RABIES. Zeliha Koçak Tufan, MD, Assoc. Prof. Yildirim Beyazit University Infectious Diseases & Clinical Microbiology Department

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1 RABIES Zeliha Koçak Tufan, MD, Assoc. Prof. Yildirim Beyazit University Infectious Diseases & Clinical Microbiology Department

2 Please focus on the pathogenesis and prophylaxis plus wound care!!

3 What is Rabies? Rabies is an acute viral disease of the central nervous system that is transmitted to humans by infected animals. After a prodromal phase, rabies manifests most often as encephalitis or less frequently as a paralytic form of the disease and then progresses to coma and death Harrison s Infect Dis

contain a single-strand, nonsegmented, negative-sense

4 The virus Rabies virus--neurotropic viruse-- Rhabdoviridae Family, Genus Lyssavirus Enveloped virions contain a single-strand, nonsegmented, negative-sense RNA Lyssaviruses have a predilection for nerves, along which they spread

5 Rhabdos, mean rodlike CDC

6 EPIDEMIOLOGY Almost all cases of rabies are transmitted from rabid animals through a bite. In developing countries, dogs account for 90 percent or more of reported cases transmitted to humans, whereas bats account for most rabies cases in the United States.

7 Almost all rabies infections of domestic animals are result of spillover from wildlife reservoirs Bats, raccoons, skunks, and foxes

8 Rare cases: -Non-bite exposure----aerosolized virus -Via transplantation of tissue from a donor with unrecognized rabies (Transplanted corneal tissue has been the source of eight cases of human rabies; In 2004, three deaths resulted from transplantation of solid organs and another death from transplantation of a vascular conduit from a donor who was initially thought to have died from an intracranial hemorrhage but was retrospectively diagnosed with rabies)

First rabies vaccine ------1885, Coordinated vaccination and surveillance programs have essentially eliminated the

9 First rabies vaccine , Coordinated vaccination and surveillance programs have essentially eliminated the rabies reservoir in dogs in North America and Europe Wildlife species?? 30,000-70,000 people die worldwide of rabies each year

10 PATHOGENESIS Virions are first amplified near the site of inoculation and subsequently enter local motor and sensory nerves Viruses then migrate centrally in a retrograde direction within the axoplasm of peripheral nerves until reaching the spinal cord and brain ( mm/day) NEURONAL DYSFUNCTION!

11 After CNS infection is established, there is centrifugal spread along peripheral nerves to other tissues, including the salivary glands, liver, muscle, skin, adrenal glands, and heart. Rabies virus replication in acinar cells of the salivary glands results in viral excretion in the saliva of rabid animals.

12 The virus is known to bind to nicotinic acetylcholine receptors Experimental evidence also supports a role for the neural cell adhesion molecule and the p75ntr neurotrophin receptor as receptors for rabies virus.

nucleocapsids embedded in an amorphous substance or matrix.

13 The most characteristic pathologic finding in rabies is the Negri body! Eosinophilic cytoplasmic inclusions in brain neurons and are composed of randomly oriented rabies virus nucleocapsids embedded in an amorphous substance or matrix. These inclusions occur in a minority of infected cells, are most commonly present in Purkinje cells of the cerebellum and in pyramidal cells in the hippocampus, and are less frequently seen in cortical neurons and in the brainstem

14 Factors that may affect host susceptibility to infection include The size of the inoculum, Proximity of the bite to the central nervous system, Host genetic variations.

15 Clinical Findings Three general phases: Prodrome, Acute neurologic phase, Coma/death

16 The average incubation period is one to three months The prodrome consists of nonspecific flu-like symptoms including malaise, anorexia, irritability, low grade fever, sore throat, headache, nausea, and vomiting.

17 There may also be specific neurologic signs and symptoms at the site of virus entry that are suggestive of rabies infection, including paresthesias, pain and pruritus.

18 An acute neurologic syndrome of either encephalitic or paralytic rabies follows the prodrome and typically lasts for two to seven days. Encephalitic rabies (80%) hyperactivity, persistent fever, fluctuating consciousness, painful pharyngeal or inspiratory spasms, autonomic stimulation (hypersalivation), hydrophobia and seizures Paralytic rabies (20%) is characterized by quadriparesis and sphincter involvement.

19 6YGB hyperexcitability

20 Hydrophobia: involuntary, painful contraction of the diaphragm and accessory respiratory, laryngeal, and pharyngeal muscles in response to swallowing liquids or a draft of air (aerophobia).

