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Virology > TA Review > Flashcards

TA Review Flashcards

1
Q

4 Basic Properties

A

-obligate parasite -composed of nucleic acids -small, pass through filters -cannot be directly observed

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2
Q

Lytic vs. chronic vs. latent

A

Lytic –> Virus is replicating, with symptoms Chronic –> Virus is replicating, asymptomatic presentation Latent –> Virus is not replicating, asymptomatic

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3
Q

General Stages of Replication Cycle

A
  1. Attachment and penetration 2. Uncoating 3. Fusion 4. Replication/translation/maturation 5. Assembly 6. Budding
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4
Q

Ebola Replication Cycle

A
  1. Attachment 2. Macropinocytosis 3. Fusion at endosome 4. Negative strand with RNA virus transcription –> translation into viral proteins. 5. Negative strand RNA virus replication 6. Assembly of parts from 4 and 5 7. Budding
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5
Q

RNA Virus classification card

A
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6
Q

DNA Virus Classification Card

A
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7
Q

What are DNA Viruses

A

HHAPPPP(y)

Hepadna (HBV), Herpes, Adeno, Pox, Parvo_, P_apilloma, _P_olyoma

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8
Q

Characteristics of DNA Viruses

A
  • Double-stranded (except parvo – it’s only “ part of” a virus)
  • Replicate in nucleus (except pox – it’s weird)
  • Are Icosahedral (except pox – it’s weird)
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9
Q

Geography of Ebola

A

West Africa

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10
Q

Transmisison of Ebola

A

Direct Contact: Blood, secretions, organs, & other body fluids –

Indirect Contact: Contaminated environment –

Airborne Transmission: During aerosol generating procedures –

Individuals are Infectious as long as Ebola virus present in blood, breast milk, and other secretions.

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11
Q

Diagnosis of Ebola

A

Presenting Symptoms: ELISA; PCR; virus isolation –

Late in Disease or After Recovery: IgM and IgG antibodies

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12
Q

Ebola incubation period

A

2-21 days

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13
Q

Ebola presenting symptoms

A
  • Acute Onset: Fever, Myalgia, Headache
  • After 5 days: N&V, Abdominal pain, Diarrhea, Chest pain, Cough, Pharyngitis
  • Other Symptoms: Photophobia, Lymphadenopathy, Conjunctivitis, Jaundice, Pancreatitis, CNS Symptoms (decreased mental status, delirium, coma)
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14
Q

Ebola disease progression

A

Erythematous maculopapular rash: face, neck, trunk, arms with desquamation

  • Bleeding Manifestations: petechiae, ecchymosis, & hemorrhage (less common).
  • Fatal Progression: Shock, DIC, liver & renal failure. Death between 6-16 days.
  • Protracted Convalescence: Arthralgia, orchitis, uveitis, transverse myelitis
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15
Q

Tx Ebola

A

Current: Supportive

Investigational: Zmapp (3 monoclonal antibodies) after onset of treatment; Vaccines

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16
Q

Pathogenesis of Ebola

A

Infects macrophages and dendritic cells –> Leads to supression of Type I IFN, and systemic dissemination –> Causes direct tissue injury in liver, spleen, and adrenals–> Host IR causes damage also via cytokines.

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17
Q

Influenza Virus A/B/C family

A

Orthomyxoviridae

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18
Q

Influenzae Morphology

A

Enveloped

Single Strand RNA virus

Negative sense

Segmented

Helical Capsid

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19
Q

Influenzae pathogenesis/infectious properties

A

Hemaagglutin (HA) –> Binds Sialic Acid which leads to endocytosis into respiratory endothelium and agglutination of RBCs

Neuroaminidase (NA) –> Cleaves HA sialic acid bond and allows for spread of viral copies

M2 –> forms a proton channel, facilitates uncoating

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20
Q

Standard clinical manifestation of influenzae

A

Primarily: “flu symptoms” including malaise and myalgia

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21
Q

Clinical complications of Influenzae

A

pneumonia/secondary bacterial pneumonia

otitis media

Reye’ s syndrome (w/aspirin in peds) –> Rash, vomiting, liver damage due to swelling in liver and brain

Encephalitis

myositis/cardiac involvment

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22
Q

Diagnosis of Influenzae

A

Often made on clinical grounds

Rapid antigen, culture, serotyping are available

GO back to lecture for this!! more info on slides.

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23
Q

Influenzae Antigenic Shift

A

(major reassortment, Flu A only). Responsible for Pandemics, happen every 50 years

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24
Q

Antigenic Drift Influenzae

A

(yearly changes/mutations). Three strains: A, B, and C. Responsible for yearly outbreaks

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25
Q

Treatment of Influenzae

A

NA Inhibitors (Tamiflu/Oseltamavir) and M2 Channel Blockers (Amantadine) Vaccines (live + inactivated)

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26
Q

Virus in family paramyxoviridaie

A

Parainfluenzae

RSV

hMPV

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27
Q

Adenovirus morphology

A

Nonenveloped

linear

dsDNA

Icosahedral capsid

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28
Q

Adenovirus infectious properties

A

HA (hemaglutinin) –> binds sialic acid and mediates endocytosis

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29
Q

Transmission of Adenovirus

A

Fecal Oral

*(TA Review is wrong when it says Fomites, Droplet, contact)

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30
Q

Epidemiology of adenovirus

A

Outbreaks in congregate settings, different serotypes target different tissues

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31
Q

Clinical presentation of adenovirus

A

• Pharyngitis, pneumonia, & other respiratory tract infections •

Common Cold (#3 cause) •

Conjunctivitis (“pink eye”) •

Gastroenteritis (#2 viral cause of diarrhea), hemorrhagic cystitis (hematuria & dysuria)

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32
Q

Adenovirus diagnosis

A

DFA (direct fluorescent antibodies); PCR; culture

Not routinely done –> check on this in lecture

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33
Q

Tx and Prevention of adenovirus

A

Supportive. Live attenuated vaccine used in military (congregate setting)

Cidofovir used in immunocompromised hosts

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34
Q

Coronavirus morphology

A

Enveloped,

(+) ss RNA;

helical capsid (RNA genome + N protein)

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35
Q

Coronavirus infectious properties

A

E2 glycoproteins form “halo-like” projections surrounding the envelope (crown!)

