Showing papers on "Visceral leishmaniasis published in 1982"

Prevalence and disease spectrum in a new focus of visceral leishmaniasis in Kenya.

Abstract: A cross-sectional community study was conducted in the village of Kivaa in Machakos District, Kenya, to determine the prevalence and disease spectrum of visceral leishmaniasis. The disease was first diagnosed in 1978. Demographic data was collected from 50 households comprising 374 individuals. Clinical examination, laboratory investigations and leishmanin skin tests were performed. The results showed that in spite of the presence of a susceptible population, visceral leishmaniasis occurred with a low prevalence in Kivaa as evidenced by the small number of individuals with active disease (0·30%), a low leishmanin positivity rate (7·2%) and the presence of leishmanial antibodies in only 3·7% of the population. The infection affected individuals in homesteads with or without nearby termite hills. Leishmanial antibodies and leishmanin positivity were found among asymptomatic household contacts of patients as well as in isolated individuals in non-infected homesteads. These findings suggest the existence of a spectrum of disease ranging from asymptomatic to self-healing to severe clinical illness. Furthermore, there was significant clustering of leishmanin reactors in the households of patients. The aetiology of this striking focality of visceral leishmaniasis remains obscure. Possible explanations are discussed.

Susceptibility of clinically sensitive and resistant Leishmania to pentavalent antimony in vitro

Abstract: Standard courses of pentavalent antimonials frequently fail to cure cutaneous, mucocutaneous, and visceral leishmaniasis, and characteristically fail to cure diffuse cutaneous disease. We have determined the in vitro sensitivity of clinical isolates of Leishmania to pentavalent antimony to determine if inherent drug resistance of the parasite is responsible for treatment failures in human beings. Intracellular amastigotes resulting from promastigote-initiated infection of human macrophages were exposed to pentavalent antimony for 6 days at 34.5-35 degrees C. Amastigotes from clinically sensitive simple cutaneous lesions exhibited a range of in vitro sensitivity. Four strains were greater than or equal to 90% eliminated and two strains were 70-75% eliminated in vitro by concentrations of antimony (15-20 micrograms Sb/ml), comparable to peak achievable serum levels in humans. Amastigotes from initially clinically resistant simple cutaneous lesions showed a wider range of sensitivities. Five strains were greater than or equal to 90% eliminated, but one strain was only 40% eliminated and another strain was completely insensitive in vitro. The clinically resistant diffuse cutaneous strain was 61% eliminated. The techniques described herein permit determination of the in vitro antimicrobial susceptibility of Leishmania from all major human forms of leishmaniasis. The data from this series indicate that in a minority of initially resistant cases parasite resistance to the drug may be contributing to clinical resistance, and use of non-antimonial drugs might be recommended for future therapy.

Leishmaniasis in beige mice.

Abstract: The courses of two protozoal diseases, cutaneous and visceral leishmaniasis, were examined in three groups of C57BL/6J mice. One group of mice was homozygous recessive for the beige gene (bg/bg). Beige mice are the genetic homologue of the human Chediak-Higashi syndrome and, among other defects, are profoundly deficient in natural killer cell activity. Wild-type (+/+) mice, which respond to experimental cutaneous or visceral leishmaniasis by eventually eliminating their parasites, and heterozygous beige (bg/+) mice served as controls; both are phenotypically normal in natural killer cell activity, which is particularly high in the spleen. In bg/bg mice, the course of Leishmania tropica, a causative agent of cutaneous leishmaniasis, was similar to that in control mice after both primary and challenge inoculations. All groups of mice expressed similar humoral and cellular immune responses to L. tropica antigen. However, bg/bg mice failed to eliminate amastigotes of Leishmania donovani, a causative agent of visceral leishmaniasis, from their spleens over an observation period of 56 days, in contrast to bg/+ and +/+ controls. Similar levels of anti-leishmanial antibody were produced by all groups of mice, and all mice responded comparably to footpad injections of L. donovani antigen. The results of this study suggest a possible role for natural killer cells in recovery from L. donovani but not from L. tropica infection.

Leishmaniasis in Brazil: XVIII. Further evidence incriminating the fox Cerdocyon thous (L) as a reservoir of Amazonian visceral leishmaniasis.

Abstract: Major endemic areas of visceral leishmaniasis in Brazil are located in the drier, poorly forested regions, principally in the northeastern States such as Ceara and Bahia. Cases of the human disease in the Amazon Region are rare, very sporadic, and seldom present opportunities for epidemiological study. Following the report of a fatal case near Salvaterra, the Island of Marajo, Para State, a preliminary investigation has resulted in the isolation of a parasite regarded as Leishmania donovani chagasi from the viscera and skin of an apparently healthy fox, Cerdocyon thous, captured in the same locality. This represents the third recorded isolation of the parasite from this species of fox in the Amazon Region. The inapparent nature of the infections supports the suggestion that this canid may represent the primitive natural host of L. d. chagasi. C. thous is commonly associated with forested or wooded areas, and enzymic profiles for the enzymes ASAT, ALAT, PGM, GPI, MDH, MPI, G6PD, PEP and ACP failed to distinguish an isolate of L. d. chagasi from this animal in Para from others obtained from cases of human visceral leishmaniasis in the neighbouring States of Maranhao, Ceara and Bahia. This suggests that the major, present-day endemics may have originated from a primary silvatic enzootic.

