Mycoplasma agalactiae infections
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PicturesTop of page
IdentityTop of page
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
OverviewTop of page
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).
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 AffectedTop of page
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).
DistributionTop of page
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 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.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease not reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||Disease never reported||OIE, 2009|
|Bhutan||No information available||OIE, 2009|
|Cambodia||No information available||OIE, 2009|
|China||No information available||NULL||Wang et al., 1988; OIE, 2009|
|-Hong Kong||No information available||OIE, 2009|
|-Xinjiang||Present||Wang et al., 1988|
|India||Disease never reported||NULL||Konsam et al., 1989; Sikdar and Uppal, 1996; OIE, 2009|
|Indonesia||Disease not reported||OIE, 2009|
|Iran||Present||NULL||OIE, 2000; OIE, 2009|
|Iraq||No information available||NULL||AlGraibawi et al., 1989; OIE, 2009|
|Israel||Disease not reported||200803||OIE, 2000; OIE, 2009|
|Japan||Disease not reported||OIE, 2009|
|Jordan||Disease never reported||OIE, 2009|
|Kazakhstan||Disease not reported||OIE, 2009|
|Korea, Republic of||No information available||OIE, 2009|
|Kuwait||Disease not reported||OIE, 2009|
|Kyrgyzstan||Disease not reported||OIE, 2009|
|Laos||Disease never reported||OIE, 2009|
|Malaysia||Disease not reported||OIE, 2009|
|Mongolia||Present||NULL||Damdinsuren Ch, 1989; OIE, 2009|
|Myanmar||Disease never reported||OIE, 2009|
|Nepal||No information available||OIE, 2009|
|Oman||Disease not reported||OIE, 2009|
|Pakistan||Disease not reported||OIE, 2009|
|Philippines||Disease never reported||OIE, 2009|
|Qatar||Absent, reported but not confirmed||OIE, 2009|
|Saudi Arabia||Disease not reported||OIE, 2009|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||Disease not reported||OIE, 2009|
|Tajikistan||Disease not reported||OIE, 2009|
|Thailand||No information available||OIE, 2009|
|Turkey||No information available||NULL||Otlu et al., 1997; OIE, 2009|
|United Arab Emirates||No information available||OIE, 2009|
|Vietnam||Disease never reported||OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease not reported||NULL||Belaid et al., 1990; OIE, 2009|
|Angola||No information available||OIE, 2009|
|Benin||No information available||OIE, 2009|
|Botswana||Disease not reported||OIE, 2009|
|Burkina Faso||No information available||OIE, 2009|
|Cameroon||Present||Martrenchar et al., 1995|
|Chad||No information available||OIE, 2009|
|Congo||No information available||OIE, 2009|
|Djibouti||Disease not reported||OIE, 2009|
|Egypt||Disease never reported||OIE, 2009|
|Eritrea||Present||NULL||OIE, 2000; OIE, 2009|
|Ethiopia||No information available||OIE, 2009|
|Gabon||No information available||OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||Disease never reported||OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||No information available||OIE, 2009|
|Lesotho||Disease not reported||OIE, 2009|
|Madagascar||Disease never reported||OIE, 2009|
|Malawi||No information available||OIE, 2009|
|Mali||No information available||OIE, 2009|
|Mauritius||Disease never reported||OIE, 2009|
|Morocco||No information available||OIE, 2009|
|Mozambique||Disease not reported||OIE, 2009|
|Namibia||No information available||OIE, 2009|
|Nigeria||Disease never reported||OIE, 2009|
|Rwanda||No information available||OIE, 2009|
|Senegal||No information available||OIE, 2009|
|South Africa||Disease never reported||OIE, 2009|
|Sudan||Disease not reported||OIE, 2009|
|Swaziland||Disease not reported||OIE, 2009|
|Tanzania||No information available||OIE, 2009|
|Togo||No information available||OIE, 2009|
|Tunisia||Disease not reported||OIE, 2009|
|Uganda||No information available||OIE, 2009|
|Zambia||No information available||OIE, 2009|
|Zimbabwe||Disease never reported||OIE, 2009|
|Canada||Disease never reported||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease never reported||OIE, 2009|
|USA||Restricted distribution||OIE, 2009|
Central America and Caribbean
|Belize||Disease not reported||OIE, 2009|
