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Mycoplasma agalactiae infections

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Datasheet

Mycoplasma agalactiae infections

Summary

  • Last modified
  • 11 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Mycoplasma agalactiae infections
  • Overview
  • Mycoplasma agalactiae (Ma) is considered the classical agent of contagious agalactia (CA) and is one of the principal mycoplasmoses of small ruminants and has also been reported in ibex (

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Pictures

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PictureTitleCaptionCopyright
Udder of a goat with contagious agalactia,
TitleSymptoms on udder
CaptionUdder of a goat with contagious agalactia,
CopyrightJohn B. Bashiruddin
Udder of a goat with contagious agalactia,
Symptoms on udderUdder of a goat with contagious agalactia,John B. Bashiruddin
Hardening of the tissue, abscess formation and eventual fibrosis resulting in total loss of normal mammary tissue may be seen in the sectioned udder.
TitleSectioned udder
CaptionHardening of the tissue, abscess formation and eventual fibrosis resulting in total loss of normal mammary tissue may be seen in the sectioned udder.
CopyrightJohn B. Bashiruddin
Hardening of the tissue, abscess formation and eventual fibrosis resulting in total loss of normal mammary tissue may be seen in the sectioned udder.
Sectioned udderHardening of the tissue, abscess formation and eventual fibrosis resulting in total loss of normal mammary tissue may be seen in the sectioned udder.John B. Bashiruddin
Milk from animals with contagious agalactia. The milk sample at (B) is discoloured, and although usually yellowish, here it is also tinged with blood, and contains clotts.  (A) is a normal sample.
TitleMilk from animals with contagious agalactia
CaptionMilk from animals with contagious agalactia. The milk sample at (B) is discoloured, and although usually yellowish, here it is also tinged with blood, and contains clotts. (A) is a normal sample.
CopyrightJohn B. Bashiruddin
Milk from animals with contagious agalactia. The milk sample at (B) is discoloured, and although usually yellowish, here it is also tinged with blood, and contains clotts.  (A) is a normal sample.
Milk from animals with contagious agalactiaMilk from animals with contagious agalactia. The milk sample at (B) is discoloured, and although usually yellowish, here it is also tinged with blood, and contains clotts. (A) is a normal sample.John B. Bashiruddin
Goat showing swollen carpal joint caused by Mycoplasma agalactiae.  Arthritis and lameness were the overt clinical signs, and the organism was isolated from joint fluid.
TitleSwollen carpal joint
CaptionGoat showing swollen carpal joint caused by Mycoplasma agalactiae. Arthritis and lameness were the overt clinical signs, and the organism was isolated from joint fluid.
CopyrightJohn B. Bashiruddin
Goat showing swollen carpal joint caused by Mycoplasma agalactiae.  Arthritis and lameness were the overt clinical signs, and the organism was isolated from joint fluid.
Swollen carpal jointGoat showing swollen carpal joint caused by Mycoplasma agalactiae. Arthritis and lameness were the overt clinical signs, and the organism was isolated from joint fluid.John B. Bashiruddin
Sheep with contagious agalactia showing keratoconjunctivitis caused by Mycoplasma agalactiae.
TitleKeratoconjunctivitis
CaptionSheep with contagious agalactia showing keratoconjunctivitis caused by Mycoplasma agalactiae.
CopyrightJohn B. Bashiruddin
Sheep with contagious agalactia showing keratoconjunctivitis caused by Mycoplasma agalactiae.
KeratoconjunctivitisSheep with contagious agalactia showing keratoconjunctivitis caused by Mycoplasma agalactiae.John B. Bashiruddin

Identity

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Preferred Scientific Name

  • Mycoplasma agalactiae infections

International Common Names

  • English: agalactia; arthritis; contagious agalactia; contagious agalactia, mycoplasmal agalactia in sheep - exotic; keratoconjunctivitis; mastitis

Local Common Names

  • Italy: agalasia contagiosa; mal di sito

English acronym

  • CA

Overview

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Mycoplasma agalactiae (Ma) is considered the classical agent of contagious agalactia (CA) and is one of the principal mycoplasmoses of small ruminants and has also been reported in ibex (González-Candela et al., 2006; Tardy et al., 2012). The disease in which one of the symptoms is agalactia is a complex syndrome mainly of mastitis, arthritis and keratoconjunctivitis. M. agalactiae occurs in every continent and is the major cause of CA in Mediterranean Europe, but several other mycoplasmas, M. mycoides subsp. capri,M. capricolum subsp. capricolum (Mcca), and sometimes M. putrefaciens (Mput), may also produce a similar syndrome and may be the predominating cause in other geographical locations. M. agalactiae is characterized biochemically by the absence of glucose and mannose catabolism, arginine and gelatin hydrolysis, the presence of phosphatase activity, tetrazolium reduction anaerobically and aerobically, and haemadsorption. The genome of PG2 strain is 877438 bp, which codes for 714 genes and has a G+C content of 29.7% (Sirand-Pugnet et al., 2007); strain 5632 is 130kbp larger (Nouvel et al., 2010).

History


CA has been known for nearly 200 years in Europe and was known as 'mal di sito' ('illness of the place') in Italy because animals became infected after grazing on pasture where other sick animals had previously been. Although the clinical syndrome was attributed to a mycoplasma and described by Metaxa in 1861 (cited in Bergonier et al., 1997), the main causative organism, M. agalactiae, was not isolated and cultured until 1925 by Bridre and Donatien (Cottew and Leach, 1969). It was the second mycoplasma to be discovered, 27 years after the isolation of the mycoplasma that causes contagious bovine pleuropneumonia.

From the Pyrenees where the disease has been reported since 1891, M. agalactiae spread throughout Europe in the 1900s and reached Italy in 1979. It entered Sardinia in 1980, Brazil in 1986 and the Canary Islands in 1992. It is present in all continents of the world (Cottew, 1979; Jones, 1987). M. agalactiae and contagious agalactia have been detected in the USA (DaMassa, 1983), but neither the organism nor the disease have been reported recently in that country.

Hosts/Species Affected

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All breeds and sexes of sheep are susceptible to infection with M. agalactiae. Pregnant ewes, especially during the last trimester of gestation, are more susceptible than other groups. Although lambs can contract the disease, they are more resistant than adult sheep. Goats of all breeds, sexes and ages are more susceptible than corresponding groups in sheep. In endemic areas, both sheep and goats usually develop CA. It has also been reported in ibex (González-Candela et al., 2006; Tardy et al., 2012).

Distribution

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CA has occurred in most continents of the world but in Europe the disease caused by M. agalactiae has only persisted in the Mediterranean basin (Cottew, 1979; Jones, 1987; OIE, 1994). It is present in France (Bergonier et al., 1997), Spain (Rodríguez et al., 1996; Gil et al., 1999a), including the Basque country and the province of Navarre (Ramírez et al., 2001), Gran Canaria (Real et al., 1994; Andrada et al., 2001), Portugal (Atalaia et al., 1986), Romania, Bulgaria, Hungary (Bajmocy et al., 1998), the Russian Federation, Italy (Tola et al., 1997; De Santis et al., 1999), the Former Yugoslavian Republic of Macedonia (Cokrevski et al., 2001), Albania, Greece (Tsaknakis et al., 1992, Petsaga-Tsimperi and Sarris, 1997), and Switzerland (Marino-Ode et al., 1984). The estimated prevalence of M. agalactiae in Europe ranges from 0.03 to 9 cases per 10,000 sheep and goats (Woodhead and Morgan, 1993). M. agalactiae has been reported in Israel (Rapoport et al., 1999), Turkey (Erdag, 1989), Iran, Iraq, Morocco, Malaysia, Brazil and Eritrea. It is present in India (Singh et al., 1974; Banerjee et al., 1979), Africa, for example Nigeria (Egwu et al., 2001), and was in USA (DaMassa 1983; Kinde et al, 1994).

