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SMP - MIM Part 2 > Lecture 6 - Enterics > Flashcards

Lecture 6 - Enterics Flashcards

1
Q

What are enterics?

A

Facultative Gram negative, rod-shaped bacteria common to or occurring as pathogens in the intestinal tract

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2
Q

Other name for enterics?

A

Enteric bacilli

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3
Q

Gaseous requirement of enterics?

A

Facultative anaerobe

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4
Q

What are 12 medically important (esp. in nosocomial infections) genera of the family enterobacteriaceae?

A
  1. Escherichia
  2. Salmonella
  3. Shigella
  4. Yersinia
  5. Proteus
  6. Providencia
  7. Morganella
  8. Citrobacter
  9. Enterobacter
  10. Pantoea
  11. Serratia
  12. Klebsiella
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5
Q

What body sites can enterobacteriaceae infect?

A

ANY

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6
Q

What are some infections that enterobacteriaceae cause?

A
  1. Common community acquired infections:
    - Enteritis/colitis
    - Cystitis/pyelonephritis
  2. Nocosomial infections (all categories)
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7
Q

What body site does Escherichia infect?

A

CNS

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8
Q

What body site does Salmonella infect?

A

GIT

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9
Q

What body site does Shigella infect?

A

GIT

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10
Q

What 2 enterobacteriaceae infect the CNS?

A
  1. Escherichia

2. Citrobacter

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11
Q

What 3 enterobacteriaceae infect the lower respiratory tract?

A
  1. Klebsiella
  2. Enterobacter
  3. Escherichia
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12
Q

What 3 enterobacteriaceae infect the bloodstream?

A
  1. Klebsiella
  2. Enterobacter
  3. Escherichia
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13
Q

What 4 enterobacteriaceae infect the GIT?

A
  1. Salmonella
  2. Shigella
  3. Escherichia
  4. Yersinia
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14
Q

What 4 enterobacteriaceae infect the urinary tract?

A
  1. Escherichia
  2. Proteus
  3. Klebsiella
  4. Morganella
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15
Q

What enterobacteriaceae is responsible for 90% of UTIs acquired in community conditions?

A

Escherichia

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16
Q

What are the 2 physical features of enterobacteriaceae?

A
  1. Gram negative rods (0.5 x 2 microns)

2. Motility: when motile by peritrichous flagella (Klebsiella and Shigella are the only non-motile)

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17
Q

What are peritrichous flagella?

A

Multiple flagella emanating from all aspects of the cell periphery (in contrast to polar flagella localized to one end of the cell)

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18
Q

What are the 3 biochemical/metabolic features of enterobacteriaceae?

A
  1. Facultative anaerobes
  2. Ferment glucose
  3. Oxidase negative
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19
Q

What is an oxidase test?

A

Test that distinguishes Enterobacteriaceae from other important enteric pathogens, Vibrios and Campylobacter, which are oxidase positive

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20
Q

What are the media for selective isolation and differentiation of enterobacteriaceae?

A

Many of them (do not need to know names) that use bile salts or dyes that inhibit other organisms (typically gram + bacteria) and contains a differentiating compound that some species can use and others cannot (e.g. lactose)

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21
Q

What is the difference between Lac positive and Lac negative enterobacteriaceae?

A
  1. Lac positive: cells that can ferment lactose

2. Lac negative: cells that cannot ferment lactose

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22
Q

What are 4 prominent Lac negative enterics?

A
  1. Salmonella
  2. Shigella
  3. Yersinia
  4. Proteus
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23
Q

What are fecal coliforms?

A

Lac positive enterics, primarily E. coli indicative of fecal contamination

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24
Q

What is speciation of enterobacteriaceae based on?

A

Based on metabolic/biochemical reactions during which enterobacteriaceae react with different compounds to produce different color compounds, gases, etc.

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25
Q

Purpose of API strips?

A

Speciation of enterobacteriaceae

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26
Q

What test is done once an enterobacteriaceae is speciated?

A

Subtyping based on serotyping with the:

  1. O-antigen: LPS
  2. H-antigen: flagellum
  3. K-antigen: capsule
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27
Q

What is the K-antigen called in Salmonella?

A

Vi-antigen

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28
Q

What is the most abundant facultative anaeroble in the gut?

A

E. coli

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29
Q

What vitamin does E. coli produce?

A

Vitamin K2

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30
Q

What are disease associated subtypes of E. coli? Other name for them?

A

Subtypes of E. coli that have acquired virulence genes through horizontal gene transfer

= pathovars

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31
Q

Important E. coli pathovars to know?

A
  1. Uropathogenic
  2. Neonatal meningitis
  3. Large collection that produces GIT diseases
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32
Q

What is the clinical significance of E. coli pathovars?

