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Neuroimaging and Clinical Manifestations of Bilateral Temporal Encephalopathy Secondary to Murine Typhus Infection

2005; Lippincott Williams & Wilkins; Volume: 84; Issue: 4 Linguagem: Inglês

10.1097/01.phm.0000157106.73355.90

1537-7385

Henry L. Lew, Barton Lane, Harriet K. Zeiner,

Infectious Encephalopathies and Encephalitis

A 49-yr-old white male who lived on a tropical island experienced a high fever (39.4°C) approximately 1 wk after noticing a flea bite to his leg. He was brought to a local emergency room where a skin rash and bloody diarrhea were clinically prominent. Laboratory testing revealed anemia, thrombocytopenia, and hyponatremia. During the ensuing day, he developed acute renal failure, generalized seizures, ultimately lapsed into a coma, and was intubated and transferred to the hospital intensive care unit. Initial magnetic resonance imaging of the brain showed extensive cortical swelling of bilateral temporal and parietal lobes (Fig. 1, top), with extension to medial temporal cortices (Fig. 1, bottom). Acyclovir was initiated under the assumption of herpes encephalitis. In the second week of admission, serologic testing showed positive antimurine typhus immunoglobulins G and M. Thus, doxycycline treatment was initiated and the patient’s medical status gradually stabilized. After 3 wks of coma, the patient eventually awoke and was transferred to an inpatient rehabilitation unit in the continental United States.FIGURE 1: T2 axial magnetic resonance images at the level of the midbrain and lateral ventricles. Top, extensive T2 signal abnormality consistent with edema of lateral temporal cortex and medial (hippocampal) cortex. Bottom, insular and parietal lobe cortices demonstrate T2 hyperintensity bilaterally. This pattern of involvement is most consistent with diffuse encephalitis, either viral or rickettsial.On initial evaluation at the time of transfer, the patient was confused and agitated (Rancho Los Amigos Level 4). Throughout the entire hospitalization course, he was incapable of interactive communication, wandered constantly around his room, and had no predictable sleep cycle. He did not respond to various attempts at oral feeding and repeatedly pulled on his gastric feeding tube. Due to a lack of ability to learn new information, he was transferred to a long-term subacute care facility. A follow-up computed tomographic scan, 8 mos after onset of symptoms, showed extensive bitemporal encephalomala-cia with atrophic changes in the limbic system. Murine typhus, caused by Rickettsia typhi, is an arthropod-borne infection, with fleas, rats, and possums as reservoirs.1 Rickettsial infection typically occurs in temperate and subtropical costal areas and can induce systemic endothelial vasculitis affecting multiple organs.1,2 After a 1- to 2-wk incubation period, nonspecific clinical symptoms develop, including fever, chills, headache, diffuse pain, and a maculopapular rash. Laboratory findings often include leukopenia, elevated hepatic transaminases, hypocalcemia, hyponatremia, and hypoalbuminemia. Serologic tests may detect specific Rickettsia typhi antibodies, which typically become positive during the second week of infection.1 The treatment of choice is tetracycline, although quinolones are also an effective alternative.1 However, even with treatment, neurologic complications can occur in 15–45% of infected patients.1,3,4 Due to the severity and location of the infective lesions, this patient’s memory and learning remained severely impaired. The magnetic resonance imaging/com-puted tomographic findings assisted the rehabilitation team and family members in understanding the patient’s clinical features and prognosis.