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PubMed1985

Progressive disseminated penicilliosis caused by Penicillium marneffei. Report of eight cases and differentiation of the causative organism from Histoplasma capsulatum.

Eight patients with fatal penicilliosis caused by Penicillium marneffei are reported. All were natives of southern rural Guangxi, and none had a predisposing illness or evidence of altered immunity. The distinctive features of P. marneffei include proliferation of yeast-like cells within histiocytes, followed by the development of focal necrosis and, eventually, large abscesses. Outside the histiocytes, the fungi elongate, become slightly curved, and form septa. In vitro, P. marneffei produces a red pigment which diffuses into the culture medium. The differentiation between P. marneffei and Histoplasma capsulatum is described, and possible reservoirs for P. marneffei are discussed.

Adolescent↗
PubMed1996

Unilateral adrenal enlargement due to Histoplasma capsulatum.

Human infection with Histoplasma capsulatum runs the gamut from asymptomatic to disseminated disease. CT-directed fine-needle aspiration of bilaterally enlarged adrenal glands has been used in diagnosing serious infections with this ubiquitous organism. Three cases have previously been reported in which H. capsulatum infection caused unilateral adrenal enlargement; this enlargement was diagnosed post-mortem. We describe three patients with unilateral adrenal enlargement due to H. capsulatum whose conditions were diagnosed antemortem. We encourage clinicians to include infection with H. capsulatum as well as other granulomatous diseases and tumors in the differential diagnosis of unilateral adrenal enlargement.

Adrenal Glands↗
PubMed1994

Case report: fluconazole therapy in histoplasma mediastinal granuloma.

A 41-year-old man presented with night sweats, fever, and substernal chest pain approximately 5 months after being treated for community-acquired pneumonia. Chest radiograph revealed a mediastinal mass that was confirmed by computed tomography (CT) of the thorax. During surgery, enlarged paratracheal lymph nodes and a mass surrounding the right lower lobe bronchus and bronchus intermedius were found. Multiple biopsies from the mass showed that it consisted mainly of acellular fibrous tissue, but a small number of fungal forms typical of Histoplasma capsulatum were seen at the edged of the fibrotic reaction. The lymph nodes contained granulomatous inflammation and areas of necrosis, but no organisms were identified. The patient was treated with fluconazole for 6 weeks with resolution of symptoms. After completion of therapy, a follow-up CT scan of the thorax showed involution of the mediastinal mass. There has been no recurrence of symptoms or radiographic abnormalities for 24 months since cessation of fluconazole. This case illustrates isolated mediastinal involvement by histoplasmosis and suggests that therapy with fluconazole at this stage may prevent the often devastating late complications of mediastinal fibrosis.

Adult↗
PubMed1996

Histoplasma capsulatum necrotizing myofascitis of the upper extremity.

Necrotizing myofascial fungal infections of the upper extremity is a rare event even in immunocompromised hosts. We report the course of a renal transplant patient who developed extensive necrotizing myofascial infection of an upper extremity secondary to Histoplasma capsulatum. Initial, functional, upper limb salvage was achieved after aggressive surgical debridement and high doses of amphotericin B. The patient ultimately succumbed to systemic fungal sepsis. The etiology and treatment of these infections are discussed.

Amphotericin B↗
PubMed1980

Histoplasma capsulatum endocarditis requiring aortic valve replacement for aortic insufficiency.

A patient with valvular heart disease was found to have disseminated histoplasmosis and Histoplasma endocarditis. Refractory congestive heart failure secondary to severe progressive aortic insufficiency and the presence of a large valvular vegetation necessitated aortic valve replacement, which was timed to coincide with the midpoint of a course of therapy with 4 gm of amphotericin B. The patient has done well since the completion of treatment.

Aortic Valve↗
PubMed1999

Potential association between calcified thoracic lymphadenopathy due to previous Histoplasma capsulatum infection and pulmonary Mycobacterium avium complex disease.

