Campylobacteriosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Campylobacter organisms are curved or spiral, motile, non–spore-forming, gram-negative rods. The known routes of transmission are fecal-oral, person-to-person sexual contact, raw milk and poultry ingestion, and waterborne (ie, through contaminated water supplies). Exposure to sick pets, especially puppies, has also been associated with outbreaks.
Pathophysiology
- Campylobacter organisms are curved or spiral, motile, non–spore-forming, gram-negative rods.
- C jejuni appears to invade and destroy epithelial cells. Some strains of C jejuni produce a cholera-like enterotoxin, which is important in the watery diarrhea observed in infections.
- The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism.
- In patients with HIV, infections may be more frequent, may cause prolonged or recurrent diarrhea, and may be more commonly associated with bacteremia and antibiotic resistance. T
- The severity and persistence of infection in patients with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection.
- The exact pathogenesis by which it causes colitis after transmission is not fully understood. However, it is hypothesized that requirement for C. jejuni virulence include (1) motility, (2) drug resistance, (3) host cell adherence, (4) host cell invasion, (5) alteration of the host cell signaling pathways, (6) induction of host cell death, (7) evasion of the host immune system defenses, and (9) acquisition of iron which serves as a micronutrient for growth and works as a catalyst for hydroxyl radical formation.[1]
- C. jejuni also secretes proteins that may contribute to the ability of the bacterium to invade the host epithelial cells.[1]