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

AfghanistanNo information availableOIE, 2009
ArmeniaDisease not reportedOIE, 2009
AzerbaijanDisease not reportedOIE, 2009
BahrainDisease never reportedOIE, 2009
BangladeshDisease never reportedOIE, 2009
BhutanNo information availableOIE, 2009
CambodiaNo information availableOIE, 2009
ChinaNo information availableNULLWang et al., 1988; OIE, 2009
-Hong KongNo information availableOIE, 2009
-XinjiangPresentWang et al., 1988
IndiaDisease never reportedNULLKonsam et al., 1989; Sikdar and Uppal, 1996; OIE, 2009
IndonesiaDisease not reportedOIE, 2009
IranPresentNULLOIE, 2000; OIE, 2009
IraqNo information availableNULLAlGraibawi et al., 1989; OIE, 2009
IsraelDisease not reported200803OIE, 2000; OIE, 2009
JapanDisease not reportedOIE, 2009
JordanDisease never reportedOIE, 2009
KazakhstanDisease not reportedOIE, 2009
Korea, Republic ofNo information availableOIE, 2009
KuwaitDisease not reportedOIE, 2009
KyrgyzstanDisease not reportedOIE, 2009
LaosDisease never reportedOIE, 2009
LebanonPresentOIE, 2009
MalaysiaDisease not reportedOIE, 2009
MongoliaPresentNULLDamdinsuren Ch, 1989; OIE, 2009
MyanmarDisease never reportedOIE, 2009
NepalNo information availableOIE, 2009
OmanDisease not reportedOIE, 2009
PakistanDisease not reportedOIE, 2009
PhilippinesDisease never reportedOIE, 2009
QatarAbsent, reported but not confirmedOIE, 2009
Saudi ArabiaDisease not reportedOIE, 2009
SingaporeDisease never reportedOIE, 2009
Sri LankaDisease never reportedOIE, 2009
SyriaDisease not reportedOIE, 2009
TajikistanDisease not reportedOIE, 2009
ThailandNo information availableOIE, 2009
TurkeyNo information availableNULLOtlu et al., 1997; OIE, 2009
United Arab EmiratesNo information availableOIE, 2009
VietnamDisease never reportedOIE, 2009
YemenNo information availableOIE, 2009

Africa

AlgeriaDisease not reportedNULLBelaid et al., 1990; OIE, 2009
AngolaNo information availableOIE, 2009
BeninNo information availableOIE, 2009
BotswanaDisease not reportedOIE, 2009
Burkina FasoNo information availableOIE, 2009
CameroonPresentMartrenchar et al., 1995
ChadNo information availableOIE, 2009
CongoNo information availableOIE, 2009
DjiboutiDisease not reportedOIE, 2009
EgyptDisease never reportedOIE, 2009
EritreaPresentNULLOIE, 2000; OIE, 2009
EthiopiaNo information availableOIE, 2009
GabonNo information availableOIE, 2009
GambiaNo information availableOIE, 2009
GhanaNo information availableOIE, 2009
GuineaDisease never reportedOIE, 2009
Guinea-BissauNo information availableOIE, 2009
KenyaNo information availableOIE, 2009
LesothoDisease not reportedOIE, 2009
MadagascarDisease never reportedOIE, 2009
MalawiNo information availableOIE, 2009
MaliNo information availableOIE, 2009
MauritiusDisease never reportedOIE, 2009
MoroccoNo information availableOIE, 2009
MozambiqueDisease not reportedOIE, 2009
NamibiaNo information availableOIE, 2009
NigeriaDisease never reportedOIE, 2009
RwandaNo information availableOIE, 2009
SenegalNo information availableOIE, 2009
South AfricaDisease never reportedOIE, 2009
SudanDisease not reportedOIE, 2009
SwazilandDisease not reportedOIE, 2009
TanzaniaNo information availableOIE, 2009
TogoNo information availableOIE, 2009
TunisiaDisease not reportedOIE, 2009
UgandaNo information availableOIE, 2009
ZambiaNo information availableOIE, 2009
ZimbabweDisease never reportedOIE, 2009

North America

CanadaDisease never reportedOIE, 2009
GreenlandDisease never reportedOIE, 2009
MexicoDisease never reportedOIE, 2009
USARestricted distributionOIE, 2009

Central America and Caribbean

BelizeDisease not reportedOIE, 2009
Costa RicaDisease never reportedOIE, 2009
CubaDisease never reportedOIE, 2009
Dominican RepublicDisease never reportedOIE, 2009
El SalvadorDisease never reportedOIE, 2009
GuadeloupeNo information availableOIE, 2009
GuatemalaDisease never reportedOIE, 2009
HaitiNo information availableOIE, 2009
HondurasNo information availableOIE, 2009
JamaicaDisease never reportedOIE, 2009
MartiniqueNo information availableOIE, 2009
NicaraguaDisease never reportedOIE, 2009
PanamaNo information availableOIE, 2009

South America

ArgentinaDisease never reportedOIE, 2009
BoliviaNo information availableOIE, 2009
BrazilDisease not reportedOIE, 2009
ChileDisease not reportedOIE, 2009
ColombiaDisease never reportedOIE, 2009
EcuadorDisease never reportedOIE, 2009
French GuianaNo information availableOIE, 2009
PeruDisease never reportedOIE, 2009
UruguayDisease never reportedOIE, 2009
VenezuelaDisease never reportedOIE, 2009

Europe

AlbaniaPresentNULLOIE, 2000; OIE, 2009
AustriaNo information availableOIE, 2009
BelarusDisease not reportedOIE, 2009
BelgiumDisease not reportedOIE, 2009
BulgariaDisease not reported2000OIE, 2000; OIE, 2009
CroatiaDisease not reportedOIE, 2009
CyprusPresentOIE, 2009
Czech RepublicDisease not reportedOIE, 2009
DenmarkDisease never reportedOIE, 2009
EstoniaDisease never reportedOIE, 2009
FinlandDisease never reportedOIE, 2009
FranceNo information availableNULLWiele Avan de, 1994; Bergonier et al., 1997; OIE, 2009
GermanyDisease never reportedOIE, 2009
GreeceRestricted distributionNULLTsaknakes et al., 1992; Petsaga-Tsimperi and Sarris, 1997; OIE, 2009
HungaryDisease not reported2003Bajmócy et al., 1998; OIE, 2009
IcelandDisease never reportedOIE, 2009
IrelandDisease never reportedOIE, 2009
ItalyPresentNULLMontagna and Goffredo, 1989; Brajon et al., 1991; OIE, 2009
LatviaDisease never reportedOIE, 2009
LiechtensteinDisease not reportedOIE, 2009
LithuaniaDisease never reportedOIE, 2009
LuxembourgDisease never reportedOIE, 2009
MacedoniaAbsent, reported but not confirmedNULLCokrevski et al., 2001; OIE, 2009
MaltaDisease not reportedOIE, 2009
MontenegroDisease never reportedOIE, 2009
NetherlandsDisease never reportedOIE, 2009
NorwayDisease never reportedOIE, 2009
PolandDisease never reportedOIE, 2009
PortugalAbsent, reported but not confirmedOIE, 2009
RomaniaDisease not reported2004OIE, 2000; OIE, 2009
Russian FederationDisease never reportedOIE, 2009
SerbiaPresentOIE, 2009
SlovakiaDisease not reportedOIE, 2009
SloveniaDisease not reportedOIE, 2009
SpainRestricted distributionNULLGoncer and Rodríguez, 1990; Real et al., 1994; Pérez et al., 1996; Rodríguez et al., 1996; OIE, 2009
SwedenDisease never reportedOIE, 2009
SwitzerlandDisease not reported199902OIE, 2000; OIE, 2009
UKDisease not reportedOIE, 2009
UkraineDisease never reportedOIE, 2009

Oceania

AustraliaDisease not reportedOIE, 2009
French PolynesiaDisease not reportedOIE, 2009
New CaledoniaDisease never reportedOIE, 2009
New ZealandDisease never reportedOIE, 2009

Pathology

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The main target organ of these mycoplasmas is the mammary gland and this is manifested by a fall in, or complete loss of milk production in dairy breeds, sometimes within 2-3 days, and morbidity and mortality in young animals of meat breeds. The milk may appear yellow and granular and take on a thick consistency with milk clots that may obstruct the teat duct (see Pictures for an example). The causal mycoplasmas can be isolated from milk when mastitis is present. The udder may become hot, swollen and tender (see Pictures). In the later stages of CA, the udder atrophies, caused by extensive fibrosis of the secretory tissue. The severity of arthritis/polyarthritis may range from stiffness of the joints to severe lameness in which joints, typically the tarsus and carpus, are swollen with accumulation of synovial fluid (see Pictures). This fluid is often a rich source of specific antibody, often present at a higher titre than in the serum, and of the causal mycoplasmas themselves. The first signs associated with ocular lesions are conjunctivitis and congestion, lacrimation and photophobia, followed by vascularization of the cornea, inflammatory foci and parenchymatous keratitis (see Pictures). Severe cases can lead to blindness. Pneumonia has also been reported in cases of CA especially in young animals where it may represent the only external sign.

