1. Breeding stock should be maintained in a closed unit. If new birds are purchased, a thorough physical examination should be performed with appropriate diagnostic procedure before delivery.
2. New birds should be quarantined for at least sixty days in a separate facility, and monitored for the presence of disease.
3. Ratite producers should limit visits to other farms. A complete body cleaning, and change of all clothing and shoes, should take place before interacting with home stock.
4. Visitors should be provided with rubber boots and coveralls before entering pens.
5. Care should be taken when decontaminating the interior and exterior of transport vehicles.
6. A very important policy of a ratite facility is to confine activities to one species, due to the danger of cross-transmission of infectious organisms between ratites, water fowl, exotic birds and livestock.
7. All water should be free of pathogens and should be analyzed annually to confirm quality.Bird pens should be placed in a well-drained area, and fence posts should be on the outside of the pen.
8.  A structure placed in the middle of the pen will reduce exposure to wind and precipitation, and will protect food trays.
9. Sufficiently-high, strong wire fencing will reduce injuries to birds and prevent attack by wild animals. Fences should reach down to the ground if a perimeter fence is not in place, to reduce exposure to wild animals or stray dogs.
10. At most ostrich facilities, producers prefer to leave a space for escape under the bottom line of the fence, and a perimeter fence should therefore be in place. Electric fences and dogs have been used with success in keeping out unwanted animals which may injure livestock.

Arthropods

Ticks are common parasites of the ostrich in its native African environment, and include the following genera/species: Amblyomma spp., Haemaphysalis punctata, Hyalomma spp., Rhipicephalus turanicus and Argus spp. Ticks have been implicated in transmission of viral diseases, and heavy infestations cause ill thrift, slow growth and low egg production. Treatment is best achieved with 5% carbaryl dust at fourteen-day intervals. Pterolichus bicaudatus (ostrich quill mite) and Struthiolipeurus struthionus (ostrich louse) may cause pruritis and/or excessive preening and feather loss. Infestation with these external parasites causes stress and predisposes birds to secondary infections and gastrointestinal disorders (e.g. impactions). Treatment for mites is accomplished with ivermectin, and lice are treated in a similar manner to tick infestations.

Miscellaneous arthropod infestations – e.g. Struthiobosca struthionis in ostriches, Struthiodiperus rheae in rheas, and Culicoides spp. and Simulium spp. in emus – cause blood loss, irritation and stress, and transmit other parasites. Pyrethrin sprays may help to prevent extreme exposure to many of the flying arthropod parasites.

Helminths

Helminth parasites found in ratites include the following: Baylisascaris spp., Libyostrongylus douglassi, Paraonchocerca struthionus, Struthiofilaria megalocephala, Ascaridia orthocerca, Deletrocephalus dimidiatus, Deletrocephalus casarpintoi, Dicheilonema rheae, Paradeletrocephalus minor and Chandlerella quiscali. Baylisascaris spp. have been identified in ostriches and emus (7, 14). The definitive hosts for this parasite are skunks and raccoons, which shed the eggs in faecal material; the eggs can remain infective in the soil for several years. Birds suffering from Baylisascaris spp. infections show ataxia, muscle weakness, recumbency and death, due to visceral larval migration into the brain and spinal cord. Diagnosis is made at necropsy by observation of the parasite in brain or spinal cord tissue sections. Baylisascaris spp. cause a zoonotic parasitic disease and can provoke severe physical damage through visceral larval migration if eggs are ingested. Reduction of definitive host populations around a facility and proper feed storage will help to reduce exposure to this dangerous parasite.

A helminth parasite which affects young emus in a similar manner is Chandlerella quiscali. This parasite is transmitted by Culicoides midges, and visceral larval migration occurs before the birds reach one year of age. Generalized neurological signs accompany Chandlerella spp. infestation, and diagnosis is made at necropsy. Libyostrongylus douglassi (wireworm) is a proventricular parasite which is extremely deadly to young ostrich chicks. Prevention of this parasite from infesting a ratite facility is very important. The life cycle is direct, and pasture rotation is recommended as a control measure. Fenbendazole, levamisole and ivermectin may be effective in the control of this deadly parasite.

The other helminth parasites listed should be treated as mentioned for L. douglassi. Prevention of parasite exposure is the primary management measure recommended in all ratite operations. Once a parasite has become established on a facility, diligent testing and treatment – especially in young birds – will limit economic losses and bird mortality.

 Protozoa

The blood protozoa Leucocytozoon struthionis and Plasmodium spp. have been identified in ostriches (7), and are transmitted by flying arthropod vectors. These parasites do not generally cause significant clinical illness, and treatment is usually more problematic than the infestation. The intestinal protozoa Balantidium struthionis, Cryptosporidium spp., Histomonas meleagridis, Hexamita spp., Giardia spp. and Trichomonas spp. cause gastrointestinal problems which result in wasting, anorexia, diarrhoea and death for all ratite species, especially rheas. Direct faecal and intestinal content examinations are essential in diagnosing these parasitic diseases (7). Appropriate treatment with anti-protozoal drugs will reduce losses in an outbreak; but proper husbandry practices will limit incidence, thus reducing labour and other expenses.

Tapeworms and flukes

Houttuynia struthionis (ratite tapeworm) primarily affects younger birds. Ostriches and rheas seem to be the most common ratite species affected, and the recommended treatment is fenbendazole. The adult ratite fluke (Philophthalmus gralli) is found outside the nictitating membrane in affected birds. The intermediate host of the fluke is a freshwater snail, and ratites acquire the parasite through ingestion of freshwater crustaceans or other solid objects. It is recommended that ratite exposure to standing water be restricted, thus reducing the risk of intermediate host exposure.

