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D&T 2 Exam 2 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Clostridium difficile is a particular problem where

A

in hospitals

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2
Q

characteristics of clostridium difficile

A

large gram-positive rods single or in chains that form spores/endospores.

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3
Q

what are the two major spore forming bacteria

A

clostridium and bacillus
clostridium is anaerobic
Bacillus is aerobic

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4
Q

what are spores resisnt to

A

drying, boiling, chemicals, radiation

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5
Q

clostridium are (aerobic/anaerobic)

A

obligate anaerboes

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6
Q

what are the different species of clostridium

A

histotoxic clostridia

enterotoxic clostridia

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7
Q

what is contained within histotoxic clostridia

A

C perfringens

C difficile

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8
Q

what clinical outcome comes from C perfringens

A

cellultis and gas gangrene

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9
Q

what clinical outcome comes from C difficile

A

pseudomembraneous

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10
Q

what does enterotoxic clostridia cause

A

food poisining/ diarrhea

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11
Q

the disease produced is dictated by the

A

exotoxins that are being produced

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12
Q

clostridium perfrinigens causes

A

gas gangrene

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13
Q

clostridium perfrinigens is (aerobic/anaerobic)

A

anaerobic but oxygen tolerant

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14
Q

where is clostridium found

A

soil and in the GI tract in the normal microbiota of humans and animals

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15
Q

(important)* what do clostridium perfringens look like

A

large gram positive rods in a boxcar shape

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16
Q

in a spore stain what does clostridium perfringens look like

A

spores = blue

vegitative cells = red

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17
Q

in gram stian what do teh spores and vegetative cells look like

A

spores are colorless and vegetative cells are purple

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18
Q

what is characteristic about what clostridium perfringens produces

A

it produces gas during growth : CO2, H2 + foul smelling volatile amines such as putrescine and cadaverine

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19
Q

40% of gas gangrene comes from what species of clostridium

A

C. Novyi

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20
Q

the type A strains of clostridium are the

A

major human pathogen common in intestines of humans and animals
+ soil

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21
Q

the toxin of the type A strians of C perfrinigens in C diff are

A

alpha a toxin

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22
Q

what is the alpha toxin

A

a phosphilipase C - used to digest the membranes of cells

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23
Q

hw do you detect alpha toxin / what is the nagler rxn

A

plate on egg yolk agar, and the alpha will cleave off the phosphatidly choline and insoluble diglyceride comes out

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24
Q

what is the result of alpha toxin of C perfrinigens

A

dermonecrotic-widespread destruction of tissue cells

hemolytic- B hemolysis so kills phagocytic cells

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25
Q

WHAT is kappa toxin

A

toxin found in type A strains of perfrinigens that is a collagenase –> tissue destruction

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26
Q

what is the theta toxin

A

toxin of type A C perfrinigens oxygen labile hemolygen that kills phagocytic cells as part of th hemolytic rxn

  • gives the smaller more intense clearing zone on blood agar
  • outer=alpha
  • inner=theta
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27
Q

what % of type A strains make enterotoxin

A

1-5% of type A strains make enterotoxin

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28
Q

how does the enterotoxin of C perfrinigens work

A

it binds to tigh j(x) proteins and leads to increased permeability and fluid loss

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29
Q

what is the clincal manifesration of C. perfrinignes

A
  1. anareobic cellulitis where the organism only grows int he dead tissue
  2. myonecrosis: where new tissue is killed and spread into

the more alpha toxin, the more it will go towards myonecrosis + new tissue destruction

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30
Q

anaerboic cellulitis

A

usually traumatic and may be non traumatic that has a gradul onset following tissue trauma, localized in damaged soft tissue with gas formation

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31
Q

who does anaerobic callulitis occur in

A

diabetes and poor circulation

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32
Q

describe myonecrosis/ gas gangrene

A

acute onset with severe pain, alpha toxin production that kills tissue

gas production that ay progress to blood stream invasion and septicemia

can be fatal in 12 hrs

gas filled bullae

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33
Q

treatment of myonecrosis from clostridium perfringens

A

debridment with maggots?!?!? (it works but gross)

high dose IV penicillin

hyperbaric oxygen: makes it less favorable for anaerobes the grow

no vaccine

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34
Q

enterotoxic clostridia will cause

A

diarrhea and fever with rare vomiting

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35
Q

clostridium difficle characteristics

what they look like etc

A

gram positive rods that are thinner than C perfingens with terminal spores causing a drumstick like appearance

they sporulate well in the intestines

obligate anaerobes, grow in the intesstinal tract `

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36
Q

what are the 2 toxins ofclostridium difficile

A

Toxin A and Toxin B
Toxin A = enterotoxin
Toxin B = cytotoxin

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37
Q

what do Toxin A and B of C difficle do

A

covalent glucosylation of cellular GTPase that interferes with intracellular signaling –> 1)inhibition os actin polymerization and

2) disruption of tight junctions leading to fluid loss
3) cell death from apoptosis

leading to cell death, fluid secretion and inflammation

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38
Q

cell toxin A

A

binds to the apical surface of epithelial cells and interferes with tight Jx and allows toxin B the get into the cell –> release of inflammatory mediators that effect neutrophils resulting in inflamation and neutrophils accumulation

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39
Q

fever and diarrhea think

A

C difficile

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40
Q

is toxin A or B more cytotoxin?

