Leishmaniasis is a zoonosis caused by an intracellular parasite belonging to the genus Leishmania. In Europe, Africa, South America and China,
visceral leishmaniasis is caused by L. infantum. The vectors of
leishmaniasis are phlebotomine sandflies belonging to the genera Phlebotomus. According to the World Health Organization there are 2 million new cases each year and 1/10 of the world's population is at risk of
infection.
Leishmaniasis is considered a zoonosis and human are generally accidental hosts. The animal reservoir includes rodents, dog and other mammals. Several studies have indicate that half of the dogs with antileishmanial
antibodies have no signs of disease although, animal with
subclinical infections are potentially infectious to sand flies. The factors determining susceptibility or resistence to
visceral leishmaniasis remain unclear, but the genetics of the host may play a major role. Clinical signs are: intermittent
fever, hepatosplenomegaly, skin lesions and
ulcers,
alopecia, onychogryphosis,
anemia,
thrombocytopenia and
hypergammaglobulinemia. In mice, the outcome of
infection depends on the polarized activation of one of two subsets of CD4+ T cells, Th1 or Th2, the subdivision into Th1 and Th2 cells is based on the pattern of
cytokines that they produce. Th1 cells produce
gamma interferon (IFN-gamma) and
interleukin -2 (IL-2), whereas Th2 cells produce
IL-4,
IL-5, and
IL-10. An important difference between susceptible and resistant mice is that the resistant mice are able to switch to a Th1 profile and control the disease. An important factor in the "decision" to form a Th1 or Th2 phenotype is the early
cytokine environment, and
IL-12 is one of the
cytokines that contributes significantly to the establishment of the Th1 phenotype. Canine leishmaniosis is endemic in the Mediterranean basin and, in most cases is caused by the parasite Leishmania infantum. The main clinical findings are skin lesions, local or generalized lymphoadenopathy, loss of
body weight, glomerulopathy, ocular lesions,
epistaxis and lameness. Non pruritic skin lesions are the usual manifestation and several forms have been described, such as
exfoliative dermatitis and
alopecia, and ulcerative, nodular and pustular
dermatitis. Seroepidemiological studies of canine
leishmaniasis have revealed a large number of asymptomatic seropositive animals. Moreover in areas where
leishmaniasis is highly endemic, high proportion of apparently healthy animals show low levels of anti-Leishmania
antibodies. Others have regressive forms of the desease, and their antibody levels will decrease in the following months or years; still others maintain low levels of
antibodies without developing the desease for many years. However, the total number of infected animals is unknown. Canine
leishmaniasis is a major zoonosic
parasitic disease, enzootic in the Mediterranean area, caused by the intracellular protozoan Leishmania infantum. The dog is the main reservoir host of the parasite. However, most infected dogs do not present any clinical signs, and there is evidence that
Leishmania infection prevalence rates in areas of endemicity are higher than those ascertained by serological studies.
Visceral leishmaniasis is becoming a real problem of public health because it is an
opportunistic infection in immunocompromised patients and in human immunodeficiency virus-positive subjects. The detection of the extent of the
infection, particularly among asymptomatic dogs, is of great importance for the control of
leishmaniasis. PCR has been applied successfully in recent years to detect Leishmania spp. even in the cases with any of the clinical manifestation of
leishmaniasis. Very recently, real-time PCR for Leishmania has been applied to evaluate the parasitic load of dog tissues both at the time of the diagnosis and during follow-up of the
therapy and to measure
cytokine mRNA levels in different clinical samples of infected and uninfected dogs.