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PubMed1967

Agar-gel precipitin-inhibition technique for histoplasmosis antibody determinations.

The agar-gel precipitin-inhibition technique has been modified to detect antibodies of Histoplasma capsulatum in sera from human clinical cases and experimental animals infected with this organism. By use of this modified technique, the histoplasmosis can be detected more consistently and reliably than with the direct agar-gel diffusion test, and titers are comparable to those attained by the complement-fixation serological technique.

Animals↗
PubMed1979

Immunoregulatory responses in experimental disseminated histoplasmosis: lymphoid organ histopathology and serological studies.

To study immunoregulatory mechanisms in systemic histoplasmosis, a highly reproducible model of infection was established in C3H/Anf mice. Intravenous inoculation of 6- to 8-week-old mice with from 5 x 10(5) to 10 x 10(5) cells of yeast-phase Histoplasma capsulatum strain G-217B produced disseminated infection that resolved over an 8-week period without therapeutic intervention. Serological studies demonstrated complement-fixing antibody production to yeast- and mycelial-phase antigens of H. capsulatum. Complement-fixing antibody to the former was detected at week 1, and it peaked at week 3 and declined thereafter. Complement-fixing antibody to mycelial-phase antigen(s) appeared later (week 3) and did not peak until week 18. Grossly, the spleens of infected mice were enlarged from three to four times normal size during peak infection, whereas the thymuses were markedly involuted. Conversely, at week 8 the average spleen size was considerably smaller and the thymic mass was increased relative to the mass at week 3. Histopathologically, the paracortical regions of lymph nodes and the white pulp (periarteriolar lymphocyte sheaths) and marginal zones of the spleen were heavily infiltrated by granulomata at week 1. By week 8, the infiltrates in these areas had largely resolved. Thymocytes were severely depleted from the cortical lobules of the thymus at week 1; however, thymic cellularity was restored by week 8. These reciprocal changes in cellularity of the thymus and spleen during active infection may be of importance with reference to the disturbances of immunoregulation that we have observed in Histoplasma-infected mice.

Animals↗
PubMed1979

Immunoregulatory responses in experimental disseminated histoplasmosis: depression of T-cell-dependent and T-effectory responses by activation of splenic suppressor cells.

The cellular immune responses of mice with disseminated histoplasmosis are markedly diminished in association with the generation of potent immunosuppressor activity by spleen cells. The zenith of suppressor activity was observed during most active infection, from 1 to 3 weeks after inoculation. During this time there was: (i) depression of the delayed-type hypersensitivity response to sheep erythrocytes and histoplasmin, (ii) impairment of concanavalin A- and histoplasmin-induced blastogenic transformations by splenocytes in vitro, (iii) depressed cytotoxic activity of spleen cells from infected mice, and (iv) marked suppression by splenocytes from infected mice of the primary antibody response to sheep erythrocytes by normal spleen cell cultures. With resolution of the infection by week 8, there was a shift of immunoregulatory function from dominant suppressor activity to expression of helper activity. At this time, delayed-type hypersensitivity responses to the above antigens were vigorous; furthermore, the cytotoxic activity and plaque-forming cell response of splenocytes from 8-week-infected mice were equal to or greater than normal control values. The shift in the immunoregulatory response from a suppressor to a helper mode indicated that the net amount of help or suppression measured at any given time during infection represented the algebraic sum of both helper and suppressor activities mediated by different populations or subpopulations of cells within the splenic microenvironment of infected mice.

Animals↗
PubMed1980

Immunoglobulin E in histoplasmosis.

Immunoglobulin M, G, A, and E serum levels were quantitated in 20 patients with active histoplasmosis (group I), 24 healthy subjects who were skin test positive to histoplasmin (group II), and 47 healthy persons who were skin test negative to histoplasmin (group III). The results established that patients with this disease have increased immunoglobulin G (P less than 0.05), immunoglobulin A (P less than 0.001), and immunoglobulin E (P less than 0.01) serum levels when compared with the 71 healthy subjects in groups II and III.

