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| __NOTOC__ | | __NOTOC__ |
| | {{About1|Rabies virus}} |
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| '''For patient information click [[Rabies(patient information)|here]]''' | | '''For patient information click [[Rabies(patient information)|here]]''' |
| {{Taxobox | color=violet | | {{Taxobox | color=violet |
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| }} | | }} |
| {{Rabies}} | | {{Rabies}} |
| {{CMG}}; {{MJM}} | | {{CMG}}; {{AE}} {{MIR}} {{IQ}} {{HK}} |
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| {{SK}} Rabies virus infection | | {{SK}} Rabies virus infection; Mad dog disease; Hydrophobia |
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| ==[[Rabies overview|Overview]]== | | ==[[Rabies overview|Overview]]== |
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| ==[[Rabies causes|Causes]]== | | ==[[Rabies causes|Causes]]== |
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| ===Cause===
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| [[File:Rabies Virus EM PHIL 1876.JPG|thumb|[[Transmission electron microscopy|TEM]] [[micrograph]] with numerous rabies [[virion]]s (small, dark grey, rodlike particles) and [[Negri bodies]] (the larger [[pathognomonic]] cellular inclusions of rabies infection)]]
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| Rabies is caused by a number of ''[[lyssavirus]]es'' including: [[rabies virus]] and [[Australian bat lyssavirus]].<ref>{{cite web|title=Rabies, Australian bat lyssavirus and other lyssaviruses|url=http://www.health.gov.au/internet/main/publishing.nsf/Content/ohp-rabies-consumer-info.htm|work=The Department of Health|accessdate=1 March 2014|date=Dec 2013}}</ref>
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| The rabies virus is the [[type species]] of the Lyssavirus [[genus]], in the family'' [[Rhabdoviridae]]'', order ''[[Mononegavirales]]''. Lyssaviruses have helical symmetry, with a length of about 180 [[nanometre|nm]] and a cross-section of about 75 nm.<ref name=Sherris>{{cite book | author = Drew WL | chapter= Chapter 41: Rabies | editors = Ryan KJ, Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th | pages=597–600 | publisher = McGraw Hill | year = 2004 | isbn = 0-8385-8529-9 }}</ref> These viruses are [[Viral envelope|enveloped]] and have a single-stranded [[RNA]] genome with [[negative-sense#Negative-sense|negative sense]]. The genetic information is packed as a [[ribonucleoprotein]] complex in which RNA is tightly bound by the viral nucleoprotein. The [[RNA genome]] of the virus encodes five genes whose order is highly conserved: nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G), and the viral RNA polymerase (L).<ref name="pmid15885837">{{cite journal | author = Finke S, Conzelmann KK | title = Replication strategies of rabies virus | journal = Virus Res. | volume = 111 | issue = 2 | pages = 120–31 | date = August 2005 | pmid = 15885837 | doi = 10.1016/j.virusres.2005.04.004 | url = }}</ref>
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| Once within a muscle or nerve cell, the virus undergoes replication. The trimeric spikes on the exterior of the membrane of the virus interact with a specific cell receptor, the most likely one being the [[acetylcholine]] receptor, [[acetyl]]. The cellular membrane pinches in a procession known as [[pinocytosis]] and allows entry of the virus into the cell by way of an [[endosome]]. The virus then uses the acidic environment, which is necessary, of that endosome and binds to its membrane simultaneously, releasing its five proteins and single strand RNA into the cytoplasm.<ref name=CDC_Rabies_PEP />
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| The L protein then transcribes five mRNA strands and a positive strand of RNA all from the original negative strand RNA using free nucleotides in the cytoplasm. These five mRNA strands are then translated into their corresponding proteins (P, L, N, G and M proteins) at free ribosomes in the cytoplasm. Some proteins require post-translative modifications. For example, the G protein travels through the rough [[endoplasmic reticulum]], where it undergoes further folding, and is then transported to the [[Golgi apparatus]], where a sugar group is added to it ([[glycosylation]]).<ref name=CDC_Rabies_PEP />
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| Where there are enough proteins, the viral polymerase will begin to synthesize new negative strands of RNA from the template of the positive strand RNA. These negative strands will then form complexes with the N, P, L and M proteins and then travel to the inner membrane of the cell, where a G protein has embedded itself in the membrane. The G protein then coils around the N-P-L-M complex of proteins taking some of the host cell membrane with it, which will form the new outer envelope of the virus particle. The virus then buds from the cell.<ref name=CDC_Rabies_PEP />
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| From the point of entry, the virus is [[neurotropic virus|neurotropic]], traveling quickly along the neural pathways into the [[central nervous system]]. The virus usually first infects muscle cells close to the site of infection, where they are able to replicate without being 'noticed' by the host's immune system. Once enough virus has been replicated, they begin to bind to acetyl choline receptors (p75NR) at the neuromuscular junction. <ref>http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1004348</ref> The virus then travels through the nerve cell axon via retrograde transport, as its P protein interacts with dynein, a protein present in the cytoplasm of nerve cells. Once the virus reaches the cell body it travels rapidly to the Central Nervous System (CNS), replicating in motor neurons and eventually reaching to the brain. <ref name=Robbins/> After the brain is infected, the virus travels centrifugally to the peripheral and autonomic nervous systems, eventually migrating to the salivary glands, where it is ready to be transmitted to the next host.
