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any one of several infectious diseases of man and animals caused by rickettsiae, which are spread by bloodsucking arthropods.
In man. In man, rickettsioses include epidemic (louse) typhus; its recrudescent louse-borne form, Brill’s disease; and endemic, or flea (murine), typhus, which is harbored and disseminated by rats and mice and transmitted by fleas. In another form of the disease, Marseilles or Mediterranean (boutonneuse) fever, ticks and dogs are the carriers and ticks the transmitters. In Central Asian hemorrhagic fever, rodents and ticks are the carriers and ticks the transmitters. The carriers of North Queensland tick typhus are small wild animals and the transmitters are ticks. In rickettsialpox, mice are the carriers and ticks the transmitters; in scrub typhus (also called Japanese river fever and tsutsugamushi fever), rodents and ticks are the carriers and ticks the transmitters. In Q fever, ticks and many species of wild and domestic animals are the carriers and the chief transmitters are ticks. Still other forms of rickettsiosis in man are trench fever (also called Volhynia fever and five-day fever), in which man is the carrier and body lice the transmitters, and paroxysmal rickettsiosis, in which rodents are the carriers and ticks the transmitters. Among these diseases, epidemic and endemic typhus, trench fever, Q fever, rickettsialpox, and paroxysmal rickettsiosis have been reported at different times in the USSR.
Rickettsiosis sets in after tick bites or penetration into cuts, scratches, and mucosa of infected feces from lice and fleas. Some rickettsioses, such as Q fever, are spread by the urine, feces, or milk of infected animals. The carriers of rickettsioses, except in the case of typhus and trench fever, are animals, chiefly wild ones and especially rodents. Blood-sucking insect transmitters become infected by the infected animals. Ticks are also natural carriers of many rickettsioses, in which rickettsiae may be transmitted transovarially from generation to generation. The existence of natural carriers has caused most rickettsioses to be classified as naturally endemic diseases. In some rickettsioses, such as epidemic typhus, man is the source of infection.
Rickettsioses in man are febrile diseases varying in severity and symptoms; a rash is characteristic of some forms. Fleaborne murine typhus, whose causative agent is Rickettsia mooseri, develops after infected louse feces settle in scratches on the skin. The incubation period is five to 15 days. The characteristic symptom is a bright pink rash that appears on the trunk, extremities, and face four to five days after the disease’s onset. The course of fleaborne murine typhus is milder than that of epidemic typhus.
The incubation period of rickettsialpox is one to two weeks. A week before the fever develops, an induration with a blister in its center appears at the site of the tick bite. The induration later becomes covered with a black crust and surrounded by a hyperemic zone. When areas of the rash dry, they form dark crusts. The incubation period of paroxysmal rickettsiosis is seven to ten days. Recurrences of fever are characteristic. There is usually no rash and no induration at the site of the tick bite.
Such serologic methods as agglutination, hemagglutination, and complement fixation are used in the laboratory diagnosis of rickettsioses. Bacteriological studies are sometimes made. Treatment is effected mainly with antibiotics. Prevention entails control of the transmitters, such as lice in the case of typhus, disinsectization, the use of repellents and protective clothing, and restrictions on the use of milk and meat from infected animals. Active immunization is used to prevent some rickettsioses, including typhus and Q fever.
REFERENCEZdrodovskii, P. F., and E. M. Golinevich. Uchenie o rikketsiiakh i rikketsiozakh, 3rd ed. Moscow, 1972.
V. L. VASILEVSKII
In animals. The commonest forms of rickettsiosis encountered by veterinarians are infectious hydropericarditis (heart-water), Q fever, rickettsial keratoconjunctivitis, and rickettsial monocytosis (canine rickettsiosis). Infectious hydropericarditis is a disease of cattle and swine that was first described in South Africa in 1838 by F. Trichardt. The causative agents are Cowdria ruminantium in ruminants and C. suis in swine. The source of the causative agent is infected and convalescent animals and the transmitters are ixodid ticks. Heartwater is manifested by fever, cardiac and respiratory disturbances, diarrhea, and convulsions; the acute form of the disease is usually fatal. A characteristic pathologicoanatomic symptom is the accumulation of an exudate in the pericardium and body cavities. There is no specific treatment for the disease. Preventive measures include isolation of infected animals, control of ticks, and vaccination.
Rickettsial keratoconjunctivitis occurs in cattle, camels, swine, and poultry. It was first described in 1931 in South Africa by D. W. A. Coles. Diseased animals are the source of the causative agent, Ricolesia bovis, which is transmitted through the air in droplets of moisture. The disease is characterized by swelling of the eyelids, photophobia, and conjunctivitis. The course is benign, the animals recovering within eight to ten days. Solutions of colloidal silver and zinc sulfate and antibiotic ointments are used for therapy. Preventive measures include isolation of infected animals and disinfection of their living quarters.
Rickettsial monocytosis occurs in cattle and dogs. It was first described in 1935 in Algeria. The causative agents are Rickettsia bovis and R. ovina in cattle and R. canis in dogs. Infected animals are the source of the agents, and ixodid ticks are the carriers. The disease is manifested by fever. A characteristic symptom is the presence of rickettsiae in the monocytes. The animals generally recover, but they remain long-term carriers of rickettsiae. Sulfanilamides are used for therapy. Preventive measures include isolation of infected animals, eradication of ticks, and disinfection of the animal’s living quarters.