lecture exam 3 you got this!

Transient- occupy body for short period. Skin surface

Resident- more permanently. Fluctuate with health, age, hormone, drugs

Microbial antagonism- microbes against intruder microbes

Deep of epidermis, gland, follicle

Staphylococcus, corynebacterium, propionibacterium, yeast

Resident microbiota/indigenous microflora/ commensal

colonized on outer surface without penetrating sterile tissue

Infection- microbe penetrated sterile tissue and multiplied. Microbe is now a pathogen

Infectious disease- cause damage to tissue/organ

Sterile

heart, ovaries, bones, lung, muscle

Resident microbs

skin, vagina,GI tract, respitatory

When water breaks

Baby:First solid food, teeth erupt,

Adults: puberty/menopause, long antibiotic, diet, disease

on epidermis, gland follicle, not dermis

•Staphylococcus, Streptococcus, Pseudomonas, Micrococcus, Propionibacterium, corynebacterium

Fungi: Candida, malassezia

Arthropods: demodex mite

Mouth: Very diverse environment

 Streptococcus

 S. mutans & S. sanguinis = cavities sticky dextran slime

Large intestine

 Obligate anaerobes (no air),  Clostridium, bacteroides, bifidobacterium

Coliform (gram - , Facultative anaerobes that ferment lactose)  E. coli, enterobacter, citrobacter in small #

Little microbiota in Esophagus/stomach/small intestine- digestive enzyme and violent swallowing

Pharynx- oral streptococci. 

Nasal entrance- Staphylococcus aureus

in mucous membrane of nasopharynx- Neisseria 

None in bronchi and lung

Kidney, ureter is sterile through urine

Female- Vagina and urethra 

Urethra- nonhemolytic streptococci, staphylococci,

diphtheroid, escherichia, gardnerellla, corynebacteria

Vagina shift to acid producing lactobacilli

Males- outer urethra

•True pathogens (primary): Capable of making a person with a functioning immune system 

flu, plague, cold, malaria, rabies

(high virulence factor)

Opportunistic pathogens: Only capable of causing disease in a weakened host or they are established somewhere not natural to them

Old age, organ transplant, chemotherapy

Pseudomonas, candida albican (

(low virulence factor)

Virulence- ability of microb to establish into host and cause damage

Finding a portal of entry,- skin GI 

attaching firmly- fimbriae, capsules

surviving host defense- avoid phagocytosis

cause of damage and disease- direct(enzyme) and indirect (host response is inappropriate)

existing host- respiratory tract, fecal

Streptococcus and staphylococcus, S. aureus s can enter multiple ways, some need specific

Conjunctiva/ broken skin- chlamydia trachomatis, staphylococcus

Gastrointestinal- salmonella, shigella, hept A

Respiratory- mumps, streptococcal sore throat

Urogenital- UTI, STD, STI

Pregnancy through placenta- STORCH(syphilis, toxoplasmosis, (HIV,hepB), rubella, cytomegalovirus, herpes) common for infants

Exogenous- microb enter from environment

Endogenous- microb already in body 

Infectious Dose:  The number of individual microbes needed to initiate infection

low- locally and immediately; high need to travel through body

salmonella need high ID to cause infection (acid kills)

adhesion: fimbriae, capsules, spike, hooks etc.

Virus- specialized receptors.

Can’t bind= non infectious

Virulence factor- microbe characteristics that help(antiphagocytic, enzyme, toxin)

Antiphagocytic factor- how pathogen avoid/kill phagocytes. 

Ex. strep and staph produce leukocidins that are toxic to WBC.

pathogen avoid/kill phagocytes. 

Ex. strep and staph produce leukocidins that are toxic to WBC.

