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STI Pathogens:
Pathogen
Chlamydia trachomatis
General Characteristics
Obligate intracellular bacteria:
but NOT an energy parasite
(has own ATP transportersonly requires host ATP for
persistent infection)
Cell wall similar to G(-): but
lacks peptidoglycan
Affects more females than
males
Conditions Caused
Often asymptomatic
Serotypes D-K cause urogenital
infection:
Females:
-Cervicitis
-Salpingitis (lead to PID)
-Urethritis
-Chronic pelvic pain
Males:
-Urethritis
-Epididymitis
Neonates:
-Conjunctivitis
-Pneumonia
Virulence Factors
Developmental Cycle:
Elementary Body: infectious,
enters cells and is enclosed in
vacuole (resist fusion with
lysosome)
Reticulate Body: non-infectious
and metabolically active;
replicated in vacuoles to form
inclusion bodies
-Inclusions derived from more
than 1 EB fuse in the cell to form
a single inclusion
-Mutations (ie. in lnc gene) can
prevent fusion
Serotypes L1-L3 cause
Lymphogranuloma Venereum
(LGV):
-Increases risk for HIV coinfection
-Treat the same way as
Chlamydia
-No good treatment for systemic
infection
Neisseria gonorrhoeae
Non-motile, G(-), diplococcic
Facultative intracellular
bacterium: replicates in PMNs
and subepithelial tissue;
humans are the only host
Fastidious growth
requirements:
-Inhibited by FAs
-CAP or Thayer-Martin plates
-37 degrees, CO2 enriched
Affects roughly equal
amounts of men and women
Infections facilitate transmission
of chlamydia and HIV: assume
chlamydial co-infection and treat
for it
Males:
-Urethritis (most common)
-Epididymitis
Females:
-Cervicitis (most common)
-Progress to PID
Disseminated Infection: rare
-Bacteremia
-Arthritis, dermatitis, endocarditis
Pili:
-Function:colonization
-Phase varation: expression vs.
non-expression
-Antigenic variation: change
pilus subunit expressed
Opa proteins:
-Function: close contact after
pili bind and anchor
-Phase variation: expression
(opaque colonies) vs. nonexpression
-Constitutively transcribed: but
translation controlled by CTCTT
frameshifts
Pathogenesis
Disease sequelae due to
inflammatory response
Disseminates from
primary site of infection:
in mononuclear cells
Can become persistent:
organism present and
viable but not culturable
-Reduced expression of
MOMP
-Increased expression of
stress proteins (hsp60,
hsp10) and LPS (chronic
inflammation)
-May be induced by IFN-γ
or the use of penicillin
LGV:
-Local: small papule on
external genitalia/anus,
swollen LN, mucoid anal
discharge
-Systemic: fever, rashes,
nausea (possibly
meningitis or arthritis)
-Can become serious
chronic/systemic disease
Adherence: to mucosal
surface following sexual
contact
Invasion: can invade
epithelial cells, but do not
always
Mucosal Damage: due to
granulocyte response
Clinical ID
Epithelial cells from infected
site
-Scrapings
-First-catch urine
-Pus from genital lesions (LGV
only)
Direct Detection:
-Fluorescent Abs to MOMP or
LPS
-PCR
-Ligase chain reaction (LCR)
-Multiplex reactions (detect
multiple STIs)
Direct Gram Smear:
-Only sensitive for
symptomatic men
Culture:
-Diplococci within PMN
diagnostic
Oxidase (+)
Direct Detection:
-Enzyme immunoassays
-DNA/RNA hybridization
-Multiplex PCR to detect
chlamydia as well
LOS:
-Structure: lipid A w/o O Ag
-Variation: sialyation confers
serum resistance
(dissemination)
-Proinflammatory
OMP1: used for serotyping
-Porin
IgA Protease:
-Cleaves IgA1 (secretory and
non-secretory)
-Adherence in presence of IgA
-Loss of protease does not affect
infectivity
Treponema pallidum
(Syphilis)
Obligate human pathogen
G(-) spirochete
Outer glycosaminoglycan
coating
Very motile (corkscrew)
Difficult to culture and does
not stain by routine methods
Highly unstable: rapid death in
environment and high
sensitivity to antimicrobials
Metabolically crippled
organism
Infects more men than
women
Chancres increase susceptibility
to HIV transmission
Transferrin: iron acquisition
