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Week 4 Quiz Flashcards

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1
Q

Papillomaviridae-

  1. DNA/RNA, ds/ss,
  2. enveloped/non enveloped,
  3. capsid
  4. Replication
  5. Species that can be infected?
A
  1. dsDNA- circular genome
  2. Non enveloped
  3. Capsid is icosahedral with L1 (80%) and L2 (20%) proteins
  4. in nucleus of cells in differentiated skin
  5. Only humans
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2
Q

Papillomavirus Infection subtypes

A
  1. Skin
  2. Mucosa
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3
Q

Papillomavirus skin infection

A
  • HPV 1-4 : Benign skin proliferation on soles of hands and feet.
    • wart types: plantar, flat, and common warts
  • 3-4 month incubation
  • contact only contagious if open wound
  • Regresses without therapy,
  • recurrence common
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4
Q

Papillomavirus Mucosal infection types

A
  1. Single oral papillomas- most common benign tumor of oral cavity, RARELY RECUR after removal.
  2. Laryngeal papillomas-HPV-6 and HPV 11 can obstruct airway= life threatening. Can RECUR after surgical removal
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5
Q

Papillomavirus genital warts (AKA?)

  1. HPV types that caus it?
  2. Epidemiology?
A

Condylomata acuminata

HPV-6 and HPV-11 spread by sexual contact.

Epidemiology: 1% of sexually active US population, mostly age 15-40

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6
Q

Cervical dysplasia and neoplasia

  1. HPV types
  2. How does it cause cancer?
  3. % of cervical cancer from HPV
A
  1. HPV 16, 18, 31, 45 –infection of female genital tract.
  2. HPV breaks E1/E2 genes= decreased inhibition of E6/E7 E6/E7 =oncogenic proteins, inactivate p53 and RB genes= decreased apoptosis.
  3. 85% of cervical cancer has HPV-DNA
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7
Q

HPV type of infection outcome

A
  1. Productive infection- Early= production of viral DNA capsid proteins. Late= only in terminally differentiated cells of epidermis–>KOILOCYTOSIS
  2. Latent infection - no signs or symptoms. Basal layer of epidermis invaded by HPV. months-years
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8
Q

Koilocytes

A

DIAGNOSTIC= Multinucleation, nuclear enlargement, hyperchromasia, irregular outline, and perinuclear halo HPV infection

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9
Q

HPV transmission

A

Via fomites, shedding through

  1. open wound
  2. sex
  3. birth
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10
Q

HPV Control

A
  1. Creams
  • Podphyllin and podofilox= lotion/gel to remove warts–they stop the growth cycle
  • Aldara= stimulates immune cells to make cytokines and interferons
  1. Vaccines-
  • ​GARDASIL= prophylactic (preventative), contains L1 proteins that assemble into VPL (virus like particles) that look like HIV. VPLs for 6, 11, 16, 18
  • CERVARIX = VPL 16, 18
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11
Q

Polyomaviridae

  1. DNA/RNA, ds/ss,
  2. enveloped/non enveloped
  3. capsid
  4. Replication
  5. Species that can be infected?
A
  1. dsDNA
  2. non enveloped
  3. n/a (compared to papillomaviridae)
  4. Nuclear (probably?)
  5. immunocompromised humans, also reactivated during pregnancy with no effects on fetus
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12
Q

JC infection

A
  • Progressive multifocal leukoencephalopathy (PML)
  • infection of oligodendrocytes–> decreased myelin in brain
  • speech, vision coordination, mentation affected –>paralysis and death.
  • Die within 1-4 months, most die within 2 years.
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13
Q

BK virus infection–2 different types of transplant patients

A
  1. Ureteral stenosis in renal transplant recipients
  2. Hemorrhagic cystitis in bone marrow recipients
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14
Q

Polyomavirus pathogenesis

A
  1. Enter respiratory tract and the multiply
  2. Primary viremia
  3. replicate in kidney
  4. transient secondary viremia
  5. If immunodeficient: Reactivation =
  • JC- viremia and CNS infection = PML
  • BK- latent infection in kidney. Viruria=shedding through urine, can cause hemorrhagic cystitis
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15
Q

