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Frequently Asked Questions - Rabies

• Does a person bitten by a rabid person need to be given anti-Rabies immunization?

• What is the difference between the observation period and the incubation period?

• Do we need to kill the dog immediately?

• Is rubbing the bite wounds with garlic and vinegar useful in the prevention of Rabies?

• Is “tandok” effective in the prevention of Rabies?

• Is Rabies preventable?

• Is Rabies curable?

• What is active and passive immunization?

• What is Rabies post-exposure treatment?

• If bitten by a stray animal, what should be properly done?

Question: Does a person bitten by a rabid person need to be given anti-Rabies immunization?

Answer:  Print

 Yes. A rabid person can transmit the Rabies virus to another person and need to be given anti-Rabies

immunization

Question: What is the difference between the observation period and the incubation period?

Answer:  Print

 The observation period is the period of time that the dog or cat is observed for signs of Rabies. The

observation period for dogs or cats is usually 14 days starting from the day the animal has bitten a person.

Studies have shown that a dog or cat, which is rabid at the time of the bite usually, dies within 14 days. If it

remains to be alive within that period, it means that it is not rabid and has not transmitted the virus to the

person.

Question: Do we need to kill the dog immediately?

Answer:  Print

No. If the dog is apparently healthy, it should not be killed immediately and should instead be kept on a leash

or caged for observation for 14 days.

Question: Is rubbing the bite wounds with garlic and vinegar useful in the prevention of Rabies?

Answer:  Print

No. Garlic and vinegar need not be applied on the bite wound for they will cause more injury (swelling,

irritation, further introducing dirt into the wound). By washing the wound immediately with soap and clean

water, the risk of Rabies infection will be greatly reduced.

Question: Is “tandok” effective in the prevention of Rabies?

Answer:  Print

No. “Tandok” is folk medicine done by placing a deer horn over the wound. This is believed to suck out the

Rabies virus. Records have shown that patients who received “tandok” treatment died either of Rabies or

 Tetanus, which only means that “tandok” is not effective.

Question: Is Rabies preventable?

Answer:  Print\

 Yes. By administering vaccine and immunoglobin at the right time to an animal bite victim, Rabies can be

prevented. One important measure that will be of big help in reducing the risk of getting Rabies is by

immediately washing the bite wound with soap and water.

Question: Is Rabies curable?

Answer:  Print

No. Once signs of brain involvement are manifested, the Rabies victim dies within 1-3 days.

Question: What is active and passive immunization?

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Answer:  Print

Active immunization or vaccination aims to induce the body to develop antibodies against Rabies whose

effect lasts for 1 to 3 years.Passive immunization is the process of giving an antibody to persons with

Category III exposure (head and neck bites, multiple/single deep bites, contamination of mucous membranes,

licks of the eyes, lips and mouth) in order to provide immediate protection against Rabies, which should be

administered within the first seven days of active immunization. The effect of the immunoglobulin is only

short term.Question: What is Rabies post-exposure treatment?

Answer:  Print

Post-exposure treatment is given to persons who are exposed to rabid animals. It consists of local wound

treatment, active immunization (vaccination) and passive immunization (administration of rabies

immunoglobin).

Question: If bitten by a stray animal, what should be properly done?

Answer:  Print

a. Immediately wash the bite wound with soap and clean water. Antiseptics may be applied. b. Consult a

physician or go to your nearest Animal Bite Center for immunization. The victim may also be given antibiotics

and anti-tetanus immunization, if indicated.c. Consult a veterinarian for the management of the biting dog.

Viral Zoonoses Slide Set

Pathogenesis of Rabies Infection

 

C. Pathogenesis

The commonest mode of transmission in man is by the bite of a rabid animal or the contamination of scratch wounds by virus- infected saliva. However, other routes have been implicated in the past, suchas through mucous membranes of the mouth, conjunctiva, anus and genitalia. Infection by aerosoltransmission had been demonstrated in experimental animals and has been implicated in humaninfection in rabies-infected bat caverns and in several laboratory accidents. Man to man transmission by transplantation of infected corneas were reported in 5 instances. Rabies is an acute infection of theCNS which is almost invariably fatal. The virus is similar to VSV of cattle. Following inoculation, thevirus replicates in the striated or connective tissue at the site of inoculation and enters the peripheralnerves through the neuromuscular junction. It then spreads to the CNS in the endoneurium of theSchwann cells. Terminally, there is widespread CNS involvement but few neurons infected with thevirus show structural abnormalities. The nature of the profound disorder is still not understood.

