REVIEW ARTICLE

 

Approach in sexually transmitted diseases

 

 

Walter Belda Junior^I; Ricardo Shiratsu^II; Valdir Pinto^III

^IResponsible for the Department of Sexually Transmitted Diseases /AIDS, Brazilian Society of Dermatology. Post-doctorate Degree in Dermatology, Universidade Estadual de Campinas (UNICAMP). Assistant Professor, Ph.D., Department of Dermatology, Faculdade de Medicina da Universidade de Sao Paulo (FMUSP) – Sao Paulo (SP), Brazil.
^IIVolunteer Assistant Professor, Department of Dermatology, Universidade Federal de São Paulo (UNIFESP) – Sao Paulo (SP), Brazil
^IIIMinistry of Health. National Program of Sexually Transmitted Diseases

Mailing Address

 

 

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ABSTRACT

Nowadays, sexually transmitted diseases are one of the most common public health issues. Among its consequences are the possibility of transmission from mother to baby – which may cause miscarriages and congenital disease, male and female infertility, and the increase of HIV infection risk. Therefore, the main goal of these guidelines is to contribute to the improvement of the treatment for sexually transmitted diseases patients by presenting to the medical community how today's science stands on the matter and also what the recommendation for diagnosing and treating a patient are.

Keywords: Chancroid; Gonorrhea; Granuloma inguinale; Lymphogranuloma venereum; Sexually transmitted disease; Sexually transmitted disease/diagnosis; Sexually transmitted disease/etiology; Sexually transmitted disease/therapy

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INTRODUCTION

In 1999, the World Health Organization (WHO) estimated a total of 340 million new cases of curable sexually transmitted diseases (STD) per year all over the world among subjects aged 15 to 49 years amounting to 10 to 12 million cases in Brazil. Other some millions of incurable STD (viral), including genital herpes, human papilloma virus infections, hepatitis B and HIV infections occur annually ¹.

Among women with untreated infections by gonorrhea/ Chlamydia, 10 to 40% develop pelvic inflammatory disease (PID). Among them, more than 25% will become infertile – considering that the rate of infertility caused by non-infectious causes is estimated 3 to 7%. Studies conducted in developed countries indicate that women who have had PID are six to ten times more likely to have ectopic pregnancy, being that ectopic pregnancy contributes to more than 15% of maternal death ².

Spontaneous abortions, stillbirths, low birth weight, congenital and perinatal infections are associated with untreated STD in pregnancy ³. Among men, Chlamydia has become an important cause of fertility if not properly treated ^{4, 5, 6.}

Despite that, sexually transmitted diseases have only regained importance as a public health issue after the AIDS epidemics. Studies have shown that people with STD and non-ulcerative genital infections have 5 to 10 times higher risk to get infected by HIV, which is 18 times higher for those with ulcerative diseases ⁷.

Conversely, if HIV holder also has STD, HIV will be more easily transmitted to his partners. The mean concentration of HIV in seminal liquid is eight times greater in men with urethritis, without any difference in serum concentration. After treatment, seminal concentration is comparable again ⁸. HIV is also present in cervical-vaginal concentration in a frequency twice higher among women with gonorrhea, three times greater in the presence of Chlamydia and four times greater if there is ulceration of cervix or vagina ⁹. Bacterial vaginosis of endogenous origin doubles the risk of HIV infection, and it has significant implications in the gestational period, increasing the risk of prematurity and puerperal infection ^{10, 11, 12}.

Notifiable STD in Brazil are AIDS, HIV in pregnancy and exposed child, syphilis in pregnancy and congenital syphilis. To other STD, there is no system of required notification and the absence of population study hinders the visibility of the problem and the implementation of priority interventions and assessment of their effectiveness ¹³.

MAIN CLINICAL SYNDROMES

• ACQUIRED SYPHILIS

Chronic infectious disease, transmitted by sexual intercourse and sometimes by the placenta. It is characterized by long periods of clinical remission and the capacity to reach multiple organic systems, producing skin, mucosa, cardiovascular and nervous lesions.

Etiology

Treponema pallidum is a microorganism deprived of cell membrane, small and thin (5 x 15 x 0.2nm), of regular spires never over 12, with thinned extremities. It has rotation, flexion and contraction, as well as translation movements. It is not visible under optical microscopy, except if stained by argentum impregnation (Fontana's technique).

Epidemiology

It is a universal disease that affects all social-economic classes. The infection source is exclusively human and primary and secondary syphilis manifestations are contagious. It does not provide immunity, which means that re-infection and over-infection are possible. It normally affects mostly young people, aged 15 to 25 years, because they are more sexually active ^{14, 15}.

Transmission

Transmission takes place by direct contact with open lesions, transfusion of blood contaminated with acquired syphilis and via transplacental transmission in congenital syphilis. Treponema is capable of penetrating through normal skin and mucosa, but its penetration is facilitated when there is continuity solution. It quickly multiplies on the infected epithelium, and by lymphatic route it attacks the regional ganglia, where it is also quickly multiplies. Its dissemination is also immediate by hematogenic route. Thus, it invades the whole organism, and even when symptoms are local, generalized infection takes few hours. There are reports of accidental inoculation by manipulation of contaminated lesions by physicians, dentists and laboratory technicians.