A

B is 100x more cytotoxin than toxin A

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41
Q

what are NAP1

A

these are hypertoxogenic C diff strains that produce 10x more of both toxin A and B

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42
Q

non-toxic C difficile

A

has neither toxin A or B

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43
Q

what is th additional virulence factor of NAP1 strains of C dif

A

Binary toxin - actin specific ADP-ribosyltransferase

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44
Q

where is C diff found

A

soil, but can get into the intestines

normal flora of infants, minor in adults

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45
Q

what causes C diff

A 
antibiotic treatment with 
clindmycin 
ampicillin
cephalosporins
fluoroquinolones (most severe)

(c/linda with her big CEPHalus is sitting on an amp(icillin) and holding a flower(fluoroquino)

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46
Q

what antibiotics are not likely to casue c diff

A

vancomycin or metronidazole

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47
Q

most common transmission of C diff

A

hospital

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48
Q

describe the clinical manifestation of c diff

A

fever, cramping, foul smelling, rarely bloody diarrhea with colitis

> 3 unformed stooler/24h for 2 days

yellow pseudomembrane

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49
Q

treatment of C diff

A

discontinue the antibiotis and then begin metrinidazole or
vancomycin - fidaxomaxin

fecal transplants given via NG tube

toxoid vaccine in phase III trials

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50
Q

what is bezlotoxumab (zinplava)

A

human mAB that binds to toxin B that can prevent reoccurrence of C diff in pts w severe infection

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51
Q

what will you most often find in a bite wound

A

mix of anaerobes and aerobes - the aerobe uses up the O2 so the anerobe can grow

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52
Q

where are bacteroides and anaerboes found

A

found in normal microbiota + bite wound ifnections + GI tract + skin wound infections

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53
Q

bacteroides are

A

gram negative rods

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54
Q

peptostreptococcus are

A

gram positive anaerboic cocci seen in human infections

in singles, pairs, tetrad, groups

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55
Q

actinomyces are

A

gram positive filamentous branching rods

not acid fast

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56
Q

what do bacteroides and other anaerboes cause clinically

A 
abscesses in brain, lung, liver, intra-renal 
peritonitis
dental and oral infections 
necrotizing pneumonia
pelvic inflammatory disease
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57
Q

predisposing factors to infection with bacteroides / anaerobes

A

reduction in tissue oxidation-reduction tissue due to trauma from loss of blood or growth of a facultative bacteria to use up the O2.

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58
Q

3 clues to possible anaerobic infection

A

1) fould smelling discharge
2) nothing shows on routine aerobic culture
3) gas in tissue or discharge

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59
Q

acceptable clincal specimens for bacteroides

A

aspirated pus, tissue, body fluids- cerebrospinal, pleural, pericardial, synovial, transtracheal aspirate

NOT: throat swab, gingival or vag swab or urine –> too much risk of finding other things

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60
Q

treatment of baceroides/ anaerobes

A

drainage / debriment + antibiotic therapy

metronidazole- god for bacteroides
carbapenems
B lactam/b-lactamase inhibitor

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61
Q

bacteroides/porphyromonas/provotella characteristics + where is each found

A

group of pale staining gram negative rods

bacteroides - intestinal
porphyromonas-oral
provetella-oral

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62
Q

porphyromonas gingivalis

A

normal microbiota of gingival flora and when it overgrows –> gingivitis and periodontitis . will see gingival pockets

can cause local or systemic abscesses due to poor oral hygeine

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63
Q

povotella melaninogenica looks like:
is plated on:
requires:

A

tan to black pgimentation on blood agar

requires vitamin K and hemin

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64
Q

povotella melaninogenica can cause

A

gingivitis and periodontitis +

can spread from oral tissue into soft tissue –> lung abscesses and genital infections. can go systemic

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65
Q

bacteroides fragilis is found

A

in the intestinal tract - most commonly isolated anaerobes

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66
Q

major virulence factor for invasion for B fragilis

A

polysaccharide capsule

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67
Q

what are the 6 distinctive properties/ virulence factors of B fragilis

A

1) polysacharide capsule
2) LPS- no endotoxin activity
3) neuraminidase- tissue degregdation
4) SOD: resist O2 toxicity
5) enterotoxin (ETBF enterotoxin bacteroides fragilis))
6) zinc metalloproteases

