Ornithosis and Psittacosis

JOHN P. DELAPLANE.

PEOPLE can get ornithosis--or psittacosis--through contact with sick birds, notably parrots and other birds of the psittacine, or parrot, family. Epidemics have occurred since 1879 in Switzerland, Germany, France, England, and the United States.

The disease used to be known as 'parrot fever" because people thought parrots and parakeets were the only sources of infection. Now we know that some 70 species of birds can get the infection.

Since 1938, epidemics in people traceable to contacts with fulmars, petrels, chickens, ducks, pigeons, shore birds, pheasants, and turkeys have been recorded.

K. F. Meyer, of the Hooper Foundation, University of California, has suggested that "psittacosis" be used to designate infections that have parrot or psittacine origin and "ornithosis" to designate the infections that arise from nonpsittacine birds.

Diagnoses of the epidemics in 1948, 1951, and 1952 among workers in poultry-dressing plants in Texas were based on positive complement-fixation serological tests. Turkeys were suspected as the source of infection in man because the incubation period of the disease indicated repeatedly that the infection followed the processing of turkeys. The isolation of the virus from turkeys and the fact that the virus infected laboratory technicians who worked with it proved that turkeys were the source of those epidemics. Thereafter persons concerned with Problems of public health and poultry diseases became deeply interested. About 200 workers in poultry-dressing Plants got the disease in 1954.

The first description of a disease marked by an atypical pneumonia was reported in 1879 among persons having contact with sick parrots. A severe and sometimes fatal atypical pneumonia was observed in various European countries and the United States in later years. An unusually severe epidemic occurred in Paris in 1892. Then the disease was thought to originate as a result of gram-negative bacterial organisms, which could be isolated readily from the tissues of the sick and dead parrots. The subsequent failure of investigators to find the gram-negative bacterial organism consistently in sick or dead parrots created doubt that the organism actually caused the disease. We now recognize that the organism originally reported was merely a common complicating agent, rather than one of primary significance.

The name "psittacosis" was suggested for the disease in 1895. From 1895 to 1929 the disease was recognized as single or group infections in Europe and the United States.

An epidemic involving more than 100 cases of atypical pneumonia, diagnosed as psittacosis, occurred in Argentina in 1929. A year later epidemics in Europe and the United States were traced to parrots newly imported from South America, and the virus character of the psittacosis disease agent was found by scientists in England and the United States.

They discovered that white mice could be infected with the virus and would therefore be used in laboratory studies. The finding contributed greatly to our knowledge of the disease.

We refer to the ornithosis and psittacosis agents as large, particle-size viruses they can be seen with an ordinary microscope and are susceptible to antibiotics, while true viruses cannot be seen or are not affected by antibiotics.

An epidemic of pneumonitis among persons who were processing fulmars and petrels in the Faroe Islands in 1938 was found to be a "psittacosis-like" disease. The finding emphasized the importance of birds other than parrots as sources of human infections.

A highly virulent virus isolated from snowy egrets in Louisiana and indistinguishable from the one causing a severe human pneumonitis in that State in 1944 suggests that this bird was the possible source of the infection in man.

Since the 1930's, ornithosis and psittacosis viruses have been found to be closely related to a group of agents affecting mammals, such as bovine sporadic encephalomyelitis, lymphogranuloma venereum, mouse pneumonitis, feline pneumonitis, and agents isolated from calves, ewes, and opossums.

THE CLINICAL SYMPTOMS and pathology of the disease are better known in psittacine birds than in turkeys.

Latent infections occur in most species of birds. Virus may be shed from time to time and can infect man and other birds.

The infection may or may not be apparent in psittacines. The sick birds seem to be sleepy and have ruffled feathers, fits of shivering, labored breathing, and a rapid loss of body weight. Diarrhea, with greenish stools, may soil the feathers. Nestlings become infected through feeding. Virus has been recovered from eggs, but the importance of a direct transmission through the egg has not been well established among these birds.

The mortality among parakeets is 5 to 10 percent when they are raised under satisfactory conditions; otherwise, the mortality rate may be higher. Stress factors, such as changes in environment, shipping, exposure to cold, and unfavorable temperatures, are thought to excite latent infections into activity.

The incubation period upon contact exposure usually is 5 to 20 days, but it might take as long as 100 days for infection to occur in individuals exposed to contamination.

The disease may persist for weeks in an individual and may be marked by frequent relapses.

The gross pathological changes observed in typical specimens include enlarged, saffron-colored livers, with many partly healed, whitish foci. The spleen is usually enlarged during the various stages of the disease. The air sacs show catarrhal inflammation and accumulations of whitish exudates. Degenerative changes may be seen in the kidneys. Occasionally there is evidence of pericarditis.

Microscopic studies of the various tissues show changes in the normal structure of the spleen, with increased numbers of white blood cells, which are recognized as body defense mechanisms in combating infections such as psittacosis. The large spleens commonly seen in diseased psittacines occur from the increases of blood and the large numbers of white blood cells.

The liver has many small, distinct areas of whitish, dead cells irregularly distributed throughout the organ. In lesions of longer duration, collections of leucocytic types of white blood cells are observed. The serous membranes covering the liver become affected, and depositions of a thin film of fibrin (false membranes) may cover the surface of this organ. More frequently this type of film on the surface of the liver is referred to as "plastic exudate."

The lesions found in other birds, such as the pigeon, are similar fundamentally to those in psittacine birds.

IN MAN the disease is characterized by an atypical pneumonia with the incubation period of 7 to 15 days after contact with the infective birds. The symptoms parallel those of influenza. Fever may persist 3 or 4 weeks. Cough may be slight or absent.

Relapses following recovery are not uncommon. Death may result from toxemia or pulmonary insufficiency.

The use of broad-spectrum antibiotic therapy, such as Aureomycin, Terramycin, and Chloromycetin will bring the disease readily under control. Relapses have occurred when the antibiotic therapy has been stopped.