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Infectious Disease > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Herpes viruses

3 families, what viruses?

A

1) Alpha-herpes viruses = HSV1, HSV2, VZV
2) Beta-herpes viruses = CMV, HHV6, HHV7
3) Gamma-herpes viruses = EBV, HHV8 (KSHV)

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2
Q

Herpes Viruses Shared Features

1) shape?
2) envelope?
3) labile or stable?
4) genome?
5) capsid?

A

1) Spherical

2) Lipid Envelope - derived from host golgi
- Coated with surface glycoproteins for cell-binding, cell-cell spread, and immune evasion

3) Labile, easy to kill in environment → spread requires close contact
4) dsDNA linear
5) icosahedral capsid

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3
Q

Primary infection with herpes viruses typically results in __________ infection in specific cells

Reactivation of herpes virus infection typically results in _________ infection

All herpes virus infections are more severe in patients with ______________

A

Primary infections → LATENT infection in specific cells

Reactivation → LYTIC infection

Infections more severe in patients with T cell disorders

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4
Q

Features of reactivation infection with herpes viruses

A

Reactivation → LYTIC infection - can be subclinical (shedding) or cause clinical disease resulting in spread of infection to new hosts

Less severe than initial infection

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5
Q

Alpha Herpesvirus:

A

HSV1, HSV2, VZV

think NEURONS

Replicate quickly and lyse epithelial cells

Neurotropic (like to infect neurons) and establish latency in neurons

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6
Q

Pathogenesis of HSV1 and HSV2:

1) Invasion through _____________ → replicate in ______ and ______ _______ cells → lyse, provoke inflammatory response → PAPULE
2) Lysis of many cells and production of cytokines → virus-filled fluid collection between dermis and epidermis → _________
3) Leukocytes enter vesicle and transform lesion to ___________
4) Forms a scab = _______________

A

1) Invasion through BREAK in mucous membranes/skin → replicate in BASAL and INTERMEDIATE EPITHELIAL cells → lyse, provoke inflammatory response → PAPULE
2) Lysis of many cells and production of cytokines → virus-filled fluid collection between dermis and epidermis → VESICLE
3) Leukocytes enter vesicle and transform lesion to PUSTULE
4) Forms a scab = DISEASE RESOLUTION (no virus in there)

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7
Q

Latency reservoir of HSV1

A

trigeminal ganglion

Can shed without any symptoms

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8
Q

Characteristic disease of HSV1

A

ORAL lesions

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9
Q

Herpetic gingivostomatitis

A

Typically due to HSV1

systemic symptoms, multiple painful oral/perioral lesions, tender adenopathy

Occurs in 20% of people during primary infection

Lasts 5-7 days then heals

Responds to antiviral therapy

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10
Q

HSV1 reactivation lesions

A

Mild tingling/pain for 6-12 hours → tender papule → vesicle formation → crusting/ulcer formation

Triggered by fever and sun exposure

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11
Q

HSV1 infection complications (2)

A

1) Keratitis

2) Herpes virus encephalitis

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12
Q

Keratitis

A

typically due to reactivation, involves cornea and can cause scarring

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13
Q

Herpes virus encephalitis

A

due to reactivation, causes necrotizing encephalitis traveling via trigeminal ganglion

Typically due to HSV1*

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14
Q

Latency reservoir of HSV2

A

sacral sensory ganglion

Can have asymptomatic shedding

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15
Q

Characteristic disease of HSV2

A

Genital lesions (sexually transmitted)

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16
Q

Primary infection with HSV2

A

usually asymptomatic

Headache, painful genital lesion, painful urethritis with tender inguinal adenopathy

Within first year of primary infection with get 3-4 recurrences of lesions/year

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17
Q

Complications associated with HSV2 infection (4)

A

usually with first episode

1) Viral meningitis (HSV2)
2) Urethritis
3) Candida superinfection
4) Anal and rectal HSV

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18
Q

Diagnosis of HSV1 and HSV2

A

PCR: detect HSV in late lesions - MOST COMMON

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19
Q

VZV pathogenesis:

initially infects __________ –> spreads to _____ and ________ via _______ and ______ cells

Infection then remains latent in _____________

A

initially infects upper respiratory epithelium → spreads to lymph nodes and RES (liver/spleen) via dendritic and T cells

Latency reservoir: Dorsal root ganglion

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20
Q

Primary chickenpox:

spread how?
symptoms?

