VIRUSES Flashcards
(51 cards)
Hepatitis B (dsDNA)
Causative organism: Hepadnavirus (HBV)
Classic Clinical Presentation: Serum hepatitis B, liver cell carcinoma
Pathogenesis: Gapped dsDNA
Treatment/interventions: Pooled IgG
Adenovirus (dsDNA)
Clinical Syndrome: Adenovirus Causative Organism: Adenovirus Classic Clinical Presentation: viral conjunctivitis (very red eyes), fever, pharyngitis Transmission: pool water Epi: kids in pools Pathogenesis: serotypes 3, 7 Method of diagnosis: Treatment/Interventions Treatment mechanism/Adverse effects:
Human Papillomavirus (HPV) (dsDNA)
Clinical Syndrome: HPV Causative Organism: Papillomavirus (HPV) Classic Clinical Presentation: genital warts, cervical cancer Transmission: sexual Epi: Pathogenesis: Method of diagnosis: Treatment/Interventions: vaccine available Treatment mechanism/Adverse effects:
JC virus (aka polyomavirus) (dsDNA)
Clinical Syndrome: PML (progressive multifocal leukoencephalopathy)
Causative Organism: JC virus (aka polyomavirus)
Classic Clinical Presentation: progressive multifocal leukoencephalopathy (PML) in HIV
Transmission: 90% of us have it in genome
Epi: AIDS
Pathogenesis: oligodendroglial cells
Method of diagnosis:
Treatment/Interventions:
Treatment mechanism/Adverse effects:
Variola major
dsDNA
Clinical Syndrome: smallpox
Causative Organism: variola major
Classic Clinical Presentation: vesicular rash limbs and face > trunk (chickenpox more on trunk!)
Transmission: aerosol, person-to-person, very contagious
Epi: eradicated, but bioterrorism
Pathogenesis:
Method of diagnosis: PCR, culture
Treatment/Interventions: live vaccine (dryvax; cidofovir)
Treatment mechanism/Adverse effects: flu-like symptoms common
Parvovirus B-19
ssDNA
Clinical Syndrome: 5th disease (erythema infectiosum)
Causative Organism: Parvovirus B-19
Classic Clinical Presentation: slapped cheek + glove/stocking rash; aplastic crises in sickle-cell disease patients; miscarriage, hydrops fetalis in pregnant women
Transmission: respiratory secretions, blood
Epi: < 10 years old
Pathogenesis: replicates in RBC (binds to P antigen), destroys RBC –> anemia
Method of diagnosis: IgM sero, PCR
Treatment/Interventions: no vaccine
Treatment mechanism/Adverse effects:
HSV1 –> oral herpes (labialis)
Herpes alpha (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Clinical Syndrome: oral herpes (labialis)
Causative Organism: HSV-1
Classic Clinical Presentation: oral herpes (oral vesicles), keratitis/blindness
Transmission: respiratory secretions, saliva
Epi: infect sensory ganglia (painful) HSVs can reactivate and travel to skin (lesions) or to CNS (encephalitis) along motor neurons or olfactory neurons; infect T cells; neuronal dissemination (hematogenous dissemination in neonates, AIDS)
Pathogenesis: latent in trigeminal ganglion (oral lesions because latent near face)
Method of diagnosis: clinical, PCR, serology (IgG, IgM); HSV-1 encephalitis: CSF, PCR=gold!, EEG, MRI, RBCs in CSF*
Treatment/Interventions: Acyclovir (HSV1 > HSV2 > VZV); valacyclovir to decrease transmission to partner
Treatment mechanism/Adverse effects: nucleoside analogues block DNA synthesis; Adverse effects: GI, headache
HSV1 –> temporal lobe encephalitis
Herpes alpha (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Clinical Syndrome: Temporal lobe encephalitis
Causative Organism: HSV-1
Classic Clinical Presentation: necrotizing encephalitis, hemorrhagic necrosis (RBCs in CSF), personality changes bc temporal lobe
Transmission: respiratory secretions, saliva
