11_Rabies, Polio, Pox Flashcards
Rabies virus:
- causes what disease?
- type of virus and resulting symptoms?
- transmission
- epidemiology?
- rabies
- neurotropic virus –> causes acute viral infxn of the CNS; fatality rate of ~100%
- transmitted by animal bites
- occurs worldwide, most cases occur in Africa and Asia as a result of exposure to dogs in rabies-endemic areas
structure of rabies virus?
- single stranded, negative-sense RNA virus in the genus Lyssavirus, family Rhabdoviridae
- bullet-shaped (75x180 nm)
- enveloped, single stranded RNA genome (12 kb)
Pathogenesis of rabies after an animal bite
- incubation period of rabies: 20-90 days or longer; most of this period is a delay in progression of infxn from the site of inoculation
- virus spreads via peripheral nerves to CNS, and then w/in CNS by fast axonal transport along neuroanatomical connections
- after development of CNS infxn, the virus spreads centrifugally along sensory & autonomic nerves to multiple organs
what is the clinical course and timeframe of rabies in humans?
- Exposure
- Incubation period: 20-60 days
- 1st symptom
- Prodrome: 2-10 days
- fever, anorexia, HA, malaise, pain, numbness (at bite site)
- 1st neurological sign
- Acute neurologic phase: 2-7 days
- anxiety, CNS signs, paralysis, hydrophobia, delirium, hallucinations
- Onset of coma
- Coma: 0-14 days
- pituitary dysfxn, hypotension, cardiac arrhythmia, cardiac arrest, coma
- Death
Differences between Encephalitic rabies and Paralytic rabies?
-
Encephalitic rabies: furious form ~80%
- *KEY SIGN: HYDROPHOBIA
- prodromal sxs
- paresthesias/pain/pruritis at site of bite
- episodes of generalized arousal or hyperexcitability separated by lucid periods
- autonomic dysfxn
-
Paralytic rabies: dumb form (~20%) –> *FATAL OUTCOME
- paresthesias/pain/pruritis at site of bite
- early flaccid muscle weakness (often begins in bitten extremity –> progresses to produce quadriparesis –> bilateral facial weakness
- sensory exam in usually normal
- sphincter is involved
which form of rabies is often misdiagnosed as Guillain-Barre syndrome?
Paralytic rabies - “dumb form”
how to diagnose rabies infection?
- lab tests to determine whether an animal is rabid; determined by multiple tests:
- RT-PCR used to test saliva for rabies virus or by isolation of the virus (RT-PCR is reverse transcription-polymerase chain reaction)
- histologically: Negri bodies are characteristic, which are eosinophilic intracytoplasmic inclusions formed by aggregates of nucleocapsids in neurons of about 50-80% of infected humans; found in purkinje cells of the cerebellum
- serology (neutralizing serum or CSF Abs in unvaccinated person are diagnostic but usually are only detectable late in disease)
describe the post-exposure prophylaxis for rabies infxn
- wound site: immediate thorough cleansing of all wounds w/ soap & water; tetanus prophylaxis; Abx
- human rabies immune globulin (RIG): 20 IU;kg body weight; given IM at site distant from vaccine
- rabies vaccine: IM (1 mL) in the deltoid area on days 0, 3, 7, 14, and 28)
how to control and eliminate Rabies?
-
After a recognized exposure –> post exposure prophylaxis (PEP)
- consists of immediate wound cleansing, active immunization with multiple doses of rabies vaccine, and passive immunization with human rabies immune globulin, injected into and around the wound and intramuscularly.
- PEP prevents rabies virus from gaining access to the nervous system.
- Latin America is an example of a region in which several countries have successfully controlled rabies.
- This has been achieved predominately by mass vaccination of over 45 million dogs annually.
Poliovirus:
structure
strains
- (+)ss-RNA genome and a protein capsid
- (genome is a single-stranded positive-sense RNA genome that is about 7500 nucleotides long)
- 3 serotypes of poliovirus—
- poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3)
- *each with a slightly different capsid protein all three are extremely virulent and produce the same disease symptoms.
- PV1 is the most commonly encountered form, and the one most closely associated with paralysis.
describe the dissemination pathways of poliovirus in humans
oral ingestion of the virus –> virus multiplies in alimentary mucosa (&possibly in the tonsils and Peyer’s patches)–> virus then moves into the blood stream (viremia).
2 possible dissemination routes through which the circulating polio-virus can enter the CNS:
- virus permeation through the blood-brain barrier (BBB), or
- virus transmission via peripheral nerves
The circulating virus invades the CNS and replicates in neurons, particularly motor neurons.
Poliovirus symptoms:
initial sxs
sequelae
- 90% of pts are asymptomatic, or v mild sxs
- Initial sxs can incl: fever fatigue, HA, vomiting, stiffness in neck, pain in limbs
- Sequelae:
-
acute flaccid paralysis (AFP): 1 in 200 infxns; irreversible paralysis, usually in legs
- virus enters blood stream –> invading CNS –> as it multiplies, virus destroys the nerve cells that activate muscles;
- the affected muscles no longer fxnal and limb becomes floppy and lifeless
-
bulbar polio: more extensive paralysis, involving trunk and muscles of thorax and abdomen –> can result in quadriplegia
- poliovirus attacks nerve cells of the brain stem, reducing breathing capacity and causing difficulty swallowing and speaking;
- among those paralyzed, 5-10% die when their breathing muscles become immobilized
-
acute flaccid paralysis (AFP): 1 in 200 infxns; irreversible paralysis, usually in legs
when did incidence of poliomyelitis in US start dropping?
after Salk vaccine in 1955, and decreased further after Sabin vaccine in ~1960S
what are the many future benefits of polio eradication?
- success will mean that no child will ever again suffer the terrible effects of lifelong polio-paralysis
- Economic modelling has found that the eradication of polio would save at least US$ 40–50 billion between 1988 and 2035, mostly in low-income countries.
small pox:
etiologic agent
symptoms
when eradicated?
- caused by Orthopoxvirus (OPV) variola virus (VARV) –> 1-30% case-fatality rates of smallpox (strictly human disease)
- infxn began w/ systemic aches and fever that peaked in ~1 week;
- as fever broke –> oropharyngeal enanthema (eruption of mucous surface) developed –> exanthema (skin rash of virus-filled, “shotty” pustules)
- eradicated by 1980
Pox virus:
structure
categorizations
- large, ds-DNA viruses;
- genomes contain 135-360 kb and contain up to 328 predicted open reading frames (ORFs)
- 2 subfamilies:
- chordopoxvirinae, which infect vertebrates, and
- entomopoxvirinae, which infect insects.
how does small pox virus replicate?
- grows in the cytoplasm of an infected cell
- Thin section of infected chick embryo cell.
- Mature virions are brick-shaped.
- Magnification approximately x25,000
varicella life cycle?
What condition can complicate Zoster?
What are the manifestations of this?
VZV vasculopathy due to productive viral infection of cerebral arteries can complicate Zoster
VZV Vasculopathy:
diagnosis and treatment
Compare and Contrast the Shingles vaccinations that are available