Salmonella spp. are ubiquitous organisms which reflect contamination of facilities through contact with rodent or wild bird reservoirs. Various Salmonella spp. have been isolated from the gastrointestinal tracts of all ratite species, but the incidence of paratyphoid Salmonella spp. (e.g. S. Typhimurium) is very rare. It must be remembered that certain Salmonella organisms are zoonotic, and precautions should be taken when handling a suspect case. Emus can be infected with S. Pullorum – a pathogen which persists in game fowl – and develop antibodies against this pathogen. The importance of S. Pullorum in ratites is unknown at this time, as no documented field cases have been identified. Salmonella organisms can be transmitted horizontally by infected birds via the faecal/oral route, or through contamination of equipment or the environment. Vertical transmission via faecal contamination of eggs has also been described as a method of Salmonella infection in the poultry industry. As Salmonella bacteria can be transmitted through eggs or contaminated equipment, care must be taken when receiving birds or eggs after interstate or international shipment. Most birds suffering from Salmonella spp. infections show no specific clinical signs, and are diagnosed through microbiological screening at necropsy. Treatment of infected birds with an appropriate antibiotic will generally suppress the clinical infection, but may lead to an asymptomatic carrier state. To reduce the risk of subclinical carriers developing, a whole-blood S. Pullorum agglutination test should be performed prior to shipment, and routine screening of birds by cloacal swabs during quarantine is also suggested.

Erysipelas

Emus have been reported to be susceptible to infection by Erysipelothrix rhusiopathiae. Infection with this soil organism occurs via small skin lacerations, caused by trauma, or insect vectors. Acute deaths usually occur due to a bacterial septicaemic condition, but penicillin or quinolone antibiotics may help mildly-affected birds. If erysipelas is a problem within a region or at a particular production facility, ratites should be immunized using a commercial, formalin-inactivated bacterin (with aluminium hydroxide adjuvant) licensed for turkeys. No adverse reaction has been noted in emus vaccinated with this inactivated turkey vaccine. In areas where erysipelas is endemic, birds should receive the first vaccine subcutaneously at six weeks of age, a second dose at six months of age, and an annual booster.

Colibacillosis

Escherichia coli serotypes are widely distributed; the degree of pathogenicity depends on the condition of the bird(s) exposed. In general, emus seem to be more susceptible to E. coli gastroenteritis infection than other ratite species.

Transmission usually occurs via the faecal/oral route, and the agent may be identified via culturing of cloacal swabs. Appropriate antibiotics are essential in treating an E. coli infection in ratite species. Autogenous bacterins are available, which may be used when colibacillosis becomes a health problem on a farm. These bacterins use cultures isolated from affected birds to help boost immunity in the resident animals. The efficacy of these bacterins in ratite and other avian species is unknown at present. The best prevention measures for colibacillosis infections are proper management and nutrition, and stress reduction in the flock or transported birds.

Pasteurellosis

There have been rare occurrences of Pasteurella spp. isolation in ratite species.

Intensive farming may increase occurrence, and this organism should therefore be monitored closely. Environmental exposure and direct contact with recovered Pasteurella carriers provide ample opportunity for acquisition of this bacterium in an immune suppressed ratite flock. Non-specific respiratory signs may be noted in the clinically-diseased bird, while generalized vascular congestion is seen on gross necropsy specimens. At present, no vaccination measures are recommended, but high standards of biosecurity are required to prevent introduction of infections into flocks.

Mycoplasmosis

Mycoplasma cloacale has been isolated from tracheal swabs of ostriches and emus, while there has been no isolation from these species of the three pathogenic Mycoplasma spp. found in commercial poultry. Intensification of the ratite industry, and concentration of birds in feedlots, may lead to the emergence of mycoplasmosis as a disease of economic significance due to the ease of transmission of this pathogen. Clinical signs accompanying mycoplasmal infection include nonspecific upper respiratory conditions and/or arthritis (27). Identification of Mycoplasma in other avian species is performed through isolation of the organism from joint aspirates or respiratory discharge, or through serological screening using the serum plate agglutination test. At present, a highly-sensitive polymerase chain gene probe assay can be used for identification of Mycoplasma galliseptium and M. synoviae in a few diagnostic laboratories (27). Treatment of confirmed cases is usually accomplished using tylosin or tetracycline antibiotics. Producers and transporters are encouraged to identify potential cases before the animals are placed in holding facilities, to reduce the risk of exposure of non-infected birds.

Tuberculosis

Mycobacterium avium has been diagnosed in ostriches and emus in the USA and Canada, and in emus in the USA. M. avium persists in wild bird populations and can infect pigs, cattle and immunosuppressed humans; it is therefore classified as a zoonotic disease. Transmission of M. avium occurs through infected faeces shed by clinically-ill birds. The organism can remain viable in the soil for up to twelve months, making sanitation after a clinical case difficult for the owner. The highly-mobile ratite industry enables dissemination of the organism via transport, holding facilities, quarantine houses and auction barns.

As M. avium generally affects the avian gastrointestinal system, clinical signs are usually those of non-specific wasting. Emus may develop leukocytosis with or without cloacal prolapse. Confirmation of the infection is usually accomplished at necropsy, unless an intensive ante-mortem physical examination is performed, isolating the acid-fast organism from a bacterial granuloma or a faecal screen. Screening tests using faecal acid-fast methods are unreliable; intradermal testing is therefore recommended, together with the maintaining of closed flocks, examination of newly-acquired breeding stock and good management. Tuberculosis is a potential zoonotic disease for which no treatment is available; a flock maintained within a production facility must therefore be free from tuberculosis.

