Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide

Datasheet

contagious bovine pleuropneumonia

Toolbox

Datasheet

contagious bovine pleuropneumonia

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • contagious bovine pleuropneumonia
  • Overview
  • 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...

Don't need the entire report?

Generate a print friendly version containing only the sections you need.

Generate report

Pictures

Top of page
PictureTitleCaptionCopyright
Typical stance of cattle affected with CBPP showing an extended and arched back, extended head and abducted elbows. It has difficulty breathing and shows 'heave marks' from the strain.
TitleSymptoms
CaptionTypical stance of cattle affected with CBPP showing an extended and arched back, extended head and abducted elbows. It has difficulty breathing and shows 'heave marks' from the strain.
CopyrightAlain Provost
Typical stance of cattle affected with CBPP showing an extended and arched back, extended head and abducted elbows. It has difficulty breathing and shows 'heave marks' from the strain.
SymptomsTypical stance of cattle affected with CBPP showing an extended and arched back, extended head and abducted elbows. It has difficulty breathing and shows 'heave marks' from the strain.Alain Provost
Adhesions between lobes of the lung in cattle with CBPP.
TitlePathology
CaptionAdhesions between lobes of the lung in cattle with CBPP.
CopyrightJohn B. Bashiruddin
Adhesions between lobes of the lung in cattle with CBPP.
PathologyAdhesions between lobes of the lung in cattle with CBPP.John B. Bashiruddin
Adhesions between the visceral pleura and the chest wall in cattle with CBPP. A large part of the infected, necrotic and marbled parts of lung can be seen attached to the chest wall; the necrotic area is probably part of a large sequestrum, deep red areas of consolidation and marbled lung tissue are active sites of infection.
TitlePathology
CaptionAdhesions between the visceral pleura and the chest wall in cattle with CBPP. A large part of the infected, necrotic and marbled parts of lung can be seen attached to the chest wall; the necrotic area is probably part of a large sequestrum, deep red areas of consolidation and marbled lung tissue are active sites of infection.
CopyrightJohn B. Bashiruddin
Adhesions between the visceral pleura and the chest wall in cattle with CBPP. A large part of the infected, necrotic and marbled parts of lung can be seen attached to the chest wall; the necrotic area is probably part of a large sequestrum, deep red areas of consolidation and marbled lung tissue are active sites of infection.
PathologyAdhesions between the visceral pleura and the chest wall in cattle with CBPP. A large part of the infected, necrotic and marbled parts of lung can be seen attached to the chest wall; the necrotic area is probably part of a large sequestrum, deep red areas of consolidation and marbled lung tissue are active sites of infection.John B. Bashiruddin
View of chest cavity of a bovine infected with CBPP showing a collection of several litres of straw-coloured pleural fluid. This liquid is particularly rich in mycoplasma organisms and is the sample of choice for diagnostic purposes. Pure cultures of M. m. mycoides SC may be obtained from it, and it is suitable for use in rapid molecular confirmatory tests.
TitlePathology
CaptionView of chest cavity of a bovine infected with CBPP showing a collection of several litres of straw-coloured pleural fluid. This liquid is particularly rich in mycoplasma organisms and is the sample of choice for diagnostic purposes. Pure cultures of M. m. mycoides SC may be obtained from it, and it is suitable for use in rapid molecular confirmatory tests.
CopyrightJohn B. Bashiruddin
View of chest cavity of a bovine infected with CBPP showing a collection of several litres of straw-coloured pleural fluid. This liquid is particularly rich in mycoplasma organisms and is the sample of choice for diagnostic purposes. Pure cultures of M. m. mycoides SC may be obtained from it, and it is suitable for use in rapid molecular confirmatory tests.
PathologyView of chest cavity of a bovine infected with CBPP showing a collection of several litres of straw-coloured pleural fluid. This liquid is particularly rich in mycoplasma organisms and is the sample of choice for diagnostic purposes. Pure cultures of M. m. mycoides SC may be obtained from it, and it is suitable for use in rapid molecular confirmatory tests.John B. Bashiruddin
Fibrinous pleural deposits in the chest cavity of a bovine infected with CBPP. Yellow fibrinous deposits may be seen with pleural adhesions to the chest wall.
TitlePathology
CaptionFibrinous pleural deposits in the chest cavity of a bovine infected with CBPP. Yellow fibrinous deposits may be seen with pleural adhesions to the chest wall.
CopyrightJohn B. Bashiruddin
Fibrinous pleural deposits in the chest cavity of a bovine infected with CBPP. Yellow fibrinous deposits may be seen with pleural adhesions to the chest wall.
PathologyFibrinous pleural deposits in the chest cavity of a bovine infected with CBPP. Yellow fibrinous deposits may be seen with pleural adhesions to the chest wall.John B. Bashiruddin
Lung of affected cattle with chronic CBPP. Superficial view of a lobe showing distension of the lung caused by a sequestrum. Hepatization of the lobules and may be seen in parts of the lung and there is a thickening of the pleura.
TitlePathology
CaptionLung of affected cattle with chronic CBPP. Superficial view of a lobe showing distension of the lung caused by a sequestrum. Hepatization of the lobules and may be seen in parts of the lung and there is a thickening of the pleura.
CopyrightJohn B. Bashiruddin
Lung of affected cattle with chronic CBPP. Superficial view of a lobe showing distension of the lung caused by a sequestrum. Hepatization of the lobules and may be seen in parts of the lung and there is a thickening of the pleura.
PathologyLung of affected cattle with chronic CBPP. Superficial view of a lobe showing distension of the lung caused by a sequestrum. Hepatization of the lobules and may be seen in parts of the lung and there is a thickening of the pleura.John B. Bashiruddin
Lung of affected cattle in acute CBPP. An incision through a lesion showing hepatization of the lobules and oedema with thickening of the interlobular septa resulting in a marbled appearance.
TitlePathology - CBPP
CaptionLung of affected cattle in acute CBPP. An incision through a lesion showing hepatization of the lobules and oedema with thickening of the interlobular septa resulting in a marbled appearance.
CopyrightJohn B. Bashiruddin
Lung of affected cattle in acute CBPP. An incision through a lesion showing hepatization of the lobules and oedema with thickening of the interlobular septa resulting in a marbled appearance.
Pathology - CBPPLung of affected cattle in acute CBPP. An incision through a lesion showing hepatization of the lobules and oedema with thickening of the interlobular septa resulting in a marbled appearance.John B. Bashiruddin
Immunohistochemical staining of sections on CBPP-affected lung with the peroxidase-anti-peroxidase (PAP) method and rabbit hyperimmune serum against M. m. mycoides SC. Distended zone of cellular infiltration in a nectrotic area with concentrated staining, (original x20). Brown colour indicates areas of stain deposition indicative of the presence of mycoplasma antigen.
TitleHistology
CaptionImmunohistochemical staining of sections on CBPP-affected lung with the peroxidase-anti-peroxidase (PAP) method and rabbit hyperimmune serum against M. m. mycoides SC. Distended zone of cellular infiltration in a nectrotic area with concentrated staining, (original x20). Brown colour indicates areas of stain deposition indicative of the presence of mycoplasma antigen.
CopyrightJohn B. Bashiruddin
Immunohistochemical staining of sections on CBPP-affected lung with the peroxidase-anti-peroxidase (PAP) method and rabbit hyperimmune serum against M. m. mycoides SC. Distended zone of cellular infiltration in a nectrotic area with concentrated staining, (original x20). Brown colour indicates areas of stain deposition indicative of the presence of mycoplasma antigen.
HistologyImmunohistochemical staining of sections on CBPP-affected lung with the peroxidase-anti-peroxidase (PAP) method and rabbit hyperimmune serum against M. m. mycoides SC. Distended zone of cellular infiltration in a nectrotic area with concentrated staining, (original x20). Brown colour indicates areas of stain deposition indicative of the presence of mycoplasma antigen.John B. Bashiruddin
Immunohistochemical staining of sections on CBPP-affected lung with the peroxidase-anti-peroxidase (PAP) method and rabbit hyperimmune srum against M. m. mycoides SC. Positive specific reactivity surrounding a small blood vessel with a perrivascular 'cuff' of lymphocyte infiltration and endothilial damage (original x40). Brown colour indicates areas of stain deposition indicative of the presence of mycoplasma antigen.
TitleHistology
CaptionImmunohistochemical staining of sections on CBPP-affected lung with the peroxidase-anti-peroxidase (PAP) method and rabbit hyperimmune srum against M. m. mycoides SC. Positive specific reactivity surrounding a small blood vessel with a perrivascular 'cuff' of lymphocyte infiltration and endothilial damage (original x40). Brown colour indicates areas of stain deposition indicative of the presence of mycoplasma antigen.
CopyrightJohn B. Bashiruddin
Immunohistochemical staining of sections on CBPP-affected lung with the peroxidase-anti-peroxidase (PAP) method and rabbit hyperimmune srum against M. m. mycoides SC. Positive specific reactivity surrounding a small blood vessel with a perrivascular 'cuff' of lymphocyte infiltration and endothilial damage (original x40). Brown colour indicates areas of stain deposition indicative of the presence of mycoplasma antigen.
HistologyImmunohistochemical staining of sections on CBPP-affected lung with the peroxidase-anti-peroxidase (PAP) method and rabbit hyperimmune srum against M. m. mycoides SC. Positive specific reactivity surrounding a small blood vessel with a perrivascular 'cuff' of lymphocyte infiltration and endothilial damage (original x40). Brown colour indicates areas of stain deposition indicative of the presence of mycoplasma antigen.John B. Bashiruddin
Lung of affected cattle with chronic CBPP. Incision of sequestrum showing necrotic lung material encapsulated by fibrotic capsule. The sequesrtum contains degraded lung tissue, pus and mycoplasma organisms. Diagnostic samples are taken from the edge of the sequestrum next to the fibrous capsule where the greatest concentration of viable mycoplasma are present.
TitlePathology
CaptionLung of affected cattle with chronic CBPP. Incision of sequestrum showing necrotic lung material encapsulated by fibrotic capsule. The sequesrtum contains degraded lung tissue, pus and mycoplasma organisms. Diagnostic samples are taken from the edge of the sequestrum next to the fibrous capsule where the greatest concentration of viable mycoplasma are present.
CopyrightJohn B. Bashiruddin
Lung of affected cattle with chronic CBPP. Incision of sequestrum showing necrotic lung material encapsulated by fibrotic capsule. The sequesrtum contains degraded lung tissue, pus and mycoplasma organisms. Diagnostic samples are taken from the edge of the sequestrum next to the fibrous capsule where the greatest concentration of viable mycoplasma are present.
PathologyLung of affected cattle with chronic CBPP. Incision of sequestrum showing necrotic lung material encapsulated by fibrotic capsule. The sequesrtum contains degraded lung tissue, pus and mycoplasma organisms. Diagnostic samples are taken from the edge of the sequestrum next to the fibrous capsule where the greatest concentration of viable mycoplasma are present.John B. Bashiruddin
Lung of affected cattle with chronic CBPP. Incision of sequestrum demonstrating the presence of possible connections from the necrotic lung tissue to the outside envirnment through the bronchial passages.
TitlePathology
CaptionLung of affected cattle with chronic CBPP. Incision of sequestrum demonstrating the presence of possible connections from the necrotic lung tissue to the outside envirnment through the bronchial passages.
CopyrightJohn B. Bashiruddin
Lung of affected cattle with chronic CBPP. Incision of sequestrum demonstrating the presence of possible connections from the necrotic lung tissue to the outside envirnment through the bronchial passages.
PathologyLung of affected cattle with chronic CBPP. Incision of sequestrum demonstrating the presence of possible connections from the necrotic lung tissue to the outside envirnment through the bronchial passages.John B. Bashiruddin
The extended neck and head is due to respiratory distress and coughing.
TitleExternal symptoms
CaptionThe extended neck and head is due to respiratory distress and coughing.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
The extended neck and head is due to respiratory distress and coughing.
External symptomsThe extended neck and head is due to respiratory distress and coughing.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Enlarged joint is due to tendosynovitis and arthritis resulting from a mycoplasma.
TitlePathology
CaptionEnlarged joint is due to tendosynovitis and arthritis resulting from a mycoplasma.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Enlarged joint is due to tendosynovitis and arthritis resulting from a mycoplasma.
PathologyEnlarged joint is due to tendosynovitis and arthritis resulting from a mycoplasma.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
The thoracic wall is reflected; there is excessive fibrin on the parietal and visceral pleurae and a cloudy fluid in the thoracic cavity.
TitlePathology
CaptionThe thoracic wall is reflected; there is excessive fibrin on the parietal and visceral pleurae and a cloudy fluid in the thoracic cavity.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
The thoracic wall is reflected; there is excessive fibrin on the parietal and visceral pleurae and a cloudy fluid in the thoracic cavity.
PathologyThe thoracic wall is reflected; there is excessive fibrin on the parietal and visceral pleurae and a cloudy fluid in the thoracic cavity.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Pneumonic lesion in CBPP is not uncommonly unilateral.
TitlePathology
CaptionPneumonic lesion in CBPP is not uncommonly unilateral.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Pneumonic lesion in CBPP is not uncommonly unilateral.
PathologyPneumonic lesion in CBPP is not uncommonly unilateral.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Area of coagulation necrosis in a section of lung affected with CBPP.
TitlePathology
CaptionArea of coagulation necrosis in a section of lung affected with CBPP.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Area of coagulation necrosis in a section of lung affected with CBPP.
PathologyArea of coagulation necrosis in a section of lung affected with CBPP.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)

