COVER
RECOGNISING CBPP
A Field Manual for Recognition



CONTENTS


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CONTENTS

THE PURPOSE OF THE MANUAL

OBTAINING FURTHER COPIES

GENERAL FEATURES OF CBPP

The disease
The cause
Natural hosts
Geographical distribution
Transmission and spread
Appearance of the disease in a herd
Prevention and control

CLINICAL SIGNS

POST-MORTEM APPEARANCE

INVESTIGATION OF FIELD OUTBREAKS

Epidemiological investigation
Clinical examination
Post-mortem examination
Laboratory confirmation
Samples for laboratory confirmation
Interpretation of laboratory results

DIFFERENTIAL DIAGNOSIS

ACKNOWLEDGEMENTS

COLOUR PLATES

THE PURPOSE OF THE MANUAL

Contagious bovine pleuropneumonia (CBPP) is one of the great plagues which continue to devastate cattle herds on which so many people are dependent in Africa. In recent years the disease has emerged from areas where it has been persisting in endemic form to reinvade others from which it had previously been eradicated. In addition to these newly-infected areas, even the endemic areas are experiencing an upsurge in the incidence of CBPP.

Recent dramatic events confirm that early recognition of the disease after its introduction or reintroduction to a country, or previously free zone of an infected country, is essential if control and elimination is to be achieved rapidly. Only if the introduction is detected rapidly can stamping out by slaughter of infected herds, undoubtedly the most cost-effective option in the long term, be considered an affordable strategy for many countries. Because of the nature of the disease any delay can result in widespread dispersal of infection complicating and greatly increasing the costs of any control measures adopted.

Vigilance is required whether it be at the national or district level to ensure that the disease does not escape detection. This manual presents the most important features of CBPP to enable the disease to be recognised both by clinical and post-mortem examination. It is intended for use by all veterinary and paraveterinary staff in the front line of defence against the disease and also to assist in informing farmers of the risk.

Early warning is the key to early reaction for containment, control and rapid elimination to prevent epidemics.

OBTAINING FURTHER COPIES

The booklet is one of a series being prepared by the FAO EMPRES Unit as an aid to emergency preparedness for the major epidemic diseases of livestock.

For details and to obtain additional copies contact:

EMPRES (Livestock)
FAO Animal Health Service
Animal Production and Health Division
Viale delle Terme di Caracalla
00100 Rome, Italy

Tel: +39 6 57054798/6772
Fax: +39 6 57053023
E-mail: empres-livestock@fao.org

CONTAGIOUS BOVINE PLEUROPNEUMONIA

GENERAL FEATURES OF CBPP

CBPP is a serious threat to livestock production in Sub-Saharan Africa and some Asian countries. It is a serious obstacle to livestock development. Once introduced to a new area, initial losses in pastoral communities can be very high and its eradication is very difficult requiring major expenditure for control.

The disease

Contagious bovine pleuropneumonia (CBPP) is an infectious and highly contagious disease of cattle and water buffaloes considered to be amongst the most important infectious diseases. Affected animals have difficulty in breathing due to damage to the lungs, lose condition and a proportion die. All ages of cattle are susceptible but young cattle develop joint swellings rather than lung infections. Many cattle show no disease signs despite being infected and others recover quickly after a transient mild disease, yet they can carry infection for as long as two years and may be responsible for passing on infection at a later date.

The Cause

The disease is caused by a bacterium called Mycoplasma mycoides var. mycoides which is difficult to see even with a light microscope but growth of the organism can be seen when infectious material is cultured in the laboratory.

Natural hosts

Cattle of all types (both Bos taurus and Bos indicus) are susceptible; domestic buffaloes are generally more resistant. CBPP has been reported in Asian yaks and in American bison but never in African buffaloes (Syncerus caffer). Sheep and goats are resistant to the disease.

There are variations in breed susceptibility in cattle, for example, trypanotolerant breeds seem to be more susceptible.

Geographical distribution

CBPP is widespread in Africa and is recognised to be present in some countries of Asia and Europe.

