Microbiology Exam 1 Flashcards

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0
Q

What are virulence factors

A

molecules or activities that permit the processes of pathogens, including adherence factors, toxins, inflammatory mediators, anti-host enzymes, bacterial capsules.

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1
Q

Pathogens are organisms with capability to do what three things

A
  1. colonize host
  2. overcome host immunity
  3. replicate within the host environment and/or cause host tissue damage
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2
Q

What are the 3 domains of life and some examples of each

A
  1. eukaryotes: all non-microscopic life: mammals, fungi, algae, plants as well as some microscopic life such as protozoa
  2. bacteria: gram+ gram-; rods, cocci, etc
  3. archaea: geyers at yellowstone!
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3
Q

What is the difference between gram+ and gram-

A

gram+ have thick outer cell wall and a single inner plasma membrane

gram- have a thin cell wall sandwiched between two cell membranes, the outer wall contains major virulence factor - LPS (lipopolysaccharide) which is toxic an thus termed an endotoxin

difference in gram staining between these two results from different wall sizes, both take up a crystal violet stain, but only the gram- are destained by an alcohol wash

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4
Q

Are viruses living?

what are their two categories and provide an example of each?

A

non-living

enveloped and non-enveloped

enveloped are much less hardy than non-enveloped. ex) herpes, hepatitis B, influenza, rubella, mimps, HIV

non-enveloped: Hep-A, polio, papilloma, rotaviruses

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5
Q

what are prions?

What is an example?

A

Prions are small “infectious” proteins whose modes of actions are poorly understood, also non-living
ex: mad cow disease

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6
Q

what are the surface molecules anchored in the cell wall of bacteria of bacteria and what do they do?

A

Pili aka **fimbrae: used for attachment and conjugation
Flagella: used for locomotion
capsule: used to protect from phagocytosis
LPS: major virulence factor found in the outer membrane of gram- bacteria

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7
Q

why do bacteria secrete digestive enzymes?

A

because only small molecular weight molecules can pass through the cell wall and cell membrane. The digestive enzymes break down carbs and proteins to small sugars and amino acids which can then be taken in through the pores

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8
Q

what is the role of the bacterial cell wall?

What is it made of?

A

protects the bacterial cell, wraps around the fragile-balloon like plasma membrane and protects it from osmotic pressure within cytoplasm, by preventing the bacterial cell from swelling up and breaking open

it is made of rope-like, linear, polysaccharide chains cross-linked by peptides. The polysaccharide chains are formed by repeating, modified glucose-dimers called N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM).

The wall molecule is a peptidoglycan that is constantly being synthesized and degraded by autolysins

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9
Q

discuss the ways that LPS can cause serious problems if present in large amounts.

A

in small amounts, LPS is excellent at activating the innate immune reaction

in large amounts:
-in blood vessels, large amounts of LPS can activate the clotting system, leading to disseminated intravascular coagulation. This can completely obstruct blood flow in the affected blood vessels, causing damage or death to the underlying tissues.

-Macrophages also respond to LPS in their environment by becoming activated, LPS-activated Macrophages secrete “drool” various noxious compounds onto the surrounding tissues, which includes proteases that breakdown the extracellular matrix (e.g. collagen, etc.) in the area. They also produce pro-inflammatory mediators, such as PGE2 and TNF. PGE2 can activate osteoclasts to reabsorb bone and TNF signals endothelial cells to produce more NO, which causes pre-capillary sphincters to relax (inflammation) If there are too many capillaries in the body opened at one time, this will cause the blood pressure to fall dramatically, and can lead to hypovolemic shock (septic shock)

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10
Q

What are the four different glucose polysaccharides in nature?
what are the major functions of large glucose polysaccharides?

A

1) starch (plants)/glycogen (animals)
2) cellulose (plants): structural
3) chitin (animals) : major structure that makes up the ectoskeleton of bugs/insects/fungs
4. Peptidoglycan (bacterial cell wall) modified glucose disaccharides: NAG-NAM building blocks, macrophages have lysosomes that are designed to break dimers

***amylase used by plants to breakdown starch between glucose bonds

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11
Q

what are antibiotics?

