Contagious Agalactia and Other Mycoplasmal Mastitides of Small Ruminants: Introduction

Known for nearly 200 years, contagious agalactia is primarily a disease of dairy sheep and goats. In lactating female animals, it is characterized by mastitis. Males, young animals, and nonlactating females develop arthritis, keratoconjunctivitis, and respiratory problems. Pregnant females can abort. It is mainly caused by Mycoplasma agalactiae but in recent years, M capricolum capricolum (Mcc), M mycoides mycoides LC (Mmm LC), and M putrefaciens have also been isolated in many countries. The clinical signs of these infections are sufficiently similar to those of contagious agalactia for the OIE to include them as causes of this list B disease.

Etiology and Epidemiology:

Sheep and goats are equally susceptible to M agalactiae , but goats are additionally affected by Mcc, Mmm LC, and M putrefaciens . Reports from north Africa indicate that Mcc may also be a problem in sheep. In general, clinical disease is more pronounced in goats. Antibodies to Mmm LC and Mcc have been detected in South American camelids, but no mycoplasmas have yet been isolated. As alpacas, llamas, and vicunas develop polyarthritis, pneumonia, and pleuritis, it is likely that mycoplasmas may eventually be found. Mmm LC have also been isolated from cattle, although its role in disease in this species is not clear.

Contagious agalactia has been reported in southern Europe, in particular France, Portugal, Spain, Greece, and Italy; Turkey and many parts of the Middle East; India; USA; South America; and north central, and eastern Africa. Recently Mmm LC has also been reported in arthritic goats and cattle in New Zealand and in goat kids with polyarthritis in Hungary.

The disease predominantly affects milking sheep and goats. It often appears in a herd soon after lactation begins in the spring, and probably represents the activation of latent infection. Young ruminants become infected directly while suckling; adults are contaminated via the milker’s hands, milking machines, or by bedding, which often provides a rich source of mycoplasmas. Transmission by aerosol in infective exudates over short distances and ingestion of contaminated water may also lead to infection. Organisms can persist for >1 yr after clinical recovery in infected animals. The introduction of such carriers into a susceptible flock can cause high morbidity (30-60%) and mortality, especially in lambs and kids (40-70%).

M putrefaciens is common in milking goat herds in western France where it can be isolated from animals with and without clinical signs, although milk production is usually severely affected. It has also been associated with a large outbreak of mastitis and agalactia leading to severe arthritis in goats accompanied by abortion and death in California. M putrefaciens was the major finding in an outbreak of polyarthritis in kids in Spain.

Clinical Findings and Lesions:

The course of disease is more likely to be chronic with M agalactiae , while in goats, Mmm LC, Mcc, and M putrefaciens usually produce acute or hyperacute infection, often with respiratory complications. Animals in the early acute stage of disease show a general malaise that corresponds to septicemia. In <1 wk, animals can become hyperthermic (>41°C), prostrated, and show inappetence. Pregnant females near term may abort. While some animals die without showing any other signs, most develop severe mastitis followed by arthritis and keratitis. An unusual feature of outbreaks caused by M putrefaciens is the lack of fever in affected does and kids.

The main target organ of contagious agalactia is the mammary gland, in which a fall in or complete loss of milk production, sometimes within 2-3 days, can be seen. The milk may appear yellow and granular and take on a thick consistency with milk clots that may obstruct the teat duct. The causative mycoplasmas can be isolated from milk when mastitis is present. The udder may become hot, swollen, and tender. In the later stages, the udder atrophies due to extensive fibrosis of the secretory tissue. The severity of arthritis/polyarthritis may range from joint stiffness to severe lameness in which joints—typically the tarsus, carpus, and hock—are swollen with accumulations of synovial fluid. This fluid can be a rich source of specific antibody (often at a higher titer than in the serum) and the causative mycoplasmas themselves. Ocular lesions begin with conjunctivitis and congestion, lacrimation, and photophobia, followed by vascularization of the cornea, inflammatory foci, and parenchymatous keratitis. Severe cases can lead to blindness. Pneumonia has also been reported in cases of contagious agalactia, especially in young animals in which it may represent the only external sign.

Diagnosis:

Clinical diagnosis in a severely infected flock is easy as the 3 major signs—mastitis, arthritis, and keratoconjunctivitis—are present within a flock, though rarely in the same animal. However, an acute form, in which there is septicemia without specific local signs, can confuse the diagnosis.

Laboratory diagnosis is the only means of confirmation. Preferred samples from living animals include nasal swabs and secretions, milk from mastitic does or from apparently healthy does when there is a high rate of mortality and morbidity in kids, joint fluid from arthritic cases, eye swabs from cases of ocular disease, and blood for antibody detection from affected and nonaffected animals. The ear canal is a rich source of pathogenic mycoplasmas. Mycoplasmas may be isolated from blood during the acute stage of the disease. 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.

Detection of antibodies in serum by complement fixation test or ELISA provides rapid diagnosis but may not be very sensitive in chronically affected herds and flocks. Indirect ELISA, some of which are commercially available, have been used routinely in control programs to screen herds for M agalactiae but less so for Mmm LC and Mcc. Confirmation of infection by isolation and identification is usually necessary in areas believed to be free of contagious agalactia. Serologic tests are not widely available for M putrefaciens .

A number of other mycoplasmas such as M arginini , M serogroup 11 , and M bovis have occasionally been isolated from mastitic milk, eye swabs, and joint fluids, but their pathogenicity is unknown. 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:

Antibiotics, such as the penicillins, that inhibit cell wall synthesis are not effective against contagious agalactia. Tetracyclines and macrolides can sometimes bring about clinical improvement, but there is always the danger of creating inapparent carriers. Furthermore, erythromycin and tylosin can cause destruction of milk-producing tissue in small ruminants. In many disease-free countries and regions, a confirmed infected herd would be slaughtered.

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.

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. New developments with recombinant vaccines and improved adjuvants may eventually help to improve control.