Family Rhabdoviridae.

-ssRNA with helical capsid and bullet-shaped envelope.

Genus Lyssavirus.

Rabies.

Transmission: animal bite, direct contuct with saliva.

Reservoir: wild animals: fox, badger, raccoons, skunks, bats, coyotes, feral dogs.
Domestic dogs and cats.

Pathogenesis:
Bite-attachment to the acetylcholine receptors and retrograde travelling via neurone
into the spinal chord and up to the brain. Replication in the neurons of the CNS and
formation of the Negri bodies. Virus also travels to the salivary glands and insures
transmission.

Clinical presentation: after incubation period (12 days to 12 months) the wound gets
swollen, red and painful.
Flue-like symptoms.
Mood changes, depression and hallucinations.
Then neurological symptoms occur: hydrophobia, aerophobia, psycho-motor
aggravation.
Painful contractions of the larynx and pharynx. Hypersalivation.
Paralytic stage: flaccid peripheral paralysis and bulbar paralysis with 100% mortality.

Treatment: Immunoglobulin (HRIG) + killed rabies vaccine at day 0,3, 7,14, 28.

Family Filoviridae: Hemorrhagic Fevers.

Marburg virus. Ebola virus.

Transmission: close contact with body fluids, especially blood.
Natural reservoir is unknown. Wild animals, monkeys-main suspect.
Pathogenesis: severe haemorrhagic s-me due to increased vascular permeability.
Treatment: supportive.
D-s: Serological tests (ELISA).

Enveloped Segmented –ssRNA Viruses: Orthomyxoviridae, Bunyaviridae,

Arenaviridae.

Influenza: A, B, C.

A-people and animals.

B-people only.

C-insignificant.

Spanish flu H1N1.- 50 millions died 1918-1919.

Avian influenza: H5N1-potentially pandemic.
Swine flu:

Genome is segmented (8 RNA molecules).

Envelope surface GP: NA and HA.
Antigenic drift: HA or NA small mutations, within the same strain.. Cause epidemics.
Antigenic shift: emerging of the new strain of NA or HA. Occur in the host that is
infected with2 different strains. Results in a formation of the completely new strain,
causes pandemics.

Transmission: via respiratory route (aerosol droplets)

Pathogenesis:
HA-attachment to sialic acid receptors, fusion between virus and host cell (respiratory
epithelium).
NA-breaking the mucin barrier, exposing sialic acid binding sites.

Clinical presentation: fever, headache, mialgia, faryngotracheitis.

Mild, moderate and severe forms.
Severe form can result in toxic miocarditis, toxic shock and death.
Complications- secondary bacterial infections (pneumonia, sinusitis, otitis).

D-s: Virus isolation. For genetic and antigenic analysis.

Detection of viral proteins. Express-test.
Detection of viral RNA. (PCR)
Serological method: 4-fold increase in AB in 2 weeks.
Treatment:
Amantadine, rimantadine- prevent the uncoating of virus A.
Sanamavir, oseltamavir- inhibit NA.

Vaccine: inactivated, against few most probable strains.

Family bunyaviruses.
Segmented (3 segments), -ssRNA.
ARBO
Vector- mosquito.
Rift valley fever (vaccine developed).
California encephalitis
Hemorrhagic fevers.

Exception Hantaviruses: respiratory rout with dust particles.

Reservoir: mouse.
Hantavirus pulmonary syndrome

Treatment- not available.

D-s: ELISA.

Family Arenaviridae.
2 segments _RNA.
Haemorrhagic fevers (Lassa, Junin, Machupo).
Lymphocyticchoriomeningitis .

Hepatitis D.

Naked Segmented ds RNA

REOVIRIDAE

Rotaviruses
Transmission: fecal-oral.
Children 1-st year of life.
Gastroenteritis with severe dehydration.
Treatment- dehydration.
Vaccine: after 2005.

Coltiviruses. Colorado tick fever.

RBC infected. Self-limiting. ELISA