Viral Infections 1 Flashcards
Aseptic meningitis
A short-lived, self-limited, CNS syndrome characterized by meningeal symptoms and a sterile CSF.
Nothing grows when submit CSF sample to lab - will not grow on plate
identifying the cause is important for proper treatment - multiplex PCR on CSF samples - only big hospitals have
Viral meningitis
A viral infection associated with acute onset of meningeal symptoms (classical triad!).
Aseptic vs Viral Meningitis
All viral are aseptic but not all aseptic are viral
viral meningitis = aseptic meningitis
aseptic meningitis ≠ viral meningitis
they are used interchangeably
Most of aseptic meningitis cases are caused by
viruses
Bacterial vs viral meningitis
Viral encephalitis
inflammation of the brain parenchyma caused by a virus
Usually is a complication of viral meningitis (meningoencephalitis) [but symptoms are overwhelmingly of encephalitis]
Accounts for ~70% of all confirmed cases of encephalitis
Viral myelitis
inflammation of the spinal cord due to a virus that can be diffuse or localized to a specific region
Usually acute (symptom onset occurs within hours to days of infection)
When there is involvement of spinal nerve roots (or PNS) is referred to as myeloradiculitis
spinal cord inflamed - nerves coming out also affected
Viral CNS infections (ways get in/process of infection)
1) Viruses are either inhaled (Mumps), ingested (non-polio Enteroviruses), or injected (arboviruses)
2) Infect the oropharyngeal [inhaled], gastrointestinal [ingested], or skin-associated lymphoid tissues [injected]
3) Viruses gain entry to CNS by directly infecting BMECs [across monolayer], through infected immune cells that cross into the brain [through continuous tissue], or migration through peripheral sensory or motor neurons [nerve hoping]
4) Usually meningeal cells are infected first - results in inflammation and
meningeal syndrome of symptoms - classical triad
5) Intact adaptive [T, B, Treggs, antibodies] response is required to control and clear the infection [inane fagocites do not do - need adaptive response]
6) Without proper immune control can spread to parenchyma of brain and spinal cord
7) Treat the symptoms - antiviral treatment only if effective drug exists [if not antiviral cannot do anything except treat symptoms]
Antivirals
have very few side effects because very specific for virus - better to start before know if sure
incidence of viral meningitis
unknown given that most cases are self-limited and go unreported because we have robust and effective immune responses that should clear the infection
type of virus that causes vast majority of viral meningitis
Enteroviruses - gut related (enteric system) - babies touch a lot of things and put into mouth
Coxsackie viruses - hand-foot-and-mouth disease
Other common causes of viral meningitis
Arboviruses (arthropod-borne viruses), and HIV [ reason cannot cure is because microglia serve as a reservoir for - alway develop neurological disorders - not nessarily always develop AIDS]
Other less common causes of viral meningitis
lymphocytic choriomeningitis virus (LCV), Cytomegalovirus (CMV), type II herpesvirus (HSV-2), Measles virus, Mumps virus, Epstein–Barr (EBV), and influenza viruses [before vaccine - measles/mumps - most common - mostly due b/c CNS infection]
Viral meningitis is usually preceded by
flu-like respiratory, gastrointestinal, or joint/muscle pain symptoms (depending on the viral route of infection)
symptoms point to how was aquired
Non-polio enteroviruses
cases ___
why so common ___
Up to 61% of cases (90% in countries with Mumps vaccinations)
> 110 genetically distinct enteroviruses have been identified - maybe why so common
Non-polio enteroviruses
Risk Factors
Risk factors: neonates and infants, summer months, day care setting
Seasonal - tend to manifest in late summer and early autumn
Non-polio enteroviruses
therapy/treatment/progression
No specific antiviral therapy exists
~99% of cases is self-limiting and involves complete recovery
In the < 1% that results in death, brainstem inflammation is almost always involved
how do Non-polio enteroviruses get into the CNS
many pathways
Target multiple receptor for entry, including ones in BMECs
Trojan horse transit is possible
Neurons (and neural stem cells) highly susceptible to infection
- Latency and reactivation!
Depending area of entry - meningitis or encephalitis
Mumps virus
incedence
type(s)
common manifestation
Up to 15% of cases
12 genotypes, with the majority of meningitis cases due to genotypes B and G (not the most common)
- Vaccine (MMR) provides limited protection towards the neurotropic strains
common manifestation is inflammation of the parotid (salivary) glands – 15% of the cases will involve CNS
Mumps virus meningitis onset
occurs ~6 days after the appearance of parotid gland symptoms - classical triad, plus swollen and painful testis, and joint
and muscle pain
Fever lasts from 3 to 7 days, with eventual recovery after fever subsides
Mumps virus meningitis how occour
Viremia important for dissemination
- neurotropic strains will cause CNS infection in >50% patients
Ependymal cells very susceptible – seeds the CSF - can use same ways to infect but mostly chord plexi (high blood - gross well in ependymal cels - lyice - access CSF)
respiratory - salivary and lymph tissue - blood - spread to spleen and liver - infected - keep spreading - goes into CNS
Arboviruses
area
meningitis cases
yousto be restricted to areas now expanding - exposed population is also expanding
< 1% of cases (healthy individuals will restrict infection to meninges) - Immunosuppressed individuals cannot, will disseminate - encephalitis
West nile virus (arboviruses - geographical and clinical clues)
Dengue (arboviruses - geographical and clinical clues)
bone crushing fever
blood test - low platlets - hemoregic fever
Chikingunya (arboviruses - geographical and clinical clues)
Zika (arboviruses - geographical and clinical clues)
Viral meningitis
non-polio enteroviruses
mumps, hiv, others
arboviruses
