First of all a few basic facts. Syphilis is a bacteria. It is transmitted via direct skin contact with contagious Syphilitic lesions. What are considered contagious Syphilitic lesions you say? Well, they are ulcers caused by Syphilis (known as a Chancres) and the skin rash that occurs in secondary Syphilis. The ulcers are generally single and painless (except in HIV positive patients where the ulcers can be multiple and painful). They can appear anytime between 9 to 90 days post infection. Most commonly they appear at about 4 weeks post infection. The ulcers are found at the site of bacterial entry. So they can be anywhere but they are most frequently found in the anogenital region. The rash caused by secondary Syphilis is called the Great Imitator because it can look like any rash. It appears 3 to 6 weeks after the initial Syphilitic ulcer (Chancre) has subsided. Since it can look like anything, it is hard to differentiate from other rashes (eg eczema). It is usually a macula-papular rash that involves the trunk more than the limbs and also involves the palms and soles.

At this point some of you are asking ‘If what you say is true, then Syphilis is not necessarily sexually transmitted.’ To that I say ‘You are absolutely right.’ There was a user on the forum (www.askdrtan.com) who caught Syphilis from her client. She is a masseuse. Direct skin contact with infectious lesions remember?

Next I want to clear up some technical terms. Often people throw words at me like ‘Early Primary Syphilis’ and ‘Latent Secondary Syphilis’. This shows that there is a lot of confusion in the terminology out there. So let’s set the record straight.

There are 2 stages of Syphilis: Early and Late. The definition of early Syphilis VARIES depending on which guidelines you read. According to the US CDC, if the Syphilis infection was within the past 1 year, it is considered Early Syphilis. According to the WHO it is 2 years. Why does this matter? It determines what treatment a patient gets. Early Sypphilis requires less medicines than Late Syphilis. So far confusing enough? It gets worse.

Early Syphilis is divided into 3 clinical stages. Primary Syphilis, Secondary Syphilis and Latent Syphilis (also known as Early Latent Syphilis). The stages are characterized as such: Primary Syphilis – presence of Chancre, Secondary Syphlis – presence of rash, Latent Syphilis – no symptoms.

Late Syphilis is divided into 2 clinical stages. Tertiary Syphilis and Latent Syphilis (also known as Late Latent Syphilis). The stages are characterized as such: Tertiary Syphilis – End organ involvement including aneurysms, Latent Syphilis – no symptoms.

There are 2 other types of Syphilis we will not be discussing in this post and they are Neuro-Syphilis (Syphilis involving the nervous system) and Syphilis in the Newborn.

Remember we said Syphilis is a bacteria? To be more precise, Syphilis is the disease caused by a bacteria and this bacteria is called Treponema Pallidum. The special thing about T. Pallidum is that is cannot be cultured. In other words, you cannot grow it in a dish. In other words, the only way to prove it is there is either to see the live bacteria directly or by using indirect evidence of its presence (something known as serology tests which are essentially bood tests).

To see the live bacteria you first need an active lesion. Next, you need a skilled person to sample bacteria from the lesion. Next you need special equipment and specially trained medical professionals to use this special equipment to look for the bacteria. Because the case load of Syphilis for most countries is rather low, most labs either do not have the equipment or the training. Also, because if the high rate of false negatives from these tests, patients suspected of Syphilis are required to follow up with serology testing anyway. In other words, these tests are rather useless except in very specific settings.

Serology tests are the mainstay of diagnosing Syphilis. There are basically 2 types of serology tests: Treponemal Tests and Non-Treponemal tests. There are many types of Treponemal Tests (eg TPHA, FTA-Abs etc). There are also many types of Non-Treponemal tests (VDRL, RPR, HEAT etc). For ease of discussion we will consider all Treponemal tests the same and all Non-Treponemal tests the same.

The one very important thing to remember is that there is no such thing as one perfect ‘most accurate’ test for Syphilis. This is what most people look for and it is really just chasing a rainbow.

Treponemal tests are very good at screening for Syphilis. They are as good as 100% accurate in diagnosing Syphilis except under 3 conditions. The first is very early Syphilis. When I say very early I mean less than 12 weeks from the date of infection. Although Treponemal tests are as good as conclusive at 4 weeks, the recommendation is still to retest at 12 weeks. The second is very late latent Syphilis. How late? Nobody knows. The accuracy of Treponemal tests is late latent Syphilis drops from 100% to 70% over several years. The third and last condition under which Treponemal tests are of no use is if a person has been previously infected with Syphilis. Even if this person has been treated successfully, the Treponemal test will still remain positive. So there is no way to know if this person has been re-infected or not using Treponemal tests.

