Psittacosis is a specific infection of birds produced by a microbial agent whose precise classification is currently in question. When transmitted to man this agent can produce asymptomatic infection, a transient influenza like illness, or serious pneumonic disease characterized by high fever, headache, cough, myalgia, pulmonary infiltrates, and a significant mortality. Because it is now recognized that many species of birds other than the order Psittaciformes transmit psittacosis or “Bedsonia” agent, ornithosis has been suggested as a more accurate title. Usage has made psittacosis the accepted term for the human disease.
In 1879, Ritter, a Swiss physician, described seven cases of an unusual pneumonia that occurred after contact with tropical birds. Morange, in 1894, established the parrot as a vector and termed the disease psittacosis after the Greek psittakose (the parrot). During the year 1929-1930 a serious epidemic of pneumonia occurred in Europe, America, and Asia following shipments of infected South American parrots. This epidemic led to clearer recognition of psittacosis as a human disease.
The etiologic agent was demonstrated to be a filterable agent by Bedson, Western, and Simpson in 1930. Subsequent studies have shown that over 90 species of birds can harbor the agent, and its worldwide distribution has been documented. Since the lifting of quarantine restrictions on the importation of psittacine birds in 1951, there has been a significant increase in cases in the United States.
Etiology, How Is Psittacosis Transmitted To Humans
The psittacosis agent is an obligate intracellular parasite. It is morphologically and serologically related to lymphogranuloma venereum and to a number of mammalian agents producing pneumonitis, meningoencephalitis, and abortion in their native hosts. To date, these agents have not been shown to produce human disease. Because of their large size (250 to 400 m.ju.), possession of both RNA and DNA, a demonstrable cell wall containing muramic acid, division by binary fission, and their susceptibility to chemotherapeutic agents known to inhibit bacterial enzyme systems, these agents more closely resemble Rickettsia or bacteria than true viruses.
Parrots and parakeets are the most common carriers and until recently represented the major source of human infection. With better control of psittacine disease in aviaries, other birds now contribute more human infections with psittacosis, and cases have resulted from contacts with turkeys, pigeons, ducks, chickens, pheasants, finches, and other fowl. Although individuals of both sexes and all ages are susceptible, overt clinical infections in children are uncommon. Persons working with birds are at greatest risk of infection, and there is an increased incidence of psittacosis in pet shop employees, pigeon handlers, and poultry workers.
The agent is present in the blood, tissue, and discharges of infected birds. It is hardy and can withstand drying. Although the avian disease can be fatal, infected birds frequently show only minimal evidence of illness, such as ruffled feathers, lethargy, and failure to eat. Birds having tixo disease, but asymptomatic carriers are common, and birds that recover can shed transmissible agent for many months. In general, human psittacosis acquired from psittacine birds or turkeys has been more severe than that acquired from pigeons, ducks, chickens, or pheasants. Bird ectoparasites can harbor the agent and may serve as a source of reinfection for domestic flocks. Antimicrobials incorporated in bird foodstuffs have not eradicated psittacosis from infected parrots or parakeets.
Psittacosis is generally acquired by the respiratory route through inhalation of infected dried bird excreta, more rarely by handling the feathers and the tissues of infected birds. On rare occasion the disease may be acquired through an open lesion or the bite of a bird. Small epidemics have
been attributed to aerosols of dust laden with dried excreta. Cases have been reported after only brief exposure to birds. There is some evidence that the incubation period may be shortened by a large inoculum. Person to person transmission of psittacosis, although rare, has been documented. These cases of “human” strain psittacosis have been severe, with high mortality.
Pathology of Psittacosis.
In birds, the principal sites of disease are the liver, spleen, and pericardium. In man, the lung is most commonly involved. Although the psittacosis agent generally gains access to the human bod;.’ via the respiratory route, there is clear evidence that it rapidly enters the blood and produces systemic disease involving the lungs and the reticuloendothelial tissues. The agent can be isolated from the blood of infected humans during the first two weeks of illness, and has been found in the spleen in fatal cases. The mature pulmonary lesion is a lobular pneumonitis.
The process is initiated by inflammation and progressive edema of the alveolar cells. Exudation is often accompanied by small hemorrhages. Polymorphonuclear leukocytes appear early in the process. Later inflammatory exudates show lymphocytes and large numbers of mononuclear leukocytes within the alveoli and interstitial spaces. The mucosa of the trachea and bronchi generally remains intact cot is edematous and invaded with mononuclear cells Thick, gelatinous plugs of mucus may fill major and minor bronchi and may account for the severe cyanosis, and progressive anoxia seen in fatal cases. Foci of necrosis may occur in more severely affected areas of the lung and are sometimes associated with capillary thrombi.
The process is generally most severe in dependent bronchopulmonary segments. Large monocytes and macrophages containing cytoplasmic inclusion bodies, which may represent the agent L.C.L. bodies), are characteristic of psittacosis infection. Vasculitis and thrombosis may account for many findings. Hyperplasia and monocytic infiltration of pulmonary and hilar lymph nodes and splenic enlargement with occasional areas of focal necrosis may occur. Rarely the liver may show intralobular focal necrosis and swollen Kupffer cells containing the psittacosis elementary bodies. Changes in the myocardium, pericardium, meninges, brain, adrenals, and kidneys have been reported.
