Bacterial Infections of the GI Tract 3 Flashcards Preview

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Flashcards in Bacterial Infections of the GI Tract 3 Deck (23):
1

Vibrio spp:

1. Gram stain

2. Aerobic abilities

3. Shape

4. Free living in           ?

5.                temperature range of growth

6. Requires                          for growth (compound)

7. Grow at a                range of pH

8. Susceptibility to stomach acid

 

1. Gram negative

2. Facultative anaerobes

3. Comma (curve shaped)

4. Free living in water

5. Broad  temperature range of growth

6. Requires sodium chloride for growth

7. Grow at a wide/broad range of pH

8. Definitely susceptible to stomach acid which is why a high infectious dose is needed to cause illness

2

Vibrio cholerae

1. Symptom range

2. Incubation period

3. Duration

4. Key symptom

5. How much fluid can a patient lose?

6. What does the diarrhea look like

7. What actually kills the patient?

1. Symptoms range from asymptomatic to severe watery diarrhea

2. Incubation is 2-3 days

3. Duration is up to 7 days...unless it kills you

4. 5-25% of patients develop severe watery diarrhea

5. Can lose up to 250ml/kg body weight/day

6. Diarrhea looks like rice water

7. Dehydration can kill within hours

3

Vibrio cholerae

1. How does cholera spread?

2. Long-term immunity?

3. Associated with what?

4. Typing is based on what?

5. What type caused the first 6 cholera pandemics?

6. Which one is causing the 7th?

1. Spreads through contaminated water

2. Long-term, O antigen specific immunity

3. Associated with epidemics, pandemics, and natural disasters

4. Typing is based on O antigens (O1-O200)

5. Type O1 caused the first 6 pandemics

7. El Tor biotype is causing the 7th

4

Vibrio Cholerae

1. How does v. cholerae adhere to intestinal epithelial cells?

2. How does the cholera toxin work?

3. Pathogenesis is similar to what other disease?

1. Toxin co-regulated pilus (TCP) helps v. cholerae adhere to intestinal epithelial cells

2. Cholera toxin is an AB toxin. The toxin causes an activation of adenylate cyclase which increases the amount of cAMP. An increase in cAMP causes massive efflux of sodium, chloride, potassium, water, and bicarbonate.

3. Very similar to ETEC LT toxin

5

Vibrio Cholerae

1. Diagnosis method and what requirements are being tested for

2. Treatment

3. How high is the mortality rate without rehydration therapy

1. Diagnosis made by culture on differential media. Vibrio Cholerae is a facultative anaerobe, has a wide temp and pH growth range, and requires sodium chloride

2. Treatment is rehydration therapy (oral and IV)

3. Mortality rate can reach 90% without adequate rehydration

6

Vibrio parahaemolyticus

1. Inflammatory or not so much?

2. Primary symptoms (5)

3. Virulence/pathogenesis

1. Definitely inflammatory

2. Common symptoms are explosive watery diarrhea, nausea, vomiting, abdominal cramps/discomfort, and a low grade fever

3. Kanagawa hemolysin induces chloride secretion so watery diarrhea

7

Vibrio parahaemolyticus

1. Vibrio parahaemolyticus is the most common cause of                             in Japan and SE Asia

2.                    associated                     in the U.S.

3. Associated with the consumption of                     

1. Vibrio parahaemolyticus is the most common cuase of bacterial gastroenteritis in SE Asia

2. Seafood associated gastroenteritis in the U.S.

3. Associated with the consumption of raw shellfish

8

Vibrio parahaemolyticus

1. Treatment and Prevention

Vibrio parahaemolyticus is self limiting. Prevention would be properly cooking shellfish

9

Yersinia enterocolitica

1. Gram stain

2. Shape

3. Most isolates are virulent or avirulent?

4. Spread by ingestion of contaminated           and             especially,             

1. Gram negative

2. Shape is coccobacilli

3. Most isolates are avirulent

4. Spread by ingestion of contaminated water and food, especially pork

 

10

Yersinia enterocolitica

1. Range of symptoms

2. Duration of disease

3. Treatment

1. Range of symptoms is from fever, abd cramps, and watery diarrhea all the way to explosive, bloody diarrhea

2. Duration is 1-2 weeks

3. Treatment: disease is usually self-limiting. If not then TMP-SMZ or aminoglycosides. That last part wasn't part of the lecture

11

Yersinia enterocolitica

1. Pathogenesis

2. Pathogenesis is similar to what other disease

3. Produces what type of toxin?

4. Diagnosis

1. Pathogenesis is poorly understood but it does attack M-cells

2. Process is similar to Salmonella but injects YOPs (yersinia outer proteins) via T3SS mechnism rathat than SPSs

3. Produces a heat-stable enterotoxin

4. Diagnosis is via stool culture

12

Clostridium difficile

1. Where does C. diff do its dirty work?

2. Gram stain

3. Aerobic abilities

4. Invasive or not so much?

5. Inflammatory or not so much?

6. What does C. diff do that explains why is spreads to easily and why it is so hard to kill?

 

1. C. diff does its dirty work in the large intestine

2. *Gram stain positive*

3. Anaerobic

4. Non-invasive

5. Definitely inflammatory

6. C. diff is spore forming which makes it so difficile...HAHAHAHA!

13

Clostridium difficile

Describe the symptom varying and degrees of virulence

How does someone usually acquire C. diff?