BACKGROUND: Among patients with pulmonary disease due to Mycobacterium avium complex (MAC) seen recently at our center, a substantial number have had extensive calcified mediastinal, hilar, and peribronchial lymphadenopathy, a finding historically inconsistent with pulmonary MAC disease. METHOD: We retrospectively studied the frequency of calcified lymphadenopathy in the chest and prevalence of known risk factors for MAC infection in 79 patients with pulmonary MAC disease who were referred to our hospital over a 1-year period. RESULTS: Calcified intrathoracic adenopathy was present in 25 of the 79 patients (32%). Residential histories revealed that 20 of the 25 patients (80%) with such calcified chest adenopathy reported living for substantial periods in the regions indigenous for Histoplasma capsulatum. In contrast, the residences of patients without calcified chest adenopathy were more evenly distributed throughout the country. Nineteen of these 25 patients (76%) with calcified chest adenopathy had no known predisposing risk factor for the infection; in contrast, the proportion of patients with no calcified adenopathy who also had no identifiable classic risk factor tended to be lower (32/54, 59%). CONCLUSION: In this retrospective study, we observed that (1) a large number of patients with pulmonary MAC disease had no identifiable risk factor, (2) calcified chest adenopathy was present in one third of the patients, (3) the residential history of those with calcified adenopathy mirrored the endemic region of histoplasmosis, and, (4) conversely, those patients with pulmonary MAC who lived outside the histoplasmosis belt had no such adenopathy. Thus, we hypothesize that previous fungal infection may predispose the lungs of certain patients to subsequent invasion by MAC, presumably by airway distortion and/or parenchymal damage.

Aged↗
PubMedDate not supplied

Histoplasma capsulatum osteomyelitis in the cat.

Seven cats with osseous lesions as the primary manifestation of disseminated Histoplasma capsulatum infection were evaluated. The major clinical signs in these cats were related to the bony lesions and included lameness, bone pain, and soft tissue swelling of limbs and joints. Other clinical and pathologic findings were similar to previously reported forms of disseminated histoplasmosis in the cat. The radiographic appearance of the lesions was predominantly osteolytic; periosteal and endosteal new bone production was present in some cases. Infection occurred primarily in bones of the appendicular skeleton with a predilection for sites below the elbow and stifle joints.

Animals↗
PubMed1970

Uptake of Cystine by the Yeast Phase of Histoplasma capsulatum.

This report deals with factors affecting the uptake of cystine by the yeast phase of Histoplasma capsulatum. The kinetics of uptake showed a saturation at 70 muM and an average K(m) value of 3 x 10(-5)m. The optimal pH and temperature for transport of cystine were 6.5 and 37 C, respectively. The energy of activation was 14.1 kcal/mole, and the temperature coefficient value was 2.1. A requirement for energy supplied by metabolic activity was demonstrated by the inhibition of incorporation of the amino acid by cells preincubated with either 2,4-dinitrophenol or sodium azide. Although uptake was not inhibited by any single amino acid, a combination of amino acids did cause a decrease in uptake. Thus, the data show that the uptake of cystine by yeast cells of H. capsulatum has the characteristics of a system of transport that requires the expenditure of energy by the cells.

Journal Article↗
PubMed1970

Incorporation of Cystine by Yeast Cells of Histoplasma capsulatum.

This report deals with the incorporation of cystine into macromolecules by yeast cells of Histoplasma capsulatum. The results show that at saturating concentrations of cystine in a rich medium, total uptake of the cystine occurs in 10 hr, whereas the amount of label in the cold trichloroacetic acid-soluble material reaches a maximum at 3 to 4 hr and remains at this value. The amount of label in the cold acid-insoluble material accumulates linearly for 4 to 5 hr and reaches a plateau at 7 to 9 hr. A chemical fractionation of labeled cells shows that 25% of the cystine taken up remains as low-molecular-weight components, of which cystine comprises 60 to 75%. Approximately 30% of the total label incorporated is ethanol-soluble, and polyacrylamide gel electrophoresis of this material shows a rather uniform incorporation of the amino acid into many proteins. The combined hot KOH fractions account for 40% of the total label incorporated. The amount of hot KOH-insoluble material almost doubles in a 10-hr pulse, whereas there is an increase in hot KOH-soluble material. Hence, the greatest amount of label from cells pulsed with (14)C-cystine is recovered from cell wall material.

Journal Article↗
PubMed1978

Histoplasma capsulatum infection in nude mice.

Congenitally athymic nude (nu/nu) mice, when injected intraperitoneally with Histoplasma capsulatum, developed a rapidly fatal disseminated infection characterized by heavy parasitization of reticuloendothelial tissues. In contrast, their heterozygous (nu/X) littermates, which possessed a functioning thymus, developed only a low-grade infection which was apparently self-limited and rarely fatal. Transplantation of thymic tissue into nu/nu mice diminished greatly the severity of infection and reduced mortality by about 50%. These studies emphasize the importance of cell-mediated immunity in host defense against histoplasmosis and suggest that the nude mouse may be a valuable model for the study of this chronic intracellular infection.

Animals↗
PubMed1992

Alterations in murine macrophage arachidonic acid metabolism following ingestion of nonviable Histoplasma capsulatum.

