Viruses Flashcards
1
Q
Where do enteric viruses primarily replicate?
A
distal ileum
2
Q
What enteric infections are agammaglobulinemia patients prone to?
A
chronic EV infections of CNS
3
Q
Typical EV incubation period? Exception?
A
- 3-6 days
- acute hemorrhagic conjunctivitis = 1-3 days
4
Q
Who gets asymptomatic EV infections?
A
50% - usually older kids and adults
5
Q
MOst common EV clinical manifestation?
A
non-specific febrile illness
6
Q
Which EV causes herpangina and stomatitis/anterior mouth lesions?
A
Coxsackie A strains and Cox A16 (HFMD)
7
Q
What is pleurodynia?
A
- Bornholm disease = resp EV manifestation
- fever, sharp episodic pain in chest/upper abdomen
- young adults
- Cox B3, B5
8
Q
How common are GI Sx in EV infections?
A
- 1/3 patients
- vomiting and diarrhea are common but are rarely severe
9
Q
What 2 virus types can commonly cause hemorrhagic conjunctivitis?
A
EV and adenoviruses
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
11
Q
Viral exanthems are common with EV infections. Who gets them?
A
expression inversely related to age
12
Q
What is the most common neurologic manifestation of EV infections?
A
- aseptic meningitis –> EV accounts for 80-92% of AM cases
13
Q
Who gets aseptic EV meningitis? When?
A
- summer and fall
- <1 year but also older children
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
15
Q
What is the most profound of serious EV disease? Mimics?
A
- severe neonatal infection
- may mimic bacterial sepsis, disseminated/CNS HSV infection
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)
17
Q
Common viral cause of gastroenteritis in children worldwide?
A
Rotaviruses (decreasing due to vaccination, especially in US)
18
Q
Morphology of rotaviruses?
A
- reoviridae
- segmented, non-enveloped, dsRNA
- 2 shell nucleocapsid containing structural proteins
19
Q
What ages get most severe RV GI disease?
A
3-24 months, milder disease throughout life
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
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
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)
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)
24
Q
Which 2 caliciviruses are associated with disease in humans?
A
- norovirus
- sapovirus
25
What is most common cause of outbreaks of gastroenteritis in closed populations?
norovirus
26
Who do sapoviruses commonly occur in?
children with sporadic diarrhea
27
Morphology of caliciviruses?
- non-enveloped ssRNA
- diverse genetically and antigenically
- classified into genogroups and genotypes
28
Most common cause of foodborne illness and foodborne disease outbreaks in US?
norovirus
29
When do calicivirus infections occur?
cold months
30
Course of calicivirus infections?
- older = more vomiting
- V and D; usually don't have fever and lasts 1-4 days
- incubation 12-48 hours
31
Shedding of calicivirus?
- viral excretion peaks 4 days after exposure and may persist for 3 weeks (worse in IC)
32
Adenovirus morphology?
- dsDNA, non-enveloped
- NO seasonality
- many manifestations, mild to severe
33
What does adenovirus gastroenteritis look like in children?
- 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
Astrovirus morphology?
- non-enveloped ssRNA
35
Who gets astroviruses? Presentation?
- children >4, late winter/early spring
- mild diarrhea lasting 5-6 days + V, fever, ab pain
- outbreaks can occur in closed populations
36
Where is inflammation primarily observed in acute hepatitis? What is seen?
- portal triad
- intracellular cholestasis
- piecemeal necrosis with Councilman apoptotic bodies
- ballooning degeneration
37
What percent of fulminant hep cases are caused by viral hep?
12%
38
What two HV's commonly lead to chronic hep?
- HCV = most common
| - HBV = younger age at infection is assoc w/ inc risk of chronicity
39
What HV is assoc with a carrier state?
HBV
40
IP and general presentation of HAV?
- 3-6 weeks
| - benign, self-limited; flu-like syndrome with RUQ pain with mild-severe icteric phase
41
How is HAV primarily transmitted?
