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Chapter 41 : Rhabdoviruses

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Rhabdoviruses, Page 1 of 2

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Abstract:

Rabies is an acute encephalomyelitis of humans and animals caused by infection with rabies virus. Rabies virus is usually transmitted by an animal bite. Worldwide, dogs are the most important rabies vector, whereas in North America wild animals, especially bats, are the main threat to humans. After a delay at the site of entry, rabies virus spreads through the nervous system within axons by fast axonal transport. Rabies can be very effectively prevented after a recognized animal exposure with wound cleansing and administration of rabies vaccine and rabies immune globulin. Rabies typically develops after an incubation period of 20 to 90 days following the exposure. There are both encephalitic and paralytic forms of rabies and the disease is virtually always fatal after clinical onset. Hydrophobia is a characteristic clinical feature of encephalitic rabies. Progressive weakness involving the limbs and face occurs in paralytic rabies, which often begins close to the site of the wound. Pathological changes in rabies include the presence of eosinophilic inclusions called Negri bodies in the cytoplasm of neurons and inflammatory changes. Imaging studies may be normal and do not show specific abnormalities. A laboratory diagnosis can be made antemortem with the detection of rabies virus antigen or RNA in tissues (e.g., skin) and/or body fluids (e.g., saliva) and with serological testing. There have been rare survivors of rabies, but there is no known effective therapy.

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41
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Figures

Image of FIGURE 1
FIGURE 1

Schematic representation of the rabies virus particle. Viral proteins: N for nucleoprotein, P for phosphoprotein, M for matrix protein, G for glycoprotein, and L for large protein; their length in amino acids are indicated. The viral membrane is covered by the glycoprotein G, whereas M is located beneath the membrane. N is bound to the genomic RNA and together with P and L forms the ribonucleoprotein, which constitutes the active viral replication unit. (Reproduced with permission from Albertini AAV et al.: Rabies virus transcription and replication, in Research Advances in Rabies, Alan C. Jackson (ed), Advances in Virus Research 79:1–22, 2011. Copyright Elsevier.)

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41
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Image of FIGURE 2
FIGURE 2

Schematic diagram showing the sequential steps in the pathogenesis of rabies after an animal bite/peripheral inoculation of rabies virus. (Reproduced with permission from Jackson AC, Fu ZF: Pathogenesis, in Rabies: scientific basis of the disease and its management, Third Edition, edited by AC Jackson, 2013, Elsevier Academic Press, Oxford, UK, pp 299–349. Copyright Elsevier.)

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41
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Image of FIGURE 3
FIGURE 3

Three large Negri bodies in the cytoplasm of a cerebellar Purkinje cell from an 8-year-old boy who died of rabies after being bitten by a rabid dog in Mexico. (Reproduced with permission from AC Jackson, E Lopez-Corella, N Engl J Med 335:568, 1996. Copyright Massachusetts Medical Society.)

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41
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Image of FIGURE 4
FIGURE 4

Reported cases of rabies involving bats (A), raccoons (B), and skunks (C) by county, 2013. Adapted from JL Dyer et al., J Am Vet Med Assoc 245:1111–1123, 2014. (Centers for Disease Control and Prevention.)

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41
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Image of FIGURE 5
FIGURE 5

Distribution of the major rabies virus variants among wild terrestrial reservoirs in the United States and Puerto Rico, 2009 to 2013. * Potential host shift event. AZ = Arizona. CA = California. NC = North central. SC = South central. TX = Texas. Reproduced from JL Dyer et al., J Am Vet Med Assoc 245:1111–1123, 2014. (Centers for Disease Control and Prevention.)

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41
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Tables

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TABLE 1

Cases of human rabies associated with organ transplantation in the USA (19 ), Germany ( ), and Kuwait/Saudi Arabia (22a). (Adapted with permission from Jackson AC: Human disease, in Rabies: scientific basis of the disease and its management, Third Edition, edited by AC Jackson, 2013, Elsevier Academic Press, Oxford, UK, pp 269–298. Copyright Elsevier.)

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41
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TABLE 2

Cases of human rabies with treatment failures that used the main components of the “Milwaukee protocol.” (Updated from Jackson AC: Therapy in human rabies, in Research Advances in Rabies, Alan C. Jackson (ed), Advances in Virus Research 79:365 – 375, 2011. Copyright Elsevier.)

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41
Generic image for table
TABLE 3

Cases of human rabies with recovery. (Adapted from Jackson AC: Therapy of human rabies, in Rabies: scientific basis of the disease and its management, Third Edition, edited by AC Jackson, 2013, Elsevier Academic Press, Oxford, UK, pp 573–587. Copyright Elsevier).

Citation: Jackson A. 2017. Rhabdoviruses, p 967-979. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch41

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