Sexually Transmitted Diseases Introduction


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Sexually Transmitted Diseases Introduction

  1. 1. Sexually transmitted diseases INTRODUCTION Sexually transmitted diseases (STDs) have been described as ―hidden epidemics,‖ comprising 5 of the top 10 most frequently reported diseases in the United States. An estimated 12 million new cases of STDs occur each year in the U.S., which has the highest rate among all developed countries. In the developing world, STDs are an even greater public health problem as
  2. 2. the second leading cause of healthy life lost among women between 15 and 44 years of age. The STD epidemic in the developing world, where atypical presentations, drug resistant organisms, and co-infections (especially with HIV) are common, can have a potentially larger impact on our population due to increased international travel and migration. The health consequences of STDs occur primarily in women, children and adolescents especially among racial/ethnic minority groups. In the
  3. 3. U.S., more than a million women are estimated to experience an episode of pelvic inflammatory disease (PID) per year. The number of ectopic pregnancies has been estimated as 1 in 50, and approximately 15% of infertile American women are thought to have tubal inflammation as a result of PID. Adverse outcomes of pregnancy due to untreated STDs include neonatal ophthalmia, neonatal pneumonia, physical and mental developmental disabilities, and fetal
  4. 4. death from congenital syphilis. Among all age groups, adolescents (10- to 19-year-olds) are at greatest risk for STDs, because of a greater biologic susceptibility to infection and a greater likelihood of having multiple sexual partners and unprotected sexual encounters. Minority groups such as African- Americans and Hispanic Americans have the highest rates of STDs. STDs and human immunodeficiency virus (HIV) infections share common risk factors for transmission. Genital
  5. 5. ulcer disease increases the risk of HIV acquisition and transmission by 2- to 5- fold; urethritis and cervicitis increase the risk by 5-fold. Treatment and control of STDs at the population level may result in decreases in HIV incidence among populations with high rates of STDs. STD control should be considered an important component of HIV prevention in public health as well as clinical practice. Effective clinical management of STDs
  6. 6. should include screening of sexually active individuals with appropriate laboratory tests, providing definitive diagnosis and treatment, client- centered risk reduction and education, and evaluation and treatment of partners. Screening of asymptomatic patients is of utmost importance in order to prevent sequelae. Screening for STDs among sexually active women, especially pregnant women, is essential since roughly 70% of chlamydial infections and 50% of
  7. 7. gonococcal infections are asymptomatic in this population. Unfortunately, the barriers to effective STD prevention are multiple, including the biological characteristics of STDs, lack of public awareness regarding STDs, inadequate training of health professionals, and sociocultural norms related to sexuality that can lead to misperception of recognized risk and consequences. GENITAL ULCER Figure 1
  8. 8. DISEASES: Reported cases of OVERVIEW syphilis by stage of infection: A genital ulcer is defined United States, as a breach in the skin or 1941–2006 CDC mucosa of the genitalia. Genital ulcers may be single or multiple and may be associated with inguinal or femoral lymphadenopathy. Sexually transmitted pathogens that manifest as genital ulcers are Herpes simplex virus (HSV), Treponema pallidum, Haemophilus ducreyi, L-serovars of Chlamydia trachomatis and Calymmatobacterium
  9. 9. granulomatis. Genital ulcer diseases facilitate enhanced HIV transmission among sexual partners. In the presence of genital ulcers, there is a 5-fold increase in susceptibility to HIV. In addition, HIV infected individuals with genital ulcer disease may transmit HIV to their sexual partners more efficiently. HSV is the most common cause of genital ulcers in the US among young sexually active persons. T. pallidum is the next most common
  10. 10. cause of GUD, and should be considered in most situations despite the decline in cases of syphilis nationwide (figure 1). Chancroid, caused by H. ducreyi has infrequently been associated with cases of GUD in the US, but has been isolated in up to 10% of genital ulcers diagnosed from STD clinics in Memphis and Chicago. Chancroid is the most common genital ulcer disease in many developing countries. Lymphogranuloma venereum or LGV caused by L-serovars of
  11. 11. C. trachomatis and granuloma inguinale (donovonosis) caused by Calymmatobacterium granulomatis are endemic in tropical countries and should be considered in the differential diagnosis of genital ulcers from a native in the tropics or in travelers. The prevalence of pathogens that cause GUD varies according to the geographic area and the patient population. A single patient can have genital ulcers caused by more than one pathogen. Despite laboratory
  12. 12. testing, approximately 25% of genital ulcers will have no identifiable cause. There is considerable overlap in the clinical presentation of herpes, primary syphilis and chancroid, the three most common causes of genital ulcers in the U.S. Inguinal lymphadenopathy is present in about 50% of the patients with genital ulcer diseases. Genital herpes typically presents with multiple, shallow ulcers and bilateral lymphadenopathy. Primary syphilis can
  13. 13. usually be differentiated from genital herpes by the presence of a single deep, defined ulcer with induration. A distinction may be made between syphilis and chancroid, which commonly presents with a painful, undermined ulcer with a purulent base and tender lymphadenopathy unlike syphilis. The cause of genital ulcers cannot be based on clinical findings alone. Diagnosis based on the classic presentation is only 30% to 34% sensitive but 94% to 98% specific.
