Contagious Caprine Pleuropneumonia

Caused by Mycoplasma capricolum subsp. capricolum and occasionally M. mycoides subsp. capri or M. mycoides subsp. mycoides

• Occurs in Africa and Turkey
• Pneumonia, fibrinous pleurisy, pleural exudate, consolidated and emphysematous lungs
• Aerosol transmission; highly contagious

Health and Production Compendium

Selected sections for: contagious caprine pleuropneumonia Identity Pathogen/s Overview Distribution Distribution Table Hosts/Species Affected Host Animals Systems Affected List of Symptoms/Signs Epidemiology Zoonoses and Food Safety Pathology Diagnosis Disease Course Disease Treatment Table Disease Treatment Prevention and Control References Images

Datasheet Type(s): Animal Disease Identity

Preferred Scientific Name contagious caprine pleuropneumonia

International Common Names

English acronym CCPP

English contagious caprine pleuropneumonia, mycoplasma - exotic

Pathogen/s

Mycoplasma capricolum subsp. capripneumoniae

Overview The causative agent of contagious caprine pleuropneumonia (CCPP) is Mycoplasma capricolum subsp. capripneumoniae(Mccp), which was previously known by the strain name of its type species, F38. It is a member of the Mycoplasma mycoides cluster which includes M. mycoides subsp. mycoides SC (MmmSC), M. mycoides subsp. mycoides LC (MmmLC), M. mycoides subsp. capri (Mmc), M. capricolum subsp. capricolum (Mcca) and Mycoplasma species bovine group 7 (Bg7), an uncharacterized bovine isolate, which causes other diseases of ruminants. CCPP is a significant disease of goats in Africa, the Middle East and Western Asia, and is characterized primarily by its contagious nature. The disease causes interstitial, fibrinous pleuropneumonia, interlobular oedema and hepatization of the lung causing high mortality rates of up to 80%. Definite diagnosis is made by culture of the causative agent from lung samples or pleuritic fluid taken at postmortem. Liquid and solid mycoplasma media are inoculated and filtered subcultures from liquid medium may be required if there is evidence of bacterial contamination. Isolates may be identified by biochemical, immunological and molecular tests. Serological tests for the detection of specific antibodies have relied on the complement fixation test which is the test prescribed by the Office International des Epizooties (OIE) for international trade. A latex agglutination test is also available, and is used routinely in some parts of Africa.

History

CCPP is an infectious disease which affects only goats, and was first described in the late 19th century (Hutcheon, 1889; McMartin et al., 1980). Before the isolation and identification of Mycoplasma strain F38 by MacOwan (1976), and the subsequent demonstration of its causal relationship with CCPP (MacOwan and Minette, 1976), M. mycoides subsp. capri was considered to be the aetiological agent of CCPP (Edward, 1953; Jonas and Barber, 1969). So far M. capricolumsubsp. capripneumoniae is the only mycoplasma that fulfils Koch’s postulates for CCPP and is believed to be the sole cause of CCPP (MacOwan, 1984). Mycoplasma strain F38 has recently been reclassified and now all F38-like mycoplasmas are known as Mycoplasma capricolum subsp. capripneumoniae (Leach et al., 1993). This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's Handistatus database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.

Distribution Although a precise description of the distribution of CCPP is not available, the clinical disease has been reported in 30 countries mainly in Africa and Asia (Thiaucourt and Bölske, 1996). The only African countries where M. capricolum subsp. capripneumoniae has been isolated are Chad (Lefèvre et al., 1987a), Eritrea, Ethiopia (Thiaucourt et al., 1992), Kenya (MacOwan and Minette, 1976), Niger, Sudan (Harbi and El-Tahir, 1981), Tanzania (Kusiluka et al., 2000), Tunisia (Perreau et al., 1984), and Uganda (Bölske et al., 1995). In Asia and the Mediterranean, isolations have been reported in Oman (Jones and Wood, 1988), Turkey (Jones and Wood, 1988), the United Arab Emirates, and Yemen (Rurangirwa et al., 1987b). In Mali, goats have been suspected of infection based on serological evidence (Rurangirwa et al., 1990).

