>-{{c1::AG detection}}</div><div>-{{c1::Gram stain}}</div><div>Therapy:&nbsp;</div><div>{{c1::Penicillin &amp; ceftriaxon.&nbsp;}}</div>
Two types of moraxella and disease<div>Moraxella lacunata --&gt; {{c1::conjunctivitis}}</div><div>Moraxella catarrhalis --&gt; {{c1::pneumonia}}, {{c1::endocarditis}}, {{c1::mengitis}}, {{c1::otitis media}}, {{c1::sinusitis}}</div><div>Will produce beta-lactamase. Treatment --&gt; {{c1::amoxicillin+ clavulanic acid}}</div>
Which mucosal immunoglobin isotope predominates? {{c1::IgA}}
Intestinal lymphocytes responses are <u>induced in </u>the {{c1::organized tissues (peyer's patch)}}<div>Scattered lymphocytes within the {{c1::lamina propria}} carry out <u>effector functions</u></div>Organized lymphoid tissues includes peyer's patch, lymphoid follicles, appendix, tonsils, adenoids
Crohn's and celiac disease result from {{c1::dysregulated mucosal immune responses}}
The {{c1::glycocalyx}} is a mucinous thick barrier on mucus membranes that traps pathogens and is full of {{c1::IgA}} immunoglobins"<img src=""paste-6419ef0d6dd29f5bfa35b6ad989e529cc3dcaeea.jpg"">"
How do proteolytic enzymes (like pepsin and trypsin) act as an innate immune defense?<div>{{c1::break down to peptides less immunogenic&nbsp;}}</div><div>{{c1::kill pathogens themselves}}</div>
Antimicrobial molecules and effect:<div>Lactoferrin: {{c1::Binds to iron and inhibits bacterial growth}}</div><div>Lysozyme: {{c1::Cleaves cell wall of gram positive bacteria&nbsp;}}</div><div>Defensins: {{c1::causes lysis of bacteria and fungi&nbsp;}}</div>
Commensal organisms protect us by {{c1::competing with pathogens for space and nutrients}}, {{c1::degrading toxins}}, {{c1::establishing the GALT}}
"Under an electron microscope inspection of the peyer's patches you view areas not covered by glycocalyx made out of thin cells with no microvilli<div><img src=""paste-973009747958e25445cc274eacc79ca0ee39fd82.jpg""><br></div><div>What are they and what's their function?</div><div>{{c1::M cells. uptake of antigens and delivery to dendritic and B cells}}</div><div><br></div>""<img src=""paste-a5d921fa1d014a539050ca2d0372039bc00f091f.jpg"">"
"you are viewing intraepithelial lymphocytes under the microscope.&nbsp;<br><div><img src=""paste-a7d6e0d4df620d8c51f60ca651311edcebc451e8.jpg""></div><div>what kind of T cell is it and which type of TCR does it produce?</div><div>{{c1::CD8 positive Alpha-Beta TCR}}</div>"
lamina propria lymphocytes are {{c1::CD4:: Which T cell marker?}} effector/ memory T cells<div>They have a {{c1::weak:: Strong or weak?}} proliferative response to antigens</div>
Blood IgA exists as a {{c1::monomer:: Dimer or monomer?}}<div>Mucosal IgA exists as a {{c1::dimer:: Dimer or monomer?}}</div><div>Mucosal IgA binds to {{c1::polymeric Ig receptor (PIgR}} on the basolateral surface and transported to the glycocalyx</div>
The {{c1::Secretory component}} of the IgA receptor protects it from proteolytic cleavage and acts as a glue to bind to the glycocalyx
Functions of IgA in the gut:<div>-{{c1::Neutralizes pathogens and toxins in the glycocalyx and in endosomes}}</div><div>-{{c1::Exports toxins}}</div><div>-{{c1::Imports toxins for dendritic detection and processing}}</div>
Anti-inflammatory mechanism of sIgA:<div>-Unable to activate {{c1::compliment system}}</div><div>-Inhibits {{c1::phagocytosis&nbsp;}}</div><div>-Down regulates {{c1::TNF-alpha}} and {{c1::IL-6}}</div>
Mucosal immune system responds to {{c1::pathogens}}, but normally not to {{c1::dietary antigens}}
Dietary antigens induce the production of {{c1::Tregs}} which maintain non-responsiveness to oral antigens. this is called {{c1::mucosal oral tolerance}}
<div>Two signals are required for B cell activation.&nbsp;</div><div>Signal 1: {{c1::Antigen recognition via BCR}}</div><div>Signal 2 can be two things:&nbsp;</div><div>{{c1::Thymus dependent antigen response where T follicular helper cells are required&nbsp;}}</div><div>Or</div><div>{{c1::Thymus independent antigen response where the part of the antigen itself such as LPS will activate the B cell}}</div>
{{c1::linked recognition}} is a process in which<span>&nbsp;an epitope is processed and expressed by a B cell, then recognized by a T helper cell.&nbsp;</span>
Polysaccharides are not recognized by {{c1::T helper}} cells in linked recognition. to combat this is to {{c1::conjugate it with a protein}}, so B cells can take it up, break it down and express the protein part for T cells to recognize&nbsp;&nbsp;
Where do activated B cells undergo affinity maturation and isotype switching? {{c1::in the germinal centers}}
"<div><br></div>Where do B cells rapidly divide? {{c1::dark zone}}<div>where do B cells interact with follicular dendritic cells? {{c1::light zone}}</div><div><img src=""paste-4a981eedd598bbd73e5f7b4c855cd88e4707e319.jpg""><br></div>"
To activate B cells, T helper cell will express {{c1::CD40L}} and secrete cytokines.&nbsp;<div>{{c1::IL-21:: Which IL-}} will activate STAT3 which enhances B cell proliferation.&nbsp;</div>
"You are viewing a cell with an extensive amount of rough ER and eccentric nucleus.&nbsp;<div><img src=""paste-b88f9b8028a6af777ef6d2ee796652ba37c67e05.jpg""><br></div><div>What is it most likely? {{c1::Plasma cell}}</div>"
Isotype // Signal for production // effect<div>IgM // {{c1::None needed}} // {{c1::Compliment activation}}</div><div>IgG // {{c1::IFN-g}} // {{c1::attach and induce phagocytosis &amp; compliment activation}}</div><div>IgE // {{c1::IL-4}} // {{c1::Helmniths attachment &amp; mast cell degranulation}}</div><div>IgA // {{c1::TGF-beta}} // {{c1::mucosal immunity}}</div>
Plasma cells express which antibody in<div>Primary infections: {{c1::IgM}}</div><div>Secondary infection: {{c1::IgG}}</div><div>{{c1::Affinity maturation}} is increased binding of antibody to antigen due to somatic hypermutation</div>
Thymus independent B cell activation divided into two:&nbsp;<div>TI-1 {{c1::where the concentration of LPS will activate B cell regardless of T cells. Antibodies are IgM alone}}</div><div>TI-2 {{c1::where dendritic cells activate instead of T cells. Antibodies are IgM and IgG}}</div>
Children below the age of five cannot respond to {{c1::TI-2:: TF // TI-1 // TI-2}} antigens, which is why they need to be conjugated
You {{c1::upregulate:: Upregulate or downregulate?}} the immune system in the case of vaccination or to treat cancer.<div>You {{c1::downregulate}} the immune system in translpant patients or autoimmune diseases</div>
Which cells have an enhanced response after re-exposure to an offending agent?&nbsp;<div>{{c1::CD4/8 T cells &amp; B cells}}</div>
Immunization acts to increase the concentration of {{c1::antibodies and effector T cells}} specifically against the reactive agent
Immunization before exposure is called {{c1::immunoprophylaxis}}, and intends to prevent infection<div>Immunization during an active infection is called {{c1::immunotherapy}}, and intends to cure the infection&nbsp;</div>immunotherapy best if immuno-compromised patients. do NOT give them live vaccines
Passive immunization via transfering {{c1::antibodies}} to the patient like maternal milk&nbsp;<div>Drawback is that it has {{c1::no immunological memory}}</div><div>Active immunization either by {{c1::natural infection}} or {{c1::vaccination}}</div>"<img src=""paste-9bed5e1ea9fc161a16c3095a50aee0fd4f7b1e75.jpg"">"
Passive immunization examples:<div>Natural: {{c1::IgA transfer from breast feeding// IgG placental cross-over}}</div><div>Medical: {{c1::Extracted antibodies as a prophylaxis or cure}}</div><div>Blocking: {{c1::prevent erythroblastosis fetalis by preventing sensitization (RhoGam)}}</div>
Are vaccines usually given only once? {{c1::Nope. Need boosters&nbsp;}}
What must be considered with designing a vaccine?&nbsp;<div>{{c1::Efficacy}}, {{c1::Toxicity}} &amp; {{c1::safety&nbsp;}}</div><div><br></div>
In designing a vaccine:<div>which type has the highest efficacy? {{c1::Attenuated}}<div>Which has the highest toxicity?<span>{{c1::Attenuated}}</span></div><div>Which has the lowest safety<span>{{c1::Attenuated}}</span></div></div>
Side effect of using anti-TNF agents is a {{c1::reactivated TB}} infection
{{c1::Natalizumab}} used to treat multiple sclerosis by binding and blocking the alpha 4 chain
{{c1::Hypersensitivity}} is an excessive immune response against foreign antigens caused by the adaptive immune system.&nbsp;
Hypersensitivity will occur during the {{c1::second:: First, second, third?}} exposure to the antigen
{{c1::Haptens}} are chemical compounds too small to elicit an immune response themselves, but are capable of conjugating to our antigens and alienate them from our body, thus creating hypersensitive responses"<img src=""paste-b2a8dbee3098ce61e33834d80a59a4d47a561cde.jpg""><div>Like penicillin is capable of eliciting type 2 and type 3 hypersensitive reactions</div>"
Type I hypersensitivity:<div>Requires the cytokines and signals: {{c1::CD40/CD40L IL-4 &amp; IL-13 (Th2)}}<br><div>Sensitisation product: {{c1::IgE immunoglobins}}</div><div>Effector mechanism upon re-exposure: {{c1::IgEs will activate mast cells and cause degranulation}}</div><div>Reaction: {{c1::irritation to systemic anaphylaxis&nbsp;}}</div><div>{{c1::Atopic}} individuas have an inherited predisposition</div></div>
Effector phase of IgE mediated allergic response:<div>Immediate: {{c1::Histamine release}}</div><div>Minutes: {{c1::Arachadonic acid products}}</div><div>Hours: {{c1::Gene activation of new cytokine production (Eosinophil production and Th2 amplification)}}</div>
Mast cell degranulation effects:<div>GI: {{c1::increased fluid secretion and peristalsis&gt;&gt; Diarrhea and vomiting}}</div><div>Airways: {{c1::constriction and mucus secretion&gt; Phlem and difficulty breathing}}</div><div>BVs: {{c1::vasodilation&amp; increased permeability&gt; Edema and increased flow}}</div>
Eosinophils activated by the signals: {{c1::IL-5/ eotaxins 1-3, C3a and C5a}}
Systemic anaphylaxis caused by allergens that reach the {{c1::blood stream and activate mast cells throughout the body}}
Treatment for anaphylactic shock:<div>Early phase: {{c1::IM Epinephrine&nbsp;}}<span>and</span><span>&nbsp;</span>{{c1::antihistamines}}<span>&nbsp;&nbsp;</span></div><div>Late phase: {{c1::Corticosteroids}}</div>
Type II hypersensitivity<div>Immunoglobin type: {{c1::IgG}} and<span>&nbsp;</span>{{c1::IgM}}<span>&nbsp;</span></div><div>trigger agent: {{c1::Cell+ hapten}}</div><div>Response: {{c1::Complement mediated lysis}}/ {{c1::ADCC}}/ {{c1::Phagocytosis&nbsp;}}</div><div><br></div>Can cause intravascular hemolytic anemia, drug induced thrombocytopenia, granulocytopenia, rheumatic heart disease&nbsp;
Type III hypersensitivity<div>Immunoglobin type: {{c1::IgG}}</div><div>Trigger: {{c1::Soluble antigen}}</div><div>response: {{c1::forms complexes generally cleared by phagocytosis in liver and spleen. May deposit in basement membrane&nbsp;}}</div>
Type III hypersensitivity may form complexes directly in tissues called {{c1::Arthus}} reaction which activates the complement sytem and creates C5a (attracts {{c1::neutrophils}}) May lead to farmers lung<div><br></div>
Time for hypersensitivity reaction<div>Type I: {{c1::Immediatly or minutes}} after exposure</div><div>Type II &amp; III<span>&nbsp;{{c1::3-6 hours}} after exposure</span></div><div>Type IV: {{c1::48}} hours after exposure</div>
Arthus reactions happen when theres an {{c1::antigens excess and deposit in the tissues:: Antigen excess, antigen antibody ratio is 1, antibody excess}}
Beta lactam antibiotics 4 main categories includes<div>-{{c1::Penicillins}}</div><div>-{{c1::Cephalosporins}}</div><div>-{{c1::Carbapenems}}</div><div>-{{c1::Monobactams}}</div><div><br></div>
Penicillins arent usualy effective against pseudomonas, except {{c1::Carbenicillin}}, {{c1::Piperacillin}} and&nbsp;{{c1::Ticarcillin}}<div>Extended or broad spectrum penicillins include {{c1::Ampicillin}} and {{c1::amoxicillin}}</div>Antipseudomonal mnemonic: somebody came into the car to kill pseudomonas with Pipe and tic
Penicillins work on bacteria by inhibiting the {{c1::cross linking}} of the peptidoglycan. it inhibits the enzyme {{c1::transpeptidase}}
Ampicillin is a first line drug for:<div><span>{{c1::Meningitis}}, {{c1::gonorrhea}}&nbsp;</span>{{c1::urethritis}}&nbsp;<span>and</span> {{c1::cholecystitis bc it gets concentrated in bile&nbsp;}}<div>Side effects include diarrhea, skin rashes, failure of contraceptives and food interferes absorption</div><div><br></div><div><br></div></div>Amoxicillin has better oral absorption, no interferance with food, less diarrhea.&nbsp;
Carbenicillin &amp; ticarcillin useful for:&nbsp;<div>Pseudomonas and {{c1::proteus}} (Burns, UTIs, spepticemia)</div><div><br></div><div>Pipercillin:&nbsp;</div><div>Pseudomonas and {{c1::klebsiella}} (Neutropenic and immunocompromised patients)</div>
Amoxicillin is combined with the beta lactamase inhibitor {{c1::clavulenic acid&nbsp;}}<div>Ampicillin is combined with the beta lactamase inhibitor {{c1::sulbactam}} and {{c1::tazobactam&nbsp;}}</div>Beta lactamase inhibitors alone dont do anything. they are added to bacteria which gained resistance to beta lactams&nbsp;
Penicillins work for:<div>Streptococcal {{c1::pharyngitis (Scarlet fever)}}&nbsp;</div><div>{{c1::Fusospirochetal infections}}&nbsp;</div><div>{{c1::<span>Rat bite fever</span><span>}}&nbsp;</span></div><div>{{c1::<span>Lyme disease&nbsp;&nbsp;</span><span>}}</span></div><div>{{c1::Vulvular heart disease&nbsp;}}</div>Pneumococcal (meningitis. pneumona)<div><br><div>Streptococcal pharyngitis, meningitis, arthritis, endocarditis, pneumonia</div></div>
Group 3 penicillins are anti {{c1::staph}}<div>Group 5 penicillins are anti {{c1::pseudomonas}}</div>
With increased cephalosporin generation, theres an {{c1::increased:: Increased or decreased?}} gram negative, and an {{c1::decreased}} gram positive activity
Cephalosporins not recommended in combination with {{c1::nephrotoxic drugs (Aminoglycosides)}}<div>Contraindicated to combine with {{c1::diuretics}}</div>
Carbepenems<div>Imapenem must be administered together with {{c1::cilastatin}}</div><div>Excreted by {{c1::kidneys}}.&nbsp;</div><div>Has a high incidence of seizures compared to meropenem</div><div>other carbepenems include meropenem and doripenem&nbsp;</div><div>have a very wide spectrum of activity.&nbsp;</div>used for nosocomial infections.&nbsp;
Monobactam aztreiban active only against {{c1::Gram negative aerobic}} bacteria.&nbsp;
Macrolides are {{c1::bacteriostatic:: Bacteriocidal or static}} and {{c1::broad}}&nbsp;spectrum antibiotics<div>They are used to treat atypicals like {{c1::chlamydia}} {{c1::Mycoplasma}} and {{c1::legionella}}</div><div>Best macrolide? {{c1::Clarithromycin}}.</div><div>Clarithromycin is eliminated via {{c1::kidneys}}. other macrolides via the {{c1::liver}}</div><div>Erythromycin and clarithromycin ONLY will inhibit cytochrome P450, {{c1::<u>azithromycin will not</u>}}</div><div><br></div>Erythromycin has most side effects, ranging from GI to cholestatic hepatitis and thrombophlebitis&nbsp;
the ketolide telithromycin is a reversible inhibitor of {{c1::CYP3A4}} and is not recommended due to {{c1::hepatotoxicity}}. Only indication is {{c1::community acquired pneumonia (CABP)}}
Linezolid has a bioavailability of {{c1::100%}}, and CSF penetration of 70%. Eliminated via {{c1::renal and nonreal pathways}}<div>Patients should avoid foods with large quantities of {{c1::tyramine}}, and drugs such as {{c1::serotonergics}} &amp; {{c1::adrenergics}}</div>
Streptogramins: a combination of two drugs, first is quinupristin and the second dalfopristing in a {{c1::30:70}} ratio&nbsp;<div>Used for vancomycin resistand {{c1::enterococci}} and methicillin resistant {{c1::S. aures}}</div><div>Dose adjustment needed with {{c1::hepatic}} impairment&nbsp;</div>
Chloramphenicol not often used because of massive {{c1::toxicity}}.&nbsp;<div>adverse effects are bone {{c1::marrow depression}} and {{c1::<u>gray baby syndrome</u>}}</div><div>Uses: {{c1::pyogenic meningitis}}</div><div>{{c1::Anaerobic infections (Bact. fragilis)}}</div><div>{{c1::Massive conjunctivitis&nbsp;}}</div>second choice in Brucellosis, UTI, rickettsial infections, conjunctivitis,<br>external ear infections<br>
aminoglycoside antibiotics are bactericidal by binding to the {{c1::30s}} ribosomal subunit and inhibiting {{c1::protein}} synthesis&nbsp;<div>Enter cells the cell via {{c1::passive diffusion}} and {{c1::proton pumps (oxygen dependent)}}. transport is blocked by reducing {{c1::pH and in anaerobic environment&nbsp;}}</div><div>Has a {{c1::low:: high or low}} margin of safety</div><div><br></div><div>Elimination via kidneys, and excretions is directly proportional to {{c1::creatinine}} clearance</div><div>does it cross the BBB? {{c1::No}}</div><div>aminoglycoside antibiotics share toxicities such as:&nbsp;</div><div>-{{c1::Ototoxicity}}, {{c1::nephrotoxicity}}, {{c1::neuromuscular blockage}} and skin reaction</div>
Tetracyclins have a {{c1::broad}} spectrum of activity<div>Long acting tetracyclins: {{c1::Doxycycline}} and {{c1::minocycline}}</div><div>need to avoid {{c1::dairy products}} when using them.&nbsp;</div><div>Adversereactions: Gi disturbance/ phototoxicity, super infection, liver damage, kidney damage,<u> fancony like syndromes</u>,&nbsp;&nbsp;</div><div>do NOT give to: {{c1::Children}}, {{c1::pregnant women&nbsp;}}</div>Gramp positive, neg, actinomycetes, atypicals&nbsp;
"You take a swab from a patient presenting with sinusitis. After gram stain and microscopic investigation you view grampositive diplococci surrounded by a capsule. this bacteria caused alpha hemolysis, and has C polysaccharide. after further testing you conclude that the strain is sensitive to optochin, and is bile soluble&nbsp;<div><img src=""paste-c40f91159b81267f681a9bb046b5cf40508863b9.jpg""><br></div><div><img src=""paste-067bb0a4bef229c450c5344f95af79eb7f1898d8.jpg""><br></div><div>What is the most likely bacteria? {{c1::Streptococcus pneumoniae (Pneumococcus)}}</div><div><br></div>"
Alpha hemolysis seen in pneumococcus is caused by {{c1::pneumolysin&nbsp;}}
Pneumococcus causes disease first by colonizing the oropharynx by the means of {{c1::surface protein adhesins}}
Pneumococcus can become invasive and cause:<div>-{{c1::Pneumonia}}&nbsp;</div><div>-{{c1::Bacteremia&nbsp;}}</div><div>-{{c1::Meningitis&nbsp;}}</div><div>MUST take a blood culture&nbsp;</div><b>In the case of meningitis and you see gram positive diplococci NOT INSIDE PMNS think pneumococcus&nbsp;</b>
Pneumococcus diagnosis in the case of pneumonia is is done by {{c1::sputum}} or {{c1::brachoalveolar lavage (BAL)}}<div><br></div><div>In the case of meningitis diagnosis is done by {{c1::CSF}}</div>
Therapy of pneumococcus is done by beta lactams Penicillins, cephalosporins, macrolides and newer quinolones<div>Prevention by {{c1::polysaccaride vaccine}} for adults, and {{c1::polysaccharide conjugated to protein}} for those below 2 years</div>
You are culturing bacteria from a patient with a UTI, and after gram staining and microscopic investigation you view gram positive diplococci. after further investigation you notice that the bacteria is optochin resistant, not bile soluble, and is VERY resistant. has a group D carbohydrate antigen<div>Most likely bacteria? {{c1::Enterococcus (Faecium// faecalis)}}</div>
Enterococci have a {{c1::low:: High or low?}} level of virulence, and usually colonize the {{c1::GIT}}. they are very resistant to antimicrobials, and are frequent nosocomial pathogens
Vancomycin resistant enterococci (VRE) can be acquired by modifying glycopeptides from D-Ala-D-ALA to<div>{{c1::&nbsp;D-ALA-D-LAC}} or {{c1::D-ALA-D-SER}}. this prevents vancomycin from binding to it</div>
99% of the human flora is {{c1::anaerobic:: Aerobic or anaerobic? }}
Anaerobic bacterial collection is done via&nbsp;{{c1::swab in anaerobic transport system}}<span>,&nbsp;</span>{{c1::pus collection,}}<span>&nbsp;or&nbsp;</span>{{c1::abscess aspiration}}Must keep the bacteria away from oxygen
Anaerobes arent usually collected from stool, except for {{c1::C. <i>difficile</i>}}clostridiun difficile is associated with diarrhea and hemorrhagic collitis&nbsp;
characteristics of anaerobic infections include:<div>- infection results when anaerobes are introduced to {{c1::damaged or devitalized tissue}}</div><div>- infections are {{c1::polymicrobial:: Mono or polymicrobial? }}</div><div>-bacteria usually derived from {{c1::patients normal flora&nbsp;}}</div><div>-{{c1::foul odor::odor?}}</div>
Antimicrobials active against anaerobes:&nbsp;<div>-{{c1::Metronidazole (Anti-protozoal drug)}}</div><div>-{{c1::Penicillins +Beta lactamase inhibitors}}</div><div>-{{c1::Carbepenems}}&nbsp;</div><div>-{{c1::Clindamycin&nbsp;}}</div><div>{{c1::Aminoglycosides}} DO NOT WORK against anaerobes</div>
After a perforated appendix followed by an appendectomy a patient developed high fever and peritonitis. after an abdominal fluid culture you view anaerobic gram negative bacterium which forms no spores, and has a very large capsule. what is the MOST LIKELY offending agent? {{c1::Bacteroides fragilis.&nbsp;}}Bacteroides fragilis is the most common pathogenic species in the GIT.&nbsp; it accounts for 0.5% of the normal flora (seems small, but remember that the amount of colonies in the gut is HUGE)<div>It infects areas below the diaphragm&nbsp;</div>
"you are viewing gram negative filamentous bacteria under the microscope. they have pointed ends and have a central swelling.&nbsp;<div><img src=""paste-a23db3f7e831668fe65091967d0d5004625020ea.jpg""><br></div><div>most likely bacteria: {{c1::Fusobacterium spp.}}</div>"This one causes pleuropneumonia and facial infections. rarely causes jugular vein thrombosis, which occur after prolonged pharyngitis.&nbsp;<div>fusobacteria are anaerobes but tolerate up to 6% oxygen</div>
{{c1::Propionibaterium acnes}} is a normally part of the skin flora, and can result in acne. they are gram positive rods&nbsp;
A patient presents with a granulomatous infection of the skin. the pathogen is gram positive, non-acid fast bacterium with branching rods. <b>after inspecting the pus you view sulfur granules</b>.&nbsp; most likely offending agent? {{c1::actinomycetes (israelii // propionica)}}this bacteria is usually found in soil, oral and GIT flora<div>treat with penicillin and surgical debridement and drainage</div>
Occult skull fracture will result in recurrent {{c1::meningitis}}
Lysozyme will break bonds within the peptidoglycan exposing the cell membrane to other antimicrobials.&nbsp;<div>it affects {{c1::both gram positive and negative:: Gram positive or neg?<span>}}&nbsp;</span></div>affects positive more bc of the greater accessibility of peptidoglycan&nbsp;
Innate immune system recognizes PAMPS by using {{c1::toll-like receptors}}
function of complements:<div>{{c1::C3b}} will lead to&nbsp;<span>opsonization&nbsp;</span><span>and lead to phagocytosis&nbsp;</span></div><div>{{c1::C3a and C5a&nbsp;}}&nbsp;<span>have a chemokine function&nbsp;</span><br></div><div>Can also lead to complement mediated cytolysis by the formation of&nbsp;<span>{{c1::&nbsp;membrane attack&nbsp;</span><span>complexes (MAC)&nbsp;}}</span></div>Complements are also useful for making people blush. Actually do it right now. compliment someone. <b>consider this a break you deserve it</b>.&nbsp;
Enterobacteria are gram negative and have the LPS serogroup {{c1::O}} antigen<div>Possible other antigens:&nbsp;</div><div>-{{c1::Capsular (K antigen)}}</div><div>-{{c1::Flagellum (H antigen)}}</div><div>-{{c1::Fimbria (pilus)}}</div>
UTIs are most commonly caused by {{c1::E.coli&nbsp;}}
E.coli can cause extraintestinal diseases such as&nbsp;<div>UTI due to the virulence factors: {{c1::adhesins/ apha-hemolysin/ capsule}}</div><div>Septicaemia due to virulence factors: {{c1::siderophores (Fe3+) &amp; alpha-hemolysin}}</div><div>Neonatal meningitis due to {{c1::<u>K1 capsular PS</u>}}</div>
Diarrhea causing E.coli acronym and meaning<div>EPEC --&gt; {{c1::Enteropathogenic Ecoli}}</div><div>ETEC<span>&nbsp;</span><span>--&gt;&nbsp;</span>{{c1::Enterotoxigenic Ecoli}}<span>&nbsp;</span></div><div>EIEC<span>&nbsp;</span><span>--&gt; </span>{{c1::Enteroinvasive Ecoli}}<span>&nbsp;</span></div><div>EHEC<span>&nbsp;</span><span>--&gt;&nbsp;</span>{{c1::Enterohemorrhagic Ecoli}}<span>&nbsp;</span></div><div>VTEC<span>&nbsp;</span><span>--&gt;&nbsp;</span>{{c1::Verotoxin producing Ecoli}}<span>&nbsp;</span></div><div>STEC<span>&nbsp;</span><span>--&gt;&nbsp;</span>{{c1::Shiga toxin producing Ecoli}}<span>&nbsp;</span></div><div>EAEC<span>&nbsp;</span><span>--&gt;&nbsp;</span>{{c1::enteroaggregative Ecoli}}<span>&nbsp;</span></div>
"You are examining an intestinal biopsy of a two-year-old with diarrhea and inflammation. the bacterium seems to have bundle forming pilli. Gene sequencing shows that the pathogen has the gene intimin, and is closely adhering to the gut epithelium.<div><img src=""paste-0116292de3185c9aef2112b22ff07b31775b2145.jpg""><br></div><div>Diagnosis? {{c1::Enteropathogen E. <i>coli </i>(EPEC)}}</div>"Only infects of those below 3 years.&nbsp;<div>causes decreased surface absorption</div>
"You are examining a case of diarrhea without inflammation of a man who recently came back from traveling abroad. After carefully examining the strain you find colonization factor antigens (mostly fimbriae) and that the bacterium produces heat stable and heat labile enterotoxins&nbsp;<div><img src=""paste-35544be1f83e46bb2df290504496362cb41bd842.jpg""><br></div><div>Diagnosis? {{c1::Travellers diarrhea by enterotoxinogenic E. <i>coli&nbsp; (</i>ETEC<i>)</i>}}</div>"enterotoxinogenic Ecoli from animals dont infect humans because their adhesion factors target different receptors than us humans.&nbsp;<div>LT/ ST increases salt and water production, thus causing diarrhea&nbsp;</div>
A patient presents with diarrhea with present fresh blood. further tests shows a bacterial strain coding for shiga toxin, and intimin. the patients state deteriorated and he developed HUS. You later on found out that the cause was a contaminated beef burger.&nbsp;<div>Possible diagnosis:&nbsp;</div><div>{{c1::<div>Enterohemorrhagic E.coli</div><div>Shiga toxin E.coli</div><div>Vero Toxin E. coli</div>}}<br></div>Do not give antibiotics. Will induce more toxin release.&nbsp;<div>Most common serogroup in the US is O157:H7</div>
"You are seeing a patient with chronic diarrhea. After further investigation you see bacteria with a variety of adhesins and biofilm&nbsp;<div><img src=""paste-15dcd2bada702a373e022bd7d6ba89ecf773d5b6.jpg""><br></div><div>Diagnosis? {{c1::Enteroaggregative E.coli}}</div>"
A patient comes with a bloody diarrhea. after further investigation you notice that the insulting bacteria invade the basal lamina by being taken up by M cells and ulcered the mucosa. Later you find out that the bacteria has enzymes polymerizing the actin pool propelling it forward<div>diagnosis? {{c1::Enteroinvasive E. coli (shigella)}}</div>
"An immunocompromised patient on assisted ventilation developed right lung pneumonia<div><img src=""paste-4c3ca325caed36023636ca788d4582648b418962.jpg""><br></div><div>You culture the sputum and find highly mucoid bacteria which are highly resistant&nbsp;</div><div><img src=""paste-f5608edcffbf7a99d6cc1aecff31f15bd4e20a3b.jpg""><br></div><div>Most likely diagnosis? {{c1::Klebsiella&nbsp;}}</div>"
"A patient presenting with a UTI with increased urine pH due to urease. Patient also preseted with struvite (kidney) stones. you cultured the infecting agent and it appears to be moving in waves&nbsp;<div><img src=""paste-61c50c93521cb6d6cb7707e8f18fdc80f14ed8c8.jpg""><br></div><div>Diagnosis? {{c1::Proteus}}</div>"Urease is used for identification.&nbsp;<div>Contains Antibiotic R</div>
"After prolonged hospital stay a patient developed a nosocomial infection (UTI, wound or airway infection in this case).&nbsp;<div>after cell culture you find out that this bacteria produces a red pigment, and contains ESBL and carbapenemases.&nbsp;</div><div><img src=""paste-fba657d78d0e88475e1582ede716fcb4dc1c7db5.jpg""><br></div><div>Possible diagnosis? {{c1::Enterobacter serratia}}</div>"It's a nosocomial opportunistic bacteria.&nbsp;
there are two salmonella species. the one relevant to us is {{c1::S. <i>enterica</i>}}
"A patient comes to you complaining of intestinal cramps, moderate fever, vomiting and diarrhea. a culture was taken and you find this&nbsp;<div><img src=""paste-0040562e600225366cc2e7d887e1414534bd316f.jpg""><br></div><div>The patient then tells you he ate not well prepared chicken before symptoms.</div><div>offending agent? {{c1::Salmonella}}</div>"Presence of WBCs not characteristic
Salmonella can be put into three categories. Give examples<div>Non-host adapted: {{c1::S. Enteritidis &amp; S. Typhimurium}}</div><div>Animal adapted: {{c1::S. Cholaraesuis}}</div><div>Adapted to human: {{c1::S. Typhi &amp; S. Paratyphi (A/B/C)}}</div>Adapted to human salmonella cannot infect animals. causes enteric fever and typhoid <i>(dont confuse with typhus by rickettsiae)</i>