Identity

Top 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

English acronym

  • CBPP

French acronym

  • PPCB

Overview

Top 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 Animals

Top of page
Animal nameContextLife stageSystem
Bos grunniens (yaks)Domesticated host, Wild hostCattle & Buffaloes: All Stages
Bos indicus (zebu)Domesticated hostCattle & Buffaloes: All Stages
Bos mutus (yaks, wild)Domesticated host, Wild hostCattle & Buffaloes: All Stages
Bos taurus (cattle)Domesticated hostCattle & Buffaloes: All Stages
Bubalus bubalis (Asian water buffalo)Domesticated hostCattle & Buffaloes: All Stages

Systems Affected

Top of page respiratory diseases of large ruminants

Distribution

Top 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.


Europe


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).

 

Africa

 

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 

Country

Outbreaks

Cases

Deaths

Slaughtered

Destroyed

Burkina Faso

4

203

45

0

0

Cameroon

8

384

16

41

0

Central African Republic

43

3674

1270

0

0

Chad

17

342

200

37

18

Congo, DRC

15

8277

458

1361

0

Cote d'Ivoire

18

595

215

13

7

Ethiopia

29

457

112

12

0

Gabon

3

       

Ghana

75

127

1

115

0

Mali

4

204

82

119

0

Niger

6

41

10

0

0

Nigeria

22

489

96

221

9

Somalia

12

69

16

0

0

Sudan

2

202

92

108

0

Tanzania

8

399

177

0

0

Togo

9

13

3

1

0

Uganda

22

1330

193

67

0

Zambia

7

30

21

0

1

Total (18)

304

16836

3007

2095

35

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.

