RATITES 0749-0720/98 $8.00 + .

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INFECTIOUS DISEASES AND

PARASITES OF RATITES
Simon M. Shane, BVSc, PhD, MBL

As the production of ostriches becomes commercialized, diseases

and parasitism will become more significant in this species, especially
in large, multi-age flocks or feed lots. Emus and rheas will be presented
for treatment by owners of small flocks and individual pairs representing
the remnants of the speculative multiplication period during the early
1990s.
The study of diseases and parasites of ratites in the United States
has been impeded by the previously high cost of multiplier stocki which
precluded experiments to determine susceptibility to specific pathogens.
Factors that have hindered epidemiologic investigations include the
wide distribution of small units throughout the United States and Can-
ada, incomplete records provided by owners or reluctance to provide
data, high turnover of birds in multiplier flocks, and inconsistencies in
both identification of birds and diagnostic procedures carried out by
practitioners and referral laboratories. Diagnostic procedures have con-
centrated on gross postmortem examination, histopathology, and at-
tempts at aerobic and anaerobic bacteriology and mycology. Isolation
and identification of viral agents has been limited by the nonavailability
of suitable egg-embryo, tissue culture, and laboratory systems to propa-
gate pathogens. Diagnosticians in the United States have applied earlier
reports from the Republic of South Africa and Israel, where large-scale
farming preceded the multiplication boom during the early 1990s.
Most knowledge relating to diseases of ostriches and emus has
been extrapolated from the epidemiology and pathology of commercial
poultry. Following the trends in the US broiler and egg industries

From the Department of Epidemiology and Community Health, Louisiana State University
School of Veterinary Medicine, Baton Rouge, Louisiana

VETERINARY CLINICS OF NORTH AMERICA: FOOD ANIMAL PRACTICE

VOLUME 14' NUMBER 3 • NOVEMBER 1998 455

456 SHANE

through the 1940s to the present time, it is anticipated that diseases and
parasites associated with intensification will assume economic signifi-
cance in ratites. Disease syndromes will follow the sequence of viral
immunosuppression followed by exposure to primary, respiratory, and
systemic pathogens and terminating in secondary bacterial infection
with opportunist organisms. Stress associated with climatic extremes,
nutritional deficiencies, mismanagement, or stocking at high density
predisposes flocks to the effects of protozoal and metazoan parasites. It
is anticipated that feed lot conditions will give rise to pasteurellosis,
salmonellosis, erysipelas, clostridial enteritis, helminthiasis, and coccidi-
osis. Maintaining large populations of birds in a limited geographic area
will facilitate the adaptation of poultry pathogens to ostriches and emus.
This is exemplified by the occurrence of velogenic Newcastle disease in
ostriches in Israel and isolation of avian influenza from emus and rheas
in the United States and Europe.

BIOSECURITY

The commonality between disease agents in commercial poultry

and those in ratites suggests that preventive measures used in the
broiler and egg industries are necessary to prevent disease in commercial
ostriches and in individual emu flocks.
The following principles of biosecurity, which limit the introduction
and dissemination of disease, are critical to the productivity and profit-
ability of the US poultry industry.
• Conceptual biosecurity involves location of farms in isolated areas,
operation of single-species units, and limiting the age spread of
birds using all-in-all-out placement cycles.
• Structural biosecurity encompasses investment in fencing, decon-
tamination equipment, and facilities, which reduce the probability
of introduction of disease by wildlife reservoirs, personnel, and
equipment.
• Operational biosecurity includes the routine procedures relating
to hygiene and decontamination in the operation of breeding and
grow-out units, which limit the introduction of disease agents.
A detailed description of the methods of transmission of pathogens
associated with ratites and a review of procedures to limit the introduc-
tion and spread of disease are included in texts on biosecurity in the
poultry industry3o,41 and in texts specifically for ratites. 34

CLASSIFICATION OF RATITE DISEASES

BY ORGAN SYSTEM

Classifying diseases by organ system facilitates the recognition and

diagnosis of specific diseases by practitioners. The documented and
 INFECTIOUS DISEASES AND PARASITES OF RATITES 457

recognized diseases of ratites are therefore reviewed in relation to the

principal organ systems.

RESPIRATORY SYSTEM

Mycoplasmosis

Etiology and Occurrence. Mycoplasmas other than those occurring

in chickens (Mycoplasma synoviae and M. gallisepticum) have been isolated
from ostriches. The clinical significance of these isolates is unknown. It
is possible that with intensification of the industry, mycoplasmas may
emerge as potential primary pathogens or interact synergistically with
other viral and bacterial respiratory agents.
Transmission. Mycoplasma spp are transmitted in poultry by the
transovarial vertical route and by lateral contact between infected and
susceptible birds. The organism can be transmitted by fomites, although
the mycoplasmas are sensitive to environmental exposure.
Epidemiology. Multiple-age production programs, maintenance of
ratites of different species in close contact with domestic poultry, contact
with free-living birds, and introduction of new stock without quarantine
all contribute to infection of flocks.
Clinical Signs. Other than a single case of arthritis in an emu, there
is no specific syndrome associated with Mycoplasma infection in ratites.
Pathology. A potentially pathogenic Mycoplasma sp could cause
airsacculitis or seropurulent arthritis, by analogy with commercial poul-
try.
Diagnosis. A diagnosis can be made by isolation and identification
of Mycoplasma spp from air sac or tracheal swabs or synovial fluid.
There is no evidence of any commercial ratite species showing
antibodies on the rapid serum plate agglutination test using either M.
gallisepticum or M. synoviae antigen.
Treatment. If treatment is required, tylosin or a fluoroquinolone
antibiotic should be administered by the parenteral or oral route.
Prevention. Appropriate preventive measures include adequate bio-
security, maintenance of closed flocks, and quarantine of newly acquired
birds with appropriate screening.

Coryza

Etiology and Occurrence. Haemophilus spp have been isolated from

outbreaks of sinusitis in ostriches in Israe1. 25 Cases have not been re-
ported in the United States, although the infection is endemic in the
commercial egg industry in some states, including California.
The following information is based on the disease in chickens,
which are susceptible to H. paragallinarum.
Transmission. Haemophilus infection is transmitted directly from
458 SHANE

infected to susceptible birds. Recovered chickens remain permanent

carriers. Although the organism is sensitive to environmental exposure
and does not survive for longer than 24 hours outside the host, contami-
nated equipment, trailers, clothing, and feed bags can transmit infection.
Epidemiology. Direct and indirect contact between ratites and in-
fected commercial or backyard chickens may predispose birds to infec-
tion.
Clinical Signs. Affected ostriches in Israel showed lachrymation
and seropurulent nasal exudate. Chronic cases showed sinusitis.
Pathology and Diagnosis. Affected birds show rhinitis and sinusitis.
The organism can be cultured from choanal swabs and from sinus
exudate by aspiration biopsy or at postmortem examination. Appro-
priate media and microbiologic techniques are required to isolate and
identify Haemophilus spp.
Treatment. Administration of trimethoprim-sulfa or penicillin dihy-
drostreptomycin suppresses clinical signs.
Prevention. Appropriate biosecurity, including quarantine of ac-
quired stock, reduces the probability of introduction of this disease.
If coryza emerges as a problem in commercial flocks, an autogenous
bacterin may be required to vaccinate immature ostriches before transfer
to feed lots.

