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PRESENTED BY: HADIA RASHID
BIOMEDICAL SCIENCES
B22F0148BMS033
RABIES VIRUS
TABLE OF CONTENT
HISTORICAL BACKGROUND
EPIDEMIOLOGY
SPECIFICATIONS
TAXONOMY
RABIES VIRION
ROUTE OF TRANSMISSION
REPLICATION STRATEGY
PATHOGENESIS
SYMPTOMS
DIAGNOSIS
PREVENTION AND TREATMENT
VISUAL DEMONSTRATION
HISTORICAL
BACKGROUNG
 Rabies virus was first isolated by scientists
Paul Remlinger and Adelchi Negri. Negri
bodies, characteristic intracellular inclusions,
were identified as indicators of rabies
infection.
 Louis Pasteur successfully developed the first
rabies vaccine in 1885.
 The first recorded outbreaks of rabies
occurred in Europe.
EPIDEMIOLOGY
 It causes tens of thousands of deaths every
year, mainly in Asia and Africa.
 Victims are mostly children under 15 years
of age.
 In Pakistan, 97,000 dog-bites cases were
reported(2016) causing rabies, especially in
rural areas of Sindh, with three cities
accounting for 85% of the total reported
cases: Karachi, Peshawar, and Hyderabad.
SPECIFICATIONS
NEUROTROPIC
VIRUS
BULLET SHAPED
75 nm Diameter
BALTIMORE GROUP
V
12 kbp GENOME
SIZE
ENVELOPED VIRUS
BIOSAFETY LEVEL 2
TAXONOMY
FAMILY: RHABDOVIRIDAE
SPECIE: RABIES VIRUS
GENUS: LYSSAVIRUS
RABIES VIRION
Envelope: Present. Virus envelope contains glycosylated G-protein
spikes embedded in a lipid membrane derived from the host cell.
Matrix (M) protein: The membrane or matrix (M) protein layer lies
beneath the envelope. Virus nucleoprotein (N) which tightly binds the
viral RNA to form the nucleocapsid core lies inside to matrix protein.
Viral genome: The core of the virion consists of helical unsegmented,
ss (-) sense RNA and an RNA-dependent RNA polymerase.
 It is a simple virus with genome encoding for only 5 proteins.
RABIES VIRION
GENOME
PROTEINS
Route of transmission
Bites of rabid
animal most
common
Usually lab workers
and researchers
Non bite exposureof
saliva with mucous
surfaces such as eyes
,nose and open
wounds
In very cases during
diagnosis and research
coming in contact with
infected aerosols
Rabies transmission
through corneal and solid
organ transplants have
been recorded,very rare.
PATHOGENESIS
PATHOGENESIS
Zoonotic disease: Rabies
INCUBATION
PRODROME
ACUTE NEUROLOGIC PERIOD
COMA
DEATH
Few days to several years
2 to 4 days
2 to 10 days
 Muscles become paralyzed
 Respiratoryfailure
 Weakness
 Paralysis
 Loss of coordination
 Coma
SYMPTOMS
 Fever
 Headache
 Malaise
 Fatigue
 Pain, itching, or tingling at
the site of the original
wound (where the virus
entered the body)
 Restlessness
 Agitation
 Aggression
 Hallucinations
 Hydrophobia
 Hypersalivation
(excessive salivation)
PRODROMALPHASE FURIOUS PHASE PARALYTIC PHASE
DIAGNOSIS
SPECIMENS
 Saliva
 Blood samples
 Spinal fluid
 Nervous tissue biopsy
 Skin samples
TECHNIQUES
 Clinical observations
 PCR
 FAT(fluorescence antibody test)
 Virus isolationby culturing it in mice
PREVENTION
Pre-exposure prophylaxis with rabies
vaccine is recommended.
 Minimize contact with potentially rabid animals.
 Do not approach or handle wild or stray animals.
 Vaccinate pets and livestock againstrabies.
TREATMENT
 Post-exposure prophylaxis (PEP) is the emergency
response to a rabies exposure. This prevents the virus from
entering the central nervous system, which would
invariablyresult in death.
