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PubMed1975

Ocular lesions in the Earth Day, 1970, histoplasmosis epidemic.

The relationship between systemic histoplasmosis and this particular clinical picutre of a central choroiditis with peripheral atrophic lesions in the fundus was postulated by Woods in 1960 [19]. Since that time there have been many studies attempting to substantiate his hyptthesis [1, 3-5, 7-18]. In a large study performed in Walkersville, Maryland, which is an area endemic for histoplasmosis [14], the prevalence of the characteristic peripheral histoplasmic lesion in the fundus was 27 per 1000 population. The prevalence was 44 per 1000 population with positive histoplasmosis skin tests. In a similar study done in sothern Ohio, the prevalence of peripheral fundus lesions was 1.6 percent of 1417 patients examined [1]. Several generalizations can be made from the information obtained in studying the students involved in the Willis flu, and these can be compared with information from the control students from Bellingham. First, the acute infection at Willis School did not cause significant ocular abnormalities. This finding is supported by the fact that no significant differences occurred in the fundus lesions seen in the control group of students who lived in the same geographic area but were not clinically ill from histoplasmosis. Our evidence shows that the eyegrounds of the individuals living in this area were different from those of the students who lived outside the central Ohio area. How do we account for the similarity of ocular lesions in the affected students and the Delaware control group? Perhaps by the age of 11 or 12, a person living in the histoplasmosis belt will have already been exposed to histoplasmosis, resulting in the characteristic scars that are seen. If, in fact, histoplasmosis is the etiological agent in the patients who are diagnosed as having presumed ocular histoplasmosis, difficulty arises in understanding why those individuals involved in the epidemic did not have more scars than the control group. Perhaps the numbers of patients examined were not large enough to reflect the difference that really may exist. An interesting observation is that 4 (67 percent) of our control students with significant lesions had negative histoplasmosis skin tests. Of course, other organisms may have caused these lesions which have not yet been implicated as causative agents in the presumed ocular histoplasmosis syndrome.

Adolescent↗
PubMed1985

Humoral and cellular immune response in ocular histoplasmosis.

We have compared several humoral and cellular immune responses in ocular and in acute histoplasmosis syndromes. T-lymphocyte subset analysis revealed elevated ratios of T-helper/T-suppressor lymphocytes in ten of 22 patients with ocular histoplasmosis, whereas ratios were depressed in 18 of 22 with acute histoplasmosis syndromes. Lymphocyte transformation responses to mitogens and to histoplasma antigens were similar in both acute and ocular histoplasmosis. However, histoplasma antibody levels as measured by immunodiffusion, complement fixation, and radioimmunoassay were elevated in only three of 22 patients with ocular histoplasmosis, compared with 18 of 22 with acute histoplasmosis. Natural killer cell cytotoxicity was depressed in ten of 20 patients with ocular histoplasmosis compared with none of 18 with acute histoplasmosis. These findings support the clinical observations that ocular histoplasmosis and acute histoplasmosis syndrome are seldom, if ever, seen in the same patient.

Antibodies, Fungal↗
PubMed2004

Histoplasmosis in a pediatric oncology center.

OBJECTIVE: To understand the presentation and current management of histoplasmosis in a pediatric oncology center. Study design Retrospective review of clinical features of patients with histoplasmosis at a tertiary-care cancer center in an endemic area. RESULTS: Between 1988 and 2001, 57 patients with cancer had 61 episodes of acute histoplasmosis. Of these, 76% were male, and 64% had acute lymphocytic leukemia (ALL). Most were not neutropenic and had nonspecific febrile illnesses. The most rapid and specific tests for histoplasmosis in patients with cancer were histopathologic examination of lung biopsy specimens in patients with localized pulmonary infection and Histoplasma sp. antigen detection in the urine of patients with disseminated histoplasmosis (DH). The mean times to diagnosis were 20.6+/-15.2 days (pulmonary) and 18.6+/-8.2 days (disseminated) after the onset of symptoms. Most patients were treated with amphotericin B (AmB) followed by azole drugs for a mean of 8.5+/-3.1 weeks (pulmonary) and 10.4+/-7.9 weeks (disseminated). No patient died of histoplasmosis, but cancer therapy often was modified because of the infection. Most received unnecessary antibacterial drugs. CONCLUSIONS: Most readily available diagnostic tests for histoplasmosis lack sensitivity in these patients. Delay in diagnosis of histoplasmosis complicates care. No deaths were attributed to histoplasmosis; outcomes after treatment are good.