  14. 14. Therefore, diagnostic testing should be performed when possible. Serologic testing for syphilis should be considered even when lesions appear atypical. If available, darkfield examination or direct immunofluorescence on the lesion material should be performed as the definitive tests for T. pallidum. Genital herpes can be diagnosed in the presence of typical lesions and/or positive serology, but herpes culture should be performed when the
  15. 15. diagnosis is uncertain. GENITAL HERPES SIMPLEX Figure 2 Transmission Genital herpes simplex electron virus infection affects up micrograph of to 60 million people in herpes simplex the U.S. and can be virus caused by both herpes CDC/Dr. Erskine simplex virus type 1 Palmer (HSV-1) and type 2 (HSV-2) (figure 2). The Figure 3 seroprevalence of HSV-2 Genital herpes — has increased over the Initial visits to past three decades to physicians’ 22% among individuals offices: United 15 to 74 years of age States, 1966–2006 (figure 3). Behavioral factors correlated with Figure 4 seroprevalence include
  16. 16. Genital herpes on cocaine use, multiple the penis © sexual partners and early Australian Herpes sexual activity. Most Management Forum patients (40%) infected with genital HSV-2 and two-thirds of the patients Figure 5 infected with HSV-1 are Genital herpes on asymptomatic. Hence the penis © genital herpes is often Australian Herpes acquired from Management Forum individuals who have never been clinically Figure 6 diagnosed with herpes. Classical primary Transmission of HSV genital herpes between sexual partners affecting the vulva. has been estimated at This clinical picture 12% per year but can be is seen in a minority as high as 30% among of cases © women who are partners Australian Herpes of infected men. Women have a 5% to 10% higher
  17. 17. Management Forum seroprevalence of HSV-2 than men, suggesting the increased risk of acquisition. Genital lesions acquired through sexual contact are typically caused by HSV-2 (figure 4-6), while oropharyngeal lesions acquired through non-genital personal contact are most commonly due to HSV- 1. However, both viruses can cause genital and oral infections. HSV-2 causes the vast majority of genital herpes in the U.S., but HSV-1 accounts for 5% to 30%
  18. 18. of first-episode cases. After mucosal or cutaneous contact, HSV replicates in the dermis and epidermis and ascends through the sensory nerve fibers to the dorsal root ganglia. Once established in the sensory ganglia, the virus remains latent for life with periodic reactivation and spreads through the peripheral sensory nerves to the mucocutaneous sites. Most patients seropositive for HSV-2 have subclinical, undiagnosed genital
  19. 19. herpes. About one fourth of the patients with first episode of genital herpes have positive HSV-2 serology suggesting prior asymptomatic infection. Thus, the first clinical episode of genital herpes could reflect either primary infection or a first recognized episode of a past infection. Primary infection with HSV-2 is characterized by a prodrome of systemic symptoms including fever, chills, headache and malaise. Pain and paresthesias around the outbreak site precede the appearance
  20. 20. of lesions by 12 to 48 hours. The hallmark of genital herpes consists of grouped vesicles or pustules that lead to shallow ulcers. Atypical lesions of genital herpes include linear fissures of the vulva, cervical ulcerations, vaginal discharge, papules and crusts. Patients may have accompanying tender inguinal lymphadenopathy. Urethritis, rectal or perianal symptoms may be present if there is urethral or rectal involvement. Immunocompromised
  21. 21. patients may present with extensive perianal and rectal manifestations. Extragenital manifestations of HSV include ulcerative lesions of the buttock, groin, thighs, pharyngitis, aseptic meningitis, transverse myelitis and sacral radiculopathy. Primary infection with HSV-1 is manifested by genital ulcers in about one-third of patients. Another one-third may present with orolabial lesions or pharyngitis and the remaining patients are
  22. 22. asymptomatic. The genital lesions caused by HSV-1 are indistinguishable from those of HSV-2. Recurrent genital herpes is usually a milder syndrome than primary infection. The recurrence rate of genital herpes due to HSV-2 is much more frequent than due to HSV-1. Similarly, the recurrence rate of orolabial infection due to HSV-1 is much more frequent than due to HSV-2.