Aspergillosis
Etiology and Occurrence. Mycotic pneumonia and airsacculitis is
caused by Aspergillus fumigatus and other Aspergillus spp. The condition
occurs in neonates, resulting in death or stunting in both emus and
ostriches. Losses may be extensive, involving a high proportion of the
annual crop, or the infection may be confined to individual birds.
Transmission. Aspergillosis is a congenital condition acquired either
by penetration of the eggshell by spores after oviposition or following
contamination during incubation. By analogy with commercial poultry,
infection may be acquired within the first 48 hours after hatch if chicks
are brooded on contaminated litter.23
Epidemiology. Delay in collection of eggs, especially when oviposi-
tion occurs in contaminated and damp nesting areas, contributes to shell
penetration by Aspergillus spores. Defective hatchery hygiene results in
high levels of Aspergillus spores in setters and hatching compartments,
which will infect neonates. The practice of retaining chicks in the hatch-
ing compartment for longer than 12 hours predisposes them to infection.
Clinical Signs. Affected chicks may show dyspnea within the first
few days after hatch. Recovered birds are invariably stunted. Morbidity
and mortality are influenced by the extent of egg-borne infection and
hatchery contamination.
Pathology. Dead chicks show 1- to 3-mm-diameter, yellow to white
granulomas in the lungs or adherent to the air sacs and viscera. Chronic
cases show large confluent granulomas adherent to the serosa of viscera,
 INFECTIOUS DISEASES AND PARASITES OF RATITES 459

air sacs, and peritoneum. Aspergillus spp can be isolated from lesions
using Sabouraud's dextrose agar. Characteristic hyphae are observed on
histologic examination of specially stained sections.
Treatment. Treatment with ketoconazole provides variable results 6
and is not recommended for commercial flocks, based on cost in relation
to clinical response.
Prevention. Frequent collection of eggs and maintenance of an
appropriate level of hygiene in the hatchery reduce the probability of
Aspergillus infection in chicks. Routine monitoring of hatcheries using an
air sampler or exposure of petri dishes containing Sabouraud's dextrose
medium is recommended.

Respiratory Helminths

Etiology and Occurrence. Syngamus trachea has been described in

the trachea of ostriches. Cyathostoma variegatum occurs in the bronchi
of emus.
Transmission. Ingestion of third-stage larvae encysted within snail
or beetle intermediate hosts or direct infection with mature ova con-
taining third -stage larvae in soil.
Epidemiology. Free-living birds, including passeriforms and galli-
forms, serve as definitive hosts.
Clinical Signs. Affected ostriches and emus show dyspnea and
head shaking.
Pathology and Diagnosis. Mature Syngamus worms are observed
in the trachea, and Cyathostoma organisms are found in the major bronchi
of emus on postmortem examination. Double operculated ova are identi-
fied in fecal flotation preparations.
Treatment. Ivermectin (200 I-1g/kg), fenbendazole, or mebendazole
can be used for treatment.

DISEASES OF THE GASTROINTESTINAL TRACT

Salmonellosis

Etiology and Occurrence. A variety of paratyphoid Salmonella spp

have been isolated from emus, ostriches, and rheas. S. arizonae has been
identified in the ovary of an ostrich. This has implications relating to
vertical transmission, by analogy to the turkey industry. Emus infected
with S. pullorum under experimental conditions develop antibodies to
the pathogen, and ratites are considered susceptible to this vertically-
transmitted pathogen of galliform birds.
Transmission. Salmonella can be transmitted by direct contact with
infected carriers. Indirect infection occurs through contaminated cloth-
ing, equipment, housing, or ingestion of feed containing viable Salmo-
460 SHANE

nella spp. Rodents, free-living birds, and possibly insects serve as reser-
voirs of infection. Vertical, nonovarian transmission of Salmonella in
emus has been documented. Recovered carriers disseminate infection to
younger, susceptible ratites in a flock by direct or indirect contact.
Epidemiology. Deficiencies in biosecurity predispose to infection.
Introducing newly acquired birds directly into the flock can result in
extensive infection. Trading and speculation in stock, which character-
ized the industry during the early years of this decade, resulted in
distribution of Salmonella, especially in birds passing through auction
barns. Improper hygiene procedures relating to collection and incubation
of eggs may result in congenital salmonellosis.
Clinical Signs. Affected neonates and juveniles show depression or
may die acutely without obvious clinical abnormalities. There are no
specific signs attributed to Salmonella infection.
Pathology. There are no specific lesions associated with salmo-
nellosis. Neonates may show omphalitis, and with progressing age,
enlargement of the spleen and liver are evident. Generalized vascular
congestion and the presence of granulomas in the viscera may be ob-
served in chronic cases.
Diagnosis. Appropriate microbiologic examination reveals the pres-
ence of Salmonella. The isolation of Salmonella spp from the intestinal
tract of a ratite does not necessarily imply that the organism was respon-
sible for the death of a patient. Farming practices predispose birds to
intestinal colonization, which may not be of significance in otherwise
clinically unaffected birds. Isolation of Salmonella is a function of diag-
nostic intensity. All cases submitted for postmortem examination, irre-
spective of presentation, should be screened for Salmonella by culturing
heart-blood swabs and sections of intestine and liver. Submission of
Salmonella isolates to a reference laboratory for speciation and serotyping
is recommended if salmonellosis emerges as a flock problem. Cloacal
and oviduct swabs from mature breeders and swabs from eggs and the
hatchery environment should be examined if the yolk sacs of chicks and
neonates yield Salmonella spp.
Treatment. Young chicks with systemic salmonellosis can be treated
with fluoroquinolone antibiotics and supportive therapy. Although ther-
apy suppresses mortality, treated birds invariably become chronic carri-
ers, intermittently excreting Salmonella.
Prevention. Biosecurity procedures to limit the possibility of intro-
duction of Salmonella spp include decontamination of personnel, trailers,
and equipment. Newly acquired birds should be quarantined and
screened for Salmonella by examination of fecal and cloacal swabs during
a 4-week period. The whole-blood Salmonella pullorum/gallinarum aggluti-
nation test should also be performed during quarantine to detect anti-
bodies to Salmonella type D infection. Veterinarians should assist clients
in complying with the requirements of the National Poultry Improve-
ment Plan, which now recognizes ostriches as a commercial species.
Monitoring of the environment of flocks, including soil, water, incuba-
 INFECTIOUS DISEASES AND PARASITES OF RATITES 461

tors, and brooding areas, should be carried out at intervals or should be

incorporated into surveillance programs in the event of outbreaks of
salmonellosis. The water supply to flocks should be chlorinated at a
level of 1 to 2 ppm. Feed should be free of Salmonella contamination.

Campylobacteriosis
Etiology and Occurrence. Campylobacter jejuni is widely distributed
in commercial poultry and in free-living avian species. 31 C. jejuni is not
a primary pathogen in commercial chickens and turkeys. Toxigenic and
invasive strains of the organism may act synergistically with viral and
protozoal enteropathogens. C. jejuni is pathogenic to humans, and ostrich
and emu meat may serve as a vehicle for food-borne infection.
Transmission. Campylobacter can be transmitted to commercial
flocks by free-living birds, rodents, and contaminated water.
Epidemiology. C. jejuni is sensitive to desiccation and does not
survive in a dry environment for longer than a few hours. The organism
can persist in moist biological material for up to 5 days and for longer
periods in water and biological films lining piping and tanks. The
epidemiology of Campylobacter infection in commercial poultry has not
been clearly defined, although it is assumed that reservoirs, including
rodents, free-living birds, and possibly cattle, may serve as a source of
infection.
Clinical Signs. No specific clinical condition of ratites has been
attributed to C. jejuni, although the organism is frequently isolated
from the intestinal tract or liver of ratites submitted for postmortem
examination. Lawsonia spp, which is related to Campylobacter, was iso-
lated from a single case of cloacitis and intestinal prolapse in immature
emus on a farm in Louisiana. 21
Pathology and Diagnosis. No specific descriptions of lesions associ-
ated with Campylobacter infection in ratites is available.
Sections of ligated intestine on ice or culturette swabs placed in a
transport medium are required, because Campylobacter is sensitive to
desiccation. Isolation requires a special selective medium and incubation
for 24 to 48 hours at 42°C in a microaerophilic environment.
Treatment. Erythromycin is considered to be the antibiotic of choice
if treatment of Campylobacter is required.
Prevention. The water supply to the flock should be chlorinated.
Appropriate biosecurity procedures limit the probability of infection.
These include elimination of rodents, reduction of contact with free-
living birds, decontamination of equipment and footwear, and mainte-
nance of single-species operations.

