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Genital Warts

(venereal warts, condyloma, condylomata acuminata)

Definition & Overview:

Genital warts is a highly contagious sexually transmitted disease caused by the

human papillomavirus (HPV) during vaginal, oral or anal sex. There are over 75
different strains of the HPV virus but only 10 of them are responsible for causing
genital warts.

Also known as venereal warts, condyloma, condylomata acuminata, genital

warts appear as small white, pink, red, or flesh-colored bumps that range in size
from unnoticable, to single lesions to clusters similar in appearance to a cauliflower.
In men, genital warts can grow on the penis, near the anus, between the anus and
scrotum. In women, genital warts may grown on the vulva, perineum, in the vagina
and on the cervix. Genital warts can also develop in the mouth or throat of a person
who has oral sex with someone infected with HPV causing virus. Genital warts is a
leading cause of cervical cancer in women and can cause penile cancer in men.


Genital warts are caused by the HPV virus. Although there are more than 75 strains
of the virus, 2 strains (HPV 6 and HPV 11) are responsible for 90 percent of the
cases of genital warts. Approximately 8 more strains can cause genital warts and
ALSO have a higher potential for causing cancer. Strains HPV 16, 18, 31 and 45
together account for 80 percent of cervical and genital cancers.

Approximately 2 out of 3 of the people who have sexual contact with a person
infected with the HPV virus ALSO become infected with the HPV virus.

"The viral particles are able to penetrate the skin and mucosal surfaces through
microscopic abrasions in the genital area, which occur during sexual activity. Once
cells are invaded by HPV, a latency (quiet) period of months to years may occur."

The latency period just means the HPV virus is in an incubation period. Having sex
with a partner whose HPV infection is in the incubation period still leaves you
vulnerable to becoming infected yourself. In other words, just because one can't
see the genital warts, doesn't mean they are not there. The incubation period can
last from 3 months to 2 years.

Common warts (that usually appear on the hands) are caused by different strains of
the HPV virus and are not the same as genital warts.

Genital warts are generally painless, but are a nuisance due to their location, size
and itching/irritation.

When genital warts grow from their incubation period, they often start out as small,
gray, pink, red or white swellings in the genital area. The often begin as single
lesions approximately 1 to 2 mm in size, but if left untreated, can rapidly grow in
clusters which when form together, can be large and appear similar to a cauliflower

Besides itching, genital warts can cause pain during intercourse and in some cases,

Tests & Diagnosis

Genital warts are often diagnosed through an examination by a doctor. However, in

some cases, genital warts are only detectable through tests and techniques which

• Lesions are visibly enhanced with the application of a chemical called acetic
acid solution which causes them to become white for about 5 to 10 minutes.
• A pap test for women can detect changes to the cervix which may occur as a
result of the HPV virus.
• Magnification, also called colposcopy, may be used to see lesions that are not
visible to the eye.
• Pelvic examination for women.


Genital warts can be removed, however the HPV virus that causes genital warts can
not be cured. The virus continues to live inside your skin and may cause the warts
to return. Genital warts may need to be removed more than once.

Removal methods of genital warts include:

• Cryotherapy: A process that uses liquid nitrogen to "freeze off" the warts.
• Loop electrosurgical excision procedure (LEEP) involves a sharp instrument,
shaped like a loop, which is passed underneath the wart and then used to cut
it out from the skin.
• Laser treatment to physically destroy the lesion.
• Electric current to physically destroy the lesions.

Besides physical removal, your doctor may prescribe certain topical medications
that are applied to the skin to treat the virus. As outlined by eMedicineHealth, these

• Podophyllum resin (Pod-Ben-25, Podofin)

• Podofilox (Condylox) - Can be topically applied at home, higher cure rates
than Podophyllum resin, useful for prevention
• Trichloroacetic acid – Topically applied, response is often incomplete and
recurrence is higher, may cause pain and burning
• 5-Fluorouracil (Efudex) – Applied as a cream, long treatment time, can cause
burning and irritation, many side effects
• Interferon alpha-n3 (Alferon N) – Used as an injection for warts that do not
respond to other therapies, many side effects
• Imiquimod (Aldara) – New treatment, applied as a cream, local skin irritation
is a common side effect.
Genital warts MUST be treated by a doctor. Over the counter topical medications for
other types of warts must never be used.


Since no treatment for genital warts is 100 percent effective, prevention should be
a top concern whether you are infected with the HPV virus or not.

Condoms do not offer iron-clad protection against genital warts since the infected
spot may not be covered by a condom."Skin near the warts and around the
genitals, anus, and other areas can pass the virus from one person to the next.
Therefore, male and female condoms cannot fully protect you...Nonetheless,
condoms should still be used. They reduce your chances of getting or spreading

Abstinence and monogamous sex with partner not infected with the HPV virus is the
best method for prevention.

A new vaccine known as Gardasil offers protection from the most dangerous types
of HPV. The Food and Drug Administration (FDA) approved the vaccine in June
2006. The national Advisory Committee on Immunization Practices recommends
routine vaccination for girls age 11 and 12, as well as girls and women ages 13 to
26 if they haven't received the vaccine already. The vaccine is most effective if
given to girls before they become sexually active.


In worst cases, the HPV virus can lead to cancer of the cervix. Some experts
believe that HPV is responsible for 90 percent of all cases of cervical cancer. (5)
Certain types of the HPV strains have been associated with cancer of the vulva, anal
cancer, rectal cancer and cancer of the penis.

Genital warts can lead to a number of different problems during pregnancy to


• Difficulty urinating
• Warts on the vaginal wall may reduce the vagina's ability to stretch
• Transmission of the virus to the baby, to include the baby's throat. Surgery
may be needed to prevent airway obstruction.


Chlamydia infection (from the Greek, χλαμύδος meaning "cloak") is a common

sexually transmitted infection (STI) in humans caused by the bacterium Chlamydia
trachomatis. The term Chlamydia infection can also refer to infection caused by any
species belonging to the bacterial family Chlamydiaceae. C. trachomatis is only
found in humans. Chlamydia is a major infectious cause of human genital and eye

Chlamydia infection is one of the most common sexually transmitted infections

worldwide — it is estimated that about 2.3 million individuals in the United States
are infected with chlamydia.[2] It is the most common bacterial STI in humans.[3]

C. trachomatis is naturally found living only inside human cells. Chlamydia can be
transmitted during vaginal, anal, or oral sex, and can be passed from an infected
mother to her baby during vaginal childbirth. Between half and three-quarters of all
women who have a chlamydia infection of the neck of the womb (cervicitis) have no
symptoms and do not know that they are infected. In men, infection of the urethra
(urethritis) is usually symptomatic, causing a white discharge from the penis with
or without pain on urinating (dysuria). Occasionally, the conditions spreads to the
upper genital tract in women (causing pelvic inflammatory disease) or to the
epididymis in men (causing epididymitis). If untreated, chlamydial infections can
cause serious reproductive and other health problems with both short-term and
long-term consequences. Chlamydia is easily treated with antibiotics.

Chlamydia conjunctivitis or trachoma is a common cause of blindness worldwide.

The World Health Organization estimates that it accounted for 15% of blindness
cases in 1995, but only 3.6% in 2002.

Related conditions

Genital disease

Chlamydial cervicitis in a female patient characterized by mucopurulent cervical

discharge, erythema, and inflammation.

Chlamydial infection of the neck of the womb (cervicitis) is an asymptomatic

sexually transmitted illness for about 50-70% of the female population. Of those
who have an asymptomatic infection that is not detected by their doctor,
approximately half will develop pelvic inflammatory disease (PID), a generic term
for infection of the uterus, fallopian tubes, and/or ovaries. PID can cause scarring
inside the reproductive organs, which can later cause serious complications,
including chronic pelvic pain, difficulty becoming pregnant, ectopic (tubal)
pregnancy, and other dangerous complications of pregnancy. Chlamydia causes
250,000 to 500,000 cases of PID every year in the United States. Women infected
with chlamydia are up to five times more likely to become infected with HIV, if

Chlamydia is known as the "Silent Epidemic" because in women, it may not cause
any symptoms in 75% of cases, and can linger for months or years before being
discovered. Symptoms that may occur include: unusual vaginal bleeding or
discharge, pain in the abdomen, painful sexual intercourse (dyspareunia), fever,
painful urination or the urge to urinate more frequently than usual (urinary

Male patients may develop a white, cloudy or watery discharge (shown) from the
tip of the penis.