Try to guess which is typhoid salmonella and which non-typhoid salmonella.&nbsp;<div>Case1</div><div>Patient comes with watery stool, few PMNs. this one is typically seen causing gastroenteritis, but rarely develops into a systemic infection. you dont usually give antibiotic UNLESS its systemic.&nbsp;</div><div>which type is it? {{c1::Non-Typhoid salmonella}}</div><div><br></div><div>Case 2&nbsp;</div><div>Inflammation is dominated by lymphocytes in stool, as well as in blood. diarrhea may not be present. easily becomes systemic and causes septicemia, <u>infects kupfer cells</u> and causes perforation. Antibiotics is a must.&nbsp;</div><div>Which type? {{c1::Typhoid salmonella&nbsp;}}</div>
Yersenia pseudotuberculosis causes mesenteric {{c1::lymphadenitis.}}<div>Yersenia enterocolitica causes {{c1::enterocilitis.&nbsp;}}</div><div>systemic infections and enteric fever may also occur</div><div>Yersenia pestis causes {{c1::plague}}</div>Y.pestis contains many virulent factors. Capsule, coagulase, fibrinolysin.&nbsp;<div>resevoir is wild rodents or rats, and the vector is the rat flea</div>
"A patient suffering third degree burns comes to your unit and is treated accordingly. after a few days you notice <u>greenish discharge</u> coming from the burn wounds with very distinctive <u>fruity odor</u>. the bacteria is aerobic, gram negative and has polar flagella.&nbsp;<div><img src=""paste-f04f2851fffffb62fe0f73a6d37b306cb72e4aaf.jpg""><br></div><div><img src=""paste-fa65965a427932a1d700237a4d5dbf17cdb565b3.jpg""><br></div><div>Diagnosis? {{c1::Pseudomonas}}</div>"
"Which pseudomonas species is seen in the agar plate below?<div><img src=""paste-609148b833b6ae2cbe36711c2180eaa0c6c2ca2a.jpg""><br></div><div>{{c1::P. <i>aeruginosa</i>}}</div>"Distinct by this shade of green. Produces the pigments pyocianin and pyoverdin&nbsp;
Toxins produced by pseudomonas:&nbsp;<div>-{{c1::Cytotoxin (Leukocidin)&nbsp;}}</div><div>-{{c1::Phospholipase C (Hemolysin)}}</div><div>-{{c1::Pyocianin (pigment too)}}</div><div>-{{c1::<u><b>Exotoxin A</b></u> (protein synthesis inhibitor)}}</div><div>Do an antibiotic susceptibility test and treat with aminoglycoside + AntiPS beta lactam (ceftazidime or imipenem)</div>Also produces biofilm which makes it hard for antimicrobials to reach it
Bulkholderia cepacia is a gram negative aerobe frequently causing rot in onions. has the frequency of causing pneumonia and septicemia in children with {{c1::cystic fibrosis&nbsp;}}
Stenotrophomonas maltophilia is an opportunistic gram negative aerobe which is inherently resistant to {{c1::carbepenems&nbsp;}}<div>Treat with {{c1::trimethoprim-sulphametoxazole&nbsp;}}</div>
Legionella are gram negative aerobes which stain weakly. they are naturally found in {{c1::amoebas}}.&nbsp;<div>When they infect humans they infect alveolar macrophages via {{c1::coiling phagocytosis&nbsp;}}</div><div>Can manifest clinically as either {{c1::pontiac fever}} or {{c1::legionnaires' disease&nbsp;}}</div><div><br></div><div>Diagnosis by gram stain (weak staining) and nucleic acid amplification rest (PCR of BAL). antigen detection of L. pneumophilia serotype 1 seen in {{c1::urine}}</div>Infection associated frequently with air conditioning systems&nbsp;<div>S.pneumophilia serotype 1&amp;6 cause 90% of human infections</div>
"Non-fermenting gram negative rods include:&nbsp;<div>-{{c1::Pseudomonas}}</div><div>-{{c1::Bulkholderia cepacia&nbsp;}}</div><div>-{{c1::Stenotrophomonas maltophilia}}<b><div style=""display: inline !important;"">&nbsp;</div></b></div>-{{c1::Acinetobacter}}<div>-{{c1::Legionella <u>(SPREADS VIA AC)</u>}}</div>"
Spore forming anaerobes include:<div>-{{c1::C. <i>difficile&nbsp;</i>}}</div><div>-{{c1::C. <i>botulinum&nbsp;</i>}}</div><div>-{{c1::C. <i>tetani&nbsp;</i>}}</div><div>-{{c1::C. <i>perfringens&nbsp;</i>}}</div>
Before surgery a patient was given too many antibiotics to prevent infection. A few days later the patient develops a bloody diarrhea. After further testing you confirm the presence of glutamate dehydrogenase and toxin A/B<div><div>offending agent? {{c1::C. <i>difficile</i>}}<i>&nbsp;</i></div></div>"<div><img src=""paste-5445490dc861fea0fb671b593911c43edce8ce2b.jpg""><br></div>This bacteria has varying severity from antibiotic associated diarrhea to pseudomembranous colitis<div>&nbsp;</div>"
Treatment for C. <i>difficile</i>?<div>-{{c1::the infection started bc of the broad spectrum antibiotic treatment. stop that and let the gut flora push it back.}}</div><div>-{{c1::Metronidazol&nbsp;}}</div><div>-{{c1::Oral vancomycin}}&nbsp;</div><div>-Fidaxomicin</div><div>-{{c1::Fecal transplant}}</div>
"After ingesting tinned food, a patient develops nausea and stomach ache. later symptoms appear to be bilateral ptosis, a change in the voice, mouth dryness, constipation, positive romberg test.&nbsp;<div>Cell culture of the tinned food seen below</div><div><img src=""paste-7d840d8ec1f5576e160c24bb3d60e1c3cebd30b9.jpg""><br></div><div>Offending agent?&nbsp;</div><div>{{c1::C. <i>botulinum&nbsp;</i>}}</div>"it's gram positive and releases botulinus toxins (Botox) which blocks ACH from exiting nerves --&gt; Flaccid paralysis&nbsp;
C. botulinum can infect infants which are fed {{c1::honey}}. Will colonize the gut (not seen in adults)<div>Therapy is {{c1::trivalent Antitoxin A/B/C}}</div><div><br></div>
"A 5 year old was playing in the playground but slipped and scraped his chin. Thinking nothing of it he got up and continued playing. A few days later he developed muscle spasms and appeared with an arched back and a fixed trismus ""smile""&nbsp;<div><img src=""paste-9a0ab0b6da2d5d0e9bb09f75d3dbfa80f3e76c27.jpg""><br></div><div><img src=""paste-2ceea251e360eea04b19e9ad0316379e9b9231de.jpg""><br></div><div>Offending agent?</div><div>{{c1::C. tetani --&gt; tetanus}}</div><div><i>Dont judge these pictures representing a 5-year-old&nbsp;</i><br></div>"<div><br></div>Toxin of C. tetani will travel in retrograde and inhibits the release of GABA causing spastic paralysis.&nbsp;<div>Neonatal tetanus from umbilical infections due to unvaccinated mother.&nbsp;</div><div><br></div><div><br></div>
"A patient came presenting with myonecrosis (gas gangrene) has an open wound wich came in contact with soil. after culture and gram stain you see gram positive anaerobes with double hemolysis and few PMNs. after further investigation you notice that the strain produces lecithinase<div><img src=""paste-a5bc51e50f3c2dddc1d399d61dbf45d80e985431.jpg""><br></div><div><img src=""paste-d835f8eae4ba5380a5ff25f249bee396609c6358.jpg""><br></div><div>Offending agent?&nbsp;{{c1::C. <u>perfringens</u>}}</div><div>Treatment? {{c1::Proper wound care (hydrogen peroxide}}</div>"Type A strain in soil and GI, whereas type B-E strain only found in GI.&nbsp;<div>alpha toxin (phospholipase or lecithinase) increases vascular permeability, hemolysis and tissue destruction</div><div>Beta toxin causes necrosis in necrotising enteritis</div><div>Epsilon toxin causes vascular permeability in GIT</div><div>Iota toxin causes necrosis and increased vascular permeability.&nbsp;</div>
C. perfringens<u><b> type A strain causes food poisoning</b></u> (painful watery diarrhea without fever) enterotoxins by type A strains are activated by {{c1::trypsin&nbsp;}}<div><br><div>Beta toxin is produced by type&nbsp;C&nbsp;strains. people unaccustomed to high&nbsp;{{c1::protein}}&nbsp;diet dont have enough trypsin to destroy the toxin <u>will cause enteritis necrotisans</u></div></div>
Mycobacterium tuberculosis contains a unique fatty acid in it's wall called {{c1::mycolic acid&nbsp;}}"<img src=""paste-a0809888e98ffd3fdefedbc839018179bd34d061.jpg"">"
Which stain is used to stain mycobacteria? {{c1::Ziehl-Neelsen staining}}&nbsp;This is used for all acid fast bacteria&nbsp;
<div>M. tuberculosis&nbsp;</div><div>{{c1::are obligate aerobes.:: Aerobes or anaerobes}}&nbsp;</div>{{c1::intracellurly in phagosomes of non-activated macrophages:: Where do they reside in the body?}}<div>{{c1::grow temperature range 35 - 37^oC ::Temperature of growth?}}<br></div><div>{{c1::Take 8-10 weeks to grow in cultures:: How long does it take to culture them? }}</div>
Sulfatides, polyanionic trehalose glycolipids of M. tuberculosis will {{c1::prevent fusion of phagosomes with lysosomes thus promoting bacterial growth:: Action? }}
Pathology of M. tuberculosis is due to {{c1::host response, not microbial toxic factors&nbsp;}}
Reservoir for&nbsp;<span>M. tuberculosis is {{c1::human}} and transmission is&nbsp;</span>{{c1::airborne (droplet nuclei)}}<div><span><br></span><div><span>Reservoir for&nbsp;</span>M. bovis is {{c1::cattle}} and transmission is via {{c1::contaminated milk}}</div></div>
M. tuberculosis uses {{c1::mannose capped glycolipids:: Antigen?}}, which are recognized and phagocytosed by macrophages via mannose receptors
Which lymphocyte subtype is activated in the case of a M. tuberculosis infection? {{c1::Th1 CD4 cells.}}&nbsp;IL-12 produced by APCs promote differentiation of Th1 cells&nbsp;<div>IFN-g produced by by Th1 will initiate intracellular killing of MTB</div>
If a competent immune system is unable to contain an MTB infection it will try to contain it by forming a {{c1::granuloma}}.<div>Containment fails in the case of {{c1::old age, malnutrition, AIDS or progressed HIV}}</div>When containment fails the granuloma opens up and spills MTB out into the airways. This facilitates aerosol spread.&nbsp;
Primary MTB infection is you get the infection for the first time, and get a caseation in the infected lobe and lymph node.&nbsp;<div>what happens in the case of:&nbsp;</div><div>the organism being not viable? {{c1::You get rid of the infection and develop a scar}}</div><div><br></div><div>The organism becomes suppressed and dormant? {{c1::formation of granuloma and a latent lesion}}</div><div><br></div><div>Immune system cannot control the lesion? {{c1::Progressive primary TB, meningitis and miliary TB in organs&nbsp;}}</div><div><br></div>"<div>Ghon complex is you have caseation and involvement of hilar lymph nodes with the MTB.&nbsp;</div><div>Infection of primary MTB usually occurs in the lower upper lobe or the upper lower lobe&nbsp;</div><div><img src=""paste-d7508c44ebbecd6941672c2be19d49a7193a4b9b.jpg""><div><br></div></div>"
Secondary TB arises usually from {{c1::dormant primary lesions or re-infections}}&nbsp;<div>It usually affects the {{c1::apex of the upper:: Which lobe}} lobe</div><div>This is usually seen in {{c1::immunosuppressed patients&nbsp;}}</div>"<img src=""paste-6ad7d3d8f9a6b6829cc70f67851d4e2bfc3e0c50.jpg"">"
Cutaneous TB infects skin or mucous membranse. the initial lesion is called {{c1::tuberculous chancre}} which appear as a firm shallow ulcers with granular bases. it usually appears in about {{c1::2-4}} weeks after initial infection
"Causes of cutaneous tuberculosis:&nbsp;<div>{{c1::<div>Lupus vulgaris - most common and seen on face and neck. Firm, translucent brown nodules. spreads laterally&nbsp;</div><div><img src=""paste-f5f5e44b4d53a0a3fcb602024b852b8a17d4eedb.jpg""></div>}}<br></div><div><br></div><div>{{c1::<div>Scrofuloderma. Spreads from underlying caseous lymph nodes or joints. (deeper). overlying lymph nodes.&nbsp;&nbsp;</div><div><img src=""paste-c0e9b5df3b6acdae42086948bf3a1528b36c93fe.jpg""></div>}}<br></div><div><br></div><div>{{c1::<div>Warty tuberculosis- Common in developing countries. causes warty plaques on hands, knees or buttocks&nbsp;</div><div><img src=""paste-79a5210653f0b3c2d13e540c2b8ea641994d75e6.jpg""></div>}}<br></div><div><br></div>"
<div>Atypical mycobacteria&nbsp;</div><div><br></div><div>M. marinum - AKA {{c1::fish tank granuloma}}&nbsp;</div><div><br></div><div>Those infected with M. avium or M. intracellulare should be tested for {{c1::immunocompetence or AIDS}}</div><div><br></div><div><br></div>M. marinum if infected while cleaning a fish tank.&nbsp;<div><br></div>
"A patient describes that his painless erythmatous nodule became necrotic and ulcerated. His history says that he works in areas with vegetation and water, and he suspects the trauma he's gotten is the main cause.<br><div><img src=""paste-ed20d19455f3227746b2c3ca553445a36aea27f1.jpg"">&nbsp;</div><div>You are suspecting a mycobacterial etiology, but which is it? {{c1::M. ulcerans&nbsp;}}</div>"
If the sputum of a TB patient is positive, what does it indicate? {{c1::the patient is definitely infectous.&nbsp;}}<div><br></div>
{{c1::Flourescence auramine staining}} is more sensitive for diagnosing TB than looking for Ziehl neelsen positivity in sputumIt takes 10⁴ AFB/ml for ZN positivity -&gt; not sensitive
Diagnosis of mycobacterium.&nbsp;<div>For culture --&gt; non sterile cultures need {{c1::decontamination}}&nbsp;</div><div>Sterile cultures put directly in {{c1::Löwenstein-Jensen medium (LJ)}}<span>&nbsp;</span></div><div>For sputum --&gt; homogenized with mucolytic agents&nbsp;</div><div><br></div><div>The advantage of PCR over culture is that it is {{c1::faster}}. look for rif gene for rifampin resistance</div>decontamination of specimen done by adding NaOH followed by neutralization and centrifusion.&nbsp;
Tuberculin test is positive in the case of {{c1::previous infection}}, or {{c1::vaccination (BCG)}}Testing develops delayed type hypersensitivity
IFN-g release assay measuring mycobacterial infection is not positive in the case of {{c1::BCG vaccination}}
First line TB drugs:&nbsp;<div>Isoniazid&nbsp;</div><div>Rifampicin</div><div><span>Ethambutol</span></div><div>Pyrazinamid&nbsp;</div><div><br></div><div>Regimen for 6 months:&nbsp;</div><div>{{c1::INH + RMP + EMP + PZA}} for 2 months&nbsp;</div><div>{{c1::INH + RMP}} for additional 4 months&nbsp;</div><div><br></div><div>Multidrug resistance if it's resistant to {{c1::INH and RMP}}</div><div>Extetensive resistance if resistant to {{c1::flouroquinolones and injectible drugs}}</div>
M. avium and slow growing atypical mycobactes are resistant to anti-mycobacterial drugs. {{c1::macrolides}} are needed<div><br></div>
Does a BCG vaccination make you completely immune to TB? {{c1::It doesnt make you completely immune, but it reduces the risk of infection}}
Once a Ghon complex of TB undergoes fibrosis and calcification, radiologists call it {{c1::ranke complex}}
"A patient with suspected TB has his sputum taken which was stained by ZN stain. after a look under the microscope you see this&nbsp;<div><img src=""paste-d4532fca0c5ef2a8c33c973cc23918c1c2661370.jpg""><br></div><div>Which mycobacterium do you suspect and which further tests should you do? {{c1::Mycobacterium avium-intracellulare complex (MAC). Check for AIDS}}</div>""<b style="""">Normally you only see a few mycobacteriae, but in this case its too many indicating immunosuppression</b>"
Leprosy is caused by {{c1::mycobacterium leprae}}. The pathogen gets engulfed by alveolar macrophages, and disseminates to replicate in {{c1::cool:: Warm or cool?}} tissuesTissues such as earlobes and feet<div><br></div>
Tuberculoid leprosy seen in {{c1::immunocompetent:: Immunocompetent or immunocomprimised?}} patients. Asymmetric peripheral nerve involvement<div><br><div>lepromatous leprosy seen in {{c1::immunocompromised}} patients. Symmetric skin nodules&nbsp;</div></div>
"An immunocompromised patient with TB comes in for surgery. you open up the patient and see dotted organs.&nbsp;<div><br><div><img src=""paste-b1091b3a16d91bf22e24d5aa15010da3c30d175b.jpg""><br></div><div>What do you see?&nbsp;</div></div><div>{{c1::Miliary TB}}</div>"
<div>Vibrio cholera spreads by {{c1::ingesting contaminated food or water}}<br></div><div><br></div>Outbreaks are caused by serogroups {{c1::O1}} and {{c1::O139}}.&nbsp;<div><br><div>The {{c1::El Tor}} biotype of the disease survives better in the environment and causes asymptomatic carriers compared to the classical biotype.</div></div><div><br></div>
Main virulence factors of Vibrio cholera includes:<span>&nbsp;</span><div><div>-{{c1::Cholera toxin (phage coded)&nbsp;}}</div><div>-{{c1::Toxin-coregulated pilus}}</div></div>Cholera toxin works by keeping adenyl cyclase switched on, caused increased cAMP and increased secretions of Na, K, Cl, HCO3 and water into the gut lumen. Causes dehydration, hypokalemia and metabolic acidosis&nbsp;
"<div>All the cases below revolve around vibrio.</div><div>Case1:</div>A Japanese patient comes with a watery diarrhea after consumption of raw seafood. which pathogen do you suspect? {{c1::Vibrio <i>parahaemolyticus</i>}}<div><br></div><div>Case2:</div><div>A patient develops bacteremia with cellulitis after contact with seafood</div><div><img src=""paste-30afec9bc52cbf89c44cd88b43d101a265468d1e.jpg""><br></div><div>This pathogen is highly fatal in people with iron storage disease and alcoholics (liver problems)&nbsp;</div><div>what do you suspect? {{c1::Vibrio <i>vulnificus&nbsp;</i>}}</div><div><br></div><div>Case3</div><div>A patient came with severe dehydration, metabolic acidosis, hypokalemia and diarrhea. the characteristic of the stool can be best described as ""rice water stool"".</div><div><img src=""paste-bc9aa05a6fed84d999e4f6847813b1c74a6b71c4.jpg""></div><div>&nbsp;You later found out the patient recently came back from his vacation from bengal. What do you suspect? {{c1::Vibrio <i>cholera</i>}}</div>"
Culture of Vibrio cholera is done on {{c1::alkaline:: Acid or alkaline}} enriched media<div>Use {{c1::TCBS}} selective differentiating agar plates</div><div>Therapy is mainly done by {{c1::<u>oral rehydration fluid (ORF)</u>}}</div><div><br></div>TCBS: Thiosulfate citrate bile salts sucrose<div>Cholera isnt routinely cultured here, so you need to ask for it&nbsp;</div>
Vibrio, campylobacter and helicobacter are all gram {{c1::negative}} curved rods<div><br><div><br></div></div>
Campylobacter reservoir is animals, especially {{c1::poultry}}risk is eating raw chicken&nbsp;
Campylobacter enteric infections most commonly caused by {{c1::C. <i>jejuni&nbsp;</i>}}<div><br></div><div>Campylobacter systemic infections most commonly caused by {{c1::C. <i>fetus&nbsp;</i>}}</div>
Post infectious sequelae of campylobacter jejuni includes:&nbsp;<div>-{{c1::Reactive arthritis}}</div><div>-{{c1::Guillain-Barré syndrome}}</div>Guillain-Barré syndrome includes ascending flaccid paralysis due to molecular mimicry C. jejuni LPS and peripheral nerve gangliosides
"A patient comes to you with a severe case of bloody diarrhea. After further investigation you are seeing gram negative S shaped rods within the stool.&nbsp;<div><img src=""paste-c54446ccef76b5c507fa08055db77c64804d8c64.jpg""><br></div><div>this cuture grows under microaerophilic conditions and loves hot temperatures (42^oC)</div><div><br></div><div>What is it, and what do you treat it with (remember, this is severe)</div><div>{{c1::Most likely campylobacter jejuni. Treat with macrolides}}</div>"
An older patient comes to you complaining of a stomach ache. after further investigation you find a gram negative curved rod colonizing the gastric mucosa. <b>you find out that this pathogen is urease positive</b>, and produces toxins such as cagA and VacA. Which pathogen do you suspect? {{c1::Helicobacter pylori&nbsp;}}"<img src=""paste-5cb01be699e8c280546b719a95e3e33e8af3f705.jpg""><div>This one is transmitted oral-fecally.&nbsp;</div><div>acute infections cause gastritis, but might develop into peptic ulcers, atrophic gastritis, gastric adenocarcinomas or MALTomas&nbsp;</div>"
Flouroquinolones is derived from adding flourine to {{c1::nalidixic acid (Quinolone) }}<div>Old FQs were good for gram {{c1::-ve}} organisms including {{c1::pseudomonas}}.&nbsp;</div><div>New FQs for both gram negative and positive, MRSA, and intracellular bacteria&nbsp;</div>FQs end with the suffix -floxacin
What is the MOA of glucocorticoids ?&nbsp;indirectly inhibit phospholipase A2 by inducing synthesis of <b>lipocortin 1</b>Pharmacology
Aspirin belongs to which class of NSAIDs ?&nbsp;SalicylatesPharmacology
What is the MOA of NSAIDs ?inhibit <b>cyclo-oxygenase </b>pathway of arachidonic acid which leads to decreased synthesis of prostanoids (prostaglandins, thromboxane, prostacyclins)Pharmacology
Relief from pain following NSAID use is due to decreased&nbsp;{{c1::prostaglandin}} mediated <b>vasodilation</b>also note that decreased prostaglanding generation means less synthesis of inflammatory mediators such as <b>bradykinin</b>&nbsp;and <b>5-hydroxytryptamine</b>Pharmacology
COX1 predominant in&nbsp;{{c1::gastric mucosa}}
Aspirin <u>acetylates</u>&nbsp;COX (at ser530) and is therefore&nbsp;{{c1::irreversible}}note that other NSAIDS block COX channels by forming <u>hydrogen bonds</u>&nbsp;with arginine halfway through
Most NSAIDs are eliminated by the&nbsp;{{c1::kidney}}
Paracetamol is preferred as an antipyretic because it {{c1::lacks GI effects}}<br>Note that:&nbsp; Aspirin is not indicated for fever because of its association with <b>Reye's Syndrome</b>
Acetaminophen (paracetamol), unlike NSAIDs, has&nbsp;{{c1::weak::weak/strong}} anti-inflammatory effects
COX2 Inhibitors have been associated with increased risk of&nbsp;{{c1::MI}} and&nbsp;{{c1::Stroke}} because they do not inhibit platelet aggregationRemember that: COX2 inhibitors are contraindicated in cardiovascular disease
Ketorolac use is limited because of its&nbsp;{{c1::GI}} and&nbsp;{{c1::renal}} side effects
Flouroquinolones characteristics:<div>-Concentration dependence inhibition like {{c1::aminoglycosides:: Which type of antibiotics?}}&nbsp;</div><div>- Bioavailability 80-95% almost like {{c1::linezolid (100%)}}</div><div>-oral absorption impaired by divalent cations (antacids) like {{c1::tetracyclines&nbsp;}}</div><div>-Elimination is via {{c1::kidneys}}</div><div>-Have limited CSF penetration, better use {{c1::cephalosporines&nbsp;}}</div>
FQs mechanism of action:&nbsp;<div>-{{c1::Inhibits DNA gyrase (topoisomeraseII)}}&nbsp;</div><div>-{{c1::Inhibits topoisomerase IV}}</div>
In diarrheal diseases give the FQs {{c1::ciprofloxacin}} or {{c1::norfloxacin}}.&nbsp;<div>If you dont know the cause give ciprofloxacin and metrozinadole&nbsp;</div>
{{c1::Diclofenac}} and&nbsp;{{c1::Sulindac}} are associated more with liver function abnormalities (NSAIDs)<br>
You have an athlete with an infection. Which antimicrobial category do you NOT prescribe? {{c1::Fluoroquinolones}}.&nbsp;Causes tendon rupture. dont give to children under 18y either. affects MMP.&nbsp;
Quinolones side effect:&nbsp;<div>-{{c1::GABA inhibition}}&nbsp;</div><div>-{{c1::Cation complexation}}</div><div>-{{c1::CYP450 inhibition}}&nbsp;</div><div>-{{c1::Phototoxicity}}&nbsp;</div><div><u>-Torsades de pointe: paroxysm of ventricular tachycardia</u></div><div><br></div><div>Drug interactions with antidepressants, caffiene, warfarin and NSAIDs</div>
NSAIDs can counteract effect of many {{c1::antihypertensives}} such as diuretics, ACE inhibitors and AR antagonists
Intrinsic FQ resistance seen in {{c1::streptococci due to homolouge PmrA protein&nbsp;}}
Common <u>Adverse</u>&nbsp;Gastrointestinal effects of NSAIDs include {{c1::esophagitis}},&nbsp;{{c1::erosions}},&nbsp;{{c1::peptic ulceration}}, gastric irritation and&nbsp;{{c1::bleeding}}
Common <u>Renal</u>&nbsp;adverse effects associated with NSAIDs include&nbsp;{{c1::sodium and water}} retention, chronic renal&nbsp;{{c1::failure}} , and nephritis
NSAID <u>Hematological</u> adverse effects include&nbsp;{{c1::<b>thrombocytopenia</b>}} and&nbsp;{{c1::hemolytic anemia}}
{{c1::Elicitation::Sensitization/Elicitation}} stage of the Delayed Type Hypersensitivity response is directed by mediators released from&nbsp;{{c2::TH1}}<br>
Foreign body granulomas distinguished based on {{c1::absence of lymphocytes}} in the lesion
{{c1::IFNγ}} and {{c1::TNF}} are required for granuloma formation<br>
Susceptibility to Systemic Lupus Erythematosus is associated with HLA-{{c1::DR2/3}}
Altered Stability of the HLA-DQ molecule is caused by a substitution of&nbsp;{{c1::aspartic acid}} to an uncharged residue (alanine, valine, serine). <i>This change increases suseptibility to diabetes</i>
Co-trimoxazole is a folate synthesis inhibitor consisting of two combined sulfonamides {{c1::trimethoprim}} + {{c1::sulfamethoxazole&nbsp;}}<div>both have a {{c1::synergistic:: synergistic or additive}} effect and are bacteriocidal.&nbsp;</div><div>{{c1::Trimethoprim}} crosses the BBB&amp; placenta but {{c1::sulfamethoxazole}} doesnt&nbsp;</div>"<img src=""paste-6a1e311b8c58d7a5450e354be74ae97e4ca45e59.jpg"">"
Grave's diseases is caused by&nbsp;{{c1::autoantibodies specific for TSH receptor}} which&nbsp;{{c1::stimulate::inhibit/stimulate}} production of thyroid hormone
Myasthenia Gravis is caused by&nbsp;{{c1::autoantibodies that bind alpha subunit of Acetylcholine receptor}} which results in receptor internalization and degradation
GoodPasture's Syndrome is caused by&nbsp;{{c1::autoantibodies reacting with GBM}}
Polymorphisms in PTPN-22 gene associated with&nbsp;{{c1::Rhuematoid Arthritis}} and&nbsp;{{c1::DM1}}. This disease variant leads to excess lymphocyte activation.
Polymorphism in NOD-2 associated with&nbsp;{{c1::Crohn's}}.&nbsp;Explanation: NOD2 is a cytoplasmic sensor of microbes expressed in epithelial cells. Mutation causes <b>ineffective sensing of intestinal microbes</b> which leads to an inflammatory response against commensal flora.
Infections can contribute to autoimmunity through (1) upregulation of&nbsp;{{c1::costimulators}} on APCs (2)&nbsp;{{c1::molecular mimicry}} (ex. rheumatic heart disease) (3)&nbsp;{{c1::polyclonal activation of b cells}} in <u>viral</u> infections (4) tissue damage which leads to <b>release of self antigens</b>
Most common causes of death in SLE patients are&nbsp;{{c1::renal failure}} and&nbsp;{{c1::Infections}}
Most of the visceral lesions in SLE are caused by&nbsp;{{c1::immune complexes}}Note: SLE is a type III hypersensitivity
Sulfonamides arent usually prescribed alone.&nbsp;<div>Indications for only sulfonamide use:&nbsp;</div><div>{{c1::Sulfasalazine}} for IBD and regional enteritis.&nbsp;</div><div>{{c1::sulfacetamide}} in opthalmic preperation</div><div>{{c1::silver sufadiazine}} topically to reduce infections for burns, not deep infections</div><div>{{c1::mafenide}}: for burns&nbsp;</div>
The treatment of choice for pneumocystis pneumonia (PCP) is {{c1::TMP-SMX oral (co- trimoxazole)}}co-trimoxazole is trimethoprim + sulfamethoxazole
{{c1::<u>Hydralazine</u>}}, {{c1::Procainamide}}, and {{c1::D-penicillamine}} are drugs that induce an SLE like response<br>
Antibodies to&nbsp;{{c1::dsDNA}} and&nbsp;{{c1::Smith Ag}} are diagnostic of Systemic Lupus Erythematosus
{{c1::Antiphospholipid}} Antibodies are present in 50% of the patients with systemic lupus erythematosis<br>
All sulfonamide except {{c1::sulfasalazine}} is rapidly absorbed from the GIT<div>All are distributed uniformly except {{c1::sulfadiazine}}</div><div><br></div><div>Sulfanomides contraindicated in:</div><div>-{{c1::Hypersensitivity}}</div><div>-{{c1::Impaired renal/hepatic functions}}</div><div>-{{c1::Pregnancy &amp; lactation}}</div><div><br></div><div>Drug interactions with:</div><div>Oral anticoagulants, sulfonylurea and anticonvulsants. <u>they potentiate their effect, need dose adjustment</u></div>
Adverse drug reactions to sulfonamides:<br><div><span>{{c1::</span>Crystallurea &amp; urinary obstruction --&gt; Drink more water! (stay hydrated in general. I cant stress this enough<span>&nbsp;)</span></div>}}<div>Acute hemolytic anemia &amp; agranulocytosis ---&gt; in {{c1::G6PD}}</div><div>Kernicterus in {{c1::newborns}}. billirubin disassociates from plasma albumin&nbsp;</div>
Streptococcus pneumonia AKA {{c1::pneumococcus}}
SLE Diagnostic Criteria (Mnemonic: IM DAMN SHARP)"<img src=""Screen Shot 2019-11-01 at 6.53.31 PM.png""><div><br></div><div>IM DAMN SHARP: Immunologic disorder, Malar rash, Discoid rash, Antinuclear antibody, Mucositis, <b>Neurologic disorder (50%)</b>, Serositis, <b>Hematologic disorder (100%),</b> <b>Arthritis (90%)</b>, <b>Renal disorder (50%)</b>, Photosensitivity<br></div>"important
Skin Manifestation in SLE presents as interface {{c1::dermatitis}} with&nbsp;{{c1::fullhouse of antibodies}} (IgAm, IgM, IgG, C1q, C4)Note: complements and immunoglobulins are deposited at <b>dermoepidermal junction</b>
"<img src=""Screen Shot 2019-11-01 at 7.17.08 PM.png"">"Lupus Panniculitis&nbsp;
SLE Heart manifestations include&nbsp;{{c1::Valvular}} abnormalities, accelerated&nbsp;{{c1::coronary atherosclerosis}}, and&nbsp;{{c1::myocarditis}}Note: valvular abnormalities in lupus include <b>leaflet thickening with susbsequent dysfuntion</b> (steneosis, regurgitation) which usually affects the mitral or aortic valve, and <b>libman-sacks endocarditis</b>&nbsp;important
Pulmonary manifestations in SLE include&nbsp;{{c1::Pleuritis}} and&nbsp;{{c1::Pleural Effusions}} (most common), can also include chronic interstitial fibrosis and secondary pulmonary hypertensionimportant
SLE can present with enlarged lymph nodes with hyperplastic follicles or {{c1::necrotizing lymphadenitis}}important
<b>Chronic Discoid</b> Lupus Erythematosis affects mainly the skin of the&nbsp;{{c1::face}} and&nbsp;{{c1::scalp}}Note: patients can develop multisystem disease after years (5-10%); ANA may be positive in 35% of the cases
<b>Subacute Cutaneous </b>Lupus Erythematosis affects mainly the skin and tends to be&nbsp;{{c1::widespread}},&nbsp;superficial and nonscarring. It has a strong association with&nbsp;{{c1::SS-A}} and&nbsp;{{c1::HLA-DR3}}.
