contagious bovine pleuropneumonia
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- contagious bovine pleuropneumonia
International Common Names
- English: contagious bovine pleuropneumonia, mycoplasma mycoides - exotic; Infection with Mycoplasma mycoides subsp. mycoides SC; lung sickness; lungsickness
- French: peripneumonie contagieuse du boeuf
Local Common Names
- Italy: peripulmonite contagiosa dei bovini; polmonera
OverviewTop of page
The causative agent of contagious bovine pleuropneumonia (CBPP) is Mycoplasma mycoides subspecies mycoides SC (small colony); the first mycoplasma to be described. Phylogenetically it is a member of the Mycoplasma mycoides cluster which are pathogens of ruminants, and include M. mycoides subsp. capri, M.capricolum subsp. capripneumoniae, M. capricolum subsp. capricolum and Mycoplasma leachii. 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).
CBPP is a respiratory illness characterized by the presence of sero-fibrinous, interstitial pneumonia, interlobular oedema and hepatization giving a marbled appearance of the lung and capsulated lesions termed sequestra in the lungs of affected cattle. The occurrence of subacute, symptomless infections and chronic carriers after the clinical phase of the disease are generally believed to create major problems in the control of this disease. CBPP is present in the Middle East, Asia, and is now considered the most significant disease of cattle in Africa. The last reported occurrence of CBPP in Europe was in Portugal in 1999.
The Consultative Group on CBPP was reconvened for the first time in over 25 years in October 1998 by the OIE (1998) to discuss the deteriorating situation of the disease in Africa. Over the previous decade, an alarming spread of the disease was seen in Africa along two fronts: one in the east where it had invaded the whole of Tanzania, the north of Zambia threatening Malawi and Mozambique; and the other on the south-west where CBPP appeared after a long absence in Botswana in 1995 and subsequently in west Zambia. Simultaneously, the incidence of CBPP continues to increase in the endemic areas of West and Central Africa as well as in the Horn of Africa. The meeting concluded that CBPP "can now be considered as the most important threat to the cattle industry in Africa". The group met again in October 2000 to review the situation in Africa and the conclusion remained unchanged. Although deterioration could not be demonstrated it was noted that the inadequacy of veterinary services which led to a lack of epidemiological knowledge, and the failure to control coupled with the lack of regional coordination, and civil unrest contributed to the spread of CBPP in the African continent. Further meetings in 2003 and 2006 recommended research into improving vaccines and assessing the possible use of antibiotic treatments as an option to control CBPP. They also recommended carrying out serological prevalence studies and using mathematical modelling in CBPP research. The meeting in 2006 went as far as recommending the use of antibiotics in defined scenarios, but abattoir surveillance, culling, zoning and controlling cattle movement along with vaccination are the main holistic strategies for controlling CBPP.
Tambi et al. (2006) estimated the cost of CBPP in twelve sub-Saharan African countries to 3.7 million Euros per country and suggested an investment of 14.7 million Euros to control CBPP would prevent the loss of 30 million Euros.
Definite diagnosis is made by culture of the causative agent from lung samples or pleuritic fluid taken at postmortem. Pleural fluid was described as the sample of choice (Nicholas and Baker, 1998), but recent reports from an experimental infection indicate detection as low as 25% in pleural fluid (Schnee et al., 2011). Liquid and solid mycoplasma media are inoculated and filtered subcultures from liquid media 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 and more recently the competition ELISA which are tests prescribed by the Office International des Epizooties (OIE) for international trade. Both these tests are only reliable for herd diagnosis. The immunoblotting test has been developed and is useful as an additional specific serological test to support other serological diagnostic methods. A penside latex agglutination test has also been developed and is commercially available (Churchward et al., 2007).
The preferred method for the control of CBPP is the restriction of animal movement and stamping out by slaughter of entire infected herds. There is only one vaccine, T144, recommended by the OIE and FAO. Antibiotic therapy is discouraged on the basis that it may promote the formation of carriers. In vitro minimum inhibition concentration tests indicate tilmicosin, oxytetracycline and the fluroquinolones are active against M. m. mycoides SC (Ayling et al., 2007). In vivo studies have demonstrated that danofloxacin, a fluoroquinolone was effective at treating a CBPP outbreak in Namibia and no further cases occurred (Nicholas et al., 2007). Treatment of infected animals with oxytetracycline was shown to have a positive impact on the course of the disease and prevent the spread of disease to in-contact animals, however M. m. mycoides SC could still be recovered from the treated animals (Niang et al., 2007).
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. For information on this disease from OIE, see the website: www.oie.int.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Bos grunniens (yaks)||Domesticated host, Wild host||Cattle & Buffaloes: All Stages|
|Bos indicus (zebu)||Domesticated host||Cattle & Buffaloes: All Stages|
|Bos mutus (yaks, wild)||Domesticated host, Wild host||Cattle & Buffaloes: All Stages|
|Bos taurus (cattle)||Domesticated host||Cattle & Buffaloes: All Stages|
|Bubalus bubalis (Asian water buffalo)||Domesticated host||Cattle & Buffaloes: All Stages|
Systems AffectedTop of page respiratory diseases of large ruminants
DistributionTop of page
CBPP appears to have existed in the ancient world according to early classical writings (Provost et al., 1987). It was referred to as polmonera by Gallo in Italy and was confined to the Alps and Pyrenees in the 16th Century. The disease was reported in Britain by Barker in 1736; the clinical signs of CBPP were correctly described for the first time by Bourgelat in 1765, and Albert de Haller recommended mass slaughter for its control in 1773 (Egwu et al., 1996).
Cattle movements in the early 19th Century caused by Napoleonic military campaigns and the general increase in international cattle trading led to the rapid spread of CBPP throughout Europe, mainly via Swiss and Dutch cattle which were preferred at that time for breeding. As a consequence, Britain became re-infected in 1840 following the introduction of an infected bull from the Netherlands. From Britain, CBPP spread to Scandinavia and the USA in 1843. In February 1879 the British government placed restrictions on cattle from USA because of CBPP. The specially created Bureau of Animal Industry, using basic procedures of quarantine, slaughter, and disinfection eradicated CBPP from the USA in 1892 after an 8-year campaign.