Clostridial Enteritis
Etiology and Occurrence. Clostridium spp, including C. perfringens,
have been isolated from the intestines of dead ostriches and emus. C.
462 SHANE

chauvoei enterotoxemia, associated with paralysis, has been recorded in

ostriches housed in a ZOO.22 C. difficile has been identified as the cause of
mortality in 20-day-old ostrich chicks. 35
Transmission. Clostridium spp are spore-forming organisms that
persist in soil for long periods. The organism is ingested by chicks,
which are geophagous and coprophagous. Many nonpathogenic Clostrid-
ium spp are probably normal inhabitants of the intestinal tract.
Epidemiology. Clostridial enterotoxemia results from excessive in-
traluminal proliferation of toxigenic Clostridium spp. Any factor that
affects normal intestinal motility predisposes to enterotoxemia. Move-
ment of immature birds among pens, transport stress, abrupt change in
diet, deprivation of feed and water, or ingestion of large quantities of
substrate or vegetation resulting in impaction or delayed intestinal pas-
sage can predispose to enterotoxemia. The condition is analogous to
clostridial enteritis in commercial poultry.33
Clinical Signs. No specific clinical presentation has been described.
Mortality may be acute, or young birds may die, showing anorexia and
depression indistinguishable from ventricular impaction.
Pathology and Diagnosis. By analogy with chickens, lesions can
range from mild hyperemia of the intestinal mucosa to pseudomembra-
nous enteritis. Confirmation of the diagnosis is based on histologic
examination of affected sections of intestine, which show necrosis associ-
ated with the presence of gram-positive bacteria. Isolation and identifi-
cation of Clostridium spp using anaerobic culture is suggested in cases
involving commercial feed lot operations. An evaluation of managemen-
tal factors that predispose to infection and implementation of diagnostic
procedures to detect concurrent protozoal or viral enteric infections are
recommended.
Treatment. For extensive outbreaks, zinc bacitracin can be adminis-
tered in drinking water to reduce mortality in affected flocks.
Prevention. Under commercial conditions, necrotic enteritis is sup-
pressed in broilers by including zinc bacitracin in feed at a level of 30
g/ton. Approval by the US Food and Drug Administration (FDA) would
be required for this compound to be added to ratite rations. Appropriate
trials to demonstrate safety and effectiveness will be necessary to obtain
approval.

Necrotizing Typhlocolitis of Rheas

Etiology and Occurrence. A series of outbreaks of necrotizing

typhlocolitis were attributed to concurrent infection with a trichomonad
and a spirochete. The condition has been diagnosed in rhea flocks in the
midwest. 28
Transmission. Immature birds are exposed to the presumptive
causal protozoal and bacterial pathogens by ingestion of soil or by
contact with clinically healthy carriers.
Epidemiology. The cases recorded in the literature all involved
 INFECTIOUS DISEASES AND PARASITES OF RATITES 463

multispecies farms, and it is presumed that organisms innocuous in a

natural definitive host are pathogenic in a recently introduced species
such as the rhea, especially when subjected to stress.
Clinical Signs. Affected juvenile rheas show depression and an-
orexia. Flock mortality rate may exceed 80%.
Pathology and Diagnosis. Acute cases show marked distension of
the terminal colon and ceca, with the accumulation of intraluminal fluid.
Advanced cases show fibronecrotic and pseudomembranous colitis. Ce-
cal cores similar to those observed in histominiasis in turkeys are ob-
served in chronic cases.
The condition is diagnosed by histologic examination using Periodic
Acid-Schiff (PAS) stain for protozoa and Warthin-Starry stain for spiro-
chetes.
Treatment. Oral metronidazole in combination with parenteral lin-
comycin reduced mortality in affected flocks.
Prevention. Rheas should be raised on a single-species farm, with
separation of neonate, juvenile, and adult birds. Appropriate hygiene
and disinfection of brooding pens should be carried out. It may be
necessary to use concrete flooring in brooding pens to facilitate intercycle
decontamination.

Viral Enteritidis

Etiology and Occurrence. A number of viral infections have been

implicated in mortality in ostrich and rhea chicks. These include coro-
naviruses. 13 It is noted that numerous cases of high mortality and stunt-
ing occur in ostriches and emus without identification of a specific
bacterial or protozoal agent. The isolation and identification of viruses
from the intestinal tract is a function of diagnostic intensity. It is antici-
pated that viral agents, including adenoviruses, circoviruses, and arena-
viruses, will be described following the emergence of intensive ostrich
production and feed lot management systems.
Transmission. Viruses associated with enteritis in juvenile ratites
may be transmitted directly from adult carriers or be acquired through
environmental contamination or indirect infection from fomites.
Epidemiology. Maintaining large numbers of ratites in multi-age or
multispecies farms predisposes to the perpetuation of infection. Environ-
mental conditions favoring the proliferation and persistence of protozoal
and bacterial pathogens exacerbate primary viral enteric infection.
Clinical Signs. Generally, affected chicks are anorexic and depressed
and die acutely, showing diarrhea and dehydration.
Pathology and Diagnosis. Chicks show evidence of dehydration
and absence of ingesta in the anterior gastrointestinal tract. The jejunum
may be distended with clear to turbid fluid. Intercurrent observations
may include nephrosis owing to reduced water intake, atrophy of the
spleen and thymus following immunosuppression, delayed feather de-
velopment and rickets, and stunting secondary to malabsorption. Histo-
464 SHANE

logic examination may show varying degrees of villous atrophy and the
presence of inclusion bodies in enterocytes or hepatocytes, depending
on the nature of the pathogen. Electron microscopy of intestinal tissue
or feces may reveal the presence of viruses, which can be tentatively
identified on the basis of morphology.
Treatment. No specific recommendations can be provided other
than operation of facilities on a separate-species basis with all-in-all-out
brooding of chicks. Epidemiologic evaluation to determine the possibil-
ity of vertical transmission of agents should be performed, and appro-
priate preventive measures, implemented. Biosecurity may limit the
dissemination of the agent to other farms. Thorough decontamination of
brooding facilities may reduce the exposure of young chicks to environ-
mental agents.

Zygomycosis

Etiology and Occurrence. Infection with fungi of the genera Basidia,

Rhizopus, and Mucor can result in stomatitis ventriculitis and systemic
mycosis.
Transmission. Infection is transmitted by ingestion of the infective
agent from contaminated soil and feeders.
Epidemiology. Zygomycosis is encountered in immature ratites sub-
jected to environmental stress, prolonged antibiotic therapy, immuno-
suppression, or intercurrent gastrointestinal infection and parasitism.
Clinical Signs. Stomatitis may be evident, but generally, birds show
depression, anorexia, and stunting, without specific signs or obvious le-
sions.
Pathology and Diagnosis. Focal stomatitis, esophagitis, proventicu-
litis, and ventriculitis are observed. Ulcers may occur in the proventicu-
Ius and ventriculus in advanced cases. A diagnosis of zygomycosis is
based on histologic examination of affected tissue using an appropriate
staining technique. Fungi can be cultured on Sabouraud's dextrose agar.
Treatment. Ketoconozole or nystatin are recommended as specific
therapy. Supportive treatment, including broad-spectrum antibiotics,
may be indicated to suppress concurrent bacterial infection. Extended
oral antibiotic therapy is contraindicated, because this suppresses the
normal intestinal flora and predisposes to mycosis.
Prevention. Obvious risk factors should be identified and elimi-
nated.

