Contagious Caprine Pleuropneumonia

Contagious Caprine Pleuropneumonia is also known as Pleuropneumonia contagiosa and Abunini disease in animals.

Contagious Caprine Pleuropneumonia is a classical and contagious disease of goats resembles the contagious bovine pleuropneumonia. It develops pleuropneumonia in sheep and goats.

Etiology

Contagious Caprine Pleuropneumonia is caused by M. capricolum subspecies Capripneumoniae.

The causative agent is previously known as Mycoplasma strain F38. It is difficult to differentiate from M. mycoides subspecies Capri.

Mycoplasma mycoides subspecies Caprae, M. mycoides subspecies mycoides, M.galactiae, M. arginini and M. capricola have been considered as the principal cause of pleuropneumonia in kids upto 6 months.

Epidemiology

Prevalence of Infection

• It is widespread in tropical countries.
• Reported from Chennai, Assam, Mumbai, Haryana, Uttarpradesh, Bihar, West Bengal in India.
• It is a fatal disease of goats distributed in about 38 countries in Asia and Africa.
• Infectivity is high with a morbidityrate 100%.
• Mortality rate is f 60-100%.

Economic Impact

The direct losses of the disease result from its high mortality, reduced milk and meat yield, cost of treatment, control, disease diagnosis and surveillance. In addition to this, there are indirect losses due to the imposition of trade restrictions.

Source of infection

• By carrier or infected animals.
• Organism do not live long outside of animal body.

Transmission

• The disease spread through inhalation of organism present in soil and environment.
• The bot fly have been found to spread the infections.
• Experimental transmission is possible.

Host Affected

• Goats are highly susceptible when compared to sheep.
• Goat strain is not transmissible to cattle.

Pathogenesis

In animals with primary infection, the illness lasts for about two days and death ensues, while in other cases it may last several days.

The primary clinical signs are cough with animals tending to lie down or lag behind the flock.

Affected animals continue to graze for some time but eventually become anorexic, breathing becomes laboured with painful grunting and a rise in temperature up to 41°C.

Gradual respiratory signs progress and accelerated, painful, and is followed by severe cough. In the terminal cases, the animals are unable to move.

Affected animals have abducted legs, the stiff neck and extended downward. Saliva drools from mouth and nose is obstructed by mucopurulent discharge. The tongue protrudes and bleat distressingly.

In fully susceptible flocks that encounter an outbreak, morbidity is usually 100% and mortality is up to 70%.

The organism is reported to affect majorly the respiratory tract of goats.

In endemic areas subacute and chronic cases are common and the symptoms are milder, dominated by intermittent coughing.

Clinical Signs

Acute Form

• It is a highly fatal disease in sheep and goats.
• Mortality varies from 60-100%.
• Incubation period is about 6-10 days.
• Anorexia, dullness, depression, nasal discharge, abdominal respiration, fever and dry painful cough.
• Animal may die but no pathological changes in lungs.
• Nasal discharge is watery in early stage and turns to thick mucopurulent to white  in later stage.

Chronic Form

• Clinical signs are mostly similar to cattle CCPP restricted to the respiratory tract.
• Cough, dyspnoea, lagging behind, lying down a lot but the animal can stand and walk.
• Fever 40.5 ° C to 41.5 ° c (104-106)

Terminal stage: Mouth breathing, tongue protrusion and frothy salivation with death in two or more days. In adverse climatic conditions  disease occurs as septicemic with little signs or with evidence of pneumonia.

Necropsy Findings

Usual findings are similar to bovine but in caprine sequestra are not formed in the lungs.

Lesions are restricted to lungs and pleura with hepatization of part of the lung and increase in pleural fluid with a fibrinous pleuritis. The lesions may be confined with lung.

Diagnosis

• Based on clinical signs and necropsy findings.
• Interstitial interlobular septa seen.
• More effective detection is by PCR performed on samples of pleural fluid dried on filter paper.
• Detection of antigen from lung tissues. Pleural fluid has to be examined by PCR.
• Antibody detection by CFT, ELISA and Latex agglutination test.
• A blocking ELISA using monoclonal antibody is highly specific for detection of CCPP.
• Sample collection Mycoplasma are fragile and should be freeze dried and has to be a transported in time.
• Serum, lung tissues, pleural fluid, nasal discharges.

Differential Diagnosis

• Other pulmonary mycoplasmoses
• Chronic respiratory diseases

Treatment

• Oxytetracycline, rolitetracycline, chlortetracycline and tylosin.
• The organism is highly sensitive to Oxytetracycline 15mg/kg body weight /day.
• Tiamutin 36mg/kg body weight is satisfactory.
• Tylosin tartrate @ 10mg/kg body weight i/m along with cotrimaxazole tablet for 5-7 days for the treatment with alincomycin gave satisfactory result. 
• The macrolides (erythromycin, spiramysin, and tylosin), tetracyclines and quinolones are active against M. capricolum subspecies capripneumoniae.

Prevention

• Vaccine consists of live culture of M. caprae.
• Dose 0.2 ml at tip of the ear.
• Saponin killed lyophilised vaccine can be used for revaccination at 6 months interval.

Control

• Bio-security to prevent contact with infected animal is important.
• Vaccination with an inactivated mycoplasma F38 vaccine induces an immune response which is effective in reducing morbidity and mortality rates.
• A booster dose / month after the first vaccination provides an additional protection.
• Immunity is generally short lived.
• Maternal antibody may interfere with the development of immunity and kids born to does that have been vaccinated while pregnant should themselves not be vaccinated prior to 12 weeks of age.
• Control measures include prevention of mixing and good hygiene.
• Movement restrictions and slaughtering infected animals are recommended for countries that are newly infected.