 Chlamydiosis

Chlamydia psittaci is an intracellular bacterium which has been identified as the causative agent in deaths of commercial rheas. Infected rheas usually die peracutely, while emus seem to be refractory to the organism isolated from species flocks. Pigeon strains of C. psittaci have been identified in outbreaks of the disease in Texas, and may have caused other rhea deaths in the southern USA. Diagnosis is made at necropsy through bacterial isolation. The gross pathological signs of psittacosis include splenomegaly, hepatomegaly, pericarditis and fibrinous airsacculitis. Extreme care should be taken by the veterinarian during treatment and/or necropsy of a C. psittaci case, in view of the zoonotic potential of the organism. The psittacosis bacterium is highly infectious to humans and causes severe pneumonia and death if not treated appropriately. Treatment of ratites and humans is best achieved with the tetracycline class of antibiotics. Reduction of wild bird access to feed and water areas will reduce the exposure of ratites to potential carriers of the Chlamydia organism.

Clostridial enteritis

A number of clostridial organisms have been isolated from various ratite species, including Clostridium perfringens, C. colinum, C. chauvoei and C. difficile. There is no published information on the frequency of isolation of Clostridium spp. from the intestinal tract of normal ratites, but clostridial enteritis usually occurs following proliferation of a toxin-forming Clostridium spp. in other avian species. Diagnosis of clostridial enteritis is usually made at necropsy through microbiological identification. Anaerobic culture methods should be recommended by the clinical veterinarian if such procedures are not commonly performed on bacterial culture specimens by the diagnostic laboratory. Outbreaks of clostridial infections can be treated with the addition of zinc bacitracin in feed at a rate of 30 g/ton (27).

 Infectious coryza

Haemophilus spp. are transmitted horizontally and have been isolated from ostriches in Israel. Clinical signs are concentrated in the upper respiratory system and are treated with appropriate antibiotics from microbiological culture, and antibiotic sensitivity results. Proper management and quarantine of newly-acquired birds will reduce the risk of exposure and infection from this bacterial organism.

Anthrax

Although rare, Bacillus anthracis has been diagnosed in South African ostriches. In areas where anthrax has been identified as a cause of livestock deaths, ratite producers are advised to have any bird which dies peracutely necropsied by a veterinarian or pathologist, due to the highly zoonotic nature of this organism. Diagnosis is usually made at necropsy. Affected birds have extreme splenomegaly, hepatomegaly and vascular congestion (27). There is no treatment for this disease, and ostriches or other ratite species should not be maintained on farms with a history of anthrax.

Aspergillus spp. has been identified as a primary cause of death in juvenile emus and ostriches. The most susceptible individuals are young birds in enclosed facilities with exposure to dust or to hay which is alternately wet and dry. Aspergillus spp. exposure can occur through egg contamination but, under current conditions in the industry, poorly-managed intensive chick facilities seem to be the most likely place for an outbreak to occur. Affected chicks usually die suddenly, or exhibit severe dyspnoea prior to death.

Aspergillus granulomas are detected in the lungs and/or airsacs on gross post-mortem examination. In a highly intensive farming operation, treatment may not be costeffective, but itraconizole is the drug of choice. Although a ubiquitous organism, Aspergillus spp. can cause infection in humans, and face-masks must therefore be worn to reduce human exposure. Management procedures which reduce juvenile stress and exposure to dust and hay will alleviate much potential exposure to the fungal organism.

Zygomycosis

Basidia, Mucor and Rhizopus are genera of zygomycetes which affect the upper gastrointestinal system of ratites. Zygomycotic infections occur when the organism is ingested and is allowed to overwhelm the bird, due to suppressed immune status or concurrent bacterial, viral or parasitic infections.

Non-specific clinical signs accompany a zygomycotic infection, and diagnosis is usually made on post-mortem examination. Although these fungal infections have been noted in the USA and Israel, there is a real potential for exposure in other countries due to the ubiquitous nature of this organism (13). To prevent or reduce exposure to zygomycotic organisms, the producer should eliminate stress, primary viral or bacterial infections, and fungal contamination of feed and substrate.

Candidosis

Stomatitis characterized by white raised lesions in the oral cavity extending down the oesophagus is usually associated with a Candida spp. infection (27). The two main Candida organisms isolated from ratite species are C. albicans and C. mucor. Candida spp. are opportunistic organisms and usually indicate a primary bacterial, viral, parasitic or management problem which is reducing the ability of the bird to fight infection. Diagnosis can be made through Gram’s staining, direct scraping of the oral plaques and viewing the characteristic budding yeast forms. Treatment and prevention are achieved by using nystatin, fluconizole or ketoconizole, with adjunct supportive therapy. It is essential for the veterinarian to identify and treat the underlying primary immune suppressive problem affecting the individual bird or flock to ensure proper treatment of the secondary fungal infection. To provide treatment in large-scale production operations, copper sulfate may be added to the drinking water at a level of 1:2,000 in a large-scale feedlot operation .