In Africa it is found in an area south of the Sahara, from the Tropic of Cancer to the Tropic of Capricorn and from the Atlantic to the Indian Ocean. Endemic infection extends throughout the pastoral herds of much of western, central and eastern Africa, with Angola and northern Namibia in southern Africa. Newly-infected areas in the 1990s include much of Uganda, parts of Kenya, the lturi Region of the Democratic Republic of Congo and most of Tanzania, where recently the disease has spread alarmingly; Rwanda (1994), Botswana (1995, now free), Burundi (1997) and Zambia (1997) were recently reinvaded but Lesotho, Malawi, Mozambique, South Africa, Swaziland, and Zimbabwe are currently free.

In Asia CBPP has been reported in recent times from Assam in India, Bangladesh and Myanmar. Sporadic outbreaks have been recognised in the Middle East most likely from importations of African cattle.

CBPP was eradicated from the USA in 1892, Zimbabwe in 1904, South Africa in 1924, Australia in 1972 and the Peoples Republic of China in the 1980s.

After virtual elimination from Europe in the 19th century the disease reappeared in Portugal and Spain in 1951 and 1957, respectively. Outbreaks have been reported in southern France on a few occasions, the latest being in 1984. In Italy the disease reappeared in 1990 but was eliminated by 1993.

Transmission and spread

CBPP is invariably introduced into a herd by contact with an infected animal; transmission occurs from direct, close, repeated contacts between diseased and healthy animals in shared night accomodation or at water holes, dip tanks, markets, common grazing and gathering places for mass vaccination campaigns. Indirect transmission from pastures and water or by carriage, for example, on people and feed sacks, are thought not to be important.

The causative agent is present in liquid droplets in the breath and in urine and, although the CBPP organisms are killed rapidly in hot, dry environments, air-borne transmission appears possible over distances up to 200 metres.

Transmission is favoured by close crowding of cattle and outbreaks are more common and extensive when cattle are housed or have been transported by train or truck and trekked on foot in groups.

Chronically infected and symptomless animals play an important role in the persistence and spread of the disease. In this context pastoral herds are especially significant since they may contain many chronically infected animals. Herdsmen fleeing from a focus of disease with apparently healthy animals have been known to spread disease widely.

Appearance of the disease in a herd

Typically, when first introduced into a herd CBPP is severe and mortality relatively high. A small proportion of cattle may die rapidly without showing any signs other than fever. It may be possible to link the onset of disease to previous contact with other cattle three to six weeks earlier but this is not always the case as the incubation period may appear to be as long as six months. Clinical signs may become apparent only several months after the contact. Thus, the disease can become established in a herd before it is noticed and tracing back to the origin can be difficult. This is particularly so where routine vaccination has been practised with long intervals between campaigns and where antibiotics have been used to treat clinical cases. Both reduce the incidence of clinical disease, making its recognition more difficult, but do not prevent infection occurring in the herd.

After some time, the disease in the herd becomes chronic, the clinical signs become less severe and the mortality rate falls. However, losses do continue.

Prevention and control

Ideally, CBPP control is achieved by eliminating the whole cattle herd population wherever the disease is detected i.e. stamping-out. However, this may not prove realistic and quarantine coupled with vaccination is the most frequently used CBPP control measure. Yet, to be effective vaccination must target 100 per cent of cattle within an epidemiologically and geographically definable area. Vaccination must be repeated, initially at short intervals and thereafter annually over several years, i.e. not less than 3 to 5 years. Such vaccination must be maintained until evidence of CBPP eradication is demonstrated by structured surveillance. Live attenuated vaccines (T1 strain) are widely used in Africa and only those with PANVAC certification should be used. Vaccine quality control is, thus, an essential element of CBPP control programmes.

CLINICAL SIGNS

Not all the animals are affected in the same way and often the disease has a chronic course from its onset.

The hyperacute form, involving up to 10 per cent of infected animals, may be observed at the onset of an outbreak, death is sudden and is often not accompanied by any other signs. Clinical diagnosis is difficult.