Epi: infect sensory ganglia (painful) HSVs can reactivate and travel to skin (lesions) or to CNS (encephalitis) along motor neurons or olfactory neurons; infect T cells; neuronal dissemination (hematogenous dissemination in neonates, AIDS)
Pathogenesis: retrograde up trigeminal nerve to brain instead of skin
Method of diagnosis: clinical, PCR, serology (IgG, IgM); HSV-1 encephalitis: CSF, PCR=gold!, EEG, MRI, RBCs in CSF*
Treatment/Interventions: Acyclovir (HSV1 > HSV2 > VZV); valacyclovir to decrease transmission to partner
Treatment mechanism/Adverse effects: nucleoside analogues block DNA synthesis; Adverse effects: GI, headache
HSV2
Herpes alpha (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Clinical Syndrome: genital herpes meningitis
Causative Organism: HSV2
Classic Clinical Presentation: genital or neonatal herpes; meningitis in immunocompromised; neonate: skin-eye-mouth vesicles, CNS
Transmission: sex (mucous membrane contact), perinatal
Epi: infect sensory ganglia (painful) HSVs can reactivate and travel to skin (lesions) or to CNS (encephalitis) along motor neurons or olfactory neurons; infect T cells; neuronal dissemination (hematogenous dissemination in neonates, AIDS)
Pathogenesis: latent in sacral ganglia; thus genital lesions
Method of diagnosis: clinical, PCR, serology (IgG, IgM
Treatment/Interventions: Acyclovir (HSV1 > HSV2 > VZV); valacyclovir to decrease transmission to partner
Treatment mechanism/Adverse effects: nucleoside analogues block DNA synthesis; Adverse effects: GI, headache
VZV
Herpes alpha (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Clinical Syndrome: 1) Varicella (chickenpox); 2) Zoster (Shingles)
Causative Organism: VZV
Classic Clinical Presentation:
Varicella: itchy vesicular rash (1-3 dermatomes on one side); severe in immunocompromised, fetus (encephalitis, pneumonia)
Zoster: unilateral rash, encephalitis (in immunocompromised)
Transmission: respiratory secretions; environmental virions aerosolized from skin lesions
Epi: infect sensory ganglia (painful) HSVs can reactivate and travel to skin (lesions) or to CNS (encephalitis) along motor neurons or olfactory neurons; infect T cells; neuronal dissemination (hematogenous dissemination in neonates, AIDS)
Pathogenesis: all ganglia: Mannose-6-phosphate sorts into endosome; respiratory mucosa –> T cells –> blood –> skin –> sensory neurons –> ganglia
Method of diagnosis: clinical, PCR, serology (IgG, IgM)
Treatment/Interventions: VZV vaccine: live attenuated Oka strain (avoid in pregnancy or if immunocompromised); VariZIG-Zosterig for immunocompromised post-1st exposure
Treatment mechanism/Adverse effects: nucleoside analogues block DNA synthesis; Adverse effects: GI, headache
Cytomegalovirus (CMV in AIDS)
Herpes beta (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Causative organism: CMV
Classic Clinical Presentation: AIDS: retinitis/blindness, GI ulcers + inflammation, encephalitis
Transmission: Person-to-person in basically every way imaginable; 50% of people sero-positive
Epi: prenatal, neonate, severe AIDS, immunocompromised
Pathogenesis: CMV infects GU, GI, or RT –> leukocytes take up virus, hematogenous dissemination –> latent in hematopoietic stem cells (HSCs?), monocytes –> reactivate only if immunocompromised, stress
Method of Diagnosis: AIDS: PCR
Treatment/Interventions: Prenatal: immunoglobulin; Neonatal/AIDS: Gangciclovir or Valganciclovir
Treatment mechanism/Adverse effects: Nucleoside analogues block viral DNA polymerase + replication; Heme/renal/neurotoxicity
Congenital CMV
