Riemerella anatipestifer infection
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Riemerella anatipestifer infection
International Common Names
- English: anatipestifer syndrome; duck septicaemia; duck septicemia; goose influenza; infectious serositis; new duck disease; polyserositis; riemerella anatipestifer in birds, duck septicemia, infectious serositis; riemerellosis; septicaemia; septicemia; serositis; sinusitis
Local Common Names
- Germany: septicemia anserum exudativa
OverviewTop of page
Riemerella anatipestifer infection is a septicaemic (acute, peracute, sometimes chronic) disease of primarily ducks and geese, but it also affects turkeys, chickens, pheasants, guinea fowls, quails and swans. The infection causes serious losses in ducks and geese due to high mortality. It usually occurs in young birds of 1-8 weeks of age. In addition to mortality, it causes carcass condemnation and weight loss. The disease was first reported in the USA in 1932 (Henricksen and Hilbert, 1932) in ducks in an area of intensive duck farming where it was known as ‘new duck disease’. Other synonyms are infectious serositis (Dougherty et al., 1955), anatipestifer syndrome and duck septicaemia. A similar disease in goslings ‘septicaemia anserum exudativa’ was reported by Riemer in 1904. Later, it was known to be caused by the same bacterium that is responsible for the disease in ducklings. R. anatipestifer infection has been reported worldwide.
R. anatipestifer infection is caused by a Gram-negative bacterium named initially as Pfeifferella anatipestifer. Because of its uncertain taxonomic status, it was placed under various genera and named as Moraxella anatipestifer, Pasteurella anatipestifer and species incertae sedis. On the basis of its DNA base composition and cellular fatty acid profile, it was transferred to Flavobacterium-Cytophaga group (Piechulla et al., 1986). Segers et al., (1993) reported significant differences between this organism and other members of Flavobacterium and Weeksella, and suggested the name Riemerella anatipestifer in honor of Riemer (1904) who initially reported the disease ‘septicaemia anserum exudativa’ in geese.
The control of this infection is rather difficult because R. anatipestifer has at least 21 known serotypes, and different serotypes do not provide cross-protection against each other. Very often, more than one serotype are responsible for disease in a flock or on a farm. An effective vaccine has to be multivalent to provide protection against predominant serotypes. The infection can be treated with antibiotics, but is mostly controlled through vaccination. The infection is not of any public health importance, and is not reportable to regulatory authorities.
Hosts/Species AffectedTop of page
Riemerella anatipestifer infection is primarily a disease of ducks and geese. It has also been reported in turkeys (Zehr and Ostendorf, 1970; Helfer and Helmboldt, 1977), chickens (Rosenfeld, 1973), pheasants (Bruner et al., 1970), swans (Munday et al., 1970), guinea fowls and quails (Pascucci et al., 1989).
DistributionTop of page
Information given in the Geographical Distribution table shows the occurrence of Riemerella anatipestifer infection in countries that produce ducks, geese and turkeys. The disease is widespread in intensive duck producing areas of China, Thailand, Taiwan, USA, UK, Germany and Hungary. The infection has also been reported from Canada, Denmark, Italy, France, Netherlands and Australia. Sporadic cases have been reported from India, Bangladesh, Singapore, Israel, Korea, Egypt, Russia and New Zealand.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Bangladesh||Present||Mustafa et al., 1985|
|China||Widespread||Cheng et al., 2003|
|-Anhui||Widespread||Hu et al., 2001|
|-Fujian||Widespread||Huang et al., 1999|
|-Guangdong||Widespread||Guo Yujiang, 1983; Gao and Guo, 1988; Zhang et al., 1999|
|-Hebei||Widespread||Gao and Guo, 1988; Zhang and Guo, 1999|
|-Jiangsu||Widespread||Hu et al., 1997|
|-Jiangxi||Widespread||Zhu et al., 2001|
|-Sichuan||Widespread||Cai et al., 2001; Wang et al., 2002|
|-Yunnan||Widespread||Wang et al., 2001|
