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CORRESPONDENCE COLUMN |
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| Year : 2006 | Volume
: 51
| Issue : 1 | Page : 63-65 |
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| Primary cutaneous histoplasmosis in an immunocompetent host from a non-endemic area |
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S Nanda, C Grover, A Goel, D Kapoor, BSN Reddy, N Khurana
Department of Dermatology and S.T.D. and Pathology, Maulana Azad Medical College and Lok Nayak Hospital, New Delhi -110 002, India
Correspondence Address:
S Nanda
Department of Dermatology and S.T.D. and Pathology, Maulana Azad Medical College and Lok Nayak Hospital, New Delhi -110 002
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0019-5154.25208
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How to cite this article:
Nanda S, Grover C, Goel A, Kapoor D, Reddy B, Khurana N. Primary cutaneous histoplasmosis in an immunocompetent host from a non-endemic area. Indian J Dermatol 2006;51:63-5 |
How to cite this URL:
Nanda S, Grover C, Goel A, Kapoor D, Reddy B, Khurana N. Primary cutaneous histoplasmosis in an immunocompetent host from a non-endemic area. Indian J Dermatol [serial online] 2006 [cited 2023 Nov 29];51:63-5. Available from: https://www.e-ijd.org/text.asp?2006/51/1/63/25208 |
A 40 year old female presented to us in May 2001 with two asymptomatic, umbilicated lesions over the right cheek and forehead for the past 6 months. A provisional diagnosis of giant molluscum contagiosum was made and exterpation was done. No molluscum bodies were found and the lesions did not subside, so an excision biopsy was performed for one of the lesions and specimen was sent for histopathology. Biopsy revealed acanthotic epidermis with mild papillomatosis. A diffuse dermal infiltrate comparising predominantly of histiocytes admixed with plasma cells and few lymphocytes and eosionophils characterized and lesions. Majority of the histiocytes revealed intracellular small (2-3 l) sized eosinophilic round to ovoid organisms, at places completely filled the cells. Few areas showed a clear halo around those organisms [Figure - 3] (H&E, 1000x).
Intense staining with periodic Acid Schiff technique and silver methanine showed morphology suggestive of histoplasmosis [Figure - 2]. Small size of the organisms and absence of carminophilia of capsule with mucicamine staining reaction ruled out he possibility of cryptococcosis. The infiltrate was extending into the deeper dermis and around the skin appendages with areas showing granulomatous aggregates of histocytes, all showing intercellular yeast of histoplasma. Patient is a kabadi (junk dealer) by occupation working in a damp moist basement. Rest of the mucocuatneous and systemic examination was within normal limits.
Thorough investigation, including blood sugar, Mantoux test and HIV revealed no underlying immunosuppression. CD4 counts were normal.
Culture for histoplasma revelaed no growth. Skin antigent for histoplasma could not be carried out due to non availability of the same. CT scan, bronchoscopy reveled no abnormality. The patient was kept under follow up. In Dec. 2003, the patient again presented to us with a single skin colored, asymptomatic lesion over the upper lip [Figure - 1]. An excision biopsy was done, the specimen was sent for both histopathology as well as fungal culture. Histopathology ws again consistent with histoplasmosis while culture revealed no growth. Repeat blood sugar, Mantoux test, HIV and CD4 counts were found to be normal. Serology for histoplasmosis could not be performed due to non-availability of the same.
Histoplasmosis is an endemic mycosis, which is most prevalent in the Ohio and Mississippi river valleys of North America, though there are rare reports of this myoses from non-endemic regions too. [1],[2],[3] There are reports of this disease in both immuno-suppressed as well as immuno-competent host.[4],[5] The causative agent Histoplasma capsulatum is found globally in soil especially in soil containing high concentrations of bird and bat droppings.[6] The clinical spectrum is variable, ranging from a severe multisystem illness involving the bone marrow, liver, spleen and lungs, to an indolent infection localized to the gastrointestinal tract, skin, adrenal glands, brain, meninges or other extrapulmonary tissue. Acute pulmonary infectin, chronic pulmonary and progressive diseminated histoplasmosis are the most commonly recognized clinical manifestations, pericarditis, rheumatologic syndromes, esophageal compression and sarcoid like manifestations are well recognized complications of histoplasmosis. Cutaneous histoplasmosis occurs in upto 17% of American patients with disseminated histoplasmosis.[7]
Diagnostic modalities include cultures, fungal stains of tissue or body fluids and tests for antigens and antibodies. Serologic tests for antibodies provide the basis for diagnosis in patients with maild infections, but require at best a month to appear after the initial exposure. Patients with milder manifestations or chronic complications have a lower fungal burben, reducting the chances for diagnosis by antigen detection or culture, as was seen in the present case. In such cases serologic tests are valuable.8 The diagnosis can be established by isolation of H. capsulatum from the sputum or bronchoscopy specimens in 60% to 85% of cases. Chest X-ray usually show diffuse infiltrates but are normal in 25 to 33% of cases.
Skin biopsy can prove to be useful in establishing the diagnosis especially in set up like ours where facilities for serodiagnosis are not readily available. Also most of these tests would be of little or no use in cases of pure cutaneous histoplasmosis.
Although excellent laboratory methods are available, histoplasmosis in nonendemic regions, might pose a diagnostic challenge and an astute clinician and good laboratory backup is required in such cases. Unusual clinical presentations with limited physical findings may compound the difficulty in diagnosis. Physicians must be aware of the clinical syndromes and take advantage of the epidemiologic clues, namely activities or occupations that expose the patient to sites contaminated that expose the patient to sites contaminated with bat or bird droppings. Also, clinicians must be familiar with the uses and limitations of the diagnostic tests for fungal diseases.[8]
| References | |  |
| 1. | O'Hara CD, Allegretto MW, Taylor GD, et al. Epiglottic histoplasmosis presenting in a nonendemic region. Arch Pathol Lab Med 2004; 128:574-7.  |
| 2. | Minamoto GY, Rosenberg AS. Fungal infections in patients with acquired immunodeficiency syndrome. Med Clin North Am 1997; 81:381-409. |
| 3. | Taylor GD, Fanning EA, Ferguson JP et al . Disseminated histoplasmosis in a nonendemic area. Can Med Assoc J 1985; 133:763-5. |
| 4. | Wolf J, Blumberg HM, Leonard MK. Laryngeal histoplasmosis. Am J Med Sci 2004 Mar; 327(3):160-2. |
| 5. | Rosenberg JD, Scheinfeld NS. Cutaneous histoplasmosis in patients with acquired immunodeficiency. Cutis 2003 Dec.; 72(6):439-5. |
| 6. | Cano MVC, Hajjeh RA. The epidemiology of histoplasmosis: a review. Seminars in respiratory infections 2001; 16(2):109-18. |
| 7. | Wheat JL, Connoly-Stringfield, Baker PA, et al. Disseminated histoplasmosis in the acquired immunodeficiency syndrome: clinical findings, diagnosis and treatment and review of the literature. Medicine (Baltimore) 1990; 69:391-74. |
| 8. | Wheat LJ. Laboratory diagnosis of histoplasmosis: Update 2000. Seminars in respiratory infections 2001; 16(2):131-40. |
Figures
[Figure - 1], [Figure - 2], [Figure - 3] |
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