CBPP was introduced into southern Australia from Britain in 1858 and spread in Victoria unnoticed for a year. It then underwent rapid spread northward and reached Queensland by 1864, and fuelled by the increasing demand for meat in the Southern States, it repeatedly cycled from North to South carried by cattle trekked down to meet these demands. Almost a hundred years later an eradication campaign commenced in 1961 and with the last lesions seen in 1967, Australia was declared free of CBPP in 1973 (Newton, 1992). From Australia CBPP spread to New Zealand, India, China, Mongolia, Korea, Hong Kong and Japan in the late 19th Century and early 20th Century (Laak, 1992). South Africa became infected in 1854 from either Britain (Hutyra et al., 1938) or the Netherlands (Provost et al., 1987). Britain eradicated CBPP in 1898 using a stamping out approach.
Although sporadic outbreaks continued on the French/Spanish borders until the 1920s CBPP was eradicated from most parts of Western Europe by the beginning of the 20th Century by prohibiting cattle movement, slaughtering diseased and contact cattle (Hutyra et al., 1938). The outbreak of the First World War was a major set back for disease control particularly in Eastern Europe; residual disease in Russia, Romania and Poland spread to Austria and Germany, where it was eventually suppressed. CBPP persisted in Russia and Poland until the late 1930s. Doubts remain as to whether it was completely eradicated from Eastern Europe. Today, in the absence of effective surveillance systems, these concerns persist, with continued unsubstantiated claims of CBPP in Eastern Europe.
Nicholas and Palmer (1994) argued that the disease was never truly eradicated from western Europe as was suggested by Provost et al. (1987) but instead stubbornly persisted in the Iberian Peninsula where it was reported as late as 1958 in Portugal (Ferronha et al., 1990). Further outbreaks occurred in 1961 in Spain and then in the Department des Pyrènèes-Orientales in France in 1967, 1980, 1982 and 1984 (Provost et al., 1987) where some mortality was recorded in three herds (Laak, 1992). Infection was reported to be widespread in Portugal in 1983 (Ayling et al., 1999). CBPP was endemic in north western parts of Portugal around Porto, but outbreaks subsequently decreased significantly. Spain began reporting cases of CBPP from 1989. Whilst the first cases occurred around Madrid and Segovia, the majority of outbreaks were in the northern coastal areas bordering the Bay of Biscay (Laak, 1992). In 1990 Italy reported its first outbreak for over 100 years in Piedmonte in the north. The disease quickly spread to most major cattle areas of Italy. However, as a result of abattoir surveillance, movement control linked to serological monitoring, and slaughter of infected and contact animals, no cases have been reported since September 1993. For the first time for over 20 years, no outbreaks were reported in Europe in the year 2000 and it has remained CBPP free since (November 2011).
There are a number of different theories to explain the spread of CBPP into eastern Africa. It may have been present in pre-colonial times and some workers cite Thomson’s description of a cattle disease resembling CBPP in Maasai cattle in the1880s in eastern Africa (Thomson, 1885). It has been suggested that, after its arrival in South Africa from Europe, CBPP spread into East Africa by Boer settlers who trekked their cattle to the Kenyan highlands around the turn of the 20th century. An alternative or additional route of infection into Africa was the introduction of CBPP into Ethiopia and Sudan with infected Indian cattle belonging to the British Expeditionary Force in the late 19th Century. The disease would then have spread into Eastern and possibly Western Africa via well established trade routes. Today, CBPP is endemic in much of sub-Saharan Africa and its incidence is increasing. South Africa, countries bordering the Mediterranean and those such as Gambia, Senegal, Zambia, Malawi, Zimbabwe, Swaziland and Madagascar were purportedly still free of CBPP in 1993 (Laak, 1992; OIE, 1993).
By the end of 1999, CBPP was present in at least 27 countries in equatorial, central and southern Africa although it is difficult to be certain due to the discrepancies between official and non-official reports. A more accurate estimate of distribution was provided by Masiga et al. (1998) who examined the number of countries reporting the disease over the last 20 years. Overall, it appears that the number of countries now infected is similar to that seen 23 years ago. During that period there was a steady but slow decline to a low of about 15 countries in the late 1970s and early 1980s when many countries were immunising extensively with either the T1 44 broth vaccine or the combined rinderpest/CBPP freeze dried vaccine.
While relatively accurate data can be gathered on which countries are infected, what is less clear is the prevalence of infection within these countries, as reported cases are notoriously inaccurate and subjective. An examination of the number of outbreaks reported by African countries in the late 1990s showed that large increases in incidence occurred in Burkina Faso and Ghana in West Africa, Ethiopia, Kenya and Tanzania in East Africa, and Namibia and Zambia as well as Botswana between 1995 and 1996 in Southern Africa. Outbreaks of CBPP in previously uninfected areas occurred in Kenya, Rwanda, Tanzania, Botswana, Zambia, Burundi and West Guinea. The reasons for the increase in CBPP incidence relate to the decrease in efficiency and financing of national veterinary services and specifically to reduced funding for vaccination, possibly linked to the success of the rinderpest campaign, changes in vaccines and vaccine usage, cost recovery for CBPP vaccination and reduced disease surveillance. In addition, the usual generic problems contribute: severe droughts leading to changes in cattle movements; war and civil unrest; and even reduction in hostilities leading to the destruction of border fences and increased border movements of cattle, as seen recently with the importation of the disease from Namibia into Botswana (Amanfu et al., 1998).
In 2011, CBPP was reported to the AU-IBAR in 18 African countries; spreading across the west, central, east and southern Africa regions. During the reporting period, 304 epidemiological units were affected by CBPP across Africa involving 16,836 cases and 3007 deaths, with an estimated case fatality rate of 17.9% (see table below). The highest number of CBPP outbreaks was reported in Ghana (75), followed by Central African Republic (43) and Ethiopia (29).
Countries in Africa reporting CBPP to the AU-IBAR
Central African Republic
Out of the 18 affected countries listed in the table above, all except DRC and Gabon have been reporting the disease over the past four years, while Congo DR and Gabon reported the disease for the first time in 2010.
