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We report the isolation of Histoplasma capsulatum from a culture of the viscera of Didelphis albiventris, one of the marsupial species found in Brazil. To our knowledge, this is the first report of the isolation of this fungus from this mammalian species. This finding confirms the ubiquitous presence of H. capsulatum in nature.
The epidemiological, clinical and therapeutical findings are described in a case of recurrent pulmonary histoplasmosis due to Histoplasma capsulatum. The patient, a bulldozer-operator, worked in Africa for a long period in extremely dusty conditions without any protection. Three different episodes of H. capsulatum pneumonia recurred during eighteen months after his return from Africa. A full dose treatment by Amphotericin B failed to eliminate disease recurrence on three occasions. The high concentration of airborne H. capsulatum spores inhaled could have been the main cause of the difficulty obtaining a rapid sterilization of the microorganism by Amphotericin B and disease recurrence. The late start of the treatment or the unexplained ability of some persons to develop repeated infections even with normal immunological parameters could be another explanation for the reported phenomenon.
The classification of microbial strains is currently based on different typing methods, which must meet certain criteria in order to be widely used. Phenotypic and genotypic methods are being employed in the epidemiology of several fungal diseases. However, some problems associated to the phenotypic methods have fostered genotyping procedures, from DNA polymorphic diversity to gene sequencing studies, all aiming to differentiate and to relate fungal isolates or strains. Through these studies, it is possible to identify outbreaks, to detect nosocomial infection transmission, and to determine the source of infection, as well as to recognize virulent isolates. This paper is aimed at analyzing the methods recently used to type Histoplasma capsulatum, causative agent of the systemic mycosis known as histoplasmosis, in order to recommend those that yield reproducible and accurate results.
We present a case of colonic histoplasmosis in a young HIV antibody-positive homosexual male who presented with acute diarrhea. The diagnosis was made by flexible sigmoidoscopy with biopsy which revealed organisms morphologically consistent with Histoplasma capsulatum, and was later confirmed by fungal culture of the biopsy specimens. At colonoscopy, skip areas with plaques, ulcers, and a pseudopolyp were observed. The colitis resolved endoscopically after a 6-wk course of intravenous amphotericin B, and the patient has had no recurrence of symptoms while on maintenance therapy with amphotericin B. However, the organisms continue to be noted on biopsies of normal-appearing areas in the rectum and sigmoid 5 months after diagnosis. Colonic involvement with H. capsulatum, an organism endemic to the Midwest, may be seen more frequently as the total number of cases of HIV-infected individuals increases in this region.
Histoplasma capsulatum can, sometimes, simulate sarcoidosis, clinically and pathologically. A case is reported in which disseminated histoplasmosis is proved only by fungus granulomatous tissue. Another similar cases of the literature incite to propose the practice of special stains, above all Gomori-Grocott technical, before sarcoid-like lesions. Lesions pathogeny was discussed. In our case it's not possible to eliminate the role of primary sarcoidosis in disseminated histoplasmosis.
A widespread maculo-papular cutaneous rash appeared on a HIV-positive young bisexual Cambodian man. He was treated for Mycobacterium tuberculosis and Pneumocystis carinii infections. He had been residing in France for seven years. Histology showed, within the dermis, abundant extracellular and intramacrophagic yeast-like organisms suggestive of histoplasmosis. Cultured specimens produced a growth of colonies after three weeks on Sabouraud 4 p. 100 dextrose agar at 25 degrees C. Numerous macroconidia were found which made the species diagnosis of Histoplasma capsulatum possible. Despite initiation of therapy with amphotericin B the patient died. Cutaneous involvement with or without specific features is uncommon in disseminated histoplasmosis. The specific cutaneous lesions are protean. They rarely are the presenting sign of initial infection. Disseminated histoplasmosis has a poor prognosis in acquired immunodeficiency syndrome: amphotericin B is not curative. Maintenance suppressive therapy with ketoconazole has been recommended following amphotericin B completion, although break-through has been reported.
