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Systemic salmonellosis in patients with disseminated histoplasmosis. Case for 'macrophage blockade' caused by
Abstract:
Five patients are described with disseminated histoplasmosis and systemic salmonellosis. Four of these patients were also immunocompromised because of the acquired immunodeficiency syndrome in two patients and renal transplantation in another two patients. Histologic studies in two patients showed histiocytes that were heavily laden with Histoplasma capsulatum yeast-phase organisms. We postulate that diffuse parasitization of the reticuloendothelial system (RES) by Histoplasma organisms may cause "RES blockade," which then predisposes to systemic salmonellosis, as reported in certain other infections and in sickle cell anemia.
Insights
Disseminated histoplasmosis, particularly in immunocompromised patients, may lead to systemic salmonellosis. This occurs due to Histoplasma capsulatum overwhelming the reticuloendothelial system, causing a blockade that facilitates Salmonella infection.
Area of Science:
- Infectious Diseases
- Immunology
- Pathology
Background:
- Disseminated histoplasmosis is a serious fungal infection.
- Immunocompromised individuals are at higher risk for severe infections.
- Co-infections with bacterial pathogens can complicate fungal diseases.
Observation:
- Five patients presented with disseminated histoplasmosis and systemic salmonellosis.
- Four patients were immunocompromised due to acquired immunodeficiency syndrome (AIDS) or renal transplantation.
- Histologic examination revealed extensive Histoplasma capsulatum within macrophages.
Findings:
- A strong association between disseminated histoplasmosis and systemic salmonellosis was observed.
- The reticuloendothelial system (RES) was heavily parasitized by Histoplasma.
- This extensive parasitization is hypothesized to cause RES blockade.
Implications:
- RES blockade by Histoplasma may predispose individuals to systemic salmonellosis.
- Understanding this interaction is crucial for managing co-infections in immunocompromised patients.
- Further research into RES blockade mechanisms could reveal new therapeutic targets.