In terms of seasonality, CBPP appears to have no defined trend in 2011 with the disease having been reported throughout the year. There is, however, a small variability in the number of reported outbreaks between the months of the year.
CBPP control remains a big challenge for many affected countries. The available control measures include vaccination and movement control, but there is reasonable evidence to suggest that a number of cattle owners have resorted to the indiscriminate use of antibiotics to treat clinical cases (AU-IBAR, 2011). Spread of the disease is largely attributed to uncontrolled movement of cattle.
Against this background, there is need to critically evaluate the effectiveness and efficiency of the current methods being employed to control CBPP in Africa.
Very little meaningful data exist for the prevalence of CBPP in the Middle East and the rest of Asia today, as surveillance systems are ineffective or non-existent, so the exact status of the disease in Asia is not known. Information on CBPP in China has only recently been published (Xin et al., 2012) indicating that CBPP was present in China from 1919 until 1989 when 178,570 cattle died of CBPP. The disease was eventually eradicated using a novel attenuated vaccine applied to over 74.5 million cattle (Xin et al., 2012). Lefèvre (1991) and Laak (1992) thought the disease was present in a swath of Asia running from Sinkiang, in the west of China, south-eastwards towards Thailand and Vietnam covering Mongolia, Tibet, Bangladesh, Sichuan, Bhutan, Myanamar, Burma, Cambodia and Assam; CBPP is suspected in Pakistan and Nepal. In Assam, regions of high incidence include Akajan, Sissiborgaon, Dhemaji and Dhakuakhana, which lie in the Brahmaputra valley (Choudhary et al., 1987). It is believed that sporadic outbreaks still occur in the Yemen, United Arab Emirates, Saudi Arabia, Kuwait and Lebanon mainly as a result of cattle imported from Africa (Lefèvre 1991; Laak 1992). Jordan is also thought to be infected (Mlengeya, 1995).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|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 never reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||Disease not reported||NULL||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Bhutan||No information available||NULL||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||NULL||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|China||No information available||NULL||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|-Hong Kong||Disease never reported||OIE, 2009|
|Georgia (Republic of)||Last reported||1932||OIE Handistatus, 2005|
|India||Disease not reported||1990||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Indonesia||Disease never reported||OIE, 2009|
|Iran||Disease never reported||OIE, 2009|
|Iraq||Disease never reported||OIE, 2009|
|Israel||Disease not reported||OIE, 2009|
|Japan||Disease not reported||OIE, 2009|
|Jordan||Disease never reported||NULL||Mlengeya, 1995; 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||Disease not reported||1991||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Kyrgyzstan||Disease never reported||OIE, 2009|
|Laos||Disease not reported||OIE, 2009|
|Lebanon||Disease not reported||NULL||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Malaysia||Disease never 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||1973||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Myanmar||No information available||NULL||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Nepal||No information available||OIE, 2009|
|Oman||Disease not reported||OIE, 2009|
|Pakistan||Disease not reported||OIE, 2009|
|Philippines||Disease never reported||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||Disease not reported||2006||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||Disease not reported||OIE, 2009|
|Taiwan||Disease never reported||OIE Handistatus, 2005|
|Tajikistan||Disease never reported||OIE, 2009|
|Thailand||Disease never reported||NULL||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Turkey||No information available||OIE, 2009|
|Turkmenistan||Disease never reported||OIE Handistatus, 2005|
|United Arab Emirates||Disease not reported||1990||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Uzbekistan||Disease never reported||OIE Handistatus, 2005|
|Vietnam||Disease never reported||NULL||Lefèvre, 1991; Laak, 1992; OIE, 2009|
|Yemen||Disease not reported||OIE, 2009|
|Algeria||Disease never reported||OIE, 2012|
|Angola||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Benin||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Botswana||Disease not reported||OIE, 2009|
|Burkina Faso||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Burundi||Disease not reported||Masiga et al., 1998; Kané, 2000; OIE Handistatus, 2005|
|Cameroon||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Cape Verde||Disease never reported||OIE, 2012|
|Central African Republic||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Chad||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Congo||No information available||Masiga et al., 1998; Kané, 2000; OIE, 2009|
|Congo Democratic Republic||Present||Masiga et al., 1998; Kané, 2000; AU-IBAR, 2011|
|Côte d'Ivoire||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Djibouti||Disease not reported||OIE, 2012|
|Egypt||Disease not reported||1971||OIE, 2012|
|Eritrea||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Ethiopia||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Gabon||Restricted distribution||OIE, 2012|
|Ghana||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Guinea||Disease not reported||2006||Masiga et al., 1998; Kané, 2000; OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Lesotho||Disease never reported||OIE, 2012|
|Libya||Disease never reported||OIE Handistatus, 2005|
|Madagascar||Disease never reported||OIE, 2012|
|Malawi||Disease never reported||OIE, 2012|
|Mali||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Mauritania||Reported present or known to be present||Masiga et al., 1998; Kané, 2000|
|Mauritius||Disease never reported||OIE, 2009|
|Morocco||Disease never reported||OIE, 2009|
|Mozambique||Disease never reported||OIE, 2009|
|Namibia||Restricted distribution||Bamhare, 2000; OIE, 2009|
|Niger||Reported present or known to be present||Masiga et al., 1998; Kané, 2000; OIE Handistatus, 2005|
|Nigeria||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Réunion||Disease never reported||OIE Handistatus, 2005|
|Rwanda||2010||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Sao Tome and Principe||Disease not reported||OIE Handistatus, 2005|
|Senegal||Disease not reported||1977||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Seychelles||Disease not reported||OIE, 2012|
|Somalia||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|South Africa||Disease not reported||1924||OIE, 2012|
|Sudan||Present||Masiga et al., 1998; Kané, 2000; AU-IBAR, 2011|
|Swaziland||Disease never reported||OIE, 2012|
|Tanzania||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Togo||Present||Masiga et al., 1998; Kané, 2000; OIE, 2009|
|Tunisia||Disease never reported||OIE, 2012|
