Sexually Transmitted diseases Flashcards
1
Q
Physical shape of syphilis
A
-long, very thing spirochete
2
Q
Visualization of syphilis
A
- fixed tissues by silver stain
- visualize live by dark field microscope
3
Q
Sheath surrounding syphilis
A
glycosaminoglycan surrounding whole cell
4
Q
Motility of syphilis
A
- endoflagella within periplasm
- 3 at each end
5
Q
Three other bacteria that have characteristic of spirochete
A
- treponema
- leptospira
- borrelia
6
Q
Envelope of syphilis
A
- no LPS, loosely anchored OM with cardiolipin
- mostly IM lipoproteins, few OM proteins
7
Q
Cultivability of syphilis
A
- unculturable in lab
- survive a few weeks, but no growth
- microaerophilic metabolism
8
Q
The stages of syphilis
A
Primary, secondary, and tertiary
9
Q
Description of the primary stage of syphilis
A
- ulcerated, defined papule at site of infection = chancre
- regional lymph nodes well
- usually genital, oral/anal 10-20%
- heals spontaneously, org. remains
10
Q
Description of the secondary stage of syphilis
A
- red macular/maculopapular rash occurring anywhere(in. soles and palms)
- condylomas in moist areas
- spont. heals
- recurrence
- long latent period
11
Q
Similarity between primary and secondary stages of syphilis
A
- unusual primary site indicative of overlap between both stages
- chin, tonsil, ear, neck, fingers, chest, arm
12
Q
Description of the tertiary stage of syphilis
A
- lesions in tissues throughout body(due to immune response)
- skin: gummas
- bones: porous, fragile
- heart: aorta swells, ruptures
- liver damage
- CNS: paresis, tabes dorsalis
13
Q
Birth defects related to syphilis
A
- abortion or stillbirth
- Hutchinson’s triad: interstitial keratitis, 8 nerve deafness, H. teeth
- saddlenose, neural defects, bone deformation
14
Q
Epidemiology of syphilis
A
- exclusively human and STD
- contagious for 3-5yrs after infection
15
Q
Pathogenesis of syphilis
A
- highly infectious
- hyaluronidase facilitates spread and invasion of tissues
- rapid motility
- few surface proteins
16
Q
Primary and secondary lesions full of
A
T.pallidum
17
Q
Tertiary lesions
A
Presentation is a hyperimmune response
18
Q
Control of syphilis
A
- Serologic tests for syphilis: STS, VDRL
- indirect test
- Fluorescent treponema antibody
19
Q
Describe indirect test for syphilis
A
- T pallidum induces formation of ‘reagin’ in host(IgM + IgA)
- add cardiolipin to patient serum
- if +, reagin causes cardiolipin to clump
- lots of false positives
20
Q
Describe the fluorescent treponema antibody
A
- can be indirect, detect anti-treponema antibodies
- bind T.pallidum to slide and add serum from patient
- add fluorescent anti-human to detect antibody in serum
21
Q
Treatment of syphilis
A
- treat with penicillin G
- one i.m. injection for early disease
- 3 injections for latent disease
22
Q
Physical shape of neisseriae
A
- gram negative
- coffee bean shaped diplococcus
- seen in both inter cellularly and in PMNs
23
Q
Growth of neisseriae
A
- fastidious
- aerobic
- cytochrome c oxidase positive
- 2 identical chromosomes
24
Q
Clinical presentation of neisseriae
A
- invades mucus membranes of UGT, rectum, eye, throat
- proctitis
- pharyngitis
- arthritis
25
Male clinical presentation of neisseriae
- urethritis; painful urination, drip of pus from urethra
| - 40% asymptomatic
26
Female clinical presentation of neisseriae
- urethritis
- vaginitis
- cervicitis
- salpingitis, PID, peritonitis
- fallopian tube scarring, infertility
- 60% asymptomatic
27
Neonate clinical presentation of neisseriae
-conjunctivitis from infected birth canal
28
Epidemiology of neisseriae
- exclusively a human STD
- -75% infection rate
- 50% after one encounter
- co infection chlamydia
- large number of asymptomatic carriers
29
Diagnosis for neisseriae
- males: gram stain of urethral drip
| - females: culture of cervical swab or vaginal swab
30
Pathogenesis of neisseriae- light binding
1. attachment
- pili
- pilus antigenic variation by recombination
- 1 promoter(pilE), many genes(pilS)
- recombine new pilS gene or part of gene with pilE to make new pili
31
Pathogenesis of neisseriae-tight binding
- Opa(protein II)
- named for opacity phenotype of colonies
- antigenic variation by DNA slippage of repeats
- infections in females change Opas during menstrual cycle
32
Three proteins involved in the evasion process of neisseriae
-Por, Rmp, IgA protease
33
Function of Por in neisseriae
Por(protein 1): outer membrane porin, but also prevents phagolysosome fusion in host
34
Function of Rmp in neisseriae
Rmp(protein 3): Host abs binds to it, prevents Ab binding to Por and LOS in outer membrane
35
Function of IgA protease
IgA is the bactericidal, complement activating, first response Ab in mucus membranes
36
Toxicity associated with neisseriae
LOS
-lipid A part is toxic
-oligosaccharide mimics host cell membrane structure
-NANA transferase to sialylate bacterial LOS with host NANA
PG
-released by autolysis at low temp or alkaline pH
Fbp
-scavenges Fe from human lactoferrin and transferrin
37
Control of neisseriae
- resistance acquired very easily
- PPNG produce B-lactamases
- Pan resistant
38
Treatment of neisseriae
- cephtriaxone or cefixime
- doxycycline or erythromycin for co-infections
- tetracycline drops in eyes of newborns
39
Difference of neisseria meningitidis
-spread via aerosol transmission and not via STD
40
Physical appearance of neisseria meningitidis
-gonococcus, but also has a polysaccharide capsule
41
Clinical presentation of neisseria meningitidis
- invades bloodstream, meningococcemia
- presents as purpura and small hemorrhages as blood vessels become permeable
- toxic effects of LOS, soluble PG
42
Involvement of meninges of neisseria meningitidis
- acute headache, vomiting, stiff neck
- disoriented, lethargic
- coma, death
- PMNL found in CSF, BS permeability
- brain covered with purulent exudate
- progress to DIC and circulatory collapse, meningococcal septicemia
43
Epidemiology of neisseria meningitidis
- transient or resident flora in 10%
- pilin modification with phosphatidylgylcerol disrupts micro colony of Nm
- spread via respiratory droplets
44
Treatment of widespread neisseria meningitidis
-prophylaxis is necessary in epidemic settings
45
Pathogenesis of neisseria meningitidis
- like gonococcus(pili, prot I,II,III, LOS)
- antiphagocytic polysaccharide capsule
- antigen B is sialylated, much more disguised than the others
- special pili attach to BBB endothelial cells and recruit junctional complexes
- additional adhesins
46
Vaccines of neisseria meningitidis
- ACWY conjugate vaccine
| - 2 NmB vaccines
47
Medical treatment for neisseria meningitidis
- 3rd generation Cephlasporin
- initial broad spectrum with vancomycin
- acyclovir if herpes present
- Rifampin or 3rd generation Ceph for prophylaxis
- high dose Cipro
48
Description of Moraxella catarrhalis, a type of Neisseria
- 50% carrier rate in school age
- opportunistic sinusitis, bronchitis, pneumonia
- present as otitis media in children
- COPD problems
- B lactamases production
49
Treatment of Moraxella Catarrhalis
- 3rd generation Ceph
| - Ciproxin
