Morbidity and Mortality Weekly Report - Human rabies—Indiana and California, 2006
Rabies is a viral infection that causes acute, progressive encephalitis and is considered to be universally fatal. However, during 2004, an unvaccinated Wisconsin patient received a new medical treatment and became the first documented survivor of rabies* who had not received preexposure vaccination or postexposure prophylaxis (PEP), suggesting the possibility of successful future interventions (1). This report describes two recent patients with rabies who were treated using therapy similar to that used for the Wisconsin patient; both treatments were unsuccessful. The report also describes the concomitant epidemiologic investigations by the Indiana State Department of Health (ISDH), California Department of Health Services (CDHS), and CDC, and the local public health responses in Marshall County, Indiana, and San Joaquin and Alameda counties in California. The findings in this report underscore the continuing need for enhanced clinical awareness of possible rabies exposure to ensure prompt PEP and timely diagnosis of rabies, especially if treatment is attempted.
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Indiana
Case report. On September 30, 2006, a girl aged 10 years had pain in her right arm, and her parents noticed a skin eruption on her trunk and extremities. On October 3, she began vomiting and had increased arm pain and occasional arm numbness. During her initial visit to her family’s primary health-care provider on October 4, radiographs of her arm and clavicle were normal. Three to five days after her initial symptoms began, the patient’s speech became difficult to understand, and she had a decreased appetite, sore throat and neck pain, and temperature of 101[degrees]F. She became irritable and agitated. A rapid Group A streptococcal antigen test and slide heterophil antibody assay were negative on October 6. The patient was hospitalized on October 7 at a community hospital, where she was found to have difficulty swallowing secretions. Her tongue had a whitish coating and was protruding from her mouth. Her complete blood count and electrolytes were normal. She was prescribed methylprednisolone for possible glossitis and fluconazole for mucosal candidiasis.
On October 8, neurologic involvement became more evident, and the attending physician arranged for transfer to a university-affiliated tertiary care pediatric hospital. On arrival at the pediatric hospital, the patient was irritable, with intermittent moments of alertness, altered mental status, and lethargy. She had slurred speech and difficulty swallowing secretions and complained of a drowning sensation. Because of difficulty breathing, low oxygen saturation, and excess secretions, the patient was intubated and placed on a mechanical ventilator. A lumbar puncture was performed, indicating a white blood cell (WBC) count of 26 cells/[mm.sup.3] (normal: 0-7 cells/[mm.sup.3]), a red blood cell (RBC) count of 1 cell/[mm.sup.3] (normal: 0 cells/[mm.sup.3]), a protein level of 28 mg/dL (normal: 15-45 mg/dL), and a glucose level of 89 mg/dL (normal: 40-70 mg/dL). Vancomycin, cefotaxime, and acyclovir were administered for the presumptive diagnosis of meningoencephalitis. On the second day of hospitalization, the patient experienced episodes of lethargy, somnolence, generalized skin flushing (associated with vancomycin administration), and hypersalivation.
Initial interviews of family members indicated that the patient frequently was exposed to healthy-appearing household cats and dogs but to no other animals. On the third day of hospitalization, the patient’s primary-care physician told staff members at the pediatric hospital that a babysitter suggested the patient might have sustained an animal scratch or bite during June 2006. Family members did not know what type of animal might have scratched her. However, in spite of her endotracheal intubation, the patient was able to indicate that a bat had scratched or bit her. On the same day, serum, saliva, cerebrospinal fluid, and a skin biopsy from the nape of the neck (nuchal sample) were sent to CDC for rabies virologic testing, and a serum rabies-virus-specific antibody test was positive. Reverse transcription-polymerase chain reaction (RT-PCR) performed on saliva and skin samples also were positive for rabies virus amplicons, and direct fluorescent antibody (DFA) staining of the skin biopsy was positive for detection of rabies virus antigens. The patient had not received a rabies vaccine or rabies PEP.
After rabies was confirmed, the Wisconsin rabies treatment protocol (1) was initiated, including antiexcitatory and antiviral therapy with phenobarbital, midazolam, ketamine, and amantadine with aggressive supportive care. On the sixth day of hospitalization, ribavirin was administered intravenously, under a Food and Drug Administration (FDA) emergency use investigational new drug protocol. ([dagger]) Coenzyme Q10, L-arginine, tetrahydrobiopterin, and vitamin C also were administered in an attempt to replenish neurotransmitter substrates. During hospitalization, the patient experienced multiple complications, including increased intracranial pressure, bouts of diabetes insipidus, syndrome of inappropriate secretion of antidiuretic hormone (SIADH), reversible pancreatitis secondary to ribavirin, intracranial venous sinus thrombosis, and cerebral and cerebellar herniation. In spite of a reduction in sedation drugs, the patient never regained consciousness. Because of a deteriorating clinical condition and poor prognosis, life support was withdrawn. The patient died on November 2, 2006, on the twenty-sixth day of hospitalization. Rabies virus antigen was detected in brain tissue collected postmortem.