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36
Q

Transmisison of coronavirus

A

Fomites, person:person

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37
Q

Clinical presentation/epidemiology/diagnosis of coronavirus

A

Common Cold (#2 cause) & other respiratory infections; –>Diagnosis is clinical picture, seen all over the world

Gastroenteritis

  • Severe Acute Respiratory Syndrome (SARS): fever, respiratory distress & pneumonia, diarrhea; 10% mortality. Diagnosis is done via PCR/EM/Antibody Assay, seen in Asia did spread from China to worldwide.
  • Middle East Respiratory Syndrome (MERS): fever, respiratory distress & pneumonia, diarrhea. Diagnosis is done via PCR/EM/Antibody Assay. Seen in Saudi Arabia.
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38
Q

SARS/MERS

A

Both caused by coronavirus

  • Severe Acute Respiratory Syndrome (SARS): fever, respiratory distress & pneumonia, diarrhea; 10% mortality. Diagnosis is done via PCR/EM/Antibody Assay, seen in Asia did spread from China to worldwide.
  • Middle East Respiratory Syndrome (MERS): fever, respiratory distress & pneumonia, diarrhea. Diagnosis is done via PCR/EM/Antibody Assay. Seen in Saudi Arabia.
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39
Q

TX coronavirus

A

All treated with supportive care

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40
Q

Parainfluenzae Virus morphology

A

Enveloped,

ss (-) linear,

non-segmented RNA;

helical capsid

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41
Q

Respiratory Syncytial Virus (RSV) morphology

A

Paramyxoviridae:

Enveloped,

ss (-) linear,

non-segmented RNA;

helical capsid

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42
Q

Human Metapneumovirus (hMPV) morphology

A

Paramyxoviridae:

Enveloped,

ss (-) linear,

non-segmented RNA;

helical capsid

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43
Q

Parainfluenzae Infectious Properties

A

HN protein functions with combined HA and NA activity: mediates fusion and endocytosis (H) and cleaving for spread (N)

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44
Q

Parainfluenza Transmission

A

Respiratory droplets & Contact

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45
Q

Parainfluenzae clinical presentation/epidemiology

A

Croup (laryngotracheobronchitis – barking seal cough) –> See the steeple sign on xray, the narrowing of the airway

seen in kids age 3-5, most people get it by age 5. Seen in Fall and Spring.

bronchiolitis Pneumonia in kids (URI + LRI);

Common cold in adults (URI only)

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46
Q

Diagnosis of Parainfluenzae

A

DFA and PCR and culture

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47
Q

Treatment of Parainfluenza

A

Supportive and corticosteroids to open up the airway

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48
Q

RSV infectious properties

A

G protein mediates attachment and release, instead of HA/NA in other parmyxoviruses (such as parainfluenze and hMPV)

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49
Q

Transmission of RSV

A

Fomites or direct contact with secretions

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50
Q

Clinical presentations of RSV

A
  • Kids/Infants: Pneumonia & bronchiolitis
  • Immunocompetent Adults: Common Cold
  • Immunocompromised Adults: Pneumonia
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51
Q

Epidemiology of RSV

A

Most infected by 2 years of age. Reinfection throughout life is common.

  • Risk Groups: Premature / Elderly, Congenital Heart Defects, Bronchopulmonary Dysplasia (BPD – formerly chronic lung disease of infancy)
  • Outbreaks in winter & spring
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52
Q

Diagnosis of RSV

A

Rapid antigen test, DFA, PCR (not used clinically)

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53
Q

Treatment of RSV

A
  • Supportive care.
  • Prevention of severe RSV disease for high risk infants: palivizumab (vs F protein). High risk infants are pre-mes, congenital heart defect babies, infants with bronchopulmonary dysplasia
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54
Q

hMPV clinical presentation

A

Bronchiolitis Pneumonia in kids, elderly, and immunocompromised;

URI in healthy adults

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55
Q

Epidemiology/Transmission of hMPV

A

Outbreaks: Jan-April (winter).

Recurrent infections throughout life.

Highest risk: immunocompromised, preemies, transplant, cardiopulmonary disease.

Transmission by contact with contaminated secretions.

