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Pathology -- Infectious Disease > Infectious Disease -- Bacteria III - Enteric Pathogens > Flashcards

Infectious Disease -- Bacteria III - Enteric Pathogens Flashcards

1
Q

Are enteric pathogens very common?

Very deadly?

A

Yes common

Few kilers

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2
Q

Top three most common food-bourne domestically acquired pathogens

A

Norovirus
Salmonella
C. perfringens

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3
Q

Top three most common foodbourne illness pathogens requiring hospitalization

A

Salmonella
Norovirus
Campylobacter

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4
Q

Top five foodbourne illnesses resulting in death

A 
Salmonella
Toxoplasma gondii
Listeria monocytogenes
Norovirus
Campylobacter
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5
Q

Based on the bacterial stats name two bacteria that are common contaminants, but do not cause serious disease

A

Clostridium perfringens

Staph. aureus

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6
Q

List two bacteria who are much less common, but cause fatal disease

A

E Coli O157:H7

Listeria

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7
Q

Enteric viruses – list three

A

Norwalk Virus
Enterovirus
Polio Virus

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8
Q

Four enteric parasites

A

Giardia
Amoebae
Ascaris
Cryptosporiosis

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9
Q

Six more frequently discussed enteropathic bacteria

A 
E Coli
Cholera
Shigella
Salmonella (enteritidis, typhi)
Campylobacter
Yersnia
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10
Q

Three types of pathogenesis typically seen with enteropathic bacteria

A

Ingestion of enterotoxins
Infection by colonizing toxigenic organisms
Direct invasion of the gut wall

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11
Q

What happens when enterotoxins are ingested

A

Absorption of pre-formed toxins

Symptoms in a very short incubation time

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12
Q

What happens with the infection by colonizing toxigenic organisms pathogenesis method

A

Hypersecretion reaction from bacterial adherence and toxin secretion
Incubation: 1-3 days

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13
Q

Incubation time for the direct invasion of the gu wall pathogenesis

A

Days-weeks

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14
Q

Three most important traits of virulence factors for enteropathic bacteria

A

Adherence to mucosal cells
Production of enterotoxin
Capacity of invade

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15
Q

Specific virulence factors involved in adherence to mucosal cells?

A

Pili

Flagella

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16
Q

Specific virulence factors involved in production of enterotoxins

A

Prototype secretagogue toxin (cholerae)
Cytotoxins (Shiga toxin – Shigella, O157:H7)
Superantigens (Staph)

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17
Q

Mechanisms involved in for capacity to invade tissue

A

Intracellular proliferation, cell lysis, cell-to-cell spread

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18
Q

Invasion of cells and lysis causes….

A

Bloody/Pussy Diarrhea (dysentery)

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19
Q

Predisposing factors for enteropathic bacteria

A 
Fecal contamination of Food
Immunosuppression
Antispasmodic drugs
Antacids
Mucosal Disease
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20
Q

Why do antispasmodic drugs and antacids promote enteropathic disease?

A

Less killed in stomach

Less movement of Intestine–> Overgrowth

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21
Q

Classic Example. Local response to absorbed toxin

A

Staph food poisoning

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22
Q

Classic Example. Systemic response to absorbed toxin

A

Botulism, O157:H7

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23
Q

Classic Example. Dysentery

A

Shigella

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24
Q

Classic Example. Systemic Illness

A

Typhoid Fever

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25
Q

Classic Example. Secretory Diarrhea

A

Cholera

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26
Q

Two causes of excess fluid in diarrhea (with example)

A 
Hypersecretion (Cholera)
Osmotic Load (Lactose Intolerance)
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27
Q

Dysentery =

A

Loose Stool + Blood + Leukocytes

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28
Q

Difference between diarrhea and dysentery.

A

Diarrhea occurs when there is either toxin with no bacteria, superficial colonization+toxin, or superficial colonization + inflammation. Dysentery occurs when the pathology extends deeper to mucosal invasion and necrosis, submucosal invasion, and/or systemic spread.

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29
Q

The detail run down on E Coli

A

G- Rod
Green Sheet on EMB agar
Coliform

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30
Q

Important Characteristics of E Coli

A

Watery diarrhea, cramping pain, fever, malaise
Invasive or cytolytic disease - dysyntery
Verotoxin (shigatoxin) – hemolytic uremic syndrome

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31
Q

What happens in hemolytic uremic syndrome

A

Renal Failure and Anemia

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32
Q

Describe effects of enterotoxic E Coli

A

Watery Traveler’s Diarrhea

Consumption of food contaminated with enterotoxin-producing strain

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33
Q

Describe the effects of enterohemorrhagic E Coli

A

Severe bloody colitis from consumption of food contaminated with invasive verotoxin (shiga toxin) strain
(Mainly O157:H7)

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34
Q

Foods assocaited with EHEC?