HPV types that cause

  1. warts
  2. condyloma acuminata
  3. cervical and genital cancer
A
  1. Warts 1, 4
  2. Condyloma acuminata= 6,11
  3. Cervical and genital cancer: 16,18
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16
Q

Hepatitis A

  1. Family (structure of virus)
  2. infection
  3. Resistance/vulnerable
A
  1. Picornavirus= +ssRNA, icosahedral, non enveloped, VPg on 5’ end.
  2. fecal/oral= Acute, not chronic (AAA= Acute, alone, asymptomatics)
  3. **Resistant to: **to: acid, solvents, water, drying, temp: 3-61C Vulnerable to: Chlorine, formalin, peracetic acid, b-propiolactone, UV radiation
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17
Q

Hepatitis A Symptoms

A
  1. Incubation: 2-6 weeks. Immune mediated damage to liver cells
  2. Prodrome: flu-like symptoms, nausea, vomiting, fatigue, headache, anorexia
  3. Icteric Phase: starts with dark urine (bilirubinuria)–> pale stool jaundice: abdominal pain, itching- symptoms wane during this period?
  4. Recovery 99%
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18
Q

**Hep A Pathogenesis **

A
  1. Ingestion
  2. Replication in GI/oropharyngeal tract
  3. Transporation/replication in liver
  4. Shed in bile= transport to intestines
  5. Shed in feces
  6. Brief viremia
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19
Q

Hep A virus time course

A
  1. 0-1 month: fecal HAV
  2. 1 month: symptoms, ALT spikes
  3. anti-IgG HAV increases for 12 months, indicates prior infection and protects against reinfection
  4. HAV IgM- peaks at 3 months, indicates acute HAV infection. Gone by about 5.5 months
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20
Q

HAV

  1. Transmission (x3)
  2. Epidemiology
  3. Control
A
  1. Transmission
  • Close contact (household contact, sex, daycare centers)
  • Contaminated food, water
  • Blood (very rare)
  1. Epidemiology
  • ​1.5 million cases worldwide- mostly south and central america, Africa, Asia, Middle East,
  • 40-70% of US people have antibodies to HAV
  1. Control- hygeine, vaccination
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21
Q

Diagnosing HAV

  1. - HAV IgG, + HAV IgM
  2. +HAV IgG, + HAV IgM
    • HAV IgG, -HAV IgM
  4. -HAV IgG, -HAV IgM
A

IgM= early marker, acute infection

IgG= Past infection or late current infection, vaccination, protects against reinfection

  1. Acute HAV infection
  2. Acute HAV infection (later stage than 1)
  3. Immunity to HAV
  4. No exposure- no acute infection or immunity (at risk)
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22
Q

Hepatitis B

  1. Family
  2. Transmission
  3. Carrier
  4. Incubation
  5. HCC risk
A
  1. hepadnavirus= dsDNA, circular, enveloped
  2. BBB=blood, birthing, babymaking,
  3. Yes
  4. Long
  5. Yes
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23
Q

Hep B

  1. Structure
  2. Replication
A
  1. dsDNA ciruclar
    • icosahedral capsid with Core protein (HBcAg) and soluble core protein (HBeAg)
    • envelope with Surface antigen (HBsAg) in three forms:
      • S- large HBsAg
      • S2-medium
      • S= small HBsAg
  2. Carries DNA polymerase and codes for reverse transcriptase
    • Nucleus: relaxed dsDNA–> CCC DNA (covalently closed circular DNA), transcription to 4 mRNA
    • Cytoplasm: translation, core proteins assembled. (-) DNA made from mRNA with encoded reverse transcriptase.
    • Budding: mRNA is degraded. Budding through ER and exocytosis
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24
Q

