Rabies aetiology pathogenesis and prevention
Rabies aetiology pathogenesis and prevention
Rabies Rabies is an acute encephalomyelitis caused by an RNAcontainingrhabdovirus. It is characterized by paroxysmsof muscle spasm that particularly affect muscle groupsassociated with swallowing and inspiration, in response toattempts to drink water, as well as the sight, sound ormention of water. For practical purposes it is invariablyfatal.
Aetiology The rabies virus is an RNA-containing rhabdovirus which,with five related viruses, comprise the Lyssavirus genus.The virus can be grown in cell culture.
Distribution and incidence Antarctica and Australasia are free of rabies, otherwise allcontinents are endemic; the UK, Scandinavia, Japan andTaiwan are free of the disease. The incidence of humanrabies is difficult to estimate. Occasional cases occur inEurope and North America. It is a considerable healthproblem in Asia, Africa, and Central and South America.
Transmission and epidemiology Rabies virus is inoculated in saliva by the bite of a rabidanimal, most often a dog, less often a cat. Lickingabraded or cut skin can transmit infection. Virus can penetratemucous membranes of the mouth and eyes. Endemiccanine rabies is the major determinant of risk for humaninfection.All mammals can become infected, but transmission tohumans is mainly related to biting animals, commonly straydogs in the tropics. Wolves, jackals, mongooses, bats (insectivorous,vampire and fruit eating), monkeys and ungulates(sheep, cattle and deer) can all become infected and posea greater or lesser degree of risk to humans. Apart frombats all species die of this infection. In Europe the red foxis the reservoir of infection. Vampire bats infect cattle inthe countries of South America, causing considerable economiclosses through cattle rabies. Human infection hasbeen acquired directly from vampire bats and followingexposure to aerosols containing virus excreted by bats inbat caves.
Pathology Virus first penetrates skeletal muscle cells and then entersnerves through the fibres supplying muscle spindles and travels centripetally to infect nerve cells. Virus replication occurs and then ruptures cells, releasing virions to infect other neurons. Neuropathological changes are not gross.Collections of inflammatory cells are seen around smallvessels; dead neurons and phagocytosis of degeneratingneurons are seen especially in the medulla and the midbrain.Viraemia is not thought to contribute to spread ofthe virus; rather, it occurs through centrifugal spread viafibres of the autonomic nervous system to cornea, skin andsalivary glands.
Clinical features The incubation period is 20-60 days on average, ranging upto 1 year. Initial symptoms are headache, fever, insomnia,anorexia and paraesthesiae or altered sensation at the siteof the bite or some peripheral site. After 2 or 3 days thepatient may become markedly agitated, hyperexcitable,anxious, confused and lucid by turns. The earliest hint ofhydrophobia may be evident at this stage, with rapid progressionto overt hydrophobia, with involuntary contractionof the main and accessory inspiratory muscles in asustained spasm brought on by attempts to drink water orat the sound, sight or mention of water. Variations of moodpersist. Saliva may be continuously spat out as it cannot beswallowed. The spasms can be provoked by fanning airacross the face. Cranial nerve palsies, paralysis and bizarrepatterns of breathing follow. Ascending paralysis withouthydrophobia occurs in a few patients, and this can poseproblems in diagnosis. Death occurs in 7-14 days fromrespiratory failure or cardiac arrhythmias.
Differential diagnosis Tetanus, other causes of ascending paralysis, and encephalitisand rabies hysteria are the main things to consider.
Laboratory diagnosis Virus may be grown from saliva, nasal washings, CSF andurine. Viral antigen can be identified in skin biopsies, preferablytaken from the hairy skin of the neck, where hair folliclescontain peripheral nerves, or less easily in cornealimpression smears using fluorescent antibody labellingtechniques. The sensitivity of this method for antemortemdiagnosis is not ideal. Corneal impression smears and skinbiopsies for antigen detection should be refrigerated immediatelyafter collection. In specialist centres PCR is availableusing reverse transcriptase PCR technology, and thismethod can detect virus in saliva. Blood and CSF shouldalso be tested for rabies antibodies, and in the unvaccinatedpatient a positive test supports the diagnosis.
Prevention, control and treatment Correct management at the time of biting prevents rabies.First aidThe wound should be washed under running water for5 minutes with soap or detergent. Where the wound iswashed with soap all traces of this must be washed away ifa quaternary ammonium compound is to be subsequentlyapplied, as soap inactivates cetrimide. Primary suture andscrubbing of the wound should be avoided if at all possible.Alcohol 40-70% or an aqueous solution of iodine or aquaternary ammonium compound with known lethal effecton rabies virus, such as 0.1% cetrimide solution, shouldthen be applied and the wound covered with a dressing.Tetanus prophylaxis should be given and antibiotics asindicated.The need for rabies vaccine must then be considered. Low risk: following licks of the skin, abrasions orscratches, minor bites on covered areas of arms, trunkand legs, start vaccine (schedules given below) if animalis rabid or suspected rabid. If the animal is rabid at thetime of exposure, or is wild or not available for observation,then vaccine plus rabies imimmoglobulin (RIG)should be started together. If the biting animal is a dogor cat and is healthy after 15 days of observation, thenfurther vaccination can be stopped.
High risk: following licks of the mucosa, major bites, i.e.multiple bites, or bites to the head, face, fingers or neckby a suspect or rabid domestic or wild animal, or by ananimal that is not available for observation, give vaccineplus rabies immunoglobulin. Again treatment can bestopped if the biting cat or dog is healthy at 15 days.Rabies vaccinationThe vaccine used now is human diploid cell vaccine(HDCV). For pre-exposure vaccination (e.g. prior to travel etc.)the recommended schedule is three doses of 1.0 mL ofHDCV given by deep subcutaneous or intramuscularinjection (deltoid region, not gluteal region) on days 0,7 and 28. For low-risk cases HDCV should be given; for those whohave not received full pre-exposure immunization givefive doses of 1.0 mL of vaccine intramuscularly, startingon the day of biting, day 0, and thereafter on days 3, 7,14 and 30. The vaccine is given by deep subcutaneous orintramuscular injection. If intramuscular, the injection isgiven into the lateral aspect of the thigh or the deltoidbut not the gluteal region. For those who have had fullpre-exposure vaccination, i.e. three doses of HDCV, twodoses of vaccine are given on days 0 and 3-7. When RIGis needed it is given as detailed below. For high-risk cases human RIG is given, 20iu/kg bodyweight, up to half infiltrated in and around the woundafter cleansing and half given intramuscularly. In someparts of the world human RIG will not be available andequine RIG will be used. As reactions to equineRIG are not uncommon a test dose should be given first.HDCV is given as five doses of 1.0mL of vaccine on days0, 3, 7, 14 and 30 to those with no or incomplete preexposurevaccination for rabies. For those with full preexposurevaccination two additional doses of 1.0 mL ofHDCV are given on days 0 and 3-7, RIG is not usuallyneeded.While patients with established rabies can be kept alive byintensive care, the fatal outcome is unaltered. Postmortemscarried out in patients managed in this way haveshown extensive destruction of nervous tissues. Practicalmanagement in an endemic area comprises sedation andpain relief. Close contacts of cases should be vaccinated.The problem of controlling reservoirs of infectionremains. The capturing and killing of stray dogs in endemicareas has reduced an important source of human rabies.Vaccination of household dogs and cats is a helpfulmeasure but does not exclude the possibility of the animalcontracting rabies. Good results have been obtained in thecontrol of fox rabies in Europe by putting down baits containingan oral antirabies vaccine. The incidence of rabiesin sentinel species has declined markedly.
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