International Journal of Public Health Science (IJPHS)

Vol.6, No.4, December 2017, pp. 343~350

ISSN: 2252-8806, DOI: 10.11591/ijphs.v6i4.10781  343

Review of Rabies Preventions and Control

Chernet Balcha, Nejash Abdela

College of Agriculture and Veterinary Medicine, School of Veterinary Medicine, Jimma University, Ethiopia

Article Info ABSTRACT

Article history: Rabies is an acute viral infection of the central nervous system, caused by a
Received Sep 18, 2017 lyssavirus in the family Rhabdoviridae. It is zoonotic viral disease that can
Revised Nov 23, 2017 affect all mammals, including humans, cats, dogs, and wildlife and farm
animals. The virus is present in the saliva of affected animals, and the most
Accepted Dec 3, 2017
frequent method of transmission to humans is by bites, scratches or licks to
broken skin or mucous membranes. The disease has a long incubation period
Keyword: (six months) and symptoms may take several weeks to appear after infection.
The first clinical symptom is neuropathic pain at the site of infection or
Control wound due to viral replication. Diagnosis can only be confirmed by
Prevention laboratory tests preferably conducted post mortem on central nervous system
Rabies tissue removed from cranium. This paper reviews the possible prevention and
Vaccine control of rabies. Essential components of rabies prevention and control
Zoonosis include ongoing public education, responsible pet ownership, routine
veterinary care and vaccination, and professional continuing education.
Control strategies include quarantine, confirmation of diagnosis, determining
the origin and spread of an outbreak. Since rabies is invariably fatal and
deadly viral disease that can only be prevented the collaborative effort
between Veterinarians and human health care professionals are needed in the
prevention and control of rabies.
Copyright © 2017 Institute of Advanced Engineering and Science.
All rights reserved.

Corresponding Author:
Nejash Abdela,
Jimma University, College of Agriculture and Veterinary Medicine,
School of Veterinary Medicine,
Jimma, Ethiopia.
Email: nejash.abdela@gmail.com

1. INTRODUCTION
Rabies is a viral disease that affects the central nervous system of warm-blooded animals, including
humans [1],[2] and it is a zoonotic viral disease that produces almost invariably fatal encephalitis in humans
and most other mammals [3]. The disease is characterized by the development of severe nervous symptoms
that lead to paralysis and death [4]. Once symptoms of the disease develop, it is invariably fatal and deadly
viral disease that can only be prevented but not cured [5]. Dogs remain the primary reservoir in developing
countries, whereas wildlife species serve as hosts in developed nations [6].
Rabies is widely distributed throughout the world with the exception of Australia, New Zealand,
Japan, a number of European countries and some Caribbean Islands. Wild animals serve as a large and
mainly uncontrollable reservoir of sylvatic rabies, which is an increasing threat to the human population and
to domestic animals in many countries [1]. Rabies is an acute viral infection of the central nervous system,
caused by a lyssavirus in the family Rhabdoviridae [4],[7].
The name Rhabdo comes from the Greek and identifies the characteristic bullet or rod-shape of the
viruses [1]. It affects all mammals, including humans, cats, dogs, wild life and farm animals. In animals,
three forms are classically described; prodromal, excitement (furious) and paralytic (dumb). The virus is
present in the saliva of affected animals, and the most frequent method of transmission to humans is by bites,
scratches or licks to broken skin or mucous membranes [8]. The virus is spread through infected saliva in

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344  ISSN: 2252-8806

bites, scratches and through licks from infected animals in open wounds or on mucosal membranes
[7],[9],[10].
Rabies infection in humans is still a major public health Problem all over the world [11]. Rabies
kills an estimated 35,000 per year, mostly in Africa, Asia and Latin America [6]. The World Health
Organization (WHO) considers rabies to be a neglected disease and declare it to be primarily a problem in
areas troubled with poverty and with a lack of economic resources [12]. With over 55 000 human deaths a
year [7] and signs of it re-emerging [9]. The domestic dog is the most important vector of human exposure
[13]. It is possible to prevent a person exposed to the virus from getting ill to rabies by neutralizing virus with
antibodies before the virus invades the nervous tissue. This is done through vaccination and/or use of
immunoglobulins, so called post-exposure prophylaxis (PEP) [7],[14]. Public awareness and an increase of
knowledge about rabies disease, first aid measures after dog bites, increased knowledge about dog behavior
and how to avoid getting bitten by dogs are suggested methods to prevent rabies in humans [7],[9]. Therefore
the main objective of this paper is to review the current information available for prevention and control of
rabies.