Asia


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 Table

Top 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/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AfghanistanNo information availableOIE, 2009
ArmeniaDisease not reportedOIE, 2009
AzerbaijanDisease never reportedOIE, 2009
BahrainDisease never reportedOIE, 2009
BangladeshDisease not reportedNULLLefèvre, 1991; Laak, 1992; OIE, 2009
BhutanNo information availableNULLLefèvre, 1991; Laak, 1992; OIE, 2009
Brunei DarussalamDisease not reportedOIE Handistatus, 2005
CambodiaNo information availableNULLLefèvre, 1991; Laak, 1992; OIE, 2009
ChinaNo information availableNULLLefèvre, 1991; Laak, 1992; OIE, 2009
-Hong KongDisease never reportedOIE, 2009
Georgia (Republic of)Last reported1932OIE Handistatus, 2005
IndiaDisease not reported1990Lefèvre, 1991; Laak, 1992; OIE, 2009
IndonesiaDisease never reportedOIE, 2009
IranDisease never reportedOIE, 2009
IraqDisease never reportedOIE, 2009
IsraelDisease not reportedOIE, 2009
JapanDisease not reportedOIE, 2009
JordanDisease never reportedNULLMlengeya, 1995; OIE, 2009
KazakhstanDisease not reportedOIE, 2009
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofDisease never reportedOIE, 2009
KuwaitDisease not reported1991Lefèvre, 1991; Laak, 1992; OIE, 2009
KyrgyzstanDisease never reportedOIE, 2009
LaosDisease not reportedOIE, 2009
LebanonDisease not reportedNULLLefèvre, 1991; Laak, 1992; OIE, 2009
MalaysiaDisease never reportedOIE, 2009
-Peninsular MalaysiaDisease never reportedOIE Handistatus, 2005
-SabahDisease never reportedOIE Handistatus, 2005
-SarawakDisease never reportedOIE Handistatus, 2005
MongoliaDisease not reported1973Lefèvre, 1991; Laak, 1992; OIE, 2009
MyanmarNo information availableNULLLefèvre, 1991; Laak, 1992; OIE, 2009
NepalNo information availableOIE, 2009
OmanDisease not reportedOIE, 2009
PakistanDisease not reportedOIE, 2009
PhilippinesDisease never reportedOIE, 2009
QatarNo information availableOIE, 2009
Saudi ArabiaDisease not reported2006Lefèvre, 1991; Laak, 1992; OIE, 2009
SingaporeDisease never reportedOIE, 2009
Sri LankaDisease never reportedOIE, 2009
SyriaDisease not reportedOIE, 2009
TaiwanDisease never reportedOIE Handistatus, 2005
TajikistanDisease never reportedOIE, 2009
ThailandDisease never reportedNULLLefèvre, 1991; Laak, 1992; OIE, 2009
TurkeyNo information availableOIE, 2009
TurkmenistanDisease never reportedOIE Handistatus, 2005
United Arab EmiratesDisease not reported1990Lefèvre, 1991; Laak, 1992; OIE, 2009
UzbekistanDisease never reportedOIE Handistatus, 2005
VietnamDisease never reportedNULLLefèvre, 1991; Laak, 1992; OIE, 2009
YemenDisease not reportedOIE, 2009

Africa

AlgeriaDisease never reportedOIE, 2012
AngolaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
BeninPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
BotswanaDisease not reportedOIE, 2009
Burkina FasoPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
BurundiDisease not reportedMasiga et al., 1998; Kané, 2000; OIE Handistatus, 2005
CameroonPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
Cape VerdeDisease never reportedOIE, 2012
Central African RepublicPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
ChadPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
CongoNo information availableMasiga et al., 1998; Kané, 2000; OIE, 2009
Congo Democratic RepublicPresentMasiga et al., 1998; Kané, 2000; AU-IBAR, 2011
Côte d'IvoirePresentMasiga et al., 1998; Kané, 2000; OIE, 2012
DjiboutiDisease not reportedOIE, 2012
EgyptDisease not reported1971OIE, 2012
EritreaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
EthiopiaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
GabonRestricted distributionOIE, 2012
GambiaPresentOIE, 2012
GhanaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
GuineaDisease not reported2006Masiga et al., 1998; Kané, 2000; OIE, 2009
Guinea-BissauNo information availableOIE, 2009
KenyaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
LesothoDisease never reportedOIE, 2012
LibyaDisease never reportedOIE Handistatus, 2005
MadagascarDisease never reportedOIE, 2012
MalawiDisease never reportedOIE, 2012
MaliPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
MauritaniaReported present or known to be presentMasiga et al., 1998; Kané, 2000
MauritiusDisease never reportedOIE, 2009
MoroccoDisease never reportedOIE, 2009
MozambiqueDisease never reportedOIE, 2009
NamibiaRestricted distributionBamhare, 2000; OIE, 2009
NigerReported present or known to be presentMasiga et al., 1998; Kané, 2000; OIE Handistatus, 2005
NigeriaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
RéunionDisease never reportedOIE Handistatus, 2005
Rwanda2010Masiga et al., 1998; Kané, 2000; OIE, 2012
Sao Tome and PrincipeDisease not reportedOIE Handistatus, 2005
SenegalDisease not reported1977Masiga et al., 1998; Kané, 2000; OIE, 2012
SeychellesDisease not reportedOIE, 2012
SomaliaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
South AfricaDisease not reported1924OIE, 2012
SudanPresentMasiga et al., 1998; Kané, 2000; AU-IBAR, 2011
SwazilandDisease never reportedOIE, 2012
TanzaniaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
TogoPresentMasiga et al., 1998; Kané, 2000; OIE, 2009
TunisiaDisease never reportedOIE, 2012
UgandaPresentMasiga et al., 1998; Kané, 2000; OIE, 2012
ZambiaPresentOIE, 2012
ZimbabweDisease not reportedOIE, 2009

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaDisease not reportedOIE, 2009
GreenlandDisease never reportedOIE, 2009
MexicoDisease never reportedOIE, 2009
USADisease not reportedOIE, 2009

Central America and Caribbean

BarbadosDisease never reportedOIE Handistatus, 2005
BelizeDisease never reportedOIE, 2009
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease never reportedOIE Handistatus, 2005
Costa RicaDisease never reportedOIE, 2009
CubaDisease never reportedOIE, 2009
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicDisease never reportedOIE, 2009
El SalvadorDisease never reportedOIE, 2009
GuadeloupeDisease never reportedOIE, 2009
GuatemalaDisease never reportedOIE, 2009
HaitiDisease never reportedOIE, 2009
HondurasDisease never reportedOIE, 2009
JamaicaDisease never reportedOIE, 2009
MartiniqueDisease never reportedOIE, 2009
NicaraguaDisease never reportedOIE, 2009
PanamaDisease never reportedOIE, 2009
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease never reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaDisease never reportedOIE, 2009
BoliviaDisease never reportedOIE, 2009
BrazilDisease never reportedOIE, 2009
ChileDisease never reportedOIE, 2009
ColombiaDisease never reportedOIE, 2009
EcuadorDisease never reportedOIE, 2009
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaDisease not reportedOIE, 2009
GuyanaDisease never reportedOIE Handistatus, 2005
ParaguayDisease never reportedOIE Handistatus, 2005
PeruDisease never reportedOIE, 2009
UruguayDisease never reportedOIE, 2009
VenezuelaDisease never reportedOIE, 2009

Europe

AlbaniaDisease not reportedOIE, 2009
AndorraLast reported1957OIE Handistatus, 2005
AustriaDisease not reportedOIE, 2009
BelarusDisease never reportedOIE, 2009
BelgiumDisease not reportedOIE, 2009
Bosnia-HercegovinaDisease never reportedOIE Handistatus, 2005
BulgariaDisease never reportedOIE, 2009
CroatiaDisease never reportedOIE, 2009
CyprusDisease never reportedOIE, 2009
Czech RepublicDisease not reportedOIE, 2009
DenmarkDisease not reportedOIE, 2009
EstoniaDisease never reportedOIE, 2009
FinlandDisease not reportedOIE, 2009
FranceDisease not reportedOIE, 2009
GermanyDisease not reportedOIE, 2009
GreeceDisease never reportedOIE, 2009
HungaryDisease not reportedOIE, 2009
IcelandDisease never reportedOIE, 2009
IrelandDisease not reportedOIE, 2009
Isle of Man (UK)Disease never reportedOIE Handistatus, 2005
ItalyDisease not reportedOIE, 2009
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease not reportedOIE, 2009
LiechtensteinDisease not reportedOIE, 2009
LithuaniaDisease never reportedOIE, 2009
LuxembourgDisease never reportedOIE, 2009
MacedoniaDisease never reportedOIE, 2009
MaltaDisease never reportedOIE, 2009
MoldovaLast reported1946OIE Handistatus, 2005
MontenegroDisease never reportedOIE, 2009
NetherlandsDisease not reportedOIE, 2009
NorwayDisease not reportedOIE, 2009
PolandDisease not reportedOIE, 2009
PortugalDisease not reportedOIE, 2009
RomaniaDisease not reportedOIE, 2009
Russian FederationDisease not reportedOIE, 2009
SerbiaDisease never reportedOIE, 2009
SlovakiaDisease not reportedOIE, 2009
SloveniaDisease never reportedOIE, 2009
SpainDisease not reportedOIE, 2009
SwedenDisease not reportedOIE, 2009
SwitzerlandDisease not reportedOIE, 2009
UKDisease not reportedOIE, 2009
-Northern IrelandLast reported1893OIE Handistatus, 2005
UkraineDisease never reportedOIE, 2009
Yugoslavia (former)Disease never reportedOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Disease never reportedOIE Handistatus, 2005