Clinical Manifestations

The first manifestation of syphilis is chancre. The period of incubation ranges from two to four weeks. When fully developed, it presents as an exulcerated lesion, round or oval, of clean and pink aspect, granulomatous and beige, which discharges transparent serous liquid rich in Treponema, without adjacent inflammatory phenomena. Satellite adenopathy of the chancre is also part of the clinical presentation of primary syphilis, always present and without phlogistic signs. The secondary stage is characterized by syphilitic roseola, condyloma acuminatum, alopecia areata, and generalized micropolyadenopathy that goes with cutaneous-mucous lesions, which may be observed in cervical, supra-clavicular, axillary, epithrochlear and inguinal-crural regions. Late symptomatic syphilis has its onset after variable periods of latency, from two months to 30 years. It comprises cutaneous lesions of benign prognosis to neurological, cardiovascular and visceral lesions. Cutaneous lesions may surge between two and seven years after the secondary presentation ¹⁶.

Laboratory Work Up

Darkfield microscopy

Considering direct tests, this one is superior because it enables observation of live, mobile Treponema pallidum with all its morphodynamic characteristics, executing rotation, torsion and flexion movements without any deformation. The main indication for darkfield microscopy is primary syphilis.

The possibility of negative results in the test may be related to:

- patient using local or systemic anti-treponema medication
- chancre older than 3 weeks of progression
- non-representative sample
- non-syphilitic process

Serologic Tests:

Non-Treponemic tests (cardiolipidic or reagins)

This type of test detects the presence of non-specific antibodies (reagins) in the serum. They appear on average three to five weeks after the onset of protosyphiloma. There are mainly two types of tests: flocculation test and complement fixation reaction. In the flocculation reaction, the most widely used and standardized is VDRL (Venereal Disease Research Laboratory), and for complement fixation the most used one is Wassermann's reaction, in addition to RPR (Rapid Plasma Reagin). Antibodies detected by those techniques start to be observed three weeks after the onset of chancre, increase their titles progressively up to a maximum in the secondary period, with practically 100% positive response in this stage. In the tertiary period, positivity is approximately 90%.

Given that they are non-treponemic reactions, they are not specific and in addition to being positive for other treponematosis such as bouba and pinta, they may be present in other diseases than syphilis; in such cases they are named biological false-positive serologic reactions, whose main causes are:

1. Error in execution of the technique
2. Acute causes

• Infectious mononucleosis
• Viral Pneumonia
• Infectious hepatitis
• Herpes simples and zoster
• Measles
• Lymphogranuloma Venereum
• Vaccination (yellow fever and typhoid fever)
• Pregnancy

3. Chronic causes

• Rheumatoid arthritis
• Systemic lupus erythematosus
• Autoimmune hemolytic anemia
• Nodous periartheritis
• Thyroiditis
• Chronic hepatitis
• Hansen's disease
• Tuberculosis
• Leptospirosis
• Malaria
• Visceral leishmaniasis
Treponemic tests

To establish the definite diagnosis of syphilis and owing to limitations of non-treponemic tests, it is necessary to confirm it using specific tests based on detection of antibodies against Treponema pallidum. These tests include direct immunofluorescence test (FTA-abs); the treponema immobilization (TPI) test; treponema hemagglutination test (TPHA), and more recently enzyme immunoassays (EIA) ^{16, 17}.

The most widely used tests are:

1. Treponema immobilization test (TPI)
2. Reiter Protein Complement Fixation (RPCF)
3. FTA-200
4. FTA-abs (Fluorescent Treponemal Antibody-absorbed Test)
5. Treponema pallidum Hemagglutination (TPHA)
6. IgM-TPHA

Management

Treponema pallidum it is one of the most sensitive microorganisms to penicillin, disappearing from lesions within 12-18 hours from its systemic administration.

Thus, the recommended dose for recent syphilis management (primary, secondary and latent with less than one year of progression) is Penicillin Benzathine 2.400.000 IU, intramuscular, single dose. For latent, late, cutaneous and cardiovascular syphilis, the recommendation is Penicillin Benzathine 7.200.000 IU, intramuscular, divided into three weekly doses of 2.400.000 IU. In cases of allergy to penicillin, the following therapeutic regimens are recommended: recent syphilis - Doxycycline 100 mg PO, BID for 15 days; Tetracycline 500 mg PO, TID for 15 days; Erythromycin 500 mg PO, TID for 15 days and, Ceftriaxone 250 mg IM/day for 10 days. In latent, late, cutaneous and cardiovascular syphilis: Doxycycline 100 mg PO, BID for 4 weeks; Tetracycline 500 mg PO, TID for four weeks and, erythromycin 500 mg PO, TID for 4 weeks. Some authors suggest the use of azythromycin to treat syphilis, but there are reports of therapeutic failures. ^{18, 19, 19}

Cure Control

Serology tests should be performed at three, six and twelve months after treatment. If serology titration does not fall four times in recent syphilis after three months of treatment, or six months in recent latent syphilis, or if clinical signs and symptoms still persist, we should acknowledge treatment failure or the possibility of re-infection. In this case, before starting new management, we should perform lumbar puncture and CSF (cerebrospinal fluid) investigation. CSF should also be tested whenever there is 4-fold increase in serology titration ¹⁶16.

