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Streptococcus and Enterococcus infections in poultry

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Datasheet

Streptococcus and Enterococcus infections in poultry

Summary

  • Last modified
  • 03 January 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Streptococcus and Enterococcus infections in poultry
  • Pathogens
  • Enterococcus
  • Enterococcus durans
  • Enterococcus faecalis
  • Enterococcus faecium
  • Enterococcus hirae
  • Overview
  • Introduction


    Streptococcal and enterococcal infections in birds have a worldwide distribution and may cause acute septicaemic and chronic infections...

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Pictures

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PictureTitleCaptionCopyright
RED patterns obtained by PFGE with Sma I of 20 E. faecalis strains recovered from two hatcheries. RED patterns of isolates from hatchery 1 are shown in lanes 1 to 13 and those of hatchery 2 in lanes 14 to 20. Lanes of the control arthropathic and amyloidogenic E. faecalis strain 6085.94 are marked with a 'C'. Strains isolated from Marek's disease vaccine suspensions sampled through injection devices are located in lanes 1, 4, 5, 6, 8 to 11 and 14 to 18. Strains derived from samples taken directly from bags are in lanes 2, 3 and 7. Strains cultured from air samples are found in lanes 12, 13, 19 and 20. The RED pattern of lane 6 closely resembles that of the amyloid arthropathy inducing control strain. The RED pattern of lane 15 and 16 also resembled closely that of the control strain.
TitleRED patterns obtained by PFGE
CaptionRED patterns obtained by PFGE with Sma I of 20 E. faecalis strains recovered from two hatcheries. RED patterns of isolates from hatchery 1 are shown in lanes 1 to 13 and those of hatchery 2 in lanes 14 to 20. Lanes of the control arthropathic and amyloidogenic E. faecalis strain 6085.94 are marked with a 'C'. Strains isolated from Marek's disease vaccine suspensions sampled through injection devices are located in lanes 1, 4, 5, 6, 8 to 11 and 14 to 18. Strains derived from samples taken directly from bags are in lanes 2, 3 and 7. Strains cultured from air samples are found in lanes 12, 13, 19 and 20. The RED pattern of lane 6 closely resembles that of the amyloid arthropathy inducing control strain. The RED pattern of lane 15 and 16 also resembled closely that of the control strain.
CopyrightWith permission from Avian Pathology, Taylor & Francis, UK
RED patterns obtained by PFGE with Sma I of 20 E. faecalis strains recovered from two hatcheries. RED patterns of isolates from hatchery 1 are shown in lanes 1 to 13 and those of hatchery 2 in lanes 14 to 20. Lanes of the control arthropathic and amyloidogenic E. faecalis strain 6085.94 are marked with a 'C'. Strains isolated from Marek's disease vaccine suspensions sampled through injection devices are located in lanes 1, 4, 5, 6, 8 to 11 and 14 to 18. Strains derived from samples taken directly from bags are in lanes 2, 3 and 7. Strains cultured from air samples are found in lanes 12, 13, 19 and 20. The RED pattern of lane 6 closely resembles that of the amyloid arthropathy inducing control strain. The RED pattern of lane 15 and 16 also resembled closely that of the control strain.
RED patterns obtained by PFGERED patterns obtained by PFGE with Sma I of 20 E. faecalis strains recovered from two hatcheries. RED patterns of isolates from hatchery 1 are shown in lanes 1 to 13 and those of hatchery 2 in lanes 14 to 20. Lanes of the control arthropathic and amyloidogenic E. faecalis strain 6085.94 are marked with a 'C'. Strains isolated from Marek's disease vaccine suspensions sampled through injection devices are located in lanes 1, 4, 5, 6, 8 to 11 and 14 to 18. Strains derived from samples taken directly from bags are in lanes 2, 3 and 7. Strains cultured from air samples are found in lanes 12, 13, 19 and 20. The RED pattern of lane 6 closely resembles that of the amyloid arthropathy inducing control strain. The RED pattern of lane 15 and 16 also resembled closely that of the control strain.With permission from Avian Pathology, Taylor & Francis, UK
Two broiler breeders with E. faecalis-associated unilateral amyloid arthropathy.
TitleSymptoms
CaptionTwo broiler breeders with E. faecalis-associated unilateral amyloid arthropathy.
CopyrightAnimal Health Service, Poultry Health Centre, Deventer, The Netherlands
Two broiler breeders with E. faecalis-associated unilateral amyloid arthropathy.
SymptomsTwo broiler breeders with E. faecalis-associated unilateral amyloid arthropathy.Animal Health Service, Poultry Health Centre, Deventer, The Netherlands
Anterior view of the hock joint of a broiler breeder chicken with unilateral E. faecalis-associated amyloid arthropathy. Note the severe swelling of hock joint. Birds of affected flocks were vaccinated in the left gastrocnemius against Marek's disease (right of picture). E. faecalis with a pulsed-field gel electrophoresis restriction endonuclease digestion pattern after Sma I digestion identical to a reference arthropathic and amyloidogenic strain was cultured from most affected joints.
TitlePathology
CaptionAnterior view of the hock joint of a broiler breeder chicken with unilateral E. faecalis-associated amyloid arthropathy. Note the severe swelling of hock joint. Birds of affected flocks were vaccinated in the left gastrocnemius against Marek's disease (right of picture). E. faecalis with a pulsed-field gel electrophoresis restriction endonuclease digestion pattern after Sma I digestion identical to a reference arthropathic and amyloidogenic strain was cultured from most affected joints.
CopyrightWith permission from Avian Pathology, Taylor & Francis, UK
Anterior view of the hock joint of a broiler breeder chicken with unilateral E. faecalis-associated amyloid arthropathy. Note the severe swelling of hock joint. Birds of affected flocks were vaccinated in the left gastrocnemius against Marek's disease (right of picture). E. faecalis with a pulsed-field gel electrophoresis restriction endonuclease digestion pattern after Sma I digestion identical to a reference arthropathic and amyloidogenic strain was cultured from most affected joints.
PathologyAnterior view of the hock joint of a broiler breeder chicken with unilateral E. faecalis-associated amyloid arthropathy. Note the severe swelling of hock joint. Birds of affected flocks were vaccinated in the left gastrocnemius against Marek's disease (right of picture). E. faecalis with a pulsed-field gel electrophoresis restriction endonuclease digestion pattern after Sma I digestion identical to a reference arthropathic and amyloidogenic strain was cultured from most affected joints.With permission from Avian Pathology, Taylor & Francis, UK
Two brown replacement pullets (4 weeks of age) from the same hatch; bird (A) is a healthy control, bird (B) was inoculated intramuscularly at hatch with 10,000,000 cfu of arthropathic and amyloidogenic E. faecalis.
TitleSymptoms
CaptionTwo brown replacement pullets (4 weeks of age) from the same hatch; bird (A) is a healthy control, bird (B) was inoculated intramuscularly at hatch with 10,000,000 cfu of arthropathic and amyloidogenic E. faecalis.
CopyrightWith permission from Avian Pathology, Taylor & Francis, UK
Two brown replacement pullets (4 weeks of age) from the same hatch; bird (A) is a healthy control, bird (B) was inoculated intramuscularly at hatch with 10,000,000 cfu of arthropathic and amyloidogenic E. faecalis.
SymptomsTwo brown replacement pullets (4 weeks of age) from the same hatch; bird (A) is a healthy control, bird (B) was inoculated intramuscularly at hatch with 10,000,000 cfu of arthropathic and amyloidogenic E. faecalis.With permission from Avian Pathology, Taylor & Francis, UK
Gross view of an affected (skinned) hock joint of a brown layer. Note the peri-articular irregular bulging areas representing orange-coloured amyloid masses deposited in the articular recesses and the joint cavity.
TitlePathology
CaptionGross view of an affected (skinned) hock joint of a brown layer. Note the peri-articular irregular bulging areas representing orange-coloured amyloid masses deposited in the articular recesses and the joint cavity.
CopyrightAnimal Health Service, Poultry Health Centre, Deventer, The Netherlands
Gross view of an affected (skinned) hock joint of a brown layer. Note the peri-articular irregular bulging areas representing orange-coloured amyloid masses deposited in the articular recesses and the joint cavity.
PathologyGross view of an affected (skinned) hock joint of a brown layer. Note the peri-articular irregular bulging areas representing orange-coloured amyloid masses deposited in the articular recesses and the joint cavity.Animal Health Service, Poultry Health Centre, Deventer, The Netherlands
Congo red stain of an amyloid arthropathic broiler breeder joint from which arthropathic and amyloidogenic E. faecalis was isolated viewed in full polarized light. The apple-green birefrigent areas represent amyloid deposits. Note the extreme hypertrophy of the synovial membrane on the right side of the picture. Amyloid deposits are located, similarly to brown layers, in the hyperthophic synovial membrane, the superficial articular cartilage and around cartilage nutritional vessels. (Note scale bar).
TitleHistology
CaptionCongo red stain of an amyloid arthropathic broiler breeder joint from which arthropathic and amyloidogenic E. faecalis was isolated viewed in full polarized light. The apple-green birefrigent areas represent amyloid deposits. Note the extreme hypertrophy of the synovial membrane on the right side of the picture. Amyloid deposits are located, similarly to brown layers, in the hyperthophic synovial membrane, the superficial articular cartilage and around cartilage nutritional vessels. (Note scale bar).
CopyrightWith permission from Avian Pathology, Taylor & Francis, UK
Congo red stain of an amyloid arthropathic broiler breeder joint from which arthropathic and amyloidogenic E. faecalis was isolated viewed in full polarized light. The apple-green birefrigent areas represent amyloid deposits. Note the extreme hypertrophy of the synovial membrane on the right side of the picture. Amyloid deposits are located, similarly to brown layers, in the hyperthophic synovial membrane, the superficial articular cartilage and around cartilage nutritional vessels. (Note scale bar).
HistologyCongo red stain of an amyloid arthropathic broiler breeder joint from which arthropathic and amyloidogenic E. faecalis was isolated viewed in full polarized light. The apple-green birefrigent areas represent amyloid deposits. Note the extreme hypertrophy of the synovial membrane on the right side of the picture. Amyloid deposits are located, similarly to brown layers, in the hyperthophic synovial membrane, the superficial articular cartilage and around cartilage nutritional vessels. (Note scale bar).With permission from Avian Pathology, Taylor & Francis, UK
Haematoxylin and eosin stain of articular recesses showing extensive cellular infiltration (Note scale bar).
TitleHistology
CaptionHaematoxylin and eosin stain of articular recesses showing extensive cellular infiltration (Note scale bar).
CopyrightWith permission from Avian Pathology, Taylor & Francis, UK
Haematoxylin and eosin stain of articular recesses showing extensive cellular infiltration (Note scale bar).
HistologyHaematoxylin and eosin stain of articular recesses showing extensive cellular infiltration (Note scale bar).With permission from Avian Pathology, Taylor & Francis, UK
Vegetative endocarditis of 12 months old layer caused by Staphylococcus aureus and Streptococcus faecalis.
TitlePathology
CaptionVegetative endocarditis of 12 months old layer caused by Staphylococcus aureus and Streptococcus faecalis.
Copyright©Sri Poernomo
Vegetative endocarditis of 12 months old layer caused by Staphylococcus aureus and Streptococcus faecalis.
PathologyVegetative endocarditis of 12 months old layer caused by Staphylococcus aureus and Streptococcus faecalis.©Sri Poernomo
At higher magnification heterophil (black arrows), lymphocytic and plasmacellular infiltrations (white arrows) are visible (Note scale bar).
TitleHistology
CaptionAt higher magnification heterophil (black arrows), lymphocytic and plasmacellular infiltrations (white arrows) are visible (Note scale bar).
CopyrightWith permission from Avian Pathology, Taylor & Francis, UK
At higher magnification heterophil (black arrows), lymphocytic and plasmacellular infiltrations (white arrows) are visible (Note scale bar).
HistologyAt higher magnification heterophil (black arrows), lymphocytic and plasmacellular infiltrations (white arrows) are visible (Note scale bar).With permission from Avian Pathology, Taylor & Francis, UK