  23. 23. SYPHILIS Figure 7 Treponema pallidum Histopathology (figure 7), a spirochete, showing Treponema is a major public health pallidum spirochetes concern because of the in testis of complications of experimentally untreated disease. In the infected rabbit. United States, the rates Modified Steiner of primary and silver stain. CDC/Dr. secondary syphilis have Edwin P. Ewing, Jr. declined significantly in the past thirty years (figure 20-21). Some Figure 8 racial and ethnic groups Clinical such as African presentation of Americans, Native syphilis Americans and Alaskan natives continue to have disproportionately high Figure 9 rates of syphilis (figure Primary syphilis. 22). The incidence of
  24. 24. Primary chancre on primary and secondary the glans The syphilis in non-Hispanic University of Texas blacks remains high at Medical Branch 17 cases per 100,000 persons which is 34 times greater than the Figure 10 rate for non-Hispanic Primary syphilis. A whites. In the U.S., the vulvar chancre and Southeast has the highest condylomata rates of syphilis perhaps acuminata The due to poor access to University of Texas health care, Medical Branch unemployment and the stigma associated with Figure 11 discussion of STDs Primary Syphilis (figure 21). Untreated Bristol Biomedical syphilis infection in Archive © University pregnancy can lead to of Bristol. Used with congenital syphilis in permission 70% of the cases. The prevalence of
  25. 25. syphilis in HIV infected Figure12 individuals ranges from This photograph 14 to 22%. Syphilis, shows a close-up along with other genital view of keratotic ulcer diseases, facilitates lesions on the transmission of HIV. A palms of this syphilitic chancre not patient’s hands only increases due to a secondary transmission of HIV by syphilitic infection causing a breakdown of CDC the skin, but also increases the number of inflammatory cells receptive to HIV. The Figure 13 transmission rate of This patient presented with a syphilis from an infected sexual partner has been secondary estimated at 30%. syphilitic rash covering his back T. pallidum is an representing the exclusive human systemic spread of pathogen that can be
  26. 26. the Treponema visualized by dark field pallidum bacteria. microscopy. It appears as These a spiral bacterium with papulosquamous corkscrew motility. After lesions often inoculation through appear as rough, abraded skin or mucus red, or reddish membranes it attaches to brown spots that the host cells and usually form on disseminates within a the palms of the few hours to the regional hands, soles of the lymph nodes and feet, the chest and eventually to the internal back, but can organs and the central nervous system. manifest upon other regions of The clinical presentation the body. CDC of syphilis is divided into primary, secondary, early latent, late latent Figure 14 and tertiary stages based Secondary syphilis - on infectiousness and for mouth mucosa purposes of therapeutic
  27. 27. Bristol Biomedical decisions and disease- Archive © University intervention strategies of Bristol. Used with (figure 8). permission Primary syphilis After an incubation Figure 15 period of 2 to 6 weeks This patient following exposure, a presented with a papule develops at the gumma of nose site of inoculation, which due to a long will then ulcerate into standing tertiary the characteristic syphilitic syphilitic chancre (figure Treponema 9-11). The classic pallidum chancre is a painless, infection. Without indurated ulcer with treatment, an well-defined borders and infected person a clean base. A chancre still has syphilis can develop on the oral even though there (figure 11) or anorectal are no signs or mucosa as well as in the symptoms. It genital mucosa (figure 9-
  28. 28. remains in the 10). Prior application of body, and it may topical antibiotics or the begin to damage use of systemic the internal antimicrobials, may organs, including change the typical the brain, nerves, appearance of the lesion. eyes, heart, blood Non-tender vessels, liver, lymphadenopathy may be present. bones, and joints. CDC Secondary syphilis Approximately 60% to 90% of patients with Figure 16 untreated primary A photograph of a syphilis will develop patient with manifestations of tertiary syphilis secondary syphilis. resulting in Secondary syphilis is a gummas seen here systemic disease that on the nose. This results from patient presented dissemination of the with tertiary treponemes. Systemic
  29. 29. syphilitic gummas symptoms include of the nose generalized mimicking basal lymphadenopathy, fever, cell carcinoma. headache, sore throat and The gummatous arthralgias. Numerous tumors are benign clinical manifestations and if properly occur 4 to 10 weeks after treated, will heal the chancre disappears and the patient (or 2 to 6 months after will recover in sexual contact). These most cases. CDC involve dermatologic (figure 12-13), central nervous system (aseptic Figure 17 meningitis, cranial Gummas, or soft neuropathy), ocular ‖gummy‖ tumors, (iritis, uveitis or are seen here on conjunctivitis), hepatic this liver specimen (hepatitis) and renal due to tertiary (immune complex syphilis. In this glomerulonephritis) image two systems.
  30. 30. gummas are seen The most common in this liver manifestation of specimen. At the secondary syphilis is the lower periphery, skin rash characterized one is seen as a by macules and papules firm, white, distributed on the head somewhat and neck, the trunk and irregular nodule. extremities including the The other is palms and soles. The hemorrhagic and rash may be confused largely necrotic. with pityriasis rosea, CDC psoriasis or drug eruption. Condyloma lata are large, raised whitish lesions that are seen in warm, moist areas which occur before or soon after the rash and are highly infectious. These need to be distinguished from condyloma
  31. 31. acuminata of human papillomavirus infections. Mucous patches are shallow, painless ulcerations that can be found on the oral or anorectal mucosa. Latent syphilis Latent syphilis is defined by reactive serology in the absence of clinical signs or symptoms. After resolution of early (primary or secondary) syphilis, mucocutaneous lesions can recur for up to 1 to 2 years in 25% of the patients. Early latent syphilis is defined as the first year from the suspected exposure when
  32. 32. the patient is still at risk for relapse of the manifestations of secondary syphilis. Late latent syphilis is defined as a time period of one year or more after the primary infection and before the onset of tertiary syphilis. Tertiary syphilis Tertiary syphilis or late syphilis can occur after primary, secondary or latent syphilis. In the pre-antibiotic era, 25% to 40% of all patients with syphilis developed tertiary syphilis. It may present with cardiovascular
