Difference between revisions of "Riemerella anatipestifer"
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|species = ''R. anatipestifer'' | |species = ''R. anatipestifer'' | ||
}} | }} | ||
| − | + | Previously Known As: '''''Moraxella anatipestifer — Pasteurella anatipestifer — Pfeifferella anatipestifer''''' | |
Disease Known As: '''''Duck Septicaemia — Goose Influenza — Infectious Serositis — New Duck Disease — Polyserositis — Riemerellosis''''' | Disease Known As: '''''Duck Septicaemia — Goose Influenza — Infectious Serositis — New Duck Disease — Polyserositis — Riemerellosis''''' | ||
==Introduction== | ==Introduction== | ||
| − | '''''Riemerella anatipestifer''''' is a '''gram negative [[Bacteria|bacterial]] pathogen causing septicaemia in ducks and geese'''. This | + | '''''Riemerella anatipestifer''''' is a '''gram negative [[Bacteria|bacterial]] pathogen primarily causing septicaemia in ducks and geese'''. This may lead to '''high mortality and significant economic losses''' both from direct fatalities and carcass condemnation. |
There are '''21 known serotypes''' with no cross-reactivity between them. Multiple serotypes are often present in one outbreak. | There are '''21 known serotypes''' with no cross-reactivity between them. Multiple serotypes are often present in one outbreak. | ||
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'''Worldwide''' – widespread in China, Thailand, Taiwan, USA, UK, Germany and Hungary and present to variable degrees in most other poultry producing countries. | '''Worldwide''' – widespread in China, Thailand, Taiwan, USA, UK, Germany and Hungary and present to variable degrees in most other poultry producing countries. | ||
| − | Transmission occurs through '''infected birds and premises''', the organism being shed in '''nasal and sinusoid secretions'''. These can contaminate water and drinkers/feeders. It can also enter through '''broken skin'''. Infection spreads fast in confined houses. Healthy ducklings may also carry the infection asymptomatically in their respiratory tracts.<ref>Ryll, M., Christensen, H., Bisgaard, M., Christensen, J. P., Hinz, K. H., Köhler, B (2001) '''Studies on the prevalence of ''Riemerella anatipestifer'' in the upper respiratory tract of clinically healthy ducklings and characterization of untypable strains'''. ''J Vet Med. Series B'', 48(7):537-546; 34</ref> | + | Transmission occurs through '''infected birds and premises''', the organism being shed in '''nasal and sinusoid secretions'''. These can contaminate water and drinkers/feeders. It can also enter through '''broken skin'''. No evidence of vertical transmission has been published. Infection spreads fast in confined houses. Healthy ducklings may also carry the infection asymptomatically in their respiratory tracts.<ref>Ryll, M., Christensen, H., Bisgaard, M., Christensen, J. P., Hinz, K. H., Köhler, B (2001) '''Studies on the prevalence of ''Riemerella anatipestifer'' in the upper respiratory tract of clinically healthy ducklings and characterization of untypable strains'''. ''J Vet Med. Series B'', 48(7):537-546; 34</ref> |
| − | == | + | ==Hosts== |
Ducks and geese are the main hosts but turkeys, chickens, pheasants, guinea-fowl, quails and swans can also be infected. | Ducks and geese are the main hosts but turkeys, chickens, pheasants, guinea-fowl, quails and swans can also be infected. | ||
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==Clinical Signs== | ==Clinical Signs== | ||
| − | Systemic infection | + | Systemic infection is common. However, infection may also become localised in joints and skin in chronic cases. In addition, localised infection of the oviduct may develop resulting in blind layers when the birds grow up. |
| − | Disease is then '''multisystemic''' and can comprise of '''greenish [[Diarrhoea|diarrhoea]]''', pyrexia, anorexia, growth retardation, nasal discharge, coughing, restlessness, polydipsia, '''ataxia, hypermetria, weakness, tremors''' and limb swelling. Nervous signs develop when the organism crosses the blood:brain barrier. Conjunctivitis, chemosis, scleral inflammation and ocular discharge sometimes also occur. In late disease, young birds may suffer from '''convulsions'''. | + | Disease is then '''multisystemic''' and can comprise of '''greenish [[Diarrhoea|diarrhoea]]''', pyrexia, anorexia, growth retardation, nasal discharge, coughing, restlessness, polydipsia, '''ataxia, hypermetria, weakness, tremors''' and limb swelling. Nervous signs develop when the organism crosses the blood:brain barrier. Conjunctivitis, chemosis, scleral inflammation and ocular discharge sometimes also occur. In late disease, young birds may suffer from characteristic '''convulsions'''. |
| − | '''High mortality up to 75% occurs in ducklings and goslings'''. In most cases, death occurs within | + | '''High mortality up to 75% occurs in ducklings and goslings'''. In most cases, death occurs within 12-24h of the onset of clinical signs. |