Identity

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Preferred Scientific Name

  • Streptococcus and Enterococcus infections in poultry

International Common Names

  • English: apoplectiform septicemia; enterococcosis; enterococcus infection in birds; Enterococcus infections in poultry; enterococcus, streptococcus suis, associated septicemia in birds; sleeping sickness; streptococcosis; Streptococcus infections in poultry

Local Common Names

  • Germany: Schlafkrankheid der Hühner

Pathogen/s

Top of page Enterococcus
Enterococcus durans
Enterococcus faecalis
Enterococcus faecium
Enterococcus hirae
Streptococcus
Streptococcus bovis
Streptococcus dysgalactiae
Streptococcus equi
Streptococcus equi subsp. zooepidemicus
Streptococcus gallolyticus
Streptococcus suis

Overview

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Introduction


Streptococcal and enterococcal infections in birds have a worldwide distribution and may cause acute septicaemic and chronic infections with varying mortality rates.

The approximately 40 recognised species of the genus Streptococcus and 17 of the genus Enterococcus are mainly found in gastrointestinal tract and mucosal surfaces of man and animals. Some species are also found in plants, soil, water and food products. This explains the worldwide occurrence of infections associated with this potentially pathogenic species which can be found as commensal or transient colonisers of the resident microflora. Such infections are regarded mostly as opportunistic in nature and occur in many different production systems.


History


The first description of streptococcosis in fowl was given by Nörgaard and Mohler in 1902 who reported the condition found as 'apoplectiform septicemia'. Mack (1908) described what most probably was the same disease. Postmortem features included enlarged, pale and friable liver, while abdominal and thoracic viscera were deeply congested with yellowish discoloration. Sero-fibrino-sanguinous exudate was present on various organs. Apoplectiform septicemia in turkeys has only been reported once (Volkmar, 1932).

Streptococcosis has also been described as a cause of peritonitis (Kernkamp, 1927; Edwards and Hull, 1937) and salpingitis (Edwards and Hull, 1937). Vegetative endocarditis associated with streptococci has been reported a number of times (Kernkamp, 1927; Povar, 1947; Jortner and Helmboldt, 1971). The occurrence of amyloidotic joint and systemic lesions associated with Enterococcus faecalis, previously named Streptococcus faecalis, were described later (Landman et al., 1994), while more recently pulmonary hypertension has been described in broilers infected with E. faecalis (Tankson et al., 2001).


Taxonomy


Both genera Streptococcus and Enterococcus were considered to belong to the same genus (Streptococcus) from 1906 (Andrewes and Horder, 1906) to 1984 (Shleifer and Kilpper-Bälz, 1984), when they were separated into two distinct groups with the help modern molecular taxonomic approaches.

Early technical developments that were used for streptococci classification consisted of the use of haemolytic reactions after culture on blood agar, the use of carbohydrate fermentation reactions, morphology, and the detection of carbohydrate antigens by serological testing introduced by Lancefield (1933). The latter method showed good correlation with classification by means of biochemical testing, although it caused some confusion in streptococcal taxonomy as some micro-organisms that were physiologically heterogeneous could have a common group antigen.

New approaches like cell wall composition studies, metabolic studies, numerical taxonomy, DNA base composition determinations, base sequence homology (DNA-DNA hybridisation) and DNA transformation enabled considerable progress on the classification of streptococci.

Major revision of the genus Streptococcus was performed after data from cell wall and lipid chemical analyses, whole genomic DNA-DNA base pairing, DNA-rRNA hybridisation and 16S rRNA oligonucleotide cataloguing were obtained (Schleifer and Kilpper-Bälz, 1987). It was concluded that the streptococci consisted of three genetically distinct groups: Streptococcus sensu stricto, the genus Enterococcus formed by members of the Lancefield D streptococci and the genus Lactococcus.

Based on 16 rDNA comparative sequence analysis approximately 40 species have been incorporated to the genus Streptococcus, most of which are allocated within one of the six species groups. According to Kawamura et al. (1995), these six species groups are 'pyogenic', 'mitis', 'salivarius', 'bovis', 'anginosus' and 'mutans'. Of the streptococci described in birds S. dysgalactiae and S. equi subsp. zooepidemicus belong to the 'pyogenic' group, S. gallolyticus and S. alactolyticus to the 'bovis' group and S. mutans to the 'mutans' group. S. suis and S. pleomorphus remain ungrouped by 16S rRNA sequence homology.

The number of species included in the genus Enterococcus is currently 17, most of which are included in one of the four species groups, as shown by 16 rDNA comparative sequence analysis. The four species groups are E. faecium (comprising E. faecium, E. durans, E. mundtii and E. hirae), E. avium (listing E. avium a.o.), E. gallinarum (including a.o. E. gallinarum and E. casseliflavus) and E. cecorum (with E. cecorum and E. columbae) (Devriese and Pot, 1995). Orphan species are E. faecalis, E. saccharolyticus, E. sulfureus, E. dispar.


Streptococcus and Enterococcus species found in poultry


S. alactolyticus (Farrow et al., 1984)

S. equi subsp. zooepidemicus formerly S. zooepidemicus and S. capsulatus gallinarum (Farrow and Collins, 1984)

S. gallolyticus formerly S. bovis synomus to S. caprinus (Latham et al., 1979; Osawa et al., 1995)

S. mutans (Schleifer et al., 1986)

S. pleomorphus (Barnes et al., 1977)

S. dysgalactiae (Garvie et al., 1983)

S. suis (Kilpper-Bälz and Schleifer, 1987)

E. avium (Collins et al., 1984)

E. casseliflavus (Collins et al., 1984)

E. cecorum (Williams et al., 1987)

E. columbae (Devriese et al., 1990a)

E. durans (Collins et al., 1984)

E. faecalis (Shleifer and Kilpper-Bälz, 1984)

E. faecium (Shleifer and Kilpper-Bälz, 1984)

E. gallinarum (Collins et al., 1984)

E. hirae (Farrow and Collins, 1985)

E. mundtii (Collins et al., 1986)

Host Animals

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Animal nameContextLife stageSystem
Anas (ducks)Domesticated host
Anser (geese)Domesticated host
Cairina (Muscovy ducks)Domesticated host
Columba livia (pigeons)Domesticated host
Gallus gallus domesticus (chickens)Domesticated host
Meleagris gallopavo (turkey)Domesticated host
Numida meleagris (guineafowl)Domesticated host

Hosts/Species Affected

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Most streptococci and enterococci associated with poultry are commensal or transient residents of the intestinal flora. Most are regarded as potential pathogens, and most of them have been incriminated in disease outbreaks in a wide range of species.

S. gallolyticus, formerly known as S. bovis and synonymous to S. caprinus is known since 1988 as a facultative pathogen for racing pigeons. It was described for the first time in Belgium (De Herdt et al., 1991) associated with acute mortality, lameness, inability to fly, weight loss and diarrhoea. S. gallolyticus has also been described in association with increased mortality in turkey poults (Droual et al., 1997). S. dysgalactiae has been isolated from broilers with cellulitis observed at processing (Messier et al., 1993). Another streptococcus associated with disease in birds is S. mutans. It has been found in a flock of geese showing septicemia and increased mortality (Ivanics et al., 1984). S. pleomorphus, an obligate anaerobe, has been isolated from the caeca of chicken, turkeys and ducks, although its role in avian pathology has not been clarified (Barnes et al., 1977). S. equi subsp. zooepidemicus, previously named S. zooepidemicus and S. capsulatus gallinarum, has been associated with massive acute mortality in eared grebes (Podiceps nigricollis) (Jensen, 1979). In chickens S. zooepidemicus was described as a cause of endocarditis, septicemia and high mortality by several authors (Damman and Manegold, 1905; Hudson1933; Genest and Nadeau, 1944; Buxton, 1952; Agrimi, 1956; Ushijima and Sato, 1958; Sato et al., 1960; Peckham, 1966), and in turkeys this micro-organism has also been associated with apoplectiform septicemia (Volkmar, 1932). Edwards and Hull (1937) describe the occurrence of exudative peritonitis and salpingitis in hens. Decreased egg production and mortality associated with S. equi subsp. zooepidemicus infection has been described in layers fed milk from cattle with mastitis (Goren et al., 1981). Chronic streptococcic peritonitis by S. pyogenes of hens is also described by Kernkamp (1927).

Enterococci are frequently involved in infections of day-old chicks. Most prominently affecting the yolk sac. These infections are often polymicrobial in nature, and the relative importance of the various species involved in the pathogenesis of such infections has not been established.