A

substances that are able to inhibit or kill another microorganism

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12
Q

why doesn’t penicillin harm human cells?

what is PBP?

A

because it blocks new bacterial cell wall synthesis and we do not make cell walls

Penicillin binding protein: takes 2 dangling side chains and covalently links them together

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13
Q

what three steps are required for penicillin to work effectively?

A

1) bacteria must be growing; requires hydrolases which cut the cell wall in order for it to expand and grow
2) penicillins & cephalosporins block the “spot-welding”; they do this by covalently binding to the transpeptidase enzyme, permanently inactivating the enzyme. If the hydrolases keep cutting up the wall, then the wall eventually falls apart.
3. the now fragile cell swells from osmotic pressure and bursts

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14
Q

what is meant by bactericidal and bacteriostatic?

A

bactericidal: penicillin is an example of a bactericidal antibiotic, which can kill bacteria directly under normal hypotonic conditions

bacteriostatic antibiotics inhibit the proliferation of bacteria, but do not generally kill them directly, and require immunity to eliminate the bacteria

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15
Q

what does penicillin have as part of it’s structure that allows it to covalently bond with transpeptidase?

A

unstable beta-lactim ring, which breaks open and renders the enzyme useless

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16
Q

What are the resistance mechanisms that bacteria can develop to penicillin?

A

1) change pore structure
2) produce penicillinase (breaks down penicillin)
3) alter transpeptidase (so penicillin won’t bind to it)
4) decrease hydrolase activity

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17
Q

what are immune hypersensitivities?

A

immune response to “harmless” things like antibiotics

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18
Q

how does penicillin help facilitate hypersensitivities?

A

when penicillin’s unstable b-lactim ring breaks open, it will quickly form a covalent bond with any nearby protein structure including host proteins, platelets, and cells (not just it’s target). When penicillin is attached to these host proteins, they take on a “foreign appearance” and our immune system can react to them to destroy them.

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19
Q

what is required for a bacteria to respire?

A

heme-proteins

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20
Q

what are obligate aerobes, microaerophic aerobes, facultative, aerotolerant and anaerobes?

A

aerobes must have oxygen to live

microaerophic aerobes compete best in environments with only very small levels of oxygen

facultative can respire if oxygen is present but can survive on fermentation if oxygen is absent

aerotolerant anaerobes are not killed by oxygen but can only ferment substrate

anaerobes are always killed by oxygen

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21
Q

living in an oxygen environment comes at a price - having to deal with toxic oxygen radicals. what two enzymes are the most important in neutralizing these oxygen radicals?

A

superoxide dismutase (SOD): produces less toxic, hydrogen peroxide (H2O2) from the very toxic O2-, making it less toxic

catalase (CAT) further converts H2O2 to water and oxygen, makes it benign

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22
Q

which bacteria have both SOD and CAT? Which have just one?

A

obligate aerobes and facultative have both

microaerophilic just have SOD

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23
Q

What are the two things that can happen when a bacteria is fed sugars? which is more energy efficient?

A

Fermentation, produce a couple of ATPs, throw out excess as acids, keytones and alcohols

Respiration, it can use oxygen to form carbon dioxide and water, 5x as energy efficient

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24
Q

how to bacteria replicate?

what is the bacterial chromosome like?

A

binary fission

it’s a circular molecule of double-stranded DNA, making it haploid (we are diploid)

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25
Q

what are plasmids?

A

extra small circular strand of DNA that can also be present in bacterial cells. They insert into bacterial host chromosome and come out again. They often carry genes that can help bacteria and harm humans; genes coding for toxins, antibiotic resistance, etc

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26
Q

Is a Virus DNA or RNA?

A

?

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27
Q

what are the three types of gene swapping (exchange of DNA between bacteria)?

A
  1. transformation: DNA is slurped up from nearby dead cell
  2. transduction: viruses transfer DNA between bacteria
  3. conjugation: “bacterial sex” DNA is directly passed from one bacteria to another. many of these exchanged genes give selective advantage to the recipient.
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28
Q

What are the 3 groups of bacterial DNA mutations

A

1) point mutations: one DNA base is changed which usually results in a different amino acid being placed into the protein at that site
2) base deletion: remove one DNA base, which will change the reading frame from that point on
3) base addition: adding one DNA base, which again changes the reading frame from that point on.

