Riemerella anatipestifer infection

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Histopathology

Histologic section of duck brain (original x50 H&E stain): Riemerella anatiperstifer causing meningitis and vasculitis in a young duck. Note inflammatory response in vessel wall.

Richard J. Julian

Gross lesions

Fibrinous airsacculitis

Tirath Sandhu

Identity

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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

Pathogen/s

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Riemerella anatipestifer

Overview

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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.

Host Animals

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Animal name	Context	Life stage
Anas (ducks)	Domesticated host; Wild host	Poultry\|Day-old chick; Poultry\|Young poultry
Anser (geese)	Domesticated host; Wild host	Poultry\|Day-old chick; Poultry\|Young poultry
Cairina (Muscovy ducks)	Domesticated host; Wild host	Poultry\|Day-old chick; Poultry\|Young poultry
Coturnix	Domesticated host	Poultry\|Young poultry
Cygnus olor (mute swan)	Wild host
ducks (breeds and production)	Domesticated host; Wild host	Poultry\|Day-old chick; Poultry\|Young poultry
Gallus gallus domesticus (chickens)	Domesticated host	Poultry\|Young poultry
Meleagris gallopavo (turkey)	Domesticated host	Poultry\|Young poultry
Numida meleagris (guineafowl)	Domesticated host; Wild host

Hosts/Species Affected

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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).

Systems Affected

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multisystemic diseases of poultry
nervous system diseases of poultry
reproductive diseases of poultry
respiratory diseases of poultry
skin and ocular diseases of poultry

Distribution

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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 Table

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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.

Last updated: 26 May 2022

Continent/Country/Region	Distribution	Reference	Notes
Africa
Egypt	Present	Bayoumi et al. (1988) Ibrahim et al. (2000)
Asia
Bangladesh	Present	Mustafa et al. (1985)
China	Present, Widespread	Cheng AnChun et al. (2003)
-Anhui	Present, Widespread	Hu QingHai et al. (2001)
-Fujian	Present, Widespread	Huang Yu et al. (1999)
-Guangdong	Present, Widespread	Guo Yujiang (1983) Gao and Guo (1988) CABI (Undated)
-Hebei	Present, Widespread	Gao and Guo (1988) Zhang DaiMing and Guo YuPu (1999)
-Jiangsu	Present, Widespread	Hu QingHai et al. (1997)
-Jiangxi	Present, Widespread	Zhu ZhiXiu et al. (2001)
-Sichuan	Present, Widespread	Cai JiaLi et al. (2001) Wang MingShu et al. (2002)
-Yunnan	Present, Widespread	Wang QiongQiu et al. (2001)
-Zhejiang	Present, Widespread	Bao GuoLian et al. (1997) Hu et al. (2003)
India	Present	Sarma et al. (1985) Murthy et al. (Undated)
-Assam	Present	Chaudhury and Mahanta (1985)
-West Bengal	Present	Sadhukhan et al. (2001)
Israel	Present, Widespread	Bendheim and Even-Shoshan (1975) Bendheim et al. (1978)
Japan	Present	Chikuba et al. (2016) Sakurai et al. (1987)
Singapore	Present, Widespread	Singh et al. (1982) Loh et al. (1992)
South Korea	Present, Widespread	Kang and Koh (1993) Kolodzieyski et al. (2002)
Taiwan	Present, Widespread	Chang (1984) Huang et al. (1991)
Thailand	Present, Widespread	Mahitanan et al. (1982) Pathanasophon et al. (1994) Kohler et al. (1997)
Europe
Czechia	Present	Rachač and Vladík (1987)
Denmark	Present	Bisgaard (1982) Bisgaard (1995)
France	Present	Saint-Aubert et al. (1972) Vallee et al. (1972) Ganiere et al. (1983)
Germany	Present, Widespread	Riemer (1904) Gerlach (1970) Ziedler et al. (1984) Floren et al. (1987)
Hungary	Present, Widespread	Bitay et al. (1979) Ivanics et al. (1996)
Italy	Present, Widespread	Pascucci et al. (1981) Giovannetti and Pascucci (1983)
Poland	Present	Gazdzinski and Minta (1978)
Russia	Present	Goroshko and Prokof'eva (1958)
Spain	Present	Leon et al. (1980)
United Kingdom	Present, Widespread	Asplin (1955) Harry (1969) Timms and Marshall (1989)
North America
Canada	Present, 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)
United States	Present	CABI (Undated a)	Present based on regional distribution.
-California	Present, Widespread	Smith et al. (1987)
-Connecticut	Present	Jortner et al. (1969)
-Illinois	Present	Graham et al. (1938) Campagnolo et al. (2001) Tripathy et al. (Undated)
-Indiana	Present, 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)
Oceania
Australia	Present, Widespread	Munday et al. (1970) Grimes and Rosenfield (1972) Rosenfeld (1973)
-New South Wales	Present, Widespread	Jackson (1972)
-Victoria	Present	Reece and Coloe (1985)
New Zealand	Present	Hemsley (1996)

Pathology

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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.

Diagnosis

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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/Signs

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Sign	Life Stages	Type
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 Course

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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).

Epidemiology

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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: Economic

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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 Safety

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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 Treatment

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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 Control

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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.

References

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Website	URL	Comment
Duck Care - a data resource for duck keepers	http://www.duckhealth.com	An information resource for duck keepers provided by Cornell University Duck Resrearch Laboratory.

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Riemerella anatipestifer infection

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