With the exception of Q fever, the clinical manifestations and pathologic effects of the rickettsial diseases are much the same, varying only in severity. Typhus may be taken as the prototype. The incubation period varies from 3 to 18 days. The onset is usually abrupt, with fever rising to extreme levels over several days; headache, often severe; and prostration. A macular rash, which resembles that of measles and involves the trunk and limbs, appears on the fourth or fifth febrile day. An important diagnostic sign in scrub typhus is the necrotic ulcer and eschar at the site of attachment of the infected mite. Delirium—followed by progressive stupor and coma, sustained fever, and occasionally focal neurologic signs and optic neuritis— characterizes the untreated cases. Stiffness of the neck is noted only rarely, and the CSF may be entirely normal or show only a modest lymphocytic pleocytosis.
In fatal cases, the rickettsial lesions are scattered diffusely throughout the brain, affecting gray and white matter alike. The changes consist of swelling and proliferation of endothelial cells of small vessels and a microglial reaction, with the formation of so-called typhus nodules.
Q fever, unlike the other rickettsioses, is not associated with an exanthem. In the few cases with which we are familiar, the main symptoms were those of a low-grade meningitis. Rare instances of encephalitis, cerebellitis, and myelitis are also reported, possibly as postinfectious complications. There is usually a tracheobronchitis or atypical pneumonia (one in which no organism can be cultured from the sputum) and a severe prodromal headache. In these respects, the pulmonary and neurologic illnesses resemble that of the other main cause of “atypical pneumonia,” M. pneumoniae. The Q fever agent (Coxiella) should be suspected if there are concomitant respiratory and meningoencephalitic illnesses and there has been exposure to parturient animals, to livestock (including abattoir workers, who are also exposed to Brucella and anthrax), or to wild deer or rabbits. The diagnosis can be made by the finding of a severalfold increase in specific immunofixation antibodies. Patients who survive the illness usually recover completely; a few are left with residual neurologic signs.
This consists of the administration of doxycycline or chloramphenicol, which are highly effective in all rickettsial diseases. If these drugs are given early, coincident with the appearance of the rash, symptoms abate dramatically and little further therapy is required. Cases recognized late in the course of the disease require considerable supportive care, including the administration of corticosteroids, maintenance of blood volume to overcome the effects of the septic-toxic reaction, and hypoproteinemia.
This disease is caused by Toxoplasma gondii, a tiny (2to 5-μm), obligate, intracellular parasite that is readily recognized in Wrightor Giemsa-stained preparations. It has assumed greater importance in recent decades because of the frequency with which it involves the brain in patients with HIV. In fact, the manifestations of toxoplasmosis are dependent on the response of the host immune system to the infection. Infection in humans is either congenital or acquired postnatally. Congenital infection is the result of parasitemia in the mother who happens to be pregnant at the time of her initial (asymptomatic) Toxoplasma infection. (Treated mothers can be assured, therefore, that there is little carryover risk of producing a second infected infant.) Several modes of transmission of the late-acquired form have been described—eating raw beef, handling uncooked mutton (in Western Europe), and, most often, contact with cat feces, the cat being the natural host of Toxoplasma. Most infections in HIV patients occur in the absence of an obvious source.