How is pseudomembranous colitis treated?

Answer: Discontinue offending drug and start metronidazole or vancomycin. Both suppress C. difficile and allow normal flora to return.

Which one of the two exotoxins produced by C. difficile is most responsible for pseudomembranous colitis?

Answer: Cytotoxin kills enterocytes causing pseudomembrane formation.

Name the two exotoxins produced by C. difficile:

1. Cytotoxin

2. Enterotoxin

What commonly causes pseudomembranous colitis?

Answer: Usage of broad-spectrum antibiotic treatment (eg, clindamycin or ampicillin) results in suppression of normal GI flora and proliferation of C. difficile. Clostridium difficile is usually acquired from the hospital environment.

How is botulism treated?

Answer: Classic botulism can be treated with respiratory care and antitoxin; as for infant botulism, infants typically recover spontaneously with supportive care.

CLOSTRIDIUM DIFFICILE Name the most common disease associated with Clostridium difficile:

Pseudomembranous colitis

What are the symptoms of classic botulism?

Answer: Cranial paralysis, including diplopia, ptosis, dysphagia, symmetric, descending motor paralysis, and death due to respiratory failure

Mnemonic:

BAFfles nerves (Botulism, Ach, Flaccid paralysis)

What usually causes infant botulism? What are its associated symptoms?

Answer: Results from infant ingestion of contaminated honey leading to lethargy, and decreased muscle tone, floppy baby syndrome; most common type of botulism in the United States

What is the mechanism of botulinum toxin in causing botulism?

Answer: The toxin blocks the release of acetyl-choline (Ach), resulting in flaccid paralysis.

What diseases does C. botulinum cause?

Answer: Clostridium botulinum causes food-borne botulism (ingestion of preformed toxin), infant botulism (ingestion of spores that germinate in gut-producing toxins), and wound botulism (injection of spores that germinate in tissue-producing toxins).

CLOSTRIDIUM BOTULINUM Do Clostridium species require oxygen?

Answer: No, they are all obligate anaerobes.

How is B. cereus treated?

Answer: The food poisoning is self-limited, so it is treated with supportive care to prevent dehydration.

What are the clinical symptoms caused by the heat-labile and heat-stable toxins?

Answer: Rapid onset (<5 hours) of vomiting and nausea following ingestion of food is classic for heat-stable toxin. Onset of voluminous, watery, nonbloody diarrhea, nausea, vomiting, and abdominal pain after an incubation period up to 16 hours is characteristic of heat-labile toxin.

Name the gram-negative rod that produces a toxin similar to the heat-labile toxin of B. cereus. What are their mechanisms of action?

Answer: Vibrio choleras cholera toxin. Both toxins trigger adenosine diphosphate (ADP)-ribosylation of G protein, stimulating adenylate cyclase and increasing cAMP. (ADP-ribosylation is a common mechanism used by various bacterial toxins.)

Name the two toxins made by B. cereus.

1. Heat-labile toxin

2. Heat-stable toxin

BACILLUS CEREUS Name the most common clinical association with Bacillus cereus:

Answer: Food poisoning from reheated rice

How is anthrax usually treated?

Answer: Penicillin, tetracyclines, and fluoro-quinolones (remember the rush to get ciprofloxacin during the anthrax terrorism crisis)

What are the clinical symptoms of gastrointestinal anthrax? What is the overall mortality rate?

Answer: Bloody vomiting, bloody diarrhea, abdominal pain, fever. Mortality rate of 25% to 60%

What are the clinical symptoms of pulmonary anthrax? What is the overall mortality rate?

Answer: First stage (first 2-3 days) consists of influenza-like symptoms such as dry cough, fever, and aches. Then sudden progression to second stage, which is characterized by difficulty breathing, substernal pressure due to bloody pleural effusion, and sepsis. Chest x-ray shows widening of the mediastinum. Mortality rate near 100% if untreated.

What are the clinical symptoms of cutaneous anthrax? What is the overall mortality rate?

Black, painless papules, and pustules erupt on skin surface, then spreading to lymph nodes and blood, resulting in sepsis if untreated. Mortality rate of 20%.

Name the three virulence factors of B. anthracis and describe their mechanism of action:

1. Capsule is antiphagocytic.

2. Edema factor exotoxin is acalmodulin-dependent adenylate cyclase that increases cyclic adenosine monophos-phate (cAMP) causing severe edema. 3. Lethal factor exotoxin is a protease, causing cells to increase tumor necrosis factor (TNF) production leading to cell death.