Epidemiology, Prevention and Control Methods of Human Rabies: Review Article

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International Journal of Basic and Applied Virology 4(1): 22-27, 2015 ISSN 2222-1298 IDOSI Publications, 2015 DOI: 10.5829/idosi.ijbav.2015.4.1.93256 Epidemiology, Prevention and Control Meods of Human Rabies: Review Article Nibret Moges Clinical Medicine Department, Faculty of Veterinary Medicine, University of Gondar, P.O. Box 196, Gondar Eiopia Abstract: Rabies is viral encephalitis, almost always fatal, caused by lyssavirus infection. It is associated wi dysfunction of e neurons after entry of e rabies virus to e central nervous system, usually in e spinal co. The only lesions are in e central nervous system and spreads from e site of infection occur only by ways of e peripheral nerves. The bite route is still regaed as e most important means of transmission. Alough wild animals can be host for rabies, dogs and cat remain a most important source of human exposure. The disease is worldwide in distribution except in Antarctica. There is lack of accurate quantitative information on rabies bo in humans and animals and little is known about e awareness of e people about e disease to apply effective control measures in many developing countries. Key wos: Epidemiology Human Rabies Prevention and Control Worldwide INTRODUCTION contains a single-stranded, negative-sense RNA genome. The virus multiplies in e salivary glands of an infected The dictionary tells us at rabies is derived from e host [3, 6]. It is transmitted to humans or oer animals by Latin rabere, To rage or to rave, as is e corresponding e bite of an infected animal whose saliva contains e adjective rabid; rabere possibly may have earlier origins virus; aerosols of e virus at can be spread in caves in e Sanskrit rabhas, for "Violence". The Greeks where bats roost; or by contamination of scratches, adopted eir own wo, lyssa, meaning "madness", abrasions, open wounds and mucous membranes wi for rabies; is in turn is still reflected in English in saliva from an infected animal [7-9]. lyssophobia, described in oxfo English Dictionary as Rabies is a zoonotic disease [10]. It is widely A morbid dread of hydrophobia, e symptoms of which distributed roughout e world wi e exception of sometimes simulate ose of e actual disease [1]. Australia, New Zealand, Japan, a number of European Rabies is an encephalomyelitis caused by a countries and some Caribbean Islands. Wild animals serve neurotrophic virus at affects all species of as a large and mainly uncontrollable reservoir of sylvatic warm-blooded animals [2, 3]. It was recognized in Egypt rabies, which is an increasing reat to e human before 2300 B.C. and in ancient Greece, where it was well population and to domestic animals in many countries described by Aristotle. Perhaps e most leal of all [6, 11]. Therefore, e objective of is paper was to infectious disease, rabies also has a destruction of having review information regaing human rabies stimulated one of e great discoveries in biomedical epidemiologyand its prevention and control meods. science. Rabies is an invariably leal; a cute viral disease of Epidemiology e central nervous system at affects all mammals and The Epidemiology of Human Rabies: An understanding at is transmitted by infected secretions [4, 5]. It is of e epizootiology of rabies is necessary in caused by a number of different strains of highly evaluating e risk of exposure and e need for rabies neurontropic viruses. Most belong to a single serotype in post exposure prophylaxis (PEP) in humans. Rabies is e genus Lyssavirus (Greek Lyssa, rage or rabies), found in mammals in all regions of e world except family Rhabdoviridae. The bullet shaped virion Antarctica [4]. Corresponding Auor: Nibret Moges, Clinical Medicine Department, Faculty of Veterinary Medicine, University of Gondar, P.O.Box 196, Gondar, Eiopia. 22