2. LITERATURE REVIEW
2.1. Etiology
The causative agent of rabies is a member of the Lyssavirus genus of the Rhabdoviridae family of
bullet-shaped viruses, which have a single-stranded RNA genome [1],[7]. The genus includes the classical
rabies virus (genotype 1) and six so-called rabies-related viruses, Lagos bat virus (genotype 2), Mokola virus
(genotype 3), Duvenhage virus (genotype 4), European bat lyssaviruses 1 and 2 (genotypes 5 and 6), and the
recently discovered Australian bat genotype 7 [15]. The genus Lyssa virus comprises rabies virus and closely
related viruses, including Mokola virus, Lagos bat virus and Duvenhage virus from Africa, European bat
virus 1 and 2 and Australian bat Lyssavirus. Each of these viruses is considered capable of causing rabies like
disease in animals and humans [1]. Rabies virus can be inactivated by sodium hypochlorite, 45-75% ethanol,
iodine preparations, quaternary ammonium compounds, formaldehyde, phenol, ether, trypsin, β-
propiolactone, and some other detergents. It is also inactivated by a very low pH (below 3) or very high pH
(greater than 11). This virus is susceptible to ultraviolet radiation. It is rapidly inactivated by sunlight and
drying, and (in dried blood and secretions) it does not survive for long periods in the environment [16].

2.2. Epidemiology
2.2.1. geographic distribution
With some exceptions (particularly islands), rabies virus is found worldwide. Some countries such
as the United Kingdom, Ireland, Sweden, Norway, Iceland, Japan, Australia, New Zealand, Singapore, most
of Malaysia, Papua New Guinea, the Pacific Islands and some Indonesian islands have been free of this
virus for many years [17]. Rabies is a serious disease threat to humans, domestic animals, and wildlife.
Worldwide rabies kills about 50,000 – 100,000 people/year and countless domestic and wild animals [18].
In Europe the red fox is the most important reservoir host and vector of rabies. An increase in incidence of
rabies in foxes result in an increase in incidence of rabies in domestic animals such as cattle, sheep, horse,
cat, dog and others.
Sylvatic and urban rabies cycles occur concurrently in some regions, while the sylvatic cycle
predominates in others. For example, wild animals accounted for more than 90% of the animal rabies cases
reported in the U.S. and Canada in 2010. Rabies can be a serious concern in some rare or endangered
species. In Africa, the Ethiopian wolf (Canis simensis) and African wild dogs (Lycaon pictus) are
threatened by this virus. Although cases of rabies tend to be sporadic, epizootics are possible [16].

2.2.2. Host range

All mammals are susceptible to rabies, but only a limited number of species also act as reservoir
hosts. They include members of the families Canidae (dogs, jackals, coyotes, wolves, foxes and raccoon
dogs), Mustelidae (e.g., skunks), Viverridae (e.g., mongooses), and Procyonidae (raccoons), and the order
Chiroptera (bats) [17]. Rabies reservoirs are generally grouped into terrestrial (i.e., land-dwelling) species
and bat species. Rabies can occur sporadically in individuals or can exist in an enzootic or epizootic state in
animal populations. In enzootic state rabies is indigenous to a reservoir species in a locality and occurs with
a relatively stable incidence rate. An epizootic occurs when the incidence of disease increases markedly in
the reservoir species. Rabies that is transmitted sporadically from reservoir to non-reservoir species is said
to “spillover”. These reservoir species are: raccoon (Procyon lotor), striped skunk (Mephitis mephitis),
coyote (Canis latrans; infected with the dog variant), gray fox (Urocyon cinereoargenteus), and Arctic fox
(Alopex lagopus) and red fox (Vulpes vulpes) [18].

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2.2.3. Transmission
A rabies exposure is any bite, scratch, or other situation in which saliva, cerebral spinal fluid, tears,
or nervous tissue from a suspect or known rabid animal or person enters an open wound, is transplanted into,
or comes in contact with mucous membranes of another animal or person. On rare occasions human rabies
has been acquired by inhalation of airborne virus in laboratories working with live rabies virus and in caves
with millions of bats. The common mode of transmission of rabies in man is by bite of a rabid animal or the
contamination of scratch wounds by virus infected saliva [19].

