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Emergency And Acute Medicine – Rabies
Rabies is a viral infection of the central nervous system affecting mammals and has the highest case fatality rate of any known infectious disease once clinical symptoms develop. It is caused by a negative-stranded RNA virus in the genus Lyssavirus of the family Rhabdoviridae. Worldwide, rabies causes approximately 30,000–70,000 deaths annually, most commonly in Southeast Asia, the Philippines, Africa, South America, and the Indian subcontinent. In the United States, 2–3 human cases occur per year, most related to foreign travel or bat exposure. In the U.S., bats are the most common reservoir; globally, dogs are the primary reservoir. Other reservoirs include raccoons, skunks, foxes, woodchucks, and groundhogs. Small rodents such as squirrels and rats have not been documented to transmit rabies to humans.
Transmission occurs through contact with infected saliva, most commonly via animal bite. Nonbite transmission may occur through saliva exposure to mucous membranes or open wounds. Bat exposures may occur without a visible bite. Organ transplantation represents the only well-documented person-to-person transmission. Casual contact such as petting an animal or contact with blood, urine, or feces is not considered a transmission risk.
After inoculation, the virus replicates locally in muscle tissue and binds to nicotinic acetylcholine receptors, then enters peripheral nerves and travels via retrograde axonal transport toward the CNS at approximately 1–4 inches per day. Once in the CNS, rapid viral replication causes encephalitis. The virus then spreads centrifugally to peripheral nerves and salivary glands.
The disease progresses through five stages: incubation, prodrome, encephalitis, coma, and death (rarely recovery). The incubation period averages 1–3 months but may range from 10 days to 1 year, depending on viral load and proximity of the exposure to the CNS. The prodrome lasts 1–7 days and includes nonspecific symptoms such as fever, headache, malaise, myalgias, nausea, and sore throat. Paresthesias or fasciculations at the bite site are highly suggestive.
The encephalitic (classic) form accounts for approximately 80% of cases. Patients develop anxiety, agitation, hallucinations, confusion, seizures, muscle spasms, and autonomic instability. Hydrophobia—painful pharyngeal spasms triggered by attempts to swallow—and aerophobia—pharyngeal spasms induced by airflow—are pathognomonic. Brainstem involvement may cause diplopia and facial paralysis. Paralytic rabies (about 20%) presents with ascending paralysis resembling Guillain–Barré syndrome. Atypical forms, often associated with bat exposures, may present with neuropathic pain or movement disorders.
Once neurologic symptoms appear, rabies is almost universally fatal. Most patients die within two weeks of symptom onset due to respiratory failure or cardiovascular collapse. Rare survivors typically have significant neurologic deficits.
Diagnosis during life relies on detection of rabies RNA by RT-PCR in saliva, virus isolation, or detection of rabies antibodies in serum (if unvaccinated) or cerebrospinal fluid (CSF). CSF may show mild pleocytosis and elevated protein. Neuroimaging is often normal but may demonstrate cerebral edema. A high index of suspicion is essential, especially in patients with unexplained encephalitis and a history of animal exposure or travel to endemic areas.
Emergency management begins with thorough wound cleansing using soap and water, which significantly reduces viral load. Tetanus immunization should be updated as indicated. Determination of need for postexposure prophylaxis (PEP) should involve consultation with local public health authorities. For domestic animals, a 10-day observation period may be appropriate. For wild animals, the animal should be tested if available. If the animal cannot be tested or exposure is high risk, PEP should be initiated.
PEP consists of both passive and active immunization. Human rabies immune globulin (HRIG) is administered at 20 IU/kg, with as much as possible infiltrated around the wound and the remainder given intramuscularly at a site distant from vaccine administration. Rabies vaccine (1 mL IM in the deltoid in adults or anterolateral thigh in infants) is given on days 0, 3, 7, and 14, with an additional dose on day 28 for immunocompromised patients. Individuals previously vaccinated require only vaccine doses on days 0 and 3 and do not require HRIG. HRIG should not be administered more than 7 days after the first vaccine dose.
Pre-exposure prophylaxis consists of vaccination on days 0, 7, and either 21 or 28 and is recommended for veterinarians, animal handlers, laboratory workers, and travelers to endemic regions. Rabies vaccination and HRIG are considered safe in pregnancy.
Patients with clinical rabies require hospital admission and supportive care. Stable patients receiving PEP may be discharged with arrangements for completion of the vaccine series. Coordination with public health authorities is essential.
The key principle is that postexposure prophylaxis is the only proven effective intervention and must be administered promptly in all high-risk exposures. Once symptoms develop, rabies is almost universally fatal.