A

spread via respiratory droplets or direct contact

Mild malaise, low grade fever → papules → vesicles → pustules → scabs (Vesicular rash)

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21
Q

Characteristics of rash present in primary chickenpox?

A

Characteristic “dew drop on a rose petal” = vesicle on erythematous base

Crops of vesicles at VARYING AGES

On trunk and face - distal extremities spared

Infectious just prior to onset, until scabbing

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22
Q

Complications associated with a primary chickenpox infection

A

1) Bacterial superinfection of skin lesions
2) Pneumonitis
3) hepatitis
4) **encephalitis (in immunocompromised)

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23
Q

The vaccine for chicken pox is made up of what?

A

LIVE ATTENUATED vaccine

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24
Q

Reactivation zoster:

clinical presentation (3)

A

1) Dermatomal rash in distribution of dorsal root nerve where it escaped latency
2) Does NOT cross midline
3) Painful prodrome can precede rash by 3-5 days

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25
Q

Complications associated with reactivation zoster (4)

A

1) bacterial superinfection
2) eye involvement (V1, includes tip of nose)
3) muscular weakness
4) Post-herpetic neuralgia → prolonged pain after

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26
Q

Reactivation zoster vaccine is for who?

A

VZV vaccine for immune competent people > 60 years (boost CD8+ T cell response which can decline with age)

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27
Q

Beta Herpesvirus:

A

CMV, HHV6, HHV7

think MYELOID LINEAGE

Replicate slowly in myeloid cells

Like to be in myeloid lineage cells and sometimes endothelial cells

Restricted to humans

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28
Q

Pathogenesis of CMV infection:

infects __________ cells –> local replication –> dissemination via ________ and ________

viral secretions in ______, _______, and ______ –> transmission

A

Infect mucosal epithelial cell surfaces → local replication → dissemination via peripheral blood monocytes and DCs

viral secretions in saliva, urine, breast milk → transmission

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29
Q

Latency reservoir for CMV virus

A

CD34+ myeloid cells

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30
Q

Mononucleosis-like syndrome

-main features (5)

A

characteristic disease of CMV infection

1) Mimics infectious mononucleosis (EBV)
2) Fever, malaise, adenopathy
3) Mild hepatitis, sore throat
4) Lymphocytes in blood
5) NO HETEROPHILE AB PRODUCED (in contrast to EBV)

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31
Q

CMV infection in immunocompromised person can cause what complications?

A

Immune compromised (T cell deficiency)→

systemic disease with end organ damage

Interstitial pneumonia common (can be fatal up to 50%)

Can also involve liver, colon, esophagus, bone marrow, retina

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32
Q

CMV Primary vs. reactivation infection in pregnant women:

which one is more likely to cause symptoms in baby?

A

FIRST CMV infection → baby more likely to be symptomatic at birth, serious illness

Reactivation → baby unlikely to have sx, but can have non-fatal sx (hearing loss) later on

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33
Q

Symptomatic congenital CMV after in utero infection (7)

A

1) Jaundice
2) enlarged liver/spleen
3) MIcrocephaly
4) seizures
5) decreased platelets
6) can be fatal
7) Can interfere with brain, eye, and ear development of fetus

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34
Q

Transmission of CMV (4)

A

1) Perinatal infection - CMV shed from mom into birth canal
2) early childhood infection via saliva
3) Adolescence - sexual transmission
4) in utero infection

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35
Q

Diagnosis of CMV (3)

A

1) PCR for CMV DNA from tissue
2) Tissue Histology of CMV Disease (viral inclusions)
3) IgM ab against CMV (IgG to CMV indicates PRIOR infection)