Candidiasis

Etiology and Occurrence. Candida spp, including C. albicans, occur

frequently in the environment of immature ratites.
Transmission. Infection is transmitted by ingestion of Candida spp
in water or contaminated feeders or from the environment.
 INFECTIOUS DISEASES AND PARASITES OF RATITES 465

Epidemiology. Candidiasis usually follows immunosuppression or

environmental stress, or it may be iatrogenic, resulting from prolonged
therapy with antibiotics including tetracyclines.
Clinical Signs. Depression, anorexia, and progressive weight loss
occur. Characteristic stomatitis may be observed on clinical examination
of the oropharynx.
Pathology and Diagnosis. Mild cases show focal stomatitis, pharyn-
gitis, and esophagitis. Advanced cases may involve ulceration or pseu-
domembranous lesions of the pharynx, esophagus, or proventiculus.
Diagnosis is based on identification of the pathogen, which can be
cultured on Sabourand's dextrose agar, or by histologic examination
using appropriate stains.
Treatment. Treatment is conducted using ketoconozole or nystatin
with appropriate supportive therapy.
Prevention. Preventive measures include alleviation of intercurrent
immunosuppressive factors where possible, upgrading of hygiene, and
decontamination of facilities in units where the condition has occurred.
In turkeys, nystatin may be incorporated into feed for a limited period
to suppress infection.

Endoparasites

A detailed description of the diagnosis and life cycle of endopara-

sites of ratites is documented by Craig and DiamondY The following
information is provided in relation to the most significant endoparasites
of the digestive tract.
Libiostrongylus douglassii is responsible for diphtheritic proventricu-
litis in young ostriches in South Africa and is responsible for mortality
rates of up to 50% of affected flocks. This parasite has been identified in
ostriches in North America. Ivermectin (200 /-1g/kg), fenbendazole (15
mg/kg), and levamazole (30 mg/kg) have been shown to be efficacious
and safe in the treatment of young ostriches.
Trichostrongylus tenuis has been identified in the cecum of the emu.
Infection results in mucoid-blood-stained diarrhea.
Houttuynia struthionis is the principal cestode of the ostrich and rhea
and causes extensive losses in the South African industry. Praziquantel
(7.5 mg/kg) is effective against cestodes of ostriches.

DISEASES OF THE INTEGUMENT

Ostrich Pox

Etiology and Occurrence. Pox has been diagnosed in ostriches in

IsraeP6 and in the Republic of South Africa. 3 An outbreak of ostrich pox
occurred in Arizona following unseasonal and excessive rainfall in 1995.
Transmission. Avian pox viruses are transmitted by mosquitoes. It
466 SHANE

is presumed that direct transmission can occur between confined pen

mates by analogy to commercial chickens.
Epidemiology. Introduction of ratites into areas with endemic pox
results in seasonal outbreaks. The occurrence of the disease is a function
of vector density and is influenced by temperature, rainfall, and the
presence of susceptible hosts.
Clinical Signs. Early cutaneous lesions appear as 3-mm- to l-cm-
diameter raised areas on the eyelids and nonfeathered skin adjacent to
the cere. The lesions of the eyelids may coalesce to produce confluent,
proliferative masses, resulting in symblepharon. The diphtheritic form
is characterized by focal pharyngitis and tracheitis causing dyspnea.
Flock morbidity may exceed 80 0/0, and losses may reach 50 0/0 in en-
demic regions.
Pathology and Diagnosis. The proliferative lesions of the skin are
characteristic. Histologic examination shows the presence of intracy-
toplasmic inclusion bodies in sections of tracheal mucosa and skin tissue.
Pox virus can be isolated from lesions by inoculating 10-day-old em-
bryonated specific pathogen free (SPF) chicken eggs via the chorioallan-
toic route.
Treatment. Application of antibacterial compounds to the dermal
lesions with supportive therapy, including administration of fluids, is
suggested. Affected birds should be separated from pen mates to avoid
persecution and the possibility of lateral transmission by direct contact.
Prevention. Under emergency conditions, pigeon pox or chicken-
strain fowl pox vaccine may be administered by intradermal stab in
birds at risk. If ostrich pox emerges as a significant problem, a specific
vaccine may be required. It is noted that the commercial ostrich industry
is concentrated in arid areas of the United States where pox is not
generally a problem, owing to environmental conditions that limit the
population of mosquito vectors.

Dermatomycosis

Etiology and Occurrence. Dermatophytes of the genera Trichophy-

ton, Microsporum, Streptomyces, and Rhizopus have been implicated in
avian dermatomycosis. Trichophyton has been identified as the cause of
mycotic dermatitis in ostriches in Canada. 12
Epidemiology. It is presumed that the various fungi responsible
for mycotic dermatitis infect young ostriches that have contact with
contaminated fomites. Columbiforms and free-ranging galliforms may
serve as reservoirs of infection.
Clinical Signs. Affected birds show cutaneous proliferation of the
skin at the angle of the beak, on the eyelids, and on the neck, associated
with depilation. Young birds with advanced dermatomycosis are an-
orexic, stunted, and lethargic.
Pathology and Diagnosis. Microscopic examination of sections of
affected tissue show orthokeratotic hyperkeratosis. With appropriate
 INFECTIOUS DISEASES AND PARASITES OF RATITES 467

staining, fungal hyphae are observed. Fungi may be cultured on Sabou-

raud's dextrose agar.
This condition should be differentiated from polychlorinated biphe-
nyl (PCB) toxicity and deficiencies of biotin and pantothenic acid, which
present as hyperkeratosis.
Treatment. Griseofulvin can be administered in drinking water.
Supportive therapy, including subcutaneous fluids and nutritional sup-
plements, may be recommended for debilitated birds.
Prevention. Appropriate biosecurity procedures and hygiene should
limit the occurrence of dermatomycosis. Thorough disinfection of the
environment and replacement of substrate is necessary to prevent infec-
tion of subsequent placements of chicks in brooding units housing
infected birds.

Conjunctivitis

Etiology and Occurrence. An outbreak of conjunctivitis attributed

to Staphylococcus hyicus has been described in Canada. 9
Clinical Signs. A single affected ostrich showed severe conjunctivi-
tis.
Diagnosis. Microbiologic examination yielded Staphylococcus hyicus.
Appropriate diagnostic procedures eliminated diagnoses of infection
with Haemophilus, Mycoplasma, and Chlamydia.
Treatment. The infection responded to topical application of a chlor-
amphenicol ointment.

Ectoparasites

The ectoparasites of ra tites are described in detail by Craig and

Diamond. 11
Ratites may be infested with ixodid and argasid ticks, mites, and
lice. Carbaryl (Sevin) dust (3% to 5%) is effective as a treatment and is
well tolerated by all ages of ratites. Label directions and precautions
must be followed. New introductions to flocks should be quarantined,
inspected for parasites, and treated with Sevin dust as a precaution.
Black flies (Simulium spp) will affect ratites, resulting in stress and
anemia. The control of these ectoparasites, including Culicoides spp
("midges"), is impossible in endemic areas. Ratites should not be located
in areas where large populations of hematophagous dipterids occur
seasonally.

DISEASES OF THE CENTRAL NERVOUS SYSTEM

Western Equine Encephalitis

Etiology and Occurrence. Western equine encephalitis in emus re-

sults from infection with an alphavirus of the family togaviradae. The
468 SHANE

agent occurs throughout the central and western regions of Canada, the
United States, and Mexico. Outbreaks have been recorded in emus in
Oklahoma and Texas from 1993 onward, and in California during 1997.10
Transmission. Culex tarsalis is considered to be the primary vector.
Emus are an accidental host.
Epidemiology. Unseasonal rainfall and elevated temperature may
result in a high density of Culex vectors. Wild passeriformes are both
reservoirs and primary hosts, and flocks of commercial poultry may
serve as amplifying hosts.
Clinical Signs. Affected birds show depression, anorexia, watery
diarrhea, and progressive ataxia. Paresis terminates in sternal or lateral
recumbency and death. A high proportion of cases recover spontane-
ously, with residual impairment of the nervous system.
Pathology and Diagnosis. Generally, there are no gross diagnostic
lesions. Microscopic changes include meningoencephalitis, multifocal
myocarditis, and leiomyositis. Diagnosis is based on isolation and identi-
fication of western equine encephalitis virus. In recovered birds, retro-
spective serology indicating a significant rise in western equine encepha-
litis antibody titer is diagnostic.
In a case described from the San Joaquin Valley of California in
1997, adult male emus showed serosal hemorrhages suggestive of east-
ern equine encephalitis.
Treatment. Isolation of affected emus in the early stages of the
disease and supportive therapy may be beneficial.
Prevention. Immunization using an inactivated equine vaccine in-
corporating both western and eastern equine encephalitis antigen is
strongly recommended in endemic areas.

