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Overview of Contagious Agalactia

By Robin A. J. Nicholas, MSc, PhD, FRCPath, Animal Health and Veterinary Laboratories Agency, United Kingdom

First recognized in Italy more than 200 years ago, contagious agalactia is primarily a disease of dairy sheep and goats and is characterized by an interstitial mastitis leading to a loss of milk production, arthritis, and infectious keratoconjunctivitis. It is more often seen on farms practicing traditional husbandry. Contagious agalactia is principally caused by the wall-less bacterium Mycoplasma agalactiae, but in recent years, M mycoides capri (Mmc; formerly known as LC), and, to a lesser extent, M capricolum capricolum (Mcc) and M putrefaciens have also been isolated from goats with mastitis, arthritis, and occasionally, respiratory disease. The clinical signs of these infections are sufficiently similar to those of contagious agalactia for the OIE to include them as causes of this listed disease.

Etiology and Epidemiology:

Mycoplasmas that cause contagious agalactia can persist for >1 yr after clinical recovery of infected animals, which are the main reservoir of the organism. The introduction of such carriers into a susceptible flock can initially cause high morbidity and mortality. Once established in a herd, young ruminants become infected while suckling. Adults are contaminated via the milkers’ hands, milking machines, or possibly by bedding. Other routes of transmission may include aerosols of infective exudates over short distances and ingestion of contaminated water.

Sheep and goats are equally susceptible to M agalactiae, but goats are additionally susceptible to Mcc, Mmc, and M putrefaciens. However these mycoplasmas may be found in both animal species in regions where they graze together. In general, clinical disease is more pronounced in goats. Antibodies to Mcc and Mmc have been detected in South American camelids, but no mycoplasmas have yet been isolated. Because alpacas, llamas, and vicunas develop polyarthritis, pneumonia, and pleuritis, it is likely that mycoplasmas may eventually be found. Mmc has also been isolated from cattle, although its role in disease in this species is not clear.

Contagious agalactia has been reported in many countries surrounding the Mediterranean, in particular Portugal, Spain, Greece, Italy, France, Turkey, Israel, and North Africa, as well as in many parts of the Middle East, most notably Iran, India, Mongolia, and parts of South America. Sporadic cases have been reported in the USA.

Clinical Findings and Lesions:

The incubation period ranges from 1 wk to 2 mo and can be followed by either an acute disease with fever, neurologic signs, and occasionally death or, more commonly, a subacute or chronic disease characterized by mastitis, arthritis, and infectious keratoconjunctivitis. The infection begins as an interstitial mastitis giving rise to a hot, swollen, and painful udder, followed by a sudden drop in the quantity and quality of milk production. The milk may appear discolored and granular, separating into watery and solid phases, or take on a thick, yellow consistency with milk clots obstructing the teat duct. After several days, the affected udder shrinks because of damage to secretory tissue. Abscesses within the udder and enlargement of the retromammary lymph nodes may also be seen. Generally the clinical condition improves after a few weeks, with partial restoration of udder function, but the quality of milk remains abnormal. In some cases, atrophy and fibrosis lead to permanent loss of milk production.

The acute syndrome may lead to abortion and weak lambs as a result of ingestion of infected milk or starvation brought about by reduced milk production. Arthritis can be seen in adults and the young who find it difficult to keep up with the flock; affected animals may be seen limping or sitting on their carpal joints because of the discomfort. In these animals, the joints are hot, swollen, and painful. Conjunctivitis presents as a discharge of clear exudates from the eyes, followed by corneal opacity, keratitis, purulent exudation, and occasionally ulceration and panophthalmitis. Severe cases may result in irreversible blindness. Necropsy often reveals generalized peritonitis among animals that die during the acute stage. The infected udder is grossly atrophic in either one or both halves. Microscopically, the chronic inflammatory reaction in the stroma shows increased fibrosis and a reduced number of glandular acini. Infected joint capsules are edematous, and the synovium may contain clumps of fibrin. Articular surfaces may be eroded and occasionally ankylosed. In early stages of keratitis, the cornea is edematous and infiltrated with leukocytes; later, abundant purulent exudate infiltrates both the cornea and the ciliary body.