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68
Q

what bateria is classic for a human bite wound

A

eikenella

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69
Q

treatment of B fragilis

A

resistance to B lactamase, so use penicillin with a B lactamase inhibitor

metronisaole
carbapenems

surgical drainage of the abscesses

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70
Q

fusobacterium is

A

pleomorphic gram negative rods found in the normal flora of the oral cavity and intestinal tract

long and thin with pointed ends -“fusiform appearance”

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71
Q

most common Fusobacterium infection

A

F. nucleatum

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72
Q

fusobacterium clinical manifestation

A

acute necrotizing ulcerative gingivitis (ANUG) where fusobact. miced w provotella and spirochetes leading to rapid estruction of the periodontal tissues that can spread to nearby tissues like the cheekcs, lips or jaw

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73
Q

F necrophorum will cause

A

normal flora of intestines and abdominal + liver abscesses

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74
Q

peptostreptococcus cause infections

A

abscesses almost anywhere in the body

can lead to bacteremia

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75
Q

actinomyces appear how in pus

A

it clumps together and will form “sulfur” granules/ clumps of yellow. the pus has lumps in it.

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76
Q

actinomyces found

A

as normla flora in oral cavity, intestines and vagina

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77
Q

clinical manifestations of actinomyces

A

chronic suppurative infections
cervico facial lesiosn
abdominal lesions
salpingitis related to intrauterine contraceptive device

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78
Q

are animal or human bites worse?

A

human!

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79
Q

eikenella corrodens characterisitcs

A

gram negative bacilli, not anaerobic (facultative anaerobe) but is normal oral flora that causes mixed infection w anaerobes

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80
Q

in what population does B fragilis cause diarrhea

A

1-5 yr olds

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81
Q

what does eikenella cause on a pitri dish

A

pitting or corroding of the agar

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82
Q

what can eikenella corrodens cause

A

endocarditis

meningitis and brain abscesses

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83
Q

pasturella is

A

normal flora found in animals

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84
Q

paseurella characteristics

A

small gram negative coccobacillis or rods that stains heavier on the ends / bipolar staining

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85
Q

what can pasturella cuase in humans

A

cellulitis @ site of animal bite
osteomyelitis
blood stream spread

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86
Q

treatment of pasturella

A

panicillin G ampicillin and cefuroxime

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87
Q

e. coli, shigella and salonella are part of what family

A

enterobacteriacae

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88
Q

what do enterobacteriacae grow on

A

blood agar

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89
Q

what do you use to isolate enterobacteriacae species from food, water and feces

A

selective differential agar : macConkey agar

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90
Q

MacConkey agar

A

is selective for gram negative bacteria and has differential color based on lactose fermentation

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91
Q

how does MacConkey agar differentiate between enterobacteriacae species

A

on MacConkey agar:

Lactose fermenting colonies produce a drop in pH leading to a pink color

Lactose non-fermenting do not change color and remina yellow

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92
Q

which enterobacteriacae are lactose fermenting

A

E. coli
Enterobacter
Klebsiella
Proteus

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93
Q

which enterobacteriacae do not ferment lactose

A

shigella and salmonella

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94
Q

what three things are used for antigenic analysis for enterobacteriacae

A

O Antigen: surface LPS

H-antigen: flagella antigen

K antigen: Capsule

pili/fimbrae

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95
Q

where is e. coli found

A

normal intestinal floura

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96
Q

which diseases are cuaed by normal flora E. coli

A

UTIs, and invasive disease like septicemia, meningitis and pneumonia

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97
Q

the E. coli that have acquired additional factors will produce

A

intestinal dieases –> diarrhea

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98
Q

type I fimbrae have adherence to

A

allnormal intestinal isolates, most common UTI isolates

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99
Q

type P fimbrae have adherence to

A

UTIand some normal intestine

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100
Q

CFA fimbrae have adherence to

A

small intestine

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101
Q

BFP fimbrae have adherence to

A

small and large intestine

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102
Q

enterotoxins of E coli

A

heat-labile toxin (LT)
Heat Stable toxin (HS)
Shiga-like toxin

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103
Q

what does heat labile toxin of E coli do

A

activates adenylate cyclase –> fluid secretion and diarrhea (identical to cholera toxin) - this is travelers diarrhea

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104
Q

how does heat stable toxin (ST) act

A

its a small peptide that stimulates guanylate cyclase –> fluid secretion and diarrhea

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105
Q

how does E coli aquire heat labie toxin and heat stable toxin

A

plasmid

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106
Q

how does e coli acquire shiga like toxin

A

bacteriophage from shigella

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107
Q

what does shiga-like toxin do

A

it causes bloody diarrhea by causing enterohemorrhagic colitis + hemolytic Uremic Syndrome

It bind to G3b receptor and inhibits protein synthesis in target cells and kills cells in the
KIDNEY, PANCREAS AND BRAIN

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108
Q

what systemic effects does shigella like toxin produce

A
  • destruction of renal endothelial cells
  • activation of blood platelets and coagulation cascade
  • clots in small vessels fo the kidney
  • microangiopathic hemolytic anemia
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109
Q

intestinal infections of E. coill are spread by

A

fecal-oral spread of new virulent strain of E. oli

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110
Q

most common diarrhea causing strain of E. coli

A

Enterohemorrhagic E. coli - EHEC

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111
Q

how is EHEC spread?