|-Zhejiang||Widespread||Bao et al., 1997; Hu et al., 2003|
|India||Present||Murthy et al., 1981; Sarma et al., 1985|
|-Assam||Present||Chaudhury and Mahanta, 1985|
|-West Bengal||Present||Sadhukhan et al., 2001|
|Israel||Widespread||Bendheim and Even-Shoshan, 1975; Bendheim et al., 1978|
|Japan||Present||Sakurai et al., 1987|
|Korea, Republic of||Widespread||Kang and Koh, 1993; Kolodzieyski et al., 2002|
|Singapore||Widespread||Singh et al., 1982; Loh et al., 1992|
|Taiwan||Widespread||Chang, 1984; Huang et al., 1991|
|Thailand||Widespread||Mahitanan et al., 1982; Pathanasophon et al., 1994; Kohler et al., 1997|
|Egypt||Present||Bayoumi et al., 1988; Ibrahim et al., 2000|
|Canada||Widespread||Taylor, 1955; Sandhu and Harry, 1981|
|-Alberta||Present||Leavitt and Ayroud, 1997|
|-Manitoba||Present||Wobeser et al., 1982|
|-Ontario||Present||Sandhu and Harry, 1981|
|-Saskatchewan||Present||Wobeser and Ward, 1974|
|USA||Present||Present based on regional distribution.|
|-California||Widespread||Smith et al., 1987|
|-Connecticut||Present||Jortner et al., 1969|
|-Illinois||Present||Graham et al., 1938; Tripathy et al., 1980; Campagnolo et al., 2001|
|-Indiana||Widespread||Sandhu and Harry, 1981|
|-Minnesota||Present||Charles et al., 1991|
|-New York||Present||Hendrickson and Hilbert, 1932|
|-Oregon||Present||Helfer and Helmboldt, 1977|
|-South Carolina||Present||Eleazer et al., 1973|
|-Utah||Present||Brogden et al., 1982|
|Czech Republic||Present||Rachac and Vladík, 1987|
|Denmark||Present||Bisgaard, 1982; Bisgaard, 1995|
|France||Present||Saint et al., 1972; Vallee et al., 1972; Ganiere et al., 1983|
|Germany||Widespread||Riemer, 1904; Gerlack, 1970; Ziedler et al., 1984; Floren et al., 1987|
|Hungary||Widespread||Bitay et al., 1979; Ivanics et al., 1996|
|Italy||Widespread||Pascucci et al., 1981; Giovannetti and Pascuccci, 1983|
|Poland||Present||Gazdzinski and Minta, 1978|
|Russian Federation||Present||Goroshko and Prokofeva, 1958|
|Spain||Present||Leon et al., 1980|
|UK||Widespread||Asplin, 1955; Harry, 1969; Timms and Marshall, 1989|
|Australia||Widespread||Munday et al., 1970; Grimes and Rosenfield, 1972; Rosenfeld, 1973|
|-New South Wales||Widespread||Jackson, 1972|
|-Victoria||Present||Reece and Coloe, 1985|
|New Zealand||Present||Hemsley, 1996|
PathologyTop of page
The infection causes septicaemic lesions in affected birds. The heart, liver and airsacs are covered with a yellowish white exudate consisting of fibrin. Both abdominal and thoracic airsacs have thin layers of dry caseous exudate. Spleen is mottled and kidneys are congested. In females, the oviduct contains caseous plugs. Lungs are rarely involved. Occasionally, caseous lesions in the nasal and infraorbital sinuses are observed (Leibovitz, 1972). Lesions in the nervous system include fibrinous meningitis. Chronic infections in ducks may occur in the joints or skin. Skin lesions are in the form of dermatitis with yellowish exudate seen between fat and skin layers, while the outside of the skin appears spongy like a honeycomb. Lesions in turkeys and chickens are similar but less severe.
Histopathological lesions include fibrinous exudate, infiltrated with mononuclear cells and heterophils on the serous surfaces of pericardium, airsacs and liver capsule. Multinuclear giant cells may be seen in airsacs and skin lesions in chronic cases. The liver cells show cloudy swelling, fatty degeneration and necrosis (Chaudhury and Mohanta, 1985). Mottling of spleen is due to an increase in size and number of germinating lymph follicles. Lesions in the central nervous system include serofibrinous inflammation of cerebral and spinal meninges. Extensive exudate in the ventricular system and leukocytic infiltration of subpial and periventricular brain tissue has been observed.
DiagnosisTop of page
Clinical signs in ducklings and goslings include lethargy, ruffled feathers, anorexia, lagging behind the flock, nasal and eye discharge, greenish diarrhoea, incoordination, falling on their back, paddle their legs, and unable to stand or walk. In later stages, affected birds suffer from convulsions of the head and neck, ataxia before death. Mortality can be as high as 75%.
