NEET-PG 2012 — Microbiology

Q: All of the following cause Fournier's gangrene except:

Clostridium. ***Clostridium*** - While *Clostridium* species (especially *C. perfringens*) **CAN be isolated** from Fournier's gangrene cases and contribute to gas formation and tissue necrosis, they are **less commonly identified as primary pathogens** compared to other organisms. - In the context of this question, *Clostridium* is considered the "except" option because it is **relatively less frequently implicated** in Fournier's gangrene compared to the other listed organisms, though it is NOT entirely excluded from the microbiology of this condition. - *Clostridium* species are more classically associated with **gas gangrene (clostridial myonecrosis)** in traumatic wounds and deep muscle tissue. *Bacteroides* - ***Bacteroides fragilis*** and other **anaerobic gram-negative bacilli** are among the **most commonly isolated organisms** in Fournier's gangrene. - They produce enzymes that facilitate tissue destruction and contribute significantly to the **polymicrobial synergistic necrotizing infection**. - Essential component of the typical microbial flora in perianal and genital infections. *Streptococcus* - ***Streptococcus pyogenes*** (Group A Streptococcus) and other streptococcal species are **frequently isolated** from Fournier's gangrene. - They produce toxins and enzymes causing **rapid necrotizing fasciitis** with systemic toxicity. - Major contributor to the aggressive nature and rapid progression of the infection. *Staphylococcus* - ***Staphylococcus aureus*** (including MRSA) is **commonly found** in polymicrobial Fournier's gangrene infections. - Contributes to local tissue destruction through toxin production and enzyme activity. - Often isolated from perianal and genital skin flora, facilitating its involvement in these infections.

Q: Classical complement is activated by:

Ag-Ab complex. ***Ag-Ab complex*** - The **classical complement pathway** is initiated by the binding of **C1q** to an antigen-antibody complex, specifically involving **IgM** or certain subclasses of **IgG**. - This binding triggers a cascade of events leading to the activation of the complement system, ultimately resulting in the **lysis of target cells**, **opsonization**, and **inflammation**. *C3 Convertase* - **C3 convertase** is an enzyme complex formed later in the complement cascade, responsible for cleaving C3 into C3a and C3b. - While essential for all complement pathways, it is a **downstream effector** and not the initial activator of the classical pathway. *C1* - **C1** is a complex protein that includes C1q, C1r, and C1s. While C1 plays a crucial role in the classical pathway, it is **activated by** the antigen-antibody complex, not an independent activator. - The activation sequence is: **Ag-Ab complex → C1q binding → C1 activation → cascade initiation**. Thus, the Ag-Ab complex is the primary trigger, and C1 is the responder. *IgA* - **IgA** primarily functions in mucosal immunity and is generally **not an activator** of the classical complement pathway. - Instead, IgA can activate the **alternative complement pathway** under specific circumstances, but not the classical pathway through direct binding to C1q.

72 Questions — Page 8 of 8

Q71

All of the following cause Fournier's gangrene except:

Q72

Classical complement is activated by: