Anaerobic infections of the GI tract: Cross, Ryan

Question 1

Anaerobic infections can be distinguished by their:

Answer 1

Smell- their metabolic byproducts (organic acids) stink.

Question 2

Name the two phyla that make up most of the anaerobic gut flora

Answer 2

Bacteriodes and Clostridium

Question 3

Bacteriodes fragilis.
Micro morph, gram stain?
MCC of?
Pathogenesis?

Answer 3

Gram (-) rod
MCC of serious anaerobic infections.
Break in mucosal layer, allows invasion of bacteria.
Antiphagocytic capsule
Host response to capsule plays role in abscess formation.

Question 4

Bacteriodes fragilis.
Clinical presentation?
Dx?
Tx?

Answer 4

Clinical: MC cause intra-abdominal infections, abscesses, or peritonitis
Found in ~25% of lung abscesses
(in general, dz below diaphragm)
Enterotoxin producing strain can cause diarrhea

Dx: Anaerobic cultures (involve stabbing test tub filled with agar)
Tx: Resistant to penicillin. Susc. to metronidazole, carbapenems, combo beta-lactams and beta-lactamase inhibitors.

Question 5

Prevotella melaninogenica:
micro morph, gram stain?
Found where?
When does it strike?
Clinical findings?

Answer 5

Gram (-) coccobacillus
Found in mouth, elsewhere in GI tract, Vagina, nasopharynx
Strikes when immune system is suppressed, other flora reduced in number (opportunistic)
Clinical: oral, periodontal abscesses, pulm abscesses, chronic otitis, sinusitis, (in general, dz above diaphragm)

Question 6

Clostridium.
Found where?
Resistant to?
Pathogenesis?

Answer 6

Found in soil (spores) and colon
Resistant to high heat and harsh environment
Patho: Exotoxins, hydrolytic enzymes

Question 7

C. perfringens:
Micro morph, gram stain?
Clinical syndromes?

Answer 7

Morph: box car gram (+) bacilli
Syndromes: Gas gangrene, food poisoning (watery diarrhea, cramps, minimal vomiting)

Question 8

C. tetani.
What does it cause?
Pathogenesis?
Tx?
Does acute illness confer immunity?

Answer 8

Tetanus…
Tetanus toxin is an AB neurotoxin–> cleaves SNAREs, doesn’t allow fusion of inhibitory neurotransmitter bearing vesicles w/ neuron membrane for release. Net effect: disinhibition of excitatory impulses–> spasms, incr. muscle tone, widespread autonomic instability.
Tx: Wound debridement to eradicate spores. Human tetanus immune globulin to neutralize toxin.
DOC metronidazole
No conferred immunity from acute illness. Need tetanus toxoid (3 injections, first at time of dx and others 2 weeks apart, after)
Booster Q10yrs

Question 9

C. botulinum.
5 different forms:

Pathogenesis:

Answer 9

Foodborne- canned foods
Infant botulism- raw honey, carpet spores
Wound botulism
Inhalational- bioterror
Iatrogenic

Patho: AB toxin
Most potent bacterial toxin
Cleaves SNARE proteins and doesn’t allow acetylcholine bearing vesicles to be released from neurons. –> no excitation at motor end plate–> flaccid paralysis.

Question 10

Clinical presentation of classic (foodborne) botulism.

Answer 10

Acute, symmetric descending flaccid paralysis
Symp. begin 12-36 hrs post ingestion
nausea, dry mouth, dysphagia, diarrhea, blurred vision
Possible death by resp. failure

Question 11

Infant botulism (Floppy Baby Syndrome) 
Clinical presentation?

Answer 11

Constipation followed by weakness, feeding difficulties, descending global hypotonia, drooling, anorexia, irritability, weak cry

Question 12

Tx for botulism:

Answer 12

Mechanical ventilation
Pts >1yo get horse antitoxin
Infants get human-derived botulism immune globulin

Wound botulism: Penicillin or metronidazole

Question 13

Describe the virulence factors of H. pylori.
Dx?
Tx?

Answer 13

VacA- vacuolating cytotoxin
PAI encoding T3SS- injects Cag and VacA into host cell
Cag: rearranges cytoskeleton
Urease

Dx: endoscopy w/ biopsy and culture, stool antigen, urea breath test, serology
Tx: Triple/ bismuth based Quad therapy
omeprazole, amoxicillin, and clarithromycin (OAC) for 10 days
bismuth subsalicylate + PPI + metronidazole + tetracycline (BMT) for 14 days