Rickets in broilers
SUMMARY
This case report describes an on-farm investigation of a
problem originally reported as "poor growth rate in broilers
associated with a change in anti-coccidial program". The
problem turned out to be so severe that some flocks were
producing almost no birds of marketable quality. One major
cause was identified, as well as contributory managemental
factors.
PRESENTING PROBLEM
An integrated company suddenly encountered a problem
characterised by a marked reduction in growth of broilers from
about 14 days of age. The farm manager claimed that this
problem occurred when the anticoccidial regimen was changed
from a straight ionophore programme to a nicarbazin/ionophore
shuttle programme.
HISTORY
Year:1984 Country: Brazil Case:84-152
Bird Species: Chicken Bird Type : Broiler
Breed: Hubbard Age: 14 days +
Clinical Signs: Reduced mobility, reduced feed and water
consumption and reduced growth rate.
Birds on farm: 250.000
Birds in flock: 60.000 (6 x 10.000)
Birds affected: almost all
Total Mortality: 25% by 30 days
Mortality last 3 days: 300
Age when problem first noted:14 days
Feed type: Mash produced on site
Water source: Artesian well
Water treatment: Automatic chlorination
Litter type: Wood shavings - new
Vaccination History:
Marek Day 1 at hatchery
Newcastle Day 1 (eye-drop) and 14 (water)
Treatment already performed : Various anti-bacterial
treatments had been tried without success.
CLINICAL AND PATHOLOGICAL INVESTIGATION
General Observations:
The organisation includes separate breeder farms and broiler
grow-out farms. The broiler grow-out farms consists of 25
houses on the same site. Distances between houses are about 25
meters. Each house has a capacity for 10.000 birds. The
birds are grown in the same house from one day old up to
slaughter (about 50 days). The parent farm on another site did
not report any problem in replacements or in egg-production
and was not visited. The feed mill and hatchery are on
adjacent sites to the broiler grow-out farm. It was decided
to visit at least six flocks roughly corresponding to birds in
each of the first six weeks of life. The objective was to
evaluate the houses and management and to select birds for
post-mortem examination.
Clinical examination:
The flocks in the first two houses entered were 3 and 10 days
old, respectively. The general level of management seemed
satisfactory. In the first house the organisation of the
brooding circle was fairly typical of that practised in the
area (circles of hard-board enclosing groups of 500 chicks
under propane brooders, with fountain type drinkers and feed
on trays). An unusual feature of the houses was the fact that
the definitive feeders (automatic chain-type) and drinkers
(automatic pendular) are placed on a slatted area raised about
25 cm from the surrounding deep litter. This is said to help
control litter humidity and is said to have been instituted
because of the warm and humid climate in the region. The
second unusual feature was that the sides of the house were
also covered in wooden slats. Normal houses in the region
(and those used for parent birds in this organisation) have
wire netting on the sides and curtains which can be raised and
lowered. This means that the houses are unusually dark and
that direct sunlight never enters. The 10 day old birds were
reasonably active, their brooding circles had been enlarged so
that they could venture on to the slatted area with the
definitive feeders and drinkers. Both the first two flocks
were considered to be clinically normal and had mortality
levels within the expected for the unit for their ages. The
next flock were 18 days old. Here there was some evidence of
poor growth rate. While there were many chicks which would be
considered normal for their age, some smaller chickens huddled
along the edges of the house. When stimulated these chicks
were disinclined to move. The next flock showed a dramatic
increase in this type of bird, and in the final two flocks
100% of the birds were well below the expected weight and had
markedly reduced mobility. It was stated that 4 previous
flocks had already been eliminated at 38 days of age. They
had not responded to the treatments used and no birds were
marketable. A sample of birds taken from each of these flocks
was brought to the feed analysis laboratory for post-mortem
examination.
Post-mortem examinations.
Flock 1 (3 days). Three birds had yolk-sac infection, one had
pericarditis, 2 had visceral gout and a further five had no
visible abnormalities. Taken in conjunction with the very low
mortality in the flock these findings were considered to be of
little significance.
Flock 2 (10 days). Some ulceration at the entrance of the
gizzard was seen in two chicks. The remaining 8 chicks were
essentially normal.
Flock 3 (18 days). Sample was composed of the smaller birds
with poor mobility. All birds had poorly-calcified bone
(shank very easily bent). The growth plate in the proximal
tibia was about 3 mm wide.
Flocks 4-6 (24-38 days). Although there was some weight gain
compared to previous flock all were markedly below the
expected weight for age. As in the previous flock there was
marked bone fragility based on the ease with which the shank
could be bent. Smaller birds had many spontaneous fractures
(especially of the ribs). A wide band of cartilage was found
in the proximal tibia. In the older birds the parathyroid
glands were easily found and, probably hypertorphied. The
appearance of the viscera was unremarkable except from some
ulceration at the entrance to the gizzard and lack of food in
the intestine of some birds. The bursal weight/bodyweight
ratios varied between 2.8 and 3.7 grams bursa per kg of
bodyweight (normal). No evidence of gross intestinal
pathology was evident. Even quite intensive scraping of the
intestinal mucosa did not reveal coccidia.
