VIRUSES Flashcards
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:
Aseptic Meningitis
Picorna (+) ssRNA
Causative organism: Coxsackie B
Classic Clinical Presentation: headache, photophobia, fever, stiff neck; Encephalitis. Resolves in kids (approximately?). More complicated in adults.
Transmission:
Epi: summer, kids
Pathogenesis:
Method of Diagnosis: lumbar puncture, PCR of CSF
Treatment/Interventions: self-limited, IV-IG (IV immunoglobulin) if recurrent
Treatment mechanism/Adverse effects:
Myopericarditis
Picorna (+) ssRNA
Causative organism: Coxsackie B (or Echovirus)
Classic Clinical Presentation: Upper respiratory tract (URT) infection seeds to heart –> local necrosis, inflammation, can cause chronic heart failure (CHF)
Transmission:
Epi: child and teen males 2:1
Pathogenesis:
Method of Diagnosis:
Treatment/Interventions: IVIG (IV immunoglobulin) if bad; worst case: transplant
Treatment mechanism/Adverse effects:
Neonatal sepsis
Picorna (+) ssRNA
Causative organism: Enterovirus
Classic Clinical Presentation: hepatic necrosis, sepsis-like symptoms, myocarditis, encephalitis, high fatality rates
Transmission: perinatal transmission from mother
Epi: newborns
Pathogenesis:
Method of Diagnosis:
Treatment/Interventions: IVIG (IV immunoglobulin)
Treatment mechanism/Adverse effects:
Non-specific rash, fever
Picorna (+) ssRNA
Causative organism: common symptoms enterovirus Classic Clinical Presentation: self-limited; most common symptoms of enterovirus infections Transmission: Epi: Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Norovirus (enterovirus)
Calicivirus (+) ssRNA
Causative organism: Norovirus (aka Norwalk virus)
Classic Clinical Presentation: 1-3 days; self-limited diarrhea, vomiting, maybe flu-like symptoms (especially cruises). causes blunting of jejunum villi.
Transmission: feca-oral, fomites, aerosol-vomitus; food-borne outbreaks. HIGHLY CONTAGIOUS (10 particles!)
Epi: causes 50% of viral gastroenteritis; cruise ships; point source outbreaks (foodborne); all ages because no immunity
Pathogenesis: no envelope, encodes 4 peptides: helicase (unwind RNA), protease (cleaves mRNA peptide), RNA polymerase, capside; no toxin
Method of Diagnosis: 1) clinical (vomiting + diarrhea > 50% of people infected); 2) RT-PCR (reverse transcriptase PCR) on stool or vomit
Treatment/Interventions: supportive (rehydration)
Treatment mechanism/Adverse effects: hard to find supportive care on a cruise ship
West Nile
Flavi (+) ssRNA
(All Arboviruses)
Causative organism: West Nile Virus
Classic Clinical Presentation: Fever, headache, myalgias, lymphadenopathy, rash, acute flaccid paralysis
Transmission: Mosquito; subacute infection in most; encephalitis in very young, old, immunocompromised
Epi: all cause ENCEPHALITIS; need mosquito presence; summer in temperate climates, tropics
Pathogenesis: hematogenous spread
Method of Diagnosis: IgM in CSF, PCR
Treatment/Interventions: supportive
Treatment mechanism/Adverse effects:
St. Louis Encephalitis
Flavi (+) ssRNA
(All Arbovirus)
Causative organism: St. Louis Encephalitis Virus
Classic Clinical Presentation:
Transmission: Mosquito; subacute infection in most; encephalitis in very young, old, immunocompromised
Epi: all cause ENCEPHALITIS; need mosquito presence; summer in temperate climates, tropics
Pathogenesis:
Method of Diagnosis:
Treatment/Interventions:
Treatment mechanism/Adverse effects:
Dengue fever
Flavi (+) ssRNA
(All Arboviruses)
Causative organism: dengue virus Classic Clinical Presentation: Transmission: mosquito; subacute infection in most; encephalitis in very young, old, immunocompromised Epi: Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Yellow fever
Flavi (+) ssRNA
(All arboviruses)
Causative organism: Yellow fever virus Classic Clinical Presentation: Transmission: mosquito; subacute infection in most; encephalitis in very young, old, immunocompromised Epi: all cause ENCEPHALITIS; need mosquito presence; summer in temperate climates, tropics Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Congenital Rubella
Toga (+) ssRNA
Causative organism: Rubella virus
Classic Clinical Presentation: deafness, cataracts, microcephaly, blueberry muffin rash, retards in-utero growth, cardiac defects
Transmission: pregnant woman inhales in 1st-2nd trimester
Epi: prenatal
Pathogenesis: C, E1, E2. Virus replicates in lymph nodes, viremia –> delayed rash. Enveloped.