|Uganda||Present||Masiga et al., 1998; Kané, 2000; OIE, 2012|
|Zimbabwe||Disease not reported||OIE, 2009|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Disease not reported||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease never reported||OIE, 2009|
|USA||Disease not 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 never 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||Disease never reported||OIE, 2009|
|Guatemala||Disease never reported||OIE, 2009|
|Haiti||Disease never reported||OIE, 2009|
|Honduras||Disease never reported||OIE, 2009|
|Jamaica||Disease never reported||OIE, 2009|
|Martinique||Disease never 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||Disease never reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Disease never reported||OIE Handistatus, 2005|
|Argentina||Disease never reported||OIE, 2009|
|Bolivia||Disease never reported||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||Disease not reported||OIE, 2009|
|Andorra||Last reported||1957||OIE Handistatus, 2005|
|Austria||Disease not reported||OIE, 2009|
|Belarus||Disease never reported||OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Bosnia-Hercegovina||Disease never 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 not reported||OIE, 2009|
|Estonia||Disease never reported||OIE, 2009|
|Finland||Disease not reported||OIE, 2009|
|France||Disease not reported||OIE, 2009|
|Germany||Disease not reported||OIE, 2009|
|Greece||Disease never reported||OIE, 2009|
|Hungary||Disease not reported||OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease not reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||Disease not reported||OIE, 2009|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Disease not 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 never reported||OIE, 2009|
|Moldova||Last reported||1946||OIE Handistatus, 2005|
|Montenegro||Disease never reported||OIE, 2009|
|Netherlands||Disease not reported||OIE, 2009|
|Norway||Disease not reported||OIE, 2009|
|Poland||Disease not reported||OIE, 2009|
|Portugal||Disease not reported||OIE, 2009|
|Romania||Disease not reported||OIE, 2009|
|Russian Federation||Disease not reported||OIE, 2009|
|Serbia||Disease never reported||OIE, 2009|
|Slovakia||Disease not reported||OIE, 2009|
|Slovenia||Disease never reported||OIE, 2009|
|Spain||Disease not reported||OIE, 2009|
|Sweden||Disease not reported||OIE, 2009|
|Switzerland||Disease not reported||OIE, 2009|
|UK||Disease not reported||OIE, 2009|
|-Northern Ireland||Last reported||1893||OIE Handistatus, 2005|
|Ukraine||Disease never reported||OIE, 2009|
|Yugoslavia (former)||Disease never reported||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Disease never reported||OIE Handistatus, 2005|
|Australia||Disease not reported||OIE, 2009|
|French Polynesia||Disease never reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease not 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 lesions of this disease are mostly confined to the thoracic cavity and lungs, and lesions are usually unilateral. In a study of 566 CBPP-affected lungs in Portugal, Nunes et al. (1990) showed 95% of lesions to be unilateral which contrasts with infections caused by Pasteurella haemolytica where both lungs are usually affected. The diaphragmatic lobe was observed to be more commonly affected than the apical lobe (Nunes et al., 1988; 1990). The thoracic cavity of affected animals may contain many litres of clear yellowish brown fluid containing some pieces of fibrin (Laak, 1992). This pleural fluid is ideal diagnostic material from which the mycoplasma can be isolated in pure colony form or on which PCR can be carried out with DNA purification (Nicholas and Bashiruddin, 1995). Caseous fibrinous deposits are observed on the parietal and visceral surfaces of the lungs (Provost et al., 1987).
The interlobular septa of the affected lung show distension with amber-coloured fluid surrounding the distended lymphatics. This fluid separates the lung lobules which vary in colour with red, grey and yellow hepatization being evident indicating different stages of inflammatory lesions (Hudson, 1971). Consolidation of the lungs with typical marbled appearance, sometimes accompanied by adhesion of the parietal and visceral surfaces is also characteristic. In chronic or advanced cases, a sequestrum consisting of necrotic lung parenchyma surrounded by a fibrous capsule which varies in size between 1 and 10 cm in thickness is formed (Martel et al., 1983; Trichard et al., 1989; Santini et al., 1992). The sequestrum may constitute a source of infection to cattle when ruptured particularly where the sequestrum is drained by a bronchus and forms an outlet for the dissemination of infected aerosol droplets (Provost et al., 1987). Such a mechanism would account for outbreaks of disease in closed herds. Windsor and Masiga (1977), however, could not experimentally induce the breakdown of sequestra and believed that it is only acutely infected animals that transmit the disease. In acutely infected animals one or more infarcts may be seen in the kidneys.
In addition to respiratory disease, affected calves may present exudative peritonitis, arthritis, bursitis and fibrinous arthritis of the carpal and tarsal joints (Provost et al., 1987). More often than not, enlargement of the suprascapular lymph nodes may accompany these changes.
Early on in the course of disease the CBPP lesion comprises a bronchiolar necrosis and oedema, progressing rapidly to an exudative serofibrinous bronchiolitis with extension to the alveoli and uptake of alveolar fluid into tissue spaces, lymph vessels and ultimately septal lymphatics ducts (Done et al., 1995). These rapidly reach saturation and the process is extended centrifugally to the tracheobronchial lymph nodes and centripetally to the pleural lymphatic ducts. The mediastinal, sternal, aortic and intercostal lymph nodes may then become enlarged, oedematous or even haemorrhagic. With stasis, lymph vessels become thrombosed and ultimately fibrosed (Buttery et al., 1980). The pulmonary lobules become consolidated with alveolar oedema, fibrin and inflammatory cells. Coagulative necrosis is common. M. m. mycoides SC can be isolated from or demonstrated in these lobules by immunohistochemistry.
Perivascular organisation foci or 'organizing centres', found in the interlobular septa, are considered pathognomonic for CBPP (Ferronha et al., 1988). They consist of a centre occupied by a blood vessel with proliferation of connective and inflammatory cells surrounded by a peripheral zone of necrotic cells. Two types of foci have been recognized (Nunes et al., 1988). Type I foci contain more proliferative cells in the central zone which is larger than the peripheral zone and probably corresponds to the success of the host immune response in resolving the infection; immunoreactive antigen is associated with macrophages. In Type II foci, the proliferative cells are scarce and the peripheral zone is relatively larger. Immunoreactive antigen can be seen in the central zone inside blood vessels and it is thought Type II foci indicate a failure of the immune response leading to aggravation of signs.
