Abstract
Developing effective therapeutics or preventive interventions for important health threats is greatly enhanced whenever accessible models can enable the assessment of clinically important outcomes. While no non-human model is ever perfect, inexpensive in vivo small animal models in such as mice are often of great help in assessing the relevant efficacy of potential interventions. In addition to acute diarrhea, the long-term growth and developmental effects of enteric infections, with or without overt diarrhea, are increasingly recognized. To address these diverse effects, inexpensive animal models are proving to be very helpful. Herein, we review the major clinical concerns with enteric parasitic and bacterial infections that are extremely common worldwide, especially in vulnerable young children living in impoverished areas, and the recently published murine models of these infections and their outcomes. We find that common dietary deficiencies seen in children in developing areas have striking effects on diarrhea and enteropathy outcomes in mice. However, these effects differ with different pathogens. Specifically, the effects of protein or zinc deficiency differ considerably with different major protozoal and bacterial pathogens, suggesting different pathogenetic pathways and intervention effects. The pathogens reviewed are the seven top parasitic and bacterial pathogens seen in children, namely, Cryptosporidium, Giardia, Campylobacter, Shigella, enterotoxigenic Escherichia coli (ETEC), enteroaggregative E. coli (EAEC), and enteropathogenic E. coli (EPEC).
Highlights
Relevant “disease” is classically seen as specific unhealthy outcomes for the “host” as a result of host and environmental determinants
(enteroaggregative E. coli), enteropathogenic E. coli (EPEC), group II norovirus, and enterotoxigenic Escherichia coli (ETEC) are each significantly associated with this marker of intestinal inflammation (Platts-Mills, unpublished personal communication with permission, 2020)
There has been a steady decline in the height-for-age Z (HAZ) scores of children in Asia, Africa, and Latin America over their first 2 years of life[4] While the causes of this early childhood stunting in poor areas is complex, it likely relates to combinations of reduced food security and repeated or even common multiple enteric infections, resulting in damage to the intestine referred to as “environmental enteropathy” (EE) or environmental enteric dysfunction (EED)
Summary
Relevant “disease” is classically seen as specific unhealthy outcomes for the “host” as a result of host and environmental determinants. Review objectively measured for assessing interventions such as effective treatments, vaccines, or preventive measures It is both overt diarrhea as well as growth, weight gains, and measurable markers of enteropathy (histologic, barrier function, or inflammatory biomarkers) that we have focused on “modeling” in this review of our experience with murine models of enteric infections and their outcomes. There has been a steady decline in the height-for-age Z (HAZ) scores of children in Asia, Africa, and Latin America over their first 2 years of life[4] While the causes of this early childhood stunting in poor areas is complex, it likely relates to combinations of reduced food security and repeated or even common multiple enteric infections, resulting in damage to the intestine referred to as “environmental enteropathy” (EE) or environmental enteric dysfunction (EED). Malnourished children experience both greater incidence and severity of diarrhea, completing a bidirectional vicious cycle of diarrhea and malnutrition.[7]
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