Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Disease entities of farmed ratites in New Zealand A review article of potential transmissible diseases in farmed ratites was recently published in Survei//ancdl).The present article details the disease entities recorded in farmed ratites in New Zealand, most of which are not infectious in origin, but are related to problems with nutrition andor management. The diseases occur at three distinct stages during the life of the bird - during the incubation and hatching periods, within the first 3 weeks of life, and later during rearing. Viruses: Nodular proliferations of nonfeathered areas of the skin are characteristic of poxvirus infections, and the nostrils and eyelids are commonly affected sited2).Infections are often transmitted by mosquitoes. A group of ten 2 to 4-month-old ostriches in a large flock of birds developed scabs around the commissures of their mouths, on their eyelids and feet. In the same flock, five birds 2 to 4 weeks of age developed similar lesions. Lesions in all the birds regressed spontaneously. Initially, it was believed that the infection may have been related to recent scabby mouth vaccination of a nearby group of sheep, but electron microscopy revealed parapox-like particles slightly different from sheep-associated virus and suggestive of OStrich-associated parapox. Unfortunately, further characterisation of the virus was not carried out. Bacteria: Various bacterial infections of ostriches and emus are presented in Table I. Fungi: Aspergillus spp, most commonly A fimigatus, are frequent causes !of mycotic pneumonia in ratite~'~). Although A fumigatus has been responsible for most cases of fungal pneumonia and/or air sacculitis of ratites in New Zealand, A niger arid A flavus have also been cultured from two separate cases. Multiple granulomas or multi-focal white nodules of caseous necrosis were seen in air sacs and the lungs, with infections noted in very young birds as well as 4-year-old adults. Candida spp are sometimes found in association with aspergillosis, being opportunistic invaders of damaged mucosal surfaces. Infections in eroded or ulcerated proventricular lesions are not uncommon, and the yeast has also been isolated from cases of air sacculitis, stomatitis, and enterifis. A mixture of Absidia, Mucor and Rhizopus spp was obtained from a case of necrotising pneumonia in a 4-week-old ostrich. Continued overleaf 10 Surveillance 25(4) 1998 Parasites: A case of air sacculitis in an ostrich was found to be due to necrotic tracts surrounded by a foreign body granulomatous reaction suggestive of aberrant parasitic larval migration. The actual cause remains unknown because there are no reports of internal parasites of ostriches in New Zealand. cially on the foot pads, around the eyes and commissures of the mouth and plugging external ear canals (Figure 1). The skin of the neck was often flaky. Histopathologically, there was marked surface and follicular ortho- and parakeratosis. Owners were made aware of the condition but reported a variable response to biotin supplementation in surviving birds. Nutritional diseases: Hatchability problems are often associated with oedema of the neck and legs, and may be due to an inade- Nutritional imbalances appear to have been quate supply of vitamin E and selenium, or responsible for bone fragility in emus. In one high humidity during i n c u b a t i ~ n ( ~ ~A( ~ ~ case ( ~ ' . in 9-month-old emus, serum calcium myopathy often occurs in conjunction with and phosphorus concentrations were adethe anasarca, resulting in the death of affect- quate, and the ratio between the two was nored chicks soon after hatching"'. The muscu- mal. However, using reference ranges for lar changes of skeletal muscle myodegenera- other species, serum copper concentrations tion and myonecrosis may be subsequent to were very low in a random sample of ten the anasarca or may be due to a nutritional birds from the flock. There is a need to estabimbalance'xi. lish a reference range and to investigate liver storage of copper in ostriches. Biotin-responsive dermatitis was reported from many ostrich farms, and primarily af- There was a case of possible thiamine deficiency in a 10-day-old chick exhibiting fected young birds (less than 3 months of age). It tended to have an insidious onset, neurological signs of ventroflexion of the with birds becoming progressively debilitat- head and flipping head over heels. ed, lame and emaciated. It was characterised