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| ===Transmission===
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| All warm-blooded species, including humans, may become infected with the rabies virus and develop symptoms. [[Bird]]s were first artificially infected with rabies in 1884; however, infected birds are largely if not wholly asymptomatic, and recover.<ref name=serological>{{cite journal |author=Shannon LM, Poulton JL, Emmons RW, Woodie JD, Fowler ME |title=Serological survey for rabies antibodies in raptors from California |journal=J. Wildl. Dis. |volume=24 |issue=2 |pages=264–7 |date=April 1988 |pmid=3286906 |doi=10.7589/0090-3558-24.2.264 |url=http://www.jwildlifedis.org/doi/abs/10.7589/0090-3558-24.2.264}}</ref> Other bird species have been known to develop rabies [[antibody|antibodies]], a sign of infection, after feeding on rabies-infected mammals.<ref name="pmid16498885">{{cite journal | author = Gough PM, Jorgenson RD | title = Rabies antibodies in sera of wild birds | journal = Journal of Wildlife Diseases | volume = 12 | issue = 3 | pages = 392–5 | year = 1976 | pmid = 16498885 | doi = 10.7589/0090-3558-12.3.392| url =http://www.jwildlifedis.org/doi/abs/10.7589/0090-3558-12.3.392}}</ref><ref name=Owls>{{cite journal |author=Jorgenson RD, Gough PM |title=Experimental rabies in a great horned owl |journal=J. Wildl. Dis. |volume=12 |issue=3 |pages=444–7 |date=July 1976 |doi=10.7589/0090-3558-12.3.444 |url=http://www.jwildlifedis.org/doi/abs/10.7589/0090-3558-12.3.444}}</ref>
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| The virus has also been adapted to grow in cells of [[poikilotherm]]ic ("cold-blooded") vertebrates.<ref>{{cite web|url=http://virology-online.com/viruses/Rhabdoviruses.htm| title=Rabies |last=Wong|first=Derek |publisher=Wong's Virology|accessdate=19 Mar 2009}}</ref><ref>{{cite book|title=Developments in Veterinary Virology: Rabies|last=Campbell |first=James B. |last2=Charlton |first2=K.M.|publisher=Springer|year=1988|page=48|isbn=0-89838-390-0}}</ref> Most animals can be infected by the virus and can transmit the disease to humans. Infected [[bat]]s,<ref name="pmid13858519">{{cite journal | author = Pawan JL | title = The transmission of paralytic rabies in Trinidad by the vampire bat (''Desmodus rotundus murinus'' Wagner | journal = Caribbean Medical Journal | volume = 21 | pages = 110–36 | year = 1959 | pmid = 13858519 | doi = }}</ref><ref name="pmid14431118">{{cite journal | author = Pawan JL | title = Rabies in the vampire bat of Trinidad, with special reference to the clinical course and the latency of infection | journal = Caribbean Medical Journal | volume = 21 | pages = 137–56 | year = 1959 | pmid = 14431118 | doi = }}</ref> [[monkey]]s, [[raccoon]]s, [[fox]]es, [[skunk]]s, [[cattle]], [[wolf|wolves]], [[coyotes]], [[dog]]s, [[mongoose]]s (normally yellow mongoose)<ref>{{cite journal | author = Taylor PJ | title = A systematic and population genetic approach to the rabies problem in the yellow mongoose (Cynictis penicillata) | journal = The Onderstepoort Journal of Veterinary Research | volume = 60 | issue = 4 | pages = 379–87 | date = December 1993 | pmid = 7777324 }}</ref> and [[cat]]s present the greatest risk to humans.