Affected turkeys appear depressed, dehydrated, lame, and have difficulty walking. Later, the birds become moribund and die. The infection causes low but lingering mortality. Similar clinical signs have been observed in chickens and other birds.
Presumptive diagnosis of Riemerella anatipestifer can be made from flock history, clinical signs and lesions. Nervous signs such as tremors of head and neck, falling on back and difficulty to stand up, incoordination and ataxia are very common in infected ducks and geese. Septicaemic lesions, typically fibrinous pericarditis, perihepatitis, airsacculitis, meningitis and salpingitis are also indicative of this infection, although some of these lesions may also be observed in infections with Pasteurella multocida, Escherichia coli or Streptococcus faecium. Similar nervous signs have also been observed in Salmonella infection in ducklings. Chlamydiosis and Coenonia anatina infection should also be considered in differential diagnosis. Confirmatory diagnosis should be based on isolation and identification of the causative organisms.
R. anatipestifer can be easily isolated from brain, heart blood, airsacs, liver, or oviduct by culturing on trypticase soy agar enriched with 0.05% yeast extract, 5% bovine serum or sheep blood. The organism can be identified by sugar, biochemical and enzymatic reactions.
R. anatipestifer isolates are serotyped by agglutination and agar-gel precipitation reactions (Sandhu and Harry, 1981). Slide agglutination test is performed by mixing a small colony with a drop of antiserum on a glass slide. If the isolate is same serotype as the antiserum, agglutination occurs in a few seconds. Tube agglutination can be done to determine antibody titres in a serum. For agar gel precipitin test, supernatant from a heated culture suspension is used as an antigen against known serotype antisera. Precipitin bands appear in 48-72 h. Antibody titres in sera can also be determined by enzyme-linked immunosorbent assays (Hatfield et al., 1987), which is more sensitive than agglutination tests.
List of Symptoms/SignsTop of page
|Digestive Signs / Abnormal colour of stool in birds, white, green, yellow faeces||Poultry:Day-old chick,Poultry:Young poultry||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Diarrhoea||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Discomfort, restlessness in birds||Poultry:Day-old chick,Poultry:Young poultry||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Poultry:Day-old chick,Poultry:Young poultry||Sign|
|General Signs / Inability to stand, downer, prostration||Poultry:Day-old chick,Poultry:Young poultry||Sign|
|General Signs / Increased mortality in flocks of birds||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Poultry:Young poultry||Sign|
|General Signs / Lameness, stiffness, stilted gait in birds||Sign|
|General Signs / Polydipsia, excessive fluid consumption, excessive thirst||Poultry:Day-old chick,Poultry:Young poultry||Sign|
|General Signs / Reluctant to move, refusal to move||Sign|
|General Signs / Swelling of the limbs, legs, foot, feet, in birds||Sign|
|General Signs / Torticollis, twisted neck||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weakness, paresis, paralysis of the legs, limbs in birds||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Tremor||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Respiratory Signs / Coughing, coughs||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sign|
|Respiratory Signs / Purulent nasal discharge||Sign|
|Skin / Integumentary Signs / Ruffled, ruffling of the feathers||Poultry:Day-old chick,Poultry:Young poultry||Sign|
|Skin / Integumentary Signs / Soiling of the feathers, vent feathers||Poultry:Day-old chick,Poultry:Young poultry||Sign|
Disease CourseTop of page
Ducks and geese usually get infected through the respiratory tract, although infections through a break in the skin have also been reported ( Leibovitz, 1972). Healthy ducklings may carry the organisms in the respiratory tract (Ryll et al., 2001). Cooper (1989) suggested transmission of infection in turkeys may be transmitted by mosquitoes, but the experimental evidence is circumstantial. After respiratory infection, the organisms gain entry into the blood circulation causing bacteraemia and systemic disease. It is not known as to how the organisms produce septicaemic lesions, although fibrinolytic enzymes, haemolysins and lipopolysaccharides have been suggested to be involved (Bangun et al., 1981; Brogden, 1989). The organisms pass through the blood-brain barrier to cause nervous signs and lesions. In most cases, death occurs within 6-12 h after showing clinical signs, although some sick birds may survive for a few more days before death. Recovered birds are stunted in growth. Chronic infections may result in localized infections of joints and/or skin. Experimental infection can be reproduced by subcutaneous, intramuscular, intravenous, intrasinus (infraorbital) or web-pad injections. The incubation period is about 2 to 5 days. Experimental infection through parenteral routes can cause clinical signs and mortality within 24-48 h. An acute form of the disease occurs in young ducklings. Turkeys usually contract the chronic form; susceptible age is 4 to 18 weeks.