A

Hamburger
Dairy Products (unpasteurized)
Fruit Juice
Agricultural products contaminated with manure (spinach)

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35
Q

Which E Coli is primarily pediatric diarrhea in impoverished nations

A

EAEC (enteroaggregative)

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36
Q

Risk of person-to-person transmission of O157-H7

A

Low.

Fecal oral transfer sometimes shows up in places like daycare centers.

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37
Q

Relationship of O157:H7 to temperature? Sorbitol?

A

Won’t ferment sorbitol

Won’t grow at 45 degrees

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38
Q

Mechanism of O157:H7 disease?

A

Small infectious dose
Bac adhere to cell membrane and colonize LI
Produce shigatoxins which damage endothelial cells
(inhibits mRNA translation, protein synthesis)

39
Q

Disease course of O157:H7?

A

Onset 3-4 days after ingestion of the organism
Severe Abdom. cramping, watery diarrhea progressing to bloody in 3-4 days
Occasioanlly Vomiting. Low or No fever.
Average duration – 8 days

40
Q

Different ways in which O157:H7 might present?

A 
Asymptomatic
Mild Illness
Dysyntery
Hemolytic Uremic Syndrome
Thrombotic Thrombocytopenic Purpura (TTP)
41
Q

Who is most vulnerable to O157:H7 hemolytic uremic syndrome

A

Children, Elderly

42
Q

Generic bacteria data for shigella?

A

G-
Non-motile
Non-coliform

43
Q

Pathogenesis of Shigella

A

Fecal/Oral Transmission (Daycares, MSM)
Invasive lesions of colonic mucosa which spreads to LN
Exotoxin causes Mucosal necrosis
Highly Virulent

44
Q

T or F. Shigella cannot cause bacteremia to distant organs

A

True

45
Q

Generic Bacteria information for Vibrio cholerae

A

Comma-shaped, G-

Alkali tolerant

46
Q

How is Vibrio cholerae transmitted?

A

Direct fecal-oral transmission

Asymptomatic Carriers

47
Q

Pathogenesis of Vibrio cholerae?

A

Enterotoxin induces the secretion of isotonic fluid

No invasive lesions

48
Q

Cause of death in Vibrio cholerae?

A

Dehydration, Hypovolemic Shock

49
Q

Mechanism of Vibrio cholerae hypersecretion

A

Subunit A binds with ADP ribosylation factors
Activates GTP-activated adenylate cyclase resulting in cAMP formation
Stimulates secretion of chloride bicarbonate

50
Q

Generic bacteria info for Salmonella.

A

G-
Non Coliform
H2S production

51
Q

Two groupings of Salmonella to separate

A

S. enteritidis, S. typhimurium

S. typhi

52
Q

Three forms of Salmonella

A

Typhoid
Enteric Fever
Salmonella Food Poisoning

53
Q

Presentation of Salmonella Food Poisoning

A

Vomiting and Diarrhea (gastroenteritis)
Superficial lesions of colon
Usually self-limiting (except immunocrompromised)

54
Q

Organisms responsible for Salmonella food poisoning

A

S. enteritis, S typhimurium

55
Q

Common origins of Salmonellosis

A

Eggs, Undercooked Chicken
Contaminated Water
Turtles/Reptiles
Cantaloupes, Mangoes

56
Q

Who should never own a reptile

A

IC, Pregnant, Kids Under Five

57
Q

Salmonella pathologic mechanism

A

Invasion of Mucosal cells, cause ulceration
No enterotoxin
Multiply in neutrophils+Macrophages
G- Sepsis

58
Q

Salmonella is a common cause of ______ in children with sickle cell anemia

A

Osteomyelitis and Sepsis

59
Q

What is paratyphoid fever (organisms, symptoms)

A

S. typhinurium, paratyphi or cholera-suis
Fever, Bacteremia, Local Lesions
Ass. w/ sickle cell disease + schistosomiasis

60
Q

Describe Typhoid Fever symptoms

A
  • Fever with “rose sports” on lower anterior chest and abdomen
  • Hepatosplenomegaly
    - Typhoid Nodules throughout immune tissues+liver
  • Diarrhea (rarely with vomiting)
  • Ulcerations of Peyer’s Patches
  • Neutropenia
61
Q

Causative organism for Typhoid Fever

A

Salmonella Typhi

62
Q

Describe a Typhoid Fever carrier state

A

3-5% achieve carrier state in Gall Bladder

Bacteria isnt dissolved by bile, so it can move up to stay there

63
Q

Generic Campylobacter jejuni information

A

G- Comma shaped

Flagellated

64
Q

Where does Campylobacter jejuni infection usually come from?