*the last two result in dramatic alterations, often fatal to the protein

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29
Q

what are the three major phagocytic cells in the body?

A

monocyte, neutrophil, macrophage

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30
Q

True or False: Is normal flora part of our innate immune system?

name some parts of our innate immune sytem

A

true

epithelium, water “flush” (tears, saliva), secreted anti-microbial molecules, basophils, eosinophils, monocytes, macrophages, neutrophils, platelets, RBCs

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31
Q

what are the three main characteristics of innate and adaptive immune system?

A

specificity of recognition: innate (broad) adaptive (very)
speed of action: innate (fast), adaptive (slow)
memory development: innate (nope), adaptive (yes)

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32
Q

Explain the pathway of inflammation

A

Injury –> release response molecules (histamines) from sentinel cells (mast cells) —> alerts body of problem, initiates inflammatory response

1) increase local capillary flow by relaxing pre capillary sphincters (heat and redness)
2) cause capillary endothelial to gap, allowing blood to flood into affected tissue (swelling)
3) cause capillary endothelial cells to show “stop signs” CAMs that cause certain inflammatory response cells to exit the capillaries and move to the site of injury, includes PMN, macrophages, phaocytic cells

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33
Q

explain the difference between primary and secondary lymphoid tissue

A

primary (bone marrow and thymus) are sites of lymphocyte development and education, B cells are made in bone marrow and T cells in thymus. Once their education is complete “graduation” they move to secondary lymphoid tissues, which consist of the lymph nodes, spleen, adenoid, tonsils, peyer’s patches, etc.

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34
Q

what do B cells do?

A

B cells use their Ag-specific surface receptors to bind to Ag and then they produce and release an Ab (which is an immunoglobulin) that binds to the problem, both coating and flagging it for destruction

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35
Q

what do T cells do?

A

T cell receptors only bind to processed proteins (Ag) presented to them on surface of other cells. Once the T cell receptor (TCR) binds, it releases one or more proteins called cytokines which act on their host cells.

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36
Q

what different things can cytokines do?

A

signal destruction of infected host cells, activation and division of host cells, modify vasculature and neural functions, change whole body temperature.

37
Q

what is an epitope?

A

small region of the antigen that actually binds to a B or T cell antigen recognition receptor.

38
Q

how does meningitis form?

A

Strep pneumonia (gram+) enters the blood, crosses the blood brain barrier and infects the meninges.

39
Q

what is an endotoxin?

A

unique to gram-, LPS, potent inflammatory agent, lipid derived, designed to stay with cell

40
Q

what are exotoxins? what are the 2 main types of exotoxins?

A

exotoxins are proteins that are designed to be secreted.a

1) cytolitic: punch holes in cell membrane –> causes cell to lyse RBC or by cleaving the charged groups of phospholipids of the membrane
2) A-B toxins: interact with membranes, has an AB enzyme binding unit that’s specific. B attaches to membrane which allows A to enter cytosol as an enzyme and damages certain cell functions. most importantly, it decreases protein synthesis. Most powerful toxin known, all it takes is 1 and they can be reused.
3) superantigen (SA): glues T helper cell to Ag receptor, regardless of fit, Th cells release lots of cytokines “cytokine storm” increases inflammation

41
Q

what does LPS activate?

A

complement cascade (initiates inflammation)
hageman factor (causing coagulation)
platelets (causing coagulation)
macrophages/monocytes (causing secretion of pro-inflammatory mediators, enzymes, and O2 radicals)

42
Q

what are the 4 major actions of the AB toxins that result in pathology?

A

1) toxin blocks (ribosylates) host protein elongation factor (EF) resulting in inhibition of protein synthesis.
2) toxin blocks (ribosylates) a G-protein, resulting in ionic imbalance and water loss
3) toxin cuts host ribosomal RNA resulting inhibition of protein synthesis
4) toxin blocks vesicle fusion and release of neurotransmitters –> leads to vasoconstriction or vasodilation

43
Q

what are the two major gram+ pyogenic cocci? what shape are they normally found in, in gram stains?