"<img src=""Screen Shot 2019-11-01 at 7.29.51 PM.png"">"Rheumatoid NodulesNote: seen in&nbsp;<b>subcutaneous tissue&nbsp;</b>at pressure points, but may also present in viscera ex. pleura
Rheumatoid Arthritis mainly affects the joints but can involve extra-articular tissue such as the&nbsp;{{c1::skin}},&nbsp;{{c1::blood vessels}}, {{c1::lungs}} and {{c1::heart}}
Sjögren Syndrome is a immune disorder that destroys the&nbsp;{{c1::salivary}} and lacrimal glands. It mainly presents with {{c1::keratoconjunctivitis sicca}} and {{c1::xerostomia}}. The disease mainly affects&nbsp;{{c1::women}} over 50 years of age. The {{c1::parotid}} gland may be enlarged in 50% of the cases. Diagnosis is made by biopsy of the lip.<div><br></div><div>Note: 40-fold increased risk of <b>marginal zone lymphoma</b></div>"<img src=""Sjögren's Syndrome.png"">"
ANA unique to Systemic Sclerosis include&nbsp;{{c1::DNA topoisomerase I}} (more likely to have <b>pulmonary fibrosis</b>) and {{c1::anti-centromere Ab}}&nbsp;(majority with <b>CREST</b> syndrome)"<img src=""69182557_780717409035701_9090486080095801725_n.jpg"">"important
Scleorderma manifestations include striking {{c1::cutaneous}} changes, <b>cardiac <u>arrhythmias</u>&nbsp;or failure</b>, <b>lung involvement</b>, dysfunction of the <u>lower</u>&nbsp;{{c1::esophageal sphincter}},&nbsp;{{c1::Raynaud's}} phenomenon, intestinal&nbsp;{{c1::obstruction}}, hypothryoidism, <b>proteinuria </b>(70% of pts). Small Intestine may be involved which results in {{c1::malabsorption syndrome}} and anemia."<img src=""99215.06e44385b70146030b9574d514b107b4_1 (1).jpg"">"important
The most severe mainfestion of systemic sclerosis is&nbsp;{{c1::malignant hypertension}}important
Most common cause of death in systemic sclerosis is&nbsp;{{c1::pulmonary disease}}
Diseases caused by staphylococcus aureus include&nbsp;{{c1::skin and soft tissue}} infections (ex. impetigo, furuncles, <u>abscess</u>, carbunucle), {{c1::osteomyelitis}}, {{c1::food poisoning}},&nbsp;{{c1::toxic shock syndrome}}, {{c1::bronchopneumonia}} which often folows viral infections, aspiration or <u>mechanical ventilation</u>, {{c1::arthritis}}, {{c1::endocarditis}} esp. with iv drug users, {{c1::bacteremia}} and brain abscesses"<img src=""73b7fb94ee1a98b1dffcada386ae33a4.png"">"
Staphylococcus Scalded Skin Syndrome (SSSS) is an infection (oral, nasal, throat or umbilical) with an&nbsp;{{c1::epidermylotic toxin}} producing strain. It mostly affects&nbsp;{{c1::children under two years}}.Note: presents with skin rash and separation of epidermis beneath the <u>granular</u>&nbsp;cell layer
Toxins involved in Staphylococcus Toxic Shock Syndrome include&nbsp;{{c1::TSST-1}} and {{c1::enterotoxins B and C}}
Staphylococcus Epidermidis is an&nbsp; {{c1::opportunistic}} pathogen which easily colonizes&nbsp;{{c1::medical devices}} and forms <b>biofilm. </b>It is part of the normal flora of the skin and throat and a frequent causative agent of&nbsp;{{c1::postoperative wound infections}}.Note that it colonizes the skin and throat
S. Saprophyticus causes&nbsp;{{c1::urinary tract infections}} in <u>young girls and women.</u>
Drug of choice for Staphylococci Infections includes&nbsp;{{c1::penicillinase resistant beta lactams}} such as <u>oxacillin and cloxacillin</u><b>&nbsp;</b>Note: adminstration of penicillinase resistant beta lactams should only be done after sensitivity testingimportant
MRSA infections are treated with&nbsp;{{c1::vancomycin}}important
beta lactam resistance in MRSA is caused by&nbsp;{{c1::acquisition of mecA or C gene coding for PBP2a}}&nbsp;important
Catalse Positive organisms include (5) ?&nbsp;"<img src=""8411fd2f450580466079af4ae6634f9c.png"">"important
Growth characteristic of staphylococcus aureus include&nbsp;{{c1::beta}} type hemolysis and formation of {{c1::bronze}} colored colonies.&nbsp;Note that: s. aureus are <b>halophilic</b> (7.5%) which is feature that can be used to selectively culture themimportant
{{c1::Clumping Factor}} (cell bound coagulase) in staphylococcus <i>aureus&nbsp;</i>hides ligands for phagocytic contactimportant
alpha toxin in s. aureus is particularly toxic to&nbsp;{{c1::monocytes}} and&nbsp;{{c1::platelets}}Note: alpha toxin can lead to increased release of cytokines and inflammatory mediators (symptoms of&nbsp;<b>septic shock)</b>
Panton-Valentine <b>Leukocidin</b> is a marker of&nbsp;{{c1::community acquired MRSA}}
{{c1::C4}} gene &amp; HLA-DR 2/3 is associated with SLE<br>
Mutations in AIRE are caused failure of&nbsp;{{c1::central tolerance}} and may lead to {{c1::Autoimmune Polyendocrine Syndrome}}
Mutations in FAS/FASL assocaited with {{c1::autoimmune lymphoproliferative syndrome(ALPS)}}
<b><u>Group A</u> streptococcus</b>&nbsp;can lead to&nbsp;{{c1::rheumatic fever}} post-infection
Borrelia burgdoferi associated with HLA-{{c1::DR2}} &amp; {{c1::DR4}} can lead to&nbsp;{{c1::chronic arthritis}} in Lyme disease
Chlamydia Trochomatis Infections associated with HLA-{{c1::B27}} can lead to&nbsp;{{c1::Reiter's Syndrome}}
Deficiencies of the early components of the classical pathway is strongly associated with&nbsp;{{c1::SLE}}
Azathioprine indicated in&nbsp;{{c1::organ transplants}} and treatment of {{c1::autoimmune diseases (<b>RA &amp;&nbsp;<u>SLE</u>)</b>}}&nbsp;
Main side effect of Azathiopurine is&nbsp;{{c1::depression of the bone marrow}} which usually manifests as&nbsp;{{c1::leukopenia}}
Drug Interactions of <u>Azathioprine </u>include&nbsp;{{c1::Rifampcin}} which&nbsp;{{c1::enhances::inhibits/enhances}} its metabolism, and&nbsp;{{c1::Allopurinol}} which {{c1::inhibits::inhibits/enhances}} its metabolism.
Methotrexate is an antimetabolite that inhibits&nbsp;{{c1::dihydrofolate reductase}} which results in decreased synthesis of {{c1::thymidine}} and {{c1::purine}}&nbsp;bases
Methotrexate OD causes&nbsp;{{c1::pneumonitis}}
<u>Cyclophosphamide </u>is an alkylating agent that is effective in&nbsp;{{c1::autoimmune disorders}} (ex. {{c1::SLE}} and multiple sclerosis);&nbsp;{{c1::AIHA}}, antibody induced pure&nbsp;{{c1::red cell aplasia}} and Wegner's granulomatosis.
All below are anaerobic non-spore forming bacteria. Order them into gram positive or negative&nbsp;<div>{{c1::<div><br></div><div>Gram positive:</div><div>-Peptostreptococcus spp</div><div>-Propionibacterium acnes</div><div>-Actinomyces&nbsp;</div><div><br></div><div>Gram negative:&nbsp;</div><div>-Fusobacterium nucleatum</div><div>-Bacteriodes fragilis</div><div><br></div>::Peptostreptococcus spp/ bacteroides fragilis/ actinomyces spp/ propionibacterium acnes/ fusobacterium nucleatum}}<br></div><div><div><br></div><div><br></div></div>
Cyclosporine is a&nbsp;{{c1::calcineurine}} inhibitor indicated in human&nbsp;{{c1::organ transplantation}},&nbsp;{{c1::autoimmune disorders}} and in the treatment of&nbsp;{{c1::graft versus host}} disease. It is also used in&nbsp;{{c1::psoriasis}} and severe cases of&nbsp;{{c1::rheumatoid arthritis}} that have not responded to methotrexate.MOA: binds cyclophilin -&gt; complex reduces activity of calcineurine -&gt; interrputs <b>translocation of NFAT</b> to nucleus (essential for induction of cytokine synthesis)
Cyclosporine Adverse Effects include: {{c1::nepHrotoxicity}},&nbsp;{{c1::Hypertension}}, {{c1::Hepatotoxicity}}, {{c1:Hirsutism}}, {{c1:gingival Hyperplasia}}, {{c1:Tremor}}, and {{c1::Neurotoxicity}}mnemonic: <u>Tim</u>&nbsp;is riding a cycle wearing 5<u>&nbsp;Hats </u>and a <u>N</u>ightshirt (Tim = tremor, cycle to remind you of cyclosporine, 5H: nepHrotoxicity, Hyperplasia of gums, Hypertension, Hirsutism, Hepatotoxicity, Nightshirst = Neurotoxicity)
{{c1::Metoclopramide}} increases cyclosporine absorption<br>mnemonic: adding METal to your cycle makes it faster (idk man)
{{c1::Calcium}} <u>Antagonists</u>&nbsp;increase plasma concentration of&nbsp;{{c2::cyclosporine}} by changing tissue distribution.<br>
Tacrolimus is a&nbsp;{{c1::macrolide antibiotic}} that acts by inhibiting&nbsp;{{c1::calcineurine}} which blocks t cell activation.&nbsp;
Sirolimus inhibts&nbsp;{{c1::mTOR}} which blocks T lymphocyte prgression at the&nbsp;{{c1::G1/S}} transition
Everolimus is indicated for&nbsp;{{c1::kidney}} and liver transplant rejection prophylaxis
Sirolimus is indicated for <u>prophylaxis</u>&nbsp;of {{c1::kidney transplant rejection}} in combination with glucocorticoids and&nbsp;{{c1::ubeoretinitis}} in combination with cyclosporine.Note: sirolimus and cyclosporine act <u>synergestically</u>&nbsp;and so adminstration must be separated by time
Adverse effects of Sirolimus include&nbsp;{{c1::hyperlipidemia}}, leukopenia and thrombocytopeniamnemonic: Sir needs HLP (sir to remind you of sirolimus, and HLP for hyperlipidemia, leukpenia, and thrombocytopenia)
Antithymocyte globulins are&nbsp;{{c1::cytotoxic polyclonal antibodies}} (derived from horses or rabbits) indicated in prophylaxis and rejection of&nbsp;{{c1::renal}} transplant and the treatment of&nbsp;{{c1::aplastic anemia}}.mnemonic: horses love Red Plastic (dont judge me)
Antithymocyte globulins cause general&nbsp;{{c1::immunosuppression}} which can lead to serious infections, especially by&nbsp;{{c1::CMV}}. They can also cause&nbsp;{{c1::myelosuppression}} and fever, rigor, urticaria, rash or serum sickness can occur.Note: long-term use can lead to increased incidence of lymphoma in kidney transplant patients
Muromunab-<b>CD3</b>&nbsp;prevents antigen recognition and inactivates t cells by inducing {{c1::internalization of TCR}}
Muromunab-CD3 can cause&nbsp;{{c1::cytokine release}} syndrome and severe {{c1::pulmonary}} edema
Basiliximab &amp; Daclizumab inhibit&nbsp;{{c1::IL2}} mediated activation and proliferation of T cellsMOA: They have a high affinity to CD{{c1::25}} (alpha subunit IL2)
<u>Anti-TNFa</u> are either monoclonal antibodies such as&nbsp;{{c1::<u>Infliximab</u>}}, {{c1::Adalimumab}} or {{c1::Golimumab}} or circulating receptor fusion protein <u>etanercept</u>MOA: bind TNFalpha and prevent synthesis of <b>IL-1 and IL-6</b>, and adhesion of <b>lymphocyte activating molecules</b>
Anti-TNFa antibodies indicated in&nbsp;{{c1::Rheumatoid Arthritis}}, ankylosing spondylitis, psoriasis and Crohn's.mnemonic: alpha CARP
Anti-TNFa drugs raise the risk of contracting&nbsp;{{c1::tuberculosis}}
Glucocorticoids have important effects on the development of&nbsp;{{c1::fetal lungs}}Important Note: <b>Betamethasone</b> (12mg IM every 24hrs for two doses) in anticipated premature delivery (before 34 weeks) reduces risk of <u>respiratory distress syndrome&nbsp;</u>
Glucocorticoids {{c1::increase::decrease/increase}} hepatic glycogen and {{c1::decrease::decrease/increase}} glucose uptake and utilization in peripheral tissues.Note: use of glucocorticoids can cause a tendency for&nbsp;<b>hyperglycemia</b>
Pathological effects of high glucocorticoid levels include&nbsp;{{c1::osteoporosis}} due to enhanced bone resorpstion.
Long term use of glucocorticoids side effects include increased susceptibility to&nbsp;{{c1::infection}}, {{c1::peptic Ulcers}}, {{c1::Hypertension}} and&nbsp;{{c1::Hyperglycemia}},&nbsp;{{c1::osteoporosis}} in post menopausal women, sodium retention with&nbsp;{{c1::edema}}, behaviorual disturbances (insomnia, depression,&nbsp;{{c1::psychosis}}), and&nbsp;{{c1::cataracts}} especially in children."<img src=""Screen Shot 2019-11-01 at 11.02.04 PM.png"">"
Betamethasone, Dexamethasone and Paramethasone are {{c1::long::short/long}} term acting glucocorticoids.
<u>Gluccorticoids </u>are mainstay in the treatment of {{c1::autoimmune and rheumatic inflammatory}} diseases and&nbsp;{{c1::systemic lupus erythematosus}}. They are also mainstay of <u>asthma therapy</u> (first line treatment).&nbsp;
<u>Glucocorticoids </u>indicated in the treatment of transplant rejection because of their ability to&nbsp;{{c1::reduce antigen expression from the grafted tissue}},&nbsp;{{c1::delay revascularization}}, interfere with the {{c2::sensitization of cytotoxic lymphocytes}} and the&nbsp;{{c2::generation of primary antibody forming cells}}
{{c1::Beclomethasone}} (corticosteroid) admintered as <u>aerosols</u> is effective in the treatment of <b>asthma</b> and as <u>nasal spray</u> for <b>allergic rhinitis</b>.<br>
High dose of intravenous {{c1::<u>methylprednisolone sodium succinate</u>}}&nbsp;is used to reverse&nbsp;{{c2::acute transplant rejection}} and&nbsp;{{c2::acute exacerbations}} of selected autoimmune disorders
Glucocorticoids inhibit transcription for genes coding for&nbsp;{{c1::cytokines}} (most importantly&nbsp;{{c1::IL2}})
<u>Dexamethasone </u>used in the treatment of <b>allergic or inflammatory conditions </b>and&nbsp;{{c1::autoimmune}} conditions. It can be<u> used to counteract allergic shock</u>Important Note: dexamethasone has no mineralocorticoid activity
Hydrocortisone used as replacement therapy in&nbsp;{{c1::adrenal insufficiency}}. Topical application used in allergic rashes, eczema and psoriasis
Alemtuzumab binds CD{{c1::52}} and causes lysis of&nbsp;{{c1::lymphocytes}} in the blood, bone marrow and organs resulting in&nbsp;{{c1::lymphocyte depletion}}Indications: CLL &amp; MS
Fingolimod changes the function of&nbsp;{{c1::adhesion molecules}} (a4/B7 integrin) in lymphocytes and is used as first line therapy in&nbsp;{{c1::multiple sclerosis}}Note: Fingolimid does not impair functions of t and b cells
Leflunomide inhibits dihydro-orotate dehydrogenase (key enzyme in&nbsp;{{c1::pyrimidine}} de novo synthesis) and is indicated in the treatment of&nbsp;{{c1::Rheumatoid Arthritis}} and&nbsp;{{c1::Psoriasis}}Note: may be useful in kidney transplantation
{{c1::low::low/high}} levels of C4 and C3 but normal levels of {{c1::factor B}} suggest activation of the classical pathway<br>
C3 and C4 concentrations should be requested in patients with&nbsp;{{c1::renal}} disease,&nbsp;{{c1::joint}} disease, and&nbsp;{{c1::multisystem disorders}} with evidence of vasculitis.
Low {{c1::C3}} and normal {{c1::C4}} seen in gram negative septicemia, and some forms of glomerulonephritis.
Streptococcus serological <u>grouping</u> is based on the&nbsp;{{c1::carbohydrate antigen}} of the cell wall (<u>Lancefield</u>&nbsp;groups A-U)Note: Serotyping based on M protein
Viridans Streptococci (S.{{c1::mitis}} and S.{{c1::mutans}}) cause&nbsp;{{c2::subacute bacterial endocarditis}} and&nbsp;{{c2::caries}}
S. milleri group vary in hemolytic properties and can be {{c1::microaeorphilic}} or anaerobs. They cause various&nbsp;{{c1::abscesses}}.
Group A Streptococci are&nbsp;{{c1::beta}} hemolytic and&nbsp;{{c1::catalase}} negative. They colonize the skin and&nbsp;{{c2::mucous membranes}}.Note: spread is airoborne or through contact
{{c1::Streptokinase}} (fibrinolysin) is used clinically to dissolve clots in acute myocardial infarctions
Spread of streptococci facilitated by virulence factors such as&nbsp;{{c1::Hyaluronidase}},&nbsp;{{c1::DNAse}} and&nbsp;{{c1::streptokinase}}
Anti-Streptolysin O (ASO) is used in serology to prove <u>previous</u>&nbsp;{{c1::GAS}} infection of the throat
Streptococcal Pyrogenic Exotoxins includes {{c1::SPE A::Erythryogenic toxin}}&nbsp; which causes <b>scarlet fever</b>&nbsp;and {{c1::SPE B &amp; C}}&nbsp;which causes&nbsp;<b>streptococcal toxic shock syndrome</b>
List the Streptococcus Pyogenes virulence factors. (Hint: SMASHED)"<img src=""paste-089b054bb5523f73275a76b4a64049b2fcd87252.jpg"">"
Diseases caused by streptococcus pyogenes include&nbsp;{{c1::pharyngitis}},&nbsp;{{c1::impetigo}},&nbsp;{{c1::scarlet fever which is usually preceded by <u>sore throat</u>&nbsp;or <u>impetigo</u>}}&nbsp;,&nbsp;{{c2::Erysipelas}}, {{c2::puerperal sepsis}} and&nbsp;{{c2::necrotizing fascitis}}mnemonic: PINESS (pharyngitis, impetigo, necrotizing fascitis, erysipelas, scarlet fever, sepsis)
Post Streptococcal diseases include&nbsp;{{c1::acute rheumatic fever}} and {{c1::acute poststreptococcal glomerulonephritis}}Important Note: ARF is after strep <u>throat</u>&nbsp;infections only, while AGN can develop after throat or <u>skin</u>&nbsp;infection
Streptococcus pyogenes is&nbsp;{{c1::Bacitracin}} sensitive !&nbsp;
Treatment of streptococcus pyogenes is by&nbsp;{{c1::<u>penicillin</u>}} or&nbsp;{{c1::erythromycin}}Important: combine penicillin with clindamycin in invasive infections
Streptococcus group C and G cause&nbsp;{{c1::sore throat}} and&nbsp;{{c1::tonsillits}}Note: they can be <b>associated with AGN</b> but NEVER with ARF
S. agalactiae (<b>GBS</b>)&nbsp; inhabits lower&nbsp;{{c1::GIT}} and female {{c1::genital tract}}. It causes&nbsp;{{c2::neonatal sepsis and meningitis}} and&nbsp;{{c2::arthritis or meningitis}} in the elderly or immunocomprimisedImportant: Diagnosis of GBS is by culture, serogroup determination and <b>CAMP test</b>
Vancomycin and Teicoplanin are&nbsp;{{c1::glycopeptides::class of antibiotic}}
Vancomycin is <u>bactericidal</u>&nbsp;except in&nbsp;{{c1::enterococcal}} infections
Vancomycin Indicated in infections with {{c1::<u>MRSA</u>}} , {{c1::coagulase negative&nbsp;staphylococi}}, {{c1::Amp resistant enterococcus}}
Vancomycin inhibits <b>transglycosylase</b>&nbsp;by binding to&nbsp;{{c1::D-ala-D-ala}} terminus of peptidoglycan.
Vancomycin is adminstered through&nbsp;{{c1::IV}} and&nbsp;{{c1::PO}}Important: oral adminstration only in cases of <u>antibiotic associated colitis caused by C. difficile</u>
vancomycin adverse reactions include&nbsp;{{c1::<u>red man syndrome</u>}},&nbsp;{{c1::nephrotoxicity}} and&nbsp;{{c1::ototoxicity}}
Teicoplanin may retain activity against vancomycin resistant&nbsp;{{c1::stpahylococcus aureus}}Note: it is <b>more active against enterococcus</b> than vancomycin
Telvancin is a&nbsp;{{c1::lipglycopeptide}} active against gram&nbsp;{{c1::positives::negatives/positives}} with reduced susceptibility to vancomycin. Approved for the treatment of&nbsp; {{c2::Skin and soft tissue infections (SSTI)}}Important: teratogenic
Polymyxin B active against {{c1::negatives::negatives/positives}}&nbsp;and is applied topically. It is combined with&nbsp;{{c2::bacitracin}} and&nbsp;{{c2::neomycin}} in OTC preparations.MOA: <b>disrupts cytoplasmic membrane</b>&nbsp;causing leakage and cell death
<u>Cycloserine </u>is a structural analogue of&nbsp;{{c1::D-alanine}} which inhibits its corporation into peptidoglycan and further cell wall synthesis by inhibiting&nbsp;{{c2::alanine reductase::enzyme}}. It is used in the treatment of&nbsp;{{c2::TB}}Important: can cause serious <b>CNS toxicity</b>
Fosfomycin is an <u>early</u>&nbsp;inhibitor of&nbsp;{{c1::cell wall synthesis}} by inhibiting cytoplasmic&nbsp;{{c2::enolpyruvate transferase::enzyme}} which blocks the addition of PEP to UDP-N-acetylglycucosamine. It is effective against {{c1::both::negatives/positives}}.Note: it is the only <u>oral</u>&nbsp;approved by FDA (single 3g dose for treatment of <b>lower UTIs in women</b>)
Bacitracin inhibits <b>cell wall formation</b>&nbsp;by interfering with&nbsp;{{c1::dephosphorylation}} in cycling of the <u>lipid carrier</u>. Indicated for <u>suppression of mixed bacterial flora in surface lesions of the&nbsp;{{c2::skin}}</u>, wounds or on mucous membranes.Important: it is highly <b>nephrotoxic</b>&nbsp;and so its only used <u>topically</u>
<u>Daptomycin </u>is a&nbsp;{{c1::cyclic lipopeptide::class}} with a fast {{c1::bactericidal::bacteriostatic/bactericidal}} action. It is an effective alternate for {{c2::vancomycin}}.&nbsp;MOA: binds membrane and causes <u>rapid depolarization</u>&nbsp;with subsequent <b>efflux of K+ </b>leading to cell death
<u>Daptomycin </u>is indicated for the treatment of complicated {{c1::SSTI}}; {{c1::MRSA}}; {{c2::staphylococcus bacteremia}} and {{c2::right sided endocarditis}}Note: not used for the treatment of pneumonia (surfactant binding inactivates drug)
Daptomycin displays {{c1::concentration::time/concentration}} dependent killing and {{c2::post antibiotic effect}} (therefore <b>once daily dosing </b><u>[4-6mg/kg]</u>). It is excreted through the kidneys and available for IV use only.&nbsp;Important: daptomycin interacts with INR assay which can result in <b>falsely high INR</b>
<u>Daptomycin </u>may cause&nbsp;{{c1::myopathy}} and&nbsp;{{c1::allergic pneumonitis}}Important: <b>needs CPK monitoring</b>
Prophylaxis for leprosy? {{c1::Dapsone}}
Influenza is an enveloped {{c1::SS RNA:: DNA/RNA?}} virus with eight segments. It infects the {{c1::upper and lower:: Upper/Lower?}} respiratory tracts. It uses it's hemagglutinin proteins (H) to bind to the {{c1::sialic acid}} receptors on epithelial cells"<div>Both inflenza A and B have eight RNA segments, but C has only one.</div><img src=""paste-dcb744b1339697bb70a4137c46dea45b5f984543.jpg"">"
Influenza virus remains restricted to the respiratory tract, meaning there is <b>NO </b>{{c1::<b>VIREMIA</b>}}.<div>Some patients can get bronchitis or pneumonia.&nbsp;</div><div><br></div><div>Secondary bacterial infections seen in {{c1::immunocompromised}} and {{c1::elderly patients}}</div><div>CNS complations due to <b>indirect </b>complications</div>"<img src=""paste-5100a7a94c5be5c0091cc984c0df16ab00f1178c.jpg"">"
Influenza serotypes (A,B,C) classified depending on differences between {{c1::nucleocaspid (NC)}} and {{c1::matrix(M)}} proteins"<img src=""paste-f8b99b834840655d34621642d010aa2f3131d784.jpg"">"
Differences in strains of influenza A depend on the two surface glycoproteins {{c1::Hemagglutinin (H)}} and {{c1::Neuraminidase (N)}}<div><br></div><div>Antigenic {{c1::drifts:: Shift/Drift?}} if there are small changes in in the glycoproteins within the natural host causing different subtypes</div><div>Antigenic {{c1::shift::Shift/Drift?}} if there is a reassortment of RNA segments between two different influenza virus resulting in a new combination of surface glycoproteins. usually happens in animals&nbsp;</div>
In influenza A there are 18 H and 11 N different glycoproteins allowing for 198 possible combinations. However, only three combinations were observed so far successfully infecting humans:&nbsp;<div>{{c1::H1N1 (Spanish flu)}}</div><div>{{c1::H2N2 (Asian flu)}}</div><div>{{c1::H3N2 (Hong Kong flu)}}</div><div><br></div><div>recently there's been a threat of the emerging avian flu,H5N1, but it is unable to infect from a human host&nbsp;</div>Generally H1,H2,H3 were observed to infect humans
A flu strain can re-infect the host if it goes through a {{c1::genetic drift}}
Influenza A is the only one undergoing genetic shifts because the other influenza's have no {{c1::animal reservoir}}
Flu vaccines:<div>{{c1::Egg based}} flu vaccines incubate the virus in hen eggs then are eother inactivated for flu shots, or attenuated for nasal sprays</div><div><br></div><div>{{c1::Culture based}} flu vaccines are produced by growing viruses in eggs, then growing them in mammalian cells, and lastly purifying it. its quicker than the previous method</div><div><br></div><div>{{c1::Recombinant}} flu vaccines does not require chicken eggs. It involves taking the HA proteins and combining it with another virus to infect the human. 100% egg free</div>Viruses are inactivated by formalin and extracted by ether<div><br></div>
Drugs for influenza treatment targets:<div><br></div><div><div>-Neuraminidase (N).&nbsp;</div><div>Function:<span>{{c1::Viruses enters and infects the cell, but cannot bud out. it decreases spread of infection.&nbsp;}}</span></div></div><div>Drug: {{c1::Oseltamivir}} &amp; {{c1::zanamivir}}</div><div><br></div><div>-M2 protein.&nbsp;</div><div>Function:<span>{{c1::Virus enters the cell but cannot uncoat. decreases infection}}.&nbsp;</span></div><div>Drugs: {{c1::Amantidine}} &amp; {{c1::Rimantidine}}</div>
The Varicella-Zoster virus is part of the&nbsp;α-herpesvirus subfamily.&nbsp;<div>First infections is usually during childhood and causes {{c1::chicken pox.}}, which then&nbsp;<span>establishes latency in the sensory ganglion.&nbsp;</span><span>Upon reactivation (usually in elderly) it causes {{c1::shingles}}</span></div><div>Transmission is via {{c1::aerosols&nbsp;}}, infects the {{c1::URT}} and replicates in the {{c1::local lymph nodes&nbsp;}}</div><div>4-6 days after infection it causes <u>viremia</u>, and starts replicating in the {{c1::liver}} and {{c1::spleen&nbsp;}}, then disseminates throughout the body via {{c1::mononuclear leukocytes}}. <i>1-2 days before the rash appears the individual becomes contagious</i>. after 10-14 days of primary infection it reaches the skin and causes the rash (<span>Xanthema).&nbsp;</span></div><div>Humoral system will provide<u> lifelong immunity</u> to {{c1::re-infection}}, not {{c1::re-activation}}&nbsp;</div><div>Treatment via acyclovir-related drugs, VZ-Ig, or the VZV vaccine (Varivax)</div>"<img src=""paste-098e4038be683796b206cea374c1772a1554b633.jpg"">"
"You are seeing a patient with infectious mononucleosis and view this under the microscope<div><img src=""paste-1924dfa5d14678608838280063f7894a863b407c.jpg""><br></div><div>Whats the offending agent? {{c1::human Cytomegalovirus (CMV)}}</div>"owl eye inclusions&nbsp;
Human Cytomegalovirus (CMV) is part of the&nbsp;β-herpesvirus, It infects {{c1::fibroblasts}}, {{c1::epithelial}} cells and {{c1::macrophages&nbsp;}}. close cell association protects the virus from antibody-mediated inactivation and produces {{c1::owl eye inclusion&nbsp;}}<div>Replication in {{c1::ductal epithelial cells}} promotes excretion in most body fluids&nbsp;</div><div><br></div><div>Spread happens via {{c1::body fluids}}, {{c1::tissue transplants}}, and {{c1::trans-placental&nbsp;}}</div><div><br></div><div>Infection is usually asymptomatic but can cause {{c1::infectious mononucleosis}}</div><div>{{c1::Immunocompromised}} patients are prone to severe CMV infections</div>
"Congenital hCMV causes {{c1::mental retardation&nbsp;}}. Infection is transmitted from mother to child either by a primary or reactivation of the infection. it is more severe if the infection happens between {{c1::4-22}} weeks of gestation. Causes <b>blueberry muffin lesions</b><div><img src=""paste-653c71d7ebe0e5e49746939dd63c217f4c7a8bcb.jpg""><b><br></b></div><div><br></div><div>abnormalities including: CNS abnormalities (e.g. microcephaly, mental retardation,epilepsy), eye (retinitis, optic atrophy), ear (deafness), lungs (pneumonitis), liver (hepatosplenomegaly)<br></div><div><br></div><div>If CMV transmission happens due to recurrent infection then the percentage of the baby being symptomatic at birth is {{c1::0%}}&nbsp;</div><div><br></div><div><br></div>"
Treatment of CMV with acyclovir is not effective because {{c1::it lacks thymidine kinase&nbsp;}}
CMV is heterophile Ig {{c1::negative:: Neg/pos?}}<div>EBV is heterophile Ig&nbsp;{{c1::Positive:: Neg/pos}}</div>
Epstein-Barr virus's DNA resides in the cell by {{c1::being an episome within the nucleus:: Integration or being an episome?}}<div>Transmission is via {{c1::close contact with saliva}}</div><div>Primary infection causes {{c1::infectious mononucleosis (Lymphadenopathy, splenomegaly, malaise and fever)}}</div><div><br></div>
<div>There are innate and adaptive antiviral responses.&nbsp;</div><div><br></div><div>-Humoral:</div><div>Innate: {{c1::Interferons&nbsp;α &amp; β}}</div><div>Adaptive: {{c1::Antibodies}}</div><div><br></div><div>-Cell-mediated:</div><div>Innate: {{c1::NK cells}}</div><div>Adaptive: {{c1::CTLs}}</div>
in viral infections the innate system (NK cells and interferons) will work to {{c1::delay and limit the viral infection:: Objective?}}<div>The adaptive system (CTLs &amp; antibodies) will {{c1::eliminate and establish immunity&nbsp;}}</div>
Intracellular innate sensors of viruses include Toll-like receptors (TLRs)<div>DNA sensors include {{c1::TLR9}}</div><div>RNA sensors includes {{c1::TLRs 3, 7 &amp; 8}}</div><div>Viral surface structures sensed via {{c1::TLRs 2&amp;4}}</div>
IFN&nbsp;α &amp; β response to viral infection induces:<div>{{c1::Blocking or viral replication}}</div><div>{{c1::Increased expression of MHC1}}&nbsp;</div><div>{{c1::Activate NK cells&nbsp;}}</div><div><br></div><div>IFN&nbsp;<span>α &amp; β will bind to 2-5(A) synthetase, which activates&nbsp;</span>{{c1::RNAse L (degrades mRNA)}}</div><div>they also activate PKR, which results in the {{c1::inhibition of viral protein synthesis&nbsp;}}</div>
CTLs perforin polymer formation steps:<div>-{{c1::Increase in intracellular Ca induces exocytosis of granules}}</div><div>-{{c1::Release of monomeric perforin between two cells}}</div><div>-{{c1::the Ca induces the imbedding of perforin into the target}}</div><div>-{{c1::In the presence of Ca perforins polymerize&nbsp;}}</div>