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56
Q

Clinical presentation of hMPV

A

Bronchiolitis Pneumonia in kids, elderly, and immunocompromised;

URI in healthy adults

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57
Q

Treatment of hMPV

A

Supportive

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58
Q

Diagnosis of hMPV

A

PCR/DFA, probably not used clinically at all

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59
Q

Measles is caused by

A

Rubeola, Morbillivirus

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60
Q

Measles/Rubeola morphology

A

single strand negative sense RNA genome

non segmented

helical capsid

enveloped

single serotype

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61
Q

Infectious properties of Measles

A

HA –> sialic acid binding, endocytosis

M protein –> assembly

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62
Q

Measles transmission

A

Aerosol, need ot keep under negative pressure isolation

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63
Q

Clinical Presentation of Measles

A
  • Incubation: 10 days;
  • Prodrome (pre-rash): 3 days of cough, coryza, conjunctivitis, photophobia (CCCP);
  • Disease: Koplik’s spots in mouth, maculopapular rash starts at head moves to feet.
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64
Q

Complications of Measles

A
  • Bacterial Superinfection, Pneumonia, Encephalitis (1 in a thousand)
  • Subacute Sclerosing Panencephalitis (1 in a million; occurs years later)
  • Transient Immunosuppression: TB susceptibility in endemic regions
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65
Q

Measles diagnosis

A

clinical findings, direct fluorescent antibody (urine)

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66
Q

measles tx and prevention

A

MMR vaccine; pooled immunoglobulins (prophylaxis in unvaccinated)

Treatment: Supportive care. Vitamin A supplementation

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67
Q

mumps morphology

A

negative sense single strand RNA, non-segmented, helical capsid, enveloped

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68
Q

infectious properties/transmisison of mumps

A

HN does both entry and exit, like parainfluenzae

Respiratory transmission

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69
Q

Clinical manifestation of mumps

A

Incubation - 7-10 days;

Viremia - 15 days

Disease manifestations – 18+ days: Parotitis (swollen parotid gland), orchitis (testis pain), mastitis, aseptic meningitis, encephalitis (Mumps gives you bumps!)

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70
Q

mumps diagnosis

A

clinical findings, serology

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71
Q

tx/prevention of mumps

A

No tx, vaccine coverage not quite as good as it was with measles. See some outbreaks amongst the vaccinated

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72
Q

Rubella/German Measles morphology

A

Togaviridae- Rubivirus,

enveloped,

(+)ssRNA,

non-segmented,

Icosahedral,

single serotype.

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73
Q

Infectious properties of Rubella

A

Only Togavirus not transmitted by Arthropod

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74
Q

Clinical presentation of Rubella

A

Fever followed by descending rash (mild disease);

Congenital rubella (toRches)- if mother infected in 1st trimester:

fetal deafness,

cataracts,

heart defects (PDA),

mental retardation,

blueberry muffin rash.

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75
Q

Rubella Diagnosis

A

Detection of IgM Rubella antibodies

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76
Q

Rubella transmission

A

respiratory droplets

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77
Q

Treatment/prevention of German measles

A

No Tx, MMR vaccine

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78
Q

Enteroviruses

A

“PERCH”

Poliovirus

Echovirus

Rhinovirus

Coxsackievirus A & B

Hepatitis A

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79
Q

Polio morphology

A

Enterovirus, Picornaviridae

non-enveloped, (+)ssRNA, nonsegmented, icosahedral

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80
Q

Infectious Properties of Polio

A

Stable at low gastric pH,

hidden binding sites,

inhibits host ribosomes

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81
Q

Clinical Presentation of Polio

A

Replicates in lymph of GI –> viremia –> anterior horn of spinal cord

Can cause meningitis and paralysis

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82
Q

Diagnosis of Polio

A

Done on Serology

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83
Q

Epidemiology of Polio

A

Fecal Oral in developing countries

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84
Q

Treatment/Prevention of Polio

A

IPV – Salk vaccine (killed)

OPV – Sabin (live attenuated)

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85
Q

Echo and Coxsackie morphology

A

Enteroviruses, picorniveridae

very small, non enveloped

Positive sense single strand RNA

nonsegmented

icosahedral

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86
Q

Infectious properties of echo and coxsackie

A

Stable at low gastric pH, hidden binding sites

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87
Q

Clinical Presentation Coxsackie A

A

herpangina, vesicular lesions, hand-foot-and-mouth diseases, throat pain, anorexia

common cold, fever, rash, meningitis in summer

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88
Q

Clinical Presentation of Coxsackie B

A

myocarditis, pleurodynia (painful pleuritic chest pain), fever,

common cold, fever, rash, meningitis in summer

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89
Q

Clinical Presentation Echovirus

A

Neonatal Disease

common cold, fever, rash, meningitis in summer

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90
Q

Epidemiology of Echo/Coxsackie

A

Fecal oral transmission, kids = hand/foot/mouth

91
Q

Treatment of Echo Coxsackie

A

Symptomatic

92
Q

Different types of Meningitis, CSF analysis

A
93
Q

Rhinovirus morphology

A

Enterovirus, picorniviridae,

very small, non enveloped

ssRNA positive sense

non segmented

icosahedral

94
Q

Infectious Properties of Rhinovirus

A

Over 100 serotypes, so reinfection of same host

95
Q

Clinical presentation of rhinovirus

Also - pharyngitis, otitis media.

Less common - bronchiolitis and pneumonia.

A

NUmber one cause of the common cold

96
Q

Diagnosis Rhinovirus

Treatment Rhinovirus

A

Diagnosis clinical

Tx supportive

97
Q

Rhinovirus epidemiology

A

Everywhere and everyone;

Transmitted by aerosols and fomites.

Hands thought to be major vector.

Early autumn and late spring.

98
Q

Rotavirus morphology

A

non-enveloped;

inner and outer capsids

Segmented dsRNA genome

dsRNA –> unique to reovirus aka this family

99
Q

Rotavirus infectious properties

A

Enterotoxin (“NSP4”) –> causes dirrhea

replication in host cytoplasm

Highly resistant to desiccation – can survive in feces for months!

