Age: 55.0
Sex: M
Vaccine: DT, RAB
Symptoms: Histology abnormal, Hypoaesthesia facial, Hypotension, Intracranial pressure increased, Lactic acidosis
Clinical narrative: Initial report received 09 November 2009 from a literature citation which involves a case of misuse (i.e., inappropriate schedule of drug administration). On 24 November 2008, the Centers for Disease Control and Prevention was notified about suspected rabies in a 55-year-old male patient who had been bitten by a bat four to six weeks prior to symptoms onset. Family members reported that they saw a bat in the rafters of the front porch for several days before it flew into the house. The patient caught the bat and allowed it to crawl up his arm and neck and was bitten on the left ear. The patient did not report the incident to public health authorities or seek medical evaluation. The patient left the bat unrestrained in the house for two days, and when the bat appeared to be well after that period, he released it outside. On 26 November 2008, infection with rabies virus variant associated with silver-haired bats was confirmed and the patient subsequently died on 30 November 2008. The following report summarizes the patient's treatments and clinical course. A 55-year-old male patient developed pruritus on 19 November 2008 on his left ear that spread to his left face and arm. Two days later on 21 November 2008, he began experiencing mild chest pain and reported to the emergency department. Testing included an electrocardiogram and cardiac enzymes which were negative for acute myocardial infarction and the patient was discharged with instructions to return if symptoms worsened. On 22 November 2008, the patient returned to the emergency department with panic attacks and anxiety associated with swallowing water. At that time, the patient reported that he had been bitten by a bat on the left ear lobe four to six weeks earlier. He received corrective treatment with rabies post-exposure prophylaxis consisting of 15.4 mL of rabies immune globulin (manufacturer, lot number not reported) and 1 mL of rabies human diploid vaccine (manufacturer and lot number not reported), and a tetanus-diphtheria vaccine booster (manufacturer and lot number not reported), and was released. The patient reported to a second emergency department on 23 November 2009 due to new numbness of the left ear and face, continuing chest pain and difficulty swallowing water. The patient also reported a history of chronic neck and back pain that occasionally featured numbness. He also informed the physician about his prior bat exposure and the PEP treatment he received the previous day. The physician explained that the PEP treatment the patient received was appropriate, but explained that treatment might not be helpful if administered late in the course of rabies disease. The patient was released from the emergency department and advised to seek medical attention if his symptoms progressed. Later that same day, the patient returned to the emergency department complaining of dehydration and he became anxious when he tried to drink fluids. On 24 November 2008, the patient was transferred to a tertiary care facility. The differential diagnosis on admission included rabies and other causes of infectious meningitis and encephalitis. A lumbar puncture yielded cerebrospinal fluid (CSF) with glucose 78 mg/dL (normal 50-80 mg/dL), protein 39 mg dL (normal 15-45 mg/dL, six red blood cells/mm3 (normal 0), and one white blood cell/mm3 (normal 0-3 cells/mm3); differential showed lymphocytic predominance of 68%, 26% monocytes, and 6% neutrophils. Complete blood cell count, metabolic panel drug screen, and computerized tomography scan of the head were unremarkable. Serum CSF, nuchal skin biopsy and saliva were collected and submitted to CDC on 24 November 2008, where a rabies diagnosis was confirmed on 26 November 2008. Viral antigen and RNA were detected by CDC in the skin biopsy by direct fluorescent antibody testing and reverse transcription polymerase chain reaction (RT-PCR), respectively. Viral RNA was also detected in the patient's saliva by RT-PCR. Serum was positive for neutralizing antibodies against rabies by rapid fluorescent focus inhibition test (RFFIT), and CSF negative by RFFIT and indirect fluorescent antibody. Rabies viral RNA amplified by RT-PCR was typed as a variant common to silver haired bats (Lasionycteris noctivagans). On 25 November 2008, the patient began rabies treatment using protocol, which included coma induction and administration of amantadine. The following day, the patient became bradycardic and hypotensive and was administered atropine and dopamine. On 28 November 2008, dopamine was replaced with norepinephrine and persistent hypotension and bradycardia. Diuretics were administered because of signs of increased intracranial pressure. On 29 November 2008, hypotension worsened and the patient developed oliguric acute renal failure with lactic acidosis and was placed on dialysis. When signs of increased intracranial pressure herniation were detected on 30 November 2008, his family elected to withdraw life support, and the patient died shortly thereafter. The autopsy (report not provided) confirmed the suspected cerebellar tonsillar herniation and moderate bilateral uncal herniation. On histological examination, multiple neurons had eosinophilic cytoplasmic inclusion bodies, particularly in specimens from hippocampi, nucleus basalis, and Purkinje cells. Documents held by sender: None.