The effect of ingestion of heat-killed Histoplasma capsulatum yeast cells on the metabolism of arachidonic acid (20:4) to prostenoids and leukotrienes was examined in murine peritoneal macrophages (M phi s). H. capsulatum-containing M phi s exhibited a metabolite profile similar to that of zymosan-challenged phagocytes; however, there were differences with respect to the relative and total amounts of products produced. While proteose peptone-elicited M phi s exposed to H. capsulatum released quantitatively less prostaglandin E2 (PGE2) and leukotriene C4 than zymosan-treated M phi s, they metabolized a greater percentage of total product to prostenoids. In addition, whereas in vitro priming with gamma interferon increased both the PGE2 and leukotriene C4 contents of zymosan-stimulated M phi supernatants, similarly primed M phi s challenged with H. capsulatum selectively increased only PGE2 production. The immunosuppressive effect of a relative excess of prostenoids in H. capsulatum-containing M phi s may contribute to the overall disturbance in cell-mediated immunity characteristic of disseminated histoplasmosis.

Analysis of Variance↗
PubMed1997

Interleukin-12 modulates the protective immune response in SCID mice infected with Histoplasma capsulatum.

Infection with Histoplasma capsulatum results in a subclinical infection in immunocompetent hosts due to an effective cellular immune response. By contrast, immunodeficient individuals can have a severe disseminated and potentially fatal disease. In a previous study, it was demonstrated that normal mice infected intravenously with H. capsulatum and treated with interleukin-12 (IL-12) at the time of infection were protected from a fatal outcome. In this study, we examined the immunomodulatory effects of IL-12 on disseminated histoplasmosis in immunodeficient SCID mice. SCID mice infected with H. capsulatum and treated with IL-12 showed an increase in survival and a reduction in the colony counts of H. capsulatum in internal organs at 14 days after infection. The protective effect of IL-12 was abrogated if animals were also treated with a neutralizing antibody to gamma interferon (IFN-gamma). IL-12 treatment also resulted in an increase in mRNA expression and protein production for IFN-gamma, tumor necrosis factor alpha (TNF-alpha), and nitric oxide from spleen cells. When IL-12 was combined with amphotericin B (AmB) treatment, there was a significant increase in survival compared with either modality alone. Moreover, combined treatment resulted in an increase in both IFN-gamma and TNF-alpha production, as well as in a substantial reduction in H. capsulatum burden at 35 and 90 days postinfection. This study demonstrates that IL-12 modulates the protective immune response to histoplasmosis in SCID mice and also suggests that IL-12 in combination with AmB may be useful as a treatment for H. capsulatum in immunodeficient hosts.

Amphotericin B↗
PubMed1997

Intrapulmonary response to Histoplasma capsulatum in gamma interferon knockout mice.

We examined the immunobiological responses to Histoplasma capsulatum in lungs of gamma interferon (IFN-gamma) knockout mice (GKO mice). Naive GKO mice succumbed by day 9 to intranasal challenge with 2.5 x 10(6) yeasts, whereas all wild-type (WT) mice survived for 45 days. Compared to lungs of WT mice, the lungs of acutely infected GKO mice exhibited dramatically elevated numbers of CFU in lungs and significantly higher levels of tumor necrosis factor alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) but not interleukin-12 (IL-12) or IL-4. To determine if IFN-gamma is necessary in reexposure histoplasmosis, GKO and WT mice were inoculated with 10(4) yeasts intranasally and given amphotericin B for 3 weeks. Six weeks later, mice were rechallenged with 2.5 x 10(6) yeasts. All GKO mice died by day 6, whereas all WT mice survived for 45 days. Lungs of GKO mice contained substantially elevated numbers of CFU and higher TNF-alpha and GM-CSF levels but not IL-12 or IL-4. Thus, IFN-gamma is requisite for control of pulmonary histoplasmosis in naive and reexposed mice.

Animals↗
PubMed2000

Interleukin-12 neutralization alters lung inflammation and leukocyte expression of CD80, CD86, and major histocompatibility complex class II in mice infected with Histoplasma capsulatum.

Histoplasma capsulatum induces a cell-mediated immune response in lungs and lymphoid organs of mammals. Resolution of primary infection in mice depends on interleukin-12 (IL-12), since neutralization of this monokine increases susceptibility to infection. The present study was designed to determine if blockade of IL-12 disrupts the protective immune response by altering the influx of lineage-specific cells into infected lungs and the numbers of cells expressing CD80, CD86, CD119, and major histocompatibility complex class II (MHC II) molecules. In mice given anti-IL-12, there was a 2.5-fold decrease in total numbers of T cells on days 3 to 10 of infection and a 4-fold increase in Mac-1/Gr-1(+) cells on days 7 and 10 compared to infected controls. CD80(+) lung cells from anti-IL-12-treated mice were 2- to 3-fold greater than those from controls on days 7 and 10, whereas the total numbers of CD86(+) cells were 2- to 3-fold less and MHC II(+) cells were 1.5- to 2-fold less on days 3 and 5. Cells expressing CD119 were reduced 1.5-fold on day 5. Treatment with monoclonal antibodies (MAb) to CD80, CD86, or both reduced the fungal burden slightly compared to that in rat immunoglobulin G-treated controls, whereas after IL-12 neutralization, blocking of CD80 reduced the tissue burden by 2. 5-fold and this correlated with a decrease in IL-4. Regardless, mortality was not altered by treatment with MAb to CD80 or CD86. We conclude that (i) IL-12 neutralization alters the nature of the inflammatory response in lungs and the expression of CD80 and CD86 on lineage-specific cells, (ii) the immune response during infection with H. capsulatum is controlled via mechanisms independent of the CD80 and CD86 costimulatory pathways, and (iii) decreased expression of CD86 and MHC II may modulate generation of optimal protective immunity.

