Lecture 55 Enteroviruses & LCMV Flashcards
Polio presentation and diagnosis
Fever and asymmetric flaccid paralysis
RT-PCR needed to confirm
Isolation of virus from fecal matter or respiratory secretions is suggestive but not definitive
Polio virus characteristics
Picorna virus
Single strand RNA
Non enveloped
Acid stable
Polio hosts
Humans are only natural host for polio
How is someone infected with Polio?
Direct or indirect fecal-oral, or direct contact with respiratory secretions
Swimming is a common cause
Pathogenesis of Polio
Enters through GI, multiplies in pharynx and small intestine
Seeds many sites and spreads to CNS
Infects anterior horn cells, brain stem, and sometimes motor cortex
How does Polio enter the CNS
Direct transfer from the blood, or retrograde axonal flow
Describe polio genome and replication
(+) sense RNA, translated into one giant polypeptide that is then cut to individual pieces
What is IRES?
IRES is: internal ribosomal entry site
Nucleotide sequence that allows swift entry into the ribosome for translation
Clinical syndromes of Polio
1) Inapparent infection
2) Abortive illness: fever, malaise, headache, drowsiness, N/V, spontaneous recovery
3) Non-paralytic poliomyelitis: fever, malaise, headache, drowsiness, N/V, stiff neck and back, spontaneous recovery
4) Paralytic Poliomyelitis: Flaccid paralysis from lower motor neuron damage, some recovery over time through muscle hypertrophy and compensating motor neurons, peak dysfunction after 2-3 days
5) Post Polio Syndrome: gradual clinical course, drop-out of motor neurons decades later in paralyzed patients
Polio bulbar paralysis
Cranial nerve involvement=> motor dysfunction in the face including difficulty swallowing, facial movements, speech, eye movements
Respiratory center depression=> respiratory paralysis
Polio prevention
Vaccine:
-IPV: Inactivated Polio Vaccine, stops paralysis but not infection or spread, less effective than OPV
-OPV: Oral, live attenuated, grown in human or monkey cells, puts virus in the community, and can mutate and cause neurovirulence
Properties of Polio that make it possible to eradicate
Humans only reservoir
Doesn’t persist well in environment
Vaccine => life-long immunity
SV 40
Not a picorna virus, came from monkey cells used to grow the Polio virus for vaccines
Causes malignant malformation => brain malignancies in kids
Causes lysis of oligodendrocytes => opportunistic PML (Progressive Multifocal Leukoencephalopathy) which is a disease of the aged and immunosuppressed
What are the 2 genera of human picorna viruses?
Enteroviruses
Rhinoviruses
Name the non-polio enteroviruses discussed
Echo
Coxsackie
General characteristics of enteroviruses
Typically assoc. with intestinal infections
Broad tissue tropism
Possible eventual neurologic disease
Most kids infected at least once by age 2
Newborns and immunocompromised at greatest risk
Same translation pattern as polio into large polyprotein
Nonenveloped
Echo Virus
Accidentally discovered in feces while looking for polio
Coxsackie Viruses
Two groups:
1) Causes diffuse myositis with acute inflammation and necrosis
2) Focal areas of degeneration of brain and skeletal muscle
Clinical manifestations of Echo/Coxsackie
Newborn:
Sudden onset, fever, vomiting, anorexia, rash, meningeal infection, Bulging of Anterior Fontanelle
Death by hepatic failure in Echo, and myocarditis in coxsackie
Older kids and adults: Fever, headache, nuchal rigidity
(outside first 2 weeks of life not usually severe)
Echo/Coxsackie diagnosis and treatment
Throat and fecal samples Up to 30% will turn up negative Caxsackie A will not grow in culture Nonsymptomatic shedding common in summer/fall RT-PCR useful Body site for isolation matters: -Feces: most sensitive, least specific -Nasopharynx: better link to disease -CSF, Blood: presence here indicates invasive disease (usually not found here?)
Echo/Coxsackie epidemiology
Infections most common in summer/fall in temperate zones
Young children primarily
Disease probability and severity inversely proportional to age (opposite to polio)
Fecal-oral transmission
Echo/Coxsackie prevention
Vaccines unlikely because of many serotypes
Careful handwashing and disinfection
LCMV general characteristics
Arenavirus group
2 RNA strands: one (-), one ambisense
Enveloped, studded with ribosomes, large
Chronic infections of rodents
LCMV clinical manifestations
Encephalitis rare
Flu-like usually
Meningitis uncommon
LCMV diagnosis and treatment
Suspected in cases of aseptic meningitis
History of exposure to mice, hamsters or other rodents
No treatment
LCMV epidemiology
Found anywhere mice are found Infection through aerosols Autumn-Winter predominance All age groups Prevent through rodent control