Internal Acariasis

with human dermatitis and other skin disorders (Hewitt et al., 1973; Krantz, 1978; Oehlschlaegel et al., 1983) and to invade various organs and body fluids of humans and other animals (Dahl, 1910). The most commonly implicated species is Tarsonemus bominis. It is generally believed that these reports represent contamination of glass slides and other materials used in preparation of tissues for microscopic examinations (Hewitt et al., 1973; Samsinâk etal, 1976).

Excluding tick-borne diseases, there are only two significant diseases of humans for which mites serve as the principal vectors: rickettsialpox and tsutsugamushi disease.

Rickettsialpox was first recognized in 1946 during an outbreak in New York City (Huebner etal., 1946). Sporadic cases had been reported as early as 1909 in Washington, DC, and other cities along the northeastern seaboard of the United States. Rickettsialpox is a relatively uncommon illness, with only 800—900 cases having been reported in the United States. Cases occur primarily in urban areas in crowded living quarters infested with the house mouse (M. musculus) that serves as the major reservoir. The pathogen is transmitted to humans by the bite of the house mouse mite, Liponyssoides sanguineus (Der-manyssidae) (Fig. 23.5). Other countries in which cases of rickettsialpox have been reported are Russia, Korea, and parts of equatorial and central Africa.

The causative agent of rickettsialpox is Rickettsia akari. It is a spotted fever group (SFG) rickettsia and is morphologically indistinguishable from R. rickettsii, the causative agent of Rocky Mountain spotted fever. The intracellular site in which it replicates in human hosts remains unknown.

Rickettsialpox is usually a mild, nonfatal illness which typically begins with the appearance of a nonpruritic, erythematous papule at each infectious bite site, usually within 24—48 hr of contact with L. sanguineus. Soon thereafter a small vesicle forms at the center of the papule, filling initially with a clear, then cloudy, fluid. The vesicle dries, producing first a crusty lesion and then a brown or black scab, or eschar, in the center of a larger, indurated area 0.5—3.0 cm in diameter. These lesions can occur on any part of the body but usually occur on the face, trunk, and extremities. They may occur on the palms and soles and on mucous membranes about the mouth. The latter include the palate and, less commonly, the general mouth cavity, tongue, and pharynx. Although there usually are only a few, as many as 100 discrete lesions have been reported in some cases.

Systemic symptoms appear about the time that eschars form, 9—14 days after the initial bites. Fever (usually peaking at 38—40° C), headache, and malaise are characteristic and may be accompanied by muscle aches, especially backaches, drenching sweats, and shaldng chills. Less common symptoms are cough, runny nose, sore throat, nausea, vomiting, enlarged and tender regional lymph nodes, and abdominal pain. Most cases resolve in 6—10 days without treatment. In some cases, however, headache and lassitude may persist for another 1 —2 weeks. Treatment with antibiotics generally alleviates the fever and other symptoms within 48 hr.

Diseases that should be included in the differential diagnosis of rickettsialpox are other members of the SFG rickettsiae, notably Boutonneuse fever, tsutsugamushi disease, Siberian tick typhus, and Queensland tick typhus. They can be distinguished, however, by their geographic occurrence and the clinical nature of the associated skin lesions. The nonrickettsial disease with which rickettsialpox is most commonly confused is chickenpox, caused by a virus. In chickenpox cases, however, the vesicles are not raised on papules, eschars are not formed, and the lesions are much more numerous. The clinical syndrome and a rise in titer of SFG-specific antibodies are generally sufficient to confirm a diagnosis of rickettsialpox. Immunity appears to be complete, perhaps lifelong, following recovery from infection. For additional information on the clinical and diagnostic aspects of this disease, see Brettman et al. (1981) and Kass et al. (1994).

L. sanguineus, the vector of the rickettsialpox agent, is primarily a parasite on the house mouse. The mite is also found on rats (Rattus spp.) and voles, although the role of these and other wild rodents in the ecology of this disease is uncertain. Whereas L. sanguineus nymphs generally take a single blood meal, adults move onto and off the host to take several blood meals. Most of the time is spent off the host in nests and runways of mouse-infested areas. Where it occurs in human dwellings, the mite seeks the warmth of furnace rooms and incinerators of old buildings, where they may occur in large numbers on the walls and ceilings. Human bites are believed to occur primarily when house mice in apartment buildings become less attractive as hosts, inducing the mites to seek alternate hosts. The occurrence oflymphocytic choriomeningitis in house mice during outbreaks of rickettsialpox in humans has been suggested as a possible factor; such infections cause changes in a mouse's body temperature, perhaps inducing the mites to abandon their natural host (Krinsky, 1983). Starved adults can live 7—8 weeks, whereas blood-fed adults can live 9 weeks or longer.

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