Diagnosis

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When a flock is severely infected, clinical diagnosis of CA is straightforward as the three major signs, mastitis, arthritis and keratoconjunctivitis, are present within a flock though not necessarily in the same animal. When fulminating outbreaks occur, in areas previously free from the disease, the initial stages of the acute form of CA may involve septicaemia and a febrile illness. Otherwise where M. agalactiae is enzootic, a discrete disease is usual which must be differentiated from viral, bacterial and other mycoplasmal causes.


Growth, Isolation and Transport Media


Laboratory diagnosis provides the only means of confirming the cause of the disease. Isolation of the organism in liquid of solid culture media presents no real problems as M. agalactiae grows well in most locally produced mycoplasma media and ME liquid and solid medium in 2-5 days. However, the quality of the media and the aseptic collection of samples are critical to the success of isolation. Some clinical samples may require several 'blind' passages in liquid medium before growth is established, and regular subcultures from these onto solid media, incubated anaerobically, may also be required before biochemical identifications can be performed (Lambert, 1987). A solid medium on which the growth of M. agalactiae results in coloured colonies is useful in the rapid presumptive diagnosis of isolates from milk. This is an excellent source of mycoplasmas (see Pictures) (Bashiruddin and Windsor, 1998; Windsor and Bashiruddin, 2000).

Occasionally, M. agalactiae will grow on blood agar when they are in pure culture, and after 48-72 hours of incubation, appear as tiny pinpoint colonies surrounded by a small zone of beta-haemolysis: this haemolysis is probably mediated by hydrogen peroxide, which M. agalactiae is known to produce (Khan et al., 2005). Other useful samples from live animals apart from milk include synovial fluid, and swabs taken from the nose and eyes. Mycoplasmas have also been isolated from the outer ear canal of sheep and mites that parasitize this site (DaMassa 1990; Gil et al., 1999b). At post-mortem, the mycoplasmas can be isolated from udder tissue, associated lymph nodes, joint fluid and lungs. The culture procedure is time-consuming and can take up to 2 weeks to achieve definite identification. Final identification is usually achieved by biochemical tests, growth inhibition and immunofluorescent tests using hyperimmune rabbit antiserum. Molecular tests such as the polymerase chain reaction (PCR) are also used.


Biochemical Tests


M. agalactiae can be distinguished from the other mycoplasmas associated with CA, by its inability to ferment glucose or to utilize arginine; it also produces film and spots on solid and liquid medium (Table 1). Commercial typing media for most of these tests are available (e.g. Mycoplasma Experience, Reigate, UK; see Websites); however, pure cultures that take time-consuming cloning and subculturing are essential for these tests. Reactions may be difficult to interpret and may result in only presumptive identification.


Table 1 


OrganismDigitonin sensitivityUrease activityGlucose fermentationArginine hydrolysisPhosphatase activityFilm & spotsCaseinolytic activity
Ma + + +
MmmLC + + +
Mcca + + + + +
Mput + + + +

Growth Inhibition Test


The growth inhibition (GI) test directly inhibits mycoplasma growth on solid media by the action of specific hyperimmune serum. The preparation of specific antisera for the GI test must take into consideration the fact that M. agalactiae shows considerable antigenic variation (Bergonier et al., 1996). Strong serological, reciprocated, cross-reactions between M. agalactiae and M. bovis were demonstrated in immunobinding and Western blotting tests with antisera against type strains, and the workers were unable to resolve the identities of several strains of M. agalactiae with simple serological tests (Gummelt et al., 1994).


Serological Tests


ELISA tests have used whole cells or subunit antigens (Levison et al., 1991; Cannas et al., 1992; Romano et al., 1995). False positives sometimes arise and methods for their elimination using protein G conjugates have been developed (Lambert et al., 1998). Newer recombinant antigens, such as the r-P48 major surface protein, have been described but their specificity and diagnostic sensitivities are not known (Rosati et al., 2000). Commercial ELISA tests are available, although reports of their sensitivity and specificity vary (Nicholas, 1995), with Pépin et al. (2003) reporting 100% sensitivity and 88-92% specificity at the flock level. However Kittelberger et al. (2006) reported sensitivities as 76.7% and 56.7% with almost 100% specificity. They also compared these two ELISA tests with the complement fixation test (CFT) and a Western blotting method and concluded that use of the CFT should be discouraged. The CFT remains as an OIE approved test and is widely used for the detection of CA at herd level. Poorly sensitive, it may not be effective for the detection of specific antibodies in small numbers of animals but its sensitivity increases with the numbers of animals sampled and especially where many chronically infected animals are present (Zavagli, 1951; Goff and Perreau, 1984).


Molecular Diagnosis

Detection by PCR tests based on the DNA fragments, 16S rRNA and uvrC genes have been used for the detection of M. agalactiae (Dedieu et al., 1995; Gonzalez et al., 1995; Tola et al., 1996; Subramaniam et al., 1998), and the test based on the uvrC gene seems ideal as shown by Bashiruddin et al. (2005). The sensitivity of these tests assessed by the addition of organisms to milk samples is about 103 cfu/ml. A PCR method using the 16S rDNA gene followed by the use of denaturing gradient gel electrophoresis has been able to detect and identify the majority of Mycoplasma species including M. agalactiae (McAuliffe et al., 2005). Other PCR methods using different genes such as the glk gene (Woubit et al., 2007); or multiplex PCR’s (Greco et al., 2001; Foddai et al., 2005) have been described. The development or real-time PCR’s has led to a number of new assays (Lorusso et al., 2007; Fitzmaurice et al., 2008; Oravcová et al., 2009; Becker et al., 2012), some combined with high resolution melting curve analysis (Rebelo et al., 2011). These tests allow the rapid detection of M. agalactiae from bacteriological cultures, milk and a variety of clinical samples.

Other diagnostic methods have also been described, these include matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) (Pereyre et al., 2013), flow cytometry (Assunção et al., 2007) and micro-arrays (Schnee et al., 2012).

Several methods of molecular typing of M. agalactiae have been developed, which enables differentiation of isolates and may help in disease tracing. These methods include variable number tandem repeat analysis (VNTR) (McAuliffe et al., 2008; Nouvel et al., 2012) and multi-locus sequencing methods (MLST) (McAuliffe et al., 2011; Manso-Silván et al., 2012). The MLST method of McAuliffe et al. (2011) is available at: http://pubmlst.org/magalactiae/ which means that the method can be used in other laboratories and the database added too.

