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Rabies
(redirected from fixed rabies virus)

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rabies (rā`bēz, ră`–) or hydrophobia (hī'drəfō`bēə), acute viral infection of the central nervous system in dogs, foxes, raccoons, skunks, bats, and other animals, and in humans. The virus is transmitted from an animal to a person, or from one animal to another, via infected saliva, most often by biting but also by the contact of torn skin with infected saliva. The virus travels from the bite or contact location to the spinal cord and brain. In humans the incubation period ranges from 10 days to a year or more. Symptoms are fever, uncontrollable excitement, and pronounced spasms of the throat muscles. Salivation is extreme, and despite great thirst the victim cannot swallow water; hence the misnomer hydrophobia (fear of water). Once symptoms develop, death (caused by convulsions, exhaustion, or paralysis) is usually inevitable.

Following a bite from a rabid or possibly rabid animal, preventive treatment involves administration of immune globulin for passive immunization followed by vaccinations over several weeks for active immunization. The only treatment after symptoms appear is rest and sedation. Dogs have been immunized from the time Louis Pasteur Pasteur, Louis , 1822–95, French chemist. He taught at Dijon, Strasbourg, and Lille, and in Paris at the École normale supérieure and the Sorbonne (1867–89).
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 demonstrated a successful vaccine in 1885. Since then, human rabies has become rare in the United States and other industrialized countries due to comprehensive vaccination programs for domestic animals. Mass vaccination of susceptible animals in the wild with vaccine-laced bait has been used in an effort to stem an increase of rabies cases in the United States and Canada that began in the late 1980s. A similar wild animal vaccination program has been used with some success in parts of Europe.


rabies

Acute, usually fatal infectious disease of warm-blooded animals that attacks the central nervous system. It is spread by contact with an infected animal's saliva, usually from a bite. The rhabdovirus that causes it spreads along nerve tissue from the wound to the brain. Symptoms usually appear four to six weeks later, often beginning with irritability and aggressiveness. Wild animals lose their fear of humans and are easily provoked to bite, as are pets. Depression and paralysis soon follow. Death usually comes three to five days after symptoms begin. In humans, death can result from a seizure in the early phase even before symptoms of central nervous system depression develop. One name for rabies, hydrophobia (“fear of water”), comes from painful throat contraction on trying to swallow. If not treated in time (within a day or two) with a serum containing antibodies and then a series of vaccinations, rabies in humans is almost always fatal. Immediate cleansing of animal bites with soap and water can remove much of the virus.


rabies
Pathol an acute infectious viral disease of the nervous system transmitted by the saliva of infected animals, esp dogs. It is characterized by excessive salivation, aversion to water, convulsions, and paralysis

rabies [′rā·bēz]
(veterinary medicine)
An acute, encephalitic viral infection transmitted to humans by the bite of a rabid animal. Also known as hydrophobia.

Rabies

An acute, encephalitic viral infection. Human beings are infected from the bite of a rabid animal, usually a dog. Canine rabies can infect all warm-blooded animals, and death usually results. See Animal virus

The virus is believed to move from the saliva-infected wound through sensory nerves to the central nervous system, multiply there with destruction of brain cells, and thus produce encephalitis, with severe excitement, throat spasm upon swallowing (hence hydrophobia, or fear of water), convulsions, and death—with paralysis sometimes intervening before death.

All bites should immediately be cleaned thoroughly with soap and water, and a tetanus shot should be considered. The decision to administer rabies antibody, rabies vaccine, or both depends on four factors: the nature of the biting animal; the existence of rabies in the area; the manner of attack (provoked or unprovoked) and the severity of the bite and contamination by saliva of the animal; and recommendations by local public health officials.

Diagnosis in the human is made by observation of Negri bodies (cytoplasmic inclusion bodies) in brains of animals inoculated with the person's saliva, or in the person's brain after death. A dog which has bitten a person is isolated and watched for 10 days for signs of rabies; if none occur, rabies was absent. If signs do appear, the animal is killed and the brain examined for Negri bodies, or for rabies antigen by testing with fluorescent antibodies. See Viral inclusion bodies

Individuals at high risk, such as veterinarians, must receive preventive immunization. If exposure is believed to have been dangerous, postexposure prophylaxis should be undertaken. If antibody or immunogenic vaccine is administered promptly, the virus can be prevented from invading the central nervous system. An inactivated rabies virus vaccine is available in the United States. It is made from virus grown in human or monkey cell cultures and is free from brain proteins that were present in earlier Pasteur-type vaccines. This material is sufficiently antigenic that only four to six doses of virus need be given to obtain a substantial antibody response. See Vaccination


Rabies 

hydrophobia, an acute infectious disease that is caused by a neurotropic virus and that affects the central nervous system. Animal rabies has been known since ancient times; it is mentioned by Democritus, Aristotle, and others. Louis Pasteur showed through his investigations that the causative agent of rabies is concentrated in the central nervous system. In 1887 the Rumanian scientist V. Babes, and in 1903 the Italian physician A. Negri discovered in the brains of dead victims of rabies special inclusion bodies measuring 1–27 microns. The nature of these inclusions—Babeş-Negri bodies—has not been fully clarified, but their detection has absolute diagnostic significance. When a person is bitten by a dog or other animal suspected of carrying rabies, the animal must be isolated for further observation. If the animal does not die within ten days, rabies is usually precluded. If it does die within this period, discovery of Babeş-Negri bodies in its brain confirms a diagnosis of rabies.

