2. Properties
The family Rhabdoviridae consists of more than 100 viruses
These can infect a wide variety of hosts, including vertebrates,
invertebrates, and plants
Common to all members of the family is a distinctive rod- or
bullet-shaped morphology.
Human pathogens of medical importance are found in the
genera Lyssavirus and Vesiculovirus.
Only rabies virus, medically the most significant member of the
genus Lyssavirus
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3. Rabies virus
Structure
The rabies virus is a negative-sense, non-segmented, single-stranded
RNA virus
measuring approximately 60 nm x 180 nm.
It is composed of an internal protein core or nucleocapsid, containing the
nucleic acid,
an outer envelope, a lipid-containing bilayer covered with
transmembrane glycoprotein spikes
RNA (4%), protein (67%), lipid (26%), carbohydrate (3%)
Replication: cytoplasm; virions bud from plasma membrane
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4. Multiplication
virus attaches to the host cell membranes via the G protein
virus penetrates the cytoplasm by fusion or pinocytosis,
virus uncoated to RNP.
The core initial primary transcription of mRNAs by using the virion-
associated RNA-dependent RNA polymerase five mRNAs
Each RNA is then translated into an individual viral protein.
replication of the genomic RNA continues with the synthesis of,
positive stranded RNA, which acts as a template for the production of
progeny negative-stranded
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7. Pathogenesis
Rabies virus is most commonly transmitted through the bite of an infected
mammals
virus may enter the peripheral nervous system directly or from muscle tissue after
entering the host
remaining at or near the site of introduction for most of the incubation period
Multiplies in muscle or connective tissue at the site of inoculation
Enters peripheral nerves at neuromuscular junctions and spreads up the nerves to
the CNS
Multiplies in the brain
Spread through peripheral nerves to the salivary glands and other tissues
Highest titers of virus submaxillary salivary gland
Pancreas, kidney, heart, retina,
Has not been isolated from the blood of infected persons
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9. Susceptibility to infection and the incubation period
– host’s age
– genetic background, and immune status
– the viral strain involved
– the amount of inoculum
– the severity of lacerations
– the distance the virus has to travel from its point of entry to the CNS
higher attack rate and shorter incubation period in persons bitten on the face
or head
the lowest mortality occurs in those bitten on the leg
Produces a specific eosinophilic cytoplasmic inclusion, the Negri body, in
infected nerve cells
- pathognomonic of rabies but is not observed in at least 20% of cases
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10. Clinical findings
Five stages of rabies infection:
Incubation period
30 to 90 days, shorter in children and in individuals bitten close to
the central nervous system
Prodromal :Clinical symptoms are first noted
Neurologic period: begins with objective signs of central nervous
system dysfunction
Coma
Death (very rare recovery)
No specific anti -rabies agent is used once clinical sign or symptoms
developed
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11. Laboratory diagnosis
Negri bodies in the brain or the spinal cord
- sharply demarcated, more or less spherical, and 2-10m in diameter
- a distinctive internal structure with basophilic granules in an
eosinophilic matrix
- rabies virus antigens
IF
Real time PCR virus genome from fixed or unfixed brain tissue
Available tissue is inoculated intracerebrally into suckling mice
- encephalitis and death
- CNS of the inoculated animal
Negri bodies and rabies antigen
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12. Prevention
No successful treatment for clinical rabies
All vaccines for human use contain only inactivated rabies
virus
Live Attenuated Viruses
Human Diploid Cell Vaccine (HDCV)
Rabies Vaccine, Adsorbed (RVA)
Purified Chick Embryo Cell Vaccine (PCEC)
Nerve Tissue Vaccine
Duck Embryo Vaccine
Post exposure prophylaxis (IgG from hyper immunized humans)
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