100
Q

Rotavirus Clinical presentation

A

Diarrhea (watery), fever, vomiting, dehydration;

worse in immunodeficient 48 hr incubation;

subsequent reinfections are milder thanks to imperfect antibodies.

101
Q

Diagnosis of rotavirus

A

ELISA, latex agglutination in stool, PCR, EM

102
Q

Epidemiology of Rotavirus

A

#1 cause of Diarrhea in kids in the US and worldwide;

almost everyone’s had it by age 4

Spread via Fecal-oral route;

patients shed virus both pre- and post-infection.

More common in winter months

103
Q

Rotavirus treatment and prevention

A

Prevent with *Live* Vaccine;

Oral Rehydration therapy in active infection

104
Q

Norovirus morphology

A

Calicivirus family.

Non-enveloped,

(+) ssRNA,

non-segmented genome

105
Q

Infectious Properties of norovirus

A

Infects the upper GI tract, replicates there

Host creates antibodies against norovirus, but they have a short effective half life

106
Q

Clinical presentation of norovirus

A

Watery diarrhea +/- fever, headache, and constitutional symptoms

More diarrhea in adults, more vomiting in kids

1-2 day incubation –> 1-2 day illness –> 2 weeks shedding

107
Q

Diagnosis of norovirus

A

Usually from clinical picture

108
Q

Epidemiology of Norovirus

A

1 cause of Adult watery diarrhea, often with large outbreaks (think cruise ships)

Fecal-oral spread; affects older children and adults

Some are asymptomatic carriers, some are totally immune (“secretor negative”)

109
Q

Treatment of norovirus

A

Supportive

110
Q

What does hepatitis look like clinically

A

upper right quadrant pain

nausea/vomiting

jaundice

itching

fatigue

111
Q

Hepatitis Morphologies

A

Hep A - Picorniviridae, non-enveloped, (+)ssRNA, nonsegmented, icosahedral

Hep B - Hepadnavirus, circular dsDNA Enveloped, icosahedral (carries own reverse txase)

Hep C - Flaviviridae, Enveloped, +ssRNA, linear, icosahedral

Hep D - Circular genome, ss-RNA

Hep E - Hepevirus (calcivirus) non-enveloped, +ssRNA, icosahedral

112
Q

Hepatitis Transmissions

A

Hep A - Fecal Oral

Hep B - Parenteral, Vertical, sexual (?)

Hep C - Parenteral (mostly)

Hep D - Parenteral, Vertical, Sexual

Hep E - Fecal Oral (waterborne)

113
Q

Incubation/clinical presentation of Hepatitis

A

Hep A - Short –> Abrupt presentation.

Hep B - Long (months).

Hep C - Long

Hep D - Depends

Hep E - Short

114
Q

Hepatitis Clinical Presentations

A

Hep A –> Mild/self limited disease. Rarely see hepatic failure secondary to host IR.

Hep B –> Acute (after the long incubation) OR

Chronic (latent carrier state possible) hepatitis: ALT > AST

Cirrhosis

HCC (hepatocellularcarcinoma) (DNA oncogene; don’t need cirrhosis)

Hep C–> 20% self limited 80% progress to asymptomatic carrier or chronic active Hep C (at risk for HCC or cirrhosis)

Hep D –> Co-infection with Hep B, causes Superinfection (worse outcomes)

Hep E –> Acute (short incubation), self-limited, NOT chronic

High mortality pregnant women in 3rd trimester

115
Q

Hepatitis Infectious Properties

A

Hep A - Stable in the soil and water

Hep B - Targets hepatocytes, but it’s mostly the immune response that causes damage

Hep C - E2 mediated cell attachment, RNA polymerase= high mutation rate, NS3/4A protease prevents IFN-b induction

Hep D - Needs Hep B for envelope proteins or else no infectious

116
Q

Hepatitis Diagnoses

A

Done with serology mostly

Hep A - anti HAV IgM (acute) anti HAV IgG (prior or vaccination)

Hep B - HBsAg – surface antigen, indicates current infection Anti-HBs – Immunity (either exposure or immunization) Anti-HBc – Indicates exposure (IgM: acute, IgG: resolved) HBeAg– Contagious

Hep C - anti-HCV Ab, PCR (HCV RNA), biopsy

Hep D - HBV and HDAg S and L

Hep E - Clinical

117
Q

Epidemiology of Hepatitis

A

Hepatitis A - Fecal oral transmission - Shellfish outbreaks Endemic areas, crowding, military, children

Hep B - Endemic S. Europe, Africa, Asia

Hep C - HIV coinfection, IV drug use

Hep D - Pts with HBV

Hep E - Developing countries

118
Q

Hepatitis treatments

A

Hep A –> Supportive/vaccine

Hep B –> Vaccine, IFNa, HBV LATTE (RT-I) which doesn’t really work that well

Hep C –> OLD: Pegylated IFN-a + Ribavirin (duration based on genotype)

Hep C –> OLD: PegIFN + Ribavirin NEW: PegIFN + Ribavirin + Protease Inhibitor (Telaprevir or Boceprivir). No Vaccine.

Hep D –> Treat Hep B

Hep E –> Supportive

119
Q

All the herpes viruses

A

Herpes Simplex Virus –> HSV-1;

HSV-2;

Varicella Zoster Virus –> VZV;

Epstein Barr Virus –> EBV;

Cytomegalovirus –> CMV;

Human Herpes Virus –> HHV-6 & HHV-7;

HHV-8

120
Q

HSV1 and HSV 2 morphology

A

dsdna, enveloped icosahedral

121
Q

HSV 1 and 2 pathogenesis

A

Surface glycoproteins: attachment and fusion, bind complement, bind Fc of IgG.