  33. 33. manifestations, gummatous lesions or CNS disease. Cardiovascular manifestations include aortic aneurysms, aortic insufficiency or coronary stenosis. Gummatous lesions are focal inflammatory areas that can involve any organ (e.g. the liver, figure 17) but usually involve the skin (figure 15-16) and bones. Neurological disease during the tertiary stage presents as general paresis or tabes dorsalis. Neurosyphilis Infection of the CNS by
  34. 34. the treponemes can occur at any time during the course of syphilis infection. In 15% to 40% of patients with untreated primary and secondary syphilis, T. pallidum was found in the CSF by animal inoculation studies. Treponemal invasion of the CNS during untreated early syphilis may have the following outcomes: spontaneous resolution, asymptomatic neurosyphilis (at any time during syphilis infection), acute syphilitic meningitis (in the first year),
  35. 35. meningovascular syphilis (5 to 12 years after primary infection), and parenchymatous neurosyphilis (18 to 25 years after primary infection). Diagnosis of syphilis The definitive diagnosis of primary syphilis is made by visualization of treponemes by dark field microscopy or by direct immunofluorescence (figure 18-19). The yield of these tests is high provided that (1) there is no prior topical or systemic antibiotic treatment and that (2) the examination is done by
  36. 36. an experienced person. To obtain a specimen, the lesion can be gently abraded with gauze. The serous exudate is then applied to a glass slide. Direct or indirect immunofluorescence is recommended for oral lesions as non- pathogenic treponemes may be confused with T. pallidum on darkfield microscopy. Serological tests are the most widely used tests for syphilis and are categorized into treponemal and non- treponemal tests. The non-treponemal tests
  37. 37. detect anti-cardiolipin antibodies and include RPR (Rapid Plasma Reagin), Toluidine Red Unheated Serum Test (TRUST) and Reagin Screen test (RST), VDRL (Venereal Disease Research Laboratory) and Unheated Serum Reagin (USR). The sensitivity of the non-treponemal tests varies from 70% in primary syphilis to 100% in secondary syphilis. These tests are advantageous because they are inexpensive, applicable for screening purposes, and their titers
  38. 38. tend to correlate with disease activity. However, confirmation of the non-treponemal tests is necessary with the specific treponemal tests. The FTA-ABS (fluorescent treponemal antibody absorption test), the MHA-TP (microhemagglutination assay) and the TP-PA (particle agglutination assay) are 80% to 100% sensitive depending on the stage of disease. However, a positive MHA-TP alone does not establish the diagnosis of primary syphilis in a patient with genital
  39. 39. ulcer, since the MHA-TP can remain positive for life. Patients suspected of having primary syphilis with a negative darkfield examination, negative RPR and MHA- TP should have follow up serologies in 2 weeks, since detection by direct microscopy depends on specimen collection and the expertise of the microscopist, and since serologies can be negative in the first two weeks after a chancre appears. False-positive non-treponemal and treponemal tests can occur in a variety of
  40. 40. disease conditions including acute viral infections, autoimmune diseases, vaccination, drug addiction and malignancy. Latent syphilis is diagnosed when a patient has a reactive RPR and a confirmatory test in the absence of signs or symptoms. The duration of disease from exposure can be estimated if the patient can recall specific signs or symptoms consistent with primary syphilis, has a history of exposure or previous serology. However, the usual scenario is that of a
  41. 41. patient with positive serology and no clinical history suggestive of syphilis. Figure 18 Dark field photomicrograph of Treponema pallidum bacteria. Nichol's strain of T. pallidum from a rabbit testicle, and stained by fluorescent antibody technique CDC Figure 19 Treponema pallidum, IFA stain for Fluorescent Treponemal Antibody
  42. 42. (FTA) antigen. CDC Figure 20 Primary and secondary syphilis — Rates: Total and by sex: United States, 1987–2006 Figure 21 Primary and secondary syphilis — Rates by state: United States and outlying areas, 2006 Figure 22 Primary and secondary syphilis — Rates by race/ethnicity: United States, 1997–2006 Figure 23
  43. 43. Primary and secondary syphilis—Age- and sex- specific rates: United States, 2006 Figure 24 CHANCROID This direct smear The incidence of microscopic exam chancroid has been revealed the steadily decreasing in the presence of US. The disease is Haemophilus endemic in some areas ducreyi indicative (New York City and of a chancroid Texas) and tends to infection. CDC occur as outbreaks in other parts of the US. Figure 25 Chancroid is a major A chancroid ulcer cause of genital ulcer on the posterior diseases in the tropics. vaginal wall in a
  44. 44. 25 year old female Haemophilus ducreyi is a due to gram-negative rod (figure 24) that requires Haemophilus ducreyi bacteria. abraded skin to penetrate The first sign of a the epidermis and cause chancroid infection. It is spread by infection is sexual contact but usually the autoinoculation of other appearance of one sites can occur. or more sores, or After an incubation raised bumps on period of 3 to 10 days, a the genital organs, papule surrounded by surrounded by a erythema develops at the narrow red border. site of inoculation (figure Eventually 27). The papule evolves rupturing, these to a pustule over 24 to 48 lesions reveal a hours and then ulcerates painful, open, pus- (figure 25-26). Men tend filled wound. to note significant pain CDC with the ulcer whereas women may not notice
  45. 45. the ulcer. About 50% of Figure 26 patients note tender This patient unilateral inguinal presented with a adenopathy (buboes). chancroid lesion Buboes (figure 29-30) of the groin and can become fluctuant, penis affecting the undergo spontaneous ipsilateral inguinal drainage (figure 28) and lymph nodes. First result in large ulcers. signs of infection Systemic symptoms are typically appear 3 usually not a feature of to 5 days after chancroid. exposure, Chancroid is a clinical although diagnosis based on: symptoms can take up to 2 weeks (1) a tender painful ulcer to appear. In men, with ragged borders they are most (2) tender common at the lymphadenopathy base of the glans (3) negative darkfield (head) of the examination of the ulcer
  46. 46. penis, though they for T. pallidum (or can appear on the negative syphilis penis shaft. CDC serology obtained at least 7 days after onset of the ulcer) (4) a negative test for herpes simplex virus The presence of a painful ulcer along with tender lymphadenopathy with suppuration is highly suspicious for chancroid. A definitive diagnosis is made by culture of H. ducreyi but appropriate culture media are not widely available.
