BackgroundThe WHO considers leishmaniasis as one of the six most important tropical diseases worldwide. It is caused by parasites of the genus Leishmania that are passed on to humans and animals by the phlebotomine sandfly. Despite all of the research, there is still a lack of understanding on the metabolism of the parasite and the progression of the disease. In this study, a mathematical model of disease progression was developed based on experimental data of clinical symptoms, immunological responses, and parasite load for Leishmania amazonensis in BALB/c mice.ResultsFour biologically significant variables were chosen to develop a differential equation model based on the GMA power-law formalism. Parameters were determined to minimize error in the model dynamics and time series experimental data. Subsequently, the model robustness was tested and the model predictions were verified by comparing them with experimental observations made in different experimental conditions. The model obtained helps to quantify relationships between the selected variables, leads to a better understanding of disease progression, and aids in the identification of crucial points for introducing therapeutic methods.ConclusionsOur model can be used to identify the biological factors that must be changed to minimize parasite load in the host body, and contributes to the design of effective therapies.

Seven hundred and twenty five female culicid mosquitoes were captured in an area of Western Spain where Dirofilaria immitis is endemic. PCR was applied for the detection of larval D. immitis DNA in mosquitoes. The ITS-2 rDNA region of the mosquito DNA was also amplified and sequenced to characterize the haplotype of infected individuals. Two Cx. pipiens showed positive reaction to D. immitis DNA, both specimens belonging to the haplotype H1. It is the first time that a culicid mosquito species is incriminated in the transmission of D. immitis and that its haplotype identified in Spain. The anthropophilic behaviour of this species, and its capture with human bait as attractant, led the authors to speculate that Cx. pipiens could be implicated in the transmission of human dirofilariosis in this endemic area.

Dirofilaria immitis is the agent of the heartworm disease in canids and felids, and of pulmonary dirofilariosis in man. Like other filariae, D. immitis harbours endosymbion Wolbachia bacteriae. In this work we analyse the response of specific IgE antibodies against both D. immitis antigens and the Wolbachia surface protein (WSP) in two groups of persons living in an area of canine endemia, one presenting high levels of total IgE (group 1) and other with normal levels (group 2). Infections with D. immitis were demonstrated by the presence of specific IgG in 228 individuals(48.8%) of the group 1 and only in one of the group 2. Specific IgE antibody response against D. immitis antigens was detected only in individuals of the group 1. IgE response against WSP was not detected in any group. The IgE response was directed mainly against two molecules of 33 and 42 kDa of the antigenic extract of D. immitis. These molecules were identified by mass spectrometry as a galectin and an aldolase, respectively. Their possible role in the survival mechanisms of the parasite and their contribution to development of allergic reactions in individuals resident in areas with heartworm disease are discussed.