Latent in CNV ganglion (HSV-1) or sacral ganglion (HSV-2)

122
Q

Transmission HSV 1 and 2

A

HSV 1: Respiratory secretions, saliva, HSV 2: Sexual, perinatal

123
Q

Clinical Presentation of HSV 1 and 2

A

Many asxatic. Oral/genital lesions- crops of small, painful blisters that ulcerate. Encephalitis.

In neonates: diarrhea, recurrent infections. (ToRCHES).

124
Q

Diagnosis of HSV 1 and 2

A

Culture, DFA, PCR, Tzanck smear (scraping of ulcer for cells)

125
Q

Epidemiology of HSV 1 and 2

A

HSV1 = most people have it,

HSV2: usually sexually transmitted

126
Q

Treatment of HSV 1 and 2

A

Acyclovir, Valacyclovir

127
Q

Varcicella Zoster Virus (“VZV,” or Human Herpes Virus-3) morphology

A

dsDNA, enveloped, icosahedral

128
Q

Pathogenesis of VZV/Zoster

A

Similar to HSV 1/2

Surface glycoproteins: bind complement, bind Fc of IgG and enter cells. Latent in DRG

129
Q

Clinical presentation/transmission of VZV/Zoster

A

Transmission: respiratory droplets
Primary (varicella): Chickenpox (“dew drop on rose petal” vesicles of different ages)

Reactivation (zoster): Shingles (vesicles & pain in dermatomal distribution from DRG) seen in Immunopromised /pregnant also with pneumonia or encephalitis

130
Q

Diagnosis of VZV/Zoster

A

Made on history of chicken pox, clinical.

131
Q

Epidemiology of Zoster/VZV

A

Primary disease worse in adults, reactivation in immunocompromised

132
Q

Treatment of VZV and Zoster

A

VZV vaccines, (Val)Acyclovir, Human Pooled IgG

133
Q

Epstein-Barr Virus (“EBV” or Human Herpes Virus-4) morphology

A

dsDNA, enveloped, icosahedral

134
Q

EBV transmssion/pathogenesis

A

TM by saliva, requires close contact.

Infects B cells via CD21, causes B cell transformation

(immortalization), remains latent in B cells for life. Can cause via this immortilazation atypical lymphocytosis (T cells).

135
Q

EBV clinical presentation

A

Mononucleosis: fatigue, fever, lymphadenopathy, pharyngitis, hepatosplenomegaly, rash (worse with amoxicillin). Resolves in 2-3 weeks. –> mono sucks, you feel really tired
Complications in immunosuppressed: lose control of transformed B cells, complications range from minor to malignancy

136
Q

Diagnosis of EBV

A

MONOspot test- IgM heterophile (nonspecific) antibody

*Not sensitive for children under 5 yrs old

137
Q

Epidemiology of EBV

A

50% of children infected, 70% of US by age 30

African endemic Burkitt’s, HIV-associated lymphomas, Hodgkin’s

138
Q

Treatment EBV/mono

A

Rest, reduce immunosupression

139
Q

CMV human herpes virus 5 morphology

A

dsdna

icosahedral

enveloped

140
Q

Pathogenesis of CMV

A

Infects lymphocytes,

Downregulates MHC I, Contains UL97 and UL 54.

141
Q

Clinical presentation of CMV

A

EBV negative Mono

Congenital infection –> (hearing loss) TORCHES CMV is the most common congenital infection

Severe disease in immunocompromised (pneumonia, retinitis, etc)

Other: Guillain-Barre syndrome

Shed in secretions, blood transmission

142
Q

TORCHES congenital infections

A

T – Toxoplasmosis / Toxoplasma gondii
O – Other infections (see below)
R – Rubella
C – Cytomegalovirus
H – Herpes simplex virus-2 or neonatal herpes simplex

The “other agents” under O include:

Coxsackievirus
Chickenpox (caused by varicella zoster virus)
Chlamydia
HIV
Human T-lymphotropic virus
Syphilis

143
Q

Diagnosis of CMV and

A

Owl’s eye inclusions, biopsy and culture, PCR, urine cultures

144
Q

Epidemiology of CMV

A

Most people are CMV positive, but disease is bad in immunocompromised.

145
Q

Treatment of CMV

A

Treatment is reserved for immunocompromised. Can treat prophylactically

1st Line: (Val)Gancyclovir.

2nd Line: Foscarnet or Cidofovir if viral TK (UL97) resistance. 2nd line drugs are very toxic, esp. Cidofovir (nephrotoxic)

146
Q

HHV-6 (and HHV-7) morphology

A

dsDNA, enveloped, icosahedral

147
Q

HHV-6 (and HHV-7) pathogenesis

A

Infects lymphocytes; Persists in Macrophage

148
Q

HHV-6 (and HHV-7) clinical presentation

A

Sixth Disease or Roseola

Roseola (Exanthema subitum): Child with 2 days of fever, then fever disappears and total body rash suddenly appears.
Febrile seizures (benign condition)
149
Q

Diagnosis of HHV-6 (and HHV-7)

A

Made on clinical presentation:

Roseola (Exanthema subitum): Child with 2 days of fever, then fever disappears and total body rash suddenly appears.
Febrile seizures (benign condition)
150
Q

