Lect 22 Flashcards
Measels multiplies in
- respiratory epithelium
- lymph nodes
Prodromal stage of measels is characterized by
- 3 C’s
- coryza
- persistent cough
- conjunctivitis
- Koplik spots on buccal mucosa
Koplik spots on buccal mucosa is diagnostic for
measels
describe rash associated with measels
- appears 3-4 days after prodrome initiates
- begins below ears and spreads
- associated with fever
what are the 3 main complications from measels
- PNA
- diarrhea
- CNS involvement
hosts of measels
- humans
- monkeys
- no healthy carrier state is known
measels primarily affects what patient population
children
- but rare < 6 m.o due to maternal immunity
how is measels transmitted
respiratory droplets
How is measels diagnosed
- rash +/- koplik spots
- FA test
- multinucleated giant cells
measels prevention
-
MMR vaccine
- 2 doses
- 15 months
- 4-6 years
- 2 doses
- immune globulin (BayGam) for exposed non-immune subjects 6 days after exposure
describe measels vaccine used in US
- MMR II: live, attenuated vaccine, not suitable for all patients
Children often escaped infection with Rubella. Why was this a problem?
led to the principal problem linked to rubella – congenital rubella syndrome when infection occurs in women during the first trimester of pregnancy
congenital rubella syndrome
- 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
does timing of infection affect outcome of congenital rubella syndrome
- yes, early in pregnancy is the worst
prevention for Rubella
- MMR vaccine
- Non-specific intravenous immune globulin (IVIG) may be provided for nonimmune women with documented exposure to rubella in first trimester.
MMR should not be given to
- pregnant women
What two unique properties influence disease capacity of Herpes simplex virus
- capacity to invade and replicate in CNS
-
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).
how does HSV become latent
- Retrograde transport of virus through sensory neurons and ultimate infection of the dorsal root ganglia (virus remains latent).
- Latency is life-long
Recrudescence of HSV will occur even in the presence of active humoral and cellular immunity and present as
“cold sores”, “fever blisters” on vermilion border of lips
Rule of thumb for HSV– probability of recrudescence is greater in individuals with
larger and more extensive initial outbreaks.
reservoir for HSV
humans
how is HSV spread
- contact with vesicular fluid, saliva, and secretions
- asymptomatic shedding is possible
Which of the HSV types occurs early in life and is common? Which type tends to occur later and correlates with sexual activity
- HSV-1
- oral herpes
- HSV -2
- genital herpes
How is HSV diagnosed
- Ballooning pathology and presence of enlarged and fused cells (Tzanck smear)
- FA assay for viral antigens
- culture in HeLa, Hep-2 cell lines