Oceania

AustraliaDisease not reportedOIE, 2009
French PolynesiaDisease never reportedOIE, 2009
New CaledoniaDisease never reportedOIE, 2009
New ZealandDisease not reportedOIE, 2009
SamoaDisease never reportedOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathology

Top of page

Gross Lesions


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.


Histopathology


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.

Diagnosis

Top of page

Laboratory Diagnosis



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).


Biochemical Tests


 

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).


Serological Tests


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).


Molecular Diagnosis

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/Signs

Top of page
SignLife StagesType
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 Course

Top 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.



Hyperacute Form


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.

Acute Form

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).


Subacute/Chronic Forms


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).

Epidemiology

Top 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: Economic

Top 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 Treatment

Top 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 Control

Top 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.

References

Top of page

Abdo EM, Nicolet J, Frey J, 2000. Antigenic and genetic characterization of lipoprotein LppQ from Mycoplasma mycoides subsp. mycoides SC. Clinical and Diagnostic Laboratory Immunology, 7(4):588-595; 35 ref.

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.

Abu-Amero K, Halablab MA, Miles RJ, 1996. Nisin resistance distinguishes Mycoplasma from Acholeplasma species and provides a basis for selective growth media. Applied and Environmental Microbiology, 62:3107-3111.

African Union-Interafrican Bureau for Animal Resources, 2011. Panafrican Animal Health Yearbook 2011. Pan African Animal Health Yearbook, 2011:xiii + 90 pp. http://www.au-ibar.org/index.php?option=com_flexicontent&view=items&cid=71&id=109&Itemid=56&lang=en

Aluotto BB, Wittler RG, Williams CO, Faber JE, 1970. Standard bacteriologic techniques for the characterization of Mycoplasma species. International Journal of Systematic Bacteriology, 20:35-58.

Amanfu W, Masupu KV, Adom EK, Raborokgwe MV, Bashiruddin JB, 1998. An outbreak of contagious bovine pleuropneumonia in Ngamiland district of north-western Botswana. Veterinary Record, 143(2):46-48; 13 ref.

Askaa G, Christiansen C, Erno H, 1973. Bovine mycoplasmas: genome size and base composition of DNA. Journal of General Microbiology, 75:283-286.

Askaa G, Erno H, Ojo MO, 1978. Bovine mycoplasmas: Classification of groups related to Mycoplasma mycoides. Acta Veterinaria Scandinavia, 19:166-178.

Ayling R, Miles RJ. Regalla J, Nicholas RAJ, 1999. Development of improved serological tests for the diagnosis of CBPP. Proceedings of the International Symposium on Mycoplasmas of Ruminants, Toulouse, France, June 2-4 1999.

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.

Ayling RD, Godinho K, Nicholas RAJ, 2007. Comparative studies on the in vitro antimicrobial sensitivities of Mycoplasma mycoides subsp. mycoides SC type and Mycoplasma bovis. In: CBPP Control: antibiotics to the rescue. FAO-OIE-AU/IBAR-IAEA Consultative Group Meeting on CBPP in Africa, 2006. Rome, Italy: FAO, 51-61.

Bamhare C, 2000. CBPP surveillance in vaccinated areas: Namibia experience with CBPP vaccines prepared from the T1-44 and T1-SR strains. Report of the second meeting of the FAO/OIE/OAU/IEAE Consultative Group on Contagious Bovine Pleuropneumonia (CBPP), FAO, Rome, 24-26 October, 2000.

Bashiruddin JB, De Santis P, Vacciana A, Santini FG, 1999a. Detection of Mycoplasma mycoides subsp. mycoides SC in clinical material by rapid colorimetric PCR. Molecular and Cellular Probes 13, 23-28.

Bashiruddin JB, De Santis P, Varga E, Stipkovits L, 2001. Confirmation of the presence of Mycoplasma bovis in Hungarian cattle with pneumonia resembling pleuropneumonia. Veterinary Record (in press).

Bashiruddin JB, Nicholas RAJ, Santini FG, Ready RA, Woodward MJ, Taylor TK, 1994. Use of the polymerase chain reaction to detect mycoplasma DNA in cattle with contagious bovine pleuropneumonia. Veterinary Record, 134(10):240-241; 5 ref.

Bashiruddin JB, Santini FG, Santis Pde, Visaggio MC, Francesco Gdi, D'Angelo A, Nicholas RAJ, 1999. Detection of Mycoplasma mycoides subspecies mycoides in tissues from an outbreak of contagious bovine pleuropneumonia by culture, immunohistochemistry and polymerase chain reaction. Veterinary Record, 145(10):271-274; 16 ref.

Bashiruddin JB, Taylor TK, Gould AR, 1994. A PCR-based test for the specific identification of Mycoplasma mycoides subspecies mycoides SC. Journal of Veterinary Diagnostic Investigation, 6(4):428-434; 14 ref.

Bashiruddin JB, Windsor GD, 1998. Development of coloured colonies as an aid to identification of certain pathogenic mycoplasmas. 12th International Congress of the International Organization for Mycoplasmology, July 22-28, Sydney, Australia.

Bashiruddin JB, Windsor GD, Regalla J, De Santis P, 1999c. Development of coloured Mycoplasma mycoides colonies on solid media as an aid to rapid diagnosis. Proceedings of the International Symposium on Mycoplasmas of Ruminants. Toulouse, France, June 2-4, 1999.

Bellini S, Giovannini A, Francesco Cdi, Tittarelli M, Caporale V, 1998. Sensitivity and specificity of serological and bacteriological tests for contagious bovine pleuropneumonia. Revue Scientifique et Technique - Office International des épizooties, 17(3):654-659; 10 ref.

Brandao E, 1995. Isolation and identification of Mycoplasma mycoides subspecies mycoides SC strains in sheep and goats. Veterinary Record, 136(4):98-99; 4 ref.

Buttery SH, Cottew GS, Lloyd LC, 1980. Effect of soluble factors from Mycoplasma mycoides subsp. mycoides on the collagen content of bovine connective tissue. Journal of Comparative Pathology, 90:303-314.

Choudhary MR, Datta BM, Das SK, Sarma DK, 1987. Screening of CBPP in Assam using complement fixation test. Indian Veterinary Journal, 64(4):345-346; 3 ref.

Churchward CP, Flint JP, Danks C, Humbert I, Hashem E, Nicholas RAJ, Ayling RD, 2007. Development and initial evaluation of a lateral flow device for the rapid detection of contagious bovine pleuropneumonia. In: Proceedings of the World Association of Veterinary Laboratory Diagnosticians, 13th International Symposium, Melbourne, Australia, 12-14 November 2007. Melbourne, Australia: World Association of Veterinary Laboratory Diagnosticians.

Costas M, Leach RH, Mitchelmore DL, 1987. Numerical analysis of PAGE protein patterns and the taxonomic relationships within the 'Mycoplasma mycoides cluster'. Journal of General Microbiology, 133(12):3319-3329; 16 ref.