Distribution Table

Country Distribution Last Reported Origin First Reported Invasive References Notes ASIA Afghanistan No information available OIE, 2009

Armenia Disease not reported OIE, 2009

Azerbaijan Disease not reported OIE, 2009

Bahrain Present OIE, 2009

Bangladesh Disease not reported OIE, 2009

Bhutan No information available OIE, 2009

Brunei Darussalam Disease not reported OIE Handistatus, 2005

Cambodia No information available OIE, 2009

China Disease never reported OIE, 2009

-Hong Kong No information available OIE, 2009

Georgia (Republic of) Disease never reported OIE Handistatus, 2005

India Restricted distribution OIE, 2009

Indonesia Disease never reported OIE, 2009

Iran Present OIE, 2009

Iraq No information available OIE, 2009

Israel Disease never reported OIE, 2009

Japan Disease never reported OIE, 2009

Jordan Disease never reported OIE, 2009

Kazakhstan Disease not reported OIE, 2009

Korea, DPR Disease not reported OIE Handistatus, 2005

Korea, Republic of Disease never reported OIE, 2009

Kuwait Present OIE, 2009

Kyrgyzstan Disease not reported OIE, 2009

Laos No information available OIE, 2009

Lebanon Absent, reported but not confirmed OIE, 2009

Malaysia Disease not reported OIE, 2009

-Peninsular Malaysia Disease never reported OIE Handistatus, 2005

-Sabah Disease never reported OIE Handistatus, 2005

-Sarawak Disease never reported OIE Handistatus, 2005

Mongolia Disease not reported OIE, 2009

Myanmar Disease never reported OIE, 2009

Nepal Disease not reported OIE, 2009

Oman Present NULL OIE, 2009; Jones & Wood, 1988

Pakistan Present OIE, 2009

Philippines Disease never reported OIE, 2009

Qatar Disease not reported OIE, 2009

Saudi Arabia Disease not reported OIE, 2009

Singapore Disease never reported OIE, 2009

Sri Lanka Disease not reported OIE, 2009

Syria Disease not reported OIE, 2009

Taiwan Disease never reported OIE Handistatus, 2005

Tajikistan Disease not reported OIE, 2009

Thailand Disease never reported OIE, 2009

Turkey No information available OIE, 2009

Turkmenistan Disease not reported OIE Handistatus, 2005

United Arab Emirates No information available NULL OIE, 2009; Rurangirwa et al., 1987b