M putrefaciens is common in milking goat herds in western France. It can be isolated from the milk of animals with or without clinical signs, and milk production is usually severely affected. The milk of affected animals has a characteristic smell of putrefaction.


When a flock is severely affected, clinical diagnosis is easy; the three major signs—mastitis, arthritis, and keratoconjunctivitis—are generally present, although rarely in the same animal. However, an acute form, in which there is septicemia without specific local signs, can confound the diagnosis.

Laboratory diagnosis is the only means of confirmation. Preferred samples from living animals include milk and udder secretions, joint fluid from arthritic cases, eye swabs from cases of ocular disease, and serum for antibody detection. The ear canal is a rich source of pathogenic mycoplasmas. Isolation of mycoplasmas from the blood during the brief mycoplasmaemia stage of the disease is rarely successful. Samples from dead animals should include udder and associated lymph nodes, joint fluid, lung tissue (at the interface between diseased and healthy tissue), and pleural or pericardial fluid. Samples should be kept moist and cool and sent promptly to a diagnostic laboratory. PCR tests, which can be performed directly on clinical samples, including milk, can be used to confirm the diagnosis.

Identification of the organism is usually achieved by the growth inhibition or immunofluorescence tests using hyperimmune rabbit antiserum and, increasingly, by PCR tests that can be performed directly on clinical samples, including milk, within hours. PCR, together with denaturing gradient gel electrophoresis, which can detect all causative mycoplasmas in a single reaction, has been described.

Detection of antibodies in serum by ELISA provides rapid diagnosis of disease but may not be very sensitive in chronically affected herds and flocks. Indirect ELISA, some commercially available, have been used routinely in control programs to screen herds for M agalactiae but less so for Mmc and Mcc. Immuno (Western) blotting can be used to confirm suspect ELISA results and can distinguish field infection from vaccine antibody. In areas believed to be free of contagious agalactia, it is usually necessary to isolate and identify the causative organism to confirm infection. Serologic tests are not widely available for M putrefaciens.

A number of other mycoplasmas such as M arginini, M bovigenitalium, and M bovis have occasionally been isolated from mastitic milk and joint fluids, but their role in disease is not known. M conjunctivae is a common cause of keratoconjunctivitis but does not affect the udder or joints. Other bacteria causing mastitis include staphylococci, streptococci, Escherichia coli, and Klebsiella; caprine arthritic encephalomyelitis virus and Erysipelothrix rhusiopathiae should also be considered in cases of arthritis.

Treatment, Control, and Prevention:

Regular laboratory monitoring of flocks/herds and replacement animals may help to prevent spread or introduction of disease and can be done on serum and/or milk (including bulk tank milk) by serology, culture, or PCR. Culling or isolation of infected animals is generally advised, because udder damage is considered permanent. When this is not possible, hygienic measures, such as improved milking hygiene and pasteurizing milk before feeding to the young, should be implemented.

Antibiotics that inhibit cell wall synthesis (eg, penicillins) are not effective against contagious agalactia. In vitro tests have shown that strains of M agalactiae are still sensitive to fluoroquinolones and macrolides. These can bring about clinical improvement, particularly if given early in the disease, but there is always the danger of promoting carrier animals. Resistance to tetracyclines has been reported for some strains of M agalactiae. The use of erythromycin and tylosin can destroy milk-producing tissue in small ruminants. In many disease-free countries and regions, a confirmed infected herd is always slaughtered.

In countries bordering the Mediterranean, 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; however, they do not prevent transmission of the mycoplasmas. Generally, the duration of immunity, particularly to the formalinized, inactivated vaccines that are used in Europe, is short. Vaccines containing two or three of the causative agents are now available, but published data on their effectiveness is scarce.

Zoonotic Risk:

There is no evidence that contagious agalactia is transmitted to people.