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To accommodate the rapid transition to external nutrients, the chick's gastrointestinal tract undergoes dramatic changes within the first few days of life. These include a rapid increase in mass, villi number and length, enterocyte number, crypt depth and proliferating cells. Concomitant with the development of digestive structures and functions a rapid development of the gut associated lymphoid tissue (GALT) occurs. This lymphoid system works within and in concert with digestive tract parenchyma, however, there is little information describing the normal development and immunological function of the avian GALT in the immediate posthatch period. The purpose of this review is to summarize current knowledge on the structure and function of the avian GALT during the early post-hatch period. At hatch, the gut is poorly populated by both innate immune leukocytes and lymphocytes. The basal numbers of lymphocytes are the result of early waves migrating from the thymus and bursa of Fabricius. Further waves of lymphocyte migration occur after 4 days of life and continue intermittently with time. In concert with this pattern of lymphocyte population adaptive immunity develops. Hence, the gut of the hatchling is unprotected by adaptive immunity during the first few days of life. Protection during this critical period might be the result of maternal antibody activity or that of the innate immune system. This system appears to be functional at this time, though much work is needed to establish this possibility. Upon maturity of the immune system, most of the immunological activity within the chick GALT is concentrated in the hindgut, and specifically so in the caeca and bursa of Fabricius. Once immune responses have become established the relevant cells disseminate systemically and to other areas of the small intestines. Finally, observations on the beneficial effects of early feeding on development of gut and GALT are discussed with reference to management of hatchlings.Ontogeny of gut associated immune competence: A. Friedman et al.

Interactions between coinfecting parasites may take various forms, either direct or indirect, facilitative or competitive, and may be mediated by either bottom-up or top-down mechanisms. Although each form of interaction leads to different evolutionary and ecological outcomes, it is challenging to tease them apart throughout the infection period. To establish the first step towards a mechanistic understanding of the interactions between coinfecting limited-term bacterial parasites and lifelong bacterial parasites, we studied the coinfection of Bartonella sp. (limited-term) and Mycoplasma sp. (lifelong), which commonly co-occur in wild rodents. We infected Bartonella-and Mycoplasma-free rodents with each species, and simultaneously with both, and quantified the infection dynamics and host responses. Bartonella benefited from the interaction; its infection load decreased more slowly in coinfected rodents than in rodents infected with Bartonella alone. There were no indications for bottomup effects, but coinfected rodents experienced various changes, depending on the infection stage, in their body mass, stress levels and activity pattern, which may further affect bacterial replication and transmission. Interestingly, the infection dynamics and changes in the average coinfected rodent traits were more similar to the chronic effects of Mycoplasma infection, whereas coinfection uniquely impaired the host's physiological and behavioral stability. These results suggest that parasites with distinct life history strategies may interact, and their interaction may be asymmetric, non-additive, multifaceted and dynamic through time. Because multiple, sometimes contrasting, forms of interactions are simultaneously at play and their relative importance alternates throughout the course of infection, the overall outcome may change under different ecological conditions.

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