Acute Disease↗
PubMed2000

Practice guidelines for the management of patients with histoplasmosis. Infectious Diseases Society of America.

OBJECTIVE: The objective of this guideline is to provide recommendations for treating patients with the more common forms of histoplasmosis. PARTICIPANTS AND CONSENSUS PROCESS: A working group of 8 experts in this field was convened to develop this guideline. The working group developed and refined the guideline through a series of conference calls. OUTCOMES: The goal of treatment is to eradicate the infection when possible, although chronic suppression may be adequate for patients with AIDS and other serious immunosuppressive disorders. Other important outcomes are resolution of clinical abnormalities and prevention of relapse. EVIDENCE: The published literature on the management of histoplasmosis was reviewed. Controlled trials have been conducted that address the treatment of chronic pulmonary and disseminated histoplasmosis, but clinical experience and descriptive studies provide the basis for recommendations for other forms of histoplasmosis. VALUE: Value was assigned on the basis of the strength of the evidence supporting treatment recommendations, with the highest value assigned to controlled trials, according to conventions established for developing practice guidelines. BENEFITS AND COSTS: Certain forms of histoplasmosis cause life-threatening illnesses and result in considerable morbidity, whereas other manifestations cause no symptoms or minor self-limited illnesses. The nonprogressive forms of histoplasmosis, however, may reduce functional capacity, affecting work capacity and quality of life for several months. Treatment is clearly beneficial and cost-effective for patients with progressive forms of histoplasmosis, such as chronic pulmonary or disseminated infection. It remains unknown whether treatment improves the outcome for patients with the self-limited manifestations, since this patient population has not been studied. Other chronic progressive forms of histoplasmosis are not responsive to pharmacologic treatment. TREATMENT OPTIONS: Options for therapy for histoplasmosis include ketoconazole, itraconazole, fluconazole, amphotericin B (Fungizone; Bristol-Meyer Squibb, Princeton, NJ), liposomal amphotericin B (AmBisome; Fujisawa, Deerfield, IL), amphotericin B colloidal suspension (ABCD, or Amphotec; Seques, Menlo Park, CA), and amphotericin B lipid complex (ABLC, or Abelcet; Liposome, Princeton, NJ).

Antifungal Agents↗
PubMed1972

Evaluation of a microtiter latex agglutination test for histoplasmosis.

Experiments were designed to evaluate a Microtiter latex agglutination (Micro-LA) test, as a serological aid in the diagnosis of histoplasmosis, and to compare this test with the conventional microtiter-complement fixation (CF) test for histoplasmosis. Sera tested were from cases of acute and chronic pulmonary and disseminated histoplasmosis, as well as from individuals not having histoplasmosis. Ninety-seven percent of the cases of acute pulmonary histoplasmosis had positive Micro-LA tests, whereas 91% had positive CF tests. Ninety-six percent of the patients having chronic pulmonary histoplasmosis showed positive Micro-LA tests and 91% had positive CF tests. In contrast, 64% of the cases of disseminated histoplasmosis had positive Micro-LA tests, whereas 82% had positive CF tests. None of these differences was statistically significant. Although there were no significant differences in complement fixing and agglutinating antibody cross-reactivity with Blastomyces antigens, more patients demonstrated CF titers than Micro-LA titers. Sera from patients with acute and chronic histoplasmosis showed higher Micro-LA titers than CF titers, whereas sera from cases of disseminated histoplasmosis showed higher CF titers. Histoplasmin skin testing has less of a boosting effect on agglutinating antibodies than on CF antibodies to histoplasmin. Anticomplementary sera can be used in the Micro-LA test. This test is simple to perform, and results can be obtained in 2 to 4 hr.

