We studied and compared the prevalence of Leishmania infection and the seroprevalence and the prevalence of canine leishmaniasis in an area where canine leishmaniasis is endemic. One hundred dogs living on the island of Mallorca (Spain) were studied. In this study, we clinically examined each dog for the presence of symptoms compatible with leishmaniasis, determined the titer of anti-Leishmania antibodies, and investigated the presence of Leishmania DNA by PCR in skin, conjunctiva, and bone marrow samples of each dog. The prevalence of the disease and the seroprevalence were 13 and 26%, respectively. In 63% of the dogs, Leishmania DNA could be detected by PCR in at least one of the tissues studied. The results of positive PCR in the bone marrow, the conjunctiva, and the skin were 17.8, 32, and 51%, respectively. The prevalence of the infection, 67%, was calculated using all animals that were seropositive and/or positive by PCR with any tissue. The results showed that the majority of dogs living in an area where canine leishmaniasis is endemic are infected by Leishmania and that the prevalence of infection is much greater than the prevalence of overt Leishmaniarelated disease.Canine leishmaniasis is a severe systemic disease of dogs caused by the protozoan parasite Leishmania infantum. Clinical manifestations of the disease include nonpruritic skin lesions, such as exfoliative dermatitis and ulcerations, local or generalized lymphadenopathy, loss of weight, poor appetite, ocular lesions, epistaxis, lameness, renal failure, and diarrhea (5,9,14,25). Leishmaniasis is a zoonotic disease for which dogs are considered the chief reservoir of the parasite. The disease is endemic in the Mediterranean basin, where seroprevalence ranges between 10 and 37% (10, 24). There are, however, several studies suggesting that the rate of infection is higher than the figures found by serological investigations. A survey performed using the PCR and immunoblotting techniques found that most dogs living in southern France had been exposed to Leishmania (3). These results agree with another study that found a rate of Leishmania infection of 65% for dogs living in Portugal by using serology and cell-mediated tests (4).The percentage of infected dogs living in an area where canine leishmaniasis is endemic has major public health implications. It was demonstrated that infected, but asymptomatic, dogs were sources of the parasite for phlebotomine vector sandflies and as a consequence play an active role in the transmission of Leishmania (15).The present study was designed to investigate and compare the prevalence of Leishmania infection, the seroprevalence and the prevalence of the disease in a canine population living in an area where canine leishmaniasis is endemic. One hundred dogs living on the island of Mallorca (Spain) were included in this study. Veterinarians clinically examined all dogs, and the titer of anti-Leishmania antibodies was determined. The presence of Leishmania DNA in each dog was investigated by PCR with three tissues: ...

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The comparative concentration profiles of the (+) and (-) albendazole sulphoxide (ABZSO) enantiomers obtained in plasma and in selected target tissues/fluids after intravenous (i.v.) administration of a racemic formulation of ricobendazole (RBZ) to cattle were characterised. Fourteen Holstein calves received RBZ (racemic solution, 150 mg/mL) by i.v. administration at 7.5 mg/kg. Jugular blood samples were collected over 48 h post-treatment (plasma kinetic trial) and two animals were sacrificed at either 4, 12, 20, 28 or 32 h post-treatment to obtain samples of abomasal/small intestine mucosal tissue, abomasal/small intestine fluids, bile, liver and lung tissue (tissue distribution study). The (-)ABZSO enantiomer was depleted significantly faster from plasma compared with the (+)ABZSO antipode. The plasma AUC for (+)ABZSO (38.3 microg. h/mL) was significantly higher (P < 0.05) compared with that obtained for (-)ABZSO (20.5 microg. h/mL). The (+)ABZSO enantiomer was the predominant antipode measured in bile, abomasal fluid and abomasal mucosa. For instance, at 12 h post-treatment the (+)/(-) concentration ratios were: 12.9 (plasma), 1.62 (abomasal mucosa), 13.0 (abomasal fluid), 2.92 (intestinal mucosa), 9.87 (intestinal fluid) and 21.5 (bile). No marked differences between the concentration profiles of both enantiomers were observed in the liver tissue. Albendazole (ABZ) was recovered from the liver, lung and gastrointestinal (GI) mucosal tissues of RBZ-treated calves up to 32 h post-treatment, probably produced by a GI microflora-mediated sulphoreduction of RBZ. An enantioselective kinetic behaviour may account both for the faster depletion of the (-) enantiomer and for the higher availabilities of the (+) antipode observed in plasma and in most of the tissues/fluids investigated. The simultaneous evaluation of the plasma kinetics and tissue concentration profiles of both enantiomeric forms reported here, may help to interpret the relationship between chiral behaviour and pharmacological action for sulphoxide derivatives of benzimidazole (BZD) methylcarbamate anthelmintics.

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Isolated dermal mast cells from atopic dogs are a valuable tool for the analysis of their functional properties in atopic dermatitis. We have characterized the histamine secretory pattern of mast cells enzymatically dispersed from the skin of dogs naturally suffering from this condition. The total histamine content found per isolated skin mast cell was higher in the allergic dogs than in nonatopic (control) animals (8.7 pg/mast cell versus 5.2 pg/mast cell). This phenomenon together with the well known higher concentration of skin mast cell number in atopic dermatitis lesions might account for the observed increase in local histamine concentration (15.0 micrograms/g versus 9.0 micrograms/g). Atopic dog-derived mast cells were highly reactive to both non-immunological (ionophore A23187) and an immunological-like (concanavalin A) stimulus. Furthermore, histamine net release induced by concanavalin A (1 mg/ml) stimulation was clearly enhanced in the atopic dogs (33.3% net release versus 15.4% in controls). These results have not been described in dermal mast cells dispersed from the skin of individuals with atopic dermatitis and clearly support the hypothesis that mast cells play a major role in causing and possibly modulating atopic dermatitis, through enhanced sensitivity or releasability. However, whether these two phenomena are primary abnormalities of atopic dermatitis, or only secondary changes, remains undetermined.