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36
Q

Treatment of CMV

A

Ganciclovir (NOT acyclovir), can become resistant to Ganciclovir → use Foscarnet

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37
Q

Latency reservoir for HHV6 and HHV7

A

Latency reservoir: B cells, myeloid progenitor cells (T cells)

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38
Q

Characteristic disease associated with HHV 6 (and sometimes 7)

A

Exanthema Subitum (Infant ROSEOLA)

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39
Q

Exanthema Subitum (Infant ROSEOLA)

3 main clinical features

A

1) HIGH FEVER

2) Rash begins as fever abruptly subsides**
- Rash: begin on trunk, spread to face, neck, extremities - No pigmentation or desquamation

3) NO conjunctivitis or pharyngeal exudate

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40
Q

Gamma Herpesvirus

A

EBV, HHV8

ATYPICAL CELLS

Replicated in lymphoid cells and undergo LYTIC replication in epithelial cells, endothelial cells, and fibroblasts

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41
Q

Pathogenesis of EBV infection?

infects _________ cells and ________ cells –> latency in ___________ cells and travels throughout the body

A

infect oral mucosal epithelial cells and adjacent B cells → latency in resting memory B cells and travels throughout the body

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42
Q

Two proteins expressed by EBV virus during latency that can be used as a marker of CHRONIC (latent, NOT ACUTE) infection?

A

Expresses EBNA1 and EBNA2 proteins during latency → ab to EBNA used as marker of CHRONIC or old infection (NOT ACUTE)

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43
Q

Latency reservoir of EBV

A

Naive B cells

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44
Q

Infectious Mononucleosis

3 main features

A

Characteristic disease of EBV

1) Fever, profound malaise
2) Exudative pharyngitis with palatal petechiae**
3) Lymphadenopathy, Splenomegaly, Hepatomegaly**

Improved within 14 days, but can have prolonged fatigue

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45
Q

Antibodies to which 2 proteins will be present during an acute EBV infection?

A

Viral capsid antigen (VCA) and Early Antigen (EA) antibodies present

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46
Q

Heterophil Antibodies

(+) indicates what?

(-) indicates what?

A

EBV induces B cells to make ab for which there is no prior immunologic memory
–> POSITIVE MONOSPOT TEST

Monospot negative IM → CMV, rubella, HepA, HHV6/7

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47
Q

EBV specific antibodies

IgG ab to VCA vs. IgM ab to VCA means what?

A

IgG ab to EBV capsid antigen (VCA) → infection has occurred (either acutely or in past)

IgM ab to VCA → acute infection

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48
Q

KSHV (HHV8) is latent in what cells?

A

B cells

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49
Q

KSHV (HHV8) causes what 2 characteristic diseases?

A

Kaposi sarcoma in HIV/AIDS patients

B cell lymphoma

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50
Q

Kaposi sarcoma in HIV/AIDS patients

A

Angioproliferative inflammatory lesion caused by HHV8 infection

sexually transmitted, and sometimes transmitted via saliva (Africa)

51
Q

Lytic replication

A

occurs in permissive cells and is CYTOPATHIC (kills cells)

52
Q

Histological features of herpes virus infection

A

1) Significant numbers of infectious particles released

2) Nuclear and cytoplasmic inclusions present
- -> Viral capsid proteins trapped in nucleus

3) Cytomegalic cells and syncytia formation

53
Q

Inclusion bodies associated with herpes viruses:

1) Intranuclear Acidophilic = ______ and _______
2) Intranuclear Basophilic = ______
3) Intranuclear and intracytoplasmic = _____ and _______

A

Intranuclear Acidophilic = Cowdry Type A (HSV, VZV)

Intranuclear Basophilic = CMV “owl eyes”

Intranuclear and intracytoplasmic = HHV6, CMV

54
Q

Replication cycle of herpes virus:

1) Attachment and entry

A

virus attaches to cell specific receptors (determines cell type of herpes infection) and dumps viral capsid into cytoplasm

55
Q

Herpes virus Viral glycoproteins

A

mediate this attachment/entry

In lipid envelope mediate cellular tropism and are targets of adaptive immune response

56
Q

Replication cycle of herpes virus:

2) Uncoating

A

Capsid transported to nucleus and dsDNA genome inserted into nucleus → forms episome (circle) → latency or acute replication

57
Q

Episome

A

Episome is where virus maintains itself during latency

circular dsDNA of herpes virus inside host cell nucleus that can either undergo latency or acute replication

58
Q

Herpes virus replicates in ____________ using ________.

