Rabies is one of the most extended diseases known to man, with instances going back 4000 years. A rabid animal bite was always fatal for most of human history. The rabies virus infects the central nervous system rapidly.
Viral encephalitis brought on by rabies kills up to 70000 individuals annually globally. Humans can contract viral encephalitis from infected animal saliva. In developed nations, there is widespread prophylaxis due to Pasteur’s rabies vaccine from 1885.
Epidemiology
Studies estimate that rabies causes 70,000 fatalities annually, with less developed nations being more severely affected. Only few human cases have been documented in the United States; however, this may be because post-exposure prophylaxis is often used, and preventative initiatives are in place.
Only 10% of rabies transmission cases in developed nations have included domesticated animals; most cases have involved wild species, including raccoons, skunks, bats, and foxes.
While rodents and members of the rabbit family are typically considered safe since they are not predicted to outlive an inoculating bite from a rabid animal, rabies has been caused by transmission from rats. Any mammal may carry rabies. Identifying the animal carriers in the region can assist decide who could benefit from prophylaxis since animal carriers differ by region.
Anatomy
Pathophysiology
After viral transmission, the rhabdovirus targets the central nervous system as it moves to the peripheral nervous system, causing encephalomyelitis. The first signs and symptoms in humans resemble any other generic viral infection, such as fever, malaise, or headache. These initially mild symptoms might develop into anxiety, agitation, and acute delirium later.
Within the first few days following a rabid bite, tingling at the bite site is one highly persistent symptom. Interestingly, the virus returns to the peripheral nervous system after first infecting highly innervated regions like the salivary glands in the central nervous system. Patients’ mouths froth because of hypersalivation, and they have acute pharyngeal muscular spasms at the sight, sound, or taste of water, characterized as hydrophobia.
The infection eventually leads to total nervous system failure, which results in immediate death. Animals typically pass away within ten days, although the incubation period can last from 2 weeks to 6 years. The viral load, the site of infection, and the severity of the lesion are determining variables for the timeframe of onset. The virus eventually impacts the central nervous system, frequently impacting the brainstem more significantly.
An inflammatory reaction produces toxic consequences, and the functional alterations are only partially understood. In the end, it is suspected that the virus affects neurotransmission, and both virus- and cell-dependent mechanisms may be involved in apoptosis. When clinical signs appear, rabies has always been fatal.
Etiology
Rabies is caused by the Rhabdoviridae virus family, which is composed of two bullet-shaped viruses. The viral envelope makes up the first component, considered more structural, while the ribonucleocapsid core is found in the second section, which is more functional.
The virus is most frequently transmitted through the bite of an infected mammal, both domestic and wild; however, saliva can also be transmitted through damaged skin or mucous membranes. Other infection methods include aerosolized viral inhalation, ingestion, transplacental transmission, and organ transplants.
Administer 20 IU/kg, infuse locally around the bite wound
If the location of the bite is uncertain or hard to access (such as fingers, knees, lips), inject the remaining vaccine volume intramuscularly into the anterolateral aspect of the thigh
If administering rabies immune globulin is challenging, or the bite location is unknown, administer it at a site far from the rabies vaccine administration site
Administer 20 IU/kg, infuse locally around the bite wound
If the location of the bite is uncertain or hard to access (such as fingers, knees, lips), inject the remaining vaccine volume intramuscularly into the anterolateral aspect of the thigh
If administering rabies immune globulin is challenging, or the bite location is unknown, administer it at a site far from the rabies vaccine administration site
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References
https://www.ncbi.nlm.nih.gov/books/NBK448076/
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Rabies is one of the most extended diseases known to man, with instances going back 4000 years. A rabid animal bite was always fatal for most of human history. The rabies virus infects the central nervous system rapidly.
Viral encephalitis brought on by rabies kills up to 70000 individuals annually globally. Humans can contract viral encephalitis from infected animal saliva. In developed nations, there is widespread prophylaxis due to Pasteur’s rabies vaccine from 1885.
Studies estimate that rabies causes 70,000 fatalities annually, with less developed nations being more severely affected. Only few human cases have been documented in the United States; however, this may be because post-exposure prophylaxis is often used, and preventative initiatives are in place.
Only 10% of rabies transmission cases in developed nations have included domesticated animals; most cases have involved wild species, including raccoons, skunks, bats, and foxes.
While rodents and members of the rabbit family are typically considered safe since they are not predicted to outlive an inoculating bite from a rabid animal, rabies has been caused by transmission from rats. Any mammal may carry rabies. Identifying the animal carriers in the region can assist decide who could benefit from prophylaxis since animal carriers differ by region.
After viral transmission, the rhabdovirus targets the central nervous system as it moves to the peripheral nervous system, causing encephalomyelitis. The first signs and symptoms in humans resemble any other generic viral infection, such as fever, malaise, or headache. These initially mild symptoms might develop into anxiety, agitation, and acute delirium later.
