|Year : 1983 | Volume
| Issue : 4 | Page : 270-3
Disseminated histoplasmosis (a case report).
SY Sane, MG Patel, BM Patel, KK Kokal
S Y Sane
|How to cite this article:|
Sane S Y, Patel M G, Patel B M, Kokal K K. Disseminated histoplasmosis (a case report). J Postgrad Med 1983;29:270-3
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Sane S Y, Patel M G, Patel B M, Kokal K K. Disseminated histoplasmosis (a case report). J Postgrad Med [serial online] 1983 [cited 2023 Oct 1 ];29:270-3
Available from: https://www.jpgmonline.com/text.asp?1983/29/4/270/5500
Histoplasmosis is a disease of world wide occurrence. In India, till now only sporadic cases are reported. Clinical manifestations of histoplasmosis are of three main types: Acute primary, chronic cavitatory and progressive disseminated. Pulmonary involvement masquarades clinical and radiological findings of tuberculosis while cases presenting with ear, nose, throat (ENT) mucosal involvement are mistaken for malignancy. Presentation as hepatosplenomegaly has to be differentiated from common infections like kalaazar and malaria. Hence, in India, disseminated histoplasmosis is rarely suspected. Herewith, we report a case of disseminated histoplasmosis treated successfully.
A 55 year old male, a resident of Nasik (district of Maharashtra), was admitted with complaints of rapid loss of 10 kg weight over a period, of 4 months, generalised asthenia, anorexia, fever with chills and pain in the right hypochondrium. There was history of nodular mass in the nose diagnosed as rhinoscleroma 6 months earlier. On examination, the patient was found to be cachetic and febrile. The pulse was 100 per minute, and B.P. was 130/90 mm of Hg. He had no lymphadenopathy. The liver was enlarged, firm, tender, and 6 cm below the costal margin. The spleen was 3 cm in size, palpable, and non-tender. He had no respiratory symptoms; cardiovascular and nervous system examinations were normal.
Haemoglobin was 13.3 gm%, total leucocyte count was 6,300/cmm with P-70%, L-2.5%, E-3% and M-2%. ESR was 92 mm at the end of one hour. Serum proteins (6.3 gm%) revealed mild increase of globulins (3.3 gm%) and albumin was 3.0 gm%. Other liver function tests were within normal limits. Routine urine and stool examinations were normal. X-ray chest revealed clear lung fields. Liver scan with 99mTc-sulphur colloid showed an enlarged liver, particularly the left lobe, with patchy uptake. The spleen was moderately enlarged with uniform uptake. Four days after admission, he developed hoarseness of voice. The ENT examination showed right vocal cord paresis and oedema with small irregular nodule on the right valeola. The clinical diagnosis was carcinoma of larynx and the nodular mass in the nose was interpreted as rhinoscleroma.
The materials surveyed at the laboratory were (1) nasal mucosa smears, (2) biopsy of the laryngeal nodule, (3) biopsy of the nasal mass and (4) liver biopsy. The smears were stained with H & E, P.A.S., Gram's and Giemsa's stain. The biopsies were processed as usual and sections were stained with H & E, P.A.S., silver stain, Wilder's reticulin and Griedley's stain. Microscopic examination of the laryngeal nodule and nasal mass revealed heavy infiltration of submucosa by lymphocytes, plasma cells, a few polymorphs and histiocytes. There were numerous organisms in histiocytes and also extra-cellularly surrounded by haloes [Fig.1] These gave vacuolated appearance to the cytoplasm. Hence the first biopsy of nasal mass was misdiagnosed as a rhinoscleroma. The morphology was better seen in the nasal smears by P.A.S. and silver stains. The histoplasma organisms appeared as oval cells, 2-4µ in size, with buds at the smaller end [Fig. 2]. The liver biopsy showed clusters of hepatocytes and some Kupffer cells with intracytoplasmic organisms.
The patient was started on injection Amphotericin B. The dose was gradually increased to 50 mg daily in infusion form. He received a total of 1650 mg of Amphotericin B. During the course of the disease, he developed a few soft. nodules on the forehead which disappeared later on. Within seven days of therapy he started improving and hoarseness of voice decreased. Three weeks after therapy vocal cord nodule completely disappeared and his liver and spleen regressed in size. The patient gained 6 kg weight during therapy. At follow up after one year, the patient was asymptomatic. The liver and spleen were not palpable anymore. The repeat liver scan was also normal.
The case was diagnosed as disseminated histoplasmosis on the basis of histology and involvement of liver, spleen, nasal mucosa and nodules on the larynx and skin. Isolation of organisms by culture was not successful but histomorphological features were characteristic for diagnosis. The differential diagnosis lay between leishmaniasis, histoplasmosis, toxoplasmosis and rhinoscleroma. The differentiation was done with the help of special stains and morphology as shown in [Table 1.]
The progressive disseminated histoplasmosis is reported to occur in one or two per 1000 patients of any age due to many predisposing factors.,  Hepatosplenomegaly was a significant mode of presentation in this case as well as in other reports by many Indian authors., , ,  Histoplasmosis is a common disease of worldwide occurrence and is endemic in great river valleys of American and African continents. It is as yet a rare disease in India. In India, Panja and Sen reported the first case of disseminated histoplasmosis. This was followed by many reports of histoplasmosis in residents of Bengal.,  Sporadic reports are from Maharashtra,  and other parts of the country.
The present case is a resident of Nasik (Maharashtra), an educated person who relates the beginning of the disease following a religious festival, Kumbh-mela, when pilgrims gather from all over the country.
Awareness of this infection is important because 100% mortality seen in untreated group comes down to 70% when adequately treated with Amphotericin-B. Local histoplasmosis is often misdiagnosed as a malignant or tuberculous lesion. Disseminated disease is to be differentiated from more common diseases like tuberculosis, leishmaniasis or systemic malignancy.
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