A
  1. Pathovars have distinct pathogenic mechanisms and, consequently, can have variable clinical presentations
  2. Future physicians will be treating, and should be alert to the appearance of, new and/or atypical enteric infections
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33
Q

What is the most common E. coli pathovar? What does it cause?

A

Enterohemorrhagic E. coli causing hemorrhagic colitis

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34
Q

3 symptoms of hemorrhagic colitis?

A
  1. Watery, progressing to grossly bloody diarrhea (after 3 days)
  2. Abdominal cramping
  3. Fever rare/low grade
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35
Q

What is life-threatening sequela of hemorrhagic colitis? How often does this happen?

A

HUS = hemolytic uremic syndrome, resulting in kidney failure and death

Happens in 15% of children below 10 yo with enterohemorrhagic E. coli infection

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36
Q

Incubation period of enterohemorrhagic E. coli infection?

A

3 days

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37
Q

Which patients are most at risk for HUS?

A

Children and the elderly

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38
Q

Where in the world are enterohemorrhagic E. coli infections more common? Why?

A

Developed nations

Due to ways cattle is raised

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39
Q

What subtype of enterohemorrhagic E. coli infection is the most common?

A

O157:H7

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40
Q

Reservoir of enterohemorrhagic E. coli?

A

Cattle and other ruminants

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41
Q

Does enterohemorrhagic E. coli cause disease in animals?

A

NOPE

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42
Q

Transmission route of enterohemorrhagic E. coli infections?

A

Fecal-oral

43
Q

Transmission vehicles of enterohemorrhagic E. coli infections?

A
  1. Ground beef
  2. Spinach
  3. Unpasteurized milk
  4. Lettuce
  5. Apple cider
  6. Radish sprouts
  7. Water: municipal, swimming
  8. Animal contact: farms, petting zoos
  9. Person to person (rare)
44
Q

Infectious dose of enterohemorrhagic E. coli?

A

10-100 bacteria (low)

45
Q

What determines the infectious dose of a particular bacteria?

A

Stomach acid provides a strong barrier to intestinal infection so acid resistant intestinal pathogens have lower infectious doses and reduced stomach acidity increases susceptibility to infection

46
Q

Describe the pathogenesis of hemorrhagic colitis.

A
  1. Bacteria directly subvert columnar epithelial cells by injecting effector proteins through a syringe-like assembly known as a type III secretion system => causing attaching and effacing (A and E) lesions => reduced absorptive surface and tight junction disruption => diarrhea
  2. Bacteria produce the shiga toxin (Stx) encoded by bacteriophage: AB toxin that binds the Gb3 receptor and deadenylates 60S rRNA (with N-glycosidase) => shuts down protein synthesis => cell and organ damage (primarily endothelial cells due to Gb3 expression) => bloody diarrhea, renal failure, and CNS manifestations
47
Q

Other name for shiga toxin produced by enterohemorrhagic E. coli? Where does the name come from?

A

Verotoxin

Resembles a toxin produced by Shigella bacteria, but in Shigella the toxin is part of the genome so treating with antibiotics does not have the risk of amplification

48
Q

2 types of shiga toxins? Which is more potent? What to note?

A

Stx 1 and 2***

NOTE: bacteria produce either or both

49
Q

What are shiga toxins encoded by?

A

λ phage in EHEC, temperate phage that lysogenize until they receive a particular signal

50
Q

3 clinical features of HUS?

A
  1. Microangiopathic hemolytic anemia
  2. Thrombocytopenia
  3. Glomerular thrombotic microangiopathy
51
Q

Treatments for enterohemorrhagic E. coli infections?

A
  1. Self-resolving 5-8 days
  2. Supportive therapy, particularly for HUS
  3. Antibiotic use controversial because it can make the situation worse due to the release of greater levels of toxins
  4. Experimental strategies: Gb3 receptor analogs and immunization against Stx
52
Q

3 microbiological features of the genus Shigella?

A
  1. Oxidase negative
  2. Lactose negative
  3. Nonmotile
53
Q

How do Shigella and E. coli relate to each other?

A

Shigella is a pathovar of E. coli

54
Q

What are 4 Shigella species?

A
  1. S. dysenteriae
  2. S. flexneri
  3. S. boydii
  4. S. sonnei
55
Q

What disease do Shigella infections cause? 2 names

A

Shigellosis = (bacillary) dysentery

56
Q

4 clinical symptoms of shigellosis? What to note?