D. Clinical Features

The incubation period is highly variable, ranging from 7 days to several years. It depends on several

factors such as;

1. Dose of inoculum2. The severity of the wound3. The length of the neural path from the wound to the brain e.g. wounds on the face have ashorter incubation period than wounds in the leg.

The illness begins with a non-specific prodrome period, comprising of fever, malaise, anorexia, N+V,sore throat, myalgia and headache. The patient nay exhibit irritability and abnormal sensations around

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the wound. The prodrome is followed by one of two basic clinical patterns: the more common "furious"form characterized by hyperexcitability, spasms and hydrophobia; or "dumb" rabies featuring anascending paralysis. Survival tends to be longer for patients with "dumb" rabies than those with"furious" rabies.

Complications involving the Cardiovacular System, CNS, and the respiratory systems eventuallydevelop and contribute to death. Cardiac dysrhythmias of all types occur and respiratory disturbances

occur in all cases. Raised intracranial pressure contributes to the decreased level of consciousness andto focal convulsions. Other CNS complications include disturbances of thermoregulation, diabetesinsipidus, autonomic dysfunction and convulsions. The differential diagnosis of rabies includes tetanus, poliomyelitis, Guillain-Barre syndrome, viral encephalitis and poisonings and drugs.

E. Laboratory Diagnosis

The diagnosis of animal and human rabies can be made by 4 methods: (1) histopathology (2) viruscultivation (3) Serology (4) virus antigen detection. Although each of the first 3 methods have distinctadvantages, none provide a rapid definitive diagnosis.

1. Histopathology - Negri bodies are pathognomonic of rabies. However, Negri bodies are only

 present in 71% of cases.2. Virus cultivation - The most definitive means of diagnosis is by virus cultivation from infected

tissue. Tissue culture lines, such as WI-38, BHK-21, or CER. Since rabiesvirus induce minimalCPE, IF is routinely used to detect the presence of rabiesvirus Ag in the tissue culture. The morecommonly used method for virus isolation is by the inoculation of saliva, salivary gland tissueand brain tissue intracerebrally into infant mice. The mice should develop paralysis and deathwithin 28 days. Upon death, the brains are examined for the presence of the virus byimmunofluorescence.

3. Serology - circulating antibodies appear slowly in the course of infection but they are usually present by the time of onset of clinical symptoms. The most commonly used serological testswere the mouse infection neutralization test (MNT) or the rapid fluorescent focus inhibition test

(RFFIT). These tests have now been largely superseded by EIAs. Serology had been reported to be the most useful method for the diagnosis of rabies.

4. Rapid virus antigen detection - in recent years, virus antigen detection by IF had becomewidely used. The potentially infected tissue is incubated with fluorescein-labeled antibody. Thecells are examined by fluorescent microscopy for the presence of fluorescent intracytoplasmicinclusions. The specimens which are usually used are corneal impressions (obtained by gentlyabrading the cornea with a microscopic slide) or neck skin biopsy (the cells examined are thesensory nerves). In an American series, IF of corneal impressions or neck skin impressions wasdiagnostic only in 50% of cases early in the course of the clinical illness.

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  Negri body in body of neuron and positive IF test for rabies antigen (Source: CDC)

 

F. Management and Prevention

Once rabies is established, there is nothing much that could be done except intensive supportive care.To date, only 2 persons with proven rabies have survived, and 3 persons with probable rabies.However, one survivor was left with severe neurological sequelae and all 3 who recovered werevaccinated beforehand. Numerous antiviral agents have been tried with no success.

