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Histoplasmosis and pneumocystosis co-infections have been reported mainly in immunocompromised humans and in wild animals. The immunological response to each fungal infection has been described primarily using animal models; however, the host response to concomitant infection is unknown. The present work aimed to evaluate the pulmonary immunological response of patients with pneumonia caused either by Histoplasma capsulatum, Pneumocystis jirovecii, or their co-infection. We analyzed the pulmonary collectin and cytokine patterns of 131 bronchoalveolar lavage samples, which included HIV and non-HIV patients infected with H. capsulatum, P. jirovecii, or both fungi, as well as healthy volunteers and HIV patients without the studied fungal infections. Our results showed an increased production of the surfactant protein-A (SP-A) in non-HIV patients with H. capsulatum infection, contrasting with HIV patients (p < 0.05). Significant differences in median values of SP-A, IL-1β, TNF-α, IFN-γ, IL-18, IL-17A, IL-33, IL-13, and CXCL8 were found among all the groups studied, suggesting that these cytokines play a role in the local inflammatory processes of histoplasmosis and pneumocystosis. Interestingly, non-HIV patients with co-infection and pneumocystosis alone showed lower levels of SP-A, IL-1β, TNF-α, IFN-γ, IL-18, IL-17A, and IL-23 than histoplasmosis patients, suggesting an immunomodulatory ability of P. jirovecii over H. capsulatum response.

Histoplasmosis is one of the systemic mycoses that can involve the Central Nervous System (CNS), and it is caused by the dimorphic ascomycete species of the Histoplasma capsulatum complex. Once in the CNS, this pathogen causes life-threatening injuries that are associated with clinical manifestations of meningitis, focal lesions (abscesses, histoplasmomas), and spinal cord injuries. The present review provides updated data and highlights a particular vision regarding this mycosis and its causative agent, as well as its epidemiology, clinical forms, pathogenesis, diagnosis, and therapy, focusing on the CNS.

Histoplasma capsulatum is a dimorphic fungus associated with respiratory and systemic infections in mammalian hosts that have inhaled infective mycelial propagules. A phylogenetic reconstruction of this pathogen, using partial sequences of arf, H-anti, ole1, and tub1 protein-coding genes, proposed that H. capsulatum has at least 11 phylogenetic species, highlighting a clade (BAC1) comprising three H. capsulatum isolates from infected bats captured in Mexico. Here, relationships for each individual locus and the concatenated coding regions of these genes were inferred using parsimony, maximum likelihood, and Bayesian inference methods. Coalescent-based analyses, a concatenated sequence-types (CSTs) network, and nucleotide diversities were also evaluated. The results suggest that six H. capsulatum isolates from the migratory bat Tadarida brasiliensis together with one isolate from a Mormoops megalophylla bat support a NAm 3 clade, replacing the formerly reported BAC1 clade. In addition, three H. capsulatum isolates from T. brasiliensis were classified as lineages. The concatenated sequence analyses and the CSTs network validate these findings, suggesting that NAm 3 is related to the North American class 2 clade and that both clades could share a recent common ancestor. Our results provide original information on the geographic distribution, genetic diversity, and host specificity of H. capsulatum.

Pulmonary surfactant is a complex fluid that comprises phospholipids and four proteins (SP-A, SP-B, SP-C, and SP-D) with different biological functions. SP-B, SP-C, and SP-D are essential for the lungs’ surface tension function and for the organization, stability and metabolism of lung parenchyma. SP-A and SP-D, which are also known as pulmonary collectins, have an important function in the host’s lung immune response; they act as opsonins for different pathogens via a C-terminal carbohydrate recognition domain and enhance the attachment to phagocytic cells or show their own microbicidal activity by increasing the cellular membrane permeability. Interactions between the pulmonary collectins and bacteria or viruses have been extensively studied, but this is not the same for fungal pathogens. SP-A and SP-D bind glucan and mannose residues from fungal cell wall, but there is still a lack of information on their binding to other fungal carbohydrate residues. In addition, both their relation with immune cells for the clearance of these pathogens and the role of surfactant proteins’ regulation during respiratory fungal infections remain unknown. Here we highlight the relevant findings associated with SP-A and SP-D in those respiratory mycoses where the fungal infective propagules reach the lungs by the airways.

