Some Selected Abstracts:


Faria DR, Gollob KJ, Barbosa J Jr, Schriefer A, Machado PR, Lessa H, Carvalho LP, Romano-Silva MA, de Jesus AR, Carvalho EM, Dutra WO. Decreased in situ expression of interleukin-10 receptor is correlated with the exacerbated inflammatory and cytotoxic responses observed in mucosal leishmaniasis. Infect Immun. 2005 Dec;73(12):7853-9.

Department of Morphology, Federal University of Minas Gerais, Belo Horizonte, Brazil.

Human infection with Leishmania braziliensis can lead to cutaneous leishmaniasis (CL) or mucosal leishmaniasis (ML). We hypothesize that the intense tissue destruction observed in ML is a consequence of an uncontrolled exacerbated inflammatory immune response, with cytotoxic activity. For the first time, this work identifies the cellular sources of inflammatory and antiinflammatory cytokines, the expression of effector molecules, and the expression of interleukin-10 (IL-10) receptor in ML and CL lesions by using confocal microscopy. ML lesions displayed a higher number of gamma interferon (IFN-gamma)-producing cells than did CL lesions. In both ML and CL, CD4+ cells represented the majority of IFN-gamma-producing cells, followed by CD8+ cells and CD4- CD8- cells. The numbers of tumor necrosis factor alpha-positive cells, as well as those of IL-10-producing cells, were similar in ML and CL lesions. The effector molecule granzyme A showed greater expression in ML than in CL lesions, while inducible nitric oxide synthase did not. Finally, the expression of IL-10 receptor was lower in ML than in CL lesions. Thus, our data identified distinct cytokine and cell population profiles for CL versus ML patients and provide a possible mechanism for the development of ML disease through the demonstration that low expression of IL-10 receptor is present in conjunction with a cytotoxic and inflammatory profile in ML.


Murray HW, Berman JD, Davies CR, Saravia NG. Advances in leishmaniasis. Lancet. 2005 Oct 29-Nov 4;366(9496):1561-77. Review.

Department of Medicine, Weill Medical College of Cornell University, New York, USA. hwmurray@med.cornell.edu

Governed by parasite and host factors and immunoinflammatory responses, the clinical spectrum of leishmaniasis encompasses subclinical (inapparent), localised (skin lesions), and disseminated infection (cutaneous, mucosal, or visceral). Symptomatic disease is subacute or chronic and diverse in presentation and outcome. Clinical characteristics vary further by endemic region. Despite T-cell-dependent immune responses, which produce asymptomatic and self-healing infection, or appropriate treatment, intracellular infection is probably life-long since targeted cells (tissue macrophages) allow residual parasites to persist. There is an epidemic of cutaneous leishmaniasis in Afghanistan and Pakistan and of visceral infection in India and Sudan. Diagnosis relies on visualising parasites in tissue or serology; culture and detection of parasite DNA are useful in the laboratory. Pentavalent antimony is the conventional treatment; however, resistance of visceral infection in India has spawned new treatment approaches--amphotericin B and its lipid formulations, injectable paromomycin, and oral miltefosine. Despite tangible advances in diagnosis, treatment, and basic scientific research, leishmaniasis is embedded in poverty and neglected. Current obstacles to realistic prevention and proper management include inadequate vector (sandfly) control, no vaccine, and insufficient access to or impetus for developing affordable new drugs.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:  

 13885.  Chargui N, Bastien P, Kallel K, Haouas N, Akrout FM, Masmoudi A, Zili J, Chaker E, Othman AD, Azaiez R, Crobu L, Mezhoud H, Babba H. Usefulness of PCR in the diagnosis of cutaneous leishmaniasis in Tunisia. Trans R Soc Trop Med Hyg. 2005 Oct;99(10):762-8.