-Loss DOES cause loss of
infectivity
Very little is known about the
organism
Primary Syphilis: chancre
development 3-4 weeks after
contact on external genitalia
-Filled with bacteria
-Hard, red, painless
Hyaluronidase: invasion
Secondary Syphilis: fever, sore
throat, rash (palms/soles/face)
-After primary lesion has healed
-Filled with bacteria
-Some resolve via immune
response, others go latent
Tpr (repeat genes): invasion
Latent Syphilis: seroreactive but
no signs or symptoms
-Variable length
-Can progress to tertiary
symptoms if untreated or
unresolved
Tertiary Syphilis: granulomatous
gummas on the skin (due to host
immune response)
-No bacteria in gummas
Outer membrane: few integral
proteins (helps evade immune
system)
Transmission:
-Direct sexual contact with
an individual with active
primary or secondary
lesion
-Transplacental
Causes disease of blood
vessels and perivascular
area: invades mucus
membranes, multiples
rapidly, and spreads to
systemic circulation
BEFORE development of
primary lesion
Darkfield microscopy: fluid
from primary and secondary
lesions
Serological:
VDRL/RPR: non-specific
-Positive during primary and
secondary stages
-Reduction indicates
successful treatment
-Many false +
Treponemal Tests:
-FTA-Abs: detects Ab specific
to T.pallidum (present for life,
so can’t be used to detect
successful treatment)
-NERA-TP:
microhemagglutination test
Genetic Probes: PCR (soon)
Congenital: anti-treponemal
IgM diagnostic (IgM does not
cross placenta- must be from
fetus)
Neurosyphilis: tabes dorsals,
seizures, dementia, NF tangles
post-mortem
CV Syphilis: commonly aortic
aneurysm
Haemophilus ducreyi
(Chancroid)
Candida albicans
(Vulvovaginal Yeast
Infection)
Fastidious G(-) rod
Strict human pathogen
Not really classified as an STI!
Fungi that is normal flora: GI
tract, mucuocutaneous sites
(vagina, mouth)
Congenital Syphilis: fetus
susceptible at ANY time during
gestation
-Often asymptomatic at birth
-Progresses to rhinitis,
pneumonia and failure to thrive
-Can be fatal if severe
Increases susceptibility to HIV:
due to chancroids
Chancroids: painful, genital ulcers
with ragged edges
Most common cause of
vulvovaginal yeast infections
Predisposing Factors:
-Pregnancy
-Diabetes
-Oral contraceptives/hormones
-Antibacterial Abx
Recurrent Infections: can be
caused even in healthy women
-Macrophage dysfunction?
Trichomonas vaginalis
(Trichomoniasis)
Highly motile, flagellated
protozoan (parasite)
No cyst form: but can survive
in moist environments
Most common STI worldwide
Men: generally asymptomatic
Women: dysuria, vaginal itching
and burning
-Severe infections produce
foamy, yellow green discharge
--
Multiple Forms: hyphae (tissue
invasion) and yeast (pathogenic
form in the body)
Adhesins: can bind fibronectin,
collagen, laminin
Invasion: proteases and
phospholipases produced by
hyphal form
Can infect abraded skin,
mucosal surface and
stratified squamous
epithelium: chancroids 214 days later
Infection requires:
-Increase in local numbers
of candida
-Compromised integrity of
epithelial surface
Antibody based detection
DNA probes
Multiplex PCR
-White-gray
pseudomembrane on vaginal
mucosa
-Yellow-white discharge
-Hyphal forms seen in vaginal
scrapings
Normal immune
response: phagocytosis by
macrophages (bind
mannan wall)
Biofilm formation: assists in
pathogenesis
SAPs: proteinases only found in
pathogenic yeast; pH regulated
activity
-Determines level of tissue
invasion
-Regulates other VFs
Coated with host-derived
macromolecules: evasion?
-α1 antitrypsin, fibrontectin,
α2macroglobulin, lipids
Phagocytosis: of bacteria, virus,
RBC, PMNs
Upsets Flora: ingest lactobacilli
Persistence: up to 90 days;
worse during menses and
pregnancy
Transmission: sexual
contact (most often)
PMN inflammatory
response: cell destruction
-Microscopic examinations of
wet mount preparations
(vaginal or urethra discharge)
-Culture of urogenital
specimens