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Viruses Flashcards

1
Q

Where do enteric viruses primarily replicate?

A

distal ileum

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2
Q

What enteric infections are agammaglobulinemia patients prone to?

A

chronic EV infections of CNS

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3
Q

Typical EV incubation period? Exception?

A
  • 3-6 days

- acute hemorrhagic conjunctivitis = 1-3 days

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4
Q

Who gets asymptomatic EV infections?

A

50% - usually older kids and adults

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5
Q

MOst common EV clinical manifestation?

A

non-specific febrile illness

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6
Q

Which EV causes herpangina and stomatitis/anterior mouth lesions?

A

Coxsackie A strains and Cox A16 (HFMD)

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7
Q

What is pleurodynia?

A
  • Bornholm disease = resp EV manifestation
  • fever, sharp episodic pain in chest/upper abdomen
  • young adults
  • Cox B3, B5
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8
Q

How common are GI Sx in EV infections?

A
  • 1/3 patients

- vomiting and diarrhea are common but are rarely severe

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9
Q

What 2 virus types can commonly cause hemorrhagic conjunctivitis?

A

EV and adenoviruses

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10
Q

CV manifestations of EV infections?

A
  • pericarditis, myocarditis, or both
  • young adults/adolescents
  • Cox B5, Echo 6
  • commonly arrhythmias, usually recover completely but may be linked to chronic cardiomyopathy
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11
Q

Viral exanthems are common with EV infections. Who gets them?

A

expression inversely related to age

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12
Q

What is the most common neurologic manifestation of EV infections?

A
  • aseptic meningitis –> EV accounts for 80-92% of AM cases
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13
Q

Who gets aseptic EV meningitis? When?

A
  • summer and fall

- <1 year but also older children

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14
Q

Course and prognosis of aseptic meningitis?

A
  • 7-14 days presenting with fever/irritability or fever/headache (photophob, NV, rash, pharyngitis)
  • <70% have nuchal rigidity
  • excellent prognosis
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15
Q

What is the most profound of serious EV disease? Mimics?

A
  • severe neonatal infection

- may mimic bacterial sepsis, disseminated/CNS HSV infection

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16
Q

How and who gets severe neonatal EV infection?

A
  • perinatal from mother with EV infection in week before delivery (late infection so no maternal AB yet)
  • <10 days (immune deficient)
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17
Q

Common viral cause of gastroenteritis in children worldwide?

A

Rotaviruses (decreasing due to vaccination, especially in US)

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18
Q

Morphology of rotaviruses?

A
  • reoviridae
  • segmented, non-enveloped, dsRNA
  • 2 shell nucleocapsid containing structural proteins
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19
Q

What ages get most severe RV GI disease?

A

3-24 months, milder disease throughout life

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20
Q

Contagious and shedding of RV illnesses?

A
  • highly contagious

- high viral concentrations in stool - shedding begins a few days BEFORE illness and can persist for 3+ weeks

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21
Q

Pathophysiology of RV infections?

A
  • attach to villus epi cells (enterocytes) in small intestine
  • replications leads to dec absorption of salt/water and failure to process/absorb complex sugars –> inc osmotic load in gut lumen
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22
Q

What is a toxin associated with RV?

A

non-structural protein 4 = enterotoxin (acts on epi receptor to potentiate Cl- secretion = secretory diarrhea)

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23
Q

Course of RV GI?

A
  • incubation 1-3 days
  • lasts 3-8 days (longer in IC)
  • fever and vomiting followed 24-48 hours by diarrhea (dehydration)
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24
Q

Which 2 caliciviruses are associated with disease in humans?

A
  • norovirus

- sapovirus

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25
Q

What is most common cause of outbreaks of gastroenteritis in closed populations?

A

norovirus

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26
Q

Who do sapoviruses commonly occur in?

A

children with sporadic diarrhea

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27
Q

Morphology of caliciviruses?

A
  • non-enveloped ssRNA
  • diverse genetically and antigenically
  • classified into genogroups and genotypes
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28
Q

Most common cause of foodborne illness and foodborne disease outbreaks in US?

A

norovirus

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29
Q

When do calicivirus infections occur?

A

cold months

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30
Q

Course of calicivirus infections?

A
  • older = more vomiting
  • V and D; usually don’t have fever and lasts 1-4 days
  • incubation 12-48 hours
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31
Q

Shedding of calicivirus?

A
  • viral excretion peaks 4 days after exposure and may persist for 3 weeks (worse in IC)
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32
Q

Adenovirus morphology?

A
  • dsDNA, non-enveloped
  • NO seasonality
  • many manifestations, mild to severe
33
Q

What does adenovirus gastroenteritis look like in children?

A
  • 4-17% of diarrhea in children <4
  • incubation 3-10 days
  • diarrhea tends to be more protracted (8-12 days) and severe than other EV diarrheas + vomiting, low-grade fever
34
Q

Astrovirus morphology?

A
  • non-enveloped ssRNA
35
Q

Who gets astroviruses? Presentation?

A
  • children >4, late winter/early spring
  • mild diarrhea lasting 5-6 days + V, fever, ab pain
  • outbreaks can occur in closed populations
36
Q

Where is inflammation primarily observed in acute hepatitis? What is seen?

A
  • portal triad
  • intracellular cholestasis
  • piecemeal necrosis with Councilman apoptotic bodies
  • ballooning degeneration
37
Q

What percent of fulminant hep cases are caused by viral hep?

