Granuloma Inguinale
Other Names: Donovanosis Granuloma inguinale is a genital ulcerative disease caused by the intracellular gram-negative bacterium Klebsiella granulomatis (formerly known as Calymmatobacterium granulomatis).
Epidemiology[edit | edit source]
The disease occurs rarely in the United States, although it is endemic in some tropical and developing areas, including India; Papua, New Guinea; the Caribbean; central Australia; and southern Africa .
Symptoms[edit | edit source]
Small, painless nodules appear after about 10–40 days of the contact with the bacteria. Clinically, the disease is commonly characterized as painless, slowly progressive ulcerative lesions on the genitals or perineum without regional lymphadenopathy; subcutaneous granulomas (pseudobuboes) also might occur. The lesions are highly vascular (i.e., beefy red appearance) and bleed. Extragenital infection can occur with extension of infection to the pelvis, or it can disseminate to intra-abdominal organs, bones, or the mouth. The lesions also can develop secondary bacterial infection and can coexist with other sexually transmitted pathogens.
Diagnosis[edit | edit source]
The causative organism of granuloma inguinale is difficult to culture, and diagnosis requires visualization of dark-staining Donovan bodies on tissue crush preparation or biopsy. No FDA-cleared molecular tests for the detection of K. granulomatis DNA exist, but such an assay might be useful when undertaken by laboratories that have conducted a CLIA verification study.
The presence of Donovan bodies in the tissue sample confirms donovanosis. Donovan bodies are rod-shaped, oval organisms that can be seen in the cytoplasm of mononuclear phagocytes or histiocytes in tissue samples from patients with granuloma inguinale. They appear deep purple when stained with Wright's stain. These intracellular inclusions are the encapsulated Gram-negative rods of the causative organisms. They were discovered by Charles Donovan.
Treatment[edit | edit source]
Several antimicrobial regimens have been effective, but only a limited number of controlled trials have been published (383). Treatment has been shown to halt progression of lesions, and healing typically proceeds inward from the ulcer margins; prolonged therapy is usually required to permit granulation and re-epithelialization of the ulcers. Relapse can occur 6–18 months after apparently effective therapy. Recommended Regimen
- Azithromycin 1 g orally once per week or 500 mg daily for at least 3 weeks and until all lesions have completely healed
- Alternative Regimens
- Doxycycline 100 mg orally twice a day for at least 3 weeks and until all lesions have completely healed
- OR
- Ciprofloxacin 750 mg orally twice a day for at least 3 weeks and until all lesions have completely healed
- OR
- Erythromycin base 500 mg orally four times a day for at least 3 weeks and until all lesions have completely healed
- OR
- Trimethoprim-sulfamethoxazole one double-strength (160 mg/800 mg) tablet orally twice a day for at least 3 weeks and until all lesions have completely healed.
The addition of another antibiotic to these regimens can be considered if improvement is not evident within the first few days of therapy. Addition of an aminoglycoside to these regimens is an option (gentamicin 1 mg/kg IV every 8 hours). Doxycycline should be avoided in the second and third trimester of pregnancy because of the risk for discoloration of teeth and bones, but is compatible with breastfeeding
For these reasons, pregnant and lactating women should be treated with a macrolide regimen (erythromycin or azithromycin). The addition of an aminoglycoside (gentamicin 1 mg/kg IV every 8 hours) can be considered if improvement is not evident within the first few days of therapy.
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