Definition
Contagious bovine pleuropneumonia (CBPP) is a highly infectious
acute, subacute, or chronic disease, primarily of cattle, affecting the lungs and
occasionally the joints, and caused by Mycoplasma mycoides mycoides.
Etiology
Contagious bovine pleuropneumonia is caused by M. mycoides mycoides small-colony type (SC type). M. mycoides mycoides large-colony type is pathogenic
for sheep and goats but not for cattle. M. mycoides mycoides (SC type) survives
well only in vivo and is quickly inactivated when exposed to normal external environmental
conditions. M. mycoides mycoides does not survive in meat or meat products and does
not survive outside the animal in nature for more than a few days. Many of the routinely
used disinfectants will effectively inactivate the organism.
Host Range
Contagious bovine pleuropneumonia is predominantly a disease of
the genus Bos; both bovine and zebu cattle are naturally infected. There are many
reported breed differences with respect to susceptibility. In general, European breeds
tend to be more susceptible than indigenous African breeds (8). There does seem to be some
age resistance, for animals less than 3 years of age are less resistant to experimental
challenge (5). In zoos the infection has been recorded in bison and yak. Although it has
been reported that the domestic buffalo (Bubalus bubalis) is susceptible, the
disease is difficult to produce experimentally in this species (7).
Geographic Distribution
Contagious bovine pleuropneumonia is endemic in most of Africa. It
is a problem in parts of Asia, especially India and China. Periodically, CBPP occurs in
Europe, and outbreaks within the last decade have occurred in Spain, Portugal, and Italy.
Contagious bovine pleuropneumonia was eradicated from the United States in the nineteenth
century. It is of historical interest that the Bureau of Animal Industries, which is the
forerunner of the USDA's Animal and Plant Health Inspection Service, was formed in 1884
specifically to eradicate CBPP. The United States was declared free of CBPP only 9 years
later in 1893. Currently, CBPP is not present in the Western hemisphere.
Transmission
Contagious bovine pleuropneumonia is spread by inhalation of
droplets from an infected, coughing animal. Consequently, relatively close contact is
required for transmission to occur. Outbreaks usually begin as the result of movement of
an infected animal into a naive herd. It is widely believed that recovered animals
harboring infectious organisms within a pulmonary sequestrum, may become active shedders
when stressed. Although this may be a factor in some outbreaks, it has not been
substantiated experimentally (9). There are limited anecdotal reports of fomite
transmission, but this means of transmission is not generally thought to be a problem.
Incubation Period
The time from natural exposure to overt signs of disease is
variable but generally quite long. It has been shown that healthy animals placed in a
CBPP-infected herd may begin showing signs of disease 20 to 123 days later (7).
Experimentally, subsequent to instillation of large quantities of infective material at
the tracheal bifurcation, the incubation period is 2 to 3 weeks.
Clinical Signs
Usually the first abnormality noticed is a depressed, inappetent
animal with fever. Coughing may be the next sign (Fig. 36) followed by evidence of thoracic pain and an increased
respiratory rate. As pneumonia progresses and animals become increasingly dyspneic,
animals are inclined to stand with elbows abducted in an attempt to decrease thoracic pain
and increase chest capacity. Auscultation of the lungs reveals any of a wide variety of
sounds, depending on how severely the subjacent pulmonary parenchyma is affected.
Crepitations, rales, and pleuritic friction rubs are all possible.
Percussion over affected areas reveals dullness. When pulmonary involvement is extensive
and severe, there will be very labored respiration and, sometimes, open-mouthed breathing.
Occasionally in calves, pneumonia may be accompanied by a polyarthritis. Animals affected
in this manner may be very reluctant to move and stand stiffly with a distinctly arched
back. Getting up and down may cause obvious discomfort. Large joints (Fig. 37) may be distended and warm on palpation. If joint pain
is severe, animals may be so reluctant to bend the joints that they lie in lateral
recumbency with legs outstretched. Contagious bovine pleuropneumonia often evolves into a
chronic disease. This form, characterized by ill thrift and recurrent low-grade fever, may
be difficult to recognize as pneumonia. Forced exercise may precipitate coughing.
Gross Lesions
The gross pathologic features of CBPP are quite characteristic
(3). If the animal dies, there is usually extensive and marked inflammation of the lung
and associated pleurae (Fig. 38). In
severe cases there can be abundant fluid in the thoracic cavity. The inflammation is not
uncommonly unilateral (Fig. 39). The
initial focus can be in any part of the lung and, in fatal cases, usually has spread
locally and extensively to include a sizable segment. The affected pulmonary parenchyma is
odorless and often has all stages of lesions with both acute and chronic inflammatory
changes adjacent to one another. The predominant gross change is consolidation, or
thickening, of individual lobules, which become encased in markedly widened interlobular
septa, resulting in the very characteristic marbled appearance (Figs. 40, 41).
Interlobular septa become distended first by edema, then by fibrin, and finally by
fibrosis. The overlying pleura may be very thickened by an irregular layering of yellow
fibrin which, with time, becomes fibrosed, often resulting in adhesions between parietal
and visceral pleurae. Not uncommonly, within an affected lung will be found a sequestrum -
a focus that has undergone coagulative necrosis (Fig. 42) and is effectively sealed off from the rest of the lung.
Such sequestra may even be found in recovered. animals. It has been shown that M.
mycoides mycoides (SC-type) can survive within these sequestra for months or possibly
longer (9).