In men, Chlamydia shows symptoms of infectious urethritis (inflammation of the

urethra) in about 50% of cases. Symptoms that may occur include: a painful or
burning sensation when urinating, an unusual discharge from the penis, swollen or
tender testicles, or fever. Discharge, or the purulent exudate, is generally less
viscous and lighter in color than for gonorrhea. If left untreated, it is possible for
Chlamydia in men to spread to the testicles causing epididymitis, which in rare
cases can cause sterility if not treated within 6 to 8 weeks. Chlamydia causes more
than 250,000 cases of epididymitis in the U.S. each year. Chlamydia is also a
potential cause of prostatitis in men, although the exact relevance in prostatitis is
difficult to ascertain due to possible contamination from urethritis.

Eye disease

Conjunctivitis due to chlamydia.

Chlamydia conjunctivitis or trachoma was once the most important cause of

blindness worldwide, but its role diminished from 15% of blindness cases by
trachoma in 1995 to 3.6% in 2002, according to WHO estimates.[6][4][5] The infection
can be spread from eye to eye by fingers, shared towels or cloths, coughing and
sneezing and eye-seeking flies.[10] Newborns can also develop chlamydia eye
infection through childbirth (see below). Using the SAFE strategy (acronym for
surgery for in-growing or in-turned lashes, antibiotics, facial cleanliness, and
environmental improvements), the World Health Organisation aims for the global
elimination of trachoma by 2020 (GET 2020 initiative).

Rheumatological conditions

Chlamydia may also cause reactive arthritis - the triad of arthritis, conjunctivitis
and urethritis (inflammation of the urethra) - especially in young men. About
15,000 men develop reactive arthritis due to chlamydia infection each year in the
U.S., and about 5,000 are permanently affected by it. It can occur in both sexes,
though is more common in men.

Perinatal infections

As many as half of all infants born to mothers with chlamydia will be born with the
disease. Chlamydia can affect infants by causing spontaneous abortion; premature
birth; conjunctivitis, which may lead to blindness; and pneumonia. Conjunctivitis
due to chlamydia typically occurs one week after birth (compare with chemical
causes (within hours) or gonorrhea (2-5 days)).
Other conditions

Chlamydia trachomatis is also the cause of lymphogranuloma venereum, an

infection of the lymph nodes and lymphatics. It usually presents with genital
ulceration and swollen lymph nodes in the groin, but it may also manifest as
proctitis (inflammation of the rectum), fever or swollen lymph nodes in other
regions of the body.



For sexually active women who are not pregnant, screening is recommended in
those under 25 and others at risk of infection. Risk factors include a history of
chlamydial or other sexually transmitted infection, new or multiple sexual partners,
inconsistent condom use.[15] For pregnant women, guidelines vary: screening
women with age or other risk factors is recommended by the U.S. Preventive
Services Task Force (USPSTF) (which recommends screening women under 25) and
the American Academy of Family Physicians (which recommends screening women
aged 25 or younger). The American College of Obstetricians and Gynecologists
recommends screening all at risk, while the Centers for Disease Control and
Prevention recommend universal screening of pregnant women. The USPSTF
acknowledges that in some communities there may be other risk factors for
infection, such as ethnicity. Evidence-based recommendations for screening
initiation, intervals and termination are currently not possible. There is no universal
agreement on screening men for chlamydia.

Laboratory detection

The diagnosis of genital chlamydial infections evolved rapidly from the 1990s
through 2006. Nucleic acid amplification tests (NAAT), such as polymerase chain
reaction (PCR), transcription mediated amplification (TMA), and the DNA strand
displacement amplification (SDA) now are the mainstays. NAAT for chlamydia may
be performed on swab specimens collected from the cervix (women) or urethra
(men), on self-collected vaginal swabs, or on voided urine. Urine and self-collected
swab testing facilitates the performance of screening tests in settings where genital
examination is impractical. At present, the NAATs have regulatory approval only for
testing urogenital specimens, although rapidly evolving research indicates that they
may give reliable results on rectal specimens.

Because of improved test accuracy, ease of specimen management, convenience in

specimen management, and ease of screening sexually active men and women, the
NAATs have largely replaced culture, the historic gold standard for chlamydia
diagnosis, and the non-amplified probe tests. The latter test is relatively insensitive,
successfully detecting only 60-80% of infections in asymptomatic women, and often
giving falsely positive results. Culture remains useful in selected circumstances and
is currently the only assay approved for testing non-genital specimens.

Chlamydia trachomatis inclusion bodies (brown) in a McCoy cell culture.

C. trachomatis infection can be effectively cured with antibiotics once it is detected.

Current Centers for Disease Control guidelines provide for the following treatments:

• Azithromycin 1 gram oral as a single dose, or

• Doxycycline 100 milligrams twice daily for seven days.
• Tetracycline
• Erythromycin
Untested Treatments

• Ciprofloxacin 500 milligrams twice daily for 3 days. (Although this is not an
approved method of treatment.)

β-lactams are not suitable drugs for the treatment of chlamydia. While they have
the ability to halt growth of the organism (i.e. are microbistatic), these antibiotics
do not eliminate the bacteria. Once treatment is stopped, the bacteria will begin to
grow once more. (See below for Persistence.)

Areas of research

Recent phylogenetic studies have revealed that chlamydia shares a common

ancestor with modern plants, and retains unusual plant-like traits (both genetically
and physiologically). In particular, the enzyme L,L-diaminopimelate
aminotransferase, which is related to lysine production in plants, is also linked with
the construction of chlamydia's cell wall. The genetic encoding for the enzymes is
remarkably similar in plants and chlamydia, demonstrating a close common
ancestry.[16] This unexpected discovery may help scientists develop new treatment
avenues: if scientists could find a safe and effective inhibitor of L,L-diaminopimelate
aminotransferase, they might have a highly effective and extremely specific new
antibiotic against chlamydia.

For Chlamydia's life cycle, see Chlamydia (bacterium)

Chlamydiae have the ability to establish long-term associations with host cells.
When an infected host cell is starved for various nutrients such as amino acids (e.g.
tryptophan), iron, or vitamins, this has a negative consequence for Chlamydiae
since the organism is dependent on the host cell for these nutrients. Long-term
cohort studies indicate that approximately 50% of those infected clear within a
year, 80% within two years, and 90% within three years.

The starved chlamydiae enter a persistent growth state wherein they stop cell
division and become morphologically aberrant by increasing in size. Persistent
organisms remain viable as they are capable of returning to a normal growth state
once conditions in the host cell improve.

There is much debate as to whether persistence has in vivo relevance. Many believe
that persistent chlamydiae are the cause of chronic chlamydial diseases. Some
antibiotics such as β-lactams can also induce a persistent-like growth state, which
can contribute to the chronicity of chlamydial diseases.


Sometimes referred to as "trich", is a common cause of vaginitis. It results both

from shared external water sources (hot tubs, wet bathing suits, wet towels and
washcloths), and as a sexually transmitted disease (STD). It is caused by the
single-celled protozoan parasite Trichomonas vaginalis. Trichomoniasis is primarily
an infection of the urogenital tract; the most common site of infection is the urethra
and the vagina in women. It is most common in women and uncircumcised men.
For uncircumcised men, the most common site for the infection is the tip of the
According to the Centers for Disease Control (CDC), an estimated 7.4 million new
cases of trichomoniasis occur in men and women every year in the United States.


Typically, only women experience symptoms associated with Trichomonas infection.

