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Microbiology > L33-35: Bacterial Infections of the GI Tract > Flashcards

L33-35: Bacterial Infections of the GI Tract Flashcards

1
Q

Diarrhea

A

Passage of 3+ loose/liquid stools per day, usually result in disease of small intestine

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2
Q

What are the host defenses that the GI tract can use to prevent disease?

A

Continuous epithelium, mucus (but sometimes triggers virulence), low pH, gut motility, shedding of epithelium, bile, secretory IgA, normal microbiota

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3
Q

Gastritis

A

Inflammation of the stomach

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4
Q

Gastroenteritis

A

Inflammation of stomach and intestines, characterized by nausea, vomiting, diarrhea, and abdominal discomfort/pain

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5
Q

Dysentery

A

Inflammatory disorder of the GI tract often causing diarrhea with blood/pus, pain, fever, abdominal cramps – normally associated with large intestine

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6
Q

Enteritis

A

Inflammation of the intestines, especially small intestine

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7
Q

Enterocolitis

A

Inflammation of the mucosa of small and large intestine

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8
Q

Colitis

A

Inflammation of the large intestine, specifically the colon

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9
Q

Inflammatory bacteria characteristics

A

Cause damage to the intestine through inflammation, more likely to see fecal occult/leukocytes or visible blood

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10
Q

Inflammatory bacteria types

A

Salmonella spp., Campylobacter jejuni, C. diff (severe cases), EHEC, EIEC, Shigella spp., Vibrio parahaemolyticus, Yersinia enterocolitica

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11
Q

Non-inflammatory bacteria characteristics

A

Pass through the intestine or adhere to intestinal epithelium – either don’t produce toxins or non-cytotoxic toxin

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12
Q

Non-inflammatory bacteria types

A

EPEC, ETEC, Vibrio cholerae, Listeria monocytogenes

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13
Q

Which bacteria cause bloody diarrhea? (sometimes or often)

A

EHEC, Campylobacter jejuni, Shigella spp., Yersinia enterocolitica, EIEC, C. diff, Vibrio parahaemolyticus

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14
Q

Which bacteria cause watery diarrhea? (rarely blood)

A

EPEC, ETEC, food poisoning, Clostridium perfringens, Bacillus cereus, Vibrio cholerae, Salmonella spp., Listeria monocytogenes

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15
Q

Which bacteria cause symptoms 1-8 hrs after ingestion and what is their mechanism?

A

Preformed toxin – S. aureus, Bacillus cereus (emetic), C. botulinum

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16
Q

Which bacteria cause symptoms 8-16 hrs after ingestion and what is their mechanism?

A

Production of toxin after ingestion – B. cereus (diarrheal), C. perfringens, C. botulinum

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17
Q

Which bacteria cause symptoms 16+ hrs after ingestion and what is their mechanism?

A

Adherence, growth and virulence factor production – Shigella, Salmonella, Listeria monocytogenes, all E. coli species, Campylobacter, Vibrio species

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18
Q

2 types of bacterial food poisoning

A
  1. Toxins produced before food is eaten

2. Large number of spores that germinate in intestine and produce toxins

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19
Q

Symptoms of bacterial food poisoning

A

Diarrhea, vomiting, but NO FEVER

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20
Q

4 main causes of bacterial food poisoning

A

S. aureus, C. botulinum, C. perfringens, Bacillus cereus

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21
Q

S. aureus in food poisoning

A

Preformed toxin, causes severe vomiting, diarrhea, and abdominal pain in 1-8 hrs – toxin is HEAT-STABLE (not well understood) – supportive treatment

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22
Q

Disease process of C. botulinum

A

Causes botulism, mediated by botulism toxin – early stage: vomiting, diarrhea, abdominal pain 1-16 hrs later, late stage: flaccid paralysis leading to progressive muscle weakness and respiratory arrest

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23
Q

Mechanism of infection of C. botulinum

A

Ingestion of preformed toxin or large number of spores

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24
Q

How does the botulism toxin work?

A

Acts at neuromuscular junction and interferes with signaling at synapses – if patient survives there can be lingering weakness and dyspnea up to a year later

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25
Q

How do adults and infants get infected with C. botulinum?

