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
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
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
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
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
6
Q
HSV diagnosis
A
- usually clinical but may use:
- Tzanck smear
- HSV culture
- Direct Fluorescent Antigen stain
- PCR of lesions
7
Q
HSV treatment
A
- severe HSV (in neonate/immunocompromised or encephalitis)–> IV acyclovir
- oral antiviral therapy
8
Q
VZV clinical syndromes
A
-2 main syndromes: chicken pox and shingles
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
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
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
12
Q
Primary VZV infection treatment
A
- usually self-limited and requires no treatment
- treatment accelerates resolution/decreases symptoms
- treatment necessary for immunocompromised patients
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)
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
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
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