Acute Disease↗
PubMed2004

Pulmonary histoplasmosis syndromes: recognition, diagnosis, and management.

Pulmonary manifestations are the hallmark of histoplasmosis. Clinical syndromes range from asymptomatic infection to diffuse alveolar disease causing respiratory difficulty and even death. Serologic tests for antibodies and antigen detection are especially helpful in the diagnosis of histoplasmosis but are frequently overlooked. Detection of Histoplasma capsulatum antigen in bronchoalveolar lavage fluid may be particularly helpful in patients with acute pulmonary histoplasmosis or disseminated disease with pulmonary involvement. Topics of special importance for pulmonary disease specialists include the approach to the exclusion of histoplasmosis in the evaluation of patients with suspected sarcoidosis, differentiation of pulmonary histoplasmosis and malignancy in those with lung masses or mediastinal lymphadenopathy, and recognition and management of chronic pulmonary and mediastinal manifestations of histoplasmosis. Although histoplasmosis is mild and self-limited in most healthy individuals, antifungal therapy is indicated in those with acute diffuse pulmonary infection, chronic pulmonary histoplasmosis, progressive disseminated disease, and perhaps mediastinal adenitis accompanied by obstructive symptoms. Antifungal therapy to prevent reactivation of histoplasmosis during immunosuppressive therapy, or transition of mediastinal adenitis to fibrosing mediastinitis, although controversial, is not recommended. Several new drugs active against H. capsulatum offer alternatives in patients failing or intolerant of current therapies.

Journal Article↗
PubMed2026

Histoplasmosis in children: emerging insights and evolving guidelines.

PURPOSE OF REVIEW: This review provides an update on the epidemiology, risk factors, clinical presentation, diagnosis, and management recommendations incorporating recommendations from recent publications including the Infectious Disease Society of America guidelines for the management of pulmonary and disseminated histoplasmosis. RECENT FINDINGS: Updates to the epidemiology of histoplasmosis indicate a broader geographic range than historically defined. Updated guidelines do not recommend routine treatment for asymptomatic, mild and moderate pulmonary histoplasmosis although itraconazole can be offered for immunocompromised children or for prolonged or worsening symptoms. Liposomal amphotericin B is recommended as initial treatment for severe histoplasmosis syndromes (severe pulmonary and disseminated histoplasmosis). Fibrosing mediastinitis, a late complication of histoplasmosis is treated with stenting of vessels and bronchi. Recent studies demonstrate that rituximab (anti-CD20 monoclonal antibody) may stop progression or lead to regression of progressive fibrosis. SUMMARY: Histoplasmosis has manifold manifestations, many of which are self-limited and do not require treatment. Severe histoplasmosis and its complications should be treated with liposomal amphotericin B followed by itraconazole. Clinical trials are needed to assess the efficacy of rituximab for the treatment of fibrosing mediastinitis.

Humans↗
PubMed1988

Progressive disseminated histoplasmosis in patients with acquired immunodeficiency syndrome.

PURPOSE: Progressive disseminated histoplasmosis is now diagnosed frequently in patients with the acquired immunodeficiency syndrome (AIDS) living in the central United States. Previous review articles of AIDS have failed to mention this infection. Herein, we describe 48 AIDS patients with progressive disseminated histoplasmosis in an effort to better understand the clinical presentation and diagnosis of the condition in this setting and to assess the efficacy of antifungal chemotherapy. PATIENTS AND METHODS: In the Houston metropolitan area, there were 66 cases of progressive disseminated histoplasmosis among 1,300 confirmed cases of AIDS from January 1983 to July 1987. Of AIDS patients in East Texas with histoplasmosis, 16 patients were available for follow-up by one of us, and the histories of 32 were obtained by examination of hospital charts and physician records. RESULTS: Fever, weight loss, and splenomegaly were the most common presenting signs and symptoms, occurring in 81, 52, and 31 percent, respectively. One-third of the patients had hematologic abnormalities. Infiltrates on chest roentgenograms were observed in 52 percent. Progressive disseminated histoplasmosis was the initial manifestation of AIDS in almost three-fourths of our patients. Biopsy and culture of the bone marrow established the diagnosis of progressive disseminated histoplasmosis in 69 percent. Clinical or autopsy proof of relapse occurred in three patients despite an initial course of more than 2 g of amphotericin B chemotherapy followed by ketoconazole suppression. CONCLUSION: Progressive disseminated histoplasmosis is often the first sign of immunodeficiency in patients with AIDS, and the diagnosis of this condition is most often established by bone marrow biopsy and culture. Because of the permanence of the immunodeficient state in these patients, progressive disseminated histoplasmosis is resistant to treatment.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Case report and review of disseminated histoplasmosis in South-East Asia: clinical and epidemiological implications.

