GI Gram Neg Flashcards

1
Q

Which bugs commonly infect the billiary tract from the large intestine? (3)

A

E coli, Bacteroides fragilis, and Clostridium spp

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2
Q

Bacterial overgrowth syndrome

A

Overgrowth of normal microbiota from large intestine invading the small intestine.

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3
Q

Which pathogens can adhere to the mucosa of the small intestine? (3)

A

V. cholerae, E coli, and Clostridium perfringens

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4
Q

Which bugs are first colonizers of large intestine in newborns?
What is added w/ breast feeding?
What comes to replace most of these?

A

1st: E coli and Strep. Create anaerobic environment.
These may be replaced by Bifidobacterium (anaerobic gram pos rod) in babies who are breast-fed.
Next comes Bacteroides (gram neg obligate anaerobe) in very high numbers.

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5
Q

Characteristics of diarrhea

A

Frequent stools. Usually painless w/o fever.

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6
Q

Characteristics of dysentery

Mediated by what?

A

Pus / blood in stool. Usually painful (cramps, tenesmus) w/ fever.
Cytotoxins may cause tissue destruction in large intestine.

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7
Q

Where are Peyer’s Patches found?

A

Ileum

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8
Q

Enteric fever

A

Systemic infection (bacteremia) originating in GI tract. Ex: typhoid fever

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9
Q

What 2 things are found in breast milk that aid in immune defense for infants?

A

IgA and lactoferrin

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10
Q

3 examples of obligate human pathogens

Mode of transmission?

A

S. typhi, Shigella, Helicobacter pylori

Fecal / oral transmission

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11
Q

4 examples of zoonotic pathogens (3).

Where are they found?

A
  • E coli – ground beef, EHEC
  • Non-typhoid Salmonella – Poultry, eggs, pet reptiles
  • Campylobacter – poultry, milk
  • Infected humans can also be source via fecal / oral
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12
Q

Preformed Toxin
Site
Clinical features
Examples (2)

A

Small bowel
Severe NVD
Staph aureus and Bacillus cereus

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13
Q

Secretory Toxin
Site
Clinical features
Examples (2)

A

Small bowel
Profuse water diarrhea, painless, usually no fever.
ETEC and V cholerae

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14
Q

Cytotoxin
Site
Clinical features
Examples (2)

A

Large bowel
Bloody diarrhea, painful cramps, fever
EHEC and some Shigella

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15
Q

Mucosal colonization / destruction
Site
Clinical features
Examples (3)

A

Small bowel
NVD, fever
EPEC, Salmonella, and Campylobacter (early)

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16
Q

Deep invasion
Site
Clinical features
Examples (3)

A

Large bowel
Purulent bloody dysentery, painful cramps, fever
EIEC, Shigella, and Campylobacter (late)

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17
Q

Systemic dissemination
Site
Clinical features
Examples

A

GI –> blood –> liver –> back to GI
Enteric fever
Salmonella typhi

18
Q

4 most common causes of bacterial enteric disease

A

1) Campylobacter (50%)
2) Salmonella (25-30%)
3) Shigella (15%)
4) E coli (5%)

19
Q

E coli transmission

A

Fecal / oral or contaminated foods (meats, fruits, vegetables).

20
Q
ETEC
Name
Disease
Transmission
Virulence factors
Sxs
Similar to which other bacterium?
A

Enterotoxigenic.
“Traveler’s diarrhea” for 3-4 days.
Mainly passed from person-to-person.
Virulence factors - plasmid-mediated secretory toxins (heat-stable ST or heat-labile LT) that cause increased cAMP → increased secretion by enterocytes.
Watery diarrhea, cramps, nausea, low fever. Similar to Vibrio cholerae.

21
Q
EPEC
Name
Site of infection
Sxs
Transmission
Similar to which other bacterium?
A

Enteropathogenic.
Colonization / destruction of mucosa of small intestine.
Causes infantile diarrhea, gastroenteritis, fever, NVD, non-bloody mucus filled stools.
Mainly passed person-to-person.
Similar to non-typhoid Salmonella.

