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{{WBRQuestion
{{WBRQuestion
|QuestionAuthor=William J Gibson
|QuestionAuthor=William J Gibson (Reviewed by  {{YD}})
|ExamType=USMLE Step 1
|ExamType=USMLE Step 1
|MainCategory=Microbiology
|MainCategory=Microbiology
|SubCategory=Musculoskeletal/Rheumatology, General Principles, Infectious Disease
|SubCategory=Musculoskeletal/Rheumatology, Infectious Disease
|MainCategory=Microbiology
|MainCategory=Microbiology
|SubCategory=Musculoskeletal/Rheumatology, General Principles, Infectious Disease
|SubCategory=Musculoskeletal/Rheumatology, Infectious Disease
|MainCategory=Microbiology
|MainCategory=Microbiology
|SubCategory=Musculoskeletal/Rheumatology, General Principles, Infectious Disease
|SubCategory=Musculoskeletal/Rheumatology, Infectious Disease
|MainCategory=Microbiology
|MainCategory=Microbiology
|MainCategory=Microbiology
|MainCategory=Microbiology
|MainCategory=Microbiology
|MainCategory=Microbiology
|SubCategory=Musculoskeletal/Rheumatology, General Principles, Infectious Disease
|SubCategory=Musculoskeletal/Rheumatology, Infectious Disease
|MainCategory=Microbiology
|MainCategory=Microbiology
|SubCategory=Musculoskeletal/Rheumatology, General Principles, Infectious Disease
|SubCategory=Musculoskeletal/Rheumatology, Infectious Disease
|MainCategory=Microbiology
|MainCategory=Microbiology
|SubCategory=Musculoskeletal/Rheumatology, General Principles, Infectious Disease
|SubCategory=Musculoskeletal/Rheumatology, Infectious Disease
|MainCategory=Microbiology
|MainCategory=Microbiology
|SubCategory=Musculoskeletal/Rheumatology, General Principles, Infectious Disease
|SubCategory=Musculoskeletal/Rheumatology, Infectious Disease
|MainCategory=Microbiology
|MainCategory=Microbiology
|MainCategory=Microbiology
|MainCategory=Microbiology
|SubCategory=Musculoskeletal/Rheumatology, General Principles, Infectious Disease
|SubCategory=Musculoskeletal/Rheumatology, Infectious Disease
|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?
|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?
|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.  
|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:
*Mistrafficking neutrophils to become unable to access infected site
*Reducing blood supply to infected tissue by vasoconstriction and platelet aggregation
*Activating arachidonic acid cascade and protein kinase C to modulate host cell metabolism


''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.
*Mistraffick neutrophils to become unable to access infected site
|AnswerA=Combination of MHC class II and T-cell receptor (TCR) to stimulate leukocytes
*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.
|AnswerA=Combination of MHC class II and T-cell receptor (TCR) to stimulate leukocytes.
|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".
|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".
|AnswerB=Phospholipase
|AnswerB=Phospholipase
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|AnswerCExp=Both botulinum and tetanus toxin cleave SNARE protein at synapses, thereby disabling neurotransmitter release at the synaptic cleft.
|AnswerCExp=Both botulinum and tetanus toxin cleave SNARE protein at synapses, thereby disabling neurotransmitter release at the synaptic cleft.
|AnswerD=Inactivation of 60S ribsosome by cleaving rRNA
|AnswerD=Inactivation of 60S ribsosome by cleaving rRNA
|AnswerDExp=The toxins produced by ''Shigella'' and ''EHEC'' inactivate the 60S ribosome by cleaving rRNA.
|AnswerDExp=The toxins produced by ''Shigella'' and EHEC inactivate the 60S ribosome by cleaving rRNA.
|AnswerE=Increase of cAMP by intrinsic enzymatic activity.
|AnswerE=Increase of cAMP by intrinsic enzymatic activity
|AnswerEExp=Edema factor toxin produced by ''[[Bacillus anthracis]]'' mimics adenylate cyclase enzyme and increases cAMP by increasing enzymatic activity.
|AnswerEExp=Edema factor toxin produced by ''[[Bacillus anthracis]]'' mimics adenylate cyclase enzyme and increases cAMP by increasing enzymatic activity.
|EducationalObjectives=''Clostridium perfringens'' produces gas gangrene and alpha toxin, a phospholipase C enzyme that degrades tissue.
|EducationalObjectives=''Clostridium perfringens'' causes gas gangrene and produces the hemolytic alpha toxin, a zinc-containing phospholipase C enzyme (lecithinase) that preferentially degrades phophatidylcholine and sphingomyelin.
|References=Titball RW, Naylor CE, Basak AK. The Clostridium perfringens alpha-toxin. ''Anaerobe''. 1999;5(2):51-64.
|References=Titball RW, Naylor CE, Basak AK. The Clostridium perfringens alpha-toxin. ''Anaerobe''. 1999;5(2):51-64.<br>
First Aid 2014 page 127
First Aid 2015 page 172.
|RightAnswer=B
|RightAnswer=B
|WBRKeyword=Microbiology, Bacteria, Toxin, Toxins, Mechanism, Gangrene,
|WBRKeyword=Bacteria, Toxin, Toxins, Gas gangrene, Clostridium perfringes, A
|Approved=Yes
|Approved=Yes
}}
}}

Latest revision as of 23:10, 27 October 2020

 
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:
  • Mistrafficking neutrophils to become unable to access infected site
  • Reducing blood supply to infected tissue by vasoconstriction and platelet aggregation
  • Activating arachidonic acid cascade and protein kinase C to modulate host cell metabolism

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.
Educational Objective: Clostridium perfringens causes gas gangrene and produces the hemolytic alpha toxin, a zinc-containing phospholipase C enzyme (lecithinase) that preferentially degrades phophatidylcholine and sphingomyelin.
References: Titball RW, Naylor CE, Basak AK. The Clostridium perfringens alpha-toxin. Anaerobe. 1999;5(2):51-64.
First Aid 2015 page 172.]]

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::