Of the enterococci E. faecalis has been most frequently associated with poultry diseases, especially endocarditis (Gross and Domermuth, 1962; Jortner and Helmboldt, 1971). Other enterococci also associated with valvular endocarditis are E. faecium and E. durans (Domermuth and Gross, 1968). E. faecalis has been considered the etiological agent of hepatic granulomas in turkeys by Hernandez et al. (1972), while Moore and Gross (1968) considered it as an contributory agent. Arthropathic and amyloidogenic E. faecalis strains have been reported as the etiological agent in some spontaneous cases of AA amyloid arthropathy and concomitant systemic amyloidosis in brown layers (Landman et al., 1994) and also, although to a lesser extend, in broiler breeders (Landman et al., 1998; Steentjes et al., 2002). E. faecalis has been isolated arthritic joints of domestic ducks (Bisgaard, 1981), while E. faecium has been incriminated in acute septicemia of white pekin ducklings (Sandhu, 1988). E. faecalis has been incriminated with ascites in hens (Huan Shu and Huan, 1997) and with pulmonary hypertension in broilers (Tankson et al., 2001).

E. durans infection in young chickens has been associated with bacteremia and encephalomalacia (Cardona et al., 1993). Another enterococcus associated with brain lesions (focal necrosis) in the young chicks is E. hirae (Devriese et al., 1991b; Randall et al., 1993). E. hirae has also been found in cases of endocarditis in four-week-old broilers (McNamee and King, 1996) and diarrhoea in first week layer chicks (Kondo et al., 1997). In chickens, E. faecalis bacterial endocarditis associated lesions of the central nervous system were described by Jortner and Helmboldt (1971).

Streptococci and enterococci in other species of birds

S. suis has been associated with septicaemia in psittacine birds (Mellopsittacus undulatus, Forpus conspillatus, Agapornis swinderniana, Agapornis roseicollis), zebrafinches (Taeniopygia guttata), bullfinches (Pyrrhula pyrrhula), canaries (Serinus canaria) and a duck (Anas platyrhynchos) (Devriese et al., 1994).

Four cases of E. hirae septicaemia have been diagnosed in psittacine birds (Devriese et al., 1992). It concerned neophemas (Neophema pulchella), a salmon-crested cockatoo (Cacatua moluccensis), nose-ringed parakeets (Psittacula krameri) and lutino-type budgerigar (Mellopsittacus undulatus).

E. faecalis has been associated with tracheitis in canaries (Devriese et al., 1990d).

Systems Affected

Top of page blood and circulatory system diseases of poultry
digestive diseases of poultry
multisystemic diseases of poultry
muscular skeletal diseases of poultry
nervous system diseases of poultry

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.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

ChinaPresentGuo et al., 1987; Guo et al., 1989
-HenanPresentWang-ZiZhen, et al., 1999
-ShanghaiPresentHuan Shu, 1997
IndiaPresentLakshmanachar and Raja, 1992; Rajesh et al., 2001
JapanPresentPresent based on regional distribution.
-HokkaidoPresentUshijima and Sato, 1958; Sato et al., 1960; Kondo et al., 1997

Africa

EgyptPresentEl-Nasser et al., 1994; Moustfa and Hussein, 1999

North America

CanadaPresentGenest and Nadeau, 1944
USAPresentPresent based on regional distribution.
-CaliforniaPresentPovar and Brownstein, 1947; Cardona et al., 1993; Droual et al., 1997
-KentuckyPresentEdwards and Hull, 1937
-MinnesotaPresentKernkamp, 1927
-New JerseyPresentHudson, 1933
-New YorkPresentMack, 1908; Sandhu, 1988
-OhioPresentVolkmar, 1932
-VirginiaPresentNörgaard and Mohler, 1902; Moore and Marten, 1944

South America

BrazilPresentPresent based on regional distribution.
-Rio Grande do SulPresentSchmidt-Hoensdorf, 1925
UruguayPresentFerrer et al., 1978

Europe

BelgiumPresentHerdt et al., 1994b; de et al., 1991
BulgariaPresentMinev and Mineva, 1971; Ilieva et al., 1987
FrancePresentPaniset and Verge, 1925
GermanyPresentDamman and Manegold, 1905; Damman and Manegold, 1907; Greve, 1908
GreecePresentParisis and Lekkas, 1970
HungaryPresentIvanics et al., 1984; Ivanics et al., 1997
IrelandPresentMcNamee and King, 1996
ItalyPresentAgrimi, 1956; Casagrande et al., 1998; Esposito, 2000; Passamonti et al., 2000; Terregino et al., 2000
NetherlandsPresentLandman et al., 1994; Dorrestein et al., 1996; Chamanza et al., 1998; Landman et al., 1998
NorwayPresentTaksdal, 1999
Russian FederationPresentPresent based on regional distribution.
-Central RussiaPresentGorbov and Machinskii, 1984
-Southern RussiaPresentKadymov and Dunyamaliev, 1986; Kadymov et al., 1989
SwedenPresentMagnusson, 1910
UKPresentBuxton, 1952; Randall and Pearson, 1991
Yugoslavia (former)PresentTopolko et al., 1973
Yugoslavia (Serbia and Montenegro)PresentVelhner et al., 1988

Oceania

New ZealandPresentBlack, 1997

Pathology

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Chickens


S. dysgalactiae along with E. coli has been incriminated in focal dermatitis and cellulitis of the postventral skin in broiler chickens. The thickened skin is discoloured and sometimes exhibits crusts with fibrinocaseous exudates in the subcutis. Lesions are characterized microscopically by thickening of the dermis with a granulomatous inflammatory reaction (Messier et al., 1993).

The macroscopic lesions described in birds dying from an acute S. equi subsp. zooepidemicus infection are characteristic of septicemia. Sanguineous fluid is to be found in pericardium, peritoneal and thoracic cavities. There is congestion of the lungs and an enlarged, friable and buff-coloured liver. A flaccid heart in diastole is frequently seen along with a dark-red enlarged and sometimes friable spleen with haemorrhages. Bloody transudate is found in the trachea and oral cavity. Breast musculature is blood stained. In chronic cases coagulated exudates in dry or laminar form and necrotic lesions dominate. Swollen wattles and joint lesions are also observed. Yellow mucoid or cheesy exudates occur in tendons of the hock joint, hock, stifle and wing joints (Buxton, 1952; Peckham, 1966). Vegetative endocarditis may occur with streptococci occurring in tissue sections of affected heart valves (Peckham, 1966). At microscopy congestion of parenchymatous organs, in which streptococci can be visualised, occurs in acute cases. Later, heterophil infiltrations are seen around hepatic vessels. In chronic cases diffuse liver necrosis and granulomas occur. Slight congestion of brain vessels and necrosis of myocardial fibres might occur.

Visceral lesions found in cases of E. faecalis endocarditis include valvular vegetations of the aortic and /or left (and sometimes right) atrio-ventricular valves. Extravalvular lesions observed are septic infarcts in the liver, spleen and myocardium. There is frequently glomerulonephritis, myocarditis, hepatocellular necrosis and fibrinoid necrosis of the adenoid sheathed arteries of the spleen. Central nervous system lesions are related to septic embolization of this organ. These lesions consist of multifocal segmental inflammation of arteries, arterioles and capillaries, with associated perivascular and intracerebral inflammatory foci, infarcts of brain tissue, and leptomeningitis (Jortner and Helmboldt, 1971). In broilers, vegetative endocarditis lesions by group D streptococcus as described by Randall and Pearson (1991) were located most frequently on the right atrioventricular valves and adjoining endocardium. Signs of congestive heart failure (carcass congestion, liver swelling and mild ascites) were prominent. The latter lesions can be confounded with genuine ascites. Lesions in E. hirae endocarditis are essentially similar to those described previously although no ascites was found (McNamee and King, 1996).

Swollen and bronze coloured livers are sometimes present in chickens with E. faecalis amyloid arthropathy at postmortem. The joints show (peri)articular orange coloured deposits, which correspond to AA amyloid deposits. At microscopy, in the naturally occurring and the induced cases, the amyloid deposits (which appear as apple green birefrigent areas when viewed with polarized light after Congo red stain) are found in the hypertrophic synovial villi and in the articular cartilage, particularly in the superficial layer and in the nutritional blood vessel walls (Peperkamp et al., 1998). Arthritis is evidenced by proliferation of synoviocytes, with purulent exudate in the articular recesses, and infiltration of the synovial membrane by lymphocytes, plasma cells and heterophils. The synovial membrane presents either irregular extensions or villous hypertrophy. Birds frequently exhibit arthritis deformans.

Lesions in E. durans encephalomalacia are mainly restricted to the medulla oblongata and cerebelum, while in cases of E. hirae encephalomalacia lesions occur in most parts of the brain except the cerebellum. In the latter cases at macroscopy, pinpoint yellowish discolourations are seen in the brainstem and other parts of the brain. Microscopically, foci of malacia, mainly in the brainstem, show some infiltrations with heterophils have been reported (Devriese et al., 1991b). No macroscopic lesions have been noted in birds with E. durans encephalomalacia. Microscopically multifocal to coalescing areas of malacia in brainstem and cerebellar white matter are found. Thrombi can be seen in capillaries within the malacic areas in the brain stem and sometimes in cerebellum. Mild lymphocytic perivascular cuffing and mild difuse gliosis can be found in malacic brainstem areas (Cardona et al., 1993).


Pigeons


Necrosis of the musculus pectoralis is pathognomonic for S. gallolyticus septicemia in pigeons. Moreover, coagulation necrosis can occur in liver, heart and kidney tissue (De Herdt et al., 1992). Arthritis of knee, hock and shoulder joint and tenosynovitis of the musculus supracoracoideus have also been reported as well as meningitis and encephalitis of the cerebellum and cerebrum.

In various organs cellular infiltrations with heterophils, lymphocytes and macrophages, and the presence of cocci has been described. Other findings are inflammation of the spleen, degenerative changes in the liver, nephritis and interstitial oedema of muscular tissue.


Ducks


Gross lesions of E. faecium-induced septicemia in ducklings include fibrinous pericarditis, perihepatitis, endocarditis, airsacculitis, hepato- and splenomegaly. Spleens exhibit haemorrhages and necrotic areas (Sandhu, 1988).


Turkeys


Gross lesions associated with S. gallolyticus infection of turkey poults include pale foci in the pectoral muscles, enlarged livers and enlarged, dark, friable or mottled spleens. At histopathology multifocal necrosis in the spleen is apparent along with Kupfer cell hypertrophy with necrosis of macrophages (Droual et al., 1997).

Postmortem lesions due to S. equi subsp. zooepidemicus in turkeys are similar to those of chickens (Volkmar, 1932).

Experimental E. faecalis septicemia results in congestion of subcutaneous tissues and serous membranes, enlarged and greenish discoloured liver, and splenomegalia. Septic trombi localized in various organs producing infarction with infiltrations of heterophils. During the subacute and chronic phase, whitish foci of varied size (maximum 10 mm) can be found throughout the liver at macroscopy. Microscopically, focal necrotic cholangial lesions followed by focal hepatitis and granulomas can be found (Hernandez et al., 1972).