A

animal-human
or
human-human related to humans

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112
Q

serotype of EHEC

A

O157:H7

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113
Q

STEC MEANS

A

shiga-toxin producing E. coli. same as EHEC

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114
Q

habitat of EHECs

A

intestinal tract of animals - mainly cattle –> contamination

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115
Q

timeine of EHEC

A

2-5 day incubation period - begins as a watery diarrhea

1-2 days later turns bloody and colonizes the large intestine

no invasion, little or no fever, no pus –> NO FEVER.

can turn into HUS- kidney failure

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116
Q

HUS cauased by

A

shiga like toxin

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117
Q

bloody diarrhea without fever think

esp with kidney failure

A

EHEC

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118
Q

how to treat EHEC

A

do not use antibiotics! If the cells are killed they release more toxin so they increase shiga toxin release

give supportive kidney care

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119
Q

what does shigamAB

A

mAB that can bind to shiga toxin

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120
Q

how to culture serotype O157

A

make macConkey agar with sorbitol instead of lactose
.
EHECs do not ferment sorbitol but E. coli does.

so colorless is O157
normal Ecoli will be red

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121
Q

wht is eculizumab used for

A

atypical hemolyic uremic syndrome- blocks complement components of C5 which lyses RBCs

122
Q

why are person to person outbreaks seen less in the US

A

since we have good clean water practices

123
Q

what is ETEC

A

enterotoxic E. coli –> montezumas revenge

124
Q

ETEC is transmitted from

A

contamined drinking water

125
Q

pathogenesis of ETEC

A

ingestion, bacteria adhere to mucosal surface of small intestines –> production of one or both enterotoxins (LT or ST)—> fluid secretion and a watery diarrhea WITH NO FEVER

126
Q

is shigella normal flora?

A

NO NEVER

127
Q

2 types of shigella

A
  1. shigella dysenteriae / type 1

2. shigella sonnei, flexneri and boydii

128
Q

what does Shiga dysenteriae cause

A

most severe disease with classic bacterial dysentery + blood

129
Q

other species of shigella (other than S. dysenteriae) cause

A

shigellosis - mild disease

130
Q

virulence factors of shigella

A

LPS
invasion plasmid antigen
shigella toxin

131
Q

what does the invasion plasmid antigen of shigella do

A

binds to epithelial cells fo colon and replicate inside th epithelial cells. ability to invate intracellularly

132
Q

s dysenteriae makes 100x more _____ than the other types of shigella

A

shiga toxin

133
Q

how is shigella transmitted

A

person:person , fecal:oral

134
Q

who is shigelosis found in

A

usually found in kids

135
Q

where is shigella dysenteria found in

A

underdevloped countries

136
Q

EHEC v shigellalosis

A

in EHEC the sgia toxin sits on the surface so no inflammation –> no fever

in shigella the shiga toxin invades the cell –> some inflammation –> fever

137
Q

classic symptoms of Shigella dystenteriae

A

small volume bloody mucoid discharge with fever along wtih large numbers of leukocytes and RBC in stools due to the invasion into the epithelial cells

lateral spread and uceration of the intestinal mucosa

138
Q

treatment of shigella

A

can use antibiotics but dont want to use antibiotics with HUS

139
Q

primary serotype of salmonella

A

salmonella enterica

140
Q

the numbers in a salmonella serotype refer to the

A

O antigens

141
Q

the last letter of the salmonella serotype refers to

A

the H antigens

142
Q

what type of salmonella causes gastroenteritis int he US and highly lethal infections in AIDS patients in Africa

A

S. typhimurium

S. Enteritidis

143
Q

what types of salmonella cause typohoid fever

A

S. typhi

S. paratyphi

144
Q

what type fo salmonella causes septicemia

A

S. cholerasuis

145
Q

what antigens are used for serotyping salmonella (4)

A

O antigen: LPS
H antigen
K antigen
Adhesion/invasion antigens: required for adhesion, uptake and intracellular growth in macrophages and epithelial cells

146
Q

what cells do salmaonella grow in

A

macrophages and some epithelial cells

147
Q

what ar the exotoins in salmonella

A

e. coli LT and ST-like toxins

148
Q

how is salmonella tramsnitted

A

animal - human
come from the intestinal flora of birds, cattle and reptiles, and then it gets into our food + water supply

for us mainly in poultry and eggs

can be person:person

149
Q

most common salmonella infection

A

gastreoenteridis

150
Q

clinical timeline of salmonella

A

incubation 12-36 hrs after injestion that begins are neausea and vomiting progressing to a diarrhea and fever.