1. Postexposure prophylaxis

In cases of animal bites, dogs and cats in a rabies endemic area should beheld for 10 days for observation. If signs develop, they should be killed and their tissue examined in the laboratory. Wildanimals are not observed but if captured, the animal should be killed and examined. The essentialcomponents of postexposure prophylaxis are the local treatment of wounds and active and passiveimmunization.

a. Wound treatment - surgical debridement should be carried out. The wound should not besutured up. Experimentally, the incidence of rabies in animals can be reduced by local treatmentalone.

 b. Passive immunization - human rabies immunoglobulin around the area of the wound; to besupplemented with an i.m. dose to confer short term protection. There is convincing evidencethat combined treatment with rabies immunoglobulin and active immunization is much moreeffective than active immunization alone. Equine rabies immunoglobulin (ERIG) is available inmany countries and is considerably cheaper than HRIG.

c. Active immunization - the human diploid cell vaccine is the best preparation available. Thevaccine is usually administered into the deltoid region, and 5 doses are usually given.

2. Preexposure prophylaxis

Persons who are regularly at high risk of exposure, such as vets, laboratory workers, animal handlersand wildlife officers should be considered for preexposure prophylaxis by active immunization with thecell culture vaccine. Immunization normally consists of 3 doses of vaccine. Antibody can bedemonstrated in the sera of virtually 100% of those vaccinated if the diploid cell culture vaccine isused. Booster doses should be offered to persons at continuing risk every one to three years. Localtreatment of wounds should always be carried out in exposed persons who have been vaccinated previously. The WHO expert committee considers that local infiltration with antiserum is optional andsystemic passive immunization contraindicated.

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3. Rabies Vaccines

Several types of live attenuated vaccines are available for use in animals, but they are considered to beunsuitable for humans. The vaccines which are available for humans are present are inactivated wholevirus vaccines.

a. Nervous tissue preparation - this consisted of a 5% suspension of infected animal nervoustissue which had been inactivated (eg. the Semple vaccine was derived from phenol-inactivatedinfected rabbit brain), These preparations are now out of date as they were associated with therare complication of demyelinating allergic encephalitis. This appears to be related to myelin basic protein in the vaccine. This complication was shown to occur in 4.6 case for 1000 personsvaccinated by the Semple vaccine. The case-fatality proportion was 3.13%. The Semple vaccineis still used in some developing countries. A suckling mouse brain vaccine is used in someCentral and S.American countries.

 b. Duck Embryo Vaccine - this vaccine strain is grown in embryonated duck eggs and isinactivated with B-propriolactone. This vaccine has a lower risk of allergic encephalitis.However, it is considerably less immunogenic and does have minor side effects. Almost allvaccinees experience local reactions, 33% have constitutional symptoms such as fever, malaise,myalgia, and generalized lymphadenopathy.

c. Human Diploid Cell Vaccine (HDCV) - HDCV was introduced in 1978. It is a grown on WI-38 (U.S.) or MRC-5 (Europe) cells. The vaccine is highly effective, in several studies,antibodies have been demonstrated in 100% of all recipients. Serious adverse reactions toHDCV are extremely rare. However, the vaccine is very expensive ( $100 for 6 doses), ashuman cell cultures are more difficult to handle than other animal cell culture systems. 5 or 6doses of the vaccine is normally i.m. However, several studies suggest than smaller intradermaldoses of HDCV may be as effective and thus it may be considered for use in poor developingcountries.

Another inactivated vaccine is widely used in China. It is derived from virus grown in primary hamster kidney cells and cost less than the other diploid cell culture vaccines. The vaccine had been shown to

 be as effective as HDCV. Efforts are being made to use other inexpensive cell culture systems such asVERO cells.

4. Failure of prophylaxis

HDCV has been used to treat many thousands of people exposed to possible rabid animals in the past12 years and its efficacy has been proven. At least 16 people treated with HDCV after exposure havedied of rabies. All of the patients had major exposures and in the majority, the incubation period wasshort, 21 days or less. Treatment was frequently not started promptly within 24 hours and only half received combined serum and vaccine. At least one person has died despite optimum treatment.

G. Rabies Control

Urban - canine rabies accounts for more than 99% of all human rabies cases and over 90% of allhuman post-exposure treatments worldwide. In the past, the Scandinavian countries were able to ridthemselves of rabies by sanitary control alone, which included stray dog control. Other countries, suchas the UK, have used these techniques allied with quarantine and/or vaccination to eradicate and thenmaintain freedom from the disease. Currently, the importation of mammals into the UK is controlled bythe Rabies order. It applies to a wide range of mammals but livestock including horses, which arecovered by separate regulations. The animals must be vaccinated on arrival. Effective animal vaccinesare available.