Acute Disease↗
PubMed1983

Protective effect of poly-2-vinylpyridine-N-oxide on susceptibility of silica-treated mice to experimental histoplasmosis.

We have studied the ability of poly-2-vinylpyridine-N-oxide (PVNO), a lysosomal stabilizing agent, to abrogate the cytotoxic effects of silica on macrophages. Male C3H/HeN mice were pretreated with PVNO and inoculated intravenously with silica particles. At 24 h after silica injection, silica-treated and -untreated mice were challenged intravenously with varying doses of live yeast cells of Histoplasma capsulatum. All mice receiving silica died when challenged with 5 X 10(5) yeast cells of Histoplasma sp. compared with no deaths in PVNO-pretreated animals and 10% mortality in controls not receiving PVNO or silica. When animals were given 2.5 X 10(5) yeast cells (a sublethal dose), the protective effect of PVNO was seen by a reduction in splenomegaly and viable Histoplasma sp. present in the spleen. Furthermore, PVNO alone showed a significant protective effect (P less than 0.05) against a lethal challenge with Histoplasma sp. Prior treatment with PVNO also protected mouse peritoneal macrophages from the cytotoxic effects of silica particles in vitro. These results indicate that PVNO abrogates the cytotoxicity of silica particles on macrophages and also increases the resistance of mice to histoplasmosis.

Animals↗
PubMed1985

Macrophage-related fibrinolysis in experimental disseminated histoplasmosis.

A model of disseminated histoplasmosis in CBA/J mice was developed. Cultures of Histoplasma capsulatum from the spleens of infected mice suggested almost complete clearance of fungi by week 3. The adherent spleen cells from infected mice showed a 2- to 20-fold increase in fibrinolysis. The increase in activity was maximal around 1 to 2 weeks and disappeared after week 3 of infection, and this paralleled the progressively decreasing number of culturable fungi from the spleen. In vitro coculture of infected spleen cells or nylon wool-purified immune T cells and proteose peptone-induced macrophages resulted in increased fibrinolysis. Peritoneal exudate cells from infected mice also showed increased fibrinolysis. The addition of soluble antigen to an in vitro culture system resulted not only in an increase in fibrinolytic activity of peritoneal exudate cells derived from infected mice but also of proteose peptone-induced macrophages. These observations suggest that spleen and peritoneal macrophages from H. capsulatum-infected mice exhibit increased fibrinolysis which in turn is indicative of macrophage activation. The mechanism of activation occurs as a result of immunologically specific T cell-macrophage interaction and by the action of histoplasma products on the macrophages. The significance of these findings and the role of the plasminogen activator assay in studies of disseminated fungal infection are discussed.

Animals↗
PubMed1991

Infection of P388D1 macrophages and respiratory epithelial cells by Histoplasma capsulatum: selection of avirulent variants and their potential role in persistent histoplasmosis.

We evaluated P388D1 macrophagelike cells as model host cells for studying the intracellular survival and strain-specific virulence of Histoplasma capsulatum. Previously characterized strains which were virulent for mice destroyed monolayers of these cells within a few days. In contrast, related avirulent "smooth" variants failed to do so even after 20 days, although they persisted within P388D1 cells for at least 7 days. On the basis of this observation, we developed a quantitative radiolabel assay to use as an initial screen for virulence. Another cell type lining the respiratory tract was then examined as a potential host for H. capsulatum. Hamster trachea epithelial (HTE) cells readily internalized a variety of strains lacking alpha-(1,3)-glucan in their cell walls; however, the tracheal cells were only rarely infected by organisms possessing this polysaccharide. We subsequently inoculated HTE cells with alpha-(1,3)-glucan-positive strains and enriched for the few yeasts infecting these cells. The progeny resembled smooth variants in terms of colony morphology, the absence of alpha-(1,3)-glucan in their cell walls, and their inability to kill macrophages. Did the HTE cells select for these variant yeasts from the parent inoculum or instigate a change from the parental phenotype? Following a 3-h uptake period, only 2% of the ingested yeasts lacked alpha-(1,3)-glucan. One day later, nearly half of the intracellular organisms lacked this polymer. This rapid conversion of a large proportion of the inoculum suggests some type of environmentally triggered change, perhaps analogous to phase variation seen in many other pathogens. Infection of epithelial cells or some other nonprofessional phagocyte during natural histoplasmosis might give rise to similar variants, thus establishing a reservoir of organisms capable of causing chronic or latent infections.