  47. 47. Figure 27 A differential diagnosis revealed that this was a chancroidal lesion, and not a suspected syphilitic lesion, or chancre. CDC Figure 28 This patient presented with a chancroid showing signs of a ruptured inguinal lymph node. The ulcers usually begin as tender, elevated bumps, or papules, that become pus-filled, open sores with eroded or ragged edges. Ruptured buboes, or swollen lymph nodes, are susceptible to
  48. 48. secondary bacterial infections. CDC Figure 29 This 52yr old female patient presented with a chancroid and spontaneous rupture of a left inguinal bubo. Chancroid is characterized by painful genital ulcers, which are associated with a unilateral painful inguinal lymphadenopathy in 50% of those infected. Left untreated, suppurative, spontaneously rupturing
  49. 49. buboes occur in approximately 25% of cases. CDC Figure 30 This photograph shows that a chancroid infection has spread to the inguinal lymph nodes, which have enlarged forming buboes. Caused by the sexually transmitted bacterium, Haemophilus ducreyi, in about half of the untreated chancroid cases, the lymph nodes in the groin develop into buboes that can enlarge until they burst through the overlying skin. CDC
  50. 50. VAGINAL Figure 31 DISCHARGE This was a case of (VAGINITIS): trichomonas OVERVIEW vaginitis revealing a copious purulent Vaginal discharge is a frequent gynecologic discharge emanating from complaint, accounting for more than 10 million the cervical os. office visits annually. Trichomonas Physiologic vaginal vaginalis, a flagellate, is the discharge is white, odorless and increases most common during midcycle due to pathogenic estrogen. Abnormal protozoan of vaginal discharge may humans in result from vaginitis or industrialized vaginosis, cervicitis and countries. This
  51. 51. protozoan resides occasionally in the female endometritis. Vaginitis lower genital tract presents with an increase and the male in the amount, odor or urethra and color of discharge and prostate, where it may be accompanied by replicates by itching, dysuria, binary fission. dyspareunia, edema or CDC irritation of the vulva. The three most common causes of vaginal discharge are bacterial vaginosis or BV (40% to 50% of cases; associated with Gardnerella vaginalis and overgrowth of various bacteria including anaerobes), vulvovaginal candidiasis (20% to 25% of cases) and
  52. 52. trichomoniasis (figure 31) (15% to 20% of cases). While trichomoniasis is a sexually transmitted disease, bacterial vaginosis occurs in women with high rates of STDs as well as in women who have never been sexually active. Vaginitis may also result from infection with Group A streptococci, Staphylococcus aureus toxic shock syndrome and severe herpes simplex virus infection. Non-infectious causes of vaginal discharge include chemical or
  53. 53. irritant vaginitis, trauma, pemphigus, and collagen vascular diseases. Vaginal discharge may result from cervicitis caused by N. gonorrhoeae and C. trachomatis. Severe genital herpes infection can cause both cervicitis and vaginitis. Figure 32 GONORRHEA Gonorrhea Rates In the United States 1941-2006 CDC 355,642 cases of gonorrhea were Figure 33 diagnosed in 1998, the A cervical smear first increase since 1985 photomicrograph (figure 32). This increase is thought to be from reveals
  54. 54. extracellular expansion of screening diplococci programs and improved determined to be surveillance, increased Neisseria sensitivity of new gonorrhoeae diagnostic tests, and an bacteria. increase in morbidity. Neisseria The risk factors for gonorrhoeae is a gonorrhea include young major cause of age (15- to 19-year- old pelvic age group in women and inflammatory 20- to 24-year old age disease, ectopic group in men), low pregnancy, and socioeconomic status, infertility. It has early onset of sexual been shown to activity, unmarried facilitate the marital status, past transmission of history of gonorrhea and the Human men who have sex with Immunodeficiency men. Recently, there Virus (HIV). have been reports of CDC/Joe Miller increased incidence of
  55. 55. rectal gonorrhea among men who have sex with Figure 34 men. The rates of Gonococcal gonorrhea are highest arthritic patient among minority races who presented such as African- with an inflammation of Americans, Hispanics, Asians and Pacific the skin of her right arm due to a Islanders. The Southeastern region of disseminated the U.S. has the highest Neisseria rates of gonorrhea in the gonorrhoeae bacterial infection. nation. Although N. Transmission efficiency gonorrhoeae can of N. gonorrhoeae infect the genital (figure 33) depends on tract, the mouth, the anatomic site of and the rectum, infection and the number they can become of sexual exposures. disseminated Transmission by penile- throughout a vaginal intercourse has
  56. 56. person’s been reported to be 50% bloodstream to 90% among women causing a who are sexual contacts widespread of infected men reaction. compared to 20% among CDC/Emory men who are sexual contacts of infected women. The latter can Figure 35 increase to 60% to 80% Gonococcal following 4 exposures. urethritis can Transmission of rectal become and pharyngeal systemically gonococcal infection is disseminated less well defined, but leading to appears to be relatively gonococcal efficient. conjunctivitis of Neisseria gonorrhoeae is the right eye almost always sexually CDC transmitted except in cases of neonatal transmission. It causes a
  57. 57. spectrum of mucosal diseases including pharyngitis (figure 40), conjunctivitis (figure 35), urethritis, cervicitis and proctitis. It also causes disseminated gonococcal infection (DGI), septic arthritis (figure 34), endocarditis, meningitis and pelvic inflammatory disease. Up to 30% people infected with gonorrhea have concomitant infection with Chlamydia trachomatis. After an incubation period of 1 to 14 days, the classic presentation of gonorrhea in men is
  58. 58. the presence of pus at the urethral meatus accompanied by symptoms of dysuria, edema or erythema of the urethral meatus. However, a fourth of the patients may only develop scant, mucoid exudate or no exudate at all. Complications of gonococcal urethritis in men include epididymitis, acute or chronic prostatitis. Men who have sex with men may also have rectal gonorrhea, which is usually asymptomatic but may be associated with tenesmus, discharge
  59. 59. and rectal bleeding. Oropharyngeal gonorrhea may manifest as acute pharyngitis or tonsillitis, the large majority of which are asymptomatic. In women, the primary site of infection is the endocervical canal, which may present with purulent or mucopurulent discharge, erythema, edema and friability of the cervix (figure 38). Concurrent urethritis, infection of the periurethral gland (Skene’s gland) or Bartholin’s gland may also be present.