Four children with orbital histoplasmosis caused by Histoplasma capsulatum var. duboisii (one of whom had been unsuccessfully treated with amphotericin-B) were treated with a combination of trimethoprim and sulphamethoxazole (Septrin) and surgical drainage. All patients improved markedly during therapy with resolution of the lesions, and with no recurrence of infection in three patients, 1 year later. The fourth patient was lost to follow-up. Treatment was devoid of side effects. These findings clearly indicate that Septrin could be a safe alternative to amphotericin-B for the treatment of African histoplasmosis, especially in patients presenting with solitary or localized lesions.
One-month-old and 1-year-old male BALB/c mice showed a lower resistance than 4.5-month-old mice to Histoplasma capsulatum infection. 4.5-month-old mice successfully resolved the infection when challenged with either a LD50 or LD100 for 1-month-old mice. A critical clinical course of experimental histoplasmosis was observed in 4.5-month-old syngeneic mice when spleen cells from 1-month-old BALB/c mice were transferred to them. Irradiated recipient mice, into which bone marrow and spleen cells were transferred, died when infected with the LD100 for 1-month-old mice. The same occurred with 4.5-month-old non-irradiated infected mice which received only spleen cells and with 1-month-old mice which were used as a control of infection. However, infected and non-transferred 4.5-month-old mice survived this dose. Thus, the adoptive transference of spleen cells from 1-month-old mice to 4.5-month-old mice suppressed the resistance of these adult mice to infection. Apparently, the transference of the suppressive state requires the presence of two cell populations, a non-adherent and an adherent and radioresistant cell present in the spleen of male 1-month-old mice.
A 65-year-old woman with disseminated histoplasmosis underwent resection of an atherosclerotic abdominal aortic aneurysm. Yeast forms of Histoplasma capsulatum were present in the aneurysm. Surgical resection and revascularization with a Dacron graft followed by systemic amphotericin B therapy and chronic ketoconazole suppressive therapy have resulted in a patient without symptoms 15 months postoperatively. It is important to be aware of the potential for artherosclerotic aortic aneurysm involvement by H. capsulatum.
A patient with oesophageal stenosis caused by Histoplasma granulomas is reported. He was treated with an initial combined course of intravenous amphotericin B and oral rifampicin. Complications included adrenal insufficiency, operative perforation of the oesophagus, amphotericin nephrotoxicity and tuberculosis. The histoplasmosis has not recurred for over 3 years.
From an observation of pulmonary histoplasmosis with Histoplasma capsulatum in a Haiti woman living in France for 2 years, the authors recall the mycological and epidemiological data of this fungus as well as the main clinical radiological and biological signs of the disease. Because of its tendancy to dissemination, histoplasmosis can have a bad prognosis. It is difficult to diagnose in our countries and facing a chronic pulmonary form, a diagnosis of tuberculosis is often thought of. But its possibility is to be envisaged in case of a journey in countries of endemia, and the disease should be confirmed by: -- several samplings to trace the fungus, bringing the mycological prove of the disease; -- serum uses; -- modalities and difficulties of the treatment by Amphotericin B are also recalled.
Report of a case of histoplasmosis observed in Zaïre with lymphatic, pulmonary and intestinal localizations. Histoplasma duboisii was abundant in the stools, sputum and lymphatic tissue. With no amphotericine B available, treatment first started with high dosage of miconazole which had no effect. Ketoconazole have been, then, tried, giving a clinical and biological improvement, but patient still in a very bad condition, died. Ketoconazole seems to have a rapid but not lasting effect, even with increased dosages.
Fungal endarteritis resulting from progressive disseminated histoplasmosis may cause arterial aneurysms, or lead to infection of pre-existing aneurysms. Three patients with Histoplasma capsulatum infections of abdominal aortic aneurysms are reported. All had previous disseminated histoplasmosis and atherosclerotic peripheral vascular disease. All were considered cured of systemic infection when their aneurysms were discovered. Atherosclerotic vascular lesions may become infected during the course of systemic fungal disease and may serve as a haven for viable organisms in patients whose dissemination recurs despite seemingly adequate antifungal therapy. In treating these patients, resection of all infected arterial tissue, revascularization through uninfected tissues, and long-term antimicrobial therapy are recommended.
