Visceral leishmaniasis in Northeast Brazil: What is the impact of HIV on this protozoan infection?

Abstract

BackgroundThe aim of this study was to compare cases of Visceral Leishmaniasis (VL) with and without HIV in a state in northeastern Brazil.MethodologyWe performed a comparative study in the state’s referral hospital for infectious/parasitic diseases located in Northeast Brazil between January 2007 and July 2017. The data obtained using this protocol were analyzed with SPSS.Principal findingsIn total, 252 patients were evaluated, including 126 with coincident VL/HIV and 126 with VL alone. Both groups primarily consisted of male patients. The most commonly affected ages were 30–39 years in the coinfected group and 19–29 years in the VL group (p < 0.001). Fever and anorexia (p = 0.001), which were more common in those with VL alone, were frequently observed, while diarrhea, vomiting, bleeding and dyspnea were more common in patients with VL/HIV coinfection (p<0.005). According to the hemogram results, leukocyte levels were lower in the VL group (p < 0.0001). Additionally, AST (aspartate aminotransferase) and ALT (alanine aminotransferase) levels differed between the groups, with higher levels in patients with VL (p < 0.001). On average, HIV was diagnosed 2.6 years before VL (p < 0.001), and VL relapse was observed only in the coinfection group (36.5% of cases). Fever (β = +0.17; p = 0.032) in the first VL/HIV episode was identified as a risk factor for relapse (R2 = 0.18). More deaths occurred in the VL/HIV group (11.1%) than in the VL group (2.4%).Conclusion/SignificanceVL/HIV was found to be prevalent among young adults, although the median patient age was higher in the VL/HIV group. The classic symptomatology of VL was more common in patients not coinfected with HIV; therefore, attention is needed in patients with HIV who present with any symptoms that suggest the presence of VL, especially in endemic areas. No cases of VL relapse occurred in patients without HIV, and death was more common in the VL/HIV co-infected group.

High seroprevalence of Leishmania infantum is linked to immune activation in people with HIV: a two-stage cross-sectional study in Bahia, Brazil

“…The geographic overlap of HIV-1 and L. infantum infections raises the possibility of co-infection, which several groups have shown to increase morbidity and mortality [7,11,52–58,13,14,19,21–23,50,51]. Several groups have studied the extent of this overlap in several Brazilian regions.…”

“…A wealth of studies worldwide [14,42,61–64] and a recent systematic review [56] have demonstrated a high frequency of relapse of VL in PWH, as well as increased mortality. Relapse of VL have been reported after anti-leishmaniasis treatment, even years after the patient was considered clinically cured, especially in PWH and/or immunosuppressive conditions [13, 51].…”

“…The few studies evaluating the prevalence of HIV-1 and L. infantum coinfection on a national level in Brazil [7, 8] have highlighted regions endemic for leishmaniasis: Distrito Federal [9], Ceará [10, 11], Maranhão [12, 13], Mato Grosso [14], Mato Grosso do Sul [15, 16], Minas Gerais [17, 18], Pernambuco [19], Piauí [20], Rio Grande do Norte [21, 22], Sergipe [23] and Tocantins [24]. Bahia is also considered an endemic area for leishmaniasis, with an incidence rate of 0.08/10,000 inhabitants for VL reported in 2018 [25].…”

Parasite Genotype Is a Major Predictor of Mortality from Visceral Leishmaniasis

“…Death is usually associated with hemorrhagic phenomena, which could be caused by bacterial coinfection ( 4 , 5 ) as a consequence of cytokine-driven systemic inflammation ( 6 ). Leishmania /HIV results in greater risks of relapse and fatality ( 7 , 8 ). Despite the range of clinical presentations, the parasite factors that determine differential virulence in humans are not well understood.…”

Parasite genotype is a major predictor of mortality from visceral leishmaniasis

“…6 Leishmania /HIV results in greater risks of relapse and fatality. 7,8 Despite the range of clinical presentations, the parasite factors that determine differential virulence in humans are not well understood.…”