Herpes beta (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Causative organism: CMV
Classic Clinical Presentation: Prenatal: respiratory problems, rash, hepatosplenomegaly, microcephaly, premature birth, brain damage –> deafness/blindness, cognitive deficits, seizures
Transmission: person-to-person in basically every way imaginable, 50% of people seropositive
Epi: prenatal, neonate, severe AIDS, immunocompromised
Pathogenesis: CMV infects GU, GI, or RT –> leukocytes take up virus, hematogenous dissemination –> latent in hematopoietic stem cells, monocytes –> reactivate only if immunocompromised, stress
Method of Diagnosis: Prenatal: IgG, amniotic PCR; Neonate: PCR
Treatment/Interventions: Prenatal: Immunoglobulin; Neonatal/AIDS: Ganciclovir or Valganciclovir
Treatment mechanism/Adverse effects: Nucleoside analogues block viral DNA polymerase + replication; Heme/renal/neurotoxicity
Cytomegalovirus Mono
Herpes beta (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Causative organism: CMV
Classic Clinical Presentation: Adult: heterophile (negative); mono symptoms
Transmission: person-to-person in basically every way imaginable; 50% of people seropositive
Epi: prenatal, neonate, severe AIDS, immunocompromised
Pathogenesis: CMV infects GU, GI, or RT –> leukocytes take up virus, hematogenous dissemination –> latent in hematopoietic stem cells, monocytes –> reactivates only if immunocompromised, stress
Method of Diagnosis: Adults: Monospot (-), PCR, serology
Treatment/Interventions: prenatal: IG; neonatal/AIDS: ganciclovir or vanganciclovir
Treatment mechanism/Adverse effects: nucleoside analogues block viral DNA polymerase + replication; heme/renal/neurotoxicity
6th Disease (Roseola) = Exanthema Subitum Herpes beta (dsDNA) all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Causative organism: HHV-6, HHV-7 Classic Clinical Presentation: high fever + seizures FOLLOWED BY fine pink rash (mostly trunk), bulging fontanelle (aseptic meningitis); can cause hepatitis, mono symptoms Transmission: respiratory secretions Epi: 6 months-3 years; latent virus can reactivate Pathogenesis: T lymphocytes Method of Diagnosis: Clinical, PCR Treatment/Interventions: Self-limited Treatment mechanism/Adverse effects:
Epstein-Barr Virus Mono
Herpes Gamma (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Causative organism: Epstein-Barr Virus (EBV)
Classic Clinical Presentation: infectious (heterophile (+)) mono; fever, pharyngitis, rash with amp; hepatosplenomegaly, fatigue; lymphoma + cancers of B cells (Burkitt’s Lymphoma)
Transmission: respiratory secretions, saliva
Epi: Burkitt’s Lymphoma = Africa; teens/college
Pathogenesis: B lymphocytes infected + site of latency
Method of Diagnosis: Monospot (+) rapid antibody; Anti-VCA (early-acute mono), Anti-EBNA (late)
Treatment/Interventions: steroids sometimes
Treatment mechanism/Adverse effects:
Kaposi’s Sarcoma
Herpes Gamma (dsDNA)
all herpes viruses: enveloped when infectious (no envelope spreading cell-to-cell); latent in DRG (HSV1,2) or lymph nodes/cells (rest); glycoprotein antigens expressed by infected cell AND on virion envelope (innate immune system), particularly affect immunocompromised. Congenital (CMV, VZV), neonatal (HSV, VZV) very bad.
Causative organism: HHV-8 (aka Kaposi’s Sarcoma Virus)
Classic Clinical Presentation: asymptomatic in most; immunocompromised: dark purple lesions, Castleman’s disease (lymphoma-like)
Transmission: sexual contact
Epi: AIDS, elderly
Pathogenesis: encodes human proteins (piracy); IL-6, Bcl2, etc.