Non-Treponemal tests are often used for screening of Syphilis in places where the prevalence of Syphilis is relatively high. This is because of the third reason given in the preceding paragraph. (Also becasue it is cheaper). So you would notice that European Guidelines recommend using Treponemal tests for screening and most Asian guidelines recommend using Non-Treponemal tests. On the whole, Non-Treponemal tests are LESS ACCURATE than Treponemal tests when used for screenig of Syphilis. They are however useful under 2 conditions. The first is when a person has been previously infected with Syphilis and we need to find out if he or she has been re-infected or not. The second is for monitoring of treatment success or failure.

So remember we said there is no one perfect test for screening of Syphilis? The trick is to do both a Treponemal as well as a Non-Treponemal test for patients. That is ideal.

If a patient has never had Syphilis before, which would be the majority of readers here, and you HAD to choose one test, than the Treponemal test is better. Remember to always test at 4 weeks and retest at 12 weeks.

I hope that added some clarity to Syphilis testing.

I would like to end off on the note that nothing in Medicine is straightforward. Just when you think you had a handle on Syphilis testing, let me tell you this: All the above serology tests mentioned above will also be POSITIVE if a person has any of the Non-Syphilitic Treponemal Diseases. You didn’t think Syphilis was an only child did you? There are other bacteria under the Treponemal family which will all test positive using the exact same tests as we use to diagnose Syphilis.

So after all this discussion, we come back to square one. The same usual boring advice I give everyone. Do not try to be your own doctor by reading the internet. If you want to know whether you have been infected with Syphilis or not, please see a doctor trained in such matters and heed his advice.

About Dr. Tan
Dr. Tan graduated from the National University of Singapore in 2001. His residency was in the two largest public hospitals in Singapore; Tan Tock Seng Hospital and Singapore General Hospital.

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Note that the positive test line takes a little longer to appear compared to the Alere Determine HIV 1/2 Test.

However, by 6 minutes, the results is unmistakable.

To view the video, click on the link below:

http://www.youtube.com/watch?v=OY1ast9Wyis&feature=youtu.be

At the end of 20 minutes, the test looked like this:

About Dr. Tan
Dr. Tan graduated from the National University of Singapore in 2001. His residency was in the two largest public hospitals in Singapore; Tan Tock Seng Hospital and Singapore General Hospital.

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 However, I get frequently asked what a positive test looks like.

 This is the reason I uploaded this video. It shows the Alere Determine HIV test in action detecting the presence of HIV antibodies in blood.

 From the timeline, it also illustrates how fast the Determine test is. Although we always wait for the official 20 minutes for the test to complete, from this video you can see that by 1 minute into the test, we can easily tell if a person is positive for HIV.

•  9 seconds – blood applied
• 24 seconds – chase buffer applied
• 58 seconds – faint line appearing in patient window
• 1 minute 30 seconds – line is obvious and unmistakable
• 4 minutes – faint line appearing in control window
• 5 minutes – both lines are obvious and unmistakable

Click on the link below to watch the video:

 http://www.youtube.com/watch?v=SLvkhCXXajQ

About Dr. Tan
Dr. Tan graduated from the National University of Singapore in 2001. His residency was in the two largest public hospitals in Singapore; Tan Tock Seng Hospital and Singapore General Hospital.

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 First of all, data on this is lacking and very hard to come by.

 There are many theories that hypothesize that PEP reduces viral replication and delays sero-conversion and therefore make HIV testing less accurate. These theories have neither been proven nor debunked.

 Furthermore, there is very limited data on the use of P24 antigen tests (including Combo/Duo tests) and viral load testing for diagnostic purposes in patient who have or undergoing PEP. In fact, studies on monkeys (and more limited studies on humans) have shown positive viral load tests in individuals who were subsequently found not to be infected. This could represent an aborted infection (which is what PEP is supposed to and designed to do) rather than a true false positive. This illustrates one of the limitations of using viral load tests to diagnose people currently on or have completed PEP.

 Official Guidelines

 The US CDC Guidelines on Antiretroviral Postexposure Prophylaxis After Sexual, Injection-Drug Use, or Other Nonoccupational Exposure to HIV in theUnited Statesrecommends that patients should be tested for the presence of HIV antibodies at baseline, 4 – 6 weeks, 3 months and 6 months post exposure.

 The Joint WHO/ILO guidelines on post-exposure prophylaxis (PEP) to prevent HIV infection recommends HIV testing at baseline, immediately after completing PEP (i.e. 4 to 6 weeks post exposure) and again ‘3 – 6 months post exposure’.

 The 2 guidelines are rather similar although the US CDC seems to be more firm on the requirement of a test at 6 months compared to the WHO guidelines.

 Very recently, the New York State Department of Health AIDS Institute’s adult HIV guidelines committee undertook a comprehensive re-evaluation of its HIV occupational PEP guidelines and issued some changes which included shortening of the time of HIV testing after exposure to 3 months if modern, blood based, standard HIV testing is performed. This is certainly promising however it refers to occupational HIV exposure only and the same data and recommendation may not be extended to non-occupational exposure.

 Summary

 In short, most official guidelines still recommend testing at 6 months for patients who have undergone PEP.

 Sometimes testing at 3 months post exposure is good enough but this really depends on what kind of test is done.

 My own experience is the test done at 4 weeks exposure (or immediately upon completion of the PEP medications) is very indicative. I will still recommend a retest at 3 months although I have yet to see the test at 4 weeks get it wrong.

 At the end of the day, the best person to advise you is still the doctor who prescribed you the PEP. He/She will be most familiar with the sensitivity of local tests available and the local guidelines.

About Dr. Tan
Dr. Tan graduated from the National University of Singapore in 2001. His residency was in the two largest public hospitals in Singapore; Tan Tock Seng Hospital and Singapore General Hospital.

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 87% effective in preventing HIV.

 Scientific studies have shown that proper use of the condom can provide anything from 60% to 95% reduction in risk of HIV transmission.

 The most often quoted study involved more than 3000 HIV 1 sero-discordant couples. Self reported use of the condom reduced the risk of HIV transmission by 78% per sex act.

 The US CDC’s condom report published in the year 2000 estimated that consistent condom use reduced the risk of HIV transmission by 85%.

 Diaphragms and Female Condoms

 No evidence that either one reduces the risk of HIV transmission

 The MIRA study recruited 5000 women to study the use of diaphragms in preventing HIV. Since women who use the diaphragm were also likely to use the male condom, interpretation of the data was not straightforward. However, it is generally accepted that diaphragms do not reduce the risk of HIV infection.

 There is very limited research on the effectiveness for female condoms to prevent HIV and STDs in both vaginal as well as anal sex. No conclusions can be drawn from the current data.

 There has been a lot of excitement over the development of an anti-viral vaginal gel that has been shown to significantly reduce the risk of HIV transmission. It is also available as a drug infused vaginal ring. This is still under investigation and is not yet commercially available. If it is as effective as it appears, it will make a huge impact on empowering women to protect themselves from HIV.

 Male Circumcision

 60% effective in preventing HIV

 There have been 3 randomized trials to study the benefits of male circumcision in preventing HIV transmission. All of them have shown consistent evidence of a 60% reduction in HIV risk that persists for years.

 Furthermore, male circumcision has also been shown to reduce the incidence of trichomniasis, bacterial vaginosis and genital ulcers in women. However, it has not been shown to reduce HIV transmission from a circumcised man to a woman.

 Circumcision has also not been shown to reduce the risk of any of the other STDs.

 Circumcision also has not been shown to reduce the risk of HIV in men who have sex with men (MSM).

About Dr. Tan
Dr. Tan graduated from the National University of Singapore in 2001. His residency was in the two largest public hospitals in Singapore; Tan Tock Seng Hospital and Singapore General Hospital.

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 One of the world’s top medical journals JAMA, recently published a study that found up to 7% resistance of Gonorrhea to Cefixime. Cefixime is one of the last oral antibiotics available to treat Gonorrhea.

 Treatment failure was not limited to urethral infections but also applies to pharyngeal (throat) and rectal infections.

 The US CDC has in fact already taken this into account and since last year has already changed their treatment guidelines to remove Cefixime from their recommendations of first line treatments. The treatment recommendation for Gonorrhea now is an injection of 250mg Ceftrixone AND Azithromycin OR Doxycycline.

 There are more than 100 million cases of proven Gonorrhea infections worldwide each year. Since the 1940’s, Gonorrhea has been on a relentless march down the road of antibiotic resistance. At this point in time, Cephalosporins are the only weapons we have left against it. Now, even this weapon is showing signs of losing effectiveness. There is currently 1 new drug being studied but the pipeline of new antibiotics is fast drying up.

 From a practical patient point of view, please make sure you visit your doctor for a test of cure after you have been treated for Gonorrhea. You have to make sure the strain you have is not antibiotic resistant and the treatment was a success. If not, you will need second line treatment. This will not only protect you, it will also protect your partner and overall lead to the slower development of antibiotic resistant Gonorrhea.

About Dr. Tan
Dr. Tan graduated from the National University of Singapore in 2001. His residency was in the two largest public hospitals in Singapore; Tan Tock Seng Hospital and Singapore General Hospital.

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At the time, there was already a technique developed to detect various antibodies in the blood. This technique was called ELISA which stood for Enzyme Linked Immuno Sorbent Assay.

This technique is based on the lock and key theory of antibodies. Basically, antibodies and antigens work like locks and keys. One key for one lock. One antibody fits one antigen. Having the antibody means the antigen is also present.

So the ELISA technique basically involves getting a little cup (aka microwell) and sticking HIV antigens (locks) all over the bottom. The cup is then filled with the serum to be tested. If the appropriate anti-HIV antibodies are present (keys), they will stick to the antigens (locks). So far so good?

Now this is the clever bit. Since these antigens and antibodies are microscopic, the scientists had to figure out a way to be able to see if the locks have captured any keys. Microscopes do not work because these antigens and antibodies are just too small. They figured out that since antibodies are proteins too, they themselves are also antigens! In other words, the other end of the key is also a lock. So the scientist developed an anti-HIV antibody antibody. So this new antibody sticks to the back of the first antibody. This second antibody is also special in the fact that an enzyme is attached to it. When a special substrate is added to the mix, the enzyme will turn the substrate a different color (usually red). So there you have it. If the serum to be tested contains anti-HIV antibodies, after all these steps, the liquid in the microwell will turn red. So elegant and so simple. This came to be known as the 1^st generation HIV ELISA test.

However there were several problems associated with this test. First of all, it only detected antibodies to the HIV 1 virus, not HIV 2. Secondly, it only detected the IgG antibodies which can take some time to be produced in the body up to levels which where detectable and hence the testing window period. Thirdly, the antigen purification was not very good which led to a high level of false positives and hence the need for confirmation by Western Blot.

There wasn’t a big leap of technology going into the 2^nd generation test. Scientist just basically figured out a way to incorporate HIV 2 antigens into the test. There were also better antigen production techniques that improved the false positive rate. However the science behind the test went largely unchanged.

There was however a huge leap of technology from the 2^nd to 3^rd generation ELISAs. The main change was the 3^rd generation ELISAs could detect IgM as well as IgG antibodies. Because the body produces IgM way before it produces IgG, this significantly reduced the testing window period.

How the scientist did this was to develop what is now known as a ‘Sandwich ELISA’ technique. Similar to the previous ELISA tests, HIV 1 and 2 antigens were placed in the microwell. The anti-HIV IgM antibody would attach to the antigens. Now the thing about the IgM antibody is that it is like many keys attached to each other. In other words there are multiple antigen binding sites. This is very different from IgG that has just 1 antigen binding site. So what the scientist figured out how to do was to stick the enzyme and a HIV antigen together. So this antigen-enzyme conjugate will stick onto the other binding sites of the IgM antibody that has stuck onto the antigens in the microwell. The enzyme on the antigen then converts the substrate color thus enabling detection. Since the IgM antibody is ‘sandwiched’ between 2 antigens, the name ‘sandwich ELISA’ was coined.

Lastly, we come to the so called 4^th generation ELISA test. Not many people agree with this nomenclature because technically, it is identical to the 3^rd generation ELISA test. Basically the 4^th generation ELISA test is putting 2 different tests (i.e 3^rd generation ELISA and P24 antigen test) onto the same test strip. Because the P24 antigen is produced even earlier than the IgM antibody, this reduces the testing window period even further. So you can see that there isn’t really a ‘4^th generation ELISA’.

So now you know everything you need to know about the different generation ELISA tests. Hopefully that gives you more confidence in discussing tests and test results with your doctor.

About Dr. Tan
Dr. Tan graduated from the National University of Singapore in 2001. His residency was in the two largest public hospitals in Singapore; Tan Tock Seng Hospital and Singapore General Hospital.

