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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
Classic Example. Secretory Diarrhea
Cholera
26
Two causes of excess fluid in diarrhea (with example)
``` Hypersecretion (Cholera) Osmotic Load (Lactose Intolerance) ```
27
Dysentery =
Loose Stool + Blood + Leukocytes
28
Difference between diarrhea and dysentery.
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.
29
The detail run down on E Coli
G- Rod Green Sheet on EMB agar Coliform
30
Important Characteristics of E Coli
Watery diarrhea, cramping pain, fever, malaise Invasive or cytolytic disease - dysyntery Verotoxin (shigatoxin) -- hemolytic uremic syndrome
31
What happens in hemolytic uremic syndrome
Renal Failure and Anemia
32
Describe effects of enterotoxic E Coli
Watery Traveler's Diarrhea | Consumption of food contaminated with enterotoxin-producing strain
33
Describe the effects of enterohemorrhagic E Coli
Severe bloody colitis from consumption of food contaminated with invasive verotoxin (shiga toxin) strain (Mainly O157:H7)
34
Foods assocaited with EHEC?
Hamburger Dairy Products (unpasteurized) Fruit Juice Agricultural products contaminated with manure (spinach)
35
Which E Coli is primarily pediatric diarrhea in impoverished nations
EAEC (enteroaggregative)
36
Risk of person-to-person transmission of O157-H7
Low. | Fecal oral transfer sometimes shows up in places like daycare centers.
37
Relationship of O157:H7 to temperature? Sorbitol?
Won't ferment sorbitol | Won't grow at 45 degrees
38
Mechanism of O157:H7 disease?
Small infectious dose Bac adhere to cell membrane and colonize LI Produce shigatoxins which damage endothelial cells (inhibits mRNA translation, protein synthesis)
39
Disease course of O157:H7?
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
Different ways in which O157:H7 might present?
``` Asymptomatic Mild Illness Dysyntery Hemolytic Uremic Syndrome Thrombotic Thrombocytopenic Purpura (TTP) ```
41
Who is most vulnerable to O157:H7 hemolytic uremic syndrome
Children, Elderly
42
Generic bacteria data for shigella?
G- Non-motile Non-coliform
43
Pathogenesis of Shigella
Fecal/Oral Transmission (Daycares, MSM) Invasive lesions of colonic mucosa which spreads to LN Exotoxin causes Mucosal necrosis Highly Virulent
44
T or F. Shigella cannot cause bacteremia to distant organs
True
45
Generic Bacteria information for Vibrio cholerae
Comma-shaped, G- | Alkali tolerant
46
How is Vibrio cholerae transmitted?
Direct fecal-oral transmission | Asymptomatic Carriers
47
Pathogenesis of Vibrio cholerae?
Enterotoxin induces the secretion of isotonic fluid | No invasive lesions
48
Cause of death in Vibrio cholerae?
Dehydration, Hypovolemic Shock
49
Mechanism of Vibrio cholerae hypersecretion
Subunit A binds with ADP ribosylation factors Activates GTP-activated adenylate cyclase resulting in cAMP formation Stimulates secretion of chloride bicarbonate
50
Generic bacteria info for Salmonella.
G- Non Coliform H2S production
51
Two groupings of Salmonella to separate
S. enteritidis, S. typhimurium | S. typhi
52
Three forms of Salmonella
Typhoid Enteric Fever Salmonella Food Poisoning
53
Presentation of Salmonella Food Poisoning
Vomiting and Diarrhea (gastroenteritis) Superficial lesions of colon Usually self-limiting (except immunocrompromised)
54
Organisms responsible for Salmonella food poisoning
S. enteritis, S typhimurium
55
Common origins of Salmonellosis
Eggs, Undercooked Chicken Contaminated Water Turtles/Reptiles Cantaloupes, Mangoes
56
Who should never own a reptile
IC, Pregnant, Kids Under Five
57
Salmonella pathologic mechanism
Invasion of Mucosal cells, cause ulceration No enterotoxin Multiply in neutrophils+Macrophages G- Sepsis
58
Salmonella is a common cause of ______ in children with sickle cell anemia
Osteomyelitis and Sepsis
59
What is paratyphoid fever (organisms, symptoms)
S. typhinurium, paratyphi or cholera-suis Fever, Bacteremia, Local Lesions Ass. w/ sickle cell disease + schistosomiasis
60
Describe Typhoid Fever symptoms
- 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
Causative organism for Typhoid Fever
Salmonella Typhi
62
Describe a Typhoid Fever carrier state
3-5% achieve carrier state in Gall Bladder | Bacteria isnt dissolved by bile, so it can move up to stay there
63
Generic Campylobacter jejuni information
G- Comma shaped | Flagellated
64
Where does Campylobacter jejuni infection usually come from?