Uzbekistan Disease not reported OIE Handistatus, 2005

Vietnam Disease never reported OIE, 2009

Yemen No information available NULL OIE, 2009; Rurangirwa et al., 1987b

AFRICA Algeria Disease never reported OIE, 2009

Angola No information available OIE, 2009

Benin No information available OIE, 2009

Botswana Disease not reported OIE, 2009

Burkina Faso No information available OIE, 2009

Burundi Disease never reported OIE Handistatus, 2005

Cameroon Reported present or known to be present OIE Handistatus, 2005

Cape Verde Disease never reported OIE Handistatus, 2005

Central African Republic Disease not reported OIE Handistatus, 2005

Chad No information available NULL OIE, 2009; Lefevre et al., 1987a

Congo No information available OIE, 2009

Congo Democratic Republic No information available OIE Handistatus, 2005

Côte d'Ivoire Reported present or known to be present OIE Handistatus, 2005

Djibouti Disease not reported OIE, 2009

Egypt Disease never reported OIE, 2009

Eritrea Present NULL OIE, 2009; Thiaucourt et al., 1992

Ethiopia Present NULL OIE, 2009; Thiaucourt et al., 1992

Gabon No information available OIE, 2009

Gambia No information available OIE, 2009

Ghana No information available OIE, 2009

Guinea Disease never reported OIE, 2009

Guinea-Bissau No information available OIE, 2009

Kenya Restricted distribution NULL OIE, 2009; MacOwan & Minette, 1976

Lesotho Disease never reported OIE, 2009

Libya Reported present or known to be present OIE Handistatus, 2005

Madagascar Disease never reported OIE, 2009

Malawi No information available OIE, 2009

Mali No information available NULL OIE, 2009; Rurangirwa et al., 1990

Mauritius Disease never reported OIE, 2009

Morocco Disease never reported OIE, 2009

Mozambique Disease not reported OIE, 2009

Namibia No information available OIE, 2009

Niger Present Bloch & Diallo, 1991

Nigeria Disease never reported OIE, 2009

Réunion Disease never reported OIE Handistatus, 2005

Rwanda No information available OIE, 2009

Sao Tome and Principe Disease not reported OIE Handistatus, 2005

Senegal No information available OIE, 2009

Seychelles No information available OIE Handistatus, 2005

Somalia No information available OIE Handistatus, 2005

South Africa Disease never reported OIE, 2009

Sudan Disease not reported 200602 OIE, 2009; Harbi & El-Tahir, 1981

Swaziland Disease never reported OIE, 2009

Tanzania Present NULL OIE, 2009; Kusiluka et al., 2000

Togo No information available OIE, 2009

Tunisia Disease not reported 2000 OIE, 2009; Perreau et al., 1984

Uganda Disease not reported NULL OIE, 2009; Bölske et al., 1995

Zambia No information available OIE, 2009

Zimbabwe Disease not reported OIE, 2009

NORTH AMERICA Bermuda Disease not reported OIE Handistatus, 2005

Canada Disease never reported OIE, 2009

Greenland Disease never reported OIE, 2009

Mexico Disease never reported OIE, 2009

USA Disease never reported OIE, 2009

-Georgia Disease never reported OIE, 2009

CENTRAL AMERICA Barbados Disease never reported OIE Handistatus, 2005

Belize Disease never reported OIE, 2009

British Virgin Islands Disease never reported OIE Handistatus, 2005

Cayman Islands Disease not reported OIE Handistatus, 2005

Costa Rica Disease never reported OIE, 2009

Cuba Disease never reported OIE, 2009

Curaçao Disease not reported OIE Handistatus, 2005

Dominica Disease not reported OIE Handistatus, 2005

Dominican Republic Disease never reported OIE, 2009

El Salvador Disease never reported OIE, 2009

Guadeloupe No information available OIE, 2009

Guatemala Disease never reported OIE, 2009

Haiti Disease never reported OIE, 2009

Honduras No information available OIE, 2009

Jamaica Disease never reported OIE, 2009

Martinique Disease not reported OIE, 2009

Nicaragua Disease never reported OIE, 2009

Panama Disease never reported OIE, 2009

Saint Kitts and Nevis Disease never reported OIE Handistatus, 2005

Saint Vincent and the Grenadines CAB Abstracts data mining OIE Handistatus, 2005

Trinidad and Tobago Disease never reported OIE Handistatus, 2005

SOUTH AMERICA Argentina Disease never reported OIE, 2009

Bolivia No information available OIE, 2009

Brazil Disease never reported OIE, 2009

Chile Disease never reported OIE, 2009

Colombia Disease never reported OIE, 2009

Ecuador Disease never reported OIE, 2009

Falkland Islands Disease never reported OIE Handistatus, 2005

French Guiana Disease not reported OIE, 2009

Guyana Disease never reported OIE Handistatus, 2005

Paraguay Disease never reported OIE Handistatus, 2005

Peru Disease never reported OIE, 2009

Uruguay Disease never reported OIE, 2009

Venezuela Disease never reported OIE, 2009

EUROPE Albania No information available OIE, 2009

Andorra Disease not reported OIE Handistatus, 2005