Although the proportion of rabies among other infectious diseases of animals is not great, rabies infections are found all over the world. Mammals, mainly members of the canine family, are affected by rabies under natural conditions. Among domestic animals, the most numerous of those infected are cattle (up to 55 percent), dogs (27 percent), sheep and goats (11 percent), pigs (5 percent), and horses (2 percent). In the USSR the majority of cases occur in the early months of the year (January to May). Wild carnivores play the most important role in spreading rabies among agricultural animals. Infection of animals with rabies occurs only as a result of the entry of the saliva of the infected animal through breaks in the skin or mucous membrane, usually by a bite. The latent period of rabies in animals lasts one to two months (in up to 90 percent of cases), more rarely up to six months. Its duration depends mainly on age (the younger the animal, the shorter the latent period) and the site, size, and depth of the bite (with deep, numerous, extensive wounds and bites in the head area the incubation period is shortened).

The five clinical forms of rabies that are commonly distinguished in animals are (1) abortive, in which recovery occurs after initial typical symptoms; (2) relapsing, in which the animal dies after temporary improvement; (3) atypical, which is chronic and accompanied by emaciation; (4) furious (most typical), in which aggressiveness is manifested by the animal and there is perversion of the appetite (ingestion of inedible objects) and paralysis of the pharynx; and (5) quiet, which is characterized by a less expressive period of excitement. Rabies proceeds most typically in dogs. In cats the illness usually proceeds in its furious form; in cattle, sheep, and goats, in its furious and quiet forms; in pigs, in sharply expressed violent form.

Treatment of animals infected with rabies is prohibited; they are to be immediately destroyed. Prophylaxis is directed toward immunizing animals, destroying stray dogs and cats, and shooting and trapping animals that make up reservoirs of rabies.

Infection of man with rabies occurs by a bite or lick on the skin or mucous membranes by a rabid animal whose saliva contains the causative agent of rabies. Especially dangerous for man are bites of a rabid animal on the head, face, or neck; in such cases the incubation period of the disease is shortened and the illness proceeds with special virulence. Having penetrated the human body through a wound inflicted by the bite of a rabid animal (or a licked scratch), the virus spreads along nerve trunks toward the central nervous system, affecting the nerve centers and the cerebral cortex.

The following are distinguished in the clinical history in man: (1) the stage of depression of the central nervous system, lasting from several hours to 48 hours; (2) the stage of excitement, hallucinations, and motor agitation (from four to seven days); (3) the stage of paralysis (from several hours up to two to three days), ending in the death of the patient. The latent (incubation) period calculated from the moment of the bite or lick by a rabid animal to the first manifestations of the disease lasts from 15 to 55 days. At first a dull aching pain begins at the site of the bite, continuing even when the wound is closed. The patient’s mood is depressed, his sleep is restless. Various hallucinations appear—visual, auditory, and olfactory—usually menacing in character. After a comparatively short period of depression, motor excitement and noisy breathing develop, and the patient is excited and alarmed and complains of lack of air. Then muscular convulsions develop, mostly of the musculature of the pharynx; at the mere sight of a glass of water or at the sound of running water the patient develops reflex spasms of the pharyngeal musculature, making ingestion of food and drink impossible. All the senses, including vision and hearing, are significantly sharpened; any stimuli (a light breeze blowing, the touching of the patient’s body’, the effects of bright light or loud sounds) lead to the development of muscle convulsions and spasms of the pharyngeal musculature. Beginning with the second or third day of the illness, speech becomes incoherent, hallucinations are intensified, the patient thrashes around in bed, tries to run away, and so on. Convulsive attacks become more frequent as the disease progresses. Abundant salivation is noted. Soon paralysis of the upper and lower extremities occurs; the patient dies of paralysis of the heart. The temperature remains normal or is slightly elevated (37.3°–37.4° C) for the duration of the disease.

Treatment consists of symptomatic measures that prevent convulsions and act as analgesics and somnifacients. Feeding is done artificially. Prophylaxis consists of injection of a person who has been bitten by a rabid animal with antirabies vaccine; vaccination must be started as early as possible and without fail before the 14th day from the moment of infection, since it produces nonsusceptibility to rabies in the patient no earlier than two to three weeks from the beginning of its injection. Given in good time, the injections are a reliable means of preventing the development of rabies.

REFERENCES

Rudnev, G. P. Zoonozy, 2nd ed. Moscow, 1959.
Bunin, K. V. Diagnostika infektsionnykh boleznei. Moscow, 1965.
Nazarov, V. P. Beshenstvo zhivotnykh. Moscow, 1961.

K. V. BUNIN



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