Animals↗
PubMed2002

Discordance between T-cell receptor expression and effector function in mice infected with Histoplasma capsulatum.

V beta 10(+) and V beta 14(+) T cells were selectively increased 7 to 14 days following infection in the lungs of naive mice infected with Histoplasma capsulatum. Following secondary challenge of immune mice, V beta 1(+) and V beta 8.1(+) cells were sporadically increased. Elimination of V beta 10(+) and V beta 14(+) cells from naive mice did not alter the course of infection over a period of 21 days. Thus, overexpression of V beta families does not necessarily signify a key role in host defense.

Animals↗
PubMed2003

Overexpression of interleukin-4 in lungs of mice impairs elimination of Histoplasma capsulatum.

Protection against the pathogenic fungus Histoplasma capsulatum requires Th1 cytokines. Since interleukin-4 (IL-4) can inhibit both Th1 cytokine production and activity, we examined the effects of overproduction of IL-4 in the lung on the course of pulmonary histoplasmosis. IL-4 lung transgenic mice manifested a higher fungal burden in their lungs, but not spleens, compared to wild-type infected controls. Despite the higher burden, the transgenic animals were ultimately capable of controlling infection. The adverse effects of IL-4 on H. capsulatum elimination were not observed during the early phase of infection (days 1 to 3) but were maximal at day 7 postinfection, prior to the induction of cell-mediated immunity. Analysis of total body and lung cytokine levels revealed that gamma interferon and tumor necrosis factor alpha production were not inhibited in the presence of excess IL-4. Our results with transgenic mice were supported by additional in vivo studies in which allergen induction of pulmonary IL-4 was associated with delayed clearance of H. capsulatum yeast and increased fungal burden. These findings demonstrate that excess production of endogenous IL-4 modulates protective immunity to H. capsulatum by delaying clearance of the organism but does not prevent the generation of a Th1 response that ultimately controls infection.

Animals↗
PubMed1969

Effect of antilymphocyte serum on animals experimentally infected with Histoplasma capsulatum or Cryptococcus neoformans.

The anti-mouse and anti-guinea pig antilymphocyte sera (ALS) prepared for this study were shown to contain cytoxic and leucoagglutinating antibodies, and were capable of producing severe lymphopenia in these animals. Guinea pigs treated weekly with ALS were more susceptible to development of fatal infection when inoculated with Histoplasma capsulatum. No fatalities occurred in guinea pigs infected with equal doses of H. capsulatum but treated with normal rabbit serum (NRS) or saline. The time necessary to reach 50% fatality in mice infected with Cryptococcus neoformans was greatly reduced by pretreatment with ALS in comparison with infected controls treated with NRS or saline. When low dosages were used (0.1 ld(50)), the effect was even more pronounced. Spleen homogenates from mice infected with equal dosages of H. capsulatum and treated with ALS or NRS were cultured. More than 150 times as many organisms were present in the spleens of the ALS-treated group. Similar results were obtained from culturing the lungs and liver. Delayed hypersensitive skin reactions were radically decreased or abrogated in H. capsulatum-infected guinea pigs inoculated intraperitoneally with ALS 12 hr before skin testing with histoplasmin. When ALS was given weekly, the influence on skin reactivity was less notable. Given intradermally, ALS was shown to inhibit the delayed reaction to histoplasmin within a radius of 40 mm.

Animals↗
PubMed1997

Histoplasma capsulatum sinusitis.

Sinusitis is commonly reported in patients with AIDS. In addition to the usual bacterial pathogens isolated from immunocompetent patients, sinusitis in patients with AIDS may be caused by a variety of unusual bacteria, viruses, fungi, parasites, and mycobacteria. Histoplasma capsulatum has not typically been associated with sinusitis in either group of patients. We report a case of sinusitis caused by H. capsulatum in a patient with AIDS.

Acquired Immunodeficiency Syndrome↗