The risk of developing rabies depends on e e second-highest rate, followed by Thailand; in ese anatomic site and severity of e bite, e species countries to e virus is primarily transmitted rough inflicting e wound and probably e rabies virus variant canines (Feral dogs and oer wild canine species). [1]. Even e very severe exposure associated wi wolf Recent reports suggest at wild rabid dogs are roaming bites involving e head does not lead inevitably to rabies e streets. Because much cheaper pre-vaccination is not encephalitis. In is case, about 50-60 percent of e commonly administered in places like Thailand, e victims will develop rabies if ey are not given expense for lack of preparation wi far more costly post-exposure treatment wi lesser bite, e risk is around post-exposure prophylaxis can hit families ha [11,12]. 10-40 percent however, modern post-exposure treatment, In Eiopia, during e last 3 years (1999-2002), instituted on e day of e bite can reduce e risk to post exposure antirabies treatment was given to 7,755 virtually zero [12]. peoples in Addis Ababa and 137 fatal human rabies cases When a person is exposed to an animal suspected were recoed at e zoonoses laboratory of EHNRI [15]. of having rabies, e risk of rabies transmission In addition to deas caused by rabies, millions of should be evaluated carefully. Risk assessment should persons annually receive post exposure treatment (PET) include consideration of e species of animal involved, for potential exposure to rabies virus. Many of ese e prevalence of rabies in e area wheer exposure individuals receive vaccines of nervous tissue origin sufficient to transmit rabies occurred and e current (NTO); which potentially result in ousands of serious status of e animal and its availability for diagnostic adverse reactions. Along wi e potential for adverse testing [13]. reactions wi vaccines of NTO, ere is concern over variability in antigen content. Experience in Pakistan and Mortality and Morbidity Estimates: In most areas of e Nigeria wi antirabies vaccines of little or no potency world, accurate estimates of human rabies deas are indicate at ineffective or even take (Lackingany impossible to obtain because surveillance systems and antigenic value) biologicals may at times circulate in a regional laboratories are inadequate or nonexistent. number of countries [1]. Annual report of 2000 human deas in Bangladesh, Most human cases are reported in cities and are 1014 in china and 30,000 in India in e 1990s convey a caused by e bites of rabid dogs. In ose countries rough estimate of e magnitude of mortality associated at have managed to control or eradicate canine rabies, wi rabies worldwide [1]. In Eiopia, a total of 322 even ough ey still have a wild cycle, e number of reported human deas were recoed between 1990 and human cases has been reduced to very low level. Such is 2000 at zoonoses laboratory of EHNRI wi an annual e situation in e US, where in 1938 ere were 47 human range of 17 to 54 cases and 95% of ese were acquired cases, but recently e number has been down to between from dogs. Among e reported fatal human rabies cases, 0 and 3 a year [10]. 38.82% were children 45.03% adults, 13.98% old people and 2.17% were unknown age [14]. Rabies in Developing and Developed Nations: From e Rabies is now present in all mainland Africa public perspective, rabies remains a major reat only wi countries, including Madagascar. In 1998 only Libya and in regions of Asia, Africa and Sou America where some African islands reported no cases of rabies. domestic dogs act as e major reservoir for e virus and Human rabies is grossly underreported in Africa. In 1998, e primary source for human exposures rough animal only 204 cases were notified to WHO, 91 percent were bite. Wiin e broad category of developing countries, attributable to dog bites. The largest number, 43, e geographic area of e tropics accounted for more occurred in Eiopia [12, 14]. an 99% of human deas and approximately 90% of There are an estimated 55,000 human deas annually PETs for Rabies in 1985. The trend towa increasing from rabies worldwide, wi about 31,000 in Asia and global urbanization has meant at in 2000, approximately 24,000 in Africa. One of e sources of recent flourishing one half e world s human population lives in cities of rabies in East Asia is e pet boom. China introduced compared wi one-i in e 1970s. Disease such as in e city of Beijing e One-Dog Policy in November rabies at are prone to transmission in crowded urban 2006 to control e problem. India has been reported as centers wi inadequate public heal infrastructures having e highest rate of human rabies in e world, remain a constant or increasing reat in much of e primarily because of stray dogs. As of 2007, Vietnam had world [16]. 23