Hepatitis B Symptoms

  1. Acute
  2. Chronic
A
  1. Acute:
    • Incubation= 1-6 months,
    • Majority asymptomatic, during replication phas
    • some develop jaundice= fatigue, anorexia, nausea
    • Rarely develop fulminant hepatitis =may develop GI bleeding, hepatic encephalopathy, ascites
    • recovery= lifetime immunity
  2. Chronic:
    • Infection lasted >6months
    • Asymptomatic or symptomatic (nausea, anorexia, fatigue, upper quadrant pain) carriers
    • Complications: liver damag–> cirrhosis–> cancer–> death
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25
Q

HBV pathogenesis

Acute vs Chronic

A

Acute

  1. HBV infects liver
  2. Antibodies kill infected cells= Acute disease symtpoms (jaundice, release of enzymes)
  3. Resolution

Chronic

  1. HBV infects liver
  2. Immune response is insufficient
  3. Develop fulminant hepatitis, primary hepatocellular carcinoma, cirrhosis
26
Q

Acute HBV - markers/time course

  1. HBeAg
  2. AntiHBC IgM
  3. AntiHBC IgG
  4. AntiHBs
  5. Anti HBe
A
  1. **HBeAg= active viral replication- very contagious: **4weeks-24 weeks, peaks at 10
  2. IgM AntiHBc=acute/recent infection- 6-32 weeks, peaks at 16 weeks**only marker during window period
  3. AntiHBc IgG- prior exposure or chronic infection
  4. **AntiHBs- immunity to HepB- **starts rising at 32 weeks, peaks at 36 and slowly decreases
  5. AntiHBe- antibody to HBeAG= low transmissibility. if acute infection, peaks within 4 months, chronic-years
27
Q

What markers would you find in

  1. Acute HBV
  2. Window
  3. Chronic HBV (high infectivity)
  4. Chronic HBV (low infectivity)
  5. Recovery
  6. Immunized
A
  1. Acute: HBsAg, **HBeAg, **Anti-HBc (IgM)
  2. Window: (**Anti-HBe-maybe) **AntiHBc (IgM)–ALWAYS MARKER FOR WINDOW
  3. Chronic (high) IgG Anti HBc, HBsAg, HBeAg
  4. Chronic (low) Anti HBeAg, IgG Anti-HBc, HBsAg
  5. Recovery: AntiHBs, AntiHBe, IgG Anti-HBc
  6. Immunized: ** AntiHBs**
28
Q

What do these markers indicate?

  1. HBs-Ag
  2. AnitHBs
  3. HBcAg
  4. AntiHBc
  5. HBeAg
  6. AntiHBe
A
  1. HBs-Ag-on HBV surface, indicates hep B infection
  2. AnitHBs-immunity to hep B
  3. HBcAg-Core HBV protein
  4. AntiHBc-
    • IgM= acute/recent infection, window periord
    • IgG= previous infection or chronic infection,
  5. HBeAg-soluble core protein that indicates active replication= high infectivity
  6. AntiHBe- low infectivity
29
Q

HepB treatment and control

A
  1. Treatment
    • Acute: No treatment
    • Chronic: reverse transcriptase inhibitors Lamivudine and Adefovir (+ alpha-interferon)
  2. ​Control
    • ​​screening donated blood
    • universal blood body fluid precautions
    • HBsAg vaccinations (3 series)
    • HAV, HVB vaccination (twintix)
30
Q

HBC Infection

  1. Family
  2. Transmission
  3. Carrier
  4. Incubation
  5. HCC risk
A
  1. RNA flavivirus
  2. blood, (IVDU, post- transfusion)
  3. Yes
  4. Long
  5. Yes- CCC= Chronic, Cirrhosis, Carcinoma, carrier
31
Q

Hep C

  1. Structure
  2. Replication
A
  1. Enveoloped, ss+ RNA linear, icosahedral
    • 6 genotypes, 1= 75%, 2= 10%, 3=10%
  2. CYTOPLASM= Receptor endocytosis and binding, fusion, uncoating, translation, RNA replication, Assembly and budding through ER and membrane.
32
Q