38
Q

What two HV’s commonly lead to chronic hep?

A
  • HCV = most common

- HBV = younger age at infection is assoc w/ inc risk of chronicity

39
Q

What HV is assoc with a carrier state?

40
Q

IP and general presentation of HAV?

A
  • 3-6 weeks

- benign, self-limited; flu-like syndrome with RUQ pain with mild-severe icteric phase

41
Q

How is HAV primarily transmitted?

A
  • fecal-oral in contaminated water/shellfish/food
42
Q

How is HAV detected?

A
  • IgM anti-HAV = acute (inc assoc with peak of Sx)

- IgG (total anti-HAV) = convalescent

43
Q

5 manifestations of HBV?

A
  • Sx or asym acute hep
  • fulminant hep
  • chronic hep w/ cirrhosis and HCC progression
  • carrier state
44
Q

What HBV patients usually progress to chronic disease?

A

those infected early in life (90% progression) vs. only 5% infected as adults

45
Q

3 ways to transmit HBV?

A
  • parenteral
  • intimate (STD)
  • perinatal (endemic)
    1/3 unknown
46
Q

IP of HBV? Icteric phase marked by?

A
  • 6-16 weeks

- inc LFT’s, dark urine

47
Q

What causes ground glass appearance in HBV?

A
  • cytoplasm packed with spheres and tubules of HBsAg
48
Q

When is HBsAg detected in acute disease?

A
  • appears before onset

- peaks during overt disease then declines to undetectable levels in 3-6 months?

49
Q

When is HBsAg detected in chronic disease?

A
  • increases during acute infection

- remains persistently elevated

50
Q

When does anti-HBs appear in acute disease?

A
  • does not rise until acute infection is over
  • usually not detectable for weeks-months after HBsAg has disappeared
  • may persist for life
51
Q

When does HBeAg appear?

A
  • soon after HBsAg
  • signifies active viral replication
  • persistence indicates continued rep, infectivity and probably progression to chronic disease
52
Q

What does the appearance of anti-HBe mean?

A

implies that acute infection has peaked and is waning

53
Q

Pattern of IgM anti-HBc appearance?

A
  • becomes detectable shortly before onset of symptoms
  • concurrent with elev LFT’s
  • IgM replaced by IgG over months (seen as inc total anti-HBc)
54
Q

How is HCV transmitted?

A
  • parenteral (IVDA most common RF)
  • possible sexual
  • 23% unknown
55
Q

Three outcomes of HCV infection?

A
  • acute with recovery = 15%
  • fulminant rare
  • chronic = 85%
56
Q

Complications in patients with chronic HCV?

A
  • 80% stable disease

- 20% cirrhosis and possible HCC

57
Q

What makes HCV chronic progression more rapid?

A

EtOH, toxins

58
Q

Which HCV genotype is most prevalent in US? Why is this a problem?

A
  • HCV type 1

- most difficult to treat

59
Q

IP of HCV? What marks chronic disease?

A
  • 6-8 weeks

- asymp periods alt with periods of active disease

60
Q

Serologic pattern in chronic HCV?

A
  • initial symptomatic infection marked by elev LFT’s, HCV RNA (PCR)
  • takes months for anti-HCV to develop
  • chronic disease has active periods with elev LFT’s and HCV RNA
61
Q

What is limiting and unique about HDV?

A

dependent upon HBV to assist in replication and packaging into infective virions

62
Q

Primary form of transmission of HDV?

A

parenteral

63
Q

What determines disease presentation of HDV?

A
  • when infection is acquired relative to HBV
  • co-infection = both
  • superinfection = HBV then D
64
Q

Manifestation of D/B co-infection?

A
  • acute or fulminant hep

- 95% recover (rare progression to chronic disease)

65
Q

Manifestation of B-D superinfection?

A
  • new acute/fulminant infection
  • 7-10% die from fulminant
  • 10-15% recover from acute hep
  • 80% go on to have chronic HBV and HDV infections
66
Q

Which zoonotic virus is associated with fecal-oral water transmission?

67
Q

IP and typical presentation of HEV?

A
  • 2-9 weeks
  • flu-like syndrome and icteric phase
  • usually self-limited
68
Q

What is associated with high HEV mortality?

A
  • pregnancy

- 15% of patients gets fulminant hep

69
Q

Which LFT is elevated more in viral hep?

70
Q

What 4 serologies are included in acute panel?

A
  • HBsAg
  • IgM HBc
  • HAV IgM
  • HCV EIA (PCR if +)
71
Q

What 3 hepatitis etiologies should always be at the top of your DDx?

A

viral
drug-induced
toxic (occ, hobby)

72
Q

Max neut band %?

73
Q

What type of anemia is Fe deficiency? MCH/MCV?

A
  • microcytic, hypochromic

- low

74
Q

What type of anemia is folate deficiency? MCV?

A
  • megaloblastic

- high

75
Q

Upper normal limits of ALT, AST, alk phos?

A
  • 40, 40, 120
76
Q

Quick and dirty assessment of lab hepatic vs. biliary disease?

A

look at ratios between patient values and upper normal limits

77
Q

How do AST and ALT elevations compare in EtOH disease?

A

AST:ALT = 2:1

78
Q

What 3 viruses are blood borne pathogen concerns?

A

HIV, HBV, HCV

GI (5 decks)

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