Method of Diagnosis: Clinical
Treatment/Interventions:
Treatment mechanism/Adverse effects:
Rotavirus (Winter Vomiting Disease)
dsRNA
(segmented Reovirus = “repeat-o-virus”
Causative organism: Rotavirus
Classic Clinical Presentation: most common cause of kid GEitis; self-limited vomiting then 4-8 day watery diarrhea, abdominal pain, low fever, high mortality in developing world (dehydration)
Transmission: fecal-oral, fomites
Epi: kids in winter; teens/adults asymptomatic
Pathogenesis: segmented dsRNA, no envelope, has RNA-dependent RNA polymerase; Enterotoxin NSP4 –> Ca2+ efflux, villi death, malabsorption, inflammation
Method of Diagnosis: clinical; Wheels on microscopy; stool ELISA
Treatment/Interventions: vaccine; RotaTeq, Rotarix; Rehydration therapy; good hygiene
Treatment mechanism/Adverse effects: DO NOT USE anti-diarrheal medications
Poliomyelitis
Picorna (+) ssRNA
Causative organism: Poliovirus
Classic Clinical Presentation: 90% asymptomatic; 8% flu-like symptoms; 2% viremia –> CNS via vagus nerve –> meningitis (stiff neck, photophobia); <1% paralytic polio (CNS: neuronal necrosis, respiratory paralysis +/- asymmetrical paralysis/weakness (peripheral limbs), 10% die
Transmission: fecal-oral (shedding even while asymptomatic)
Epi: summer; sustained transmission (?) only in 4 countries
Pathogenesis: acid-resistant virus passes through stomach, hematogenous spread, 1% infects CNS
Method of Diagnosis: PCR (oropharynx first, stool if negative); serology
Treatment/Interventions: IPV (inactivated polio vaccine-3 shots + 5 year booster); OPV-(oral polio vaccine, not in US); herd immunity
Treatment mechanism/Adverse effects: OPV has small risk of vaccine-associated polio/VAPP (but confers lifelong + intestinal immunity, better herd immunity)
Bulbar paralytic poliomyelitis
Picorna (+) ssRNA
Causative organism: Poliovirus
Classic Clinical Presentation: CN necrosis (esp CN 9 + 10) –> dysphagia, altered speech, paralyzed CNS vasomotor + respiratory centers, 50% fatality
Transmission: fecal-oral (shedding even while asymptomatic)
Epi: summer; sustained transmission (?) only in 4 countries
Pathogenesis: acid resistant virus passes through stomach, hematogenous spread, 1% infects CNS
Method of Diagnosis: PCR (oropharynx first, stool if negative); serology
Treatment/Interventions: IPV-inactivated polio vaccine (3 shots + 5 year booster); OPV- Oral live vaccine (not in U.S.); herd immunity
Treatment mechanism/Adverse effects: OPV has small risk of vaccine-associated polio/VAPP (but confers lifelong + intestinal immunity, better herd immunity)
Enterovirus exanthems
Picorna (+) ssRNA
Causative organism: Echovirus Classic Clinical Presentation: morbilliform rash, maculopapular (red area with confluent bumps); roseoliform rash: discrete macules (color change, flat) + papules (raised bumps) Transmission: Epi: Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Encephalitis
Picorna (+) ssRNA
Causative organism: Echovirus Classic Clinical Presentation: Encephalitis Transmission: Epi: Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Common cold
Picorna (+) ssRNA
Causative organism: Rhinovirus Classic Clinical Presentation: common cold Transmission: Epi: Pathogenesis: Method of Diagnosis: clinical Treatment/Interventions: Treatment mechanism/Adverse effects:
Conjunctivitis
Picorna (+) ssRNA
Causative organism: Coxsackie A (or enterovirus 70)
Classic Clinical Presentation: self-limited acute hemorrhagic conjunctivitis
Transmission: VERY CONTAGIOUS: fingers, fomites
Epi: VERY CONTAGIOUS: fingers, fomites
Pathogenesis:
Method of Diagnosis:
Treatment/Interventions:
Treatment mechanism/Adverse effects:
Hand-Foot-Mouth Disease
Picorna (+) ssRNA
Causative organism: Coxsackie A (or Enterovirus 70)
Classic Clinical Presentation: painful vesicles on hand, foot, mouth
Transmission: person-to-person
Epi: kids, Asian outbreaks
Pathogenesis:
Method of Diagnosis: clinical
Treatment/Interventions: self-limited, supportive care
Treatment mechanism/Adverse effects: