Micro 9 Ex 2

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Rhabdoviridae genome

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Enveloped with large peplomers
Helical cylindrical nucleocapsid-giving the virus the
bullet (conical) shape
Non segmented single-stranded negative-sense RNA

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only significant human pathogen among rhabdoviruses

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Lyssavirus
includes rabies and rabies-like viruses

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rhabdovirus (Lyssavirus) virion characteristics

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Single envelope glycoprotein, called G; trimers of G form spikes covering virion; viral attachment protein; elicits neutralizing antibodies
Rhabdovirus replicates in cytoplasm

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Rabies is usually transmitted in

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saliva and is acquired from the bite of a rabid animal.
Rabies virus is not very cytolytic and seems to remain cell-associated

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Where does the rabies virus replicate?

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replicates in the muscle at the site of the bite, with minimal or no symptoms (incubation phase).

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The length of the incubation phase is determined by

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by the infectious dose and the proximity of the infection site to the central nervous system and brain

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What is the rabies prodrome phase

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After weeks to months, the virus infects the peripheral nerves and travels up the CNS to the brain

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What is the neurologic phase of rabies?

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Infection of the brain causes classic symptoms, coma, and death

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During the neurologic phase, the virus spreads to

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the glands, skin, and other body parts, including the salivary glands, from where it is transmitted

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Rabies infection does not elicit an antibody response until

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the late stages of the disease, when the virus has spread from the CNS to other sites.
Antibody can block the progression of the virus.

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The long incubation period of rabies allows

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active immunization as a postexposure treatment.

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fever, nausea, vomiting, loss of appetite, headache, lethargy, pain at site of bite, describe which phase of rabies?

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Prodrome Phase

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hydrophobia, pharyngeal spasms, hyperactivity, anxiety, depression, describe which phase of rabies

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Neurologic Phase. CNS symptoms: loss of coordination, paralysis, confusion, delirium
virus in brain and other sites (high titre)
detectable antibody in serum and CNS

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Patients with rabies may die due to

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coma: cardiac arrest, hypotension, hypoventilation, secondary infections
virus in brain and other sites (high titre)

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Postexposure prophylaxis is possible because of long incubation phase.

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-initiated for anyone exposed by bite, or contamination of open wound or mucous membrane to saliva or brain tissue of an animal suspected of rabies infection; unless animal is tested and shown to be negative for the virus.
-Wound should be washed with soap and water (inactivates free virus); also recommended to instill antirabies serum around the wound.
- Passive immunization with either equine antirabies serum or human rabies immune globulin (HRIG) in combination with vaccination with killed-virus recommended

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Antigen detection via

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immunofluorescence or presence of Negri bodies in brain tissue commonly used tests.

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Vaccine given in series of five shots (IM); produced in

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human diploid cells or rhesus fetal lung cells; given 0, 3, 7, 14, 28 days after exposure.

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Preexposure vaccination of at risk individuals (about 2 yr protection).

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Animal workers and laboratory workers who handle potentially infected tissues and animals.
Those traveling to endemic areas.

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Domestic pets were the ones causing rabbies, until vaccination was mandatory the incidence went down. Now the wild animals are the problem. The major carriers are

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Skunk and racoon are the major carriers of rabbies

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Rabies Virus transmission

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Zoonosis:
Reservoir: wild animals
Vector: wild animals and unvaccinated dogs and cats
Source of virus:
major: saliva in bite of rabid animal
minor: aerosols in bat caves containing rabid bats

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Rabies Virus Geography/Season

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Virus is found worldwide, except in some island nations: no seasonal incidence

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Rabies Virus Modes of Control

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Vaccination program for pets; vaccination available for at-risk personnel; vaccination programs implemented to control rabies in forest animals

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Togavirus and Flavivirus genome

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Enveloped virus containing a single-stranded RNA genome; positive sense genome

Viruses replicate in the cytoplasm except for rubella

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Alphavirus (Arboviruses) and Rubivirus
(Rubella virus) bud at

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plasma membrane
-replication includes early (nonstructural) and late (structural) protein synthesis

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Flavivirus bud at

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internal membranes

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Alpha and Flaviviruses have a very broad host range

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Infect vertebrates and invertebrates

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the flu-like symptoms of infection of Togavirus and Flavivirus can be accounted for by

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inducing of interferon

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Flaviviruses can infect cells of the

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the monocyte-macrophage lineage

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Non-neutralizing antibody can enhance flavivirus infection via

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receptors on the macrophage.