Other birds


The main pathological manifestation of birds with S. suis and E. hirae infection is septicaemia.

The trachea of canaries suffering from E. faecalis infections shows a chronic productive inflammation. The epithelium becomes metaplastic and infiltrated with lymphocytes which can form aggregates; propria mucosa causing stenosis, which explains the stridor found in some cases (Devriese et al., 1994).

Diagnosis

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Isolation and identification of the micro-organism is essential for the diagnosis of both streptococcosis and enterococcosis. Therefore bacteriological analysis of yolk, embryo fluids, affected organs and joints, valvular vegetations, blood samples from septicaemic individuals and any suspected lesion should be performed. Bacteriology of intestinal contents and faeces is not of diagnostic value as most streptococci and enterococci species are part of the normal intestinal flora of birds and are found in the environment. Therefore, care should be taken that material for examination is not contaminated.

In capillary and venous diffusion studies of E. coli K12 and E. faecalis in chickens after intravenous inoculation, bacteria were found to persist most in capillaries (Labarthe et al., 1986, 1988); this is in agreement with the capillary trapping hypothesis (Knudson and Alden, 1980). It follows that capillary microblood culture could account for higher sensitivity than venous blood culture. Cytology of organ smears provides additional help in diagnosis as macrophages and Gram-positive cocci are easily detected.

Identification of streptococci and enterococci after culture on sheep or ox blood agar, selective blood agar and MacConkey agar with aerobic incubation at 37°C for 24-48 hours, is mostly performed by means of rapid tests such as the API 20 Strep (bioMérieux sa, Marcy-l'Etoile, Lyon, France) galleries and Streptex (Murex Biotech Limited, Temple Hill, Dartford, Kent, UK) after 24 h incubation. Due to recent changes in taxonomy not all species are correctly identified by such means. With the aid of identification tables provided by various text books on bacteriology (Barrow and Feltham, 1993; Holt, 1994; Quinn et al., 1994) proper species cataloguing can be achieved.

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Abnormal colour of stool in birds, white, green, yellow faeces Poultry:All Stages Diagnosis
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Poultry:All Stages Diagnosis
Digestive Signs / Ascites, fluid abdomen Poultry:All Stages Sign
Digestive Signs / Diarrhoea Poultry:All Stages Diagnosis
Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly Poultry:All Stages Sign
Digestive Signs / Malformation of jaw, brachygnathia, prognathia Poultry:All Stages Sign
General Signs / Ataxia, incoordination, staggering, falling Sign
General Signs / Dehydration Poultry:All Stages Sign
General Signs / Discomfort, restlessness in birds Poultry:All Stages Diagnosis
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Fever, pyrexia, hyperthermia Poultry:All Stages Diagnosis
General Signs / Inability to stand, downer, prostration Poultry:All Stages Sign
General Signs / Increased mortality in flocks of birds Poultry:All Stages Diagnosis
General Signs / Lack of growth or weight gain, retarded, stunted growth Poultry:All Stages Diagnosis
General Signs / Lameness, stiffness, stilted gait in birds Poultry:All Stages Diagnosis
General Signs / Neck weakness, paresis, paralysis, limp, ventroflexion Sign
General Signs / Opisthotonus Sign
General Signs / Regression of the comb, wattles in birds Poultry:All Stages Sign
General Signs / Sudden death, found dead Poultry:All Stages Diagnosis
General Signs / Swelling of the limbs, legs, foot, feet, in birds Poultry:All Stages Diagnosis
General Signs / Torticollis, twisted neck Sign
General Signs / Torticollis, twisted neck Sign
General Signs / Trembling, shivering, fasciculations, chilling Poultry:All Stages Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Poultry:All Stages Diagnosis
General Signs / Weakness, paresis, paralysis of the legs, limbs in birds Sign
General Signs / Weakness, paresis, paralysis, drooping, of the wings Sign
General Signs / Weight loss Poultry:All Stages Sign
Musculoskeletal Signs / Abnormal curvature, angulation, deviation of legs, limbs, feet of birds Poultry:All Stages Diagnosis
Musculoskeletal Signs / Ankylosis, arthrogryposis decreased joint mobility in birds Poultry:All Stages Diagnosis
Musculoskeletal Signs / Bone exposure, back, thorax, chest, ribs Poultry:All Stages Diagnosis
Musculoskeletal Signs / Decreased, absent mobility, back region or joints Poultry:All Stages Diagnosis
Musculoskeletal Signs / Relative shortening of the limbs, legs, of birds Poultry:All Stages Sign
Nervous Signs / Circling Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Poultry:All Stages Diagnosis
Nervous Signs / Excessive or decreased sleeping Poultry:All Stages Diagnosis
Nervous Signs / Tremor Poultry:All Stages Sign
Pain / Discomfort Signs / Pain of the limbs, legs, foot, feet in birds Poultry:All Stages Diagnosis
Reproductive Signs / Decreased hatchability of eggs Poultry:Embryo Sign
Reproductive Signs / Decreased in size, small ovary, ovaries Poultry:Mature female Diagnosis
Respiratory Signs / Change in voice, vocal strength Poultry:All Stages Sign
Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding Poultry:All Stages Diagnosis
Skin / Integumentary Signs / Ruffled, ruffling of the feathers Poultry:All Stages Diagnosis
Skin / Integumentary Signs / Soiling of the vent in birds Poultry:All Stages Diagnosis

Disease Course

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Chickens


Most streptococcal and enterococcal infections in chickens occur in two different clinical forms; acute and subacute/chronic.

In the acute form of the disease birds may die suddenly without clinical signs, although cyanosis and diarrhoea may be seen. The chronic stage is characterized by listlessness, growth suppression or loss of body weight, lameness and ruffled feathers. The somnolent behaviour cited in early descriptions of S. equi subsp. Zooepidemicus-associated chronic disease prompted some scientists to name the condition ‘sleeping sickness’ (Damman and Manegold, 1905).

Adult chickens with spontaneous E. faecalis endocarditis described by Jortner and Helmboldt (1971) are found dead without symptoms. In broilers increased mortality due to endocarditis of group D enterococcus was observed between 14 and 21 days according to Randall and Pearson (1991).

E. faecalis-induced amyloid arthropathy frequently occurs during rearing from 5 to 6 weeks onwards associated with impaired growth. The affected birds are smaller in size, make a peeping sound, like that of younger chickens, have ruffled feathers and show a characteristic stiff gait. Mostly the stifle and hock joints are bilaterally and sometimes unilaterally swollen. When adult birds are affected, weight loss can occur depending on the severity of disease. The disease has a chronic onset (Landman et al., 1994, 1998).

The only clinical symptoms found in E. hirae-associated encephalomalacia is torticollis and affected chicks are called 'stargazers'. On average 1-4% of the flock is affected and symptoms appear between the third and eighth day of age (Chamanza et al., 1998). In cases of E. durans encephalomalacia increased mortality starts from the fourth until the tenth day of age. Clinical symptoms, being more varied, include severe depression, paralysis, leg tremors and increased mortality (Cardona et al., 1993).


Pigeons


S. gallolyticus-associated clinical signs include acute mortality, inability to fly, lameness, weight loss and slimy green diarrhoea. Other signs observed are inability to stand, polyuria/polydypsia, distended abdomen, rattles, dullness, weight loss and muscular necrosis on the breast area (Devriese et al., 1990c; De Herdt et al., 1994b).


Ducks


E. faecium has been reported as a cause of acute septicemia and mortality (ranging from 0.5 to 5% in field outbreaks) in 1 to 2 week-old white pekin ducklings. Birds were listless and anorectic before death (Sandhu, 1988).


Turkeys


Although S. gallolyticus has been reported in association with increased mortality in turkey poults ranging from 1 to 3 weeks of age, no further description of clinical symptoms has been given (Droual et al., 1997).

The onset of S. equi subsp. zooepidemicus septicemia in turkeys is quite sudden. Affected birds may appear drowsy and sleepy, show diarrhoea and loss of appetite. Mostly, death occurring without prodromal clinical symptoms (Volkmar, 1932).

Experimentally induced E. faecalis septicemia in turkeys is characterized by high mortality (greatest at day 6 post-inoculation) during the acute phase of infection with clinical signs of anorexia, (head) shaking, depression and ruffled feathers. Transition to a chronic phase follows without further clinical symptoms, although liver lesions develop (Hernandez et al., 1972).


Other birds


The only clinical symptoms associated with S. suis septicemia are acute mortality, sometimes concerning young birds with a filled crop.

In the case of E. hirae mortality to infectious septicemia can occur over several months, affecting both young and adult birds. The course of the disease can be acute or chronic.

In cases of E. faecalis-associated tracheitis in canaries, birds show varying degrees of respiratory problems. Their song changes and becomes hoarse or disappears completely.

Epidemiology

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Both streptococci and enterococci are intestinal inhabitants of birds and mammals, which explains their worldwide occurrence. The diseases associated with them are considered to be opportunistic, where predisposing factors influence the disease associated with these potential pathogens.

Enterococci associated with chicken intestinal flora include E. faecalis, E. faecium (Barnes et al., 1958; Molitoris et al., 1986), E. gallinarum (Kaukas et al., 1986), E. cecorum (Dutta and Devriese, 1982; Williams et al., 1989), E. durans and E. hirae (Devriese et al., 1987). Of these species E. faecalis and E. faecium dominate the intestinal flora in the day-old chick, while in 3- to 5-week-old broilers E. faecium and S. alactolyticus seem to dominate, followed by E. hirae and E. durans. More rarely isolated in day-old chicks were E. durans, E. mundtii and S. alactolyticus and in older broilers it was E. hirae, E. durans, E. cecorum, E. faecalis, E. gallinarum, E. mundtii and E. casseliflavus. In layers and parent stock older than 12 weeks E. cecorum and S. alactolyticus dominate the intestinal flora. Other species found in this category of birds include E. faecalis, E. faecium, E. hirae, E. avium, E. mundtii and S. bovis (Devriese et al., 1991a). Kaukas et al. (1986) found a decrease in E. faecalis isolates during the first week of life, with a corresponding increase in E. faecium and in contrast to Devriese et al. (1991a) also an increase in E. gallinarum.

S. zymogenes (E. faecalis) has also been found as a component of the ovaric and oviduct flora of apparently healthy hens (Dhokarikar et al., 1985).

Streptococci have also been described as part of the microflora of the bursa of Fabricius in chickens (Kimura et al., 1986). Qualitative and quantitative analysis of the bacterial flora of the trachea of healthy chicks showed the presence of Streptococcaceae (Dho and Mouline, 1983).

