Common Viral Pathogens Flashcards Preview

Disease & Defense - Unit 3 > Common Viral Pathogens > Flashcards

Flashcards in Common Viral Pathogens Deck (38):

Virus vs. Bacteria

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


Common laboratory tests looking for actual virus

-culture w/in tissue
-assay to look for antigens
-PCR to amplify portion of viral genome


Common laboratory test looking for host immune response to virus

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


8 herpes viruses which infect humans

-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


Clinical manifestations of HSV-1/HSV-2

-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


HSV diagnosis

-usually clinical but may use:
-Tzanck smear
-HSV culture
-Direct Fluorescent Antigen stain
-PCR of lesions


HSV treatment

-severe HSV (in neonate/immunocompromised or encephalitis)--> IV acyclovir
-oral antiviral therapy


VZV clinical syndromes

-2 main syndromes: chicken pox and shingles


Clinical manifestations of primary VZV infection

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


Pathogenesis of primary VZV infection

-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


Prevention of HSV-1/HSV-2

-no vaccine
-hand hygiene/physical barriers
-avoid contact
-prevent reinfection w/lower doses of acyclovir on daily basis


Primary VZV infection treatment

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


VZV varicella prevention/prophylaxis

-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)


Pathogenesis of VZV latency and reactivation

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


VZV reactivation infection clinical manifestations

-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


VZV reactivation (Zoster) diagnosis

-usually diagnosed clinically
-also: Direct IFA, PCR, or culture


VZV reactivation (Zoster) treatment

-acyclovir decreases number/duration of lesions and pain
-pain treated w/NSAIDs, opiates, sometimes steroids


VZV reactivation (Zoster) prevention/prophylaxis

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


EBV primary infection clinical manifestations

-usually early childhood
-asymptomatic or mild febrile illness
-"infectious mononucleosis"=clinical syndrome in older children/teens/adults
-incubation 4-6 weeks
-transmission via saliva


Infectious mononucleosis signs and symptoms

-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


EBV pathogensis

-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


EBV diagnosis

-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)


EBV Prevention/Prophylaxis

-no vaccine
-prevent contact w/infectious saliva


Cancers associated w/EBV

-Burkitt's Lymphoma
-Hodgkin's lymphoma
-Nasopharyngeal carcinoma
-lymphoproliferative disease


EBV treatment

-normal hosts=usually supportive
-steroids for overly enlarged tonsils
-attempt to restore immune function in immunocompromised hosts


Primary CMV infection clinical characteristics

-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


CMV latency and reactivation

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


CMV and pregnancy

-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


Congenital CMV syndrome signs/symptoms

-low birth weight
-hearing loss
-mental impairment
-skin rash ("blueberry muffin spots")


CMV diagnosis

-serology (CMV IgM and IgG)
-viral culture
-direct fluorescence test
-tissue histology: cells have "owl's eye" appearance b/c intranuclear inclusion bodies


CMV treatment

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


CMV prevention/prophylaxis

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


RSV general characteristics

-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)


RSV clinical manifestation in young children

-bronchiolitis in children lower respiratory involvement
-seasonal peak in winter


RSV pathogenesis

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


Rotavirus general characteristics

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


Rotavirus pathogenesis

-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


Rotavirus clinical presentation

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