**1. Introduction**

The fungus incriminated in pulmonary histoplasmosis is *Histoplasma Capsulatum* (*H. Capsulatum*), a dimorphic organism. Having two forms, the mycelial one is observed at ambient temperatures, while at body temperatures, the inhaled microorganism converts to yeast, which is the case of terminal bronchioles and alveoli [1]. Regarding the epidemiology, the most endemic zones of the world are those with temperate climates such as eastern and southern Europe, eastern Asia, Australia, regions of Africa and in the river valleys of the north and central part of the United States [2].

The immunity to *H. Capsulatum* is cell-mediated by IFN-g production from CD4 T lymphocytes and activated macrophages. The macrophages containing the infection lead to granuloma formation. The immune response is given mainly by IL 12, IFN-g, and tumor factor necrosis (TNF)-a [1].