An immunocytochemical study of CBPP infected Italian cattle (Scanziani et al., 1997), showed that the severity of lung lesions correlated with the severity of changes in the lymph nodes. In the acute stage of the disease, specific antigen was detected in the lobular periphery and in the cytoplasm of alveolar macrophages. In chronic lesions, immunoreactivity was seen in the fibrotic areas and in macrophages located in the lobular septa. Necrotic debris and macrophages located in the inner part of the sequestra were specifically stained. Immunoreactive material was also seen in the centrofollicular areas of the broncho-associated lymphoid tissue structures and in the lymph node follicles. Furthermore, electron microscopy of the mediastinal lymph nodes of a chronically affected calf showed degenerating mycoplasmas and a few apparently intact mycoplasmas in the macrophages.
DiagnosisTop of page
The isolation and growth of M. m. mycoides SC is essential for the diagnosis and confirmation of outbreaks of CBPP. Subsequently, it is also a requirement of the OIE for countries wishing to declare freedom from CBPP under the recommended standards for epidemiological surveillance systems for the disease (OIE, 1997). Nasal swabs, bronchoalveolar lavage and blood may be taken from live animals and tissue samples from edge of pulmonary lesions, broncho-pulmonary lymph nodes, pleural fluid, and joint fluid from calves may be taken at postmortem.
Growth, Isolation and Transport Media
M. m. mycoides SC, is facultatively anaerobic, growing well in both anaerobic and aerobic environments at a pH of 7.6-7.8. It usually grows well in sealed liquid broth cultures, especially if the broth level is a few inches deep to allow for an oxygen or air gradient. Gentle aeration increases the growth rate and yield of M. m. mycoides (Rodwell and Mitchell, 1979). In actively growing cultures, M. m. mycoides is filamentous which is the result of genetic division preceding cytoplasmic division. At the end of growth, however, short beaded filaments predominate and ultimately only coccoid bodies are seen (Razin, 1978). M. m. mycoides SC is not intrinsically difficult to grow but requires a fully functioning bacteriological laboratory with access to specialist mycoplasma media. Many media have been described which enable the growth of M. m. mycoides SC (for example, Hudson, 1971; Freundt, 1983; Nicholas and Baker, 1998; Rice et al., 2000b). A number of commercially prepared media for the isolation and identification of mycoplasmas of veterinary importance are also available, for example, Mycoplasma Experience, Reigate, UK. Isolation media for M. m. mycoides SC also traditionally serve as transport media and are based on conventional growth media with the addition of inhibitors such as ampicillin, bacitracin, penicillin G, polymyxin B, and thallium acetate to stop the growth of cell-walled bacteria. Nisin, a bacteriocin that inhibits the growth of certain cell-walled bacteria may be particularly useful as it inhibits Acholeplasma as well (Abu-Amero et al., 1996). The growth of arginine-hydrolysing mycoplasmas may be inhibited by citrulline, lysine and ornithine (Ozcan et al., 1999).
The sensitivity to digitonin indicates the requirement for sterol; members of the genus Mycoplasma are digitonin sensitive, and this test is performed after the initial isolation of suspicious mycoplasmas. A series of biochemical tests standardized by Aluotto et al. (1970) follow, and M. m. mycoides SC strains may be identified by the fermentation of glucose, the reduction of tetrazolium aerobically and anaerobically, and the digestion of casein; they do not hydrolyse arginine, liquify coagulated serum, produce film and spots, and have no phospatase activity.
Final identification of mycoplasmas is usually achieved by growth inhibition (GI) and/or immunofluorescence (IF) tests which are carried out on agar with specific antiserum. The tests are relatively specific; they can identify the two subspecies of M. mycoides but cannot distinguish between SC and M. m. capri
Recently, a nitroblue tetrazolium (NBT) reduction technique has been described for the detection of substrate metabolism by washed cell suspensions and may be suitable for use in routine laboratories to differentiate M. m. capri, and SC strains (Miles and Agbanyim, 1998).
Bashiruddin et al. (1999c) and Bashiruddin and Windsor (1998) developed a medium in which M. m. mycoides colonies were coloured red due to tetrazolium reduction (CBPP Diagnostic Medium, Mycoplasma Experience, Reigate, UK). Using clinical material and isolated mycoplasmas to inoculate plates, M. m.capri colonies were dark red after 3 days, whereas M. m. mycoides SC colonies were much lighter coloured and only became dark red after approximately 7 days. This medium may be useful in the primary isolation of M. m. mycoides SC from clinical material, enabling immediate identification of colonies for subsequent testing by standard and molecular methods (Bashiruddin et al., 1999c; Bashiruddin and Windsor, 1998).
The results of substrate oxidation studies have also led to the development of rapid tests for the utilization of maltose and glycerol by members of the M. mycoides cluster. The inability to use maltose differentiates M. m. mycoides SC strains (32/32 strains negative) from other M. mycoides strains (32/35 strains +ve). A test was developed based on hydrolysis of a colourless, chromogenic alpha-glucosidase (maltase) substrate, p-nitrophenyl-a-D-glucopyranoside (pNPG), to give a brightly coloured, yellow product (p-nitrophenol). It can be carried out using cells washed and resuspended in buffer or by simply adding pNPG (100 mM) to colonies on agar plates; colonies of maltose-utilising strains become coloured in about 40 min (Rice et al., 2000a).
Glycerol utilising ability leads to the production of hydrogen peroxide, which may be detected in colorimetric assays (Houshaymi et al., 2000). These tests confirmed that European M. m. mycoides SC strains did not oxidise glycerol (i.e. there was no hydrogen peroxide produced), and high rates of hydrogen peroxide production were observed for non-European M. m. mycoides SC strains, subsp. mycoides LC and subsp. capri strains. In qualitative assays using colonies grown on serum agar (72-96 h), plates were flooded with a reagent prepared by mixing glycerol, 3,3’ diaminobenzidine and peroxidase. Plates were then incubated at 37°C and observed for red coloration of colonies. The time for development of colour was 45-135 min for European M. m. mycoides SC strains, but 1-20 min for other strains of M. mycoides (Houshaymi et al., 2000).
