Microbiology PreTest Self-Assessment and Review by Matthew Grisham

Author:Matthew Grisham
Language: eng
Format: epub
Publisher: McGraw-Hill Education
Published: 2014-11-15T00:00:00+00:00

211. The answer is a. (Brooks, pp 270-272. Levinson, pp 143-145. Murray, pp 317-320. Ryan, pp 376-377.) Cholera is a toxicosis. The mode of action of cholera toxin is to stimulate the activity of adenyl cyclase, an enzyme that converts ATP to cyclic AMP. Cyclic AMP stimulates the secretion of chloride ion, and affected patients lose copious amounts of fluid. A drug that inhibits adenyl cyclase thus might block the effect of cholera toxin. Water and electrolyte replacement are primary management mechanisms, while oral tetracycline may help reduce stool output. Many antimicrobial agents are effective against V. cholerae, notably oral tetracycline. A sensitivity test would be needed for choosing the best drug to kill the bacteria. Fluid secretion would be lessened if adenyl cyclase was inhibited. Our patient would not die with the described medical treatment, but be helped to overcome the infection. Reduction of bacterial motility has no association with bacterial virulence.

212. The answer is d. (Brooks, pp 226-228. Levinson, pp 106-110. Murray, pp 210-223. Ryan, pp 263-264.) Certain strains of staphylococci elaborate an enterotoxin that is frequently responsible for food poisoning. Typically, the toxin is produced when staphylococci grow on foods rich in carbohydrates and is present in the food when it is consumed. The resulting gastroenteritis is dependent only on the ingestion of toxin and not on bacterial multiplication in the GI tract. Characteristic symptoms are nausea, vomiting, abdominal cramps, and explosive diarrhea. The illness rarely lasts more than 24 hours. Campylobacter perfringens toxin contributes to a form of food poisoning, but the organism is ingested and grows in the patient, then releasing the toxin. Campylobacter perfringens also have toxins that can damage various tissues (gas gangrene). Staphylococcus aureus produces coagulase that clots plasma and does not contribute to S. aureus food poisoning. Penicillinase (β-lactamase) does not contribute to food poisoning symptoms. Leukocidin inactivates WBCs in the laboratory, but clinical significance is uncertain.

213. The answer is e. (Brooks, pp 224-229. Levinson, pp 106-110. Murray, p 222, Ryan, pp 269-270.) Staphylococci are gram-positive, non-spore-forming cocci. Clinically, their antibiotic resistance poses major problems. Many strains produce β-lactamase (penicillinase), an enzyme that destroys penicillin by opening the lactam ring. Drug resistance, mediated by plasmids, may be transferred by transduction. No known allergic reactions occur by release of staphylococcal proteins. Even if the penicillin penetrates the S. aureus membrane, external penicillinase would probably have broken the β-lactam ring, inactivating the drug. S. aureus most likely contains penicillin-binding proteins (PBPs) but nothing happens if the penicillin is inactivated. Acetyl is CH3CO. The acetylase would break this bond, but it is uncertain whether this inactivates penicillin like β-lactamase does.

214. The answer is c. (Brooks, p 207. Levinson, pp 127-128, 492. Murray, pp 383-386. Ryan, pp 320-322.) Campylobacter botulinum growing in food produces a potent neurotoxin that causes diplopia, dysphagia, respiratory paralysis, and speech difficulties when ingested by humans. The toxin is thought to act by blocking the action of acetylcholine at neuromuscular junctions. Botulism is associated with high mortality; fortunately, C. botulinum infection in humans is rare.

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