In ducklings less than eight weeks old the enterococcus flora of intestines consists of E. faecalis and E. faecium, while beyond that age E. gallinarum is included (Saikia et al., 1995).

Studies on the phallus flora of ganders showed that Escherichia coli and Streptococcus D were the commonest isolates (60.5% and 51.7%, respectively), suggesting that the majority were derived from the intestinal flora (Marius-Jestin et al., 1987).

Non-haemolytic streptococci and a-haemolytic streptococci have been found as components of the bacterial flora of clinically normal conjunctivae in the domestic duckling (Chalmers and Kewley, 1985).

S. equi subsp. zooepidemicus apoplectic septicemia in chickens can be induced by intravenous, intraperitoneal, intramuscular and infraorbital sinus inoculation according to Peckham (1966). Nörgaard and Mohler (1902) showed transmission of disease by streptococci by feeding bread soaked in bouillon cultures, although refractivity to the oral route was shown by other authors (Damman and Manegold, 1905; Hudson, 1933). Transmission of disease after intravenous, intraperitoneal and intrasinus inoculation was also shown by Edwards and Hull (1937). Damman and Manegold (1905) reported on transmission by inhalation and subcutaneously. Hudson (1933) demonstrated transmission of S. equi subsp. zooepidemicus and induction of a highly fatal septicemia after intranasal inoculation. Transmission of this pathogen and clinical disease was achieved after its intravenous or intraperitoneal inoculation by Sato et al. (1960).

In ducks transmission only occurs after intravenous inoculation and not through the oral, subcutaneous or intramuscular route (Nörgaard and Mohler, 1902). Volkmar (1932) showed transmission of isolates from turkey to chicken after intravenous, intraperitoneal, oral and intramuscular inoculation.

The occurrence of S. gallolyticus septicemia in pigeons was already suspected long before it was first reported, however the streptococcus species was not identified (Madej, 1961). S. gallolyticus has been found as an important component of human and other mammal’s intestinal flora, where it is regarded as a pathogen. It has been shown to occasionally induce septicemia and endocarditis (Devriese et al., 1990b). Studies in Belgium showed that S. gallolyticus is as important as Salmonella as a cause of septicemia in pigeons (Devriese et al., 1990c). It was also shown that S. gallolyticus seems to form part of the normal pigeon intestinal flora, thus occurring widely and often asymptomatically in the pigeon population. The prevalence of S. gallolyticus is significantly higher from January to August. This has been related to the start of the breeding season during which period hygienic conditions are often poor in pigeon lofts and the stocking density is high (De Herdt et al., 1994b). Normal infection routes for S. gallolyticus are not known. Experimentally, clinical disease can be induced in 90% of intravenously inoculated birds with 109 cfu S. gallolyticus field isolate (De Herdt et al., 1992). It is speculated that repeated oral uptake of S. gallotyicus might play a role in clinical outbreaks. Intracellular survival and replication of virulent S. gallolyticus strains in macrophages might be of importance in the pathogenesis as shown by experimental studies (De Herdt et al., 1995). Also adhesion to fibronectin and collagen type IV seem to be of importance in disease expression. Collagen IV surrounds myofibrils explaining the occurrence of muscular lesions, while fibronectin has been found in tendons that are frequently affected.

Domermuth and Gross (1969) found that E. faecalis induces vegetative endocarditis in chickens at a much higher rate than E. faecium and E. durans after intravenous inoculation. The valvular vegetations consisted of streptococcal masses enmeshed in fibrin. A single intravenous injection of high doses (108 cfu) of E. faecalis not only induced endocarditis and visceral lesions, but central nervous system lesions as well probably by septic embolization to the brain (Jortner and Helmboldt, 1971). Studies on the epidemiology and pathogenesis of arthropathic and amyloidogenic E. faecalis have been performed by Landman et al. (1998; 1999; 2000; 2001) and Steentjes et al. (2002). E. faecalis strains involved in cases of amyloid arthropathy in both brown layers and broiler breeder birds were found to have an identical DNA restriction endonuclease digestion pattern after digestion by Sma (Serratia marcescens) I and analysis by pulsed-field electrophoresis (Landman et al., 1998; Steentjes et al., 2002) indicating they belong to the same clone and suggesting they are the same pathotype. The strains originated from several European countries and one from California. During studies of the pathogenesis of infections with arthropathic and amyloidogenic E. faecalis in brown layers, intravenous, intra-articular and intraperitoneal inoculation of 6-week-old brown layer pullets resulted in amyloid arthropathy, while intramuscular, oral and intratracheal inoculation did not. Similar to studies of other authors mentioned above, oral inoculation of 1-day-old chickens did not cause any pathology. However, intramuscular inoculation with 106 cfu resulted in severe growth retardation and arthritis in 60% of the birds, and amyloid arthropathy in approximately 40% (Landman et al., 1999a). This anticipated possible infection through contaminated Marek’s disease vaccine suspensions. Indeed samples of hatchery air (hatcher and processing room), Marek’s disease vaccine suspensions and injection needles collected during chick processing, revealed variable levels <500 to 106 colony forming units (cfu)/m3 air, <10 to 106 cfu/ml vaccine suspension, and 9500 to 61,000 cfu/needle) of E. faecalis contamination. Pulsed-field gel electrophoresis (PFGE) DNA restriction endonuclease fragment analysis after Sma I digestion of E. faecalis strains obtained from two hatcheries revealed a predominant PFGE pattern in one hatchery, while three isolates with an almost identical PFGE pattern to an amyloid arthropathy inducing isolate were found (Landman et al., 2000). Recently, a series of outbreaks of E. faecalis-associated unilateral amyloid arthropathy were found in broiler breeders which were suspected to have been caused by E. faecalis-contaminated Marek’s disease vaccine suspensions (Steentjes et al., 2002). In egg transmission studies, neither egg dipping, nor inoculation of the air chamber with E. faecalis reproduced the condition, although a few chicks became septicaemic. Yolk sac inoculation of 6-day-old embryos caused embryonic death within 2 days. In contrast, egg albumen inoculation with E. faecalis led to arthritis in 1/6 of the progeny, indicating the possibility that vertical transmission of E. faecalis by the oviductal route could lead to arthritis (Landman et al., 1999a). Subsequently, the vertical transmission of an amyloid arthropathy-inducing E. faecalis strain was demonstrated at a small scale experimentally and in a field case (Landman et al., 1999b; 2001a). More recently the induction of E. faecalis arthritis after intratracheal inoculation of day-old chicks has been demonstrated. These results prompted the study of aerosol transmission. Although E. faecalis bacteraemia was induced after aerosol exposure to this micro-organism, arthritis was not induced (Landman and Van Eck, 2001b; Landman et al., 2001c). From comparison with intratracheally infected birds, this was explained by a difference in dose exposure. The effective aerosol dose for the colonisation of joints in immunosuppressed birds may be lower than for normal birds.

Virulent strains of E. faecalis have been incriminated in the pathogenesis of hepatic granulomas in turkeys induced with Catenabacterium spp, by causing desquamation of intestinal epithelium of mainly the duodenum after oral inoculation (Moore and Gross, 1968). In contrast, Hernandez et al. (1972) considered E. faecalis as an etiological agent and reproduced the condition inoculating high doses (108 cfu) orally. Although liver lesions were induced intravenously, no granulomas were recorded.

In a retrospective study it was shown that chickens on feed restriction and subjected to an 'adequate' level of stress could better withstand an E. faecalis infection than when fed ad libitum and not stressed (Katanbaf et al., 1987). Siegel et al. (1987) investigated genotype-housing interactions and responses of chickens to E. faecalis. High weight lines were found to be most susceptible to infection suffering higher mortality and weight loss after intravenous inoculation of high doses (108 cfu), whilst the effect of cage vs. floor housing varied according to genetic line.

Zekarias et al. (2000) studied differences in susceptibility for E. faecalis-induced AA or reactive amyloid arthropathy between white and brown layers which could not be explained by differences in the gene coding for the amyloid precursor protein serum amyloid A (SAA) (Ovelgönne et al., 2001). The leucocyte responses, type of inflammatory pattern and predicted cytokine profile indicated that susceptibility to amyloid arthropathy is associated with immunological response patterns. White layers being less susceptible to the disease showed a cell-mediated type response, which could be a result of "Th1" tilted CD4+ response, whereas brown layers have features of a "Th2" dominated response.

E. hirae adherence to enterocytes of the duodenum has been postulated to play a role in pathogenesis of diarrhoea and associated mortality in layer pullets (Kondo et al., 1997). An attempt to reproduce E. hirae-associated brain lesions in four-day-old chickens through intravenous or intratracheal inoculation (with approx. 108 cfu) proved unsuccessful (El-Shukon and Abdul-Aziz, 1993), nor was this species pathogenic for chicken embryos (102-3 cfu) and betamethasone-treated chicks (approx. 108 cfu) (Abdul-Aziz and El-Shukon, 1994).

E. faecium septicemia in white pekin ducklings can be induced after parenteral (subcutaneous, intravenous or intrasinus) inoculation of high doses (107 cfu), while the oral route was refractory (Sandhu, 1988).

Impact: Economic

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Diseases associated with streptococci or enterococci have been relatively uncommon, despite their worldwide distribution. Their economic importance and impact was therefore considered small with the exception of occasional severe outbreaks, although no data are available.

In the Netherlands, where arthropathic and amyloidogenic E. faecalis affected mainly brown layers an epizooty occurred affecting 1-5% of layer farms with a prevalence varying from less than 1% up to 30% or more in some cases.

Zoonoses and Food Safety

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Although enterococci and streptococci have been isolated from poultry carcasses (Geornaras et al., 1996; Kruse et al., 1999; El-Dengawy and Nassar, 2001; Borgen et al., 2001) no incrimination in cases of food poisoning in humans has been described.

In recent studies, a high prevalence of vancomycin-resistant enterococci (VRE) in broiler and turkey carcasses was detected 6 months to 1 year (Robredo et al., 1999) and even 3 years after banning avorpacin as growth promotor (Borgen et al., 2001). In contrast other investigations report on the decreased incidence of VanA-type vancomycin-resistant enterococci isolated from poultry meat and from faecal samples of humans in the community after discontinuation of avoparcin usage in animal husbandry. (Klare et al., 1999; Pantosti et al., 1999).

In any case these studies suggest that the food chain could be a source of VRE colonization in man and thus a source of VRE infections acting as a potential reservoir. It underlines the role of animal products in the spread of resistant bacteria and transferable resistance genes to humans in the community.