Austria No information available OIE, 2009

Belarus Disease never reported OIE, 2009

Belgium Disease not reported OIE, 2009

Bosnia-Hercegovina Disease not reported OIE Handistatus, 2005

Bulgaria Disease never reported OIE, 2009

Croatia Disease never reported OIE, 2009

Cyprus Disease never reported OIE, 2009

Czech Republic Disease not reported OIE, 2009

Denmark Disease never reported OIE, 2009

Estonia Disease never reported OIE, 2009

Finland Disease never reported OIE, 2009

France Disease never reported OIE, 2009

Germany Disease never reported OIE, 2009

Greece Disease not reported OIE, 2009

Hungary Disease never reported OIE, 2009

Iceland Disease never reported OIE, 2009

Ireland Disease never reported OIE, 2009

Isle of Man (UK) Disease never reported OIE Handistatus, 2005

Italy No information available OIE, 2009

Jersey Disease never reported OIE Handistatus, 2005

Latvia Disease never reported OIE, 2009

Liechtenstein Disease not reported OIE, 2009

Lithuania Disease never reported OIE, 2009

Luxembourg Disease never reported OIE, 2009

Macedonia Disease never reported OIE, 2009

Malta Disease not reported OIE, 2009

Moldova Disease not reported OIE Handistatus, 2005

Montenegro Disease not reported OIE, 2009

Netherlands Disease never reported OIE, 2009

Norway Disease never reported OIE, 2009

Poland No information available OIE, 2009

Portugal Disease not reported OIE, 2009

Romania Disease never reported OIE, 2009

Russian Federation Disease not reported OIE, 2009

Serbia No information available OIE, 2009

Slovakia No information available OIE, 2009

Slovenia Disease never reported OIE, 2009

Spain Disease not reported OIE, 2009

Sweden Disease not reported OIE, 2009

Switzerland Disease never reported OIE, 2009

Ukraine Disease never reported OIE, 2009

United Kingdom

-Northern Ireland Disease never reported OIE Handistatus, 2005

United Kingdom Disease never reported OIE, 2009

Yugoslavia (former) No information available OIE Handistatus, 2005

Yugoslavia (Serbia and Montenegro) Disease not reported OIE Handistatus, 2005

OCEANIA Australia Disease never reported OIE, 2009

French Polynesia Disease not reported OIE, 2009

New Caledonia Disease never reported OIE, 2009

New Zealand Disease never reported OIE, 2009

Samoa Disease never reported OIE Handistatus, 2005

Vanuatu Disease never reported OIE Handistatus, 2005

Wallis and Futuna Islands No information available OIE Handistatus, 2005

Hosts/Species Affected CCPP has been reported to affect only goats (Thiaucourt and Bölske, 1996) and it does not cause disease in sheep, neither spontaneously nor experimentally (McMartin et al., 1980). However, there are some reports describing the isolation of M. capricolum subsp. capripneumoniae from healthy sheep in Kenya that have been in contact with goat herds affected by CCPP (Litamoi et al., 1990), and from sick sheep mixed with goats in Uganda suffering from the disease (Bölske et al., 1995). The isolation of M. capricolum subsp. capripneumoniae from cattle with mastitis has also been reported (Kumar and Garg, 1991), and these reports confound the perceived host specificity of M. capricolum subsp.capripneumoniae.

Host Animals

Animal name Context Capra hircus (goats) Domesticated host, Wild host

Systems Affected

Respiratory - Small Ruminants

List of Symptoms/Signs

Sign Life Stages Type Digestive Signs Anorexia, loss or decreased appetite, not nursing, off feed S1 ( All Stages ) Diagnosis [C] General Signs Weight loss S1 ( All Stages ) Diagnosis [C] Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift S1 ( All Stages ) Sign [C] Sudden death, found dead Sign [C] Stiffness or extended neck Sign [C] Inability to stand, downer, prostration Sign [C] Fever, pyrexia, hyperthermia S1 ( All Stages ) Diagnosis [C] Exercise intolerance, tires easily S1 ( All Stages ) Diagnosis [C] Lack of growth or weight gain, retarded, stunted growth S1 ( All Stages ) Sign [C] Reluctant to move, refusal to move Sign [C] Nervous Signs Dullness, depression, lethargy, depressed, lethargic, listless S1 ( All Stages ) Diagnosis [C] Pain/Discomfort Signs Pain, chest, thorax, ribs, sternum S1 ( All Stages ) Sign Reproductive Signs Mastitis, abnormal milk Sign [C] Agalactia, decreased, absent milk production S1 ( All Stages ) Sign [C] Respiratory Signs Purulent nasal discharge S1 ( All Stages ) Diagnosis [C] Mucoid nasal discharge, serous, watery S1 ( All Stages ) Diagnosis [C] Dyspnea, difficult, open mouth breathing, grunt, gasping S1 ( All Stages ) Diagnosis [C] Increased respiratory rate, polypnea, tachypnea, hyperpnea S1 ( All Stages ) Diagnosis [C] Coughing, coughs S1 ( All Stages ) Diagnosis [C] Skin/Integumentary Signs Rough hair coat, dull, standing on end S1 ( All Stages ) Sign [C]