List of Symptoms/Signs

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SignLife StagesType
Cardiovascular Signs / Muffled, decreased, heart sounds Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sheep & Goats:All Stages Sign
Digestive Signs / Diarrhoea Sheep & Goats:All Stages Sign
General Signs / Fever, pyrexia, hyperthermia Sheep & Goats:All Stages Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sheep & Goats:All Stages Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area Sheep & Goats:All Stages Sign
General Signs / Generalized lameness or stiffness, limping Sheep & Goats:All Stages Diagnosis
General Signs / Hindlimb lameness, stiffness, limping hind leg Sheep & Goats:All Stages Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area Sheep & Goats:All Stages Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia Sheep & Goats:Mature female Diagnosis
General Signs / Opisthotonus Sign
General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass Sheep & Goats:All Stages Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Sudden death, found dead Sign
General Signs / Swelling skin or subcutaneous, mass, lump, nodule Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Weight loss Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sheep & Goats:All Stages Sign
Ophthalmology Signs / Blepharospasm Sheep & Goats:All Stages Sign
Ophthalmology Signs / Blindness Sheep & Goats:All Stages Diagnosis
Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling Sheep & Goats:All Stages Diagnosis
Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature Sheep & Goats:All Stages Sign
Ophthalmology Signs / Conjunctival, scleral, redness Sheep & Goats:All Stages Sign
Ophthalmology Signs / Corneal edema, opacity Sheep & Goats:All Stages Sign
Ophthalmology Signs / Corneal neovascularization, pannus Sheep & Goats:All Stages Diagnosis
Ophthalmology Signs / Corneal swelling, mass, nodule Sheep & Goats:All Stages Diagnosis
Ophthalmology Signs / Corneal ulcer, erosion Sheep & Goats:All Stages Diagnosis
Ophthalmology Signs / Hypopyon, lipid, or fibrin, flare, of anterior chamber Sheep & Goats:All Stages Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Ophthalmology Signs / Photophobia Sheep & Goats:All Stages Sign
Ophthalmology Signs / Purulent discharge from eye Sign
Pain / Discomfort Signs / Forelimb pain, front leg Sign
Pain / Discomfort Signs / Hindlimb pain, hind leg Sign
Pain / Discomfort Signs / Ocular pain, eye Sheep & Goats:All Stages Sign
Pain / Discomfort Signs / Pain mammary gland, udder Sheep & Goats:Mature female Diagnosis
Reproductive Signs / Abortion or weak newborns, stillbirth Sheep & Goats:Gimmer,Sheep & Goats:Mature female Diagnosis
Reproductive Signs / Agalactia, decreased, absent milk production Sheep & Goats:Mature female Diagnosis
Reproductive Signs / Firm mammary gland, hard udder Sign
Reproductive Signs / Mastitis, abnormal milk Sheep & Goats:Mature female Diagnosis
Reproductive Signs / Purulent discharge, vulvar, vaginal Sign
Reproductive Signs / Warm mammary gland, hot, heat, udder Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign
Respiratory Signs / Coughing, coughs Sign
Respiratory Signs / Decreased, muffled, lung sounds, absent respiratory sounds Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Sign
Respiratory Signs / Purulent nasal discharge Sign
Respiratory Signs / Sneezing, sneeze Sign
Skin / Integumentary Signs / Rough hair coat, dull, standing on end Sign
Skin / Integumentary Signs / Warm skin, hot, heat Sign

Disease Course

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CA is predominantly a disease of milking sheep and goats. It often appears in a herd in the spring soon after lactation begins and probably represents the activation of latent infection. The young ruminants become infected directly at suckling, whereas the adults are contaminated via the milker's hands, milking machines or by bedding, which often provides a rich source of mycoplasmas. Transmission is by aerosol of infective exudates over short distances and drinking contaminated water may also lead to infection.

The course of disease is more likely to be chronic with M. agalactiae, whereas in goats, M. mycoides subsp.  capri which includes the former M. mycoides subsp mycoides large colony type (MmmLC) (Manso-Silván et al., 2009), M. capricolum subsp. capricolum (Mcca), and M. putrefaciens (Mput) usually produce acute or hyperacute infection, often with respiratory complications. An unusual feature of outbreaks caused by Mput is the lack of pyrexia in the affected nannies and kids. Females seem to be affected more than males (Toshkov et al., 1975). Animals in the early acute stage of disease with M. agalactiae show a general malaise, and a hyperthermia of 41 to 42°C that corresponds to septicaemia. The animals may become prostrated and show in appetence, and some may die. Pregnant females near term may abort. Enteritis may be observed in severe cases (Lambert, 1987). Typically, in a flock the occurrence of signs peaks after the time of parturition in both dams and young. Most animals survive and the organism may then localize in the udder, joints or eyes and most ewes develop severe unilateral or bilateral mastitis followed by arthritis and keratoconjunctivitis. A rapid drop in milk production results and high numbers of organisms are shed in milk. Complete agalactia eventually results from infection of the mammary gland. Subsequent re-infections may be in apparent or result in minor clinical symptoms, but large numbers of M. agalactiae may be shed in milk and other body fluids for weeks and sometimes years. M. agalactiae has been associated with granular vulvo-vaginitis in Indian goats (Singh et al., 1975).

The severity of the symptoms is thought to be related to the route of infection and the immune and hormonal status of the host. Experimental infections via the subcutaneous route, resembling wound infection, were more severe than those produced by the intramammary, intravenous or oral routes, and pregnant animals fared worst of all (Hasso et al., 1993). Because M. agalactiae infections may be persistent, they surmised that the increase in progesterone early in pregnancy allowed clinical signs to appear during pregnancy, which continued until birth. The continuous presence of testosterone in males and the absence of testosterone in castrated males allowed symptomless or subclinical infections (MacOwan et al., 1984). Experimental infection by the conjunctival route produced a disease that resembled natural infection. It confirmed many of the stages of M. agalactiae infection and the persistence of the organism in the symptomless and immunologically unresponsive host. Because of this it has been developed as an animal model for further studies on virulence, immune mechanisms, and pathogenesis (Sanchis et al., 1998).

Epidemiology

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The main reservoir of mycoplasmas causing CA is the infected animal in which the organisms can persist for over a year after clinical recovery. The introduction of such carriers into a susceptible flock can cause high morbidity and mortality. In 1993, an outbreak involving 600 goats in California, introduced by a single clinically normal lactating nanny goat infected with M. agalactiae, resulted in 15% mortality (Kinde et al., 1994). Several reports have confirmed the presence of M. agalactiae in ear mites collected from the external ear canal of goats affected with CA and clinically normal goats (DaMassa, 1990; Gil et al., 1999b). One possible source of infection is semen; M. agalactiae was detected in goat bucks (de la Fe et al., 2009). The ability of the organism to form a biofilm indicates an ability to survive in the environment longer than previously thought (McAuliffe et al., 2006).

Impact: Economic

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The disease syndrome caused by M. agalactiae is considered to be a significant economic problem not because of mortality it causes but because of the high morbidity associated with CA. In naive herds it has caused mortalities of up to 50% (Real et al., 1994). Economic losses result from deaths, reduced physical condition, lowered milk production, abortions, animal welfare problems of arthritis and conjunctivitis, and expensive preventative and treatment procedures.

Zoonoses and Food Safety

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CA is not a zoonotic disease.

Disease Treatment

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Chemotherapy


Frequent therapeutic failures have cast doubts on the value of antibiotic therapy for CA. The reasons for this include the lack of knowledge of the sensitivities of antibiotics for M. agalactiae, underdosage, and the high cost of treatment compared with culling. Whether or not antibiotics can effect a complete mycoplasma sterilization by antibiotics in general is also under contention. Oxytetracycline at 14 mg/kg given for 3 days (Nicolet, 1994) can sometimes bring about clinical improvements but there is always the danger of promoting inapparent carrier animals. Although the use of erythromycin at 25 mg/kg and tylosin at 10 mg/kg bring about clinical cure (Nicolas et al., 1982; Kinde et al., 1994), they can also lead to the destruction of milk-producing tissue in small ruminants. Tiamulin at 10 mg/kg will maintain effective inhibitory dosage in the udder for 12 h (Ziv et al., 1983), but twice that dosage is required for apparent clinical cure and bacteriological clearance (Ojo et al., 1984).

In vitro minimum inhibition concentration (MIC) studies have demonstrated that antibiotics are effective against M. agalactiae in the laboratory and these include oxytetracycline, tylosin, enrofloxacin, spiramycin and lincomycin-spectinomycin (Loria et al., 2003), and clindamycin (de Garnica et al., 2013). However Antunes et al. (2008) found two M. agalactiae isolates had high MIC values for tetracycline, which was also detected by Filoussis et al. (2013); Regnier et al. (2013) found two isolates with high MIC values for florfenicol. This indicates that M. agalactiae is capable of developing antibiotic resistance, which was also indicated by Paterna et al. (2013).

Prevention and Control

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Vaccines


In Europe both attenuated and inactivated vaccines have been used with mixed success. Some have provided protection from clinical disease and have been useful in endemic areas but the problems of encouraging the carrier state still apply. Some autogenous vaccines have dubious efficacy, and some preparations have been responsible for the spread of scrapie (Carmelli et al., 2001). Generally, the duration of immunity is short. There is some experimental evidence of the persistence of antibodies for about 1 year with the alleviation of clinical signs; however, M. agalactiae was shed in milk (Buonavoglia et al., 1998). Some phenol- and saponin-inactivated vaccines have been effective in limiting the spread of M. agalactiae (Tola et al., 1999b; de la Fe et al., 2007a, 2007b). A commercial vaccine containing aluminium hydroxide also induced high levels of antibody for at least 5 months and did not reduce the excretion of M. agalactiae in milk (Pépin et al., 2001). Experimental trials using an inactivated mineral-oil adjuvanted M. agalactiae vaccine was described as having long-term immunogenicity (five months after the second vaccination) which induced full-protective immunity (Buonavoglia et al., 2010).