Method of Diagnosis: IgM serology; PCR
Treatment/Interventions: Prevention only; avoid live virus vaccine (if pregnant?)
Treatment mechanism/Adverse effects: live vaccine can cause disease
Rubella (German measles)
Toga (+) ssRNA
Causative organism: Rubella virus
Classic Clinical Presentation: posterior auricular lymph nodes inflamed (posterior auricular lymphadenopathy); low fever. Milder measles symptoms. Rash on head –> toe in 24 hours
Transmission: inhalation
Epi: kids
Pathogenesis: C, E1, E2. Virus replicates in lymph nodes, viremia –> delayed rash. Enveloped.
Method of Diagnosis: PCR, IgM serology (4 times titer inc 2 weeks apart).
Treatment/Interventions: Vaccine: MMR
Treatment mechanism/Adverse effects:
East/West Equine Encephalitis
Toga (+) ssRNA
Causative organism: Alphavirus Classic Clinical Presentation: Transmission: mosquito Epi: Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
SARS
(+) ssRNA
Causative organism: Coronavirus Classic Clinical Presentation: Transmission: Epi: Pathogenesis: Enveloped; propagated epidemic Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Flu
Orthomyxo
(-) ssRNA; segmented
all (-) RNA viruses carry their own RNA-dependent RNA polymerases within virion to do: (-) ssRNA –> mRNA or (+) ssRNA –> dsRNA –> (-) ssRNA for replication
Causative organism: Influenza A
Classic Clinical Presentation: “Flu-like symptoms” 4-8 days –> fever, chills, headache, myalgias, arthralgias, dry cough, nasal discharge.
Complications: bacterial pneumonia, bacterial superinfection, bacterial sepsis, myositis (muscle), Reye’s syndrome
Transmission: respiratory secretions
Epi: genetic drift (random mutations, small change) & genetic shift (genome segments trade in co-infection, huge change) –> new strains annually
Pathogenesis: Hemagluttanin, Neuraminidase, M2 (M2 is A-only, makes ion channel); infects & destroys columnar epithelial cells in upper respiratory tract (increased mucous, ciliary stasis)
Method of Diagnosis: clinical, nasal secretions: culture, rapid antigen testing (PCR only used for H1N1). Check for pneumonia co-infection
Treatment/Interventions: Amantadine (A-only: blocks M2); Neuraminidase inhibitors (oseltamavir, zanamavir); vaccines: TIV (dead > 6 months of age) or LAIV (live, nasal, 2-50 yo)
Treatment mechanism/Adverse effects: decreased uncoating via M2 proteins, decreased budding
Flu
Orthomyxo
(-) ssRNA; segmented
all (-) RNA viruses carry their own RNA-dependent RNA polymerases within virion to do: (-) ssRNA –> mRNA or (+) ssRNA –> dsRNA –> (-) ssRNA for replication
Causative organism: Influenza B
Classic Clinical Presentation: “flu-like symptoms” 4-8 days –> fever, chills, headache, myalgias, arthralgias, dry cough, nasal discharge
Complications: bacterial pneumonia, bacterial superinfection, bacterial sepsis, myositis (muscle), Reye’s
Transmission: respiratory secretions
Epi: genetic drift (random mutation, small change) & shift (genome segments trade in co-infection, large change) –> new strains annually
Pathogenesis: Hemagluttanin, Neuraminidase, M2 (M2 is A-only, makes ion channel); infects & destroys columnar epithelial cells in upper respiratory tract (increased mucous, ciliary stasis)
Method of Diagnosis: clinical, nasal secretions: culture, rapid antigen testing, (PCR only used for H1N1). Check for pneumonia co-infection
Treatment/Interventions: Amantadine (A only; blocks M2); Neuraminidase inhibitors (oseltamavir, zanamavir); vaccines: TIV (dead, > 6 months old) or LAIV (live, nasal, 2-50 yo)
Treatment mechanism/Adverse effects: decreased budding
Avian Flu
Orthomyxo
(-) ssRNA; segmented
all (-) RNA viruses carry their own RNA-dependent RNA polymerases within virion to do: (-) ssRNA –> mRNA or (+) ssRNA –> dsRNA –> (-) ssRNA for replication
Causative organism: Classic Clinical Presentation: Transmission: Epi: Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Bronchiolitis Pneumonia
Paramyxo
(-) ssRNA