2.3. Pathogenesis
Rabies virus enters the body through wounds or by direct contact with mucosal surfaces. It cannot
cross intact skin. Rabies virus replicates in the bitten muscle (local viral proliferation in non-neural tissue)
and gains access (viral attachment) to motor endplates and motor axons to reach the central nervous system
[20]. Virions are carried in transport vesicles [21] and travel to the central nervous system (CNS) exclusively
by fast retrograde transport along motor axons, with no uptake by sensory or sympathetic endings [22].
Following centrifugal transport along efferent cranial nerves, the salivary glands become infected
and virus particles are shed in the saliva. Infection of the brain commonly leads to behavioural changes that
induce the host to bite other animals, thereby transmitting the virus. The widespread central nervous system
infection almost inevitably leads to death, usually through respiratory paralysis, but also through secondary
circulatory, metabolic or infectious processes [23],[24].
Viruses can also enter motor axons in peripheral nerves directly during a penetrating injury. The
incubation period varies from 5 days to several years (usually 2–3 months; rarely more than 1 year),
depending on the amount of virus in the inoculum, the density of motor endplates at the wound site and the
proximity of virus entry to the central nervous system [25].
The incubation period is less than 50 days if the patient is bitten on the head or neck or if a heavy
inoculum is transferred through multiple bites, deep wounds, or large wounds. A person with a scratch on the
hand may take longer to develop symptoms of rabies than a person who receives a bite to the head. In dogs
and cats, the incubation period is 10 days to 6 months; most cases become apparent between 2 weeks and 3
months. In cattle, an incubation period from 25 days to more than 5 months has been reported in vampire bat-
transmitted rabies. In humans, the incubation period can be a few days to several years. Most cases become
apparent after 1-3 months [17].

2.4. Clinical signs

The clinical picture can be highly variable between different species, individuals of the same
species, and even within the course of the disease in a particular individual. As the disease progresses,
animals with rabies may show strange behavior. Any clinical suspicion of rabies must be confirmed by
laboratory examination [5].
The initial clinical signs are often nonspecific and may include fearfulness, restlessness, anorexia or
an increased appetite, vomiting, diarrhea, a slight fever, dilation of the pupils, hyperreactivity to stimuli and
excessive salivation. The first sign of post-vaccinal rabies is usually lameness in the vaccinated leg. Animals
often have behavioral and temperament changes, and may become either unusually aggressive or
uncharacteristically affectionate [17].

2.4.1. Prodromal stage

After a certain incubation period, the onset of clinical symptoms follows. During this first stage
which usually lasts for about 1-3 days minor behavioral changes might occur, i.e. aggressiveness in tame
animals, daytime activities in nocturnal animals, no fear of humans in wild animals or abnormalities in
appetite [26].

2.4.2. Excitement (furious) phase

Eventually, the prodromal stage is followed by a period of severe agitation and aggressiveness. The
animal often bites any material. Rabid dogs, for example, may develop a typical high barking sound during
furious rabies. Death may follow convulsions even without the paralytic stage of the disease [17].
The furious form is characterized by restlessness, wandering, howling, polypnea, drooling and
attacks on other animals, people or inanimate objects. Affected animals often swallow foreign objects such as
sticks and stones. Wild animals frequently lose their fear of humans, and may attack humans or animal
species they would normally avoid (e.g., porcupines). Nocturnal animals may be visible during the day. In
cattle, unusual alertness can also be a sign of this form [17].

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2.4.3. Paralytic (dumb) phase

The “dumb” form of rabies is characterized by progressive paralysis. In this form, the throat and
masseter muscles become paralyzed; the animal may be unable to swallow, and it can salivate profusely.
Laryngeal paralysis can cause a change in vocalization, including an abnormal bellow in cattle or a hoarse
howling in dogs. There may also be facial paralysis or the lower jaw may drop. Ruminants may separate from
the herd and can become somnolent or depressed. Rumination may stop. Ataxia, incoordination and
ascending spinal paresis or paralysis are also seen [17]. This stage is characterized by the inability to
swallow, leading to a typical sign of foaming saliva around the mouth. Some animals may develop paralysis
beginning at the hind extremities. Eventually, complete paralysis is followed by death [26].

