Histoplasmosis: Laboratory Diagnosis

The diagnosis of histoplasmosis is based on clinical, imaging, and laboratory evidence of the disease. The gold standards of laboratory diagnosis are the presence of the fungus in the pathological examination of tissues and its isolation (direct microscopy, histopathology, cytopathology) in mycological culture (4–6 weeks required) by clinical specimens. The antibody test, sometimes negative in immunocompromised patients, must be performed at least four weeks after acute infection to be positive. The antibody test is most useful in subacute and chronic forms of histoplasmosis. The antigen test is the most common method for establishing the diagnosis of acute pulmonary histoplasmosis or progressive disseminated histoplasmosis. The antigen test in urine or serum has good sensitivity, better in bronchoalveolar lavage fluid. There are skin sensitivity tests with low sensitivity that are used only for epidemiologic studies and are not recommended for diagnosis. Molecular diagnosis has improved the sensitivity of clinical specimens. Laboratory PCR assays with different molecular targets have been developed. Currently, the main procedure for molecular diagnosis of histoplasmosis is the application of a rapid DNA probe on a fungus isolated from a culture. This chapter summarizes the currently available tools for the laboratory diagnosis of histoplasmosis, focusing on the complexity of the assays and their performance in different clinical contexts

The Influence of Protease Inhibitors on the Evolution of Hepatitis C in Patients with HIV and HCV Co-Infection

Prevalence of hepatitis C in HIV infected patients is much higher than in the general population. There is the possibility of viral clearance HCV, in some patients co-infected HIV and HCV, in the phase of immune reconstruction after antiretroviral treatment (ART). There are patients’ anti-HCV positive who initially did not show HCV viral load detected and after the start of ART becomes HCV viral load detectable. There are studies that described that immune restoration with increase in CD4+ and CD8+ T cells, from ART, was important in control of HCV viremia. Has been proposed hypothesis that direct or indirect effect of ART on HCV replication play a role in spontaneous resolution of HCV infection. We evaluated the co-infected patients with HIV and HCV under combined antiretroviral treatment, containing PI boosted with ritonavir in terms of immunological and virological status (for both infection) and also liver disease. Patients were evaluated for liver damage by non-invasive methods. We have shown that a small percentage of patients have severe liver damage. We demonstrated the negative role of HCV on immunological status and in liver fibrosis in co-infected patients. A high proportion of these HIV and HCV co-infected patients had no detectable viremia, higher than other studies published

Epidemiology of Histoplasmosis

More prevalent than initially considered, histoplasmosis is primarily a non-contagious disease of the reticuloendothelial system, producing a broad spectrum of clinical manifestations, ranging from asymptomatic or self-limited infection, in immunocompetent patients to life-threatening, disseminated disease in immunocompromised ones. The causative agent is H. capsulatum, a thermally dimorphic, intracellular fungus, discovered in 1906, by the pathologist Samuel Darling, when examined tissues from a young man whose death was mistakenly attributed to miliary tuberculosis. Since then, histoplasmosis was described on six continents, with high and low endemicity areas. H. capsulatum is a soil-based fungus, commonly associated with river valleys in the temperate zone, and with the presence of bird and bat guano. Infection occurs when saprophytic spores are inhaled and change to the pathogenic yeast in the lungs, where H. capsulatum overcomes many obstacles to cause host injuries. Depending on geographic distribution, morphology, and clinical symptoms, three varieties have been historically recognized, two of them (var. capsulatum and var. duboisii) being pathogen to humans, and the third (var. farciminosum) has predominantly been described as an equine pathogen. In endemic areas, patients with AIDS or people who receive immunosuppressive therapies should be counseled to avoid high-risk activities; otherwise, precautionary measures should be taken

Colonization, Infection and Risk Factors for Death in an Infectious Disease ICU in Romania

Knowing the bacterial strains in the intensive care unit (ICU) is important for reducing the rate of bacterial transmission and the risk of healthcare-associated infections (HAIs), allowing for targeted interventions to reduce the risk of death by HAIs. We performed a retrospective case-control study in a single center that included 320 bacteriologically screened patients from the ICU of the Infectious Diseases Hospital in Constanta between September 2017 and March 2020. Sixty-five secondary bacterial infections were identified as the cause of hospital admission and 60 bacterial colonizations. There were 20 cases and 300 controls for the mortality rate and risk factors for death. Multivariate analysis identified that hospitalization of patients for HIV infection (OR 11.82, 95% CI: 1.69-83.62, P ≤0.05) and Clostridioides difficile infection (OR 7.38, 95% CI: 1.39 -39.22, P ≤ 0.05) were independent risk factors associated with death. We observed that the number of colonizations or secondary infections in the ICU was similar, and the mortality rate in the ICU was influenced by HIV infection or Clostridioides difficile infection

High Risk of Secondary Infections Following Thrombotic Complications in Patients With COVID-19

Background. This study’s primary aim was to evaluate the impact of thrombotic complications on the development of secondary infections. The secondary aim was to compare the etiology of secondary infections in patients with and without thrombotic complications. Methods. This was a cohort study (NCT04318366) of coronavirus disease 2019 (COVID-19) patients hospitalized at IRCCS San Raffaele Hospital between February 25 and June 30, 2020. Incidence rates (IRs) were calculated by univariable Poisson regression as the number of cases per 1000 person-days of follow-up (PDFU) with 95% confidence intervals. The cumulative incidence functions of secondary infections according to thrombotic complications were compared with Gray’s method accounting for competing risk of death. A multivariable Fine-Gray model was applied to assess factors associated with risk of secondary infections. Results. Overall, 109/904 patients had 176 secondary infections (IR, 10.0; 95% CI, 8.8–11.5; per 1000-PDFU). The IRs of secondary infections among patients with or without thrombotic complications were 15.0 (95% CI, 10.7–21.0) and 9.3 (95% CI, 7.9–11.0) per 1000-PDFU, respectively (P = .017). At multivariable analysis, thrombotic complications were associated with the development of secondary infections (subdistribution hazard ratio, 1.788; 95% CI, 1.018–3.140; P = .043). The etiology of secondary infections was similar in patients with and without thrombotic complications. Conclusions. In patients with COVID-19, thrombotic complications were associated with a high risk of secondary infections