13: Sexually Transmitted Diseases

Chapter 13

Sexually Transmitted Diseases

Sexually transmitted diseases (STDs) continue to be a major health problem worldwide and, in many instances, are on the increase. In the United States, some of the highest rates of infection occur in adolescents and young adults. More than 25 STDs have been identified and are listed in < ?xml:namespace prefix = "mbp" />Table 13-1. Current estimates predict that more than 65 million Americans are infected with one or more STDs, and 19 million new infections occur annually.1 The morbidity and mortality associated with STDs vary, with clinical consequences ranging from minor inconvenience or irritation to severe disability and death. The diagnosis of an STD also has psychosocial effects.

TABLE 13-1 Sexually Transmitted Diseases

Disease Pathogen
Acquired immunodeficiency syndrome (AIDS) Human immunodeficiency virus (HIV)55
Amebiasis Entamoeba histolytica
Bacterial vaginosis Bacteroides spp., Mobiluncus spp.
Chancroid Haemophilus ducreyi
Condyloma acuminatum (genital warts) Human papillomavirus (HPV-6, HPV-11)
Cytomegalovirus infection Cytomegalovirus
Enterobiasis Enterobius vermicularis
Epididymitis, mucopurulent cervicitis, lymphogranuloma venereum, nongonococcal urethritis, pelvic inflammatory disease, Reiter’s syndrome Chlamydia trachomatis
Epididymitis, gonorrhea, mucopurulent cervicitis, pelvic inflammatory disease Neisseria gonorrhoeae
Genital herpes Herpes simplex viruses (HSV-1, HSV-2)
Giardiasis Giardia lamblia
Granuloma inguinale (donovanosis) Calymmatobacterium granulomatis
Hepatitis B Hepatitis B virus (HBV)
Molluscum contagiosum Poxvirus
Nongonococcal urethritis, nonspecific vaginitis Trichomonas vaginalis
Nongonococcal urethritis Ureaplasma urealyticum
Pediculosis Pediculus pubis
Salmonellosis Salmonella spp.
Shigellosis Shigella spp.
Streptococcal infection Group B streptococci
Syphilis Treponema pallidum
Vulvovaginal candidiasis Candida spp., Torulopsis spp.

STDs have important implications for clinical practice in dentistry:

STDs are transmitted by intimate interpersonal contact, which can result in oral manifestations. Dental health professionals need to be cognizant of these manifestations as a basis for referral of patients for proper medical treatment.

Some STDs can be transmitted by direct contact with lesions, blood, or saliva, and because many affected persons may be asymptomatic, the dentist should approach all patients as though disease transmission were possible and must adhere to standard precautions.

A single STD is accompanied by additional STDs in about 10% of cases, and STD-associated genital ulceration increases the risk for human immunodeficiency virus (HIV) infection.13

Pathogens responsible for STDs can exhibit antimicrobial resistance, thus proper treatment is essential.1,4

Some STDs are incurable, but all are preventable.

Patient interaction with dental health care workers can be an important component of STD control by providing opportunities for diagnosis, education, and information regarding access to treatment.

Although most STDs have the potential for oral infection and transmission, discussion in this chapter is limited to gonorrhea, syphilis, and select human herpesvirus and human papillomavirus infections, because these entities are of special interest or importance in the provision of dental care and serve to illustrate basic principles. Chapters 10 and 18 present information about hepatitis B and HIV infections.



Gonorrhea is an STD of worldwide distribution that is caused by Neisseria gonorrhoeae. It produces symptoms in men that usually cause them to seek treatment soon enough to prevent serious sequelae, but maybe not soon enough to prevent transmission to others. Infections in women often do not produce recognizable symptoms until complications have emerged. Because gonococcal infections among women frequently are asymptomatic, an important component of gonorrhea control in the United States continues to be the screening of women who are at high risk for STDs. Of note, patients infected with N. gonorrhoeae often are coinfected with Chlamydia trachomatis.