A
  1. Initial watery diarrhea
  2. Subsequent abdominal cramping
  3. Fever
  4. Bloody, mucoid discharge with prominent fecal leukocytes

NOTE: symptoms can be mild to severe depending on species: sonnei < flexneri < dysenteriae

57
Q

Fatality rate of shigellosis due to S. dysenteriae? What causes death?

A

5-15%

Due to hemorrhaging and ulceration of the colon

58
Q

Definition of dysentery?

A

Triad of symptoms:

  1. Abdominal cramps
  2. Tenesmus
  3. Frequent, small-volume bloody, mucoid discharge
59
Q

What is the significance of fecal leukocytes?

A

Invasive enteric pathogens, like Shigella, Salmonella, Yersinia, and Campylobacter, provoke a inflammatory response resulting in high fecal leukocyte count

60
Q

Primary reservoir of Shigella?

A

Humans

61
Q

Infectious dose of Shigella infections?

A

< 200 bacteria (low)

62
Q

What species are most Shigella infections in the US due to?

A

S. sonnei

63
Q

What populations are most at risk of Shigella infections?

A
  1. Children < 15 yo due to outbreaks in daycares and institutional settings
  2. Traverler’s diarrhea
64
Q

What are secondary attacks? What infections have a high rate of these?

A

High chance of additional cases after one focus case in a household

Shigella infections

65
Q

Are Shigella infections more common in the US or the rest of the world?

A

Rest of the world: 15,000 vs 150 million cases/year

66
Q

What species are most Shigella infections in the world due to?

A

S. flexneri

67
Q

Describe the pathogenesis of Shigella infections.

A

Bacteria is phagocytosed by microfold cells of the GIT lumen and transcytosed to the basal aspect of the cells and are either phagocytosed by activated macrophages or interact with the basal surface to induce their own phagocytosis by the epithelial cells => they replicate in the epithelial cells => use the actin cytoskeleton of the cell to push themselves from one cell to the next => intracellular infection spreads throughout the epithelial layer of the colon => epithelial cells eventually killed => bloody, mucoid discharge

68
Q

Which only Shigella species produces a toxin? What is it? Effects?

A

S. dysenteriae Type I produces shiga toxin => bloody diarrhea and renal failure

69
Q

Treatment for Shigella infections?

A

Antibiotics

70
Q

Transmission vehicles of Salmonella infections? Most common?

A
  1. Tomatoes
  2. Jalapenos
  3. Cilantro
  4. Papaya juice
  5. Chicken eggs and poultry***
  6. Peppers
  7. Peanuts
  8. Cereal
  9. Water
71
Q

Why are there so many transmission vehicles of Salmonella?

A

Because they are universally present in the environment: human and animal GITs, water, soil, etc.

72
Q

4 microbiological features of the Salmonella genus?

A
  1. Oxidase negative
  2. Lactose negative (99%)
  3. Motile (phase variable)
  4. H2S producer (hydrogen sulfide)
73
Q

What are the 2 taxonomic nomenclatures for the genus Salmonella?

A
  1. Traditional: based on O and H antigens => ~2,500 species organized into serogroups A to I = Kauffman-White scheme
  2. Current: 2 species => S. enterica (with 6 subspecies) and S. bongori
74
Q

Host range and diseases of Salmonella infections?

A

Depends on Salmonella serotype:

  1. Some have a broad host range, e.g. S. Typhimurium, S. Enteritidis, infect diverse animal species, and typically cause gastroenteritis in humans
  2. Some have a narrow host range, are specifically adapted to a preferred host and rarely manifest as gastroenteritis (e.g. S. choleraesuis in pigs and S. Typhi and Paratypihi ONLY in humans)
75
Q

Disease caused by S. Typhi and Paratypihi? Which causes more severe cases?

A

Typhoid fever

S. Typhi causes more severe cases

76
Q

What is salmonellosis? Transmission? Clinical manifestation?

A

Infection with a member of the genus Salmonella typically transmitted through fecal contaminated food or water

Clinical manifestations vary with serotype

77
Q

2 possible clinical manifestations of non-typhoid salmonellosis?

A
  1. Gastroenteritis: watery diarrhea often with fever, nausea and vomiting
  2. Bacteremia
78
Q

Incubation period and duration of gastroenteritis due to salmonellosis?

A

6-48 h incubation period

2-7 day duration and self-resolving

79
Q

What % of patients with non-typhoidal salmonellosis have bacteremia?

A

8%

80
Q

What patients are at high risk of having bacteremia due to non-typhoidal salmonellosis? What is this called?

A

AIDS patients at high risk (recurrent bacteremia AIDS defining)

81
Q

Incidence of non-typhoidal salmonella serotypes in the US? What to note?