FVER usually present
rarely bloody

151
Q

what cells does salmonella infect

A

invade and replicate in epithelial M cells of small and large intestines and multiplication in macrophages

into the LNs and lymphatics in HIV patients

152
Q

name of autoimmune disease following salmonella

A

reiter’s syndrome: reactive arthritis
cant see
cant pee
cant climb a tree

153
Q

how will salmonella present on selective MacConkey agar

A

it will appear yellow scine it does not ferment lactose

154
Q

on XLD agar salmonella will appear

A

BLACK due to H2S production

155
Q

antigens specific to the S typhi serotype

A

Kapsular antigen: Vi antigen: special capsule found only on S typhi

156
Q

transmission of S. Typhi

A

only person:person spread via fecal-oral transmission

157
Q

who has increased susceptibility to typhoid fever

A

people with hemolytic anemia since they have more iron released from cells floating around in blood - the iron is beneficial to the typhoid

158
Q

how does S typhi infect?

A

invades through M cells through peyers patches of M cells and replicates in macrophages

disseminates thrgouh LNs –> blood stream and then goes to other places w maccrophages like spleen,liver and BM

159
Q

clinical disease from S. Typhi

A

initial spread is asymptomiatic

increased bacteria in liver etc leads to sustained bacteremia with high fever

followed by kidney, gall bladder, peyer’s patches, and skin

sepsis in severe cases

160
Q

if you survive typhoid the body can remove S. typhoid from every organ except the

A

gall bladder

161
Q

treatment of typhoid fever

A

ciprofloxacin or 3rd gen cephalosporin

162
Q

are there vaccines for typhoid and if so what

A

yes!
1- purified Vi capsule polysacharride
2- live attenuated Ty 21a strain

163
Q

vibrio and campylobacter can be described as

A

enteric gram negative curved and spiral rods

164
Q

Vibrio characteristics

A

curved gram negative rod with a single polar flagella

165
Q

where is vibrio found

A

common in surface water

166
Q

major pathogen of vibrio

A

vibrio cholera

167
Q

ingestion of raw fish/ shellfish in japan leads to what type of vibrio infection

A

V parahaemolyticus

168
Q

which vibrio found in oysters

A

V vulnificus

169
Q

V. vulnificus leads to

A

food borne bactermia and skin lesions from handling shell fish

170
Q

virulence factors of Vibrio cholerae

A

LPS: O antigens (O and O139)
Pilli
some minor antigens

171
Q

the O1 antigen of vicrio chloerae causes

A

classical cholera

172
Q

the non O1 antigens of vibrio cholera cuases

A

mild diarrhea

173
Q

the O139 antigen of vibrio cholera causes

A

cholera 2

174
Q

exotoxins of vibrio cholera

A

cholera enterotoxin identical to E coli LT

175
Q

what are important features of the cholera enterotoxin, whihc is similar to E coli LT

A

it is a multiple subunit toxin (A+5b)

the A subunit is an adenylate cyclase tha increases cAMP that stimulates fluid secretion -in intestinal epithelial cells

The B part is invovled in binding to the target cell and is the main antigen

176
Q

transmission of vvibrio cholera

A

person to personf rom drinking fecal contaminated water or food - can survivei well in environmental water

177
Q

how vibrio cholera infects an organism

A

organism goes to the SMALL INTESTINE and DOES NOT invade the tissue. it sits on the surface and pumps out tons of cholera toxin

178
Q

clinical minifestation of vibrio cholera

A

massive diarrhea, rice water stools leading to dehydration and electrolye imbalance en of cholera

179
Q

treatm

A

fluid replacement + rehydration salts

doxycycline + cipro

180
Q

is there a vaccine for cholera?

A

yes. oral live attenuated strain where the A subunit has been deleted fromt he toxin and keep the B gene intact, which sit he immunogenic portion.

single dose age 18-64

181
Q

dukoral

A

is an oral inactivated O1 bacteria and cholera toxin B subunit so has some cross protection against eneterotoxic ecoli

182
Q

1 food poisoning disease

A

campylobacter

183
Q

what is a ded end host

A

where a parasite does not replicate or transmit, but dies

184
Q

what are the features of Helicobacter

A

gram negative spirally curved rod

185
Q

what does H pylori cause

A

colonization of the stomach –> gastritis + peptic ulcers, eventually leading to gastric adenocarcinoma

186
Q

virulence factors of H pylori (4)

