Kala-azar Epidemiology and Control, Southern Sudan

Kolaczinski, Jan; Hope, Andrew; Ruíz, José Antonio López; Rumunu, John; Richer, Michaleen; Seaman, Jill

doi:10.3201/eid1404.071099

Cited by 30 publications

(31 citation statements)

References 12 publications

(12 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…AVL caused by L. donovani occurs mainly in Sudan [15] and Somalia [16], but probably also in Yemen and Saudi Arabia, where no accurate data are available. The disease is also endemic in neighbouring Ethiopia, Kenya and Uganda.…”

Section: Anthroponotic Visceral Leishmaniasismentioning

confidence: 99%

Leishmaniasis in the World Health Organization Eastern Mediterranean Region

Postigo

2010

International Journal of Antimicrobial Agents

260

218

View full text Add to dashboard Cite

Section: Anthroponotic Visceral Leishmaniasismentioning

confidence: 99%

Leishmaniasis in the World Health Organization Eastern Mediterranean Region

Postigo

2010

International Journal of Antimicrobial Agents

260

218

View full text Add to dashboard Cite

“…Malnutrition was identified as a risk factor for severe disease and death from VL in both children (OR 5.0) and adults (OR 11.0) [100]. Malnutrition-related VL is particularly evident in displaced and impoverished populations [101, 102], and the recently described movement of transmission into peri-urban slums is likely to lead to an increase in the malnutrition-infection synergism [103]. Although the immunopathogenic basis for the malnutrition-related risk of VL has not been investigated, investigations in a murine model of polynutrient deficiency (deficient protein, energy, zinc, and iron) [104–106], which closely mimicked moderate acute malnutrition, revealed an increased rate of early dissemination following cutaneous infection with L. donovani [105].…”

Section: Spectrum and Immunopathogenesis Of Progressive Vl In Humansmentioning

confidence: 99%

Immunopathogenesis of non-healing American cutaneous leishmaniasis and progressive visceral leishmaniasis

2012

View full text Add to dashboard Cite

The outcomes of Leishmania infection are determined by host immune and nutrition status, parasite species, and co-infection with other pathogens. While subclinical infection and self-healing cutaneous leishmaniasis (CL) are common, uncontrolled parasite replication can lead to non-healing local lesions or visceral leishmaniasis (VL). It is known that infection control requires Th1-differentiation cytokines (IL-12, IL-18, and IL-27) and Th1 cell and macrophage activation. However, there is no generalized consensus for the mechanisms of host susceptibility. The recent studies on regulatory T cells and IL-17-producing cells help explain the effector T cell responses that occur independently of the known Th1/Th2 cell signaling pathways. This review focuses on the immunopathogenesis of non-healing American CL and progressive VL. We summarize recent evidence from human and animal studies that reveals the mechanisms of dysregulated, hyper-responses to Leishmania braziliensis, as well as the presence of disease-promoting or the absence of protective responses to Leishmania amazonensis and Leishmania donovani. We highlight immune-mediated parasite growth and immunopathogenesis, with an emphasis on the putative roles of IL-17 and its related cytokines as well as arginase. A better understanding of the quality and regulation of innate immunity and T cell responses triggered by Leishmania will aid in the rational control of pathology and the infection.

show abstract

“…Health coverage in this country is so minimal that some patients must walk for several days to obtain the most basic of services 32 . Ongoing civil war and unrest have had a devastating effect on healthcare delivery; however, a Comprehensive Peace Agreement between northern and southern Sudan was signed in 2005 32 .…”

Section: Cost Of Leishmaniasis Treatment In Sudanmentioning

confidence: 99%