Fas pathway steps:&nbsp;<div>-{{c1::Fas/FasL ligation --&gt; Binding with FADD&nbsp;}}</div><div>-{{c1::Cleaving Caspase8}}</div><div>-{{c1::Release of cytochrome C causing the activation of caspase9}}</div><div>-{{c1::Activation of caspase3--&gt;apoptosis&nbsp;}}</div>"The granzyme B pathway is very similar, and starts by activating caspase8<div><img src=""paste-794bae6a626e3d119cd002d3cc916ae0c036f630.jpg""><br></div>"
{{c1::FasL}} associated killing is used by both NK &amp; CTLs to kill infected cells. It is upregulated when theyre activated.<div><br></div><div>The outcome of TNF on the other hand depends on the target. If it is an infected cells it {{c1::induces apoptosis}}. If it was a macrophage or endothelial cell it {{c1::induces activation of transciption genes (that activate NF-κB,)}}</div>
IFN-gamma does two things:&nbsp;<div>{{c1::Upregulates MHC1 expression}}&nbsp;</div><div>{{c1::Activates killing by NK cells}}</div>
Infected cells express the stress molecules {{c1::MICA}} &amp; {{c1::MICB}}, which are recognized by the killer activation receptors (KAR) on the NK cells.&nbsp;<div>if KAR/MHC1 binding is insufficient {{c1::NK cell}} kills the cell</div><div>If KAR/MHC1 binding is too much then {{c1::CTL}} kills the cell&nbsp;</div>
NK cells express the FC receptor {{c1::FCgIII}}, which recognises IgG on infected cells and triggers killing. Macrophages have the same receptor which which triggers opsonization&nbsp;
{{c1::primary Immunodeficiencies}} result from monogenic disorders of the immune system characterized by increased susceptibility to infections, increased autoimmunity, autoinflamation, or malignancies
An immunodeficient patient comes to your clinic. what characteristics do you expect his infections to have?&nbsp;<div>- Frequent</div><div>- {{c1::Severe/ resistant to treatment}}&nbsp;</div><div>- {{c1::Without symptom-free interval}}</div><div>- {{c1::Caused by unusual organisms (usually opportunistic)}}</div>
Immunodeficiency due to {{c1::B cell abnormality (nearly 50%):: Abnormality in which part of the immune system?}} is the most common primary immune deficiency&nbsp;"<img src=""paste-3dae6969906c3d731f07165fdf54383f426de879.jpg"">"
Primary immune deficiencies are usually first observed in {{c1::infants/ children:: Which age group?}}
Primary immune deficiencies are mostly inherited in an {{c1::X-linked fashion}} and affects mainly {{c1::males (70% of PIDs in males):: Males/Females?}}
{{c1::Secondary (acquired):: Primary/secondary?}} immune deficiency results in a previously normal individual, and is reversible if the underlying cause is treatedSec immune deficiencies are more common than primary.&nbsp;
A previously healthy 30 year old comes to you with increased recurrence of infection, and was diagnosed with acquired immune deficiency. you suspect the offending agent is viral, what is it most likely? {{c1::HIV}}
If you see a patient with an immune deficiency you check for two things:&nbsp;<div>-{{c1::Number of cells}}</div><div>-{{c1::Function of cells}}</div>Sometimes the number is normal but the function is abnormal&nbsp;
Severe combined immunodeficiencies (SCID) is characterized by a defect {{c1::both B &amp; T lymphocytes:: Which immune component?}}It affects T cells, but because T cells have a vital role in activating B cells they are also either absent or severely decreased&nbsp;
When do patients with SCID develop signs of immunodeficiencies? {{c1::usually at 3 months of age}}Since it is mainly a T cell (also affects B cells) it manifests at 3 months&nbsp;
X-linked SCID results from a mutation in the {{c1::gamma chain of IL-2}}, which is responsible for T cell development (and indirectly affects B cells).&nbsp;<div>Treatment is with IG and antibodies, but {{c1::BMT}} is curative&nbsp;&nbsp;</div>GammaC gene is encoded by the X-chromosome --&gt; more prevalent in males
SCID can be inherited in an autosomal recessive way, like {{c1::Adenosine deaminase deficiency (ADA)}} or {{c1::Purine nucleotide phosphorylase (PNP)}}
Adenosine deaminase/ Purine nucleotide phosphorylase are enzymes used in the {{c1::purine salvage}} pathway. deficiency causes SCID which is inherited {{c1::autosomal recessively&nbsp;}}<div>this deficiency leads to accumulation of toxic purine metabolites and inhibition of DNA synthesis in lymphocytes&nbsp;</div>
Recombinase deficiencies (RAG1 and 2) causes SCID of the T-B- phenotype.&nbsp;<div>this can be viewed as {{c1::absence of cortico-medullary differentiation within the thymus&nbsp;}}</div>"<img src=""paste-82cb179e6d041beaa15967a696ed14d35db22cd5.jpg"">"
Omenn syndrom is a form of SCID with a T⁺/B^- phenotype due to {{c1::partial RAG deficiency&nbsp;}}
<div>Forms of SCID and causes&nbsp;</div><div><br></div>T+B- phenotype<br>– Omenn Syndrome {{c1::(partial RAG deficiency)}}<br><br>• T+B+ phenotype<br>– Bare Lymphocyte Syndrome Type I or II {{c1::(no MHC class I or II)}}<br>– ZAP-70 deficiency {{c1::(defective T cell signaling)}}<br><br>• Multisystem Disorders<br>– Wiskott-Aldrich Syndrome (mutation in gene for {{c1::WASP protein}})<br>– Ataxia Telangiectasia (mutation in gene for {{c1::ATM protein}})
A patient with SCID comes to you with normal T/B cell numbers, but an inverse in CD8/CD4 (only CD8 seen present in blood, no CD4s). what is the underlying syndrome and the cause? {{c1::Bare lymphocyte syndrome. APCs do not express MHCII (including in the thymus), so cells do not develop into CD4s, but into CD8s&nbsp;}}
A patient comes to you with recurrent infections, eczema &amp; thrombocytopenia. they present with small, defective platelets due to an abnormality in a gene responsible for cytoskeletal organization, also affecting T:B interactions. Antibody testing shows elevated levels of IgE &amp; IgA, normal IgG, low IgM.&nbsp;<div><br></div><div>What is this syndrome called, and the underlying cause? {{c1::Wiskott-Aldrich Syndrome due. Due to a defect in WASP (WAS protein)</div><div>Inheritence is X-linked recessive}}</div>"<div>Causes increased susceptibility to pyogenic infections, and has a poor response to polysaccharide antigens</div><img src=""paste-b3da9c3ce969eaa00e0d73de538d7f48ab00a851.jpg"">"
{{c1::X-linked agammaglobulinemia}} is the most severe B cell immune deficiency. characterized by IgG level &lt;100mg/dL, absent or low IgA, IgM, IgD, IgE. Low or absent CD19+ cells, and very small tonsils, increased encapsulated pyogenic bacterial infections, but otherwise normal cell-mediated immunity&nbsp;
X-linked agammaglobulinemia is due to a defect in the {{c1::bruton tyrosine kinase (BTK)&nbsp;}} responsible for B cell development. BM contains {{c1::Pre-B (B220⁺)}} cells but development doesnt go further.&nbsp;
{{c1::Transient hypogammaglobinemiaof infancy }}&nbsp;happens usually between 3 months an 1 year of age where IgG levels are low, but not due to pathologic reasons. Completely normal.&nbsp;"<div>Maternal IgGs are catabolized. should recover by the second year of life</div><img src=""paste-40319e81a89506763857a82bc4de41d5de0c9df5.jpg"">"
{{c1::Selective IgA deficiency}} is the most common and mildest humoral immunodeficiency. characterized by the absence or reduction of IgA, but normal levels of other Abs.&nbsp;<div>usually sporadic, and asymptomatic. but may have recurrent respiratory infections, diarrhea or allergy.</div>
If patients with selective IgA deficiency were exposed to IgA via plasma transfusion they will develop {{c1::anti-IgA antibodies}}. patients may have IgG2/IgG4 subclass immunodeficiency . Pts have increased susceptibility to {{c1::pyogenic bacterial}} infections<div>Treatment is {{c1::not necessary}}</div>
Hyper IgM syndrome is characterized by elevated levels of IgM (duh), decreased {{c1::IgG:: Immunoglobin}} and {{c1::IgA::Immunoglobin}}, intermittent neutropenia, normal B cell number, and increased susceptibility to pyogenic infections, gram positive bacteria and oppotunistic infection
There are two forms of Hyper IgM Syndrome:&nbsp;<div>X-linked due to {{c1::defective expression of CD40L on T cells}}</div><div>Autosomal recessive due to {{c1::absence of CD40 on APCs&nbsp;}}</div><div><br></div><div>It is characterised by the inability of {{c1::isotype switching}}</div>
DiGeorge syndrome is characterized by the absence or hypoplasia of the {{c1::thymus}}, leading to partial or complete T cell deficiency. (B cell are normal/near normal)<div>it is cauzed by the deletion of chromosome {{c1::22q}}</div><div>Patients can present with defects in parathyroid, aortic arch, lips, ears, heart.&nbsp;</div><div>this affects {{c1::both sexes:: Which sex?}}</div><div>Can be corrected by {{c1::fetal thymic transplant or HLA-identica BM transplant&nbsp;}}</div>"<img src=""paste-d08b71963112d6075a21d4872e49c74ee725a6b0.jpg"">"
"A patient presents with recurrent infections and deep abscesses caused by catalase + organisms. NTB test is done and this is seen:&nbsp;<div><br><div><img src=""paste-2793c7967fd7516db43f6a8d183b210328c14b24.jpg""><br></div></div><div>Diagnosis? {{c1::Chronic granulomatous disease}}</div>"&nbsp;Catalase+ organisms include S.aures, aspergillus, serratia and nocardia&nbsp;<div><br></div>
CGD presents due to {{c1::the absence of oxidative burst (no generation of superoxide)}} leading to defective bacterial killing<div>2/3 of inheritence is XL, 1/3 is autosomal recessive.&nbsp;</div>
Complement deficiencies&nbsp;<div><br></div><div>deficiency in the classical pathway (C1,C2,C4) leads to {{c1::immune complex disease}}</div><div><br></div><div>Def in MBL pathway leads to {{c1::bacterial infections during childhood}}</div><div><br></div><div>Def in alternative pathway leads to increased {{c1::pyogenic infections and neisseria&nbsp;}}</div><div><br></div><div>Def in membran attack components (MAC) (C5-C9) leads to {{c1::icreased neisseria infections ONLY}}</div>
Superficial mycosis caused by {{c1::dermatophytes}} and {{c1::candida}} infections<div>Can be seen infecting the skin, nail, hair (keratin in general), and mucous membranes</div>
Candida infections come mostly from {{c1::the patients own digestive tract}}
Subcutaneous mycosis often caused by {{c1::dimorphic}} fungi. It goes deeper than superficial mycosis, affecting the {{c1::dermis}}, {{c1::subcutis}}, and {{c1::adjacent bones}}<div><br></div><div>Localized in {{c1::immunocompetent}} patients, but spreads in {{c1::immunocompromised}} patients</div>
Dermatophytosis is the infection of the skin, hair or nail caused by {{c1::keratino}}-philic fungi&nbsp;<div><br></div><div>Offending agents include:</div><div><br></div><div>-{{c1::Microsporum (hair and skin)}}</div><div>-{{c1::Epidermophytom (Nail and skin)}}</div><div>-{{c1::<u>Trichrophyton (Nail, Hair, skin)</u>}}</div>
"You see a patient with athlete's foot and suspect a fungal etiology.&nbsp;<div><br><div><img src=""paste-47e27108ebb17b47d0b9faa3d8ee799016095587.jpg""><br></div></div><div>Most likely fungus? {{c1::Tinea pedis&nbsp;}}</div>"
Culture of dermatophytes is done on {{c1::sabouraud agar}}<div><br><div><u>skin </u>infections are treated with {{c1::<u>topical </u>azoles or terbinafine}}</div><div><u>Nail or hair</u><b> </b>infections treated with {{c1::<u>oral </u>azoles, terbinafine or griseofluvin}}</div></div>Growth on sabouraud agar varies depennding on fungus growth time and temperature.&nbsp;
"You see a patient with a superficial chronic infection of the stratum corneum with a lipophilic yeast.&nbsp;<div>Clinical findings show hyperpigmented trunk</div><div><img src=""paste-c53f9abf5ee197f3aa6fc3bc7f086f9451bbbf3e.jpg""><br></div><div>and upon microscopy you see short hiphae and yeast cells. colonization was done on sabouraud agar supplemented with olive oil&nbsp;</div><div><img src=""paste-e1a573e2f87a5d6320e0d301f053db9fc411b93d.jpg""><br></div><div>Whats the condition called, and the offending agent? {{c1::Pityriasis versicolor. caused by Malassezia furfur&nbsp;}}</div>"
"You are seeing a patient with a superficial infection of the stratum corneum, which appears as a brownish macule on the palm/ finger or face.&nbsp;<div><img src=""paste-f967702b3632a61687c05b1827f94d35588407e3.jpg""><br></div><div>Whats this called and underlying cause?&nbsp;</div><div>{{c1::Tinea nigra, caused by hortae (exophiala) or weneckii (pigmented)}}</div>"
"You are seeing a patient with a fungal infection of the scalp hair. it appears as a black nodule&nbsp;<div><img src=""paste-1ae8a35b2429f07ea0fe3a9191ea9e3372a5c277.jpg""></div><div>culture shows brown to black colonies.&nbsp;</div><div>What is the condition called, etiology and treatment?&nbsp;</div><div>{{c1::Black piedra caused by piedrae hortae. treat with a haircut and azole shampoo}}</div>"
"You are investigating a patient with a fungla infection of the facial, axillary and genital hairs. the fungus appears to be white to yellowish nodules loosly attached to the hair.&nbsp;<div><img src=""paste-3d85db0d17f1e7403b243569ef7824ffc42a85bc.jpg""><br></div><div>Upon culturing you view intertwined septate hyphae</div><div><img src=""paste-bf2312a63510af714d5ce0cf8b8f2ccbcfee7c3c.jpg""><br></div><div><br></div><div>Whats the condition and etiology of this? {{c1::White piedra caused by trichosporon}}</div>"
Subcutaneous mycosis is mainly caused by:<div>- {{c1::Sporotrichosis&nbsp;}}</div><div>- {{c1::Chromoblastomycosis&nbsp;}}</div><div>- {{c1::Mycetoma&nbsp;}}</div>
"A gardener comes to you presenting with skin necrosis.&nbsp;<div><img src=""paste-5fe2ddc3018db43a1a682375710f551eb5f17939.jpg""><br><div>You culture the offending agent and find out that it is thermally dimorphic. At 37^o its round, and at 25^o it is a septated hyphae&nbsp;<div><br><div><img src=""paste-9ddd86918d46267640646c6e4662bc59d543c0b4.jpg""><img src=""paste-573caa062e52fcbce494855331ba0a2ef96ba2ff.jpg""><br></div><div>Offending agent?&nbsp;</div><div>{{c1::<div>Sporothrix schenkii. Subcutaneous mycosis (sporotrichosis)</div><div>Can undergo systemic dissemination or pulmonary in chronic alcoholics</div>}}<br></div></div></div></div>"
Treatment of sporotrichosis:&nbsp;<div>if cutaneous: {{c1::Potassium iodide (topical or oral)}}</div><div>If disseminated: {{c1::Amphotericin B}}</div>
"A hiker in tropical areas presents to you with papules and verrucous cauliflower-like lesions on the lower extremities.&nbsp;<div><div><img src=""paste-430ed2a3fede94d5d2a65ef14e645b3f31d82935.jpg""><br></div><div>Upon further investigation you view <u>sclerotic cells in tissues</u> (globe shaped cigar colored thick walled structures)</div></div><div><img src=""paste-0821d20746c0d94cf711d7a314e7c88a845247a5.jpg""><br></div><div>Culture shows slow growing dark velvety colored septated hiphae&nbsp; with a black obverse</div><div><img src=""paste-114982ebea2bd1077a50e433ac970d89ad0a3f49.jpg""><br></div><div>Diagnosis? {{c1::Chromoblastomycosis&nbsp;}}</div>"
"A patient with a history of trauma to the foot comes to you with a deformed foot containing abscesses and granules within the draining sinuses.&nbsp;<div><img src=""paste-42b337f9eec74a775c29977e93b3aebb9facf547.jpg""><img src=""paste-61afb905270f360e31e82d2c473820c87934c629.jpg""><br></div><div>What is your diagnosis? {{c1::Mycetoma (madura foot)}}</div><div>Possible causitive agents:</div><div>Bacterial: {{c1::Actinomyces (bacteria)}}</div><div>Fungal: {{c1::Saptophytic fungi&nbsp;}}</div><div><br></div>"
The three main proteins which are produced by all retroviruses are {{c1::Gag}}, {{c1::Pol}} &amp; {{c1::env}}Gag: Core &amp; matrix proteins<div>Pol: reverse transcriptase, protease &amp; integrase</div><div>Env: Transmembrane gp&nbsp;</div>
{{c1::P24}} is the most abundant viral antigen for HIV and can be detected by ELISA to diagnose HIV
HIV includes {{c1::two:: Number}} copies of viral genomic RNA and {{c1::three:: Number}} viral enzymes<div>The viral matrix is surrounded by a matrix protein called {{c1::P17}} which lies underneath the envelope</div>Viral enzymes include RT, protease and integrase&nbsp;
When HIV infections are on mucosal surfaces they get internalized via {{c1::M}} cells by binding to {{c2::CCR5}} and {{c2::galactosylceramide}}.<div><br></div>"<img src=""paste-07535b919870debcbd5bec0f885a499bb5f01d19.jpg"">"
HIV patients develop symptoms if CD4 T cell levels go below {{c1::500}} cells/μL<div>HIV develops into AIDS if&nbsp;<span>CD4 T cell levels go below&nbsp;</span>{{c1::200}}&nbsp;<span>cells/</span><span>μL</span></div>"<img src=""paste-99c5d353f0502baa21761444e3ec7970ebf05189.jpg"">"
We suspect that the main reason for the declining viremia after the acute phase HIV infection is the development of {{c1::HIV-specific CTL (CD8)}}<div><br></div>"<img src=""paste-95cefd0cf7a5a2744a408c3d5dc38bb653b6803c.jpg"">"
Two phases for the HIV-1 infection:&nbsp;<div>-First phase where CD8 response is high and the virus resides within {{c1::monocytes}} and {{c1::memory CD4 cells}}</div><div><br></div><div>-Second phase when the virus escapes the CD8 response through mutations and starts infecting {{c1::naive CD4 T cells}}</div><div><br></div><div>AIDS appears with the depletion of {{c1::CD4 T cells (Count less than 200/)}}</div><div><br></div>
What is the reason for increased mutations in HIV? {{c1::RT has no proofreading}}
HIV will infect cells expressing the receptor CD4 and chemokine receptors including {{c1::CCR5}} and {{c1::CXCR4}}
CCR5 are expressed on {{c1::monocytes, DC, and memory CD4 cells}}<div>CRCX4 is expressed on {{c1::Naive CD4 cells&nbsp;}}</div>
Acute viremia of HIV is associated with the {{c1::R5}} strain of the virus<div>{{c1::Memory CD4 T}} cells are the reservoir for HIV</div>Two strains present: R5 and X4 strains.&nbsp;<div>Acute infection is with the R5 strain. AIDS has the X4 strain&nbsp;</div>
{{c1::Delta32}} is a mutant allele of the CCR5 receptor which exhibits slow HIV progression in carriers<div>Having the HLA alleles {{c1::B*27}} &amp; {{c1::B*57}} will delay the progression to AIDS, but having {{c1::B*35}} will accelerate it</div>
HIV escapes the immune system when {{c1::it gathers mutations and escapes CD8 detection&nbsp;}}
Once patients with HIV develop AIDS the main cause of mortality are {{c1::opportunistic infections}}<div>AIDS patients are also susceptible to cancers such as {{c1::Kaposi's sarcoma}}</div>Such as PJP/PCP(same thing) and MAC
Two retroviruses infecting humans:<div>-{{c1::HIV}}</div><div>-{{c1::HTLV}}</div><div><br></div>HIV is a lentivirus (slow grower)<div><br></div>
{{c1::HTLV}} is the only retrovirus known to cause malignancy (has an oncogene)
HIV has two proteins on the viral evelope:<div>One transmembrane protein called the fusion protein aka {{c1::gp41:: gp(x)}} which facilitates fusion with the host cell</div><div>One surface protein called attachment protein aka {{c1::gp120<span>:: gp(x)</span><span>}}&nbsp;</span><span>which&nbsp;</span>facilitates&nbsp;<span>binding with the host cell</span></div>
HIV major capsid protein is {{c1::P24}}<div>The outer matrix protein is {{c1::P17}}</div>"<img src=""paste-5b3782dba7ec29872599245ee6463d37cfa90d98.jpg"">"
The first phase of HIV replication includes {{c1::reverse transcription}} and {{c1::integration}} using virally encoded proteins<div><br></div><div>The second phase of HIV replication includes {{c1::transcription}} and {{c1::translation}} using host cell mashinery</div>
Gp120 infects CD4 receptors which are found on {{c1::helper T cells}}, {{c1::lymphocytes}}, {{c1::monocytes}}, {{c1::macrophages}} and {{c1::dendritic cells}}
Function of reverse transcriptase includes:&nbsp;<div>{{c1::RNA dependant DNA polymerase}}</div><div>{{c1::RNAse&nbsp;}}</div><div>{{c1::DNA dependant DNA polymerase&nbsp;}}</div>
The genomic sequence of HIV has two phases:&nbsp;<div>RNA phase found in the {{c1::cytoplasm or virus virus itself }}</div><div>DNA phase found in the {{c1::nucleus}}</div><div>DNA is inserted <b>randomly </b>by integrase. once inserted its caled a {{c1::provirus}}<br></div>
The HIV provirus is transcribed into one full length mRNA via the host cell mashinery called {{c1::RNA polymerase II}}Some full length become Viral RNA for packaging whereas others get translated&nbsp;
Envelope polyprotein gp160 is cleaved into gp120 &amp; gp41 by {{c1::host:: Viral or host?}} cellular protease
Normally HIV release from cells causes death EXCEPT in {{c1::macrophages}}
HIV Gag-pol polyproteins are cleaved by {{c1::viral:: Viral or host?}} proteases&nbsp;This can be targeted by Anti-proteases leading to immature viruses&nbsp;
In HIV, the initial cells that are infected within the genital tract are {{c1::macrophages}}
During the AIDS period coinfection by {{c1::herpesvirus 6}} can trans-activate transcription of silent HIV provirus, increasing replication&nbsp;
{{c1::PCR}} is the most sensitive method of detecting HIV in the bloodQuantitative PCR can estimate the viral load and estimate the stage of disease
ELISA can be used in HIV to detect viral {{c1::antigens and antibodies (but most commonly the antigen p24):: Antigens/antibody?}}
ELISA can be used to look detect hiv and is sometimes called HIV enzyme immunoassay. the drawback is {{c1::that it can be false positive}}<b>If an ELISA come out positive you must do a western blot to confirm it (more specific)</b>
In HIV treatment includes a combination of drugs which include {{c1::protease inhibitors}}, {{c1::RT inhibitor}}, {{c1::integrase inhibitor.&nbsp;}}The combination therapy includes HAART or cART (three drugs used)
In HIV treatment, protease inhibitors are used to interfere with the processing of {{c1::Gag/pol polyprotein}} which results in immature viruses unable to infect.&nbsp;<div><br></div><div>Resistance to protease inhibitors results in {{c1::lipodystrophy}} and {{c1::hyperglycemia}}</div><div><br><div>It does not affect the integrated provirus.&nbsp;</div></div>
The {{c1::viral load}} is a prognostic indicator of the rate of progression to AIDS
HAARt or cART therapy to pregnant women is given during the {{c1::second and third}} trimester, followed by administration to the newborn. Transmission via milk is also possible&nbsp;
HTLV is the only known retrovirus to cause cancers,&nbsp;<div>Cancers caused by HTLV1 {{c1::adult T cell leukemia}} and {{c1::HTLV associated myelopathy (HAM)}}</div><div>HTLV2 causes myelopathy and suspected to cause hairy cell leukemia.&nbsp;</div><div><br></div><div>Both HTLVs infect {{c1::CD4 T}} cells</div>
<div>HTLV</div>ATL presents in 2-5% of infected patients after {{c1::20-40}} years<div>HAM develops {{c1::a few}} years after infection.&nbsp;</div><div><br></div><div>HAM produces anti-HTLV-1 antibodies in the CSF, lymphocyte infiltration and {{c1::demyelination}} of spinal cord.&nbsp;</div><div><br></div><div>HAM characterised by progressive {{c1::spasticity}}, weakness of {{c1::extremities}}, {{c1::urinary and fecal}}&nbsp; incontinence</div>HAM stands for HTLV associated myelopathy
Systemic mycosis can be caused by primary pathogens such as:<div><br><div>-{{c1::Cryptococcus gattii}}</div></div><div>-{{c1::Histoplasma capsulatum&nbsp;}}</div><div>-{{c1::Blastomyces dermatitidis}}</div><div>-{{c2::Coccidiodes immitis}}</div><div>-{{c2::Paracoccidiodis brasiliensis&nbsp;}}</div><div><br></div><div>Opportunistic infections caused by any fungus in immunocompromised patients&nbsp;</div>
Primary fungal pathogens are thermal dimophs, meaning they have two phases:<div>Saprobic phase: in the form of {{c1::hyphae/mold}} in the soil at room temperature&nbsp;</div><div>Parasitic phase: in the form of {{c1::yeast}} at 37^o</div>
Blastomyces dermatitidis is an endemic in the {{c1::southeastern USA and Oio-mississipi valley around the great lakes}}"<img src=""paste-2256ed82a72f919e45b5aeceb3e0d667c754ca82.jpg"">"
Infection by systemic fungi is done by {{c1::inhalation}} of the conidia&nbsp;
Blastomyces dermatitidis yeast cells resist phagocytosis by shedding cell wall glycoprotein {{c1::(BAD1)}} and incoporporating a large amount of&nbsp;{{c1::α-1,3-glucan}}.<div><br></div><div>Host defence is cell mediated, specifically {{c1::Th1&nbsp;}}</div>α-1,3-glucan makes it difficult for detection.&nbsp;
"Possible clinical syndromes by blastomycis dermatitidis include:<div>{{c1::Pulmonary blastomyces dermatiditis (Looks like TB or lung cancer)}}</div><div><img src=""paste-8f8ebf3e86fa0a661c434ede8cce4fa0b0215ce4.jpg""><br></div><div>{{c1::<div>Disseminated blastomycosis: affects skin, bones GUT &amp; CNS</div><div></div>}}<br></div><div><img src=""paste-8d8183c2938a2e1d3439fe181127c1234f9eaaec.jpg""><br></div>"
Blastomyces dermatitidis can be stained by PAS and GMS stains.&nbsp;<div><br></div><div>Treatment in severe cases via {{c1::amphotericin B}}, and in mild cases by {{c1::itraconazole}}</div>
Histoplasma capsulatum is an endemic in southeasterns USA and ohio-mississipy valleys around the great lakes. It is common in areas contaminated with {{c1::bird/bat guano (droppings)}}<div><br></div><div>H.capsulatum survives and multiplies within {{c1::macrophages&nbsp;}}</div><div><br></div><div>Immune response is mediated by {{c1::CD4}} cells</div>
H. capsulatum is an <i>intracellular </i>infection of the {{c1::reticuloendothelial system}}<div>It can cause {{c2::chronic pulmonary cavity}}, {{c2::chronic mediastinal fibrosis}}, {{c2::chronic disseminated disease}}, {{c2::or acute disseminated disease (fatal septic shock-like)&nbsp;}}</div><div><br></div><div>Treatment via {{c1::amphotericin B}} followed by {{c1::itraconazole&nbsp;}}</div><div><br></div><div><br></div>
"Coccidiodes immitis is acquired by inhalation in {{c1::arid desert:: Tropical/ dry}} areas in USA mexico and south america<div>The primary infection is in the {{c1::lung}}</div><div>Anthroconidia will convert to <u>spherules </u>in the lung which produce endospores&nbsp;</div><div><img src=""paste-c4a135599a77027e2394a82eb5db5a28b460fad2.jpg""><br></div><div>Most cases are asymptomatic, but in severe cases it can form {{c1::san joaquin valley fever}} or {{c1::rheumatism}}</div><div><br></div><div>Treatment with amphotericin B and itraconazole. In meningeal involvement use {{c1::fluconazole}}</div>"
"Paracoccidiodes brasiliensis is acquired by inhalation or traumatic inoculation in {{c1::humid rainforests:: Desert/ rainforest?}}<div><br></div><div>It is rarely progressive. different manifestations depending on age:</div><div>young and immunocompromised patients: {{c1::lymphadenopathy}}, {{c1::organomegaly}} &amp; {{c1::bone marrow involvement&nbsp;}}</div><div>In adults: {{c1::Chronic pulmonary}} + oral {{c1::mucosal involvement&nbsp;}}</div><div><img src=""paste-fc973362b8a3e2671d246bed844e673d60e1febe.jpg""><br></div><div>Treat with itraconazole.&nbsp;</div>"
Cryptococcus gattii causes disease in {{c1::healthy:: Healthy/ immunocompromised?}} individuals found in tropical or subtropical areas.&nbsp;<div><br></div><div>Virulence determinant by the {{c1::polysaccharide capsule}} and {{c1::the ability to grow at 37^o}}</div><div><br></div><div>Can cause lung infection or miningitis</div><div><br></div><div>&nbsp;</div>
Difference btween C. gattii and C. neoformans: neoformans is {{c1::opportunistic}} whereas gatti infects {{c1::healthy individuals&nbsp;}}<div><br></div><div>How to differentiate between the strains? {{c1::Use&nbsp;CGB agar (canavanine-glycine-bromthymol blue)}}<span>&nbsp;&nbsp;</span></div><div><span>Both can cause meningitis&nbsp;</span></div>
{{c1::MHC (HLA)}} molecules are major determinants of graft rejection
Tempo of rejection reaction<div>(Type // Time // Cause)</div><div><br></div><div>{{c1::<u>Hyperacute</u>}} // minutes-hours // {{c1::<u>Preformed antibodies</u>}}</div><div><br></div><div>{{c1::Accelerated}} // Days // {{c1::Reactivation of sensitized T cells}}</div><div><br></div><div>{{c1::Acute}} // Days - Weeks // {{c1::Primary T cell response&nbsp;}}</div><div><br></div><div>{{c1::Chronic}} // Months-years // {{c1::Minor histocompatability antigens --&gt; CD8 response}}</div>Hyperacute reactions happen due to preformed antibodies which were induced by previous exposure&nbsp;
Recognition of alloantigens happens in 2 different ways:<div>- Direct allorecognition --&gt; {{c1::Foreign MHC presents foreign peptides (STRONG REACTION)}}</div><div>- Indirect allorecognition --&gt; {{c1::Own MHC presents foreign peptides of the donor}}</div>
