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1.
Secondary
à Condyloma latum (DO NOT CONFUSE with Condyloma acuminatum or genital
warts– two completely different conditions) =
secondary syphilitic eruption of flat-topped papules at
the anus or wherever contiguous folds of skin produce
heat and moisture
2.
Tertiary
à Gummas (granulomatous)
ii.
Histology
à Plasma cells clustering around blood vessels although not
a definitive diagnosis
b.
Chancroid
à
STD
i.
Caused
by Hemophilus ducreyi, a gram negative bacillus
ii.
Presents clinically as painful ulcers
iii.
Less
common in the
US
c.
Granuloma inguinale
à
i.
Caused
by Calymmatobacterium granulomatis, a gram
negative rod
ii.
Can
form a painless ulcer
iii.
Donovan bodies
(organisms within macrophages; according to Dr. Heller
they look like safety pins) on Wright/Giemsa are
diagnostic
d.
Chlamydia
à
i.
Causes
2 different types of STDs
1.
Non-gonococcal
urethritis
a.
More
common
b.
Caused
by Chlamydia of serotypes D – K
c.
Begins
with inguinal swelling
2.
Lymphogranuloma venereum (LGV)
a.
Caused
by serotypes L1, L2 & L3
b.
Not
very common
ii.
Outcomes of Chlamydia infections
1.
Draining sinuses
2.
Ulcers
3.
Fibrosis
4.
Malignant potential = vulvar cancer later on
e.
Chlamydia
that we
are going to see with and presents similarly to
Gonorrhea:
i.
Men are symptomatic (burning, dysuria, discharge)
ii.
Women are asymptomatic = bad since can get an ascending infection that results in
scarring of the tubes
iii.
Causes
of Pelvic Inflammatory Disease (PID), infertility due to
scarring of the fallopian tubes, and increased risk of
tubal pregnancies (can result in death)
f.
Herpes
à
i.
Type I
or II
ii.
May be
contagious without lesions
iii.
High
neonatal risks especially if child is vaginally
delivered since child can get overwhelming herpes sepsis
and die– opt for C-section if mother has active
infection
iv.
Can
occur as primary and recurrent attacksà
first time with clinical infection is usually painful
resulting in urinary retention (patients were placed in
a bath and told to urinate into the water for treatment
of urinary retention); recurrent attacks are less
difficult
v.
Diagnosed by
characteristic intranuclear inclusions that have two
different characteristics
1.
Cowdry’s type A inclusions
= multinucleated with ground glass appearance best seen
on a glass slide = classic herpes
2.
Multinucleated inclusion bodies
g.
Human
papillomavirus
à
i.
There
are ~100 types (with more constantly being discovered
constantly) with 60 affecting the lower genital tract of
both men and women
ii.
Both
men and women are asymptomatic with women more likely to
show signs of infection
iii.
HPV 6, 11 = causes Condyloma acuminatum or genital warts
1.
Low
risk or not likely to progress to cancer
2.
Causes
warts on the vulva
iv.
HPV 16, 18 = cause 100% of the cervical cancers
1.
High
risk for pre- and invasive neoplasms
2.
Not all
relate to genital diseases
v.
HPV
facts (she stressed that we do not have to memorize the
numbers; simply appreciate them)
1.
One of
the 3 most common STDs
along with Gonorrhea and Chlamydia
2.
History
of HPV: Was believed to arise from “impure” coition in
the 1700s; differentiated from Syphillis and Gonorrhea
in the 1800s. Summation = it has been with us for a long
while
3.
20-40%
of sexually active women have HPV
à
not all of them associated with warts or cancers since
most healthy individuals clear the virus from their
bodies within 2 years
4.
5.5
million new infections/yr in US = it is all over the
place
5.
Estimated total prevalence in US is 20 million
a.
1950s
13/100,000 US women had warts
b.
1970s
106/100,000 US women had warts (free love anyone)
c.
Currently estimated to affect 20-50% of sexually active
women
6.
Once
HPV gets into the cell it can manifest as these 2 basic
formsà
a.
Episomal-nonintegrated, productive infection (warts)
= it is in the car but it is not the driver (Dr.
Heller’s analogy); someone infected can still pass it on
to his/her partner
b.
Integrated into host DNA-nonprodctive infection
(malignant potential)
= it is the driver of the car and can steer the wheel
(again, Dr. Heller’s analogy)
7.
Virtually all HPV infection disappears and is
non-detectable by PCR, usually within 2 yrs
8.
The
mechanism of latency and re-emergence is less well-known
but it occurs with HPV nevertheless so you cannot blame
your significant other for cheating on you since he/she
may have contracted it before he/she met you.
9.
You can
get HPV from other methodologies other than sexual
intercourse
10.
If
children present with HPV infection think sexual abuse
although a mother who is not hygienically clean can pass
it on to her child after diapering, etc.
11.
Can
also present in the perianal region of both men and
women. Dr. Heller was not sure if this was related to
sexual practices although homosexual men often present
with warts in this area more frequently
vi.
Risk factors for HPV genital infection
1.
Exposure to virus
2.
Immune
status – HIV+ patients find it difficult to eradicate
due to immunosuppression
3.
Pregnancy
– possibly due to hormonal status and transient
immunosuppression (the facts are still undiscovered)
4.
Long-term OCP
use that causes increased estrogen and progesterone
receptors (ER & PR)
5.
Nutritional status
– you need to be well-nourished to fight this infection
vii.
Diagnosis
1.
Clinically = lumpy, bumpy
2.
Microscopically
a.
Papillomatosis due to lumpy, bumpy appearance
b.
Koilocytes (Greek word for “empty”) = squamous cells
demonstrating nuclear change = a “rasionoid” nuclei
(enlarged) = present with perinuclear halo or space as a
result of both the cells’ naturally high glycogen
storage capacity (space-occupying) and the nuclear
activities
c.
KI-67 =
a proliferation antigen used to stain HPV = a
confirmatory diagnosis of Condyloma a. if proliferation
occurs in the basal region of the epithelium
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