Hep C Symptoms

A
  • Usually asymptomatic (75%)
  • Symptoms (15%)= jaundice= fatigue, myalgia, low grade fever, right upper quadrant pain, vomiting
  • Injecting drug useres more likely to develop jaundice than other patients
33
Q

HCV Pathogenesis

A
  • Symptoms due to cell mediated immune response–> inflammation of liver
  • Parenchumal cell degeneration
  • Hepatocyte necrosis
  • macrophage accumulation near dying hepatocytes
34
Q

HCV transmission

A
  1. birth
  2. sex
  3. needle stick injuries (6x higher transmission compared to HIV sticks)
35
Q

HCV Control/treatment

A
  1. Treatment:
    • Interferon/Ribavirin combination
    • Pegylated Interferon a/ribavirin
    • Boceprevir or telaprevir (protease inhibitors)
  2. Control: No vaccine
36
Q

Hepatits D Virus

  1. Family
  2. Transmission
  3. Carrier
  4. Incubation
  5. HCC risk
A
  1. RNA Deltavirus (enveloped, ss - circular RNA with unknown capsid)
  2. Blood, birth, sex
  3. Yes
  4. Infection dependent on HBV infection:
    • Superinfection= HDV after HBV= short incubation
    • Coinfection= HDV+ HBV= long infection
  5. Yes
37
Q

HDV

  1. Structure
  2. Replication
A
  1. Structure:
    • Envelop= from HBV
    • ss - RNA, enclosed in circle
    • Capsid-delta antigen
  2. Replication: needs HVsAg for replication, only encodes for/makes delta antigen
38
Q

HDV Symptoms

A
  1. Co-infection
    • Severe Acute disease:
      • fulminant liver failure in 1% of patients
      • complete recover from HBV and HDV is common
    • Low risk chronic infection= <5% patients
  2. super infection- HDV in HBsAg + patient
    • 5% patients- fulminant hepatitis
    • 80-90% : chronic HDV –>rapid cirrhosis –> HCC
39
Q

HDV

  1. treatment
  2. Control
A
  1. Chronic infection treatment: alpha interferon + lamivudine
  2. prevention of HBV infection
40
Q

HBE Virus

  1. Family
  2. Transmission
  3. Carrier
  4. Incubation
  5. HCC risk

EEE?

A
  1. RNA hepevirus- non enveloped, ss+RNA
  2. Fecal/oral, especially water
  3. No
  4. Short
  5. No

EEE= enteric, expectant (hgiher mortality), epidemic

41
Q

**HBE **

  1. Structure
  2. Replication
A
  1. icosahedral, non enveloped, ss+RNA, 4 genotypes, 1 caues human disease
  2. entry via GI tract, replication in liver, exits via stool to infect more water
42
Q

HEV Symptoms

A

Prodromal Phase

Icteric Phase= jaundice, fatigue, abdominal pain, loss of appetitie, nausea/vomiting, joint pain, dark urine

More serious in pregnant women and transpalnt patients.

**unknown if IGg antibodies protect against reinfection**

43
Q

HEV

  1. Epidemiology
  2. Prevention
A
  1. Low sanitation= higher incidences
    • Central and south-east asia, north and west africa, mexico
    • Anywhere drinking water is contaminated with feces
  2. proper treatment and disposal of human waste, improved hygeine, water treatment.
44
Q

Herpes Virus 1-2

  1. Subfamily
  2. Primary target cell
  3. site of latency
  4. Means of spread
A
  1. alpha-herpes virus= HSV 1,2,3
  2. Mucosepithelial
  3. Neuron
  4. Close contact
45
Q

Herpes virus

  1. Structure
  2. Replication
A
  1. dsDNA, linear, enveloped. Glycoprotein spikes on capsid
  2. Protein phases–replication in nucleus, envelop from nucleus
    • Early proteins (a)= needed for transcription regulation ,cell takeover
    • early proteins (b) = transcription factors, enzymes, DNA polymerase
    • late proteins (gamma) =structural proteins,
46
Q