A

Adults: improperly canned food items
Infants: honey

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26
Q

Infant botulism (floppy baby syndrome)

A

Occurs between birth-6 months; germination of C. botulinum spores in intestines leads to toxin production (due to permeability of intestinal mucosa)

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27
Q

Treatment for botulism

A

Supportive or IV anti-toxin administration if severe

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28
Q

Clostridium perfringens characteristics

A

Gram+ rod that forms spores

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29
Q

C. perfringens disease process

A

Mediated by C. perfringens enterotoxin, associated with meat/gravies held below standard temp and begins 8-16 hrs after ingestion

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30
Q

Pathogenesis of C. perfringens

A

Survive cooking, grow in food, ingested and sporulate –> enterotoxin produced –> diarrhea

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31
Q

Treatment for C. perfringens

A

Supportive therapy

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32
Q

Bacillus cereus characteristics

A

Gram+ rod, spore-forming

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33
Q

Emetic form of Bacillus cereus

A

Vomiting, nausea, and abdominal cramps 1-8 hrs due to ingestion of preformed heat-stable enterotoxin – related to improper storage of rice

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34
Q

Diarrheal form of Bacillus cereus

A

Diarrhea, nausea, and abdominal cramps 8-16 hrs later, production of heat-liable enterotoxin in intestine – comes from meat, vegetables

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35
Q

What is the main difference between the pathogens that cause food poisoning and those that cause other disease?

A

The bacteria that cause food poisoning do so by release of toxin but cannot actually bind to the digestive tract

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36
Q

Helicobacter pylori characteristics

A

Gram- curved rod, microaerophilic, produce flagella and uses urease to cause disease

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37
Q

What disease does Helicobacter pylori cause?

A

Ulcers and chronic gastritis (related to stomach cancer)

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38
Q

Pathogenesis of Helicobacter pylori

A

Penetrates the stomach epithelium and produces NH3 using its urease (neutralizes acid of stomach), then exposes underlying tissue due to damage and this is where ulcers can form

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39
Q

Diagnosis of Helicobacter pylori

A

Urea breath test (or biopsy)

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40
Q

Treatment of Helicobacter pylori

A

Only treat after positive test – combination of antibiotics and proton pump inhibitor

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41
Q

Listeria monocytogenes characteristics

A

Gram+ facultative anaerobic, short rods, intracellular – can persist in the cold!!!

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42
Q

Epidemiology of Listeria monocytogenes

A

Animal reservoirs such as mammals, birds, and fish; contaminated food is primary source (ready to eat meats, cheeses), high risk of infection in pregnant women, elderly, immunocompromised – passed mother to fetus

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43
Q

Clinical manifestation of Listeria monocytogenes

A

Usually asymptomatic in adults (but fever); causes bacteremia or meningitis/encephalitis in immunocompromised adults

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44
Q

Listeria monocytogenes and pregnant women

A

May develop nausea, fever, diarrhea; should check if fever with no obvious infection – can be passed to newborn

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45
Q

Neonatal Listeria monocytogenes infection

A

Granulomatosis infantiseptica = pyogenic granulomas all over body, meningitis, encephalitis, can be early (in utero – premature or death) or late onset

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46
Q

Pathogenesis of Listeria monocytogenes

A

Adhere and induce uptake into the cell with IntA, internalized in endocytic vacuole which activates Listeriolysin O (LLO) – can spread by replicating in host cell cytosol and using ActA-mediated actin polymerization to spread

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47
Q

Where can Listeria monocytogenes spread?

A

First to neighboring cells and blood stream, then to liver, spleen, and CNS

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48
Q

Diagnosis of Listeria monocytogenes

A

Microscopy is too sensitive, best is cold enrichment selection (because it grows in the cold)

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49
Q

Treatment of Listeria monocytogenes

A

Beta-lactam or trimethoprim-sulfamethoxazole (no vaccine, cook properly)

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50
Q

MacConkey agar test

A

Tests for lactose fermentation – positive = red (E. coli, etc.), negative = white (Salmonella, Shigella, etc.)