  60. 60. Symptoms of gonococcal infection in women may include vaginal discharge, dysuria, menorrhagia or intermenstrual bleeding. However, the majority of women with gonorrhea have few symptoms. Approximately one-third of women with gonococcal cervicitis may also have positive rectal cultures usually due to perineal contamination with gonococci or due to rectal intercourse. About 10% to 20% of women with acute gonorrhea develop acute salpingitis
  61. 61. or pelvic inflammatory disease (see section on pelvic inflammatory disease, below). Systemic complications of gonorrhea include perihepatitis (Fitz-Hugh- Curtis syndrome), disseminated gonococcal infection (DGI), endocarditis and rarely meningitis. The incidence of DGI is 0.5% to 3% among patients with untreated gonorrhea. Bacteremia begins 7 to 30 days after infection. In the majority of patients mucosal infection is often asymptomatic which
  62. 62. may lead to underdiagnosis of DGI. The most common involvement is the skin and joints (figure 36-37), which leads to arthralgias or arthritis, tenosynovitis, and tender necrotic nodules with an erythematous base in the distal extremities (gonococcal arthritis- dermatitis syndrome). Patients with DGI should also be examined for endocarditis or meningitis. Gonorrhea can also be maternally transmitted (figure 41).
  63. 63. Figure 36 This patient presented with a cutaneous gonococcal lesion due to a disseminated Neisseria gonorrhea bacterial infection. CDC Figure 37 This cutaneous ecthyma was caused by a systemically disseminated Neisseria gonorrhea infection. When N. gonorrhea bacteria become disseminated throughout the body, they then can cause centers of infection
  64. 64. in all bodily regions. In this patient’s case, the bacteria caused the formation of a skin infection known as a pyoderma, or ecthyma. CDC Figure 38 This colposcopic view of this patient’s cervix reveled an eroded ostium due to Neisseria gonorrhea infection. A chronic Neisseria gonorrhea infection can lead to complications, which can be apparent such as this cervical inflammation, and some can be quite
  65. 65. insipid, giving the impression that the infection has subsided, while treatment is still needed. CDC Figure 39 This patient presented with urogenital complications from a case of gonorrhea including penile paraphimosis. Due to the accompanying inflammation brought on by the Neisseria gonorrhoeae infection, the foreskin becomes adherent to the glans penis resulting in a
  66. 66. condition known as phimosis, and cannot be retracted in order to expose the entire glans. CDC Figure 40 This patient presented with symptoms later diagnosed as due to Gonococcal pharyngitis. Gonococcal pharyngitis is a sexually-transmitted disease acquired through oral sex with an infected partner. The majority of throat infections caused by gonococci have no symptoms, but some can suffer from mild to severe sore throat. CDC
  67. 67. Figure 41 This was a newborn with gonococcal ophthalmia neonatorum caused by a maternally transmitted gonococcal infection. Unless preventative measures are taken, it is estimated that gonococcal ophthalmia neonatorum will develop in 28% of infants born to women with gonorrhea. It affects the corneal epithelium causing microbial keratitis, ulceration and perforation. CDC
  68. 68. Figure 42 CHLAMYDIA Chlamydia TRACHOMATIS trachomatis taken INFECTION from a urethral scrape. Untreated, Infections due to C. chlamydia can trachomatis (figure 42) cause severe, are one of the most costly prevalent STDs. The reproductive and rates of chlamydia other health infection among males problems and females are highest including both in the age groups short- and long- between 15 to 24 years term (figure 44). The majority consequences, i.e. of chlamydia urethritis in pelvic men and cervicitis in inflammatory women are disease (PID), asymptomatic. Women infertility, and endure the most
  69. 69. potentially fatal morbidity and the most tubal pregnancy. costly outcomes of CDC/ Dr. chlamydia infection due Wiesner, Dr. to pelvic inflammatory Kaufman disease (PID), ectopic pregnancy, tubal Figure 43 infertility and chronic pelvic pain. In men, This woman’s chlamydia was formerly cervix has manifested signs considered to be the of a erosion and cause of most cases of erythema due to non-gonococcal urethritis (NGU) but chlamydial recent data suggest that infection. only 10% to 20% of An untreated cases of NGU are caused chlamydia by Chlamydia (see infection can section on urethritis in cause severe, men). costly reproductive and Transmissibility of C. other health trachomatis has not been
  70. 70. problems well studied. However, a including both recent study has shown short- and long- that 68% of male term partners of infected consequences, i.e. women and 70% of pelvic female partners of inflammatory infected men are positive disease (PID), by PCR for C. infertility, and trachomatis suggesting potentially fatal that transmission from tubal pregnancy. men or women is equally efficient. CDC/ Dr. Lourdes Fraw, Jim Pledger C. trachomatis infects the columnar or squamocolumnar epithelium of the urethra, cervix, rectum, conjunctiva and the respiratory tract (in the neonate). All chlamydiae contain DNA, RNA and