Dedieu L, Mady V, Lefevre PC, 1994. Development of a selective polymerase chain reaction assay for the detection of Mycoplasma mycoides subsp. mycoides S.C. (contagious bovine pleuropneumonia agent). Veterinary Microbiology, 42(4):327-339; 12 ref.

Done SH, Nicholas R, Palmer N, 1995. Contagious bovine pleuropneumonia (CBPP). An emerging disease in Europe. Cattle Practice, 3(1):13-20; 10 ref.

Egwu GE, Nicholas RAJ, Ameh JA, Bashiruddin JB, 1996. Contagious bovine pleuropneumonia: an update. Veterinary Bulletin, 66:875-888.

Ferronha MH, Nunes Petisca JL, Sousa Ferreira H, Machado M, Regalla J, 1988. Localizacão de antigenios Mycoplasma mycoides subspecies mycoides nas lesoes do pulmao de bovinos com peripneumonia. Repositorio de Trabalhos do Laboratorio Nacional de Investigacao Veterinaria. Numero Especial, 25-36.

Ferronha MH, Nunes Petisca JL, Sousa Ferreira H, Machado M, Regalla J, Penha GonÇalves A, 1990. Detection of Mycoplasma mycoides subsp. mycoides immunoreactive sites in pulmonary tissue and sequestra of bovines with contagious pleuropneumonia. Contagious bovine pleuropneumonia. A seminar in the Community Programme for the Coordination of Agricultural Research, held in Lisbon on 7 and 8 December, 1988., 17-25; [Report No. EUR 12065 EN]; 14 ref.

Freundt EA, 1955. The classification of the pleuropneumonia-like group of organisms (Borrelomycetales). International Bulletin of Bacteriological Nomenclature and Taxonomy, 5:67-78.

Freundt EA, 1983. Culture media for classic mycoplasmas. In: Razin S, Tully JG, eds. Methods in Mycoplasmology Vol. 1. Mycoplasma characterization. New York, USA: Academic Press, 127-135.

Goff Cle, Thiaucourt F, 1998. A competitive ELISA for the specific diagnosis of contagious bovine pleuropneumonia (CBPP). Veterinary Microbiology, 60(2/4):179-191; 40 ref.

Gonçalves R, Regalla J, Ayling RD, Nicholas RAJ, 2008. Impact of Mycoplasma bovis infection on serosurveillance for contagious bovine pleuropneumonia. Veterinary Record, 163(21):632-633. http://veterinaryrecord.bvapublications.com/archive/

GonÇalves R, Regalla J, Nicolet J, Frey J, Nicholas R, Bashiruddin J, Santis Pde, GonÇalves AP, 1998. Antigen heterogeneity among Mycoplasma mycoides subsp. mycoides SC isolates: discrimination of major surface proteins. Veterinary Microbiology, 63(1):13-28; 27 ref.

Gosney F, Corrò M, Iob L, McAuliffe L, Nicholas RAJ, 2011. Variable number tandem repeat (VNTR) typing of strains of Mycoplasma mycoides subspecies mycoides small colony isolated from the north-eastern regions of Italy between 1990 and 1993. Veterinary Microbiology, 147(1/2):220-222. http://www.sciencedirect.com/science/journal/03781135

Gourlay RN, Howard CJ, 1983. Respiratory mycoplasmosis. Advances in Veterinary Science and Comparative Medicine, 26:289-332; 6pp. of ref.

Guadagnini PF, Simone Fde, Panina GF, Gaffuri A, Bugnetti M, Finazzi M, Mandelli G, Sironi G, Belloli A, 1991. Contagious bovine pleuropneumonia (CBPP). A review with field observations. Selezione Veterinaria, 32(1):3-31; 16 ref.

Hamsten C, Tjipura-Zaire G, McAuliffe L, Huebschle OJB, Scacchia M, Ayling RD, Persson A, 2010. Protein-specific analysis of humoral immune responses in a clinical trial for vaccines against contagious bovine pleuropneumonia. Clinical and Vaccine Immunology, 17(5):853-861. http://cvi.asm.org/cgi/content/abstract/17/5/853

Hotzel H, Sachse K, Pfützner H, 1996. A PCR scheme for differentiation of organisms belonging to the Mycoplasma mycoides cluster. Veterinary Microbiology, 49(1/2):31-43; 21 ref.

Houshaymi B, Rice P, Agbanyim C, Khan L, Nicholas RAJ, Miles R, 2000. Biochemical characterisation of Mycoplasma mycoides subspecies mycoides small colony strains and the development of rapid diagnostic biochemical tests. In: Bergonier D, Frey J, eds. COST 826. Agriculture and biotechnology. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics. Volume IV. Luxembourg, Germany: Office for official publications of the European Communities.

Hudson JR, 1971. Contagious bovine pleuropneumonia. Rome, Italy: FAO.

Hudson JR, Cottew GS, Adler HE, 1967. Diseases of goats caused by mycoplasmas: a review of the subject with some new findings. Annals of the New York Academy of Sciences, 143:287-297.

Hutyra F, Marek J, Manninger R, 1949. Special pathology and therapeutics of the diseases of domestic animals. London, UK: Bailliere, Tindall and Cox.

Johansson KE, Persson A, Persson M, 1998. Diagnosis of contagious caprine and contagious bovine pleuropneumonia by PCR and restriction enzyme analysis. Towards livestock disease diagnosis and control in the 21st century: proceedings of an International Symposium on Diagnosis and Control of Livestock Diseases Using Nuclear and Related Techniques, Vienna, Austria, 7-11 April 1997., 137-158; 35 ref.

Kané M, 2000. Long endemicity of CBPP in West and Central Africa. Report of the second meeting of the FAO/OIE/OAU/IEAE Consultative Group on Contagious Bovine Pleuropneumonia (CBPP), FAO, Rome 24-26 October, 2000.

Kusiluka LJ, Semuguruka WD, Kazwala RR, Ojeniy B, Friis NF, 2000. Demonstration of Mycoplasma capricolum subsp. capripneumonae and Mycoplasma mycoides subsp. mycoides, small colony type in outbreaks of capine pleuropneumonia in eastern Tanzania. Acta Veterinaria Scandinavica, 41(3):311-319.

Kusiluka LJM, Sudi FF, 2003. Review of successes and failures of contagious bovine pleuropneumonia control strategies in Tanzania. Preventive Veterinary Medicine, 59(3):113-123.

Laak EAter, 1992. Contagious bovine pleuropneumonia, a review. Veterinary Quarterly, 14(3):104-110; 41 ref.

Leach RH, Costas M, Mitchelmore DL, 1989. Relationship between Mycoplasma mycoides subsp. mycoides ('Large-colony' strains) and M. mycoides subsp. capri, as indicated by numerical analysis of one-dimensional SDS-PAGE protein patterns. Journal of General Microbiology, 135(11):2993-3000; 17 ref.

Lefèvre PC, 1991. [Atlas of infectious diseases of ruminants.] Atlas des maladies infecteuses des ruminants. Maisons Alfort, France: Institut d'Elevage et de Medicine Veterinaire des pays Tropicaux.

Lesnoff M, Laval G, Bonnet P, Chalvet-Monfray K, Lancelot R, Thiaucourt F, 2004. A mathematical model of the effects of chronic carriers on the within-herd spread of contagious bovine pleuropneumonia in an African mixed crop-livestock system. Preventive Veterinary Medicine, 62(2):101-117.

Manso-Silván L, Vilei EM, Sachse K, Djordjevic SP, Thiaucourt F, Frey J, 2009. Mycoplasma leachii sp. nov. as a new species designation for Mycoplasma sp. bovine group 7 of leach, and reclassification of Mycoplasma mycoides subsp. mycoides LC as a serovar of Mycoplasma mycoides subsp. capri. International Journal of Systematic and Evolutionary Microbiology, 59:1353-1358.

