Abstract

Cryptosporidium, a protozoan parasite in the phylum Apicomplexa, is the etiological agent of cryptosporidiosis, an intestinal infection characterized by profuse watery diarrhea. Over 30 species of Cryptosporidium are recognized, some host specific whereas others infect a broader host range. Cryptosporidium hominis and Cryptosporidium parvum are the species most commonly associated with human infection; C. hominis is largely associated only with human infections, but C. parvum is also associated with infection in animals, especially young ruminants. In some regions, cryptosporidiosis is a serious veterinary problem, particularly for calves, and lambs. Many outbreaks of human cryptosporidiosis have been associated with zoonotic transmission following contact with infected animals. In Africa, where cryptosporidiosis is a major contributor to pediatric morbidity and mortality, evidence suggests transmission is principally anthroponotic. Given the frequent close contact between humans and animals in Africa, the apparent predominance of human-to-human transmission is both interesting and puzzling. In this article, after a brief “text book” introduction to the parasite, we consider in separate sections the different aspects of relevance to Cryptosporidium transmission in African countries, describing different aspects of the various species and subtypes in human and animal infections, considering livestock management practices in different African countries, and looking for any characteristic “hot spots” where zoonotic transmission has apparently occurred. Studies where transmission networks have been investigated are particularly relevant. Finally, in a separate section, we try to gather these different strands of evidence together in order to assess the reasons behind the apparent predominance of anthroponotic transmission in Africa. Reviewing the available evidence provides an opportunity to re-think transmission pathways, not only in Africa but also elsewhere, and also to pose questions. Does the predominance of human-to-human transmission in Africa reflect a relative absence of zoonotic C. parvum in African livestock? Are Africans less susceptible to zoonotic Cryptosporidium infection, perhaps resulting from early immunostimulation by C. hominis or due to inherent genetic traits? Is the African environment—in all its variety—simply more detrimental to oocyst survival? Will the so-called hypertransmissible subtypes, currently relatively rare in Africa, be introduced from Europe or elsewhere, and, if so, will they fade out or establish and spread? Our intention with this manuscript is not only to summarize and consolidate diverse data, thereby providing an overview of data gaps, but also to provide food for thought regarding transmission of a parasite that continues to have a considerable impact on both human and animal health.

Highlights

  • Addressing the Zoonotic Transmission EnigmaWhen Cryptosporidium was first discovered it was considered primarily as a parasite of animals, with the first human cases not identified until some 70 years later

  • Considering the three articles that we considered showed relatively strong evidence of zoonotic transmission of C. parvum, only the one from Egypt [105] mentions breed; the authors state that, in general, most livestock in the region of the study were native crossbreeds, the animal breeds in the study, or in the two specific farms where zoonotic transmission was suggested, were not stated

  • Exposure to Cryptosporidium early in life may be relevant for limiting future infection, including with zoonotic species, other risk factors may occur in Africa that may increase infection likelihood

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Summary

INTRODUCTION

When Cryptosporidium was first discovered it was considered primarily as a parasite of animals, with the first human cases not identified until some 70 years later. A comprehensive contact-network analysis study conducted in 4 African countries [Gabon, Ghana, Madagascar, and Tanzania; [76]], reported that C. hominis predominated among human isolates (from children below 5 years), and that C. hominis occurred not infrequently in their animal contacts (goats, sheep, cows, dogs) Given that these animals may well have ingested feces of infected children, it is unclear whether we can infer zoonotic transmission here rather than carriage in those animals in which C. hominis DNA was detected (12 cows, 5 goats, 1 sheep, and 3 dogs), given how rarely this species has previously been identified in animal infections.

Evaluation of evidence*
CONCLUSIONS
Findings
EFSA BIOHAZ
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