Two commercial broiler pure lines that were previously identified to differ
in their susceptibility to Marek's disease (MD) were line-crossed to gener
ate an F-1 population. Eight F-1 males were randomly mated to four or five
F-2 females to produce an F, test: population that would be segregating for
genes affecting MD. All F-2 progeny (four hatches) were pedigreed at hatch
and placed in colony houses as nonvaccinated. At 5 days of age, they were
challenged intraabdominally with MD virus RB1B. Clinical signs, mortality a
nd gross and microscopic lesions were recorded during the MD challenge. At
8 wk postchallenge, all remaining birds were euthanatized and necropsied. D
uring the MD challenge of the first two hatches, we observed that several s
everely stunted broilers originated from certain families and the differenc
es in body weight among birds appeared as early as 3 wk postchallenge. To c
onfirm this observation, body weight at G wk postchallenge was determined f
or all surviving birds in hatches 3 and 4 (n = 242). Genetic variation in b
ody weight among broiler sire families was apparent; the average body weigh
t for males at this rime was 2.07 kg, whereas with females, it was 1.87 kg.
At lease 12.2% of the broilers, including both sexes, weighed less than I
kg ("severely stunted") at this time. The incidence of these growth-stunted
birds within each broiler sire family ranged from 0 co 26% and for dam fam
ilies, 0 to 60%. Correlation analyses between stunting and other MD-associa
ted traits revealed chat the incidence of stunting had a significant and po
sitive association with paralysis (r = 0.50). Therefore, the data suggest t
hat there may be a genetic component affecting body weighs loss during MD i
nfection. The genetic component is speculated to affect susceptibility to M
D paralysis with an indirect effect on the body weight of birds. The signif
icance of this finding is best exemplified by the identification of a broil
er sire family with over 26% of its progeny affected by this MD-associased
trait.