In general, rabies poses e greatest risk cities raccoons, skunks and foxes) or occurs in travelers bitten where dog and human populations reach eir by dogs elsewhere in e world. The increase in wildlife highest population densities. Rural or sylvatic rabies, rabies in e United States and some oer developed involving rabies virus transmission from indigenous wild countries present a far greater risk to human an do dogs life, is a lesser reat in most regions of e world. Even in or cats [17]. rural locations, dogs remain e most significant reat In several countries of central and Sou America for rabies virus transmission to humans. In Mexico, vampire-bat rabies is a reat to livestock and to e where vampire bat and dog rabies co-occur, dog human population [11]. Among human rabies cases in e exposures account for approximately 81% of cases United States attributed to bat-associated variants, (Mainly urban) and vampire bats for approximately 11% of about 70% were caused by e silver-haired bat and cases (Mostly rural). During an outbreak of rabies in eastern pipistrelle bat variants. However, only two cases Zimbabwe from 1980 to 1983, e majority of documented were associated wi a history of bat bite, as most bat animal cases occurred in jackals, but dogs were e most exposures go undetected. Bat caves may contain serious reat to humans [1]. aerosols of rabies virus and present a risk to spleunkers. Accoing to Jackson and Wunner[1] in countries Migrating fruit eating bats exist in many countries and are where canine rabies is highest among human males and a source of infection for many animals and human [17]. among individuals less an 20 years of age. The age and As Jackson and Wunner [1] a disturbing trend in sex distribution of human rabies deas generally mirrors recent cases of human rabies in e United States has e age distribution of dog bite victims, wi a large been e inability to elicit a history of animal bite from e proportion of victims under e age of 15 years. As Knipe victim or close family members. Public heal experts and Howley[16] in ese countries, very large numbers of believe at a bat bite is still e most plausible doses of human vaccines are used and ere is a explanation for ese cases because documented continuing need for comprehensive, professionally instances of non bite routes of infection are exceedingly organized and publicly supported rabies control agencies. rare and generally have occurred under exceptional The actual risk of human exposure to rabies virus in situations at are not comparable wi ose described developing countries is difficult to estimate. Surveys for recent cases. based on e experiences of foreign citizens from The most common explanation for e lack of history developed nations traveling or working overseas provide of a bat bite obtained from recent rabies patients or eir a range of values for rabies virus exposure or post close personal contacts are at patients failed to report exposure treatments of 0.2-6.2 per 1000 persons per an event perceived as insignificant or at e bat bite mon. These values vary wi location and may not went unnoticed. The phenotype of rabies virus variants accurately reflect e risk to indigenous populations. In associated wi bats may promote transmission via Thailand, it is estimates at over 200,000 persons superficial wounds inflicted to peripheral body sites. received PET using tissue culture-derived vaccines in All persons bitten by bat must receive post exposure 1997 at a cost of approximately 10 million U.S. dollars [1]. rabies prophylaxis [17]. In most developed countries, even ose wi modest disease buen, publicly supported rabies control Routes of rabies virus transmission to humans: agencies operate by different ways [16]. Human rabies in Accoing to information provided by CDC, ere are two developed countries where tissue culture-derived possible routes of exposure to rabies; bite and non bite. vaccines and rabies immunoglobulin are available is a Any penetration of e skin by tee of a rabid animal very rare disease. In e United States, e number of constitutes a bite exposure. Nonbite exposure include human rabies cases has declined dramatically since 1950s, scratches, abrasions, open wounds, or mucous concomitant wi e decline of canine rabies. There has membranes at come in contact wi saliva or oer been a median of ree human cases of rabies per year potentially infectious material, example-brain or spinal since 1990 and is number is higher an figures from co tissue, from a rabid animal [18, 19]. Europe or Canada [1]. Rabies virus cannot penetrate intact skin. Infection is In e United States, Canada and Western Europe, usually e result of mammal bite, but is also possible if where canine rabies has been controlled, dogs are saliva contaminates damaged skin or even intact responsible for very few cases. Raer, human rabies mucous membranes. On very rare occasions, virus has develops from bites of wild animals (Especially bats, been inhaled as an aerosol. Those who handle infected 24