Animals↗
PubMed1993

Local immunity in lung-associated lymph nodes in a murine model of pulmonary histoplasmosis.

Local immunity against acute pulmonary histoplasmosis was studied in the lung-associated lymph nodes of normal nonimmune mice infected intratracheally with live Histoplasma capsulatum yeasts. The phenotypes and distribution of cells in lung-associated lymph nodes and spleens were determined by flow cytometry. In addition, the immune responsiveness of these cells was evaluated by in vitro blastogenesis. Anti-H. capsulatum antibodies in serum and H. capsulatum antigen in tissue were measured by immunoassays. Cellular immune responses were greater in the lymph nodes than in the spleens. In lymph nodes 7 days after infection, a marked increase in the number of B lymphocytes caused the percentage to rise to 43%, compared with 26% in controls, and it remained elevated throughout the course of infection. A CD3+ cell that did not express CD4 or CD8 increased in number until it constituted 21% of lymph node cells, compared with 5% in controls, by day 14. The numbers of CD4+ and CD8+ T lymphocytes were modestly increased from days 7 to 35, but their percentages dropped because of the greater numbers of B lymphocytes and CD3+4-8- cells. Macrophages consistently constituted 2 to 3% of lymph node cells during the study. In spleens 7 days after infection, the percentage of macrophages in infected mice rose to 21%, compared with 9% in controls, but the total spleen cell number did not increase until day 14, when all cell subsets were nearly double in number. The in vitro blastogenic response of lymph node cells to H. capsulatum peaked at day 7, but spleen cell response was minimal during the course of infection. Histoplasma-specific serum immunoglobulin G antibodies reached peak levels by day 21 and remained high to the end of the study. In contrast, levels of antigen-specific immunoglobulin M antibodies were very low. These data suggest that antigen-specific immune responses occur in lung-associated lymph nodes and that this draining lymph node response may be an important component in host defense against Histoplasma lung infection.

Acute Disease↗
PubMed1995

Vaccination with recombinant heat shock protein 60 from Histoplasma capsulatum protects mice against pulmonary histoplasmosis.

HIS-62 is a glycoprotein that has been isolated from the cell wall and cell membrane fraction of the pathogenic fungus Histoplasma capsulatum. It is a target of the cellular immune response to this fungus, and it protects mice against a lethal intravenous inoculum of H. capsulatum yeast cells. In this study, we cloned the gene encoding this antigen to reveal its biological nature and studied the immunological activity of recombinant antigen. The amino acid sequences of the NH2 terminus and internal peptides were obtained by Edman degradation. Degenerate oligonucleotides were used to isolate a gene fragment of HIS-62 by PCR. One 680-bp segment that corresponded to the known peptide sequence was amplified from H. capsulatum DNA. This DNA was used to screen a genomic library, and the full-length gene was isolated and sequenced. The deduced amino acid sequence of the gene demonstrated approximately 70 and approximately 50% identity to heat shock protein 60 (hsp 60) from Saccharomyces cerevisiae and hsp 60 from Escherichia coli, respectively. A cDNA was synthesized by reverse transcription PCR and was expressed in E. coli. Recombinant protein reacted with a monospecific polyclonal rabbit antiserum raised against native HIS-62, with monoclonal HIS-62-reactive T cells, and with splenocytes from mice immunized with viable yeast cells. Moreover, vaccination with the recombinant protein conferred protection in mice against a lethal intranasal inoculation with yeast cells. Thus, HIS-62 is a member of the hsp 60 family, and the recombinant hsp 60 is protective against pulmonary histoplasmosis in mice.