Newcastle Disease

Etiology and Occurrence. Paramyxovirus type 1 strains are respon-

sible for Newcastle disease in domestic poultry. The most severe form
(velogenic viscerotropic), which is exotic to the United States, is endemic
in Latin America, including Mexico, and in central Europe, Asia, and
Africa. Outbreaks of velogenic viscerotropic Newcastle disease, which
presents as a condition of the central nervous system, have been reported
in commercially reared ostriches in Israel.
Transmission. Newcastle disease virus can be spread by wind for
distances of up to 4 miles. Contaminated equipment and clothing, trans-
port of infected stock, and concentration of birds from diverse sites at
auction barns could all be potentially involved in dissemination of
infection.
Epidemiology. Ostriches and presumably other ratites may become
infected if housed in close proximity to commercial poultry.29 It is antici-
pated that lentogenic (mild) Newcastle disease may become endemic in
commercial ostrich units, based on the wide distribution of the virus in
 INFECTIOUS DISEASES AND PARASITES OF RATITES 469

the US domestic poultry population. Backyard chickens and free-living

birds serve as reservoirs for infection.
Clinical Signs. Velogenic viscerotropic Newcastle disease infection
results in 100% morbidity and up to 50% mortality in immature os-
triches. Clinical signs include torticollis, incoordination, recumbency, and
diarrhea.
Pathology and Diagnosis. No specific gross lesions have been docu-
mented other than generalized venous congestion and nephrosis associ-
ated with water deprivation. In commercial poultry, hemorrhagic enteri-
tis and petechial and echymotic hemorrhages occur in the serosa of
the viscera. Histologic examination shows neuronal degeneration and
perivascular lymphocytic cuffing in brain tissue.
Newcastle disease virus can be isolated from brain tissue of affected
birds on both tissue culture and in embryonated SPF chicken eggs, but
serial passage may be necessary to demonstrate the presence of the
virus. If ostriches survive longer than 10 days after infection, elevated
antibody titers can be quantified using either hemagglutination inhibi-
tion or enzyme-linked immunosorbent assay.
Treatment. Supportive therapy is appropriate in areas where there
is no obligatory slaughter and disposal of flocks infected with Newcastle
disease virus.
Prevention. In areas where velogenic viscerotropic Newcastle dis-
ease is endemic, vaccination programs paralleling those used in chicken-
breeding stock are applied. In Israel, successive doses of attenuated live
Newcastle disease vaccine (Hitchner B1 strain) is administered by the
intraocular route at 14 and 30 days of age. This is followed by an
inactivated oil emulsion vaccine as a booster at approximately 45 to 50
days of age by the subcutaneous route.
Ostriches should not be vaccinated in the United States, because
there is currently no risk of infection with the velogenic viscerotropic
virus. In the event of a surveillance program, ostriches with antibodies
to Newcastle disease virus induced by vaccination will be quarantined
and may even be slaughtered. Live, lentogenic vaccine, although stable
in chickens and turkeys, may undergo reversion if introduced into novel
species such as emus and ostriches.

Borna Disease

Etiology and Occurrence. Bornavirus is responsible for mortality in

ostrich chicks in Israel. 40
Transmission. It is presumed that insect vectors transmit the virus
to young ostriches from a free-living reservoir.
Epidemiology. The disease was described in the brooding units
housing large numbers of ostrich chicks operated by a collective farm in
Israel, commencing during the late 1980s. Morbidity and mortality ex-
ceeded 50% of annual production on some farms. Borna disease has not
been diagnosed in the western hemisphere.
470 SHANE

Clinical Signs. Affected chicks show depression progressing to

paresis and paralysis, with death occurring within 8 days owing to
dehydration.
Pathology and Diagnosis. No specific gross lesions are associated
with borna virus infection. Microscopic examination of brain tissue
shows lymphocytic perivascular cuffing and neuronal degeneration. An
enzyme-linked immunosorbent assay has been developed in Israel as a
diagnostic procedure to detect antigen in brain tissue.
Treatment. Hyperimmune serum has been shown to reduce mortal-
ity in early cases. Supportive therapy is indicated.
Prevention. An inactivated vaccine has been used in Israel since
1992 with success. Chicks are vaccinated at approximately 3 weeks of
age, following the decline in maternal antibody.

Baylisascaris Encephalitis

Etiology and Occurrence. Baylisascaris procyonis and B. columnaris

are causal agents of cerebral and nematodiasis in emus.
Transmission. Nematodes are acquired by ingestion of mature ova
from soil.
Epidemiology. B. procyonis and B. columnaris are parasites of rac-
coons and skunks, respectively. Eggs voided by the definitive hosts
remain viable in soil for many years. Larvae emerge from the ova in the
intestinal tract and migrate to the brain.
Clinical Signs. Affected emus show incoordination progressing to
paresis and paralysis. 1s
Pathology. No gross lesions are observed other than the secondary
effects of dehydration and inanition. Histologic examination may show
the presence of the larvae in the brain or spinal cord.
Treatment. No treatment is effective after the parasites have entered
the central nervous system.
Prevention. The only practical preventive measure is excluding
raccoons and skunks from emu pens.

Chandlerella Encephalitis

Etiology and Occurrence. The filarid parasite Chandlerella quiscali is

an aberrant parasite of emus. The condition has been described in
Louisiana, Mississippi, and Texas. 2o
Transmission. The microfilaria are believed to be transmitted by
Culicoides crepuscularis. The natural reservoirs are the grackle, blue jay,
cowbird, and starling, which are parasitized without adverse effects.
Emus are accidental hosts.
Clinical Signs. Young affected emus show depression and progres-
sive incoordination. Torticolis is a prominent sign, and recovered birds
 INFECTIOUS DISEASES AND PARASITES OF RATITES 471

show scoliosis owing to unilateral paralysis of cervical and thoracic

musculature.
Pathology and Diagnosis. Histologic examination of the spinal
column and brain may show the presence of microfilarid parasites 70 to
100 f.1m in size.
Treatment. No treatment is possible once parasites have migrated
to the central nervous system, owing to the inhibitory effect of the
blood-brain barrier on anthelmintics.
Prevention. Experience in Louisiana and Mississippi has shown that
administration of ivermectin at a dose of 200 f.1g/kg by the subcutaneous
route at 3-week intervals protects young emus from larval migration to
the central nervous system, effectively suppressing clinical signs. Adult
emus are apparently refractory to infection, although the mechanism for
resistance is unknown.

SYSTEMIC DISEASES

Bacterial and viral pathogens characterized by septicemia or multisys-

tem involvement are reviewed under this disease category.

Anthrax

Etiology and Occurrence. Bacillus anthracis is responsible for acute

mortality in ostriches in South Africa.
Transmission. Infection is transmitted by ingestion of viable organ-
isms, which persist for many years in soil in the spore form.
Epidemiology. Ostrich flocks are at risk if exposed to pens where
soil has been contaminated by improper disposal of carcasses of rumi-
nants and equines that died owing to anthrax. The susceptibility of emus
and rheas is unknown.
Clinical Signs. The literature records peracute mortality in imma-
ture and mature ostriches.
Pathology and Diagnosis. It is necessary to include anthrax in the
differential diagnosis in mature ostriches and possibly emus that die
acutely without a history or evidence of trauma. A peripheral blood
smear should be examined in these cases to exclude the possibility of
anthrax before commencing a postmortem examination. Postmortem
changes include venous congestion and splenomegaly. The diagnosis of
anthrax can be presumed by demonstrating characteristic square-ended
bacilli in a stained-blood smear. The organism can be isolated and
identified in swabs derived from peripheral blood, spleen, and liver for
confirmation.
Treatment. Because the condition is characterized by peracute mor-
tality, treatment is impractical.
Prevention. Ostriches (and possibly emus) should not be main-
tained on farms with a history of anthrax. Contact birds should be
472 SHANE

moved from pens where anthrax mortality has occurred and should be
treated with dihydrostreptomycin as a prophylactic measure. Carcasses
of dead birds should be disposed of by deep burial or complete incinera-
tion. In endemic areas, flocks should be immunized using an inactivated
vaccine approved by state or federal veterinary authorities.