There are two OIE approved serological tests, the complement fixation test (CFT) and the competitive ELISA. The CFT is specific but lacks sensitivity. With a positive result being any reaction at 1/10 or higher, CFT is also far from robust. In a thorough examination of CFT in which over 33,000 sera from healthy herds were tested between 1991-1994 in Italy, Bellini et al. (1998) reported that CFT was 98% specific while its sensitivity, based on nearly 600 cattle with specific lesions from 11 infected herds, was only 64%. Isolation of the causative mycoplasma from affected animals was even more insensitive at 54%. During the Italian outbreaks, abattoir surveillance detected nearly as many outbreaks as serological monitoring (see section on Pathology for indicators), while clinical examination was much less useful (Regalla et al., 1996). It followed that by using CFT as a screening test, some CBPP affected cattle, in the early or later stages of infection were missed, accounting for the persistence of the disease in Portugal. A competitive (c)ELISA developed at CIRAD-EMVT, Montpellier, may have advantages in terms of ease of testing and standardisation of results, but it has sensitivity levels similar to CFT (Goff and Thiaucourt, 1998). Gonçalves et al. (2008) reported that Mycoplasma bovis is one of the causes of false positive CBPP CFT results.
Immunoblotting tests (IBT) were described by Goncalves et al. (1998) in which the simultaneous presence of five antigens (110, 98, 95, 62/60 and 48) was highly characteristic of sera from infected cattle. These tests were compared to the CFT in an examination of sera from Portuguese herds affected by CBPP (ca 170 cattle). There was 79% agreement between CFT and IBT. In a study of 88 cattle with CBPP lesions, IBT detected 80 and CFT detected 72 (Ayling et al., 1999).
Abdo et al. (1998; 2000) identified a 48 kDa protein, named LppQ, which was found in the type strain and European, African and Australian field strains. They used the protein in an immunoblotting test for the serodetection of M. m. mycoides SC in experimentally infected cattle.
A penside latex agglutination test, which can give a result in two minutes is now produced commercially as BOVILAT, AHVLA (Churchward et al., 2007). This is based on the carbohydrate antigen and gives similar sensitivity and specificity to the CFT, but confirmation of positive results using other tests is advised.
Muuka et al. (2011) reported on an experimental infection study and stated that no single serological test can detect CBPP positive animals at all stages of infection.
Antigen Detection Systems
Rodriguez et al. (1996) reported a monoclonal antibody-based sandwich ELISA that could detect as little as 105 CFU/ml of both M. mycoides biotypes within two hours. Sensitivity could be improved significantly by incubating samples for 48 hours. This test could not distinguish between the M. m. mycoides SC and M. m capri, but coupled with pathological and serological information from affected animals the test could prove very useful.
Immunocytochemistry (ICC) is increasingly used to confirm the diagnosis of CBPP particularly where the causative organism, M. m. mycoides SC, is not recoverable (often following long transport distances), where the animal has died of acute disease or where serology is not possible or unclear (Ferronha et al., 1990; Scanziani et al., 1997). However, the sensitivity of ICC using polyclonal serum can be low and non-specific results frequently occur (Bashiruddin et al., 1999b).
Powerful 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. m. mycoides SC. An arbitarily-primed PCR (AP-PCR) of M. m. mycoides SC with Mlip1 and Mlip4 primers produced a fingerprint with little genomic polymorphism and thus of limited epidemiological use. Two bands of 900 bp and 100 bp for strains PG1, PO, KH3J and Fatick were produced, although the later had a faint band at 400 bp, in contrast to the five M. capricolum subsp. capricolum strains tested which produced four different patterns (Rawadi et al., 1995). These tests were designed from sequences of unknown functions or from known genes (Bashiruddin et al., 1994b; Dedieu et al., 1994; Hotzel et al., 1996; Miserez et al., 1997; Rodriguez et al., 1997; Persson et al., 1999). With many of these tests, confirmation of the presence of M. m. mycoides SC or the production of the expected amplification product was possible by the digestion of the product with specific restriction enzymes. In some cases the standard detection of PCR products by agarose gel electrophoresis was replaced with enhanced methods which improved the sensitivity and allowed some degree of automation (Bashiruddin et al., 1999a; Persson et al., 1999). They have been used for the detection and identification of M. m. mycoides SC from culture and clinical materials including nasal mucous, pleural fluid, tissue from lung, lymph node, kidney, spleen, and semen from bovines (Bashiruddin et al., 1994a; 1994b; Nicholas et al., 1994; Bashiruddin et al., 1999a; 1999b; Stradaioli et al., 1999); and from the milk and respiratory tract of small ruminants (Brandao, 1995; Kusiluka et al., 2000; Srivastava et al., 2000). In some cases they had superior diagnostic sensitivities compared with conventional diagnostic tests. Particularly sensitive nested PCR systems have been used for the detection of M. m. mycoides SC from culture and clinical material where the target organism may be in low numbers such as in nasal swab samples (Hotzel et al., 1996; Miserez et al., 1997).
Miles et al. (2006) developed PCR assays that will detect M. m. mycoides SC and differentiate European and African/Australian isolates. More recent technological advances have resulted in the use of real-time PCR assays. Vilei and Frey (2010) describe a TaqMan real-time PCR which they designed specifically to target the LppQ gene, which may be useful if a LppQ devoid vaccine was successfully developed. Schnee et al. (2011) describe a novel multiplex real-time PCR which they demonstrated to be specific and sensitive when assessed using experimentally infected cattle. A LAMP assay which can be used without expensive equipment and can give results in a relatively short time has been developed and is currently being trialled (Unger, IAEA; personal communication).