Epidemiology of HHV-6 (and HHV-7)

A

Most children have it by age 3 (95%)

151
Q

Treatment of HHV-6 (and HHV-7)

A

Treating Sixth Disease or Roseola

Gets better on its own, supportive

152
Q

HHV-8 is also called

A

(Kaposi Sarcoma Associated Herpesvirus)

153
Q

Morphology of HHV-8

(Kaposi Sarcoma Associated Herpesvirus)

A

dsDNA, enveloped, icosahedral

154
Q

Pathogenesis of HHV-8

A

Infects B cells primarily, encodes growth and anti-apoptotic factors

155
Q

Clinical presentation of HHV-8

A

Kaposi Sarcoma: Vascular lesions w/bleeding and hemosiderin deposition

Primary effusion lymphoma –> lymphoma in body cavities
Castleman’s disease –> proliferation of lymph nodes

156
Q

Diagnosis of HHV 8

A

History of Aids, Clinical presentation:

Kaposi Sarcoma: Vascular lesions w/bleeding and hemosiderin deposition

Primary effusion lymphoma
Castleman’s disease

157
Q

Epidemiology of HHV-8

A

In the US: associated with HIV/AIDS, MSM, and drug users

Endemic in Africa, Mediterranean

158
Q

Treatment of HHV-8

A

Antiretrovirals for HIV (or chemo if invasive)

159
Q

Human Papilloma Virus (HPV) morphology

A

Unenveloped, circular dsDNA

160
Q

HPV virulence factors

A

– Does not infect APCs–>limited immune detection

– Viral proteins E6 and E7 inhibit tumor suppressor genes –> oncogenicity

161
Q

Clinical presentation of HPV

A

– Most asymptomatic

– Strains 6, 11 –> Genital warts (condyloma accuminatum)

– Strains 16, 18 –> Cervical cancer

162
Q

Diagnosis of HPV

A

– Cytology (“Pap smear”): look for characteristic changes (koilocytes)

– Biopsy (if abnormal cells seen on pap): look for degree of cervical endothelial dysplasia

163
Q

Epidemiology of HPV

A

– Exposure is EXTREMELY common; sexually active are at risk for high risk strain

infection.
– 99% of all cervical cancers assoc with HPV infection (also anal cancers

164
Q

Treatment/Prevention of HPV

A

Bivalent (16, 18) and tetravalent (6, 11, 16, 18) vaccines available for women and men ages

Treat malignancy with chemoradiation

165
Q

HIV morphology

A
  • Enveloped, with 2 copies of + sense ssRNA
  • Carries its own reverse transcriptase, a protease, and “integrase –> targets for drugs
166
Q

Infectious properties/pathogenesis of HIV

A
  • A retrovirus: Inserts its genetic material into the host’s genome
  • Selects for immune cells: CD4+ Helper T-Cells & Macrophages
  • Evades effective immune response due to hyper-variability of envelope proteins & downregulation of MHC
167
Q

Clinical course of HIV without HAART (aka AIDS)

A
  • Acute Infection (~2-4 weeks) –> Asymptomatic Period (avg ~8 yrs) –> AIDS (~13 yrs)
  • Opportunistic infections, increased risks of cancer, dementia, kidney disease, more.
168
Q

Diagnosis of HIV

A
  • ELISA for anti-HIV antibodies,

confirm with Western blot;

PCR for plasma viral RNA

169
Q

Epidemiology of HIV

A

In US, highest risk is in MSM, IV drug users, and Immigrants from endemic areas
- Most new infections are in Blacks & Latinos; increasing % through heterosexual contact

170
Q

Treatment of HIV

A
  • Highly Active Anti-Retroviral Therapy (“HAART”)

will go into specifics on other cards

171
Q

Specific important proteins/genes of HIV virus

A

p24 –> capsid protein encoded for by gene gag

gp41 --> fusion and entry

gp120 –> attachment to host T cell

gp41 and gp120 are both envelope proteins (outermost layer, surrounding capsid) encoded for by gene env

Reverse transcriptase –> encodes dsDNA from (+) ssRNA encoded for by gene pol

Integrase –> inserts dsDNA into host genome

172
Q

Time course of HIV infection

A

Primary Infection –> Low viral load, High T cell count

Acute HIV syndrome (wide dissemination of virus and seeding of lymphoid tissue) –> High viral load and mid-low T cell count. Three weeks after primary infection.

Clinical Latency –> Can last months to years. Viral load drops after acute HIV syndrome and then starts rising slowly. T cell count starts dropping slowly.

Constitutional symptoms –> Happens when T cell count gets low enough/viral load gets high enough

Opportunistic Infections –> When T cell count gets really low. Viral load very high.

Death –> Usually due to an opportunistic infection/other sequealae.

173
Q

Common opportunistic infections

A
174
Q

Principles of HAART

A
  • Strongly recommended for all pts at time of dx
  • Required for pts CD4 count <500 cells/mm3, or AIDS-defining illness

Use exactly 3 drugs:
- Use at least two different classes of drugs

  • Usually: 2 NRTI + 1 integrase inhibitor

Lack of maintenance –> breeding resistance to drugs.

175
Q

Life Cycle and linked Drugs

A
  1. Attachment (Maravoric)
  2. Fusion/Uncoating (Enfurvitide)
  3. Reverse Transcription (NRTIs Exs: Abacavir, Tenofovir), NNRTIs Exs: NeVIRapine, EfaVIRenz, and EtraVIRine )
  4. Integration (Integrase Inhibitor, Ex: Raltegravir)
  5. Assembly
  6. Maturation (Protease Inhibitors ex: idinavir all ___-navir)
176
Q

NRTIS mechanism of action and names and toxicities

A

Molecules that look like a normal nucleosides and competitively inhibit reverse transcriptase.