Eastern equine encephalomyelitis (EEE), western equine encephalomyelitis (WEE) and St Louis encephalitis viruses have been isolated from ratites in the USA. Initial reports indicated that emus were the only birds affected on multi-species farms. A recent report indicates that an apparent outbreak of EEE occurred in a flock of rheas in southern Florida.The concentration of non-native avian species adjacent to wooded land, swamp or irrigated areas provides an environment suitable for mosquitoes and other earthropod vectors. Mosquitoes transmit infection from passeri form reservoirs to emus and rheas which are accidental hosts.

The clinical manifestation of EEE in emus is a peracute haemorrhagic gastroenteritis. Cases of WEE and St Louis encephalitis develop the typical neurological signs of progressive depression and paralysis. The encephalitis viruses are zoonotic, and appropriate precautions should be taken when performing necropsy procedures on viraemic subjects. Ratites are not involved as amplifiers of equine encephalitis or St Louis encephalitis viruses within endemic areas. Vaccinated birds develop a protective antibody titre of unknown duration. It is currently recommended that a bivalent EEE/WEE inactivated tissue-culture origin vaccine be administered twice-yearly to emus and rheas raised in an area endemic for these arboviruses. Young birds should receive the first dose at six weeks of age, with a booster four weeks later. Unvaccinated birds should be vaccinated twice, at four-week intervals, before being subjected to the twice-yearly programme. A full dose of the equine vaccine should be administered to birds of all ages. This is not an approved vaccine for ratites in the USA, and administration is subject to the ethical and legal restraints of using the vaccine in non-approved species. Owners must receive relevant information before informal consent is granted for vaccination. Antibody response to vaccination can be monitored using the complement fixation procedure.

Avian influenza in Emu

Type A orthomyxoviruses are classified according to haemagglutinating and neuraminidase activity of glycoprotein in the viral envelope. A range of avian influenza strains have been isolated from ostriches in South Africa and rheas in the USA exhibiting various clinical syndromes ranging from high mortality to in apparent infection.

The ability of avian influenza virus to mutate and spread among avian species makes this a potentially dangerous infection for commercial poultry. Transmission can occur from wild birds coming into contact with ratites, from newly-introduced, non quarantined stock or indirectly via the clothing of visitors and transport trailers. The risk of exposure can be reduced by operating closed facilities with strict bio-security measures, including control over entry of personnel.

Infection with influenza strains of low pathogenicity may be treated with supportive therapy. Virulent strains result in high mortality in young ostriches, which die despite administration of fluids and antibiotics. Prevention requires application of bio-security measures and quarantine of newly-introduced birds, which should be monitored for the presence of antibodies using the agar gel precipitation procedure prior to purchase or delivery. It is possible that inactivated vaccines against specific strains of influenza may be permitted by the United States Department of Agriculture, Animal and Plant Health Inspection Service, which is the Federal agency responsible for control of exotic and catastrophic diseases in the USA.

Newcastle disease virus in Emu

Newcastle disease (ND) is caused by paramyxovirus type 1, which affects galliforms, passeriforms and psittacines in addition to other families, including ratites. Velogenic viscerotropic ND (VVND) has been isolated from ostriches Showing high mortality in Israel and from rheas in Brazil. The disease manifests clinically as nervous signs, and 80% mortality occurs experimentally with infected ostrich chicks. Countries which are free of VVND, such as the USA, maintain restrictions on the importation of domestic, companion and exotic bird species, together with quarantine at the point of entry. The disease is spread by direct and indirect contact with infected carriers and fomites. Air-borne dissemination of virus may occur for up to 4 km.

Ratites should be vaccinated only in areas where VVND is endemic. Vaccinated ratites produce antibodies which will be detected if a test and depletion control programme is implemented in a non-endemic area. This may result in compulsory slaughter or rigid and extended quarantine.

 Adenovirus in Emu

Adenoviruses have been implicated as the cause of wasting disease in youngostriches in the USA . The clinical signs associated with these outbreaks included non-specific wasting, anorexia and depression. Specific adenoviruses are pathogenic in poultry and are responsible for haemorrhagic enteritis in turkeys, and inclusion body hepatitis/hydropericardium syndrome and egg drop syndrome in chickens.

Adenoviruses are transmitted vertically by the transovarian route. Adenoviral infection may remain dormant in chickens until onset of production or exposure to an environmental stress. In the cases observed in the USA, mortality in ostriches occurred at approximately two months of age. Affected birds showed anorexia, emaciation and diarrhoea. Isolation and identification of an adenovirus from moribund or dead birds is required to confirm the diagnosis. It is noted that adenoviruses are ubiquitous, and considerable research is still required to define the role of the agent in the ‘fading chick’ syndrome. There is no diagnostic procedure to determine the carrier status of an asymptomatic breeder ostrich. Poultry producers in countries other than the USA administer homologous, inactivated oil-emulsion vaccine to control specific infections including

egg drop syndrome, which is exogenous to the USA. At this time, it is considered advisable to maintain a closed breeding flock or purchase immature ostriches from a facility known to be free of the condition. Custom hatching and brooding may disseminate the infection, which can be spread by lateral exposure to ‘shedders’. The total impact of adenovirus infections in the ratite industry is not known at this time, but bio-security measures are required to prevent adenoviral infection restraining the expansion of production, especially in the large units required for commercial multiplication of slaughter stock.