2.5. Diagnosis
Laboratory diagnosis of rabies in humans and animals is essential for timely post-exposure
prophylaxis. Rabies diagnosis may be carried out either in vivo or postmortem [27]. Infection with rabies
virus can be difficult to diagnose ante-mortem. Although hydrophobia is highly suggestive, no clinical signs
of disease are pathognomonic for rabies. Historical reliance on the detection of accumulations of Negri-
bodies is no longer regarded as suitable for diagnostic assessment because of low sensitivity and alternative
laboratory-based tests based have been developed to conclusively confirm infection [4].
Most diagnostic tests for rabies virus in animals need brain material for diagnosis and as such are
often only possible post mortem [28]. The diagnosis of rabies in animals can be made by taking any part from
the affected brain. But in order to rule out rabies, the test must include tissues from at least two locations in
brain, from the brain stem and cerebellum. There are many diagnosis methods for detection of rabies in
animals like (Table 1); direct florescent antibody, mouse inoculation technique, tissue culture infection
technique, and polymerase chain reaction [29]. Brain samples are most readily taken by breaching the skull
and sampling directly. Brain smears or touch impressions are used for the meni detection of virus antigen
with the fluorescent antibodytest (FAT) for both human and animal samples. In animals the direct fluorescent
antibody test (dFAT) is the recommended diagnostic test. This test detects the presence of rabies antigens in
brain tissue. Other diagnostic techniques include reverse transcription polymerase chain reaction (RT-PCR),
direct rapid neur immunohistochemistry test (dRIT) and serological tests (Fluorescent antibody neutralization
test, rapid pres fluorescent focus inhibition test). In humans, the rabies recommended test is dFAT on brain
tissue. Other diagnostic tests that have been used are RT-PCR and dRIT [4].
Clinical diagnosis of rabies divided upon three stages in human; prodromal, excitement (furious) and
paralytic (dumb). But all these stages cannot be observed in an individual. The very first clinical symptom is
neuropathic pain at the site of infection or wound due to viral replication. Following by the prodromal phase
either or both the excitement or paralytic forms of the disease may be observed in the particular species. It is
also documented that cats are more likely to develop furious rabies than dogs [29]. In some cases, no signs
are observed and rabies virus has been identified as the case of sudden death [30]. Diagnosis can only be
confirmed by laboratory tests preferably conducted post mortem on central nervous system tissue removed
from cranium [31].
Rabies must be considered in the differential diagnosis of any suspected mammalian meningitis/
encephalitis, distemper, infectious canine hepatitis and cerebral cysticercosis (Taenia solium) in dogs,
sporadic bovine encephalomyelitis (Chlamydia psittaci), heartwater in cattle and sheep. Other conditions like
mineral/ pesticide poisoning and Plant poisoning from Pennisetum clandestinum (kikuyu grass) in cattle,
Cynanchum spp (monkey rope) in sheep should be considered [23].

Table 1. Diagnostic techniques for rabies

Technique Specimen Advantage/Disadvantage
Direct Fluorescent Antibody Target organs, such as brain, salivary glands, Applicable with most tissue sources. Not
Technique (DFA) liver, spleen, pancreas, nuchal skin, brain is the applicable in decomposed tissue
most appropriate sample
Mouse Inoculation Similar to DFA Only use fresh tissues
Technique (MIT)
Tissue Culture Infection Similar to DFA Only use fresh tissues
technique (TCIT)
Polymerase Chain Reaction Similar to DFA including body fluids, saliva, Applicable in all tissue conditions
(PCR) urine, CSF Expensive
Need experienced technicians
Source: (Yousaf et al., 2012) [29]

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2.6. Prevention and control

There is no certain cure for rabies except supportive care. Rabies can be prevented before the latent
symptoms can develop, consists of giving a person an injection of rabies immune globulin and another
injection of rabies vaccine as soon as possible after the bite or exposure to saliva from an infected animal
[29].

2.6.1. Principles of rabies prevention and control

2.6.1.1. Case definition
An animal is determined to be rabid after diagnosis by a qualified laboratory and confirmation either
by a positive direct fluorescent antibody test (preferably performed on central nervous system tissue) or
Isolation of rabies virus in cell culture or in a laboratory animal.

2.6.1.2. Rabies exposure

Rabies is transmitted when the virus is introduced into bite wounds, open cuts in skin, or onto
mucous membranes from saliva or other potentially infectious material such as neural tissue [32].

2.6.1.3. Public health education

Essential components of rabies prevention and control include ongoing public education, responsible
pet ownership, routine veterinary care and vaccination, and professional continuing education. The majority
of animal and human exposures to rabies can be prevented by raising awareness concerning: rabies
transmission routes, and avoiding contact with wildlife. Prompt recognition and reporting of possible
exposures to medical professionals and local public health authorities is critical [32].