The herpes virus acquires its capsid in the _______ resulting in what?

A

Replicates in NUCLEUS using viral-encoded DNA polymerase and gets capsid in nucleus

**Intranuclear inclusions (accumulated viral capsid proteins) often present in herpesvirus infection

59
Q

3 major sets of genes expressed by the herpes virus during genome replication

A

1) Immediate early genes
2) Early genes
3) Late genes

60
Q

Immediate early genes

A

transcribed soon after viral entry, set up environment conducive for viral replication

61
Q

Early genes

A

encode replication enzymes (DNA POLYMERASE) and nonstructural viral proteins

62
Q

Late genes

A

encode viral structural proteins needed for packaging new virion and egress from infected cell

*Capsid proteins are transported into the nucleus for ENCAPSIDATION → nuclear viral inclusions

63
Q

Latent replication

A

Genome persistence in NUCLEUS of specific cells

Small subset of viral genes expressed, but NO infectious particles are produced

REACTIVATION = source of majority of disease

64
Q

Antiviral Therapy for Herpesviruses:

what is the general mechanism by which they act?

A

Mechanism: NUCLEOSIDE ANALOGS → interrupt viral DNA synthesis by integrating into growing viral DNA and preventing chain elongation

1) Acyclovir
2) Ganciclovir

65
Q

Acyclovir

activated by _________

used to treat _______ and ______, but not _______

A

nucleoside analog activated by thymidine kinase → treat HSV/VZV

NO activity against CMV (no thymidine kinase)

66
Q

Ganciclovir

activated by _________

used to treat _______

A

nucleoside analog activated by viral UL97 protein kinase → treat CMV and B-herpesviruses

67
Q

Mechanism to resistance of herpes viruses to acyclovir of ganciclovir?

A

mutations or deletions of viral kinase required for initial phosphorylation/activation of prodrug

68
Q

Neisseria gonorrhoeae

gram \_\_\_\_\_
shape?
aerobe/anaerobe?
oxidase?
catalase?
capsule?
intra or extracellular?
A 
Gram-negative diplococci
Strictly aerobic
Oxidase +
Catalase +
NO CAPSULE
Facultative intracellular (often found within neutrophils)
69
Q

Neisseria gonorrhoeae

culture medium?

A

5% Co2 atmosphere on Thayer Martin agar (VPN) (selective medium for pathogenic Neisseria)

Rapid autolysis at 25 C and alkaline pH

70
Q

Neisseria gonorrhoeae

main virulence factors?

A

1) Produces IgA protease → allows oropharynx colonization
- Cleaves Fc portion of IgA → prevent opsonization

2) Pili (fimbriae)

71
Q

Neisseria gonorrhoeae

Pili (fimbriae)

A

→ attachment to mucosal surface and prevention of phagocytosis

Highly variable → allows for recurrent infection in same person

Can use phase variation to switch on/off expression of pili

72
Q

Neisseria gonorrhoeae

deficiency in _________ predisposes to Neisseria bactermia

A

Deficiency in complement factors C5-C9 (MAC) predisposes to Neisseria bacteremia

73
Q

N. Gonorrhoeae can ferment ________ while N. Meningitis can ferment ___________

A

N. Gonorrhoeae can ferment glucose

N. meningitidis can ferment maltose AND glucose

74
Q

Gram stain of urethral/endocervical exudates when diagnosing N. gonorrhea will show what?

A

diplococci WITHIN PMNs

75
Q

Gold standard for diagnosing gonorrhea?