A

~40-50K cases/year

Actual: 1-1.5 M, but most cases do not get reported AND seasonal pattern with most cases in late summer/early fall

82
Q

Populations at higher risk of non-typhoidal Salmonella infections?

A
  1. Children < 5 yo

2. Elderly

83
Q

7 clinical symptoms of typhoid strains of Salmonell infections?

A

Enteric (typhoid) fever: severe systemic illness that spreads through the bloodstream

  1. Protracted fever for 3-4 wks
  2. Insidious onset
  3. Headache
  4. Anorexia
  5. Myalgia 10-14 days post-exposure
  6. GIT symptoms 1 week later
  7. “Rose spots” = maculopapular rash on trunk
84
Q

Transmission of typhoid strains of Salmonella?

A
  1. Person to person with some individuals being asymptomatic chronic carriers (gallbladder is infected) that pass the bacteria in their feces for over a year and transmit it in areas where there is not proper sanitation (1-4% of untreated patients) => low infectious dose
  2. Food and water
85
Q

Mortality rate of typhoid fever? What causes death?

A

10-15% mortality in untreated cases due to ileal perforation & hemorrhaging

86
Q

Incidence of typhoid salmonella infections in the US? What to note?

A

400-500 cases/year

NOTE: traveler’s disease in 75% of cases

87
Q

Incidence of typhoid salmonella infections in the world? What to note?

A

26 M cases/year

NOTE: mostly in South Asia, 80% due to S. Typhi and 200-600K deaths/year

88
Q

Reservoir of typhoid Salmonella?

A

Humans

89
Q

Describe the pathogenesis of Salmonella gastroenteritis.

A

Bacteria transgresses GIT epithelial layer through the microfold cells => inflammatory response with macrophages and PMNs secreting leukocytes => inflammatory diarrhea

90
Q

Describe the pathogenesis of Typhoid fever.

A

Bacteria transgresses GIT epithelial layer through the microfold cells => inflammatory response with macrophages => bacteria survives the macrophages and grows in them, so macrophages serve as a vehicle for dissemination through the mesenteric lymph nodes => blood => liver and spleen => gallbladder => back to GIT

91
Q

Why does the fever in typhoid fever take 10-14 days to appear?

A

Doesn’t appear until the macrophages start to lyse and release the bacteria in the bloodstream => bacteremia

92
Q

Why is the genus campylobacter important?

A

Causes almost as many infections as Salmonella

93
Q

8 microbiological features of the genus Campylobacter?

A
  1. Gram negative
  2. Curved/helical rod
  3. Single polar flagellum
  4. Microaerophilic (5-10% O2)
  5. Oxidative metabolism (do not utilize carbohydrates)
  6. Optimal growth at 42 C (some species)
  7. Oxidase positive
  8. Polysaccharide capsule
94
Q

4 primary species of clinical importance in the genus Campylobacter? Most important one?

A
  1. C. jejuni***
  2. C. coli
  3. C. upsaliensis
  4. C. fetus
95
Q

Why was the genus Campylobacter not recognized for a while?

A
  1. Because it only needs 5-10% O2 and need 42 degrees so wouldn’t survive under typical culture conditions
  2. Very small and can pass through a sterilization filter
96
Q

Where are Campylobacters found?

A

GIT of animals and birds

97
Q

Transmission vehicles of Campylobacter? Most common?

A
  1. Undercooked poultry*** (50-70% of sporadic cases)
  2. Raw milk
  3. Surface waters
  4. Beef
  5. Clams
  6. Cheese
  7. Direct contact with infected animals and pets
98
Q

US incidence of Campylobacter infections? What to note?

A

> 2 million/yr (not reportable)

NOTE: seasonal, summer to early fall and higher in rural communities

99
Q

In what population is a Campylobacter infection symptomatic?

A

Symptomatic infection in children and asymptomatic in adults

100
Q

Pathogenesis of Campylobacter infection? What is it similar to?

A

Invasive organism that provokes a strong inflammatory response

Similar to Salmonella infection

101
Q

Sequella of Campylobacter infection? How does this work?

A

Guillain-Barre syndrome = flaccid peripheral neuropathy due to inflammatory demyelination

Campylobacter sialic acid containing LOS (lipooligosaccharide: similar to LPS, but lacking outer O antigen repeats) induce cross-reactive antibodies to GM1, GM2, GD1a = “molecular mimicry”

102
Q

How often does a Campylobacter infection develop into GBS?

A

Approx. 1 in 2000 C. jejuni infections and 30-66% of GBS cases have antecedent C. jejuni infection

103
Q

3 most common infections in US?

A
  1. Salmonella
  2. Campylobacter
  3. Shigella

SMP - MIM Part 2 (13 decks)

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