Histopathology of the brain and spinal cord by thickening and crusting of the skin, espe- was unremarkable. Species Age Diseasellesions Isolate Ostrich Embryos Dead-in-shell E coli Ostrich 1 5 wk Omphalitidperitonitis (often in association with delayed yolk sac resorption)" E coli, Staphylococcus aureus, Pseudomonas stutzeri, Klebsiella oxytoca, Enterococcus faecium, Bacillus licheniformis Necrotising enteritis ~_ Clostridiumperfringens Ostrich 1-4 wk ~ ~~ ._ Ostrich 2 of 3 wks Acute suppurative enteritis E coli Ostrich 1 mth Meningoencephalitis, cerebellar necrosis Probably Lisferia spp Ostrich 1 mth Cerebellar meningoencephalitis, heoatitis. mvocarditis Ostrich 3 mth Haemorrhages. ?Terminal septicaemidbacteraemia Gram positive cocci: ?Streptococcusspp Ostrich 3 mth Enteritis, multi-focal hepatic necrosis CI peifringens, Acute focal suppurative hepatitis, pneumonia, haemorrhages . --- - ?Acute septicaemia ..__________ ~ ~ ___________ Campylobacterjejuni C jejuni, E coli ~ ~~~~~~~~ Emu 4 mth Ostrich 5 mth Enteritis C1perfringens Ostrich 4 Yr Nephrosis, hepatic necrosis, Droventricular ulcers E coli ~~~ ~~~~~ ~~~~~~~ ~ _________~~~~ ~ ~ Ostrich 4 Yr Pneumonia ~_ Necrotising hepatitis .-~ Ostrich Emu Ostrich ~~~ Emu Ostrich Mixed bacteria - -- - ~ -- Necrotising ulcerative colitis, multifocal hepatic necrosis, pancreatitis Campylobacterspp Acute focal myositis and hepatitis __ _____~ Enterococcus faecab Faeces of clinically normal birds - _ _ _ _ ~ Faeces of clinically normal birds ~ ~ ~ ~ ~ _ _ _ Salmonella Typhimurium -__ ~ ~ _ _ _ S Choleraesuis ___ a The yolk sac should be fully resorbed by 10 days of age following hatching. Environmental contaminants are usually involved - Figure 1: Biotin-responsive hyperkeratosis. Thick crusts are present around the eyes and commissures of the mouth. Neoplasia: Lymphosarcoma has been diagnosed in two ostriches and an emu. A 7-yearold female ostrich presented with difficulty defaecating and a prolapsed clitoris due to a 4 cm firm ulcerated mass partially occluding the lumen of the cloaca. It appeared to be similar to lymphoid leucosis in poultry, in that there was histopathological evidence of lymphatic spread. In another case, a 20month-old male ostrich died suddenly, and on necropsy there was a multi-lobulated subcutaneous lymphoma at the base of the neck just cranial to the thoracic inlet. Similar nodules were observed throughout the lung, liver and spleen. The kidneys were diffusely pale and enlarged and there was evidence of extensive visceral gout due to renal failure. A 6-month-old emu presented with a skin lump which was highly suggestive of lymphosarcoma on cytological examination. Management-related and miscellaneous problems: There has been an emerging pattern of acute hepatopathies in ostriches throughout New Zealand. Affected birds range in age from 3 months to 3 years, with the majority of cases at about 7 months of age. Histories included either loss of weight before death or sudden death. While multiple pale foci were sometimes noted in the liver at postmortem, many birds had no significant gross lesions. Histopathologically, there was an acute multifocal necrotising hepatitis, occasionally in association with intralesional bacteria. Special stains did not reveal any association of fungi or Ebrio spp with the lesions. Bacteria associated with necrotising hepatitis in ostriches include E coli and Pseudomonas spp'", Clostridium chauvoei'"), C1 sordellii("', Campylobacter jejuni('*', and Salmonella Choleraesuis('", but cultures performed on the livers in these cases were inconclusive. Virus isolation also produced negative results. A small number of cases appeared to be bacterial in origin, secondary to septicaemia from an enteritis via the portal circulation. However, the main histological features of many of the undiagnosed hepatopathies suggested a toxigenic aetiology. A similar outbreak in ostriches in South Africa was investigated about 15 years ago, but no conclusive cause was ascertained. One notable feature of the disease in Surveillance 25(4) 1998 11 South Africa was the presence of green urine, probably due to severe liver damage(I4).Histopathological changes in livers were similar to those seen in New Zealand. Ostriches like to feed amongst leaf litter, which sometimes contains high concentrations of Pithomyces chartarum, suggesting a mycotoxin as a possible aetiology (M Collett, Massey University, pers comm). In general, because of strict hygiene and cleaning practices, errors