The fungus Histoplasma capsulatum causes histoplasmosis, which is spread mostly through the respiratory tract. During the autopsy of a patient from Martinique with a disseminating disease characterized as a general protozoan infection in 1906, Samuel Taylor Darling, a pathologist at Ancon Hospital in the Panama Canal Zone, first described H. capsulatum. Darling's microbe was first identified as yeast rather than protozoa by Rocha-Lima, a Brazilian studying in Hamburg in 1912. Since then, it's been more common to be diagnosed with the disease. The diagnosis of histoplasmosis had always been done post mortem until 1934, when Dodd and Tompkins discovered it in a living new-born. Vanderbilt University's De Monbreun isolated and analyzed the fungal culture from this case.De Monbreun discovered the fungal etiology and dimorphism of H. capsulatum. H. capsulatum has recently arisen as a major opportunistic infection in patients with immunodeficiency, primarily HIV (Human Immunodeficiency Virus) in H. capsulatum endemic areas. In typical youngsters, this disease is frequently self-limiting and does not require treatment [1]. Children with weakened immune systems are more likely to contract a serious illness.

The dimorphic fungus H. capsulatum can be found in areas of North, Central, and South America, as well as Africa and Asia. There have, however, been reports of instances all around Europe. In pigeon and poultry breeders, tunnels where bats frequent, and abandoned construction sites, outbreaks have been discovered. Because most research on the problem has been limited to places where outbreaks of histoplasmosis have occurred and are dependent on skin testing, the true incidence of histoplasmosis is unknown. Furthermore, certain studies were carried out on specialized groups, such as hospitalized patients or recruits. In 1948, soil was contaminated with chicken excreta, resulting in the first environmental isolation [2]. The native habitat of H. capsulatum is soil, particularly soil tainted by bat or bird droppings, which produces a nitrogen-rich environment. High carbohydrate concentrations, cationic salts, acidic pH, soil temperatures ranging from -18 8°C to 37 8°C, and a moisture content of 12 percent are among the other environmental requirements. 

Hundreds of thousands of people are infected with H. capsulatum each year in the United States and Central America. The majority of people are unaware that they have a fungal infection. Only until the introduction of a skin test antigen that could be used in epidemiological research was the full amount of H. capsulatum infection in the Ohio and Mississippi River valleys determined. Christie and Peterson and Palmer discovered the link between Histoplasma skin test positivity and lung calcifications in tuberculin-negative people in their seminal investigations. Following large-scale population surveys conducted by the Public Health Service, it was shown that over 80% of young individuals in the states surrounding the Ohio and Mississippi Rivers had previously been infected with H. capsulatum. People living in endemic areas are quite likely to be exposed to H. capsulatum, but clinical illness is rare [3]. The great majority of people infected with histoplasmosis shows no symptoms or has a very mild sickness that is never diagnosed as histoplasmosis. The clinical signs detailed below are those that occur in the tiny percentage of people infected with H. capsulatum who develop symptoms.

Most patients with acute histoplasmosis do not require treatment; however, persistent forms of the virus and severe acute pulmonary histoplasmosis must [4]. Amphotericin B deoxy cholate was the only treatment option until the azole period began in the 1990s. Since then, the number of treatment alternatives has risen dramatically. In the 1950s and 1960s, the National Communicable Disease Center (forerunner of the Centers for Disease Control and Prevention) Cooperative Mycoses Study Group and the Veterans Administration-Armed Forces Cooperative Study on Histoplasmosis conducted a series of clinical trials to prove the effectiveness of amphotericin B. During the same time period, researchers at the National Institutes of Health and the Missouri State Sanatorium published reports on their experiences using amphotericin B to treat disseminated histoplasmosis [5]. These early investigations established some essential aspects regarding the chronic cavity pulmonary and chronic progressive disseminated forms of histoplasmosis, despite the fact that they were neither controlled nor randomized.

Antifungal therapy should be administered to all individuals with persistent pulmonary histoplasmosis. Without treatment, the condition will most certainly proceed to respiratory insufficiency, resulting in the death of many individuals. Amphotericin B has been replaced as the treatment of choice with itraconazole, 200 mg twice daily. The majority of patients is chronically unwell and will not require amphotericin B treatment at first. The duration of Iitraconazole treatment ranges from 12 to 24 months, with close monitoring to detect relapses [6].

Conclusion

Histoplasmosis primarily affects young people who become ill during epidemics when it comes to age groups. Even when children are exposed to epidemics, they are more likely to develop asymptomatic or

Moderate infections. Infants, on the other hand, are at danger of contracting more serious illnesses or spreading diseases. Large inoculum exposure, acquired immunodeficiency from immunosuppressive medicines, malnutrition, or HIV infection are all risk factors for disseminated histoplasmosis, which can occur at any age. Primary immunodeficiency diseases that alter the function of T lymphocytes, monocytes, and macrophages can also predispose to disseminated histoplasmosis. Despite the fact that immunocompromised hosts are more prone to histoplasmosis, immunocompetent persons have developed lung and central nervous system symptoms. There is no transfer from person to person or animal to person and no isolation protocols are required. When an immunocompromised host with diminishing cell- mediated immunity is exposed to even a minor inoculum from the environment, reinfection can occur. In most cases, histoplasmosis is asymptomatic and self-limiting. When symptoms do occur, frequent symptoms include fever, cough, and malaise.

References

1. Bhatti S, Vilenski L, Tight R, Smego Jr RA (2005) Histoplasma endocarditis: clinical and mycologic features and outcomes. Journal of infection.51(1):2-9.
2. Bradsher RW, Wickre CG, Savage AM, Harston WE, Alford RH (1980) Histoplasma capsulatum endocarditis cured by amphotericin B combined with surgery. Chest.78(5):791-795.
3. Bullock WE, Artz RP, Bhathena D, Tung KS (1979) Histoplasmosis: association with circulating immune complexes, eosinophilia, and mesangiopathic glomerulonephritis. Archives internal med.139(6):700-702.
4. Dismukes WE, Bradsher Jr RW, Cloud GC, Kauffman CA, Chapman SW, George RB (1992) Itraconazole therapy for blastomycosis and histoplasmosis. The American j med.93(5):489-497
5. Kauffman CA (2007) Histoplasmosis: a Clinical and Laboratory Update. Clin microbiol rev 20: 115-132.