all (-) RNA viruses carry their own RNA-dependent RNA polymerases within virion to do: (-) ssRNA –> mRNA or (+) ssRNA –> dsRNA –> (-) ssRNA for replication
Causative organism: RSV (Respiratory Synctial Virus)
Classic Clinical Presentation: upper respiratory tract infection symptoms –> lower respiratory tract infection (50%) –> bronchiolitis (croup) or pneumonia (alveoli) –> edema, necrosis, atelectasis (mini lung collapse)
Transmission: respiratory secretions or fomites; reinfections frequent
Epi: HAI, all kids by 2 yo; severe disease if premature baby, immunosuppressed, chronic heart disease (CHD?), neonate; winter
Pathogenesis: G, F=fusion (forms syncytia); can survive on fomites
Method of Diagnosis: clinical viral culture, rapid antigen test if hospitalized
Treatment/Interventions: supportive; if high risk: prophylactic Palvizumab (Ig for Fusion protein) > RSV-IgIV
Treatment mechanism/Adverse effects: bronchodilators, steroids, antivirals don’t help
Rubeola Virus (Measles)
Paramyxo
(-) ssRNA
all (-) RNA viruses carry their own RNA-dependent RNA polymerases within virion to do: (-) ssRNA –> mRNA or (+) ssRNA –> dsRNA –> (-) ssRNA for replication
Causative organism: Rubeola virus
Classic Clinical Presentation: measles rash (face –> body, maculopapular), conjunctivitis, Koplik’s spots (oral lesions), otitis media (OM?), croup. Complications: encephalitis, sclerosing panencephalitis (years later: degenerative CNS disease)
Transmission: inhalation
Epi: kids without vaccines (especially in 6 months-1 yo)
Pathogenesis: H (hemagluttanin), F (fusion), M (matrix) proteins; Viremia –> rash 2 weeks later
Method of Diagnosis: Serology: IgM-IgG titer (4x increase)
Treatment/Interventions: vaccine (live attenuated) at 1 yo; Ribavarin: report to DOH
Treatment mechanism/Adverse effects: don’t give vaccine if immunosuppressed
Mumps
Paramyxo
(-) ssRNA
all (-) RNA viruses carry their own RNA-dependent RNA polymerases within virion to do: (-) ssRNA –> mRNA or (+) ssRNA –> dsRNA –> (-) ssRNA for replication
Causative organism: Mumps virus
Classic Clinical Presentation: parotid gland inflammation, fever, morbilliform rash (maculopapular), orchitis (inflammation of testes), meningitis, in utero heart defects
Transmission: inhalation
Epi: religious brooklyn population, anyone without vaccine
Pathogenesis: HN (hemagluttanin, neuraminidase), F (fusion), 7 structural 20 day incubation, viremia –> seeds CNS, testes, salivary glands
Method of Diagnosis: IgM-IgG titer (4x increase), PCR
Treatment/Interventions: MMR vaccine
Treatment mechanism/Adverse effects: vaccine not 100% effective
Rabies Rhabdo (-) ssRNA
Causative organism: rabies virus
Classic Clinical Presentation: encephalitis, delirium, hypersalivation, hydrophobia (pharyngeal muscles spasms) –> coma, flaccid paralysis, death (infects PNS, CNS, innervated organs)
Transmission: bite from dog or wild animal, exposure to bats
Epi: active (?) incubation 1-2 months (long!) distal from bite to brain (approximate time to symptoms)
Pathogenesis: replicate in NMJ; infect motor neurons in PNS –> CNS –> PNS again; replicate in salivary glands where sensory nerves end
Method of Diagnosis: RT-PCR (reverse transcriptase PCR) of saliva, skin biopsy neckline (lots of nerves); Negri bodies in brain, Ig in CSF
Treatment/Interventions: Pre-exposure: inactive vaccine; post-exposure: RIG (rabies immunoglobulin, passive immunity) in wound & active vaccine HDCV
Treatment mechanism/Adverse effects: if you have symptoms, you’re pretty much dead
Ebola
Filo
(-) ssRNA
Causative organism: Ebola virus Classic Clinical Presentation: hemorrhagic fever, encephalitis Transmission: Epi: Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
HIV/AIDS
Retroviruses
(+) ssRNA
Causative organism: HIV-1
Classic Clinical Presentation: Acute: asymptomatic, flu-like/mono-like symptoms, GALT loss (bacteremia). Antibodies by 6-12 weeks
Established: low viremia, NOT latent. Asymptomatic for years. Prone to HSV zoster, TB, Kaposi’s sarcoma, pneumonia.