• GONORRHEA

It is an infectious-contagious disease, pandemic, inter-human, caused by diplococcus (Neisseria gonorrhoeae) and sexual transmission, even though it may exceptionally be caused by indirect contamination, but it does not provide immunity. In general, it is a urethral or uterine cervix infection that may propagate to glands and neighboring organs by ascending route; in some few cases, primary local infection is extra-genital, causing conjunctivitis, ophthalmia, pharyngitis and anoretitis. Similarly to any infectious process, it is not always localized because depending on the immune status of the host, it may lead to sepsis and general and systemic manifestations.

Epidemiology

Its incidence is greater between the ages of 15 and 30 years, but it is common also at other age ranges. It affects both genders, with male predominance.

Etiological agent

Neisseria gonorrhoeae is a gram negative diplococcus measuring 0.6 to 1.0 mµof diameter, reniform, which are grouped in two, with adjacent concave faces. They are aerobic, immobile, do not form spores and are sensitive to most antiseptic agents currently used. They are intra-cellular organisms deprived of capsule.

Clinical Manifestations

In men, manifestations occur after a mean incubation period of two to five days. Initially, there is sensation of tingling or intra-urethral pruritus, followed by dysuria. Two to three days later there is mucous urethral discharge, which soon becomes mucopurulent, yellow or greenish, with abundant spontaneous discharge.

In women, most cases are simpler, translated only as endocervicitis ²¹.

Complications in men:

• Balanoposthitis
• Stones that cross to the urethra
• Spontaneous perineal pain
• Prostatitis
• Epididymitis
• Cystitis

Complication in women:

• Bartholinitis
• Adnexitis

• EXTRA-GENITAL GONORRHEA

Ophthalmic: It is characterized by conjunctivitis, initially serous, which becomes progressively purulent, viscous, yellowish, followed by palpebral and conjuctival edema.

Rectal: The main symptoms are tenesmus, anal pruritus, painful evacuation and mucous-purulent rectal secretion. Rectoscopy may show purple and edematous mucosa, recovered with abundant suppuration with multiple erosions.

• GONOCOCCAL PHARYNGITIS

It affects on average 10% to 20% of the subjects who practice oral sex with partners who have gonococcal urethritis.

Disseminated

Hematogenic dissemination of gonorrhea occurs in 0.3% to 3% of the cases and affects primarily the skin and the joints, and it is less frequent in cardiac valves and in the brain.

Differential diagnosis

It should be made with the processes caused by different etiological agents, such as Chlamydia trachomatis, Ureaplasma urealitycum, Trichomonas vaginalis, Herpes virus, Candida albicans, and chemical, metabolic (diabetes) and traumatic processes.

Laboratory Work Up

1) Gram staining: there are intracellular gram negative diplococcal. ²² It presents 95% sensitivity in men and 50% for cervical and rectal samples.

2) Culture: enriched and selective means are recommended, which ensures growth and development of neisseria. They require CO2 atmosphere of about 3-5% and humidity rate of 90% at temperature of 35.5º C to 36.5º C. ^23,24

Among the most used culture media there are modified Thayer-Martin, Martin Lewis and NYC (New York City). ²⁵

Management

Owing to the capacity that bacteria have to develop chromosome and/or plasmodia resistance to the different antibiotics used in treatment, it is necessary to be constantly on the watch to detect frequent failures. The drugs recommended for management are Ofloxacin 400 mg PO single dose; cefixime 400 mg PO single dose; ciprofloxacin 500 mg PO single dose; ceftriaxone 250 mg intramuscular single dose. Since 2006, the Center for Disease Control and Prevention (CDC) has not recommended the use of quinolone derivatives to treat gonorrhea owing to progressive increase of resistant strains in the USA; however, this phenomenon is not common in Brazil. ^26,27,28,29

• Canchroid

Sexually transmitted disease, of acute progression, caused by gram-negative bacillus and clinically characterized by the presence of painful ulcerations of varied sizes, irregular margins and frequently involved by bright erythematous halo located in the genital, anal or anogenital regions, followed or not by satellite adenopathy.

Epidemiology

It is a cosmopolitan disease with outbreaks in industrialized countries, but it has greater prevalence in Africa, Middle East and tropical and subtropical regions of South America. The natural source seems to be exclusive men. It has high infectivity and low pathogenicity. Its virulence is low and given that it is an infection limited to the skin and mucosa, there is no systemic involvement.