Symptoms include:

• Vaginitis - itching, burning, and inflammation of the vagina

• Cervicitis - inflammation of the cervix
• Urethritis - inflammation of the urethra
• Green/Yellow, frothy vaginal discharge

Most men with trichomoniasis do not have signs or symptoms; however, some men
may temporarily have an irritation inside the penis, mild discharge, or slight
burning after urination or ejaculation.

Some women have signs or symptoms of infection which include a frothy, yellow-
green vaginal discharge with a strong odor. The infection also may cause discomfort
during intercourse and urination, as well as irritation and itching of the female
genital area. In rare cases, lower abdominal pain can occur. Symptoms usually
appear in women within 5 to 28 days of exposure.


Trichomoniasis is diagnosed by visually observing the trichomonads via a

microscope. In women, the doctor collects the specimen during a pelvic
examination by inserting a speculum into the vagina and then using a cotton-tipped
applicator to collect the sample. The sample is then placed onto a microscopic slide
and sent to a laboratory to be analyzed. An examination in the presence of
trichomoniasisptaulas may also reveal small red ulcerations on the vaginal wall or
cervix; if occurring on the cervix, is termed "strawberry cervix."

Treatment for both pregnant and non-pregnant patients usually utilizes

metronidazole[2] (Flagyl) 2000mg oral one time by mouth. Sexual partners, even if
asymptomatic, should be concurrently treated.


Research has shown a link between trichomoniasis and two serious sequelæ. Data
suggest that:

• Trichomoniasis is associated with increased risk of transmission of HIV.

• Trichomoniasis may cause a woman to deliver a low-birth-weight or
premature infant.

Additional research is needed to fully explore these relationships.

Trichomoniasis and Pregnancy

Trichomoniasis during pregnancy raises the risk of premature rupture of

membranes (PROM) and premature delivery. Treating the infection does not appear
to reduce this risk.

Pregnant women with trichomoniasis may have babies who are born early or with a
low birth weight (under 5 pounds).

The Centers for Disease Control and Prevention (CDC) recommends that women
with trichomoniasis who have symptoms should be treated, but women without
symptoms do not necessarily need to be treated.

During the first 3 months of pregnancy, many experts feel that women shouldn't
take metronidazole (Flagyl®) because it may hurt the baby. However, most doctors
feel that metronidazole can be given safely after the end of the first trimester.

Transmission to the Baby

Transmission of trichomoniasis from mother to child is rare. Babies born to infected

mothers may contract the infection during delivery. Infants may develop fever; girls
may develop vaginal discharge. Children should be treated if diagnosed with

Interventions for trichomoniasis in pregnancy

Metronidazole is effective against a trichomoniasis infection during pregnancy, but

may increase the risk of preterm and low birthweight babies.

Trichomoniasis is a very common sexually transmitted infection. Symptoms include

vaginal itching and discharge. It is not clear if pregnant women with trichomoniasis
are more likely to give birth preterm, or have other pregnancy complications. The
review of trials found that the drug metronidazole is effective against trichomoniasis
when taken by women and their partners during pregnancy, but it may harm the
baby. Of the two clinical trials reviewed, one was stopped early because women
taking metronidazole were more likely to give birth preterm and have low-
birthweight babies. Further research into trichomoniasis treatments for pregnant
women is needed.
Prevalence and prevention

The American Social Health Association estimates trichomoniasis affects 7.4 million
previously unaffected Americans each year and is the most frequently presenting
new infection of the common sexually transmitted diseases.[3]

Use of male condoms may help prevent the spread of trichomoniasis, although
careful studies have never been done that focus on how to prevent this infection.
Refraining from sharing swimsuits or towels may also help as trichomonads survive
for up to 45 minutes outside of the body.

Nitroimidazole drugs are effective in the treatment of trichomoniasis in women.

Trichomoniasis is a sexually transmitted infection that affects about 120 million

women worldwide every year. This review examines the effectiveness of various
treatments and found that oral nitroimidazole drugs are effective in treating
trichomoniasis in women.

Trichomoniasis (trich) is treated with an oral antiprotozoal medicine, such as

metronidazole or tinidazole. The medicine is taken either as a single dose (2 grams)
or as multiple doses (250 to 500 mg) to equal a total of around 7 grams. The cure
rate in treating trich using metronidazole is 90% to 95%. The cure rate using
tinidazole is 86% to 100%.

Sex partner(s) should be treated at the same time you are being treated to
increase the cure rate and reduce the possibility of further transmission or
reinfection. Sexual intercourse should be avoided during treatment until symptoms
have gone away and until partners have been treated. Ideally, it is best to avoid sex
for 1 week after treatment with a single dose of metronidazole. Male partners may
not have symptoms but still need treatment.

People who are infected with HIV receive the same treatment for trich as those who
are HIV-negative.



Syphilis is a complex, sexually transmitted disease (STD) with a highly variable

clinical course. The disease is caused by the bacterium, Treponema pallidum. In the
United States, 36,935 cases of syphilis, including 349 cases of congenital syphilis,
were detected by public health officials in 2006. Six of the ten states with the
highest rates of syphilis are located in the southern region of the United States.
The route of transmission of syphilis is almost always through sexual contact,
although there are examples of congenital syphilis via transmission from mother to
child in utero.

The signs and symptoms of syphilis are numerous; before the advent of serological
testing, precise diagnosis was very difficult. In fact, the disease was dubbed the
"Great Imitator" because it was often confused with other diseases, particularly in
its tertiary stage.

Syphilis is passed from person-to-person through direct contact with a syphilis sore
(called a chancre). Chancres mainly occur on the external genitals, vagina, anus, or
rectum, but may also occur on the lips and in the mouth. Transmission of syphilis
occurs during vaginal, anal, or oral sex. Pregnant women with the disease can pass
it on to their babies.
Syphilis cannot be spread by toilet seats, door knobs, swimming pools, hot tubs,
bath tubs, shared clothing, or eating utensils.
The first symptoms of syphilis can appear from 10-90 days (average 21 days). The
first stage is marked by the appearance of a chancre that is usually firm, round,
small, and painless. The chancre lasts 1-5 weeks and heals on its own. The second
stage of syphilis begins when one or more areas of the skin develops a non-itching
rash. Rashes can appear as rough, "copper penny" spots on the palms of the hands
and bottom of the feet; a prickly heat rash, small blotches or scales all over the
body; a bad case of old acne; moist warts in the groin area; white patches in the
mouth; sunken dark circles the size of a nickel or dime; or as pus-filled eruptions
like chicken pox. Rashes can last 2-6 weeks and, like the chancre, heal on their
own. During the first and second stages of syphilis, an infected person can easily
pass the disease to their sex partners.

The latent (hidden) stage of syphilis begins when the secondary symptoms
disappear. If the infected person has not received treatment, he/she still has
syphilis even though there are no symptoms. Syphilis remains in the body and
begins to damage the internal organs including the brain, nerves, eyes, heart, blood
vessels, liver, bones, and joints.
An infected pregnant woman has about a 40% chance of having a stillbirth
(syphilitic stillbirth) or delivering a baby who dies shortly after birth. A baby born to
a mother with either untreated syphilis or syphilis treated after the 34th week of
pregnancy has a 40%-70% chance of being infected with syphilis (congenital
syphilis). The baby may be born without symptoms, but will develop them within a
few weeks, if not treated immediately. Some infected babies are born with very
serious health problems including skin sores, a very runny nose which is sometimes
bloody (and infectious), white patches in the mouth, inflamed arm and leg bones, a
swollen liver, anemia, jaundice, or a small head. Untreated babies may become
retarded or have seizures. About 12% of infected newborns will die because of the

Bicillin, a type of penicillin (G benzathine), will cure a person who has had
syphilis for <1 year. More doses are needed to cure someone who has had it longer.
A baby born with the disease needs daily penicillin treatment for 10 days. There are
no home remedies or over-the-counter drugs that cure syphilis. Washing the
genitals, urinating, or douching after sex does not prevent syphilis. Any unusual
discharge, sore, or rash -especially in the groin area - should be a signal to stop
having sex and to see a doctor immediately.