March JB, 2004. Improved formulations for existing CBPP vaccines: recommendations for change. In: Towards sustainable CBPP control programmes for Africa. Proceedings FAO-OIE-AU/IBAR-IAEA Consultative Group on Contagious Bovine Pleuropneumonia, Third Meeting, Rome, Italy, 12-14 November 2003. Rome, Italy: Food and Agriculture Organization of the United Nations (FAO), 102-109.

March JB, Brodie M, 2000. Comparison of the virulence of European and African isolates of Mycoplasma mycoides subspecies mycoides small colony type. Veterinary Record, 147:20-21.

March JB, Hitchen P, Morris HR, Dell A, 1999a. Analysis of the capsular polysaccharide of Mycoplasma mycoides subsp. mycoides SC, the causal agent of CBPP: purification, composition and its role in infection and immunity. In: Stipkovits L, Rosengarten R, Frey J, eds. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics. Volume III. Luxembourg, Grmany: Office for official publications of the European Communities, 69-72.

March JB, Jones GE, Williamson HS, Amanfu W, 1999. Studies on the immunological diversity of type, vaccine and wild strains of Mycoplasma mycoides subsp. mycoides SC. In: Stipkovits L, Rosengarten R, Frey J, eds. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics. Volume III. Luxembourg, Germany: Office for official publications of the European Communities, 159-162.

Mariner JC, McDermott J, Heesterbeek JAP, Thomson G, Martin SW, 2006. A model of contagious bovine pleuropneumonia transmission dynamics in East Africa. Preventive Veterinary Medicine, 73(1):55-74.

Martel JL, Perrin M, Belli P, Froget FJ, 1983. The clinical aspects of contagious bovine pleuropneumonia. The diagnosis of contagious bovine pleuropneumonia and other infections with Mycoplasma mycoides subspecies mycoides, 4-7; [Document EUR 8654]; 9 ref.

Masiga W, Rossiter P, Bessin R, 1998. Contagious bovine pleuropneumonia. I. Epidemiology: Present situation of CBPP in Africa and epidemiological trends, Proceedings of the FAO/OIE/OAU CBPP Consultative Group Meeting, FAO, Rome, 5-7 October, 1998.

Masiga WN, Domenech J, Windsor RS, 1996. Manifestation and epidemiology of contagious bovine pleuropneumonia in Africa. Revue Scientifique et Technique - Office International des Épizooties, 15(4):1283-1308.

Mbulu RS, Tjipura-Zaire G, Lelli R, Frey J, Pilo P, Vilei EM, Mettler F, Nicholas RAJ, Huebschle OJB, 2004. Contagious bovine pleuropneumonia (CBPP) caused by vaccine strain T1/44 of Mycoplasma mycoides subsp. mycoides SC. Veterinary Microbiology, 98(3/4):229-234.

Miles K, Churchward CP, McAuliffe L, Ayling RD, Nicholas RAJ, 2006. Identification and differentiation of European and African/Australian strains of Mycoplasma mycoides subspecies mycoides small-colony type using polymerase chain reaction analysis. Journal of Veterinary Diagnostic Investigation, 18(2):168-171.

Miles RJ, Agbanyim CA, 1998. Determination of substrate utilisation rates by mycoplasmas. In: Miles RJ, Nicholas RAJ, eds. Mycoplasma Protocols, Methods in Molecular Biology, Vol. 104. Totowa, New Jersey, USA: Humana Press, 95-104.

Miles RJ, Taylor RR, Varsani H, 1991. Oxygen uptake and H2O2 production by fermentative Mycoplasma spp. Journal of Medical Microbiology, 34:219-223.

Miserez R, Pilloud T, Cheng X, Nicolet J, Griot C, Frey, J, 1997. Development of a sensitive nested PCR method for the specific detection of Mycoplasma mycoides subsp. mycoides SC. Molecular and Cellular Probes, 11:103-111.

Mlengeya TDK, 1995. Current status of contagious pleuropneumonia (CBPP) in Tanzania. A paper presented at the National Conference of the Tanzanian Veterinary Medical Association, held in Arusha on 19 May, 1995, 1-11.

Morein B, 1998. Immunity and vaccination in relation to CBPP. Proceedings of FAO/OIE/OAU CBPP Consultative Group Meeting, Rome, 5-7 October, 1998.

Muuka G, Hang'ombe BM, Nalubamba KS, Kabilika S, Mwambazi L, Muma JB, 2011. Comparison of complement fixation test, competitive ELISA and LppQ ELISA with post-mortem findings in the diagnosis of contagious bovine pleuropneumonia (CBPP). Tropical Animal Health and Production, 43(5):1057-1062. http://springerlink.metapress.com/link.asp?id=103008

Newton LG, 1992. Contagious bovine pleuropneumonia in Australia: some historic highlights from entry to eradication. Australian Veterinary Journal, 69(12):306-317; 96 ref.

Niang M, Sery A, Cissé O, Diallo M, Doucouré M, Koné M, Simbé CF, Amanfu W, Thiaucourt F, 2007. Effect of antibiotic therapy on the pathogenesis of CBPP. In: CBPP Control: antibiotics to the rescue. FAO-OIE-AU/IBAR-IAEA Consultative Group Meeting on CBPP in Africa, 2006. Rome, Italy: FAO, 25-32.

Nicholas R, Bashiruddin J, Ayling R, Miles R, 2000. Contagious bovine pleuropneumonia: a review of recent developments. Veterinary Bulletin, 70(8):827-838; 4 pp. of ref.

Nicholas RAJ, Aschenborn HKO, Ayling RD, Loria GR, Lukhele O, Tijpura-Zaire G, Godinho K, Hubschle OJB, 2007. Effect of Advocin on the elimination of CBPP from the Caprivi Region of Namibia. In: CBPP Control: antibiotics to the rescue. FAO-OIE-AU/IBAR-IAEA Consultative Group Meeting on CBPP in Africa, 2006. Rome, Italy: FAO, 33-40.

Nicholas RAJ, Baker SE, 1998. Recovery of mycoplasmas from animals. In: Miles RJ, Nicholas RAJ, eds. Mycoplasma Protocols. Totowa, USA: Humana Press, 37-44.

Nicholas RAJ, Bashiruddin JB, 1995. Mycoplasma mycoides subspecies mycoides (small colony variant): the agent of contagious bovine pleuropneumonia and member of the "Mycoplasma mycoides cluster". Journal of Comparative Pathology, 113(1):1-27; 122 ref.

Nicholas RAJ, Bashiruddin JB, Santini FG, Regalla J, Taylor TK, 1994. Evaluation of a polymerase chain reaction for contagious bovine pleuropneumonia in naturally infected cattle. IOM Letters, 3:15-16.

Nicholas RAJ, Palmer NMA, 1994. Contagious bovine pleuropneumonia in Europe. State Veterinary Journal, 4:14-16.

Nicholas RAJ, Santini FG, Clark KM, Palmer NMA, Santis Pde, Bashiruddin JB, 1996. A comparison of serological tests and gross lung pathology for detecting contagious bovine pleuropneumonia in two groups of Italian cattle. Veterinary Record, 139(4):89-93; 16 ref.

Nicholas RAJ, Tjipura-Zaire G, Mbulu RS, Scacchia M, Mettler F, Frey J, Abusugra I, Huebschle OJB, 2004. An inactivated whole cell vaccine and LppQ subunit vaccine appear to exacerbate the effects of CBPP in adult cattle. In: Towards sustainable CBPP control programmes for Africa. Proceedings FAO-OIE-AU/IBAR-IAEA Consultative Group on Contagious Bovine Pleuropneumonia, Third Meeting, Rome, Italy, 12-14 November 2003. Rome, Italy: Food and Agriculture Organization of the United Nations (FAO), 91-97.

Nunes Petisca JL, Costa Durao JF, Lage M, GonÇalves JM, Azevedo Ramos MJ, Baptista R, Galo A, Monteiro M, Caiado J, Silva ER, Mota JF, Afonso A, 1990. Pathogenesis and pathological features of contagious bovine pleuropneumonia (CBPP). Contagious bovine pleuropneumonia. A seminar in the Community Programme for the Coordination of Agricultural Research, held in Lisbon on 7 and 8 December, 1988., 2-6; [Report No. EUR 12065 EN]; 11 ref.