Avibirnavirus

Infectious bursal disease virus (IBDV) is responsible for immune suppression in young chickens as a result of the destruction of immature lymphocytes in the bursa of Fabricius. Avibirnavirus identical to IBDV has been isolated from the bursa of immature ostriches in flocks in California and Florida where high flock mortality was observed. Affected birds do not show specific clinical signs, but depression and anorexia may precede death. Isolation and identification of the virus is required for confirmation. Supportive treatment and antibiotic therapy is recommended due to immune suppression. Administration of infectious bursal disease vaccines licensed for chickens is not recommended. The response of a ratite to live attenuated chicken vaccine is unknown, and the vaccine virus could be deleterious to an unnatural recipient. It must be remembered that IBDV can persist for up to ninety days in biological material, necessitating thorough disinfection of brooding facilities. Diligent bio-security is necessary to prevent exposure to the highly infectious agent.

Avipoxvirus

Pox has been diagnosed in ostriches in the USA, Israel and South Africa. The virus can be transmitted by mosquitoes or by direct contact with a pox lesion.

Immature ostrich chicks aged between two weeks and one year are most susceptible. The coetaneous form of pox is characterized by persistent proliferative lesions of 0.5-2.0 cm in size, on the eyelids, beak, wing and toes. The diphtheritic form produces tracheitis, stomatitis and a severe dyspnoea in affected birds. Pox can be confirmed by histopathological examination of affected tissue, which shows the presence of intracytoplasmic Bollinger bodies. Affected birds should be separated and given supportive therapy, including systemic and topical antibiotics, to prevent secondary bacterial infections. All unaffected birds should be vaccinated with a commercial fowlpox vaccine via the intradermal route, in accordance with the recommendation of the manufacturer for reconstitution and administration. Control of mosquitoes may be possible but rapid diagnosis and vaccination is the most appropriate preventive measure.

Viral enteritis

A wide range of bacteria and viruses have been isolated from the gastrointestinal tract of one- to three-week-old ostriches from flocks with a high level of morbidity and Mortality. Isolates include coronaviruses and adenoviruses which may not be the primary cause of death. Intra-flock transmission usually occurs rapidly through faecal/oral contamination, and may be exacerbated by high stocking density or defects in bio-security and hygiene. Clinical signs associated with viral enteritis are non-specific but generally include anorexia and diarrhoea. Due to the presence of opportunistic bacteria, it may be difficult to identify a viral agent during pathological examination. Virus identification by histopathology or electron microscopy and examination of faecal material may help in identifying the viral organism responsible for the clinical illness. Supportive therapy, intravenous fluid administration, tube feeding and antibiotics may help reduce flock deaths. The best way to prevent outbreaks of viral enteritis is through proper management hygiene before the introduction of new birds into a production unit, and through biosecurity in established flocks.

Borna disease virus

Borna disease virus (BDV) has been identified in Israel in ostrich chicks (two to eight weeks old) raised under intensive conditions. Clinical signs are initiated by paresis and general malaise, which contribute to anorexia and depression. The affected birds usually die within four to eight days, due to dehydration. Intensive farming methods seem to be a contributing factor in BDV outbreaks, with insect vectors believed to be responsible for transmission of the virus.

Histopathological lesions in affected birds show neuronal degeneration and lymphocytic perivascular cuffing. An enzyme-linked immunosorbent assay has been developed in Israel to demonstrate the presence of BDV in brain tissue of infected birds. Prevention of Borna disease outbreaks in intensive ostrich-raising facilities will require stress-reduction management programmes. For a Borna disease management programme, an inactivated viral vaccine must be developed, to immunize parent stock and thus provide maternal immunity to the offspring. At present, BDV is restricted to intensive ostrich-farming facilities in Israel, but the current popularity of ratite importation increases the likelihood of virus spread. Good husbandry, management and biosecurity will reduce the stress on birds and consequently, reduce the risk presented by this viral organism to susceptible birds in Israel and other parts of the world which are affected.

Other viruses

For some of the viral mortality associated with disease outbreaks in ratite facilities, no aetiological agent has been identified. The capacity of ratites to harbour and grow multiple pathogens within the gastrointestinal and respiratory tracts makes the isolation of unknown viral agents difficult. Rotaviruses, reoviruses, parvoviruses and picornaviruses are all potential pathogens which may contribute to ratite morbidity and mortality, but have not yet been identified in these species. With increased observation and diligence by clinical veterinarians and pathologists, other ratite viral pathogens will be discovered in the future, thereby helping to ensure healthy production within the industry.

With the increase in the numbers of farm-raised ratites throughout Australia, Asia, Africa, Europe and North America, there has been a world-wide increase in the spread of parasitic and infectious diseases associated with these birds. The three most commonly raised ratite species are ostriches (Struthio camelus), emus (Dromaius novaehollandiae) and rheas (Rhea americana). The Darwin’s rhea (Pterocnemia pennata) is of no significance in commercial production, as it is listed as an endangered species. The purpose of ratite production is to supply consumers with high-quality leather, low-fat red meat, feathers and other by-products (e.g. oils from rendered emu fat). As entrepreneurs raise birds to meet the potential demand, a world-wide interest in ratites has developed. The transport of birds across international borders has created the potential for the spread of infectious diseases. Regulatory authorities from many countries have recognized ratites as a threat to the health ofcommercial poultry. In Australia, importation restrictions permit the introduction of commercial poultry and some avian species through high-security quarantine facilities

Scientific name

Description

Of the salmonella species, S. pullorum causes pullorum disease and S. gallinarum causes fowl typhoid in poultry. In the past, these two diseases have caused significant problems, though both diseases are now very well controlled in the poultry industry. However, they may still exist in backyard poultry. There is little risk of emus being exposed to these two types of salmonella.