Epidemiology The most important distinguishing features of CCPP, with respect to the other goat respiratory mycoplasmoses, were defined by Hutcheon and are quoted as follows: (1) the disease is readily contagious to susceptible goats; (2) sheep and cattle are not affected by disease [but see below]; (3) local oedematous reactions do not occur in goats when infective inoculum is given subcutaneously (Hutcheon, 1889). In natural infections, the organisms are acquired by susceptible goats by inhalation of contaminated droplets from infected goats (MacOwan, 1984). The environment as a whole plays an important role in the appearance, evolution and severity of CCPP. Due to the high sensitivity of mycoplasmas to the external environment, close contact is essential between infected and naive animals for transmission to take place, and, overcrowding and confinement favours close contact and circulation of mycoplasmas. Stress factors due to malnutrition and transport over long distances can predispose the animal to disease. In Africa where extensive and traditional husbandry is practised, pathogens spread when animals meet at watering points and grazing areas. Breed and sex appear not to affect the epidemiology of CCPP, but age is an important factor. Though all age groups are susceptible, mortality is higher among young animals than adults. Infective M. capricolum subsp. capripneumoniae may persist in chronic, latent carriers, such as goats or sheep which have recovered from infection without becoming bacteriologically sterile, and are considered to be responsible for the perpetuation of the disease in a herd (Thiaucourt and Bölske, 1996; Wesonga et al., 1998). This aspect of the epidemiology was described as early as 1881 by Hutcheon (McMartin et al., 1980) in the case of CCPP in South Africa (Lefèvre et al., 1987b). Viruses are important factors that predispose lung tissue to invasion by mycoplasmas. In Africa the virus, peste des petits ruminants (PPR) and capripox viruses are important (Lefévre et al., 1987b).

Zoonoses and Food Safety CCPP is not a zoonotic disease.

Pathology The gross pathological lesions are localized exclusively to lung and pleura and are often unilateral. Affected lungs can be totally hepatized, and have a port wine colour (Thiaucourt and Bölske, 1996). A lung section shows a fine granular texture with various colours, but usually without any thickening of the interlobular septa. There is often an abundant pleural exudate and conspicuous pleuritis. The pleural exudates can solidify and form a gelatinous covering sometimes over the whole lung. In acute cases, the pleural cavity contains an excess of straw-coloured fluid with fibrin flocculations (Kaliner and MacOwan, 1976; Wesonga et al., 1993). In chronic cases there is a black discolouration of the lung tissue and sequestration of the necrotic lung areas. Adhesions between the lung and the pleura are very common and often very thick (MacOwan and Minette, 1977). Histological examination of the lung tissues may show acute serofibrinous to chronic fibrino-necrotic pleuropneumonia with infiltrates of serofibrinous fluid and inflammatory cells, mainly neutrophils, in the alveoli, bronchioles, interstitial septae and subpleural connective tissue. Intralobular oedema is more prominent but interlobular oedema has also been reported. Peribronchial and perbronchiolar lymphoid hyperplasia with mononuclear cell infiltration is also present (MacOwan and Minette, 1976; Kibor, 1990; Wesonga et al., 1998; Msami et al., 1998).

Diagnosis In the field, diagnosis of mycoplasma pneumonia cannot be established on clinical signs or on postmortem examinations alone. In outbreaks of classical acute CCPP, the high mortality and typical early thoracic lesions in goats are highly indicative of M. capricolum subsp. capripneumoniae infection, but all cases of caprine mycoplasmosis need additional laboratory tests to establish a presumptive diagnosis. It may be difficult to distinguish CCPP from an infection by M. mycoides subsp. mycoides LC or M. mycoides subsp. mycoides SC, which have a pulmonary location. In the case of M. mycoides subsp. mycoides LC infection, thickening of the interlobular septa may be evident. These lesions are similar to those observed in the case of CBPP. Sometimes the thickening is absent or inconspicuous and laboratory confirmation is needed. Recently, sequestra in the lungs of goats infected with M. mycoides subsp. mycoides SC have been described (Kusiluka et al., 2000).

Growth, Isolation and Transport Media

Definite diagnosis is made by the isolation of M. capricolum subsp. capripneumoniae from clinical samples, usually lung tissue and may be a long and difficult process. The success of isolation depends primarily on the attention that is given to sample collection. The main difficulties in isolating M. capricolum subsp. capripneumoniae is that it grows very poorly in vitro and samples are often contaminated by other mycoplasmas (Freundt, 1983a; Thiaucourt et al., 1996) which are generally faster growing and overgrow M. capricolum subsp. capripneumoniae. In addition to this the frequent use of antibiotic treatment has impaired the growth of these mycoplasmas from clinical material. An immunobinding assay that detects M. capricolum subsp. capripneumoniae in pleural fluids that overcomes some of these problems has been described (Guerin et al., 1993). Liquid medium and a solid agar medium which allows the presumptive identification of M. capricolum subsp. capripneumoniae by the production of coloured colonies is available commercially (Bashiruddin and Windsor, 1998). An antigen detection system using latex coated antibodies has also been described (March et al., 2000).