Erysipelas

Etiology and Occurrence. Erysipelothrix rhusiopathiae has been diag-

nosed in both emus and ostriches. The pathogen is ubiquitous in poultry
and domestic livestock.
Transmission. Infection follows ingestion of viable organisms pres-
ent in soil. Infection may also result from entry of the pathogen into
dermal abrasions and lacerations caused by toes as a result of fighting
or injury from contact with fences or equipment. Biting insects may
serve as mechanical vectors of the pathogen.
Epidemiology. Free-living birds and vermin serve as reservoirs of
infection. Maintaining emu or ostrich flocks in pastures previously occu-
pied by ranged turkeys may contribute to infection. Because the organ-
ism causes erysepeloid in humans, workers in processing plants, farmers
handling stock, and veterinarians performing postmortem exa.minations
are at risk of infection.
Clinical Signs. Death usually occurs acutely, but depression may
be a prodromal sign.
Pathology and Diagnosis. Ostriches and emus that die of erysipelas
show generalized venous congestion, hepatomegaly, and splenomegaly.
Petechiae may be present on the serosa of viscera and the pericardium.
The organism can be isolated from peripheral blood and from spleen
and liver tissue.
Treatment. Parenteral penicillin or fluoroquinolone antibiotic by the
intramuscular route will reduce mortality rates in affected flocks if cases
are identified and treated at an early stage of clinical disease.
Prevention. General management procedures to limit intragroup
fighting reduce the probability of infection on endemic farms. Repair of
fencing and damaged installations prevents skin lacerations and abra-
sions. Once erysipelas has been diagnosed in ratites on a farm, it is
recommended that all stock be vaccinated using a commercial formalin-
inactivated aluminum hydroxide adjuvant bacterin licensed for turkeys.
The first dose should be administered by the subcutaneous route at 6 to
8 weeks of age, followed by two subsequent doses at 6-month intervals
and an annual booster prior to the onset of the breeding season. Since
vaccines for ratites are administered under conditions paralleling extra-
label use of drugs, the practitioner should obtain informed consent from
the client and, where appropriate, clearance from an insurance company
before initiating a flock-vaccination program.
 INFECTIOUS DISEASES AND PARASITES OF RATITES 473

Tuberculosis

Etiology and Occurrence. Mycobacterium avium infection has been

diagnosed in ostriches and emus in North America. 32 The condition has
been described in birds held by traders and small-scale multipliers and
in ratites maintained in zoologic collections.
Transmission. Ratites are infected by ingestion of the causal organ-
ism in contaminated soil.
Epidemiology. M. avium can remain viable in soil and moist biologi-
cal material in excess of a year. Backyard poultry and free-ranging
ornamental birds, including peafowl and bantams, serve as reservoirs of
infection. Ratites may be infected when transported in contaminated
trailers and by fomites, including footwear and equipment. Purchase of
birds at auctions and extensive trading during the early 1990s possibly
contributed to dissemination of infection.
Clinical Signs. There are no specific clinical signs associated with
tuberculosis in ratites. Emus infected with M. avium show intestinal
prolapse, with granulomatis colitis evident on examination of protrud-
ing tissue.
Pathology and Diagnosis. Characteristic granulomas are observed
on the serosa of viscera and the peritoneum. Hepatomegaly and spleno-
megaly with focal disseminate granulomas are observed in advanced
cases. Granulomas, which may be present in the bone marrow of the
tibiotarsus, are pathognomonic. Acid-fast organisms in stained impres-
sions or sections of granulomas obtained by biopsy or at postmortem
examination represent a presumptive diagnosis. The organism can be
cultured and identified by specialist laboratories. A kit comprising bot-
tles of formalin and boracic acid preservative are available from the
National Veterinary Services Laboratory, which can confirm a diagnosis
of M. avium infection.
Individual live birds can be screened for exposure to tuberculosis
by the intradermal M. avium antigen-sensitivity test.
Treatment. None is recommended.
Prevention. Affected birds should be slaughtered and disposed of
by deep burial or incineration.
Maintaining closed flocks and intradermal screening of newly ac-
quired birds during quarantine should reduce the probability of intro-
duction of infection.

Chlamydiosis

Etiology and Occurrence. Chlamydia psittaci is a ubiquitous organ-

ism in free-ranging birds including passeriformes and columbiforms and
in domestic anseriforms and galliforms, especially turkeys. The literature
contains reports of chlamydiosis in rheas,7 but it is presumed that os-
triches and emu are also susceptible.
Transmission. The disease is transmitted to flocks by contact with
474 SHANE

clinically affected and latent carriers. The infective elementary body is

excreted in feces, which is ingested by susceptible birds.
Epidemiology. Serologic investigations have demonstrated that C.
psittaci in rheas can be acquired from pigeons, which serve as latent
carriers. Introduction of newly acquired birds without quarantine may
result in infection of a susceptible flock. Chlamydiosis is a well-recog-
nized zoonosis and may produce severe disease in immunosuppressed
individuals.
Clinical Signs. Affected rheas are depressed and show ocular dis-
charge and diarrhea preceding death.
Pathology and Diagnosis. Hepatomegaly and splenomegaly are
evident in acute cases, progressing to peritonitis, pericarditis, and fibro-
nous airsacculitis. Elementary bodies can be demonstrated in impression
smears or tissue sections processed with Gimenez or Machiavelli stains.
Some laboratories are equipped to perform fluorescent antibody-linked
or enzyme-linked immunosorbent assay to detect C. psittaci antigen.
Flock antibody titer can be monitored using complement fixation or a
blocked enzyme-linked immunosorbent assay procedure. 16
Treatment. Individual birds can be treated with doxycycline by the
intramuscular route. Tetracycline can be incorporated in feed at a level
of 400 g/ ton, subject to compliance with federal regulations relating to
prescription and withdrawal periods.
Prevention. It is necessary to maintain closed flocks and exercise a
high degree of biosecurity. Contact with free-ranging birds should be
discouraged by preventing spillage of feed. Newly acquired stock should
be quarantined for 60 days and subjected to C. psittaci antibody-titer
assay.

Pasteu rellosis

Etiology and Occurrence. Pasteurellosis in commercial poultry is

usually associated with Pasteurella multocida. There is only one docu-
mented case of pasteurellosis in ostriches. 1
Transmission. Transmission occurs through direct contact between
susceptible birds and clinically affected or latent carriers of infection.
Indirect transmission can occur through contaminated clothing, equip-
ment, or trailers.
Epidemiology. Pasteurellosis occurs extensively in backyard and
ornamental poultry. Free-living birds and mammals, including rodents,
are reservoirs of infection. Deficiencies in biosecurity predispose to intro-
duction of infection by the indirect route.
Clinical Signs. In commercial poultry, morbidity and mortality de-
pend on the pathogenicity of the strain of P. multicoda, level of immunity,
and environmental stress. In peracute cases, death occurs without pro-
dromal signs. Chronic cases present with depression, weight loss, arthri-
tis, and torticollis as a result of otitis intema.
Pathology and Diagnosis. Classic pasteurellosis in chickens and
 INFECTIOUS DISEASES AND PARASITES OF RATITES 475

turkeys results in splenomegaly and hepatomegaly. Petechiae may be

present on the pericardium and serosa of the viscera. In turkeys, pneu-
monia is a frequent observation. The organism can be isolated and
cultured from affected organs and heart blood. Field practitioners should
submit specimens routinely to a diagnostic laboratory for attempts at
isolation of Pasteurella spp (in addition to Salmonella, Erysipelothrix, and
Escherichia coli) from cases subjected to postmortem examination.
Treatment. Treatment involves intramuscular administration of
tetracyclines, followed by administration of the drug in drinking water.
Turkey feed containing tetracycline at 400 g/ton for 2 weeks suppresses
mortality in outbreaks occurring in breeding flocks.
Prevention. Maintaining a high standard of biosecurity reduces the
possibility of introduction of Pasteurella into commercial ratite flocks. If
pasteurellosis becomes a problem in intensive production units, autoge-
nous inactivated vaccines may be administered to suppress clinical signs
and mortality. Commercial live Pasteurella attenuated vaccines licensed
for chickens and turkeys are contraindicated for ratites because there is
no documentation on either safety or efficacy. In some species of poultry,
live vaccines produce a severe adverse reaction, resulting in systemic
Pasteurella infection and arthritis.