| + | |||
| + | ==Pathological Lesions== | ||
| + | On post-mortem, infection causes a '''yellowish-white fibrinous exudate to cover the heart, liver and air sacs.''' Air sacs may also contain a caseous exudate and oviducts caseous plugs in female birds. The same yellow exudate can be found in the nervous tissue and also in the joints and skin in chronic cases, forming honey-comb like dermatitis. Carcasses are septicaemic and congested. | ||
| + | |||
| + | On histopathology, '''mononuclear and heterophilic cells''' infiltrate the serous surfaces of pericardium, air sacs and liver. Multinuclear giant cells may develop in the air sacs and skin lesions in chronic cases. | ||
==Diagnosis== | ==Diagnosis== | ||
Presumptive diagnosis is often made from '''history, clinical signs and lesions''', based upon the nervous signs and fibrinous pericardial, perihepatic, meningeal and respiratory lesions and exudate. Although suggestive, these are not specific. | Presumptive diagnosis is often made from '''history, clinical signs and lesions''', based upon the nervous signs and fibrinous pericardial, perihepatic, meningeal and respiratory lesions and exudate. Although suggestive, these are not specific. | ||
| − | ''R. anatipestifer'' can be easily isolated, from brain, heart blood, air sacs, liver or oviduct and grows on '''soy media enriched with sheep blood or bovine serum''' forming non-haemolytic colonies. Isolates can then be serotyped with '''agglutination and agar gel precipitation'''.<ref>Sandhu, T., Harry, E. G (1981) '''Serotypes of ''Pasteurella anatipestifer'' isolated from commercial White Pekin ducks in the United States'''. ''Avian Diseases'', 25:497-502.</ref> | + | ''R. anatipestifer'' can be easily isolated, from brain, heart blood, air sacs, liver or oviduct and grows on '''soy media enriched with sheep blood or bovine serum''' forming non-haemolytic colonies. Incubation ideally under 5% carbon dioxide. Isolates can then be serotyped with '''agglutination and agar gel precipitation'''.<ref>Sandhu, T., Harry, E. G (1981) '''Serotypes of ''Pasteurella anatipestifer'' isolated from commercial White Pekin ducks in the United States'''. ''Avian Diseases'', 25:497-502.</ref> |
| + | |||
| + | A PCR-based diagnostic test has also been developed. | ||
'''[[ELISA testing|ELISA]] and serum tube [[agglutination]]''' can be used for antibody detection, of which ELISA is the most sensitive. | '''[[ELISA testing|ELISA]] and serum tube [[agglutination]]''' can be used for antibody detection, of which ELISA is the most sensitive. | ||
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==Treatment== | ==Treatment== | ||
| − | '''Enrofloxacin, Lincomycin, Novobiocin, Procaine Penicillin''' and '''Trimethoprim-Sulphonamides''' can be used, some as injectables, others in feed. | + | '''Enrofloxacin, Lincomycin, Novobiocin, Procaine Penicillin''' and '''Trimethoprim-Sulphonamides''' can be used, some as injectables, others in feed. However, current legislation in many countries does not allow the use of quinolones. Antibiotic sensitivity testing should be carried out prior to treatment. |
==Control== | ==Control== | ||
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|date =25 June 2011 | |date =25 June 2011 | ||
}} | }} | ||
| − | <br><br> | + | <br><br> |
| + | |||
| + | This article was reviewed by [http://www.bric.ku.dk/staff_dynamic/staff/description/?id=310904&f=3 Jens Peter Christensen, DVM, PhD] on 30/08/11. | ||
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[[Category:Avian Bacteria]] | [[Category:Avian Bacteria]] | ||
[[Category:Flavobacteria]] | [[Category:Flavobacteria]] | ||
[[Category:CABI Expert Review]] | [[Category:CABI Expert Review]] | ||
[[Category:Neurological Diseases - Birds]] [[Category:Alimentary Diseases - Birds]] [[Category:Respiratory Diseases - Birds]] | [[Category:Neurological Diseases - Birds]] [[Category:Alimentary Diseases - Birds]] [[Category:Respiratory Diseases - Birds]] | ||
| + | [[Category:Expert Review Completed]] | ||
Revision as of 17:12, 31 August 2011
| Riemerella anatipestifer | |
|---|---|
| Phylum | Bacteroidetes |
| Class | Flavobacteria |
| Order | Flavobacteriales |
| Family | Flavobacteriaceae |
| Genus | Riemerella |
| Species | R. anatipestifer |
Previously Known As: Moraxella anatipestifer — Pasteurella anatipestifer — Pfeifferella anatipestifer
Disease Known As: Duck Septicaemia — Goose Influenza — Infectious Serositis — New Duck Disease — Polyserositis — Riemerellosis
Introduction
Riemerella anatipestifer is a gram negative bacterial pathogen primarily causing septicaemia in ducks and geese. This may lead to high mortality and significant economic losses both from direct fatalities and carcass condemnation.