Etiology

It is a short bacillus, family Brucellaceae, genus Haemophilus, species ducreyi. It is a gram-negative bacillus, intracellular, facultative anaerobic, measuring 1 to 2µm by 0.5µm, with rounded extremities and deprived of capsule or motility. It has simple or double chains inside polymorphonuclear cells. It is difficult to culture it, which grows moderately in Agar-chocolate medium.

Clinical Manifestations

It has a short period of incubation, oscillating from 4 to 7 days, and its onset is rare with less than 3 or more than 10 days. It starts as a small inflammatory papule enveloped by dark erythematous halo, which rapidly progresses to vesicle-pustulous lesion, which is ruptured and leads to ulcerated lesion, of soft shallow basis, with irregular margins, recovered by purulent necrotic exsudate and it is involved by live erythematous halo. They are painful lesions in varied number, shape and size owing to its characteristic of self-inoculation. Inguinal ganglionar infarction may be present in up to 50% of the cases, normally unilateral, and 2/3 of the cases progress with fluctuation and fistulation with drainage of purulent material through one single fistula, which may support the differential diagnosis with venereal lymphogranuloma, in which fistulation is made through multiple orifices. ^30,31,33

Differential diagnosis

It should be made basically with other genital ulcers of infectious or parasitic origin, among which there is protosyphiloma, which is characterized by induration of its basis, normally single, non-painful, with clean area and regional non-inflammatory adenopathy always present; with lymphogranuloma venereum in which adenopathy is always present and it is the main manifestation of the disease, presenting fistulation through innumerous orifices; with donovanosis, in which ulcers are rounded, non-painful, of clean basis, bleeding easily and do not have ganglion involvement. It should also be differentiated from genital herpes lesions, folliculitis, impetigo, tegumentary leishmaniasis, paracoccidiodomycosis and genital pyoderma (phagedenic form).

Laboratory Work Up

1) Gram staining of purulent material obtained from the ulcers, showing gram negative bacilli displayed in columns or rows,

2) Culture: it is difficult to grow the bacteria, even when using the best media available. The most recommended media are Nairobi, Johannesburg and enriched agar chocolate. The addition of vancomycin antibiotic in the enriched agar chocolate medium intends to inhibit the growth of gram positive bacteria, normally present in the collected clinical sample .^33,34,35

Management

In addition to local care, such as frequent washing with water and soap, the patient should be reexamined seven days after beginning of therapy and should show improvement of the symptoms and the lesion by then. The following drugs are indicated for treatment: Thiamphenicol 500 mg TID for 5 days; 36,37 Thiamphenicol granular 5 g single dose; ^38,39 Azythromycin 1 g PO single dose ⁴⁰; Ceftriaxone 250 mg intramuscular single dose 40, Erythromycin 500 mg QID for 7 days 40; Ciprofloxacin 500 mg single dose. ⁴⁰

• LYMPHOGRANULOMA VENEREUM

Lymphogranuloma venereum (LGV) is an infectious contagious disease of inflammatory and invasive nature of the urogenital tract that is caused by Chlamydia trachomatis. In many parts of the world, VLG has become an important cause of anogenital disease among men who have sex with other men ⁴¹.

LGV is caused by invasive serotypes L1, L2 and L3 of Chlamydia trachomatis in contrast with serotypes A-C of this agent, which cause ocular infection, such as trachoma, and the more common serotypes D-K that cause genital infections ⁴².

Epidemiology

LGV is a relatively rare disease in industrialized countries, but it is endemic in parts of Africa, Asia, South America and the Caribbean ⁴³.

The incidence of infection by Chlamydia trachomatis after sexual contact is unknown, but probably it is smaller than gonorrhea and canchroid. The peak of incidence of the infection is between the second and third decades of life, the most active period of the sexual life. The period of sexual transmissibility in infected men is about three weeks after the regression of the primary lesion. Among women, the period of transmission is unknown, but it may probably last for months, given that the cervix can remain indefinitely infected ⁴⁴.

Clinical Manifestations

The incubation period ranges from 3 to 30 days ⁴⁵. In the clinical course of LGV, three stages of the disease are identified: primary stage (initial phase and early lesions), secondary stage (affection of regional lymph nodes, named inguinal syndrome), and tertiary stage (late forms or sequels of the disease or anogenital lesions). Between two and three weeks after the primary lesion there are femoral or inguinal adenomegalias, normally unilateral, painful, with fluctuation that may lead to spontaneous rupture, with or without formation of fistulas.

Two adenomegalias separated by Poupart ligament are characteristics of this disease. Male homosexuals and women after sexual anal intercourse may develop hemorrhagic proctitis or proctocolitis in acute stages of LGV. Primary symptoms are anal pruritus, mucoid rectal secretion and localized pain. The clinical landmark of anorectal LGV is revealed next: rectal muco-purulent secretion ⁴⁴. Proctitis may generate diarrhea or constipation, and in classical proctitis, tenesmus is detected. The tertiary stage refers to late complications that affect the rectum and the genitals, including elephantiasis. These late complications are more common among women and are named esthiomene ⁴⁶.

