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Discussion Starter · #1 ·
On August 2, 1996, an 18-year-old man residing in Flagstaff, Arizona, presented with a 2-day history of fever, inguinal pain, and diarrhea. His vital signs were as follows: heart rate, 126 beats per minute; respiratory rate, 20 breaths per minute; blood pressure, 130/81 mm Hg. He had left inguinal lymphadenopathy, for which he received a nonsteroidal anti-inflammatory drug (NSAID) and was sent home. The next day, the patient developed fatigue and difficulty breathing and fell unconscious while taking a shower. He was transported to the emergency room (ER) where he died shortly after arrival. On August 8, hemocultures obtained in the ER were reported to be positive for gram-negative coccobacilli resembling safety pins. Fluorescent antibody staining confirmed thediagnosis. Epidemiologic investigation established that the patient most likely became infected through flea-bites.The implicated fleas are known to become paradoxically hungrier and thus more likely to bite the more infectedblood meal they take. What bacterial factor plays a key role in this phenomenon?

A. Capsule
B. Coagulase
C. Endotoxin
D. Outer membrane protein
E. Superantigen toxin
 

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hmmm....tricky question

option C. Endotoxin looks tempting because of it being a Gram negative rod but i would go with

D. Outer membrane protein
 

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Discussion Starter · #6 ·
well...its really the difficult one.... :)
here we go....

Option B (Coagulase) is correct. The patient died of bubonic plague. The causative agent is Yersinia pestis-a gram-negative, bipolarly staining coccobacillus. Fleas acquire it while sucking blood from infected rats, squirrels, cats, and dogs. In the flea foregut (proventriculus), the bacteria proliferate, using blood nutrients, and secrete coagulase enzyme, which causes blood clotting and clumping of the organisms. Blocked proventriculus prevents nutrients from moving into the lower gut, making the infected flea hungrier.

Option A (Capsule) is incorrect. The capsule of Y. pestis is made up of polysaccharide-protein complex. It has an antiphagocytic role but plays no role blocking the proventriculus.

Option C (Endotoxin) is incorrect. Endotoxin (lipopolysaccharide [LPS]) is found in all gram-negative cell walls, including Y. pestis. It incites an inflammatory response when released systemically during septicemia but
plays no role in blocking the flea foregut.

Option D (Outer membrane protein) is incorrect. Outer membrane proteins of Y. pestis are directly injected into the human cells via type III secretion system and inhibit engulfment, phagocytosis, and cytokine production.

Option E (Superantigen toxin) is incorrect. Y. pestis produces a "murine" toxin that can contribute to blockage of the flea proventriculus; however, it does not have superantigen properties.

The rat flea (Xeopsylla cheopsis) carries infection from rat to rat and from rat to human. Y. pestis causes blood to clot in the gut of the flea, multiplies profusely in the clot and eventually blocks the lumen, so that the flea regurgitates infected material as it attempts to feed. As infected rats sicken, their fleas leave and may bite humans thus transmitting 'bubonic' plague. This disease is not generally transmitted from person to person. However, when there is extensive replication of bacteria in the lung, with bronchopneumonia and large numbers of bacteria in the sputum, the infection can spread from person to person by droplets, causing 'pneumonic' plague, with extremely rapid onset.
 
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