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Granuloma inguinale is a sexually transmitted, chronic,
superficial ulceration of the genitalia and inguinal and perianal
regions caused by Calymmatobacterium
or Klebsiella
granulomatis, a small,
encapsulated, nonsporulating, nonmotile, gram-negative bacillus.
Granuloma
inguinale is called Donovanosis because Donovan bodies are present in
the scrapings from the edge of the lesions.
The organism has been cultivated in the yolk sac of embryonated
chicken eggs and on media containing egg yolk.
The disease has been produced in
volunteers but not in laboratory animals, and there is no similar
disease in animals.
Granuloma inguinale is rare in temperate climates,
but common in the tropics and subtropics.
New Guinea, central
Australia, and India have the highest incidence.
Individual
susceptibility varies greatly, and the low level of infectivity has
sparked controversy about sexual transmission.
For instance, spouses
of infected persons often remain uninfected despite repeated sexual
contact. However, epidemiologic data favors sexual transmission.
Most
patients are 15 to 40 years of age, the period of greatest sexual
activity.
Because male homosexuals who take the passive role have only
anal lesions, and because C. granulomatis has been isolated from
faeces, the organism is thought to inhibit the intestinal tract.
It
causes granuloma inguinale through autoinoculation, anal intercourse,
or vaginal intercourse, when the vagina is colonized by enteric
bacteria.
The incubation period varies from 1 to 5 months, 2
to 4 weeks being the average.
The initial lesion may be a papule, a
subcutaneous nodule or an ulcer.
The lesion develops within several
weeks into a raised, soft, painless, beefy-red, superficial ulcer.
The
exuberant granulation tissue resembles a fleshy mass herniating
through the skin.
In heterosexual men, early ulceration of the penoscrotal skin commonly extends to genitocrural and inguinal folds.
In women ulceration spread to the perineal and
perianal skin. In
homosexual men the lesions are perineal and anal.
Regional lymphadenopathy is not a feature.
Occasionally, however, subcutaneous inflammation in the inguinal
regions may be confused with the bubo of
lymphogranuloma venereum.
Sometimes granuloma inguinale can infect the vagina and
cervix and mimic carcinoma.
Rarely, the infection disseminates to the pelvic
organs, bone, and spleen following abortion or delivery.
Extragenital lesions of the skin and mucous membranes of the oral
cavity have been reported.
Untreated granuloma inguinale follows an indolent,
relapsing course, often healing, with an atrophic scar.
Secondary fusospirochetal infection may cause ulceration, with mutilation or
amputation of the genitalia.
Massive cicatrization of the dermis and subcutis causes genital elephantiasis, probably by lymphatic
obstruction.
It is uncertain whether there is an association between granuloma inguinale and squamous cell carcinoma, because the diseases
share common risk factors, such as poor hygiene, fusospirochetal
flora, and a large number of sexual partners.
Microscopically, there is epithelial hyperplasia of
the ulcer margin.
The dermis and subcutis are infiltrated by numerous
histiocytes and plasma cells and by fewer neutrophils and lymphocytes.
The neutrophils in the ulcer bed are clustered into poorly defined
microabscesses.
Interspersed histiocytes contain many
bacteria ,
which are called Donovan bodies.
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The bacteria are difficult to see in
routinely stained sections but are clearly revealed by silver
impregnation.
In older lesions, the inflammatory cell
infiltrate is composed of lymphocytes and plasma cells, and the
organisms are difficult to find.
Diagnosis of granuloma inguinale is suggested by the
clinical appearance of the lesion and confirmed by the demonstration
of C. granulomatis in smears of ulcer scrapings or tissue sections.
A
combined regimen of trimethoprim and sulfamethoxazole is the treatment
of choice.
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