Examples: Zidovudine, Lamivudine, Emtricitabine, Abacavir,and Tenofovir

Toxicity for Entire Class: mitochondrial toxicity, peripheral neuropathy, hepatitis, lactic acidosis, dislipidemia, insulin resistance

Abacavir: Hypersensitivity reactions in pts with HLA-B5701 (we can test for this). We can test for this and prevent a possible fatal reaction.

Tenofovir: Renal toxicity, esp. if underlying renal disease; osteomalacia

Zidovudine: anemia

177
Q

NNRTIs mechanism of action, names, toxicities

A

Allosterically inhibit RT

NeVIRapine, EfaVIRenz, and EtraVIRine

Toxicities for entire class: Cytochrome p450 interactions, early resistance, rash

Nevirapine: Can cause severe hypersensitivity reaction with liver toxicity and rash, particularly in women with high CD4 counts.
Efavirenz: Teratogen, so avoid in pregnancy. Also causes neuropsychiatric symptoms like vivid dreams and/or depression; lipid elevation.

178
Q

Protease Inhibitors mechanism of action, names, toxicities

A
  • Messes up the maturation of the drugs because the proteins need to be cleaved in order to be assembled.
  • Lopinavir, Atazanavir, Darunavir, Fosamprenavir, Tipranavir
  • Can also act as a pharmokinetic booster –> Ritonavir +Cobicistat (cytochrome p450 inhibitors)

Toxicities entire class: Cause GI disturbances and metabolic syndrome (high cholesterol, diabetes, etc), lipodystrophy, CYP450 interactions.

Atazanavir: Can cause jaundice (without actually causing liver injury), kidney stones.

-

179
Q

Prophylaxis for Pneumocystic jiroveci

A

– CD4 count <200
– TMP-SMZ

180
Q

• Prophylaxis for Mycobacterium avium- complex

A

– CD4 count <50

– Azithromycin

181
Q

Immunology: Extracellular Bacteria

A

Innate Response:

– Phagocytosis
– Complement activation

Adaptive Response:

– Ab neutralization of pathogen

– Ab potentiation of innate response

  • Opsonization
  • ADCC (antibody dependent cell-mediated cytotoxicity)
182
Q

Immune evasion extracellular bacteria mechanisms

A
  • Inhibition of complement (all)
  • Resistance to phagocytosis (Strep. pyogenes)
  • Biofilm (Staph. epidermis)
  • Clot formation (Staph. aureus)
183
Q

Immunology intracellular bacteria adaptive and immune response

A

• Innate response: Transient control for a short period of time

– NK cells

– Phagocytes

• Adaptive response: Infection eradication

– Th1 cells –> IFN gamma

– IFN gamma–> phagocytes to destroy endocytosed bacteria

184
Q

Immune evasion intracellular bacteria

A
  • Intracellularity!
  • Inhibition of phagolysosome fusion (TB, Legionella)

• Destruction of phagosome membrane (Listeria)

185
Q

Immunology viruses

A
  • Innate response: Link to adaptive*
  • Adaptive response: Potential eradication**

– Th1 cells –> IFN gamma

– IFNs –> “antiviral” state
• Alpha/Beta: Recruit uninfected cells to put their defenses up, activate NKCs to kill viral infected cells.

• Gamma: Increases MHC I, II expression in all cells

186
Q

Immune evasion: Viruses

A
  • Intracellularity!
  • Inhibition of antigen presentation

• Manipulation of cytokine environment
– IL-1 blockade (all)
– Cytokine receptor decoys (poxvirus)
– Secretion immunosuppressive cytokines (EBV)

• Lysing of immune cells (HIV)

187
Q

Common immune evasion strategies

A
  • Neutralization ROS (many bacteria)
  • Multiple serotypes (bacteria & viruses)
188
Q

Viral vaccines: killed

A

Hepatitis A: Killed whole virus

Hepatitis B: Recombinant protein subunit (HBs)

HPV: Recombinant protein subunits

Rabies: Killed whole virus, Given as part of PEP

Influenza: Killed whole, Injected form only

Polio (Salk): Killed whole, Injected; 4 doses before school entrance. No mucosal immunity.

189
Q

Viral vaccines live

A

Measles/Mumps/Rubella: Live attenuated; Contraindicated in pregnant women, HIV pts with signs of immunodeficiency.

Yellow fever: Live attenuated; Given to those traveling to endemic areas

VZV: Chickenpox: Live attenuated

VZV: Shingles: Live attenuated; Given to pts >60 y/o, 10x dose of chickenpox

Polio (Sabin): Live attenuated, 3 doses provide optimal immunity; 1 provides 50%

Rotavirus: Live human-bovine reassortant (Rotateq) OR Live human attenuated (Rotarix), Rotateq is pentavalent; Rotarix is monovalent but provides cross-protection. Both multi-dose.

190
Q

Viruses we provide passive immunity for

A
  • Hepatitis A (IVIg)
  • Hepatitis B (Hepatitis B Ig)
  • Rabies (Rabies Ig)
  • Varicella (Varicella Ig)
  • RSV (palivizumab)

…and breast feeding!

191
Q

Diseases caused by prions

A

Humans: Creutzfeldt-Jakob Disease (CJD), Kuru.