Alternative names

The name "syphilis" was coined by the Italian physician and poet Girolamo
Fracastoro in his epic noted poem, written in Latin, entitled Syphilis sive morbus
gallicus (Latin for "Syphilis or The French Disease") in 1530. The protagonist of the
poem is a shepherd named Syphilus (perhaps a variant spelling of Sipylus, a
character in Ovid's Metamorphoses). Syphilus is presented as the first man to
contract the disease, sent by the god Apollo as punishment for the defiance that
Syphilus and his followers had shown him. From this character Fracastoro derived a
new name for the disease, which he also used in his medical text De Contagionibus
("On Contagious Diseases").

Until that time, as Fracastoro notes, syphilis had been called the "French disease" in
Italy and Germany, and the "Italian disease" in France. In addition, the Dutch called
it the "Spanish disease", the Russians called it the "Polish disease", the Turks called
it the "Christian disease" or "Frank disease" (frengi) and the Tahitians called it the
"British disease". These 'national' names are due to the disease often being present
among invading armies or sea crews, due to the high incidence of unprotected
sexual contact with prostitutes. It was also called "Great pox" in the 16th century to
distinguish it from smallpox. In its early stages, the Great pox produced a rash
similar to smallpox (also known as variola). However, the name is misleading, as
smallpox was a far more deadly disease. The terms "Lues" (or Lues venerea, Latin
for "venereal plague") and "Cupid's disease" have also been used to refer to
syphilis. In Scotland, Syphilis was referred to as the Grandgore. The ulcers suffered
by British soldiers in Portugal were termed "The Black Lion".

The Columbian Exchange theory holds that syphilis was a New World disease
brought back by Columbus and Martin Alonso Pinzon. Supporters of the Columbian
theory find syphilis lesions on pre-contact Native Americans and cite documentary
evidence linking crewmen of Columbus's voyages to the Naples outbreak of 1494. A
recent study of the genes of venereal syphilis and related bacteria has supported
this theory, by locating an intermediate disease between yaws and syphilis in
Guyana, South America.

Historian Alfred Crosby suggests both theories are correct in a combination theory.
Crosby's argument is built on the similarities of the species of bacteria which cause
yaws and syphilis. The bacterium that causes syphilis belongs to the same
phylogenetic family as the bacteria which cause yaws and several other diseases.
Despite a tradition of assigning yaws's homeland to sub-Saharan Africa, Crosby
notes that there is no unequivocal evidence of any related disease being present in
pre-Columbian Europe, Africa, or Asia, while there is indisputable evidence of
syphilis' presence in the pre-Columbian Americas. Conceding this point, Crosby
writes, "It is not impossible that the organisms causing treponematosis arrived from
America in the 1490s...and evolved into both venereal and non-venereal syphilis
and yaws."

However, Crosby considers it somewhat more likely that a highly contagious

ancestral species of bacteria moved with early human ancestors across the land
bridge of the Bering Straits many thousands of years ago without dying out in the
original source population. He hypothesizes that "the differing ecological conditions
produced different types of treponematosis and, in time, closely related but
different diseases." Thus, a weak, non-syphilitic bacterium survived in the Old
World to eventually give rise to yaws or bejel, while a New World version evolved
into the milder pinta and the more aggressive syphilis.
Going further than Crosby in arguing for worldwide incidence of syphilis prior to
Columbus, Douglas Owsley, the famed physical anthropologist at the Smithsonian
Institution, has written that many medieval European cases of leprosy, colloquially
called "lepra," were actually cases of syphilis. Although folklore claimed that syphilis
was unknown in Europe until the return of the diseased sailors of the Columbian

Syphilis infection

Different manifestations occur depending on the stage of the disease:

Primary syphilis

Primary syphilis is typically acquired via direct sexual contact with the infectious
lesions of a person with syphilis.Approximately 10-90 days after the initial exposure
(average 21 days), a skin lesion appears at the point of contact, which is usually
the genitalia, but can be anywhere on the body. This lesion, called a chancre, is a
firm, painless skin ulceration localized at the point of initial exposure to the
spirochete, often on the penis, vagina or rectum. Rarely, there may be multiple
lesions present although typically only one lesion is seen. The lesion may persist for
4 to 6 weeks and usually heals spontaneously. Local lymph node swelling can occur.
During the initial incubation period, individuals are otherwise asymptomatic. As a
result, many patients do not seek medical care immediately.
Syphilis can not be contracted through toilet seats, daily activities, hot tubs, or
sharing eating utensils or clothing.

Secondary syphilis

Secondary syphilis occurs approximately 1-6 months (commonly 6 to 8 weeks)

after the primary infection. There are many different manifestations of secondary
disease. There may be a symmetrical reddish-pink non-itchy rash on the trunk and
extremities. The rash can involve the palms of the hands and the soles of the feet.
In moist areas of the body, the rash becomes flat, broad, whitish lesions known as
condylomata lata. Mucous patches may also appear on the genitals or in the mouth.
All of these lesions are infectious and harbor active treponeme organisms. A patient
with syphilis is most contagious when he or she has secondary syphilis. Other
symptoms common at this stage include fever, sore throat, malaise, weight loss,
headache, meningismus, and enlarged lymph nodes. Rare manifestations include an
acute meningitis that occurs in about 2% of patients, hepatitis, renal disease,
hypertrophic gastritis, patchy proctitis, ulcerative colitis, rectosigmoid mass,
arthritis, periostitis, optic neuritis, intersitial keratitis, iritis, and uveitis.

Latent syphilis

Latent syphilis is defined as having serologic proof of infection without signs or

symptoms of disease. Latent syphilis is further described as either early or late.
Early latent syphilis is defined as having syphilis for two years or less from the time
of initial infection without signs or symptoms of disease. Late latent syphilis is
infection for greater than two years but without clinical evidence of disease. The
distinction is important for both therapy and risk for transmission. In the real-world,
the timing of infection is often not known and should be presumed to be late for the
purpose of therapy. Early latent syphilis may be treated with a single intramuscular
injection of a long-acting penicillin. Late latent syphilis, however, requires three
weekly injections. For infectiousness, however, late latent syphilis is not considered
as contagious as early latent syphilis. 50% of those infected with latent syphilis will
progress into late stage syphilis, 25% will stay in the latent stage, and 25% will
make a full recovery.

Tertiary syphilis

Tertiary syphilis usually occurs 1-10 years after the initial infection, though in some
cases it can take up to 50 years. This stage is characterized by the formation of
gummas which are soft, tumor-like balls of inflammation known as granulomas. The
granulomas are chronic and represent an inability of the immune system to
completely clear the organism. They may appear almost anywhere in the body
including in the skeleton. The gummas produce a chronic inflammatory state in the
body with mass-effects upon the local anatomy. Other characteristics of untreated
tertiary syphilis include neuropathic joint disease, which is a degeneration of joint
surfaces resulting from loss of sensation and fine position sense (proprioception).
The more severe manifestations include neurosyphilis and cardiovascular syphilis.
In a study of untreated syphilis, 10% of patients developed cardiovascular syphilis,
16% had gumma formation, and 7% had neurosyphilis.

Neurological complications at this stage can be diverse. In some patients,

manifestations include generalized paresis of the insane which results in personality
changes, changes in emotional affect, hyperactive reflexes, and Argyll-Robertson
pupil. This is a diagnostic sign in which the small and irregular pupils constrict in
response to focusing the eyes, but not to light. Tabes dorsalis, also known as
locomotor ataxia, a disorder of the spinal cord, often results in a characteristic
shuffling gait. See below for more information about neurosyphilis.
Cardiovascular complications include syphilitic aortitis, aortic aneurysm, aneurysm
of sinus of Valsalva, and aortic regurgitation. Syphilis infects the ascending aorta
causing dilation and aortic regurgitation. This can be heard with a stethoscope as a
heart murmur. The course can be insidious, and heart failure may be the presenting
sign after years of disease. The infection can also occur in the coronary arteries and
cause narrowing of the vessels. Syphilitic aortitis can cause de Musset's sign, a
bobbing of the head that de Musset first noted in Parisian prostitutes.


