Lecture 16: Sexually Transmitted Disease 2 Flashcards
1
Q
How are STI’s spread?
A
Person -> Person
- Sex
- Oral-gen
- I.V drugs
- Congenital transmission
2
Q
Harm reduction strategies
A
- Abstinence
- Safe sex
- Monogamous relationship
- Reduce the # of sex partners
- Vax
3
Q
Human Papillomavirus Virus (HPV)
A
- Most common sexually transmitted infection
- Causes genital warts and cervical cancer
- Unclear incubation period (3 months-several yrs)
- Transmits thru sex or skin-skin contact
- Condoms do not provide complete protection
- No epidemiologic data yet
4
Q
Altered risk of acquisition examples for HPV
A
a) Sex
b) Age
c) age of first sex intercourse
d) co-infections
e) male circumcision
f) condom use
g) life-time # of partners
5
Q
Type 16, 18 of HPV
A
Cause of 70% of Cervical Cancer Cases
6
Q
Type 6,11 of HPV
A
Cause of 90% of Genital Warts Cases
7
Q
Mechanism of HPV Disease
A
- Micro abrasion(s) in the mucosa
- Infects basal keratinocytes (b/c quiet -> no immune response)
- Differentiate and move to the distal mucosa
- Viral assembly as cells move to the mucosa
- Infections virus shed
- Chromosomal integration (takes yrs, causes the potential for cancer)
8
Q
HPV Diagnostic Approach and Treatment
A
- Clinical signs, pap smear, virus culture, and PCR
- b/c of high level of seroprevalence, serology is not useful
Treatment: Local therapy involving immune enhancers (imiquimod), liquid nitrogen or surgical removal
Prevention: Vaccine (can prevent strong chance of cervical cancer)
9
Q
HPV Vax
A
- we use nine-valent now
- made with recombinant tech in which proteins form virus like particles (VLPs) of the L1 protein
- noninfectious
10
Q
Herpes Simplex Viruses (HSV)
A
- HSV-1 and HSV-2 are both DNA viruses
- Very highly prevalent within a population
- HSV-1 more prevalent while HSV-2 less so
- Some people may not be aware bc its dormant and they never get lesions
- Most common cause of genital ulcers
- Painful lesions
- Contagious before lesions appear and with active lesions
- Recurrence more common w HSV-2
11
Q
Pathophysiology of HSV
A
- Large family of DNA viruses
- HSV-1 above belt
- HSV-2 below belt
- Man is only natural host
- Reactivation -> you will have antivirals that will work
- Life-long infection with periodic infections
- Replicates in host cell nucleus
- Neurotropic and neuroinvasive
- Replicates 8-16hrs
12
Q
HSV Transmission
A
- Ppl dont know their infected
- Transmission as a result of contact with mucous membrane
- HSV reactivation is linked to environmental stressors including sunlight
- Can be shared asymp.
13
Q
Clinical Complications of HSV in males and females
A
- viral meningitis
- radiculomyelopathy with sacral nerves
- risk of acquiring and shedding HIV
- extensive vesicular skin rash
14
Q
HSV treatment
A
- Life long
- Antiviral therapy as treatment for HSV
- Although not a cure - antiviral therapy can prevent or shorten outbreaks
- Antiviral therapy can reduce likelihood of transmitting to ones partner
15
Q
Genital Herpes Clinical Diagnosis and Patient Support
A
- Primary episodes more severe than recurrences
- Risk of transmission to fetus during delivery
- Virus culture for lesions - can differentiate HSV-1 from HSV-2
- PCR lesions with multiplex PCR, lesions tend to be very high in viral loads
- Patient has no lesions - concerned for HSV (viral load isn’t high enough to test +’ve) - you can’t rely on a -‘ve
- Serology - looking for an antibody response