Ascites in Broiler Chickens

LETTER TO THE EDITOR Ascites in Broiler Chickens DEAR SIR:

Late in 1984, two broiler chicken flocks in Saskatchewan suffered serious losses concurrently. The flocks had a common feed supplier and our postmortem findings were almost identical for each. These outbreaks exemplify risks which are taken when feed additives are used irresponsibly and so we feel that a brief published account of these incidents would serve a useful purpose. Within a seven day period, broilers from two flocks designated A and B were sent for postmortem examinations to the Department of Pathology at the Western College of Veterinary Medicine in Saskatoon, and the Provincial Diagnostic Laboratory in Regina. Flock A (21420 broilers) experienced abnormally high mortality by day 18, and the operator sent 15 dead birds for postmortem at day 21, and another ten dead and eight live birds at day 32. Mortality in flock B (14280 broilers in two age groups) reached abnormal levels by day 24. A total of 20 dead broilers, aged 27 and 33 days were submitted. Our pathological investigations revealed a consistent pattern of lesions. Hence 28 of 33 birds from flock A, and 18 of 20 birds from flock B had lesions consistent with the description which follows: Distended abdomens were noted before dissection. This was due to accumulation of a large volume of fluid and gelatinous clots within the abdominal cavity (Figure 1). The livers of some birds were swollen, whereas others had a small, firm nodular liver. Petechial hemorrhages were a characteristic of swollen livers. The nodular livers often had a whitish thickened opalescent capsule which was attributed to edema. The right ventricle of the heart and the vena cava were markedly dilated and thinwalled, causing significant cardiomegaly and this was often accompanied by increased clear pericardial fluid. Histopathological evaluation of sections of myocardium revealed occasional disintegrating muscle fibres. There were also diffuse degenerative changes. When compared with

Can Vet J 1986; 27: 99-100.

sections from normal broiler chickens of equal age, the myocardial fibres were swollen, and they stained less intensely with eosin. Many very large irregularly shaped nuclei were seen; these stained less intensely with hematoxylin and often appeared vesiculated. Occasional karyorrhectic nuclei were noted. The mitotic rate

was increased. Sarcoplasm immediately surrounding the nuclei was granular, and a significant increase of fat and glycogen was detected within

the muscle fibres. Sections of liver had necrosis of hepatocytes, hemorrhages, edema and, in some, fibrosis. In addition to these changes, livers from flock B had

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~ FIGURE 1. Broiler chickens with severe ascites. In A two carcases have been partially skinned to reveal marked abdominal distention. In B the body cavities of one broiler are opened, so that the large pale gelatinous clots (arrows) in the abdomen, and the pale rounded liver lobes are visible. The heart has collapsed because the right ventricle has been incised.

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TABLE I PERCENTAGE OF SALT AND ADDITIVES RATIONS

Na Cl

Flock A' Starter Grower 0.35 0.35

IN

Flock Bb Starter 0.35

Furazoli 0.017 0.033 0.033 done None 0.013 Amprolium 0.013 None 0.0099 None Monensin None None Robenidine 0.0006 aAnalysis by Agricultural Inspection Directorate of Agriculture Canada. bFigures provided by the feed supplier.

viral intranuclear inclusion bodies in hepatocytes. Virus particles were seen and tentatively identified as adenovirus based on their morphology on transmission electron micrographs. These pathological lesions suggested primary cardiotoxicity and chronic passive congestion of the liver. Inclusion body hepatitis was also diagnosed in flock B. Both flocks used starter and grower rations supplied by one feed manufacturer. Table I lists the salt and drug levels contained in the rations. A broad spectrum antibiotic (oxytetracycline) was added to the drinking water of both flocks when the increased mortality was noticed. Water analysis is not available for either flock. Saskatchewan ground waters often have high mineral content and may contribute to salt toxicity when dietary salt is excessive. The levels of furazolidone in the starter diets are the levels used for treatment (3 times the level recommended for growth promotion in the Canadian Compendium of Medicating Ingredient Brochures). Although it is true that toxicity studies have indicated that furazolidone is less cardiotoxic for chickens than for turkeys (1), other reports indicate that levels similar to those used in these flocks, if administered for a prolonged period, will induce cardiac failure in young broiler chickens (2,3,4). Flocks

