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Infectious Disease and Microbiology – Rabies
Rabies is a fatal viral infection caused by a bullet-shaped, single-stranded RNA virus belonging to the family Rhabdoviridae. The disease primarily affects the central nervous system and is almost universally fatal once clinical symptoms develop.
Rabies remains a major global public health problem. Approximately 15 million people receive postexposure prophylaxis annually worldwide. According to the World Health Organization, many cases are underreported, and annual deaths may exceed 55,000. The disease is more common in developing countries and occurs worldwide except in Antarctica and a few isolated island nations. In developing nations, dog bites are the most common mode of transmission, whereas in developed countries transmission more commonly occurs through raccoons, bats, foxes, and skunks.
Individuals at increased risk include laboratory workers involved in rabies research or vaccine production, veterinarians, wildlife officers, and people frequently exposed to wild animals. Exposure in caves may result from inhalation of aerosolized bat excreta. There is no known genetic predisposition.
The most effective preventive measure is mass vaccination of animals, especially dogs. Individuals with occupational or travel-related risk should receive preexposure vaccination. Preexposure prophylaxis consists of rabies vaccine administered intramuscularly on days 0, 7, and 21 or 28. Antibody titers should be periodically checked in high-risk individuals such as laboratory workers and wildlife officers.
The rabies virus enters the body through broken skin or mucous membranes, most commonly after an animal bite. The incubation period usually ranges from 20–90 days but may vary considerably. After entry, the virus travels centripetally through peripheral nerves by axonal transport to the central nervous system, where viral replication occurs with formation of characteristic Negri bodies. The virus then spreads centrifugally to tissues including the salivary and lacrimal glands.
Human infection usually results from bites of rabid animals, especially dogs. Because the virus is present in high concentrations in saliva, scratches or licks on broken skin may also transmit infection.
History is crucial for diagnosis. Multiple bites, bites involving the face, and deep penetrating injuries carry greater risk than superficial bites through clothing or bites to extremities. Early symptoms include paresthesias or pain at the bite site, fever, malaise, sore throat, nausea, and vomiting. This prodromal phase generally lasts 2–10 days.
Following the prodrome, encephalitis develops. Patients may exhibit fever, personality changes, agitation, hyperactivity, hallucinations, biting behavior, and autonomic instability. Characteristic findings of furious rabies include hydrophobia, in which attempts to drink or even the sight of water provoke painful pharyngeal spasms, and aerophobia, in which airflow or sensory stimuli trigger spasms. Seizures may occur, sometimes precipitated by tactile stimuli. Periods of agitation alternate with intervals of lucidity. Rapid progression to coma commonly follows. Paralysis may develop later in the disease.
Paralytic rabies presents differently and may resemble Guillain-Barré syndrome, with progressive weakness and paralysis.
Laboratory diagnosis is difficult and often secondary to clinical suspicion and exposure history. Direct fluorescent antibody testing of a skin biopsy taken from the nape of the neck remains the standard diagnostic method. RT-PCR testing of saliva, cerebrospinal fluid, or tissue specimens may also be used. Cerebrospinal fluid findings are nonspecific and may show pleocytosis. MRI may demonstrate increased T2 signal intensity in the hippocampi, hypothalamus, or brainstem, although imaging findings are not specific.
Pathologic examination reveals Negri bodies, especially in hippocampal pyramidal cells. Paralytic rabies may also show segmental demyelination resembling Guillain-Barré syndrome.
The differential diagnosis includes tetanus, viral encephalitis, acute disseminated encephalomyelitis, poliomyelitis, Guillain-Barré syndrome, and acute demyelinating polyneuropathy.
Management after exposure is critical because established rabies is almost universally fatal. Immediate wound cleansing with soap and water and irrigation with iodine-containing solutions can reduce transmission risk by approximately 90%.
For previously unvaccinated individuals, postexposure prophylaxis includes human rabies immunoglobulin at 20 units/kg administered once on day 0. As much of the dose as possible should be infiltrated around the wound, with the remainder injected intramuscularly at a site distant from vaccine administration. Rabies vaccine is administered intramuscularly in the deltoid region on days 0, 3, 7, 14, and 28.
Previously vaccinated individuals do not require rabies immunoglobulin and instead receive booster vaccine doses on days 0 and 3.
Immunocompromised patients may have inadequate vaccine responses and should undergo antibody testing 2–4 weeks after vaccination.
Hospital admission is recommended for patients with deep or multiple wounds, altered behavior, or neurologic symptoms. Supportive care, including intravenous fluids and careful nursing management, is essential in symptomatic rabies. Environmental stimuli should be minimized to reduce provocation of spasms and seizures.
Patients should be advised to observe the biting dog or animal for 10 days if possible. If the animal dies, disappears, or develops abnormal behavior during this period, health authorities should be notified immediately.
The prognosis of clinical rabies is extremely poor, with nearly 100% mortality in unvaccinated individuals once symptoms develop. In contrast, individuals who receive prompt postexposure prophylaxis after exposure generally have an excellent prognosis.
Complications include encephalomyelitis, intractable seizures, Guillain-Barré syndrome, myocarditis, arrhythmias, respiratory failure, vascular collapse, and death.