HSV 1, 2

  1. Proteins they encode
  2. Clinical manifestations (recurrent vs primary)
A
  1. Encode:
    • DNA dep DNA polymerase
    • Thymidine kinase (phosphorylates thymidine and other nucleosides)
  2. 80% asymptomatic. Recurrent infections are less sever and shorter than primary infections.
47
Q

Oral Herpes (2 types)

A
  1. Acute Herpetic gingivostomatitis
    • mostly children, HSV1
    • Incubation 3-7 days, lasts 5-7 days
    • clear lesion, ulcer is white
    • fever, gingivitis, lymphadenopathy, difficulty eating and drinking
  2. Herpes Labialis= Cold sore
    • HSV-1- common, 20-40% of population
    • recurrence at same sit
    • vesicles, ulcer (fluid is contagious), inflammation, edema, lesion crusts over and heals without scar
    • Heals in 7-10 days
48
Q

Herpes Keratitis

  1. Which HSV
  2. recurrence?
  3. Symptoms?
  4. Hallmark?
  5. treatment?
A
  1. Eye infection, mostly HSV1
  2. recurrent, can lead to blindness (most frequent cause of blindness)
  3. Unilateral red eye, pain, ocular irritation, photophobia, vesicular skin rash, follicular conjunctivitis
  4. Hallmark sign= dendritic corneal ulcer
  5. treatment: acyclovir cream 5x/day for 7 days
49
Q

Herpes Whitlow

  1. Type of herpes
  2. Symptoms?
  3. treatment
A
  1. HSV 1 or 2 secretions entering via wond on hand or wrist
    • HSV-1 mouth infection causes it in children
    • HSV-2 genittal infection causes it in adults
  2. 2-20 day incubation, pain burning, tingling of infected finger. Erythema, edema, vesicles on red base. Fever and malaise
  3. self limiting
50
Q

Herpes Gladiatorum (mat herpes)

  1. Population
  2. Symptoms
  3. treatment
A
  1. Wrestlers, contact sports–direct contact from skin lesions
  2. usually around head or neck. Cluster of blisters that may/ may not be painful
  3. acyclovir tablets/cream
51
Q

Exzema Herpeticum

  • population
  • severity?
  • Incubation?
  • treatment?
A
  • children, rare,
  • Sever disseminated disease infection at site of skin damage
  • Incubation 5-12 days
  • Treatment: Acyclovir and antibiotics (to prevent secondary infection)
52
Q

**Genital herpes **

  1. HSV types
  2. Symptoms
  3. Epidemiology
  4. Treatment
  5. Recurrence?
  6. Complication?
A
  1. HSV-2 >>>HSV 1 (10%)
  2. asymptomatic, lesions can appear
    • small red bumps, vesicles or open sores in genital and anal areas
    • pain or itching around genital area, thighs
    • flu-like symptoms
  3. 45 million people 12+ years have genital HSV (1/5)
  4. Heals within 4 weeks
  5. Reccurence 3-4x’s per year
  6. HSV meningitis
53
Q

HSV Encephalitis

  1. HSV type
  2. symptoms (which are most common?
  3. Diagnosis?
  4. Prognosis
A
  1. HSV-1- most common cause o viral encephalitis
  2. Symptoms
    • Prodrome: malaise, fever, nausea, —-> encephalopathy
    • fever> headach > psychiatric symptoms> seizure > vomiting > focal weakness > memory loss
    • Edema and hemorrhage in temporal lobe
  3. CSF has slightly elevated protein, normal glucose, high lymphocytes, some RBC
  4. If untreated, 70% mortality
54
Q

HSV Meningitis

  1. HSV type?
  2. Diagnosis (compare to HSV encephalitis)
  3. Treatment
A
  1. HSV-2>>> HSV-1—usually caused by complication of HSV2 gentical herpes infection.
  2. Meningitis vs Encephalitis CSF
    • WBC: M> E
    • RBC M<<e>
      <li>Protein: M&gt; E</li>
    </e>
  3. symptoms resolve themselves
55
Q

Neonatal Herpes

  1. HSV type?
  2. transmission
  3. symptoms (infected before birth)
  4. Symptoms (infected after birth)
A
  1. HSV-2 (80%) > HSV-1 (20%)
  2. delivery through infected mother, transplacental, hospital aquired
  3. Before birth infection
    • ​​premature, low birth weight, microcephaly, hydrocephalus, chorioretinitis, vesicular skin lesions
  4. After birth infection
    • ​​40% have herpes in skin, eyes, mouth.
    • 35% encephalitis
    • 25% disseminated disease= lungs, liver, adrenal glands, skin eye and mouth
56
Q

HSV 1 vs HSV 2?