A

Undercooked Beef

65
Q

Symptoms of Campylobacter jejuni

A

Gastritis, Diarrhea, and Dysentery

associated with guilain-barre neuropathies

66
Q

Risk of ______ in immunocompromised patients with Campylobacter jejuni infection

A

Sepsis

67
Q

Transmission of Campylobacter jejuni?

A

Contaminated Water Sources
Food-Bourne Illness
Improperly cooked chicken/Beef

68
Q

Pathogenesis of Campylobacter jejuni?

A

Toxin causes invasive lesions (colonic crypt abscesses) and adherance.
Rarely Septicemia
Causes foul smelling stools with blood/exudate

69
Q

Who is at highest risk for effects of Yersnia entercolitica

A

Pediatric Population

70
Q

Foods assocaited with Yersnia entercolitica

A

Raw, undercooked Pork

Unpasteurized milk

71
Q

Does Yersnia entercolitica influence upper or lower GI?

A

Both

72
Q

Pathological findings in Yersnia entercolitica?

A

Ulcerative intestinal lesions (similar to typhoid)
Microabscesses
Granuloma formation
Deeply invasive, potentially tethal

73
Q

Is Yersnia entercolitica a systemic disease?

A

No

74
Q

What’s the deal with Staph Aureus Enterotoxin

A

Common for pre-formed toxin poisoning
2-4 hours to activity
More Vomiting than Diarrhea
done in 24 hours

75
Q

Whats the deal with Bacilus cereus toxin

A

Fried Rice
Vomiting (1-5 hr) and Diarrhea (8-15 hours)
Caused by production of cereulide enterotoxins

76
Q

So what are Clostridial diseases all about?

A

G+ sporulating anaerobes
Highly stable in environment
Produce large amount of fermentation products and degradative enzymes

77
Q

Method of transmission of clostridial diseases

A

Gut and Soil Cycle – Spores

Contamination of Wounds or Food

78
Q

Pathologic disease mechanism for Clostridial disease

A

Local growth –> Absorption and distribution of exotoxin

Spores are difficult to kill, esp. in necrotic tissue/anerobic environment/noncompetitive env.

79
Q

So what’s the deal with C. tetani?

A

Common in puncture wounds
Local growht with toxin dissemination
Loss of sympathetic inhibition + inhibitory spinal interneurons

80
Q

Neurotoxin in C. tetani?

A

Tetanospasmin

81
Q

Which Clostridial disease is known for gengrene/necrotizing cellultis?

A

C. perfringens

82
Q

Symptoms of C. perfringens

A

Foul odor, thin/discolored exudate, and wet gangrene at site of infection
Gas gangrene
Hemolytic destruction of RBCs
Myonecrosis

83
Q

Who gets C. perferingens

A

Invasion of traumatic/surgical wounds (ex. amputation)

84
Q

C. perfringens list of extracellular necrotizing enzymes

A

Phospholipases, Proteinases, Poisons

85
Q

Describe how clostridial gastroenteritis typically occurs.

A

Spores survive high temperature preparation and sporulate with cooling. These cooled food are served without reheating (places like catered food).

86
Q

Symptoms of Clostridial gastroenteritis

A

Abdominal cramps, watery diarrhea

Incubation period – 6-24 hours

87
Q

Pseudomembranous colitis is associated with which bacteria

A

C. difficile

88
Q

Symptoms of Pseudomembranous colitis

A

Severe colitis + Pseudomembrane Formation

Diarrhea + Clinical Toxemia

89
Q

Toxins involved in C. difficile?

A

Enterotoxin A and Cytotoxin (Toxin B)

90
Q

Why do people typically get C. difficile?

A

Disruption of bowel flora by broad spectrum antibiotics

91
Q

Mechanism of Botulism disease?

A

Preformed neurotoxin – Cleaves synaptobrevin
Rarely from straight up bacterial infection
Blocks acetylcholine release

92
Q

Symptoms of botulism infection

A

Cranial never defects
Loss of muscle contractability
Eventual death from respiratory muscle paralysis

93
Q

Botulism is typically a disease without colonization. Who is the exception.

A

Babies eating honey – gives necrotizing enterocolitis.

94
Q

Symptoms of community acquired C diff

A

Suppression of Gastric Acid

Pathology -- Infectious Disease (23 decks)

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