Amino Acid Sequence↗
PubMed2001

Protective efficacy of H antigen from Histoplasma capsulatum in a murine model of pulmonary histoplasmosis.

We previously reported that immunization with H antigen from Histoplasma capsulatum did not protect mice against an intravenous challenge with yeasts. Here, we investigated the utility of H antigen to protect mice in a model of pulmonary histoplasmosis. Mice immunized with H antigen and challenged intranasally 4 weeks postvaccination were protected against sublethal and lethal challenges with H. capsulatum yeasts. If the challenge was performed 3 months after vaccination, there was a reduction in fungal burden following sublethal challenge and a modest delay in mortality in mice given a lethal inoculum. Vaccination was associated with production of gamma interferon, granulocyte-macrophage colony-stimulating factor, interleukin-4, and interleukin-10 by splenocytes. Vaccination with H antigen was not accompanied by a major expansion of CD4(+) or CD8(+) cells in spleens of mice. These results demonstrate that H antigen may be useful as a protective immunogen against pulmonary exposure to H. capsulatum.

Animals↗
PubMed1967

Effects of a single histoplasmin skin test on the serological diagnosis of histoplasmosis.

Numerous reports have indicated that a single histoplasmin skin test may stimulate humoral antibodies to Histoplasma capsulatum antigens in histoplasmin-hypersensitive individuals. Although these investigations concur that antibody elevations are evoked, they vary in the reported degree of incidence and response induced, and they cast doubt on the interpretation of serological tests in the diagnosis of histoplasmosis. Histoplasmin-hypersensitive subjects (114) were bled prior to administration of the skin test, 2 days later, at the time this test was read, and 15 and 30 days after testing. No significant antibody titers were observed at 2 days. At 15- and 30-day intervals, only 17 (15%) of the subjects demonstrated circulating antibodies. All 17 showed agar gel bands; 5 demonstrated no complement-fixation (CF) titers, 10 produced CF antibodies ranging from 1:8 to 1:16, and 2 demonstrated titers of 1:32. The data suggest that skin testing does not interfere significantly with antibody levels in sera drawn approximately 2 days after administration of antigen. However, since titers as high as 1:32 were obtained at later intervals, such reactions should be evaluated cautiously and only after consideration of clinical findings.

Antibody Formation↗
PubMed1975

Naturally occurring histoplasmosis in the chinchilla (Chinchilla laniger).

Histoplasmosis was diagnosed histopathologically in a female chinchilla. This animal had originated from a commercial chinchilla ranch in central Missouri. Seventeen of 130 animals in the colony had died within a month's period with a respiratory illness. This animal had a history of fur chewing, but this was not true of all the other animals that had died. Histoplasma capsulatum was cultured from timothy hay used for food.

Animal Feed↗
PubMed1991

43-kilodalton glycoprotein from Paracoccidioides brasiliensis: immunochemical reactions with sera from patients with paracoccidioidomycosis, histoplasmosis, or Jorge Lobo's disease.