However, the many salmonella species that can infect a wide range of hosts, including man, are more significant to the emu industry. The infection and disease that these salmonellae cause is generally known as ‘paratyphoid’.

Distribution and transmission

Salmonellae are widespread in the environment and a number of sources may infect a property, including wild birds, other emus, feed sources and other animals.

The organisms are reasonably resistant and can survive for several weeks or months in the environment in favourable conditions. They are susceptible to sunlight and drying out.

Carrier birds are the main reservoir of infection in poultry once the organism has established in a flock. These birds have been infected and survived but the organism has established itself in the intestine, where it causes the bird little problem but is regularly passed out in faeces. This is a source of contamination. Some rodents and insects also have a potential to act as reservoirs.

Paratyphoid has been detected on some emu farms in Queensland but the full extent of the problem is not known. Problems have occurred in young chicks less than two weeks old but further research is needed to determine the problem’s full impact and size. It is not known whether adult emus can become carriers, but it is known that paratyphoid affects a wide range of animals, so infection could probably become established in emu flocks.

Transmission between birds occurs mainly by ingestion. Sick birds and carriers excrete salmonella in their faeces, which can then contaminate food, water, litter and other areas.

Females can also lay eggs that are contaminated on the outside of the shell. The paratyphoid organisms are mobile and can penetrate the pores of a shell while it is still warm and moist. If these organisms are not killed through egg disinfection procedures, infected eggs will reach the hatcher. If these eggs hatch, large numbers of salmonella will be released into the hatcher.

Other chicks can become infected by inhaling organisms or eating contaminated fluff circulating round the hatcher. This can result in sickness, deaths and carrier birds from this batch of chicks.

Clinical signs

The disease has the potential to cause significant mortalities, including a high proportion of dead embryos in-shell in both pipped and unpipped stages.

After hatching, deaths may start after two to three days and continue for up to three weeks. The chicks look depressed and lethargic, and sit in one position with their heads down for long periods. They stop eating but may increase their water consumption. A profuse watery diarrhoea develops. Paralysis, blindness, eye infections and joint problems have also been reported in poultry.

In Queensland, signs in young chicks include depression and weakness, leading to death and sudden death with few preceding signs.

Diagnosis

A field diagnosis should be confirmed by sending samples to a veterinary laboratory, where the organism can be cultured and identified.

Freshly dead, whole chicks can be sent to a laboratory for examination or specific samples can be taken from post mortem. Samples should be kept chilled in a fridge and not frozen prior to dispatch.

Treatment

Therefore, it is important to consult your veterinarian regarding treatment and get samples to a laboratory as soon as possible. If a salmonella organism is cultured, the laboratory can also carry out drug sensitivity tests to identify which drugs the organism is susceptible or resistant to. This information is valuable in formulating an effective disease control program.

Prevention

If it becomes established on a property, a control program can be drawn up, which would concentrate on the areas where the disease causes the most damage, such as the incubation, hatching and brooder stages.

This program requires strict attention to hygiene and should include:

• collecting eggs daily and fumigating eggs with formaldehyde gas, which should eliminate or greatly reduce contamination on the outside of the shell. Here fumigation should be used rather than egg washing. If eggs are washed, a hot solution (43-49^oC) is used to expand the egg contents, and force air and hopefully any contamination out through the pores in the shell. The egg is then dried using hot air before the egg contents shrink back to normal size. If the egg is not dried before the contents shrink, the fluid and contamination may be sucked back through the shell’s pores
• washing hands or wearing disposable gloves when handling eggs. As outlined, salmonella are passed in the faeces and can then spread to contaminate many objects, including hands
• fumigating the hatcher between batches with formaldehyde or Virkon® S gas, or clean with a broad spectrum egg disinfectant, such as gluteraldehydes or orthosan. All fluff, dust and egg shell remains must also be removed
• observing chicks closely. Samples should be sent to a laboratory if chicks are dying or not doing well, or there is a high proportion of dead full-term embryos in shell
• using strategic antibiotic treatment to control infection in chicks
• considering additional precautions if problems are identified, such as
• regularly misting the eggs stored in the cold room with a recognised disinfectant. Eggs should not be handled or wiped until the surface has dried and/or each batch of eggs has been fumigated just before they are put into the incubator
• fumigating eggs as soon as they are put in the hatcher and before hatching begins. Advice should be sought if this option is used, as the amounts of formaldehyde and Condy’s crystals are different to other fumigations, and good ventilation is necessary.

Scientific name

Description

Aspergilla has the potential to infect a wide range of mammalian, avian and reptilian species, including humans, and is probably the most common fungal infection affecting birds.

The most common species of Aspergilla that causes diseases in birds are A. fumigatus, A. flavus and A. niger. Numerous other species of Aspergilla are present in the environment but they rarely appear as a cause of the disease.

A. flavus is a cause of aspergillosis in emus in Queensland.

How the disease occurs

Favourable conditions include:

• warm, moist areas, e.g. in litter around waterers and some types of deep litter
• mouldy or rotting areas, e.g. spoiled or damp feed and rotting vegetation.

As with other fungi, Aspergilla has a growing phase where hyphae (the appearance of white strands/lumps) grow. This is followed by the production of spores, which are resistant to environmental conditions and are very small, enabling them to be easily transported by wind and in dust particles. Favourable conditions can produce large numbers of spores.