Incidence and Prevalence

Gonorrhea is the second most commonly reported infectious disease and STD in the United States, behind chlamydial infection. An estimated 700,000 new cases are reported each year in the United States, and about half of these are reported to the Centers for Disease Control and Prevention (CDC).1,5 The reported incidence of gonorrhea in 2009 (i.e., 111 cases per 100,000 persons) was the lowest ever reported in the United States and was significantly lower than the incidence in the mid-1970s, when more than 1 million cases were reported.5,6

Humans are the only natural hosts for this disease, and its occurrence is worldwide. Gonorrhea is transmitted almost exclusively by sexual contact, whether genital–genital, oral–genital, or rectal–genital. The primary sites of infection are the genitalia, the anal canal, and the pharynx.

Gonorrhea can occur at any age, although it is seen most commonly in sexually active teenagers and young adults (8.5 per 1000 in the 15- to 29-year-old age group) and in the South. Rates of infection are similar in men and women, but differ by racial background. African Americans and Hispanics have 20.5 times higher rates of gonorrhea than whites.5 Risk factors other than age include young age at first sexual experience, multiple sexual partners, low level of education, low socioeconomic status, and living in an urban setting.1,5 At the current rate of infection, an average dental practice of 2000 adult patients can expect to provide care for 2 patients with gonorrhea.


Gonorrhea is caused by N. gonorrhoeae, a gram-negative intracellular diplococcus. N. gonorrhoeae is an aerobic microbe that replicates easily in warm, moist areas and preferentially requires high humidity and specific temperature and pH for optimum growth. It is a fragile bacterium that is readily killed by drying, so it is not easily transmitted by fomites. It develops resistance to antibiotics rather easily, and many strains have become resistant to penicillin, tetracycline, and quinolones.

Pathophysiology and Complications

N. gonorrhoeae infects columnar epithelium (as found in the mucosal lining of the urethra and cervix) and transitional epithelium (as in the oropharynx and rectum), whereas stratified squamous epithelium (skin and mucosal lining of the oral cavity) generally is resistant to infection.7 This anatomic susceptibility explains the occurrence of rectal, pharyngeal, and tonsillar infections and the relative infrequency of oral infection, and the fact that there are no reported cases of gonorrhea occurring in the skin of the fingers. Figure 13-1 depicts the areas of relative epithelial susceptibility to N. gonorrhoeae infection in the oral cavity and oropharynx.


FIGURE 13-1 Areas of relative epithelial susceptibility to infection by Neisseria gonorrhoeae within the oral cavity.

Infection in men usually begins in the anterior urethra. The bacteria invade epithelial tissues and are engulfed within polymorphonuclear leukocytes, leading to cytokine production and purulent discharge.7 The infection may remain localized or may extend to the posterior urethra, bladder, epididymis, prostate, or seminal vesicles. It spreads by means of lymphatics and blood vessels. Gonococcemia, although infrequent (occurring in 1% to 2% of cases), may occur and results in dissemination of the disease to distant body sites. Epididymitis is another complication of infection that can lead to infertility.

Infection in women occurs most commonly in the cervix and the urethra. Invasion of cervical epithelium can be associated with the production of a purulent exudate but more often leads to an ascending infection of the endometrium, fallopian tubes, ovaries, and pelvic peritoneum. The ascending infection is a common cause of pelvic inflammatory disease (PID), which affects about 1 million women each year in the United States.1 PID can be symptomatic or asymptomatic and may contribute to tubal scarring and infertility or ectopic pregnancy. Disseminated gonorrhea also can occur, with varying frequency. Vertical transmission accounts for a small percentage of cases of gonorrhea in the United States. If the infection goes untreated, it can cause blindness or joint infection in infants.

In both genders, gonorrhea of the rectum may occur after anal–genital intercourse or through direct anal contamination from genital lesions. Infection of the pharynx and oral cavity is predominantly seen in women and homosexual men after fellatio. It also occasionally is seen after cunnilingus.

Widespread dissemination is more likely in infected persons lacking select complement proteins. The gonococcemia can lead to variety of disorders, including migratory arthritis, skin and mucous membrane lesions, endocarditis, meningitis, PID, and pericarditis.

Clinical Presentation

Signs and Symptoms

In men, symptoms usually occur after an incubation period of 2 to 5 days, although they may take as long as 30 days to appear. The most common findings include a mucopurulent (white, yellow, or green) urethral discharge, burning pain on urination, urgency, and frequency. Tenderness and swelling of the meatus may occur.

