1/9. Mixed cryoglobulinemia secondary to visceral leishmaniasis.We describe a case of type II mixed cryoglobulinemia, with monoclonal IgMkappa rheumatoid factor, associated with visceral leishmaniasis caused by leishmania infantum. Involvement of Leishmania antigen(s) in the formation of cryoprecipitable immune complexes was suggested by the fact that cryoglobulinemic vasculitis subsided after antiparasite therapy and that anti-Leishmania antibodies, as well as rheumatoid factor, were enriched in the cryoprecipitate. We observed 2 additional patients with visceral leishmaniasis and cryoglobulinemic vasculitis. All 3 patients had seemingly contracted leishmaniasis in italy, were hepatitis c virus negative, and were initially diagnosed as having autoimmune disorders. These findings indicate that Leishmania can be an etiologic agent of type II mixed cryoglobulinemia. This parasitosis should be taken into consideration in the differential diagnosis of vasculitides in endemic areas.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/9. Congenital transmission of visceral leishmaniasis (Kala Azar) from an asymptomatic mother to her child.In this article, we report the case of a 16-month-old German boy who was admitted to the Children's Hospital of Stuttgart with a 4-week history of intermittent fever, decreased appetite, weakness, fatigue, and difficulty sleeping. He was healthy at birth and remained so for the first 15 months of his life. On admission, physical examination showed enlarged cervical, axillary, and inguinal lymph nodes, as well as hepatosplenomegaly. Laboratory data revealed pancytopenia, elevated liver function tests, and hypergammaglobulinemia. blood, stool, and urine culture results were negative. Viral infections and rheumatologic and autoimmune disorders were ruled out, but a positive titer for Leishmania antibodies was noted. In a liver and bone marrow biopsy, the amastigote form of the parasite could not be seen in cells. The promastigote form of Leishmania was found and the diagnosis of visceral leishmaniasis was made by combining the cultures of both the liver and the bone marrow biopsy material in 5 mL 0.9% saline on brain heart infusion agar, supplemented with defibrinated rabbit blood and incubated at 25 to 26 degrees C for 5 days. The parasite was identified by Southern blot analysis as leishmania infantum. Specific therapy with the antimonial compound sodium stibogluconate with a dose of 20 mg/kg body weight was begun immediately. Within 4 days, the patient became afebrile. The side effects of treatment, including erosive gastritis, cholelithiasis, worsening hepatosplenomegaly, elevation of liver enzymes, pancreatitis, and electrocardiogram abnormalities, necessitated the discontinuation of treatment after 17 days. On discharge 4 weeks later, the patient was stabilized and afebrile with a normal spleen, normal complete blood count, normal gammaglobulins, and decreasing antibody titers to Leishmania. During the next 24 months, the patient experienced intermittent episodes of abdominal pain, decreased appetite, recurrent arthralgia, and myalgia. But at his last examination in January 1998, he was well; all symptoms mentioned above had disappeared. Because the child had never left germany, nonvector transmission was suspected and household contacts were examined. His mother was the only one who had a positive antibody titer against leishmania donovani complex. She had traveled several times to endemic Mediterranean areas (portugal, malta, and Corse) before giving birth to the boy. But she had never been symptomatic for visceral leishmaniasis. Her bone marrow, spleen, and liver biopsy results were within normal limits. culture results and polymerase chain reaction of this material were negative. A montenegro skin test result was positive, indicating a previous infection with Leishmania. Western blot analysis showed specific recognition by maternal antibodies of antigens of Leishmania cultured from the boy's tissue. Visceral leishmaniasis is endemic to several tropical and subtropical countries, but also to the mediterranean region. It is transmitted by the sand fly (phlebotomus, Lutzomyia). Occasional nonvector transmissions also have been reported through blood transfusions, sexual intercourse, organ transplants, excrements of dogs, and sporadically outside endemic areas. Only 8 cases of congenital acquired disease have been described before 1995, when our case occurred. In our patient, additional evaluation showed that the asymptomatic mother must have had a subclinical infection with Leishmania that was reactivated by pregnancy, and then congenitally transmitted to the child. Visceral leishmaniasis has to be considered in children with fever, pancytopenia, and splenomegaly, even if the child has not been to an endemic area and even if there is no evidence of the disease in his environment, because leishmaniasis can be transmitted congenitally from an asymptomatic mother to her child.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