Recovered birds become resistant to infection with a homologous serotype. Although protective antigen(s) have not been isolated or identified, cell-free culture filtrate has been shown to provide protection in ducklings (Pathanasophon et al., 1996). Research studies showed that vaccination with a recombinant outer membrane protein was not protective in ducklings against challenge with a homologous serotype ( Huang et al., 2002).
EpidemiologyTop of page
Riemerella anatipestifer infection occurs in the respiratory tract through contact with infected birds or premises. The disease can also occur by infection through a break in skin. The birds develop systemic infection through bacteraemia. In chronic cases, the infection is localized in joints and skin. The organisms are shed through nasal or infraorbital sinus secretions aerosolizing the environments and contaminating feeders and drinkers. The infection spreads fast in flocks raised in confined houses and causes high mortality in young ducklings or goslings. There are no seasonal differences in the incidence of disease in ducks. Outbreaks are common in ducks and geese, but incidence in turkeys, chickens and other birds are sporadic. The disease is rare in older birds or breeder ducks. No vector is known, although mosquitoes have been reported to carry R. anatipestifer, and may be a possible mean of transmission in turkeys (Cooper, 1989).
Impact: EconomicTop of page
Riemerella anatipestifer causes high economic losses to the duck and goose industries of waterfowl producing countries. The losses are due to mortality, meat condemnation and weight loss. It adds the financial burden to producers of treatment and control measures, including costs of medications, vaccines and labour. Losses in other birds such as turkeys, chickens and others are low to moderate.
Zoonoses and Food SafetyTop of page
Riemerella anatipestifer infection does not have any public health significance. The carcasses of birds showing lesions of infection at the time of slaughter are usually condemned or downgraded.
Disease TreatmentTop of page
Riemerella anatipestifer infection can be treated with enrofloxacin (50 p.p.m. in drinking water) or subcutaneous/intramuscular injection of penicillin in dosages of 50,000 IU/kg bodyweight (Turbahn et al., 1997; Sandhu and Dean, 1980). Enrofloxacin should be repeated for the next 4 days at levels of 25 p.p.m. Other treatments include novobiocin, lincomycin or sulfadimethoxine-ormetoprim (5:3) in feed. Medications become less effective after prolonged use, due to development of resistant strains. Users should pay attention to the manufacturers’ recommendations regarding usage, particularly in relation to drug withdrawal periods.
Prevention and ControlTop of page
Inactivated vaccines have been used to immunize ducklings against Riemerella anatipestifer infection ( Harry and Deb, 1979; Sandhu, 2003). Autogenous inactivated vaccines are commonly used to provide protection. Since more than one serotype may occur in a hatch of ducks at a farm or in an area, vaccines are usually multivalent to provide broad-spectrum protection against major serotypes responsible for the disease. Inactivated vaccines usually consist of bacterial cells grown in broth media and killed with formalin. Some vaccines are oil-emulsified or contain aluminum hydroxide or other adjuvants. Since most ducks are slaughtered at 6-7 weeks of age, adjuvanted vaccines may produce lesions at the site of injections resulting in condemnation of a part of the carcass. Inactivated vaccines are usually administered subcutaneously in the neck at 2 and 3 weeks of age.
A live avirulent vaccine developed against R. anatipestifer serotypes 1, 2 and 5 infection provide significant protection when administered by aerosol to one-day-old ducklings (Sandhu, 1991). Laboratory data showed protection up to 7 weeks of age though in the field some commercial duck farm follow up with an inactivated vaccine at 2-4 weeks of age. Progeny of breeder ducks vaccinated with an inactivated or live vaccine are protected up to 2-3 weeks of age through maternal immunity.
Management and sanitation play a major role in the prevention of infection. Ducklings maintained under stressful conditions are predisposed to R. anatipestifer infections. Sanitation in a house with confined rearing of multiple-aged flocks is very critical. The whole house should be depopulated for a major clean and disinfection.
ReferencesTop of page
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