Clinical, haematological and biochemical findings in tigers infected by Leishmania infantum.

BACKGROUND: A large number of animal species are susceptible to Leishmania infantum (Kinetoplastida, Trypanosomatidae) in endemic areas, including domestic and wild felids such as tigers (Panthera tigris). Knowledge on the infection of this endangered species is still at its infancy, and therefore this study aims to identify clinical presentation and clinicopathological findings of tigers naturally infected by L. infantum. RESULTS: Tigers either L. infantum-positive (group A) or -negative (group B) were apparently healthy or presented visceral leishmaniasis unrelated conditions, except for one animal in which a large non-healing cutaneous lesion was observed. However, histological exam and immunohistochemistry carried out on the lesion excluded the presence of L. infantum amastigotes. Biochemical analysis showed that the average concentration of total proteins, globulins and haptoglobin were significantly higher (p < 0.01, p = 0.01 and p = 0.02, respectively), while the albumin/globulin ratio significantly lower (p = 0.05) in group A compared with group B. The biochemical alterations were partially confirmed by the serum protein electrophoresis results revealing a significant increase in the total protein value (p = 0.01) and hypergammaglobulinemia (p = 0.03) but an unmodified albumin/globulin ratio in group A. CONCLUSIONS: In this study tigers infected by L. infantum have shown to be mainly asymptomatic. The absence of clinical signs may lead veterinarians to overlook leishmaniasis in animals kept in captivity. Therefore, diagnostic and screening tests as serology should be part of routinely surveillance programs to be performed on tigers in zoological gardens located in endemic areas. Though only few protein-related laboratory abnormalities were recorded in infected animals, they could provide diagnostic clues for a first suspicion of L. infantum infection in tigers. Indeed, considering the high risk of zoonotic transmission in heavily frequented environment as zoos, a prompt diagnosis of L. infantum infection is of pivotal importance.

[Retrospective clinical and laboratory study of the toxocariasis cases hospitalised between 2005 and 2008]. / Studiu clinic si de laborator, retroprospectiv, asupra cazurilor de toxocaroza la copiii spitalizati in perioada 2005-2008.

UNLABELLED: The authors present the results of retroprospective clinical and laboratory diagnosis on toxocariasis cases hospitalized in the Paediatric Diseases Clinic of Iasi, between January 2005-June 2008. MATERIAL AND METHOD: The study included a number of 228 children. RESULTS: The most frequent clinical manifestation was pulmonary symptoms 80.70%: dyspneea, wheesing, asthma, cough, interstitial pneumonitis. The most frequent digestive symptoms were abdominal pain 41.22%, hepatosplenomegaly 29.38%; cutaneous manifestations were pruritus and urticaria. The laboratory diagnosis: hypereosinophilia was present at 94.73% childrens associated with hyperleucocytosis and hyper-gammaglobulinemia. All the patients were serologic confirmed with toxocariasis. The children responded well to treatment with albendazole.

Clinical and serological aspects of visceral leishmaniasis in northeast Brazilian dogs naturally infected with Leishmania chagasi.

Human visceral leishmaniasis is endemic in the northeast of Brazil, where the domestic dog is an important parasite reservoir in the infectious cycle of Leishmania chagasi. In this study, we evaluated the clinical signs of canine visceral leishmaniasis (CVL), serum protein profile and the antileishmanial IgG antibody production in 86 dogs living in northeast endemic areas of leishmaniasis. Thirty dogs from a leishmaniasis-free area were used as a control group. The major clinical signs of CVL seen were emaciation and skin ulcers (80%), followed by onychogryphosis and conjunctivitis (73%). Depilation was observed in 60% of animals while lymphadenomegaly, splenomegaly, liver enlargement or kidney involvement was less frequent (< or =20%). VL seropositive dogs presented with serum hyperproteinemia, hypoalbuminemia, hypergammaglobulinemia and decreased albumin/globulin ratio. A lower sensitivity and higher specificity was observed for promastigote indirect fluorescent antibody test (IFAT) (83 and 100%, respectively) compared with enzyme-linked immunosorbent assay (ELISA) (94 and 90%), which uses a crude extract of Leishmania. There was a positive correlation between IFAT and ELISA titers of antileishmanial IgG antibodies (Spearman test, P < 0.05), which was augmented in CVL dogs. This study found that the determination of serum protein, A/G ratio and the use of two different leishmanial serological tests like IFAT and ELISA are essential in CVL screening.

CD40-CD40 ligand interaction is central to cell-mediated immunity against Toxoplasma gondii: patients with hyper IgM syndrome have a defective type 1 immune response that can be restored by soluble CD40 ligand trimer.