Within the first few days following a rabid bite, tingling at the bite site is one highly persistent symptom. Interestingly, the virus returns to the peripheral nervous system after first infecting highly innervated regions like the salivary glands in the central nervous system. Patients’ mouths froth because of hypersalivation, and they have acute pharyngeal muscular spasms at the sight, sound, or taste of water, characterized as hydrophobia.
The infection eventually leads to total nervous system failure, which results in immediate death. Animals typically pass away within ten days, although the incubation period can last from 2 weeks to 6 years. The viral load, the site of infection, and the severity of the lesion are determining variables for the timeframe of onset. The virus eventually impacts the central nervous system, frequently impacting the brainstem more significantly.
An inflammatory reaction produces toxic consequences, and the functional alterations are only partially understood. In the end, it is suspected that the virus affects neurotransmission, and both virus- and cell-dependent mechanisms may be involved in apoptosis. When clinical signs appear, rabies has always been fatal.
Rabies is caused by the Rhabdoviridae virus family, which is composed of two bullet-shaped viruses. The viral envelope makes up the first component, considered more structural, while the ribonucleocapsid core is found in the second section, which is more functional.
The virus is most frequently transmitted through the bite of an infected mammal, both domestic and wild; however, saliva can also be transmitted through damaged skin or mucous membranes. Other infection methods include aerosolized viral inhalation, ingestion, transplacental transmission, and organ transplants.
Administer 20 IU/kg, infuse locally around the bite wound
If the location of the bite is uncertain or hard to access (such as fingers, knees, lips), inject the remaining vaccine volume intramuscularly into the anterolateral aspect of the thigh
If administering rabies immune globulin is challenging, or the bite location is unknown, administer it at a site far from the rabies vaccine administration site
Administer 20 IU/kg, infuse locally around the bite wound
If the location of the bite is uncertain or hard to access (such as fingers, knees, lips), inject the remaining vaccine volume intramuscularly into the anterolateral aspect of the thigh
If administering rabies immune globulin is challenging, or the bite location is unknown, administer it at a site far from the rabies vaccine administration site
https://www.ncbi.nlm.nih.gov/books/NBK448076/
medtigo
Rabies
Updated :
December 6, 2022
Rabies is one of the most extended diseases known to man, with instances going back 4000 years. A rabid animal bite was always fatal for most of human history. The rabies virus infects the central nervous system rapidly.
Viral encephalitis brought on by rabies kills up to 70000 individuals annually globally. Humans can contract viral encephalitis from infected animal saliva. In developed nations, there is widespread prophylaxis due to Pasteur’s rabies vaccine from 1885.
Studies estimate that rabies causes 70,000 fatalities annually, with less developed nations being more severely affected. Only few human cases have been documented in the United States; however, this may be because post-exposure prophylaxis is often used, and preventative initiatives are in place.
Only 10% of rabies transmission cases in developed nations have included domesticated animals; most cases have involved wild species, including raccoons, skunks, bats, and foxes.
While rodents and members of the rabbit family are typically considered safe since they are not predicted to outlive an inoculating bite from a rabid animal, rabies has been caused by transmission from rats. Any mammal may carry rabies. Identifying the animal carriers in the region can assist decide who could benefit from prophylaxis since animal carriers differ by region.
After viral transmission, the rhabdovirus targets the central nervous system as it moves to the peripheral nervous system, causing encephalomyelitis. The first signs and symptoms in humans resemble any other generic viral infection, such as fever, malaise, or headache. These initially mild symptoms might develop into anxiety, agitation, and acute delirium later.
Within the first few days following a rabid bite, tingling at the bite site is one highly persistent symptom. Interestingly, the virus returns to the peripheral nervous system after first infecting highly innervated regions like the salivary glands in the central nervous system. Patients’ mouths froth because of hypersalivation, and they have acute pharyngeal muscular spasms at the sight, sound, or taste of water, characterized as hydrophobia.
The infection eventually leads to total nervous system failure, which results in immediate death. Animals typically pass away within ten days, although the incubation period can last from 2 weeks to 6 years. The viral load, the site of infection, and the severity of the lesion are determining variables for the timeframe of onset. The virus eventually impacts the central nervous system, frequently impacting the brainstem more significantly.
An inflammatory reaction produces toxic consequences, and the functional alterations are only partially understood. In the end, it is suspected that the virus affects neurotransmission, and both virus- and cell-dependent mechanisms may be involved in apoptosis. When clinical signs appear, rabies has always been fatal.
Rabies is caused by the Rhabdoviridae virus family, which is composed of two bullet-shaped viruses. The viral envelope makes up the first component, considered more structural, while the ribonucleocapsid core is found in the second section, which is more functional.
The virus is most frequently transmitted through the bite of an infected mammal, both domestic and wild; however, saliva can also be transmitted through damaged skin or mucous membranes. Other infection methods include aerosolized viral inhalation, ingestion, transplacental transmission, and organ transplants.
https://www.ncbi.nlm.nih.gov/books/NBK448076/
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