A

streptocci and staphylococci

chains, clusters - respectively

44
Q

for Strep pyogenes and Staph aureus, describe their use/non use of O2

A

Strep pyogenes are aerotolerant bacteria that do not use oxygen, but can survive if O2 present in small amounts, often called microaerophilic

Staph auerus are facultative bacteria that use oxygen if present, and grow in a number of niches

45
Q

what’s the difference between beta-hemolytic or alpha-hemolytic? what about gamma-hemolytic?

A

beta- ability to completely lyse RBC
alpha - do not lyse RBC but cause hemoglobin to change chemically, turning green
gamma- have no effect on RBC

46
Q

what is the Lancefield classification system?

A

it uses serology (Abs) to classify Strep on basis of their different surface carbohydrates (cell wall polysaccharides)

most useful in beta-hemolytic

47
Q

what are the 4 major strep pathogens?

A

1) S. pyogenes
- beta-hemolytic, group A
- many toxins
- strep throat, rheumatic fever, cellulitis
2) S. agalactiae
- beta-hemolytic, group B
- capsule
- neonatal sepsis
3) S. pneumoniae
- alpha-hemolytic
- capsule
- pneumonia, ear infections (in toddlers)
4) Viridans Strep
- alpha- hemolytic
- endocarditis, dental caries

48
Q

what are streptolysins?

A

cytolytic toxins that can kill defensive leukocytes and destroy clots respectively

49
Q

what are the 3 ways S. pyogenes damages host?

A

1) local pyogenic infection
2) toxic systemic disease
3) immune-sequele diseases

50
Q

describe what happens as a result of a local pyogenic infection

A

local growth, damage/inflammation
local toxins and enzymes kill recruited PMNs forming pus, damage nearby cell membranes and destroy extracellular matrix
3 common diseases that result: strep throat, impetigo, cellulitis

51
Q

describe toxic systemic disease

A
systemic spread of secreted exotoxins, not of the bacteria (it's a local infection!) 
one of the major toxins, erythrogenic toxin, acts by inappropriately gluing TCRs on T cells to MHC class II macrophages, this can activate up to 10% of all our Th cells which floods our body with huge amounts of cytokines causes body-wide inflammation and systemic dysfunction - cytokine storm

common disease: scarlet fever and STTS (streptococcal toxic shock syndrome)

52
Q

describe immune sequelae diseases

A

prime examples of type II (Rheumatic Fever) and III (Glomerulonephritis) hypersensitivity host damage
some S.pyogenes epitopes resemble normal host epitopes and a few weeks after infection and immune response occurs against normal host tissue

53
Q

what is type II hypersensitivity?

A

results from direct binding of antibody to an epitope on the host tissue being damaged

cross reacting Ag –> often leads to rheumatic fever

54
Q

what is type III hypersensitivity?

A

result of immune-complex-induced “innocent-bystander” tissue damage, the Ab is not directed against the tissue that is being damaged, i.e. the damaged site is an innocent bystander

ex: glomerulonephritis from previous strep pharyngitis

55
Q

what are the two pre-existing diseases often associated with Rheumatic fever?

A

untreated s.pyogenes, strep pharyngitis and scarlet fever (more common)

caused by immune response to strep antigens (cross reactive Ag, type II damage)

56
Q

what causes glomerulonepthritis?

A

immune response to strep throat or strep impetigo, occurs when immune complexes of S. pyogenes Ag combine with S pyogenes specific antibodies to form soluble Ag-Ab immune complexes that can filter out of circulation onto the basement membrane of the kidneys. They get lodged there and complement is then activated and phagocytic cells are recruited to the area where they attempt to remove the Ag-Ab complex and in doing so damage the kidney tissues.

57
Q

what are three ways that Strep infections can produce heart damage?

