Contagious Bovine Pleuropneumonia (CBPP)

Also known as

Lung plague

Description

Contagious bovine pleuropneumonia (CBPP) is a combination of pneumonia and pleurisy (inflammation of the pleura--the lining/sac that separates the lungs from the chest wall. This contagious bacterial disease occurs in cattle, buffalo, zebu, and yaks. It is caused by the bacterium Mycoplasma mycoides, with typical signs of pneumonia and difficult, painful breathing.

Susceptible cattle usually develop signs 3 to 6 weeks after becoming exposed to these bacteria, but in highly susceptible cattle, signs may develop within 10 to 14 days. This disease is highly contagious with a high mortality rate, and causes significant economic losses. CBPP is currently a prominent cattle disease in Africa, but has been around for a long time in many parts of the world.

CBPP was first reported in Germany in 1693, one of the three greatest historic cattle plagues of the world along with Foot and Mouth Disease and Rinderpest. Efforts to eradicate CBPP have been undertaken in every country where it has appeared.

In the U.S. this disease was widespread by 1879, affecting herds from several states. The outbreak at that time was so severe that it resulted in a trade embargo by the British government, blocking U.S. cattle exports to Britain and Canada. In response, the U.S. established the Bureau of Animal Industry, which was set up in 1884 to eradicate the disease, a task that took several years to accomplish.

The U.S. has been free of this disease since 1892, the UK since 1898, Zimbabwe since 1904, South Africa (where the disease was introduced by importation of infected bulls from Holland in 1853) since 1924, Australia since 1970s and China since the 1980s.

After its elimination from Europe in the nineteenth century, the disease reappeared in Portugal in 1951 and Spain in 1957. A few outbreaks were reported in southern France, the latest in 1984. In Italy, the disease reappeared in 1990 but was eliminated by 1993, and the last case in Europe was in Portugal in 1999.

CBPP came to Australia with a shipment of 5 cattle from England in 1858, imported by one of Melbourne’s earliest settlers. Those cattle infected others on a neighboring farm, and then the disease spread to New South Wales, into Queensland and across northern Australia. It later arrived in Western Australia via a shipload of cattle. Only Tasmania remained free of that epidemic in Australia,

In 1959 a National Committee for the Control and Eradication of Pleuropneumonia was established in Australia to identify infected, protected and disease-free areas. Once these were established, restrictions were placed on movement of cattle between zones. This program employed veterinary officers, stock inspectors and police across Australia to facilitate the eradication program—which was accomplished by 1973.

This disease is still widespread in Africa, the Middle East, Southern Europe, as well as parts of Asia, however. It can be spread by airborne droplets and dust, and can travel several miles on the wind, with the right conditions.

Contagious bovine pleuropneumonia is still one of the most important infectious diseases of cattle in Africa. Naïve herds can experience losses up to 80%, and many cattle that survive remain chronic carriers--often suffering from recurrent low-grade fever, weight loss, and respiratory signs when exercising. These carriers can introduce the virus into uninfected herds.

Due to control efforts, incidence of CBPP had declined in Africa by the 1970’s but during the late 1980s and into the 1990s increased in prevalence in endemic areas. It re-emerged in some African and European countries that had been CBPP-free.

In the 1980s, almost no outbreaks were observed--due to annual combined vaccination campaigns from efforts toward control of Rinderpest. Then in the 1990’s CBPP gained wider extension in Africa and re-invaded countries such as Botswana, Tanzania, and Rwanda that had eliminated it in the past. However, Botswana succeeded in regaining a free status after very strict sanitary measures. The incidence of CBPP increased in many other countries of Africa and had been reported in at least 27 countries in equatorial, central, and southern Africa by the end of 1999.

Eradication was successful in Europe, with the most recent case reported in 1999 but CBPP remains a serious concern in Africa. The ending of widespread combined rinderpest/CBPP vaccination programs (after rinderpest eradication) may have contributed to its resurgence.

A few cattle with CBPP die suddenly with no clinical signs other than fever. Acute cases in cattle are characterized by fever, loss of appetite, depression and drop in milk production, followed by respiratory signs, which may include coughing, thick nasal discharges, and rapid respiration. Clinical signs may differ in severity between outbreaks.

Some cases progress rapidly to difficult, painful breathing; these animals react intensely if pressed between the ribs. Severely affected cattle stand with head and neck extended, back arched, and forelegs turned out at the elbows in an effort to breathe easier, breathing through the mouth, often grunting at each expiration of breath. In hot climates, an affected animal often stands by itself in the shade, with head lowered and extended.

The throat and dewlap sometimes swell. Severe bleeding from the nostrils, diarrhea and abortions have also been reported, with some animals giving birth to stillborn calves. Severely affected cattle often die, usually within three weeks from the onset of clinical signs. Animals that recover are frequently weak and emaciated, and may remain chronically infected. Subclinical infections also occur.

