FIELD OUTBREAK OF INFECTIOUS STUNTING SYNDROME IN BROILER

CHICKENS

Infectious stunting syndrome was diagnosed in 3 broiler flocks in Jordan, the first
report of the syndrome in this country. The flocks were housed in 3 houses on the
same farm, and were hatched from eggs obtained from breeding flocks on the
same farm in the beginning of their production cycle. The 3 broiler houses were
stocked with 20,000, 14,000 and 14,000 birds on 20, 28 and 30 December 1993
respectively.

The farm follows a strict all-in all-out stocking system and the houses had been
thoroughly cleaned and disinfected before re-stocking in December. At one day
of age, chicks in all flocks looked healthy and with good uniformity, but during
the second week of life, the manager noticed a marked variation in the size of
chicks; about 10% of the chicks in each flock were stunted although active.
Stunted birds were segregated. At one day of age, chicks in all flocks looked
healthy and with good uniformity, but during the second week of life, the
manager noticed a marked variation in the size of chicks; about 10% of the
chicks in each flock were stunted although active. Stunted birds were segregated
by a partition from their normal pen mates.

At 21 and 28 days of age their average body weight of the stunted chicks was
about 50% lower than that of birds growing normally. Delayed and irregular
growth of feathers was obvious on stunted chicks. From 14 to 28 days of age the
mortality in stunted chicks in each flock was 15 to 20% compared to 1-5 to 2% in
normal birds. During the fourth week of life about 3 to 5% of the stunted chicks
started to grow again.

Post-mortem examination of 40 to 50 stunted 21 to 28-day old chicks revealed

the following gross lesions. The proventriculus was strikingly and consistently
enlarged due to marked thickening of its wall; in many cases, the mucosal
surface was ulcerated and/or haemorrhagic. In most cases the small intestine
was pale and the jejunum was distended with fluid or contained partially digested
food. The pancreas of some stunted chicks showed various degrees of atrophy.
Another consistent finding wasmarked atrophy of the bursa of Fabricius and the
thymus. Fifteen to 20 chicks growing normally 'were also necropsied but none of
them had any of the gross lesions seen in the stunted chicks.

The whole pancreas and pieces of the proventriculus from some stunted and nor
really growing chicks were fixed in 10% neutral buffered formalin, embedded in
paraffin wax and sections were stained with hematoxylin and eosin for
histological examination.

Microscopic lesions were present in all proventriculi and in some pancreases of

stunted chicks but not in those of normally growing chicks. Lesions in the
proventriculi were chronic proventriculitis and hyperplasia of the ducts of
proventricular glands. The mucosa was thickened due to dense infiltration of the
lamina propria with mononuclear inflammatory cells, and the folds of the mucosal
surface markedly increased in length and appeared like villous projections.
Focal necrosis of the mucosa with hemorrhages was present in some cases. In
the submucosa there was hyperplasia of the ducts of glands; in some lobular
glands the hyperplastic ducts replaced most of the glandular alveoli. The ducts
were variable in size and shape, some were tortuous, and in most cases were
closely packed and separated only by very thin bands of a relatively dense
fibrous connective tissue. They were lined by one to 3 giving the lumina a stellate
appearance. Occasionally the ducts were separated by a dense infiltrate of
mononuclear leukocytes.

The most consistent microscopic lesion in the affected pancreases was

vacuolation of the acinar cells; in a few cases there was mild to moderate
fibroplasia. The interlobular connective tissue was variably infiltrated by a
moderate number of mononuclear leukocytes and plasma cells.

The diagnosis of infectious stunting syndrome was based on clinical signs and
gross and microscopic lesions (Bracewetl and Wyeth, 1981; BraceweU and
Randall, 1984; Page et al., 1982; Reece et al., 1984; Riddell and Derow, 1985).
Proventriculitis/proventricular hyperplasia has been described in some cases of
infectious stunting syndrome C Kouwenhoven et al., 1978; Page et al., 1982) and
lesions of the pancreas have been reported as a feature of some stunted chicks
(Randall et al., 1981; Reece et al., 1984; RiddeU and Derow, 1985).

Several authors also observed atrophy of the bursa of Fabricius and thymus in
affected chicks (Brien, 1983; Barr et al., 1983; Reece et a/., I984; Riddell and
Derow, 1985). Although softness of long bones has been noticed in chicks
affected with infectious stunting syndrome (Page et al., 1982; RiddeU and Derow,
1985), in this outbreak the long bones of stunted chicks were of normal strength.

The cause of stunting in this outbreak could not be determined, but the
epidemiological picture indicates that the syndrome was infectious in nature and
that the etiological agent was probably vertically transmitted from breeding
flocks. Wyeth and Cheetle (1985) presented experimental evidence that
infectious stunting syndrome was vertically transmitted.

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