Rabies is a viral infection of the central nervous system affecting mammals and has the highest case fatality rate of any known infectious disease once clinical symptoms develop. It is caused by a negative-stranded RNA virus in the genus Lyssavirus of the family Rhabdoviridae. Worldwide, rabies causes approximately 30,000–70,000 deaths annually, most commonly in Southeast Asia, the Philippines, Africa, South America, and the Indian subcontinent. In the United States, 2–3 human cases occur per year, most related to foreign travel or bat exposure. In the U.S., bats are the most common reservoir; globally, dogs are the primary reservoir. Other reservoirs include raccoons, skunks, foxes, woodchucks, and groundhogs. Small rodents such as squirrels and rats have not been documented to transmit rabies to humans.
Transmission occurs through contact with infected saliva, most commonly via animal bite. Nonbite transmission may occur through saliva exposure to mucous membranes or open wounds. Bat exposures may occur without a visible bite. Organ transplantation represents the only well-documented person-to-person transmission. Casual contact such as petting an animal or contact with blood, urine, or feces is not considered a transmission risk.
After inoculation, the virus replicates locally in muscle tissue and binds to nicotinic acetylcholine receptors, then enters peripheral nerves and travels via retrograde axonal transport toward the CNS at approximately 1–4 inches per day. Once in the CNS, rapid viral replication causes encephalitis. The virus then spreads centrifugally to peripheral nerves and salivary glands.
The disease progresses through five stages: incubation, prodrome, encephalitis, coma, and death (rarely recovery). The incubation period averages 1–3 months but may range from 10 days to 1 year, depending on viral load and proximity of the exposure to the CNS. The prodrome lasts 1–7 days and includes nonspecific symptoms such as fever, headache, malaise, myalgias, nausea, and sore throat. Paresthesias or fasciculations at the bite site are highly suggestive.
The encephalitic (classic) form accounts for approximately 80% of cases. Patients develop anxiety, agitation, hallucinations, confusion, seizures, muscle spasms, and autonomic instability. Hydrophobia—painful pharyngeal spasms triggered by attempts to swallow—and aerophobia—pharyngeal spasms induced by airflow—are pathognomonic. Brainstem involvement may cause diplopia and facial paralysis. Paralytic rabies (about 20%) presents with ascending paralysis resembling Guillain–Barré syndrome. Atypical forms, often associated with bat exposures, may present with neuropathic pain or movement disorders.
Once neurologic symptoms appear, rabies is almost universally fatal. Most patients die within two weeks of symptom onset due to respiratory failure or cardiovascular collapse. Rare survivors typically have significant neurologic deficits.
Diagnosis during life relies on detection of rabies RNA by RT-PCR in saliva, virus isolation, or detection of rabies antibodies in serum (if unvaccinated) or cerebrospinal fluid (CSF). CSF may show mild pleocytosis and elevated protein. Neuroimaging is often normal but may demonstrate cerebral edema. A high index of suspicion is essential, especially in patients with unexplained encephalitis and a history of animal exposure or travel to endemic areas.
Emergency management begins with thorough wound cleansing using soap and water, which significantly reduces viral load. Tetanus immunization should be updated as indicated. Determination of need for postexposure prophylaxis (PEP) should involve consultation with local public health authorities. For domestic animals, a 10-day observation period may be appropriate. For wild animals, the animal should be tested if available. If the animal cannot be tested or exposure is high risk, PEP should be initiated.
PEP consists of both passive and active immunization. Human rabies immune globulin (HRIG) is administered at 20 IU/kg, with as much as possible infiltrated around the wound and the remainder given intramuscularly at a site distant from vaccine administration. Rabies vaccine (1 mL IM in the deltoid in adults or anterolateral thigh in infants) is given on days 0, 3, 7, and 14, with an additional dose on day 28 for immunocompromised patients. Individuals previously vaccinated require only vaccine doses on days 0 and 3 and do not require HRIG. HRIG should not be administered more than 7 days after the first vaccine dose.
Pre-exposure prophylaxis consists of vaccination on days 0, 7, and either 21 or 28 and is recommended for veterinarians, animal handlers, laboratory workers, and travelers to endemic regions. Rabies vaccination and HRIG are considered safe in pregnancy.
Patients with clinical rabies require hospital admission and supportive care. Stable patients receiving PEP may be discharged with arrangements for completion of the vaccine series. Coordination with public health authorities is essential.
The key principle is that postexposure prophylaxis is the only proven effective intervention and must be administered promptly in all high-risk exposures. Once symptoms develop, rabies is almost universally fatal.
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