In calves up to six months of age, the primary sign may be polyarthritis (infection in multiple joints), especially knees and hocks, often without respiratory signs. The affected joints may be so painful that the animal is reluctant to bend them and is extremely lame.

Chronic CBPP is characterized by recurrent low-grade fever, weight loss, and respiratory signs that may be only be noticed when the animal is exercised. Many cattle eventually recover, although affected lung tissues may take a long time to heal.

Signs

• Fever
• Labored or rapid respiration
• Cough and nasal discharges
• Depression
• Lameness

Cause

Contagious bovine pleuropneumonia is caused by Mycoplasma mycoides, with at least 3 or 4 genetic groups and various strains that differ in virulence.

Cattle (Bos taurus and Bos indicus) and Asian buffalo (Bubalus bubalis) are the primary hosts for this pathogen. Clinical cases have also been reported in yaks and captive bison. Sheep and goats can be infected, but they are not thought to be important hosts. There is no evidence that humans are infected by M. mycoides.

CBPP infection is spread predominantly by direct contact between an infected and susceptible animal and droplet inhalation (from infected animals coughing) in susceptible cattle, and occasionally from ingestion of infected urine or placental membranes.

Since some animals can carry the disease without showing signs of illness, controlling the spread is difficult.

Certain management practices that include keeping cattle together in a small hut at night (for protection from predators) and mixing of herds along stock routes and at watering points help spread the disease.

The spread and impact of CBPP is also increased by long-distance trekking of cattle along stock routes, providing opportunities for frequent contact of cattle within and between herds. Dust generated by mass movement also increases pathogen spread.

The nomadic culture of many herdsmen has significantly contributed to the spread of CBPP in many African countries.

In susceptible herds the morbidity (number of animals affected) and mortality rates are variable. In a naïve herd, the outcome varies from complete recovery of all animals to death of the majority of them.

Morbidity increases with animals in close confinement, due to increase in transmission; infection rates can be as high as 50 to 100% in some situations. The mortality rate ranges from 10% to 80% and is usually about 50%, and 50% of the survivors may become carriers.

When first introduced into a herd that has not been previously challenged, CBPP usually causes many deaths. A few animals may die rapidly, showing only signs of fever. Usually clinical signs start manifesting several days to months after infection, indicating that the disease can occur in a herd long before clinical signs are seen, which makes tracing an outbreak difficult.

The severity of the illness can also be affected by the virulence of the strain involved, and other factors such as nutrition, parasitism, concurrent disease or stress. There may be breed-related differences in susceptibility.

CBPP is manifested in four forms: hyper-acute, acute, subacute, and chronic. The hyper-acute form is uncommon, but generally seen at the onset of disease outbreaks, affecting up to 10% of the herd. Signs are severe, but sudden death often occurs without clinical signs—or the animals may die after 1 to 3 weeks of severe pneumonia.

During epidemics, hyper-acute and acute forms of the disease predominate at the onset, while sub-acute and chronic clinical manifestations become more apparent as the epidemic progresses.

In the acute form (which is most common), about 20% of the herd is affected, with the disease course usually running 5 to 7 days. Surviving animals recover slowly, and fatalities are common.

Signs include fever (sudden rise in temperature), self-isolation from the herd, loss of appetite, drop in milk production, and difficult breathing that is labored and painful. Other signs may include abdominal breathing and “grunting” during expiration. Affected cattle may develop a shallow, dry, painful cough--often observed during and after exercise.

Affected animals may protest when pressure is applied between the ribs (because of pain) and sometimes react violently. Affected animals stand with nostrils dilated, mouth open, panting for air, with head and neck extended, forelegs spread apart—with elbows pointed outward to allow the chest to expand more fully.

Other signs are frothy saliva accumulation and nasal discharge, sometimes streaked with blood. Some affected animals develop swellings of the throat and dewlap in this stage.

Usually the bacteria invade only one lung. As pneumonia and pleurisy develop, the lung becomes inflamed and enlarged. In fatal cases, air passages fill with fluid, the lung becomes firm with fibrous connective tissue, followed by death of lung tissues.

The animal suffers from lack of air. Fibrous tissues connect the normally unattached outer surface of the lung to the inner chest wall. Great quantities of fluid may fill the chest cavity as lung tissues break down. These cattle become distressed, and stop chewing their cud. They may “go down,” refusing to stand up. In fatal cases, death occurs 2 to 5 weeks after first signs of disease.

In the subacute form, about 40% to 50% of the herd may be affected, with signs similar to those in the acute form, though less severe and with recurrent fever.