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51
Q

Indole test

A

Tests for indole production – positive = red (E. coli, Vibrio spp, etc.), negative = no color change (Salmonella)

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52
Q

Hydrogen sulfite (H2S) production test

A

Forms a black precipitate – positive = Salmonella, negative = Shigella

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53
Q

4 main E. coli pathogens

A 
ETEC = enterotoxigenic
EPEC = enteropathogenic
EHEC = enterohemorrhagic
EIEC = enteroinvasive
54
Q

EPEC characteristics

A

Gram-, facultative anaerobe, moderately invasive (generally non-inflammatory)

55
Q

Epidemiology of EPEC

A

Important in infants in developing country, 5-10% of pediatric diarrhea (ePec for Pediatric)

56
Q

Pathogenesis of EPEC

A
  • -EPEC finds its way into the intestines where it interacts with cells through BfpA
  • -Type III secretion system (needle injection) that injects protein Tir into cytosol and inserts into membrane to become receptor for bacteria
  • -Causes AE lesion (loss of microvilli) leading to watery diarrhea
  • -NO TOXINS used
57
Q

Diagnosis of EPEC

A

Ferments lactose (red on MacConkey agar), indole positive, PCR

58
Q

Treatment of EPEC

A

Supportive therapy

59
Q

ETEC characteristics

A

Gram- facultative anaerobe, non-invasive, causes watery diarrhea (known as traveler’s diarrhea – eTec for Traveler)

60
Q

Pathogenesis of ETEC

A

Attaches to the surface of the cell with its fimbriae, produces both LT (heat liable) and ST (heat stable) toxins

61
Q

How does ETEC’s LT toxin work?

A

AB toxin that finds its way into the cell to activate adenylate cyclase (which increases cAMP) to cause solutes and water to leave the cells – watery diarrhea

62
Q

How does ETEC’s ST toxin work?

A

Not an AB toxin – doesn’t enter cell but increases cGMP to cause watery diarrhea

63
Q

Diagnosis of ETEC

A

Clinical history is key, DNA probes can detect LT and ST encoding genes (not common yet)

64
Q

Treatment of ETEC

A

Supportive therapy

65
Q

Salmonella Typhi characteristics

A

Gram- facultative anaerobe, motile rods, flagellated (H antigen), acid tolerant, intracellular – INFLAMMATORY

66
Q

Epidemiology of S. Typhi

A

Only infects humans, fecal-oral transmission

67
Q

Symptom progression of S. Typhi

A

Fever with headache -> rising fever over 3 days –> typhoid fever (prolonged) –> GI symptoms (also it’s shed in stool)

68
Q

Pathogenesis of S. Typhi

A

M cells (in Peyer’s patches in the ilium) take antigens and present them, leading to tolerance – S. Typhi uses this and type III secretion to inject Ssps into cell, which induces membrane ruffling around bacteria that cause them to get enveloped

69
Q

Pathogenesis of S. Typhi leading to bacteremia

A

Escapes enterocytes and infects macrophages in the same way –> escapes from macrophages to cause bacteremia with prolonged fever

70
Q

Diagnosis of S. Typhi

A

Culture of stool and blood samples on selective media

71
Q

Treatment of S. Typhi

A

Antibiotic therapy based on susceptibility profile (fluoroquinolones, trimethoprim-sulfamethoxazole or broad spectrum cephlosporin)

72
Q

Prevention of S. Typhi

A

Avoid potential sources of infection (no water, raw fruits or vegetables), vaccination in endemic areas

73
Q

Nontyphoidal Salmonella types

A

Serovars Cholerasuis, Enteritidis, and Typhimurium

74
Q

Nontyphoidal Salmonella characteristics

A

Gram- facultative anaerobe, motile rods, flagellated (H antigen), acid tolerant, intracellular pathogens – SAME AS S. TYPHI

75
Q

Epidemiology of nontyphoidal Salmonella

A

Industrialized countries, higher in young children/allergies, sources of infection are contaminated food (transmission can go between humans, food, and animals)

76
Q

Clinical manifestations of nontyphoidal Salmonella

A

Begins between 6-48 hours post-ingestion, nausea/vomiting with cramps and watery diarrhea lasting for 3-4 days (can be with or without blood)

77
Q

Pathogenesis of nontyphoidal Salmonella

A

Same as S. Typhi except it does not have prolonged fever component

78
Q

Diagnosis of nontyphoidal Salmonella

A

Serology (detect anti-Vi antigen antibodies), culture from blood and stool – REMEMBER white on MacConkey (non-lactose fermenting) and H2S producing (black precipitate)

79
Q

Treatment of nontyphoidal Salmonella

A

Supportive therapy, antibiotics not recommended except for severe (enhances carrier state) – no vaccine for prevention!!