Thick capsules (streptococcus pneumoniae) difficult for WBCs to engulf 

 Some pathogens can live inside WBC (Listeria, HIV)

Exotoxin- toxin secreted by living bacteria

Toxic in small doses, specific cell type

die in heat

Eg. Hemolysins found in Staphylococcus and Streptococcus cause lysis of red blood cells

Endotoxins- toxin released after damaged/lysed

•Toxic only in high doses, not specific

toxin on lipopolysaccharide (LPS) layer of the gram -cell wall

does not stimulate antibody

fever, shock, pain…

bacteria produce this to disrupts the structure of tissue

incubation period- portal of entry to first symptom ~2-30 days

prodromal stage- discomfort, headache

Invasion - multiplies at high level, greatest toxicity, well established (fever, cough)

convalescent period- recover

Local:  Infection is restricted to a specific location(boils, skin infection, wart)

Systemic:  Infection spreads throughout body(viral: measles, aids, chickenpox)(bacterial:brucellosis, anthrax, syphilis)(rabies)

Focal:  Infection is local but effects are systemic (often due to toxins)(tuberculosis, streptococcal pharyngitis) (toxemia- localized infection but toxin carried by blood to target)

Mixed infection- infection contains more than one microb (dental caries, wound infection)

Primary:  First of multiple infections

Secondary:  Only occurs because primary infection weakens the host defenses

Eg. Chicken pox then gets Staphylococcus aureus

Acute infection- severe but short lived effects

Chronic infection- persist over long period of time

Signs are objective evidence- fever, bacteria in urine, increase heart rate (more precise)

Symptoms are subjective felt by patient - chills, itching, 

cough/sneezing, epithelial, diarrhea, semen, insect bite, remove blood

recurrent disease)- herpes

(long term damage•Long covid

•Reservoir: Primary habitat of a microbe (cow)

•only reservoir of Shigella = feces, soil and water

•Source:l source of infection acquired ex.Contaminated burger

tudy of frequency and distribution of disese in human population

Centers for Disease Control (CDC)

World Health Organization

MMWR (Morbidity Mortality Weekly Report

National Notifiable Disease Surveillance System

Occurrence of disease is tracked using two measures, Prevalence and Incidence

Carriers-People who carry pathogens without showing overt signs of disease but may pass the pathogen to others.

Asymptomatic- carrier but no symptoms, can spread to others

Chronic- carry infection for a long time after recovery (herpes, hepatitis)

Convalescent- recovering patient without symptoms. But can still spread

passive carriers- transfer of infectious agent through contact(hospital)

Vector- animals that transmit pathogens

Biological vectors:  Animals that participate/ multiply a pathogen,  (malaria)

Mechanical vector:  Animals that transport pathogen without being infected (E. coli, house fly)

Infection normally found in animals but may be spread to humans (rabies)

Sick animals reported via sentinel animals

Direct infection: microb spread through skin or mucous membrane contact.  Sex, kissing, sneezing or coughing on someone

Indirect spread: microb spread from host to object then another person.(Food, water, fomites, air)

Communicable:  May be spread person to person  (colds, sexually transmitted disease)

Contagious:  Easily spread person to person (measles, chicken pox) very communicable

Non-communicable: Not spread person to person (Tetanus)

Horizontal transmission:  spread from Person to person

Vertical transmission:  Parent to child (birth, nursing…)

indirect transmission, vehicle is contaminated with fecal and transported to mouth

pellets of mucus/ saliva from mouth and nose,extend the survivability of pathogens

fine dust/moisture in air that contain live pathogen

Surveillance- collecting, analyzing, reporting data on rate of occurrence, mortality, morbidity, and transmission of infection. Reportable and notifiable disease. 

Prevalence: # case/ total # people

Incidence: # new case/ # at risk people

Mortality rate- # death

Morbidity- # people afflicted with disease

Endemic:  Disease with a steady frequency in specific geographic 

Sporadic:  Occasional cases are seen at irregular intervals in different locations

Epidemic:  New cases rise beyond what is expected

Pandemic:  spread of epidemic across continents

- # cases per # of days

Point source- infectious agent came from a single source(bbq)(1 peak)

•Common,source epidemic- all cases came from exposure to same course (restaurnat workers everytime he works)(multiple peak)

-Propagated epidemic- disease transmitted person to person. (gradual growth in spikes overtime)

Used to link specific organisms to specific disease 

Infection of unknown etiology is isolated, pure culture is created, inoculate of test animal, observe for disease, obtain pure culture. Microbes from inital and after disease must match for postulate to be satisfied