21 Atypical rabies, which is less common than either classic form, has been most often described in patients with batassociated rabies. Neuropathic pain, Choreiform movements of the bitten limb during the prodromal phase, Focal brainstem signs, Cranial nerve palsies, Myoclonus, Seizures

22 DIAGNOSIS History- suspicion-clinical findings The clinical diagnosis of rabies is straightforward in developing countries when a nonimmunized patient presents after a bite by a known rabid animal. In developed countries, many patients have an unrecognized exposure (eg, to a bat).

23 Before death, the diagnosis of rabies can be made by virus-specific immunofluorescent staining of skin biopsy specimens, isolation of virus from the saliva, or detection of antirabies antibodies in serum or cerebrospinal fluid.

24 Since the sensitivity of any single diagnostic test for rabies is limited Antemortem diagnosis of rabies requires several specimens of saliva, skin, serum, and cerebrospinal fluid and multiple testing modalities, depending on the specimen type.

27 Differential diagnosis : The main diagnostic possibilities to consider in a patient with encephalitis rabies include West Nile virus and herpes simplex virus infections. In a patient with paralytic rabies, the main differential diagnoses include Guillain-Barré syndrome, transverse myelitis, and polio.

postexposure prophylaxis Unprovoked attacks are more

29 PROPHYLAXIS Rabies is an invariably fatal viral disease that can be prevented with proper wound care and postexposure prophylaxis Unprovoked attacks are more likely by animals that have rabies than animals without rabies.

30 The decision to initiate rabies postexposure prophylaxis depends on many factors, including the type of exposure and whether the animal can be observed or tested for rabies. The guidelines for rabies postexposure prophylaxis differ depending upon the species of animal involved and the country in which the exposure occurred.

31 No transmission of rabies has been documented from rabies-infected patients to healthcare providers or household contacts or by fomites or environmental surfaces.

32 Preexposure prophylaxis should be targeted to persons in high-risk groups, including veterinarians, laboratory workers and international travelers.

34 Rabies postexposure prophylaxis In areas without an endemic, terrestrial strain of rabies (eg, dog, raccoon, skunk, fox, mongoose) local public health authorities --- risk assessment

37 Wound care One of the most important initial steps to prevent rabies is wound care. Thorough washing of bite wounds, scratches, and non-bite exposures with soap and water is recommended, if feasible. When available, a virucidal agent such as povidone-iodine should also be used. In animal studies of rabies, wound cleansing alone reduced the likelihood of rabies up to 90 percent

38 All previously unvaccinated persons should be passively immunized with rabies immune globulin (RIG). If RIG is not immediately available, it should be administered no later than 7 days after the first vaccine dose. After day 7, endogenous antibodies are being produced, and passive immunization may actually be counterproductive. If anatomically feasible, the entire dose of RIG (20 IU/kg) should be infused at the site of the bite; otherwise, any RIG remaining after infiltration of the bite site should be administered IM at a distant site. With multiple or large wounds, the RIG preparation may need to be diluted in order to obtain a sufficient volume for adequate infiltration of all wound sites. If the exposure involves a mucous membrane, the entire dose should be administered IM. Rabies vaccine and RIG should never be administered at the same site or with the same syringe.

39 Active immunization-vaccine -Human diploid cell vaccine (HDCV, Imovax Rabies, Sanofi Pasteur) -Purified chick embryo cell vaccine (PCECV, RabAvert, Novartis Vaccine and Diagnostics) The CDC guidelines for vaccine administration for postexposure prophylaxis in unvaccinated persons exposed to rabies changed in 2010, from a five-dose schedule of vaccine (given intramuscularly) starting immediately (day 0) after exposure and on days 3, 7, 14, and 28 after the first dose to a four-dose schedule eliminating the day 28 dose of the series The WHO guidelines still recommend a five-dose schedule for intramuscular rabies immunization for category 2 or 3 exposures, but now cite the four-dose intramuscular schedule (days 0, 3, 7 and 14) as an alternative for exposed people who receive wound care plus high-quality RIG plus rabies vaccine

40 cdc.gov Uptodate.com Harrison s Infec Dis

RABIES Pr P ese e n se t n er e : J. J. K a K m a bo b n o a n a (M.B. B Ch C. h B; B M.Med e ) d

RABIES Pr P ese e n se t n er e : J. J. K a K m a bo b n o a n a (M.B. B Ch C. h B; B M.Med e ) d RABIES Presenter: J.J. Kambona (M.B.Ch.B; M.Med) OBJECTIVES At the end of this session each student will be able to: 1. Define rabies. 2. Describe the epidemiology of rabies. 3. Describe the cause of rabies.