materials should be careful to avoid accidents wi The benefits and costs of rabies preexposure contaminated knives and needles, should always wear prophylaxis for travelers to rabies endemic countries gloves and should avoid creating infective aerosols [12]. have been assessed and alough not necessarily As Greene [5] described such air borne infections economical, e practice is likely to continue for probably involve large quantities of aerosolized virus important non-economic reasons. The current under condition of poor ventilation and susceptible recommendations for U.S. residents are to consider exposed host. preexposure immunization when traveling to high risk Most commonly, transmission to humans takes place locations wi in countries where rabies is endemic and rough exposure to saliva during a bite by an infected where access to medical care could preclude e ready animal [4,19]. In a review of human rabies cases seen at availability of PET [1]. Pasteur Institutes distributed around e world from 1927 to 1946, animal bites accounted for 99.8% of e Prevention and Control Meods : Historically, several 3,920 cases. However, sporadic cases of human rabies key events have contributed to e control of human have been described following a variety of exposures. rabies: e development of a human rabies vaccine (1885), Saliva transmission by lick to mucous membranes, e discovery of e diagnosis Negribody (1903), e use transdermal scratches contaminated wi infectious of rabies vaccines for dogs (1904s), e addition of rabies material and even improperly inactivated rabies vaccines immune globulin to human postexposure vaccination have resulted in infection [1, 4]. treatments (1954), e grow of rabies virus in cultured Human to Human spread is always eoretical danger cells (1958) and e development of diagnostic fluorescent to ose close to e patient for saliva, tears, respiratory antibody test (1959) [17]. secretions and urine contains virus and patients wi rabies may cough, spit and even bite. However, There Are Two Approaches to Prevention of Rabies in transmission of rabies from one person to anoer has Humans: Pre-exposure and post-exposure. Pre-exposure been proved only in a group of patients who received vaccination is desirable for all persons who are at high infected corneal transplant grafts, transmission by breast risk of contact wi rabid animals such as veterinarians, milk and transplacentally has been proved in animals but animal care personnel, certain laboratory workers and not in humans. A number of women wi rabies spelunkers. Persons traveling to developing countries encephalitis have been delivered of healy babies [5, 12]. where rabies control programs for domestic animals are In e United States, ingestion of unpasteurized milk not optimal should be offered pre-exposure prophylaxis from rabid cows has been treated as a possible exposing [9, 17, 20, 21]. However, pre-exposure prophylaxis does to virus. Scratches from a rabid animal potentially could not eliminate e need for prompt post-exposure be contaminated wi virus shed in saliva and in e prophylaxis if an exposure to rabies occurs [17]. United States are often treated as an exposure, but So immediate treatment after exposure is essential for all documented cases of is injury leading to rabies are rare individuals known or suspected of having been exposed [1]. to a rabid animal [20]. Rabies in Travelers and Overseas Personnel from Pre-exposure Vaccine Regime: 1 dose of cell culture or Developed Nations: Many cases of rabies have been purified duck embryo vaccine on days 0, 7, 28 a few days reported in travelers, but ere are no data on e risk of variation is acceptable. The dose in 1 standa infection, Domestic animals, primarly dogs, are e major intramuscular dose (1ml or 0.5 ml accoing to vaccine transmitters of rabies in developing countries. type). The vaccine may be given intradermally (0.1ml on Several studies have shown at e risk of rabies day 0, 7, 28) except in anti malarial chemoprophylaxis posed by a dog bite in an endemic area ranges from 1 to (e.g. chloroquine) is being used concurrently, 3.6 cases per 1000 travelers per mon of stay. when intramuscular injections are preferable, since e Countries where canine rabies is highly endemic include antibody response may be impaired if e intradermal Mexico, e Philippines, Sirlanka, India, Thailand and meod is used WHO [22] and is will provide 2 years of Vietnam. Rabies vaccine is recommended for long-stay protection [21]. Booster (Or serologic confirmation of travelers, particularly children and persons who may be adequate level) is given depending on e individual s occupationally exposed to rabies in endemic areas [4]. continuing risk category [16]. 25

