Common Viral Pathogens Flashcards

1
Q

Virus vs. Bacteria

A
  • Viruses require host cells in order to replicated
  • Bacteria are living vs. Virus=infectious particle
  • viral infection=virus has replicated with host
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2
Q

Common laboratory tests looking for actual virus

A
  • culture w/in tissue
  • assay to look for antigens
  • PCR to amplify portion of viral genome
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3
Q

Common laboratory test looking for host immune response to virus

A
  • ELISA (Enzyme-Linked Immmunosorbent Assay)
  • add host serum to viral antigen
  • add tagged/immunofluorescent Ab to visualize host Ab
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4
Q

8 herpes viruses which infect humans

A
  • HHV-1: Herpes Simplex Virus-1 (HSV-1)
  • HHV-2: HSV-2
  • HHV-3: Varicella Zoster Virus (VZV)
  • HHV-4: Epstein Barr Virus (EBV)
  • HHV-5: Cytomegalovirus (CMV)
  • HHV-6: Roseola (HHV-6a, HHV-6b)
  • HHV-7: Roseola
  • HHV-8: HHV-8
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5
Q

Clinical manifestations of HSV-1/HSV-2

A
  • oral and genital herpes; HSV-1 mostly orofacial lesions and HSV-2 mostly genital lesions
  • incubation: ~4 days
  • transmission: direct shedding into mucosal surface
  • primary infection: usually asymptomatic, but may sometimes produce rash
  • reactivated infection: can be symptomatic, but usually less symptomatic than primary infection
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6
Q

HSV diagnosis

A
  • usually clinical but may use:
  • Tzanck smear
  • HSV culture
  • Direct Fluorescent Antigen stain
  • PCR of lesions
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7
Q

HSV treatment

A
  • severe HSV (in neonate/immunocompromised or encephalitis)–> IV acyclovir
  • oral antiviral therapy
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8
Q

VZV clinical syndromes

A

-2 main syndromes: chicken pox and shingles

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9
Q

Clinical manifestations of primary VZV infection

A
  • primary VZV=varicella=chickenpox
  • highly contagious
  • incubation 10-21 days
  • fever, malaise, headache
  • itchy, vesicular rash develops starting at trunk and spreading to limbs
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10
Q

Pathogenesis of primary VZV infection

A
  • entry via respiratory tract
  • spreads to regional lymph nodes and replicates for 2-4 days –> primary viremia
  • replicates in liver, spleen, etc. –> secondary viremia
  • secondary viremia spreads virus to skin 14-16 days after exposure –> rash
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11
Q

Prevention of HSV-1/HSV-2

A
  • no vaccine
  • hand hygiene/physical barriers
  • avoid contact
  • prevent reinfection w/lower doses of acyclovir on daily basis
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12
Q

Primary VZV infection treatment

A
  • usually self-limited and requires no treatment
  • treatment accelerates resolution/decreases symptoms
  • treatment necessary for immunocompromised patients
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13
Q

VZV varicella prevention/prophylaxis

A
  • varicella vaccine: live-attenuated vaccine=2 doses @ 12-15mo. and 4-6 yrs.
  • Varicella-zoster immune globulin (Varizig): reduces severity in high-risk pts w/in 4 days of exposure (=pooled Abs from people w/high VZV Ab titers)
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14
Q

Pathogenesis of VZV latency and reactivation

A
  • VZV remains latent in cranial, dorsal root, or trigeminal ganglia
  • no asymptomatic viral shedding
  • dermatomal rash along sensory nerve from ganglion
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15
Q

VZV reactivation infection clinical manifestations

A
  • VZV reactivation=zoster=Shingles
  • pain where vesicles will erupt several days later
  • lesions erupt over single dermatome
  • lesions itchy w/pain; 2 weeks before crust over
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16
Q

VZV reactivation (Zoster) diagnosis

A
  • usually diagnosed clinically

- also: Direct IFA, PCR, or culture

17
Q

VZV reactivation (Zoster) treatment

A
  • acyclovir decreases number/duration of lesions and pain

- pain treated w/NSAIDs, opiates, sometimes steroids

18
Q

VZV reactivation (Zoster) prevention/prophylaxis

A
  • vaccine=Zostavax=live-attentuated –> one dose @ age 60 to boost immune response to VZV
  • acyclovir for those w/recurrent shingles (usually immunocompromised)
19
Q

EBV primary infection clinical manifestations

A
  • usually early childhood
  • asymptomatic or mild febrile illness
  • “infectious mononucleosis”=clinical syndrome in older children/teens/adults
  • incubation 4-6 weeks
  • transmission via saliva
20
Q

