STIs Flashcards
Neisseria
Aerobic gram negative cocci Oxidase and catalase + N. meningitidis = meningitis N. gonorrhoeae = gonorrhea All look the same under the microscope We are all colonized by some non-pathogenic species
N. gonorrhoeae
(gram stain, shape, oxidase, catalase, intra/extracellular, media it grows on, transmission, what epithelia does it infect)
Aerobic gram negative diplococci
Oxidase and catalase +
Often appears intracellular on gram stain
Very fastidious (will not grow on SBA, may not survive drying and dies rapidly during transport)
Grow on Thayer Martin media
Transmission from male to female more likely
Primarily infects columnar or cuboidal epithelium
Superoxol Test
Performed with 30% H2o2
Really bubbly
One way to tell between gonorrhea and chlamydia
GC: copius discharge
C: no discharge
2 major virulence factors for N. gonorrhoeae
- Pili (adherence to mucosal surfaces, inhibit killing by neutrophils)
- Outer membrane (facilitate invasion, has endotoxin)
Sensitivity
The proportion of actual POSITIVES that are correctly identified as positive
Specificity
The proportion of NEGATIVES that are correctly identified
Positive predictive value
Proportion of patients with positive test results who are correctly diagnosed
Depends on the prevalence of the disease
Negative predictive value
Proportion of patients with negative test results who are correctly diagnosed
Gonorrhoea culture/diagnosis
Grows on chocolate agars with antibiotics (nutritous medial
Take urethral swabs from male and cervical swabs from females
Does NOT grow on SBA
GC culture vs PCR samples for males and females
Culture: males use urethral swabs, females need cervical swabs
PCR: males need 1st voided urine, females need vaginal swabs
What do we use to treat GC?
800mg Cefixime or 250mg ceftriaxone intramuscularly
Both are cephalosporins
3 primary Chlamydia pathogens
C. psittaci (resp tract infections from birds)
C. pneumoniae
C. trachomatic
Chlamydia life cycle
Biphasic Elementary bodies (infective form) attaches to host cell, endocytosed, morphs into reticulate body (undergoes multiplication by binary fission), then differentiates back to elementary body, released from cell, on to infect others
Chlamydia causes __ in men vs women
Men: urethritis
Women: cervicitis and PID
Lab Diagnosis for Chlamydia (4)
Antigen detection
Immuno-fluorescence
Cell culture
PCR
Chlamydia treatment (1st and 2nd line)
1st line: 1 gram Azithromycin (4 pills, single dose)
2nd line: 100 mg BID doxycycline (2 doses a day for 10 days)
Haemophilus ducreyi
Produces Chancroid lesions
Tender, non indurated irregular ulcers
Infection is localized, but frequently spreads to regional lymph nodes
Lymph nodes enlarged and painful
Intra or extracellular bacteria, appear as cocco-bacilli or short rods
Gram varibale
Arranged in parallel chains (school of risk or rail road track appearance)
2 hotspots: Nairobi and Winnipeg
Fastidious - grows slowly on chocolate but using 2 media is optimal
Media for H. ducreyi
Gonococcal agar based or a Mueller Hinton based medium can be used, and add:
1% IsoVitalex, 5% chocolatized horse blood or 1% hemoglobin, 5% fetal calf serum, Vanco
Molluscum contagiousum
Large enveloped DNA, poxvirus family
Only found in humans (no animal reservoir)
Diagnosis: EM, clincal appearance, PCR
Not painful but can be itchy (can lead to secondary infections and scarring)
Affects any area of the body
High incidence in children, immunocompromised, sexually active adults
Transmitted through direct contact and fomites
Long incubation period and lasts a long time, but will go away on its own (does not stay in body)
Treat with chemical or surgical removal of lesions
Clinical appearance of Molluscum contagiousum
Flesh coloured lesions
Dome-shaped with dimpled center
Diameter 1-5 mm
Herpes simplex virus
Enveloped, icosahedral capid, dsDNA
Thymidine kinase and DNA polymerase (acyclovir)
Spectrum of disease: asymptomatic, lesions, encephalitis, recurrent meningitis, ocular infections
HSV 1 versus HSV 2
1: frequently associated with oral/ocular infections (rising in cases of genital herpes though) - less reoccurrences, less asymptomatic shedding
2: most frequently associated with genital infections
Molleret’s
Meningitis from herpes
Recurrent
Will go away on its own without treatment
Latency and Reactivation of herpes
- Local replication and entry of virus into cutaneous neurons
- Centipetal migration in the axon
- Reactivation and replication
- Centrifugal migration to the epidermis
Melt curve analysis
Way to diagnose herpes
Real time PCR
Uses the primers for both 1 and 2 and based on what temperature they probes melt off you can generate a melting temperature which is characteristic for one of them
Acyclovir
Nucleoside analog - chain terminator
Blocks viral DNA polymerase
Has to be phosphorylated to be activated
First activation with HSV thymidine kinase, next 2 with host enzymes
Human Papilloma Virus
Papillomaviridae
Non-enveloped, dsDNA virus
Most prevalent STD
Cannot be grown in culture - molecular detection possible and use Pap test
Oncogenic virus
Contact transmission
Acquisition shortly after onset of sexual activity
Respiratory papillomatosis
Benign warts in the upper airway (may cause obstruction, can surgically remove)
Caused by HPV 6 and 11
Treating genital warts
Usually for aesthetic reasons
Podophyllin resin, trichloroacitic acid, cryotherapy
Burn or freeze them off
Why are only some HPV strains oncogenic?
High risk HPV has a circular gene
Gets integrated into the genome and splits a gene that regulates expression of E6 and E7
These have effects on the cell that will lead to its proliferation
E6 vs E7
E6: binds and leads to degradation of p53 (low risk types do NOT bind p53)
E7: binds the retinoblastoma TSG product so the transcription factor is free to activate the cell cycle (low risk types bind poorly to this)
Gardasil vs Cervarix
G: Types 16, 18, 6, 11
C: Types 16, 18 only
HPV L1 Virus-Like-Particle Vaccine
Give a pseudovirus from the capsid proteins Very safe (no replication)