Vaccination may have an adverse effect by favouring the spread of mycoplasma from vaccinated but clinically healthy flocks to unvaccinated or vaccinated flocks previously free of M. agalactiae infection.

References

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AlGraibawi MAA, AlShammari AJN, Sharma VK, Saed CM, 1989. Isolation and identification of Mycoplasma agalactiae from Angora goats in Iraq. Indian Journal of Comparative Microbiology, 10:156-158.

Andrada M, Déniz S, González M, Rodríguez F, Póveda JB, 2001. In: Poveda JB, Fernandez A, Frey J, Johansson K-E, eds. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics, Vol. 5. Luxembourg: Office for Official Publications of the European Communities, 126-129.

Antunes NT, Tavío MM, Assunção P, Rosales RS, Poveda C, Fé Cde la, Gil MC, Poveda JB, 2008. In vitro susceptibilities of field isolates of Mycoplasma agalactiae. Veterinary Journal, 177(3):436-438. http://www.sciencedirect.com/science/journal/10900233

Assunção P, Davey HM, Rosales RS, Antunes NT, Fe Cde la, Ramirez AS, Ruiz de Galarreta CM, Poveda JB, 2007. Detection of mycoplasmas in goat milk by flow cytometry. Cytometry A, 71(12):1034-1038. http://www3.interscience.wiley.com/cgi-bin/abstract/116834179/ABSTRACT

Atalaia V, Brandao E, Machado M, 1986. Contagious agalactia in Portugal. Repositório de Trabalhos do Laboratório Nacional de InvestigaÇao Veterinária, 18:11, 13-19; 20 ref.

Bajmócy E, Kaszanyitzky éJ, Bölske G, Matiz K, Tanyi J, 1998. Diagnosis of contagious agalactia in Hungary. Magyar állatorvosok Lapja, 120(7):390-394; 12 ref.

Banjeree M, Singh N, Gupta PP, 1979. Isolation of mycoplasmas and acholeplasmas from pneumonic lesions in sheep and goats in India. Zentralblat Veterinarmedinska B, 26:689-695.

Bashiruddin JB, Frey J, Königsson MH, Johansson KE, Hotzel H, Diller R, Santis Pde, Botelho A, Ayling RD, Nicholas RAJ, Thiaucourt F, Sachse K, 2005. Evaluation of PCR systems for the identification and differentiation of Mycoplasma agalactiae and Mycoplasma bovis: a collaborative trial. Veterinary Journal, 169(2):268-275.

Bashiruddin JB, Windsor GD, 1998. Development of coloured colonies as an aid to identification of certain pathogenic mycoplasmas. 12th International Congress of the International Organization for Mycoplasmology, July 22-28, Sydney, Australia.

Becker CAM, Ramos F, Sellal E, Moine S, Poumarat F, Tardy F, 2012. Development of a multiplex real-time PCR for contagious agalactia diagnosis in small ruminants. Journal of Microbiological Methods, 90(2):73-79. http://www.sciencedirect.com/science/article/pii/S0167701212001662

Belaid B, Goff Cle, Lefèvre PC, 1990. Epidemiological and serodiagnostic survey of contagious agalactia of sheep and goats in eastern Algeria. Revue d'élevage et de Médecine Vétérinaire des Pays Tropicaux, 43(1):37-41; 9 ref.

Bergonier D, Berthelot X, Poumarat F, 1997. Contagious agalactia of small ruminants: current knowledge concerning epidemiology, diagnosis and control. Revue Scientifique et Technique - Office International des épizooties, 16(3):848-873; 80 ref.

Bergonier D, de Simone F, Russo P, Solsona M, Lambert M, Poumarat F, 1996. Variable expression and geographic distribution of Mycoplasma agalactiae surface epitopes demonstrated with monoclonal antibodies. FEMS Microbiology Letters, 143:159-165.

Brajon G, Ferri G, Masotti GF, Tammaro A, Aleandri M, 1991. Contagious agalactia in a goat flock: somatic cell counts and bacteriological investigations of milk during two lactations. ATTI della Federazione Mediterranea Sanita e Produzione Ruminanti, 1:269-274; 5 ref.

Buonavoglia D, Fasanella A, Sagazio P, Tempesta M, Iovane G, Buonavoglia C, 1998. Persistence of antibodies to Mycoplasma agalactiae in vaccinated sheep. Microbiologica, 21(2):209-212; 8 ref.

Buonavoglia D, Greco G, Corrente M, Greco MF, D'Abramo M, Latronico F, Fasanella A, Decaro N, 2010. Long-term immunogenicity and protection against Mycoplasma agalactiae induced by an oil adjuvant vaccine in sheep. Research in Veterinary Science, 88(1):16-19. http://www.sciencedirect.com/science/journal/00345288

Cannas E, Carboni AQ, Fadda A, Manca M, Mugoni G, Puggioni G, 1992. Antibody detection by ELISA using membrane proteins of M. agalactiae. Proceedings of the Annual Meeting of the Italian Society for Veterinary Science, 46:987-990.

Caramelli M, Ru G, Casalone C, Bozzetta E, Acutis PL, Calella A, Forloni G, 2001. Evidence for the transmission of scrapie to sheep and goats from a vaccine against Mycoplasma agalactiae. Veterinary Record, 148(17):531-536; 21 ref.

Cokrevski S, Crcev D, Loria GR, Nicholas RAJ, 2001. Outbreaks of contagious agalactia in small ruminants in the Republic of Macedonia. Veterinary Record, 148(21):667; 8 ref.

Commission of European Communities (CEC), 1985. Contagious agalactia and other infections with Mycoplasma mycoides. In: Proceedings of CEC meeting, Mice 19-20 September. EUR 10984 en-87. CEC, General Directorate, Information, Market and Innovation, Luxembourg.

Cottew GS, 1979. Caprine-ovine mycoplasmas. In: Tully JG, Whitcomb RF, eds. The Mycoplasmas, Vol.2. London, UK: Academic Press, 103-132.

Cottew GS, Leach RH, 1969. Mycoplasmas of cattle, sheep and goats. In: Hayflick L, ed. The Mycoplasmatales and the L-phase of bacteria. North-Holland Publishing Co., 527-570.

DaMassa AJ, 1983. Recovery of Mycoplasma agalactiae from mastitic goat milk. Journal of the American Veterinary Medical Association, 183(5):548-549; 14 ref.

DaMassa AJ, 1990. The ear canal as a culture site for demonstration of mycoplasmas in clinically normal goats. Australian Veterinary Journal, 67(7):267-269; 14 ref.

Damdinsuren Ch, 1989. Mycoplasmosis in farm animals in Mongolia: immunization of sheep and goats against contagious agalactia. Archiv für Experimentelle Veterinärmedizin, 43(5):769-772; 4 ref.

de Garnica ML, Rosales RS, Gonzalo C, Santos JA, Nicholas RAJ, 2013. Isolation, molecular characterization and antimicrobial susceptibilities of isolates of Mycoplasma agalactiae from bulk tank milk in an endemic area of Spain. Journal of Applied Microbiology, 114(6):1575-1581. http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2672

de la Fe C, Amores J, Gómez Martín A, Sánchez A, Contreras A, Corrales JC, 2009. Mycoplasma agalactiae detected in the semen of goat bucks. Theriogenology, 72(9):1278-1281. http://www.sciencedirect.com/science/journal/0093691X

de la Fe C, Assunção P, Saavedra P, Ramírez A, Poveda JB, 2007. Field trial of a combined vaccine against caprine contagious agalactia: humoral immune response in lactating goats. Veterinary Journal, 174(3):610-615. http://www.sciencedirect.com/science/journal/10900233

de la Fe C, Assunção P, Saavedra P, Tola S, Poveda C, Poveda JB, 2007. Field trial of two dual vaccines against Mycoplasma agalactiae and Mycoplasma mycoides subsp. mycoides (large colony type) in goats. Vaccine, 25(12):2340-2345. http://www.sciencedirect.com/science/journal/0264410X

Dedieu L, Mady V, Lefevre PC, 1995. Development of two PCR assays for the identification of mycoplasmas causing contagious agalactia. FEMS Microbiology Letters, 129(2/3):243-249; 18 ref.

Egwu GO, Ameh JA, Aliyu MM, Mohammed FD, 2001. Caprine mycoplasmal mastitis in Nigeria. Small Ruminant Research, 39(1):87-91; 27 ref.