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Jugular pulse||Cattle & Buffaloes:All Stages||Sign|
|Cardiovascular Signs / Peripheral venous distention, jugular distention||Cattle & Buffaloes:All Stages||Sign|
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Cattle & Buffaloes:All Stages||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Cattle & Buffaloes:All Stages||Sign|
|Digestive Signs / Rumen hypomotility or atony, decreased rate, motility, strength||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Exercise intolerance, tires easily||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Fever, pyrexia, hyperthermia||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area||Cattle & Buffaloes:Calf||Sign|
|General Signs / Generalized lameness or stiffness, limping||Cattle & Buffaloes:Calf||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Reluctant to move, refusal to move||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Stiffness or extended neck||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Weight loss||Cattle & Buffaloes:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Pain / Discomfort Signs / Pain, chest, thorax, ribs, sternum||Cattle & Buffaloes:All Stages||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Cattle & Buffaloes:Cow||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Cattle & Buffaloes:All Stages||Sign|
|Respiratory Signs / Coughing, coughs||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Dull areas on percussion of chest, thorax||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding||Cattle & Buffaloes:All Stages||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Cattle & Buffaloes:All Stages||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Purulent nasal discharge||Cattle & Buffaloes:All Stages||Diagnosis|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Cattle & Buffaloes:All Stages||Sign|
|Skin / Integumentary Signs / Skin edema||Cattle & Buffaloes:All Stages||Sign|
Disease CourseTop of page
There is considerable variation in the degree of signs seen in cattle affected with CBPP ranging from the hyperacute through acute to chronic and sub-clinical forms. Respiratory distress and coughing, evident on stimulation of resting animals, are the main signs of CBPP (Scudamore, 1995). Experimental reproduction of the disease is difficult but is only effectively achieved by bronchial intubation; only small lesions have been reproduced with aerosol inhalation of low passage M. m. mycoides (Gourlay and Howard, 1982, Martel et al., 1983). Turner and Campbell (1937) reported a range of 29-58 days and Provost et al. (1987) stated 20 to 40 days for the incubation period. In experimental infections, Regalla et al. (1994) reported disease symptoms appearing in cattle 40 days after contact with inoculated animals; these symptoms lasted for 20 days. There is no hard evidence for any of the really short or excessively long incubation periods that litter the literature.
The clinical signs observed in the hyperacute form are greatly accelerated. The pathological signs are usually characteristic with marked pleural adhesion accompanied by exudative pericarditis (Provost et al., 1987). Affected animals may die within a few days of exhibiting classical respiratory signs.
The early stages of the disease are indistinguishable from any severe pneumonia with pleurisy (Scudamore, 1995). Animals show dullness, anorexia, and irregular rumination with moderate fever, and may show signs of respiratory distress. Coughing is usually persistent and is slight or dry. Sometimes body temperature rises from 40 to 42°C and the animal prostrates with difficulty of movement. As the lung lesion(s) develop, the signs become more pronounced with increased frequency of coughing and the animal may stand with back arched, head extended and elbows abducted. Because the pleurisy is so painfull, it is rare for animals to go off their feet until just before death. While classical respiratory signs may be evident in calves, the causal agent often localizes in the joints with attendant arthritis and involvement of tendons. Complications accompanying this disease in calves may also include valvular endocarditis and myocarditis (Martel et al., 1983).
In the subacute form, symptoms may be limited to a slight cough, only noticeable when the animal is exercised. CBPP in Europe, unlike that caused in Africa where mortality rates are typically 10-70% in epizootics, is characterized by low morbidity and low or non-existent mortality with the majority of infected cattle showing chronic lesions; this is characteristic of endemic disease (Regalla, 1984). These differences are perhaps due to the fact that European cattle are healthier, better fed, subjected to less physical stress and are often permanently housed throughout the year (Nicholas and Palmer, 1994). In Italy during the early 1990s, less than 5% of cattle in an infected herd showed clinical signs (Guadagnini et al., 1991). The use of antibiotics and anti-inflammatory drugs may help to mask clinical signs and to accelerate the formation of chronic lesions. In Africa up to a third of cases that recover from acute disease become potential carriers. This figure is probably higher in Europe where there is a far more widespread use of antimicrobial drugs (Nicholas and Palmer, 1994).
EpidemiologyTop of page
CBPP is a disease of cattle. Infection is spread to a susceptible animal by the inhalation of expired breath laden with M. m. mycoides SC from an infected animal. Thus husbandry practices that promote close contact, and environmental conditions that avoid desiccation have a bearing on the rapidity of the spread of disease. In an infected herd most animals at any given moment do not present clinical disease, and the appearance of disease in uninfected areas is usually associated with the introduction of an infected but symptomless animal. Cattle movement, either commercial, nomadic or for transhumance, is usually the cause for the spread of CBPP from herd to herd.
The source of outbreaks of CBPP in Italy (1990-1993) was never successfully traced, although France was heavily implicated by virtue of the large number of cattle exported to Italy from there and because they had experienced disease in the previous decade. Immunological evidence was presented by Poumarat and Solsona (1995) that most strains from Italy differed from those from outbreaks in western Europe leading to the suggestion that "contamination of Italy did not arise from exportation of CBPP from south western Europe" but from a resurgence in Italy itself or from some unknown foci elsewhere in Europe. However, in the study, two Italian isolates had identical patterns to those from France, Spain and Portugal; but conclusions based on the small numbers of European strains tested from these last three countries were hard to sustain. A more thorough study by Goncalves et al. (1998) confirmed that two Italian strains were similar to other European strains but others lacked the 98 kDa protein, although again the study was disadvantaged by the small number of strains from France and Spain.
Epidemiological evidence from the Italian outbreaks implicated France, as well as, unexpectedly, Germany and Poland as outbreaks were linked directly to importation of affected animals from these countries (Regalla et al., 1996). However, it seems highly unlikely that Italy, which had been free of disease for nearly 100 years, should be infected from three different countries within the space of 2-3 years, two of which had not experienced outbreaks for over 50 years. The use of variable number tandem repeat (VNTR) typing of 44 stains from nine outbreaks in Italy indicates the infection originated from a single source (Gosney et al., 2011). Perhaps the tracing of the origin of these cattle was imperfect. Of the non-infected countries in Europe, only Switzerland and Hungary have recently conducted targeted surveys to demonstrate freedom from CBPP (Bashiruddin et al., 2001), although suspicious cases of respiratory disease where other causes have been ruled out are investigated in the UK and France.