Morbidity and Mortality
The attack rate with CBPP is variable. It is not thought to be a
highly contagious disease. With increased confinement of animals, morbidity rises. The
mortality rate with CBPP is quite varied and ranges from 10 to 70 percent in various
outbreaks. As with many subacute and chronic infectious diseases, mortality may depend on
other intercurrent factors such as plane of nutrition, level of parasitism, and general
body condition
Diagnosis
Field Diagnosis
Clinical diagnosis of CBPP is difficult. At postmortem the gross
lesions of CBPP are somewhat distinct. Often there is an extensive deposition of fibrin
and a large quantity of straw-colored fluid in the thoracic cavity with a prominent
marbling of pulmonary parenchyma. Generally, all stages of pathologic changes, from acute
through to chronic, are present in one animal. In some chronic cases the nodules of
inflammation may not be readily apparent from the pleural surface but can be palpated
within the parenchyma. Unlike many other pneumonias, CBPP is often unilateral.
Specimens for Laboratory
From a live animal, nasal swabs, transtracheal washes, or pleural
fluid obtained by thoracic puncture all provide good samples for isolation attempts. From
a dead animal that has had severe clinical disease, the best specimens to submit are
affected lung, swabs of major bronchi, tracheo-bronchial or mediastinal lymph nodes, and
joint fluid from those animals with arthritis. All samples should be collected aseptically
and, if possible, placed in transport medium (heart infusion broth, 20 percent serum, 10
percent yeast extract, benzylpenicillin at 250 to 1000 IU/ml). Samples should be kept cool
and shipped on wet ice as soon as possible. If transport to the laboratory is delayed
(more than a few days), samples may be frozen (1). Blood should be collected for serum.
Laboratory Diagnosis
A definitive diagnosis is made by isolating and identifying the
organism. Serology is helpful in the diagnosis of CBPP. Because CBPP is a subacute to
chronic disease, most animals will have developed antibodies by the time of clinical
disease.
Differential Diagnosis
Clinically, CBPP may be confused with other pneumonic conditions,
most especially bovine pasteurellosis. However, bovine pasteurellosis would likely spread
much more rapidly and consequently the epidemiologic picture may be distinct.
Treatment
Mycoplasma mycoides mycoides (SC-type) is susceptible to a
variety of antimicrobials, including streptomycin, oxytetracycline, and chloramphenicol.
However, antimicrobial therapy may only serve to slow the progression of the disease or
may even in some cases favor the formation of sequestra. In the case of chronically
affected animals or subclinically affected carriers, the organisms may be in an
inaccessible location within an area of coagulative necrosis, which by definition is not
served by a blood supply.
Vaccination
A modified live vaccine is available for use in enzootic areas. A
major drawback of this vaccine is that it generates an unpredictable local reaction. For
this reason it is often given in the tail tip, which may become necrotic and slough.
Immunity subsequent to vaccination is generally good and lasts at least 12 months. The
CBPP vaccine is often given in combination with the vaccine for rinderpest.
Control and Eradication
Prevention
Because CBPP is a chronic disease that may exist subclinically in
carrier animals, it is important to maintain sufficient regulatory restrictions to prevent
its introduction in apparently healthy animals. Serologic testing of susceptible animals
for importation is a recommended safeguard.
Control and Eradication
Successful control of the spread of CBPP rests on removing
susceptible animals from any possible contact with CBPP-infected animals, whether they are
clinically affected or subclinical carriers only. On-farm quarantine of suspicious and
contact animals would be very advantageous in stemming the spread of the disease. In an
outbreak situation, testing, slaughter, and quarantine would be the methods of choice.
Public Health
There is no evidence to indicate that humans are susceptible to
this disease.
GUIDE TO THE LITERATURE
1. ANON. 1991. Contagious bovine pleuropneumonia. Tech. Off. Int.
Epizoot., 6:565-624.
2. BUTTERY, S. H., COTTEW, G. S., and LLOYD, L. C. 1980. Effect of
soluble factors from Mycoplasma mycoides subsp. mycoides on the collagen
content of bovine connective tissue. J. Comp. Path., 90:303-314.
3. COTTEW, G. S. 1979. Pathogenicity of the subspecies mycoides of Mycoplasma mycoides for cattle, sheep and goats. Zbl. Bakt. Hyg., 1. Abst. Orig.
A., 245:164.
4. DAMASSA, A. J., BROOKS, D. L., and ADLER, H. E. 1983. Caprine
mycoplasmosis: Widespread infection in goats with Mycoplasma mycoides subsp. mycoides (large-colony type). Am. J. Vet. Res., 44:322-325.
5. MASIGA, W. N., and WINDSOR, R. S. 1978. Some evidence of an age
susceptibility to contagious bovine pleuropneumonia. Res. Vet. Sci., 24:328-333.
6. ONOVIRAN, O., and TAYLOR-ROBINSON, D. 1979. Detection of
antibody against Mycoplasma mycoides subsp mycoides in cattle by an
enzyme-linked immunosorbent assay. Vet. Rec., 105:165-167.
7. PROVOST, A. 1988. Is the domestic buffalo really susceptible to
bovine pleuropneumonia? Bulletin de l'Academie Veterinaire de France., 61:165-172.
8. PROVOST, A., PERREAU, P., BREARD, A., LEGOFF, C., MARTEL, J.
L., and COTTEW, G. S. 1987. Contagious bovine pleuropneumonia. Rev. Sci. Tech. Off. Int.
Epizoot., 6:625-679.
9. WINDSOR, R. S., and MASIGA, W. N. 1977. Investigations into the
role of carrier animals in the spread of contagious bovine pleuropneumonia. Res. Vet.
Sci., 23:224-229.
Corrie Brown, D.V.M., Ph.D., Department of Pathology, College of
Veterinary Medicine, University of Georgia, Athens, GA 30602-7388
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