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Fig. 6.38 A, B. Histoplasma capsulatum var. duboisii. A The histopathology shows granulomas with many huge giant cells, up to 200 pm in diameter, packed with large yeast cells. H&E,x200. B Caseous necrosis surrounded by fibrosis with only a few giant cells. H & E, x80. (A, B from Bittencourt and Londero 1995; B was provided by Professor Kaschula, Cape Town)

Fig.6.39 A,B. Histoplasma duboisii nodules lie subcutaneously, over the chest (A) and around the lower leg, ankle, and foot (B)

Fig. 6.40 A-D. Histoplasma duboisii causes destructive bone lesions. A, B Affecting the lower end of the femur, with considerable soft tissue swelling and elevation of the periosteum. There are some small central lytic foci. C Similar destruction in the upper end of the tibia and D several foci in the skull. It can be very difficult to distinguish between this fungal or pyogenic osteomyelitis, and in some patients, neoplasm. The diagnosis must be confirmed clinically, by biopsy and preferably culture



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Histoplasmosis Duboisii

Caused by a larger species of Histoplasma, histoplasmosis duboisii is clinically, geographically, and histopathologically quite different from the more commonly known and widespread classical histoplasmosis capsulati.


African histoplasmosis. Large histoplasmosis. Largeform histoplasmosis.


African histoplasmosis is a systemic infection caused by the fungus Histoplasma capsulatum var. duboisii.

Geographic Distribution

Histoplasma capsulatum var. duboisii occurs, with very few exceptions, only on the African continent between the Tropics of Cancer and Capricorn. A few cases of histoplasmosis duboisii have been identified in Madagascar and isolated cases have been recognized in Arabia, parts of Asia, and Japan. It should be emphasized that these cases outside Africa are exceptional. It is suspected that there are clinically silent cases elsewhere, but this is not known for certain because there is no specific skin test. There is no doubt that histoplasmosis duboisii is most common in west and central Africa, particularly Nigeria, Senegal, the Democratic Republic of Congo (formerly Zaire), and Angola.

Epidemiology and Pathology

The duboisii variety of Histoplasma capsulatum was first described in 1952 (by Vanbreuseghem) named in 1960 (by Ciferri) and fully described as a clinical disease in 1964 (by Cockshott and Lucas). It was obtained from soil mixed with bat guano, as well as the bowel of bats in 1991 (Gugnani et al.). It has been identified in two species of baboons from Guinea and Senegal. The yeast cells of Histoplasma capsulatum var. duboisii average about 10 Eun in diameter, about twice the size of H. capsulatum var. capsulatum. They are thick walled and round or oval. They reproduce by a single bud which can equal the size of the parent cell, giving an hourglass appearance. Thus, in tissue, the two varieties vary in size.

H. capsulatum var. duboisii may remain viable for many years within tissues without clinical evidence of disease. Infection is spread by inhalation and affects all age groups, but particularly persons in their second decade. There is no significant racial or gender predominance. Histopathologically, the fungus is both extra- and intracellular, but tends to accumulate within large macrophages, which may contain up to 30 fungal cells, all apparently continuing to grow and bud. The fungus may also lie free within the tissues. The reaction is granulomatous, with very large giant cells full of fungi and surrounded by inflammation and fibrosis (Fig. 6.38). Caseation occurs, but unlike in histoplasmosis capsulati, calcification is not a feature. In some patients, particularly the immunodeficient with disseminated disease, the yeasts are found in large numbers within the tissue but without any significant inflammation: the extent of the reaction in each patient depends very much on their immune status. Different histological lesions can be seen at the same time in one patient, but the reason for this is unclear.

Diagnosis depends on the recognition of the fungus from a biopsy specimen or from pus or exudates. Culture may be required and there is also an immunofluorescent test.

Clinical Characteristics

There are two main clinical presentations: localized and disseminated.

Localized form: The lesions are isolated skin, bone, or lymph node infections.

They are chronic and may not become clinically apparent until after long incubation. On the skin there are small painless papules which may form plaques or nodules (Fig. 6.39), ulcerate, or become cold abscesses with a tendency to break down. The skin lesions can be single or multiple and some have a surrounding pigment halo. They may heal spontaneously, develop exuberant granulation tissue, or invade underlying bone. Lymph nodes may suppurate and bone infections occur in one?third of all patients, developing into chronic osteomyelitis with draining sinuses. Infection of the lungs, mucous membranes, or intestinal tract is uncommon except in the rapidly progressive disseminated form of histoplasmosis duboisii.

Disseminated form: There is fever, anemia, and weight loss, as well as abdominal pain and jaundice in some patients. Multiple cutaneous lesions are usually present all over the body, together with subcutaneous abscesses. Lumps may develop over the head with underlying lytic lesions of the skull, radiographically resembling multiple myeloma or tuberculosis. Multiple lymph nodes enlarge and the liver and spleen may be infected and enlarged. Infections of the urinary bladder and large bowel have been reported and have a poor prognosis. As the infection worsens, pulmonary lesions will develop. Unless treated, the patient will die.

Skin lesions are the most common clinical presentation, but bones and joints are frequently infected, the joints being involved by spread from bone lesions. The femora, ribs, skull, upper arms, and vertebrae are the bones most commonly affected.
African histoplasmosis often arises in patients already suffering from tuberculosis, schistosomiasis, malnutrition, leishmaniasis, or AIDS.


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