|Costa Rica||Disease never reported||OIE, 2009|
|Cuba||Disease never reported||OIE, 2009|
|Dominican Republic||Disease never reported||OIE, 2009|
|El Salvador||Disease never reported||OIE, 2009|
|Guadeloupe||No information available||OIE, 2009|
|Guatemala||Disease never reported||OIE, 2009|
|Haiti||No information available||OIE, 2009|
|Honduras||No information available||OIE, 2009|
|Jamaica||Disease never reported||OIE, 2009|
|Martinique||No information available||OIE, 2009|
|Nicaragua||Disease never reported||OIE, 2009|
|Panama||No information available||OIE, 2009|
|Argentina||Disease never reported||OIE, 2009|
|Bolivia||No information available||OIE, 2009|
|Brazil||Disease not reported||OIE, 2009|
|Chile||Disease not reported||OIE, 2009|
|Colombia||Disease never reported||OIE, 2009|
|Ecuador||Disease never reported||OIE, 2009|
|French Guiana||No information available||OIE, 2009|
|Peru||Disease never reported||OIE, 2009|
|Uruguay||Disease never reported||OIE, 2009|
|Venezuela||Disease never reported||OIE, 2009|
|Albania||Present||NULL||OIE, 2000; OIE, 2009|
|Austria||No information available||OIE, 2009|
|Belarus||Disease not reported||OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Bulgaria||Disease not reported||2000||OIE, 2000; OIE, 2009|
|Croatia||Disease not reported||OIE, 2009|
|Czech Republic||Disease not reported||OIE, 2009|
|Denmark||Disease never reported||OIE, 2009|
|Estonia||Disease never reported||OIE, 2009|
|Finland||Disease never reported||OIE, 2009|
|France||No information available||NULL||Wiele Avan de, 1994; Bergonier et al., 1997; OIE, 2009|
|Germany||Disease never reported||OIE, 2009|
|Greece||Restricted distribution||NULL||Tsaknakes et al., 1992; Petsaga-Tsimperi and Sarris, 1997; OIE, 2009|
|Hungary||Disease not reported||2003||Bajmócy et al., 1998; OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease never reported||OIE, 2009|
|Italy||Present||NULL||Montagna and Goffredo, 1989; Brajon et al., 1991; OIE, 2009|
|Latvia||Disease never reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease never reported||OIE, 2009|
|Luxembourg||Disease never reported||OIE, 2009|
|Macedonia||Absent, reported but not confirmed||NULL||Cokrevski et al., 2001; OIE, 2009|
|Malta||Disease not reported||OIE, 2009|
|Montenegro||Disease never reported||OIE, 2009|
|Netherlands||Disease never reported||OIE, 2009|
|Norway||Disease never reported||OIE, 2009|
|Poland||Disease never reported||OIE, 2009|
|Portugal||Absent, reported but not confirmed||OIE, 2009|
|Romania||Disease not reported||2004||OIE, 2000; OIE, 2009|
|Russian Federation||Disease never reported||OIE, 2009|
|Slovakia||Disease not reported||OIE, 2009|
|Slovenia||Disease not reported||OIE, 2009|
|Spain||Restricted distribution||NULL||Goncer and Rodríguez, 1990; Real et al., 1994; Pérez et al., 1996; Rodríguez et al., 1996; OIE, 2009|
|Sweden||Disease never reported||OIE, 2009|
|Switzerland||Disease not reported||199902||OIE, 2000; OIE, 2009|
|UK||Disease not reported||OIE, 2009|
|Ukraine||Disease never reported||OIE, 2009|
|Australia||Disease not reported||OIE, 2009|
|French Polynesia||Disease not reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease never reported||OIE, 2009|
PathologyTop of page
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.
DiagnosisTop of page
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.
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.
|Organism||Digitonin sensitivity||Urease activity||Glucose fermentation||Arginine hydrolysis||Phosphatase activity||Film & spots||Caseinolytic activity|
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).
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).
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/SignsTop of page
|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 CourseTop of page
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).
EpidemiologyTop of page
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: EconomicTop of page
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 SafetyTop of page
CA is not a zoonotic disease.
Disease TreatmentTop of page
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 ControlTop of page
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.
ReferencesTop of page
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