Erdag O, 1989. Investigations on the preparation and application of vaccine against contagious mycoplasma agalactia of sheep and goats in Turkey. International Symposium on Mycoplasmosis and Theileriosis, 11-13 October, 1989, Pendik, Turkey,., 16-22; [Pendik Animal Diseases Central Research Institute Publication No. 10].

Filioussis G, Ioannou I, Petridou E, Avraam M, Giadinis ND, Kritas SK, 2013. Isolation and analysis of tetracycline-resistant Mycoplasma agalactiae strains from an infected goat herd in Cyprus - short communication. Acta Veterinaria Hungarica, 61(3):291-296. http://www.akademiai.com/content/415353r85j052336/fulltext.pdf

Fitzmaurice J, Sewell M, King CM, McDougall S, McDonald WL, O'Keefe JS, 2008. A real-time polymerase chain reaction assay for the detection of Mycoplasma agalactiae. New Zealand Veterinary Journal, 56(5):233-236. http://www.vetjournal.org.nz

Foddai A, Idini G, Fusco M, Rosa N, Fe Cde la, Zinellu S, Corona L, Tola S, 2005. Rapid differential diagnosis of Mycoplasma agalactiae and Mycoplasma bovis based on a multiplex-PCR and a PCR-RFLP. Molecular Cellular Probes, 19(3):207-212.

Freundt EA, 1955. The classification of the pleuropneumonia-like group of organisms (Borrelomycetales). International Bulletin of Bacteriological Nomenclature and Taxonomy, 5:67-78.

Gil MC, Hermoso de Mendoza M, Rey J, Alonso JM, Poveda JB, Hermoso de Mendoza J, 1999. Aetiology of caprine contagious agalactia syndrome in Extremadura, Spain. Veterinary Record, 144(1):24-25; 13 ref.

Gil MC, Mendoza MHde, Rey J, Alonso JM, Poveda JB, Mendoza JHde, 1999. Isolation of mycoplasmas from the external ear canal of goats affected with contagious agalactia. Veterinary Journal, 158(2):152-154; 13 ref.

Glew MD, Papazisi L, Poumarat F, Begonier D, Rosengarten R, Citti C, 2000. Characterization of a multigene family undergoing high frequency DNA rearrangements and coding for abundant variable surface proteins in Mycoplasma agalactiae. Infection and Immunity, 68:4539-4548.

Goff Cle, Perreau P, 1984. Possibilities and limitations of serological diagnosis in contagious agalactia of small ruminants. Les maladies de la chèvre, colloque international, Niort (France), 9-11 octobre 1984., 271-278; [Colloques de l'INRA No. 28]; 4 ref.

Goncer Coca A, Rodríguez Ferri EF, 1990. Mycoplasmal pneumonias in sheep and goats in the Madrid region. Medicina Veterinaria, 7(11):619-622,624; 25 ref.

Gonzalez YRC, Bascuñana CR, Bölske G, Mattson JG, Molina CF, Johansson K-E, 1995. In virto amplification of the 16S rRNA genes from Mycoplasma bovis and Mycoplasma agalactiae by PCR. Veterinary Microbiology, 47:183-190.

González-Candela M, Cubero-Pablo MJ, Martín-Atance P, León-Vizcaíno L, 2006. Potential pathogens carried by Spanish ibex (Capra pyrenaica hispanica) in Southern Spain. Journal of Wildlife Diseases, 42(2):325-334. http://www.wildlifedisease.org

Greco G, Corrente M, Martella V, Pratelli A, Buonavoglia D, 2001. A multiplex-PCR for the diagnosis of contagious agalactia of sheep and goats. Molecular and Cellular Probes, 15:21-25.

Gummelt I, Hotzel H, Kirchhoff H, 1994. Differentiation betweeen Mycoplasma agalactiae and Mycoplasma bovis by biochemical and molecular-biological metods. In: 10th International Congress of the International Organisation for Mycoplasmology, IOM Letters Vol. 3. Bordeaux, France, July 19-26, 1994, 66-67.

Hasso SA, Al-Aubaidi JM, Al-Darraji AM, 1993. Contagious agalactia in goats: its severity as related to the route of infection and pregnancy. Small Ruminant Research, 10(3):263-275; 24 ref.

Jones GE, 1987. Agriculture. Contagious agalactia and other mycoplasmal diseases of small ruminants. Proceeding of a workshop held in Nice, France, on 19 and 20 September 1985. Agriculture. Contagious agalactia and other mycoplasmal diseases of small ruminants. Proceeding of a workshop held in Nice, France, on 19 and 20 September 1985., 118pp.; [EUR 10984 EN]; many ref.

Khan LA, Miles RJ, Nicholas RAJ, 2005. Hydrogen peroxide production by Mycoplasma bovis and Mycoplasma agalactiae and effect of in vitro passage on a Mycoplasma bovis strain producing high levels of H2O2. Veterinary Research Communications, 29(3):181-188. http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0165-7380

Kinde H, DaMassa AJ, Wakenell PS, Petty R, 1994. Mycoplasma infection in a commercial goat dairy caused by Mycoplasma agalactiae and Mycoplasma mycoides subsp. mycoides (caprine biotype). Journal of Veterinary Diagnostic Investigation, 6(4):423-427; 19 ref.

Kittelberger R, O'Keefe JS, Meynell R, Sewell M, Rosati S, Lambert M, Dufour P, Pépin M, 2006. Comparison of four diagnostic tests for the identification of serum antibodies in small ruminants infected with Mycoplasma agalactiae. New Zealand Veterinary Journal, 54(1):10-15.

Konsam G, Verma BB, Thakur DK, 1989. Mycoplasmosis in kids. Indian Journal of Veterinary Medicine, 9(1):38-39; 4 ref.

Lambert M, 1987. Contagious agalactia of sheep and goats. Revue Scientifique et Technique, Office International des épizooties, 6(3):681-697, 699-711; 61 ref.

Lambert M, Calamel M, Dufour P, Cabasse E, Vitu C, Pépin M, 1998. Detection of false-positive sera in contagious agalactia with a multiantigen ELISA and their elimination with a protein G conjugate. Journal of Veterinary Diagnostic Investigation, 10(4):326-330; 29 ref.

Levison S, Davison I, Caro Vergara MR, Rapoport E, 1991. Use of an ELISA for differential diagnosis of M. agalactiae and M. mycoides subspecies mycoides (LC) in naturally infected goat herds. Research in Veterinay Science, 51:66-71.

Loria GR, Sammartino C, Nicholas RAJ, Ayling RD, 2003. In vitro susceptibilities of field isolates of Mycoplasma agalactiae to oxytetracycline, tylosin, enrofloxacin, spiramycin and lincomycin-spectinomycin. Research in Veterinary Science, 75(1):3-7.

Lorusso A, Decaro N, Greco G, Corrente M, Fasanella A, Buonavoglia D, 2007. A real-time PCR assay for detection and quantification of Mycoplasma agalactiae DNA. Journal of Applied Microbiology, 103(4):918-923. http://www.blackwell-synergy.com/loi/jam

MacOwan KJ, Brand TF, McGillveray N, Hunter AR, 1984. Experimental infection of castrated lambs with Mycoplasma agalactiae. Journal of Hygiene, 93(3):455-463; 18 ref.

Manso-Silván L, Dupuy V, Lysnyansky I, Ozdemir U, Thiaucourt F, 2012. Phylogeny and molecular typing of Mycoplasma agalactiae and Mycoplasma bovis by multilocus sequencing. Veterinary Microbiology, 161(1-2):104-112.

Manso-Silván L, Vilei EM, Sachse K, Djordjevic SP, Thiaucourt F, Frey J, 2009. Mycoplasma leachii sp. nov. as a new species designation for Mycoplasma sp. bovine group 7 of Leach, and reclassification of Mycoplasma mycoides subsp. mycoides LC as a serovar of Mycoplasma mycoides subsp. capri. International Journal of Systematic and Evolutionary Microbiology, 59(6):1353-1358.

Marino-Ode U, Postizzi S, Nicolet J, 1984. Epidemiological studies on distribution of infectious agalactia in goats in the Ticino Canton. Schweizer Archiv für Tierheilkunde, 126(3):111-119; 7 ref.