The case report of a man working in a factory packaging chickens who developed an infected wound containing E. faecalis resistant to both vancomycin and teicoplanin, points at possible risks when handling contaminated products (Das et al., 1997).

Disease Treatment

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Isolates obtained from clinical cases should be subjected to sensitivity tests before treatment. A number of antibiotics have proven to be efficient, although the efficacy of treatment decreases with the progression of the disease in a flock. Treatment of chronic cases especially endocarditis and arthritis is difficult if not impossible.

Based on data of sensitivity studies amoxycillin seems in general to be the drug of first choice for streptococci and enterococci infections, although in vitro and in vivo studies on antibiotics revealed that ampicillin, doxycyclin and erythromycin are the products of choice to use in clinical outbreaks of S. gallolyticus-associated disease in pigeons (De Herdt et al., 1993).

Prevention and Control

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Good hygiene, management and housing can be used to prevent disease outbreaks; S. gallolyticus infections are more frequent in racing pigeon flocks kept on closed floors compared to slats.

Whole-cell formaldehyde-inactivated vaccines of S. gallolyticus serotype 1 supplied with mineral oil adjuvant results in some clinical protection against streptococcosis when the birds are vaccinated twice (De Herdt et al., 1999).

Due to the relatively low incidence of streptococcosis and enterococcosis in poultry, vaccination studies are scarce. Some exceptions are those performed for S. gallolyticus in pigeons as mentioned above (De Herdt et al., 1999) and S. mutans in chickens (Rho et al., 1999).

It is possible that amyloid arthropathy in chickens could, in some cases, be a man-made disease resulting from the injection of arthropathic and amyloidogenic E. faecalis from contaminated Marek’s disease vaccine suspensions into newly hatched chicks. Therefore, hatchery hygiene may contribute to the prevention of outbreaks of E. faecalis-related amyloid arthropathy. The hygienic measures concerned should comprise sufficient ventilation to reduce the E. faecalis load/m3 air during chick processing and carefully controlled Marek’s vaccination. Contamination of the Marek’s disease vaccine suspensions can be reduced by mounting filters on decompression needles used on bottles. Frequent change of needles is also recommended as is keeping of the vaccine suspensions at low temperatures. In this regard it should be remembered that enterococci can grow at low temperatures (10°C). Moreover, proper cleaning and disinfection of poultry houses and hatcheries will help to reduce exposure to pathogenic micro-organisms. A number of disinfectants such formaldehyde and ozone can be used efficiently.

Finally, it should be mentioned that reduction of stress and avoidance of immunosuppressive diseases will be of help to prevent opportunistic infections with streptococci and enterococci.

References

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Agrimi P, 1956. Studio sperimentale su alcuni focolai di streptococcosi nel pollo. Zooprofilassi, 11:491-501.

Andrewes FW; Horder J, 1906. A study of streptococci pathogenic for man. Lancet, 2:708-713.

Barnes EM, 1958. The effect of antibiotic supplements on the fecal streptococci (Lancefield group D) of poultry. British Veterinary Journal, 114:333-344.

Barnes EM; Impey CS; Stevens BJH; Peel JL, 1977. Streptococcus pleomorphus sp. Nov.: an anaerobic streptococcus isolated mainly from the caeca of birds. Journal of General Microbiology, 102:45-53.

Barrow GI; Feltham RKA, 1993. Cowan and Steel's manual for the identification of medical bacteria, edition 3. Cambridge, UK: Cambridge University Press.

Bentley RW; Leigh JA, 1995. Development of PCR-based hybridisation protocol for identification of streptococcal species. Journal of Clinical Microbiology, 33:1296-1301.

Billroth T, 1874. Untersuchungen uber die Vegetationsformen von Coccobacteria Septica. Berlin, Germany: G. Reimer.

Bisgaard M, 1981. Arthritis in ducks. Etiology and public health aspects. Avian Pathology, 10:11-21.

Black A, 1997. Bacterial and parasitic diseases of New Zealand poultry. Surveillance (Wellington), 24(4):3-5; 36 ref.

Bogaard AEvan den; Jensen LB; Stobberingh EE, 1997. Vancomycin-resistant enterococci in turkeys and farmers. New England Journal of Medicine, 337(21):1558-1559; 4 ref.

Borgen K; Sorum M; Wasteson Y; Kruse H, 2001. VanA-type vancomycin-resistant enterococci (VRE) remain prevalent in poultry carcasses 3 years after avoparcin was banned. International Journal of Food Microbiology, 64:89-94.

Buxton JC, 1952. Diseases in poultry associated with Streptococcus zooepidemicus. Veterinary Record, 64:221.

Cardona CJ; Bickford AA; Charlton BR; Cooper GL, 1993. Enterococcus durans infection in young chickens associated with bacteremia and encephalomalacia. Avian Diseases, 37(1):234-239; 9 ref.

Casagrande Proietti P; Passamonti F; Asdrubali G; Franciosini MP; Bordoni G, 1998. A report on an outbreak of Streptococcus bovis infection in meat pigeons. Selezione Veterinaria, No. 8/9:685-689; 10 ref.

Chalmers WSK; Kewley DR, 1985. Bacterial flora of clinically normal conjunctivae in the domestic duckling. Avian Pathology, 14(1):69-74; 10 ref.

Chamanza R; Fabri THF; Veen Lvan; Dwars RM, 1998. Enterococcus-associated encephalomalacia in one-week-old chicks. Veterinary Record, 143(16):450-451; 14 ref.

Collins MD; Farrow JAE; Jones D, 1986. Enterococcus mundtii sp. nov. International Journal of Systematic Bacteriology, 36(1):8-12; 20 ref.

Collins MD; Jones D; Farrow JAE; Kilpper-Bälz R; Schleifer KH, 1984. Enterococcus avium nom. rev., comb. nov.; E. casseliflavus nom. rev., comb. nov.; E. durans nom. rev., comb. nov.; E. gallinarum comb. nov.; and E. malodoratus sp. nov. International Journal of Systematic Bacteriology, 34(2):220-223; 26 ref.

Damman G; Manegold O, 1905. Die schlafkrankheid der Hühner. Deutsche Tierärztliche Wochenschrift, 13:577-579.

Damman G; Manegold O, 1907. Die Schlafkrankheid der Hühner. Arch. fur wissen u. prakt. tierhlk., 33:41.

Das I; Fraise A; Wise R, 1997. Are glycopeptide-resistant enterococci in animals a threat to human beings?. Lancet (British edition), 349(9057):997-998; 5 ref.

de Herdt P; Devriese LA; Uyttebroek E; Ducatelle R; Haesebrouck F, 1991. Streptococcus bovis infecties bij duiven. Vlaams Diergeneeskundig Tijdschrift, 60:41-54.

Devriese LA; Ceyssens K; Rodrigues UM; Collins MD, 1990. Enterococcus columbae, a species from pigeon intestines. FEMS Microbiology Letters, 71(3):247-252; 11 ref.

Devriese LA; Cruz Colque JI; Haesebrouck F; Desmidt M; Uyttebroek E; Ducatelle R, 1992. Enterococcus hirae in septicaemia of psittacine birds. Veterinary Record, 130(25):558-559; 6 ref.

Devriese LA; Ducatelle R; Uyttebroek E; Haesebrouck F, 1991. Enterococcus hirae infection and focal necrosis of the brain of chicks. Veterinary Record, 129(14):316; 5 ref.

Devriese LA; Gevaert D; Ceyssens K, 1990. Characteristics of Streptococcus bovis associated with pigeons. Avian Pathology, 19(3):425-428; 11 ref.

Devriese LA; Haesebrouck F; Herdt Pde; Dom P; Ducatelle R; Desmidt M; Messier S; Higgins R, 1994. Streptococcus suis infections in birds. Avian Pathology, 23(4):721-724; 10 ref.

Devriese LA; Hommez J; Wijfels R; Haesebrouck F, 1991. Composition of the enterococcal and streptococcal intestinal flora of poultry. Journal of Applied Bacteriology, 71(1):46-50; 21 ref.

Devriese LA; Pot B, 1995. The genus Enterococcus. In: Wood BJB, Holzapfel WH, eds. The Genera of Lactic Acid Bacteria, Vol. 2. Blackie Academic Professional, 327-367.

Devriese LA; Uyttebroek E; Ducatelle R; Viaene N; Derijcke J; Gevaert D, 1990. Tracheitis due to Enterococcus faecalis infection in canaries. Journal of the Association of Avian Veterinarians, 4(2):113-116; 5ref.

Devriese LA; Uyttebroek E; Gevaert D; Vandekerckhove P; Ceyssens K, 1990. Streptococcus bovis infections in pigeons. Avian Pathology, 19(3):429-434; 6 ref.

Dho M; Mouline C, 1983. Qualitative and quantitative analysis of the bacterial flora of the trachea of healthy chicks. Annales de Recherches Vétérinaires, 14(3):189-194; 19 ref.

Dhokarikar SD; Paranjpe VL; Ajinkya SM; Sardeshpande PD; Kulkarni AB, 1985. Studies on bacterial flora of ovary and oviduct of the fowl. Indian Journal of Comparative Microbiology, Immunology and Infectious Diseases, 6(1):48-52; 10 ref.

Domermuth CH; Gross WB, 1969. A medium for isolation and tentative identification of fecal streptococci, and their role as avian pathogens. Avian Diseases, 13:394-399.

Dorrestein GM; Buitelaar M; van der Hage M, 1996. S. bovis, a report on the isolation from avian and exotic animals. Proceedings X. Tagung der Fachgruppe Geflügelkrankheiten, Munchen, 7-8 März, 107-111.

Droual R; Ghazikhanian GY; Shivaprasad HL; Barr BC; Bland MB, 1997. Streptococcus bovis infection in turkey poults. Avian Pathology, 26(2):433-439; 10 ref.

Edwards PR; Hull FE, 1937. Hemolytic streptococci in chronic peritonitis and salpingitis of hens. Journal of the American Veterinary Medical Association, 44:656-660.

El-Dengawy RA; Nassar AM, 2001. Investigation on the nutritive value and microbiological quality of wild quail carcasses. Nahrung, 45:50-54.

El-Nasser AA; Mohmoud FM; El-Shabiny LM; Hassanein ZA; Abbas AA, 1994. Studies on major bacterial agents causing arthritis in chickens in Kaluobia Province. Veterinary Medical Journal Giza, 42(1(B)):277-285; 53 ref.