Differential diagnosis

Differential diagnosis of LGV includes other sexually transmitted diseases such as syphilis, canchroid, gonococcal proctitis, ameba dysenteriae, Chron's disease, ulcerative rectocolitis, and anal carcinoma.

Laboratory Work Up

The diagnosis depends on serology or identification of Chlamydia trachomatis in appropriate clinical samples. Whenever possible, histopathological exam of the tissue samples collected for biopsy may collaborate for the diagnosis. Serology test for Complement Fixation (CF) is gender-specific and does not differentiate species of Chlamydia, such as Chlamydia trachomatis, Chlamydia psittaci and common respiratory pathogen Chlamydia pneumonia. Microimmunofluorescence test (MIF) may differentiate infections caused by different species of Chlamydia, but it has not been used as routine because it requires a fluorescence microscope and highly trained technicians. It may detect IgM and IgG species-specific antibodies. MIF with IgG title 1:128 strongly suggests the diagnosis of LGV. Thus, most serology tests do not differentiate the infection caused by different serotypes of Chlamydia trachomatis. 43 Chlamydia trachomatis may be isolated in tissue cultures, using cell strain HeLa0229 or McCoy cells, but this technique is not widely available.

Alternatively, Chlamydia trachomatis may be identified by direct microscopic fluorescence using a conjugate of monoclonal antibodies in the material collected from the blister or ulceration. This method requires fluorescence microscope as well and a highly trained technician to execute and interpret the test ⁴³.

Management

Tetracycline 250 mg PO QID or Doxycycline 100 mg PO BID, both for 21 days (first choice). Erythromycin 500 mg PO QID for 21 days (first choice for pregnant or breastfeeding women). ⁴⁵

Other drugs may be used, such as chloramphenicol, rifampicin and Thiamphenicol.

• DONOVANOSIS

Donovanosis is a chronic, progressive and indolent bacterial disease that affects preferably the skin and genital and perigenital mucosa. It is frequently associated with sexual transmission, but it has low infectivity.

Etiology

They are gram negative coccus bacilli that get stained more markedly in the extremities than in the center, encapsulated or not, intra-cytoplasmatic and immobile (Calymmatobacterium granulomatis). Shaped as rounded cocci they measure 0.02 to 0.2 µm in the bacillary form and 1 to 2.5 µm in length. ^47,48

Epidemiology

The disease is more common in African-descendant people and in low income population, who is not fully knowledgeable about hygiene. Its geographical distribution is curious, being endemic in tropical and subtropical countries such as Papua-New Guinea, South Africa (providences of KwaZuluNatal and Transvaal Oriental), part of India and Indonesia, and among Australian aborigines ⁴⁹.

It is a disease that affects almost exclusively adults in the age range 20-40 years. Cases in children are frequently associated with contact with affected adults, not necessarily by sexual abuse.

Clinical Manifestations

The incubation period is reported as being 1-360 days, but lesions that are induced in volunteers suggest a period of about 50 days. Man is the main repository ⁵⁰.

Clinical manifestation starts with papules or subcutaneous nodules that may progress with superficial ulceration. They grow slowly, without causing pain, and become more definite, granulomatous, with centrifugal and serpiginous character, easily bleeding. They may be self-inoculated and multiple. Typically, there is no adenitis in donovanosis. In addition to anal and perianal region, the other areas of extragenital involvement are: lips, gums, jugal mucosa, mandible, palate, pharynx, larynx, neck, nose, ophthalmic region, scalp, chest (infra-mammary sulci), axilla, abdomen, arms, legs, bones (especially the tibia). Oral lesions are the most frequent ones, and teeth losses indicate bone impairment ^{50, 51}. Dissemination to abdominal cavity, intestines, spleen, liver, lungs, uterus and ovaries has already been reported and it is more frequently seen in endemic areas.

Laboratory Work Up

Cytodiagnosis: Material should be collected preferably in areas of active granulation without secondary infection, to look for Donovan's corpuscles. Giemsa, Leishman and Wright staining techniques may be used.

In addition to clinical pathology exam, transmission electron microscopy may be used to assess the ultrastructural characteristics of K. granulomatis of different species. The culture of the agent is difficult and it is not available as a routine. The combined culture with mono-layer cells has been described using human monocytes, Hep-2 cells and peritoneal macrophages of mice 52. The gene detection technique using polymerase chain reaction (PCR) that enables reclassification of donovanosis agent has its diagnostic application restricted to programs to eradicate the disease ^{53, 54}.

Management

There is no consensus about the best management approach to donovanosis.

The following therapeutic regimes are recommended: 1) Azythromycin 1 g PO in the first day, followed by 500 mg PO/day or Doxycycline 200 mg PO/day up to clinical cure. 2) Doxycycline 200 mg PO/day up to clinical cure. 3) Erythromycin 2 g PO/day up to clinical cure. 4) Tetracycline 2 g PO/day up to clinical cure. 5) Sulfamethoxazole/Trimethoprim (400/800) 2 pills PO twice a day for at least 14 days. Other antibiotics may also be used with satisfactory therapeutic responses, such as ceftriaxone, norfloxacin, trovofloxacin and Thiamphenicol ^{49,50,55,56,57}. To pregnant patients and positive HIV subjects, we should consider the addition of aminoglycoside since the beginning of treatment.