Wildlife - canine rabies can be controlled because in general, dogs live in close association with man

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and are therefore within physical reach. An attempt was made to vaccinate foxes in an attempt to createan immune barrier at the entrance to the Rhone valley in 1978. The live attenuated virus was containedin small plastic blister packages fixed under the skin of chicken heads used as a bait, and 4050 of these

were distributed over an area of 335km2. With continued field trials, Switzerland has been freed of rabies. Other field trials are being set up.

hysiology of Rabies

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Rabies is derived from the Latin wordrabies , meaning“madness.” Rabies is a central nervous system disease and is almost always fatal. The cause of rabies isa negative stranded RNA virus called Rabies Virus (RV). There are five genes that encode for the virus,which are nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G), and viral RNA polymerase (L). The fusion of the rabies virus envelope (which can be seen in Figure 1) to the host cell

initiates the infection process.Figure 1: This figure shows the bullet-shaped structure of the Rabies Virus.It is believed that the reaction of the G protein to the cell surface receptors may be involved. After thisoccurs, the virus goes through the host cell and enters the cytoplasm by pinocytosis (which can be seen inFigure 2).

Figure 2: This figure shows the process of pinocytosis, which allows the virus to enter the cytoplasm.

 The virus cumulates in large endosomes and the endosome membranes fuse together with the viralmembranes, which causes the release of viral RNP into the cytoplasm. The L gene transcribes the rabiesRNA into leader RNA and mRNAs, which are then translated into proteins. The intracellular ratio of leader RNA to the N protein stimulates the switch from transcription to replication. After replication iscomplete, the assembly process begins. The N-P-L complex surrounds negative-stranded RNA to form theRNP core. The M protein forms a capsule around the RNP. This RNP-M complex travels to a part of theplasma membrane containing glycoprotein inserts. Here, the M protein initiates coiling. The RNP-M bindsto the glycoprotein and the completed virus buds from the plasma membrane. In the central nervoussystem, there occurs preferential viral budding from the plasma membrane. However, the virus in thesalivary glands mostly buds from the cell membranes into the acinar lumen. This viral budding in thesalivary glands, as well as the aggressive biting behavior of the infected animal, increases the chance of aviral infection of a new host.

Figure 3: This figure shows the cycle of rabies infection and replication.Rabies is zoonotic, meaning that it is transferred by animals, most commonly by the bite of a rabid animal.However, it can be transferred in other manners. All warm-blooded animals are susceptible to gettingrabies. It usually has an incubation period of between 2-12 weeks, but there have been documented casesof incubation lasting up to a year. The onset of symptoms is determined by the bites proximity to the brainand the number of virus particles in the infection. Negri bodies, which are characteristic of rabies, areinclusion bodies that are commonly found in the cytoplasm of infected nerve cells.

Figure 4: This figure shows Negri bodies located in a rabies-infected nerve cell.The virus is located in the nerves as well as the saliva of an infected and symptomatic individual, however transmission between humans is rare. After a human is bitten, the virus enters the peripheral nervoussystem. The virus binds to the nerves via nicotinic acetylcholine receptors. During this time after a person isfirst infected, rabies is hard to detect and does not present symptoms. This is the time when a person can

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receive vaccination. Once the virus reaches the brain, it quickly causes encephalitis, or inflammation of thebrain. The cells in the brain that are affected include the cerebellum, the purkinje cells, the hippocampus,and the pontine nuclei. This stage of rabies is referred to as the prodromal phase and is the onset of symptoms. Once the virus moves along the nerve axons from the peripheral nerves to the central nervoussystem (through retrograde axoplasmic flow), the patient starts exhibiting symptoms. It is believed that “theneuromuscular junctions are very important during this transition, as their physical and chemical propertiesappear to direct the virus to infect the nerve cells,” (Hunt, 2009). This usually occurs through the sensory