The acute form is observed in approximately 20 per cent of the diseased animals. The course is 5 to 7 days. The earliest signs are a sudden onset of fever to 40° C or more and, in milking cows, a drop in milk yield. Sick cattle tend to isolate themselves from the herd and stop eating.

A typical respiratory disease develops; breathing is laboured and obviously painful. Abdominal breathing with a respiratory rate of 50 to 55 breaths/ min may be seen and cattle may ‘grunt’ when breathing out. Some animals develop a shallow, dry and painful cough particularly noticeable on exercise. Application of pressure between the ribs is painful and resented by affected cattle which sometimes react violently. On percussion, the ventral part of the chest sounds dull owing to the presence of fluid in the chest cavity. Acutely affected cattle stand with head and neck extended and forelegs spread apart (Plate 1), dilated nostrils and with mouth open panting for air. There may be nasal discharge, sometimes streaked with blood, and frothy saliva accumulates around the mouth. Some animals develop swellings of the throat and dewlap.

Pregnant cows and heifers may abort and diarrhoea has been recorded.

If the animal survives, the disease turns chronic; clinical recovery is only apparent.

The subacute form occurs most frequently in about 40–50 per cent of the animals affected. The symptoms resemble those of the acute form but are less severe; fever is intermittent. This form usually becomes chronic.

The chronic form is a natural evolution of both acute and sub-acute ones but in some animals it can develop directly. The clinical signs regress but cattle can still have intermittent fever together with loss of both appetite and weight.

Calves, in the first six months of life, more often show lameness from swollen, hot, painful limb joints.

The mortality rate is variable, rarely exceeding 50 per cent, and depends on a range of factors such as age, breed, nutrition, presence of other infections or infestations and the type of management.

Many affected cattle can appear to recover fully, yet the lesions in the lungs take a long time to heal fully and inside them the causative agent can survive for as long as two years. Up to 25 per cent of affected cattle can become chronic carriers of infection. They are often referred to as ‘lungers’ and are believed to play a role in initiating new outbreaks when they are moved into susceptible herds.

In summary, look for one or more animals with:

Any chronic (persistent) mild cough in cattle otherwise appearing normal or losing weight should be a reason to suspect CBPP.

POST-MORTEM APPEARANCE

Abnormalities (lesions) are generally confined to the chest cavity (Plate 2) except in young calves where inflammation of the limb joints (usually the carpal and tarsal joints), with increased fluid, is sometimes seen (Plate 3).

A most striking feature of the acute disease is the very large volume of yellow fluid (up to 30 litres) containing clots which can accumulate in the chest (Plates 2 and 4).

Usually only one lung and its pleura is affected. In most cases only the diaphragmatic lobe is involved (Plate 5); it is firm and fleshy, resembling liver more than healthy pink lung, and does not shrink as normal when the chest is opened.

In acute forms, the yellowish fluid in the chest cavity may solidify and cover the lining of the chest and surface of the lung (the pleura) with a yellow or yellowish-grey coating resembling an omelette (fibrin) (Plate 6). Under this the pleura is thickened and opaque. Accumulation of fibrin on the pleura causes the lung and chest wall to stick together (adhesion). The cut surface of the lung often shows a marbled appearance with areas of different colour (dark red, red and pale pink) separated by a network of pale bands (Plates 7 and 8); this is typical of CBPP.

In the chronic form, fluid is rarely seen in the pleural cavity but adhesions between lung lobes and between lungs and the chest wall are commonly found. Areas of dead lung tissue become surrounded by a capsule of fibrous connective tissue. This structure is called a sequestrum (Plate 9). Various intermediate stages between the acute lesion and a fully formed sequestrum can be found depending on the stage of the disease. The diameter of a sequestrum can vary from 2 to 25 cm and the capsule can be as much as 1 cm thick. Sequestra of different diameter can be detected in the same lung. When they are small and deep they can be identified only by careful palpation.

In the pink or white necrotic odourless mass that is found in the sequestrum the lobular structure of the lung may still be recognizable.