A

They can infect the same tissues, but HSV1 tends to be above the wasit, HSV2 is below the waist

57
Q

HSV 1-2 Pathogenesis

A
  1. Replication in epithelial cell= vesicle on red surface
  2. Move to trigeminal ganglia (oral HSV) or sacral ganglia (genital HSV) and replicates, then becomes latent.
  3. Lytic infection- in mucosepithelial cells, disease at site of infeciton
  4. Latent infection= innervating neurons
    • Recurrence= new blisters form
    • Asymptomatic viral shedding
  5. Persistent infection in lymphocytes and macrophages
  6. Cell pathology:
    • Cell Death: virus induced inhibition of macromolecules, degradation of DNA and cytoskeletal destruction
    • Chowdry acidophilic intranucleuar inclusion bodies
    • sunctia cells
58
Q

HSV 1- 2,

  1. Infection
  2. transmission
  3. Epidemiology?
  4. treatment
  5. Control
A
  1. Lifelong infection, recurrent at site of contagion, asymptommatic shedding.
  2. saliva, vaginal secretions, lesion fluid, orally, sexually, eyes and breaks in skin
  3. children (HSV 1) and sexually active poeple (HSV2), physicians, dentists, (finger infection= whitlow)
  4. Treatment: Antivirals (acyclovir, penciclovir, valacyclovir, adenosin arabinoside, iododeoxyurine, trifluridne)
  5. No vaccine, c-sections, no sex, avoid direct contact, etc.
59
Q

Varicella

  1. Disease progression (when contagious, symtpoms appear,
  2. complications 1
  3. Complication 2
A

HSV-3= Varicella Zoster Virus

  1. **Progression **
    • Incubation 14-16 days
    • Contagious 2-3 days before rashes appear
    • Pain and paresthesia –> vesicle, pustule, crust, scabbed lesions
      • more severe on trunk vs extremities
      • rash on scalp
  2. Bacterial superinfection and scarring if the lesions are scratched off
  3. Interstitial pneumonia- occurs in 20-30% of adult patients (Primary infection worse in adults than children)
60
Q

Herpes Zoster

A

Shingles

  1. Recurrence of latent varicella infection that was in DRG. Stress causes virus to spread peripherally down nerve.
  2. Small blisters on red base, new blisters continue to form for 3-5 days. Painful and unilateral. Ray-like distribution (dermatomal pattern)
  3. Only in older adults
61
Q

VZV pathogenesis

A
  1. inhalation–> infection of respiratory tract
  2. Primary Viremia= Spread by reticuloendothelial system to other body parts (headache, malaise, fever)
  3. Secondary viremia= virus invades capillaries of endothelial cells and epidermis= intercellular edema = vesicles
    • Progression of vesicles:
    • macules–> papules–> vesicles–>pustules–> crusts
62
Q

VZV

  1. recurrence?
  2. risk groups
  3. treatment
  4. Control
A

VZV

  1. yes, lifelong infection. Recurrence is contagious
  2. Risk groups
    • children= mild,
    • teens and adult= serious, pneumonia,
    • immunocompromised/newborn= life threatening pneumonia, encephalitis, progressive disseminated varicella
    • Old and immunocompromised= recurrent disease
  3. Treatment: antiviral drugs,
  4. Control:
    • varicella IgG for adults and immunocompromised
    • live attenuated vaccine after 2 years= prophylactic treatment (even after exposure)

Microbiology- Viruses (7 decks)

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