and motor nerves. Treatment becomes ineffective at this point and the mortality rate is almost 100%.Once the virus reaches the central nervous system the virus amplifies very quickly because of multiplecycles of replication. This stage of rabies is known as the acute neurological period. The centrifugal spreadof rabies leads to the virus overtaking very innervated areas, such as the salivary glands. Once there iscerebral infection, behavioral symptoms occur. The first symptoms to occur are usually numbness and painwhere bitten. Other early symptoms include fever, cough, sore throat, abdominal pain, and anxiety. Later symptoms that effect the central nervous system are more pronounced and include anxiety, hallucinations,delirium, hydrophobia, muscle spasms in the face, neck, and diaphragm followed by seizures, paralysis,significant fluctuations in temperature, heart rate and blood pressure, coma, and heart and respiratoryfailure. Hallucinations and delirium are the result of brain inflammation and other dysfunctions occurring inthe brain such as dopamine. Encephalitis is also known to cause seizures because the neurons firing in apatient’s brain with encephalitis misfire, causing the seizure. Paralysis occurs because of the damagebeing done to the nervous system. Death usually occurs between three and twenty days after the onset of 

symptoms. The virus is concentrated in the salivary glands, which explains why it is transferred usually bybites. The virus also damages the muscles involved in swallowing (usually paralyzing them), which causesa lot of pain. Because swallowing causes so much pain, the patient usually becomes dehydrated, and thus,very afraid of water. This is why the disease was once called hydrophobia. Dehydration causes the musclespasms that patients can have. There are two main ways in which these symptoms present themselves.The more common type is known as furious rabies. This type includes seizures, periods of anxiety,hallucinations, and violent behavior. The second form is known as paralytic rabies. This is characterized bya slow paralysis of the patient and typically these patients live a little longer than those who have furiousrabies. The result of death is usually respiratory failure.

Figure 5: This figure shows the progression of rabies from transmission onward.There are two different types of rabies prophylaxis that are effective when used before the onset of symptoms. The first, Rabies Vaccine, is an inactivated vaccine and is immunogenic. It is grown in human

diploid cells and is given by injection over a four-week period. Human Rabies Immunoglobin (HRIG),another treatment for rabies, is made from the plasma of hyperimmune donors. About half of the dose isinjected into the site of the bite and the other half is given through intramuscular injections. There twotreatments are used in conjunction with one another. These treatments should be administered no later than 2 days after the bite occurs.

It is still unknown what occurs during the long incubation period of the disease and the molecular mechanism in which the virus attacks the nervous system. However, there has been a lot of progress withthe control of rabies and the development of vaccinations. Overall, rabies is a frightening disease andhopefully one day scientists will be able to eliminate, or at least reduce its incidence rate significantly.

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Rabies (from Latin:rabies, “madness, rage, fury.” Also known as

“hydrophobia”) is a viral zoonotic neuroinvasive disease that causes

acuteencephalitis(inflammation of the brain) in mammals. It is most

commonly caused by a bite from an infected animal, but occasionally by

other forms of contact. If left untreated in humans it is almost invariablyfatal. In some countries it is a significant killer of livestock.

The rabies virus makes its way to the brain by following the peripheral

nerves. The incubation period of the disease depends on how far the

virus must travel to reach the central nervous system, usually taking a

few months.

In the beginning stages of rabies, the symptoms are malaise, headache,

and fever, while in later stages it includes acute pain, violent movements,

uncontrolled excitements, depressions, and the inability to swallow water 

(hence the name hydrophobia). In the final stages, the patient begins to

have periods of mania and lethargy, and coma. Death generally occurs

due to respiratory insufficiency.

In non-vaccinated humans, rabies is almost invariably fatal after 

neurological symptoms have developed, but prompt post-exposure

vaccination may prevent the virus from progressing. There are only six

known cases of a person surviving symptomatic rabies, and only two

known cases of survival in which the patient received no rabies-specific

treatment either before or after illness onset.

Etiologic Agent:

Rhabdovirus

1. It is a bullet-shaped filterable virus with strong

affinity to the CNS.

2. It is sensitive to sunlight, ultraviolet light, ether,

formalin, mercury, and nitric acid. The organism is

resistant to phenol, merthiolate, and common

antibacterial agents.