Esposito L, 2000. Experimental infection of layer chicks with an Enterococcus faecalis strain isolated from a case of Amyloid Arthropathy. XXXVIII Convegno della Societa Italiana di Patologia Aviare 'Risposta immunitaria in funzione di eta e tipo genetico' Forli, Italy, 30 settembre - 1 ottobre 1999. Selezione-Veterinaria, No. 8-9, 629-638.

Farrow JAE; Collins MD, 1984. Taxonomic studies on streptococci of serological groups C, G and L and possibly related taxa. Systemic and Applied Microbiology, 5(4):483-493; 32 ref.

Farrow JAE; Collins MD, 1985. Enterococcus hirae, a new species that includes amino acid assay strain NCDO 1258 and strains causing growth depression in young chickens. International Journal of Systematic Bacteriology, 35(1):73-75; 14 ref.

Farrow JAE; Kruze J; Phillips BA; Bramley AJ; Collins MD, 1984. Taxonomic studies on Streptococcus bovis and Streptococcus equinus: description of Streptococcus alactolyticus sp. nov. and Streptococcus saccharolyticus sp. nov. Systemic and Applied Microbiology, 5(4):467-482; 22 ref.

Ferrer E; Trenchi H; Riva G, 1978. Streptococcus faecalis outbreak in broiler fowl. Proceedings and Abstracts of the XVI World's Poultry Congress, Rio de Janeiro, Vol. IX, 1503-1509.

Galli D; Lottspeich F; Wirth R, 1990. Sequence analysis of pAD1-encoded aggregation substance of Enterococcus faecalis. Molecular Microbiology, 4:895-904.

Garvie EI; Farrow JAE; Bramley AJ, 1983. Streptococcus dysgalactiae (Diernhofer) nom. rev. International Journal of Systematic Bacteriology, 33:404-405.

Genest P; Nadeau JD, 1944. Observation, chez la poule, d'une epizootie due à Streptococcus zooepidemicus. Canadian Journal of Comparative Medical Veterinary Science, 8:342.

Geornaras I; Jesus AEde; Zyl Evan; Holy Avon, 1996. Bacterial populations associated with poultry processing in a South African abattoir. Food Microbiology, 13(6):457-465; 27 ref.

Gorbov YuK; Machinskii AP, 1984. The prevalence of associated diseases in farm animals and their control in the Mordovian ASSR. Parazitotsenozy i assotsiativnye bolezni., 235-252; 6 ref.

Goren E; de Jong WA; van Eck JHH, 1981. Streptococcus zooepidemicus infection in laying hens. Tijdschrift voor Diergeneeskunde, 106:715-717.

Greve L, 1908. Beitrag zur kenntnis der streptokokken-krankheit (schlafkrankheit) der Hüner. Deutsche Tierärztliche Wochenschrift, 15:213-215.

Gross WB; Domermuth CH, 1962. Bacterial endocarditis of poultry. American Journal of Veterinary Research, 23:320-329.

Guo YP; Gao F; Tian KG, 1987. Streptococcal infection of ducks. Chinese Journal of Veterinary Medicine, 13(7):14-15.

Guo YP; Gao F; Tian KG, 1989. On the streptococcosis of ducks. Waterfowl production. Proceedings of the International Symposium, September 11-18, 1988, Beijing, China., 378-382; 3 ref.

Herdt Pde; Desmidt M; Haesebrouck F; Ducatelle R; Devriese LA, 1992. Experimental Streptococcus bovis infections in pigeons. Avian Diseases, 36(4):916-925; 18 ref.

Herdt Pde; Devriese LA; Groote Bde; Ducatelle R; Haesebrouck F, 1993. Antibiotic treatment of Streptococcus bovis infections in pigeons. Avian Pathology, 22(3):605-615; 16 ref.

Herdt Pde; Ducatelle R; Haesebrouck F; Devriese LA; Groote Bde; Roels S, 1994. An unusual outbreak of Streptococcus bovis septicaemia in racing pigeons (Columba livia). Veterinary Record, 134(2):42-43; 6 ref.

Herdt Pde; Haesebrouck F; Charlier G; Ducatelle R; Devriese LA; Vandenbossche G, 1995. Intracellular survival and multiplication of virulent and less virulent strains of Streptococcus bovis in pigeon macrophages. Veterinary Microbiology, 45(2/3):157-169; 25 ref.

Herdt Pde; Haesebrouck F; Devriese LA; Ducatelle R, 1994. Prevalence of Streptococcus bovis in racing pigeons. Veterinary Quarterly, 16(2):71-74; 11 ref.

Herdt Pde; Vanrobaeys M; Devriese LA; Ducatelle R; Haesebrouck F, 1999. Efficacy of inactivated whole-cell vaccines against streptococcosis in pigeons. Avian Pathology, 28(4):355-361; 29 ref.

Hernandez DJ; Roberts ED; Adams LG; Vera T, 1972. Pathogenesis of hepatic granulomas in turkeys infected with Streptococcus faecalis var. liquefaciens. Avian Diseases, 15:201-216.

Holt JG; Kreig NR; Sneath PHA; Staley JT; Williams ST (eds), 1994. Bergey's Manual of Determinative Bacteriology, 9th edition. Baltimore, USA: Williams & Wilkins.

Huan Shu, 1997. Study on ascites in hens caused by Streptococcus faecalis infection. Chinese Journal of Veterinary Medicine, 23(5):9-10; 4 ref.

Hudson CBA, 1933. A specific infectious disease of chickens due to a haemolytic streptococcus. Journal of the American Veterinary Medical Association, 82:218-231.

Ilieva I; Lyupke V; Nikolov N; Gogov I, 1987. Outbreak of Streptococcus (Enterococcus) faecalis infection among chicks. Veterinarna Sbirka, 85(4):24-26.

Ivanics é; Bitay Z; Glávits R, 1984. Streptococcus mutans infection in geese. Magyar Allatorvosok Lapja, 39(2):92-95; [5 fig.]; 20 ref.

Ivanics é; Glávits R; Nagy E; édes I, 1997. Differential diagnosis of the commonest bacterial diseases of young geese. Magyar állatorvosok Lapja, 119(12):737-746.

Jensen WI, 1979. An outbreak of streptococcosis in eared grebes (Podiceps nigricollis). Avian Diseases, 23:543-546.

Jortner BS; Helmboldt CF, 1971. Streptococcal bacterial endocarditis in chickens associated lesions of the central nervous system. Veterinary Pathology, 8:54-62.

Kadymov RA; Agaeva EM; Dunyamaliev GE, 1989. Significance of combinations of microorganisms for the onset and course of streptococcosis in fowls. Veterinariya, Moscow, No.2:30-32.

Kadymov RA; Dunyamaliev GE, 1986. Streptococcus infection in fowls. Veterinariya, Moscow, USSR, No.9:39-42.

Katanbaf MN; Siegel PB; Gross WB, 1987. Prior experience and response of chickens to a streptococcal infection. Poultry Science, 66(Suppl. 1):123.

Kawamura Y; Hou X; Sultana F; Miura H; Ezaki T, 1995. Determination of 16s rRNA sequences of Streptococcus mitis and Streptococcus gordonii and phylogenetic relationships among members of the genus Streptococcus. International Journal of Systemic Bacteriology, 45:406-408.

Kernkamp HCH, 1927. Idiopathic streptococci peritonitis in poultry. Journal of the American Veterinary Medical Association, 23:585-596.

Kilpper-Bälz R; Schleifer KH, 1987. Streptococcus suis sp. nov., nom. rev. International Journal of Systematic Bacteriology, 37(2):160-162; 15 ref.

Kimura N; Yoshikane M; Kobayashi A, 1986. Microflora of the bursa of Fabricius of chickens. Poultry Science, 65(9):1801-1807; 15 ref.

Klare I; Badstübner D; Konstabel C; Böhme G; Claus H; Witte W, 1999. Decreased incidence of VanA-type vancomycin-resistant enterococci isolated from poultry meat and from fecal samples of humans in the community after discontinuation of avoparcin usage in animal husbandry. Microbial Drug Resistance, 5(1):45-52; 31 ref.

Knudson RP; Alden ER, 1980. Neonatal heelstick blood culture. Pediatrics, 65:505-507.

Kondo H; Abe N; Tsukuda K; Wada Y, 1997. Adherence of Enterococcus hirae to the duodenal epithelium of chicks with diarrhoea. Avian Pathology, 26(1):189-194; 8 ref.

Kruse H; Johansen BK; Rorvik LM; Schaller G, 1999. The use of avoparcin as a growth promoter and the occurrence of vancomycin-resistant Enterococcus species in Norwegian poultry and swine production. Microbial Drug Resistance, 2:135-139.

Labarthe JC; Guillot JF; Brée A; Mouline C, 1986. Quantitative study of venous and capillary blood cultures during experimental bacteraemia in chickens. Annales de l'Institut Pasteur/Microbiology, 137B(3):317-324; 9 ref.

Labarthe JC; Guillot JF; Brée A; Mouline C, 1988. Venous and capillary diffusion of Enterococcus faecalis in experimental bacteraemia in chickens. Annales de l'Institut Pasteur, Microbiology, 139(5):631-636; 7 ref.

Lakshmanachar N; Raja Rajeswari K, 1992. Report on streptococcal [Enterococcus faecalis] infection in chicks. Poultry Adviser, 25(1):61-63; 4 ref.

Lancefield RC, 1933. A serological differentiation of human and other groups of hemolytic streptococci. Journal of Experimental Medicine, 57:571-595.

Landman WJM; Eck JHHvan, 2001. Aerosolization of Newcastle disease vaccine virus and Enterococcus faecalis. Avian Diseases, 45(3):684-687; 13 ref.

Landman WJM; Feberwee A; Mekkes DR; Veldman KT; Mevius DJ, 1999. A study on the vertical transmission of arthropathic and amyloidogenic Enterococcus faecalis. Avian Pathology, 28(6):559-566; 23 ref.

Landman WJM; Feberwee A; Veldman KT; Mevius DJ, 2001a. Study on vertical transmission of arthropathic and amyloidogenic Enterococcus faecalis in a field case. Veterinary Quarterly, 23:88-91.

Landman WJM; Gruys E; Dwars RM, 1994. A syndrome associated with growth depression and amyloid arthropathy in layers: a preliminary report. Avian Pathology, 23(3):461-470; 38 ref.

Landman WJM; Mekkes DR; Chamanza R; Doornenbal P; Gruys E, 1999. Arthropathic and amyloidogenic Enterococcus faecalis infections in brown layers: a study on infection routes. Avian Pathology, 28(6):545-557; 39 ref.

Landman WJM; Vd Bogaard AEJM; Doornenbal P; Tooten PCJ; Elbers ARW; Gruys E, 1998. The role of various agents in chicken amyloid arthropathy. Amyloid: The International Journal of Experimental and Clinical Investigation, 5:266-278.