Infectious mononucleosis signs and symptoms

A
  • caused by EBV (sometimes CMV)
  • symptoms: fever, sore throat, swollen lymph nodes, fatigue
  • signs: exudative tonsillitis, enlarged cervical nodes, splenomegaly, occasional hepatomegaly
  • symptoms=4-8 wks
21
Q

EBV pathogensis

A
  • infection @ nasopharyngeal epithelium –> cell lysis –> spread to salivary glands & oropharyngeal lymphoid tissue
  • viremia –> liver, spleen, infects B cells
  • dormant/latent in n-p epithelium and B cells
  • virus can reactivate, usually w/out symptoms of illness
22
Q

EBV diagnosis

A
  • usually clinical
  • atypical lymphocytes on smear
  • monospot/heterophile tests=test for Abs that agglutinate RBCs
  • EBV serology: tests for Abs to EBV antigens (EBNA and VCA)
23
Q

EBV Prevention/Prophylaxis

A
  • no vaccine

- prevent contact w/infectious saliva

24
Q

Cancers associated w/EBV

A
  • Burkitt’s Lymphoma
  • Hodgkin’s lymphoma
  • Nasopharyngeal carcinoma
  • lymphoproliferative disease
25
Q

EBV treatment

A
  • normal hosts=usually supportive
  • steroids for overly enlarged tonsils
  • attempt to restore immune function in immunocompromised hosts
26
Q

Primary CMV infection clinical characteristics

A
  • infection via contact w/infected body fluids
  • asymptomatic in most healthy people
  • some people have mild febrile illness or mono-like syndrome
  • incubation 2 weeks - 2 months
  • serious in immunocompromised people
27
Q

CMV latency and reactivation

A
  • latent virus in monocytes/lymphocytes and can reactivate periodically
  • reactivation in normal immune systems is asymptomatic, serious in immunocompromised people
28
Q

CMV and pregnancy

A
  • primary CMV infection in pregnancy –> 3-5% chance that the child will be born with a congenital CMV infection
  • 10-15% of infected infants will show symptoms
  • vertical transmission can also occur in reactivation, but risk is lower
29
Q

Congenital CMV syndrome signs/symptoms

A
  • low birth weight
  • microcephaly
  • hearing loss
  • mental impairment
  • hepatosplenomegaly
  • skin rash (“blueberry muffin spots”)
  • jaundice
  • chorioretinitis
30
Q

CMV diagnosis

A
  • serology (CMV IgM and IgG)
  • viral culture
  • PCT
  • direct fluorescence test
  • tissue histology: cells have “owl’s eye” appearance b/c intranuclear inclusion bodies
31
Q

CMV treatment

A
  • none in normal people
  • immunocompromised: gancyclovir or valganciclovir
  • pregnant women: CMV-Ig
  • congenital: oral valganciclovir
32
Q

CMV prevention/prophylaxis

A

-in immunocompromised: CMV-Ig or Ganciclovir or valganciclovir to help prevent

33
Q

RSV general characteristics

A
  • aparamyxoviridae family
  • enveloped virus w/ssRNA
  • 2 important surface proteins:
  • G-protein=viral attachment
  • F-protein=fusion of infected cells to neighboring cells –> syncytia (giant multinucleated cells)
34
Q

RSV clinical manifestation in young children

A
  • bronchiolitis in children lower respiratory involvement

- seasonal peak in winter

35
Q

RSV pathogenesis

A
  • transmission via contact w/respiratory secretions via mucosa of eye/nose
  • incubation 5 days
  • syncytia formed through fusion of adjacent cells
  • bronchiolitis wheezing
36
Q

Rotavirus general characteristics

A
  • reoviridae family
  • dsRNA virus w/segmented genome
  • several serotypes (strains) of rotavirus
  • leading cause of sever diarrhea/gastroenteritis
  • commonly fecal-oral transmission
37
Q

Rotavirus pathogenesis

A
  • infects mature absorptive epithelial cells or enterocytes in proximal 2/3 of ileum
  • cell death –> reduced of absorptive surface, loss of enzymes that break down complex sugars, increased fluid/osmotic load –> diarrhea
38
Q

Rotavirus clinical presentation

A
  • usually infants/young children
  • first infection=sever gastroenteritis
  • subsequent infections are milder or asymptomatic
  • diarrhea, abdominal discomfort, dehydration
  • recovery 7-10 days