Class: Fundamentals II
Professor: Waites
Date: 11/15/2010
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1
Scribe: Abigail Grace Northcutt
Proof: Coty Elizabeth Cantrell
Pathology of Infectious Diseases [S1]
a. We talked about things from the microbial perspective, now we’ll talk about disease
from the host perspective
i. different types of organisms & their effects on humans
ii. bacteria, viruses, fungi, & eukaryotic parasites
1. mechanisms and presentations of disease with examples of microbes that
cause these diseases
Learning Objectives [S2]
a. Read slide
Top 10 Causes of Death [S3]
a. Why is infectious disease important?
i. Currently: cholera in Haiti  diarrheal disease
1. If they have sanitary water then you don’t have cholera (stems from poor
public health)
b. pink = infectious disease
i. has a potentially greater role than shown here b/c even with some of the other
causes of death, it is actually an infection that kills you
1. ie. Have cancer then get an infection that you can’t clear  die
2. Chronic obstructive pulmonary disease – infection gets stuck in lungs
Host Resistance to Infection [S4]
a. This is built into our bodies
b. Genetics: there are many conditions that predispose you to infection
i. ie. X-linked hypogammaglobulinemia
c. Anatomy & Physiology: important defense mechanisms
i. Ie. Clearing of urine – if you can’t empty bladder completely it can cause urinary
tract infection
1. Peripheral neuropathy, spinal chord injury, diabetes can all cause this
d. Immunocompetence
i. Ie. Coughing – if you have a trach tube put in, it bypasses the muco-ciliar cells &
introduces foreign matter which inhibits you from coughing to clear bacteria
e. Circulatory/Ventilatory Status: if you get a wound and don’t have good circulation to
clear the infection it can form an abscess
f. Underlying Disease
i. Cancer – less able to fight infection
Natural Barriers to Infection [S5]
a. Understand how all the things in our body & all our systems help protect our body
Sources of Systemic Infection [S6]
a. there are many things that circumvent these anatomical barriers
b. Skin: very important in keeping out infection; lost when you have burns
i. ie. Patients in hospital with burns have fungal infection
c. Catheter – UTI
d. Trach-tube – respiratory infection
e. Dental Work on someone with an abscessed tooth  need proper Ab coverage to
avoid a brain abscess
Host-Parasite Relationship [S7]
a. Precise symbiotic relationship with normal flora is important for normal health
i. normally don’t cause a problem unless they are disrupted
1. ie. Staph aureus in our nose
ii. ie. If you get HIV, some bacteria that have been dormant for years wake up & take
advantage of the lack of T-cells to defend the host
b. Highly virulent, produce disease, & easily established in the host = good infectious
material
i. ex. small pox: is supposedly eradicated so we don’t get vaccinated anymore –
could be used as an agent of bio terrorism
Class: Fundamentals II
Professor: Waites
Date: 11/15/2010
2
Scribe: Abigail Grace Northcutt
Proof: Coty Elizabeth Cantrell
1. if any person got small pox it could be easily spread to a lot of people
quickly & efficiently
2. has high virulence, high infectivity, and easily spread
ii. ex. candida: normal flora in body
1. if your normal flora is disrupted it can become opportunistic
2. has low virulence & infectivity but can cause problems
VIII. Infection vs. Colonization [S8]
a. Infection: reaction to invasion of microbe (to its presence or toxin)
b. Colonization: don’t get disease from all bacteria that we are colonized by
i. there are even pathogens that we can be colonized with but don’t ever get infected
IX. Exogenous vs. Endogenous [S9]
a. Endogenous: things that are in our body already (ie. Candida)
i. ie. Iatrogenic/Nosocomial (hospital infection) are usually endogenous but may be
exogenous
X. Extracellular Pathogens [S10]
a. depends on how & where they produce disease and how the body deals with the
pathogen
b. phagocyte metabolism – extracellular pathogens must avoid phagocytosis in some
way
i. S. aureus: makes leukocidins – kill leukocytes so they can’t eat Staph = important
virulence factor
ii. Crypt. Neoformans: capsule pictured on slide – masks Ag’s so immune system
doesn’t recognize them
iii. Strep. Pneum: has so many serotypes that the immune system makes specific Abs
for one type and is susceptible to all of the new types
1. “Each one is like meeting a new friend that can cause disease.”