Studies of adoptive transfer of resistance to Histoplasma capsulatum were performed with athymic nude (nu/nu) recipients and heterozygous (nu/+) donor mice. This model has the benefit of employing a recipient mouse (nu/nu) which cannot be immunized actively against H. capsulatum. Nu/nu mice were protected against H. capsulatum by whole spleen cells, fractioned T lymphocytes, and macrophages from immunized nu/+ donor mice. Similar cell populations from nonimmune nu/+ mice were not protective. Treatment with gold sodium thiomalate, an inhibitor of macrophage function, increased susceptibility to H. capsulatum in nu/+ and nu/nu mice. Adoptive transfer of immunity to H. capsulatum is multifactorial and depends on both T lymphocytes and macrophages.
A case of disseminated histoplasmosis with cutaneous lesions due to Histoplasma capsulatum is reported. The patient was a 22 years old congolese woman (Zaïre). The diagnosis was made on born narrow a few days only before she died. The cutaneous lesions were also positive for H. capsulatum.
Primitive detection of the Histoplasma duboisii accompanied with proteiform manifestations, is rare in the superior air ways. Its localisation at the larynx level is an exception and makes the very interest of our following reported observation. In front of this hard diagnostic, only the pathogenic agent visualisation gives evidence. Among serological techniques, immuno-fluorescence and E.L.I.S.A. are very helpful. Therapeutic possibilities have been improved by Miconazole which both associates efficiency and inocuity.
Previously reported cases of Histoplasma capsulatum infection of prosthetic heart valves have been first diagnosed at autopsy. A patient had an H capsulatum infection that was diagnosed by serologic means 1 1/2 years before involvement of the patient's prosthetic mitral valve was found at surgery. Numerous previous attempts to demonstrate organisms by culture and histologic study of bone marrow and liver biopsy specimens were unsuccessful. Various serologic tests were used in the diagnosis and evaluation of treatment of H capsulatum endocarditis. The management of this case was compared with 29 other previously reported cases of endocarditis caused by H capsulatum.
Histoplasma capsulatum is a pathogenic fungus found in discrete geographic locations throughout the world. The fungus invades the reticuloendothelial organs such as the spleen and liver of immunocompetent hosts where it is usually controlled. However, in individuals with immune deficiency, histoplasmosis is a severe and potentially fatal disease. Resistance to this infection is due primarily to a cellular immune response mediated by T cells and macrophages. Moreover, IFN-gamma is critical in activating macrophages to kill the organism. Herein we study the regulation of cytokine induction in mice infected with H. capsulatum and the effects of IL-12 in the course of infection. Mice infected with H. capsulatum and treated with neutralizing Abs to IFN-gamma, TNF-alpha, or IL-12 experienced accelerated mortality, indicating that endogenous production of these cytokines plays an important role in response to infection. In contrast, mice treated with IL-12 or a neutralizing Ab to IL-4 at the initiation of infection had substantially diminished mortality. Moreover, mice infected and treated with IL-12 show a two- to threefold increase in the amount of IFN-gamma following in vitro stimulation with specific H. capsulatum Ag compared with the control infected mice. The protective effect of IL-12 could be abrogated if a neutralizing Ab to IFN-gamma was given at the same time, demonstrating that the role of IL-12 in protection was mediated by IFN-gamma. Additionally, infected mice treated with IL-12 had a severalfold decrease in the colony counts of H. capsulatum in spleen cells after 5 days of infection as compared with control animals. Lastly, spleen cells from infected animals treated with IL-12 showed a striking decrease in their proliferative response to mitogen or H. capsulatum Ag. Responses could be restored by adding inhibitors of IFN-gamma or of nitric oxide to the in vitro cultures. The above observations suggest that IL-12 may be useful in immunologic intervention against this opportunistic pathogen.