Histoplasmosis

Schwarz, Jan

doi:10.1007/978-3-662-12027-9_4

Cited by 5 publications

(8 citation statements)

References 225 publications

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“…Important to the understanding of clinical disease due to H. capsulatum is the realization that most patients infected with this organism experience asymptomatic hematogenous dissemination throughout the reticuloendothelial system via parasitized macrophages (50,113). When T lymphocytes develop immunity to H. capsulatum antigens and activate macrophages to kill the organism, the host is able to control the infection (23,91,163).…”

Section: Disseminated Histoplasmosismentioning

confidence: 99%

“…The diagnosis is generally not entertained until culture of surgical material or synovial fluid yields H. capsulatum. Sites such as gall bladder, breast, thymus, and thyroid gland are rarely infected and usually discovered only at autopsy (42,113).…”

Section: Disseminated Histoplasmosismentioning

confidence: 99%

“…Finding the distinctive 2-to 4-m, oval, narrow-based budding yeasts allows a tentative diagnosis of histoplasmosis (98,113). Other organisms can mimic the appearance of H. capsulatum in tissues, but generally, the clinical picture will separate histoplasmosis from the others.…”

Section: Histopathologymentioning

confidence: 99%

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Histoplasmosis: a Clinical and Laboratory Update

2007

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SUMMARY Infection with Histoplasma capsulatum occurs commonly in areas in the Midwestern United States and Central America, but symptomatic disease requiring medical care is manifest in very few patients. The extent of disease depends on the number of conidia inhaled and the function of the host's cellular immune system. Pulmonary infection is the primary manifestation of histoplasmosis, varying from mild pneumonitis to severe acute respiratory distress syndrome. In those with emphysema, a chronic progressive form of histoplasmosis can ensue. Dissemination of H. capsulatum within macrophages is common and becomes symptomatic primarily in patients with defects in cellular immunity. The spectrum of disseminated infection includes acute, severe, life-threatening sepsis and chronic, slowly progressive infection. Diagnostic accuracy has improved greatly with the use of an assay for Histoplasma antigen in the urine; serology remains useful for certain forms of histoplasmosis, and culture is the ultimate confirming diagnostic test. Classically, histoplasmosis has been treated with long courses of amphotericin B. Today, amphotericin B is rarely used except for severe infection and then only for a few weeks, followed by azole therapy. Itraconazole is the azole of choice following initial amphotericin B treatment and for primary treatment of mild to moderate histoplasmosis.

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Section: Disseminated Histoplasmosismentioning

confidence: 99%

Section: Disseminated Histoplasmosismentioning

confidence: 99%

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Histoplasmosis: a Clinical and Laboratory Update

2007

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“…This notion was supported by the report of Caruso et al (7), who cloned the hsp70 gene from H. capsulatum and studied its expression in strains that differed in virulence and sensitivity to heat, and it was confirmed by the report of Shearer et al (35), who observed the synthesis of new proteins soon after the temperature shift from 25°C to between 34 and 41°C.…”

mentioning

confidence: 71%

“…The mycelial-to-yeast conversion is of particular interest since it is triggered by an increase in the temperature of incubation and conversion to the yeast morphology is necessary for virulence. In fact, an important pathological feature of disease is that only yeasts are found in infected tissues (25,34). Therefore, the unique ability of dimorphic fungal pathogens to change shape in order to colonize, adapt to, and survive in host tissues is a process that parallels and may be intimately involved with this developmentally regulated morphological process (24).…”

mentioning

confidence: 99%

The intron-containing hsp82 gene of the dimorphic pathogenic fungus Histoplasma capsulatum is properly spliced in severe heat shock conditions.

Minchiotti¹,

Gargano²,

Maresca³

1991

Mol. Cell. Biol.

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We have isolated and characterized a heat-inducible gene, hsp82, from the dimorphic pathogenic fungus Histoplasma capsulatum, which is a filamentous mold at 25°C and a unicellular yeast at 37°C. This gene, which has a high degree of homology with other members of the hsp82 gene family, is split into three exons and two introns of 122 and 86 nucleotides, respectively. Contrary to what has been demonstrated in Drosophila melanogaster, Saccharomyces cerevisiae, and other organisms, hsp82 mRNA in H. capsulatum is properly spliced during the severe heat conditions of 37 to 40°C in the temperature-sensitive Downs strain. Splicing accuracy was also observed at 42°C in the temperature-tolerant G222B strain, which showed no evidence of accumulation of primary transcripts. Furthermore, the intron containing the ,-tubulin gene is also properly spliced at the upper temperature range, suggesting that the lack of a block in splicing may be a general phenomenon in this organism.Histoplasma capsulatum, a common respiratory pathogen of humans, is a dimorphic fungus that exists in a multicellular filamentous state in nature and as unicellular budding yeasts in tissue (1). The transition between the multicellular and unicellular phases can be reversibly induced by shifting the temperature from 25°C (mycelial phase) to 37°C (yeast phase). The mycelial-to-yeast conversion is of particular interest since it is triggered by an increase in the temperature of incubation and conversion to the yeast morphology is necessary for virulence. In fact, an important pathological feature of disease is that only yeasts are found in infected tissues (25,34). Therefore, the unique ability of dimorphic fungal pathogens to change shape in order to colonize, adapt to, and survive in host tissues is a process that parallels and may be intimately involved with this developmentally regulated morphological process (24).Since the mycelial (saprobic)-to-yeast (parasitic) transition is induced by heat, it was suggested that the early events of the phase transition were part of a heat shock response which is followed by cell adaptation to higher temperatures (19). This notion was supported by the report of Caruso et al. (7), who cloned the hsp70 gene from H. capsulatum and studied its expression in strains that differed in virulence and sensitivity to heat, and it was confirmed by the report of Shearer et al. (35), who observed the synthesis of new proteins soon after the temperature shift from 25°C to between 34 and 41°C.To understand the effects of severe heat shock on mRNA precursor processing during the mycelium-to-yeast transition in this fungus, we cloned a heat shock 82 (hsp82) gene and investigated its expression in two strains that differ in sensitivity to temperature and virulence.In Drosophila melanogaster cells as well as in Saccharomyces cerevisiae, hsp83 mRNA processing is inhibited at the upper temperature range of the heat shock response (38, 40). * Corresponding author.In Drosophila cells, the block in RNA processing was not specific to hsp83 ...

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Histoplasmosis

Wu-Hsieh

Howard

1993

Infectious Agents and Pathogenesis

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Histoplasmosis

Cited by 5 publications

References 225 publications

Histoplasmosis: a Clinical and Laboratory Update

Histoplasmosis: a Clinical and Laboratory Update

The intron-containing hsp82 gene of the dimorphic pathogenic fungus Histoplasma capsulatum is properly spliced in severe heat shock conditions.

Histoplasmosis

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