W. A. AITKEN.
BOVINE shipping fever is an infectious respiratory disease. It is somewhat comparable clinically to influenza in man, but it has a longer incubation period and is primarily a disease of the lungs.
It has been a major disease of cattle for at least half a century. In some years it probably has caused the death of more young cattle than any disease.
Yet, because its primary cause has not been determined, it has never been given a fully satisfactory name.
Shipping fever, or the shipping-fever complex, usually is associated with the shipping of animals. It often spreads to exposed native stock, and it seems to occur occasionally in unexposed, unmoved cattle. At one time it was called stockyard disease because the animals so frequently had passed through stockyards.
It also has been called "hemorrhagic septicemia," but that name seems to have little justification because it does not indicate the cause or the primary characteristics of the disease. Hemorrhages are rather common, but septicemia infection in the blood stream-- is present only in the later stages, if at all. Furthermore, for many years the name "hemorrhagic septicemia" has been used, then abandoned, for such a variety of diseases that it has become confusing. When the true cause of shipping fever is established, a more appropriate name may be applied.
Shipping fever occurs in all parts of the United States. It may affect cattle of any age or type. A few or most of the animals in a herd may be affected. It is particularly prevalent in feeder cattle just after they have been moved from the range or from their home environment to the feed lot. Thus it is most commonly encountered in the Corn Belt and the other grain-raising areas, where most of the country's cattle are fed.
It may occur in any season, but most cases are in the fall, when most of the movement occurs. The crowded feeder cattle traffic lanes apparently become quite contaminated, thus increasing the exposure of the animals to all infections. Stockyards, sales barns and other yards, railroad cars, trucks and other vehicles, and private feeder yards become contaminated. It is possible that healthy-looking or recovered animals may carry and spread the infection.
Stress conditions are major predisposing factors for shipping fever, especially the excitement, exhaustion, and changes of feed and water that attend the shipping of animals. Irritation of the respiratory mucous membrane by dust stirred up during movement, overcrowding, long periods without feed and water, and weather changes also frequently are predisposing factors.
Calves weaned just before being shipped seem to be most susceptible, probably because they are more excitable and because they experience more marked feed changes than older cattle. Resistance increases with the age of the animals.
Good physical condition seems to afford little protection against incurring shipping fever, but it undoubtedly is a factor in avoiding complications and serious losses. Poorly nourished and highly parasitized animals usually are more seriously affected and less responsive to treatment. Deficiencies, particularly of vitamin A, could also be expected to reduce the resistance of the animals against respiratory infection.
Many authorities once believed that the bipolar bacillus, or Pasteurella organism, was the primary cause of the disease. (Before 1887 that organism was called the "bacterium septicemiae hemorrhagicum," hence the obsolete name hemorrhagic septicemia.) Certain strains of Pasteurella frequently are recovered from animals dead of shipping fever, but the general opinion is that they are secondary invaders that merely complicate the infection.
Pasteurella germs commonly are found on the mucous membranes of the respiratory tract of healthy cattle and of other animals, in many sections of the world. They vary in their ability to cause disease. Presumably, most of them do so only when the resistance of the animal is lowered.
Many strains of the organism seem to be unable to cause disease.
In a study of shipping fever in Ontario in 1954, G. R. Carter recovered Pasteurella hemolytica from the lungs of 15 of 26 affected animals, P. multocida from the lungs of 10, and pleuropneumonialike organisms from 1. Inoculation of normal calves with cultures or with suspensions made from the infected lungs failed to reproduce the disease even when the suspension was injected directly into both lungs. That would seem to indicate that the true causative agent no longer was present in the tissues. Dr. Carter later isolated P. hemolytica from nasal swabs of 27 of 33 affected animals and the pleuropneumonialike organism from 16 of the 33.
J. L. Palotay in 1953 reported on studies of shipping fever in a large feed lot in Colorado. Pasteurella were found in the lungs of about 40 percent of the animals that died and in the spleen and other organs of fewer than 7 percent. Escherichiae toll were found in the lungs of 46 percent. Cornybacterium Pyogenes, an organism that has been considered an important complicating infective agent in shipping fever, was not found. No Pasteurella or other infective organisms were discovered in the blood stream of 430 clinical cases in Colorado or in 7 cases in Ontario--an indication that shipping fever is not a septicemia.