Protective effect of glucan against visceral leishmaniasis in hamsters.

Abstract: The effect of pre- or posttreatment with glucan, a reticuloendothelial stimulant, on the course of Leishmania donovani infection was assessed in highly susceptible hamsters. Intravenous administration of glucan before or after L. donovani infection significantly suppressed proliferation of amastigote-stage parasites in liver and spleen. Glucan-activated peritoneal macrophages in vitro also significantly reduced multiplication of the intracellular parasite. Ultrastructural studies revealed a well-defined hepatic granulomatous response to glucan, with hypertrophic Kupffer cells and reduced numbers of intracellular parasites compared to the control group. In additional studies, groups of hamsters were immunized by intravenous injections of glucan with Formalin-killed promastigote-stage L. donovani cells and challenged 60 days after the last immunizing injection. This treatment regimen significantly prolonged the mean survival time of those hamsters which died after infection, relative to untreated control groups. Hamsters stimulated with the glucan-killed promastigote preparation also exhibited significant reductions in splenic amastigotes on days 10 and 21 postinfection compared with all other control groups, but on day 35, splenic amastigotes did not differ significantly from those of control animals. Our composite observations provide evidence for glucan-enhanced nonspecific resistance of hamsters to visceral leishmaniasis.

Host-parasite relationship in murine leishmaniasis: pathophysiological and immunological changes.

Abstract: The host-parasite relationship in human visceral leishmaniasis remains poorly understood. In the present study, pathophysiological and immunological changes were examined in BALB/c mice infected with Leishmania donovani. These animals developed chronic infection with massive hepatosplenomegaly and hypergammaglobulinemia. In contrast to mice inoculated with 0.8 X 10(6) or 4 X 10(6) amastigotes, mice infected with 20 X 10(6) amastigotes failed to reduce liver parasite loads during 2 to 8 weeks of observation. At 8 weeks, liver size was increased by 26, 63, and 94%, respectively, in groups infected with 0.8 X 10(6), 4 X 10(6), or 20 X 10(6) amastigotes. Serum immunoglobulin G and M levels at 8 weeks in animals with the heaviest infection were increased by 53 and 80%, respectively, compared with controls. Specific antileishmanial antibodies were detected in the absence of antigen-specific delayed-type hypersensitivity or in vitro lymphocyte responses. Infection did not suppress the in vivo responses of mice to the non-parasite-related antigens sperm whale myoglobin or pneumococcal polysaccharide. Splenic mononuclear cell responses to phytohemagglutinin were suppressed as early as 2 weeks, and by 8 weeks, mice infected with 0.8 X 10(6), 4 X 10(6), or 20 X 10(6) amastigotes had phytohemagglutinin responses which were, respectively, 27.7, 13.9, and 15.8% of controls. Decreased phytohemagglutinin responses could not be related to reductions in splenic T cells; however, splenic B cells and macrophages were increased at 8 weeks of infection. The course of L. donovani infection and disease in BALB/c mice resembles events occurring in humans and should prove useful in defining mechanisms of immune alterations in visceral leishmaniasis.

Visceral leishmaniasis of jackals and dogs in northern Iran.

Abstract: In a study carried out in northern Iran on the prevalence of visceral leishmaniasis among jackals and dogs, in parasitological examination four out of 161 examined jackals and three out of 100 examined dogs were positive. In serological examination, using IFA test, 6 out of 48 examined jackals and 6 out of 34 examined dogs had titres 1/160 to 1/320.

Bone lesions in four dogs with visceral leishmaniasis

Abstract: Skeletal radiographs of four dogs with confirmed visceral leishmaniasis were reviewed. The dogs had lived in the Mediterranean area for six to 36 months prior to returning to the United States, where they lived for an additional six to 41 months before clinical signs appeared. Clinical findings included lameness, fever, cutaneous lesions, muscle atrophy, lymphadenopathy, hepatosplenomegaly, and weight loss. The dogs exhibited two distinct radiographic patterns. Periosteal proliferation and increased intramedullary radiopacity of long and flat bones occurred in two dogs. Osteolysis of bones of the carpus, tarsus, and stifle was noted in two dogs. Differences in radiographic appearance were presumed to be due to different hematogenous routes of infection. Leishmaniasis should be considered in the differential diagnosis of dogs that have traveled in endemic areas and exhibit the described radiographic changes.

The zoonotic potential of reservoirs of leishmaniasis in the Old World.

