Susceptibility Studies in Schistosomiasis. IV. Susceptibility of Wild Mammals to Infection by Schistosoma haematobium in Egypt, with Emphasis on Rodents

Kuntz, Robert E.; Malakatis, George M.

doi:10.2307/3273805

Cited by 16 publications

(8 citation statements)

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“…Current, non-mouse animal models for urogenital schistosomiasis mostly rely on non-human primates [16] and hamsters [17], [18]. Non-human primate models, while capable of high fidelity recapitulation of human disease, are costly and difficult to use.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, the development of a mouse model of urogenital schistosomiasis, long pursued by investigators in the field, has historically failed due to the inability of S. haematobium cercariae to efficiently mature and migrate to the bladder venous plexus in the mouse [14], [15]. Thus, S. haematobium research is largely limited to primate [16] and non-murine rodent models [17], [18]. Primate models, while capable of faithful recapitulation of urogenital schistosomiasis, are prohibitively expensive and difficult to manipulate.…”

Section: Introductionmentioning

confidence: 99%

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A Novel Mouse Model of Schistosoma haematobium Egg-Induced Immunopathology

et al. 2012

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Schistosoma haematobium is the etiologic agent for urogenital schistosomiasis, a major source of morbidity and mortality for more than 112 million people worldwide. Infection with S. haematobium results in a variety of immunopathologic sequelae caused by parasite oviposition within the urinary tract, which drives inflammation, hematuria, fibrosis, bladder dysfunction, and increased susceptibility to urothelial carcinoma. While humans readily develop urogenital schistosomiasis, the lack of an experimentally-tractable model has greatly impaired our understanding of the mechanisms that underlie this important disease. We have developed an improved mouse model of S. haematobium urinary tract infection that recapitulates several aspects of human urogenital schistosomiasis. Following microinjection of purified S. haematobium eggs into the bladder wall, mice consistently develop macrophage-rich granulomata that persist for at least 3 months and pass eggs in their urine. Importantly, egg-injected mice also develop urinary tract fibrosis, bladder dysfunction, and various urothelial changes morphologically reminiscent of human urogenital schistosomiasis. As expected, S. haematobium egg-induced immune responses in the immediate microenvironment, draining lymph nodes, and systemic circulation are associated with a Type 2-dominant inflammatory response, characterized by high levels of interleukin-4, eosinophils, and IgE. Taken together, our novel mouse model may help facilitate a better understanding of the unique pathophysiological mechanisms of epithelial dysfunction, tissue fibrosis, and oncogenesis associated with urogenital schistosomiasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Novel Mouse Model of Schistosoma haematobium Egg-Induced Immunopathology

et al. 2012

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“…Historically, the primary in vivo models for UGS have been S. haematobium cercariae-infected hamsters and nonhuman primates [45]. Although these infections support the maturation of the parasite and oviposition, use of these animals as research models of human disease feature challenges.…”

Section: Hypothesis Testing Using New Animal Models Of Ugsmentioning

confidence: 99%

New Research Tools for Urogenital Schistosomiasis

Rinaldi

Young

Honeycutt

et al. 2014

Journal of Infectious Diseases

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Approximately 200,000,000 people have schistosomiasis (schistosome infection). Among the schistosomes, Schistosoma haematobium is responsible for the most infections, which are present in 110 million people globally, mostly in sub-Saharan Africa. This pathogen causes an astonishing breadth of sequelae: hematuria, anemia, dysuria, stunting, uremia, bladder cancer, urosepsis, and human immunodeficiency virus coinfection. Refined estimates of the impact of schistosomiasis on quality of life suggest that it rivals malaria. Despite S. haematobium's importance, relevant research has lagged. Here, we review advances that will deepen knowledge of S. haematobium. Three sets of breakthroughs will accelerate discoveries in the pathogenesis of urogenital schistosomiasis (UGS): (1) comparative genomics, (2) the development of functional genomic tools, and (3) the use of animal models to explore S. haematobium-host interactions. Comparative genomics for S. haematobium is feasible, given the sequencing of multiple schistosome genomes. Features of the S. haematobium genome that are conserved among platyhelminth species and others that are unique to S. haematobium may provide novel diagnostic and drug targets for UGS. Although there are technical hurdles, the integrated use of these approaches can elucidate host-pathogen interactions during this infection and can inform the development of techniques for investigating schistosomes in their human and snail hosts and the development of therapeutics and vaccines for the control of UGS.

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“…Congo, and finding no trace of infection. To the authors' knowledge, modern surveys have thus far not found naturally-acquired, non-hybrid S. haematobium infections in mammals other than primates or rodents; like S. mansoni, carnivores do not appear to be readily susceptible to infection with S. haematobium in the laboratory so there is little reason to assume they are more permissive under natural conditions (Kuntz and Malakatis, 1955b). Like Schistosoma haematobium, S. intercalatum/guineensis are considered primarily to be infections of man, and have rarely been reported from other taxa.…”

Section: Historical Records Of Schistosoma Mansoni S Haematobium Anmentioning

confidence: 99%