Histoplasmosis is considered the most important systemic mycosis in Mexico, and its diagnosis requires fast and reliable methodologies. The present study evaluated the usefulness of PCR using Hcp100 and 1281–1283 (220) molecular markers in detecting Histoplasma capsulatum in occupational and recreational outbreaks. Seven clinical serum samples of infected individuals from three different histoplasmosis outbreaks were processed by enzyme-linked immunosorbent assay (ELISA) to titre anti- H. capsulatum antibodies and to extract DNA. Fourteen environmental samples were also processed for H. capsulatum isolation and DNA extraction. Both clinical and environmental DNA samples were analysed by PCR with Hcp100 and 1281–1283 (220) markers. Antibodies to H. capsulatum were detected by ELISA in all serum samples using specific antigens, and in six of these samples, the PCR products of both molecular markers were amplified. Four environmental samples amplified one of the two markers, but only one sample amplified both markers and an isolate of H. capsulatum was cultured from this sample. All PCR products were sequenced, and the sequences for each marker were analysed using the Basic Local Alignment Search Tool (BLASTn), which revealed 95–98 and 98–100 % similarities with the reference sequences deposited in the GenBank for Hcp100 and 1281–1283 (220) , respectively. Both molecular markers proved to be useful in studying histoplasmosis outbreaks because they are matched for pathogen detection in either clinical or environmental samples.

Histoplasma capsulatum (H. capsulatum) is a thermal-dimorphic fungus, the causal agent of histoplasmosis. Its presence in the environment is related with chicken manure due to their high nitrogen and phosphorus content. In Colombia, chicken manure is the most used raw material in the composting process; however, there is no information about the capacity of H. capsulatum to survive and remain viable in a composted organic fertilizer. To address this question, this study shows three assays based on microbiological culture and the Hc100 nested PCR. First, a composting reactor system was designed to transform organic material under laboratory conditions, and the raw material was inoculated with the fungus. From these reactors, the fungus was not isolated, but its DNA was detected. In the second assay, samples from factories where the DNA of the fungus was previously detected by PCR were analyzed. In the raw material samples, 3 colonies of H. capsulatum were isolated and its DNA was detected. However, after the composting process, neither the fungus was recovered by culture nor DNA was detected. In the third assay, sterilized and nonsterilized organic composted samples were inoculated with H. capsulatum and then evaluated monthly during a year. In both types of samples, the fungus DNA was detected by Hc100 nested PCR during the whole year, but the fungus only grew from sterile samples during the first two months evaluated. In general, the results of the assays showed that H. capsulatum is not able to survive a well-done composting process.

Heat shock proteins (Hsps) are among the most widely distributed and evolutionary conserved proteins, acting as essential regulators of diverse constitutive metabolic processes. The Hsp60 of the dimorphic fungal Histoplasma capsulatum is the major surface adhesin to mammalian macrophages and studies of antibody-mediated protection against  H. capsulatum  have provided insight into the complexity involving Hsp60. However, nothing is known about the role of Hsp60 regarding biofilms, a mechanism of virulence exhibited by H. capsulatum . Considering this, the present study aimed to investigate the influence of the Hsp60 on biofilm features of H. capsulatum . Also, the non-conventional model Galleria mellonella was used to verify the effect of this protein during in vivo interaction. The use of invertebrate models such as G. mellonella  is highly proposed for the evaluation of pathogenesis, immune response, virulence mechanisms, and antimicrobial compounds. For that purpose, we used a monoclonal antibody (7B6) against Hsp60 and characterized the biofilm of two H. capsulatum strains by metabolic activity, biomass content, and images from scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM). We also evaluated the survival rate of G. mellonella infected with both strains under blockage of Hsp60. The results showed that mAb 7B6 was effective to reduce the metabolic activity and biomass of both H. capsulatum strains. Furthermore, the biofilms of cells treated with the antibody were thinner as well as presented a lower amount of cells and extracellular polymeric matrix compared to its non-treated controls. The blockage of Hsp60 before fungal infection of G. mellonella larvae also resulted in a significant increase of the larvae survival compared to controls. Our results highlight for the first time the importance of the Hsp60 protein to the establishment of the H. capsulatum biofilms and the G. mellonella larvae infection. Interestingly, the results with Hsp60 mAb 7B6 in this invertebrate model suggest a pattern of fungus-host interaction different from those previously found in a murine model, which can be due to the different features between insect and mammalian immune cells such as the absence of Fc receptors in hemocytes. However further studies are needed to support this hypothesis

