SUMMARY. Chicken anemia virus (CAV) can cause a disease syndrome characterized by severe anemia, bone marrow atrophy, and severe immunosuppression in young chicks. Maternal antibodies prevent these clinical signs but do not prevent infection, transmission of the virus, or immunosuppression. The clinical disease is rare today because of the widespread practice of vaccinating breeders, but the subclinical form of the disease is ubiquitous. The dynamics of CAV infection, CAV antibody responses, relative lymphoid organ weights, and associated lesions were studied in two broiler flocks from a commercial producer. Both groups had detectable CAV antibodies at hatch, which waned over the first 3 wk of life. Both groups had detectable CAV DNA in both thymi and bursae over the same period. At 35 days of age, virus was detectable by polymerase chain reaction in 16 of 20 chickens, and 7 of 20 had detectable antibodies. By 42 days of age, virus was detectable in 18 of 20 chickens, and 18 of 20 had antibodies to CAV. We observed a decrease in relative thymic weights beginning at 35 days of age, coincidental with the detection of CAV in the thymus. Bursal sizes began to decrease at 28 days of age, coincidental with a rise in antibody titers to infectious bursal disease virus. In this study, we demonstrated that under typical field conditions CAV infections in broilers have unique dynamics unlike those reported in egg laying strains of chickens managed under specific-pathogen-free conditions.

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