- fecal-oral in contaminated water/shellfish/food
42
How is HAV detected?
- IgM anti-HAV = acute (inc assoc with peak of Sx)
| - IgG (total anti-HAV) = convalescent
43
5 manifestations of HBV?
- Sx or asym acute hep
- fulminant hep
- chronic hep w/ cirrhosis and HCC progression
- carrier state
44
What HBV patients usually progress to chronic disease?
those infected early in life (90% progression) vs. only 5% infected as adults
45
3 ways to transmit HBV?
- parenteral
- intimate (STD)
- perinatal (endemic)
1/3 unknown
46
IP of HBV? Icteric phase marked by?
- 6-16 weeks
| - inc LFT's, dark urine
47
What causes ground glass appearance in HBV?
- cytoplasm packed with spheres and tubules of HBsAg
48
When is HBsAg detected in acute disease?
- appears before onset
| - peaks during overt disease then declines to undetectable levels in 3-6 months?
49
When is HBsAg detected in chronic disease?
- increases during acute infection
| - remains persistently elevated
50
When does anti-HBs appear in acute disease?
- does not rise until acute infection is over
- usually not detectable for weeks-months after HBsAg has disappeared
- may persist for life
51
When does HBeAg appear?
- soon after HBsAg
- signifies active viral replication
- persistence indicates continued rep, infectivity and probably progression to chronic disease
52
What does the appearance of anti-HBe mean?
implies that acute infection has peaked and is waning
53
Pattern of IgM anti-HBc appearance?
- 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
How is HCV transmitted?
- parenteral (IVDA most common RF)
- possible sexual
- 23% unknown
55
Three outcomes of HCV infection?
- acute with recovery = 15%
- fulminant rare
- chronic = 85%
56
Complications in patients with chronic HCV?
- 80% stable disease
| - 20% cirrhosis and possible HCC
57
What makes HCV chronic progression more rapid?
EtOH, toxins
58
Which HCV genotype is most prevalent in US? Why is this a problem?
- HCV type 1
| - most difficult to treat
59
IP of HCV? What marks chronic disease?
- 6-8 weeks
| - asymp periods alt with periods of active disease
60
Serologic pattern in chronic HCV?
- 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
What is limiting and unique about HDV?
dependent upon HBV to assist in replication and packaging into infective virions
62
Primary form of transmission of HDV?
parenteral
63
What determines disease presentation of HDV?
- when infection is acquired relative to HBV
- co-infection = both
- superinfection = HBV then D
64
Manifestation of D/B co-infection?
- acute or fulminant hep
| - 95% recover (rare progression to chronic disease)
65
Manifestation of B-D superinfection?
- 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
Which zoonotic virus is associated with fecal-oral water transmission?
HEV
67
IP and typical presentation of HEV?
- 2-9 weeks
- flu-like syndrome and icteric phase
- usually self-limited
68
What is associated with high HEV mortality?
- pregnancy
| - 15% of patients gets fulminant hep
69
Which LFT is elevated more in viral hep?
AST > ALT
70
What 4 serologies are included in acute panel?
- HBsAg
- IgM HBc
- HAV IgM
- HCV EIA (PCR if +)
71
What 3 hepatitis etiologies should always be at the top of your DDx?
viral
drug-induced
toxic (occ, hobby)
72
Max neut band %?
10%
73
What type of anemia is Fe deficiency? MCH/MCV?
- microcytic, hypochromic
| - low
74
What type of anemia is folate deficiency? MCV?
- megaloblastic
| - high
75
Upper normal limits of ALT, AST, alk phos?
- 40, 40, 120
76
Quick and dirty assessment of lab hepatic vs. biliary disease?
look at ratios between patient values and upper normal limits
77
How do AST and ALT elevations compare in EtOH disease?
AST:ALT = 2:1
78
What 3 viruses are blood borne pathogen concerns?
HIV, HBV, HCV