You do a {{c1::crossmatching test}} when youre in the lookout for potential organ donors. You check for antibodies to MHC class I or II antigens, and proceed with the operation if there is no reaction, or if theres a reaction to MHC class {{c1::II}} only&nbsp;
{{c1::Mixed lymphocyte reaction (MLR)}} if we take stimulators (irradiated donor mononuclear cells) and responders (recipient mononuclear cells), mix them together and look for a reaction to assess if the donor is suitable
You are doing a mixed lymphocyte reaction to find a suitable donor. currently you have three donors with different proliferation levels:&nbsp;<div><br></div><div>D1 --&gt; 10,000&nbsp;</div><div>D2 --&gt; 1,000</div><div>D3 --&gt; 100,000&nbsp;</div><div><br></div><div>Which one is the most suitable donor? {{c1::D2. Less proliferation means less reaction to the foreign organ.}}</div>
Two drugs that block that inhibit T cell co-stimulation by blocking Cd28 (CTLA4)<div>{{c1::Belatacept}} &amp; {{c1::Abatecept}}</div><div><br></div><div>Drugs that T-cell activation using CD25-specific antibodies: {{c1::Basiliximab}} &amp; {{c1::Daclizumab}}</div>
Patients scheduled for BMT must first undergo {{c1::myeloablation (irradiation)}} to destroy own diseased BM or leukemic cells
Opportunistic protozoans infect patients, and become intense if they become {{c1::immunocompromised}}Infections are not cleared and come back when patient's immunity drops&nbsp;
"The three upcoming cases are related to protozoa.&nbsp;<div><br></div><div>Case1:&nbsp;</div><div>An immunocompromised patient comes to you with diarrhea. you take a stool sample and stain it with Ziehl-Neelsen stain, and view round oocysts with 4 sporozoites within, stained in a <u>bright red color</u>.&nbsp;</div><div><img src=""paste-6e7ba7288135e561a7ccc2227dde38665895f7f0.jpg""><br></div><div>Diagnosis? {{c1::<b>Cryprospordium </b>pravum}}</div><div><br></div><div>Case2:</div><div>An immunocompromised patient comes to you with diarrhea. you take a stool sample and stain it with Ziehl-Neelsen stain, and view a <u>ghost shadow</u>. within the slide. upon further inspection you see a round oocyst with 2 sporocysts containing 2 sporozoites each.&nbsp;<br></div><div><img src=""paste-84163622c8b6e2919040587b295986a6591d6c29.jpg""><br></div><div>Diagnosis? {{c1::<b>Cyclospora </b>cayetanensis}}</div><div><br></div><div>Case3:</div><div>An immunocompromised patient comes to you with diarrhea. you take a stool sample and stain it with Ziehl-Neelsen stain, and view an <u>oval shaped</u> oocyst with 2 sporocysts containing 4 sporozoites each<br></div><div><img src=""paste-9ffc1e85f0ea2d9a8c671733317ffb3124195fa3.jpg""><br></div><div>Diagnosis? {{c1::<b>isopora </b>belli (number of sporocysts depends on maturation)}}</div>"
The infectious stage of <b>Cryptosporium </b>pravum is the {{c1::oocyst}} stage, which is transmitted via fecal-oral transmission.&nbsp;<div>Pathology which leads to diarrhea is caused by {{c1::blunting of the intestinal villi&nbsp;}}</div><div>{{c1::80}}% of the protozoa is returned to the environment whereas {{c1::20}}% persists within the body</div><div>Oocysts are highly resistant to {{c1::chlorination}}, hence why they are found in pools&nbsp;</div>
The hallmark of cryptosporidial infection is a {{c1::watery diarrhea without RBCs or leukocytes}}<div><br></div><div>In immunocompromised patients the severity depends on {{c1::CD4 lymphocyte}} levels --&gt; rapidly fatal diarrhea</div>
"You are suspecting a protozoal infection in a patient. upon further investigation you see a body with polar filament coils injecting epithelial cells with spores.<div><img src=""paste-6ca0e7894b6a2e2b407fea2b6ad140f115bd39ea.jpg""><br><div>offending agent {{c1::Microspordia&nbsp;}}</div></div>"It belongs to fungi, not protozoa&nbsp;
Treatment for microspordia is albendazole only if it {{c1::disseminates&nbsp;}}
{{c1::Naegleria fowleri}} is a free living amoeba AKA brain eating amoeba&nbsp;<div>The trophozoites multiply by {{c1::binary fission}}.&nbsp;</div><div>This one lives in still warm fresh waters and is suspected to infect humans by penetrating the {{c1::nasal cavity}}</div><div>No {{c1::cyst}} phase if found in humans, thus it is a dead end for them&nbsp;</div><div>it infects the brain and causes {{c1::primary amebic meningoencephalitis (PAM)}}</div><div>Upon diagnosis can be found in the {{c1::CSF&nbsp;}}</div>
"Acanthamoeba species are characterized by having {{c1::spikes<br><div><img src=""paste-19705448ac8cda8c623cf364a10db7fed5d09dd3.jpg"">}}</div><div>Unlike N. fowleri which is only found in the amoeba form in tissues, Acanthamoeba are found in {{c1::both cyst and amoeba(trophozoites)}} form</div><div><br></div><div>Acanthamoeba can can cause a variety of diseases such {{c1::granulomatous amebic encephalitis&nbsp;}} in immunocompromised patients OR {{c1::Acanthamoeba keratitis</div><div><img src=""paste-47326ed1bf7ddd8f5e6a473a7bf0c53d1bb1b0b1.jpg""><br></div><div>}} which is seen in immunocompetent individuals. seen as a paracentral stromal ring</div>"
3 types of mycotic infecitions:<div>{{c1::Superficial}} --&gt; affects the skin</div><div>{{c1::Subcutaneous}} --&gt; penetrates the skin</div><div>{{c1::Systemic}} --&gt; throughout the body&nbsp;</div>
Amphotericin B is a wide range antifungal and is the treatment of choice for life-threatening {{c1::systemic:: Superficial/subcutaneous/systemic?}} mycosis. It acts by binding to {{c1::ergosterol}}, which forms pores in the fungi&nbsp;<div><br></div><div>Half life is {{c1::15}} days</div><div>{{c1::Poorly:: Readily or poorly?}} crosses the BBB</div><div>Given via IV except in {{c1::GI infections(oral) }}</div><div><br></div><div>It is also used as an antiprotozoal drug for {{c1::leishmaniasis}}</div><div><br></div><div>Resistance due to {{c1::reduced ergosterol content}} or modifying the sterol target</div><div><br></div><div>Can cause toxicity due to {{c1::low therapeutic index}}</div><div><br></div><div>Side effects include {{c1::nephrotoxicity}}</div>
Nystatin is an antifungal similar in mechanism to amphotericin B. It is too toxic for systemic use, so it only used {{c1::topically}}.&nbsp;<div>Used to treat {{c1::superficial}} or {{c1::vaginal candidiasis&nbsp;}}</div>
"Flucytosine is a synthetic pyrimidine antifungal used in combination with {{c1::amphotericin B}}. this combination is used to treat systemic mycoses and meningitis caused by {{c1::cryptococcus neoformans}} and {{c1::candida albicans&nbsp;}}<div><br></div><div>Flucytosine in combination with itraconizole treats {{c1::chromoblastomycosis&nbsp;}}</div><div><br></div><div>MOA of flucytosine is by producing <i>5-fluorouracin</i> and inhibiting {{c1::thymidylate synthase&nbsp;}}, which deprives the fungus of thymidylic acid for DNA synthesis&nbsp;</div><div><br></div><div>Amphotericin acts by making the fungus more ""holy"" and allowing more 5-FC entry to the cell&nbsp;</div><div><br></div><div>Side effects might cause reversible neutropenia and bone marrow suppression, reversible hepatic dysfunction --&gt; elevated {{c1::serum transaminases and lakaline phosphatase}} severe {{c1::enterocolitis&nbsp;}}</div>"
Ketoconazole is useful for treating {{c1::systemic:: Superficial, subcutaneous or systemic?}} mycosis. Side effects include the blockage of 11 b-hydroxylase, which suppresses {{c1::cortisol}} and {{c1::testosterone}} synthesis&nbsp;<div><br></div><div>Azoles are generally fungastatic, and interact with the enzyme&nbsp;{{c1::<span>C-14 a-</span><span>demethylase (p-450</span><span>}} to block the demethylation of ianosterol to {{c1::ergosterol&nbsp;}}</span></div><div><br></div><div>Ketoconazole is antagonized by the antifungal {{c1::amphotericin B(The target is ultimately ergosterol)}}</div><div><br></div><div>Ketoconazole is most useful to treat {{c1::histoplasmosis&nbsp;}}<br><br></div><div>Administration is oral, however <i>it does not cross the BBB</i></div><div><br></div><div><i>It is also highly teratogenic&nbsp;</i></div><div><br></div><div>By inhibiting CYP450 it potentiates toxicities of drugs such as {{c1::cyclosporine&nbsp;}}, But drugs which induce p450 such as {{c1::rifampin}} will shorten the duration of action.&nbsp;</div><div>{{c1::H2-receptor blockers}} will decrease absorption of ketoconazole</div>
Unlike ketoconazole, fluconazole does not cause {{c1::endocrine side effects}} and has {{c1::excellent CNS permeability&nbsp;}}<div>It is used prophylactically&nbsp;</div><div><br></div><div><i>Fluconazole is {{c1::teratogenic}} as other azoles&nbsp;</i></div>
Itraconazole is a broad spectrum antifungal, and is the drug of choice for {{c1::blastomycosis}}, {{c1::sporotrichosis}}, {{c1::paracoccidioimycosis}} and {{c1::histoplasmosis&nbsp;}}
Echinocandins such as {{c1::caspofungin}}, {{c1::micafungim}} and {{c1::anidulafungin&nbsp;}} work by interfering of the {{c1::fungal cell wall synthesis(b (1,3)-D-glucan,).&nbsp;}}<div><br></div><div>Caspofungin is the second-line antifungal after {{c1::amphotericin B}}</div>
Fungi that cause superficial skin infections are called {{c1::dermatophytes&nbsp;}}
The drug of choice against dermatophytes and onychomycosis (nail fungal infectioon) is {{c1::terbinafine&nbsp;}}. It acts by inhibiting fungal {{c1::<b>squalene epoxidase</b>&nbsp;}} -- accumilation of squalene --&gt; fungicidal
Griseofluvin is given for superficial mycosis and works by {{c1::disrupting the microtubules and mitotic spindle, thus inhibiting mitosis&nbsp;}}. it is generally fungastatic, induces P450 and causes hepatotoxicity&nbsp;
Approaches to anti-malarian therapy<div><br></div><div>- Acute attack used to cure malaria which has no exo-erythrocytic stage like {{c1::P. falciparum&nbsp;}}</div><div>- {{c1::Chemoprophylaxis}} when visiting an area where it is an endemic&nbsp;</div><div>- {{c1::Radical cure}} which is active against parasites in the liver</div>
Anti-malarian drugs have categories such as<div><br></div><div>-Blood schizonticides:</div><div>{{c1::Chloroquine}}, {{c1::Quinine}}, {{c1::Mefloquine}}, {{c1::Halofantrine}}</div><div>Used to remove schizonts in the blood</div><div><br></div><div>Tissue schizonticides:&nbsp;</div><div>{{c1::Primaquine}}</div><div>Used to eliminate schizonts in the liver once attacks are controlled by blood schizonticides&nbsp;</div>
Chloroquine is an anti-malarian drug which reduces fever and<i> clears blood of parasites</i> within 24 hours. this results in a radical cure in parasites with no exo-erythrocytic stage such as {{c1::P. falciparum}}.<div>Parasites which form hypnozoites in the liver such as {{c1::P. vivax}} or {{c1::P. ovale}} need further treatment with tissue schizonticide such as {{c1::primaquine}}</div>
Method of action of chloroquine is preventing the polymerization of toxic heme to {{c1::hemezoin&nbsp;}}. this will kill the parasite&nbsp;
For prophylaxis against P. ovale, P. vivax and sensitive P. falciparum we use the drug {{c1::proguanil&nbsp;}}<div><br></div><div>For resistant P. falciparum we use {{c1::pyrithamine-dapsone}}&nbsp;</div>
The drug of choice for chloroquine resistant P. falciparum is {{c1::quinine&nbsp;}}<div>Not used for chemoprophylaxis</div><div><i>Side effect includes blackwater fever</i></div>
Melfoquine is an antimalarian drug used for prophylaxis and treatment of multidrug resistant {{c1::P. falciparum&nbsp;}}<div>It acts by interfering with {{c1::transport of host material into the parasites food vacuole&nbsp;}}</div><div><br></div><div>It is given {{c1::once}} per week as a prophylaxis&nbsp;</div>
Halofantrine is an antimalarian drug used as a {{c1::stand-by drug if chemoprophylaxis fails.&nbsp;}}<div>Side effects such as {{c1::serious cardiac problems&nbsp;}}<br><div><br></div></div>
Primaquine is a tissue schizonticide which is affective against the {{c1::liver hypnozoites}} and {{c1::gametocyte}} stage of malaria.<div><br></div><div><i>Primaqine should not be used during pregnancy</i></div>
Pyrimethamine is an antimalarian drug which inibits {{c1::dihydrofolate reductase&nbsp;}}.&nbsp;<div>Acts as a blood schizonticide and sporonticide.&nbsp;</div><div><br></div><div>If megaloblastic anemia appears with pyrimethamine occurs revers with {{c1::leucovorin&nbsp;}}</div>
Anti-malarian drugs which affect the folic acid pathway include {{c1::Pyrimethamine}}, {{c1::proguanil}} and {{c1::dapsone}}
Atovaquone-proguanil combination is useful against {{c1::chloroquine-resistant P. falciparum.&nbsp;}}<div><br></div><div>Atovaquone MOA is by inhibiting {{c1::mitochondrial processes&nbsp;}}</div><div><br></div><div>Proguanil produces cycloguanil, which will inhibit {{c1::dihydrofolate reductase}}</div>
You are seeing an immunocompromised patient with signs of an infection. you give antibiotic treatment but the patient doesnt respond to it. two possible reasons for that:&nbsp;<div>- {{c1::The bacteria is resistant to the therapy&nbsp;}}</div><div>- {{c1::it is not a bacterial infection (think fungal)}}</div>
Fungi causing opportunistic infections include:&nbsp;<div>{{c1::Aspergillus}}</div><div>{{c1::Candida}}</div><div>{{c1::Cryptococcus neoformans/gatii&nbsp;}}</div><div>{{c1::Pneumocystic jiroveci (PCP/PJP)}}</div><div>{{c1::zygomyces&nbsp;}}</div>Candida and aspergillus are most common
"You are seeing an immunocompromised patient with a fungal infection. upon microscopy you see yeast-like cells with pseudohyphae.&nbsp;<div><img src=""paste-f581a1378c63ea644a23d0d9882b6e9558e3d6b7.jpg""><br></div><div>Upon further investigation, once suspended in serum the fungus forms germ-tubes&nbsp;</div><div><img src=""paste-a9d749fbc25027be8aacab6747f7ff73189b5380.jpg""><br></div><div>You are now certain that this fungus is {{c1::Candida albicans&nbsp;}}</div><div><br></div>"<i>Candida albicans can be differentiated from other candida by the formation of germ-tubes&nbsp;</i>
The source of a Candida infection is usually the patients own flora, and rarely via exogenous transmission <i>EXCEPT </i>{{c1::C. auris&nbsp;}}
50-70% of nosocomial bloodstream fungal infections is caused by {{c1::C. albicans}}
Candidiasis syndromes<div><br></div><div>Chronic mucocutaneous candidiasis seen in T-cell deficiency</div><div><br></div><div>UTI common in {{c1::diabetic patients}}</div>
Candida auris transmission happens exogenously and has a high mortality rate. The main concerns include:<div>- {{c1::Multi-drug resistance}}</div><div>- {{c1::Difficult to identify with standard lab methods}}</div><div>- {{c1::causes outbreaks in healthcare settings&nbsp;}}</div>
Lab tests for C. auris includes {{c1::MALDI-TOF mass spectrometry}}
Treatment for candidiasis<div>-Mucosal and cutaneous:&nbsp;</div><div>{{c1::<div>Topical azoles ointments&nbsp;</div><div></div>}}<br></div><div>-Urinary candidiasis:&nbsp;</div><div>{{c1::Fluconazole (C. glabrata is resistant to fluconazole}}</div><div><br></div><div>-Solid organ/ hematogenous infections:</div><div>{{c1::Echinocandins&nbsp;}}</div><div>{{c1::Fluconazole oral/ IV}}</div>
"An AIDS patient comes to the clinic with signs of meningitis. CSF culture shows a yeast cell. Further staining with indian ink shows a halo corresponding with the extracellular polysaccharide capsule&nbsp;<div><img src=""paste-940f6eb6765a7c2ccac2692adc4f3bbd87e59e1d.jpg""><br></div><div>Your main suspect is a fungal infection, but which is it?&nbsp;</div><div>{{c1::Cryptococcus neoformans&nbsp;}}</div><div>What treatment do you prescribe?&nbsp;</div><div>{{c1::Amphotericin B +flucytosin for 2 weeks + 8 weeks of oral fluconazole&nbsp;}}</div>"<i>Infects patients with CD4&lt;200&nbsp;</i><div><i>Can cause pulmonary cryptococcus (bilateral or nodular infiltrates)&nbsp;</i></div><div><i>Disseminated cryptococcus</i></div><div><i>MOST COMMONLY MENINGITIS WITH CNS INF</i></div>
"A patient presents to the clinic with an allergic response similar to asthma with present eosinophilia. upon further history taking you find out he is a gardener, and that he often sees mold growing in his garden but he doesnt pay any attention to it.&nbsp;<div>You culture his sputum and find blue conidial heads</div><div><img src=""paste-e2dc0183a376abe2ae8fb44284bd63e034f73b12.jpg""><br></div><div>Diagnosis?&nbsp;</div><div>{{c1::Allergic broncho-pulmonary aspergillosis (ABPA) caused by aspergillus}}</div>"
Aspergillus can cause:&nbsp;<div>Allergic broncho-pulmonary aspergillosis (ABPA) by {{c1::inhalation of the antigen into the lungs}}</div><div>Aspergilloma by {{c1::aspergillus infection of the lungs in pre-existing cavities (after a TB infection) }}</div>
Patients at risk of developing invasive pulmonary aspergillosis (IPA) are:<div><span>{{c1::Those with persistant granulocytopenia&nbsp;}}</span><div>{{c1::<span>defective granulocyte function</span></div><div>}}</div><div>{{c1::<span>on corticosteroid therapy&nbsp;</span></div><div>}}</div><div><span>{{c1::AIDS patients&nbsp;}}</span></div></div><i>Granulocytopenia + pulmonary infiltrates on CXR + fever =&gt; IPA!!</i>
Diagnosis of <i>invasive </i>Aspergillus done mainly by {{c1::serum glactomannan test&nbsp;}}
Pneumocystis jiroveci has 3 developmental forms:&nbsp;<div>{{c1::Trophic form}}--&gt; {{c1::Precyst}}--&gt; {{c1::Cyst form}}</div>
"An AIDS patient comes to you presenting with fever, chills, non-productive cough, progressive dyspnea, wight loss and respiratory failure. BAL was taken and you were able to see cysts under the microscope&nbsp;<div><img src=""paste-e5e46023489b98aaae05c1120c671c727adfd6ae.jpg""><br></div><div>Diagnosis: {{c1::Pneumocystis jiroveci (PCP/PJP)}}</div>"<i>this organism is not culturable</i><div><i>First line treatment is trimoxazole&nbsp;</i></div>
The strongest risk factors for excess mortality in HIV infections is viral load greater than {{c1::400}} copies/ml and CD4+ levels less than {{c1::200}} cells/ml
In HIV life cycle it binds to different receptors and has a different function for each.&nbsp;<div>CD4 receptors for {{c1::binding}}</div><div>CCR5/ CXCR4 for {{c1::fusion}}</div>
NRTI mechanism of action is by interrupting HIV replication via competitive inhibition of {{c1::reverse transcriptase and termination of the DNA chain&nbsp;}}"<b><img src=""znwYRz4Fh-EIOO_U9v6vmS_Qb2toa81Hd68V1CSjUTlFI50gYS4bw8St2mbznSfoq7e0u0EBkpD84MLAW7sg4_bst3qVaWMc7OcbfVdfGS1SELsK89dF3sP3SuuuSISGO8m1.png""></b>"
NRTI's are prodrugs and absorption isnt affected by food, except {{c1::didanosine}} which must be taken on an empty stomach
Didanosine is a NRTI and should NOT be combined with {{c1::ribavirin}}
NNRTI method of action is by {{c1::noncompetitive binding to the p66 unit of reverse transcriptase at the allosteric site resulting in a conformational change.&nbsp;}}"<b><img src=""Xt_B8gTErVyWM_CP6REuuQ8WteO_lp-eUdxK65ra6M5n-dd3b10pZLzf-mAt4IR5oukdYpRTBvqe77_NcEGWAOUyjKXzkLFu-99ydC3mXkFJaUzMw02Kr-aGD4QbWUjeFu_r.png""></b>"
Protease inhibitors are an integral part of HAART and work by {{c1::competitively binding to HIV protease subsequent cleavage of gag-pol polypetide resulting in immature viruses&nbsp;}}"<b><img src=""Z4LaKzpE3mcDv3sNFdMP_r9olQjpFflwnwLseMRs5AxfzJOjxh9twtNDrvoev58x_dlgc22pMuEEopGc42ROt_NL01L7pQRwYwSTIjWafklLeHhFyfCzp1wjnoFvzINvUALl.png""></b>"
Entry inhibitors is a chemokine {{c1::CCR5}} co-receptor agonist. The best example drug for this is {{c1::maraviroc}}
An example for fusion inhibitors in HIV drugs is <b>enfuvirtide</b>. method of action is {{c1::binding to HR1 and preventing gp41 conformational change and fusion}}"<b><img src=""8udLYvPIOGJubWrKfzibU6dqPGMfgt_mxU4wtOPA8F5_WIzOE87kdv_Y4m7YabLID9El7Lu7EpLHtiWrTXslEaqOxNKIeWG39_78tqGWv17tQ7lWjBhQ3vJ0Kx0kI2HYNe1J.png""></b>"
HIV integrase inhibitors include raltegravir, elvitegravir, dolutegravir (-gravir). method of action is by {{c1::competitively inhibiting strand transfer reaction by binding metallic ions in active site}}
Arboviruses are transmitted to man via {{c1::blood sucking arthropods like mosquitoes or flies (from the initials ARthropod BOrne)&nbsp; &nbsp;}}<div>The dead end for most arboviral infections is {{c1::human (except dengue and yellow fever)}}</div>
Arboviruses belong to 3 main families:<div><br></div><div>{{c1::Togaviridae}}</div><div>{{c2::<div>+sense RNA virus. includes EEE, WEE, VEE</div><div></div>}}<br></div><div>{{c1::Bunyaviridae}}</div><div>{{c2::<div>-sense RNA virus. includes sandfly fever, RVF, CCHF</div><div></div>}}<br></div><div>{{c1::Flaviviridae&nbsp;}}</div><div>{{c2::+sense RNA. includes Dengue, yellow fever, Japanese encephalitis}}</div><i>All of them are enveloped RNA viruses&nbsp;</i>
Man-arthropod-man cycles in arboviral infections can be caused by {{c1::dengue}} or {{c1::urban yellow fever}}.&nbsp;
Arboviral infections can manifest in 3 types of illnesses:&nbsp;<div>-{{c1::Fever and rash}}</div><div>-{{c1::Encephalitis (VEE,EEE,WEE,St Louis encephalitis, Japanese encephalitis)&nbsp;}}</div><div>-{{c1::Hemorrhagic fever (yellow fever, dengue, C-CHF)}}</div>
A patient presents to you with hemorrhagic fever and shock. Serology tests show that that he was previously infected with a dengue serotype, and that this is another dengue serotype infection. explain the pathogenesis&nbsp;<div>{{c1::There are 4 different serotypes. having antibodies to serotype 1 will not neutralize serotype 2, but will exacerbate the infection by being uptaken by monocytes and producing a cytokine storm--&gt; shock }}</div>"<b>&nbsp;</b><img src=""paste-5a77966082a2d943aa04a14096a4991aa4aa3f42.jpg"">"
"A farmer comes to you with what appears to be a painless black swollen postule on his pointing finger&nbsp;<div><div><img src=""paste-ddb0045ac4f423644a57cc4025ff0472b47e8638.jpg""><br></div><div>Upon further investigation you find blunt ended gram positive streptobacilli which produce endospores in non-favorable conditions.&nbsp;</div></div><div><img src=""paste-e0f10f60dcdd2f99bbdf7b3a06b623d09ec9bc0c.jpg""><br></div><div>you find out that it is capsulated with poly-D-glutaminic acid and is non-motile and <b>non-hemolytic</b>. It produces endotoxins such as edema factor and lethal toxin&nbsp;</div><div><br></div><div>Diagnosis and offending agent? {{c1::Cutaneous anthrax infection by Bacillus anthracis&nbsp;}}</div>"<i>B. anthracis can cause cutaneous anthrax, pulmonary anthrax (via inhallation of spores--&gt; hemorrhagic lymphadenitis + pneumonia) or GI anthrax (usually in animals).&nbsp;</i>
"A patient comes to you complaining of a stomach-ache and diarrhea which was later diagnosed as food poisoning. He said that a few days ago he was strolling down the street and eating food from street vendors (possibly not under hygienic conditions) and started vomitting a couple of hours later. Stool culture shows gram positive bacilli producing enterotoxins similar to ETEC.&nbsp;<div>Blood culture shows STRONGLY hemolytic colonies&nbsp;</div><div><img src=""paste-bc251a893ab541b22177ff0ceb37ea23b99ba128.jpg""><br></div><div>Offending agent? {{c1::Bacillus cerus&nbsp;}}</div>"<i>Once the street food cools down the bacteria produces toxins which is the reason for our presentation.&nbsp;</i><div><i><br></i></div><div><i>Do not confuse with B. anthracis since this one is hemolytic, and anthracis isnt&nbsp;</i></div>
Listeria monocytogenes escapes the phagosome due to {{c1::listeriolysin O}}<div><br></div><div>It is inherently resistant to {{c1::cephalosorins&nbsp;}} treat with ampicillin and trimoxazole&nbsp;</div>
"After a mother gives birth the baby presents with meningitis and granulomatosis infatiseptica. you take the history of the mother and find out that she had a previous abortion which raises concerns. you culture the offending agent and find aerobic gram positive beta hemolytic colonies&nbsp;<div><img src=""paste-e9a030a540670f15aa28d0d934ecc22b0fda30c1.jpg""><br></div><div>The bacteria appears to be coccobacilli shaped and escape the phagosomes for some reason. They are CAMP test positive. investigation of the patients home shows that her fridge which is set to 4 ^oC harbours the same offending agent&nbsp;</div><div><br></div><div>Offending agent? {{c1::Listeria monocytogenes}}</div>"<i>They escape the phagosome due to listeroilysin O</i>
"A patient comes to you with myocarditis and neuritis. Blood cultures are negative, and the only infection you can find is in the upper respiratory tract. Upon further investigation you find out that the offending agent consists of small, non motile, not encapsulated gram positive rods.&nbsp;<div><img src=""paste-798dfbd73cf6b0055dcbb5ea634711d1d3f04188.jpg""><img src=""paste-a125976472f63078ac6a9b7a3767ec666c01d636.jpg""><br></div><div>Offending agent? {{c1::Cornynebacterium diptheriae (C. diptheriae)}}</div><div><br></div><div><br></div>"
C. diphtheriae virulence factor is a phage coded {{c1::diphtheria toxin}} which acts systemically&nbsp;<div>some are highly resistant to antibiotics (C. jeikeium) use {{c1::vancomycin&nbsp;}}</div>
"You culture diphtheria on selective mediums such as&nbsp;<div>{{c1::tellur containing medium}}</div><div>{{c1::Loeffler medium&nbsp;}}</div><div><img src=""paste-c777fc65088acb43529c7438c9e7725f0d78f1e4.jpg""><br></div><div><br></div><div>{{c2::Albert}} or {{c2::Neisser}} stains used to visualize them (looks like matchsticks)</div><div><img src=""paste-28d227dec44a6afde40924d35342426031113f47.jpg""><br></div><div><br></div>"
Nocardia is {{c1::penicillin}} resistant&nbsp;
Rod shaped aerobic gram positive bacteria include:&nbsp;<div><br><div>{{c1::Bacillus anthracis}}&nbsp;</div></div><div>{{c1::Bacillus cerus}}&nbsp;</div><div>{{c1::Listeria monocytogenes}}</div><div>{{c1::Corynebacterium diphtheria}}&nbsp;</div><div>{{c1::Nocardia&nbsp;}}</div><i>Sorry to do this to you but you gotta know em&nbsp;</i>
"All spirochaetales bacteria are culturable except {{c1::treponema&nbsp;}}<div><br></div><div>They move with the presence of an {{c1::endoflagellum}} with rotation and flexion</div><div><img src=""paste-fd49576651833d12a3e1d8d87ad8a711c6e1a6e8.jpg""><br></div><div><br></div>"
A patient with a spirochaetales infections is given antimicrobials, but for some reason develops a fever. What is this reaction called? {{c1::Jarisch-Herxheimer reaction}}
"A patient from tropical areas comes to you with what appears to be an elevated crusted skin lesion&nbsp;<div><img src=""paste-ddbaa52a947107764fca613707d70e6d63c1bb07.jpg""><br></div><div>Culture was proven to be not possible since this strain is not-culturable, but you do find a spiral shaped bacteria&nbsp;</div><div><img src=""paste-bbd7377775f0ab7718a117b9c24a01c72f786aa2.jpg""><br></div><div>Serology tests showed that the patient is positive for syphilis, but T. pallidum ssp. pallidum is not present.&nbsp;</div><div><br></div><div>What's your diagnosis and offending agent? {{c1::Yaws/ framboesia caused by Treponema pallidum ssp. pertenue&nbsp;}}</div>"
"A patient from a deserty environment (lets say Saudi Arabia) comes to you presenting with oral mucosal lesions&nbsp;<div><img src=""1-s2.0-S1286457901015131-fx4.jpg""><br></div><div>You find another patient with a later stage of the same disease forming a gumma on the skin (but can be also found in bones and nasopharynx)&nbsp;</div><div><img src=""5.jpg""><br></div><div>You later found out that the two same patients live in unhygienic conditions and share utensils&nbsp;</div><div><br></div><div>Culture was not possible since its non-culturable, but you do view spiral bacteria</div><div><img src=""paste-bbd7377775f0ab7718a117b9c24a01c72f786aa2.jpg""></div><div>Serology tests were positive for syphilis&nbsp;</div><div><br></div><div>What's the disease and whats the offending agent? {{c1::Bejel/ Endemic syphilis caused by Treponoma pallidum ssp. endemicum&nbsp;}}</div>"
"A patient from south america presents to you with pruritic papules on the skin, which later manifested into discoloration and scarring of his skin.&nbsp;<br><div><img src=""paste-f5293095512c7e8f62b2c63304c85f164bc13056.jpg""></div><div>You find out that this bacterium is non-culturable, but it is spiral shaped which gives you a lead&nbsp;</div><div><img src=""paste-bbd7377775f0ab7718a117b9c24a01c72f786aa2.jpg""></div><div>Patient said that his wife has the same condition and you know that it spreads by direct contact.&nbsp;</div><div>a serology test was done and and the patient was positive for syphilis.&nbsp;</div><div><br></div><div>Disease and offending agent? {{c1::Carate/Pinta caused by Treponema pallidum ssp. carateum&nbsp;}}</div>"
