Public health aspects of visceral leishmaniasis in Montenegro

Leishmaniasis belongs to the parasitic communicable zoo noses, caused by members of Leishmania species. The infected phlebotomies sand fly carries the parasites, which cause the different forms of disease. Retrospective/prospective review of records for documented cases of visceral leishmaniasis (VL) in period from 1992 to 2012 in Montenegro shows 83 diagnostic cases, and 1 (1.20%) case with dermal leichmaniasis. with 3 (3.61%) deaths cases. Analyses of age show: 36 (43.37%) children and 47 (56.63%) adults. Examinations are based on epidemiological, clinical, hematological, patohystological and serological investigations. Infection can be sub-clinically or clinically manifested with acute, sub-acute, and chronic type. Incubation in clinically manifested infections ranges from several weeks to several months. In our study, the prevalence of general infective syndrome is registered in all of 83 manifested cases (100%). Enlarged spleen in 79 (95.18%) cases, enlarged liver in 37 (44.57%) cases, anemia in 49 (59.04%) cases, pancytopenia in 32 (38.55%) cases, and increased activity of serum aminotransferases in 37 (44.57%) cases. The diagnosis was confirmed by an analysis of bone marrow biopsy material by direct microscopy of serial sections colored by Romanowski and Giemsa s staining, and by immune-biochemical methods. Serological diagnostic is confirmed by using agglutination test. In Montenegro (in humans and dogs) two types of leishmania (L) (L. donovani, L. infantum were presented). As to therapy treatment, the common treating is with antimony drugs: glucantime is relatively satisfactory for a long time. During 2008 there were registered cases not responding to the therapy and those were manifested with relapses after therapy. In the first line of therapy, we used meglumine antimony (Glucantime) in 78 (93.97%) patients. Resistence developed in 7 (8.97%) during treatment, and relapse occurred in 5 (6.41%) patients. It was 1 (1.20%) patient treated with Miltefosine the one who had a relapse, and with Amphotericin B (Ambisome) 4 (4.82%) patients.

[1]  E. Chatelain,et al.  Visceral leishmaniasis treatment: What do we have, what do we need and how to deliver it? , 2012, International journal for parasitology. Drugs and drug resistance.

[2]  Suman Gupta,et al.  Visceral leishmaniasis: Experimental models for drug discovery , 2011, The Indian journal of medical research.

[3]  P. Ready Leishmaniasis emergence in Europe. , 2010, Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin.

[4]  M. Oshaghi,et al.  Vector incrimination of sand flies in the most important visceral leishmaniasis focus in Iran. , 2009, The American journal of tropical medicine and hygiene.

[5]  F. Frézard,et al.  Pentavalent Antimonials: New Perspectives for Old Drugs , 2009, Molecules.

[6]  R. López-Vélez,et al.  The Relationship between Leishmaniasis and AIDS: the Second 10 Years , 2008, Clinical Microbiology Reviews.

[7]  J. Berman,et al.  Advances in leishmaniasis , 2005, The Lancet.

[8]  J. Depaquit,et al.  Sandflies (Diptera: Psychodidae) in the Bar area of Montenegro (Yugoslavia). 2. Presence of promastigotes in Phlebotomus neglectus and first record of P. kandelakii , 2004, Annals of tropical medicine and parasitology.

[9]  J. Dujardin,et al.  Culture-Independent Species Typing of Neotropical Leishmania for Clinical Validation of a PCR-Based Assay Targeting Heat Shock Protein 70 Genes , 2004, Journal of Clinical Microbiology.

[10]  Shyam Sundar,et al.  Visceral leishmaniasis: current status of control, diagnosis, and treatment, and a proposed research and development agenda. , 2002, The Lancet. Infectious diseases.

[11]  J. Blackwell,et al.  Solute carrier 11a1 (Slc11a1; formerly Nramp1) regulates metabolism and release of iron acquired by phagocytic, but not transferrin-receptor-mediated, iron uptake. , 2002, The Biochemical journal.

[12]  H. Maltezou,et al.  Visceral leishmaniasis during childhood in southern Greece. , 2000, Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.

[13]  F. Pratlong,et al.  Visceral leishmaniasis and HIV-1 co-infection in southern France. , 1995, Transactions of the Royal Society of Tropical Medicine and Hygiene.

[14]  S. Martínez,et al.  Leishmania lymphadenitis diagnosed by fine‐needle aspiration biopsy , 1993, Diagnostic cytopathology.

[15]  R. Pearson,et al.  Epidemiology of visceral leishmaniasis in northeast Brazil. , 1992, The Journal of infectious diseases.

[16]  J. Berman,et al.  Recommendations for treating leishmaniasis with sodium stibogluconate (Pentostam) and review of pertinent clinical studies. , 1992, The American journal of tropical medicine and hygiene.

[17]  T. Birkland,et al.  Soluble TNF and membrane TNF expressed on CD4+ T lymphocytes differ In their ability to activate macrophage antileishmanial defense , 1992, Journal of leukocyte biology.

[18]  J. Sypek,et al.  Antileishmanial defense in macrophages triggered by tumor necrosis factor expressed on CD4+ T lymphocyte plasma membrane , 1991, The Journal of experimental medicine.

[19]  D. Fish,et al.  Visceral leishmaniasis in HIV infection and AIDS: clinical features and response to therapy. , 1990, The Quarterly journal of medicine.

[20]  N. Reiner,et al.  Modulation of in vitro monocyte cytokine responses to Leishmania donovani. Interferon-gamma prevents parasite-induced inhibition of interleukin 1 production and primes monocytes to respond to Leishmania by producing both tumor necrosis factor-alpha and interleukin 1. , 1990, The Journal of clinical investigation.

[21]  R. Pearson,et al.  Clinical and immunological responses following accidental inoculation of Leishmania donovani. , 1988, Transactions of the Royal Society of Tropical Medicine and Hygiene.

[22]  A. Bacic,et al.  Lipophosphoglycan of Leishmania major that vaccinates against cutaneous leishmaniasis contains an alkylglycerophosphoinositol lipid anchor. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[23]  S. Turco,et al.  Cell surface lipophosphoglycan of Leishmania donovani. , 1987, Molecular and biochemical parasitology.

[24]  R. Badaró,et al.  A prospective study of visceral leishmaniasis in an endemic area of Brazil. , 1986, The Journal of infectious diseases.

[25]  J. Bouvier,et al.  The major surface protein of Leishmania promastigotes is a protease. , 1986, The Journal of biological chemistry.

[26]  D. Russell,et al.  The involvement of the major surface glycoprotein (gp63) of Leishmania promastigotes in attachment to macrophages. , 1986, Journal of immunology.

[27]  P. Manson-Bahr,et al.  East African kala-azar with special reference to the pathology, prophylaxis and treatment , 1959 .

[28]  A. Nikolić,et al.  LIFE TABLES AND REPRODUCTIVE PARAMETERS OF PHLEBOTOMUS NEGLECTUS TONNOIR, 1921 (DIPTERA, PSYCHODIDAE) UNDER LABORATORY CONDITIONS , 2010 .

[29]  S. Croft,et al.  Chemotherapy in the treatment and control of leishmaniasis. , 2006, Advances in parasitology.

[30]  D. Hill,et al.  Travel and Tropical Medicine , 2005 .

[31]  S. Reed,et al.  Human T-cell responses in Leishmania infections. , 1993, Progress in clinical parasitology.

[32]  A. Barral,et al.  Evaluation of the histopathological classifications of American cutaneous and mucocutaneous leishmaniasis. , 1991, Memorias do Instituto Oswaldo Cruz.