Some research workers have suspected that a virus is the primary infective agent in shipping fever, but the suspicion has not been confirmed. The virus theory would seem to be challenged by the fact that animals in the early stages of the diseases usually respond markedly to treatment with certain drugs, whereas most viruses that produce disease are not affected by any drugs. Some viruses, such as the one that causes psittacosis of birds and man, however, are killed by some antibiotics. It is possible also that in shipping fever a virus could cause only a mild disease but one that predisposes the animal to complicating infections. The variations in these complicating infections could account for the apparent difference in response of animals with shipping fever to the same drug when used in different geographical areas.
If the disease were caused by a single micro-organism, then the response to a certain treatment should be constant.
The symptoms of shipping fever usually appear within 10 days after the animals arrive at their destinations, which often is 5 to 14 days after the date of first possible exposure.
The first and most diagnostic signs are a tired appearance, a reduced appetite, obvious chilling, and a soft cough. The temperature at this stage is usually 105 F., or higher. Similar temperatures are frequent in animals in the groups before they reveal any symptoms.
The affected animals soon become depressed and gaunt. Their breathing rate is somewhat increased. They may have a watery discharge from the nose and eyes and a dirty, encrusted muzzle. Diarrhea may occur, but usually only if the animals have been carelessly fed or have a complicating infection, such as coccidiosis.
Some years the disease will follow a mild course, and many cases will recover in a few days without treatment unless pneumonia develops. Other animals, unless treated, may linger one to several weeks. When they do recover, they are apt to be unthrifty.
In other years, especially since 1950, the disease has been more prevalent and more severe. Many affected animals have died in 24 hours. Only the increased alertness of the attendants and the improved methods of treatment have prevented tremendous losses in these years.
The swellings under the skin of the throat and dewlap, which were commonly reported at one time, seem to be observed less often in recent years. A commoner occurrence, especially in animals that require prolonged treatment, is a nearly total loss of appetite plus constipation. That probably is the result of changed conditions for the micro-organisms of the rumen, which are so important in digestion. Those organisms may be affected adversely by the prolonged use of drugs or possibly by the lack of eating and by the fever. Such animals usually respond to transplants of rumen content (cud) from healthy animals.
Overtreatment with the sulfonamide drugs may also cause serious damage to the kidneys and result in a lingering illness, without fever, and in death.
THE LESIONS found on postmortem examination are confined chiefly to the respiratory organs. The character of the changes and the extent of involvement of other organs depend on the length of the illness and on the complicating infections.
In the most complete study made in many years, W. R. Graham in 1953 reported on 57 cattle that had died out of hundreds affected with shipping fever in Colorado feed lots. He found pneumonia present in 55, or 96.5 percent, of the fatal cases. The other two animals had a severe congestion of parts of the lungs.
He observed that shipping fever begins with a severe congestion of the lung, followed by hemorrhage and the outpouring of fibrinous exudate into the aleveoli (the air spaces of the lung) and a severe inflammation of the tract leading to the lungs. Abscesses or gangrene were present in some lungs.
Subcutaneous edema (dropsy) was found in 10 percent of the fatal cases. An inflammation of the serous membrane lining the thoracic cavity was found in most of them, and the mucous membrane of the stomach and intestine was inflamed in many.
In the later stages of the disease, bacteria apparently had invaded the blood stream in a few, producing a septicemia, which was indicated by small hemorrhages on various organs. The hemorrhages most frequently were found in the subcutaneous tissues, in the thymus gland, on the heart, and occasionally on the kidneys. The brain was congested in 22 percent of these animals, and it contained actual hemorrhages in about 10 percent.
Inclusion bodies in the tissue cells, the cell changes that indicate a virus infection, were not found.
A diagnosis of shipping fever is indicated when a respiratory illness, accompanied by a high temperature, occurs in cattle that have been shipped within about 10 days.
Cattle with pneumonia or with leptospirosis, anthrax, blackleg, certain intoxications, or even a mild digestive disorder may sometimes show similar symptoms before other symptoms more characteristic of those diseases develop. In all except the respiratory diseases, however, the characteristic coughing is usually absent.