Contagious caprine pleuropneumonia (CCPP) is an important and distinct disease limited to goats in certain areas of the world. Similar clinical signs may occur with infection by other species of Mycoplasma worldwide. These organisms may be responsible for severe pneumonia outbreaks in goat herds. Polyarthritis, mastitis, neurologic signs, high fever, and sudden death may accompany signs of respiratory disease or may be the dominant clinical signs of Mycoplasma infection.
Etiology of Mycoplasma Pneumonias in Goats
Contagious caprine pleuropneumonia is a severe and highly fatal disease that is due to Mycoplasma capricolum capripneumoniae, or Mccp(previously Mycoplasma biotype F38), in areas of Africa, Asia, and the Middle East. In naive herds, morbidity is often 100%, and mortality may reach 80%.
Mycoplasma capricolum capripneumoniae is related to the causative agent of contagious bovine pleuropneumonia Contagious Bovine Pleuropneumonia Contagious bovine plueuropneumonia is highly contagious and generally accompanied by pleurisy. It is present in Africa, with minor outbreaks occurring in the Middle East. The USA has been free... read more (CBPP), Mycoplasma mycoidesmycoides (previously referred to as the small colony, Mmm SC, or SC variant). There are many other closely related species, such as Mycoplasma capricolumcapricolum and members of the Mycoplasma mycoides cluster, including M mycoidescapri (previously M mycoidesmycoides large colony type, or Mmm LC) that can produce similar lesions. Mycoplasma agalactia, Mycoplasma bovis, Mycoplasma ovipneumoniae, Mycoplasma putrefaciens, and Mycoplasma conjunctivae are also capable of producing disease in goats, including respiratory disease, polyarthritis, conjunctivitis, and mastitis. Clinical signs and isolates vary by geography and husbandry, but they affect goat herds worldwide.
Contagious caprine pleuropneumonia is transmitted via aerosol droplets. Although goats are the primary host, infection of sheep and wild ruminants has been documented. carriers are thought to be uncommon but possible sources of disease transmission.
Other Mycoplasma spp are transmitted through the milk of infected does (or via infected supplemental cow's milk in the case of M bovis), aerosol droplets, and respiratory secretions.
Clinical Findings of Mycoplasma Pneumonias in Goats
In CCPP, weakness, anorexia, cough, tachypnea, and nasal discharge, accompanied by fever (40.5°–41.5°C [104.5°–106°F]), are typical. Exercise intolerance progresses to respiratory distress, with open-mouth breathing and frothy salivation. Sudden death without obvious respiratory signs may develop after septicemia in a minority of cases; however, unlike other Mycoplasma spp, disease is typically limited to the respiratory tract.
On postmortem examination, there is typically appreciable straw-colored pleural effusion and acute fibrinous pneumonia. Consolidation is sometimes confined to one lung. The distention of interlobular septa by serofibrinous fluid, commonly observed in infections that are due to M mycoides capri, is rarely evident in CCPP. In antimicrobial-treated or recovered animals, a sequestrum similar to that observed in CBPP may develop.
Lethargy, anorexia, cough, tachypnea, fever, and nasal discharge may accompany clinical signs of other body systems with other Mycoplasma spp. Polyarthritis and respiratory disease in kids, plus agalactia as a result of mastitis in does, are the typical triad of signs in other Mycoplasma outbreaks in goat herds. Less frequently, neurologic signs and sudden death may be clinical signs of infection.
In addition to nonspecific clinical signs of inflammation, dehydration, and sepsis, changes in hematologic and serum biochemical parameters may include alterations in the WBC count, thrombocytopenia, and decreased total protein concentration. Postmortem findings may reveal pleuropneumonia similar to CCPP, bronchopneumonia, or interstitial pneumonia. Evidence of septicemia (microthrombi, hemorrhages, and microabscesses) as well as inflammation of the joints, nervous system, or mammary glands in adults may be present.
Diagnosis of Mycoplasma Pneumonias in Goats
The clinical signs, epidemiological characteristics, and necropsy findings may be enough to establish a diagnosis in endemic areas for CCPP and other Mycoplasma spp outbreaks. The causative organism should be isolated and identified for definitive diagnosis; however, isolation may be difficult, and special media and extended incubation times are required for culture of Mycoplasma spp. PCR assay, which can be performed directly on the pleural fluid or affected lung, has greatly facilitated the diagnosis of CCPP. PCR assays of milk, nasal swabs, otic swabs, or tissue may be helpful for the diagnosis of other infections caused by Mycoplasma spp. Serologic tests include complement fixation, passive hemagglutination, and ELISA; the latex agglutination test can be done in the field directly on whole blood as well as on serum samples in the laboratory. These tests are best used for herd-level surveillance rather than diagnosis of acute cases. Serologic cross-reactions may occur, and differentiation of closely related species can be difficult.
Control of Mycoplasma Pneumonias in Goats
Quarantine of affected flocks and strict biosecurity protocols for introduction of new animals are necessary to limit transmission and losses due to CCPP and other Mycoplasma spp. Vaccines are available in some countries, and good to excellent protection has been reported. Macrolides, tetracyclines, fluoroquinolones, and florfenicol may successfully treat Mycoplasma infections if administered early in the course of disease. Tylosin (10 mg/kg, IM, every 24 hours for 3 days) or oxytetracycline (15 mg/kg, IM, every 24 hours for 3 days) is effective in the treatment of CCPP.
Contagious caprine pleuropneumonia is a severe, infectious disease with high morbidity and mortality rates that can cause important economic losses in goat herds in endemic areas.
Other Mycoplasma spp can cause pneumonia outbreaks and affect the production of sheep and goat herds worldwide.
Accurate diagnosis, strict biosecurity, and prompt treatment are essential for decreasing disease transmission and herd losses.