Healthcare associated infection-disease acquired/developed in hospital

•Water needs to be potable: No pathogens, toxins, turbidity, odor, taste

Water pick up pathogens, snow, lake, therefore it is open 

•Water is tested for indicator organisms like E. coli

•Presence of E. coli likely means other enteric organisms are present as well Giardia, Shigella, hepatitis A

•Water is tested for indicator organisms like E. coli (intestinal resident of bird)

•Coliforms (Gram negative, facultative anaerobes that ferment lactose) are indicative of fecal contamination, but testing for E. coli is best

Viable plate count- •Quick and easy but supplies minimal information, not sure bacteria

•Selective or differential media make the test more useful

 Used for “clean” water where you wouldn’t expect to find many microbes

combination of microbiology and statistics to estimate the coliform count

•Presumed, Confirmed, Completed tests

•Takes three days

1.Water is pumped from reservoir and screened.

3.Particles aggregate, settle, and Mg+ and Ca+ are reduced, pH is lowered.

8.Water is filtered through gravel, sand, anthracite.

9.Chlorine, corrosion inhibitors, fluoride (maybe) is added.

10.Storage.

•Primary: Trash is removed, smaller particles settle

•Secondary: Microbial decomposition of sludge

•Tertiary: Filtering, chlorination, disposal

1.Water arrives and is screened to remove trash.

3.Solids settle and fat/oil/grease rises to top.

5.Solids and oils are decomposed, dried and disposed of in landfill.

6.Liquid waste is decomposed, allowed to settle, and chlorinated or treated with UV light.

7.Treated water may be allowed to seep into ground, pumped to ocean, or put for industrial use.

•Food infection: The ingestion of live cells that grow within the intestine, undercooked food. Hard to track

•Typically involves diarrhea, vomiting

•Salmonella, E. coli, hepatitis A

2 weeks, hard to track

•Food intoxication: Illness is due to the ingestion of toxins in food

•Microbes may be dead but toxins remain

•Illness may occur throughout body

•Staphylococcus aureus, Clostridium botulinum

•Food intoxication more quickly than food infection

4°C or above 60°C

•Flash pasteurization 72°C for 15 seconds

•Ultra high temperature (UHT) pasteurization 138°C for 2 seconds

•Irradiation: UV (serilize surfaces)

Ionizing (penetrates meat, vegetables)pathogens

•Addition of salts, acids, nitrates = Desiccation (keep things from growing) not reliable microbicidal method

•Clean: Clean hands, surfaces and food

•Separate: Reduce cross-contamination

separate utensils on raw meat, poultry, seafood, eggs

•Cook: Temperatures high enough to kill cells (145°-165°F)

•Mixed food (casseroles, ground beef) requires higher temperatures than whole cuts

•Toxins may still be present after cooking

•Botulism toxin can be destroyed by boiling for a few minutes

•S. aureus enterotoxin impossible to destroy

•Chill: within 1-2 hours to prevent growth of microbes

First- physical(skin, coughing), chemical (Ph, lysozyme, digestive) genetic barrier, block portal of entry. Nonspecific 

Second- inflammation and phagocytosis. (fever, interferon, complement)

Third-. Foreign substance encounter lymphocyte. Acquired immunity, very specific. Develops memory (B and T lymphocyte, antibodies)

•Physical: Skin desquamated, coughing, sneezing, ciliated epithelial cells

•Chemical: Stomach acid, skin ph,Tear has lysozyme hydrolyze peptidoglycan in cell wall of bacteria. Saliva has defensin are peptide that damage/ lyse cell

•Genetic: Humans are immune to many animal viruses.•Sickle cell disease protects against malaria•A genetic mutation against  HIV

WBC or leukocyte survey tissue for pathogen with their receptors (patern recognition receptors PRR) (Toll like receptor TLR) feel for (pathogen associated molecular pattern PAMP) that are common on pathogen protein

1.Mononuclear phagocyte system (MPS)- network of fibers that allows white blood cells to pass  through “solid” organs. 