A

*NAATs (Nucleic Acid Amplification Tests)

76
Q

Asymptomatic carriers of gonnorhea:

Men vs. women?

A

WOMEN much more likely to be asymptomatic →risk of developing PID

Problem for control of gonorrhea transmission

77
Q

Clinical Manifestations of gonorrhea infection: (6)

A

1) Cervicitis, Urethritis
2) Septic arthritis
3) Neonatal conjunctivitis
4) Pelvic inflammatory disease
5) Fitz-Hugh Curtis Syndrome
6) **Increases likelihood that HIV and other STDs may be more efficiently transmitted through unprotected sex

78
Q

Gonorrhea: Cervicitis, Urethritis (3 sx)

A

1) Pain/discomfort with urination
2) Pain during sex
3) Yellow/white thick mucopurulent discharge from urethra or vagina (chlamydia is clear/watery discharge)

79
Q

Gonorrhea: Septic arthritis

A

most common cause of septic arthritis in sexually active people
Usually affects the knee

80
Q

Gonorrhea: Neonatal conjunctivitis

timeline of infection?

A

(Ophthalmia neonatorum)

Eye infection of neonate born to infected mothers

Occurs 1-5 days after birth (Chlamydia is 5-12 days after birth)

81
Q

Gonorrhea: Pelvic inflammatory disease

A

N. gonorrhoeae infection that ascends genital tract and infects uterus, oviduct, and ovaries

82
Q

Gonorrhea: Fitz-Hugh Curtis Syndrome

A

perihepatitis, infection of liver capsule and peritoneal surfaces of anterior RUQ
SX = patchy purulent and fibrinous exudate = “Violin String” adhesions

can also occur with Chlamydia

83
Q

Treatment of gonorrhea

A

ceftriaxone (single IM dose) + doxycycline or azithromycin (for possible coinfection with chlamydia)

Patients infected with N. gonorrhoeae often co-infected with C. trachomatis

MUST treat known sexual contacts of a patient with this disease

84
Q

Chlamydia trachomatis

Does not gram stain because it is ___________ and lacks ___________

stains with ________

A

OBLIGATE INTRACELLULAR
-CANNOT synthesize ATP or oxidize NADP → COMPLETELY dependent on host cell for energy production

Lacks peptidoglycan due to absence of MURAMIC ACID component of bacterial cell walls → penicillin resistant

Can visualize by staining infected cells with Giemsa stain

85
Q

Chlamydia trachomatis:

Virulence factors: (3)

A

1) Lipopolysaccharide: group antigen common to all Chlamydia
2) Specific outer membrane proteins → serotype chlamydia
3) Survives in endosomes in cells by inhibiting endosome/lysosome fusion

86
Q

Biphasic life cycle of Chlamydia:

A

1) Elementary bodies = infectious

2) Reticulate bodies = multiply (replicate by BINARY FISSION)

87
Q

Elementary bodies

A

infectious form, enter epithelial cells by endocytosis and phagocytosed by macrophages

Form reticulate bodies (dividing type)

EBs are INFECTIOUS, but metabolically inert outside human cell

88
Q

Reticulate bodies

A

divide by binary fission, and reorganize into EBs within cytoplasmic inclusions

Cell fills with cytoplasmic inclusions → cell bursts → release EBs to infect nearby cells

89
Q

C. Trachomatis: A-C

A

“above the belt”

trachoma, conjunctivitis - transmitted by hand-eye contact

90
Q

Chlamydia: Trachoma

A

chronic keratoconjunctivitis → progressive scarring of conjunctiva and cornea, can lead to blindness

91
Q

Chlamydia: Inclusion conjunctivitis

A

acute disease in infants and adults (usually neonatal conjunctivitis in US)
Mucopurulent conjunctivitis 7-12 days after delivery
Infection can disseminate and cause pneumonia

92
Q

C. Trachomatis: D-K

5 types of manifestations

A

Infects columnar epithelium of GU tract, common co-infection with gonorrhea

1) Urethritis, Cervicitis
2) PID
3) Fitz-Hugh-Curtis Syndrome (perihepatitis)
4) Neonatal conjunctivitis and atypical pneumonia (due to infected mother)
5) Reactive arthritis (Reiter’s Syndrome)

93
Q

Chlamydia urethritis/cervicitis symptoms?