This is typical of the disease and differs from lung lesions due to tuberculosis or abscesses. The contents of sequestra shrinks and becomes dry although they may later become liquid.

Lymph nodes in the chest may be enlarged and wet (oedematous), with small necrotic foci and pin-point haemmorrhages, the difference between cortex and medulla may be indistinguishable.

In the kidney cortex, white spots of dead tissue of variable size, called infarcts, can sometimes be seen (Plate 10).

In summary, look for:

Because the lesions are so characteristic, slaughterhouse monitoring is a powerful tool to use in detecting introduction and spread of the disease.

INVESTIGATION OF FIELD OUTBREAKS

Investigation leading to a conclusive decision will rely on a combination of the following activities:

  1. Epidemiological investigation to obtain a general picture of the way the disease has behaved in the herd;

  2. Clinical examination: how the animals of a herd are affected by the disease;

  3. Post-mortem examination to observe the characteristic lesions in organs of dead and\or slaughtered animals;

  4. Laboratory examination to confirm the presence of infection..

Epidemiological investigation

When CBPP is suspected, the questions asked should include the following to obtain a picture of the way the disease is behaving (in itself this can be as characteristic as the clinical signs and pathology):

  1. What species of animal are present on the livestock holding (or village), how many of each are present and which species are affected?

    Cattle, sheep, goats, pigs, wild animals, etc. If domestic or wild animals other than cattle or water buffaloes are affected a condition other than CBPP should be considered.

  2. What ages of cattle/domestic buffaloes are affected?

    Record the animals by age class: under 6 months, 7 to 18 months, over 18 months. In CBPP the more severe respiratory forms are observed in adult animals.

  3. Have the cattle been vaccinated against CBPP or other epidemic diseases and when did the last vaccination take place? Which vaccine was used? How many animals were vaccinated? Who conducted the vaccination?

    If all the cattle have been vaccinated with a quality-assured CBPP vaccine at appropriate time intervals they should not develop the disease. However, CBPP can still occur in non-vaccinated cattle in partially-vaccinated herds and even in vaccinated cattle which have not been revaccinated in time.

  4. When did the first signs of disease appear? Is this the first time that this disease has occurred? If not, what are the approximate dates of previous episodes?

    This can help to indicate whether the disease is endemic or newly-introduced and can help to calculate when infection entered the herd.

  5. Have other cattle been bought or introduced for any reason during the six months before the disease was first noticed? If so, from where? Did any become sick?

    The answer can provide an explanation of how the disease might have entered the farm/herd.

  6. Were replacement animals vaccinated before or after their entering the herd for CBPP or other diseases?

    This provides information why sickness might be limited to a particular group of animals.

  7. Was the herd exposed to another herd, even for a short time, during the six months before the disease was first noticed. Do nomadic herds pass through the area? If so, when and from where?

    Nomadic herds can be a CBPP reservoir. The answers can also provide an explanation of how the disease might have entered the farm/herd.

  8. Is the disease known to the community and does it have a local name?

    Pastoralists are often able to provide a useful guide to disease conditions they have encountered in the past.

  9. Have the infected animals been treated with antibiotics? If so, which ones?

    Antibiotics may mask the clinical appearance of CBPP and alter the progression of disease in a herd; their use also complicates diagnosis.

  10. What are the signs observed in diseased animals?

    Respiratory signs are more evident in adult animals whereas enlargement of joints may be present in calves under 6 months of age.

  11. How many animals are clinically sick out of the total?

  12. How many animals have died since the infection occurred - out of the herd and out of the affected group?

  13. What is the health state in neighbouring herds?

    To decide if CBPP is present in the area, the answers should be checked by visiting neighbouring herds.

  14. Have animals been sold, transferred or given on loan in the last six months?

    The answer to this question might give important information about spread of the disease and assist in tracing.

  15. Are grazing lands, water holes, drinking-troughs or dipping tanks shared even temporarily with other nomadic or sedentary herds?