Martrenchar A, Zoyem N, Ngangnou A, Bouchel D, Ngo Tama AC, Njoya A, 1995. Study of the main infectious agents involved in the aetiology of pulmonary diseases of small ruminants in Northern Cameroon. Revue d'élevage et de Médecine Vétérinaire des Pays Tropicaux, 48(2):133-137; 15 ref.

McAuliffe L, Churchward CP, Lawes JR, Loria G, Ayling RD, Nicholas RAJ, 2008. VNTR analysis reveals unexpected genetic diversity within Mycoplasma agalactiae, the main causative agent of contagious agalactia. BMC Microbiology, 8(193):(07 November 2008). http://www.biomedcentral.com/1471-2180/8/193

McAuliffe L, Ellis RJ, Lawes JR, Ayling RD, Nicholas RAJ, 2005. 16S rDNA PCR and denaturing gradient gel electrophoresis; a single generic test for detecting and differentiating Mycoplasma species. Journal of Medical Microbiology, 54(8):731-739.

McAuliffe L, Ellis RJ, Miles K, Ayling RD, Nicholas RAJ, 2006. Biofilm formation by mycoplasma species and its role in environmental persistence and survival. Microbiology (Reading), 152(4):913-922. http://mic.sgmjournals.org

McAuliffe L, Gosney F, Hlusek M, Garnica MLde, Spergser J, Kargl M, Rosengarten R, Ayling RD, Nicholas RAJ, Ellis RJ, 2011. Multilocus sequence typing of Mycoplasma agalactiae. Journal of Medical Microbiology, 60(6):803-811. http://jmm.sgmjournals.org/

Montagna CO, Goffredo G, 1989. Contagious agalactia of sheep and goats in Apulia and Basilicata. Obiettivi e Documenti Veterinari, 10(3):17-20; 8 ref.

Nicholas R, 1995. Contagious agalactia. State Veterinary Journal, 5(2):13-15.

Nicolas JB, Chauchef S, Parbelle M, Ferial ML, 1982. Les mycoplasmoses caprines vues par un laboratoire de diagnostic. Revue Médicine Véterinaire, 133:423-426.

Nicolet J, 1994. Mycoplasma infections in cattle, sheep and goats: methods for diagnosis and prophylaxis. Comprehensive reports on technical items presented to the International Committee or to Regional Commissions 1994., 31-66; 5 ref.

Nouvel LX, Marenda MS, Glew MD, Sagné E, Giammarinaro P, Tardy F, Poumarat F, Rosengarten R, Citti C, 2012. Molecular typing of Mycoplasma agalactiae: tracing European-wide genetic diversity and an endemic clonal population. Comparative Immunology, Microbiology & Infectious Diseases, 35(5):487-496. http://www.sciencedirect.com/science/article/pii/S0147957112000604

Nouvel LX, Sirand-Pugnet P, Marenda MS, Sagné E, Barbe V, Mangenot S, Schenowitz C, Jacob D, Barré A, Claverol S, Blanchard A, Citti C, 2010. Comparative genomic and proteomic analyses of two Mycoplasma agalactiae strains: clues to the macro- and micro-events that are shaping mycoplasma diversity. BMC Genomics, 11(86):(2 February 2010). http://www.biomedcentral.com/1471-2164/11/86

OIE, 1994. Office of International Epizootics figures: Animal health status and disease control methods.

OIE, 2000. Tables on animal health status and disease control methods. Paris, France: Office International des Epizooties.

OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int

Ojo MO, Kasali OB, Bamgboye DA, 1984. In vitro and in vivo activities of tiamulin against caprine mycoplasmas. Les maladies de la chèvre, colloque international, Niort (France), 9-11 octobre 1984., 287-293; [Colloques de l'INRA No. 28]; 10 ref.

Oravcová K, López-Enríquez L, Rodríguez-Lázaro D, Hernández M, 2009. Mycoplasma agalactiae p40 gene, a novel marker for diagnosis of contagious agalactia in sheep by real-time PCR: assessment of analytical performance and in-house validation using naturally contaminated milk samples. Journal of Clinical Microbiology, 47(2):445-450. http://jcm.asm.org/

Otlu S, Aydin F, Genc O, Tas C, 1997. Clinical and bacteriological studies on contagious agalactia in sheep. Pendik Veteriner Mikrobiyoloji Dergisi, 28(1):33-38; 17 ref.

Paterna A, Sánchez A, Gómez-Martín A, Corrales JC, Fe Cde la, Contreras A, Amores J, 2013. In vitro antimicrobial susceptibility of Mycoplasma agalactiae strains isolated from dairy goats. Journal of Dairy Science, 96(11):7073-7076. http://www.sciencedirect.com/science/article/pii/S0022030213006164

Pépin M, Dufour P, Lambert M, Aubert M, Valognes A, Rotis T, Wiele Avan de, Bergonier D, 2003. Comparison of three enzyme-linked immunosorbent assays for serologic diagnosis of contagious agalactia in sheep. Journal of Veterinary Diagnostic Investigation, 15(3):281-285.

Pépin M, Sanchis R, Abadie G, Lambert M, Dufour P, Guibert J-M, 2001. Experimental vaccination against Mycoplasma agalactiae using an inactivated vaccine. In: Poveda JB, Fernandez A, Frey J, Johansson K-E, eds. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics, Vol. 5. Luxembourg; Office for Official Publications of the European Communities, 162-165.

Pereyre S, Tardy F, Renaudin H, Cauvin E, Machado Ldel PN, Tricot A, Benoit F, Treilles M, Bébéar C, 2013. Identification and subtyping of clinically relevant human and ruminant mycoplasmas by use of matrix-assisted laser desorption ionization-time of flight mass spectrometry. Journal of Clinical Microbiology, 51(10):3314-3323. http://jcm.asm.org/content/51/10/3314.abstract

Pérez Gómez S, San Martín Larraya M, Arriaga Oroquieta A, 1996. Epidemiology of contagious agalactia in Lacho sheep in Navarra province, Spain. Medicina Veterinaria, 13(1):55-60; 15 ref.

Petsaga-Tsimperi V, Sarris K, 1997. Mycoplasmosis of sheep and goats in northern Greece. Veterinarski Glasnik, 51(1/2):49-53; 6 ref.

Pettersson B, Tully JG, Bölske G, Johansson K-E, 2001. Re-evaluation of the classical Mycoplasma lipophilum cluster (Weisburg et al., 1989) and description of two new clusters in the hominis group based on 16S rDNA sequences. International Journal of Systematic and Evolutionary Microbiology, 51:633-643.

Ramírez AS, García M, Díaz-Bertrana L, Fernández A, Poveda JB, 2001. Goat and sheep abortions associated with Mycoplasma agalactiae in Northern Spain. In: Poveda JB, Fernandez A, Frey J, Johansson K-E, eds. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics, Vol. 5. Luxembourg; Office for Official Publications of the European Communities, 122-125.

Rapoport E, Flitman-Tene R, Yogev D, Levisohn S, 1999. Outbreaks of contagious agalactia in Israel. Clinical and epizootiological aspects. In: Stipkovitz L, Rosengarten R, Frey J. COST 826 Agriculture and biotechnology Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics, Vol. 3. EUR 18756 EN Luxembourg, 120-123.

Razin S, Yogev D, Naot Y, 1998. Molecular biology and pathogenicity of mycoplasmas. Microbiological and Molecular Biological Reviews, 62:1094-1156.

Real F, Déniz S, Acosta B, Ferrer O, Poveda JB, 1994. Caprine contagious agalactia caused by Mycoplasma agalactiae in the Canary Islands. Veterinary Record, 135(1):15-16; 14 ref.

Rebelo AR, Parker L, Cai HY, 2011. Use of high-resolution melting curve analysis to identify Mycoplasma species commonly isolated from ruminant, avian, and canine samples. Journal of Veterinary Diagnostic Investigation, 23(5):932-936. http://vdi.sagepub.com/content/23/5/932.abstract

Regnier A, Laroute V, Gautier-Bouchardon A, Gayrard V, Picard-Hagen N, Toutain PL, 2013. Florfenicol concentrations in ovine tear fluid following intramuscular and subcutaneous administration and comparison with the minimum inhibitory concentrations against mycoplasmal strains potentially involved in infectious keratoconjunctivitis. American Journal of Veterinary Research, 74(2):268-274. http://avmajournals.avma.org/loi/ajvr

Rodríguez JL, Poveda JB, Rodríguez F, Espinosa de los Monteros A, Ramírez AS, Fernández A, 1996. Ovine infectious keratoconjunctivitis caused by Mycoplasma agalactiae. Small Ruminant Research, 22(1):93-96; 19 ref.