Undercooked Beef
65
Symptoms of Campylobacter jejuni
Gastritis, Diarrhea, and Dysentery | associated with guilain-barre neuropathies
66
Risk of ______ in immunocompromised patients with Campylobacter jejuni infection
Sepsis
67
Transmission of Campylobacter jejuni?
Contaminated Water Sources Food-Bourne Illness Improperly cooked chicken/Beef
68
Pathogenesis of Campylobacter jejuni?
Toxin causes invasive lesions (colonic crypt abscesses) and adherance. Rarely Septicemia Causes foul smelling stools with blood/exudate
69
Who is at highest risk for effects of Yersnia entercolitica
Pediatric Population
70
Foods assocaited with Yersnia entercolitica
Raw, undercooked Pork | Unpasteurized milk
71
Does Yersnia entercolitica influence upper or lower GI?
Both
72
Pathological findings in Yersnia entercolitica?
Ulcerative intestinal lesions (similar to typhoid) Microabscesses Granuloma formation Deeply invasive, potentially tethal
73
Is Yersnia entercolitica a systemic disease?
No
74
What's the deal with Staph Aureus Enterotoxin
Common for pre-formed toxin poisoning 2-4 hours to activity More Vomiting than Diarrhea done in 24 hours
75
Whats the deal with Bacilus cereus toxin
Fried Rice Vomiting (1-5 hr) and Diarrhea (8-15 hours) Caused by production of cereulide enterotoxins
76
So what are Clostridial diseases all about?
G+ sporulating anaerobes Highly stable in environment Produce large amount of fermentation products and degradative enzymes
77
Method of transmission of clostridial diseases
Gut and Soil Cycle -- Spores | Contamination of Wounds or Food
78
Pathologic disease mechanism for Clostridial disease
Local growth --> Absorption and distribution of exotoxin | Spores are difficult to kill, esp. in necrotic tissue/anerobic environment/noncompetitive env.
79
So what's the deal with C. tetani?
Common in puncture wounds Local growht with toxin dissemination Loss of sympathetic inhibition + inhibitory spinal interneurons
80
Neurotoxin in C. tetani?
Tetanospasmin
81
Which Clostridial disease is known for gengrene/necrotizing cellultis?
C. perfringens
82
Symptoms of C. perfringens
Foul odor, thin/discolored exudate, and wet gangrene at site of infection Gas gangrene Hemolytic destruction of RBCs Myonecrosis
83
Who gets C. perferingens
Invasion of traumatic/surgical wounds (ex. amputation)
84
C. perfringens list of extracellular necrotizing enzymes
Phospholipases, Proteinases, Poisons
85
Describe how clostridial gastroenteritis typically occurs.
Spores survive high temperature preparation and sporulate with cooling. These cooled food are served without reheating (places like catered food).
86
Symptoms of Clostridial gastroenteritis
Abdominal cramps, watery diarrhea | Incubation period -- 6-24 hours
87
Pseudomembranous colitis is associated with which bacteria
C. difficile
88
Symptoms of Pseudomembranous colitis
Severe colitis + Pseudomembrane Formation | Diarrhea + Clinical Toxemia
89
Toxins involved in C. difficile?
Enterotoxin A and Cytotoxin (Toxin B)
90
Why do people typically get C. difficile?
Disruption of bowel flora by broad spectrum antibiotics
91
Mechanism of Botulism disease?
Preformed neurotoxin -- Cleaves synaptobrevin Rarely from straight up bacterial infection Blocks acetylcholine release
92
Symptoms of botulism infection
Cranial never defects Loss of muscle contractability Eventual death from respiratory muscle paralysis
93
Botulism is typically a disease without colonization. Who is the exception.
Babies eating honey -- gives necrotizing enterocolitis.
94
Symptoms of community acquired C diff
Suppression of Gastric Acid

Pathology -- Infectious Disease (23 decks)

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