    This is to indicate possible contacts with animals from other herds allowing tracing of the origin of infection and early warning of disease spread onwards.

Clinical examination

As the clinical appearance can differ so much between individuals in a herd depending on the different stages of disease development, it is important to examine as large a number of animals as possible to obtain a full picture. A general examination of the herd is needed to record breeds and age classes, grouping animals as under 6 months, 7 to 18 months and adults. A notebook is essential to record all the findings to refer to later.

1. Record the farmer's observations

Ask for the animal attendant's description of the disease seen.

Has any treatment been used? Antibiotics such as tylosin and the tetracyclines can be effective in producing an apparent cure.

[Conventional understanding is that antibiotic therapy is contraindicated in outbreaks of CBPP because it is believed that its use leads to the generation of a high proportion of “lungers” in the herd and that these can later spread infection to susceptible cattle. This may be true, but in most countries in which CBPP occurs antibiotic therapy is a fact of life. Disagreement over its use should not be allowed to create a barrier between animal health worker and livestock owner.]

Have any cows been observed to abort?

2. Observe the animals at rest

Before touching the animals, check if they are alert or depressed, if lameness is present and if the body condition is satisfactory for the time of year and husbandry system.

Do any stand with the neck and head extended, forelegs spread apart, mouth open panting for air? It is worth remembering that this happens to:

  1. CBPP severely affected animals - acute cases; but also to
  2. animals with respiratory diseases other than CBPP.

Is breathing difficult, rapid and painful? If breathing is difficult the nostrils are generally dilated and clear or blood-stained discharge may be seen.

Check the character and rate of respiration. Is it fast (more than 20 per minute)?

Do any animals cough?

Is there a discharge from the eyes and nose? A clear discharge may be present.

3. Physical examination

Take the rectal temperature: in acute cases it can rise above 40°C.

Check the surface lymph nodes: enlargement is not a feature.

Check the mouth, including the lining of the lips, the tongue, cheek papillae and the hard palate - lesions are not found, unlike in rinderpest and FMD, although saliva may dribble from the mouth.

4. Force the animals to run for a few minutes and examine them again

CBPP symptoms can be more clearly seen after a few minutes exercise - especially the cough and lameness.

Post-mortem examination

The severity of clinical signs observed often contrasts markedly with the extent of lesions seen at post-mortem examination; advanced lesions may be seen in older cattle showing only mild clinical signs.

Lesions are usually confined to the chest where the presence of an accumulation of yellow fluid, uncollapsed lung and marbled lung sticking to the chest wall, are very strongly indicative of acute CBPP. Sequestra indicating the chronic stage of CBPP might not be detected without careful sectioning of the lung. In young calves only a hot painful swelling of joints might be found.

Laboratory confirmation

The presence of the disease can be detected in two ways: detection of the causal organism in affected tissue and detection of serum antibodies to the organism.

The causal organism, Mycoplasma mycoides, can be demonstrated in the fluid present in the chest and in diseased lung by culture, by antigen detection tests (interface precipitin test or agar gel immunodiffusion test) and by a polymerase chain reaction (PCR).

The rapid slide agglutination test using whole blood or serum for antibody detection can be a useful test to detect infected herds; it can be used in the field to give rapid results. It is performed by mixing a drop of a suspension of killed and stained Mycoplasma mycoides organisms with a drop of serum or blood on a glass slide; in a positive result aggregates form within one minute.

At present, the laboratory test of choice for detecting serum antibodies is the complement fixation test (CFT). Great care is needed in collecting and storing sera to be used for this test which is complex to perform. A competitive ELISA test is undergoing evaluation as a test for antibodies.

Histopathology of affected lung fixed in formalin can also help in confirming the diagnosis. The peroxidase-antiperoxidase (PAP) test is an excellent confirmatory test.

Samples for laboratory confirmation

Infected tissue is used to demonstrate the presence of the Mycoplasma organisms. Usually the samples required will be chest fluid and diseased lung kept on ice during transport to the laboratory. Additional samples may be fixed in 10 per cent formalin solution for histopathology.

