The only other mite reported as a possible vector of R. ctkari is Ornithonyssus bacoti, based on experimental transmission studies using laboratory white mice {Lackman, 1963; Philip and Hughes, 1948).

Tsutsugamushi disease is a mite-borne rickettsiosis of humans that is endemic in eastern and southern Asia, the western Pacific region, along the northern coast of Australia (Queensland and Northern Territory), and the Indian subcontinent. Cases may occur as far west as Afghanistan, Pakistan, and neighboring areas of the former Soviet Union. It is also known as scrub typhus and chigger-bome rickettsiosis. The causative agent is Orientia tsutsugamushi (formerly Rickettsia tsutsugamushi) transmitted by the bite of trombiculid larvae, or chiggers (Pig. 23.10).'

Tsusugamushi disease was recognized as early as the fourth century AD, when it was described in clinical manuals as an illness associated with mites. It was not until 1930, however, that Japanese workers first isolated and identified the pathogen as a rickettsia. This disease first caught the attention of the Western world during World War II when the Allied Forces were severely affected during operations in the Pacific Theater. The number of cases of tsutsugamushi disease exceeded that of direct wartime casualties among the military forces in that region. Fatality rates as high as 27-35% occurred among troops on the islands of Goodenough and Finchhaven in New Guinea (Philip, 1948; Philip and Kohls, 1945). With the advent of effective antibiotics for treatment, the incidence of tsutsugamushi disease decreased dramatically in the region during the late 1940s and 1950s. However, sudden increases have occurred since that time in Japan (ca. 1975), Korea (ca. 1985), and other areas. For comprehensive reviews on this important mite-borne disease, see Traub and Wisseman (1974) and Kawamura et al. (1995).

The causative agent of tsutsugamushi disease is considered to be distinct enough from related rickettsial organisms to be placed in its own genus, Orientia (Tamura et al., 1995). Like Rickettsia species, it is an obligate intracellular parasite that multiplies in the cytoplasm of host cells. The clinical picture is complicated, however, by a multitude of antigenic variants, or strains, that exhibit various degrees of pathogenicity to humans. Among the better characterized strains are Gillian, Karp, Kato, Kawasaki, Kuroki, and Shimokoski. The relationships among the different strains and their mite vectors remain largely unknown.

The classic form of tsutsugamushi disease varies from a mild to severe illness. It begins with the development of a small papule at the bite site of an infected chigger.

FIGURE 23.23 Leptotrombidium akamushi (Trombiculidae), chigger vector of Orientia tsutsttgamusln, the causative agent of tsutsugamushi disease isi Japan. (Modified from Baker et al., 1956.)

The skin reaction varies from hardly noticeable or mildly itchy to painful. The latter discomfort is characteristic of bites of the mite Leptolrumbid-mm, akamushi (Fig. 23.23) and has been likened to a tiny thorn that has penetrated the skin and induces pain when it is rubbed. This sensation, called ira in endemic areas of Japan, usually appears about 10—20 hr after the bite and is believed to be caused by an inflammatory eruption associated with formation of a feeding tube (stylostome) by the attached mite. Bites occur most frequently in the folds of soft skin of the axillary region, upper legs, and abdomen. Other common sites include webs between the fingers, skin behind the knees, genitalia, under breasts, and skin constricted by clothing. The bites become ulcerated and form hard, black scabs (eschars), typically accompanied by fever and a maculopapular rash.

Following an incubation period of about 10 days (range, 5—20 days), symptoms generally include loss of appetite, fever, headache, muscle aches, and general malaise; regional or generalized lymphadenopathy is also common. The more virulent strains of Orientia tsutsugamushi can cause hemorrhaging, intravascular coagulation, and other blood disorders as the rickettsiae multiply in epithelial cells of the vascular system. This can lead to microthrombi in the kidneys, lungs, and heart, contributing to fatalities. Mortality varies widely from 3 to 60%, depending on the strain and geographic region. Cases of tsutsugamushi disease can be treated effectively with antibiotics. However, in severe cases with hemorrhagic complications, heparin therapy and platelet transfusion may be necessary. Immunity following recovery is not lasting, such that reinfections are common in endemic areas.

Although cases of tsutsugamushi disease occur throughout the year, they often are seasonal in certain areas, reflecting the activity of local mite vectors. In some

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