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A and B were both maintained from day 1 on this high dietary level. At day 23, flock A was switched to grower ration (0.017% furazolidone). It is of interest that another flock on the same farm was fed the same starter ration from day I to day 17, then switched to a starter containing no furazolidone. In the latter flock, no abnormal mortality was experienced, although a few cases of "water belly" were reported. Other drugs in the diets could have contributed to the cardiac failures. Monensin was present in the diet of flock B and is known to cause myocardial injury in chickens (5,6) as it can in other species. The estimated dose (less than 5 mg per bird daily) is well below the LD 50 of this drug for chickens (200 mg per kg). However this drug is considered compatible with furazolidone when the latter is present at the 0.0055% level (7). This compatibility may not apply when furazolidone is added at the therapeutic levels as it was here. Amprolium is considered compatible with 0.011% furazolidone (7) and experimental results using 0.040% furazolidone showed no increased toxicity when amprolium was added (3). Robenidine (present in the starter for flock A) is considered incompatible with amprolium or furazolidone (7). The estimated loss for each flock is tabulated in Table II. High dietary levels of furazolidone, continued over a period of more than three weeks, can likely be blamed for these losses, possibly aided by inappropriate combination with other drugs. Losses of this magnitude are obviously

incompatible with profitability. Add to this the cost of drugs, not to mention the illegality of including furazolidone at 0.033% of an animal ration without a veterinary prescription. This all adds up to a very unprofitable situation. Yours sincerely, J.P. ORR K.S. LITTLE Department of Veterinary Pathology Western College of Veterinary Medicine University of Saskatchewan Saskatoon, Saskatchewan S7N 0 WO

M. SCHOONDERWOERD Pathology Branch Laboratory Services OS Longman Building 6909 - 116 Street Edmonton, Alberta T6H 4P2

A.J. REHMTULLA Provincial Diagnostic Laboratory 4840 Wascana Parkway Regina, Saskatchewan S4S OBI

References 1. JENSEN LS, CHANG CH, WASHBURN KW. Differ-

ential response in cardiomyopathy of chicks and turkeys to furazolidone toxicity. Avian Dis 1975; 19: 596-602. 2. HARWOOD PD, STUNZ DI, WOLFGANG RW. The

efficacy of furazolidone as a coccidiostat against Eimeria tenella, and Eimeria necatrix. Proceedings of 2nd National Symposium on Nitrofurans in Agriculture. Athens, Georgia 1958: 107-117. 3. FERON VJ, VAN STRATUM PGC. The effect of furazolidone on broiler chickens fed rations containing amprolium or zoalene. Tijdschr

Diergeneeskd 1966; 91: 571-579. 4 MUSTAFA Al, IDRIS SO, ALI BH, MAHDI BM, ABU

ELGASIM Al. Furazolidone poisoning associated with cardiomyopathy in chickens. Vet Rec 1984; 115: 251. 5. HANRAHAN LA, CORRIER DE, NAQU SA. Monen-

sin toxicosis in broiler chickens. Vet Pathol 1981; 18: 665-671.

TABLE II CALCULATED LOSSES FOR FLOCKS A AND B

6. WAGNER DD, FURROW RD, BRADLEY BD.

Flock A

Flock B

Subchronic toxicity of monensin in broiler chickens. Vet Pathol 1983; 20: 353-359.

15%

16.6%

2.5% 17.5%

2.5% 19.1%

Died or culled Slaughter condemnations Total losses

7. CANADIAN COMPENDIUM OF MEDICATING INGREDIENT BROCHURES 5th ed. Feed and

Fertilizer Division, Agriculture Canada, Ottawa, 1984.