Serum, used for antibody tests, is obtained by allowing blood to clot at room temperature and then collecting the clear liquid which is produced when the clot contracts. This usually takes a few hours and during this time the blood samples should be kept at ambient temperature. Separated sera should be kept on ice, not frozen, and transported quickly to a laboratory.

Interpretation of laboratory results

Culture and antigen detection tests provide conclusive confirmation of the diagnosis.

It must be emphasised that none of the available antibody tests can reliably discriminate between infected and healthy individuals - they are herd tests.

It is important to remember that Pasteurella species bacteria can be cultured frequently from any pneumonic lung (and even from normal lung), thus, their isolation does not indicate a diagnosis of pasteurellosis nor does it rule out the diagnosis of CBPP.

The slide agglutination test can give false positive results in uninfected animals and also antibodies become undetectable by this test as the disease progresses. Therefore, it cannot be used reliably for individual animals, yet is useful in detecting infected herds early in the course of the disease. The CFT is the most reliable test currently available but it should be noted that false negative results can be found early and late in the disease course.

DIFFERENTIAL DIAGNOSIS

In carrying out a CBPP diagnosis it is necessary to differentiate this disease from other diseases which may present similar clinical signs or lesions. Remember that the way the disease behaves in the herd is as important as the findings in a single animal when carrying out an investigation. Some sources of confusion are:

Rinderpest: The confusion with rinderpest results from the fever and discharges observed from the eyes, nose and mouth. However, the characteristic lesions of rinderpest which are essentially erosions in the mouth and throughout the digestive tract, together with the profuse, often bloody, diarrhoea in advanced cases, should enable easy differentiation from CBPP in which these are not seen. Lung lesions are seen in more chronic cases of rinderpest and these consist of red areas of collapse together with emphysema of lung lobules and the septa separating them. At this stage the erosive lesions of rinderpest may have healed.

Foot-and-mouth disease: Salivation, lameness and fever are the cause of confusion.

Haemorrhagic septicaemia (HS): This is a very acute disease and most affected animals die within 6 to 72 hours after the onset of clinical signs. Buffaloes are particularly susceptible. Oedema of the throat and neck to the brisket is often very pronounced. The lung lesions seen in animals that survive the longest can appear very similar to the marbling lesion of CBPP, there may be yellow fluid in the chest and the affected lung may adhere to the inside of the rib cage. Thus, in the individual case distinguishing between HS and CBPP can be difficult.

Bacterial or viral broncho-pneumonia: Clinical signs may resemble closely those of acute CBPP. Post mortem examination shows usually both lungs to be affected, fibrinous exudate may be present but not to the same extent as in CBPP. While dark, solid areas of lung may be seen, these are usually restricted to the anterior lobes (not the diaphragmatic lobe as in CBPP) and marbled lungs are not often seen.

Theileriosis (East Coast Fever): Coughing, nasal and ocular discharge and diarrhoea are observed. Affected cattle show general enlargement of superficial lymph nodes and especially those of the head. The lungs contain much clear liquid which is also present in the chest cavity; the airways in the lung may be filled with white froth. Cigarette burn-like ulcers are seen in the abomasal folds. Neither pneumonia nor inflammation of the pleura are present.

Ephemeral fever: In most cases this is a self-limiting disease of short duration; most affected cattle recover quickly, even those which are severely affected. The fever fluctuates with two or more peaks. Pneumonia is not a main feature of the disease but a secondary pneumonia can occur with lung oedema and emphysema in a small proportion of cases. Confusion with CBPP arises from the presence of fever, discharges from the eyes and dripping of saliva from the mouth, lameness and swollen joints (but in animals of all ages unlike CBPP).

Abscesses: They can be mistaken for sequestra. When cut open the contents of abscesses may have an offensive smell, and be purulent or liquid. A total destruction of the lung tissue occurs. In sequestra the contents often retain typical lung structure. Old thickly encapsulated hydatid cysts can also cause some confusion.