A
  1. flagella for penetration through gastric mucus to avoid acid
  2. adhesins to mediate binding to cells
  3. CagA protein- MOST IMPORTANT
  4. LPS
187
Q

what does CagA of H pylori do

A

surface pilus/needle syringe complex tht injects CagA into host cells, and is lethal by effecting tight junctions –> stimulation of inflammation

gastric mucosal injury

188
Q

Exotoxins of H pylori

A
  1. Urease which neutralizes gastric acids
  2. Mucinase to degrade gastric mucosa
  3. vacuolating cytotoxin (VacA)
189
Q

what does VacA do

A

it is found in H pylori as an exotoxin and induces vaculozation and cell death/apoptosis in EPITHELIAL CELLS

it also stimulates neutrophil migration leading to overall inflammation

it promotes urea diffusion across the spithelial surface

190
Q

how H pylori colonizes

A

bacteria use flagella to move beneath the mucin layer and attach to gastric epithelium –> colonization

the urease releases ammonia to keep Ph@ 7

colonization uually asymptomic but can led to inflammation, gastritis and ulcers –> gastric cancer

191
Q

best way to diagnose H pylori

A

breath test and confirm w gastric biopsy

192
Q

treatment of H pylori

A

antibiotics
now: step 1: Rabeprazole + amoxicillin 5 days
step 2: rabeprazole + clarithro + tinidazole 5 days

must confirm erdication of active ifnection after 4 wks therapy

193
Q

chracteristics of Reovirus

A

dsRNA, segmented, naked

Respiratory Enteric Orphan viruses

194
Q

the type of Reovirus that causes the most human diesease is

A

rotavirus

195
Q

what are the three viruses within reocirus

A

reovirus
rotavirus
Colorado tick Fever

196
Q

how does Rotavirus infect a cell

A

intestinal trypsin is needed to cleave the spike protein VP4 to expose a hydrophobic domain and allow entry and the outer most shell is removed releasing the double coated virus into the cytoplasm

the viral RNa dependent RNA pol is brought into the cell int he virion which is then used to make mRNA from the segmented dsRNA

the mRNA does into the cytoplasm to make viral proteins

in a cytoplasmic inclusion the viral proteins make the first shell encapsulating the 11 different mRNAs

then the virus uses the viral RNA dependent RNA pol to make dsRNA

the virus will acquire its second shell

197
Q

rotavirus infects what type of cells

A

enterocytes of the small intestine

198
Q

what is the enterotoxin associated with rotavirus

A

cholera like exotoxin: NSP4 is excreted from the infected cell and increases the intracellular calcium levels in the cell. resulting in compensatory chloride secretion and secretory diarrhea.

199
Q

to what point are maternal antibodies in a child effective @ protection

A

first 3 months of life

200
Q

calcivirus includes

A

norovirus and saprovirus

201
Q

characteristics of calcivirus

A

plus strand RNA virus

non-eveloped

202
Q

best method to wash hands of noro virus

A

soap + water

203
Q

1 cause of gastroenteritis in children <5

A

norovorus

204
Q

the vaccine for norovirus is

A

live attenuated

205
Q

bad side effect of newer rotavirus vaccines / Rotashield

A

intussusception

206
Q

route of spread of noro virus

A

person:person, food and water

207
Q

what are Kaplan’s criteria used for and what are they

A

vomiting in more than half of symptomiatic cases

mean incubation period of 24-48 hrs

mean duration of illness 12-60 hrs

no bacterial pathogen osolated in stool culture

208
Q

what are the characteristics of listeria

A

theya re gram + rods or coccobacilli that do not form spores with falgella

faculative anaeroe that can grow in vacuum packed foods - intracellular

b hemolytic

209
Q

habitat of Listeria

A

are commonly found in soil plant environments and can infect humans and animals –> can persist as disease or normal flora

210
Q

major pathogen of listeira

A

Listeria monocytogenes

211
Q

what temp does listeria prefer

A

37 / cooler temps like the refrigorator!

212
Q

what does the listeriolysin do

A

it lyses phagosomal membranes and allows bacteria to escape the phagosome and enter macrophages

213
Q

describe the distinctive properties of ActA - of listeria

A

it is a cell wall protein that acts as an actin polymerization active site + polymerizes actin @ one end of the cell

it pushes the bacteria from one cell to the next without exiting

214
Q

what bacteria uses the same mechanism of intracelular replication as listeria

A

shigella

215
Q

primary way that humans get infected with listeria

A

via ingestion of food specifically ready to eat meat products
transplacental transmissionf rom mother to fetus

216
Q

highest death rate from any of the food poisonings from

A

listeria

217
Q

clinical manifestations of listeria infection

A

asymptomatic or flu-like diarrhea - symptoms assocaited w dose

immunocompromised get invasion into the submucosa via M cells and replication in macrophages –> diarrhea, fever, headache and nausea

blood stream invasion, septicemia and meningitis

218
Q

effects of listeria on a pregnant woman

A

20x higher risk of infection with bloodstream invsion and transplacental spread to the fetus