M. m. mycoides SC has been identified from small ruminants in Africa (Ojo, 1976; Okoh and Ocholi, 1986) and some isolates have been shown to be pathogenic to cattle (Hudson et al., 1967). This makes more likely the possibility of cross transmission of this mycoplasma between small and large ruminants (Taylor et al., 1992). Recently, M. m. mycoides SC strains were isolated from healthy and diseased sheep and goats in Europe, Asia and Africa from countries with recent histories of CBPP (Brandao, 1995; Santis et al., 1999; Kusiluka et al., 2000; Srivastava et al., 2000). Although the role of small ruminants in the epidemiology of CBPP remains unclear, the possibility of carriage and transmission to cattle can not be discounted.
Impact: EconomicTop of page
The economic effects of CBPP can be enormous, resulting in heavy losses in cattle populations. In Britain 187,000 cattle died of CBPP in 1860 (Hutyra et al., 1938). In the Netherlands nearly 65,000 cattle died of CBPP between 1833-1850 (Laak, 1992). Over 100,000 cattle died within two years of the introduction of CBPP into South Africa (Trichard et al., 1989). In the early 1860s when the disease spread rapidly throughout Australia, it behaved as a virulent epidemic with losses of up to 75% of animals in an affected herd amounting to 1.4 million head. Consideration of the true costs of control and eradication of CBPP in Central and Southern Africa have been detailed recently (Windsor and Wood, 1998).
Disease TreatmentTop of page
Historically it has been indicated that antibiotics have no role in the eradication of CBPP either at farm level or, more importantly, nationally and internationally. Antibiotics can of course alleviate clinical signs, enabling some improvement in condition. For the individual farmer, particularly the nomad, this prevents the loss of often their only form of income and livelihood; the fact that these animals provide a constant source of infection to all those they come into contact with is not the farmer’s primary concern. Strategically, it could be argued that any reduction in mycoplasma excretion inevitably leads to a reduction in disease incidence. However this needs to be balanced against the damage caused by symptomless cattle spreading disease within and across international boundaries, which often results in explosive outbreaks among susceptible populations.
The reality is that in spite of official condemnation, antibiotics are used, so advice is necessary on which are the most effective. Ayling et al. (2000) carried out an in vitro trial of the effects of five commonly used antibiotics on a number of strains of M. m. mycoides SC, and concluded that tilmicosin and danofloxacin were effective both in terms of mycoplasmastatic and mycoplasmacidal activity; florfenicol and a tetracycline provide intermediate effectiveness while spectinomycin was ineffective against some strains. The use of fluoroquinalones, such as danofloxacin, is causing concern amongst regulatory authorities that feel these drugs should be restricted to human use because of rapid increases in microbial resistance.
More work needs to be done on the effectiveness of using antibiotics to control CBPP. Undoubtedly treatment of single animals will not control the spread of disease among infected herds, so strategic treatment plans need to be investigated as stated by the FAO-OIE-AU/IBAR-IAEA. Consultative Group Meeting on CBPP in Africa 2006. Understandably any recommendation to use antibiotics raises concerns about inducing antibiotic resistance in bacteria and any possible subsequent effect on future disease treatment in animals and man.
Prevention and ControlTop of page
Immunization and Vaccines
The currently approved product is a live attenuated vaccine, T144, which has been in constant use for nearly 40 years. It suffers from a short duration of efficacy, adverse reactions and cold chain dependence. Endobronchial inoculation of the vaccine has been shown to lead to CBPP (Mbulu et al., 2004). Furthermore, there has been suspicion that this vaccine and its variants have lost efficacy during the past 10 years and that the vaccination campaigns of 1995 and 1996 did not provide expected levels of protection. In 1995, such were the doubts about the identity and potency of the widely used streptomycin resistant variant, T144-SR that its use was discouraged (Tulasne et al., 1996). Various suggestions were made to explain vaccine failure including loss of immunogenicity, increased virulence of outbreaks and insufficient vaccine titres. March (2004) recommended improved buffering of the vaccine would improve the viable dose of the vaccine.
The development of new vaccines for CBPP has been problematical. Two approaches were used initially with the first concentrating on immunostimulating complexes (ISCOMs) as carriers for subunit vaccines. Whole detergent-solubilised cells of M. m. mycoides SC consisting mainly of membrane proteins have been used to obtain strong and long lasting immunity in mice and in vaccinated cattle. However field trials were less successful with poor immune responses although some protection to challenge was seen in vaccinated animals (Morein, 1998). A second approach focussed on the capsular polysaccharide of M. m. mycoides SC. Early work by March et al. (1999) suggests this complex may have a potential as a vaccine.
Since then work has been carried out using saponised whole cells and different purified proteins, however these approaches have generally resulted in no protection and even exacerbation of disease (Hamsten et al., 2010; Nicholas et al., 2004).
An understanding of the immunology associated with CBPP and the protective response may help in the formulation of a more effective vaccine. Scacchia et al. (2007) indicated that cyclosporine suppressed the immune response which impacted on the disease outcome. Information on the immune response can appear contradictory, with Totté et al. (2008) indicating CD4+ T cells have a major contribution in animals that have recovered from infection whereas Sacchini et al. (2011) say CD4+ T lymphocytes have a minor role in the control of a primary infection of CBPP in cattle.
ReferencesTop of page
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Abdo EM, Nicolet J, Miserez R, GonÇalves R, Regalla J, Griot C, Bensaide A, Krampe M, Frey J, 1998. Humoral and bronchial immune responses in cattle experimentally infected with Mycoplasma mycoides subsp. mycoides small colony type. Veterinary Microbiology, 59(2/3):109-122; 29 ref.
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Ayling RD, Baker SE, Nicholas RAJ, Peek ML, Simon AJ, 2000a. Comparison of in vitro activity of danofloxacin, florfenicol, oxytetracycline, spectinomycin and tilmicosin against Mycoplasma mycoides subsp. mycoides small colony type. Veterinary Record, 146:243-246.
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