Tuberculosis: Tubercular nodules can superficially resemble sequestra but they are degenerative cheese-like lesions, sometimes calcified. The lung tissue is destroyed. The same lesions are also seen in lymph nodes in the chest. The capsule of the tubercular nodules is not well defined when compared to that of sequestra.

Farcy: The lung lesions of farcy differ from sequestra as they are filled with foul smelling purulent material as described for abscesses. Similar lymph node lesions are always present.

Actinobacillosis: Lesions are generalized and seldom present in lungs but when found, could be mistaken for sequestra.

Echinococcal (hydatid) cysts: These cysts have a double wall and contain a clear liquid, often calcified when old.

Foreign body pericarditis: Although the two conditions present clinical and pathological similarities, only one animal is usually affected.

ACKNOWLEDGEMENTS

This guide was prepared by the staff of FAO EMPRES (Livestock). Some source material was provided by the Istituto Zooprofilatico Sperimentale dell'Abruzzo e del Molise “G. Caporale”, Teramo (IZST), Italy, and some additional text was modified from “Contagious Bovine Pleuropneumonia (Lungsickness) - a guide to recognition and action” produced by Dr A.A. Majok and Dr L. Tyler of the Veterinary Epidemiology and Economics Unit of the Department of Animal Health and Production (DAHP), Ministry of Agriculture, Botswana. Their contribution is gratefully acknowledged.

Colour plates appear by kind permission of the following:

Front coverDr Alain Provost
Plates 2, 3 and 9Dr Roger Windsor
Plates 5, 10IZST
Plates 1, 4, 6 and 7DAHP, Botswana
Plate 8Dr Abdelali Benkirane

COLOUR PLATES

Plate 1

Plate 1 Clinical case of CBPP

This animal is having difficulty in breathing. It stands with its head and neck extended and legs widely placed. Often the elbows are turned out. Inflammation of the membranes surrounding the lungs causes pain in the chest resulting in abdominal breathing movements.

Plate 2

Plate 2 Early stage of CBPP: abnormalities in the chest

The diaphragm has been removed to allow a view into the chest from behind.

The right lung (1) is normal and has collapsed as the chest was opened. The left lung (2) has not collapsed; it is firm and fleshy. It is coated with a yellow deposit which is also present on the inside of the ribs. Also visible are the remains of the large amount of yellowish fluid (3) which was present in the chest.

Plate 3

Plate 3 Swollen knee joints of a calf with acute CBPP

The joints are inflamed by the CBPP infection causing swelling, pain and lameness.

Plate 4

Plate 4 Early stage of CBPP: fluid in the chest

The chest has been opened to show the large volume of yellowish fluid it contains. This can be sufficient in life to interfere with breathing.

Plate 5

Plate 5 The lungs in early CBPP

The lung at the bottom is normal and has collapsed when the chest was opened. The affected lung at the top is firm and fleshy, like liver, and has not collapsed. Clotted fibrin is visible on its surface.

Plate 6

Plate 6 “Omelette” like material in chest at a later stage

In this case much of the fluid in the chest has coagulated in one large clot which resembles an omelette. The yellow fibrin is also visible coating the lung which is severely affected and on the membrane covering the inside of the ribs.

Plate 7

Plate 7 CBPP: marbled lung

The lung has been cut open to reveal the marbled appearance of the fleshy, diseased lung. Areas of dark red lung are separated by a network of pale bands. This is typical of CBPP.

Plate 8

Plate 8 Early CBPP: marbled lung

In addition to the marbled appearance of the cut lung, individual areas between the pale bands vary in colour from deep red to pale pink depending on how badly affected they are.

Plate 9

Plate 9 Old case of CBPP with a sequestrum in the lung

The dead lung tissue has changed into a solid material which is surrounded by a thick layer of fibrous tissue. Many recovered cattle have one or more of these sequestra in their lungs. This is a typical sign of CBPP to be looked for during meat inspection.

Plate 10

Plate 10 Early case of CBPP: kidney

Areas of dead tissue (infarcts) clearly stand out as white spots against the background of the red normal kidney tissue.

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