with temperature and humidity cause more problems than bacterial infections during incubation. Malpositioning of eggs so that the air cell is not located at the top of the shell, may also be responsible for mortality of chicks that fail to hatch‘4). Tibiotarsal rotation is thought to be due to farm-related factors such as pen design, access to water and nutrition(15). Gastrointestinal impaction (especially of sand) is of particular concern, and most cases encountered have occurred in chicks 3 months of age or younger. Large numbers of young birds may be affected, partly because of the chicks’ inquisitiveness and fossicking habits, and partly because of the absence of older birds to set an example for younger birds to mimic(4).Clinical signs include sudden depression and death within 1 or 2 days, or ill-thrift in chronically affected birds. Proventricular and ventricular impaction lead to gastric stasis and koilin hypertrophy(I6).The ingestion of metal objects may cause “hardware disease”(17). Aortic rupture was recorded in both a young and an adult ostrich. In the younger bird, a nutritional deficiency, such as vitamin E deficiency, may have played a part. The disease was associated with excess weight and lack of exercise. 12 Surveillance 25(4) 1998 A case of pancreatic ductal ectasia and associated stones was recorded in a 5-year-old female rhea. Visceral gout cases are occasionally encountered. Gout is caused by either an increase in the rate of synthesis of purine precursors of urate or the reduced elimination of urate by the kidney. Predisposing factors include increased dietary protein, certain chemicals, toxins, feed ingredients, infectious agents, vitamin A deficiency and genetic predisposition to the disease. References (1) Christensen NH. Potential for appearance of transmissible diseases in farmed ratites in New Zealand. Surveillance 24(1), 1621, 1997. (2) Raidal SR, Gill JH, Cross GM. Pox in ostrich chicks. Australian Veterinary Journal 73, 32-3, 1996. (3) Marks SL, Stauber EH, Ernstrom SB. Aspergillosis in an ostrich. Journal of the American Veterinary Medical Association 204, 784-5, 1994. (4) Philbey AW. Laboratory investigations of diseases of ostriches. Perspective No 4, 16-8. (5) Ley DH, Morris RE, Smallwood JE, Loomis MR. Mortality of chicks and decreased fertility and hatchability of eggs from a captive breeding pair of ostriches. Journal of the American Veterinary Medical Association 189, 1124-6, 1986. (6) Deeming DC. The incubation requirements of ostrich (Struthio camelus) eggs and embryos. In: Ostrich Odyssey, University of Sydney Post-Graduate Committee in Veterinary Science, Proceedings No 217. Pp 1-66. 1993. (7) Philbey AW, Button C, Gestier AW, Munro BE, Glastonbury JRW, Hindmarsh M, Love SCJ. Anasarca and rnyopathy in ostrich chicks. Australian Veterinary Journal 68, 237-40, 1991. (8) van Heerden J, Hayes SC, Williams MC. Suspected vitamin E-selenium deficiency in two ostriches. Journal of the South African Veterinary Association 54, 53-4, 1983. (9) Miller R, Sullivan N. A retrospwtive analysis of ostrich diseases in Queensland and New South Wales (1992-1994). In: Ostrich Odyssey 94, Veterinary Seminar Proceedings, Canberra, Australia. Pp 49-66. 1994. (10) Lublin A, Mechani S, Horowitz HI, Weisman Y. A paralytic-like disease of the ostrich (Struthio camelus masaicus) associated with Clostridium chauvoei infection. Veterinary Record 132, 273-5, 1993. (11) Poonacha KB, Donahue JM. Acute clostridial hepatitis in an ostricli. Journal of Veterinary Diagnosis and Investigation 9, 208-10, 1997. (12) Huchzermeyer FW. Transmissible diseases. In: Huchzermeyer F’N (ed). Ostrich diseases. Pp234. Agricultural Research Council, Onderstepoort, 1994. (13) Welsh RD, Vanhooser SL, Dye LB, Nieman RW. Salmonella infection in ratites: Diagnosis, epidemiology, and clinical significance. Veterinary Medicine 92, 193-8, 1997. (14) Worthington B. Ostriches bring new risk of disease. Hawkes Bay Herald lribune 151 4/97. (15) Squire BT, More SJ. Factors on farms in eastern Australia associated with the development of tibiotarsal rotation in ostrich chicks. Australian Veterinary Journal 76, 110-7, 1998. (16) Shakespeare AS. Recumbency in ostriches. The Compendium 01 Continuing Education for the Practising Veterinarian 17, 1440-6, 1995. (17) Samson J. Prevalent diseases of ostrich chicks farmed in Canada. Canadian Veterinary Journal 38, 425-8, l997. MichZ.le Cooke MAF Quality Management Batchelar Animal Health Laboratory Email: [email protected]