Clinical Manifestations of Psittacosis.
Wide variations can occur in the clinical picture. The incubation period ranges I to 15 days . Probably asymptomatic infection or mild influenza-like infections are the rule. Moderate or severe infections, although less frequent, are more commonly diagnosed. The onset of illness may be insidious, but it often starts with chills and a fever that rises slowly from initial levels of 101 or 102 to 103 to 105° F. during the first week of illness. Headache is severe. Malaise, anorexia, severe myalgias, particularly in the neck and back, and arthralgias are common. Cough is generally prominent but may be delayed until Late in the first week.
Small amounts of mucoid sputum with occasional blood streaking are the rule, and pleuritic pain is rare. Changes in mentation are often seen. Delirium or stupor may occur in severe cases toward the end of the first week, and is usually associated with severe pulmonary involvement, cyanosis, and other evidences of anoxia. Other neurologic manifestations are uncommon. Nausea and vomiting are frequent. Epistaxis may occur early in the course of the illness. A macular rash resembling that seen in typhoid has occasionally been described. Jaundice and progressive nitrogen retention have been reported in severe cases. Severe dyspnea, tachypnea, tachycardia, cyanosis, jaundice, delirium, and stupor are all poor prognostic signs.
The physical findings of pneumonia are often sparse. Chest roentgenograms may reveal evidence of infiltrates not detected at the bedside. Examination may reveal only fever, painful muscle groups, an elevated respiratory rate, and a relative bradycardia. Fine, crepitant rales may be heard in localized areas over the lungs. Frank percussion or auscultatory changes suggestive of true consolidation are less common. Pleurisy with effusion can occur but is unusual. Mild hepatomegaly is frequent. A palpable spleen has been reported in 5 to 70 per cent of patients. An erythematous pharynx may be noted. In rare instances there may be signs of pericarditis or myocarditis. In prolonged, severe illness, thrombophlebitis and pulmonary infarction have been reported as late complications.
Patients with mild cases may recover in 7 to 8 days. More severe infections may last 12 to 21 days without specific treatment. Fever is ordinarily sustained or remittent, and when accompanied by bradycardia, resembles the fever seen in untreated typhoid infections. Defervescence is generally slow, and prolonged convalescence is common. Secondary bacterial infections are rare.
Simple laboratory studies are not helpful in establishing a diagnosis. The leukocyte count is usually normal, but leukopenia or low-grade leukocytosis ranging to over 20,000 cells per cubic millimeter may occur. The erythrocyte sedimentation rate is generally elevated. Proteinuria is common during the febrile period. Chest roentgenograms generally show soft patchy infiltrates radiating outward from the hilum, which tend to be more prominent in dependent lobes or segments. Occasionally diffuse miliary, nodular, or frank lobar distribution of infiltrates is seen.
A specific diagnosis can be made by serologic studies. The agent is present in the blood and sputum during the first two to three weeks, but isolation is hazardous, and should not be attempted except in special laboratories. Diagnosis is generally made by a diagnostic rise in complement-fixing antibodies against a heat-stable group antigen prepared from psittacosis agent grown in eggs. Paired acute and convalescent sera should always be tested. A significant change in antibody titers is generally present by the twelfth to four-by 30 days, then slowly disappear. Treatment can deal or suppress antibody response. There is considerable cross reaction between antigens prepared from psittacosis and lymphogranuloma venereum viruses. False positive complement- fixation tests may occur with Q fever or brucellosis. Cutaneous hypersensitivity to the Frei antigen may develop during psittacosis.
Psittacosis Differential Diagnosis.
Specific diagnosis of psittacosis is of extreme importance because of its potential severity (reported fatality rates range from 5 to 40 per cent), its response to antimicrobials, an,d the public health significance of psittacosis infection. The syndrome of viral pneumonia accompanied by protracted high fever, unusually severe headache, and relative bradycardia should suggest psittacosis. Often a history of contact with birds is the only clue to diagnosis. When pneumonic symptoms are prominent, psittacosis must be differentiated from viral pneumonias, mycoplasmal pneumonia, influenza, Q fever, tuberculosis, histoplasmosis, coccidioidomycosis, bacterial pneumonia, and other processes that produce pulmonary infiltrates. If pneumonic symptoms are not prominent, psittacosis can be confused with other systemic febrile illnesses such as typhoid fever, brucellosis, infectious mononucleosis, infectious hepatitis, miliary tuberculosis, or the viral meningo encephalitides.
Treatment of Psittacosis.
The tetracyclines are the drugs of choice, and early diagnosis and initiation of treatment may be life-saving. Following institution of therapy with 2 to 3 grams daily, both fever and symptoms are generally controlled within 48 to 72 hours. Chloramphenicol appears to be less effective. Although the disease apparently responds to penicillin in doses above 2 million units daily, tetracycline remains the drug of choice. Treatment should be continued for at least 10 days. The high fever and progressive anoxia secondary to extensive pulmonary involvement in severe cases may require appropriate measures directed at these problems.