Fungal infections of the respiratory system are life-threatening complications for immunocompromised patients. Invasive pulmonary aspergillosis, caused by the airborne mold Aspergillus fumigatus, has a mortality rate of up to 50% in this patient population. The lack of neutrophils, a common immunodeficiency caused by, e.g., chemotherapy, disables a mechanism of sequestering iron from the pathogen, an important virulence factor. We construct and parameterized an agent-based model (ABM) of the immune response to Aspergillus fumigatus. We were able to obtain all the parameters a-priori from the literature creating a solid model. The parameters acquisition can be divided into direct and indirect. The former refers to parameters reported in the literature, such as the initial number of macrophages. In the indirect, we had to create mathematical models to obtain parameters hidden behind an experimental procedure. Upon parameterization, we fully validate the model with novel data. The model’s main prediction is that the critical reason why macrophages are unable to control the infection in the absence of neutrophils is the onset of hemorrhaging, as the fungus punctures the alveolar wall. The result is that the fungus gains access to heme- bound iron. At the same time, the macrophage response to the fungus is impaired. We show that these two phenomena together enable the infection to be successful.