Essential complementary actions

They include the following general measures:

1) To counsel and provide tests for anti-HIV, VDRL serology and hepatitis B and C;
2) To vaccinate against hepatitis B if the patient is younger than 30 years;
3) To suspend sexual intercourse until treatment is finished and symptoms have disappeared;
4) To emphasize constant use of condoms.

If it is not possible to define the correct etiological diagnosis of the process, it is recommended to use the syndromic approach advocated by the Ministry of Health, as shown below.

Syndromic approach in genital ulcers – Flow chart of genital ulcers (Figure 1).⁵⁶

 

 

For the first episode of genital herpes, start treatment as early as possible with Acyclovir 200 mg, 4/4 h, five times a day for 7 days or 400 mg PO, TID for seven days OR Valacyclovir 1 g PO BID for 7 days OR Famciclovir 250 mg PO, TID for seven days. In cases of recurrent genital herpes, start early management with Acyclovir 400 mg PO, TID for 5 days OR Valacyclovir 500 mg PO, BID for five days OR Famciclovir 125 mg PO, BID for 5 days.

In the absence of vesicle lesions, we recommended preventive treatment for the two most frequent causes of genital ulcers – primary syphilis and canchroid, with Penicillin G Benzathine 2.4 million IU, intramuscular, single dose + azythromycin 1 g PO single dose OR ciprofloxacin 500 mg PO, BID for 3 days OR erythromycin estearate 500 mg PO, QID for 7 days.

If lesions last more than 4 weeks, start suspecting of donovanosis, lymphogranuloma venereum or neoplasm. Refer to or perform a biopsy for investigation. Simultaneously, start treatment for donovanosis - Doxycycline 200 mg/day PO until clinical cure OR azythromycin 1 g PO single dose, followed by 500 mg PO/day for 3 weeks.

 

REFERENCES

1. World Health Organization. Guidelines for the management of sexually transmitted infection. Geneva: Switzerland; 2003. 89p.         [ Links ]

2. World Health Organization. Global strategy for prevention and control of sexually transmitted infections:2006 –2015. Geneva: Switzerland; 2007. 60p.         [ Links ]

3. Gutman L. Gonococcal diseases in infants and children. In: Holmes KK, Mardh P-A, Sparling PF, Weisner PJ, Cates W Jr, Lemon SM, et al., eds. Sexually transmitted diseases. New York: McGraw-Hill Inc; 1999. p.1146.         [ Links ]

4. Karinen L, Pouta A, Hartikainen AL, Bloigu A, Paldanius M, Leinonen M, et al. Association between Chlamydia trachomatis antibodies and subfertility in the Northern Finland Birth Cohort 1966 (NFBC 1966), at the age of 31 years. Epidemiol Infect. 2004;132:977-84.         [ Links ]

5. Mardh PA. Tubal factor infertility, with special regard to chlamydial salpingitis. Curr Opin Infect Dis. 2004;17:49-52.         [ Links ]

6. Eley A, Pacey AA, Galdiero M, Galdiero M, Galdiero F. Can Chlamydia trachomatis directly damage your sperm? Lancet Infect Dis. 2005;5:53-7.         [ Links ]

7. Fleming DT, Wasserheit JN. From epidemiological synergy to public health policy and practice: the contribution of other sexually transmitted diseases to sexual transmission of HIV infection. Sex Transm Infect. 1999;75:3-17.         [ Links ]

8. Cohen MS, Hoffman IF, Royce RA, Kazembe P, Dyer JR, Daly CC, et al. Reduction of concentration of HIV-1 in semen after treatment of urethritis: implications for prevention of sexual transmission of HIV-1. AIDSCAP Malawi Research Group. Lancet. 1997;349:1868-73.         [ Links ]

9. Ghys PD, Fransen K, Diallo MO, Ettiègne-Traoré V, Coulibaly IM, Yeboué KM, et al. The associations between cervicovaginal HIV shedding, sexually transmitted diseases and immunosuppression in female sex workers in Abidjan, Côte d'Ivoire. AIDS. 1997;11:85-93.         [ Links ]

10. Sewankambo N, Gray RH, Wawer MJ, Paxton L, McNaim D, Wabwire-Mangen F, et al. HIV-1 infection associated with abnormal vaginal flora morphology and bacterial vaginosis. Lancet. 1997;350:546-50.         [ Links ]

11. Klebanoff MA, Hauth JC, MacPherson CA, Carey JC, Heine RP, Wapner RJ, et al. Time course of the regression of asymptomatic bacterial vaginosis in pregnancy with and without treatment. Am J Obstet Gynecol. 2004;190:363-70.         [ Links ]