The South-East Asian region is not known to be a major endemic area for histoplasmosis. We have recently diagnosed several cases of disseminated histoplasmosis in patients from this region. We report on a well documented indigenous case of disseminated histoplasmosis in a 62-year-old poultry farmer and review the literature for other reported cases of clinical histoplasmosis in the South-East Asian region. Sporadic cases of indigenous chronic pulmonary and non-meningeal disseminated histoplasmosis in immunocompetent hosts have been reported as well as examples of disseminated histoplasmosis in immunocompromised hosts. These reports suggest that histoplasmosis is endemic to certain areas in South-East Asia and that there may be a large number of undiagnosed and subclinical cases. The recent advances in diagnostic tests for histoplasmosis are also reviewed with reference to the experience of using these tests in the reported case.

Amphotericin B↗
PubMed2000

Ovarian histoplasmosis in systemic lupus erythematosus.

Histoplasma capsulatum is a pathogenic fungus endemic to North, Central, and South America. Histoplasmosis is primarily acquired by inhalation and in immunocompetent hosts infection is generally limited to the lungs. Histoplasmosis may disseminate systemically in hosts with defective cell-mediated immunity or massive inoculation. Systemic lupus erythematosus (SLE) is an autoimmune disorder associated with multiple primary and drug-related immunological defects that predispose patients to infections. Disseminated histoplasmosis has only rarely been described in association with SLE. We describe a 32-year-old woman with SLE who had a 2-year history of irregular menses and a confirmed anovulatory state, secondary to ovarian histoplasmosis. The ovarian histoplasmosis was discovered incidentally at surgery for a persistent colo-cecal fistula, which had developed 6 months earlier and was originally associated with an Actinomyces and Fusobacterium pelvic abscess. The patient had no evidence of active pulmonary histoplasmosis and her disseminated histoplasmosis likely resulted from re-activation of latent disease. This is the first description of disseminated histoplasmosis presenting as ovarian dysfunction in a patient with SLE.

Adult↗
PubMed1992

Histoplasmosis in Indianapolis.

Recurrent outbreaks of histoplasmosis in Indianapolis since 1978 have expanded our understanding of histoplasmosis. Histoplasmosis has emerged as the leading opportunistic infection in patients with AIDS from Indianapolis. Clinical manifestations of histoplasmosis are influenced by host factors. Underlying lung disease predisposes to chronic pulmonary histoplasmosis, and immunosuppressive medications or disorders predispose to dissemination. Inflammatory manifestations, including arthritis, erythema nodosum, and pericarditis, commonly occur with acute histoplasmosis. Diagnosis of histoplasmosis requires understanding of the accuracy and limitations of cultural and serological methods. More recently, radioimmunoassay for polysaccharide antigen has offered a new diagnostic approach. Amphotericin B remains the gold standard for treatment and is highly effective, even in immunocompromised individuals. Itraconazole shows promise as an alternative to amphotericin B for treatment of less severely ill patients. The role of fluconazole in therapy remains unknown until ongoing clinical trials are completed. Histoplasmosis cannot be cured in individuals with AIDS and in a small proportion of other individuals with other underlying immunosuppressive conditions. In such cases, long-term maintenance treatment is required to prevent relapse. Antigen detection has proven useful for following progress during treatment and for identifying relapse.