XI. Facultative Intracellular Pathogens [S11]
a. want to be taken up by phagocytes in order to hide from Immune cells
b. can live & some can even multiply inside the phagocyte until they are ready to leave
the cell
c. tend to produce chronic disease
d. don’t need capsule or toxin because they don’t care if they get eaten
e. resistant to phagocytic compounds
f. ex. Listeria: primarily food borne pathogen
XII. Obligate Intracellular Pathogens [S12]
a. Facultative: live as extra or intracellular pathogens
b. may need to use host cell machinery to carry out their functions
i. more difficult to culture in the lab b/c they need an environment similar to that
inside the cell
ii. Ehrlichia: parasitizes human WBC’s, Rickettsia like organism
1. transmitted by ticks & causes neurological disease
XIII. Other Examples of How Microbes Evade Host Immune Response [S13]
a. bacteria’s goal is to survive & reproduce so they need to conceal themselves from
host
b. C. difficile: most common cause of diarrhea in the hospital, anaerobic
i. usually in a patient that is given Ab’s which kill off normal flora in colon
1. especially antibiotics that treat/kill other anaerobic bacteria
ii. recognizes the environment that it can now grow in  damages colon  bloody
diarrhea
iii. lives in the mucous layer so it is not seen by the immune system
c. E. coli: If you don’t get lysed by complement “you can go on and be an E. coli”
d. Shift presents new flavors of influenza each year b/c our body is only immune to the
exact type we’ve already seen
e. HIV kills Thelper cells, If T-cells can’t stimulate immune system, the virus gets the
upper hand, can result in many opportunistic infections
Class: Fundamentals II
Professor: Waites
Date: 11/15/2010
3
Scribe: Abigail Grace Northcutt
Proof: Coty Elizabeth Cantrell
f. IgA secretory immunoglobulin is broken down by N. gonorrhoeae before the IgA can
get to it
XIV. Transmission & Communicability [S14]
a. better to prevent infections from happening than to treat it after you get it
i. What’s the cause, what are the properties of the microbe, how is it spread, how do
we recognize it?
b. many diseases can be spread in more than one way
c. Direct Spread: mucosa to mucosa (sexually or vertically)
d. Droplets: common cold; cough or touch a surface
e. Water: cholera
f. Food: meat, dairy
g. Soil: fungal organism, if breathed in the form of dust – may cause respiratory
infection
h. fomites: on surfaces, ie. sharing needles
i. Transplacental: from mother to fetus = vertical transmission
j. Perinatal: transmitted at the time of delivery – may or may not be vertical
k. Animal: rabies transmitted by animal bite (in saliva of animal) – bats & skunks can
carry the virus for prolonged periods
i. salmonella is also zoonotic – “That’s why you should never kiss your turtle.”
l. Arthropod: malaria - mosquitos, rocky mnt spotted fever – ticks
m. “Think about everything you can catch just by going about your daily lives.”
XV. Histopathological Responses to Infection [S15]
XVI.
1. Exudative [S16]
a. empyema = pus in a body cavity instead of in tissue
b. abscess = pus in tissue, acute infection
c. gram + (Ie. Staph or strep)
XVII. 2. Necrotizing [S17]
a. toxin that causes necrosis of tissue
i. lots of necrotic activity but doesn’t have a lot of immunologic response
b. Gas Gangrene: highly eosinophilic muscle fibers – muscles are dead or dying =
brighter red staining
i. Clostridial toxins kill muscle cells
c. anaerobic bacteria – produces lots of metabolic bi-products which causes bubbles in
tissue
d. may see some WBCs or bacteria but the main thing is the necrosis caused by the
toxin
e. Mentioned Diptheria case in IP Lab
XVIII. 3. Granulomatous [S18]
a. foreign bodies & diseases (sarcoidosis)
b. typically chronic infections
c. made of monocytes that become macrophages then turn into epitheloid cells & Giant
cells
d. acid fast stain of this tissue may show bacteria in the granuloma
XIX.
