WBR0055

Author	PageAuthor::William J Gibson
Exam Type	ExamType::USMLE Step 1
Main Category	MainCategory::Microbiology
Sub Category	SubCategory::Musculoskeletal/Rheumatology, SubCategory::General Principles, SubCategory::Infectious Disease
Prompt	[[Prompt::A soldier suffers an open leg wound after an explosion. He is immediately treated upon returning to the military base and underwent an emergent surgery. Two days after his surgery, he develops a high grade fever and painful swelling and blisters at the wound site. CT scan of the involved leg shows gas formation arising in nearby muscles and subcutaneous tissue. What is the mechanism of action of the toxin involved in this patient's complication?]]
Answer A	AnswerA::Combination of MHCII and TCR together to stimulate leukocytes.
Answer A Explanation	[[AnswerAExp::This is the mechanism of the Toxic Shock Syndrome (TSS) toxin by S. aureus and endotoxin A of S. pyogenes. Because of their unique ability to stimulate leukocytes without co-stimulatory factors, these toxins are called "super antigens".]]
Answer B	AnswerB::Phospholipase
Answer B Explanation	AnswerBExp::''Clostridium perfringens'' causes gas gangrene and produces the hemolytic alpha toxin, a zinc-containing phospholipase C enzyme (lecithinase) that preferentially degrades phophatidylcholine and sphingomyelin.
Answer C	AnswerC::Cleavage of SNARE protein
Answer C Explanation	AnswerCExp::Both botulinum and tetanus toxin cleave SNARE protein at synapses, thereby disabling neurotransmitter release at the synaptic cleft.
Answer D	AnswerD::Inactivation of 60S ribsosome by cleaving rRNA
Answer D Explanation	AnswerDExp::The toxins produced by ''Shigella'' and ''EHEC'' inactivate the 60S ribosome by cleaving rRNA.
Answer E	AnswerE::Increase of cAMP by intrinsic enzymatic activity.
Answer E Explanation	[[AnswerEExp::Edema factor toxin produced by Bacillus anthracis mimics adenylate cyclase enzyme and increases cAMP by increasing enzymatic activity.]]
Right Answer	RightAnswer::B
Explanation	[[Explanation::The patient is most likely suffering from gas gangrene (clostridial myonecrosis), caused by Clostridium perfringens. C. perfringens is found in soil and the environment as spores, which can enter open wounds. Clostridium perfringens causes gas gangrene and produces the hemolytic alpha toxin, a zinc-containing phospholipase C enzyme (lecithinase) that preferentially degrades phophatidylcholine and sphingomyelin. The toxin has 3 roles in the pathogenesis of gas gangrene: Mistraffick neutrophils to become unable to access infected site Reduce blood supply to infected tissue by vasoconstriction and platelet aggregation Activate arachidonic acid cascade and protein kinase C to modulate host cell metabolism Infections can progress rapidly, leading to myonecrosis and the formation of gas as tissue is destroyed. Potentially lethal sepsis can ensue within few hours without proper treatment. The treatment for gas gangrene is wound debridement, and often amputation of the affected area, with adjuvant penicillin. Educational Objective: Clostridium perfringens produces gas gangrene and alpha toxin, a phospholipase C enzyme that degrades tissue. References: Titball RW, Naylor CE, Basak AK. The Clostridium perfringens alpha-toxin. Anaerobe. 1999;5(2):51-64. First Aid 2014 page 127]]
Approved	Approved::Yes
Keyword	WBRKeyword::Microbiology, WBRKeyword::Bacteria, WBRKeyword::Toxin, WBRKeyword::Toxins, WBRKeyword::Mechanism, WBRKeyword::Gangrene
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