Amphotericin B↗
PubMed1997

Markedly elevated serum lactate dehydrogenase levels are a clue to the diagnosis of disseminated histoplasmosis in patients with AIDS.

Disseminated histoplasmosis is a common late manifestation of AIDS, but the diagnosis may be unsuspected in some patients because the clinical presentation of histoplasmosis may mimic other opportunistic infections. High serum lactate dehydrogenase (LDH) levels have been associated with disseminated histoplasmosis. We therefore evaluated whether markedly increased LDH levels were useful for making a diagnosis of disseminated histoplasmosis by comparing admission LDH levels for 15 patients with culture-proven disseminated histoplasmosis with those for 30 patients with advanced AIDS who were admitted to the hospital for evaluation of pulmonary infiltrates and fever. The mean admission LDH level in patients with disseminated histoplasmosis was 1,356 IU/L (range, 145-5,410 IU) whereas it was 332 (range, 77-832 IU) in the patients with other pulmonary processes. Admission LDH levels were >600 IU in 11 (73%) of the 15 patients with disseminated histoplasmosis vs. 3 (10%) of controls (P < .001). We conclude that markedly elevated admission LDH levels may be a clinical clue to the diagnosis of disseminated histoplasmosis in patients with AIDS.

AIDS-Related Opportunistic Infections↗
PubMed1984

Cavitary histoplasmosis occurring during two large urban outbreaks. Analysis of clinical, epidemiologic, roentgenographic, and laboratory features.

We have compared risk factors for cavitary histoplasmosis in 62 patients with that manifestation of the infection and in 679 patients with other forms of histoplasmosis, and we have evaluated the clinical and laboratory findings in 45 patients with cavitary histoplasmosis who were cared for at the Indiana University Medical Center hospitals during two large histoplasmosis outbreaks. Chronic obstructive lung disease and old age were the strongest risk factors for cavitary histoplasmosis but male sex, white race and immunosuppression were also important in certain patient groups. Fever, sweats, weight loss, productive cough, anemia, lymphopenia, and alkaline phosphatase elevation were common findings. The patients were occasionally incorrectly treated for presumed class 3 tuberculosis. Cultures were positive in 58% of patients, with sputum samples providing the highest yield (61%). Histoplasmal serologic tests provided useful clues to the diagnosis, positive in over 90% of cases. About one-third of patients recovered spontaneously while another 35% improved following treatment. About 4% developed chronic untreated cavitary histoplasmosis characterized by clinical and roentgenographic exacerbations and remissions. Of the deaths in four patients with untreated disease, one was caused by disseminated histoplasmosis while three died of other causes. Ketoconazole appeared effective in three of seven patients while its effect in three additional patients was uncertain. Toxicity precluded completion of ketoconazole therapy in one patient. Only amphotericin B has been proven to be effective therapy for cavitary histoplasmosis.

Adolescent↗
PubMed2005

Presumed ocular histoplasmosis syndrome.

PURPOSE OF REVIEW: Presumed ocular histoplasmosis syndrome remains a significant cause of visual morbidity. We review recent literature on the pathogenesis and particularly on the treatment of complications of presumed ocular histoplasmosis syndrome. RECENT FINDINGS: The pathogenesis of presumed ocular histoplasmosis syndrome remains mysterious; although some recent molecular evidence suggests a direct link between Histoplasma capsulatum and presumed ocular histoplasmosis syndrome, other reports document nearly identical disease occurring in the absence of H. capsulatum seropositivity. Treatment options have advanced rapidly in the past few years. Small case series and clinical trials suggest excellent efficacy for photodynamic therapy in the treatment of subretinal neovascularization associated with presumed ocular histoplasmosis syndrome. Preliminary studies also suggest efficacy of intravitreal corticosteroids. A large randomized controlled clinical trial failed to show efficacy for subretinal surgery in the management of presumed ocular histoplasmosis syndrome, however. SUMMARY: Despite continued debate on the etiology of presumed ocular histoplasmosis syndrome, there have been significant advances in treatment of the blinding complications of presumed ocular histoplasmosis syndrome.

Choroidal Neovascularization↗