2.6.1.4. Human rabies prevention

Human rabies can be prevented by a) eliminating exposure to rabies virus, b) providing appropriate
rabies pre-exposure prophylaxis, and c) prompt local treatment of bite wounds combined with appropriate
rabies post-exposure prophylaxis [32]. Inactivated human vaccines are available for at risk veterinary staff,
other animal handlers, wildlife officers, laboratory workers and others at high risk of exposure.

2.6.1.5. Mestic animal rabies control

The primary components of a rabies control program for companion animals are: immunization and
licensing; stray animal control; reporting, investigation, and isolation of animals involved in bite incidents;
and public education. Multiple vaccines are licensed for use in domestic animal species. Vaccines available
include: inactivated or modified live virus vectored products; products for intramuscular and subcutaneous
administration; products with durations of immunity from one to 4 years; and products with varying
minimum age of vaccination [32].

2.6.1.6. Animal bites reporting

The local health officer or designee shall be immediately notified of any person or animal bitten by
or potentially exposed to a rabid or suspected rabid animal. In addition, the local health officer or designee
shall be notified when any person is bitten by a mammal. Potential human rabies exposures are then
evaluated and rabies post-exposure prophylaxis (PEP) recommendations made [32].

2.6.1.7. Stray animals

Stray dogs, cats, and ferrets should be removed from the community. Local health departments and
animal control officials can enforce the removal of strays more effectively if owned animals are required to
have identification and are confined or kept on leash. Strays should be impounded for at least 3 business days
to determine if human exposure has occurred and to give owners sufficient time to reclaim animals [33].

2.6.1.8. Isolation of animals exposed to rabies

Any animal bitten by, scratched by, or having direct contact with a wild mammal that is not
available for rabies testing should be regarded as having been exposed to rabies. All livestock species-horses,
cattle, sheep, goats, llamas/alpacas, and swine are susceptible to rabies infection. Cattle and horses are the
livestock species most frequently diagnosed with rabies. Unvaccinated livestock bitten by or exposed to a
rabid or suspect rabid animal should be euthanized [32].

2.6.1.9. Wild animal rabies control

Principles of rabies prevention should focus on excluding wild animals from areas of human and
domestic animal habitation and activity, and avoidance of contact with possibly rabid wild animals. Public

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education on the risks of rabies transmission from wild animals is paramount to effective disease prevention.
Immunization of wildlife by widespread distribution of vaccine-impregnated oral baits has shown variable
success toward arresting the propagation of rabies in raccoons and coyotes in other states. The use of oral
rabies vaccines (ORV) for the mass vaccination of free-ranging wildlife should be considered in selected
situations [32].

2.6.2. Animal pre-exposure vaccination

A number of recently developed, highly-effective, thermo stable, inactivated vaccines are available
for veterinary use. The duration of immunity conferred varies from one to three years. Most veterinary
vaccines are only registered for use in specific species, for example dogs. All rabies vaccines registered for
human and animal use must conform to established potency standards. A minimum antigenic potency of 2.5
IU per dose is mandatory [34].
The vaccines may be used in young pups, but they must be boosted at three months of age and again
within the following year. Revaccination must be carried out every three years thereafter. Cattle and sheep
may be vaccinated annually or every two to three years, depending on the vaccine manufacturer's
instructions. Following an outbreak in domestic livestock, vaccination of animals without visible bite wounds
is strongly recommended [35].
There are currently 17 parenteral animal rabies vaccines licensed by the U.S. Department of
Agriculture (USDA) for use in dogs, cats, sheep, cattle, horses, and/or ferrets. Some are approved for dogs or
cats for a multi-year immunity period and others for only a 1-year period. All dogs and cats should be
revaccinated 12 months after initial vaccination regardless of the length of immunity period of the initial
vaccine. Obtaining a booster vaccination immediately following an exposure to a rabid animal is important to
ensure adequate protection against the virus [35].

2.6.3. Animal post-exposure treatment

Findings from a study conducted by Hanlon .et al., 2002 suggested that 5 doses of canine rabies
vaccine administered on days 0, 3, 14, 21 and 35 along with murine anti-rabies antibody on day 0 may be
effective in protecting a previously unvaccinated animal exposed to rabies. Regardless of the age of the
animal at initial vaccination, a booster vaccination should be administered 1 year later [5]. If signs suggestive
of rabies develop (e.g., paralysis, seizures, etc.), the animal should be euthanized and the head shipped for
testing [36].

