contagious caprine pleuropneumonia
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- contagious caprine pleuropneumonia
International Common Names
- English: contagious caprine pleuropneumonia, mycoplasma - exotic; Goat disease
OverviewTop of page
The causative agent of contagious caprine pleuropneumonia (CCPP) is Mycoplasmacapricolum 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 leachii an uncharacterized bovine isolate, which causes other diseases of ruminants. Note that M. mycoides subsp. mycoides large colony has now been reclassified as a serovar of M. mycoides subsp. capri and M. leachii is the new species designation for Mycoplasma bovine group 7 (Manso-Silvan et al., 2009). 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. A specific competitive enzyme-linked immunosorbent assay has been developed (Thiauourt et al., 1996).
CCPP is an infectious disease which mainly affects 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. capricolum subsp. 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). The genome sequence for Mycoplasma capricolum subsp. capripneumoniae strain M1601 (Chu et al., 2011) is 1,018,102 bp with a GC content of 23.29%. A study by Fischer et al. (2012) analysed partial sequences from seven housekeeping genes from 118 strains from the M. mycoides cluster and suggested that the M. mycoides cluster originated about 10,000 years ago which coincided with the domestication of livestock.
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 WAHID 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.
Hosts/Species AffectedTop of page
CCPP has been reported to affect only goats (Thiaucourt and Bölske, 1996) however reports have described cases of CCPP in wildlife in a preserve in the State of Qatar. The wild goat (Capra aegagrus), Nubian ibex (Capra ibex nubiana), Laristan mouflon (Ovis orientalis laristanica) and Gerenuk (Litocranius walleri) were affected (Arif et al., 2007), elsewhere in the United Arab Emirates captive Rhim and Dumani Gazelles and other deer species have been affected (Nicholas et al., 2008).
McMartin et al. (1980) reported that it does not cause disease in sheep, neither spontaneously nor experimentally However, there are some reports describing the isolation of M. capricolum subsp. capripneumoniae from sheep with respiratory disease returning to Eritrea with refugees from Sudan (Houshaymi et al., 2002) and 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). In a serological survey for CCPP in Northern Ethiopia 25 (18.3%) of 137 sheep tested were seropositive (Hadush et al., 2009).
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.
DistributionTop of page
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), Mauritius (Srivastava et al., 2010), 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 China (Li et al., 2007), 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) and Pakistan based on molecular tests (Awan et al., 2010).
According to AU-IBAR (2011) seven countries reported the occurrence of CCPP in 2011, with Ethiopia, Somalia and Tanzania having reported the disease since 2008. The disease seems to be confined to the central and eastern Africa regions based on the reports received. It is, however, impossible to rule out the presence of CCPP in other parts of the continent due to possible under-reporting of cases, and lack of adequate laboratory support to correctly diagnose the disease.
AU-IBAR (2011) reported that the disease affected 280 epidemiological units on the continent causing 5833 cases and 1342 deaths, with a case fatality rate of 23%. The highest fatalities were recorded in Somalia with 567 deaths of goats followed by Ethiopia and Chad with 486 and 213 deaths, respectively.
Countries reporting CCPP in AU-IBAR (2011): Pan African Animal Health Yearbook.
Charting the monthly occurrence reports of CCPP in 2011 revealed that higher incidence of the disease was recorded in the second half of the year, suggesting that risk factors such as movement of goats are more prevalent from July to December in the affected countries. However, CCPP was also reported to have occurred in the first half of 2011 at relatively lower levels.
For current information on disease incidence, see OIE's WAHID Interface.