"<div><span>Case1:</span><br></div><div>A man came in presenting with a chancre on his penis.&nbsp;</div><div><img src=""syphilis_primary_male.png""><br></div><div>This lesion appears to be hard and painless, but nontheless the patient is worried. You go for a swab and see lots of exudate coming out.&nbsp;</div><div>upon biopsy you see peri and onliterative endarteritis&nbsp;</div><div>You ask the patient about his sexual life and and he says that he actively visits prostitutes without using condoms.&nbsp;</div><div>Diagnosis and offending agent?<span>{{c1::</span><span>&nbsp;Primary syphilis caused by Treponema pallidum ssp. pallidum&nbsp;}}</span></div><div><br></div><div>Case2:&nbsp;</div><div>A woman comes to you complaining of rash on her torso and limbs that comes and goes.&nbsp;</div><div><img src="".jpg""><br></div><div>You ask about the sexual history and find out that one of her previous partners has the same symptoms.&nbsp;</div><div>Serological testing is positive for syphilis.&nbsp;</div><div>Diagnosis and offending agent?&nbsp;</div><div>{{c1::Secondary syphilis by Treponema pallidus ssp. pallidus}}</div><div><br></div>"<i>Trust me It's more painful coming up with this case than reading it.</i>
"How do you diagnose treponema species since theyre not culturable?&nbsp;<div>{{c1::<div>Use direct fluorescent antibody&nbsp;</div><div><img src=""FTA-ABS-Test-Result.jpg""></div>}}<br></div><div>OR&nbsp;</div><div>{{c1::<div>Dark field microscopy&nbsp;</div><div><img src=""UnpleasantAdorableGnat-max-1mb.gif""></div>}}<br></div>"Holy shit gifs work here<div>Can also use many other tests&nbsp;</div>
"Non-treptonemal tests include:&nbsp;<div><br></div><div>{{c1::Rapid plasma reagin (RPR) used for screening&nbsp;}}</div><div><img src=""paste-30474bb2b4b0117466f81b2981b49a5420fb14b5.jpg""><br></div><div><br></div><div>{{c1::Veneral disease research laboratory (VDRL) used for screening/therapy monitoring&nbsp;}}</div><div><img src=""paste-99169e9674f2fac07efbde5d5f6d4b80837252ae.jpg""><br></div>"
"Treponemal tests include:&nbsp;<div><br></div><div>{{c1::Treponema immobilization (TPI)}}&nbsp;</div><div><img src=""paste-1d55070089b24d05b7e70b34aaa327e24cc380dc.jpg""><br></div><div><br></div><div>{{c1::Fluorescent treponemal antibody absorption (FTA-Abs) (separates pathogenic antibodies from non-pathogenic treponema antibodies<span>}}</span></div><div><img src=""paste-07c166f0908196e699b9ca462505ae7b79e8b198.jpg""><br></div><div><br></div><div>{{c1::Treponema passive hemagglutination (TPH)}}</div><div><img src=""paste-d17422cc00f70547e2d22a31fb536b68eefc0e93.jpg""><br></div><div><br></div><div>+ Immunoblot &amp; ELISA&nbsp;</div>"
Treatment of syphilis is {{c1::penicillin}} or tetracycline
{{c2::Borrelia recurrentis's}} vector is the {{c1::human body louse}} and causes {{c1::epidemic relapsing fever<div></div>}}<div>{{c2::Borrelia burgdorferi's}} vector are {{c1::ticks}} and causes {{c1::lyme disease&nbsp;}}</div>
"You are a prison's physician in some backwards third world country with poor hygiene. You notice that your prisoners are developing relapsing fever, and some&nbsp; are dying of myocarditis, cerebral hemorrhage and liver failure. upon investigation you notice that your prisoners are infested with the human body louse. You check the peripheral for bacteria and culture spiral-like bacteria with large coils stained by giemsa (but can be stained with wright too)<div><img src=""paste-a634e6287433445f114c96077c7c1e526d355a90.jpg""><br></div><div>Disease &amp; offending agent?&nbsp;</div><div>{{c1::Epidemic relapsing fever caused by Borrelia recurrentis&nbsp;}}</div><div><br></div>"
"Explain the relapsing fever of B. recurrentis.<div>{{c1::<div>B. recurrentis has the ability to change the antigens which the antibodies target. Once most the bacteria are killed you appear normal, but it changes the antigen, previous antibodies are useless and get fever again</div><div><img src=""paste-896228d66faf5e02840784196322a9711dd6c202.jpg""></div>}}<br></div>""<i>This is why serology is of no use</i><div><img src=""who_the_fuck_are_you_identify_yourself.png""><i><br></i></div>"
"Imagine this:&nbsp;<div>You are a resident somewhere near a forest &amp; tall grass, and see a patient appearing with a bullseye like skin rash&nbsp;</div><div><img src=""paste-98332056169d63c22251d18e16953a2cb9f5b096.jpg""><br></div><div>What's the diagnosis, offending agent and vector?&nbsp;</div><div>{{c1::Lyme disease, caused by Borrelia burgdorferi and transmitted by ticks (found in forests/ tall grass)}}</div>"
To grow leptospira needs&nbsp;<div>{{c1::oxygen (obligate aerob)}}</div><div>{{c1::30 ^oC}}&nbsp;</div><div>{{c1::Protein rich medium (fletcher)}}</div><div>{{c1::High pH}}</div>
"Imagine this:&nbsp;<div><br></div><div>You are a physician in some third-world country. a patient appears with flu-like symptoms but is dismissed because it doesnt appear to be that serious. About 3 weeks later the patient presents with severe icterus (jaundice)</div><div><img src=""paste-ee6ab637bff16e54ea3defde1a281f1d333993f2.jpg""><br></div><div>and hepatocellular necrosis, renal failure, and pulmonary hemorrhage (Weil disease) You couldnt detect the offending agent in the blood at this time, but could have when the patient appeared with flu-like symptoms.&nbsp;</div><div><br></div><div>What's the offending agent and how do you prevent this?&nbsp;</div><div>{{c1::Leptospira interrogans. Prevent by vaccinating animals}}</div><div><br></div>"
Crimean- congo HF is an endemic in {{c1::congo/ eastern europe &amp; asia&nbsp;}}<div><br></div><div>The reservior includes domestic and wild animals (cattle)</div><div><br></div><div>Transmission is via {{c1::ticks}} or {{c1::direct contact with blood/fluid}}</div>
"A patient which works in a slaughterhouse comes to you with a sudden headache, fever, chills, myalgia, dizziness, neck pain, stiffness and pharyngitis.&nbsp;<div>Upon inspection you see that he developed petechia and ecchymosis.&nbsp;</div><div><img src=""Crimean-Congo-Hemorrhagic-Fever-CCHF-650x360.jpg""></div><div><br></div><div>The patient says he has epistaxis, hemoptysis (coughing out blood), hematouria, conjunctivitis and appears flushed in the face.&nbsp;</div><div>You dont know how to manage this patient, and he dies during the second week due to multi-organ failure.&nbsp;</div><div><br></div><div>What was the disease?</div><div>{{c1::<div>Crimean-congo HF</div><div><div></div></div>}}<br></div>"Incubation period is 3-9 days.&nbsp;
<div>Imagine this: you are a sheep herder somewhere in africa and you notice that all your sheep 100% abort their pregnancies. almost 90% of your young sheep die and 50% of the older animals die too. <i>(this is just an african horror story)</i></div><div><br></div><div>Now imagine this: you are now the physician of said sheep herder and notice that he developed hemorrhagic fever, retinitis and encephalitis about 2 weeks after his tragedy.</div><div>The herder didnt slaughter the animals, but you know that the mosquito Aedes is present in the environment.&nbsp;</div><div><br></div><div>What's the disease?&nbsp;</div><div>{{c1::<div>Riff valley hemorrhagic fever.<span>}}</span></div></div><u>Hemorrhagic fever presents in &lt;1% of infected individuals, and mortality rate is &lt;5%.&nbsp;</u><div><u>Retinitis and ecephalitis develops 1-4 weeks following infection.&nbsp;</u></div><div><u>Transmission via infected blood contact/ mosquito aedes&nbsp;</u></div>
"Imagine this: you are a health worker somewhere in central africa and you see a sudden surge in severe hemorrhagic fever. Patients are first presenting with a headache, fatigue and fever then develop into vomitting blood, bruising, bleeding from the nose, mouth and anus, and lastly they develop seizures, massive internal bleeding and die on the 12th day.<div>Your colleagues started taking precautions and are wearing hazmat suits to look for the underlying cause. what they found is a virus infection monocytes, macrophages, dendritic, endothelial and epithelial cells.&nbsp;</div><div><img src=""648x364_Ebola_Virus_and_Disease.jpg""><br></div><div>This is what they found.&nbsp;</div><div>Cause? {{c1::Ebola&nbsp;}}</div>"
A patient comes to you with an entamoeba histolytica infection. what conditions do you expect him to have? {{c1::Amebic colitis}} and {{c1::liver abscesses&nbsp;}}<i>E. dispar &amp; E. moshkovskii do NOT cause pathogenesis, but look like E. hiistolytica&nbsp;</i>
E. histolytica infections usually seen in developing or under developed countries, and its is more commonly seen in {{c1::men:: Men/ Women?}}, but affects children equally&nbsp;
"A patient comes to you presenting with bloody diarrhea, right upper quadrant pain due to liver abscesses and amebic colitis. Upon taking a biopsy of the colon you see a flask-shaped ulcer<div><img src=""36875tn.jpg""><br><div><span>Further investigation shows an invasive trophozoite with one nucleus with multipe RBCs within the cytoplasm&nbsp;</span><br></div><div><div><img src=""36871tn.jpg""><br></div><div>What's the offending agent?&nbsp;</div><div>{{c1::Entamoeba histolytica&nbsp;}}</div></div></div>"<i>The cyst form has multipe nuclei and is infective</i><div><i>the trophozoite form has one nucleus and is invasive (can form&nbsp;<span>abscesses</span><span>&nbsp;throughout the body)</span></i></div>
E. histolytica treatment<div><br></div><div>If patient is colonized with the parasite:&nbsp;</div><div>{{c1::<div>Iodoquinol (amebocide) + paromomycin (antibiotic)<span>}}</span></div></div><div><br></div><div>Invasive amebiasis:</div><div>{{c1::Nitroimidazole}}</div><div><br></div>
Giardia is resistant to {{c1::chlorination (just like cryptospordium)}} and has a low inoculum of about {{c1::10-25}} cysts
"A patient comes to you presenting with malabsorption, diarrhea, foul-smelling stools and gas, boating and abdominal cramps.&nbsp;<div>Upon stool examination you&nbsp;<span>find cyst forms of said organism&nbsp;</span></div><div><img src=""31XzWv4eJzL._SX342_.jpg""><br></div><div><br></div><div>You look into the small intestine of the same patient and find&nbsp;<span>a flagellated kite shaped body with two nuclei</span></div><div><img src=""Giardia_trophs.jpg""></div><div><br></div><div>Organism? {{c1::Giardia lamblia&nbsp;}}</div>"
Picornaviruses can be divided into two groups:&nbsp;<div>{{c1::Enteroviruses (includes polio &amp; HepA)}}</div><div>{{c1::Rhinoviruses&nbsp;}}</div>
Enterovirus pathogenesis:&nbsp;<div><br></div><div>Entry via: {{c1::aerosols or ingestion}}</div><div>Replication in the {{c1::oropharynx}}, {{c1::tonsils}} &amp; {{c1::peyers patches.}}</div><div><br></div><div>Primary viremia within the {{c1::circulation}}, secondary viremia in {{c1::targeted tissues&nbsp;}}</div>"<img src=""paste-19187899cbe576805689a9f58958867b7430c1d3.jpg"">"
Poliovirus is a {{c1::naked:: Naked// Enveloped?}} capsid making it resistant to acid, bile and detergents<i>Will survive stomach acid when ingested</i>
Poliomyelitis is an acute enteroviral infection of the {{c1::spinal cord}} causing {{c1::neuromuscular paralysis&nbsp;}}"Infects the ventral horn<div><img src=""paste-b9bd19223cd1881bbe8aedcba16e4c2866ca0cc9.jpg""><br></div>"
Most poliovirus infections {{c1::are subclinical.:: are subclinical// cause poliomyelitis?}}In serious acute infections of the CNS causes poliomyelitis. other than that its rare&nbsp;
Poliovirus features:<div><br></div><div>-{{c1::RNA:: DNA/RNA?}} virus</div><div>-{{c1::Naked:: Enveloped or non?}}</div><div>-Require {{c1::primate}} specific membrane receptor</div><div>-{{c1::Humans the the only natural host:: List the natural hosts}}</div><div>-{{c1::3:: How many}} antigenic subtypes</div><div>-{{c1::Fecal-oral}} route of transmission&nbsp;</div>
Poliovirus infections syptoms are mostly {{c1::subclinical}} or {{c1::with mild gastroenteritis}}<div><br></div><div>For successful invasion of CNS it needs a {{c1::viremic phase or travels via nerve endings of the gut}}</div><div><br></div><div>After CNS invasion symptoms include {{c1::aseptic meningitis with back pain and muscle spasm&nbsp;}}</div><div><br></div><div>Once it reaches the CNS the outcomes are devastating because of {{c1::the highly cytopathic nature of the virus&nbsp;}}</div>
Poliovirus affect all age groups, but {{c1::childern:: Adults or childern?}} are more susceptible<i>Adults have qcquired immunity</i>
Once poliovirus reaches the CNS it preferentially replicates within the {{c1::motor neurons located in the anterior horn}} of the spinal cord. The virus leads to death of the neuron --&gt; paralysis&nbsp;
Patients infected with the poliovirus can manifest a range of symptoms, including:<div><br></div><div>-{{c1::Asymptomatic (95%)}}</div><div>-{{c1::Abortive poliomyelitis (mild febrile illness )}}</div><div>-{{c1::non-paralytic poliomyelitis (aseptic meningitis)&nbsp;}}</div><div>-{{c1::Paralytic meningitis (flaccid paralysis. death of motor neurons. Can be fatal if infecting the brain stem--&gt; respiratory paralysis)}}</div>"<img src=""paste-a4f3b05d9ed28b13f3262d12ba542aca0c9d3bc5.jpg"">"
A patient with crutches comes to you presenting with mid-day fatigue, progressive weakness, decreased muscle mass and pain, all with unclear pathogenesis. you are then informed that she suffered from poliomyelitis several years prior. what does she have?&nbsp;<div><br></div><div>{{c1::Postpolio syndrome (PPS) presenting 25-30 years after the resolution of illness}}</div>
Poliovirus can be isolated from throat swabs,feces ad rectal swabs, but rarely from {{c1::CSF}}<div><br></div><div>Requires molecular techniques to differentiate between {{c1::wild}} and {{c1::vaccine}} type</div><div><br></div><div>Immunity to strain after infection or vaccination is {{c1::permanent:: Permanent// transient? }}</div>
Why is oral polio vaccination preferred over injection?&nbsp;<div><br></div><div>-{{c1::interrupts oral route of transmission by inducing IgA in GI&nbsp;}}</div><div>-{{c1::More readily accepted than the injected killed vaccine}}</div><div><br></div>
quarantine of patient with polio is NOT effective because {{c1::fecal excretion occurs prior to onset of symptoms}}
Chlamydia are {{c1::obligatory intracellular parasites:: Intra/extracellular?}}&nbsp;<div><br></div><div>They are gram {{c1::negative}}</div><div><br></div><div>They have almost no {{c1::peptidoglycan&nbsp;}}</div>
Chlamidia uses the {{c1::elementary}} body to infect cells.&nbsp;<div>once infected, they turn into {{c1::reticulate}} bodies to multiply</div><div>Duplication happens within the {{c1::inclusion}} body or vacuoule</div>
Chlamidia trachomatis has 3 biovariantst:&nbsp;<div>MoPn --&gt; {{c1::pneumonia of mice (no human significance)&nbsp;}}</div><div>TRIC --&gt; {{c1::inclusion conjunctivitis}}</div><div>LGV --&gt; {{c1::Lymphogranuloma venerum (STD)}}</div>
"A patient comes to you with what seems to be conjunctivitis which moved to the cornea causing scarring, pannus and blindness<div><img src=""paste-53d052c60094326b9c1690420e68bf1509b71a6f.jpg""><br></div><div>You look for an offending agent and found a small gram negative bacteria with no peptidoglycan. it is an obligatory intracellular bacteria which forms inclusion bodies. there was no genital involvement</div><div><img src=""paste-7abc9328ae767cc53090c197c99177839e477d76.jpg""><br></div><div>What is the disease, the offending agent and the biovariant of the offending agent?&nbsp;</div><div>{{c1::Trachoma caused by chlamidia trachomatis biovariant TRIC}}</div>"
Chlamidia trachomatis biovariant TRIC serovariant D-K can cause various {{c1::genital}} and {{c1::eye}} infectionsSerovariants A,B,Ba,C cause trachoma only.&nbsp;
"A patient comes to you with enlarged lymph nodes, bubos and fistulas in the inguinal region. Transient ulcerations are also present. Upon biopsy you notice a small gram negative bacteria with no peptidoglycan. they are obligatory intracellular and form inclusion bodies&nbsp;<div><img src=""paste-7abc9328ae767cc53090c197c99177839e477d76.jpg""><br></div><div>Upon further questioning you are informed that this person doesnt use condoms&nbsp;</div><div>Whats the condition, offending agent and biovariant?&nbsp;</div><div>{{c1::Lymphogranuloma venerum caused chlamydia trachomatis LGV biovariant. possibly by serotypes L1-L3}}</div>"
A bird handler came to you with pneumonia, meningoencephalitis and pericarditis &amp; myocarditis. Initially his symptoms started to be flu-like but it progressed into pneumonia.&nbsp;<div><br></div><div>Upon BAL you find small gram negative intracellular bacteria with no peptidoglycans.&nbsp;</div><div><br></div><div>Causitive agent?&nbsp;</div><div>{{c1::Chlamydia psittaci&nbsp;}}</div>
Chlamydia includes 3 important species:&nbsp;<div><br></div><div>{{c1::C. trichomatis --&gt; (Incusion conjunctivits and LGV)}}</div><div>{{c1::C. pneumoniae --&gt; ..pneumonia}}</div><div>{{c1::C. psittaci --&gt; pneumonia, meningoencephalitis, pericarditis/myocarditis}}</div>
Rickettsiacea has two species with distinguishable traits:&nbsp;<div><br></div><div>Rickettsia has {{c1::peptidoglycan and LPS}}</div><div>Orienta has no {{c1::peptidoglycan or LPS}}</div>
Rickettsiaceae grow intracellularly and degrade phagosomes by the aid of {{c1::phospholipase}}"<img src=""paste-7ebfa26e44f51031d5bdffe4e1b0f1f3cfa1d05b.jpg"">"
Rickettsiaceae causes systemic infection and replicates within {{c1::capillary endothelium}}&nbsp;Will cause vasculitis, fever and exanthema&nbsp;
Rickettsiaceae has 3 major groups:&nbsp;<div><br></div><div>Typhus group released by {{c1::cell lysis R. prowazekii/ R. typhi}}</div><div>Spotted fever group&nbsp;<span>released by&nbsp;</span>{{c1::focal lysis R. Rickettsii}}<span>&nbsp;</span></div><div>Scrub typhus group&nbsp;<span>released by&nbsp;</span>{{c1::budding off R.tsutsugamushi}}</div>"<img src=""paste-de19caea8143b423d7cb89cb5c851f3357e18313.jpg"">"
Rickettsiacea typhus group includes two species:&nbsp;<div><br></div><div>Prowazekii --&gt; Causes {{c1::epidemic::<span>&nbsp;</span><span>Epi or endemic</span><span>}} typhus</span></div><div>Reservoir: {{c1::Man}}</div><div>Vector: {{c1::Body louse}}</div><div><br></div><div>Typhi --&gt; causes {{c1::endemic:: Epi or endemic}} typhus&nbsp;</div><div>Reservoir: {{c1::Mice/rats}}</div><div>Vector: {{c1::Fleas}}</div><div><br></div><i>Brill-zinsser disease is a milder form of epidemic typhus returning 10-20 years after survival&nbsp;</i>
R. rickettsii presents as {{c1::Rocky mountain spotted fever (exanthemas first on the periphery then trunk)}}<div><br></div><div>{{c1::Ticks}} are the reservoir and vectors&nbsp;</div><div><br></div><div><br></div>
Rickettsial-pox is caused by {{c1::R. akari&nbsp;}}
Epidemic typhus shares antigens with {{c1::proteus}}Weil-felix reaction is a tube agglutination reaction with proteus&nbsp;
Ehrlicha, Anaplasma are small intracellular bacteria which replicate in {{c1::phagosomes&nbsp;}}<div><br></div><div>The vector for the disease includes {{c1::ticks}}, and reservoirs are wild and domestic animals&nbsp;&nbsp;</div>
"Ehrlichia chaffeensis causes {{c1::human monocytic ehrlichiosis (HME)<br><div><img src=""paste-d489604a7723ed0f9eadb4cc6b74397fbe073139.jpg"">}}<div><br></div><div>Ehrlichia ewingii causes {{c1::human granulocytic ehrlichiosis (HGE)</div><div><img src=""paste-ab1ea0f92bc113047bd7768c16a778996a3fde93.jpg"" style=""background-color: rgb(255, 255, 255);"">}}</div><div><br></div><div>Anaplasma phagocytophilum causes {{c1::human anaplasmosis}}</div></div>"<i>They are intracellular bacteria replicating in phagosomes carried by <u>ticks</u></i>
<div>Coxiella bacteria are obligate intracellular.&nbsp;</div>Coxiella burnetii causes {{c1::Q fever}}<div><br></div><div>Acute symptoms: {{c1::flu-like symptoms}}/ {{c1::interstitial pneumonia}}</div><div>Chronic symptoms: {{c1::Endocarditis}}, {{c1::hepatitis}}, {{c1::pulmonary disease&nbsp;}}</div>
Bartonella is a {{c1::facultative intracellular:: Intra/extra cellular}} pathogen that stains gram {{c1::negative}}<div><br></div><div>The most typical disease it causes is {{c1::cat-scratch disease&nbsp;}}</div>
A patient comes to you with regional lymphadenopathy. nothing about his history seems relevant, but he does mention that he has a few cats at home. what do you suspect the disease to be and the cause?&nbsp;<div><br></div><div>Cat-scratch disease caused by {{c1::Bartonella henselae}}</div>"The bacteria can cause stimulation of angiogenesis in patients with a weakened immune system&nbsp;<br><img src=""paste-0e860c7eb11d34d78a6317a73b2cb8653bdcb83f.jpg""><img src=""paste-107b96eb2dd8d0da9114c2c1a24c3c5248ab41d4.jpg""><br>"
"Imagine this:&nbsp;<div>you are a doctor somewhere out there in the world, and see a patient presenting to you with bacteraemia, focal and systemic skin leasions</div><div><img src=""05-0874-F3.jpg""><br>Upon taking the history of the patient you find out he is not grooming himself, and infested with the body louse.&nbsp;</div><div><br></div><div>What do you suspect the offending agent to be?&nbsp;</div><div>{{c1::<div>Bartonella quintana&nbsp;</div><div></div>}}<br></div>"
Blood-culture-negative endocarditis can be caused by most commonly {{c1::B. quintana}}, then {{c1::B. henselae}}
The smallest bacteria are {{c1::mycoplasma}}. an important characteristic is that they have no {{c1::cell wall ( no LPS or peptidoglycan)}}
Mycoplasma that cause disease in humans are<div><br><div>{{c1::M. hominis}}</div></div><div>{{c1::M. Pneumoniae}}</div><div>{{c1::M. genitalum}}&nbsp;</div><div>{{c1::U. urealyticum&nbsp;}}</div><div><br></div><div>They cause soft tissue infections bc they lack petidoglycan&nbsp;</div>
A patient presents a respiratory tract infection, otitis meadia, bronchitis and <u>primer atypical pneumona with dry coughs.</u>&nbsp;sputum samples came out to be with leukocytes but no bacteria. Blood test shows he has developed an antibody response with&nbsp;<u>cold IgM agglutinins.</u>&nbsp;&nbsp;<div>What do you suspect the offending agent to be?&nbsp;</div><div>{{c1::Mycoplasma pneumoniae&nbsp;}}</div>presenting age usually 5-15 years<div>ELISA test enough to confirm.</div><div>Uses P1 protein to attach to bronchial epithelial cells sialic acid receptors</div>
Possible causes of pelvic inflammatory disease (PID)?&nbsp;<div>{{c1::Chlamydia}}, {{c1::gonorrhea}}, {{c1::mycoplasma}}</div>
Whats the typical appearance of mycoplasma under the microscope? {{c1::Fried egg shape}}
ad90be700ed94ef982f6e1bcf08ed0a7-ao-1Trypanosoma species have a single large mitochondriend containing mitochondrial DNA called"<img src=""tmpq7y30dro.png"" />""<img src=""ad90be700ed94ef982f6e1bcf08ed0a7-ao-1-Q.svg"" />""<img src=""ad90be700ed94ef982f6e1bcf08ed0a7-ao-1-A.svg"" />""<img src=""ad90be700ed94ef982f6e1bcf08ed0a7-ao-O.svg"" />"
Tsetse flies carry trypanosoma species. there are 22 species, but only 2 are relevant to us:<div><br></div><div>T. b. gambiense seen in {{c1::forests and river banks}}</div><div>T. b. rhodesiense seen in {{c1::savanas}}</div><div><br></div><div>Once the fly is infected with trypanosoma its infected for life&nbsp;</div><div><br></div>"<img src=""paste-37f7867308dbbd8ba415e14706b4a1a5554aeb2e.jpg"">"
Tsetse flies prefer the color {{c1::black}}I dont know if this is racism or not I mean they <i>DO </i>like it&nbsp;
Human African Trypanosomiasis (HAT) is carried by the {{c1::tsetse fly:: Vector?}}
Overlap of Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense can only be seen in {{c1::uganda:: Country?}}&nbsp;
"A patient from <u>Uganda </u>comes to you presenting with intermittent fever and a rash. she has posterior cervical adenopathy and meningoencephalitis. The patient seems very sick, and the locals describe it as ""sleeping sickness""<div><img src=""paste-057000b7d6e7a41c86b1a30930daa7880383c568.jpg""><br></div><div>what pathogen species do you suspect?</div><div>{{c1::Since it's uganda the presence of both species is possible (Trypanosoma gambiense// Trypanosoma rhodesiense)}}</div>"
Diagnosis of Human African Trypanosoma can be done via&nbsp;<div>Serology:</div><div>-{{c1::up to 16 times elevation of serum IgM&nbsp;}}</div><div>-{{c1::CATT (card agglutination test for trypanosoma)}}</div><div><br></div><div>Microscopy:</div><div>-{{c2::Lymph node aspirate}}</div><div>-{{c2::wet smear or giemsa stain}}</div><div>-{{c2::MOST SENSITIVE mAECT (miniature anion-exchange centrifusion technique)}}</div><div><br></div><div>Lumbar puncture:&nbsp;</div><div>-{{c3::elevated CSF WBC &amp; proteins}}</div><div>-{{c3::Mott cells}}</div>
American Trypanosomiasis AKA chagas disease is transmitted by the {{c1::triatome (kissing bug)}} and the pathogen is {{c1::Trypanosoma cruzi}}"<img src=""paste-bb201dbd8318c9aca3de475434ea9b13fdbe83ba.jpg""><div>what a romantic</div>"
Immunocompromised patients infected with T. cruzi develop brain abscesses and may be difficult to be distinguished from those with {{c1::cerebral toxoplasmosis}}
"A patient from latin america has a chagoma on his limb<div><img src=""paste-492ed1f6992e4672acf0a12f428f331c5920bd61.jpg""><br><div>and presents with romana's sign</div></div><div><img src=""romana_sign.jpg""><br></div><div>the patient also presents with fever hepatosplenomegaly, lymphadenopathy and peripheral lymphocytosis. for some reason the health workers couldnt find out the cause, but it resolved within 4 weeks so they thought nothing of it.&nbsp;</div><div><br></div><div>Years later on the disease progressed into the chronic stage where the same patient presents with congestive heart failure, rhythm disturbances, thromboembolis and cardiomegaly. Upon biopsy of the heart you can see intracellular amastigotes of the parasite</div><div><img src=""paste-2cc095ff36468a021ab9f96dc3ea45515cc7c9af.jpg""><br></div><div>Whats the disease and the causative agent?&nbsp;</div><div>{{c1::Chagas disease caused by Trypanosoma cruzi&nbsp;}}</div>"
American trypanosomiasis (chagas disease) can have 3 types of manifestations in the chronic phase:&nbsp;<div><br></div><div>{{c1::Cardiac only (cardiopathy)}}&nbsp;</div><div>{{c1::Digestive only (Megadisease)}}</div><div>{{c1::Cardiac + Digestive}}</div>
Leishmania is transmitted via the {{c1::sand fly}}"<img src=""paste-7d089247027fab326cd50a3567988fb486d57e7e.jpg"">"
"Leishmania can manifest into three different types:&nbsp;<div>-{{c1::Cuteneous leishmania</div><div>Wet/pizza like often seen in L. major or L. braziliensis. Dry lesions seen in L. tropica</div><div><img src=""paste-d8f1f1c752983bcd497d9855524718a734f67bea.jpg"">}}</div><div>-{{c1::Mucosal leishmania. Is the most disfiguring.&nbsp; seen in L. tropica.</div><div>ٍ<img src=""paste-d442fdcb88d465382f599b288fab6792cc5b8005.jpg""><span>}}</span></div><div>-{{c1::Visceral leishmania. Associated with fever, hepatosplenomegaly, abdominal enlargement.</div><div><img src=""paste-35b7e69c5592b597b2b6bd6348bdf96bc41f774c.jpg"">}}</div>"
What is a sign that a person survived visceral leishmaniasis? {{c1::Post-Kala-Azar dermal leishmaniasis&nbsp;}}"<img src=""paste-0dc1df0a1fd5e87c2aef4f2a76845844d47570b9.jpg"">"
"Haemophilus are {{c1::gram negative coccobacilli:: Gram//shape}}.&nbsp;<div>To grow they need both {{c1::X (haemin)}} and {{c1::V (NAD)}} factors.</div><div>They can also be grown on a blood agar alongside {{c1::S. aures since they produce NAD</div><div><img src=""paste-43bde8e96bb7ea5fc34db3d691aad11de6e264b0.jpg"">}}</div>"
H. influenza is exclusively human, and infecs the {{c1::nasopharynx}} or {{c1::throat}}. Most are non-capsulated, but the most pathogenic strain is the capsulated type {{c1::B}}
Type B H. influenza most commonly infects the age group between 2 months and 2 years.&nbsp;<div>Can cause:&nbsp;</div><div>{{c1::Meningitis}}</div><div>{{c1::Epiglottitis}}</div><div>{{c1::bacteremiae&nbsp;}}</div><div>{{c2::septic arthritis}}&nbsp; &nbsp;</div><div>{{c2::Pneumonia}}</div><div>{{c2::Facial cellulitis}}</div>
The most common cause of community acquired typical pneumonia is {{c1::S. pneumonia}}. The second most common is {{c1::Non-capsulate H. influenza}}
Asplenia/ sickle cell syndrome increases the risk of {{c1::encapsulated bacterial}} infectionsLike H. influenza, strep pneumonia, and Neisseria meningitidis&nbsp;
Non-invasive (usually non-capsulated) H. influenza infections are can manifest as:&nbsp;<div>{{c1::Otitis media}}&nbsp;</div><div>{{c1::Sinusitis}}</div><div>{{c1::Exacerbation of COPD}}<br></div>
H. influenza has a polysaccharide vaccine which children dont respond well to. needs to be {{c1::conjugated}}
