Mycoplasma Polyarthritis in Goats

Evelyn MacKay

■ Definition and Etiology Mycoplasma are small bacteria without a cell wall responsible for a multitude of diseases affecting domestic ruminant herds worldwide.

■ Clinical Signs and Differential Diagnoses Incuba­tion period can range from a few days to weeks, depending on species, management practices, and environmental factors. Initial signs of infection in kids include fever, lethargy, anorexia, and weakness.⁵ Polyarthritis, keratoconjunctivitis, and pneu­monia develop following initial bacteremia.⁶ Meningitis and sudden death have been reported in some outbreaks.⁷ Polyar­thritis most commonly occurs in the carpal and tarsal joints; multiple joints often become warm, swollen, and painful.^3,5 Differential diagnoses include environmental organisms coloniz­ing the joints after bacteremia.

Clinical signs in does include alterations in the appearance of milk, agalactia or drop in milk production, supramammary lymphadenopathy, fibrosis of the mammary gland, fever, anorexia, and lethargy.¹ Agalactia and mastitis of does must be differentiated from other causative agents of mastitis, including environmental coliforms, S. aureus, fungal organ­isms, and caprine arthritis encephalitis virus. Adults may also develop polyarthritis, keratoconjunctivitis, and pneumonia, and infection is not limited to females. Mycoplasma can colonize the reproductive tract and has been isolated from abortions and semen.^3,9 Infected herds may have decreased reproductive performance.²

■ Clinical Pathology and Diagnosis Hematologic changes are variable and may depend on severity of disease and Mycoplasma species. Changes in experimentally infected kids included leukopenia, decreased erythrocyte count, throm­bocytopenia, decreased clotting factors, and increased clotting times consistent with disseminated intravascular coagulation.¹⁰ Total protein and albumin concentrations may be decreased in infected animals.⁶ Arthrocentesis will reveal a fibrinosup- purative arthritis.¹ Culture can be obtained from synovial fluid or milk, which requires special medium and extended time intervals for growth. M. agalactiae colonies typically resemble a “fried egg” on agar.

In endemic areas, a presumptive diagnosis may be based on clinical signs. Antemortem diagnosis can be made with samples of milk, blood, urine, and auricular, nasal, and ocular secretions.³ Species and subspecies differentiation can be challenging, and techniques used include serology and molecular diagnostics such as PCR and genome sequencing.¹¹ Biochemical tests are not useful due to extreme similarity between species.

■ Pathophysiology and Epidemiology Infection of kids usually occurs through ingestion of infected milk and colostrum from the doe or supplemented bovine milk in the case of M. bovis.¹ Disease may also spread via oral and nasal secretions of infected animals or contaminated milking equip­ment.³ Polyarthritis develops after systemic bacteremia. Strain virulence, immune and nutritional status of animals, and environmental factors all play a role in severity and spread of the disease. Morbidity is often high, but mortality varies greatly. An asymptomatic carrier introduced into the herd is often responsible for outbreaks. Disease occurs in wild ruminants, and they may represent a reservoir for transmission to domestic animals.²

■ Necropsy Findings Affected joints are swollen with decreased range of motion. Fibrin deposits and hemorrhage of the articular cartilages can be seen.¹ Microscopically, neu­trophils and mononuclear cells infiltrate the synovium.⁵ Gross pulmonary lesions may include diffuse interstitial pneumonia, bronchopneumonia, fibrinous pleuritis, or a combination of lesions.^5,12 Microthrombi may be present diffusely in vasculature, and microabscesses may be found in the spleen and kidney.¹⁰

■ Treatment and Prognosis Mortality and morbidity vary based on the isolate but can climb above 90% in kids. An outbreak in a dairy resulted in the euthanasia of 700 goats.⁷ Treatment is often unrewarding, and resources may be best directed toward prevention and control of infection. As Mycoplasma lack a cell wall, treatment with antimicrobials that disrupt cell wall synesthesia are ineffective. Antimicrobials used include tetracyclines, macrolides, fluoroquinolones, and flor- fenicol. There is evidence of existing resistance to antimicrobials, and even susceptible isolates may not be eliminated with appropriate antimicrobial therapy.² Damage to joints may be permanent and crippling by the time antimicrobial therapy is initiated.

■ Prevention and Control A closed herd with careful screening of new animals is the best method to prevent infection. Recommended screening strategies include PCR or culture of ear swabs; serology may be performed, but asymptomatic carriers are often negative.^2,9 Hygienic milking practices help reduce spread between does, and sanitization of supplies and housing is recommended. Feeding of colostrum and milk replacers reduce likelihood of transmission to kids, though pasteurization will reduce mycoplasma numbers.² Culling of affected animals or complete depopulation of herds has been used in control efforts.^7,11 Killed and attenuated live vaccines exist and have shown efficacy in reducing clinical signs and shedding, but these are not commercially available in the United States.¹³