Streptococcus and Enterococcus infections in poultry
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PicturesTop of page
IdentityTop of page
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/sTop of page Enterococcus
Streptococcus equi subsp. zooepidemicus
OverviewTop of page
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.
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).
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 AnimalsTop of page
|Animal name||Context||Life stage||System|
|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 AffectedTop of page
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 AffectedTop 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 TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Egypt||Present||El-Nasser et al. (1994); Moustfa and Hussein (1999)|
|China||Present||Guo et al. (1987); Guo et al. (1989)|
|-Henan||Present||CABI (Undated)||Original citation: Wang-ZiZhen, et al. (1999)|
|-Shanghai||Present||Huan Shu (1997)|
|India||Present||Lakshmanachar and Raja Rajeswari (1992); Rajesh Chahota et al. (2001)|
|Japan||Present||CABI (Undated a)||Present based on regional distribution.|
|-Hokkaido||Present||Ushijima and Sato (1958); Sato et al. (1960); Kondo et al. (1997)|
|Belgium||Present||Herdt et al. (1994); CABI (Undated)|
|Bulgaria||Present||Minev and Mineva (1971); Ilieva et al. (1987)|
|Federal Republic of Yugoslavia||Present||Topolko et al. (1973)|
|France||Present||CABI (Undated)||Original citation: Paniset and Verge (1925)|
|Germany||Present||Damman and Manegold (1905); Damman and Manegold (1907); Greve (1908)|
|Greece||Present||Parisis and Lekkas (1970)|
|Hungary||Present||Ivanics et al. (1984); Ivanics et al. (1997)|
|Ireland||Present||McNamee and King (1996)|
|Italy||Present||AGRIMI (1956); Casagrande Proietti et al. (1998); Esposito (2000); Passamonti et al. (2000); Terregino et al. (2000)|
|Netherlands||Present||Landman et al. (1994); Dorrestein et al. (1996); Chamanza et al. (1998); Landman et al. (1998)|
|Russia||Present||CABI (Undated a)||Present based on regional distribution.|
|-Central Russia||Present||Gorbov and Machinskiĭ (1984)|
|-Southern Russia||Present||Kadymov and Dunyamaliev (1986); Kadymov et al. (1989)|
|Serbia and Montenegro||Present||Velhner et al. (1988)|
|United Kingdom||Present||BUXTON (1952); Randall and Pearson (1991)|
|Canada||Present||GENEST and NADEAU (1944)|
|United States||Present||CABI (Undated a)||Present based on regional distribution.|
|-California||Present||POVAR and BROWNSTEIN (1947); Cardona et al. (1993); Droual et al. (1997)|
|-Kentucky||Present||EDWARDS and HULL (1937)|
|-New Jersey||Present||HUDSON (1933)|
|-New York||Present||Mack (1908); Sandhu (1988)|
|-Virginia||Present||Nörgaard and Mohler (1902); MOORE and MARTEN (1944)|
|New Zealand||Present||Black (1997)|
|Brazil||Present||CABI (Undated a)||Present based on regional distribution.|
|-Rio Grande do Sul||Present||Schmidt-Hoensdorf (1925)|
|Uruguay||Present||Ferrer et al. (1978)|
PathologyTop of page
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).
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.
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).
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).
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).
DiagnosisTop of page
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/SignsTop of page
|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 CourseTop of page
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).
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).
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).
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).
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.
EpidemiologyTop of page
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: EconomicTop of page
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 SafetyTop of page
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 TreatmentTop of page
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 ControlTop of page
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.
ReferencesTop of page
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