Introduction

• Cause: contagious bovine pleuropneumonia (CBPP) is caused by a bacterium called Mycoplasma mycoides subsp. mycoides Small Colony (MmmSCSC).
• Signs:
  • CBPP is characterized by nonspecific signs of fever, loss of appetite, depression and a drop in milk production, followed by respiratory signs, which may include coughing, purulent or mucoid nasal discharges, and rapid respiration.
  • Pregnant animals may abort the fetus or give birth to stillborn calves.
  • Severely affected cattle often die, typically within three weeks.
  • In calves up to six months of age respiratory signs of CBPP are less common and the primary sign is polyarthritis, especially of the carpal and tarsal joints, and resultant edema. Pain in the affected joint results in the animal being reluctant to move.
• Diagnosis:
  • Isolation and identification of MmmSC from clinical samples.
  • Polymerase Chain Reaction (PCR) based assays are commonly used for confirmation of the identity of the bacteria.
  • Less commonly older biochemical and serologic methods are used (growth inhibition, immunofluorescence, dot immunobinding on a membrane filter [MF-dot] test, agar gel immunodiffusion).
  • Post mortem investigation will reveal abnormalities within the chest cavity, including; gross pathologic lesions of the lung (often affecting only one lung),  the accumulation of a large volume of yellow fluid (often containing large fibrinous clots) and enlarged lymph nodes.
• Treatment:
  • Antibiotics of the tetracycline, macrolide and fluoroquinolone families can be effective in treatment; however in some cases the bacteria is not completely eliminated and subclinically infected carriers can develop.
• Prognosis:
  • The mortality rate of CBPP rate ranges from 10% to 80%, although mortality greater than 50% is rare unless in naïve herds.
  • Animals that recover are frequently weak and emaciated, and may remain chronically infected.
  • Euthanasia, on welfare grounds, should be considered for some cases.

Pathogenesis

Etiology

• The causative agent of CBPP is the bacterium MmmSC.
• Studies have shown that the disease originated in Europe in the 1700s and was spread to other continents during colonization.
• Molecular epidemiology studies have shown that there are two distinct subtypes; those isolated from European outbreaks (post 1980) and those isolated from African outbreaks.

Predisposing factors

General

• Subclinical bovine carriers with chronic infection can retain viable bacteria within sequestra in the lungs for up to two years. These carriers are a major source of infection as they can shed viable bacteria when they become stressed or immunosuppressed.
• Outbreaks usually begin as the result of animal movements and contact of an infected animal with a naive herd.

Pathophysiology

• The disease causing mechanisms are not well elucidated. Two of the main factors in the disease formation of CBPP are the capsular polysaccharide, galactan and the membrane protein, L-alpha-glycerophosphate oxidase (GlpO).
• Galactan has cytopathic and vaso-active effects and results in pulmonary edema, capillary thrombosis and collagen deposition.
• The membrane protein L-alpha-glycerophosphate oxidase (GlpO) plays central role in cytotoxicity by catalysing the oxidation of glycerol-3-phosphate, to release hydrogen peroxide (H2O2) which causes direct damage to cells and tissues and, in addition, triggers an inflammatory response.

Timecourse

• Under natural conditions the incubation period of the disease is usually 1–4 months, but can be longer.

Epidemiology

• The main form of transmission of MmmSC is through respiratory aerosols and close, repeated contact is generally required for infection. However, MmmSC might be spread over longer distances (up to 200 meters) under favourable climatic conditions.
• The organism also occurs in saliva, urine, fetal membranes and uterine discharges.
• Subclinical carriers with chronic infection can retain viable bacteria within sequestra (lesions) in the lungs for up to two years. These carriers are a major source of infection as they can shed viable bacteria when they become stressed or immunosuppressed.

Diagnosis

Treatment

Prevention

Outcomes