2.6.4. Outbreak prevention and control

The emergence of new rabies virus variants or the introduction of non-indigenous viruses poses a
significant risk to humans, domestic animals, and wildlife [37]. A rapid and comprehensive response includes
the following measures [38]:
 Characterize the virus at the national reference laboratory.
 Identify and control the source of the introduction.
 Enhance laboratory-based surveillance in wild and domestic animals.
 Increase animal rabies vaccination rates.
 Restrict the movement of animals.
 Evaluate the need for vector population reduction.
 Coordinate a multiagency response.
 Provide public and professional outreach and education.

2.6.5. Rabies control strategies

According to Bishop et al., (2003) Rabies Control Strategies includes quarantine, confirmation of
diagnosis, determining the origin and spread of an outbreak, and specific measures to terminate
transmission [23]. It is absolutely essential to confirm the diagnosis of rabies. When an outbreak has
been confirmed, the responsible state veterinarian decides on the area requiring vaccination.

2.6.5.1. Large-scale vaccination

Large-Scale Vaccination is the initial response to rabies outbreaks in endemic high-risk areas. The
aim should be to vaccinate at least 70 % of the animal population at risk in a single campaign within
as short a period as possible. Where this cannot be achieved, two or more campaigns should be
conducted within a year.

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2.6.5.2. Cordon vaccination

The aim of cordon vaccination is to create a barrier of animal immunity. This approach has
become increasingly important during the second phase of canine rabies elimination, particularly in the
vicinity of international borders and national as well as provincial game reserves. This is necessary to
prevent reinfection of areas currently free from rabies and to protect rabies-free wildlife areas. A cordon of
20 to 30 km is usually sufficient for this purpose

2.6.5.3. Ring vaccination

In areas where an isolated case has been diagnosed, ring vaccination with a radius of 20 to 30
km, where at least 70 % of dogs are vaccinated, has proven successful in controlling or eliminating rabies

2.6.5.4. Door-to-door vaccination

Vaccination on a home-to-home basis is generally more expensive, resource intensive and
time consuming, but coverage is invariably better. An example of the success of this approach is
illustrated by a campaign in Eerstehoek, a rural district in Mpumalanga. In 1998, 20 officials
vaccinated 6498 dogs in 30 villages extending over 594 km2 on a home-to-home basis. All
vaccinated dogs were identified with neckbands.

2.6.5.5. Central-point vaccination

These campaigns are usually conducted at least annually in areas where rabies is endemic and the
prevalence of outbreaks is high. The public are requested to bring their pets to identified venues.
Accurate epidemiological information, good advertising and adequate planning are of paramount
importance to ensure high coverage. Results vary from 20 to 80 % and depend on the degree of attention
to detail. Coverage is generally better if the campaign follows shortly after a well-publicised rabies
outbreak.

2.6.5.6. Oral vaccination

Sylvatic rabies has been successfully eradicated in Switzerland and other European countries
using bait vaccine. A bait containing a live, avirulent rabies virus mutant, SAG2, has been formulated
specifically for dogs and the first field trials were conducted in South Africa.

3. CONCLUSIONS AND RECOMMENDATIONS

Rabies is a fatal viral zoonotic disease and a serious public health problem. Though its
occurrence is worldwide, it is important in developing countries like Ethiopia. This is because of
widespread occurrence of large number of stray dogs. In Africa, the Ethiopian wolf (Canis simensis) and
African wild dogs (Lycaon pictus) are threatened by this virus. It is transmitted only when the virus is
introduced in to bite wound or mucus membrane. The disease is incurable but preventable. In animals,
rabies prevention is based on vaccination and the avoidance of contact with infected animals. The
majority of animal and human exposures to rabies can be prevented by raising public awareness on
rabies transmission routes, and avoiding contact with wildlife. Based on the above conclusions the
following recommendations could be forwarded.
Raising awareness of the community on the mode of transmission, prevention and control of
rabies is of paramount importance. Use of international law to support the control of communicable
diseases. Regulations for stray dog management should be adopted and Strict control of free-ranging dogs
and mandatory rabies vaccination should be enforced.

ACKNOWLEDGEMENTS
Above of all we would like to thanks almighty God for guiding us in every day of our life in every
direction. Next we would like to acknowledge Jimma University College of Agriculture and Veterinary
Medicine, and school of veterinary medicine for their facility support and internet access.

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