The adherence of Histoplasma capsulatum yeasts to lung, spleen, liver, gut, and trachea cryosections of Artibeus hirsutus bats and inbred BALB/c mice (control) was studied after in vitro yeast-tissue incubations. Candida albicans yeasts were used as a well-known adherent fungal model in the mice host, and latex beads were used as a negative adherence control. Adhered yeast cells were identified by using crystal violet staining and the immunoperoxidase method with specific antibodies. H. capsulatum yeasts adhered to all tissues tested, mainly in the lung. Moreover, H. capsulatum yeasts adhered preferentially to white and red spleen pulp, in contrast to the dispersed distribution of C. albicans yeasts. H. capsulatum yeasts were mostly found on the sinusoidal face of hepatocytes. In general, the gut showed a higher number of adhered H. capsulatum yeasts than the trachea in both bats and mice. H. capsulatum and C. albicans yeasts developed high selectivity for the lamina propria of the gut. In addition, H. capsulatum yeasts interacted better with the lamina propria and adventitia of the trachea. The number of H. capsulatum yeast cells that adhered to each tissue section type was always greater than the corresponding number of C. albicans yeast cells, and latex beads never adhered to the tissue sections. Controls with anti-H. capsulatum and normal rabbit sera showed a significant blockage of H. capsulatum yeast adherence to lung tissue. This is the first study describing the patterns of H. capsulatum yeast adherence to different bat and mouse tissues.

The ascomycete Histoplasma capsulatum is the causative agent of systemic respiratory mycosis histoplasmosis, which sometimes develops acute disseminated or chronic clinical forms, with the latter usually associated with granuloma formation. The present report shows differential histopathological changes in the pulmonary inflammatory response of mice infected intranasally with the mycelial morphotype of H. capsulatum strains with distinct genotypes, EH-46 and G-217B, classified as LAm A2 and NAm 2 phylogenetic species, respectively. Infected male BALB/c mice were sacrificed at different postinfection times, and their serial lung sections were stained with periodic acid–Schiff and analyzed via microscopy. In mice infected with the LAm A2 strain, the results showed progressive changes in the inflammatory infiltrate of the lung parenchyma during the first hours and days postinfection as well as granulomas with macrophages containing intracellular yeast cells, which prevailed at 14 and 21 days postinfection. Bronchiolar-associated lymphoid tissue was induced in mice infected with both strains, primarily in mice infected with the NAm 2 strain. Several lung sections from mice infected with the LAm A2 strain showed PAS-positive yeast cells aggregated in a perinuclear crown-like arrangement in macrophages from 3 h to 21 days postinfection. These findings highlight differences in the host pulmonary inflammatory response associated with distinct H. capsulatum species.

Background Histoplasma capsulatum and Pneumocystis organisms cause host infections primarily affecting the lung tissue. H. capsulatum is endemic in the United States of America and Latin American countries. In special environments, H. capsulatum is commonly associated with bat and bird droppings. Pneumocystis -host specificity has been primarily studied in laboratory animals, and its ability to be harboured by wild animals remains as an important issue for understanding the spread of this pathogen in nature. Bats infected with H. capsulatum or Pneumocystis spp. have been found, with this mammal serving as a probable reservoir and disperser; however, the co-infection of bats with both of these microorganisms has never been explored. To evaluate the impact of H. capsulatum and Pneumocystis spp. infections in this flying mammal, 21 bat lungs from Argentina (AR), 13 from French Guyana (FG), and 88 from Mexico (MX) were screened using nested-PCR of the fragments, employing the Hcp100 locus for H. capsulatum and the mtLSUrRNA and mtSSUrRNA loci for Pneumocystis organisms. Results Of the 122 bats studied, 98 revealed H. capsulatum infections in which 55 of these bats exhibited this infection alone. In addition, 51 bats revealed Pneumocystis spp. infection of which eight bats exhibited a Pneumocystis infection alone. A total of 43 bats (eight from AR, one from FG, and 34 from MX) were found co-infected with both fungi, representing a co-infection rate of 35.2% (95% CI = 26.8-43.6%). Conclusion The data highlights the H. capsulatum and Pneumocystis spp.co-infection in bat population’s suggesting interplay with this wild host.