Landman WJM; Veldman KT; Mevius DJ; Doornenbal P, 2000. Contamination of Marek's disease vaccine suspensions with Enterococcus faecalis and its possible role in amyloid arthropathy. Avian Pathology, 29(1):21-25; 12 ref.

Landman WJM; Veldman KT; Mevius DJ; van Eck JHH, 2001c. Aerosol transmission of arthropathic and amyloidogenic Enterococcus faecalis. Avian Diseases, 45.

Latham MJ; Sharpe ME; Weiss N, 1979. Anaerobic cocci from the bovine alimentary tract, the amino acids of their cell wall peptidoglycans and those of various species of anaerobic Streptococcus. Journal of Applied Bacteriology, 47:209-221.

Mack WB, 1908. Apoplectiform septicemia in chickens. American Veterinary Review, 33:330-332.

Magnusson H, 1910. Uber eine fur Europa neune Huhnerseuche. Apoplektische Septikamie der Huhner. Centralblatt fur Bakteriologie, Abt. I, 441-428.

Marius Jestin V; Thibault E; Moisan JC; L'Hospitalier R; le Menec M, 1987. Normal phallus flora of the gander. Journal of Veterinary Medicine, B Infectious Diseases, Immunology, Food Hygiene,Veterinary Public Health, 34:67-78.

McNamee PT; King DC, 1996. Endocarditis in broiler breeder rearers due to Enterococcus hirae. Veterinary Record, 138(10):240; 5 ref.

Messier S; Quessy S; Robinson Y; Devriese LA; Hommez J; Fairbrother JM, 1993. Focal dermatitis and cellulitis in broiler chickens: bacteriological and pathological findings. Avian Diseases, 37(3):839-844; 16 ref.

Minev M; Mineva I, 1971. Streptococcal infection in fowls (associated with Str. faecalis var. zymogenes. Second Congress of Microbiology, Sofia, 1969. Part 2, 309-313.

Molitoris E; Krichevsky MI; Faberberg DJ; Quarles CL, 1986. Effects of dietary tetracycline on the antimicrobial resistance of broiler fecal Streptococcaceae. Journal of Applied Bacteriology, 60:185-193.

Moore EN; Marten EA, 1944. The roles of microorganisms in reproductive disorders of the chicken. American Journal of Veterinary Research, 5:256.

Moore WEC; Gross WB, 1968. Liver granulomas of turkeys - causative agents and mechanism of infection. Avian Diseases, 12:417-422.

Moustfa FA; Hussein SZ, 1999. Gram positive cocci causing septicaemia in chickens in Assiut Governorate. Assiut Veterinary Medical Journal, 41(82):227-238; 30 ref.

Nörgaard VA; Mohler JR, 1902. Apoplectiform septicemia in chickens. U.S. Department of Agriculture, Bureau of Animal Industry, Bulletin 36.

Ovelgönne JH; Landman WJM; Gruys E; Gielkens ALJ; Peeters BPH, 2001. Identical amyloid precursor proteins in two breeds of chickens which differ in susceptibility to develop amyloid arthropathy. Amyloid, 8(1):41-51.

Paniset and Verge, 1925. Sur une septicemie du pigeon. Revue Generale de Medecine Veterinaire, 34:368-371.

Pantosti A; Grosso Mdel; Tagliabue S; Macrì A; Caprioli A, 1999. Decrease of vancomycin-resistant enterococci in poultry meat after avoparcin ban. Lancet (British edition), 354(9180):741-742; 5 ref.

Parisis E; Lekkas S, 1970. Streptococcus infections of birds. Proceedings of the 3rd Symposium on Bacteriology University of Athens, Greece, 306-318.

Passamonti F; Asdrubali G; Proietti PC; Rossi E del; Battistacci L, 2000. Agents of zoonosis in wild city pigeons and in meat pigeons. Agenti di zoonosi in piccioni di citta e in piccioni di allevamento. XXXVIII Convegno della Societa Italiana di Patologia Aviare 'Risposta immunitaria in funzione di eta e tipo genetico' Forli, Italy, 30 settembre - 1 ottobre 1999. Selezione-Veterinaria. No. 8-9, 795-803.

Peckham MC, 1966. An outbreak of streptococcosis (apoplectiform septicemia) in white rock chickens. Avian Diseases, 10:413-421.

Peperkamp NHMT; Landman WJM; Tooten PCJ; Ultee A; Voorhout WF; Gruys E, 1997. Light microscopic, immunohistochemical, and electron microscopic features of amyloid arthropathy in chickens. Veterinary Pathology, 34(4):271-278; 29 ref.

Povar ML; Brownstein B, 1947. Valvular endocarditis in the fowl. Cornell Veterinary, 37:49-54.

Quinn PJ; Carter ME; Markey BK; Carter GR, 1994. Clinical veterinary microbiology. London, UK: Wolfe Publishing.

Rajesh Chahota; Singh SP; Katoch RC; Gupta VK; Arvind Mahajan; Subhash Verma, 2001. Spontaneous bacterial endocarditis in a broiler chicken. Indian Journal of Animal Sciences, 71(1):28-29; 5 ref.

Randall CJ; Pearson DB, 1991. Enterococcal endocarditis causing heart failure in broilers. Veterinary Record, 129(24):535; 2 ref.

Randall CJ; Wood AM; MacKenzie G, 1993. Encephalomalacia in first-week chicks. Veterinary Record, 132(16):418; 2 ref.

Rho JH; Kim YB; Han CK; Lee NH; Sung KS; Shon DH, 1999. The effect of age and vaccination of hens on the level of anti-Streptococcus mutans specific IgY in eggs. Korean Journal of Animal Science, 41(5):563-574; 22 ref.

Robredo B; Singh KV; Baquero F; Murray BE; Torres C, 1999. Vancomycin-resistant enterococci isolated from animals and food. International Journal of Food Microbiology, 54:197-204.

Saikia PK; Dutta GN; Devriese LA; Kalita CC, 1995. Characterisation and antimicrobial susceptibility of Enterococcus species from the intestines of ducks in Assam. Research in Veterinary Science, 58(3):288-289; 14 ref.

Sandhu TS, 1988. Fecal streptococcal infection of commercial white pekin ducklings. Avian Diseases, 32(3):570-573; 9 ref.

Sato G; Miura S; Ushijima J, 1960. An outbreak of haemolytic-streptococcal infection among chickens of a flock. II. Characters of the isolated streptococci. Japanese Journal of Veterinary Research, 8:285-294.

Schleifer KH; Kilpper-Bälz R, 1984. Transfer of Streptococcus faecalis and Streptococcus faecium to the genus Enterococcus nom. rev. as Enterococcus faecalis comb. nov. and Enterococcus faecium comb. nov. International Journal of Systematic Bacteriology, 34(1):31-34; 28 ref.

Schleifer KH; Kilpper-Bälz R, 1987. Molecular and chemotaxonomic approaches to the classification of streptococci, enterococci and lactococci: a review. Systematic and Applied Microbiology, 10(1):1-19; many ref.

Schleifer KH; Kilpper-Bälz R; Kraus J; Gehring F, 1986. Relatedness and classification of Streptococcus mutans and "mutans-like" streptococci. Journal of Dental Research, 63:1047-1050.

Schmidt-Hoensdorf F, 1925. Geflugelseuchen in Sudbrasilien. Deutsche Tierärztliche Wochenschrift, 33:818-820.

Siegel PB; Katanbaf MN; Anthony NB; Jones DE; Martin A; Gross WB; Dunnington EA, 1987. Responses of chickens to Streptococcus faecalis: genotype-housing interactions. Avian Diseases, 31(4):804-808; 19 ref.

Steentjes A; Veldman KT; Mevius DJ; Landman WJM, 2002. Molecular epidemiology of unilateral amyloid arthropathy in broiler breeders associated with Enterococcus faecalis. Avian Pathology, 31(1):31-39; 14 ref.

Taksdal T, 1999. Diagnoses from the Veterinary Institute. Norsk Veterinærtidsskrift, 111(10):646-647.

Tankson JD; Thaxton JP; Vizzier-Thaxton Y, 2001. Pulmonary hypertension syndrome in broilers caused by Enterococcus faecalis. Infection and Immunity, 69(10):6318-6322; 49 ref.

Terregino C; Catelli E; Zanoni R; Giordano S; Sanguinetti V, 2000. Causes of early broiler chick mortality. Rivista di Avicoltura, 69:34-40.

Topolko S; Fras A; Karlovic M, 1973. Valvular endocarditis in hens on poultry farms in Yugoslavia. VeterinarskiArhiv, 43:182-187.

Ushijima J; Sato G, 1958. An outbreak of haemolytic-streptococcal infection among chickens of a flock. I. Pathological study on the naturally infected cases. Journal of the Japanese Veterinary Medical Association, 11:315.

Vanrobaeys M; de Herdt P; Charlier G; Ducatelle R; Haesebrouck F, 1999. Ultrastructure of surface components of Streptococcus gallolyticus strains of differing virulence isolated from pigeons. Microbiology, 145(2):335-342.

Vanrobaeys M; Herdt Pde; Ducatelle R; Creten W; Haesebrouck F, 1997. Extracellular proteins and virulence in Streptococcus bovis isolates from pigeons. Veterinary Microbiology, 59(1):59-66; 10 ref.

Velhner M; Nikolovski J; Domi X, 1988. The health situation and disease problems in poultry production in Serbia in the period 1985-87. Peradarstvo, 23(7-8):198-202; 5 ref.

Volkmar F, 1932. Apoplectiform septicemia in turkeys. Poultry Science, 11:297-300.

Wang ZiZhen; Chen-LiYing; Wang-YaBing; Wang-XuGuang; Liu-JinXin; Zhang-Han; Wang ZZ; Chen LY; Wang YB; Wang XG; Liu JX; Zhang H, 1999. A report on the diagnosis [in 1998] of Streptococcus disease on poultry farms in the province of Henan. Journal of Henan Agricultural Sciences, 12:27-28.

Williams AM; Farrow JAE; Collins MD, 1989. Reverse transcriptase sequencing of 16S ribosomal RNA from Streptococcus cecorum. Letters in Applied Microbiology, 8:185-190.

Zekarias B; Landman WJM; Tooten PCJ; Gruys E, 2000. Leukocyte responses in two breeds of layer chicken that differ in susceptibility to induced amyloid arthropathy. Veterinary Immunology and Immunopathology, 77(1/2):55-69; 45 ref.

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