Nunes Petisca JL, Duraco JFC, Lage M, Gonçalves JMM, Ramos MJA, Baptista R, Galo R, Monteiro M, Caido J, Silva ER, Mota JF, Alfonso A, 1988. [Pathogenesis and pathology of contagious bovine pleuropneumonia in Portugal.] Patogenia e anatomia atologica de peripneumonia contagiosa dos bovinos (PPCB) em Portugal. Repositorio des Trabalhos do Laboratorio Nacional de Investigacão Veterinaria (Lisbon), Numero special, 1-10.

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

OIE, 1993. Meeting of the ad hoc group on contagious bovine pleuropneumonia surveillance systems: recomended standards for epidemiological surveillance of contagious bovine pleuropneumonia. OIE, Paris, France, 7-9 June 1993.

OIE, 1997. Revue Scientifique et Technique: Office International des Epizooties, 16:898-904.

OIE, 1998. Proceedings of FAO/OIE/OAU on CBPP Consultative Group Meeting, FAO, Rome, Italy, 5-7 October, 1998.

OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int

OIE, 2012. World Animal Health Information Database. Version 2. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home

Ojo M, 1976. Caprine pneumonia IV. Pathogenicity of Mycoplasma mycoides subspecies capri and caprine strains of Mycoplasma mycoides subsp. mycoides for goats. Journal of Comparative Pathology, 86:519-529.

Okoh AEJ, Ocholi RA, 1986. Disease associated with Mycoplasma mycoides, subspecies mycoides in sheep in Nigeria. Veterinary Record, 118(8):212; 11 ref.

Ozcan S, Rice P, Al-Sheikhly D, Suchak A, Patel P, Miles R, 1999. Approaches to the development of selective media for Mycoplasma agalactiae and Mycoplasma bovis. In: Stipkovits L, Rosengarten R, Frey J, eds. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics. Volume III. Luxembourg, Grmany: Office for official publications of the European Communities, 105-108.

Persson A, Pettersson B, Bölske G, Johansson KE, 1999. Diagnosis of contagious bovine pleuropneumonia by PCR-laser-induced fluorescence and PCR-restriction endonuclease analysis based on the 16S rRNA genes of Mycoplasma mycoides subsp. mycoides SC. Journal of Clinical Microbiology, 37(12):3815-3821; 30 ref.

Plackett P, Buttery SH, Cottew GS, 1963. Carbohydrates of some mycoplasma strains. Proceedings of the 8th International Congress for Microbiology, Montreal, 1962. Recent Progress in Microbiology, 8:535-547.

Poumarat F, Solsona M, 1995. Molecular epidemiology of Mycoplasma mycoides subsp. mycoides biotype Small Colony, the agent of contagious bovine pleuropneumonia. Veterinary Microbiology, 47(3/4):305-315; 36 ref.

Provost A, Perreau P, Bréard A, Goff Cle, Martel JL, Cottew GS, 1987. Contagious bovine pleuropneumonia. Revue Scientifique et Technique, Office International des épizooties, 6(3):565-679; 99 ref.

Pyle LE, Taylor T, Finch LR, 1990. Genomic maps of some strains within the Mycoplasma mycoides cluster. Journal of Bacteriology, 172(12):7265-7268; 20 ref.

Rawadi G, Lemercier B, Roulland-Dussoix D, 1995. Application of an arbitrarily-primed polymerase chain reaction to mycoplasma identification and typing within the Mycoplasma mycoides cluster. Journal of Applied Bacteriology, 78(6):586-592; 28 ref.

Razin S, 1978. The mycoplasmas. Microbiological Reviews, 42:414-470.

Razin S, Barile MF, Harasawa R, Amikam D, Glaser DG, 1983. Characterisation of the mycoplasma genome. Yale Journal of Biological Medicine, 56:357-366.

Regalla J, 1984. Epidemiological aspects of the contagious bovine pleuropneumonia in Portugal. Repositório de Trabalhos do Laboratorio Nacional de InvestigaÇao Veterinaria, 16:13, 15-18; [4 pl., 4 maps]; 2 ref.

Regalla J, Caporale V, Giovannini A, Santini F, Martel JL, Penha GonÇalves A, 1996. Manifestation and epidemiology of contagious bovine pleuropneumonia in Europe. Revue Scientifique et Technique - Office International des épizooties, 15(4):1309-1329; 28 ref.

Regalla J, Gonçalves R, Penha Gonçalves A, 1994. Humoral immune response kinetics of cattle submitted to contact transmission with animals experimentally infected with Mycoplasma mycoides subsp. mycoides SC. IOM Letters, 3:107-108.

Rice P, Houshaymi BM, Nicholas RAJ, Miles RJ, 2000a. A rapid biochemical test to aid identification of Mycoplasma mycoides subsp. mycoides small colony (SC) strains. Letters in Applied Microbiology, 30:70-74.

Rice P, Obeid O, Miles R, 2000b. The development of improved media for the isolation and cultivation of Mycoplasma mycoides subspecies mycoides small colony strains. In: Bergonier D, Frey J, eds. COST 826 Agriculture and biotechnology. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics. Vol. 4. Luxembourg, Germany: Office for official publications of the European Communities, 147-149.

Rodriguez F, Ball HJ, Finlay D, Campbell D, Mackie DP, 1996. Detection of Mycoplasma mycoides subspecies mycoides by monoclonal antibody-based sandwich ELISA. Veterinary Microbiology, 51(1/2):69-76; 20 ref.

Rodriguez JL, Ermel RW, Kenny TP, Brooks DL, DaMassa AJ, 1997. Polymerase chain reaction and restriction endonuclease digestion for selected members of the "Mycoplasma mycoides cluster" and Mycoplasma putrefaciens. Journal of Veterinary Diagnostic Investigation, 9(2):186-190; 17 ref.

Rodwell AW, Mitchell A, 1979. Nutrition, growth and reproduction. In: Razin S, Tully JG, eds. The Mycoplasmas. Vol 1. New York, USA: Academic Press.

Rweyemamu M, Paskin R, Benkirane A, Martin V, Roeder P, Wojciechowski K, 2000. Emerging diseases of Africa and the Middle East. Annals of the New York Academy of Sciences [Tropical veterinary diseases: Control and prevention in the context of the New World Order. Proceedings of the Fifth Biennial Conference of the Society for Tropical Veterinary Medicine, held on June 12-16, 1999, in Key West, Florida, USA.], 916:61-70.

Sacchini F, Naessens J, Awino E, Heller M, Hlinak A, Haider W, Sterner-Kock A, Jores J, 2011. A minor role of CD4+ T lymphocytes in the control of a primary infection of cattle with Mycoplasma mycoides subsp. mycoides. Veterinary Research, 42(77):(12 June 2011). http://www.veterinaryresearch.org/content/pdf/1297-9716-42-77.pdf

Santini FG, D'Angelo AR, Scacchia M, Giannatale Edi, Visaggio MC, Farinelli G, Francesco Gdi, Guarducci M, 1992. A domestic buffalo with a pulmonary sequestrum caused by Mycoplasma mycoides subsp. mycoides SC: isolation, pathology and immunohistochemistry. Veterinaria Italiana, 28(4):4-10; 17 ref.

Santis Pde, Bashiruddin JB, Tittarelli M, Visaggio MC, Gianvincenzo D, 1999. Mycoplasmas in a problem flock of sheep with contagious agalactia. In: Stipkovits L, Rosengarten R, Frey J, eds. COST 826 Agriculture and biotechnology. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics. Vol III. Luxembourg, Germany: Office for official publications of the European Communities, 124-126.