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Togaviruses and Flaviviruses Viruses are associated with

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mild-systemic disease, encephalitis, arthrogenic disease, or hemorrhagic disease.

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Female mosquitoes acquire Alphaviruses and Flaviviruses by

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taking a blood meal from a viremic host.
Infects epithelial cells in midgut of mosquito and spreads to salivary glands.
There it sets up a persistent infection.

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Yellow fever

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characterized by severe systemic disease, with degeneration of the liver, kidney, and heart as well as hemorrhage. Liver involvement causes jaundice (hence the disease name). Massive gastrointestinal hemorrhage results in a “black vomit”. Mortality rate associated with yellow fever epidemics can be as high as 50%.

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Symptoms of high fever, headache, rash, and back and bone pain; also known as break bone fever.

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dengue hemorrhagic fevef (DHF)

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On rechallenge with one of four related strains, dengue can also cause

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dengue shock syndrome (DSS). Caused by production of non-neutralizing Abs, which promote uptake of virus into macrophages. Activated T-cells initiate hypersensitivity reactions, and weakening and rupture of the vasculature. Internal bleeding and loss of plasma lead to shock.

In 1981 in Cuba, dengue-2 virus infected a population previously exposed to dengue-1 virus causing an epidemic of DHF/DSS.

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Togavirus/Flavivirus must stay wet and can be inactivated by

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drying, soap, and detergents.
Virus can infect mammals, birds, reptiles, and arthropods.
Asymptomatic or nonspecific (flu-like fever or chills), encephalitis, hemorrhagic fever, or arthritis.

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Transmission
Togaviruses and flaviviruses

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specific arthropod vector characteristic for each virus (zoonosis; arbovirus).

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Who is at Risk togaviruses and flaviviruses?

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People in the ecological niche of the arthropod vector

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Geographic Distribution/Season Togaviruses and flaviviruses

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Endemic regions for each arbovirus are determined by habitat of arthropod vector.
More common in summer

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Modes of Control togaviruses and flaviviruses

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No treatment for disease other than supportive care.
Vector control: eliminate mosquito breeding grounds
Live attenuated vaccines for yellow fever. Killed vaccines for Japanese encephalitis virus, EEE, WEE, Russian spring-summer encephalitis viruses are available.

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Rubella virus has the same structural properties and mode of replication as

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as the other Togaviruses.
Unlike other Togaviruses, Rubella virus is a respiratory virus and only infects humans.

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Rubella Virus infection of fetus

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can cause severe congenital defects.

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Rubella virus infects the upper respiratory tract and then spreads to the

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local lymph nodes, which coincides with a period of lymphadenopathy.

Establishment of viremia spreads the virus throughout the body.

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Rubella in children

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Rash last for about 3 days in children; maculopapular or macular. Accompanied by swollen glands

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Infection in adults can

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be more severe and include bone and joint pain (arthralgia and arthritis), thrombocytopenia and postinfectious encephalitis (rare outcomes).
Immunopathologic effects contribute to severe forms of rubella in adults.

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Maternal antibody to rubella prevents

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the spread of virus to the fetus.
Natural infection results in lifelong immunity

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Prominent Clinical Findings in Congenital Rubella Syndrome

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Cataracts and other ocular defects
Heart defects
Deafness
Intrauterine growth retardation
Failure to thrive
Mortality within the first year
Microcephaly
Mental retardation

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Rubella Virus Modes of Control

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Live attenuated vaccine is administered as part of measles, mumps, and rubella (MMR) vaccine