Some cattle may directly go into the chronic stage, or become chronic after acute and subacute stages. The clinical signs gradually regress, though affected cattle may still show fever, lack of appetite, and weight loss. Young calves may have swollen, hot, and painful limb joints that result in lameness.

These animals may be reluctant to move; they stand stiffly with arched back. Getting up and down may cause obvious discomfort. Joints may be enlarged and warm on palpation. If joint pain is severe, animals may be so reluctant to bend the joints that they lie on their sides with legs outstretched.

African and recent European isolates of these bacteria may differ in virulence. When first introduced into a naïve herd, African isolates usually cause acute disease, severe clinical signs and high mortality rates. Once the disease has become established in a herd or region, with more animals exposed, mortality rate drops and the number of animals with chronic disease rises.

Milder illnesses were reported during recent outbreaks in Europe, and the affected animals usually developed subacute or chronic disease rather than dying. The morbidity rate was generally low (sometimes less than 5%), and only a few animals died.

The decreased severity of CBPP in Europe might also be related to better animal husbandry and the availability of antibiotics and anti-inflammatory drugs to treat the sick animals.

Incubation period is 20 to 123 days but most cases show signs within 3 to 8 weeks. This organism can be found in respiratory discharges, saliva, urine, fetal membranes and uterine discharges. Close contact is generally thought necessary for transmission but these pathogens can be spread over longer distances if climatic conditions are favorable.

Carrier animals, including sub-clinically infected cattle, can harbor viable organisms in encapsulated lung lesions for several months or more—sometimes up to two years. These animals are thought to be capable of shedding organisms periodically for a long time, particularly when stressed. Trans-placental transmission from dam to fetus is also possible.

Diagnosis is based on isolation of M. mycoides from samples such as nasal swabs and/or lung washings or pleural fluid obtained by puncture and aspiration through the chest wall, or necropsy samples. Clinical examinations, post-mortem inspections, and laboratory analyses through culture and isolation procedures, and serological analyses can aid diagnosis.

Prevention

The main challenges for prevention or eradication are the frequent occurrence of subacute or unapparent infections and the persistence of chronic carriers after the clinical phase.

In most countries, control strategies are based on early detection of outbreaks, control of animal movement and a stamping-out policy. These methods successfully eliminated the disease from North America and Europe. In Africa, control of the disease is currently based mainly on vaccination campaigns.

Surveillance of the disease through slaughterhouse inspection is also a very efficient method of detecting clinical cases.

Quick response and reporting of this disease is vital for containing outbreaks in regions that are currently free of contagious bovine pleuropneumonia. Veterinarians who encounter or suspect this disease should follow their national or local guidelines for disease reporting. In the U.S., state or federal veterinary authorities should be informed immediately.

CBPP is most likely to be introduced into new areas by an infected animal or embryos, as the organism does not survive long outside the body. Quarantines and serological testing of imported animals can help in prevention.

Outbreaks can be halted with on-farm quarantines of affected animals and any animals that have been in contact with them, movement controls, slaughter of infected and in-contact animals, and cleaning and disinfection or premises. Vaccines can be used to control CBPP in endemic areas.

Traditionally, CBPP has been controlled by the live T1/44 vaccine, which has been used in Africa for over 60 years. Vaccination has been successful when used on the entire cattle population of a country or region and maintained over successive years.

Drawbacks are the fact that the vaccine provides only short-term immunity, can cause severe adverse reactions and is rarely effective in the face of a severe outbreak. Even a mass vaccination program over a five-year period is unlikely to achieve eradication unless other strategies are also used.

For vaccination programs, another problem is that the quality of vaccines used to control CBPP has declined in recent times, due to problems of independent quality control by some manufacturers in Africa, inadequate handling of vaccines during vaccination campaigns, and usage of vaccines with sub-optimal quantities of Mycoplasma mycoides strains. The consequence has been occurrence of post-vaccination reactions in a few vaccinated cattle and occasional deaths.

Post injection, localized inflammation many occur. If reaction becomes extreme, antibiotics are necessary or the animal may die. In areas free from CBPP or with low occurrence, vaccination is not recommended.

Treatment

Tetracyclines, macrolides and fluoroquinolones have been reported useful in treatment, but individual drugs may differ in their effects. Complete elimination of mycoplasmas using antibiotics is rare, and treatment is controversial; some countries do not permit antibiotics to be used. Antibiotics are ineffective in chronic cases.

Treatment of affected animals with antibiotics can result in healthy looking animals that are still infected and able to spread the disease, so antibiotic treatment is usually not recommended. Also, these bacteria have higher mutation rates than most, which means they can rapidly develop resistance to antimicrobials.

Antibiotics have not been shown to stop the spread of disease; they only limit clinical signs in animals already infected.