22
Q
EHEC
Name / number
Inoculum
Transmission (specific foods)
Population
Sxs
Mediated by?
Similar to what other bacterium?
What is contraindicated?
Tx
A

Enterohemorrhagic.
Especially caused by O157:H7.
Small inoculum required (1-100 bugs).
Transmitted via cow intestines or infected humans. May also be caused by alfalfa sprouts, unpasteurized milk, cheese, or cider.
Most often affecting kids in warm months.
Causes severe cramps, hemorrhagic colitis, HUS, and thrombocytopenic purpura (TPP).
Absence of bloody stools does not rule out EHEC.
Mediated by cytotoxins (verotoxin and Shiga-like toxin, which are used for diagnosis) which inhibits protein synthesis → cell death.
Similar to Shigella.
Do NOT use AB’s –> lysis / toxin release
Tx w/ fluids

23
Q
HUS
Name
Cause / mechanism
Sxs
Population
A

Hemolytic uremia syndrome.
Mainly associated w/ EHEC, but also some Shigella.
E coli cytotoxins (verotoxin and Shiga-like toxin) produced in intestinal lumen enters blood circulation → systemic disease. Toxins cause inflammation, thrombosis, attach to endothelial cells, inhibit protein synthesis, and induce apoptosis.
May cause thrombotic microangiopathy, hemolytic anemia, and thrombocytopenia w/ renal lesions / failure.
Rare, but highest risk in kids and elderly.

24
Q
EIEC
Name
Mechanism
Sxs
Similar to what other bacterium?
A

Enteroinvasive.
Plasmid-mediated deep invasion of large intesetinal mucosa causes bacillary dysentery (blood and pus in poop).
Causes fever, cramps, watery diarrhea, and dysentery.
Similar to Shigella.

25
Q

Inoculum for Salmonella

Population

A

Large inoculum due to being sensitive to acid.

Most common in children during warm months.

26
Q
Salmonella typhi
Reservoir
Transmission
Virulence factors
Enteric Fever mechanism / sxs
Other causes of enteric fever
Timing for lab cultures
2 types of vaccines
A

•Obligate human pathogen.
•Transmission – Human-human transmission via fecal / oral route (food handlers or contaminated water).
•Virulence factors – endotoxin and Vi polysaccharide capsule
•Enteric fever – systemic dissemination. Bugs enter through Peyer’s Patches → macrophages → lymphatics → bacteremia → replicate in liver → return to gut via common bile duct.
Sxs include fever / abdominal pain, followed by diarrhea. 30% of pxs have maculopapular rash on trunk (rose spots). Enlarged liver / spleen may be present.
•Other causes of enteric fever include Salmonella paratyphi, Salmonella enteritidis, Yersinia enterocolitica, and late Campylobacter jejuni, or non-cholera Vibrio.
•Labs: blood cultures positive w/in 1 week, stool w/in 3 weeks, urine by 4th week (due to hematogenous seeding of kidneys). Ab titer positive b/w week 2-6.
•Vaccination is available for high-risk travel or occupations. 2 types: oral live-attenuated vaccine or injected capsular polysaccharide vaccine. Neither prevents non-typhoid enteric fever. Only 50-70% effective.

27
Q
Salmonella enterica
Transmission
Mechanism of invasion
Similar to what other bug?
Sxs
Resistance
A

•Transmission – Animal infection via consumption of food products (eggs, poultry, dairy) or direct contact (reptiles / turtles).
•Organisms invade epithelial cells of small intestine and can replicate inside macrophages.
•Gastroenteritis – due to mucosal colonization / destruction. Similar to EPEC. Abdominal pain, low grade fever, non-bloddy diarrhea. “Rotten Egg” odor of stool due to sulfhydryl compounds (H2S).
Semi-resistant to bile salts.