Sera from patients with paracoccidioidomycosis (PCM), histoplasmosis (HP), or Jorge Lobo's disease (JL) were titrated against purified gp43 from Paracoccidioides brasiliensis by using both enzyme-linked immunosorbent assay (ELISA) and immunoprecipitation (IPP) reactions with 125I-labeled antigens. In IPP, PCM sera and other sera could be distinguished on the basis of serum titers, whereas in ELISA, 53% of the HP sera and 29% of the JL sera reacted similarly to the PCM sera. To investigate the possible role of the carbohydrate epitopes in these reactions, we compared the reactivities of sera from several patients with native and deglycosylated gp43. Competition experiments were carried out with monosaccharides as inhibitors. The results suggest that greater than 85% of the reactions of the PCM sera with gp43 involved peptide epitopes. Cross-reactions with HP and JL sera in ELISA were predominantly attributed to periodate-sensitive carbohydrate epitopes containing galactosyl residues. HP and JL sera which reacted strongly with gp43 in ELISA were only weakly reactive or did not react in IPP with labeled antigens in solution. Moreover, ELISA reactions could be significantly inhibited either by monosaccharides or by periodate treatment. Apparently, carbohydrate epitopes in gp43 are more accessible to the antibodies when the molecule is bound to a plastic substrate than when it is in solution. Structural changes in the gp43 antigen arising by N deglycosylation abolish reactivity with PCM sera and support the existence of conformational peptide epitopes.

Blastomycosis↗
PubMed1976

Blocking effect of rheumatoid factor and cold agglutinins on complement fixation tests for histoplasmosis.

The blocking effect of rheumatoid factor (RF) and cold agglutinins (CA) on the detection of complement-fixing (CF) antibodies for Histoplasma capsulatum using a mycelial (histoplasmin) and a yeast antigen was studied. Sera from 213 patients serologically positive for histoplasmosis were screened for the presence of RF or CA. CF antibodies to H. capsulatum in sera containing RF or CA were studied before and after removal of these factors (RF and CA) by treatment with dithiothreitol. Results suggest that RF or CA may interfere with the CF reaction to the yeast antigen of H. capsulatum but not to the mycelial antigen (histoplasmin).

Agglutinins↗
PubMed2005

Molecular evidence of recurrent histoplasmosis with 9-year latency in a patient with Addison's disease.

We present a case of fatal histoplasmosis in a patient with Addison's disease and long-term use of corticosteroid. The patient acquired Histoplasma capsulatum in China and initially presented with a laryngeal mass. He developed fulminant pneumonia and respiratory failure 9 years later. Nucleotide sequences of internal transcribed spacer regions of rRNA genes of the H. capsulatum isolate recovered from biopsied lung tissue and of the extracted fungal DNA from the laryngeal lesion were identical, indicating the recurrent nature of infection.

Addison Disease↗
PubMed1975

Acute presumed histoplasmosis of the optic nerve head.

A 38-year-old man from the Ohio Valley area presented to the Ophthalmology Cinic at a west coast hospital (USA) because of sudden loss of the right inferior temporal visual field after severe right frontal headache of several hours' duration. During the following months, diffuse peripapillary atrophy and peripheral punched-out lesions developed. When he had been seen initially, the fundus of the left eye had also revealed extensive, diffuse, peripapillary atrophy and scarring. All laboratory tests were normal except a histoplasmin intradermal skin test. The clinical appearance of both eyes 8 months after the acute episode in the right eye supports the diagnosis of presumed ocular histoplasmosis.

Acute Disease↗
PubMed1989

Presumed ocular histoplasmosis syndrome and linear streak lesions.

Five cases of subretinal neovascular membranes in the macula associated with punched out chorioretinal scars and linear streaks were seen in five Dutch patients. Clinically the fundus lesions are consistent with those of presumed ocular histoplasmosis syndrome (POHS) seen in the United States of America. Cutaneous serological testing for histoplasmin reactivity was negative in the three patients tested. Of special interest is the presence of linear streaks in association with POHS. They have not been previously described in patients from Europe with this syndrome.

Adult↗
PubMed1977

Disseminated histoplasmosis in an English patient with diabetes mellitus.

Histoplasma capsulatum is not endemic in Britain. We report a case of disseminated histoplasmosis in an English man who had not ventured out of northern Europe for 30 years. The disease presented as painful mouth ulcers and hepatosplenomegaly six months after he had developed maturity-onset diabetes. The origin of the infecting fungus may have been from within the United Kingdom or alternatively it may have existed as an intraoral saprophyte for over 30 years.

Diabetes Complications↗