Scacchia M, Sacchini F, Filipponi G, Luciani M, Lelli R, Tjipura-Zaire G, Provvido Adi, Shiningwane A, Ndiipanda F, Pini A, Caporale V, Hübschle OJ, 2007. Clinical, humoral and IFNgamma responses of cattle to infection with Mycoplasma mycoides var. mycoides small colony and attempts to condition the pathogenesis of the infection. Onderstepoort Journal of Veterinary Research, 74(3):251-263.

Scanziani E, Paltrinieri S, Boldini M, Grieco V, Monaci C, Giusti AM, Mandelli G, 1997. Histological and immunohistochemical findings in thoracic lymph nodes of cattle with contagious bovine pleuropneumonia. Journal of Comparative Pathology, 117(2):127-136; 22 ref.

Schnee C, Heller M, Jores J, Tomaso H, Neubauer H, 2011. Assessment of a novel multiplex real-time PCR assay for the detection of the CBPP agent Mycoplasma mycoides subsp. mycoides SC through experimental infection in cattle. BMC Veterinary Research, 7(47):(12 August 2011). http://www.biomedcentral.com/content/pdf/1746-6148-7-47.pdf

Scudamore JM, 1995. Contagious bovine pleuropneumonia. State Veterinary Journal, 5, 13-16.

Srivastava NC, Thiaucourt F, Singh VP, Sunder J, Singh VP, 2000. Isolation of Mycoplasma mycoides small colony type from contagious caprine pleuropneumonia in India. Veterinary Record, 147(18):520-521; 15 ref.

Stradaioli G, Sylla L, Mazzarelli F, Zelli R, Rawadi G, Monaci M, 1999. Mycoplasma mycoides subsp. mycoides SC identification by PCR in sperm of seminal vesiculitis-affected bulls. Veterinary Research, 30(5):457-466; 42 ref.

Tambi NE, Maina WO, Ndi C, 2006. An estimation of the economic impact of contagious bovine pleuropneumonia in Africa. Revue Scientifique et Technique - Office International des Épizooties, 25(3):999-1011.

Taylor TK, Bashiruddin JB, Gould AR, 1992. Relationships between members of the Mycoplasma mycoides cluster as shown by DNA probes and sequence analysis. International Journal of Systematic Bacteriology, 42(4):593-601; 19 ref.

Thiaucourt F, Yaya A, Wesonga H, Huebschle OJB, Tulasne JJ, Provost A, 2000. Contagious bovine pleuropneumonia. A reassessment of the efficacy of vaccines used in Africa. Annals of the New York Academy of Sciences [Tropical veterinary diseases: Control and prevention in the context of the New World Order. Proceedings of the Fifth Biennial Conference of the Society for Tropical Veterinary Medicine, held on June 12-16, 1999, in Key West, Florida, USA.], 916:71-80.

Totté P, Rodrigues V, Yaya A, Hamadou B, Cisse O, Diallo M, Niang M, Thiaucourt F, Dedieu L, 2008. Analysis of cellular responses to Mycoplasma mycoides subsp. mycoides small colony biotype associated with control of contagious bovine pleuropneumonia. Veterinary Research, 39(1):1-11. http://www.vetres.org/

Trichard CJV, Basson PA, Lugt JJvan der, Jacobsz EP, 1989. An outbreak of contagious bovine pleuropneumonia in the Owambo Mangetti area of South West Africa/Namibia: microbiological, immunofluorescent, pathological and serological findings. Onderstepoort Journal of Veterinary Research, 56(4):277-284; 24 ref.

Tryon VV, Baseman JB, 1992. Pathogenic mechanisms and determinants. In: Maniloff J, McElhaney RN, Finch LR, Baseman JB, eds. Mycoplasmas: molecular biology and pathogenesis. Washington DC, USA: American Society for Microbiology, 457-471.

Tulasne JJ, Litamoi JK, Morein B, Dedieu L, Palya VJ, Yami M, Abusugra I, Sylla D, Bensaid A, 1996. Contagious bovine pleuropneumonia vaccines: the current situation and the need for improvement. Revue Scientifique et Technique - Office International des épizooties, 15(4):1373-1396; 53 ref.

Turner AW, Campbell AD, 1937. A note on the application of the complement-fixation test to the control of bovine pleuropneumonia. Australian Veterinary Journal, 13:183-186.

Vilei EM, Frey J, 2010. Detection of Mycoplasma mycoides subsp. mycoides SC in bronchoalveolar lavage fluids of cows based on a TaqMan real-time PCR discriminating wild type strains from an lppQ- mutant vaccine strain used for DIVA-strategies. Journal of Microbiological Methods, 81(3):211-218. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T30-4YT6CY4-1&_user=3325428&_coverDate=06%2F30%2F2010&_rdoc=2&_fmt=high&_orig=browse&_srch=doc-info(%23toc%234932%232010%23999189996%231963690%23FLA%23display%23Volume)&_cdi=4932&_sort=d&_docanchor=&_ct=11&_acct=C000050221&_version=1&_urlVersion=0&_userid=3325428&md5=e0943497035450598b83148850c15413

Weisburg WG, Tully JG, Rose DL, Petzel JP, Oyaizu H, Yang D, Mandelco L, Sechrest J, Lawrence TG, Etten Jvan, Maniloff J, Woese CR, 1989. A phylogenetic analysis of the mycoplasmas: basis for their classification. Journal of Bacteriology, 171(12):6455-6467; 50 ref.

Windsor RS, Masiga WN, 1977. Investigation into the role of carrier animals in the spread of contagious bovine pleuropneumonia. Research in Veterinary Science, 23:224-229.

Windsor RS, Wood A, 1998. Contagious bovine pleuropneumonia. The costs of control in central/southern Africa. Annals of the New York Academy of Sciences, 849:299-306; 13 ref.

Xin J, Li Y, Nicholas RAJ, Chen C, Liu Y, Zhang MJ, Dong H, 2012. A history of the prevalence and control of contagious bovine pleuropneumonia in China. Veterinary Journal, 191(2):166-170.

Links to Websites

Top of page
WebsiteURLComment
CFSPH: Animal Disease Informationhttp://www.cfsph.iastate.edu/DiseaseInfo/index.php"Animal Disease Information" provides links to various information sources, including fact sheets and images, on over 150 animal diseases of international significance.
OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animalshttp://www.oie.int/en/international-standard-setting/terrestrial-manual/access-online/The Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (Terrestrial Manual) aims to facilitate international trade in animals and animal products and to contribute to the improvement of animal health services world-wide. The principal target readership is laboratories carrying out veterinary diagnostic tests and surveillance, plus vaccine manufacturers and regulatory authorities in Member Countries. The objective is to provide internationally agreed diagnostic laboratory methods and requirements for the production and control of vaccines and other biological products.
OIE Technical Disease Cardshttp://www.oie.int/animal-health-in-the-world/technical-disease-cards/An updated compilation of 33 technical disease cards, containing summary information, mainly directed to a specialised scientific audience, including 32 OIE-listed priority diseases. USDA-APHIS (USA) are also credited with contributing to the maintenance of the cards.
Recognizing contagious bovine pleuropneumoniahttp://www.fao.org/docrep/005/Y4142E/Y4142E00.HTMFAO publication. CBPP often causes an explosive epidemic with high mortality in cattle populations. In endemic situations, the disease is known for its insidious spread and debilitating effects on cattle production. This booklet has large pictures of clinical signs and gross pathology of CBPP, as a means of assisting those dealing with the disease to recognize it, make a proper diagnosis and take appropriate action.
USAHA: Foreign Animal Diseases. Seventh Editionhttp://www.aphis.usda.gov/emergency_response/downloads/nahems/fad.pdfCopyright © 2008 by United States Animal Health Association ALL RIGHTS RESERVED. Library of Congress Catalogue Number 2008900990 ISBN 978-0-9659583-4-9. Publication with 472pp. aimed at providing information for practitioners within the USA to prevent and or mitigate the incursion of foreign animal diseases into that country. Contains general chapters on surveillance, diagnosis, etc. as well as 48 chapters covering individual diseases, mostly those notifiable to the OIE.

Distribution Maps

Top of page
You can pan and zoom the map
Save map