In women, a significant percentage of cases may be asymptomatic or only minimally symptomatic. Symptomatic infection may demonstrate vaginal or urethral discharge, dysuria with frequency and urgency, and burning pain when urinating. Backache and abdominal pain also may be present.

Approximately 50% of women and 1% to 3% of men are asymptomatic or only mildly symptomatic. This is unfortunate because patients may not seek medical care for their problem and as a result constitute a large reservoir of infection.

Gonococcal infection of the anal canal commonly is less intense than genital infection, but similar signs and symptoms, including a copious purulent discharge, soreness, and pain, may be noted.

Within the oral cavity, the pharynx is most commonly affected.8 Pharyngeal infection is reported to occur in 3% to 7% of heterosexual men, 10% to 20% of heterosexual women, and 10% to 25% of homosexual men.9 It usually is seen as an asymptomatic infection with diffuse, nonspecific inflammation or as a mild sore throat. The likelihood of transmission of pharyngeal gonorrhea to the genitalia seems much less than that of genital–genital transmission.10,11 Of significance, however, is the fact that N. gonorrhoeae has been cultured in expectorated saliva from two thirds of patients with oropharyngeal gonorrhea.10

Gonococcal stomatitis or oral gonorrhea is uncommon; case reports in the literature are limited.9,1215 Acute temporomandibular joint arthritis caused by disseminated gonococcal infection from a genital site has been described.16

Laboratory Findings

Laboratory diagnosis of a genital N. gonorrhoeae infection can be made based on the finding of gram-negative diplococci within polymorphonuclear leukocytes in a smear of urine or of purulent discharge in symptomatic mean (Figure 13-2). In women and asymptomatic men, nucleic acid amplification testing (NAAT) of urine is recommended because of its high sensitivity and specificity, and it can be used to simultaneously test for C. trachomatis.1,17 Culture is also available for diagnosis of N. gonorrhoeae from rectal and pharyngeal specimens. In suspected cases of oropharyngeal gonorrhea, because other species of Neisseria are normal inhabitants of the oral cavity, NAAT is more specific than a gram stain.


FIGURE 13-2 Smear demonstrates gram-negative diplococci within a leukocyte.

(Courtesy University of Iowa, Iowa City, Iowa, and Gary E. Kaiser, PhD, The Community College of Baltimore County, Baltimore, Maryland)

Medical Management

The CDC recommendations1 offer several choices for the treatment of uncomplicated gonococcal infection of the cervix, urethra, and rectum. The single-dose regimens are: injectable ceftriaxone 250 mg (intramuscularly [IM]) in a single dose) or oral cefixime 400 mg in a single dose. Alternatively, a single-dose of injectable cephalosporin plus azithromycin 1 gram orally or doxycycline 100 mg a day for 7 days is recommended. Since patients infected with N. gonorrhoeae are often coinfected with Chlamydia trachomatis dosing regimens that include either azithromycin 1 g given orally in a single dose, or doxycycline 100 mg orally two times a day for 7 days is recommended. For patients who cannot take ceftriaxone, spectinomycin (2 g IM) or azithromycin 2 g are recommended alternatives. A very low (0.8%) treatment failure rate has been reported with ceftriaxone-doxycycline in the United States, and follow-up cultures are not considered essential unless symptoms persist. After antibiotic therapy is begun, infectiousness is diminished rapidly (within a matter of hours).11,17 Infections detected after treatment are generally the result of reinfection by a sexual partner—not treatment failure. Due to widely disseminated quinolone-resistant strains (QRNs) quinolones are no longer recommended for treatment of gonorrhea.

The clinician should be aware that gonococcal pharyngitis is more difficult to eradicate than infections at urogenital and anorectal sites.17 Few antimicrobial regimens can reliably cure such infections more than 90% of the time, and IM cefixime 250 mg plus azithromycin 1 g single oral dose or doxycycline 100 mg a day for 7 days is recommended.1 As with all STDs, all sex partners of patients who have N. gonorrhoeae infection should be assessed and treated.



Syphilis is an acute and chronic STD, caused by Treponema pallidum, that produces skin and mucous membrane lesions in the acute phase and bone, visceral, cardiovascular, and neurologic disease in the chronic phase. The variety of systemic manifestations associated with the later stages of syphilis resulted in its historical designation as the “great imitator” disease. As with gonorrhea, humans are the only known natural hosts for syphilis. The primary site of syphilitic infection is the genitalia, although primary lesions also occur extragenitally. Syphilis remains an important infection in contemporary medicine because of the morbidity it causes, and because it enhances the transmission of HIV.18


Incidence and Prevalence

Syphilis is the fifth most frequently reported STD in the United States today, surpassed only by chlamydial infection, gonorrhea, salmonellosis, and AIDS. In 1990, the incidence of primary and secondary syphilis reached 50,223 cases.5 The number of cases of primary and secondary syphilis dropped to 6,000 in 2000. Since then, the rate has been steadily climbing. In 2009, almost 13,997 cases were reported, a rate of decline of 4.6 cases per 100,000 population.4,5,19 A disproportionately high number of cases continue to occur in the South and among Hispanic and non-Hispanic African American men and women. Syphilis occurs more commonly in persons aged 25 to 39 years. Its incidence in males is greater than in females, with a ratio of almost 6 : 1.19

Congenital syphilis occurs when the fetus is infected in utero by an infected mother. In 2008, a total of 431 cases of congenital syphilis were reported to the CDC. This represents a rate of 10.1 per 100,000 live births—higher than the 8.2 cases per 100,000 live births in 2005—but still a dramatic decline from the peak of 107.3 cases per 100,000 live births in 1991.19


The etiologic agent of syphilis is Treponema pallidum, which is a slender, fragile anaerobic spirochete. It is transmitted predominantly sexually, including by oral–genital and rectal–genital contact with contaminated sores. However, transmission also can occur through nonsexual means such as kissing, blood transfusion, or accidental inoculation with a contaminated needle. Indirect transmission by fomites is possible but uncommon, because the organism survives for only a short time outside the body.1,20 T. pallidum is easily killed by heating, drying, disinfecting, and using soap and water. The organism is difficult to stain, except with use of certain silver impregnation methods. Demonstration is best done with darkfield microscopy on a fresh specimen.


Available evidence suggests that T. pallidum does not invade completely intact skin; however, it can invade intact mucosal epithelium and gain entry through minute abrasions or at the hair follicles. Within a few hours after invasion, bacterial spread to the lymphatics and the bloodstream occurs, resulting in early widespread dissemination of the disease. The early response to bacterial invasion consists of endarteritis and periarteritis.20 The risk of transmission is during the primary, secondary, and early latent stages of disease, but not in late syphilis.21 Overall, patients are most infectious during the first 2 years of the disease.

Clinical Presentation

Signs and Symptoms

Manifestations and descriptions of syphilis are classically divided according to stages of the disease, with each stage having its own specific signs and symptoms related to disease duration and antigen-antibody responses. The stages are primary, secondary, latent, tertiary, and congenital. Of note, many infected persons do not develop symptoms for years, yet remain at risk for late complications if the infection is not treated.

Primary Syphilis

The classic manifestation of primary syphilis is the chancre, a solitary firm, round, granulomatous lesion that develops at the site of inoculation with the infectious organism. The chancre usually occurs within 2 to 3 weeks (range, 10 to 90 days) after exposure (Figure 13-3). Patients are infectious, however, before it appears. The lesion begins as a small papule and enlarges to form a surface erosion or ulceration that commonly is covered by a yellowish hemorrhagic crust and teems with T. pallidum. It typically is painless. Associated with the chancre are enlarged, painless, hard regional lymph nodes. The chancre usually subsides in 3 to 6 weeks without treatment, leaving variable scarring in the form of a healed papule.20,22 The genitalia, oral cavity (lips, tongue), fingers, nipples, and anus are common sites for chancres. Figure 13-4 shows examples of extragenital syphilitic chancres (lip and tongue). If adequate treatment is not provided, the infection progresses to secondary syphilis.


FIGURE 13-3 Primary syphilis: Chancre of the penis.

(From Swartz MH: Textbook of physical diagnosis, ed 6, Philadelphia, Saunders, 2010.)


FIGURE 13-4 Primary Syphilis.

A, Chancre on tongue seen in primary syphilis. B, Extragenital chancre of the lip.