3/9. Pancreatic involvement in co-infection visceral leishmaniasis and hiv: histological and ultrastructural aspects.The involvement of the gastrointestinal tract in the co-infection of hiv and Leishmania is rarely reported. We report the case of an hiv-infected adult man co-infected with a disseminated form of leishmaniasis involving the liver, lymph nodes, spleen and, as a feature reported for the first time in the English literature, the pancreas. light microscopy showed amastigote forms of Leishmania in pancreatic macrophages and immunohistochemical staining revealed antigens for Leishmania and also for hiv p24. Microscopic and ultrastructural analysis revealed severe acinar atrophy, decreased zymogen granules in the acinar cytoplasm and also nuclear abnormalities such as pyknosis, hyperchromatism and thickened chromatin. These findings might correspond to the histologic pattern of protein-energy malnutrition in the pancreas as shown in our previous study in pancreas with AIDS and no Leishmania. In this particular case, the protein-energy malnutrition may be due to cirrhosis, or, Leishmania or hiv infection or all mixed. We believe that this case represents the morphologic substratum of the protein energy malnutrition in pancreas induced by the hiv infection. Further studies are needed to elucidate these issues.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
4/9. Clinical expression of 'silent' hepatitis b virus infection in a patient with visceral leishmaniasis.A 69-year-old male was hospitalized in January 1999 because of visceral leishmaniasis. He had also suffered from anti-hepatitis c virus (HCV)-positive chronic hepatitis for years. All serum hepatitis b virus (HBV) antigens and antibodies were negative except for anti-HBc. The patient was treated with amphotericin b cholesteryl sulfate (2 mg/kg twice a day for 7 days, iv). fever disappeared on the 3rd day of treatment, the clinical condition improved rapidly and the patient recovered. In May 1999 the patient developed icteric HBsAg-negative acute hepatitis (aspartate aminotransferase 722 U/l; alanine aminotransferase 988 U/l). Anti-HBc IgM was positive and HBV-dna was detected in serum by PCR. Anti-HAV IgM was negative. A serum sample obtained on presentation and stored at -80 degrees C was retrospectively tested and found positive for HBV-dna. In July 1999, complete remission of acute hepatitis and seroconversion to anti-HBs was observed. We suppose that a moderate depression of the immune system, probably associated with leishmaniasis, may have enhanced HBV replication in the patient who had an HBsAg-negative 'silent' HBV infection. Restoration of the immune system after successful antiprotozoan therapy might have induced cell-mediated necrosis of the HBV-infected hepatocytes and seroconversion to anti-HBs.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
5/9. Imported visceral leishmaniasis: diagnostic dilemmas and comparative analysis of three assays.The present study evaluates the performances of three noninvasive serological assays for the detection of immunoglobulin g antibodies to leishmania antigen for the diagnosis of imported cases of kala azar (visceral leishmaniasis [VL]) in a country, kuwait, where the disease is not endemic. A total of 323 individuals including 21 patients with documented cases of VL, 72 individuals with suspected cases of VL, 155 patients with other parasitic infections, and 75 healthy control individuals were tested by indirect hemagglutination assay (IHA; Behring Diagnostics GmbH, Marburg, germany), indirect fluorescent-antibody assay (IFA; bioMerieux sa, Marcy l'Etoile, france), and a qualitative membrane-based immunoassay with recombinant leishmania antigen K39 (strip-test; Intersep Ltd, Berkshire, United Kingdom). Our data show that IHA is the most sensitive test (100%), followed by IFA (86.6%) and the strip-test (80.0%). The strip-test was the most specific (100%) of the three assays, followed by IFA (93.0%) and IHA (86.0%). However, the strip-test failed to detect at least three confirmed cases of VL. We conclude that IHA is preferred over IFA and the strip-test for the screening of individuals with suspected cases of VL, especially in a country where VL is not endemic and where the number of cases is regular but limited. The details about some of the patients with VL are presented to highlight the diversity of clinical presentations and problems encountered in the diagnosis of VL in a country where VL is not endemic.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