PEP consists of:
 extensive washing of wound with water and soap for at least
15 minutes
 a course of potent and effective rabies vaccine that meets
WHO standards (Active immunity)
 the administrationof rabies immunoglobulin(RIG) or
monoclonal antibodies into the wound (Passiveimmunity)
 Supportive care is provided to manage symptoms,
especially during the later stages of the disease
SUMMARY
QUOTE OF THE DAY
LYSSA VIRUS(RABIES) :Deadly neurotropic virus.pptx

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LYSSA VIRUS(RABIES) :Deadly neurotropic virus.pptx

  • 1. PRESENTED BY: HADIA RASHID BIOMEDICAL SCIENCES B22F0148BMS033 RABIES VIRUS
  • 2. TABLE OF CONTENT HISTORICAL BACKGROUND EPIDEMIOLOGY SPECIFICATIONS TAXONOMY RABIES VIRION ROUTE OF TRANSMISSION REPLICATION STRATEGY PATHOGENESIS SYMPTOMS DIAGNOSIS PREVENTION AND TREATMENT VISUAL DEMONSTRATION
  • 3. HISTORICAL BACKGROUNG  Rabies virus was first isolated by scientists Paul Remlinger and Adelchi Negri. Negri bodies, characteristic intracellular inclusions, were identified as indicators of rabies infection.  Louis Pasteur successfully developed the first rabies vaccine in 1885.  The first recorded outbreaks of rabies occurred in Europe.
  • 4. EPIDEMIOLOGY  It causes tens of thousands of deaths every year, mainly in Asia and Africa.  Victims are mostly children under 15 years of age.  In Pakistan, 97,000 dog-bites cases were reported(2016) causing rabies, especially in rural areas of Sindh, with three cities accounting for 85% of the total reported cases: Karachi, Peshawar, and Hyderabad.
  • 5. SPECIFICATIONS NEUROTROPIC VIRUS BULLET SHAPED 75 nm Diameter BALTIMORE GROUP V 12 kbp GENOME SIZE ENVELOPED VIRUS BIOSAFETY LEVEL 2
  • 7. RABIES VIRION Envelope: Present. Virus envelope contains glycosylated G-protein spikes embedded in a lipid membrane derived from the host cell. Matrix (M) protein: The membrane or matrix (M) protein layer lies beneath the envelope. Virus nucleoprotein (N) which tightly binds the viral RNA to form the nucleocapsid core lies inside to matrix protein. Viral genome: The core of the virion consists of helical unsegmented, ss (-) sense RNA and an RNA-dependent RNA polymerase.  It is a simple virus with genome encoding for only 5 proteins.
  • 9. Route of transmission Bites of rabid animal most common Usually lab workers and researchers Non bite exposureof saliva with mucous surfaces such as eyes ,nose and open wounds In very cases during diagnosis and research coming in contact with infected aerosols Rabies transmission through corneal and solid organ transplants have been recorded,very rare.
  • 11. PATHOGENESIS Zoonotic disease: Rabies INCUBATION PRODROME ACUTE NEUROLOGIC PERIOD COMA DEATH Few days to several years 2 to 4 days 2 to 10 days
  • 12.  Muscles become paralyzed  Respiratoryfailure  Weakness  Paralysis  Loss of coordination  Coma SYMPTOMS  Fever  Headache  Malaise  Fatigue  Pain, itching, or tingling at the site of the original wound (where the virus entered the body)  Restlessness  Agitation  Aggression  Hallucinations  Hydrophobia  Hypersalivation (excessive salivation) PRODROMALPHASE FURIOUS PHASE PARALYTIC PHASE
  • 13. DIAGNOSIS SPECIMENS  Saliva  Blood samples  Spinal fluid  Nervous tissue biopsy  Skin samples TECHNIQUES  Clinical observations  PCR  FAT(fluorescence antibody test)  Virus isolationby culturing it in mice
  • 14. PREVENTION Pre-exposure prophylaxis with rabies vaccine is recommended.  Minimize contact with potentially rabid animals.  Do not approach or handle wild or stray animals.  Vaccinate pets and livestock againstrabies.
  • 15. TREATMENT  Post-exposure prophylaxis (PEP) is the emergency response to a rabies exposure. This prevents the virus from entering the central nervous system, which would invariablyresult in death. PEP consists of:  extensive washing of wound with water and soap for at least 15 minutes  a course of potent and effective rabies vaccine that meets WHO standards (Active immunity)  the administrationof rabies immunoglobulin(RIG) or monoclonal antibodies into the wound (Passiveimmunity)  Supportive care is provided to manage symptoms, especially during the later stages of the disease