Biochemical Tests

Only a limited number of biochemical tests perform a useful function as a preliminary screening system and are based on specific enzyme activities or nutritional capabilities. For instance, digitonin sensitivity distinguishes mycoplasmas from acholeplasmas, and serum digestion differentiates members of the M. mycoides cluster from all other small ruminant mycoplasmas (Freundt, 1983b). Also, phosphatase production separates M.capricolum subsp. capricolum from other members of the cluster (Bradbury, 1983). Substantial metabolic differences between M.capricolum subsp. capricolum andM. capricolum subsp. capripneumoniae exist, but differences in glucose metabolism were described between strains of M. capricolum subsp. capripneumoniae (Abu-Groun et al., 1994). These tests can not differentiate M. capricolum subsp.capripneumoniae from all members of M. mycoides cluster (Bölske, 1995). The interspecies variation in some biochemical reactions is often considerable, rendering their application valueless (Jones, 1989; Rurangirwa, 1996).

Growth Inhibition Test

The growth inhibition (GI) test is the simplest and most specific, but the least sensitive of the tests available. It depends on the direct inhibition of mycoplasma growth on solid media by specific hyperimmune serum, and detects primary surface antigens (Dighero et al., 1970). The GI test is particularly useful in identifying M. capricolum subsp. capripneumoniaebecause they appear to be serologically homogeneous, and antiserum to the type strain produces wide inhibition zones free of ‘breakthrough’ colonies against field isolates from diverse sources. M. capricolum subsp. capripneumoniae cross-reacts with Leach’s Bg7, M. equigenitalium and M. primatum in the GI test, but since these cross-reactive species do not occur in goats, they present no difficulties when identifying field isolates. However, a small proportion of M. capricolum subsp. capripneumoniae isolates also cross-react in the GI test with antiserum to M.capricolum subsp. capricolum which may confuse the identification of field isolates. A monoclonal antibody has been produced which specifically inhibits the growth of M. capricolum subsp. capripneumoniae but not of other members of the M. mycoidescluster (Rurangirwa et al., 1987c). It was later demonstrated that this monoclonal antibody was not specific. Cross-reactions with some strains of Bg7 were observed with the GI test and with a strain of M.capricolum subsp. capricolumin the immunofluorescence test (Belton et al., 1994).

Fluorescent Antibody Test

The direct and indirect fluorescent antibody tests are among the most effective, simple and rapid serological methods of identification for most mycoplasma (Rosendal and Black, 1972). Several forms have been described, the most commonly used one is the indirect fluorescent antibody (IFA) test which is applied to unfixed colonies on agar.

Serological Tests

The complement fixation test (CFT) is used for the detection of CCPP infection (MacOwan, 1976; MacOwan and Minette, 1977), and it was found to be more specific, though less sensitive, than the indirect haemagglutination test (Muthomi and Rurangirwa, 1983). The latex agglutination test uses latex beads sensitized with the polysaccharide produced by M. capricolum subsp. capripneumoniae in culture supernatant in a slide agglutination test (Rurangirwa et al., 1987a). The use of the more defined antigen such as the polysaccharide provides greater sensitivity without cross-reactivity with sera against the other three principal caprine mycoplasmas. The indirect haemagglutination test (IHA) (Cho et al., 1976) has been used for the detection of antibodies to the agent causing CCPP (Muthomi and Rurangirwa, 1983). The specificity of IHA test for the M. mycoides cluster has been evaluated and results were found to show cross-reactivity between these organisms (Jones and Wood, 1988). An indirect immunosorbent assay (ELISA) was developed to screen goat sera at a single dilution of antibody to M. capricolum subsp. capripneumoniae (Wamwayi et al., 1989). Some problems due to cross-reactions from other members of the M. mycoides cluster were encountered, but in spite of these, ELISA was more sensitive than CFT in detecting antibodies in serum. More recently, a competition ELISA (c-ELISA) was developed which permitted the specific detection of antibodies in sera from animals affected by CCPP (Thiaucourt et al., 1994). Analysis of field sera showed that seroconversion did not occur in all animals, whatever test was used. The percentage positive animals in affected herds varied between 30 and 60% with this test. The tests were therefore unsuitable as individual screening tests (Thiaucourt et al., 1996).