  71. 71. cell walls that resemble those of gram-negative bacteria and require multiplication in eukaryotic cells. C. trachomatis causes a spectrum of lower and upper genital tract diseases in women: urethritis, Bartholinitis, cervicitis (figure 43), endometritis, salpingitis, tubo-ovarian abscess, ectopic pregnancy, pelvic peritonitis and perihepatitis (Fitz-Hugh- Curtis syndrome). About 75% to 90% of cases of chlamydial cervicitis are asymptomatic and may persist for years. Among
  72. 72. women with gonorrhea, 30% to 50% have concomitant Chlamydia infection. Approximately 40% to 50% of men with chlamydial urethritis may be symptomatic with dysuria or minimal urethral discharge. In 1% of men, urethritis may lead to epididymitis. C. trachomatis serovars L1-3 cause Lymphogranuloma venereum (LGV), which is characterized by a genital papule followed by unilateral tender inguinal lymphadenopathy. Other genital ulcer diseases
  73. 73. such as syphilis, chancroid or herpes should be considered in the differential diagnosis of LGV. While LGV is common in the tropical countries it is uncommon in the United States. Figure 44 Chlamydia — Age- and sex-specific rates: United States, 2006 Figure 45 Chlamydia — Rates: Total and by sex: United States, 1987–2006 CDC
  74. 74. PELVIC Figure 46 INFLAMMATORY Generalized DISEASE peritonitis due to what was Pelvic inflammatory diagnosed as a disease (PID) signifies pelvic abscess. inflammation of the A differential upper female genital diagnosis included tract and its related pelvic structures. PID can inflammatory manifest as endometritis, disease (PID), salpingitis, adnexitis, which if it had tubo-ovarian abscess, been the root pelvic peritonitis (figure cause, could begin 46) or perihepatitis. The with a pelvic most common origin, and manifestation of PID is become salpingitis, and these disseminated terms are used throughout the synonymously in the abdominopelvic literature. PID is one of
  75. 75. cavity, thereby, the most common causes causing a of hospitalization among generalized women of reproductive peritonitis. age. Risk factors for PID CDC/ Dr. James include young age, Curran multiple sexual partners, use of intrauterine devices, vaginal douching, tobacco smoking, bacterial vaginosis, HIV infection and STDs with gonorrhea or chlamydia. Use of oral contraceptives has been associated with a decreased rate of PID, especially from infection with C. trachomatis. Most cases of PID are secondary to C.
  76. 76. trachomatis or N. gonorrhoeae. C. trachomatis is the most common cause of PID in the United States. C. trachomatis is implicated with the entity of ―silent salpingitis‖ or subclinical PID. Approximately 10% of women with chlamydial cervicitis, and between 10% and 19% of women with gonococcal cervicitis, can develop acute PID. The pathogenesis of PID is not well understood. In advanced cases, numerous bacterial species are typically
  77. 77. present as ―secondary invaders,‖ including anaerobes and aerobic ―bowel flora‖ bacteria. The chronic sequelae of chlamydia-induced PID, such as ectopic pregnancy and tubal infertility, are thought to be due to an inflammatory reaction to the chlamydial heat shock protein (HSP-60). Certain characteristics of gonococcal strains such as the serovar, the formation of transparent colonies on agar, and penicillin resistance have been correlated with a propensity for causing
  78. 78. tubal infection. Women with PID and gonococcal infection tend to present with pain during the first part of the menstrual cycle suggesting the ascent of gonococci into the upper genital tract through a cervix with scant mucus during the menstrual cycle. URETHRITIS IN MALES Figure 47 This patient Urethritis (inflammation presented with a of the urethra) is case of non- characterized by a specific urethritis burning sensation during urination or itching or with discharge at the urethral accompanying
  79. 79. meatitis, and a meatus. The exudate mucopurulent (figure 47) may be urethral discharge. mucoid, mucopurulent or Non-specific purulent. Traditionally, urethritis merely urethritis has been means that upon differentiated into presentation, the gonococcal or cause of this given nongonococcal urethritis. case of urethral When N. gonorrhoeae inflammation is cannot be detected, the unknown. A syndrome is called non- differential gonococcal urethritis diagnostic process (NGU). In the United will help to States, the rates of NGU narrow the have surpassed that of possible causes by gonococcal urethritis in ruling out those the past 20 to 30 years. possibilities that The 20- to 24-year-old do not provide age group has the highest respective positive incidence of gonococcal test results. CDC and non-gonococcal
  80. 80. urethritis. Up to 25% to 30% of men with gonococcal urethritis also have concurrent Chlamydia infection. In the past, the prevalence of C. trachomatis as the cause of NGU has ranged form 23% to 55%. Recent studies showed that up to two-thirds of cases of NGU remain undiagnosed. Ureaplasma urealyticum, Mycoplasma genitalium and occasionally Trichomonas vaginalis and Herpes simplex virus have also been shown to
  81. 81. cause NGU. Gonococcal urethritis usually presents with a purulent discharge and dysuria whereas NGU usually presents with a scant, mucoid discharge. However, in some patients the inflammatory exudate may not be apparent on examination. Patients with NGU may have a discharge that is noted only in the morning or as crusting at the meatus or as a stain on the underwear. It is difficult to distinguish gonococcal and non- gonococcal urethritis