Abstract: A 'good' reservoir of leishmaniasis in the Old World is judged according to five criteria: contact with man, chronic susceptibility, good presentation of the disease organism, intimate contact with the phlebotomine sandfly vector and major source of blood meals for the vector. The endemics of cutaneous leishmaniasis in Soviet Asia and of visceral leishmaniasis in the South of France are examined in the light of these criteria. Other special examples of the criteria are highlighted and the exceptions cited. A table lists the present knowledge of the existence of reservoirs of Old World leishmaniasis.

Therapeutic Potential of Liposomes as Carriers in Leishmaniasis, Malaria, and Vaccines

Abstract: Since the first suggestion, approximately ten years ago, that lipid vesicles might have practical uses in medicine, liposomes have been a treatment in search of a disease. The approach of my laboratory since 1976 has been to search for clinical applications among infectious diseases. Because parenterally injected liposomes natually travel in great amounts to the liver and spleen I felt, at least at the beginning of our research, that attempts to tailor liposomes to particular diseases by artificially targeting the vesicles to areas other than the liver and spleen, might be difficult. Therefore, my colleagues and I have concentrated only on diseases in which the liver and spleen play an important, or even a crucial, role.

Retinal hemorrhages in kala-azar.

Abstract: We describe a patient with kala azar who presented with retinal hemorrhages. The hemorrhages resolved during treatment with pentavalent antimony.

Parasites in Sudanese cutaneous and mucosal leishmaniasis.

Abstract: Amastigotes from 18 Sudanese cases of visceral, cutaneous and mucosal leishmaniasis were measured, their immunodiffusion reactions tested and their infectivity examined in mice and hamsters. All 18 strains were serologically identical. Their amastigotes varied in size but the mucosal parasites more closely resembled the visceral than the cutaneous parasites, which were also the largest. The cutaneous parasites behaved like the Leishmania of zoonotic cutaneous leishmaniasis, being virulent to mice and producing skin lesions in both mice and hamsters following intradermal inoculation. After intraperitoneal inoculation the infection spread to the genitalia, lymph nodes, viscera and skin. In contrast, mucosal leishmaniasis parasites were indistinguishable from the visceral parasites, both types failing to infect mice by intradermal or intraperitoneal inoculation and able to infect hamsters only by the intraperitoneal injection. All inoculated hamsters developed visceral disease, usually accompanied by lymph n...

Kala-azar in Afghanistan.

Abstract: The first three cases of kala-azar from Afghanistan are reported. Two girls (aged 4 and 5 years) and a 5-year-old boy reported from Kabul and Badghis Province with classical features of visceral leishmaniasis. The diagnosis was based on the demonstration of amastigotes in the bone marrow.

Bioecologic aspects of Phlebotomine sandflies in relation to human and canine visceral leishmaniasis in northern Tunisia.

Abstract: In northern Tunisia 29 sandfly collecting places were studied for two years, in five human leishmaniasis foci, seven canine foci and in the nature. Nine species were found among the 4942 specimens collected. P. perniciosus, the well known vector of visceral leishmaniasis and the herpetophile S. minuta parroti were commonest. The sandfly season extended from april to october. P. perniciosus showed a numerical curve with one peak. It occupied various types of shelters in nature and human settlements, but prefer shady and humid shelters. In settlements it is frequently found around dwellings and has been identified in human and canine leishmaniasis foci. The highest sandfly densities and greatest species diversity were noticed in towns, especially in the cracks of the old walls or old inhabited ruins, where rodents as well as the small domestic animals provide a favourable environment for the sandflies. The historical urban ruins are the main biotope of the sandfly vectors. Infantile visceral leishmaniasis occurs during summer when the children sleep in front of the houses or in large, opened rooms exposed to P. perniciosus flies which have bitten infected dogs.

Ultrastructure of amastigotes of Leishmania donovani in the bone marrow of a dog.

Abstract: Visceral leishmaniasis was diagnosed in a dog which had been in Spain for 4 years before being brought to Florida. A bone marrow aspirate from the dog was examined by electron microscopy. Phagocytized amastigotes by macrophages had an electron-dense plasma membrane and contained ribosomes, rough endoplasmic reticulum, a well-developed Golgi apparatus, an intracellular flagellum, lipid, a kinetoplast, a row of microtubules immediately beneath the cell membrane, and a nucleus with marginated chromatin. Mean diameter and microtubule number of the dog isolate were similar to those reported for Leishmania donovani amastigotes of human origin. Plasma cells were congregated in the vicinity of parasitized macrophages.

The Distribution of Radiolabelled Drug in Animals Infected with Cutaneous Leishmaniasis: Comparison of Free and Liposome-Bound Sodium Stibogluconate

Abstract: The success of liposomes in the therapy of experimental models for visceral leishmaniasis has been demonstrated recently in several laboratories (Alving et al. 1978, Black et al. 1977, New et al. 1978), and may be attributed to the fact that both liposomes and the leishmanial parasite are taken up from the bloodstream by the Kupffer cells of the liver, so that a high concentration of liposomallyentrapped drug is brought into close contact with the parasite.