Molecular Diagnosis

Until recently, isolation was the only way to confirm the presence of CCPP. A DNA probe which differentiates M. capricolum subsp. capripneumoniae from other members of the M. mycoides cluster was developed (Taylor et al., 1992). Diagnostic systems based on PCR have been developed for the rapid detection, identification and differentiation of members of the M. mycoides cluster and the specific identification of M. capricolum subsp. capripneumoniae (Bashiruddin et al., 1994; Hotzel et al., 1996). The sequence of the gene for 16S ribosomal RNA has also been used to develop a PCR-based test where the final identification of M. capricolum subsp. capripneumoniae is made dependant on the pattern of the products after digestion of the PCR product with the restriction enzyme Pst1 (Bascuñana et al., 1994; Bölske et al., 1996).

Disease Course Acute cases can be observed in regions where CCPP is introduced for the first time into naive populations. Particularly 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. Gradually, the respiratory symptoms become prominent, respiration is accelerated and painful, and is followed by violent coughing (McMartin et al., 1980; Thiaucourt and Bölske, 1996). In the terminal stages, the animals are unable to move. They stand with their legs abducted, the neck is stiff and extended downward, saliva continuously drips from their mouth and their nose is obstructed by mucopurulent discharge. The tongue protrudes and the animals bleat distressingly. In fully susceptible flocks that encounter an outbreak, morbidity is usually 100% and mortality is up to 70% (McMartin et al., 1980). The organism is not reported to affect organ systems other than the respiratory tract. In endemic areas subacute and chronic cases are common and the symptoms are milder, dominated by intermittent coughing.

Disease Treatment Table

Drug Dosage, administration and withdrawal times Life stages Adverse affects Drug resistance Type streptomycin 30 mg/kg. Follow veterinary advice. All Stages No Drug tetracycline 15 mg/kg. Follow veterinary advice. All Stages No Drug tiamulin 30 mg/kg. Follow veterinary advice. All Stages No Drug tylosin 11 mg/kg. Follow veterinary advice. All Stages No Drug

Disease Treatment The macrolides (erythromycin, spiramysin, and tylosin), tetracyclines and quinolones are active against M. capricolumsubsp. capripneumoniae. Tylosin, tetracyclin, tiamulin or streptomycin are recommended (Hassan et al., 1984; Onovarian, 1974) but their success depends on early intervention and treatment.

Prevention and Control An experimental vaccine inactivated with saponin that protects goats for approximately a year has been produced in Kenya (Rurangirwa et al., 1984). Movement restrictions and slaughtering infected animals are recommended for countries that are newly infected.

References

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Images

Picture Title Caption Copyright

	Pathology 	Lung of a goat affected with CCPP showing a fibrinous covering over the lobe. 	L. J. M. Kusiluka, Sokoine University of Agriculture, Tanzania 
	Pathology 	Lung of a goat affected with CCPP. Superficial view of the lung showing necrosis and consolidation of the lobe. The infected regions often appear grey, hence the common name of 'grey lung' for this disease. 	G. E. Jones, Yaba Ltd, UK 
	Pathology 	Lung of a goat affected with CCPP. Superficial view of the lung showing the scar of an adhesion between the lobe and the thoracic wall. 	G. E. Jones, Yaba Ltd, UK 
	Pathology 	Lung of a goat affected with CCPP. View of a dissected lobe showing hepatization of the lobules, thickening of the interlobular septa, and thickening of the pleura. 	G. E. Jones, Yaba Ltd, UK 
	Histology 	Histological section of a lung lesion stained with haematoxylin and eosin, showing necrosis of pulmonary tissue with inflamatory luminal exudate, septal distension, and epithelial hyperplasia. 	G. E. Jones, Yaba Ltd, UK 
	Histology 	Histological section of a lung lesion stained with haematoxylin and eosin showing acute fibrinous pneumonia with precipitates of fibrin mixed with inflamatory cells in the alveoli. 	G. E. Jones, Yaba Ltd, UK 
	CCPP Diagnostic Media 	Mycoplasma capricolum subsp. capripneumoniae strain F38 colonies after 7 days of incubation on CCPP Diagnostic Media (Mycoplasma Experience, Reigate, UK) showing dark pigmentation and red crystalline deposits. 	Mycoplasma Experience, Reigate, UK 
	Pathology 	Lung is covered with fibrin and there is excessive fluid in the thoracic cavity. 	USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service 

Date of report: 03/04/2011

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