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Microbiology Part 2 > Lec 27 Enteroviruses > Flashcards

Lec 27 Enteroviruses Flashcards

1
Q

What are picomaviruses? What are the 3 types of picomavirus?

A

picomavirus = small RNA virus
enteroviruses
rhinoviruses
hepatitis A

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2
Q

What are the common types of enterovirus?

A
  • poliovirus 1-3
  • coxsackie A and B
  • echoviruses
  • numbered enteroviruses
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3
Q

When do enterovirus infections occur and where?

A

in temperate climates: summer and fall

in tropics: year round

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4
Q

Who gets enteroviruses?

A

most cases in children

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5
Q

What are symptoms of enterovirus?

A
  • most are asymptomatic or cause non-specific fever with mild resp symptoms
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6
Q

What are the viral characteristics of enterovirus?

A
  • pos sense
  • single strand
  • RNA
  • icosahedral capsid
  • no envelop
  • resistnat to harsh environmental conditions –> survives in sewage, broad pH range, GI, detergents
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7
Q

What is aseptic meningitis?

A

have symptoms and WBCs on spinal tap but using convential bacterial media, nothing grows

means the meningitis is due to something else [like a virus!]

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8
Q

What is role of canyon in center of enteroviruses?

A
  • contains VP1 capsid protein receptor binding sites –> means RBS is hidden from antibodies
  • VP1 RBS is responsible for adherence to host cell receptors
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9
Q

Can viruses with or without envelope survive in environment longer / harsher?

A

no envelope

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10
Q

How are enteroviruses transmitted?

A
  • enter through GI tract via fecal-oral route

- except rhinovirus which is via nasal secretions

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11
Q

What is the pathogenesis of enterovirus and what is replication cycle like?

A
  • enters GI and causes infection there, if pt does not have secretory IgA to virus –> get primary viremia in blood stream –> goes to target tissues
  • receptor it binds to [and thus type of cell it invades] depends on type of virus, binds via VP1
  • replication occurs in cytoplasm [no nuclear]
  • usually cytolytic = ends up killing cell as it leaves [except hep A which is more immune mediated]
  • inhibit host cell RNA synthesis
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12
Q

What is pathogenesis of polio?

A
  • travels via nerves from muscle to motor neurons in anterior horn and brainstem
  • get meningitis, encephalitis, paralytic disease
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13
Q

What is pathogenesis of HAV?

A
  • travels to liver and get hepatitis
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14
Q

What is pathogenesis of coxsackle?

A
  • goes to brain and get encephalitis
  • cox A/B go to muscle and get myocarditis, pericarditis, pleurodynia
  • cox A goes to skin and get hand food and mouth, rash, herpangina
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15
Q

What is pathogenesis of Echo?

A
  • myocarditis
  • in neonatal –> myocarditis, liver failure, death
  • also meningitis/cold/fever/rash in summer
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16
Q

What are possible target tissues of enteroviruses?

A
  • skin infections
  • muscle –> heart
  • brain
  • meninges
  • liver
  • can cross placenta and infect fetus
17
Q

For how long are enteroviruses still contagious in pt infected?

A

may have symptoms for a few days but still shed virus in nasal secretions and stool for weeks

18
Q

What are the mech of enterovirus injury?

A

cytolytic except in hep A

immune mediated in hep A

19
Q

What are the roles of secretory IgA and serum IgG in enterovirus immune response?

A

sec IgA: prevents establishment of initial infection

serum igG: prevent/control viremia

20
Q

What are the symptoms of polio?

A

90% asymptomatic
5% minor febrile illness
non-paralytic aseptic meningitis 1-2%
paralytic 2% –> get asymmetirc flaccid paralysis

21
Q

What are the two polio vaccinces?

A

inactivated [IPV]: IM, get serum IgG antibodies, does not cause disease
live [OPV]: oral, get both secretory IgA antibodies and serum IgG, cell mediated + long lasting, possibility of getting sick

22
Q

Which polio vaccine do we get?

A
  • in places where we don’t really have polio we use inactivated
  • use activated in places where polio is still common
23
Q

Where is polio endemic?

A

afghanistan
nigeria
pakistan

24
Q

What are clinical syndromes associated with enteroviruses other than polio?

A
  • exanthems [widespread rash
  • febrile illness
  • URI
  • acute hemorrhagic conjunctivitis
  • aseptic meningitis and encephalitis

= fever + rash often is enterovirus

25
Q

what are clinical syndromes associated with echo?

A

overwhelming neonatal disease

26
Q

What are specific clinical signs associated with coxsakie?

A 
herpangina [coxsakie A]
hand food and mouth [cox A]
pleurodynia [cox B]
myocarditis and pericarditis [cox B]
neonatal disease [cox B]
27
Q

What are specific clinical signs associated with coxsakie A?

A

herpangina = infection of back of mouth [vs herpes gives infection in front of mouth]

hand food and mouth [rash, papules in palms, soles, and mouth]

28
Q

What are specific clinical signs associated with coxsakie B?

A

pleurodynia [significant sharp pain with inspiration, fever]

myocarditis and pericarditis

neonatal disease

29
Q

How are enterovirus infections diagnosed?

A

usually just clinically diagnosed

for meningitis –> high WBC in CSF, lymphocytic predominance, normal glucose and protein

less routinely may do diagnostic testing:
culture –> nasopharynx/ stool
PCR –> of blood, CSF

30
Q

What are enterovirus infections commonly?

A

summer months!

31
Q

What is treatment for enteroviruses?

A

supportive

32
Q

What is Kuru?

A
  • type of prion disease
  • disease associated with ritual cannibalism in papua new guinea
  • uniformly fatal
  • get vacuole formation in brain
  • neurons replaced by amyloid plaques
33
Q

What are types of prion disease?

A
  • Kuru
  • cretuzfeldt-jacob disease [CJD]
  • variant CJD [vCJD] in younger = mad cow in humans get it from cow with BSE
  • animal: bovine spongiform encephalopathy [BSE]
34
Q

What are characteristics of prion diseases?

A
  • long incubation period
  • slow but progessive neuro deterioration
  • uniformly fatal over period of months
35
Q

What are common pathologic findings of prion diseases?

A
  • minimal inflammatory response
  • neuronal degeneration
  • astrocyte proliferation
  • vacuoles within cells
36
Q

What is a prion protein [PrP]?

A
  • infectious protein that lack nucleic acid or virus like structure
  • mech of transmission of prion diseases
  • conformational isomer of normal host protein
  • accumulated in brain of affected individual
  • resistant to chemical or physical inactivation
37
Q

How are prion diseases transmitted?

A
  • transmitted by prion protein in infected brain tissue, consume infected brain tissue and it triggers you
  • can be genetic
  • can be iatrogenic –> prion disease transmitted from donor cadaver to pt, from unclean tools, etc

Microbiology Part 2 (30 decks)

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