Incubation Period:

1. One week to seven and a half months in dogs.

2. Ten days to fifteen years in human.

3. Incubation period depends upon the following

factors:

a. Distance of the bite to the brain

 

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b. Extensiveness of the bite

c. Specie of the animal

d. Richness of the nerve supply in the area of the

e. Resistance of the host

Period of communicability:

The patient is communicable from three to five days before onset of symptoms until the entire course of illness.

Pathogenesis:

1. From the site of the bite, the organism proceeds to the CNS through the exoplasm of the peripheral nerves.

2. Experimental studies have shown that the virus stays for sometimes in the inoculation site, and the multiplication of the

virus occurs in the myocytes.

3. It has been observe that the period between inoculation and nerve invasion is the only time when prophylactic vaccine is

effective.

4. Once the virus infects the individual, the spread is both centripetal and centrifugal.

5. After infection of the CNS, the virus spreads though the peripheral nerves, to the salivary glands, and also to other organs

such as the lungs, the adrenals, the kidneys, the bladder, and the testicles (priapism).

Pathology:

1. Rabies virus causes widespread changes throughout the CNS.

2. This consists of neural necrosis and mononuclear cellular infiltration specially in the thalamus, hypothalamus, pons, and

medulla.

3. The cranial nerve nuclei are extensively damaged.

4. Neural changes are present in the spinal cord especially in the posterior horns.

5. Negri bodies are most abundant in the hypocampus, basal ganglia, pons, and medulla, and are found in the degenerating

neurons of the salivary glands (pathologic sign for rabies).

Clinical Manifestations:

1. Prodromal/Invasion phase

a. The phase is characterized by fever, anorexia, malaise, sore throat, copious salivation, lacrimation, perspiration, irritability,

hyperexcitability, apprehensiveness, restlessness, sometimes drowsy, mental depression, melancholia, and marked insomia.

b. There is pain at the original site of the bite. Headache and nausea may be present.

c. The patient becomes sensitive to light, sound and temperature.

d. There are pain and aches in different parts of the body.e. Anesthesia, numbness, tingling, burning, and cold sensation maybe felt along the peripheral nerves involved and the site

of the bite.

f. Mild difficulty in swallowing.

2. Excitement or neurological phase

a. This phase is characterized by marked excitation, and apprehension. Terror may even occur.

b. There is delirium associated with nuchal rigidity, involuntary twitching or generalized convulsions.

c. The patient may exhibit maniacal behavior, eyes are fixed and glossy, and the skin is cold and clammy.

d. There is a severe and painful spasm of the muscles of the mouth, pharynx, and larynx, on attempt to swallow water or food

or even at the mere sight of them.

e. There is aerophobia or intense fear or dislike of flying.

f. There is profuse drooling of saliva.

g. There is tonic or clonic contraction of the muscles.

h. Death may occur during the episode of spasm or from cardiac/respiratory failure.

i. If patient survives during this phase, patient deteriorates rapidly and enters to the terminalphase.

3. Terminal/paralytic phase

a. The patient becomes quiet and unconscious.

b. There is loss of bowel and urinary control.

c. Spasm ceases with progressive paralysis.

d. There is tachycardia, labored, or irregular respiration.

e. Death occurs due to respiratory paralysis, circulatory collapse, or heart failure.

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Diagnostic Procedures:

1. Virus isolation from the patient’s saliva or throat.

2. Fluorescent rabies anti-body (FRA) provides the most definite diagnosis.

3. Presence of negri bodies in the dog’s brain.

Modalities of Treatment:

1. Thoroughly wash the wounds from the bite and scratches of dog with soap and running water for at least three minutes.

2. Check the patient’s immunization status. Give tetanus toxoid if needed.

3. Give tetanus antiserum infiltrated around the wound-or given intramuscularly after a negative skin test.

4. Give anti-rabies vaccine, both passive and active, depending upon the site and extensiveness of the bite as well as the

health condition of the biting animal.

Nursing Management:

1. Isolate the patient.

2. Give emotional and spiritual support.

3. Provide optimum comfort.

4. Darken the room and provide a quiet environment.

5. Patient should not be bathed and there should not be any running water in the room or within the hearing distance of the

patient.

6. If IV fluid has to be given it should be wrapped and needle should be securely anchored in the vein to avoid dislodging in

times of restlessness.