Distribution TableTop of page
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease not reported||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|
|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|
|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||Jones and Wood, 1988; 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||Rurangirwa et al., 1987b; OIE, 2009|
|Uzbekistan||Disease not reported||OIE Handistatus, 2005|
|Vietnam||Disease never reported||OIE, 2009|
|Yemen||No information available||NULL||Rurangirwa et al., 1987b; OIE, 2009|
|Algeria||Disease never reported||OIE, 2012|
|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|
|Cape Verde||Disease never reported||OIE, 2012|
|Central African Republic||Disease not reported||OIE Handistatus, 2005|
|Chad||Present||Lefevre et al., 1987a; OIE, 2012|
|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, 2012|
|Eritrea||Present||Thiaucourt et al., 1992; OIE, 2012|
|Ethiopia||Present||Thiaucourt et al., 1992; OIE, 2012|
|Gabon||No information available||OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||Disease never reported||OIE, 2012|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||Restricted distribution||MacOwan and Minette, 1976; OIE, 2012|
|Lesotho||Disease never reported|
|Libya||Reported present or known to be present||OIE Handistatus, 2005|
|Madagascar||Disease never reported||OIE, 2012|
|Malawi||No information available||OIE, 2009|
|Mali||No information available||NULL||Rurangirwa et al., 1990; OIE, 2009|
|Morocco||Disease never reported||OIE, 2012|
|Mozambique||Disease not reported||OIE, 2009|
|Namibia||Disease never reported||OIE, 2012|
|Niger||Present||Bloch and Diallo, 1991|
|Nigeria||Disease never reported||OIE, 2009|
|Réunion||Disease never reported||OIE, 2012|
|Sao Tome and Principe||Disease not reported||OIE Handistatus, 2005|
|Senegal||No information available||OIE, 2009|
|Seychelles||No information available||OIE Handistatus, 2005|
|Sierra Leone||Present||OIE, 2012|
|South Africa||Disease never reported||OIE, 2012|
|Sudan||Disease not reported||200602||Harbi and El-Tahir, 1981; OIE, 2009|
|Swaziland||Disease never reported||OIE, 2012|
|Tanzania||Present||Kusiluka et al., 2000; OIE, 2012|
|Tunisia||Disease not reported||2000||Perreau et al., 1984; OIE, 2012|
|Uganda||Disease not reported||NULL||Bölske et al., 1995; OIE, 2009|
|Zambia||No information available||OIE, 2009|
|Zimbabwe||Disease not reported||OIE, 2009|
|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|
Central America and Caribbean
|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|
|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|
|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|
|UK||Disease never reported||OIE, 2009|
|-Northern Ireland||Disease never reported||OIE Handistatus, 2005|
|Ukraine||Disease never reported||OIE, 2009|
|Yugoslavia (former)||No information available||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Disease not reported||OIE Handistatus, 2005|
|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|
PathologyTop of page
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).
DiagnosisTop of page
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. capri or M. mycoides subsp. mycoides SC, which have a pulmonary location. In the case of M. mycoides subsp. capri 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. 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).
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 and M. 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. capripneumoniae because 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 Mycoplasma leachii, 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. mycoides cluster (Rurangirwa et al., 1987c). It was later demonstrated that this monoclonal antibody was not specific. Cross-reactions with some strains of Mycoplasma leachii were observed with the GI test and with a strain of M.capricolum subsp. capricolum in 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.
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). A latex agglutination test (CapriLAT) is now available commercially. 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. This test was therefore unsuitable as individual screening tests (Thiaucourt et al., 1996) but it has recently been modified.
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; Woubit et al., 2004). 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). More recently specific real-time PCR assays have been developed (Lorenzon et al., 2008) and Schnee et al. (2012) describe a microarray for Mycoplasma species that can also differentiate members of the M. mycoides cluster.
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sheep & Goats:All Stages||Diagnosis|
|General Signs / Exercise intolerance, tires easily||Sheep & Goats:All Stages||Diagnosis|
|General Signs / Fever, pyrexia, hyperthermia||Sheep & Goats:All Stages||Diagnosis|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sheep & Goats:All Stages||Sign|
|General Signs / Reluctant to move, refusal to move||Sign|
|General Signs / Stiffness or extended neck||Sign|
|General Signs / Sudden death, found dead||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sheep & Goats:All Stages||Sign|
|General Signs / Weight loss||Sheep & Goats:All Stages||Diagnosis|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sheep & Goats:All Stages||Diagnosis|
|Pain / Discomfort Signs / Pain, chest, thorax, ribs, sternum||Sheep & Goats:All Stages||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Sheep & Goats:All Stages||Sign|
|Reproductive Signs / Mastitis, abnormal milk||Sign|
|Respiratory Signs / Coughing, coughs||Sheep & Goats:All Stages||Diagnosis|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sheep & Goats:All Stages||Diagnosis|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sheep & Goats:All Stages||Diagnosis|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sheep & Goats:All Stages||Diagnosis|
|Respiratory Signs / Purulent nasal discharge||Sheep & Goats:All Stages||Diagnosis|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Sheep & Goats:All Stages||Sign|
Disease CourseTop of page
Acute cases can be observed in regions where CCPP is introduced for the first time into naïve 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.
EpidemiologyTop of page
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).
M. capricolum subsp. capripneumoniae has two rRNA operons which have been used to subtype strains based on single point mutations (Pettersson et al., 1998). This method identified two distinct African types I and II, but isolates from the Middle East were all type II, but they could be subdivided further. Lorenzon et al. (2002) amplified and sequenced a 2400 bp fragment of a putative membrane protein “H2” to give four defined lineages. Since then a multi-locus sequence analysis method using the H2 locus and seven new loci has been used (Manso-Silván et al., 2011). This essentially confirmed two evolutionary lineages which were comprised of five groups which showed good correlation with geographic origin.
Impact: EconomicTop of page
Goats are important commodities to a large segment of the world’s population as a source of meat, milk, and skin. CCPP is a disease of major economic importance in Africa and Asia, posing a major constraint to goat production. 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.
Zoonoses and Food SafetyTop of page
CCPP is not a zoonotic disease.
Disease TreatmentTop of page
The macrolides (erythromycin, spiramysin, and tylosin), tetracyclines and quinolones are active against M. capricolum subsp. 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 ControlTop of page
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.
ReferencesTop of page
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Distribution MapsTop of page
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