2.Extracellular fluid- (ECF) bathes cells in the body and allow communication

3.Bloodstream- 45% cells, in 55% liquid (plasma)

4.Lymphatic system- part of circulatory system. Lymph thansport through lymph node

3.Bloodstream- 45% cells, in 55% liquid (plasma)

•Plasma: liquid clotted blood, produced in liver, 92% water, protein, clotting 

•Serum:  liquid that lacks cloting

•Red cells (erythrocytes) 45%: Transport oxygen and carbon dioxide

•White cells (leukocytes) 1%: Immune function

Hematopoiesis: in embryonic membrane, liver as a fetus, red bone marrow as an adult. Form from stem cell in bone barrow

•Five lobed nucleus, Small purple horseshoe granules

•Primary phagocytes (numbers increase during bacterial infection)

•50%-90% of WBCs

•Bilobed nucleus orange granules

•Attack large eukaryotes (worm)

•1%-3% of WBCs

•Constricted nucleus, 2 Large blue/black granules

•allergy

•0.5% of WBCs

•Similar in form/function to basophils(•Constricted nucleus, 2 Large blue/black granules)

•allergy

•Non-motile

First defense

•largest size, Kidney-shaped nucleus

•Primary phagocytes

• present foreign molecules to lymphocytes

Mature into:

Macrophage-specific phagocytic function

Dendritic-  early immune reaction

•Secretion of compound that control the immune system

•3% - 7% of WBCs

Nucleus fills most of cell

•20% - 35% of WBCs

•T lymphocytes (T cells): Cell mediated immunity- kill foreign cell directly

•B lymphocytes (B cells): Humoral (antibody mediated) immunity

active=plasma cell that produce antibodies to find to invaders

no specificity for single antigen

-specific and non specific phagocytic killing, housekeepers

-process and present foreign substance to lymphocyte

-secret compound that assist/ attract immune cells

•Return extracellular fluid to the circulatory system

•Drain fluid that from inflammatory response

•Provide an additional route through body for cells of the immune system

 same as blood plasma except rbc(water, WBs, salt, protein, debris)

 lymphatic capillaries thin walls and parallel cardiovascular system

. 1 way flow contraction of skeletal muscle to heart, high in hands, breast

swelling is from blockage from filarial worm and prevent going to circulatory system

•Primary Lymphoid Organs- origin

Bone marrow

Site of development for all blood cells

Thymus

•Site maturation of T lymphocytes, children need it for immunity

Release into secondary

•Secondary Lymphoid Organs- encounter microbs

•Spleen: protection against encapsulated bacteria like Streptococcus. filter blood

•Lymph nodes: Filter lymph to remove foreign particles and WBCs that have phagocytized pathogens, located especially in armpit, groin and neck 

tip of sternum

•Site maturation of T lymphocytes, children need it for immunity

Filter lymph to remove foreign particles and WBCs that have phagocytized pathogens, located especially in armpit, groin and neck 

filter for blood

protection against encapsulated bacteria like Streptococcus. filter blood

MALT- mucosal associated lymphoid tissue-bundle of lymphocyte(breast, tonsils, rapid response to microb entering) 

Galt-  lymphoid tissue- in appendix, peyer’s patch in small intesting

SALT- skin associated lymphoid tissue

BALT- bronchial associated lymphoid tissue

•Rubor:  Redness

•Calor:   Heat

•Tumor:   Swelling

•Dolor:  Pain

•Recruitment of cells and chemicals to the site of injury

•Repair of damage and removal of damaged tissue

•Preventing further invasion by microbes

Immediate Reactions

•Vasoconstriction

•mast cell release Cytokines, chemokines(affect white blood cell

•C Reactive protein (CRP)- early indicator of inflammation, attaches to PAMP. released by liver

•Vascular reactions

•Blood vessels dilate

•Repair of damage and removal of damaged tissue

•Preventing further invasion

Late stages

•Swelling (edema) due to fluids and neutrophils (pus)

•Dilute toxins

•Deliver WBCs, oxygen, and fibrin to the site of the injury

•Resolution

•Wound is ‘cleared by macrophages

•Swelling gradually decreases as fluid is drained by lymphatic system

•if bad infection: B and T lymphocytes may be engaged 

•Chemotaxis: Movement of WBCs in response to chemicals

•This allows WBCs to travel through the bloodstream toward the site of an infection

•Diapedesis: The ability of WBCs to pass between the endothelial cells of the blood vessels and enter the tissues. 