Neurosyphilis refers to a site of infection involving the central nervous system

(CNS). Neurosyphilis may occur at any stage of syphilis. Before the advent of
antibiotics, it was typically seen in 25-35% of patients with syphilis.

Neurosyphilis is now most common in patients with HIV infection. Reports of

neurosyphilis in HIV-infected persons are similar to cases reported before the HIV
pandemic. The precise extent and significance of neurologic involvement in HIV-
infected patients with syphilis, reflected by either laboratory or clinical criteria, have
not been well characterized. Furthermore, the alteration of host immunosuppression
by antiretroviral therapy in recent years has further complicated such
Approximately 35% to 40% of persons with secondary syphilis have asymptomatic
central nervous system (CNS) involvement, as demonstrated by any of these on
cerebrospinal fluid (CSF) examination:

An abnormal leukocyte cell count, protein level, or glucose level

Demonstrated reactivity to Venereal Disease Research Laboratory (VDRL) antibody
There are four clinical types of neurosyphilis:

• Asymptomatic neurosyphilis
• Meningovascular syphilis
• General paresis
• Tabes dorsalis

The late forms of neurosyphilis (tabes dorsalis and general paresis) are seen much
less frequently since the advent of antibiotics. The most common manifestations
today are asymptomatic or symptomatic meningitis. Acute syphilitic meningitis
usually occurs within the first year of infection; 10% of cases are diagnosed at the
time of the secondary rash. Patients present with headache, meningeal irritation,
and cranial nerve abnormalities, especially the optic nerve, facial nerve, and the
vestibulocochlear nerve. Rarely, it affects the spine instead of the brain, causing
focal muscle weakness or sensory loss.

Meningovascular syphilis occurs a few months to 10 years (average, 7 years) after

the primary syphilis infection. Meningovascular syphilis can be associated with
prodromal symptoms lasting weeks to months before focal deficits are identifiable.
Prodromal symptoms include unilateral numbness, paresthesias, upper or lower
extremity weakness, headache, vertigo, insomnia, and psychiatric abnormalities
such as personality changes. The focal deficits initially are intermittent or progress
slowly over a few days. However, it can also present as an infectious arteritis and
cause an ischemic stroke, an outcome more commonly seen in younger patients.
Angiography may be able to demonstrate areas of narrowing in the blood vessels or
total occlusion.
General paresis, otherwise known as general paresis of the insane, is a severe
manifestation of neurosyphilis. It is a chronic dementia which ultimately results in
death in as little as 2-3 years. Patients generally have progressive personality
changes, memory loss, and poor judgment. More rarely, they can have psychosis,
depression, or mania. Imaging of the brain usually shows atrophy.


While abstinence from any sexual activity is very effective at helping prevent
syphilis, it should be noted that T. pallidum readily crosses intact mucosa and cut
skin, including areas not covered by a condom. Proper and consistent use of a latex
condom may be effective against the spread of syphilis through sexual contact,
although this cannot be guaranteed due to the ease with which non-genital body
parts can be infected.

Individuals sexually exposed to a person with primary, secondary, or early latent

syphilis within 90 days preceding the diagnosis should be assumed to be infected
and treated for syphilis, even if they are currently seronegative. If the exposure
was more than 90 days before the diagnosis, presumptive treatment is
recommended if serologic testing is not immediately available or if follow-up is
uncertain. Patients with syphilis of unknown duration and nontreponemal serologic
titers ≥1:32 may be considered as having early syphilis for purposes of partner
notification and presumptive treatment of sex partners. Long-term sex partners of
patients with late syphilis should be evaluated clinically and serologically and
treated appropriately. All patients with syphilis should be tested for HIV. Patient
education is important as well.

Human immunodeficiency virus (HIV)

Human immunodeficiency virus (HIV) is a lentivirus (a member of the

retrovirus family) that can lead to acquired immunodeficiency syndrome (AIDS), a
condition in humans in which the immune system begins to fail, leading to life-
threatening opportunistic infections. Previous names for the virus include human T-
lymphotropic virus-III (HTLV-III), lymphadenopathy-associated virus (LAV), and
AIDS-associated retrovirus (ARV).

Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-
ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free
virus particles and virus within infected immune cells. The four major routes of
transmission are unprotected sexual intercourse, contaminated needles, breast
milk, and transmission from an infected mother to her baby at birth (Vertical
transmission). Screening of blood products for HIV has largely eliminated
transmission through blood transfusions or infected blood products in the developed

HIV infection in humans is now pandemic. As of January 2006, the Joint United
Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization
(WHO) estimate that AIDS has killed more than 25 million people since it was first
recognized on December 1, 1981. It is estimated that about 0.6 percent of the
world's population is infected with HIV. In 2005 alone, AIDS claimed an estimated
2.4–3.3 million lives, of which more than 570,000 were children. A third of these
deaths are occurring in sub-Saharan Africa, retarding economic growth and
increasing poverty. According to current estimates, HIV is set to infect 90 million
people in Africa, resulting in a minimum estimate of 18 million orphans.
Antiretroviral treatment reduces both the mortality and the morbidity of HIV
infection, but routine access to antiretroviral medication is not available in all

HIV primarily infects vital cells in the human immune system such as helper T cells
(specifically CD4+ T cells), macrophages, and dendritic cells. HIV infection leads to
low levels of CD4+ T cells through three main mechanisms: firstly, direct viral
killing of infected cells; secondly, increased rates of apoptosis in infected cells; and
thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize
infected cells. When CD4+ T cell numbers decline below a critical level, cell-
mediated immunity is lost, and the body becomes progressively more susceptible to
opportunistic infections.

Eventually most HIV-infected individuals develop AIDS. These individuals mostly die
from opportunistic infections or malignancies associated with the progressive failure
of the immune system. Without treatment, about 9 out of every 10 persons with
HIV will progress to AIDS after 10-15 years. Many progress much sooner.
Treatment with anti-retrovirals increases the life expectancy of people infected with
HIV. Even after HIV has progressed to diagnosable AIDS, the average survival time
with antiretroviral therapy (as of 2005) is estimated to be more than 5 years.
Without antiretroviral therapy, death normally occurs within a year. It is hoped that
current and future treatments may allow HIV-infected individuals to achieve a life
expectancy approaching that of the general public.


HIV is a member of the genus Lentivirus, part of the family of Retroviridae.

Lentiviruses have many common morphologies and biological properties. Many
species are infected by lentiviruses, which are characteristically responsible for
long-duration illnesses with a long incubation period. Lentiviruses are transmitted
as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target
cell, the viral RNA genome is converted to double-stranded DNA by a virally
encoded reverse transcriptase that is present in the virus particle. This viral DNA is
then integrated into the cellular DNA by a virally encoded integrase, along with host
cellular co-factors, so that the genome can be transcribed. After the virus has
infected the cell, two pathways are possible: either the virus becomes latent and
the infected cell continues to function, or the virus becomes active and replicates,
and a large number of virus particles are liberated that can then infect other cells.

There are two strains of HIV known to exist: HIV-1 and HIV-2. HIV-1 is the virus
that was initially discovered and termed LAV. It is more virulent, relatively easily
transmitted, and is the cause of the majority of HIV infections globally. HIV-2 is less
transmittable and is largely confined to West Africa.

Comparison of HIV species

Species Virulence Transmittability Prevalence Purported origin

HIV-1 High High Global
HIV-2 Lower Low Sooty Mangabey


HIV is thought to have originated in non-human primates in sub-Saharan Africa and

transferred to humans early in the 20th century. The first paper recognizing a
pattern of opportunistic infections was published on 4 June 1981.

Two species of HIV infect humans: HIV-1 and HIV-2. Both species of the virus are
believed to have originated in West-Central Africa and jumped species (zoonosis)
from a non-human primate to humans. HIV-1 is thought to have originated in
southern Cameroon after jumping from wild chimpanzees (Pan troglodytes
troglodytes) to humans during the twentieth century. It evolved from a Simian
Immunodeficiency Virus (SIVcpz)[20] HIV-2, on the other hand, may have
originated from the Sooty Mangabey (Cercocebus atys), an Old World monkey of
Guinea-Bissau, Gabon, and Cameroon.
New World Monkeys are an interesting exception to the transmission of HIV. Their
immunity is believed to be caused by retrotransposition of the Cyclophilin gene into
an intron of TRIM5. The result is fusion gene that provides the owl monkey with
resistance to HIV-1 infection.


Estimated per-act risk for acquisition

of HIV by exposure route
per 10,000
Exposure Route
to an infected
Blood Transfusion 9,000
Childbirth 2,500
Needle-sharing injection drug use 67
Percutaneous needle stick 30
Receptive anal intercourse* 50
Insertive anal intercourse* 6.5
Receptive penile-vaginal
Insertive penile-vaginal
Receptive oral intercourse*§ 1
Insertive oral intercourse*§ 0.5
* assuming no condom use
§ source refers to oral intercourse
performed on a man

Three main transmission routes for HIV have been identified. HIV-2 is transmitted
much less frequently by the mother-to-child and sexual route than HIV-1.

The majority of HIV infections are acquired through unprotected sexual relations.
Sexual transmission can occur when infected sexual secretions of one partner come
into contact with the genital, oral, or rectal mucous membranes of another. In high-
income countries, the risk of female-to-male transmission is 0.04% per act and
male-to-female transmission is 0.08% per act. For various reasons, these rates are
4 to 10 times higher in low-income countries.

The correct and consistent use of latex condoms reduces the risk of sexual
transmission of HIV by about 85%. However, spermicide may actually increase the
male to female transmission rate due to inflammation of the vagina.

A meta-analysis of 27 observational studies conducted prior to 1999 in sub-Saharan

Africa indicated that male circumcision reduces the risk of HIV infection. However, a
subsequent review indicated that the correlation between circumcision and HIV in
these observational studies may have been due to confounding factors. Later trials,
in which uncircumcised men were randomly assigned to be medically circumcised in
sterile conditions and given counseling and other men were not circumcised, have
been conducted in South Africa, Kenya and Uganda showing reductions in HIV
transmission for heterosexual sex of 60 percent, 53 percent, and 51 percent
respectively. As a result, a panel of experts convened by WHO and the UNAIDS
Secretariat has "recommended that male circumcision now be recognized as an
additional important intervention to reduce the risk of heterosexually acquired HIV
infection in men." Research is clarifying whether there is a historical relationship
between rates of male circumcision and rates of HIV in differing social and cultural
On the other hand, some South African medical experts have expressed concern
that the repeated use of unsterilized blades in the traditional circumcision of
adolescent boys may actually be spreading HIV.
Bugchasing and giftgiving is the active pursuit to contract and transmit HIV,
Blood or blood product

In general if infected blood comes into contact with any open wound, HIV may be
transmitted. This transmission route can account for infections in intravenous drug
users, hemophiliacs and recipients of blood transfusions (though most transfusions
are checked for HIV in the developed world) and blood products. It is also of
concern for persons receiving medical care in regions where there is prevalent
substandard hygiene in the use of injection equipment, such as the reuse of needles
in Third World countries. Health care workers such as nurses, laboratory workers,
and doctors have also been infected, although this occurs more rarely. People who
give and receive tattoos, piercings, and scarification procedures can also be at risk
of infection.
Since transmission of HIV by blood became known medical personnel are required
to protect themselves from contact with blood by the use of Universal precautions.


The transmission of the virus from the mother to the child can occur in utero during
pregnancy and intrapartum at childbirth. In the absence of treatment, the
transmission rate between the mother and child is around 25 percent. However,
where combination antiretroviral drug treatment and Cesarian section are available,
this risk can be reduced to as low as one percent.
Breast feeding also presents a risk of infection for the baby.

Other routes

HIV has been found at low concentrations in the saliva, tears and urine of infected
individuals, but there are no recorded cases of infection by these secretions and the
potential risk of transmission is negligible.

Multiple infections

Unlike some other viruses, infection with HIV does not provide immunity against
additional infections, particularly in the case of more genetically distant viruses.
Both inter- and intra-clade multiple infections have been reported, and even
associated with more rapid disease progression. Multiple infections are divided into
two categories depending on the timing of the acquisition of the second strain.
Coinfection refers to two strains that appear to have been acquired at the same
time (or too close to distinguish). Reinfection (or superinfection) is infection with a
second strain at a measurable time after the first. Both forms of dual infection have
been reported for HIV in both acute and chronic infection around the world.

Diagram of HIV
HIV is different in structure from other retroviruses. It is roughly spherical with a
diameter of about 120 nm, around 60 times smaller than a red blood cell, yet large
for a virus. It is composed of two copies of positive single-stranded RNA that codes
for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of
the viral protein p24. The single-stranded RNA is tightly bound to nucleocapsid
proteins, p7 and enzymes needed for the development of the virion such as reverse
transcriptase, proteases, ribonuclease and integrase. A matrix composed of the
viral protein p17 surrounds the capsid ensuring the integrity of the virion
particle.This is, in turn, surrounded by the viral envelope which is composed of two
layers of fatty molecules called phospholipids taken from the membrane of a human
cell when a newly formed virus particle buds from the cell. Embedded in the viral
envelope are proteins from the host cell and about 70 copies of a complex HIV
protein that protrudes through the surface of the virus particle.This protein, known
as Env, consists of a cap made of three molecules called glycoprotein (gp) 120, and
a stem consisting of three gp41 molecules that anchor the structure into the viral
envelope. This glycoprotein complex enables the virus to attach to and fuse with
target cells to initiate the infectious cycle. Both these surface proteins, especially
gp120, have been considered as targets of future treatments or vaccines against

HIV test

Many HIV-positive people are unaware that they are infected with the virus. For
example, less than 1% of the sexually active urban population in Africa have been
tested and this proportion is even lower in rural populations. Furthermore, only
0.5% of pregnant women attending urban health facilities are counselled, tested or
receive their test results. Again, this proportion is even lower in rural health
facilities. Since donors may therefore be unaware of their infection, donor blood and
blood products used in medicine and medical research are routinely screened for

HIV-1 testing consists of initial screening with an enzyme-linked immunosorbent

assay (ELISA) to detect antibodies to HIV-1. Specimens with a nonreactive result
from the initial ELISA are considered HIV-negative unless new exposure to an
infected partner or partner of unknown HIV status has occurred. Specimens with a
reactive ELISA result are retested in duplicate. If the result of either duplicate test
is reactive, the specimen is reported as repeatedly reactive and undergoes
confirmatory testing with a more specific supplemental test (e.g., Western blot or,
less commonly, an immunofluorescence assay (IFA)). Only specimens that are
repeatedly reactive by ELISA and positive by IFA or reactive by Western blot are
considered HIV-positive and indicative of HIV infection. Specimens that are
repeatedly ELISA-reactive occasionally provide an indeterminate Western blot
result, which may be either an incomplete antibody response to HIV in an infected
person, or nonspecific reactions in an uninfected person. Although IFA can be used
to confirm infection in these ambiguous cases, this assay is not widely used.
Generally, a second specimen should be collected more than a month later and
retested for persons with indeterminate Western blot results. Although much less
commonly available, nucleic acid testing (e.g., viral RNA or proviral DNA
amplification method) can also help diagnosis in certain situations. In addition, a
few tested specimens might provide inconclusive results because of a low quantity
specimen. In these situations, a second specimen is collected and tested for HIV

See also Antiretroviral drug

Abacavir - a nucleoside analog reverse transcriptase inhibitors

(NARTIs or NRTIs). There is currently no vaccine or cure for HIV or AIDS. The only
known method of prevention is avoiding exposure to the virus. However, a course of
antiretroviral treatment administered immediately after exposure, referred to as
post-exposure prophylaxis, is believed to reduce the risk of infection if begun as
quickly as possible. Current treatment for HIV infection consists of highly active
antiretroviral therapy, or HAART. This has been highly beneficial to many HIV-
infected individuals since its introduction in 1996, when the protease inhibitor-
based HAART initially became available. Current HAART options are combinations
(or "cocktails") consisting of at least three drugs belonging to at least two types, or
"classes," of antiretroviral agents. Typically, these classes are two nucleoside
analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease
inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). New classes of
drugs such as Entry Inhibitors provide treatment options for patients who are
infected with viruses already resistant to common therapies, although they are not
widely available and not typically accessible in resource-limited settings. Because
AIDS progression in children is more rapid and less predictable than in adults,
particularly in young infants, more aggressive treatment is recommended for
children than adults. In developed countries where HAART is available, doctors
assess their patients thoroughly: measuring the viral load, how fast CD4 declines,
and patient readiness. They then decide when to recommend starting treatment.
HAART neither cures the patient nor does it uniformly remove all symptoms; high
levels of HIV-1, often HAART resistant, return if treatment is stopped. Moreover, it
would take more than a lifetime for HIV infection to be cleared using HAART.
Despite this, many HIV-infected individuals have experienced remarkable
improvements in their general health and quality of life, which has led to a large
reduction in HIV-associated morbidity and mortality in the developed world. One
study suggests the average life expectancy of an HIV infected individual is 32 years
from the time of infection if treatment is started when the CD4 count is 350/µL. In
the absence of HAART, progression from HIV infection to AIDS has been observed
to occur at a median of between nine to ten years and the median survival time
after developing AIDS is only 9.2 months. However, HAART sometimes achieves far
less than optimal results, in some circumstances being effective in less than fifty
percent of patients. This is due to a variety of reasons such as medication
intolerance/side effects, prior ineffective antiretroviral therapy and infection with a
drug-resistant strain of HIV. However, non-adherence and non-persistence with
antiretroviral therapy is the major reason most individuals fail to benefit from
HAART. The reasons for non-adherence and non-persistence with HAART are varied
and overlapping. Major psychosocial issues, such as poor access to medical care,
inadequate social supports, psychiatric disease and drug abuse contribute to non-
adherence. The complexity of these HAART regimens, whether due to pill number,
dosing frequency, meal restrictions or other issues along with side effects that
create intentional non-adherence also contribute to this problem. The side effects
include lipodystrophy, dyslipidemia, insulin resistance, an increase in cardiovascular
risks and birth defects.

The timing for starting HIV treatment is still debated. There is no question that
treatment should be started before the patient's CD4 count falls below 200, and
most national guidelines say to start treatment once the CD4 count falls below 350;
but there is some evidence from cohort studies that treatment should be started
before the CD4 count falls below 350. In those countries where CD4 counts are not
available, patients with WHO stage III or IV disease should be offered treatment.
Anti-retroviral drugs are expensive, and the majority of the world's infected
individuals do not have access to medications and treatments for HIV and AIDS.
Research to improve current treatments includes decreasing side effects of current
drugs, further simplifying drug regimens to improve adherence, and determining
the best sequence of regimens to manage drug resistance. Unfortunately, only a
vaccine is thought to be able to halt the pandemic. This is because a vaccine would
cost less, thus being affordable for developing countries, and would not require
daily treatment. However, after over 20 years of research, HIV-1 remains a difficult
target for a vaccine.

Treatments in development

Promising new treatments include Cre recombinase and the enzyme Tre
recombinase, both of which are able to remove HIV from an infected cell. These
enzymes promise a treatment in which a patient's stem cells are extracted, cured,
and reinjected to promulgate the enzyme into the body. The carried enzyme then
finds and removes the virus.
Media reports in 2008 and a publication in the New England Journal of Medicine in
2009, described the anecdotal case of an HIV-positive patient of a Berlin doctor,
Gero Hütter. The patient, who had both acute myelogenous leukemia (AML) and
HIV had been "functionally cured" of his HIV following a bone marrow transplant for
AML. The bone marrow donor had been selected to have a CCR5-Δ32 mutation.
After 600 days without antiretroviral drug treatment, no HIV was detectable in the
patient's blood, bone marrow or bowel (although it is likely to be present in other
tissues). The patient himself was heterozygous for CCR5-Δ32. Following
transplantation, his peripheral CD4+ T-cells were homozygous for CCR5-Δ32. The
macrophages in his bowel, which continued to express wildtype CCR5 (because
they hadn't been replaced yet from bone marrow precursors), also had no
detectable virus.
The mortality risk associated with bone marrow transplants is thought to
contraindicate the use of this experimental treatment for HIV-positive individuals
without leukemia or lymphoma. Resistance to CCR5 inhibition may be less
important if CXCR4 strains of HIV emerge (these use CXCR4 rather than CCR5 as a
coreceptor, from which they become independent), though before the treatment
Hütter's patient carried the CXCR4 virus at low levels. People without CCR5 appear
to be more sensitive to some infections such as West Nile virus.


Note: At the time of diagnosis with HIV, many people have not experienced any

Acute HIV infection can appear like infectious mononucleosis, flu, or other viral

Any of the following symptoms can occur:

• Decreased appetite
• Fatigue
• Fever
• Headache
• Malaise
• Swollen lymph glands
• Muscle stiffness or aching
• Rash
• Sore throat
• Ulcers of the mouth and esophagus

Signs and tests

• Blood differential may show abnormalities.

• HIV ELISA/Western blot is usually negative or undetermined during the acute
infection and will become positive over the next 3 months.
• HIV RNA viral load is positive in patients with acute HIV infection.
• Lower than normal CD4 count may indicate suppression of the immune
system. The CD4 count usually improves 1 - 2 months after acute infection.
• P24 antigen blood test is often positive.

Expectations (prognosis)
HIV is a long-term medical condition that can be treated but not yet cured. There
are effective means of preventing complications and delaying (but not preventing)
progression to AIDS. At the present time, not all cases of HIV have progressed to
AIDS, but time has shown that the vast majority do.

• AIDS (acquired immune deficiency syndrome)
• Autoimmune diseases
• Cancers, typically Kaposi's sarcoma and lymphomas
• Opportunistic infections (unlikely to occur in early stages of HIV disease)
• Bacillary angiomatosis
• Candidiasis
• Cryptosporidium or other protozoal enterocolitis
• Cytomegalovirus infection
• Pneumocystis carinii pneumonia
• Mycobacterium avium complex (MAC)
• Progressive multifocal leukoencephalopathy
• Salmonella infection of the bloodstream
• Toxoplasmosis
• Tuberculosis


Herpes simplex virus

Group: Group I (dsDNA)

Family: Herpesviridae
Subfamily: Alphaherpesvirinae
Genus: Simplexvirus

Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) are two species of the
herpes virus family, Herpesviridae, which cause infections in humans. Eight
members of herpes virus infect humans to cause a variety of illnesses including cold
sores, chickenpox or varicella, shingles or herpes zoster (VZV), cytomegalovirus
(CMV), and various cancers, and can cause brain inflammation (encephalitis). All
viruses in the herpes family produce life-long infections.

They are also called Human Herpes Virus 1 and 2 (HHV-1 and HHV-2) and are
neurotropic and neuroinvasive viruses; they enter and hide in the human nervous
system, accounting for their durability in the human body. HSV-1 is commonly
associated with herpes outbreaks of the face known as cold sores or fever blisters,
whereas HSV-2 is more often associated with genital herpes.

An infection by a herpes simplex virus is marked by watery blisters in the skin or

mucous membranes of the mouth, lips or genitals. Lesions heal with a scab
characteristic of herpetic disease. However, the infection is persistent and
symptoms may recur periodically as outbreaks of sores near the site of original
infection. After the initial, or primary, infection, HSV becomes latent in the cell
bodies of nerves in the area. Some infected people experience sporadic episodes of
viral reactivation, followed by transportation of the virus via the nerve's axon to the
skin, where virus replication and shedding occurs.

Herpes is contagious if the carrier is producing and shedding the virus. This is
especially likely during an outbreak but possible at other times. There is no cure
yet, but there are treatments which reduce the likelihood of viral shedding.


