Download Disease entities of farmed ratites in New Zealand

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.
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MichZ.le Cooke
MAF Quality Management
Batchelar Animal Health Laboratory
Email: [email protected]