  82. 82. based on physical examination alone. Patients with gonococcal urethritis present with acute urethritis and usually present within 4 days of onset of symptoms. Patients with non-gonococcal urethritis may present after 1 to 5 weeks after infection. Both groups may have asymptomatic infection. Some patients present with recurrent urethritis characterized by persistent symptoms or frequent recurrences. The symptoms of classic urinary tract infection such as fever, chills,
  83. 83. frequency, urgency, hematuria is not a feature of urethritis. Differential diagnosis of cystitis, prostatitis, epididymitis, Reiter’s syndrome and bacterial cystitis should be considered when evaluating a patient with urethritis. HUMAN PAPILLOMAVIRUS Figure 48 INFECTION This patient Human papillomavirus presented with (HPV) is the most chemical common viral sexually dermatitis of the transmitted disease perineum due to worldwide. The her extensive prevalence ranges from treatment for
  84. 84. labial venereal 20% to 46% in young warts. women worldwide. In Condylomata the U.S., 1% of sexually acuminata, or active persons between genital warts, is a the ages of 15 to 49 sexually years are estimated to transmitted have genital warts from disease caused by HPV. The incidence of the Human HPV infection is high Papilloma Virus, among college students (HPV), which (35% to 43%) especially manifests as among minority races, bumps or warts on individuals with multiple the genitalia, or sexual partners and within the perineal alcohol consumption. region. Immunocompromised CDC/JoeMillar persons including those with HIV infection have increased prevalence of HPV infection. Figure 49 This patient Most genital HPV
  85. 85. presented with a infections are subclinical penile tumor and are transmitted differentially primarily through sexual diagnosed as giant contact. Several condyloma of transmission studies Buschke and noted that 75% to 95% Löwenstein of male partners of (GCBL). Though women with HPV- cancerous, giant genital lesions also had condyloma of genital HPV infection. Buschke and Vertical transmission can Löwenstein cause laryngeal (GCBL) is seldom papillomatosis in infants metastatic. It is and children. Digital most commonly transmission of genital warts can also occur. found originating on the glans penis, Human papillomavirus is but may be found a double-stranded DNA on other perineal virus that infects the surfaces including squamous epithelium. It the anorectal, and causes a spectrum of
  86. 86. vulvovaginal clinical disease ranging mucosae. Though from asymptomatic the etiology is infection, benign plantar unknown, a viral and genital warts (figure cause is highly 48), squamous intra- suspect, and may epithelial neoplasia include human (bowenoid papulosis, papilloma virus, erythroplasia of Queyart, or Bowen’s disease of the cause of condylomata. the genitalia) and frank CDC malignancy (Buschke- Lowenstein tumor (figure 49), a form of verrucous squamous cell Figure 50 carcinoma) in the This HIV-positive anogenital region. External genital warts patient was exhibiting signs of have various morphological a secondary manifestations such as condyloma condyloma acuminata acuminata
  87. 87. infection, i.e., (cauliflower-like), venereal warts. smooth dome-shaped This intraoral papular warts, keratotic eruption of warts and flat warts condyloma (squamous intra- acuminata, or epithelial neoplasia). venereal warts Condyloma acuminata was caused by the tend to occur on moist human papilloma surfaces while the virus. Though oral keratotic and smooth HPV is a rare warts occur on fully occurrence, HIV keratinized skin. Flat reduces the body’s warts can occur on either immune response, surface. and therefore, Approximately one such secondary hundred types of HPV infections can have been identified. The manifest thirty types that infect themselves. CDC/ the anogenital area can Sol Silverman, Jr., be divided into low-risk DDS (e.g., 6, 11, 42, 43, 44)
  88. 88. and high-risk types (e.g., 16, 18, 31, 33, 35, 39, 45, 52, 55, 56, 58) based on their association with anogenital cancer. Types 6 and 11 are commonly associated with external genital, cervical, vaginal, urethral and anal warts as well as conjunctival, nasal, oral and laryngeal warts. While HPV types 6 and 11 are found in 90% of condyloma acuminata, they are rarely associated with squamous cell carcinoma of the external genitalia. On the other hand, HPV types 16, 18, 31, 33, 35 have been associated
  89. 89. with malignant transformation, squamous intraepithelial neoplasia and squamous cell carcinoma of the vulva, vagina, cervix, penis and anus. About 95% of squamous cell carcinomas of the cervix contain HPV-DNA. Most HPV infections do not cause any clinical manifestations and mixed types can be found in each lesion. Most genital warts are asymptomatic but they may cause itching, burning, pain and bleeding. Condyloma acuminata (figure 50)
  90. 90. can present as multiple nodules or large, exophytic, pedunculated, cauliflower like lesions in the anogenital area. They are usually noted on the penis, vulva, vagina, cervix, perineum and the anal region. Flat condylomas are usually subclinical and not visible to the naked eye. They are most commonly noted on the cervix, but may also be present on the vulva and the penis. They may also present as white plaque like lesions in the anogenital region.