13886.  Fontes CO, Carvalho MA, Nicoli JR, Hamdan JS, Mayrink W, Genaro O, Carmo LS, Farias LM.  Identification and antimicrobial susceptibility of micro-organisms recovered from cutaneous lesions of human American tegumentary leishmaniasis in Minas Gerais, Brazil. J Med Microbiol. 2005 Nov;54(Pt 11):1071-6.

13887.  Guddo F, Gallo E, Cillari E, La Rocca AM, Moceo P, Leslie K, Colby T, Rizzo AG. Detection of Leishmania infantum kinetoplast DNA in laryngeal tissue from an immunocompetent patient. Hum Pathol. 2005 Oct;36(10):1140-2. 

13888.   Passos S, Carvalho LP, Orge G, Jeronimo SM, Bezerra G, Soto M, Alonso C, Carvalho EM. Recombinant leishmania antigens for serodiagnosis of visceral leishmaniasis. Clin Diagn Lab Immunol. 2005 Oct;12(10):1164-7.

13889.   Singh R, Subba Raju BV, Jain RK, Salotra P. Potential of direct agglutination test based on promastigote and amastigote antigens for serodiagnosis of post-kala-azar dermal leishmaniasis. Clin Diagn Lab Immunol. 2005 Oct;12(10):1191-4.

13890.   Theinert SM, Basu R, Forgber M, Roy S, Sundar S, Walden P. Identification of new antigens in visceral leishmaniasis by expression cloning and immunoblotting with sera of kala-azar patients from Bihar, India. Infect Immun. 2005 Oct;73(10):7018-21.

13891.   Van der Meide WF, Schoone GJ, Faber WR, Zeegelaar JE, de Vries HJ, Ozbel Y, Lai A Fat RF, Coelho LI, Kassi M, Schallig HD. Quantitative nucleic acid sequence-based assay as a new molecular tool for detection and quantification of Leishmania parasites in skin biopsy samples. J Clin Microbiol. 2005 Nov;43(11):5560-6.


13892.     Barnett PG, Singh SP, Bern C, Hightower AW, Sundar S. Virgin soil: the spread of visceral leishmaniasis into Uttar Pradesh, India. Am J Trop Med Hyg. 2005 Oct;73(4):720-5.

13893.   Padmanabhan PK, Mukherjee A, Singh S, Chattopadhyaya S, Gowri VS, Myler PJ, Srinivasan N, Madhubala R. Glyoxalase I from Leishmania donovani: a potential target for anti-parasite drug. Biochem Biophys Res Commun. 2005 Dec 2;337(4):1237-48. 


13894 .     Breton M, Tremblay MJ, Ouellette M, Papadopoulou B. Live nonpathogenic  arasitic vector as a candidate vaccine against visceral leishmaniasis. Infect Immun.  005 Oct;73(10):6372-82.


13895.     Barratt G, Legrand P. Comparison of the efficacy and pharmacology of formulations of amphotericin B used in treatment of leishmaniasis. Curr Opin Infect Dis. 2005 Dec;18(6):527-30. Review.

13896.    Bimal S, Singh SK, Das VN, Sinha PK, Gupta AK, Bhattacharya SK, Das P.   Leishmania donovani: effect of therapy on expression of CD2 antigen and secretion of macrophage migration inhibition factor by T-cells in patients with visceral leishmaniasis. Exp Parasitol. 2005 Oct;111(2):130-2. 

13897.    Olliaro PL, Guerin PJ, Gerstl S, Haaskjold AA, Rottingen JA, Sundar S.  Treatment options for visceral leishmaniasis: a systematic review of clinical studies done in India, 1980-2004. Lancet Infect Dis. 2005 Dec;5(12):763-74. Review.

13898.    Wasunna MK, Rashid JR, Mbui J, Kirigi G, Kinoti D, Lodenyo H, Felton JM, Sabin AJ, Horton J. A phase II dose-increasing study of sitamaquine for the treatment of visceral leishmaniasis in Kenya. Am J Trop Med Hyg. 2005 Nov;73(5):871-6.