80
Q

Campylobacter jejuni characteristics

A

Gram- rod, curved or seagull shaped, microaerophilic (needs less O2), in many animal reservoirs – INFLAMMATORY

81
Q

Disease of Campylobacter jejuni

A

Ulceration and acute enteritis, watery diarrhea, can lead to sepsis and GBS – not much is known about pathogenesis

82
Q

Guillain-Barre syndrome (GBS) and Campylobacter jejuni

A

C. jejuni is not the only cause of GBS but it does cause it by mimicking something on neurons that causes the immune system to start attacking neurons – progressive muscle weakness accompanied by absent or depressed deep tendon reflexes with varied symptoms related to paralysis

83
Q

Diagnosis of Campylobacter jejuni

A

Culture (done routinely) on selective media in microaerophilic environment

84
Q

Treatment of Campylobacter jejuni

A

Supportive therapy, antibiotics only used for invasive disease

85
Q

Vibrio spp. characteristics

A

Gram- facultative anaerobe, comma shaped, live in water, have wide range of growth abilities – 3 types: V. cholerae and V. parahaemolyticus (3rd type not important) – INFLAMMATORY

86
Q

Disease of V. cholerae

A

Cholera – can be asymptomatic all the way to severe watery diarrhea (abrupt onset and can kill within hours, “rice water” stool)

87
Q

Epidemiology of V. cholerae

A

Spread through contaminated water, important cause of diarrheal disease, infection leads to long-term immunity (O-antigen specific)

88
Q

Cholera pandemics

A

O1 serotype causes these – classic biotypes seen in pandemics 1-6, El Tor biotype seen in current pandemic

89
Q

Pathogenesis of cholera

A

Due to cholera toxin – AB toxin that activates adenylate cyclase to increase cAMP –> massive efflux of watery secretions but does not cause significant cell damage (similar to ETEC LT toxin)

90
Q

Diagnosis of V. cholerae

A

Culture (in places where not common)

91
Q

Treatment of V. cholerae

A

Rehydration therapy is very important!!! (otherwise will kill)

92
Q

Disease of V. parahaemolyticus

A

Causes explosive watery diarrhea, nausea, vomiting, abdominal cramps, low grade fever

93
Q

Virulence factor of V. parahaemolyticus

A

Kanagawa hemolysin – induces chloride secretion –> watery diarrhea

94
Q

Epidemiology of V. parahaemolyticus

A

Associated with consumption of raw shellfish, common cause of bacterial gastroenteritis associated with seafood

95
Q

Treatment and prevention of V. parahaemolyticus

A

Proper cooking of shellfish, self-limiting

96
Q

Yersinia enterocolitica characteristics

A

Gram- coccobacilli, inflammatory

97
Q

Epidemiology of Y. enterocolitica

A

Widespread in nature and animals, most isolates avirulent and spread by ingestion of contaminated food/water

98
Q

Sypmtoms of Y. enterocolitica

A

Fever, abdominal cramps, watery-bloody diarrhea – lasts 1-2 weeks

99
Q

Pathogenesis of Y. enterocolitica

A

Poorly understood, but binds to and invades M cells (like Salmonella) and involves T3SS, injects Yops into cells – produces heat-stable enterotoxin

100
Q

Diagnosis of Y. enterocolitica

A

Stool culture

101
Q

Treatment of Y. enterocolitica

A

Self-limiting (supportive therapy)

102
Q

C. diff characterisitics

A

Gram+ anaerobe, non-invasive, SPORE-FORMING, emerging pathogen

103
Q

Disease/symptoms of C. diff

A

Causes pathology in the COLON – varies a lot – asymptomatic carriage is least severe, CDAD, pseudomembrane colitis, most severe is fulminant colitis (causes necrosis) leading to toxic megacolon

104
Q

Asymptomatic C. diff carriage

A

No adverse affects

105
Q

C. diff associated diarrhea (CDAD)

A

Causes watery diarrhea with fecal leukocytes and sometimes occult blood; symptoms include nausea, anorexia, fever, malaise, dehydration, leukocytosis with left shift; abdominal distension and tenderness are seen; sigmoidoscopic exam shows diffuse or patchy nonspecific colitis