•Fever: Body temperature is regulated by the hypothalamus and temp may be reset by pyrogens. 

•Inhibition of temperature sensitive microbes

•Reducing availability of iron from macrophages

•Increases metabolism/immune reaction

Survey tissue and target microb

Ingest materials

Extract antigens from foreign matter

Professional” phagocytes

•Neutrophils (bacterial infection)

•NETS (neutrophil extracellular traps)- death of neutrophil, 

•Monocyte become Macrophages and Dendritic : Circulating and fixed

•Phagocytes engulf foreign particles(PAMP) and then fuse phagosome (pocket) with a lysosome= phagolososome, destroying the contents

•Respiratory burst (oxidizing agents)- punch

•Hydrolytic enzymes- injure bacteria cell membrane

•DNase

•RNase

Proteases

.Cell dies from virus/ cancer but Prevent translation of viral protein by sending IFN to nearby cell

•alpha, by lymphocyte 

-Membrane attack complex- kill pathogen directly

-Coating of pathogen with molecule that makes them attractive to phagocytes (opsonization

-Recruitment of inflammatory cell 

Third line of defense- long term protection. B T lymphocyte against antigens 

Acquired immunity is specific- antibodies against chicken pox won’t work for other 

Memory- lymphocyte can recall the first engagment

•HLA human leukocyte antigen aka MHCs (major histocompatibility complex) molecules determinant of self

unique to each individual

•Class I HLA are found on all nucleated cells

•Class II HLAs are found on antigen presenting cells

•B cells

•Macrophages

•Dendritic cells

•Each antibody is made of protein and consists of two (identical) heavy chains and two (identical) light chains variable region and a  constant region

•Antibody genes are found in segments within the DNA of the cell randomly combined 

•Variable

•Diversity

•Joining

Constant

image

•Clonal selection involves the receptor on a cell recognizing an antigen

•Clonal expansion involves the selected clone multiplying and differentiating into cells that can fight back against a pathogen

T cells

Mature in thymus, high #, T cell receptors, require MHC, produce helper and cytotoxic t cell, kill foreign cell

B cells- mature in bone marrow, low #, does not require MHC, produces plasma and memory, produce antibodies to target antigen

Antigen- Anything that can induce an immune response in the body

Good antigens are •Big•Complex

•Bad antigen are small and/or repetitive

Epitope- •An antibody only recognizes a this small portion of an antigen,

•Alloantigens: Found on only some members of a population (blood type)

Superantigens Bacterial proteins that cause extreme stimulation of T-cells

Response of subset T cell for backup

TH1, TH2, TH17, Treg, Tc

•Antigen Presenting Cells (APCs) engulf an antigen, display epitopes on the outside of the cell (dendritic cells, macrophages, or B cells)

•Selection of a specific T cell requires

1.Binding of the antigen/MHC complex on the APC by the T cell receptor

2.Release of IL-12 by the APC

Antigen presenting cell engulf microb. Combine with MHCII receptor to display to T cell (T receptor and CD4 that recognizes self/nonself). Release interlukin 12 activates T cell 

Depending on interleukin from APC, a bound T cell displaying CD4 receptors may differentiate into

•Memory T cell: Maintains memory of the antigen for many years

•T helper 1 cell (TH1): Increases stimulation of T cells. Tumor necrosis and macrophage (increase immune system)

•T helper 2 cell (TH2): Decreases T cell activity, stimulates B cells.increase antibody Drives B cell( decrease immune system)

•T helper 17 cell (TH17): Promotes inflammation and secrete IL-17 (increase immune system)

•T regulatory cell (T reg): Prevents overactive immune reaction. Development of immune tolerance (decrease immune) 

T cytotoxic TC- destroy cancer 

•With a signal from APC and TH1 cells, T cells with CD8 receptors may differentiate into

•Memory CD8 cells

•Cytotoxic T cells (TC cells)

•TC cytotoxic cells destroy self cells that have become cancerous or infected with a virus by releasing perforins (destroy membranes) and granzymes (induce apoptosis, genetically programmed death of nucleus)  

Natural killer target cancer and virus infected cell, lack antigen receptor, so not specific