"Haemophilus ssp other than influenza cause {{c1::endocarditis}}<div><br></div><div>Haemophilus ducreyi is another ssp which is an STD causing a {{c1::painful soft ulcer</div><div><img src=""paste-bc77bf9c797e188c52bebc999eb82597ee26b515.jpg"">:: Soft/hard painful or non painful ulcer?<span>}}</span></div>"A hard and painless ulcer caused by treponema pallidum &gt;&gt; Syphilis&nbsp;
Bordetella produce localized infections with systemic effect. they love staying at {{c1::ciliated airway mucosa&nbsp;}}"<img src=""paste-600d8410bdb37930a58f8253b24b6f6cbafb3e69.jpg"">"
Bordetella has 3 relevant species that we care about:&nbsp;<br><div>{{c1::B. pertussis&nbsp;}}</div><div>{{c1::B. parapertussis&nbsp;}}</div><div>{{c1::B. bronchiseptica --&gt; is opportunistic&nbsp;}}</div>
B. pertussis inhibits phagocytic functions via the {{c1::pertussis toxin (Only found in B. pertussis)}}
"A child presents with rhinorrhea, lacrimation low fever and a dry non-productive cough. The coughs usually end with the child gasping for air, and locals call it the ""donkey cough"".&nbsp;<div>You took a nasopharyngeal swab and see small gram negative coccobacilli. You ask the mother about current vaccination, and find out she skipped the DPT vaccine bc of some facebook group she follows.&nbsp;</div><div><img src=""paste-8529016ecfc6d7c3ca8b5660ef5b397433e24d8a.jpg""><br></div><div>Whats the disease and offending pathogen?&nbsp;<span>{{c1::</span><span>Whooping cough caused by B. pertussis&nbsp;}}</span></div>"You can hear the kid gasping for air at the end.<div>&nbsp;https://www.youtube.com/watch?v=S3oZrMGDMMw<div><br></div></div>
Prevention of whooping cough via vaccine done by:&nbsp;<div>{{c1::merthiolate-killed whole cell vaccines --&gt; DPT (Diphtheria, pertussis and tetanus)}}</div><div>{{c1::acellular vaccines}}</div>
Brucella are small {{c1::gram negative coccobacilli :: gram//shape?}}<div>The most serious species is {{c1::B. melitensis}}, and {{c1::B. suis}} found in pig is associated with abscess formation</div><div>Growth is VERY SLOW. Need to inform lab that you suspect it.</div><div>Risk factor is {{c1::drinking unpasteurized milk}}</div><div>Undulent fever seen too.&nbsp;</div><div><br></div>
Three major groups oh helminiths:&nbsp;<div>{{c1::Nematodes}}</div><div>{{c1::Trematodes}}</div><div>{{c1::Cestodes}}</div><div><br></div><div>Antihelminithic drugs are aimed at the {{c1::metabolic targets}}, that are different than that of the host</div>
"Nematodes are roundworms with a head, anus and completed digestive tracts. they infect the {{c1::intestine}} as well as {{c1::blood vessels&nbsp;}}<div><img src=""paste-441517cad33dc1e5ab133fa56595f4e6dea0d8a3.jpg""><br></div>"
Mebendazole is an anti-{{c1::nematode}} drug with a wide spectrum. it works by interfering with the {{c2::syntheis of parasitic microtubules}} and {{c2::decreases oral glucose uptake}}<div><br></div><div>Contraindicated in&nbsp;<span>{{c2::</span><span>pregnant women --&gt; embryotoxic and teratogenic&nbsp;}}</span></div>Useful for treating whiphworm, pinworm, hookworm, and roundworm&nbsp;
Pyrantel pamoate is an anti-nematode drug agains roundworm, pinworm, and hook worm. it acts as a {{c1::depolarizing neuromuscular blocking agent--&gt; paralysis of worm}}
Thiabendazole is effective against strongyloidiasis and trichinosis. it works by affecting {{c1::microtubular aggregation}}.&nbsp;<div>Adverse effects include dizzinesss, anorexiam nausea and vomitting, but can be really severe and cause {{c1::erythema multiforme (erythema of unknown origin)}} or {{c1::stevens-johnson syndrome}}</div>Stevens-Johnson syndrome&nbsp;is a rare, serious&nbsp;disorder&nbsp;of your skin and mucous membranes. It's usually a reaction to a medication or an infection. Often, it begins with flu-like symptoms, followed by a painful red or purplish rash that spreads and blisters
Ivermectin is the drug of choice for {{c1::onchocerciasis&nbsp;}} and works by targeting the {{c1::parasite's GABA receotors --&gt; paralysis}}. does not readily cross the BBB.&nbsp;<div>Contraindicated in {{c1::pregnancy}}</div><div><br></div><div>Should be avoided in patients already taking {{c1::benzodiazepines}} or {{c1::barbiturates}} since they also act on GABA receptors&nbsp;</div><div><br></div><div>Adverse effects&gt;&gt; {{c1::Mazzotti reaction}}<br><div><br></div></div>Mazzotti reaction (fever, headache, dizziness, somnolence, and hypotension). Give antihistamines ot steroids&nbsp;
Praiquantel is an anti-trematode that is the drug of choice against {{c1::schistosomiasis}}, but can be used for cestode infections such as cysticercosis BUT NOT {{c1::OCULAR CYSTICEROS--&gt; damage of the eye}}<div><br></div><div>It works by increasing {{c1::permeability of cell membrane to calcium --&gt; contracture and paralysis&nbsp;}}</div><div><br></div><div>Dont administer praiquantel to {{c1::pregnant/ nursing mothers&nbsp;}}</div>
Cestodes have a flat segmented body that attaches itself to the {{c1::hosts intestine}}. It lacks a mouth and a digestive tract.&nbsp;<div><br></div><div>{{c1::Niclosamide}} is the drug of choice for cestode infections</div>
Niclosamide is the drug of choice for {{c1::cestode}} infections.<div>it acts by inhibiting&nbsp;<span>{{c1::</span><span>the parasites&nbsp;</span><span>mitochondrial anaerobic</span></div>phosphorylation of ADP--&gt; no ATP}}<div>Needs to be taken with {{c1::a laxative}}</div>
Albendazole is an anti-cestodal drug that is used against {{c1::cysticercosis&nbsp;}} and {{c1::hydatid disease}}
The vector for malaria is the female {{c1::Anopheles mosquito}}&nbsp;
"Although the UAE has been certified ""malaria free"", the majority of reported cases are due to plasmodium {{c1::vivax:: Falciparum//Vivax//Ovale//Malariae}}"
The malarian life cycle has a sexual and an asexual reproductive phase.&nbsp;<div>In the human it is {{c1::asexual}}.&nbsp;</div><div>In the mosquito's salivary glands it is {{c1::sexual&nbsp;}}.</div>
The infective stage of malaria are the {{c1::sporozoites}}&nbsp;<div><br></div><div>The dormant phase are the {{c1::hypnozoites}} within the liver</div>2 species stay dormant for a longer period of time: P. vivax &amp; P. ovale
The malaria parasite will infect mainly two things: {{c1::hepatocytes}} and {{c1::RBCs}}
{{c1::P. falciparum}} is the most dangerous type of malaria species. It has the shortest incubation period, shows a malignant tertian rhythm and if not treated will lead to death.&nbsp;
The fever in malaria coincides with the {{c1::RBC rupture (depends on cycle length)}}<i>Tertian fever (Falciparum/ ovale/ vivax)--&gt; Every 2 days</i><div><i>Quartian fever (malariae) --&gt; Every 3 days&nbsp;</i></div>
Symptoms of malaria:&nbsp;<div>-{{c1::Cyclic fever}}</div><div>-{{c1::Chills}}</div><div>-{{c1::Hepatosplenomegaly}}</div><div>-{{c1::Fatigue}}</div><div>-{{c1::Headache}}</div>
"Plasmodium falciparum is unique because when it infects RBCs it promotes the formation of knobs<div><img src=""paste-ed2bc370978135692858f9a9b74437ecd416fb4e.jpg""><br></div><div>these knobs promote:&nbsp;</div><div>-<span>{{c1::</span><span>the formation of rosettes&nbsp;</span></div><div><div><img src=""paste-1396799ce0d980e56014daf0393b12a4d17c961b.jpg""><span>}}</span></div></div><div>-{{c1::Clumping --&gt; tissue and organ necrosis&nbsp;}}</div><div><br></div>"
In malaria, uptake of infected RBCs by spleen macrophages leads the release of pro-inflammatory cytokines which leads to the expression of {{c1::adhesion molecules&nbsp;}}. this will lead to coagulation and lead to sequestration of the parasite or the infiltration of leukocytes.<div>sequestration can cause:<span>&nbsp;</span></div>{{c1::<span>-Cerebral malaria}}</span><div></div><div>{{c1::-Placental malaria}}<br></div><div><br></div><div>All this can also lead to kidney damage leading to:&nbsp;</div><div>{{c1::Increased glycolysis and lactic acid accumulation}}</div><div>{{c1::hypoxia}}</div><div>{{c1::hyperventilation}}</div><div><br></div>
{{c1::Proquanil}}, {{c1::chloroquine}} and {{c1::quinine}} are safe drugs for dealing with malaria during pregnancy
"Difference between malaria and babesia:<div>Replication:&nbsp;</div><div>malaria replicate via {{c1::schizogony}} whereas babesia via {{c1::budding}}</div><div><br></div><div>Hemozoin production:&nbsp;</div><div>Malaria {{c1::do}} whereas babesia {{c1::dont}}</div><div><br></div><div>Babesia</div><div>Infectious parasitic bodies released when ruptured are called {{c1::vermicules}}</div><div><br></div><div><i>Babesia also forms the maltese-cross</i></div><div><img src=""paste-bc4f9c684a424a94733f2dfe5e06c3e5cca91394.jpg""><i><br></i></div>"
"Lyme, Babesia, Granulocytic Ehrlichiosis and tickborne encephalitis are transmitted by ticks in the {{c1::Ixodes}} genus<div><img src=""paste-819b988d447d2c4bfed280885204a5d3505e5f23.jpg""><br></div>"
People with {{c1::G6PD deficiency}}, {{c1::Thalassemia}}, {{c1::sickle cell anemia}} have some immunity against malaria&nbsp;
"A patient comes to your clinic presenting with a fever every 2 days. He is anemic, has headaches, vomitting and diarrhea. you also find hepatosplenomegaly, and upon ultrasound find out that it is homogeneous. LDH levels are increased, but ALT/ AST are within normal ranges. Blood smear shows RBCs with little inclusions<div><img src=""paste-a386781d39c840dfd0263f679b8498c638de6d28.jpg""><br></div><div>You are later informed that the patient recently came back from africa&nbsp;</div><div>Disease? {{c1::Malaria (probably P. falciparum)}}</div>"
"(You are a physician in the US) A patient comes to you presenting with malaria-like symptoms. The patient denies that he travelled anywhere outside the country, so this seemed weird. you investigate the peripheral blood smear you see this:<div><img src=""335966fc858318ab666ea03b3914e052--maltese-cross-lyme-disease.jpg""><br></div><div>What does the patient have and what is the vector?</div><div>{{c1::Babesia transmitted via ticks&nbsp;}}</div>"
{{c1::Climate}}, {{c1::water quality}} and {{c1::factors regulating snail population}} determine the distribution of schistosomiasis&nbsp;<i>You control the snail population you control schistosoma</i>
"In the case of schistosoma, the eggs in water release miracidia which will infect {{c1::snails}}. Later on they they develop into {{c1::cecariae}} which readily infect humans and cause a phenomenon called {{c1::""swimmers itch""}}"
6149283fca1144448edb84ece3d0ccde-oa-2Below you see schistosoma eggs belonging to different species. Identify them and where thy can be isolated from&nbsp;"<img src=""tmp_ghmjvk8.png"" />""<img src=""6149283fca1144448edb84ece3d0ccde-oa-2-Q.svg"" />""<img src=""6149283fca1144448edb84ece3d0ccde-oa-2-A.svg"" />""<img src=""6149283fca1144448edb84ece3d0ccde-oa-O.svg"" />"
"Below you see both a female and a male blood fluke (schistosoma)&nbsp;<div><img src=""paste-aaced3c2802306d476def311b1dbf68d951c86d9.jpg""><br></div><div>Which one is the female, and how did you know that?</div><div>{{c1::The smaller one with black dots (eggs)}}</div>"
"Symptoms of schistosomiasis:&nbsp;<div>upon infection with cercariae which penetrate the skin will cause local {{c1::dermatitis ""swimmers itch""}}</div><div><br></div><div>Migration of immature worms takes from 4-10 weeks and causes {{c1::fever aka katayama fever (seen in S. japonicum and S. haematobium)}}</div><div>Migration through lung causes {{c1::cough and hemoptysis&nbsp;}}</div><div>Migration to the liver causes {{c1::acute hepatitis}}</div><div><br></div><div>Once the blood flukes settle either near {{c1::mesenteric}} or {{c1::vesicular}} venules they start laying eggs. Eggs induce the formation of {{c1::granulomas (hoeppli reaction) and fibrosis}}&nbsp;</div>"
Different schistosoma subspecies&nbsp; cause different chronic presentations like bloody stool or bloody urine<div><br></div><div>S. mansoni --&gt; {{c1::Bloody stool}}</div><div>S. haematobium --&gt; {{c1::Bloody urine}}</div><div>S. japonicum --&gt; {{c1::Bloody stool&nbsp;}}</div>
S. mansoni and S. japonicom infections can lead to multiple clinical manifestations including:&nbsp;<div>-{{c1::hepatosplenic schistosomiasis &gt; periportal pipe-stem fibrosis}}<div>-{{c1::ectopic lesions}}</div><div>-{{c1::oesophageal varices}}</div></div><div>- {{c1::Toxic and allergic symptoms}}</div>
S. haematobium clinical manifestation includes:&nbsp;<div>- {{c1::No initial toxic or allergic symptoms&nbsp;}}</div><div>- Cystitis and calcification</div><div>- Genital schistosomiasis&nbsp;</div><div>- Obstructive uropathy</div>
"A patient went swimming in a lake and once he came out he had local dermatitis.<div>&nbsp;<img src=""paste-5bd8d99b69faa9e3493d14b5d2dffdf77c6ec2e5.jpg""></div><div>Whats the condition called and what caused it?</div><div>{{c1::swimmer's itch caused by schistosoma}}</div>"
Schistosoma worms are initially handled by Th1 cells, but once eggs are produced theyre handled by {{c1::Th2 cells}}
Diagnosis of schistosoma depends on {{c1::eggs}}, and treatment is {{c1::praziquantel&nbsp;}}
Most hepatitis viruses are RNA viruses except {{c1::HepB}}<div><br></div><div>It is a rule in hepatitis viruses that those infecting via fecal-oral route cause {{c1::acute:: Acute//Chronic?}} infections, whereas those that infect via parental routes cause {{c1::chronic<span>:: Acute//Chronic?</span><span>}} infections</span></div>
Hepatitis B virus contains three types of particles which include infectious and non infectious particles.&nbsp;<div><br></div><div>Infectious particles includes: {{c1::Dane particles}}</div><div>Non-Infectious particles: {{c1::Spheres}} and {{c1::filaments}}</div>Dane particles includes Outer shell (containing HbsAg), the inner core (removed with NP40 detergent), the core (contains HBcAg) and polymerase<div><br></div><div>Sphere is made exclusively out of HBsAg. Although it is not infectious, it is more immunogenic than danes particles.&nbsp;</div>
Although HepB virus contains DNA, it carries it's own {{c1::reverse transcriptase&nbsp;}}
The function of the sphere and filaments in HepB is to {{c1::absorb neutralizing antibodies&gt; shield the Dane particles from host defences}}
Diagnostic test for HepB virus infection is the direct antigen detect of {{c1::HBsAg}}<div>All 3 particles in HBV contain HBsAg, but spheres got the most.&nbsp;</div>Just like when you look for p24 in HIV
Every nucleotide of the HBV is within a coding region, so whenever it breaks and integrates the consequence is that {{c1::it wont be able to continue it's life cycle}}<i>The DNA is highly compact and genes overlap. a single break can ruin 1-4 genes&gt; no more assembly</i>
HepB virus DNA contains 4 open reading frames:&nbsp;<div><br></div><div>ORF S: Encodes {{c1::HBsAg}}</div><div>ORF C: Encodes {{c1::HBcAg}}</div><div>ORF P: Encodes {{c1::viral polymerase}}</div><div>ORF X: Encodes {{c1::regulatory protein that trans-activates viral and cellular gene&nbsp;transcription}}</div>
The pathogenesis of acute and chronic HBV is the result {{c1::of cell-mediated and humoral immune responses}}<i>not a direct cytopathic effect of the virus unlike HAV (viral only) and HCV (both viral and cell mediated)</i>
Mothers who are positive for {{c1::HBeAg:: Which viral antigen}} are more likely to transmit HepB to the fetusIt indicates active replication of the virus --&gt; Higher viral load<div><br></div><div>transmission occurs via blood transfusions mostly, but can occur via saliva/ sexual intercourse&nbsp;</div>
In HepB infections (Acute/ chronic/ Hepatic carcinoma)<div>75-90% are {{c1::acute infections leading to complete recovery}}</div><div>10-25% {{c1::lead to chronic carrier state}}</div><div>1% {{c1::will progress to hepatic carcinoma&nbsp;}}</div>
The chronic HepB viral infection is defined by the {{c1::continued presence of HBsAg&nbsp; for over six months and and absence of Anti-HBs}}
A hepatitis patient is tested for antigens, and came out as positive for HBsAg and HBeAg for six months, but did not develop an antibody response. What is the current status of the patient, and what is the likelyhood of developing hepatic cell carcinoma?<div>{{c1::Asymptomatic hepatitis B carrier. Will not develop HCC}}</div><div><br></div>HCC \happens as a result of the immune response. no immune response&gt; no HCC
In viral hepatitis, the cell proliferation potentiates the action of exogenous environmental factors such as {{c1::aflatoxin}} and {{c1::alcohol}}Normally hepatic cells are dormant&gt; these factors dont do anything. But in HepB the cells are proliferating which creates the chance of mutations
Both the presence of mitogenic factors such as HepB, and mutogenic factors like aflatoxin are required for {{c1::carcinogenesis&nbsp;}}<i>Aflatoxin will mutate oncogenes or tumor suppressor genes (P53)</i>
The HBV vaccines consist of high concentrations of {{c1::HBsAg}}
HepA cellular damage is due to {{c1::direct viral action}}<div>HepB cellular damage is due to {{c1::immune response}}</div><div>HepC cellular damage is due to {{c1::both viral action and immune response}}</div>
HepA infections provide an immune response and a {{c1::non-lifelong:: Lifelong//Non-Lifelong}} immunity<div>HepB infections provide an immune response and a {{c1::lifelong<span>:: Lifelong//Non-Lifelong</span><span>}} immunity</span></div>
&nbsp;HepC (Acute/ Chronic)<div>Most are asymptomatic, but if symptoms appear then:<br><div>25% of infections are {{c1::acute}}</div><div>75% of infections are {{c1::chronic&nbsp;}}</div></div><i>Its the opposite of HepB&nbsp;</i><div><i>Transmission is mainly via hemodialysis/transfusions/ transplants, but sexual contact is also possible&nbsp;</i></div>
In HepC, the {{c1::core protein}} has been associated with developing high rates of HCC since it induces oxidative stress and suppresses apoptosis.&nbsp;<div><br></div><div>Also, the {{c1::NS5A}} protein is able to sequester p53, activate STAT3, and inhibit TNF-alpha mediated apoptosis&nbsp;<br><div><br></div></div>
Difference between HepB and HepC:&nbsp;<div><br></div><div>{{c1::HepB integrates, HepC doesnt.&nbsp;}}</div><div>{{c1::HepB mutates P53 but rarely mutates Beta-catenin, the opposite is true for HepC}}</div>
A patient with hepatitis is found to be positive for hepatitis D. Which co-infection are 100% sure he also has? {{c1::HepB}}HepD only happens with the co-infection of HepB
Which viral protein does HepD encode for? {{c1::Delta antigen HDAg ONLY}}It needs HBsAg of HepB which is why they need to be together.&nbsp;
Superinfection of HepD occurs in the scenario of: {{c1::Getting a primary HepD infection on a pre-existing chronic HepB infection--&gt; Fulminant hepatitis }}
HepE are {{c1::enterically transmitted water-borne:: Transmission }}<div>Both HepA and HepE dont have a chronic stage&nbsp;</div>
HPV has tropism for {{c1::epithelial}} cells, specifically {{c1::terminally}} differentiated cells
The HPV proteins {{c1::E6}} &amp; {{c1::E7}} are carcinogenic&nbsp;<div><br></div><div>Classification of the virus depends on the sequence of the {{c1::L1}} protein</div>"E6 will degrade P53 and E7 will bind to Rb<div><img src=""paste-b2c37774bdc83149cebd2bfe307c57e0f88c07bb.jpg""><br></div>"
Prevalence of HPV is increased in {{c1::females:: Gender?}}Most commonly seen between the ages of 20-24
Circumcision decreases the risk of {{c1::HPV (STD's in general)}} infections in males
HPV-associated diseases:&nbsp;<div><br></div><div>HPV 1: {{c1::plantar warts}}</div><div>HPV 2: {{c1::palmar warts}}<br></div><div>HPV 6: {{c1::genital warts}}<br></div><div>HPV 11: {{c1::genital warts}}<br></div><div>HPV 16: {{c1::cervical cancer}}<br></div><div>HPV 18: {{c1::cervical cancer}}<br></div>
Most cervical cancers are caused due to {{c1::HPV infection (mostly 16 &amp; 18)}}
Nematodes characteristics:<div><br></div><div>Shape: {{c1::Elongated/ cylindrical}}</div><div>Sexes: {{c1::seperate}}</div><div>Heads: {{c1::No suckers/ hooks}}</div><div>GIT: {{c1::Present and complete}}</div><div>Body cavity: {{c1::Present}}</div>
Trematodes characteristics:<div><br></div><div>Shape: {{c1::Leaf-like unsegmented}}</div><div>Sexes: {{c1::not seperate}}</div><div>Heads: {{c1::No suckers/ has hooks}}</div><div>GIT: {{c1::Present but incomplete}}</div><div>Body cavity: {{c1::absent}}</div>
cestodes characteristics:<div><br></div><div>Shape: {{c1::Tape-like segmented}}</div><div>Sexes: {{c1::not seperate}}</div><div>Heads: {{c1::No suckers/ no hooks}}</div><div>GIT: {{c1::absent}}</div><div>Body cavity: {{c1::absent}}</div>
The nematode Enterobiasis aka pinworm clinical manifestations include {{c1::perianal itching}}, {{c1::vomiting}} and {{c1::appendicitis}}.&nbsp;<div>Transmission is {{c1::via fecal-oral route&nbsp;}}</div><div>Diagnosis via {{c1::scotch tape&nbsp;}}</div>
The nematode trichuris aka whipworm has a {{c1::barrel}}-shaped egg (diagnostic)&nbsp;<div>Clinical manifestations usually asymptomatic, but in heavy infections can include: {{c1::frequent diarrhea (nocturnal stooling)}}</div><div>{{c1::Rectal prolapse}}</div><div>stool consists of {{c1::mucus and blood}}</div><div><br></div>"<img src=""paste-3b360c6bf41035e0e070a2222aae059c5fb28bf8.jpg"">"
"Ascariasis infections happen by {{c1::ingesting fertile eggs}}<div><br></div><div>Clinical manifestations include:&nbsp;</div><div><br></div><div>{{c1::Pulmonary ascariasis (eosinophilia)}}</div><div>{{c1::Intestinal ascariasis (pain/vomiting/ obstruction)}}</div><div>{{c1::Hepatobiliary and pancreatic ascariasis}}</div><div><br></div><div>Ascariasis cannot tolerate fever, so they {{c1::exit lumens</div><div><img src=""paste-6ab47e557e2f723f5fdd7ffa3ec14ec09a250dfb.jpg""><span>}}&nbsp;</span><br></div><div><br></div>"
"A patient starts seeing this on their foot<div><img src=""paste-ffc838dcd32e5f66f0592328d99a8592f223760c.jpg""><br></div><div>he describes that he often goes around barefoot&nbsp;</div><div>Likely diagnosis?&nbsp;</div><div>{{c1::Hookworm}}</div>"A. duodenale can also infect via ingestion of egg
Hookworms such as N. americanus or A. doudenale cause {{c1::anemia&nbsp;}}<div><br></div><div>Most hookworms infect via penetrating the soles of the feet but N. americanus {{c1::infects via egg ingestion}}</div>
Strongyloides infections are mostly asymptomatic except in {{c1::immunocompromised patients (will disseminate into extraintestinal organs --&gt; 85% mortality)}}<div>Infection happens via: {{c1::penetratiion of foot soles or auto-infection of peri-anal area.&nbsp;}}</div><div>This parasite likes to travel everywhere and can invite other secondary infections (gram-neg polymicrobial meningitis)</div><div>Humans will only shed larvae (no eggs)</div>"<img src=""paste-e9ca6890c12b6f1a39d271b0f5307d19dee2582a.jpg"">"
Filariasis is a {{c1::lymphatic :: Lymphatic// blood borne// GIT related }}infection<div><br></div><div>It can be caused by three parasitic nematodes:&nbsp;&nbsp;</div><div>{{c1::Wuchereria bancrofti}}</div><div>{{c1::Brugia malayl }}</div><div>{{c1::loa loa}}</div><div><br></div><div>Filarial worms carry the endosymboint {{c1::wolbachia&nbsp;}}, and depletion by antibiotics can kill the worm&nbsp;</div><div><br></div><div>Transmission is via {{c1::anopheles mosquito}} in the case of&nbsp;<span>Wuchereria bancrofti and&nbsp;</span><span>Brugia malayl</span></div><div><span>In the case of loa loa via&nbsp;</span>{{c1::tabanid(red) fly}}<span>&nbsp;</span></div>"<img src=""paste-fd3ee08601d91b8ee1f3c19efdccf10052034581.jpg""><div><img src=""paste-9a364b7e06e8996786f6b26ac615323fa0c4b9f3.jpg""><br></div><div><img src=""paste-e91449403d6873cd9b637a8986763e8da7b37b8b.jpg""><br></div>"
"Clinica filarial manifestation of&nbsp;<div><br><div>Wucheria bancrofi &amp; brugia malayi:</div><div>{{c1::Lymphedema (in extremeties like elephantitis)}}</div><div>{{c1::Genitourinary tracts (hydroceles and lymphedema)&nbsp;}}</div><div><img src=""paste-03ffda43a92f57b9651f5cded6f45d55da3ddceb.jpg""><br></div><div>In Loa loa&nbsp;</div><div>{{c1::Calaber swelling}}</div><div>{{c1::found in conjunctiva&nbsp;}}</div></div><div><img src=""paste-167d661252d74100e2069dbf2b584d9748594cfe.jpg""><br></div><div><img src=""paste-b0bf268fed1d1c84e50077953089a2d073abccd0.jpg""><br></div><div><br></div>"
Onchocerciasis aka river blindness is caused by the nematode <i>onchocerca volvulus,</i> and transmitted by {{c1::black flies (simulium damnosum)}}<div>Microfilariae will migrate through the {{c2::skin and the eye}}&nbsp;</div><div>Adult worms live coiled in {{c2::subcutaneous or deep intramuscular tissue}}</div><div><br></div><div>Clinical manifestations include:&nbsp;</div><div>Subcutaneous nodules filled with worms</div><div>Dermatitis</div><div>Lymphadenopathy&nbsp;</div><div>blindness (chronic)</div><div><br></div><div>Mazotti reaction happens when you treat with {{c2::diethylcarbamazine (DEC).}}</div>"<img src=""paste-06575a8340572dc37f3be9f587c97185a6c84002.jpg"">"
Guinea worm disease aka dracunculiasis is caused by the parasite {{c1::dracunculus medinesis&nbsp;}}<div>Infection happens by drinking water contaminated with copepods called {{c1::cyclops or water fleas}}</div><div><br></div><div>After maturation, the worm will form a painful blister to release larvae in water&nbsp;</div>"<img src=""paste-8ab399aa70fea5c25f0dd13f71d7f6614a02a1ce.jpg"">"
"Toxocara migrans is a migratory worm which when ingested can migrate to organs such as liver, spleen, lungs and the eye causing:&nbsp;<div>{{c1::Eosinophila}}, {{c1::hepatosplenomegaly}}, {{c1::retinal granulomas}}</div><div><br></div><div>Eggs are found in {{c1::dog stool</div><div><img src=""paste-9683e98955519f05e17ee68ab2a691c29c39ee99.jpg"">}}&nbsp;</div><div>Prevent by {{c1::deworming pets}}</div>"
"Trichinella spiralis is a migratory worm found in {{c1:: undercooked pork/horse meat}}<div>It resides within {{c1::striated muscles</div><div><img src=""paste-6922d6ae14c9d12b636d2591a168195e8088e87f.jpg"">}}<div>symptoms include {{c1::circumorbital edema</div><div><img src=""paste-bc4b52446d015d230c2836031a44b0d651b22460.jpg"" style=""background-color: rgb(255, 255, 255);"">}}, {{c1::splinter hemorrhage in nails</div><div><img src=""paste-f832d8a789f5885104dd178ec79aed194604b61a.jpg"" style=""background-color: rgb(255, 255, 255);"">}},&nbsp; due to vasculitis&nbsp;{{c1::<span>}}</span></div></div><div><br></div><div>can be fatal if it involves the heart, lung and CNS</div><div>Humans are the dead end</div>""<div><img src=""paste-463fc516f6d2bbe29818363eee99ce5cbde231b9.jpg""><br></div><div><br></div>"
"Clonorchis sinensis aka {{c1::chinese liver fluke&nbsp;}} is a trematode found in east asia.<div><br></div><div>Infection happens by {{c1::the ingestion of food infected by it</div><div><img src=""3-s2.0-B9780124159150000108-f10-03-9780124159150.jpg"">}}</div><div><br></div><div>It sticks to the GI using {{c1::small suckers}}</div><div>Complications include: {{c1::functional impairment of the liver}}, {{c1::biliary obstruction}} &amp; {{c1::<i>cholangiocarcinoma</i>}}</div>""<img src=""Clonorchis_sinensis_2.png""><div><br></div>"
"Fasciola hepatica and F. gigantica are {{c1::liver flukes (trematodes)}}<div><br></div><div>Way of infection is by ingesting {{c1::metacercaria found on vegetation</div><div><b><img src=""zGjBoIyCHabO5L5TkNepklJQVwywO3K2cEZA3jpH4-S_j7GIxf4mMfbvS8FLhbPaXKyoyYHU94VF9Xtobth7REeFzo0f9HlG9zcoZ82o9VlxVsWX2YF8ug-gzkcpw4uMLR_L.jpg""></b><br></div><div>}}</div><div>The main reservoir is {{c1::cattle}}</div><div><br></div><div>Eggs of F. hepatica can be confused for those of the intestinal fluke {{c1::fasciolopsis buski}}</div><div><br></div><div>Clinical manifestation</div><div>Acute hepatic stage (invasive): {{c2::Hepatomegaly and tunnel like branching within the liver}}</div><div>Chronic biliary stage (obstructive): {{c2::migration to the common bile duct lumen.&nbsp;}}</div>""<b><img src=""zDYHxiAh7znreaH0-HYYLbqm-R_7PVVZLu5JCaur3rGr2d_izGuLgfPDG4OmU4fcH_fQf1rJJOPrTWGA-Pt9I5ryydtXU23mjSdfvhiAgVQzfo7t3td1Jm5-2TSsjMPGF_dz.png""><img src=""gesM6b2E5fmGR7a9hRAp3XUk4mQwh7EOB5chuCX0SxgIkAgq9gs1Ar8XmKfVK01XM2IxN-c9Su7JEKL7bPNO-l6iaNNkk6YbRyVlMjBvfGbjNIENlQtTEeuaDNgq0lE-FD7P.png""><img src=""ZDDxiifdSs1ceeDclXmRCEzB41AnyuGvzm-zr7Vp0n80QaMpOpBq1rpPzDQVHAlROXd9ywVBx1m8ZtME12NNkmjch8HQUqpFTx07O_6vibGaHq-b4LRUdgtEA_gpX6ZCQlXF.png""><br><div>F<br></div></b><br>"