Romano R, Buonavoglia D, Montagna CO, Tempesta M, Buonavoglia C, 1995. Use of an ELISA to detect antibodies to Mycoplasma agalactiae in ovine serum samples. Acta Medica Veterinaria, 41(1/2):75-80; 7 ref.

Rosati S, Robino P, Fadda M, Pozzi S, Mannelli A, Pittau M, 2000. Expression and antigenic characterization of recombinant Mycoplasma agalactiae P48 major surface protein. Veterinary Microbiology, 71(3/4):201-210; 24 ref.

Sanchis R, Abadie G, Lambert M, Cabasse E, Dufour P, Guibert J-M, Pépin M, 2000. Inoculation of lactating ewes by the intramammary route with Mycoplasma agalactiae: comparative pathogenicity of six field strains. Veterinary Research, 31:329-337.

Sanchis R, Abadie G, Lambert M, Cabasse E, Guibert J-M, Calamel M, Dufour P, Vitu C, Vignoni M, Pépin M, 1998. Experimental conjunctival-route infection with Mycoplasma agalactiae in lambs. Small Ruminant Research, 27:31-39.

Santis Pde, Bashiruddin JB, Tittarelli M, Visaggio MC, Gianvincenzo D, 1999. Mycoplasmas in a problem flock of sheep with contagious agalactia. In: Stipkovits L, Rosengarten R, Frey J, eds. COST 826 Agriculture and biotechnology. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics. Vol III. Luxembourg, Germany: Office for official publications of the European Communities, 124-126.

Schnee C, Schulsse S, Hotzel H, Ayling RD, Nicholas RAJ, Schubert E, Heller M, Ehricht R, Sachse K, 2012. A novel rapid DNA microarray assay enables identification of 37 Mycoplasma species and highlights multiple Mycoplasma infections. PLoS ONE, 7(3):e33237. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0033237

Sikdar A, Uppal PK, 1996. Antibiogram of respiratory mycoplasmas of caprine and ovine origin. Indian Journal of Animal Health, 35(2):185-187; 4 ref.

Singh N, Rajya BS, Mohanty GC, 1974. Granular vulvovaginitis (GVV) in goats associated with Mycoplasma agalactiae. Cornell Veterinarian, 64: 435-442.

Singh N, Rajya BS, Mohanty GC, 1975. Pathology of Mycoplasma agalactiae induced granular vulvovaginitis (GVV) in goats. Cornell Veterinarian, 65:363-373.

Sirand-Pugnet P, Lartigue C, Marenda M, Jacob D, Barré A, Barbe V, Schenowitz C, Mangenot S, Couloux A, Segurens B, Daruvar Ade, Blanchard A, Citti C, 2007. Being pathogenic, plastic, and sexual while living with a nearly minimal bacterial genome. PLoS Genetics, 3(5):e75.

Solsona M, Lambert M, Poumarat F, 1996. Genomic, protein homogeneity and antigenic variability of Mycoplasma agalactiae. Veterinary Microbiology, 50(1/2):45-58; 43 ref.

Subramaniam S, Bergonier D, Poumarat F, Capaul S, Schlatter Y, Nicolet J, Frey J, 1998. Species identification of from Mycoplasma bovis and Mycoplasma agalactiae based on the uvrC genes by PCR. Molecular and Cellular Probes, 12:161-169.

Tardy F, Baranowski E, Nouvel LX, Mick V, Manso-Silvàn L, Thiaucourt F, Thébault P, Breton M, Sirand-Pugnet P, Blanchard A, Garnier A, Gibert P, Game Y, Poumarat F, Citti C, 2012. Emergence of atypical Mycoplasma agalactiae strains harboring a new prophage and associated with an alpine wild ungulate mortality episode. Applied and Environmental Microbiology, 78(13):4659-4668. http://aem.asm.org/content/78/13/4659.abstract

Tola S, Angioi A, Rocchigiani AM, Idini G, Manunta D, Galleri G, Leori G, 1997. Detection of Mycoplasma agalactiae in sheep milk samples by polymerase chain reaction. Veterinary Microbiology, 54(1):17-22; 15 ref.

Tola S, Idini G, Manunta D, Galleri G, Angioi A, Rocchigiani AM, Leori G, 1996. Rapid and specific detection of Mycoplasma agalactiae by polymerase chain reaction. Veterinary Microbiology, 51(1/2):77-84; 22 ref.

Tola S, Idini G, Rocchigiani AM, Manunta D, Angioi PP, Rocca S, Cocco M, Leori G, 1999. Comparison of restriction pattern polymorphism of Mycoplasma agalactiae and Mycoplasma bovis by pulsed field gel electrophoresis. Journal of Veterinary Medicine. Series B, 46(3):199-206; 19 ref.

Tola S, Idini G, Rocchigiani AM, Rocca PP, Manunta D, Leori G, 2001. A physical map of the Mycoplasma agalactiae strain PG2 genome. Veterinary Microbiology, 80:121-130.

Tola S, Manunta D, Cocco M, Turrini F, Rocchigiani AM, Idini G, Angioi A, Leori G, 1997. Characterization of membrane surface proteins of Mycoplasma agalactiae during natural infection. FEMS Microbiology Letters, 154(2):355-362; 21 ref.

Tola S, Manunta D, Rocca S, Rocchigiani AM, Idini G, Angioi PP, Leori G, 1999. Experimental vaccination against Mycoplasma agalactiae using different inactivated vaccines. Vaccine, 17(22):2764-2768; 20 ref.

Toshkov AS, Shirova L, Mihailova L, Shabanov M, 1975. Studies on the infection and immunization process in Mycoplasmoses. V. Experimental infection with Mycoplasma agalactiae in lambs. Acta Microbiol. Virol. Immunol., 2:42-47.

Tsaknakes E, Kontos P, Mpouptze E, Mega A, Sarres K, 1992. Epidemiological studies on contagious agalactia in sheep and goats in Chalkidiki, northern Greece. Deltion tes Ellenikes Kteniatrikes Etaireias = Bulletin of the Hellenic Veterinary Medical Society, 43(4):250-254; 18 ref.

Wang D, Zhang LC, Liu ZX, Yao JL, Huang ZC, Wu FD, 1988. Identification of Mycoplasma agalactiae using an indirect surface immunofluorescent antibody test. Chinese Journal of Veterinary Medicine, 14(10):4-6; 12 ref.

Weisburg WG, Tully JG, Rose DL, Petzel JP, Oyaizu H, Yang D, Mandelco L, Sechrest J, Lawrence TG, Etten Jvan, Maniloff J, Woese CR, 1989. A phylogenetic analysis of the mycoplasmas: basis for their classification. Journal of Bacteriology, 171(12):6455-6467; 50 ref.

Wiele Avan de, 1994. Management of an outbreak of contagious agalactia in Ossau Valley. épidémiologie et Santé Animale, No. 26:17-28.

Windsor GD, Bashiruddin JB, 2000. Coloured colonies of mycoplasmas frequently isolated from ruminants on solid agar medium. In: Bergonier D, Berthelot X, Frey J, eds. COST 826 Agriculture and biotechnology Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics, Vol. 4. EUR 19245 EN Luxembourg, 239-241.

Woodhead V, Morgan KL, 1993. Identification and analysis of the risk of contagious agalactia being introduced into the UK. Society for Veterinary Epidemiology and Preventive Medicine: Proceedings of a meeting held at the University of Exeter, March 31st- April 2nd 1993., 48-60; 24 ref.

Woubit S, Manso-Silván L, Lorenzon S, Gaurivaud P, Poumarat F, Pellet MP, Singh VP, Thiaucourt F, 2007. A PCR for the detection of mycoplasmas belonging to the Mycoplasma mycoides cluster: application to the diagnosis of contagious agalactia. Molecular and Cellular Probes, 21(5-6):391-399.

Zavagli V, 1951. L'agalactie contagieuse des brebis et des chèvres. Bulletin Office International des Epizooties, 36:336-362.

Ziv, et al. , 1983. Clinical pharmacology of tiamulin in ruminants. Journal Veterinary Pharmacological Therapy, 6:23-32.

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