12. Leitich H, Bodner-Adler B, Brunbauer M, Kaider A, Husslein P. Bacterial vaginosis as a risk factor for preterm delivery: a meta-analysis. Am J Obstet Gynecol. 2003;189:139-47.         [ Links ]

13. Ministério da Saúde. Manual de controle das doenças sexualmente transmissíveis. 4 ed. Brasília: UNESCO; 2006. 142p.         [ Links ]

14. Morton RS. The treponematoses. In.: Rook A, Wilkinson DS, Ebling TJG, Champion RH, Burton L, eds. Textbook of Dermatology. 4th ed. Oxford: Blackwell Scientific Publications; 1986.         [ Links ]

15. Rhodes AR, Luger AFH. Syphilis and treponematoses. In.: Fitzpatrick TB, Eisen AZ, Wolf K, Freedberg JM. Austen KF, eds. Dermatology in General Medicine. New York: Mcgraw Hill; 1987.         [ Links ]

16. Rivitti EA. Sífilis adquirida. In: Belda Jr W. Doenças sexualmente transmissíveis. São Paulo: Atheneu; 1999. p.9-21.         [ Links ]

17. Nogueira JM, Camarena JJ. Diagnóstico microbiológico de la sífilis del adulto y de la sífilis congênita. In: Vilata JJ, ed. Enfermedades de transmision sexual. Barcelona: JR Prous Editores; 1993.         [ Links ]

18. Centers for Disease Control and Prevention. Azithromycin treatment failures in syphilis infections – San Francisco, California; 2002-2003. MMWR Morb Mortal Wkly Rep. 2004;53:197-8.         [ Links ]

19. Holmes KK. Azithromycin versus penicillin G benzathine for early syphilis. N Engl J Med. 2005;353:1291-3.         [ Links ]

20. Passos MRL, Benzaken AS, Coelho ICB, Rodrigues GHS, Dutra JC, Varella R, et al. Estudo de equivalência entre azitromicina e penicilina G benzatina no tratamento da sífilis. DST J Bras Doenças Sex Transm. 2004;16:52-66.         [ Links ]

21. Olmos L, Vázquez JA. Infecciones gonocócicas. In: Vilata JJ, ed. Enfermedades de transmission sexual. Barcelona: JR Prous Editores; 1993.         [ Links ]

22. Siqueira LFG. O laboratório nas doenças sexualmente transmissíveis. Bol Inf Union. 1984;9:4.         [ Links ]

23. Martins Jr JE, Jackson RL. A biological environment chamber for the culture of Neisseria gonorrhoeae. J Am New Dis Anal. 1975;2:28-30.         [ Links ]

24. Siqueira LFG. O laboratório nas doenças sexualmente transmissíveis. Bol Inf Union. 1985;10:4-5.         [ Links ]

25. Siqueira LFG, Melles HHB. Uretrites gonocócicas e não gonocócicas – diagnóstico laboratorial. In: Belda Jr W, ed. Doenças sexualmente transmissíveis. São Paulo: Atheneu; 1999. p.59-69.         [ Links ]

26. Bauer HM, Mark KE, Samuel M, Wang SA, Weismuller P Moore D, et al. Prevalence of and associated risk factors for fluoroquinolone-resistant Neisseria gonorrhoeae in California, 2000-2003. Clin Infect Dis. 2005;41:795-803.         [ Links ]

27. Center for Disease Control and Prevention. Fluoroquinolone-resistance in Neisseria gonorrhoeae, Hawaii, 1999 and decreased susceptibility to azithromycin in N. gonorrhoeae. Missouri, 1999. MMWR Morb Mortal Wkly. 2000;49:833-7.         [ Links ]

28. Ng LK, Sawatzky P, Martin IE, Booth S. Characterization of ciprofloxacin resistance in Neisseria gonorrhoeae isolates in Canada. Sex Transm Dis. 2002;29:780-8.         [ Links ]

29. Belda Jr W, Velho PENF, Arnone M, Fagundes LJ. Emergence of fluoroquinolone-resistant Neisseria gonorrhoeae in São Paulo - Brazil. Braz J Microbiol. 2007;38:293-5.         [ Links ]

30. Ronald AR, Albritton WC. Chancroid and Haemophilus ducreyi. In: Holmes KK, Mardh PA, Sparling PF, ed. Sexually transmitted diseases. New York: McGraw-Hill Book Co; 1984. p.385-93.         [ Links ]

31. Belda Jr W, Siqueira LFG. Cancro Mole. In: Doenças sexualmente transmissíveis. Belda Jr W, ed. São Paulo: Atheneu; 1999. p.47-51         [ Links ]

32. Morse AS. Chancroid and haemophilus ducreyi. Clin Microbiol Rev. 1989;2:137-57.         [ Links ]

33. Hammond GW, Lian CJ, Ronald AR. Comparison of specimens collections and laboratory techniques for isolation of Haemophilus ducreyi. J Clin Microbiol. 1978;39-43.         [ Links ]

34. Hannah P, Green Wood JR. Isolation and rapid identification of Haemophilus ducreyi. J Clin Microbiol. 1982;16:861-4.         [ Links ]

35. Shawar R, Sepulveda J, Clarrige JE. Use of the rapl D-ANA system and sodium polyanetholesulfonate disk susceptibility testing in identifying Haemophilus ducreyi. J Clin Microbiol. 1990;28:108-11.         [ Links ]

36. Belda W, Santos Jr MFQ, Belda Jr W, Siqueira LFG, Fagundes LJ, Lombardi C. Novos rumos no tratamento do cancro mole – Experimentação clinica com thiamfenicol. An Bras Dermatol. 1984;59:147-9.         [ Links ]

37. Belda Jr W, Santi CG, Mirandez AA. Tratamento do cancróide com tianfenicol. Rev Bras Med. 1985;42:204-5.         [ Links ]

38. Belda W, Santos Jr MFQ, Siqueira LFG, Belda Jr W. Emprego do tianfenicol granulado em dose única de 5 g no tratamento do cancro mole. An Bras Dermatol. 1984;59:209-12.         [ Links ]

39. Belda Jr W, Siqueira LF, Fagundes LJ. Thiamphenicol in the treatment of chancroid. A study of 1128 cases. Rev Inst Med Trop Sao Paulo. 2000;42:133-5.         [ Links ]

40. Centers for Diseases Control and Prevention. Sexually transmitted diseases treatment guidelines. MMWR Morb. Mortal Wkly. 1993;42:20-2.         [ Links ]

41. van Hal SJ, Hillman R, Stark DJ, Harkness JL, Marriott D. Lymphogranuloma venereum: an emerging anorectal disease in Australia. Med J Aust. 2007;187:309-10.         [ Links ]

42. Herring A, Richens J. Lymphogranuloma venereum. Sex Transm Inf. 2006;82 Suppl 4:iv23-5.         [ Links ]

43. Mabey D, Peeling RW. Lymphogranuloma venereum. Sex Transm Infect. 2002;78:90-2.         [ Links ]

44. Ahdoot A, Kotler DP, Suh JS, Kutler C, Flamholz R. Lymphogranuloma venereum in human immunodeficiency virus-infected individuals in New York City. J Clin Gastroenterol. 2006;40:385-90.         [ Links ]

45. Da Costa JB, Domingues D, Castro R, Exposto F. Genital ulcers caused by sexually transmitted diseases: current therapies, diagnosis and their relevance in HIV pandemy. Acta Med Port. 2006;19:335-42.         [ Links ]

46. Gupta S, Ajith C, Kanwar AJ, Sehgal VN, Kumar B, Mete U. Genital elephantiasis and sexually transmitted infections - revisited. Int J STD AIDS. 2006;17:157-65.         [ Links ]

47. Galarza C. Donovanosis. Dermatol Peru. 2000;10:35-8.         [ Links ]

48. Fonseca A, Souza EM. Donovanose in Dermatologia Clínica. Rio de Janeiro: Guanabara Koogan; 1984. p.167-9.         [ Links ]

49. Department of Health and Human Services. Centers for Disease Control and Prevention. Granuloma inguinale (donovanosis) in sexually transmitted diseases treatment guidelines. MMWR Morb Mortal Wkly. 2006;55:20-1.         [ Links ]

50. O'Farrell N. Donovanosis. Sex Transm Infect. 2002;78:452-7.         [ Links ]

51. Veeranna S, Raghu TY. Oral Donovanosis. Int J STD AIDS. 2002;13:855-6.         [ Links ]

52. Kaimal S, Thappa DM. Methods of specimen collection for the diagnosis of STIs. Indian J Dermatol Venereol Leprol. 2007;73:129-32.         [ Links ]

53. Richens J. Donovanosis (granuloma inguinale). Sex Transm Infect. 2006;82(Suppl4):iv21-2.         [ Links ]

54. Mackay IM, Harnett NJ, Bastian I, Sriprakash KS, Siebert D, Sloots TP. Detection and discrimination of herpes simplex viruses, Haemophilus ducreyi, Treponema pallidum, and Calymmatobacterium (Klebsiella) granulomatis from genital ulcers. Clin Infect Dis. 2006;42:1431-8.         [ Links ]

55. Jardim ML, Melo ZO. Tratamento da donovanose com o tiamfenicol. An Bras Dermatol. 1990;65:93-4.         [ Links ]

56. Ministério da Saúde. Secretaria de Vigilância em Saúde. Programa Nacional de DST/AIDS. Donovanose in manual de controle de Doenças Sexualmente Transmissíveis: DST. 4 ed. Brasília, DF: Série Manuais; 2006. p.68:50.         [ Links ]

57. Belda W Jr, Velho PE, Arnone M, Romitti R. Donovanosis treated with thiamphenicol. Braz J Infect Dis. 2007;11:388-9.         [ Links ]

 

 

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How to cite this article: Belda Jr. W, Shiratsu R, Pinto V. Abordagem nas doenças sexualmente transmissíveis. An Bras Dermatol. 2009;84(2):151-59.