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| Rabies may also spread through exposure to infected [[livestock|domestic farm animals]], [[groundhog]]s, [[weasel]]s, [[bear]]s, and other [[Carnivora|wild carnivorans]]. Small [[rodent]]s, such as [[squirrel]]s, [[hamster]]s, [[guinea pig]]s, [[gerbil]]s, [[chipmunk]]s, [[rat]]s, and [[mice]], and [[lagomorphs]] such as [[rabbit]]s and [[hare]]s, are almost never found to be infected with rabies and are not known to transmit rabies to humans.<ref>{{cite web | url=http://www.cdc.gov/rabies/exposure/animals/other.html | title=Rabies. Other Wild Animals: Terrestrial carnivores: raccoons, skunks and foxes. | accessdate=2010-12-23 | publisher=[[Centers for Disease Control and Prevention]](CDC) }}</ref> The [[Virginia opossum]] is resistant but not immune to rabies.<ref>{{cite journal | author = McRuer DL, Jones KD | title = Behavioral and nutritional aspects of the Virginian opossum (Didelphis virginiana) | journal = The veterinary clinics of North America. Exotic animal practice | volume = 12 | issue = 2 | pages = 217–36, viii | date = May 2009 | pmid = 19341950 | doi = 10.1016/j.cvex.2009.01.007 }}</ref>
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| The virus is usually present in the nerves and [[saliva]] of a symptomatic rabid animal.<ref>''The Merck Manual'', 11th Edition (1983), p. 183</ref><ref>''The Merck manual of Medical Information. Second Home Edition'', (2003), p. 484.</ref> The route of [[infection]] is usually, but not always, by a bite. In many cases, the infected animal is exceptionally aggressive, may attack without provocation, and exhibits otherwise uncharacteristic behavior.<ref>{{cite web | last = Turton | first = Jenny | title = Rabies: a killer disease | publisher = National Department of Agriculture | year = 2000 |url = http://www.nda.agric.za/docs/rabies/rabies.htm}}</ref> This is an example of a viral pathogen [[Behavior-altering parasites and parasitoids|modifying the behavior of its host]] to facilitate its transmission to other hosts.
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| Transmission between humans is extremely rare. A few cases have been recorded through [[organ transplant|transplant surgery]].<ref>{{cite journal | author = Srinivasan A, Burton EC, Kuehnert MJ, Rupprecht C, Sutker WL, Ksiazek TG, Paddock CD, Guarner J, Shieh WJ, Goldsmith C, Hanlon CA, Zoretic J, Fischbach B, Niezgoda M, El-Feky WH, Orciari L, Sanchez EQ, Likos A, Klintmalm GB, Cardo D, LeDuc J, Chamberland ME, Jernigan DB, Zaki SR | title = Transmission of rabies virus from an organ donor to four transplant recipients | journal = [[New England Journal of Medicine|N Engl J Med]] | volume = 352 | issue = 11 | pages = 1103–11 | date = March 2005 | pmid = 15784663 | doi = 10.1056/NEJMoa043018 | url = http://www.nejm.org/doi/pdf/10.1056/NEJMoa043018 | format = PDF }}</ref> After a typical human infection by bite, the virus enters the [[peripheral nervous system]]. It then travels along the [[Afferent nerve fiber|afferent nerve]]s toward the [[central nervous system]].<ref>{{cite book |author=Jackson, Alan C., Wunner, William H.|title=Rabies|url=http://books.google.com/books?id=p8rMezRaD4oC&pg=PA290 |year=2002|publisher=Academic Press|isbn=978-0-12-379077-4|page=290}}</ref> During this phase, the virus cannot be easily detected within the host, and vaccination may still confer cell-mediated immunity to prevent symptomatic rabies. When the virus reaches the [[brain]], it rapidly causes [[encephalitis]], the prodromal phase, and is the beginning of the symptoms. Once the patient becomes symptomatic, treatment is almost never effective and mortality is over 99%. Rabies may also inflame the [[spinal cord]], producing transverse [[myelitis]].<ref>Joanne Lynn, M.D. (October 1997) [http://www.myelitis.org/tm.htm ''Transverse Myelitis: Symptoms, Causes and Diagnosis''] The Transverse Myelitis Association</ref><ref>{{cite book|author1=Larry Ernest Davis|author2=Molly K. King|author3=Jessica L. Schultz|title=Fundamentals of neurologic disease|url=http://books.google.com/books?id=moRp2jWZp0QC&pg=PA73 |date=15 June 2005|publisher=Demos Medical Publishing|isbn=978-1-888799-84-2|page=73}}</ref>
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| ==[[Rabies differential diagnosis|Differentiating Rabies from other Diseases]]== | | ==[[Rabies differential diagnosis|Differentiating Rabies from other Diseases]]== |
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| ==Diagnosis== | | ==Diagnosis== |
| [[Rabies history and symptoms|History and Symptoms]] | [[Rabies physical examination|Physical Examination]] | [[Rabies laboratory tests|Laboratory Findings]] | [[Rabies CT|CT]] | [[Rabies other diagnostic studies|Other Diagnostic Studies]] | | [[Rabies history and symptoms|History and Symptoms]] | [[Rabies physical examination|Physical Examination]] | [[Rabies laboratory tests|Laboratory Findings]] | [[Rabies x ray|Chest X-ray]] | [[Rabies CT|CT]] || [[Rabies MRI|MRI]] | [[Rabies other diagnostic studies|Other Diagnostic Studies]] | [[Rabies other imaging findings|Other Imaging Findings]] |
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| ==Treatment== | | ==Treatment== |
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| {{Viral diseases}} | | {{Viral diseases}} |
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