1st trimester = spontaneous abortion
laterstages: stillbirth or seriously ill newbron

219
Q

what are the two bacterium that can be transmitted transplacentally and cause infection in utero

A

listeria monocytogenes and tremponema pallidum/styphilis

220
Q

in the neonate what can lilsteria cuase

A

meningitis, septicemia and pneumonia

221
Q

things used to diagnose literia

A

monocytosis in the peripheral blood and CSF
GRam stain of CSF
b hemolytic on blood agar

222
Q

treatment of listeria

A

ampicillin and gentamycin

223
Q

what are listeria resistant to

A

cephalosporins

224
Q

presenting with diarrhea and lymphadnitis

A

Y enterocolitica

225
Q

describe yersinia

A

gram negative rods/coccobacilli

with bipolar stainng/ safetypin appearearance that stains heavier in the poles than in the middle

226
Q

what species of yersinia causes the bubonic plague

A

Yersinia Pestis

227
Q

what species o yersinia causes acute enterocolitis

A

Yersinia enterocolitica

228
Q

virulence factors of yersinia pestis

A

gram negative so has endotoxin –> septicemia via TLR4

Fra1 - capsular antigen

LerV antigen

Yops

229
Q

what is Fra 1

A

anti phagocytic part of yersinia capsule that is essential for extracellular growth

only procued @ 37 degres

230
Q

what is Yops of yersinia

A

it is a toxin of yersinia that is injected into the host cell (macrophages, PMNs, etc) directly and is anti phagocytic –> a decreased immune response.

231
Q

in what cell does yersinia pestis live in

A

intracellular in macrphages

232
Q

how is yersinia pestis transmitted

A

by fleas + wild rodents especailly prarie dogs

rare: if in lungs can give to other people

233
Q

how does yersinia pestis cause the bubonic plague

A

bubonic phase developed 2-6 days after flea bite with no local infection. Get into the drainng lymphatics, travels to the LNs and get inflammation taking place (like inguinal LNs) –> intracellular replication in macrphages –>breaks out of those cells –> blood steam and disseminates as an extracellular disease

eventually get septicemia

234
Q

septicemic paguse leads to

A

DIC, and necrosis of finers and extremtities. “the black death”

235
Q

pneumonic plague

A

spread of bacteria from bloodstream to lungs –. infection of many other persons very virulent!

236
Q

how to diagnose yersinia

A

antibody titeer to Fra1

237
Q

treatment of yersinia pestis

A

gentamycin or streptomycin IM or IV

238
Q

Y entercolitica and Y rseudotuberculosis has what virulence factor

A
  • adehesins and invasins for binding and crossing epithelial surface
  • LerV
  • Yops- to inject things
  • antiphagocytic

no capsule

239
Q

Y entercolitica and Y rseudotuberculosis found in who

A

pepole preparing chitlins and children

240
Q

Y entercolitica and Y rseudotuberculosis causes

A

fever and diarrhea - presents like salmonella and campylobacter

sometimes abscesses in the liver

241
Q

tuleriemia is caused by

A

Francisella tularensis

242
Q

francisella tularensis stains how

A

bipolar stains

243
Q

if you see bipolar stainig think

A

yersinia
francisella tularensis
pasturella multocida

244
Q

virulence factors of francisella tularensis

A

Capsule: anti phagocytic

245
Q

francisella tularensis isfound where

A

in rabbits and in the environment

246
Q

who gets francisella tularensis

A

hunters or job related

247
Q

francisella tularensis found where

A

ozark area

248
Q

what does francisella tularensis cause

A

tuleremia: focal ulcer at site of entry then regional lymphadenopathy.

ocular granular form of diseae

get a focal ulcer @ the site of entry! while in yersinia dont see that

oropharyngeal disease
pneumonia

249
Q

prevention of francisella tularensis

A

vaccine

250
Q

Brucella

A

undulant fever, malta fever and Bang’s disease

251
Q

chacracteristics of brucella

A

smll, weekly stainng, gram negatve coccobacilli

faculative intracellular

252
Q

what is brucella growth stimulated by

A

erythitol

253
Q

where does brucella replicate

A

in macrophageS only

254
Q

transmission of brucella

A

from infected animals urine, milk, vaingal secretion and plcental tissue

255
Q

target organs of brucella

A

lungs, LNs, spleen, liver and BM

256
Q

if you see lung and liver involvement think

A

brucella

257
Q

treatment of brucellosis

A

prolonged treatment of doxycylicine and streptomycin

258
Q

what does virus like bacteria mean

A

it is obligate intracellular! the rickettsia groups are represenative of this

259
Q

what are the 3 primary characteristics of the rickettsial group

A

1 - obligate intracellular
2-zoonotic infection
3-transmitted via arthropod vectors