There are 21 known serotypes with no cross-reactivity between them. Multiple serotypes are often present in one outbreak.
Riemerella anatipestifer is not zoonotic.
Distribution
Worldwide – widespread in China, Thailand, Taiwan, USA, UK, Germany and Hungary and present to variable degrees in most other poultry producing countries.
Transmission occurs through infected birds and premises, the organism being shed in nasal and sinusoid secretions. These can contaminate water and drinkers/feeders. It can also enter through broken skin. No evidence of vertical transmission has been published. Infection spreads fast in confined houses. Healthy ducklings may also carry the infection asymptomatically in their respiratory tracts.[1]
Hosts
Ducks and geese are the main hosts but turkeys, chickens, pheasants, guinea-fowl, quails and swans can also be infected.
Birds 1-8 weeks old are usually affected.
Clinical Signs
Systemic infection is common. However, infection may also become localised in joints and skin in chronic cases. In addition, localised infection of the oviduct may develop resulting in blind layers when the birds grow up.
Disease is then multisystemic and can comprise of greenish diarrhoea, pyrexia, anorexia, growth retardation, nasal discharge, coughing, restlessness, polydipsia, ataxia, hypermetria, weakness, tremors and limb swelling. Nervous signs develop when the organism crosses the blood:brain barrier. Conjunctivitis, chemosis, scleral inflammation and ocular discharge sometimes also occur. In late disease, young birds may suffer from characteristic convulsions.
High mortality up to 75% occurs in ducklings and goslings. In most cases, death occurs within 12-24h of the onset of clinical signs.
Pathological Lesions
On post-mortem, infection causes a yellowish-white fibrinous exudate to cover the heart, liver and air sacs. Air sacs may also contain a caseous exudate and oviducts caseous plugs in female birds. The same yellow exudate can be found in the nervous tissue and also in the joints and skin in chronic cases, forming honey-comb like dermatitis. Carcasses are septicaemic and congested.
On histopathology, mononuclear and heterophilic cells infiltrate the serous surfaces of pericardium, air sacs and liver. Multinuclear giant cells may develop in the air sacs and skin lesions in chronic cases.
Diagnosis
Presumptive diagnosis is often made from history, clinical signs and lesions, based upon the nervous signs and fibrinous pericardial, perihepatic, meningeal and respiratory lesions and exudate. Although suggestive, these are not specific.
R. anatipestifer can be easily isolated, from brain, heart blood, air sacs, liver or oviduct and grows on soy media enriched with sheep blood or bovine serum forming non-haemolytic colonies. Incubation ideally under 5% carbon dioxide. Isolates can then be serotyped with agglutination and agar gel precipitation.[2]
A PCR-based diagnostic test has also been developed.
ELISA and serum tube agglutination can be used for antibody detection, of which ELISA is the most sensitive.
Treatment
Enrofloxacin, Lincomycin, Novobiocin, Procaine Penicillin and Trimethoprim-Sulphonamides can be used, some as injectables, others in feed. However, current legislation in many countries does not allow the use of quinolones. Antibiotic sensitivity testing should be carried out prior to treatment.
Control
A multivalent vaccine is available in live and inactivated forms. The live form is administered as an aerosol spray at one day of age and the inactivated as two injections at 2 and 3 weeks of age.
Management, sanitation and minimisation of stress also play major roles in prevention.
| Riemerella anatipestifer Learning Resources | |
|---|---|
 Test your knowledge using flashcard type questions |
R. anatipestifer Flashcards |
References
- ↑ Ryll, M., Christensen, H., Bisgaard, M., Christensen, J. P., Hinz, K. H., Köhler, B (2001) Studies on the prevalence of Riemerella anatipestifer in the upper respiratory tract of clinically healthy ducklings and characterization of untypable strains. J Vet Med. Series B, 48(7):537-546; 34
- ↑ Sandhu, T., Harry, E. G (1981) Serotypes of Pasteurella anatipestifer isolated from commercial White Pekin ducks in the United States. Avian Diseases, 25:497-502.
|
This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project. The datasheet was accessed on 25 June 2011. |
This article was reviewed by Jens Peter Christensen, DVM, PhD on 30/08/11.