AIDS: CD4 < 200; Opportunistic Infection: CD4 < 300
Opportunistic Infections: PCP, toxoplasmosis, TB, CMV, MAC, IRIS, cryptococcus, PML, lymphoma, peripheral neuropathy, dementia
Transmission: person-to-person via sex, mom to fetus or breastmilk, blood-to-blood contact (IV drug users)
Epi: MSM, IV drug users; ave patient; VLSPn is about 30,000 HIV RNA/mL at six months
Pathogenesis: gp120 binds CD4+ R5/X4, gp41 mediates fusion, DNA integrates into genome of CD4. Homozygous CCR5- (negative) 32 deletion = immune to R5 (strain of HIV); heterozygous HLA = controller
Method of Diagnosis: Acute: Plasma HIV RNA culture or PCR, follow up with antibody test. Established: ELISA + WB to confirm AIDS if CD4 < 200 (normal 800-1200)
Treatment/Interventions: if CD4 <500: HAART: 2 nucleoside reverse transcriptase inhibitors (NRTI) + (NNRTI=non-nucleoside reverse transcriptase inhibitors or INSTI=integrase inhibitor or PI=protease inhibitor + Ritonavir); New York State: treat at any CD4 level
Treatment mechanism/Adverse effects: Calculate CD4: WBC x lymph% x CD4%
ATLL (adult T cell leukemia/lymphoma)
Retroviruses
(+) ssRNA
Causative organism: HTLV (human T lymphotropic virus) Classic Clinical Presentation: strongyloides hyperinfection Transmission: Epi: Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Hantavirus
Emerging
Causative organism: Sin Nombre virus Classic Clinical Presentation: Transmission: Epi: southwestern U.S. Pathogenesis: Method of Diagnosis: Treatment/Interventions: Treatment mechanism/Adverse effects:
Variant Creutzfeldt-Jakob Disease (vCJD)
Emerging
Causative organism: Prions (HuPrPSc)
Classic Clinical Presentation: Spongiform encephalopathy, dementia, ataxia, death
Transmission: eat cow that ate offal
Epi: Brit that eats beef
Pathogenesis: normal prion protein PrPc gets converted to Beta-pleated form, which forms plaques in brain
Method of Diagnosis: holes in brain WITHOUT INFLAMMATION
Treatment/Interventions:
Treatment mechanism/Adverse effects:
Anthrax
Bioterrorism
Causative organism: Bacillus Anthracis
Classic Clinical Presentation: ALL: sepsis, meningitis (esp inhaled). Cutaneous: painless vesicles –> ulcers –> painless black eschars; Inhaled: pleural effusion, necrotizing mediastinitis, respiratory failure; Intestinal: local necrosis, lymphadenitis, ascites, peritonitis; Injected: severe soft tissue infection
Transmission: cutaneous, inhalation, ingestion (undercooked or contaminated meat)-working with animal hides, drums. Spores phagocytized by macrophages.
Epi:
Pathogenesis: spores (viable for years) enter body; 3 exotoxins (LT = PA + LF; ET = PA + EF)…(PA=protective antigen; EF=edema factor; LF=lethal factor) –> phagocytosis by macrophages –> local necrosis, regional lymphadenitis, septicemia, seeds organs, meningitis, death (20-60%).
Method of Diagnosis: Cutaneous: skin biopsy best (PCR)/vesicular fluid aspiration; Inhalation: chest xray (CXR) to assess for adenopathy/effusions; PCR blood, CSF, sputum
Treatment/Interventions: Ciprofloxacin (quinolone) + doxycycline (or meropenem, ampicillin, or vancomycin) for 60 days, or 10 days cutaneous; clindamycin for toxin production; Anthrax Ig for very sick patients; mortality high for inhaled!
Treatment mechanism/Adverse effects:
Disseminated MAC
Bacterial
Causative organism: Mycobacterium avium
Classic Clinical Presentation: fever, weight loss, anemia and diarrhea, hepatosplenomegaly
Transmission: ingest from soil, water
Epi: AIDS CD4 < 50
Pathogenesis:
Method of Diagnosis: biopsy of infected organs, blood culture
Treatment/Interventions: azithromycin + ethambutol
Treatment mechanism/Adverse effects:
