Sexually Transmitted Infections

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. Causes: 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. Symptoms:

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 head. Besides itching, genital warts can cause pain during intercourse and in some cases, bleeding. 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 include: • • • •

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.

Treatment 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 include: • • • • • •

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. Prevention 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 STDs." 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. Complications 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 include: • • •

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.

Reference: http://www.cdc.gov/std/HPV/STDFact-HPV.htm www.wikipedia.com

Chlamydia

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 disease. 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 exposed. 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 urgency) 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. Diagnosis Screening 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. Treatment 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. Pathophysiology 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. Reference: wikipedia.org/wiki/Chlamydia

Trichomoniasis

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 penis. 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. Symptoms 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, yellowgreen 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. Diagnosis 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 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. Complications 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 trichomoniasis. 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 lowbirthweight 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. Reference:

en.wikipedia.org/wiki/Trichomoniasis

SYPHILIS

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 disease. 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 voyages, 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 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 HIVinfected 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 characterization. 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 test 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. Prevention 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. Reference: www.wikipedia.com http://www.cdc.gov/std/stats/syphilis.htm

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 lifethreatening opportunistic infections. Previous names for the virus include human Tlymphotropic 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, preejaculate, 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 world. 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 countries. 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, cellmediated 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. Classification 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 HIV-1

High

High

HIV-2

Lower

Low

Prevalence Purported origin Common Global Chimpanzee West Sooty Mangabey Africa

History 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. Transmission Estimated per-act risk for acquisition of HIV by exposure route

Estimated infections per 10,000 Exposure Route exposures to an infected source 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 10 intercourse* Insertive penile-vaginal 5 intercourse* 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. Sexual 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 highincome 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 contexts. 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, respectively.

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. Mother-to-child 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. 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. 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 infection.

Treatment

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 HIVinfected individuals since its introduction in 1996, when the protease inhibitorbased 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 nonadherence. 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. Symptoms Note: At the time of diagnosis with HIV, many people have not experienced any symptoms. Acute HIV infection can appear like infectious mononucleosis, flu, or other viral illnesses. 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.

Complications 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 •

Reference: www.wikipedia.com www.aids.com

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. Transmission 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: HSV-1 • • • • •

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

HSV-2 • • • • • •

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

Causes: 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. Diagnosis: 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: HSV-1 •

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

HSV-2 •

• • •

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 visible) 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. Lifestyle 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. Medications 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. •

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

HIV or AIDS 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

Reference: www.wikipedia.com www.pdfcoke.com