Presumptive diagnosis:
The appearance of the chicks and the relatively late onset of
the problem militated against a diagnosis of management error
or runting/stunting as a cause of this problem. The most
likely diagnosis seemed to be a serious nutritional problem
related to calcium/phosphorus.
Further examinations:
Based on the above presumptive diagnosis the results of recent
raw material and feed analyses were reviewed with the
nutritionist. No explanation for the marked bone pathology
was encountered here. A visit was now paid to the feed mill.
As part of a general review of raw-material storage, premix
preparation and storage, mixing technique and sample taking, a
visit was paid to the store where vitamins and trace elements
were held. Because of the nature of the problem particular
attention was paid to the stock of Vitamin D3. The
manufacturer indicated on the label was unknown to the
investigator. On close examination of the actual product it
was evident that it was a very light powder, not the normal
granular material. This indicated that the product was not
protected by the normal gelatin coating. Enquiry confirmed
that the acquisition of this batch coincided with the
beginning of the problems in the broilers. The switch from
the normal supplier had been made for the sake of economy. A
sample was taken for analysis. The drum bore a recent
certificate of analysis from a laboratory in Rio de Janeiro
stating that the potency of the product was 120.000
international units per gram.
Immediate action :
Based on the clinical signs, the lesions and the suspicious
appearance of the Vitamin D all broiler flocks were to receive
a 5 day treatment in the drinking water with a poly-vitamin
product with high levels of vitamin D. The Vitamin D in the
feed was to be substituted as soon as possible.
Outcome:
The flocks which were clinically unaffected at the time the
remedial action was taken developed normally. Older flocks
improved markedly in mobility, though it was necessary to
eliminate many stunted birds.
Laboratory Analysis:
This was obtained about one month after the problem was
solved. The sample of vitamin D was found to have only 10.000
i.u. per gram, less than 10% of that which it should have
been. The fact that it was an unprotected formulation could
have meant that almost no vitamin was reaching the birds.
Assay of 6 feed samples showed that the concentration of
coccidiostat was within 5% of the predicted level in all
cases.
Diagnosis : Primary rickets.
Discussion:
Poor growth rate and related problems could be related to
changes in anticoccidial program by two distinct mechanisms:
1. The new program could be less efficient, thus allowing the
direct deleterious effects of coccidiosis, and indirect
effects of poor absorption of nutrients.
2. The new drugs could have a direct toxic effect, either due
to improper dosage (many drugs), interaction with other drugs
(ex. tiamulin and some ionophores), or with nutrients which
are marginal (ex. monensin and methionine).
In this case it was possible to exclude the original suspicion
of the anti-coccidial program because the levels of
anti-coccidial were within the expected range, nicarbazin
toxicity is not potentiated by tiamulin, tiamulin was not
being used in the birds, and finallly, no evidence of clinical
or sub-clinical coccidiosis was shown to be associated with
the field problem.
A notable feature of this case was the very dramatic effects
on the broiler birds, while the parent birds supplemented with
the same vitamin preparation showed no clinical effect
(neither osteoporosis, nor deformed or soft-shelled eggs).
This fact had, at first, weighed against the hypothesis of a
nutritional deficiency. There are a number of possible
explanations :
1. The different side walls to the houses allowed more
sunlight into the house of the parent birds, facilitating
synthesis of vitamin D in the skin.
2. The parent birds had accumulated a sufficient store of the
vitamin in the previous months, and that clinical effects did
not become evident because it had become sufficiently
depleted.
3. There is a slightly smaller requirement in adult birds
compared to those in rapid growth.
A possible reason for the very dramatic manifestation of the
rickets in this case was the unusual management setup whereby
the young birds were being fed and watered on the raised
slatted area. Any nutritional cause of decreased mobility
could then lead to a vicious circle whereby it reduced feed
intake and thus resulted in further deficiency. The
possibility that the problem was precipitated by enteric viral
infection (runting-stunting syndrome, malabsorption syndrome)
was considered, especially since it was a large multiple-age
farm. However the lack of evidence of uneven growth in the
first two weeks and of feathering abnormalities and/or
intestinal/pancreatic pathology, argued against this. The
rapid response to the specific remedial action confirmed that
we were dealing with a simple deficiency disease.
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Paul Mc Mullin MVB CertPMP MRCVS
MSD AGvet
Hertford Road
Hoddesdon
Herts
Current (10/98) Contact Details (7/98):
E-mail:PaulMcMullin@Compuserve.com
Note for Certificate Candidates:
This copy of the case-histories were prepared for the RCVS library after
the examination. The author is identified. Materials to be presented for examination should however, be anonymous.
Acknowledgments should be provided separately
(see examination regulations forfurther details).