Rickettsialpox is a mite-borne rickettsial disease, mild and self-limited, which is characterized by an initial eschar-like lesion and a fever of a week’s duration accompanied by headache, backache, and a generalized papulovesicular rash.
The disease is caused by Rickettsia akari, a member of the spotted fever group of rickettsia. Although R. akari possesses an antigen in common with Rickettsia rickettsi, it is most closely related to Rickettsia australis theof North Queensland tick tvxhus, The txrzsmism is transmitted to ‘man, with an incubation period of 10 to 24 days, by the bite of the mouse mite, Allodermanyssus sanguineus.
Incidence and Distribution.
The incidence of the disease is difficult to determine. In the first thtee years after the disease was described in 1946, 500 cases were reported in the United States, most of them from New York City. Reporting of the disease has decreased markedly since that time. It is likely that small numbers of cases continue to occur without being reported because the disease is one in which national reporting is not required. The disease has been reported from Boston, West Haven, Connecticut, New York, Philadelphia, Pittsburgh, and Cleveland in the United States, and from the U.S.S.R.
When the disease was first described in 19.46-1947, in a New York apartment housing project, the investigators demonstrated the presence of the agent in both the commensal mouse, Mus musculus, and its mite ectoparasite, A. sanguineus, both of which were present in large numbers. The single piece of information that was missing from the initial study was the manner in which the disease agent, R. akari, entered the mouse and mite populations. The subsequent isolation from a field mouse in Korea of a rickettsial agent indistinguishable from R. akari suggests that the agent may be widely distributed among feral rodents and their ectoparasites. If this view is correct, the disease may be expected to occur in areas of expanding suburbia where man and commensal populations of domestic mice come into contact with feral mice and their ectoparasites.
Because rickettsialpox is a benign infection with no reported deaths, pathologic examination has been limited to biopsy material. The initial lesion or eschar resembles the eschars of scrub typhus and boutonneuse fever. The skin lesion of the early rash is characterized by perivascular infiltration with mononuclear cells. During the later stages of the rash when vesicula- lation occurs, the histologic changes are highly characteristic and consist of necrosis of the superficial epithelial cells leading to an intra-epidermal vesicle. Clinical laboratory findings are limited to a minimal Jeukopenia during the febrile period.
Clinical Manifestations of Rickettsialpox.
The first sign of infection is the initial lesion or eschar, which appears approximately a week before onset of fever. Most patients are unaware of the small papule that develops at the site of the infecting mite bite or, if they note it, they interpret it as a “pimple.” The lesion begins as a small papule that enlarges slowly to 0.5 to 1.5 cm. in diameter, develops a central vesicle, and finally forms a dark crust without pustulation. Except for the lack of itching, tenderness, or pustulation, the lesion resembles that of a primary vaccinia react;on. and usually leaves a small scar. When searched for carefully, the initial lesion will be found in over 90 per cent of cases.
with chills or chilly sensations ana’ drencflmg sweats. After approximately a week the fever gradually subsides. The early febrile period is characterized by headache, photophobia, marked lassitude, and muscle pains, including backache. Beginning on the first to fourth days of fever a maculopapular rash appears, which develops into a vesiculopapular rash. The vesicles are firm, sometimes surrounded by erythema, and on drying form a dark crust that falls off without leaving a scar. In contrast to chickenpox, the rashfappears on many areas of the body at almost the same time and does not itch; it is absent from the palms and soles.
Physical examination during the febrile period yields little additional information. An enlarged spleen or lymphadenopathy will be found in only a few cases. The differential diagnosis very early in the disease should include measles, chickenpox, and smallpox; with the appearance of the vesicles only the latter two diseases need be considered. The presence of an initial lesion, the more superficial position of the vesicle, and the persistence of the papular base throughout the period of rash argue strongly for rickettsialpox rather than chickenpox. Smallpox lesions resemble those of rickettsialpox, but progress to pustules. In addition, the constitutional symptoms of most patients with smallpox are considerably more severe than those of patients with rickettsialpox.
Diagnosis of Rickettsialpox.
The clinical characteristics of the disease are so distinctive that in most patients a presumptive diagr. :sis may be made on clinical grounds. Chickenpov in adults poses the most difficult diagnostic problem. Laboratory confirmations of the diagnosis is possible by isolation of the agent from blood obtained during the acute phase of illness and also by complement-fixation tests on paired specimens of serum. Because the agent of rickettsialpox is closely related to that of Rocky Mountain spotted fever, complement-fixa- tion tests may be performed with antigen prepared from either organism. A fourfold or greater rise in antibody titer may be expected in patients with rickettsialpox when the acute phase specimen is collected early in the febrile period and the convalescent specimen is collected three to.four weeks after onset of disease. The Weii-Felix agglutination reaction is of no diagnostic value in rickettsialpox.
Rickettsialpox Treatment and Prognosis.
The disease may be so mild in some patients that no specific treatment may be indicated. When therapy is desirable, the tetracyclines may be used in oral doses:of 25 mg. per kilogram per day for three or four days. Response to treatment is rapid; most patients become afebrile in 2-4 to 36 hours. Relapses of infection have not been reported. The is excellent.
The principal target of preventive measures is the mite vector of the disease, A. sanguineus, which may be controlled by the use of residual insecticides (DDT or dieldrini in areas of mouse harborage. Vector control should be achieved prior to initiating mouse control measures to avoid further dispersal of the mites in their search for food. No vaccine is currently available.