Rabies is a fatal viral infection caused by a bullet-shaped, single-stranded RNA virus belonging to the family Rhabdoviridae. The disease primarily affects the central nervous system and is almost universally fatal once clinical symptoms develop.
Rabies remains a major global public health problem. Approximately 15 million people receive postexposure prophylaxis annually worldwide. According to the World Health Organization, many cases are underreported, and annual deaths may exceed 55,000. The disease is more common in developing countries and occurs worldwide except in Antarctica and a few isolated island nations. In developing nations, dog bites are the most common mode of transmission, whereas in developed countries transmission more commonly occurs through raccoons, bats, foxes, and skunks.
Individuals at increased risk include laboratory workers involved in rabies research or vaccine production, veterinarians, wildlife officers, and people frequently exposed to wild animals. Exposure in caves may result from inhalation of aerosolized bat excreta. There is no known genetic predisposition.
The most effective preventive measure is mass vaccination of animals, especially dogs. Individuals with occupational or travel-related risk should receive preexposure vaccination. Preexposure prophylaxis consists of rabies vaccine administered intramuscularly on days 0, 7, and 21 or 28. Antibody titers should be periodically checked in high-risk individuals such as laboratory workers and wildlife officers.
The rabies virus enters the body through broken skin or mucous membranes, most commonly after an animal bite. The incubation period usually ranges from 20–90 days but may vary considerably. After entry, the virus travels centripetally through peripheral nerves by axonal transport to the central nervous system, where viral replication occurs with formation of characteristic Negri bodies. The virus then spreads centrifugally to tissues including the salivary and lacrimal glands.
Human infection usually results from bites of rabid animals, especially dogs. Because the virus is present in high concentrations in saliva, scratches or licks on broken skin may also transmit infection.
History is crucial for diagnosis. Multiple bites, bites involving the face, and deep penetrating injuries carry greater risk than superficial bites through clothing or bites to extremities. Early symptoms include paresthesias or pain at the bite site, fever, malaise, sore throat, nausea, and vomiting. This prodromal phase generally lasts 2–10 days.
Following the prodrome, encephalitis develops. Patients may exhibit fever, personality changes, agitation, hyperactivity, hallucinations, biting behavior, and autonomic instability. Characteristic findings of furious rabies include hydrophobia, in which attempts to drink or even the sight of water provoke painful pharyngeal spasms, and aerophobia, in which airflow or sensory stimuli trigger spasms. Seizures may occur, sometimes precipitated by tactile stimuli. Periods of agitation alternate with intervals of lucidity. Rapid progression to coma commonly follows. Paralysis may develop later in the disease.
Paralytic rabies presents differently and may resemble Guillain-Barré syndrome, with progressive weakness and paralysis.
Laboratory diagnosis is difficult and often secondary to clinical suspicion and exposure history. Direct fluorescent antibody testing of a skin biopsy taken from the nape of the neck remains the standard diagnostic method. RT-PCR testing of saliva, cerebrospinal fluid, or tissue specimens may also be used. Cerebrospinal fluid findings are nonspecific and may show pleocytosis. MRI may demonstrate increased T2 signal intensity in the hippocampi, hypothalamus, or brainstem, although imaging findings are not specific.
Pathologic examination reveals Negri bodies, especially in hippocampal pyramidal cells. Paralytic rabies may also show segmental demyelination resembling Guillain-Barré syndrome.
The differential diagnosis includes tetanus, viral encephalitis, acute disseminated encephalomyelitis, poliomyelitis, Guillain-Barré syndrome, and acute demyelinating polyneuropathy.
Management after exposure is critical because established rabies is almost universally fatal. Immediate wound cleansing with soap and water and irrigation with iodine-containing solutions can reduce transmission risk by approximately 90%.
For previously unvaccinated individuals, postexposure prophylaxis includes human rabies immunoglobulin at 20 units/kg administered once on day 0. As much of the dose as possible should be infiltrated around the wound, with the remainder injected intramuscularly at a site distant from vaccine administration. Rabies vaccine is administered intramuscularly in the deltoid region on days 0, 3, 7, 14, and 28.
Previously vaccinated individuals do not require rabies immunoglobulin and instead receive booster vaccine doses on days 0 and 3.
Immunocompromised patients may have inadequate vaccine responses and should undergo antibody testing 2–4 weeks after vaccination.
Hospital admission is recommended for patients with deep or multiple wounds, altered behavior, or neurologic symptoms. Supportive care, including intravenous fluids and careful nursing management, is essential in symptomatic rabies. Environmental stimuli should be minimized to reduce provocation of spasms and seizures.
Patients should be advised to observe the biting dog or animal for 10 days if possible. If the animal dies, disappears, or develops abnormal behavior during this period, health authorities should be notified immediately.
The prognosis of clinical rabies is extremely poor, with nearly 100% mortality in unvaccinated individuals once symptoms develop. In contrast, individuals who receive prompt postexposure prophylaxis after exposure generally have an excellent prognosis.
Complications include encephalomyelitis, intractable seizures, Guillain-Barré syndrome, myocarditis, arrhythmias, respiratory failure, vascular collapse, and death.
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