A four-house broiler breeder farm of approximately 35-wk-old hens was diagnosed with egg drop syndrome (EDS’76) utilizing PCR and hemagglutination inhibition (HI) testing. Based on communication with local practitioners, the geographic area near where this flock was located had numerous EDS’76 cases in table egg layers at the time of diagnosis. An egg production drop was seen in the broiler breeder flock over a 7-day period, which prompted an investigation. During this investigation, a significant number of shell-less, wrinkled, and pale eggs were noted, but no increases in mortality or respiratory signs were observed. The disease and subsequent production drops spread horizontally across the farm over a 5-wk period. Production returned to approximately the breed standard egg production 4 wk after initial egg production drop. However, hatching egg utilization continued to be reduced for another 2 wk because of the number of thin-shelled eggs. A similar pattern of drop in egg production and subsequent return was observed in the other houses. No significant lesions were noted in the tissues submitted for histopathology. Differential diagnoses that could cause shell abnormalities and egg production drops were ruled out by submitting appropriate samples for diagnostic investigation. Egg drop syndrome 76 PCR was performed on shell-less eggs and EDS’76 was detected by PCR at two separate laboratories. Subsequently, serum was submitted for HI and positive results were found in each house as they showed egg production drop concurrent with shell abnormalities. At the time the flocks returned to breed standard production, EDS’76 titers were consistent with a uniformly exposed and seroconverted flock. The authors suspect that immunosuppression as pullets played a role in this flock being impacted by EDS. No other farms in the company’s system were observed with production drops or shell abnormalities similar to this case.

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