A

75% of women and 50% of men asymptomatic

Lower abdominal pain = PID
Dysuria = urethritis
Genital discharge = cervicitis

Males → watery/mucous discharge, dysuria, unilateral testicular pain (epididymitis)

94
Q

PID caused by chlamydia can result in what complications?

A

scarring of fallopian tubes causing ectopic pregnancy, infertility, and chronic pelvic pain

95
Q

C. Trachomatis

L1-L3

A

causes Lymphogranuloma venereum

96
Q

Lymphogranuloma venereum:

A

Necrotizing granulomatous inflammation of inguinal lymphatics and lymph nodes

PAINLESS genital ulcers + PAINFUL lymphadenopathy (buboes) → fibrosis that can lead to rectal strictures with perianal involvement

Typically occurs in Africa and South America (rare in North America)

97
Q

C. Psittaci

A

pathogenic for birds → transmitted to humans via inhalation of bacteria in droplets or dust = psittacosis

98
Q

Primary Syphilis - presentation?

A

PAINLESS CHANCRE

One or more CHANCRE - painless, ulcerating papule, non-exudative, clean, hard base with indurated margins (punched out base with rolled edges)

99
Q

Secondary syphilis

A

weeks to months after primary infection = PAINLESS RASH (palms of hands and soles of feet)

100
Q

Secondary syphilis

5 main symptoms?

A

1) Maculopapular rash: discrete copper, red, or reddish-brown on trunks and extremities, notable on PALMS and SOLES
2) Condyloma lata:
3) Systemic symptoms (fever, headache, malaise, myalgias)
4) Generalized lymphadenopathy
5) Hepatitis

101
Q

Condyloma lata

A

raised, infectious, gray/white wart-like lesion in moist areas and mucous membranes (mouth, perineum)

102
Q

Tertiary Syphilis can include what 3 main things

A

not infectious anymore

1) CNS (neuro) syphilis
2) Gumma formation on skin, bones, and internal organs
3) Cardiovascular (aortitis)

103
Q

Neurosyphilis

demyelination of ________

4 main manifestations?

A

demyelination of posterior column

1) Broad-based ataxia
2) Argyll Robertson pupil (eye accommodates to near objects, but does not react to light)
3) Positive Romberg sign
4) Charcot joints

104
Q

Syphilis Gummas

A

Gumma formation on skin, bones, and internal organs

Gumma = ulcers or granulomatous lesions with round, irregular shape, visceral gumma is a mass lesion

105
Q

Syphilis Aortitis

A

affects ascending thoracic aorta, presents as dilated aorta and aortic valve regurgitation

Proliferative endarteritis affecting vaso vasorum of aorta → medial necrosis and loss of elastic fibers

Tree barking

106
Q

Congenital Syphilis

A

maternal syphilis → neonate (TORCHeS)

Can result in stillbirth, early congenital syphilis, and late congenital syphilis

107
Q

Early congenital syphilis: 5 main manifestations

A

1) Hepatomegaly, jaundice, cholestasis
2) Rhinitis (“snuffles”) - discharge contains spirochetes
3) Maculopapular lesions on palms and soles
4) Generalized lymphadenopathy
5) Anemia, thrombocytopenia

108
Q

Late congenital syphilis: 8 main manifestations

A

due to scarring or persistent inflammation from early infection

1) Gumma formation in various tissues
2) Frontal bossing, saddle nose
3) Interstitial keratitis
4) Sensorineural hearing loss
5) Hutchinson teeth, mulberry molars
6) Intellectual disability
7) Saber shins
8) Paroxysmal cold hemoglobinuria

109
Q

Yaws

A

T. pallidum infection - destructive lesions of skin and bone

Endemic among children in humid, TROPICAL countries

Ulcerating papule on legs or arms → scar formation, bone destruction

110
Q

Endemic syphilis or Bejel

A

T. pallidum
Children in Africa, Middle East, SE Asia (Desert)
Skin lesions

111
Q

Syphilis:

Direct visualization via _______ or ________

A

Direct visualization- darkfield microscopy or direct fluorescent antibody testing

112
Q

VDRL test can be falsely positive in what 6 cases?