Coli bacillosis

Etiology and Occurrence. Escherichia coli is ubiquitous in poultry,

companion and exotic birds, and domestic animals. Specific strains with
high pathogenicity have been identified in poultry.
Transmission. Transmission occurs by ingestion of E. coli from con-
taminated drinking water. Fecal-oral infection occurs following move-
ment of young stock to contaminated brooding sheds or pens or through
contact with feces voided by free-living birds or older ratites.
Congenital infection can occur as a result of contamination of the
egg shell with feces, or infection may occur during hatching, resulting
in omphalitis.
Epidemiology. Shallow wells contaminated with sewage or runoff
from pens contain high levels of E. coli. Placing stock in brooding units
or pens that have not been decontaminated after housing older and
potentially infected flocks can result in indirect infection.
Clinical Signs. Chicks with omphalitis are depressed, huddle, and
are disinclined to eat and drink. Mature birds with colibacillosis or
peritonitis show depression, but they may mask clinical signs and die
acutely without any indication of disease.
Pathology and Diagnosis. Chicks with omphalitis show an enlarged
nonresorbed yolk sac with viscous or turbid contents. Birds that die of
colibacillosis show hepatomegaly, splenomegaly, and generalized venous
congestion. Most cases show peritonitis, airsacculitis, or pericarditis.
Necrotizing enteritis has been described in emus. 5
476 SHANE

E. coli peritonitis may follow foreign-body penetration of the pro-

ventriculus in ostriches or the ventriculus in emus.
In commercial poultry, E. coli is responsible for salpingitis in older
breeding hens. This condition has not been described in commercial
ratites, but cases of salpingitis in mature ratite hens should be evaluated
by microbiologic examination.
Treatment. Surgical removal of the yolk sac is indicated in valuable
ostriches. 37 Antibiotic therapy with a fluoroquinolone compound may be
attempted, but response is generally limited to transitory suppression of
infection.
Prevention. Water should be chlorinated at a level of 2 ppm. Appro-
priate egg handling and hatchery hygiene should reduce the possibility
of congenital E. coli infection. 38

Viscerotropic Eastern Equine Encephalitis

Etiology and Occurrence. This is caused by an alpha togavirus and

results in viscerotropic infection in emus. 39
Transmission. The virus is transmitted by mosquito vectors, includ-
ing Culiseta melanura and Aedes spp.
Epidemiology. Passeriform birds serve as reservoirs of eastern
equine encephalitis virus. Emus, horses, and humans are accidental
hosts. Location of emu flocks in the vicinity of swampy areas is contrain-
dicated. Unseasonal rain followed by high ambient temperature in-
creases the density of vectors and predisposes to infection.
Clinical Signs. Eastern equine encephalitis in susceptible emus is a
peracute disease. Affected birds show sudden onset of depression, rap-
idly proceeding to sternal recumbency. Blood-stained diarrhea and termi-
nal emesis of blood-stained ingesta are characteristic signs.
Pathology and Diagnosis. Petecheal and ecchymotic hemorrhages
are noted on the serosa of viscera and beneath the pericardium. The
intestinal lumen may contain up to 500 ml of unclotted blood.
The causal virus can be isolated from spleen, liver, blood, and
intestine. A state or federal veterinarian will provide information on the
protocol and packaging for submission of specimens to the National
Veterinary Service Laboratory or other designated facility for confirma-
tion of the diagnosis. It is noted that eastern equine encephalitis is a
zoonotic disease, and because emus are viremic at the time of death,
there is considerable risk of contacting infection from performing post-
mortem examinations or through handling specimens without appro-
priate precautions.
Since birds generally die acutely, retrospective serology is not practi-
cal. The few survivors of eastern equine encephalitis virus infection have
extremely high antibody titers.
Treatment. Supportive treatment of peracute and acute cases is
 INFECTIOUS DISEASES AND PARASITES OF RATITES 477

unrewarding. A few early-stage cases have recovered following aggres-

sive fluid replacement and antibiotic therapy.
Prevention. Emus should not be located in swampy or low-lying
areas with a seasonal high density of vectors and reservoirs of the virus.
A commercial bivalent eastern/western equine encephalitis virus-
inactivated vaccine has been shown to protect flocks when administered
by the intramuscular route according to the following schedule: 6 weeks,
10 weeks, 16 weeks of age, and at 6-month intervals thereafter in April
and September. Because the use of the equine vaccine in emus is not
approved according to the vaccine label, informed consent from the
owner must be obtained before initiating an immunization program. No
adverse effects have been noted following administration of inactivated
equine vaccine, especially during the period when emus were of high
value and flocks were regularly immunized. In recent years, owners
have neglected to immunize stock, and outbreaks have been recorded in
states bordering the Gulf of Mexico.

Avian Influenza

Etiology and Occurrence. Type A orthomyxoviruses occur in a wide

range of free-living migratory waterfowl and may cause variable mild to
high losses in commercial poultry. Avian influenza viruses are classified
according to the hemagglutinating (H) and neuraminidase (N) glycopro-
teins of the viral envelope. A highly pathogenic strain of H7Nl influenza
A resulted in 80% mortality in young ostrich chicks in South Africa and
Israe1. 2 A mild H5N2 virus has been isolated from rheas and emus in
the United States. 36
Transmission. Influenza virus may be contracted through direct
contact with free-living and migratory birds, which serve as reservoirs
and are fecal excreters of virus. Indirect contact occurs from defects in
biosecurity. Contaminated clothing, vehicles, and equipment can trans-
mit avian influenza virus from infected to susceptible flocks. Introduc-
tion of infected ratites into a flock will result in rapid dissemination
of virus.
Epidemiology. Studies conducted in the Republic of South Africa
demonstrated that periodic outbreaks of avian influenza occur in the
ostrich industry in the Klein Karoo Valley. It is possible that avian
influenza may emerge as an endemic condition in intensive ostrich-
rearing areas in the United States.
Serologic surveys in the United States have shown exposure of
ratites to numerous serotypes of avian influenza. Many flocks were
infected during 1993 as a result of purchase of stock from two auction
sites in Texas.
Because avian influenza is of extreme significance to the US and
international poultry industries, it is anticipated that state and federal
regulatory authorities will monitor for the presence of virus in birds
478 SHANE