Other animals: Scrapie, Bovine spongiform encephalopathy, chronic wasting disease

192
Q

Infectious Properties seen in Prions

A

Infectious form of normal brain protein (PrP).

Domino effect: one misfolded molecule acts as template for other molecules to misfold.

Misfolded proteins are resistant to proteases. Accumulation leads to tissue damage and cell death.

193
Q

Clinical presentation of prion diseases

A

Long incubation period, slow but progressive neurologic deterioration (dementia, myoclonus, etc.). Uniformly fatal; most patients die within 6 months of symptom onset.

194
Q

Diagnosis of Prion diseases

A

Clinical; can perform EEG, MRI, CSF analysis.

195
Q

Epidemiology of prion diseases

A

Most cases are sporadic. Brain eaters, exposure to animal form, rarely familial.

196
Q

Treatment for prion diseases

A

none

197
Q

Arboviruses (arthropod borne viruses) types and names

A

Need to Know bolded ones

Family: Togaviridae (ss +RNA) Genus: Alphavirus

Viruses: EEE*, WEE*, VEE

Family: Flaviviridae (ss +RNA) Genus: Flavivirus:
Viruses: Dengue virus, West Nile Virus, Yellow fever, SLE*

Family: Bunyaviridae (ss -RNA) Genus: Bunyavirus:
Viruses: La Crosse*, Hantaviruses (rodents)

* are causes of mosquito borne encephalitis. EEE has very high mortality.

198
Q

Dengue Fever morphology/serotypes

A

Flavivirus, enveloped, (+)ss RNA, linear.

4 serotypes.

199
Q

Dengue Fever Clinical Presentation

A 
Less severe (Dengue Fever): aka “Break-bone fever” due to muscle & joint pain. Also: fever, rash, bone marrow suppression.
More severe (Dengue Hemorrhagic Fever and Dengue Shock Syndrome): Severe hemorrhagic disease, leaky capillaries and multiorgan involvement.
200
Q

What causes more severe presentation of Dengue Fever

A

(Severe disease usually occurs with second infection with a different serotype (four serotypes), due to antibody-mediated immune enhancement = exacerbated cytokine release.)

201
Q

Diagnosis of Dengue Fever

A

Detection of anti-DenV IgM in serum, PCR

202
Q

Epidemiology of Dengue Fever

A

Tropical Areas where there are mosquitos. S. America, parts of Africa, South Asia/ South East Asia

203
Q

Vector of Dengue Fever

A

Aedes aegypti mosquitos. Human and Monkey host.

204
Q

Treatment of Dengue Fever

A

Supportive care, vaccine trials ongoing

205
Q

Yellow Fever Morphology

A

Flavivirus, enveloped, (+)ss RNA, linear

206
Q

Yellow Fever Clinical Presentation

A

Majority: mild illness with fever, H/A, N/V, chills, back pain
Minority: enter a toxic phase with fever, jaundice (liver damage), GI hemorrhage

207
Q

Epidemiology of Yellow Fever

A

Africa, S. America, Central America

208
Q

Vector of Yellow Fever

A

Aedes aegypti mosquitos (same as Dengue)

Monkeys and Human reservoirs

209
Q

Treatment of Yellow Fever

A

Live attenuated vaccine available.

210
Q

West Nile Virus morphology

A

Flavivirus, enveloped, (+)ss RNA, linear

211
Q

Clinical presentation of West Nile Virus

A

Most cases are asymptomatic (80%)

Rarely can progress to neuroinvasive disease: flaccid paralysis, aseptic meningitis or severe encephalitis (<1%)

212
Q

Epidemiology of West Nile Virus

A

Has become more wide-spread over the years within the United States, from 2000 to now. Now see cases in every state. In 2000 saw just in the north east.

More severe infection with age and immunosupression.

213
Q

Vector for West Nile Virus

A

Mosquito- Culex sp.

Human and Bird Host

214
Q

Treatment of west nile virus

A

Supportive care. No vaccine available.

Prevention with good mosquito control.

215
Q

Mosquito Borne encephalitis (other then west nile)

A

EEE (highest mortality) seen in Eastern NA, SA

WEE seen in Central and Western US, SA

SLE Americas. Seen in Urban epidemics.

La Crosse

216
Q

Rabies morphology

A

Rhabdovirus, (-)ssRNA, linear, enveloped,

Helical capsid with “Bullet shaped” appearance

217
Q

Rabies clinical presentation

A

Prolonged incubation in muscle (months to years).
Then, virus travels proximally to CNS via axons, causing acute encephalitis: mental status changes, delirium, paresthesias, pain, and death.
Onset of symptoms to death ~18days!

218
Q

Diagnosis of Rabies

A

DFA (direct fluorescent antibody test) on nape of neck biopsy, PCR, Negri bodies in brain (viral sharply lined eosinophilic nucleocapsid inclusions in cytoplasm of some infected cells)

219
Q

Epidemiology of Rabies

A

Rare in US, related to exposure to bats, raccoons, skunks, wild dogs

220
Q

Transmission of Rabies

A

Exposure of non-intact skin to saliva of infected animal ~2 cases/ year in USA

221
Q

Treatment of Rabies

A

Vaccine (prevention and as part of PEP)
IgG Post-exposure prophylaxis (administer w/in 72 hours)

222
Q

Viruses with helical capsid

A

-Myxo’s (para,ortho)

  • Corona
  • Rabies

Mumps

Measles/Rubeola

223
Q
A

Virology (1 decks)

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