(A, From Ibsen DAC, Phelan JA: Oral pathology for the hygienist, ed 5, St. Louis, Saunders, 2009.)

Secondary Syphilis

The manifestations of secondary syphilis appear 6 to 8 weeks after initial exposure. The chancre may or may not have completely resolved by this time. The symptoms and signs of secondary syphilis include fever, arthralgia and malaise, generalized lymphadenopathy, and patchy hair loss and develop in 80% of patients. Generalized eruptions of the skin and mucous membranes also occur (Figure 13-5, A) and include condyloma lata or wart-like growths on the genitalia. The papules of the rash are well demarcated and reddish brown and have a predilection for the palms and soles; they typically are not itchy. Oral manifestations of secondary syphilis include pharyngitis, papular lesions, erythematous or grayish-white erosions (mucous patches) (see Figure 13-5, B), irregular linear erosions, and, rarely, parotid gland enlargement. The lesions of skin and mucous membranes are highly infectious.20,22 Without treatment, clinical manifestations of secondary syphilis ultimately resolve; however, infection progresses to latent or the tertiary stages.


FIGURE 13-5 Lesions of Secondary Syphilis.

A, Profuse papular rash. B, Mucous patch of the lower lip

(A, From Habif TP, et al: Skin disease: diagnosis and treatment, ed 3, St. Louis, 2011, Mosby.)

Latent Syphilis

Latent syphilis is defined as an untreated infection in which the patient displays seroreactivity but no clinical evidence of disease. This stage of the infection is divided into early latent syphilis (disease acquired within the preceding year) and late latent syphilis (disease present for longer than 1 year) or latent syphilis of unknown duration. During the first 4 years of latent syphilis, patients may exhibit mucocutaneous relapses and are considered infectious. After 4 years, relapses do not occur, and patients are considered noninfectious (except for blood transfusions and pregnant women).7,22 The latent stage may last for many years or, in fact, for the remainder of the person’s life. In some untreated patients, however, progression to tertiary syphilis occurs.

Tertiary (Late) Syphilis

The tertiary (late) stage occurs in roughly 1/3 of untreated persons, generally several years after disease onset.23 It is the destructive stage of the disease that involves mucocutaneous, osseous, and visceral structures). Signs and symptoms of this stage do not occur until years after the initial infection.

More than 80% of manifestations of tertiary syphilis are essentially vascular in nature and result from an obliterative endarteritis. Cardiovascular syphilis most commonly manifests as an aneurysm of the ascending aorta.

The benign tertiary stage of syphilis is classically characterized by the formation of gummas. These localized nodular, tender lesions may involve the skin, mucous membranes, bone, nervous tissue, and/or viscera. They are thought to be the end result of a delayed hypersensitivity reaction. Pathologically, they consist of an inflammatory granulomatous lesion with a central zone of necrosis. Gummas are not infectious but can be destructive.

The oral lesions of tertiary syphilis consist of diffuse interstitial glossitis and the gumma. Interstitial glossitis should be considered a premalignant condition. The tongue may appear lobulated and fissured with atrophic papillae, resulting in a bald-appearing and wrinkled surface. Leukoplakia frequently is present. The oral gumma is a rare lesion that most commonly involves the tongue and palate. It appears as a firm tissue mass with central necrosis. Palatal gummas may perforate into the nasal cavity or maxillary sinus.

Neurosyphilis can occur during any stage of syphilis. It can produce a meningitis-like syndrome, Argyll Robertson pupils (which react to accommodation but not to light), altered tendon reflexes, general paresis, tabes dorsalis (degeneration of dorsal columns of the spinal cord and sensory nerve trunks), difficulty in coordinating muscle movements, cognitive dysfunction or insanity.

Congenital Syphilis

Syphilis or its sequelae occur in the newborn if the mother is infected while carrying the child. The disease is transmitted to the fetus in utero, usually after the 16th week, because before this time, the placenta prevents transmission of bacteria. The disease persists worldwide because a substantial number of women do not receive serologic testing for syphilis during pregnancy, or they may undergo testing too late in pregnancy to receive prenatal care.24 Physical manifestations vary according to the time of infection. The sequelae of early infection include osteochondritis, periostitis (frontal bossing of Parrot), rhinitis, rash, and ectodermal changes. