WBR0055
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| Author | [[PageAuthor::William J Gibson (Reviewed by Yazan Daaboul, M.D.)]] |
|---|---|
| Exam Type | ExamType::USMLE Step 1 |
| Main Category | MainCategory::Microbiology |
| Sub Category | SubCategory::Musculoskeletal/Rheumatology, SubCategory::Infectious Disease |
| Prompt | [[Prompt::A 32-year-old male soldier suffers from an open leg wound following an explosion. He is immediately stabilized upon returning to the military base and is admitted for emergent surgery. Two days later, the patient develops high-grade fever with painful swelling and blisters at the wound site. CT scan of the involved leg is remarkable for gas formation in nearby muscles and subcutaneous tissue. What is the mechanism of action of the toxin responsible for this patient's complication?]] |
| Answer A | AnswerA::Combination of MHC class II and T-cell receptor (TCR) 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:
Infections can progress very rapidly, resulting in the development of myonecrosis and the formation of gas as more tissue is progressively destroyed. If left untreated, potentially lethal sepsis can ensue within few hours. The treatment for gas gangrene is wound debridement, and often amputation of the affected area, with adjuvant penicillin therapy. |
| Approved | Approved::Yes |
| Keyword | WBRKeyword::Bacteria, WBRKeyword::Toxin, WBRKeyword::Toxins, WBRKeyword::Gas gangrene, WBRKeyword::Clostridium perfringes, WBRKeyword::A |
| Linked Question | Linked:: |
| Order in Linked Questions | LinkedOrder:: |