A

1) if major pathogens like S.pyogenes get it into the blood from pharyngitis, pneumonia, a wound, etc they may land on normal heart tissue and cause acute bacterial endocarditis
2) immune response to S.pyogenes can cross react and attach heart and cause heart damage (ex: rheumatic fever)
3) individuals with prior heart damage have sticky heart sites that can offer opportunists the ability to cause sub-acute bacterial endocarditis

58
Q

what is acute bacterial endocarditis

A

usually occurs in a normal heart
caused by strep pyogenes and staph aureus
they get into blood and form colonies, secrete many enzymes and toxins that causes a strong inflammatory response that can damage heart tissues and lead to death

59
Q

what is sub-acute bacterial endocarditis?

A

occurs in previously damaged heart
involves opportunists - i.e. viradans strep and staph epidermidis
previously damaged tissues provides sticky surface for the bacteria to attach and colonize. They secrete less toxic substances so it’s a slow process but can be just as severe as acute bacterial endocarditis and lead to death
3 ports of entry:
-drug abuse
-dental viridans
-surgery enterics

60
Q

how can you prevent endocarditis?

A

antibiotics: amoxicillin or erythromycin

amoxicillin (a penicillin) can causes hypersensitivity in many people due to it’s reactive B-lactim ring structure

61
Q

what are the three major staphylococci pathogens, give some characterisics

A

1) staph aureus
- coagulase+, yellow colony
- protein A, many secreted enzymes and toxins, can neutralize Abs our body makes
- frequently drug resistant, MRSA (methsilin resistant staph aureus)
- food poisoning, osteomyelitis, toxic shock syndrom, nosocomial infections, skin infections: abscesses (stye, boil, carbuncle) and impetigo
2) s. epidermidis; skin “dry epithelium”
- no coagulase, white colony
- capsule
- frequently drug resistant
- catheter and prosthetic implant infections
3) S. saprophyticus
- no coagulase, white colony
- urinary track infections in young women

62
Q

what are some virulence factors of staph aureus? (over 32 factors recognized)

A

1) fibrin binding proteins on cell wall that help bacteria colonize cell and tissues
2) protein A, which binds Fc of IgG —> blocking opsonization
3) enzymes “spreading factors” secreted
4) cytolitic toxins secreted that kill nearby host cells, including PMN defenders
5) superantigen secreted, which activate Th cell and macrophage cytokine production which can lead to TSS and food poisoning

63
Q

what are the 2 major effects of coagulase?

A

1) it will bind fibrin to the surface of the bacterial cells –> which provide camouflage from the immune system for the bacteria
2) can cause large amounts of fibrin to deposit around a local infection —> walls off bacterial colony from body and restricts access of the immune system to infection site “creates a fort”

64
Q

what is the difference between food poisoning and true food poisoning?

A

food poisoning: bacteria that get inside the boy and cause infection slow - takes days, someone with is infectious
true food poisoning: enterotoxin does the poisoning, not the bacteria, quick - takes hours, someone with is non-infectious

65
Q

what is the main group of medically important gram- bacteria?

A

enteric bacilli

66
Q

how do enteric gram- rods infect the gut?

A

transfer from the 5 F’s: food fluid fingers flies and feces, emphasis on feces

67
Q

what is one of the most important characteristics of enteric gram- rods?

A

their ability to share virulence factors (i.e. exotoxin, antibiotic resistance) by gene transfer via plasmids, conjugation, transformation or by bacteriophage transduction

this also results in the spread of antibiotic resistance among pathogens and produces variant strians of typically normal flora, such as E.coli

68
Q

what does zoonotic means?

A

a disease or microbe that normally exists in other animals, but can be transmitted and infect humans.

69
Q

what are some of the characteristics of enteric gram- rods?

A

non-fastidious (but sensitive to drying)
metabolically diverse
facultative anaerobes
normally found in GI tract of humans and other animals
major GI tract normal flora + non-normal flora pathogens

70
Q

what is antigen variation?

A

multiple genes are available for each antigen and an individual bacterium can change back and forth between these genes to change the epitopes on the cell surface. a way that bacteria can better evade the adaptive immune response.

71
Q

what are the three major groups of antigens for enteric gram- rods?

A

1) flagella H-Ag
2) Capsule K-Ag
3) LPS/wall (endotoxins) O-Ag

72
Q

what is Ag phase variation?

A

ability of a microorganism (Ag) to turn on or off (be expressed or not be expressed)

phase variation protects the bacteria from Ab-mediated damage or death

73
Q

what is a major cause of malabsorption in infants primarily in developing countries

A

EPEC; enteropathogenic E. coli which attaches to the brush border of small intestine mucosal cells, causing localized flattening and destruction of microvilli, which causes malabsorption

74
Q

what is the role of LPS?

A

causes massive activation of macrophages (and other cells) resulting in production of huge amounts of pro-inflammatory cytokine mediators such as IL-1 and TNF alpha

75
Q

what type of exotoxins do enteric gram- bacteria mostly secrete

A

mostly A-B, though they secrete a variety

76
Q

what is one of the major ways to test whether our drinking water has been contaminated with fecal materials?

A

look for the presence of enteric gram- rods, especially E.coli in the water

77
Q

what is the equation for disease causing potential of any microorganism?

A

(virulence x dose) / host resistance

78
Q

what is disease caused by enteric gram- rods highest?

A

summer months, primarily related to warm weather, picnics, swimming, contact with animals

79
Q

in what population is shigellosis most common? where does it most often colonize? what is the mechanism of colonization? is it a local or systemic issue? what is a typical symptom?

A

primarily a disease of children
colonizes in the mucosal epithelium of the colon, it’s very acid resistant, only a few bacteria necessary to establish disease
mechanism is via bacterial-directed endocytosis or actin directed pseudopodia
it’s local
dysentery: blood and pus in stool

80
Q

what is a shiga toxin?

what is the mechanism of pathology?

what is hemolytic uremic syndrome?

A

A-B exotoxin produced by S. dysenteriae that cleaves ribosomal RNA, disrupting protein production in the cell

primary manifestation is damage to the intestinal epithelial cells, but in a small number of pt’s, it can get into blood stream in high enough concentration where it mediates damage to the glomerular endothelial cells, resulting in renal failure - HUS

81
Q

why is salmonella typhi more serious than shigella? what major disease does it cause?

A

it can break through the gut epithelium and enter phagocytic cells which then act as macrophage taxis to take pathogens throughout the body

typhoid fever – often fatal

82
Q

is salmonella infection local or systemic? where do they colonize? what is a common symptom? what strain can use macrophages as taxis? what is the common pathology?

A

typically it’s a localized infection of the small intestine mucosal epithelium, invade and replicate in gut epithelium. results in dirrhea. S. typhi is able to resist digestion as use macrophages as taxis to spread systemically throughout the body - typhoid fever a result.

83
Q

what is EHEC (0157:H7)

A

enterohemorrhagic E.coli
shiga-like exotoxin (verotoxin) gene
Bloody dysentery
HUS (hemolytic uremic syndrome)

84
Q

what are the most common cause of UTIs?

what type of infection is a UTI infection? (ascending/descending)

A

uropathogenic strains of E.coli, which produce specialized adhesions that allow them to adhere within the urinary track

UTI is an ascending infection (originates in colon, contaminates urethra, and ascends to bladder and can migrate to kidney)

85
Q

what is a reservoir?

A

normal host required for a microbe’s existance

86
Q

what is a vector?

A

transfers microbe (usually from reservoir to new host) ex: blood sucking insects - tropical

87
Q

what is the cause of plague in humans? what is pneumonic plague?

A

yersinia pestis

when the primary infection occurs in the lungs, it’s pneumonic plague - close to 100% mortality

88
Q

what is passive immunity?

A

injection of preformed Ab into a person to give them a specific immune response. can be used to neutralize snake venom, tetanus toxin and hepatitis viruses

IgG is another form of passive immunity - when it crosses the placenta, giving infant immunity for first month’s of life

89
Q

how does vibrio cholerae cause disease?

A

if large numbers are consumed in contaminated water or food they can adhere and colonize the small intestine. they produce A-B to bind to gut epithelial cells and then release the A-unit which enters the cells and activates adenylate cyclase, resulitn gin hypersecretion of water and electrolytes. huge fluid loss results in diarrhea.