Cell-mediated immunity that results in IL-12/IFN-gamma production is essential to control infections by intracellular organisms. Studies in animal models revealed contrasting results in regard to the importance of CD40-CD40 ligand (CD40L) signaling for induction of a type 1 cytokine response against these pathogens. We demonstrate that CD40-CD40L interaction in humans is critical for generation of the IL-12/IFN-gamma immune response against Toxoplasma gondii. Infection of monocytes with T. gondii resulted in up-regulation of CD40. CD40-CD40L signaling was required for optimal T cell production of IFN-gamma in response to T. gondii. Moreover, patients with hyper IgM (HIGM) syndrome exhibited a defect in IFN-gamma secretion in response to the parasite and evidence compatible with impaired in vivo T cell priming after T. gondii infection. Not only was IL-12 production in response to T. gondii dependent on CD40-CD40L signaling, but also, patients with HIGM syndrome exhibited deficient in vitro secretion of this cytokine in response to the parasite. Finally, in vitro incubation with agonistic soluble CD40L trimer enhanced T. gondii-triggered production of IFN-gamma and, through induction of IL-12 secretion, corrected the defect in IFN-gamma production observed in HIGM patients. Our results are likely to explain the susceptibility of patients with HIGM syndrome to infections by opportunistic pathogens.

[Hyperreactive malarial splenomegaly in a European returning from Africa]. / Splénomégalie malarique hyperréactive chez un Européen revenant d'Afrique.

INTRODUCTION: Hyper-reactive malarial splenomegaly (HMS) syndrome related to abnormal immunologic response to repeated malarial infections is unusual in European expatriates. EXEGESIS: We report the case of a 72-year-old white male patient who had been residing in the Congo and developed a typical clinical features of hyperactive malarial syndrome characterized by massive splenomegaly with hypersplenism, high titers of malarial IgM antibodies, IgM macroglobulinemia, liver and medullary lymphocytic proliferation, and a clinical and immunological response to long-term chloroquine therapy. CONCLUSION: Criteria for the diagnosis of hyper-reactive malarial splenomegaly are useful. However, making a distinction from malignant lymphoproliferative disorders is difficult, as a sustained response to chloroquine is required. Therefore, chloroquine appears to have a regulatory effect on the immune system.

[Immunology and immunopathology of African trypanosomiasis]. / Immunologie et immunopathologie de la trypanosomose Africaine.

Human African trypanosomiasis (HAT) is characterized by a major deregulation of the immune system. Hypergammaglobulinemia, auto-antibodies, and immunodepression are cardinal features. Parasitemia occurs in waves due to the successive appearance of parasites with different variable glycoprotein surface antigens (VGSA). Antigenic variation enables parasites to elude the host's immune defenses. Although high levels of immune complexes have been detected during HAT, it seems unlikely that they play a significant pathophysiological role. Numerous auto-antibodies have been detected. B lymphocyte activation is uncommon. In vitro T lymphocytes do not proliferate normally, but synthesize cytokines, such as interferon-g which enhance parasite development. Macrophages bind and destroy parasites in the presence of antibodies. They also synthesize large quantities of TNF-alpha which promote parasite destruction but also increase the severity of clinical symptoms. Nitric acid synthesized by activated macrophages has an antiparasitic effect but induces immunosuppression. In the meningoencephalitic stage of HAT, a severe inflammatory reaction is observed. This event is preceded by astroglia which could be induced by astrocytes secreting TNF-a and IL-1. Auto-antibodies against the central nervous system (e.g. anti-galactocerebrosides, anti-tryptophan-like auto-antibodies) may also be involved in the development of encephalitis. VGSA play a key role in the immunopathology of HAT (antigenic variation, induction of cytokine and autoantibody production). Successive relapses occur with the appearance of new antigenic variants and production of antibodies. The resulting continuous stimulation of the immune system leads to deregulation of immunoglobulin production and cytokine network.

Infections with Babesia canis and Ehrlichia canis in dogs in Zimbabwe.

Of 105 dogs examined at a veterinary hospital in Harare, Zimbabwe, 52 per cent had antibodies reactive with Ehrlichia canis in indirect fluorescent antibody tests, 26 per cent had Babesia canis parasites in peripheral blood smears and 17 per cent had both infections. None of the dogs with serological evidence of ehrlichiosis had typical E canis morulae detectable in blood smears. The infections were regarded as incidental findings not readily related to the reasons for examination in 46 per cent of the dogs with antibodies to E canis and 17 per cent of the dogs with both infections. The most common laboratory abnormalities were anaemia and thrombocytopenia and the prevalence and severity of these in concurrent infections were intermediate to those found in individual infections. There were no pathognomonic clinical signs or laboratory abnormalities which could be used to distinguish between individual and concurrent infections. However, there was a significantly higher prevalence of non-regenerative anaemia in dogs with antibodies to E canis than in dogs with both infections. The prevalence of thrombocytopenia was significantly higher in dogs with babesiosis than in dogs with antibodies to E canis and the prevalence of hyperglobulinaemia was significantly higher in dogs with both infections than in dogs with antibodies to E canis.