A

1) Mononucleosis, hepatitis
2) Drugs (hydralazine, procainamide)
3) IV drug use
4) Rheumatic fever
5) Lupus
6) Leprosy

113
Q

Serologic testing for syphilis includes… (2)

A

RPR test (cardiolipin coated carbon particles)

VDRL test

114
Q

Treatment of syphilis

A

Penicillin G benzathine (IM, slow release into muscle)- unless allergic, then use Azithromycin

115
Q

Jarisch-Herxheimer reaction

A

complication of penicillin therapy due to release of endotoxin-like factors from lysis of T. pallidum organisms

Fever, headache, sweating, exacerbation of syphilitic lesions 6-12 hrs after penicillin therapy

Associated with treatment of secondary syphilis

116
Q

Pediatric vaccine schedule: at what age are these vaccines given? what kind of vaccine are they?

HepB
Rotavirus
DTaP
Tdap
H. influenza
A

1) Hep B = SUBUNIT VACCINE birth-18 months

2) Rotavirus = LIVE ATTENUATED
1-2 months

3) DTaP = POLYSACCHARIDE 2-6 months
4) Tdap = POLYSACCHARIDE give only > 7 years
5) H. Influenza = type B CONJUGATE VACCINE 1-2 months

117
Q

Pediatric vaccine schedule: at what age are these vaccines given? what kind of vaccine are they?

Inactivated poliovirus
Influenza
MMR
Varicella
HepA
HPV
Meningococcal
A

Inactivated Poliovirus: 2 months

Influenza: > 6 months, annually

  • intranasal = LIVE ATTENUATED
  • IM = KILLED VACCINE

MMR = LIVE ATTENUATED 12 months

Varicella = LIVE ATTENUATED 12 months

HepA = KILLED VACCINE 12 months

HPV = SUBUNIT VACCINE - 11-12 years

Meningococcal = CONJUGATE VACCINE 11-12 years

118
Q

Adult vaccine schedule:

Adults > 60 –> ?

Adults > 65 –> ?

A

Adults > 60 years → Zoster

Adults > 65 years → Pneumococcal (13-valent conjugate), Pneumococcal polysaccharide

119
Q

Which vaccines are contraindicated in pregnancy (3)

A

Varicella
Zoster
MMR

120
Q

Key contraindications to giving a live attenuated vaccine? (3)

A

Leukemias

immunosuppression

Pregnancy (low risk contraindication)

121
Q

HPV vs. Herpes Virus:

  • who makes its own DNA-dependent DNA polymerase?
  • who has an envelope?
  • what genes do they each express
A

HPV:

  • no envelope
  • no DNA-dependent DNA-polymerase (relies on host cell)
  • Expresses early genes and late structural genes (L1, L2)

Herpes virus:

  • enveloped
  • encodes DNA-dependent DNA polymerase
  • Expresses immediate early, early, and late genes
122
Q

What kind of immune response is important for herpes virus?

A

BOTH antibody-mediated and cell-mediated immunity important to herpesvirus

Neutralizing antibodies prevent systemic spread of infection - prevent virus spread beyond cells innervated by reactivating neuron

Cell-Mediated Immunity (CD8+ T cells) critical for clearance of virus from lesions

123
Q

Genomes:

Rotavirus
Calciviruses (norovirus)
HPV
Herpes virus

A

Rotavirus = dsRNA (11 genome segments)

Calciviruses (norovirus) = (+) sense ssRNA (nonsegmented)

HPV = naked, nonenveloped, dsDNA

Herpes virus = enveloped, dsDNA

Infectious Disease (9 decks)

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