Lect 22 Flashcards

1
Q

Measels multiplies in

A
  • respiratory epithelium
  • lymph nodes
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2
Q

Prodromal stage of measels is characterized by

A
  • 3 C’s
    • coryza
    • persistent cough
    • conjunctivitis
  • Koplik spots on buccal mucosa
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3
Q

Koplik spots on buccal mucosa is diagnostic for

A

measels

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4
Q

describe rash associated with measels

A
  • appears 3-4 days after prodrome initiates
  • begins below ears and spreads
  • associated with fever
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5
Q

what are the 3 main complications from measels

A
  1. PNA
  2. diarrhea
  3. CNS involvement
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6
Q

hosts of measels

A
  • humans
  • monkeys
  • no healthy carrier state is known
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7
Q

measels primarily affects what patient population

A

children

  • but rare < 6 m.o due to maternal immunity
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8
Q

how is measels transmitted

A

respiratory droplets

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9
Q

How is measels diagnosed

A
  • rash +/- koplik spots
  • FA test
    • multinucleated giant cells
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10
Q

measels prevention

A
  • MMR vaccine
    • 2 doses
      • 15 months
      • 4-6 years
  • immune globulin (BayGam) for exposed non-immune subjects 6 days after exposure​
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11
Q

describe measels vaccine used in US

A
  • MMR II: live, attenuated vaccine, not suitable for all patients
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12
Q

Children often escaped infection with Rubella. Why was this a problem?

A

led to the principal problem linked to rubella – congenital rubella syndrome when infection occurs in women during the first trimester of pregnancy

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13
Q

congenital rubella syndrome

A
  • Maternal infection (viremia) may lead placental infection and fetal infection substantial risk to fetus
  • Cardiac defects - pulmonary artery stenosis, patent ductus arteriosis
  • Eye defects - cataracts, glaucoma
  • Hearing loss - may be profound CNS involvement
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14
Q

does timing of infection affect outcome of congenital rubella syndrome

A
  • yes, early in pregnancy is the worst
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15
Q

prevention for Rubella

A
  • MMR vaccine
  • Non-specific intravenous immune globulin (IVIG) may be provided for nonimmune women with documented exposure to rubella in first trimester.
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16
Q

MMR should not be given to

A
  • pregnant women
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17
Q

What two unique properties influence disease capacity of Herpes simplex virus

A
  1. capacity to invade and replicate in CNS
  2. ability to establish latent infections
    • HSV will cause a primary infection (may be asymptomatic) that will resolve and establish a quasi-stable state of latency subject to reactivation (recrudescence).
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18
Q

how does HSV become latent

A
  • Retrograde transport of virus through sensory neurons and ultimate infection of the dorsal root ganglia (virus remains latent).
    • Latency is life-long
19
Q

Recrudescence of HSV will occur even in the presence of active humoral and cellular immunity and present as

A

“cold sores”, “fever blisters” on vermilion border of lips

20
Q

Rule of thumb for HSV– probability of recrudescence is greater in individuals with

A

larger and more extensive initial outbreaks.

21
Q

reservoir for HSV

22
Q

how is HSV spread

A
  • contact with vesicular fluid, saliva, and secretions
  • asymptomatic shedding is possible
23
Q

Which of the HSV types occurs early in life and is common? Which type tends to occur later and correlates with sexual activity

A
  1. HSV-1
    • oral herpes
  2. HSV -2
    • genital herpes
24
Q

How is HSV diagnosed

A
  • Ballooning pathology and presence of enlarged and fused cells (Tzanck smear)
  • FA assay for viral antigens
  • culture in HeLa, Hep-2 cell lines
25
varicella-zoster virus causes both
* chicken pox * shingles
26
clinical presentation * Asymmetrical vesicular rash that sometimes follows an obvious dermatomal pattern. * Fever, malaise, headache, neuralgia with **pruritic lesions** that are often secondarily infected.
varicella zoster virus infection
27
Varicella virus transmission
* conjunctiva * respiratory tract mucosa * present in vesicles
28
Where does varicella replicate
1. Replicates in regional lymph nodes, primary viremia 4-6 days after infection 2. Virus replicates in liver and spleen generating a secondary viremia (coincident with rash) 10-14 days after infection.
29
reservoir for varicella
humans
30
What medication should a patient with varicella not take
* ASA * reyes syndrome risk
31
chickenpox prevention
* **Varivax**: live attenuated virus * **immune globulin (Varizig)** for high risk persons exposed to infection
32
clinical presentation * burning, searing pain precedes rash * rash in unilateral dermatomal distribution * 10% have involvement of ophthalmic branch of 5th cranial nerve
shingles: recrudescence of VZV
33
most common complication from shingles
postherpetic neuralgia
34
Patient with shingles MUST have had
* chicken pox or varivax vaccine * shingles is not directly transmissible
35
shingles prevention
* zostavax * patients \> 50 * high potency to boost immunity
36
Exanthem subitum (Roseola Infantum or 6th Disease)- a sequence of high fever followed by a rose-colored rash is associated with
herpes virus 6
37
how is herpes virus 6 diagnosed
* Detection of IgM antibody by EIA * DNA sequence detection by PCR amplification
38
Fifths disease or erythema infectiosum is caused by
Parvovirus B19
39
clinical presentation * Prodromal illness of several days duration with mild symptoms; fever, headache, malaise, myalgia, respiratory symptoms, sometimes nausea, vomiting. * Prodrome is followed by a skin rash with a characteristic **slapped cheek** with circumoral sparing manifestation - resolves in 1-2 weeks * A **“lacey” maculopapular rash** may also involve limbs and trunk * Connective tissue manifeststions **Arthalgia** and/or **arthritis** may follow skin eruption
Parvovirus B19
40
how is Parvovirus B19 diagnosed
* facial rash * detection of anti B19 IgM antibody
41
What HPV types are responsible for ano-genital warts?
HPV 6 and 11
42
What HPV types are responsible for cervical dysplasia
HPV 16 and 18
43
prevention HPV
* Gardasil * Cervarix * males and females ages 9-26