28
Q
Shigella
Reservoir
Population
Inoculum
Transmission / setting
Mechanism
Sxs
Virulence factor
Similar to which other bugs?
Tx
A
  • Obligate human pathogen
  • Most common in kids
  • Small inoculum required (1-100)
  • Transmission – fecal / oral (food or person-to-person), common in DAYCARE, anal sex
  • Deep invasion of large intestine causes bacillary dysentery (similar to EIEC). Less often gastroenteritis. Does NOT invade blood stream.
  • Some strains make cytotoxin (Shiga toxin, similar to EHEC) → epithelial cell death.
  • Tx w/ rehydrating fluids. AB’s (TMP-sulfa) usually only given if young, however the main problem is the toxins. AB’s may actually cause lysis of bugs → further toxin release. Don’t give anti-motility drugs due to possibility of increased toxin absorption.
29
Q
Campylobacter jejuni
Impressive stat
Morphology
Temp
Oxygen requirements
Transmission (specific foods)
Sxs
Similar to which other bugs?
Virulence factor
Diagnosis
A
  • Most common bacterial enteric infection in US. Curved GNR, grows best at 42 degrees (chicken body temp). Microaerophile.
  • Transmission – fecal / oral, contaminated food (unpasteurized milk or meat, especially POULTRY), or domestic animal contact (cattle, chickens, dogs).
  • Causes early gastroenteritis due to mucosal colonization / destruction (similar to EPEC). Sometimes late dystentery w/ enterocolitis from deep infection (similar to EIEC). Rare enteric fever. Affects both small and large intestine. Has cholera-like enterotoxin.
  • Diagnosis – characteristic darting motility seen microscopically in stool samples due to polar flagellum. Slightly curved GNR. WBCs may be found in stool.
30
Q

Yersinia enterocolitica / pseudotuberculosis
Transmission
Sxs (4 things)

A
  • Transmission – fecal / oral or animals. Usually infects during cold months. Rare in US. Human-human transmission via fleas or respiratory droplets → plague.
  • Causes gastroenteritis, diarrhea, terminal ileitis, and sometimes pseudoappendicitis
31
Q
Vibrio cholerae
Transmission
Virulence factor / mechanism
Similar to what other bug?
Sxs
Risk factors
Tx
A

Very large inoculum required
•Transmission – fecal / oral, ingestion of contaminated food / water.
•Secretory toxin (cholera toxin) → constant cAMP production → massive water / electrolyte secretion. Similar to ETEC. No invasion, just mucosal colonization.
•Produce 10-20L of diarrhea / day. “Rice water stools” due to mucus flakes. May cause shock / death.
•Risk factors – lack of water / sewage treatment or host gastric achlorhydria (due to malnutrition / drugs)
•Treat w/ hydration and electrolytes. No AB’s.

32
Q

Vibro parahemolyticus
Transmission
Sxs
Geography

A

Transmission - salt water, shellfish, and sushi
Causes gastroenteritis.
Occurs in northeast / northwest US coast

33
Q

Vibrio vulnificus
Transmission
Sxs
Population

A
  • Transmission – salt water, shellfish, and skin abrasion
  • Does NOT cause GI problems.
  • Would infection → bullous lesions. Septicemia is deadly.
  • Most common in immunocompromised and alcoholics.
34
Q
Helicobacter pylori
Reservoir
Transmission
Population
Mechanism / virulence factor
Sxs
Diagnosis
Tx
Prevention
A
  • Obligate human pathogen.
  • Transmission – fecal / oral
  • Common in kids abroad and adults in US.
  • Long term / lifelong colonization of stomach. May be asymptomatic. Avoids / survives acidic environment by releasing urease → hydrolyzes urea to CO2 + ammonia → increased pH. Also aided by mucosal secretions of stomach lining.
  • Causes gastritis, gastric / duodenal ulcers, gastric cancer.
  • Urease used for diagnosis.
  • Tx: 2+ AB’s (amoxicillin and clarithromycin), PPI (kills bugs and reduces damage)
  • If not infected, don’t use antacids, H2 antagonists, or PPI’s to prevent infection.
35
Q

Reactive arthritis

Cause

A

Complication occurring 1-4 weeks after Salmonella, Shigella, Campylobacter, or Yersinia GI infection. Also seen after GU infection. AB’s not helpful.

36
Q

AB’s are usually not used for enteric infections. Exceptions
Tx for those exceptions

A

Exceptions: At risk pxs (old, young, immunocompromised) or prolonged / severe infections.
Use fluoroquinolones.

37
Q

What does PMN’s in stool indicate?

A

Bacterial infection

38
Q

What 4 bacteria cause dysentery?

A

Shigella, enterohemorrhagic E coli, Campylobacter, and Salmonella (severe)

39
Q

What special characteristic of Staph allows it to grow on ham?

A

Salt-tolerant.

40
Q

How do you treat Staph aureus food poisoning?

A

Fluids and possibly anti-emetics. NOT AB’s due to toxin release.

41
Q

What bacterium causes food poisoning in rice?

A

Bacillus cereus