HSV is transmitted during close contact with an infected person who is shedding
virus from the skin, in saliva or in secretions from the genitals. This horizontal
transmission of the virus is more likely to occur when sores are present, although
viral shedding, and therefore transmission, does occur in the absence of visible
sores. In addition, vertical transmission of HSV may occur between mother and
child during childbirth, which can be fatal to the infant. The immature immune
system of the child is unable to defend against the virus and even if treated, the
infection can result in inflammation of the brain (encephalitis) that may cause brain
damage. Transmission occurs when the infant passes through the birth canal, but
the risk of infection is reduced if there are no symptoms or exposed blisters during
delivery. The first outbreak after exposure to HSV is commonly more severe than
future outbreaks, as the body has not had a chance to produce antibodies; this first
outbreak carries a low (~1%) risk of developing aseptic meningitis.

Signs and Symptoms:


• Small, painful blisters filled with fluid around the lips or edge of the mouth
• Tingling or burning around the mouth or nose (often a few days before
blisters appear)
• Fever
• Sore throat
• Swollen lymph nodes in neck

• Small red blisters or open sores on genitals or inner thighs; in women, often
occur inside the vagina
• May be painful or not
• In women, vaginal discharge
• Fever, muscle aches
• Headache Painful urination
• Swollen lymph glands in the groin


HSV-1 is transmitted through saliva. Kissing, using the same eating utensils,
sharing personal items (such as a razor), and receiving oral sex from someone who
has HSV-1 can cause you to contract the virus.

HSV-2 is a sexually transmitted disease.

Both herpes viruses can be contagious even if the infected person does not have
active symptoms or visible blisters.

Also, a mother can pass the infection to her baby during vaginal birth, especially if
there are active blisters around the vagina at the time of delivery.

Risk Factors:

Oral herpes (cold sores)

Everyone is at risk for oral herpes from HSV-1. In fact, studies suggest that by
adolescence 62% of Americans are infected with HSV-1 and by the time people are
in their 40s, 90% have been infected.

Genital herpes

All sexually active people are at risk for genital herpes. Having multiple sexual
partners puts you at even greater risk. Women have a greater risk of being infected
after sex with an unprotected partner than men do. Estimates of how many
Americans are infected range from 20% to 30%.

Other factors

People with weakened immune systems, such as people with HIV/AIDS or those
who take immunosuppressant drugs to treat an autoimmune disease or because of
organ transplant, are at increased risk for severe cases of herpes.


In many instances, your doctor is able to make the diagnosis of herpes from
examining you and no tests are required. If your doctor is not 100% certain,
however, then he or she make take a sample from the blisters to test for the virus.
Finally, there is a blood test that may be helpful for making a diagnosis, especially if
your doctor suspects herpes but you don't have an active infection.

Preventive Care:


• Avoiding kissing people with visible core sores

• Don't share personal items
• Wash your hands frequently
• If you have HSV-1, be careful touching your eyes and genitals; don't perform
oral sex on your partner
• Use sunscreen
• Reduce stress


• Avoid having sex if you or your partner has an outbreak (active infection) of
herpes. Herpes outbreaks are not always obvious and your partner may be
contagious without you knowing it. Anyone involved in an ongoing sexual
relationship with a partner infected with HSV-2 should get counseling from a
healthcare practitioner on how to best keep yourself safe.
• Avoid touching the sores
• Use or have your partner use a latex condom (even when sores are not
• Limit the number of sex partners

Treatment Approach:

Herpes cannot be cured, so the goals of treatment are to reduce the number of
outbreaks and to lessen symptoms when you do have an outbreak.

Cold sores usually go away by themselves in no more than 1 to 2 weeks. Using

medications may shorten the outbreak and decrease discomfort.

Antiviral medications for genital herpes can reduce outbreaks and help speed
recovery when an outbreak does occur. They can also lessen the chances of
spreading the virus.

Coping with the emotional and social aspects of having genital herpes is part of
treatment. Relaxation techniques and support groups can help.


For cold sores, applying either heat or cold to blisters may help relieve pain. Try ice
or warm compresses.

For genital herpes, wear cotton underwear and avoid tight fitting clothes as they
can restrict air circulation and slow the healing of lesions.

Be sure to tell your partner or potential partner that you have herpes.


Antiviral medicines — may help shorten the duration of a herpes outbreak and
suppress recurring outbreaks. For genital herpes, there are two types of therapy:
episodic and suppressive. With episodic therapy, you take medication at the first
sign of an outbreak and for several days to shorten the duration or prevent a full
outbreak. With suppressive therapy, you may take medication daily to keep
outbreaks from occurring. Antiviral medications include:

• Acyclovir (Zovirax)
• Famciclovir (Famvir)
• Valacyclovir (Valtrex)
Topical medications (for oral herpes) — include the antiviral cream Penciclovir
(Denavir) and an over-the-counter cream, docosanol (Abreva).

Nutrition and Dietary Supplements

Because supplements may have side effects or interact with medications, they
should be taken only under the supervision of a knowledgeable healthcare provider.

• Lysine (1 to 3 g per day) — Although not all studies agree, several studies
suggest that lysine may help reduce the number of recurring outbreaks of
cold sores and possibly genital herpes. Most of the studies have involved
people with cold sores or with both cold sores and genital herpes. A few
studies also suggest that lysine may help shorten the duration of an
outbreak. The evidence is somewhat stronger for cold sores: the research to
date is not entirely conclusive, lysine supplements have been used to help
treat or prevent mouth and genital lesions caused by herpes. Taking lysine
supplements or increasing lysine in your diet (from foods like fish, chicken,
eggs, and potatoes) may speed recovery time and reduce the chance of
recurrent breakouts of the herpes infection. If you have high cholesterol,
heart disease, or high triglycerides (type of fatty material in the blood,
generally measured when you have your cholesterol checked), it is best, at
this point, not to use lysine because animal studies suggest that this
supplement may raise cholesterol and triglyceride levels.
• Propolis — A resin made by bees, propolis is loaded with flavonoids
(antioxidants that help fight infection and boost immune function). Test tube
studies show it can stop HSV-1 and HSV-2 from reproducing. One small
study of people with genital herpes compared an ointment made from
propolis to Zovirax ointment. People using propolis saw the lesions heal
faster than those using topical Zovirax. More studies are needed to say for
sure whether propolis works.
• Zinc — In test tubes, zinc is effective against HSV-1 and HSV-2. In one small
study in people, those who applied zinc oxide cream to cold sores saw them
heal faster than those who applied a placebo cream.

Other Considerations:


Herpes viruses can be transmitted to a newborn during vaginal delivery, especially if

the mother has active lesions in the vagina at the time of delivery. Herpes infections
in newborns can be life-threatening or cause disability. Delivery by cesarean section
(C-section) will be recommended to avoid infecting the baby.

Special Populations

Newborns – herpes infections contracted during delivery from the mother can lead
to meningitis, herpes infection in the blood, chronic skin infection, and may even be

You are more likely to have severe, frequent outbreaks and to experience
complications from herpes if your immune system is suppressed from:

• Chemotherapy for cancer
• Long-term use of high doses of corticosteroids
• Medications that intentionally suppress the immune system
Warnings and Precautions

If you are diagnosed with genital herpes, you should be tested for other sexually
transmitted diseases such as chlamydia and gonorrhea.

Prognosis and Complications

Herpes is a chronic, recurrent infection. The initial symptoms usually appear within
1 to 3 weeks of exposure to the virus and last 7 to 10 days (for cold sores) or 7 to
14 days (for genital lesions). Usually the number of outbreaks is greatest in the first
year and higher for HSV-2 genital lesions than HSV-1 cold sores. Each year after
that, the number of outbreaks usually goes down and they become less severe. But
you can never completely get rid of the virus.

Complications of herpes include:

• Herpetic keratitis – herpes infection of the eye leading to scaring within the
cornea and possible blindness
• Persistent herpes infection, without lesion-free periods
• Herpes infection in the esophagus
• Herpes infection of the liver which can lead to cirrhosis (liver failure)
• Encephalitis and/or meningitis (serious brain infections)
• Lung infection
• Eczema herpetiform – widespread herpes across the skin