In more an 99% of human rabies cases, e virus was transmitted by e bite of a dog and over 90% of persons who receive postexposure treatment live in areas where canine rabies is present. WHO advocates canine rabies control as e only long term, cost effective means of eliminating or preventing most human cases [23]. Increased travel of humans, along wi intentional and unintentional translocation of animal (Including known potential rabies-reservoir species), has made e recognition of clinical rabies and its prevention of increasing importance [4]. RECOMMENDATIONS Unvaccinated dogs and cats exposed to a rabid animal should be euanized immediately. If e owner is unwilling to have is done, e animal should be placed in strict isolation for 6 mons and vaccinated 1 mon before being released. Animals wi expired vaccinations need to be evaluated on a case-by-case basis. Dogs and cats at are currently vaccinated should be revaccinated immediately, kept under e owner s control and observed for 45 days. In unvaccinated humans, rabies is almost always fatal after neurological symptoms have developed, but prompt post-exposure vaccination may prevent e virus from progressing [24]. The first protective measure is local treatment of e wound. The wound should be washed immediately wi soap and water, detergent, or anoer substance at inactivates e virus. The World Heal Organization Expert Committee on Rabies also recommends e installation of antirabies serum around e wound [16, 21]. The pre-exposure schedule for rabies vaccination is 3 doses, given at e following times; Dose 1: As appropriate Dose 2: 7 days after Dose 1 Dose 3: 21 days or 28 days after Dose 1 For laboratory workers and oers who may be repeatedly exposed to rabies virus, periodic testing for immunity is recommended and booster doses should be given as needed [21]. REFERENCES 1. Jackson, A.C. and W.H. Wunner, 2002. Rabies. United States: Elsevier science, pp: 71-82. Intl. J. Basic & Appl. Virol., 4(1): 22-27, 2015 CONCLUSIONS 2. Lahunta, A.D., 1983. Veterinary Neuroantonomy and nd Clinical Neurology. 2 ed. Canada: Saunders, 83: 383 and 406. 3. Prescott, L.M., J.P. Harley and D.A. Klein, 2002. Microbiology. 5 ed. United States: McGraw Hill, pp: 888-889. 4. Kasper, D.L., A.S. Fauci, D.L. Longo, E. Braunwald, S.L. Hauser and J.L. Jameson, 2005. Harrison s principle of Internal Medicine. 16 ed. Vol.1. United States: McGraw Hill, pp: 1155-1160. 5. Greene, C.E., 2006. Infectious Disease of e dog and cats. 3 ed. Canada: Elsevier Science, pp: 167-183. 6. Hirsh, D.C., N.J. Maclachlan and R.L. Walker, 2004. nd Veterinary Microbiology. 2 ed. United States: Blackwell science, pp: 377-380. 7. Jaweiz, E., J.L. Melnick and E.A. Adelberg, 1980. Review of Medical Microbiology. 14 ed. California: Lange Medical Publications, pp: 432-437. 8. Nelson, R.W. and C.G. Couto, 2003. Small Animal Internal Medicine. 3 ed. China: Mosby, pp: 1016. 9. Levinson, W., 2004. Medical Microbiology and Immunology. 8 ed. United States: McGraw Hill, pp: 271-272. 10. Acha, P.N. and B. Szyfres, 2003. Zoonoses and Communicable Disease Common to Man and Animals. 3 ed. Vol.2. Washington: Pan American Heal Organization, pp: 246-270. 11. Quinn, P.J., M.E. Carter, B.K. Markey and G.R. Carter, 1994. Clinical Veterinary Microbiology. Spain: Mosby, pp: 464-465. 12. Parry, E., R. Godfrey, D. Mabey and G. Gill, 2004. Principle of Medicine in Africa. 3 ed. Singapore: Cambridge University press, pp: 714-721. 13. Aiello, S.E., 1998. The Merck Veterinary Manual. 8 ed. United States: Merck and Co., INC, pp: 966-970 14. Eshetu, Y., N. Betelehem, T. Girma, M. Yared, B. Yosef, Z. Badeg, B. Mekero and B. Abebe, 2002. Situation of Rabies in Eiopia, a retrospective study 1990-2000. Eiopia. J. Heal Dev., 16(1): 105-112. 15. Paulos, A., Y. Eshetu, N. Betelehem, B. Abebe, Z. Badeg and B. Mekoro, 2003. A study on e prevalence of Animal Rabies in Addis Ababa during 1999 2002. Eiopian veterinary Journal, 7(1 and 2): 69-76 16. Knipe, D.M. and P.M. Howley, 2001. Fields Virology. 4 ed. Vol. 1. London: Wolter Kluwer heal. 17. Brooks, G.F., J.S. Butel and S.A. Morse, 2004. Medical Microbiology. 23 ed. Singapore: McGraw Hill, pp: 575-581 26

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