subjected to interstate transport. It is noted that the People's Republic of

China placed an embargo on importation of processed poultry from the
United States in 1997 as a result of reports of ratite flocks showing
antibody to avian influenza virus in Texas. This was disruptive to the
broiler industry and resulted in financial losses to integrators and export-
ers. Surveillance programs and quarantine will be initiated in the event
of outbreaks of clinical influenza in either ratites or commercial poultry.
Clinical Signs. Immature ostriches infected with H7Nl influenza in
South Africa showed 100% morbidity and 80% mortality. Losses were
indirectly proportional to age. Affected birds showed diarrhea and respi-
ratory distress and voided copious green-colored urine.
Emus and rheas infected with H5N2 influenza virus in Texas
showed ocular and nasal discharge and diarrhea.
It is emphasized that there is no characteristic clinical presentation
for avian influenza.
Pathology and Diagnosis. Ostriches that died of H7Nl influenza in
South Africa showed fibrinous airsacculitis and multifocal hepatic necro-
sis and nephrosis.
Avian influenza virus can be isolated from tracheal and cloacal
swabs. The National Veterinary Service Laboratory will receive materials
submitted through a state or federal veterinarian and will conduct the
requisite series of laboratory procedures to identify the virus and deter-
mine the pathogenicity of isolates in chickens. Antibodies to avian influ-
enza can be detected using the agar gel precipitin test, which is group
specific. Serum virus neutralization is used by research laboratories to
determine the serotype (H and N components) of field viruses.
Treatment. Flocks infected with highly pathogenic strains of avian
influenza are subject to slaughter and disposal under current federal
policy. Mild cases of avian influenza could be treated with supportive
therapy, including parenteral fluids and antibiotics. The experimental
use of amantadine to treat chickens in Pennsylvania during the 1984
outbreak resulted in the rapid emergence of resistant H5N2 avian influ-
enza strains.
Prevention. Biosecurity procedures, including restrictions relating
to introduction of new stock, reduce the probability of introduction of
infection. Biosecurity precautions should be intensified in endemic areas
or when outbreaks of avian influenza occur in commercial poultry or
other ratite flocks.
It is possible that the use of homologous inactivated vaccines may
be authorized by the US Department of Agriculture Annual Plant Health
Inspection Service (APHIS) if outbreaks of mild influenza occur in rat-
ites. Currently, the turkey industry has achieved success in reducing
losses associated with virus transmitted from migratory waterfowl using
inactivated vaccines. Current federal policy relating to outbreaks of
highly pathogenic avian influenza mandate quarantine and depopula-
tion of infected farms with disposal of carcasses.
Future prevention may involve genetically engineered vector vac-
 INFECTIOUS DISEASES AND PARASITES OF RATITES 479

cines, which were successfully evaluated during the 1994-1995 outbreak

of H5N2 Highly Pathogenic Avian Influenza (HPAI) in Mexico.

Adenovirus Infection

Etiology and Occurrence. Adenoviruses are ubiquitous in poultry

and have been documented in cases of high mortality in ostrich chicks
in Oklahoma. 27
Transmission. Adenoviruses in poultry are transmitted vertically
both by the transovarian route and laterally from infected to susceptible
chicks. In commercial chicken hens and breeders, adenoviral infection
can remain latent until onset of production.
Epidemiology. Contract hatching and rearing, trading in birds, and
failure to maintain single-species operations with separation of different
age groups all contribute to the possibility of introduction and dissemi-
nation of infection. Adenoviruses may interact with immunosuppressive
agents, including avibirnaviruses and mycotoxins, or with systemic and
enteric viral or bacterial pathogens to produce clinical conditions such
as fading-chick syndrome. As with poultry, it is presumed that a carrier
state exists in birds that have recovered from adenoviral infection.
Clinical Signs. Acute mortality occurs in ostrich chicks from 6
weeks of age onward. Mortality exceeding 90% has been documented
on some farms.
Pathology and Diagnosis. No specific lesions are noted but may
include enteritis, fibrinous airsacculitis, and pulmonary congestion.
Lymphoid depletion of the spleen and bone marrow suggests an immu-
nosuppressive component of the disease syndrome. Hyperplasia of bile
duct epithelium noted in some cases may be owing to previous exposure
to aflatoxins. Adenovirus has been isolated from cases of fading-chick
syndrome using tissue culture systems developed by specially equipped
laboratories.
Treatment. Supportive therapy can be implemented but is probably
of minimal value.
Prevention. Because the epidemiology and control of adenoviral
infection in ostriches and other ratites is unknown at the present time,
only general recommendations relating to biosecurity can be provided.
Studies have indicated that specific hens in flocks produce chicks that
die of the condition. Based on the presumption of vertical transmission,
these hens should be eliminated from breeding programs.

Crimean-Congo Hemorrhagic Fever

Etiology and Occurrence. The causal agent is a tick-borne arbovirus.

An outbreak of Crimean-Congo hemorrhagic fever resulted in closure of
the Klein Karoo Cooperative abattoir in Oudtshoorn in November 1996. 4
480 SHANE

This disease is endemic in Asiatic Russia, the Middle East, and specific
countries in eastern sub-Saharan Africa.
Transmission. Ostriches are infected by Hyalomma spp ticks, which
are vectors of the disease.
Epidemiology. The outbreak in South Africa followed unseasonal
rains in the normally arid Klein Karoo Valley of the Republic of South
Africa. This resulted in a proliferation of the wild hare population and a
consequential increase in numbers of Hyalomma ticks, which parasitized
ostriches. Viremic ostriches processed at the Klein Karoo Cooperative
plant at Oudtshoorn infected workers involved in slaughtering and
skinning.
Clinical Signs. There are no clinical signs in ostriches, which show
transitory viremia.
Prevention. Authorities in the European Union imposed an em-
bargo on ostrich meat of South African origin following the outbreak.
Studies conducted in South Africa showed that the virus was extremely
labile and did not survive for longer than 24 hours in refrigerated meat
derived from infected birds. Practical steps to avoid infection of birds
included secure fencing of growing pens to prevent ingress of wild
animals, including hares, treatment of ostriches with an approved acari-
cide (Sevin 5% powder) 14 days prior to slaughter, and inspection of
birds to ensure freedom from tick infestation at the time of delivery to
the abattoir.

Infectious Bursal Disease

Etiology and Occurrence. An avibimavirus, believed to be in com-

mon with the strains responsible for infectious bursal disease in chick-
ens, has been isolated from dead ostrich chicks with fading-chick syn-
drome in California and Florida. 8
Transmission. It is presumed that the disease can be transmitted by
direct contact between infected poultry and susceptible ratites and by
indirect infection through contaminated fomites.
Epidemiology. Infectious bursal disease of chickens is widespread
throughout the world and is responsible for extensive losses arising
from immunosuppression, which renders flocks susceptible to other
viral pathogens and secondary bacterial infection. The virus is relatively
resistant to environmental exposure and can remain viable in pens and
housing for periods in excess of 90 days.
Clinical Signs. Chicks with fading-chick syndrome show depres-
sion, anorexia, and diarrhea over a 3- to 5-day period before assuming
sternal recumbency followed shortly by death.
Pathology and Diagnosis. No specific gross lesions are observed,
but pulmonary congestion, enteritis, and airsacculitis are documented.
Histologic examination of the bursa of Fabricius showed atrophy paral-
leling the situation in chickens. Virus was isolated from affected birds
using conventional tissue culture techniques.
 INFECTIOUS DISEASES AND PARASITES OF RATITES 481

Treatment. Supportive therapy is suggested but will probably be

unproductive.
Prevention. Maintaining separation between commercial poultry
and ratites is necessary to prevent introduction and adaptation of viral
and bacterial diseases of poultry to ratites. Although infectious bursal
disease in chickens is controlled using live attenuated vaccines, prac-
titioners and owners should be strongly dissuaded from attempting
vaccination of ratites. It is possible that adaptation of the vaccine virus
to ostriches or emus may occur, resulting in the emergence of highly
pathogenic strains in these species.

Protozoal Infections

The literature relating to protozoal infections of ratites has docu-

mented cases of Leukocytozoon, Plasmodium, and Aegyptianella as hemo-
parasites in ostriches. Giardia, Histomonas, Trichomonas, and Hexamita
have been identified as the principal sarcomastigophora of the digestive
tract of ostriches and rheas. Coccidia, including Cryptosporidium and
Isospora, have been identified in ostriches. Ciliate protozoan parasites of
ostriches include Balantidium. ll
There is no documentation concerning the pathogenicity of these
parasites under commercial conditions. Most of the information in the
literature is composed of case reports and incidental observations made
from zoo specimens. A report from South Africa confirms that Crypto-
sporidium was associated with cloacal prolapse in young ostriches. 24

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Address reprint requests to

Simon M. Shane
School of Veterinary Medicine
Louisiana State University
Baton Rouge, LA 70803