4. Interstitial (Mononuclear) [S19]
a. Coxsackie viruses  myocarditis
i. child got the virus & went into heart failure a few days later
ii. virus caused inflammation in the heart – myocardial cells interspersed with
aggregates of lymphocytes & monocytes (no neutrophils)
1. seen in acute viral meningitis or pneumonia
iii. Interstitial = usually virus
XX. Cytotoxic/Cytoproliferative [S20]
a. Cytomegalovirus: viral inculsions, may also have
i. herpes & CMV can also produce inclusions
ii. pic = kidney tissue from neonate that died from CMV disease: enlarged cells with
viral nucleic acids
Class: Fundamentals II
Professor: Waites
Date: 11/15/2010
4
Scribe: Abigail Grace Northcutt
Proof: Coty Elizabeth Cantrell
Pathogenesis – Bacterial Infections [S21]
Pathogenesis of Pyogenic Bacterial Infections [S22]
a. bacteria must attach & multiply
b. often produce exotoxins when they attach
i. also stimulate neutrophils to respond which can also damage tissue
c. abscess is often a result of the bacteria’s actions as well as the body’s response to
the infection
XXIII. Tissue Penetration [S23]
a. when bacteria penetrate the cells you can get a spreading infection = cellulitis
b. H. influen = bacterial infection of the eye; orbital cellulitis
XXIV. Tissue Penetration & Toxin Production [S24]
a. Strp pyo: shows necrosis of skin in association with protease producing virulent
toxins
i. spreading throughout the tissue & causing fasciitis
1. may have to cut off limb
XXV. Attachment to Host Cell Surface Adhesins & Receptors: Mycoplasma pneumoniae
[S25]
a. No cell wall – appears serpentine
b. elaborate organelle allows it to attach to specific receptors on respiratory tract
i. cause cilia to stop beating
c. stimulates Ab formation – can measure Ab response to this bacteria
d. sialic acid receptor = integral for it to produce disease
XXVI. Multiplication of Organisms: Streptococcus pneumoniae [S26]
a. Don’t have to produce toxins
b. lung fills with fluid which allows bacteria to grow in alveoli
c. changes pH of lung & alters host metabolism
XXVII. Chronic Infections [S27]
a. allows for chronic & often asymptomatic infections
XXVIII. Autoimmune Reactions [S28]
a. A lot of damage is due to our body’s reaction to the pathogen
b. Mitral valve = most commonly affecteb by Rheumatic valvular heart disease
c. Ab’s produced by strep are cross-reactive with Ag in heart tissue can result in two
effects
i. Rubber valve (stiff & thickened) or Stenotic  heart failure
ii. Damaged valve is at risk for infection
iii. “Step has done long ago left” but you still have the effects due to host response
not bacteria
1. 90% host and only 10% bacteria
iv. Sarchoidosis? Diabetes? Pathogen?
XXIX. Exotoxins vs. Endotoxins [S29]
a. b/c of LPS all Gram – have endotoxin & only gram – have endotoxin
i. b/c LPS is found in cell wall
b. exotoxins made by bacteria & secreted
XXX. Exotoxins: Cholera Toxin [S30]
a. cholera interferes with electrolyte reabsorption in the gut mediated by cyclic AMP
i. loose tremendous amounts of fluid
ii. most at risk of mortality = elderly & young children
b. treatment = restoration of fluid
c. usually kills elderly & young
XXXI. Bacterial Endotoxins [S31]
a. endotoxin produces lots of different effects b/c it effects many aspects of the body
XXXII. Biological Actions of Endotoxin in Septic Shock [S32]
a. don’t have to memorize this, just know that endotoxin can cause many varied effects
i. endotoxin from many different pathogens can cause these effects
ii. all these effects come together to cause Septic Shock
XXI.
XXII.
Class: Fundamentals II
Professor: Waites
Date: 11/15/2010
5
Scribe: Abigail Grace Northcutt
Proof: Coty Elizabeth Cantrell
b. impaired temp regulation = fever
c. Meningococcal meningitis causes profound circulatory distress & DIC
XXXIII. DIC – gangrene of digits in meningococcal sepsis [S33]
XXXIV. Bacterial superantigens [S34]
a. tremendous outpouring of cytokines which can cause many manifestation
b. ie. Toxic shock syndrome
[End 51:37 mins]