7. Concurrent and terminal disinfection should be carried out.

Prevention and Control:

The eradication of rabies should be on global scale and should include measures to prevent and control the disease in

animals and wildlife.

1. Vaccination of all dogs

2. Enforcement of regulations for pickup and destruction of stray dogs

3. Confinement of any dog that has bitten a person for ten to fourteen days

4. Availability of laboratory facilities for observation and diagnosis

5. Providing public education, especially among children, in avoiding and reporting all animals that appear sick.

Post-exposure prophylaxis

Treatment after exposure, known as post-exposure prophylaxis or “P.E.P.”, is highly successful in preventing the disease if administered promptly, generally within six days of infection. Thoroughly washing the wound as soon as possible with soap

and water for approximately five minutes is very effective at reducing the number of viral particles. “If available, a virucidal

antiseptic such as povidone-iodine, iodine tincture, aqueous iodine solution or alcohol (ethanol) should be applied after 

washing.” Exposed mucous membranes such as eyes, nose or mouth should be flushed well with water. In the United States,

patients receive one dose of immunoglobulin and five doses of rabies vaccine over a twenty-eight day period. One-half the

dose of immunoglobulin is injected in the region of the bite, if possible, with the remainder injected intramuscularly away from

the bite. This is much less painful compared with administering immunoglobulin through the abdominal wall with a large

needle, as was done in the past. The first dose of rabies vaccine is given as soon as possible after exposure, with additional

doses on days three, seven, fourteen, and twenty-eight after the first. Patients that have previously received pre-exposure

vaccination do not receive the immunoglobulin, only the post-exposure vaccinations on day 0 and 3. Since the widespread

vaccination of domestic dogs and cats and the development of effective human vaccines and immunoglobulin treatments, the

number of recorded deaths in the U.S. from rabies has dropped from one hundred or more annually in the early twentieth

century, to 1–2 per year, mostly caused by bat bites, which may go unnoticed by the victim and hence untreated.

P.E.P. is effective in treating rabies because the virus must travel from the site of infection through the peripheral nervous

system (nerves in the body) before infecting the central nervous system (brain and spinal cord) and glands to cause lethal

damage. This travel along the nerves is usually slow enough that vaccine and immunoglobulin can be administered to protect

the brain and glands from infection. The amount of time this travel requires is dependent on how far the infected area is from

the brain: if the victim is bitten in the face, for example, the time between initial infection and infection of the brain is very

short and P.E.P. may not be successful.

Pre-exposure prophylaxis

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Currently pre-exposure immunization has been used on domesticated and normal non-human populations. In many

 jurisdictions, domestic dogs, cats, and ferrets are required to be vaccinated. A pre-exposure vaccination is also available for 

humans, most commonly given to veterinarians and those traveling to regions where the disease is common, such as India.

Most tourists do not need such a vaccination, just those doing substantial non-urban activities. However, should a vaccinated

human be bitten by a carrier, failure to receive subsequent post-exposure treatment could be fatal, although post-exposure

treatment for a vaccinated human is far less extensive than that which would normally be required by one with no pre-

exposure vaccination.

In 1984 researchers at the Wistar Institute developed a recombinant vaccine called V-RG by inserting the glycoprotein gene

from rabies into a vaccinia virus. The V-RG vaccine has since been commercialised by Merial under the trademark Raboral.

It is harmless to humans and has been shown to be safe for various species of animals that might accidentally encounter it in

the wild, including birds (gulls, hawks, and owls).

V-RG has been successfully used in the field in Belgium, France, and the United States to prevent outbreaks of rabies in

wildlife. The vaccine is stable under relatively high temperatures and can be delivered orally, making mass vaccination of 

wildlife possible by putting it in baits. The plan for immunization of normal populations involves dropping bait containing food

wrapped around a small dose of the live virus. The bait would be dropped by helicopter concentrating on areas that have not

been infected yet. Just such a strategy of oral immunization of foxes in Europe has already achieved substantial reductions in

the incidence of human rabies. A strategy of vaccinating “neighborhood dogs” in Jaipur, India, (combined with a sterilization

program) has also resulted in a large reduction in the number of human cases.