Birds usually become infected when they inhale the spores. The infection is not transferred from bird to bird. A bird’s immune system can control the infection if they have inhaled only a relatively small number of spores. Infection results if the immune system is deficient, such as in very young chicks where the immune system is still developing, or in birds that have been stressed by other disease problems, overcrowding, or insufficient food and water. Infection can also result in normal birds if they inhale a massive numbers of spores and their immune system is overwhelmed.

In Queensland, aspergillosis has been found in young chicks and caused deaths in the 3-8 week age group. There appears to be a strong association between infection and the presence of dust from litter in the atmosphere of the brooder shed. This dust can be raised when the litter is shovelled out or raked over, and even the passage of older chicks raises dust from the litter.

Clinical signs

The chicks appear to get infected in the brooder house very early in life. Initially, there are no signs, but then affected chicks will gradually appear unthrifty and less active than other chicks in the group. They will show signs of gasping and respiratory distress if forced to exercise. In the final stages, the chick is obviously depressed, doesn’t move much and shows laboured respiration, which is an exaggerated movement of the ribs and chest in and out with each breath, possibly combined with open-mouthed breathing. This is the terminal stage and the chick usually dies soon after.

These signs are caused by spores hatching and growing in the lungs. Firm, round, white nodules form in the lung tissue and grow steadily. As they grow they occupy lung space and disrupt the lung’s normal functioning. This reduces the oxygen supply to the chick to the point where it can no longer survive. These nodules may also be found in other sites, including the air sacs attached to the rib cage, liver and abdominal cavity.

Reports from the ostrich industry indicate that, as well as causing problems in chicks, aspergillosis can also infect the air sacs of older birds, causing a chronic, debilitating disease.

Diagnosis

Treatment

Prevention

Prevention should be aimed at three broad areas:

• Removal or control of favourable areas for fungal growth. This would include removing wet litter, not using damp or mouldy straw or hay as litter or food, not using and removing spoiled grain, and regular provision of fresh non-dusty litter
• Dust control in brooder sheds. This is an important area, as dust in the air of brooder sheds is closely related to infection of young chicks. As dust is most likely to be raised when litter is removed or raked over, lightly damping down the litter may prevent dust being raised when moved. Good quality litter also helps. A coarse litter of wood chips or pine wood shavings appears to work well. Litter that is already dusty may only contribute to the problem
• Hygiene. This can prevent aspergilla numbers building up to a point where problems occur. Attention needs to be paid to hygiene in all stages to the end of the brooder stage. Eggs should be fumigated and/or washed in a recognised egg sanitiser and used according to directions. The cold storage room, incubator and hatcher should be fumigated or cleaned regularly with a recognised disinfectant active against fungi. The brooder house should be cleaned and disinfected before the hatching season begins. If individual pens are cleaned out during the breeding season, they should be disinfected each time as well. Disinfectants that are active against aspergilla include those containing gluteraldehyde as an active constituent, Virkon ® S.

The above areas will also control other diseases that may cause problems during incubation, hatching and brooding. ]]> https://www.haf.bz/aspergillosis-emu-health/feed/ 0 https://www.haf.bz/emus-nutritional-requirements-for-breeding/ https://www.haf.bz/emus-nutritional-requirements-for-breeding/#comments Wed, 04 Jul 2012 06:52:25 +0000 admin http://www.haf.bz/?p=1718 Digestive system

Anatomical studies have revealed that the emu’s digestive system is comprised of an oesophagus, proventriculus, gizzard, a small intestine (duodenum, jejunum and ileum), caeca, rectum and cloaca. In this respect, they are similar to poultry with the exception that they do not have a distinct crop. However, the proventriculus is quite distensible and possibly could serve as an organ for food storage. The total length of the emu’s digestive tract is relative to its live weight and is approximately 10 times less than that of domestic fowl.

The amount of time food takes to pass through the digestive tract is variable, depending in part on the nature of the item ingested. Plant matter will take an average of five to six hours; intact wheat grains will take from less than a day up to two days. Glass marbles have been observed to be retained for 100 days. It would be expected that large particles of insoluble grit would be retained for a period in the gizzard and be effective in aiding the physical maceration of food.

Nutritional Requirements

Emus, like other birds, need essential nutrients to grow and reproduce.

Energy

Ingredients high in carbohydrates and/or fats are energy sources and can include cereal grains and full-fat soy bean meal.

Protein

Feed protein is broken down in the intestines into its constituent amino acids, which may then be absorbed into the blood and used for muscle growth. There are more than 20 amino acids of which about 11 cannot be manufactured by the emu and must therefore be present in their feed. Of these, methionine, lysine, threonine, isoleucine and tryptophan are likely to be in shortest supply in emu diets.

Vitamins

These are substances that are distinct from protein, carbohydrate or fat, but are essential in small amounts for normal growth, development and health. They must be present in the diet although some vitamins may be obtained by coprophagy or be synthesised by micro-organisms in the intestinal tract.

Minerals

These are essential for normal growth, development and health. They must be present in the diet either in relatively small amounts, for example calcium, phosphorus, manganese, sodium and chloride or only trace amounts, for example potassium, iron, copper, iodine, zinc, selenium.

Fibre

Emus can digest only about 20% of the cellulose and lignin in their diet. It is estimated that the energy derived from this can satisfy about 11% of their energy requirement for maintenance. Their limited capacity to digest fibre is consistent with the observation that, in the wild, emus eat large insects, small vertebrates and those parts of plants in which nutrients are concentrated such as growing shoots, flowers, fruits and seeds. Some fibre is necessary to promote healthy gut function, but in nutritional terms its value is low.

