pathophysiology of Chlamydia

[IDoIt4Love]

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A question asks for the mechanism of action of a C. trachomatis infection. I was very surprised when the correct answer turned out to be "cytotoxic cell mediated hypersensitivity."

First of all, I thought "cytotoxic" hypersensitivity was a Type II reaction, mediated by antibodies. Since C. trachomatis is an obligate intracellular pathogen, I ruled that answer choice out.

However, in the explanation, they describe this "cytotoxic cell mediated hypersensitivity" as a type IV hypersensitivity! I thought type IV hypersensitivity was Th cell mediated, not cytoxic cell mediated! Furthermore, I had never even heard that C. trachomatis induced a hypersensitivity reaction before, and can't find where that is explained in First Aid.

I think this q-bank question is in error, but I don't know where the error lies:

Is the infection a cytotoxic (type II) hypersensitivity?
Is the infection a delayed (type IV) hypersensitivity? If so, is type IV actually mediated by cytotoxic T cells or helper T cells?

Please help; I'm really confused.

 

[ijn]

CD4 TH1/macrophage granulomas aren't the only form of type IV hypersensitivity reactions. Cytotoxic CD8 T-cells are involved in type IV hypersensitivity reactions. The classic example is viral hepatitis where the CD8 cells are inducing apoptosis in infected hepatocytes.

 

[johndoe3344]

Type 4 HSR is mediated by Th1 which can activate CTLs. These are both components of cell mediated immunity.

Type 2 HSR is indeed called "cytotoxic" but you're confused. This cytotoxic refers to the damage to the cells (classically by ADCC) that have the antibodies bound to them. Type 2 HSR is mediated entirely by humoral immunity.

 

[Morsetlis]

Intracellular pathogens generate a Type IV hypersensitivity response. In exemplis, Mycobacterium tuberculosis. Type IV HSR are termed "cytotoxic" because Th1 cells mediate them.

Type II HSR are mediated by Antibodies versus (usually) fixed antigens, such as TSH-R (Grave's disease) or glomerular basement membrane (Goodpasteur's). Th1 cells are usually NOT involved, and cytotoxicity is only involved if there is ADCC by NK cells, via the FcyR--Fcy of IgG interaction. There can be phagocytosis and complement activation, however.

" The initial response to infected epithelial cells is a neutrophilic infiltration followed by lymphocytes, macrophages, plasma cells, and eosinophilic invasion. The release of cytokines and interferons by the infected epithelial cell initializes this inflammatory cascade.

Infection with chlamydial organisms invokes a humoral cell response, resulting in secretory immunoglobulin A (IgA) and circulatory immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies and a cellular immune response. Recent studies have implicated a 40-kd major outer membrane protein (MOMP), as well as 10- and 60-kd chlamydial heat-shock proteins (cHSP), in the immunopathologic response, but further studies are needed to better understand these cell-mediated immune responses."

Chlamydia generates both Type II and Type IV responses, with Type IV responses predominantly responsible for the pelvic inflammatory disease state.