260
Q

what type of cell does rickettsiae replicate in

A

vascular endothelial cells

261
Q

what type fo cell does Ehrlichia replicate in

A

macrophages

262
Q

what type fo cell does anaplasma replicate in

A

granulocytes

263
Q

what type fo cell does bartonella bacilliformis replicate in

A

RBCs

264
Q

what type of bacteria lives in the phagolysosome

A

coxiella bruntti

265
Q

what type od bacteria (3) escapes from the phagosome and lives in the cytosol

A

rickettsie, shigella and listeria

266
Q

what type of cell llives in the phagosome and prevent phagolysosomal fusion

A

Enrlichia

toxoplasma

267
Q

what is the principal vector of Rickettsia Rickettsii

A

domestic dog tick/ dermacentor

268
Q

how does the dermacentor infect

A

directly by biting

269
Q

how do humans get rocky mountain spotted fever

A

dogs who are ifnected by ticks give it to them

270
Q

symptoms of rickettsia rickerrsii

A

severe frontal heacahe, myalgia, and maculopapular rash

vasculitis, shock and multiple organ failure, esp renal failure

271
Q

how dos the rickettsia rickettsii rash move

A

shows up on the extremities first then moves towards the trunk

272
Q

treatment of rickerrsia rickerrsii

A

doxyclycine - must be initiated early

273
Q

rickerrsia akari is found

A

in urban areas with mice infestations

274
Q

rickisetti prowazekii causes

A

epidemic typhus

275
Q

what is the vector of rickisetti prowazekii

A

the louse, which transmits human to human

276
Q

how does the louse cause rickisetti prowazekii

A

it defectates near feeding sites and the scratching of the bite gets it into the blood

277
Q

tell me about sylvatic typhus

A

it is from rickettsia prowazekii and is transmitted by fleas from flying squirrells. it is a milder disease than epidemic typhus.

278
Q

Rickettsia typhi causes

A

endemic/ murine typhus from rickettsia. flea vector from rodents

279
Q

typhus fever from rickettsia prowazeki clinical manifestations

A

begin 7-10 days after louse with fever and headache.

rash is on th trump –> extremitities so the pams, face and soles are spared.

280
Q

rickettsia prowazeki casuing epidemic typhus pathogenesis

A

replication inside of endothelial cells –> vsculitis of small vessels of many organs, shock and organ failure

281
Q

describe orientia tsutsugamushi

A

chigger bite from mice/rodents replicate in vascular endothelial cells, and goes on the trunk first, then the extremeities

282
Q

Ehrlicia/ anaplasma cause

A

ehrlichiosis

283
Q

Human monocytic ehrlichiosis is caused by

A

Ehrlichia chaffeensis (a Ehrlicia/ anaplasma)

284
Q

what is the vector of human monocytic ehrlichiosis (HME)``

A

the lone star tick and the deer tick

285
Q

what does Ehrlichia chaffeensis / Human monocytic ehrlichiosis replicate in

A

bloodstream monocytes and tissue macrophages

286
Q

what causes Human granulocytic anaplasmosis (HGA)

A

anaplasma phagocytophilum

287
Q

vector of Human granulocytic anaplasmosis (HGA)

A

black-legged deer tick

288
Q

vector of Human granulocytic anaplasmosis (HGA) REPLICATES IN

A

GRANULOCYTES

289
Q

how does HME, human monocytotropic ehlichiosis present

A

3-4 wks after tick bite
leukopenia, thrombocytopenia with systemic inflamamtion

fever, headache, vomiting

290
Q

how does human granulocytotropic anaplasmosis (HGA) present

A

1 wk after tick bite
more acute than HME
systemic inflammation with fever, headache, confusions

291
Q

treatment of ehrlichiosis

A

doxycycline

292
Q

bartonella henselae causes

A

cat scratch disease

293
Q

how does cat scratch disease present

A

primary skin papule or pustule at inoculation site 3-10 days following a bite

then moves up lymphatics leading to painful lymphadenopaty

can resolve after 7 wks

294
Q

what hapens in a person with HIV contracts bartonella henselae

A

bacillary angiomatosis
vascular prliferative disorder of the skin and visceral organs that spreads systemically, with lesiosn that resemble karposi sarcoma. spread to liver and spleen

wide spread sepsis and and bacteremia

295
Q

treatment of bartonella

A

azithromycin

296
Q

what does Bartonella quintana cause

A

trench fever, human:human via lice

297
Q

oroya fever in the andes due to bartonella bacilliformis is transmitted by

A

a sandfly

298
Q

what causes lyme disease

A

borrelia burgdorferi

299
Q

what do the ticks reponsible for lyme disease feed on

A

white footed deer and rabbit

300
Q

name of ticks that spread lyme disease

A

ixodes scapularis

D&T 2 Exam 2 (2 decks)

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