Supplying Nutrient Requirements

The ability to supply the nutritional requirements of emus depends on the feed composition (i.e. the concentrations of the essential nutrients in the feed and the amount of feed consumed by the birds). When the emu’s diet is just comprised of a compounded feed, precise control can be had over their intake of nutrients. When a proportion of their diet is derived from range of feeds, their quantitative intake of available nutrients is less predictable.

As emus approach sexual maturity, an increasing proportion of their live-weight gain is body fat. The reproductive fitness of female emus is enhanced by ensuring only a very limited gain in body fat beyond 12 months of age. This may be achieved by giving the birds unrestricted access to a maintenance diet supplemented with lucerne pellets, hay or pasture. Close monitoring of live-weight gain together with experimental information on body composition may suggest a need to restrict the intake of the maintenance diet during this period. However, feed restriction may not be necessary, as Dr. Ravindra Bhaskaran of HAF reports, emus in their second year exhibit a marked seasonal fluctuation in feed intake. He observed feed intake to fall by as much as 40% to 50% in summer and then rise slowly during autumn and winter before increasing more sharply in late winter and spring. This reduction in appetite coupled with the onset of hot weather seems to be more than a reduced maintenance requirement for dietary energy because birds become stressed during this period, with some birds losing weight.

As the mature breeding female approaches the egg-laying season, she will require a higher plane of nutrition to meet her needs for egg formation compared with the earlier maintenance period. The time taken for an egg to develop is about five weeks for the emu and it is recommended that females be switched to a breeder diet six weeks prior to their first egg being laid. A high plane of nutrition is required also by breeding males to ensure they attain good fertility and to increase their body reserves prior to natural incubation. A suggested emu-breeder diet is given below (Table 1). This diet should contain a comprehensive poultry breeder vitamin and mineral premix.

The time taken for food to pass through the digestive tract is variable, depending in part on the item ingested. Plant particulate matter will take an average of five to six hours, intact wheat grains from less than a day up to two days. Glass marbles have been observed to be retained for 100 days. It would be expected that large particles of insoluble grit would be retained for a period in the gizzard and be effective in aiding the physical maceration of food.

Nutritional requirements

In considering nutrition we are primarily concerned with supplying the emu with all the nutrients essential to its maintenance, growth and reproduction. The nutritional requirements of emus are not yet fully understood.

Energy

Ingredients high in carbohydrates and/or fats are energy sources and include the cereal grains and full-fat soyabean meal, for example.

Protein

Feed protein is broken down in the intestines into its constituent amino acids which may then be absorbed into the blood and used for muscle growth. The emu´s requirement for protein is in effect a requirement for amino acids and it is the amino acid composition of the feed that is the crucial factor. There are more than 20 amino acids of which about 11 cannot be manufactured by the emu and so must be present in the feed. Of these methionine, lysine, threonine, isoleucine and tryptophan are likely to be in shortest supply in emu diets.

Vitamins

These are substances distinct from protein, carbohydrate or fat but which are essential in small amounts for normal growth, development and health. They must be present in the diet although some vitamins may be obtained by coprophagy or be synthesised by micro-organisms in the intestinal tract.

Minerals

These are essential for normal growth, development and health. They must be present in the diet either in relatively small amounts, for example calcium, phosphorus, manganese, sodium and chloride or only trace amounts, for example potassium, iron, copper, iodine, zinc, selenium.

Fibre

Emus can digest only about 20% of the cellulose and lignin in their diet. It has been estimated that the energy derived from this can satisfy about 11% of their energy requirement for maintenance. Their limited capacity to digest fibre is consistent with the observation that, in the wild, emus eat large insects, small vertebrates and those parts of plants in which nutrients are concentrated such as growing shoots, flowers, fruits and seeds. It also suggests that immature, rapidly growing emus should be fed diets relatively low in fibre and similar in nature to conventional poultry grower diets. Some fibre is necessary to promote healthy gut function but in nutritional terms its value is low.

Supplying Nutritional Requirements

The ability to supply emus’ nutritional requirements depends on the feed composition, that is, the concentrations of essential nutrients in the feed and the amount of feed consumed by the birds. When all of the emus’ diet comprises a compounded feed, quite precise control can be had over their intake of nutrients. When a proportion of their diet is derived from the paddock then their quantitative intake of available nutrients is less predictable.

For rapidly growing emus destined for slaughter it seems logical to reduce the dependence on paddock and instead supply compounded diets formulated to least-cost specifications.

The growth curve of emus suggests that a three-phase system of feeding may be appropriate. Phase one could be known as a starter phase and would cover the period from hatching to when the emus attained an average liveweight of approximately 10 kg (14 weeks of age). Phase two, a grower phase, would cover the period from 10 kg liveweight to 25 kg liveweight (34 weeks of age). Phase three, a finisher phase, would be that period from 25 kg liveweight through to slaughter. Dividing the growing period into phases is simply to signify periods in which the emu requires a change in its dietary nutrient composition to best meet its current level of production. However, until the appropriate nutrient response data are known, the suggestion of a three phase system is only tentative.

Leg disorders

The development of leg deformities has been cited as a common problem in captive bred emus, with clinical signs usually appearing within the first two months of life. A number of different, possibly interrelated conditions may be involved as well as calcium/phosphorus imbalance and methionine deficiency. Maternal nutrition may also be implicated. Dr. Ravindra Bhaskaran of Hindustan Animal Feeds  has observed that restricting the time of access to mixed feed to a period of only four hours each day from about 10 to 30 days of age will minimize the incidence of leg disorders in emu chicks.