106
Q

Pseudomembrane colitis (C. diff)

A

Same as CDAD but more severe – sigmoidoscopic exam shows raised, adherent yellow plaques (hence name pseudomembrane)

107
Q

Fulminant colitis (C. diff)

A

Severe or diminished diarrhea (surgical consult is required); lethargy, fever, tachycardia, dilated colon; can present as acute abdomen (sharp pain); no sigmoidoscopic exam should be performed

108
Q

Pathogenesis of C. diff

A

Toxin A and B cause damage to the mucosa and disrupt host cell cytoskeleton

109
Q

Epidemiology of C. diff

A

Often a hospitalized patient will be exposed to C. diff and if their gut flora is altered (ex. by antibiotics) they can acquire it

110
Q

Diagnosis of C. diff

A

Detect toxin in stool (culture not helpful)

111
Q

Treatment of C. diff

A

Oral vancomycin or metronidazole

112
Q

Prevention of C. diff

A

Fecal transplant

113
Q

EHEC (E. coli) characteristics

A

Infection of the large intestine – Gram- facultative anaerobe, found in animal reservoirs

114
Q

Epidemiology of EHEC

A

Sporadic cases in developed world mostly to do with hamburger or vegetables (eHec for Hamburgers)

115
Q

Disease of EHEC

A

Hemorrhagic colitis (eHec for Hemorrhagic) that causes bloody diarrhea and abdominal tenderness but no fever

116
Q

EHEC sequelae

A

Hemolytic uremic syndrome (HUS) – anemia and kidney failure

117
Q

Pathogenesis of EHEC

A

AE lesions like EPEC (Type III secretion using Tir), Shiga-like toxin that blocks translation by cleaving part of the 60S subunit of ribosome

118
Q

How does EHEC cause kidney damage?

A

Glomeruli are rich in toxin glycolipid receptor Gb3 so toxin can bind and target those tissues –> kidney damage –> kidney failure sometimes

119
Q

Diagnosis of EHEC

A

Presumptive due to bloody diarrhea without fever (can also use culture, PCR to detect Shiga toxin, or rapid diagnostic test kits)

120
Q

Treatment of EHEC

A

Supportive therapy, not antibiotics

121
Q

Why are antibiotics often contraindicated for EHEC?

A

Bacterial cell damage will lead to a lysogenic phage –> lytic lifecycle that increases toxin production and might increase HUS rate

122
Q

Prevention of EHEC

A

Properly cook hamburger, cook raw vegetables

123
Q

Shigella spp. characteristics

A

Gram- rods, facultative anaerobes, intracellular pathogens (very acid tolerant), cause dysentery – INFLAMMATORY

124
Q

Epidemiology of Shigella

A

Humans are only reservoir, transmission through fecal oral route (breakouts in daycares), incidence is directly related to hygiene, very low infectious dose needed

125
Q

Clinical manifestations of Shigellosis

A

1-3 post-ingestion, disease usually self-limiting 2-5 days post

126
Q

Strain specificity of Shigella

A

S. sonneii – fever, malaise and watery diarrhea
S. flexerni and S. dysenteriae – lead to dysentery and other typical symptoms, frequent bloody/pus-filled stools (S. dys has potential for HUS)

127
Q

Pathogenesis of Shigella

A

Very acid resistant, invades macrophages through M cells, escapes quickly from phagosome and induces apoptosis (inflammation and pus production) – interacts with basolateral face of enterocytes to induce uptake via T3SS and cause lysis of endocytic vacuole – invades other cells with actin polymerization

128
Q

Shiga toxin production (Stx) in Shigellosis

A

Binds host Gb3 receptor, inhibits translation –> cell damage –> tissue damage – glomerular endothelial cells are rich in Gb3 which is why this causes HUS

129
Q

Diagnosis of Shigella

A

Stool culture, serological tests to confirm

130
Q

Treatment of Shigella

A

Rehydration therapy, antibiotic treatment (if necessary but ampicillin resistance is common)

131
Q

Prevention of Shigella

A

No vaccine, just improved sanitation – infection does not make you immune

132
Q

EIEC

A

Another E. coli, infects large intestine – same as Shigella except no Shiga toxin

Microbiology (20 decks)

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