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 By the end of this article, I hope you are so convinced that you are running out the door to get vaccinated.

 Let’s start by understanding what HPV is. HPV is a virus that is spread through direct contact. i.e. skin to skin contact, sexual contact including vaginal sex, oral sex, anal sex, even handjobs. Basically any sexual contact and condoms offer zero protection against HPV.

 Among other things, it causes genital warts. For those of you who have not suffered from genital warts before, you might not fully appreciate the mental anguish and anxiety it brings. For those of you who have, you know exactly what I am talking about.

 Genital warts are these really ugly fleshy looking things that can grow around your pubic area, penis, vagina, anus and basically everywhere down south. They are ugly, embarrassing and very difficult to get rid of. Treatment usually involves multiple sessions of painful laser or freezing treatments. Even then, warts can still recur and are even deemed to be ‘incurable’.

 There used to be nothing we can do to prevent Genital Warts. But now, we have the HPV Vaccine called Gardasil. Gardasil is unique from its competitors in that it protects against Genital warts.

 So isn’t taking 3 jabs worth it to protect yourselves from this terrible disease?

 Still not convinced? Well, here’s more.

 HPV has also been linked to the dreaded Cervical Cancer.

 Cervical cancer is the 4^th most common cancer among women in Singapore and 3^rd most common in the world.

 PAP smears are only useful in detecting the cancer early but does nothing to prevent it. If a woman is lucky enough to detect the problem in pre-cancer stages, she only has to undergo a minor surgery to remove a chunk of her cervix. If the cancer is detected in its late stages treatment involves major surgery to remove the entire womb, radiation therapy and chemotherapy. Even with all these treatments and their terrible side effects, the prognosis is not always good.

 So which would you rather have? 3 injections or cancer?

 Still not convinced? Boy you are a hard sell.

 HPV has also been linked to vaginal and vulval cancer in women, throat and anal cancer in both men and women and penile cancer in men.

 So men and women who practice oral sex and/or anal sex are at risk. Funnily enough, and we do not know why, men are more at risk of throat cancer when they perform oral sex on a woman than vice versa. Go figure.

 So regardless of sexual orientation, everyone benefits from a HPV vaccine.

 Phew that was along article. Let’s summarize, HPV is real easy to catch. It can lead to Genital Warts, Cervical Cancer, Vaginal Cancer, Vulval Cancer, Anal Cancer and even Penile Cancer. The only way you can protect yourself is to get vaccinated with the Gardasil vaccine.

 So go get vaccinated now!

About Dr. Tan
Dr. Tan graduated from the National University of Singapore in 2001. His residency was in the two largest public hospitals in Singapore; Tan Tock Seng Hospital and Singapore General Hospital.

Find the profiles of our panel of doctors.

The good and bad of period sex are yet to be discovered. However, a number of theories suggest that the practice more of a disadvantage rather than an advantage.

The Good

In a way, it relieves menstrual cramps. How? Endorphins (a type of hormones to relieve pain and affect emotions) are secreted during orgasm and thus decrease menstrual pains.

The Bad

Naturally during menstruation, the veins of the uterus are congested and are prone to rupture easily. Vaginal walls swell as well during menstruation. This explains the dull pain in the vagina during menses and is 100% normal. Having intercourse during your period can increase the chances of irritation to the swelled up walls. The advantages of endorphins at this point mask the danger of period sex where irritation of the vaginal walls and introduction to infection are major risks. Any wound or bleeding is a fine gateway to infection.

The cervix is slightly opened during menstruation to let out blood. This heightens the risk of infection, not being limited only to the vagina, but additionally to the uterus. The penetration of the penis into the vagina during menstruation is no more than the introduction to germs at a time when the body is unable to fight them (studies have shown that immunity is decreased during menstruation).

Orgasm results in rhythmic uterine contraction. During menstruation, this helps shed blood faster and shorten your periods. A similar reaction happens when a menstruating woman lifts up heavy loads or does strenuous exercises. This explains why most athletes experience amenorrhoea (missed periods).

The Ugly

Obviously, period sex can be really, really messy and unhygienic. This fact by itself drops the interest of both parties about the idea of having sex during menstruation.

So, is period sex good or bad? Well, momentary pleasure versus risky health – you be the judge.

Dr (Ms) De Souza

MD (Russia), MMed (Obs&Gyn)