6/9. Cellular profile of cytokine production in a patient with visceral leishmaniasis: gammadelta T cells express both type 1 cytokines and interleukin-10.The cytokine profile of CD4 , CD8 T cells, gammadelta T cells and natural killer (NK) cells (CD94 CD3-) was studied in a patient with visceral leishmaniasis (VL). The otherwise healthy, human immunodeficiency virus-negative patient acquired the disease in Tuscany, italy. diagnosis was made by demonstration of high concentrations of antibodies against Leishmania antigens in serum. flow cytometry for the detection of intracellular interferon-gamma (IFN-gamma), interleukin (IL)-2, IL-4, IL-6, IL-10, IL-13 and tumour necrosis factor (TNF)-alpha expression in peripheral blood mononuclear cells stimulated with phorbol 12-myristate 13-acetate and ionomycin was performed, followed by treatment with liposomal amphotericin b. CD4 cells were identified as major cytokine-expressing cells, capable of producing both type 1 and type 2 cytokines. A high frequency of IL-4- and IL-13-expressing CD8 cells was noted. NK cells and gammadelta T cells, thought to be involved in innate host defences against Leishmania, expressed IFN-gamma and TNF-alpha. Ten per cent of gammadelta T cells expressed IL-10, predominantly together with IFN-gamma, suggesting additional immune-regulatory roles for this T-cell subset in VL.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
7/9. Atypical American visceral leishmaniasis caused by disseminated Leishmania amazonensis infection presenting with hepatitis and adenopathy.Leishmania amazonensis is widely recognised as a cause of cutaneous leishmaniasis in latin america, but it can also disseminate to produce atypical visceral leishmaniasis with hepatitis and lymphadenopathy. The patient, an 8-year-old Brazilian boy, presented with a febrile illness and hepatosplenomegaly, elevated liver enzymes and generalised adenopathy. Serological tests using antigens of L. chagasi, the typical cause of visceral leishmaniasis in latin america, were inconclusive. Leishmania amazonensis was eventually isolated in a culture of a lymph node. The patient recovered fully after treatment with meglumine antimoniate. As this case illustrates, L. amazonensis produces a spectrum of disease that includes atypical American visceral leishmaniasis with evidence of hepatocellular injury and generalised lymphadenopathy.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
8/9. Evidence of functional cellular immune impairment in an adult Belgian with visceral leishmaniasis acquired in spain.An adult Belgian patient with visceral leishmaniasis acquired while on holiday in spain is described. This patient's cellular immunity was assessed by skin testing using six different antigens and was normal just before leaving for spain. During the leishmaniasis, skin tests with the same antigens showed complete anergy. Lymphocyte transformation tests to antigens and mitogens were severely impaired but normal T cell subsets determined by OKT monoclonal antibodies were found. Immune complexes, containing antibodies to Leishmania antigen were isolated during the patient's illness. It is most likely that visceral leishmaniasis caused the functional cellular immune impairment of the patient.- - - - - - - - - - ranking = 4keywords = antigen (Clic here for more details about this article) |
9/9. Circulating factor from a kala-azar patient suppresses in vitro antileishmanial T cell proliferation.in vitro lymphocyte blastogenesis stimulated by phytohaemagglutinin (PHA), streptococcal antigens (SKSD) and leishmanial antigens were used to assess T cell responsiveness in one patient with kala-azar before and after therapy. During the illness, responses to PHA and SKSD but not to leishmanial antigens could be detected. After treatment lymphocytes responded to all three stimuli when cells were cultured in convalescent plasma, but failed to respond to leishmanial antigens when cultured in plasma obtained before treatment. These observations suggest the presence of a circulating inhibitor of anti-leishmanial T cell responsiveness in kala-azar, and warrant further investigation.- - - - - - - - - - ranking = 4keywords = antigen (Clic here for more details about this article) |