"Fasciolopsis buski is an {{c1::intestinal&nbsp;&nbsp;fluke (trematode)<br><div><b><img src=""BbnMQFf_BEL68sFmvvUEH_pNjDLoogpRenkgaaPd33UkuzjJLcwtXnCWx9BZhZbZ7W-PXXLAi1rr6UiTFwAqX67z9R6DAUVh8Mt1XuoDZcKDCmKa9EHZtCnSnw_CMgijNCfK.png""></b>}}<div>It is found growing beside {{c1::growing water plants and pigs feeding off them</div><div><img src=""paste-91ad77f84ab1a784148b8cd67d5e2f0a24c314fe.jpg""><span>}}</span><br></div><div>This parasite will attach itself to {{c1::the small intestine}}</div><div>Morphologically it lacks a {{c1::cephalic cone}}, unlike fasciola hepatica (liver fluke) However the eggs are too similar to differentiate&nbsp;</div><div><br></div><div>No clinical manifestations in light to moderate infections, but can cause {{c1::edema and obstruction}} in heavy infections</div></div>"
"Lung flukes such as {{c1::paragonimus&nbsp;}} infect the human by eating {{c1::infected crustaceans (crabs)<br><div><img src=""paste-08f407221be2aa1d0bcc5b8774561e294760c732.jpg"">}}</div><div>Paragonimus westermani flukes are brownish in color and {{c1::coffee bean shaped</div><div><img src=""paste-b2cab8b7e5592ea8f129ed66423ed10f83ca51b2.jpg"">:: Shape?<span>}}</span></div><div><span><br></span></div><div><span>The adult worm can be found in the </span><span>&nbsp;</span><span>{{c1::</span><span>lung</span><span>}}</span></div><div><span>Biopsies can be taken from stool, but also from the&nbsp;</span><span>&nbsp;{{c1::</span><span><i>sputum</i></span><span>}}&nbsp;</span></div><div><span>In the case of high eosinophilic count you can see&nbsp;</span>{{c1::charcot-leyden crystals}}<span>&nbsp;within the stool</span></div><div><span><i>Serology is sensitive and specific</i></span></div>"
Taenia saginata and taenia solium are {{c1::beef and pork tapeworms:: Type of worm and where they come from}} respectively<div><br><div>Taeniasis Infections of T. saginata and T. solium normally happens by {{c1::eating meat infected with larvae}}. Adults form in the GIT and release eggs in the stool (usualy asymptomatic but can cause discomfort)</div><div>Cystocercosis infections of T. solium if humans ingest the {{c1::eggs}}. Larvae will invade tissues (muscles/ CNS) and can cause severe symptoms (seizures/ epilepsy)</div><div>Taeniasis diagnosis by finding {{c1::proglottids}} in stool</div></div><div><br></div><div>Distinguishing the two tapeworms by the many lateral branches in saginata</div>"<img src=""paste-8fc4fc9072289c4f6ef16194a0b2346414e98786.jpg""><div><img src=""paste-c56087888e2559ad2c6d7f6b4865213939cdd747.jpg""></div><div><img src=""paste-254709f58bd8b461ee13d322e06354f77a6b2ff2.jpg""><br></div><div><br><div><br></div></div>"
"Diphyllobothrium latum is an intestinal cestode which infects humans by {{c1::eating raw/undercooked fish<div><img src=""paste-72176fa53bca1d26ae1e1514c64253301332dbf7.jpg""><span>}}</span></div><div><span><br></span></div><div><span>The primary host and reservoir is&nbsp;</span><span>{{c1::</span><span>humans</span><span>}}</span></div><div><span>Symptoms may include&nbsp;</span><span>{{c1::</span><span>vague abdominal pain and pernicious anemia</span><span>}}</span></div><div><span>Diagnosis is finding&nbsp;</span><span>{{c1::</span><span>non-motile proglottids</span><span>}}</span></div>""<img src=""paste-3bd999f1efd2fc9bcab66b4368220c26531aa304.jpg"">"
"Hymenolepis nana is an intestinal cestode infecting {{c1::humans and rodents}}<div>the cysticercoid larva develops inside a {{c1::villus of the ileum}}</div><div>The infection persists in humans via {{c1::auto-infection</div><div><b><img src=""IdKBrlqK7KoxV0dyoX7YxE0RI6ssHGfH0lEcXhUKN-s_qWvPKvZit7-Ise9gdoA2-s65I-aD-oeXHYGIYtOGlhXZnqKLaZydc9DS8Hf93d_kKp6OuzBZURbaY3hgRBMchdDQ.png""></b>}}</div><div><br></div><div>The same disease can be found in rats by the parasite {{c1::H. diminuta}}</div><div>It needs an intermediate host such as {{c1::rat flea}}, {{c1::cockroaches}} and {{c1::meal worms}}</div>""H. nana (look how happy he is to infect you)<div><b><img src=""Z4cdJACVS487h_lxb9hacdox1o4_ppplzTLT3TDiac6XjI8sDa7LhIjSzw6mIate6xrysYaPpG2NvptzlNJu5bX6OLZVtAb_zZrwxwPRobMtwF-opuCXw9pJG0TmwwXvkt9U.jpg""></b><br></div><div><b>H. diminuta</b></div><div><b><img src=""TVCnHLT4Z-A8ypz45ggx-_l3d3HoaD4ONs0PGS9yX1gqTwqMP-y6fjPGZYfuTr5BkJpmYR98xDxJEfdDGYjsu5GUAu9fuWG7O2FCqyW6cIpAz4b1Om9IOq3MybU4X3zRjwv-.jpg""></b><b><br></b></div>"
Diphylidium caninum aka {{c1::dog tapeworm&nbsp;}} can infect humans accidentally.&nbsp;<div>Transmission via {{c1::digestion of infected fleas}}</div><div>Prevent by {{c1::deworming}}</div>"<b><img src=""sxDaaC8A1qgIwiQRRxs0dJHWOVwUNrBqU5Iby6Z0pUH2lXOpsNpeAjxJojDvCWqF768zB4IumCKR8BVv987-81VwQAnijmtCW47CAMWwXie3b-k6es19RhK_qoOUglcvb5zg.png""></b>"
"Echinococcosis aka {{c1::Hydatid disease&nbsp;}} can be caused by two parasites: {{c2::E. granulosis (Dog tapeworm)}} or {{c2::E. multilocularis&nbsp;}}<div>The human host is accidental.&nbsp;</div><div><br></div><div>Depending on the spp it can have two forms:</div><div><br></div><div>Uniocular hydatid disease ( by {{c1::E. granulosus)</div><div><img src=""paste-944b6610ebd99d32197716b207bbf221822af694.jpg"">&nbsp;<img src=""Eg_cyst.jpg""><span>}}</span><br></div><div>Multiocular hydatid disease ( by{{c1:: E. multiocularis)</div><div><img src=""paste-d378502643ac44941f53cf8fcb580d42fc0bda28.jpg"">&nbsp;&nbsp;<b><img src=""8PUpQ6O87tquhkvN5Hch9wNjBa1rKMrtcMfzBtyOElO1MaNcI6nDP6TV5urz_VzB92-Rw6PZLJz9_CDD3ItuDGeLY48sNOqc5TG1TheZNNdrRF8bnq9J8pnviSF06XPxUqbc.jpg"">&nbsp;</b><span>}}</span><br></div><div><span><i>Larvae develop and enlarge as a space occupying lesion (in liver/ lung and brain etc)</i></span></div>"
Emerging vs. Re-emerging infections<div><br></div><div>Emerging: {{c1::Not previously recognized}}</div><div>Re-emerging: {{c1::Existed before but incidence increased}}</div>
Herpes viruses escape the immune system by being enveloped by {{c1::glycoprotein and fc receptors}}<div>Infections usually take place during childhood and are {{c1::lifelong:: Transient or lifelong?}}.&nbsp;</div><div>Reactivation occurs during {{c1::immunosuppression}}</div>
Herpes viruses have three classifications:&nbsp;<div><br></div><div>Alpha. characteristics: {{c1::fast growing}}, {{c1::cytolytic}}, {{c1::latency in neurons}}</div><div>Examples: {{c1::HHV-1 (<b>HSV1</b>)}}, {{c1::HHV-2 (<b>HSV2</b>)}}, {{c1::HHV-3 (<b>VZV</b>)}}</div><div><br></div><div>Beta&nbsp;<span>characteristics:&nbsp;</span>{{c2::Slow growing}}{{c2::, cytopathic effect}}<span>,&nbsp;</span>{{c2::l<span>atency in leukocytes</span><span>}}</span></div><div><span>Examples:&nbsp;</span>{{c2::HHV-5 (<b>CMV</b>)}}, {{c2::HHV-6}},<span>&nbsp;</span><span>{{c2::</span><span>HHV-7</span><span>}}</span></div><div><br></div><div>Gamma&nbsp;<span>characteristics:&nbsp;</span>{{c3::Slow growers}}<span>,&nbsp;</span>{{c3::lymphoproliferative}}<span>,&nbsp;</span><span>{{c3::</span><span>latency in lymphocytes</span><span>}}</span></div><div>Examples:&nbsp;{{c3::HHV-4 (<b>EBV</b>)}}, {{c3::HHV-8 (<b>KSV</b>)}}<span><br></span></div>HSV --&gt; Herpes simplex virus<div>VZV --&gt; Varicella zoster virus</div><div>CMV --&gt; Cytomegalovirus&nbsp;</div><div>EBV --&gt; Epstein barr virus</div><div>KSV --&gt; Kaposi's sarcoma virus</div>
Kaposi's sarcoma virus and HSV-2 are transmitted via {{c1::sexual contact}}
Once a virus infects a cell it produces three types of genes:&nbsp;<div><br></div><div>Immediate early genes: {{c1::Transcription factors}}</div><div>Early genes: {{c1::Genome and protein synthesis}}</div><div>Late genes: {{c1::structural protein synthesis&nbsp;}}</div>
There are two types of HSV<div><br></div><div>HSV-1 which infects {{c1::non-genetalia (usually mouth region)}}. latency is in the {{c1::trigeminal ganglion}}&nbsp;</div><div>HSV-2 which infects {{c1::the genetalia}}. latency in the {{c1::sacral ganglia&nbsp;}}<br></div><div><br></div><div>It prefers infecting {{c1::mucoepithelial}} cells leaving vesicles or ulcers containing the virus.&nbsp;</div><div><br></div><div>Neonatal HSV is rare, but frequently {{c2::lethal:: Asymptomatic or lethal?}}.&nbsp;</div><div>Transmission occurs either:&nbsp;<span>{{c2::In utero (transplacental)}},&nbsp;</span><span>{{c2::intrapartum}},&nbsp;</span><span>{{c2::postnatal (milk)}}</span></div><div><br></div><div>Treatment of HSV is via {{c2::acyclovir&nbsp;}}</div>"HSV2 prevalence seen more in women, black people, and increases with age<div>HSV can have severe manifestations especially in immunosuppressed patients</div><div><img src=""paste-34665b8a99f14c46a7bd2dae2e951fa5c3e7ec56.jpg""><br></div>"
VZV infections are usually self limiting. complications are rare and are more severe in {{c1::adults}} and {{c1::imunocompromised patients}}<br><br><div>In general, the most common complication is {{c1::a secondary bacterial infection of the vesicles&nbsp;}}</div>
RSV causes {{c1::LRTI::URTI or LRTI}} in children, but causes {{c1::URTI}} in adults
Rhinoviruses are {{c1::non-enveloped:: Enveloped or non?}} +ve ssRNA viruses which prefer infecting areas with {{c1::ICAM-1}} receptors<br>Most infections are {{c1::self-limiting::self-limiting or severe?}}<div>Kids are usually the reservoir</div><div>Symptoms include a runny nose, coughs and a headache, BUT NO {{c1::FEVER (uncommon)}}</div><div>Rhinoviruses with exacerbate asthma&nbsp;</div>
"Adenoviruses are non-enveloped dsDNA and infects {{c1::<b>mucoepithelial tissue</b>}}. it establishes latency in {{c1::<b>lymphoid tissue</b>&nbsp;}}<div>around 50 serogroups known.&nbsp;</div><div>Clinical manifestation include {{c2::<b>conjunctivitis</b>}} and {{c2::<b>inflamed oropharynx</b></div><div><img src=""paste-0d7558d44c7f2186bd8859d8042edb413872328c.jpg"">}}</div><div>The virus spreads via {{c3::<b>aerosols</b>}}, {{c3::<b>close contact</b>}} and {{c3::<b>fecal-oral route</b>}}</div><div>Vaccine is consists against serotypes 4&amp;7 and given to recruits of army forces&nbsp;</div>"
What do influenza and parainfluenza have in common in terms of structure? {{c1::hemagglutinin(H)}} and {{c1::neuraminidase(N) activity}}
"Respiratory syncytial virus (RSV) is an enveloped -ve ssRNA virus.&nbsp;<div>It has a protein on the surface which allows infected cells to merge producing multinucleated giant cells. that protein is called {{c1::F-protein (fusion)}}</div><div><i style="""">by the age of 3 90% of kids are already infected</i></div><div>Cases of RSV infections skyrocket during {{c1::winter because of the envelope::Season? }}</div><div>Replicates within peribronchiolar tissue leading to necrosis of bronchioles causing {{c1::bronchiolitis}}. other manifestations include {{c1::croup}} or {{c1::coryza-like illness}}&nbsp;</div><div><br></div><div>Pneumonia can be either due to {{c1::primary RSV infection}} or {{c1::secondary bacterial infection}}</div><div>Anti-RSV monoclonal antibody {{c1::palivizumab}} given to high risk infants</div>"
Measles is caused by the {{c1::<u>Rubeola (NOT RUBELLA)</u>:: }} virus
"Measles is usually an {{c1::<u>acute</u>:: Acute// chronic?}} disease with less commonly {{c1::<u>measles pneumonia</u>&nbsp;}}<div>Symptoms include {{c1::fever}}, {{c1::respiratory complications}} and {{c1::<u>a maculopapular rash</u></div><div><img src=""paste-d632d6bb4e0359fe5f58e62a91724ca114f41be9.jpg"">}}</div><div><br></div><div>Although its usually acute it can develop into {{c2::<u>post-infectious encephalitis (PIE)</u>}} or {{c2::<u>sub-acute sclerosin panencephalitis (SSPE)</u>}}</div><div>A live vaccine has been produced.&nbsp;</div>"
Envelope of measles contains two kinds of spikes: {{c1::<u>Hemagglutinin(HA)</u>}}<span>&nbsp;and&nbsp;</span>{{c1::<u>fusion protein (creates giant multinucleated cells)</u>}}<div>The receptor the virus binds to is {{c1::<u>CD46</u>}}</div><div>The natural host for measles is {{c1::<u>human (just like mumps, rubella and pox)</u>}}</div><div>Infections increase during {{c2::<u>winter and spring</u>}} seasons&nbsp;</div><div>The virus is transmitted primarily via aerosols which infects the {{c2::<u>URT</u>}}, {{c2::<u>nose</u>}} and {{c2::<u>conjunctiva&nbsp;</u>}} also spreads via urine but not really important&nbsp;</div>HA will neutralize antibodies
"Pathogenesis of measles:<div>After infection of the URT it will go to the draining lymph nodes resulting in {{c1::<u>primary viremia</u>}} which then disseminates the virus to the {{c1::<u>reticuloendothelial system especially the lymphoid tissue</u>}} resulting in another round of replication. Later a secondary viremia occurs resultng in {{c1::<u>the infection of vascular endothelium, then to the epithelium of the GI, RT and conjunctiva&nbsp;</u>}}</div><div><br></div><div>After 8-10 days of incubation the patient enters the {{c2::<u>prodromal</u>}} phase&nbsp; (fever/ malaise/rhinitis/conjunctivitis &amp; cough). Transient rash develops at the beginning of this phase, but then disappears prior to the onset of the typical {{c2::<u>exanthema (at day 14)</u>}} <i>THE PRODROMAL PHASE IS INFECTIOUS</i></div><div><i><br></i></div><div>2-4 days before the rash the patient develops {{c3::koplik's spots}} which are small raised spots with blue/whitish centers within the buccal mucosa&nbsp;</div><div>{{c3::<img src=""paste-aa055fc42dff5ce474588136a733b1be83506ed9.jpg"">}}<br></div>"
The measles rash happens approx 14 days after infection, and is due to {{c1::CTL response to infected cells in the BVs}}<div>Once youre immune it stays that way.&nbsp;</div><div>Immunity is IgG and CTL mediated, which is why children with agammaglobinemia have a {{c1::<u>normal (CTL response is more important than IgG)</u>:: Normal or abnormal?}} course of the disease&nbsp;</div><div><br></div><i>In patients with no CTL response there will be no rash</i><div><i>Children with cellular immunity deficiency do very poorly once infected.</i></div>
Complications of measles include:<div>{{c1::Post-infectious encephalitis (PIE)}}</div><div>{{c1::Sub-acute sclerosin pan-encephalitis (SSPE) is a slowly degenerating disease of the brain}}</div><div>{{c1::Measles inclusion body encephalitis (MIBE) seen in <u>immunosuppressed </u>patients (present without a rash)}}</div>"<img src=""paste-4ecac34f2c2dc7d2548c4256b45dd2c1c4675845.jpg"">"
Babies below 6 months are immune to measles due to {{c1::antibodies crossing from the mother&nbsp;}}<div><br></div><div><br></div>
Atypical measles can occur in the case of&nbsp;<div>Partially immunized individuals like {{c1::infants with residual maternal antibodies&nbsp;}}</div><div>{{c1::Failed live vaccine}}</div><div><br></div><div><br></div>
The MMR vaccine is given {{c1::twice (the second is a booster at 4-12 years):: Once, twice or thrice?}}<div>You never give the vaccine to immunocompromised or pregnant patients because {{c1::its a live attenuated vaccine}}</div><div>Quarantine isnt effective because {{c1::patient is infectious during the prodromal phase (before the rash where it looks like a normal cold)}}</div>
<u>Mumps </u>is an acute contagious disease characterized by {{c1::non-suppurative enlargment of one or both salivary glands&nbsp;}}<div>It contains two kinds of spikes on the envelope, {{c1::one acting as both hemagglutinin and neuraminidase}} and {{c1::the other as fusion protein}}</div><div>The natural host for mumps is {{c1::human (just like measles, rubella and pox) }}</div><div>Transmission is via respiratory droplets or direct contact and infects the {{c1::epithelium of the nasal or upper respiratory tract}}</div>"<div><img src=""paste-f21e72f25d64e7de56bc9ce6754051e4b6f5a8d9.jpg""><br></div><img src=""paste-413c94c636cc143e668df039c6f794bf92666f3d.jpg"">"
"Mumps is a systemic viral disease which replicates within the {{c1::epithelium of various organs}}. it can be detected in urine<div>The characteristic of this disease is the swelling of&nbsp;{{c1::<b>the parotid glands</b> associated with pain</div><div><img src=""paste-8a844124106fef4d4ed2e4c4ae891fadccb26dd0.jpg""><span>}}&nbsp;</span><br></div><div><span><br></span></div><div>Involvement of the CNS is common causing {{c1:: <b>aseptic&nbsp;meningitis</b>}} and {{c1::<b>meningoencephalitis</b>}}. Both resolve without sequel but unilateral deafness has been recorded</div><div><br></div>"
Isolation of mumps is futile because {{c1::of the presence of asyptomatic patients}}.&nbsp;<div>The vaccine should not be given to {{c1::immunocompromised patients and pregnant women}}</div>
Rubella infection results in an acute febrile illness characterized {{c1::a rash}} and {{c1::lymphadenopathy&nbsp;}}<div>It is severe in the case of pregnant women since is causes {{c1::congenital malformation and mental retardation (Like CMV and zika)}}</div><div>It is a member of the toga viruses BUT NOT TRANSMITTED VIA ARTHROPODS</div><div>The only natural host is human (MMR in general is human)</div>
The development of the rash in rubella coincides with {{c1::the development of antibodies}}. After this it is only detectable in the nasopharynx<div>Rash starts in the face then to the extremeties</div>
Rubella virus is a teratogen especially if it infects during the {{c1::first}} trimester<div>The classic triad includes: {{c1::cataracts}}, {{c1::cardiac abnormalities}} and {{c1::deafness}}</div>Women that take the vaccine must take contraceptives for the next three months (DO NOT CONCEIVE)
"There is no treatment for smallpox, only {{c1::vaccination}}&nbsp;<div>The disease infects {{c1::a wide range of hosts</div><div><img src=""paste-38d5488cfdcfe7e7baef846f5670c6c5da5d9f64.jpg"">:: different hosts or only humans?&nbsp;<span>}}</span></div><div>small pox has been eradicated since 1980 but concerns are that it will be re-introduced as a biological weapon so you gotta learn it now&nbsp;</div><div><br></div><div><br></div>""I think the RESERVOIR is human but it CAN infect various animals<div><img src=""tenor.gif""><br></div>"
The vaccinia virus is a non-pathogenic virus used as a vaccine for {{c1::smallpox}}
just like MMR smallpox's natural host is {{c1::human&nbsp;}}<div>Transmission is via {{c1::aerosols}}, {{c1::direct contact}}, or {{c1::fomites}}</div><div><br></div>
The believed pathogenesis of smallpox includes:<div>{{c1::Primary multiplication within lymphod tissue}}&gt; {{c2::transient primary viremia}}&gt; {{c1::infection of reticuloendothelial system}}&gt; {{c2::secondary intense viremia}}&gt; {{c1::febrile exanthema}}</div>Infects the reticuloendothelial system just like measles&nbsp;
"<div>In smallpox:</div>Viral replication occurs before exanthema during the {{c1::incubation period around 10-14 days after infection&nbsp;}}<div><br><div>early during the disease (around day6-9) Infectious virus originate in lesions in the {{c1::mouth}} and {{c1::URT}}. Before the exanthema they ulcerate and discharge the virus&nbsp;</div></div><div><br></div><div>After the incubation period {{c1::prodromal}} symptoms occur (fever and malaise)) for 1-5 days, then the formation of {{c1::exanthema}} occurs</div><div>{{c1::<img src=""paste-9cdb74aa35133240f5384c329c0b6a5b98d1e3ed.jpg"">}}<br></div><div><br></div><div><i>The lesions throughout the body wil be in the same stage of development (chicken pox will have different stages throughout the body)</i></div><div><br></div><div>Antibodies alone do not suffice for recovery, need {{c1::cell mediated immunity&nbsp;}}</div>""<img src=""paste-ea27c2802acb996013a440df7b5399cbc2508f61.jpg""><div>After onset of rash papules are seen on day 3 and 4, vesicles on day 5, postules of day 7 and 9, scabs on 13</div>"
Smallpox rash appears on the palms and soles, unlike {{c1::chickenpox&nbsp;}}<div>Smallpox also has more lesions on the arms and legs&nbsp;</div><div>Death due to smallpox is common.&nbsp;</div>"<img src=""paste-1c7fe73b2753c8648ca540f4a1b2866f2e89f65f.jpg"">"
Death due to chickenpox is uncommon, if it does occur though you should suspect undiagnosed {{c1::smallpox <u>(however this is an eradicated disease so I dont think this should be considered nowadays)</u><span>&nbsp;}}</span>
In smallpox, the person is contagious during the onset of the fever (prodrome phase), but is MOST contagious during {{c1::the onset of the rash}}<div>the person remains&nbsp;<span>Infectious until&nbsp;</span><span>{{c1::</span><span><b>the scabs fall off</b></span><span>}}</span></div><div><br></div><div><i>THERE ARE NO ASYMPTOMATIC CASES OR PERSISTENT CARRIERS.&nbsp;</i></div><div><br></div>
The vaccinia virus is used to vaccinate against smallpox.&nbsp;<div>It is inoculated intradermally, and the formation of a {{c1::vesicle}} indicates a success</div><div>Vaccinations stopped since 1971, and majority of people are susceptible since {{c1::they arent immune to it&nbsp;}}</div><div>It is believed that the vaccinia virus is the predecessor of the {{c1::cowpox virus}}</div><div><i>vaccinia has a broad host range</i></div>"<img src=""paste-2bf2346e5153bbf44fcf07f5204b8fc9dd29f81a.jpg""><img src=""paste-891bab42437fbd619329dff5bc7d27c1fb7ac77d.jpg"">"
"Exudate inflammation is usually made out of {{c1::pus (dead neutrophils and tissue)}}<div>Typically its caused by {{c1::localized extracellular pyogenic bacteria&nbsp;}}</div><div><img src=""paste-99da4e11bcd3e2886702e7f583518a35b13142d7.jpg""><br></div><div><br></div><div>Necrotizing inflammation results directly from {{c1::bacterial toxins}}</div><div><img src=""paste-bc9de9ad7824d3cb50ded8629cb94b3a800468c8.jpg""><br></div><div><br></div><div>Granulomatous inflammation caused by bacteria resisting death, usually are {{c1::intracellular bacteria (Like TB)</div><div><img src=""paste-9957b4caf5b29080722fd1a07f8187df9d842e66.jpg"">}}&nbsp;</div><div>Granulomas are formed when macrophages secrete {{c1::TNF-alpha and GM-CSF}}, and Th1 secrete {{c1::IL-2 and INF-gamma}}</div><div><img src=""paste-63e168bf6cc251aa465771a68277b8cb1d5cea6a.jpg""><br></div><div><br></div><div>Interstitial inflammation is a chronic non-specific inflammation with infiltrates of lymphocytes macrophages and plasma cells. This suggests a {{c1::viral, or spirocheta infection (syphilis)</div><div><img src=""paste-0e4a204c97cad5688f39046845957df0cec51d7f.jpg"">&nbsp;</div><div>(lymphocytic plasmocytic infiltration)}}</div><div><br></div><div>if it is seen with the presence of inflammation or necrosis of the vascular wall it suggests a {{c1::Rickettsia rickettsi}} infection</div><div><br></div>"
"You see a case where black rods are seen on the surface of the gastric mucosa. You notice that they exert toxins causing vacuolation. This pathogen is urease positive<div><img src=""paste-2c36cd1b5f8ad4f29e5dfe90945d826b6b7af5c6.jpg""><br></div><div>Offending agent? {{c1::H. pylori&nbsp;}}<br></div>"
"Chlamydia is an intracellular infection, which can be identified under the microscope by {{c1::eosinophilic vacules&nbsp;<div><img src=""paste-69a4c70ace96b5b3cd78a8446387f7e21c82bf6e.jpg""></div>}}"
Null reaction which is the absence of inflammation, necrosis or cytopathic signs may indicate a defect in {{c1::the host immune response}}
"Upon a cervical smear you see a bunch of cells with multiple nuclear inclusion looking like a basket of eggs.&nbsp;<div><img src=""paste-18c3296b85e9ec1eaaf40a9616719ceddf944772.jpg""><br></div><div>What do you suspect (its viral)&nbsp;</div><div>{{c1::HSV}}</div>"
"After a cervical smear you notice a sort of ""balooning"" of the cell with very clear cytoplasm&nbsp;<div><img src=""paste-de07d6c5a390cdec28bb22a486c801176b65dd44.jpg""><br></div><div>what do you suspect? {{c1::HPV}}</div>"
"A patient comes to you after a dog bite. You took a biopsy of site and find neurons with negri bodies&nbsp;<div><img src=""paste-21ae66729d24d47c9e7c023e20db645cd597c24c.jpg""><br></div><div>What't the offending agent? {{c1::Rabies&nbsp;}}</div>"
"After a renal transplant a biopsy was taken to follow up the patient. the biopsy included tubulo-interstitial nephritis and mimicked rejection, but that wasnt the case<div><img src=""paste-5b7c9ad86889a551c80d2c0c36b9e008f61bb21a.jpg""><br></div><div>Offending agent?&nbsp;</div><div>{{c1::B-K virus. Treatment is to decrease immunosuppression, rather than increase in the case of graft rejection}}</div>"
Rabies is caused by a {{c1::bullet}}-shaped unsegmented -ve RNA virus<div>It codes for {{c1::5}} core proteins<br><div>The virus is {{c1::neuro}}-tropic causing fatal encephalitis&nbsp;</div><div>The entire cycle of the virus occurs within the {{c1::cytoplasm}}. RNA polymerase and modification are virally coded.&nbsp;</div></div><div><br></div><div>The incubation period is usually {{c1::long (20-90 days but can be years)}}</div><div>Upon infection the virus travels <b>retrograde </b>via {{c1::peripheral neurons}} to the brain where it replicates within the {{c1::grey matter}}</div><div>Steps of the viral life cycle:&nbsp;</div><div>Viral Gprotein binds&gt; membrane fusion and core release&gt; Transcription and translation of mRNA&gt; accumilation of nucleocapsid protein and switch to replication&gt; Glycoprotein embeds into plasma membrane&gt; nucleocapsid associated phosphoprotein and RdRp organized into a bullte shape by matrix protein&gt; cores bud where the glycoprotein&nbsp;</div>
In rabies once clinical symptoms appear {{c1::patients deteriorate rapidly to death despite treatment (RIP):: What next?}}<div>The classic rabid sign is {{c1::hydrophobia}}</div><div>Final stages of the disease is mania, convulsions and coma&nbsp;</div>
Management of a patient exposed to rabies is either&nbsp;<div>pre-exposure prophylaxis which includes {{c1::the inactivated rabies vaccine}}</div><div>Post-exposure prophylaxis give {{c1::RIG IM at the site of bite and active immunization&nbsp;}}</div><div>Once symptoms appear its hopeless.&nbsp;</div>
DNA viruses replicate using the <b>host's </b>{{c1::DNA-dependant DNA}} polymerase&nbsp;<div>DNA-based viruses include:&nbsp;<i><span>HSV,&nbsp;</span><span>VZV,&nbsp;</span><span>HPV,&nbsp;</span><span>EBV,&nbsp;</span><span>Pox virus, Adenovirus</span></i></div><div><i><span><br></span></i></div><div>RNA viruses replicate using <b>viral </b>{{c1::RNA-dependant RNA}} polymerase</div><div>RNA-based viruses include: <i>SARS, West nile fever, Polio, measles, influenza, rhinovirus, hepatitis (except B) HIV</i></div>
Antiviral drugs:&nbsp;<div><br></div><div>Drugs that<b> inhibit uncoating</b> of the virus used for respiratory viral infections (like influenza//RSV): {{c1::<u>Amantadine</u>}} &amp; {{c1::<u>Rimantidine</u>}} --&gt; Will target M2 protein</div><div><br></div><div>Drugs that inhibit the release of viral particles from infected cells (Influenza): {{c2::Zanamivir}} &amp; {{c2::Oseltamivir}} --&gt; Inhibits Neuraminidase</div><div><br></div><div>Ribavirin is a {{c1::guanosine}} analog which inhibits RNA-dependant RNA polymerase used primarily in RSV. it is teratogenic tho</div><div><br></div><div>Palivizumab is a monoclonal antibody used to target the F glycoprotein in {{c2::RSV}}</div><div><br></div><div><br></div>
{{c1::Interferons}} are naturally produced proteins with an anti-viral function. They work by inhibiiting viral RNA translation leading to degredaton of viral mRNA and tRNA"<img src=""paste-756eaa0b866cd118308d9d828d831f759400a603.jpg"">"
Interferon {{c1::<b>alpha 2a</b>}} has been approved for the treatment of <b>chronic HepC</b>, <b>AIDS</b>, <b>Kaposi's sarcoma</b> and <b>CML</b><div><br></div><div>Interferon {{c1::<b>alpha 2b</b>}} has been approved for treatment of<b> HepB</b> and <b>acute HepC</b></div>
"{{c1::<b style="""">Lamivudine</b>}} is a <b style="""">cytosine analog</b> used to inhibiting HepB DNA polymerase&nbsp;<div><br></div><div>{{c1::<b>Entecavir</b>}} is a <b>guanosine analog</b> inhibiting HepB DNA polymerase</div><div><br></div><div>{{c1::<b style="""">Telbivudine</b>}} is a <b style="""">thymidine analog</b> inhibiting&nbsp;HepB DNA polymerase</div>"
Acyclovir is a guanosine analog activated by viral {{c1::thymidine kinase}}. it causes premature DNA chain termination&nbsp;<div>{{c1::<u>CMV</u>}} is resistant because it lacks thymidine kinase (use ganciclovir)</div><div>Acyclovir is used to treat herpes simplex encephalitis. It only affects {{c1::actively replicating}} viruses&nbsp;</div><div><br></div><div>{{c1::Foscarnet}} is a non-nucleoside analog used for acyclovir resistant herpes and CMV retinitis&nbsp;</div>
Bacterial causes of neonatal meningitis:<div>{{c1::Listeria}}, {{c1::E. coli}}, {{c1::Group B streps&nbsp;}}</div><div><br></div><div>Bacteria causing meningitis later in life:</div><div>{{c1::Neisseria meningitides}}, {{c1::H. influenza}}, {{c1::Pneumococcus}}</div>