An undercover investigation by Animal Liberation NSW

Ducks and Disease

While ducks can be fairly strong birds, the conditions they are raised in in Australia create an inviting environment for various diseases. The Department of Agriculture, Fisheries and Forestry report that the duck industry has minimal veterinary input, and that vaccines are not used(6). Total confinement systems could promote disease because of factors including the build-up of faeces, poor husbandry and the inability for ducks to clean themselves.

Outbreaks of Salmonelle, E.coli, and Pasteurella multocidia have occurred in Australia(1). The most serious disease concern for ducks is Rimerella (Pasteurella) anatipestifer(1).

In 2012, Dr Mark Simpson BVSc MANZCVSc (Avian Health) CMAVA produced a veterinary report at the request of Animal Liberation addressing issues relating to Anatipestifer Disease, Thiamine and Vitamin A deficiencies(13). Dr Simpson examined video footage of ducks within several total confinement farming facilities utilised by major Australian producers. The following passages have been extracted from this report.

By far and away the most common aetiology causing neurological disease noted within the duck broiler industry as causing this problem is Anatipestifer Disease (AD). AD is an infection with Riemerella anatipestifer which is a globally distributed, contagious disease that primarily affects young farmed ducks and turkeys. Other species of poultry and waterfowl may also be affected. In general this disease is a concern to domestic ducklings in intensive farming systems. The disease causes a variety of clinical signs including diarrhoea, lethargy, respiratory, and nervous system signs. The epidemiology and pathophysiology of the disease are, unfortunately, poorly characterised. Infection is thought to occur primarily through microtrauma to the delicate feet of the growing ducks, but may be acquired through aerosols or insect fomites (mosquitoes). Vertical transmission (through the egg) has been reported but is of unknown significance in current management systems.

Affected ducks from 14 days to 8 weeks of age often exhibit dyspnoea (difficulty breathing), ocular and nasal discharges, coughing and sneezing, tremors of the head and neck, weakness and incoordination. Poor growth rates across the affected flock are common. A severe fibrinous polyserositis, with worst lesions often occurring in the pericardium and hepatic peritoneum, is the most characteristic lesion. A fibrinous air sacculitis is common. There can be infection extending to the central nervous system, liver, spleen, and lungs. Mortality averages 5-30% but occasionally flocks can suffer losses of 75%.

Management practices are critical to the control of this disease. Poor environmental conditions such as poor ventilation, and exposure to extremes of temperature predispose to disease development. Crowding of birds may well enhance transmission. In some instances rigid sanitation and depopulation are necessary for elimination of the disease from a particular facility. Vaccines have been used overseas, with some significant improvement in outcomes. The organism has a variable pattern of antibiotic sensitivity and culture and sensitivity testing is indicated if antimicrobial therapy is considered.

The incubation period is 3-10 days after infection. Death usually ensues more quickly in younger birds, but birds approaching 6 weeks of age (age at slaughter) may last much longer. Some very young ducklings may die acutely and show no clinical signs.

The disease is highly variable, but may be loosely divided up into an early phase characterised by gastroenteritis, a mid-phase characterised by respiratory disease (with oculo-nasal discharge, sinusitis, coughing, and sneezing), and a late phase characterised by nervous system signs. These phases may not occur in every bird.

The early, gastrointestinal phase would result in green diarrhoea. The bird would feel a moderate to severe abdominal discomfort. The middle, respiratory phase would result in the pain and discomfort commensurate with a severe cold in my considered professional opinion. As the serosa surrounding the heart and liver are becoming dramatically inflamed at this stage I also expect the birds to be suffering severe pain probably perceived as an unrelenting ache originating from these organs. The delicate serosal surfaces are well recognised as highly sensitive sites of origin of pain, and are generously supplied with nociceptors (pain receptors).

Finally the birds may develop nervous system signs such as incoordination, head and neck tremors, adoption of unusual body positions (such as lying on their back with the legs paddling, opisthotonos, and torticollis), paralysis, convulsions, coma, and finally death. It is my professional opinion that birds with these clinical signs would be suffering extreme pain and discomfort, as these signs are largely the result of pathology occurring in the brain such as engorged meningeal vessels, generalised meningitis, and cerebral lesions.

Neurological signs may be due to a polyneuritis in ducks, and this may be due to a hypovitaminosis B1 (also known as thiamine deficiency). In the later stages, thiamine deficiency will lead to an accumulation of the intermediates of carbohydrate metabolism. In the initial stages of deficiency, lethargy and head tremors may be noted. A marked decrease in appetite is also seen in birds fed a thiamine-deficient diet. Poultry are also susceptible to neuromuscular problems, resulting in impaired digestion, general weakness, star-gazing, and frequent convulsions.

Vitamin A deficiency has also been recorded to produce similar clinical signs, including growth retardation, muscular weakness, pathological and inappropriate growth of endochondrial bone, ataxia, paralysis, and death. Additionally affected birds will frequently present with ruffled plumage, sinusitits, conjunctivitis, pharyngitis, and oesophagitis. Subclinical signs include an increased susceptibility to infection, most notably bumblefoot, but also aspergillosis and chlamydiosis.

As in other forms of intensive farming, there has been strong economic pressure to grow out broiler ducks more efficiently. The resulting increased growth rate, as it does in other forms of intensive farming, has led to concerns that such efficiencies increasingly impact on the welfare of the animals so changed. Unfortunately in the duck broiler segment of the market there has been very little peer-reviewed research to assess these impacts, but there is an increasing amount of concern that the domestic duck may not be as suited to intensive farming as other species. In particular the inability of these ducks to swim during the rapid growth phase of their life may change the conformation and development of bones and muscles, and predispose the birds to alterations to their anatomy. These anatomic changes could well accentuate susceptibility to other pathologies, such as bumblefoot, and contribute to problems such as ataxia and muscle weakness.

A further report by Dr Simpson in 2012 was based on post-mortems conducted on two ducks removed from a commercial duck farm in New South Wales where E. coli was found on the brain(14).

The necropsy examination (post mortem) was performed on two of the birds that had died. The hock joints in particular, were swollen and red. There were lesions on the weight-bearing pressure points of the feet suggestive of early pododermatitis (bumble foot). There were no detectable external parasites. The feathers about the vent were heavily stained with droppings, particularly fetid faeces.

The air sacs were slightly cloudy. The heart was normal. The proventriculus was slightly enlarged. The ventriculus was normal. The liver was enlarged and pale yellow, and was very friable and fatty on the cut surfaces. The spleen was mildly enlarged. The small intestine were segmentally dilated with gas and contained black/green tarry ingesta. There were focal haemorrhages on the surface of the pancreas. The colon was full of faeces.

Samples were taken from the kidneys and the brain for in-house bacteriology and samples were also sent out to an external laboratory for bacteriology.

Both in-house and external laboratories cultured Escherichia coli and Pseudomonas aeroginosa. The latter organism was isolated from the meninges while the former from the kidneys in both birds examined. The external laboratory also cultured ?-haemolytic Streptococcus from both sites, but this organism was not grown at our hospital.

These findings are consistent with a post mortem diagnosis of bacterial septicaemia and meningitis.