Asymptomatic carriage < CDAD (C. diff associatied diarrhea) < pseudomembrane colitis < fulminant colitis with toxic megacolon 

Typically a patient is hospitalized and a few things happen: they come into contact with a contaminated HCW after receiving broad spectrum antibiotics which usually happens after surgery. The normal gut flora are killed off and, if immunosuppressed, C. diff with raise its ugly head

14

Clostridium difficile

Pathogenesis: which toxins produced (2) and how do they work

Diagnosis

Treatment

Prevention

1. Toxin A and Toxin B produced which cause damage to intestinal mucosa by disrupting cellular cytoskeletons which causes diarrhea

2. Diagnosis is via *TOXIN* detection in stool. Culture is basically useless

3. Treatment is ORAL vancomycin or metronidazole

4. Prevention/Treatment is fecal transplant

15

Enterohemorrhagic E. coli (EHEC)

1. Gram stain

2. Aerobic abilities

3. Typical animal reservoir

4. How does it normally pop up? Associated with which contaminated food?

1. Gram negative

2. Facultative anaerobe

3. Usually cattle

4. Sporadic cases and outbreaks in developed world. Typcially associated with contaminated beef or vegetables (because washed with contaminated water)

16

Enterohemorrhagic E. coli (EHEC)

Symptoms and giveaway presentation

Sequelae caused by what?

Pathogenesis: name of toxin and MOA

What receptor does the toxin bind to? Location of receptor? Why aren't cattle affected?

1. Bloody diarrhea WITHOUT fever. Also marked abdominal tenderness

Sequelae caused by hemolytic uremic syndrome which can cause anemia and kidney failure

Produces Shiga-like toxin (verotoxin) which blocks translation by cleaving the 60s portion of ribosome

Verotoxin binds to Gb3 receptor in kidney. Cattle don't have Gb3 receptor. 

17

Enterohemorrhagic E. coli (EHEC)

Diagnosis (4)

Treatment and antibiotic use

Prevention

Diagnosis: 

  • Presumptive: bloody diarrhea WITHOUT fever
  • Culture (MacConkeys +)
  • PCR
  • Rapid diagnostic test kits

Treament: supportive. Antibiotics may accelerate the lytic cycle making the problem much worse

Prevention: properly cook beef and raw veggies

18

Shigella spp.

1. Gram stain

2. Shape and aerobic capabilities

3. Intracellular or extracellular

4. The deadly thing it causes?

1. Gram negative

2. Rods, facultative anaerobe

3. Intracellular pathogens

4. Causes dysentery...which kills oxen...probably

19

Shigella spp.

1. Reservoirs

2. Transmission route

3. Infectious dose

4. Incidence is directly related to              

 

1. Humans are only reservoir

2. Fecal- oral route

3. Extremely low infectious dose

4. Incidence is directly related to hygiene

20

Shigella spp.

Global Species distribution:

Which species hits developed countries?

Which species hits developing countries?

Which species hits underdeveloped tropical areas?

Which species causes the most severe infections?

S. soneii hits developed countries

S. flexneri hits developing countries

S. dysenteriae hits underdeveloped, tropical areas

S. dysenteriae causes the most severe infections

21

Shigella spp.

Symptom onset after ingestion?

Symptoms are strain specific:

S. sonneii

S. flexerni

S. dysenteriae

Symptoms usually start 1-3 days after ingestion

S. soneii: fever, malaise, and watery diarrhea

S. flexerni: dysentery, fever, malaise, watery diarrhea, abdominal cramps, tenesmus, and possibly frequent bloody and purulent stools

S. dysenteriae: all of the above plus hemolytic uremic syndrome

22

Shigella spp.

Pathogeneis combines which two disease processes?

Salmonella and EHEC

 

read the handout for everything...to much info for cards

23

Enteroinvasive E. coli

1. Common or not so much?

2. Similar to which disease? how is it different?

3. How did EIEC come about?

1. Very uncommon

2. Same as Shigella except no shiga-toxin

3. Appears E. coli obtained pathogenicity island from Shigella spp via horizontal gene transfer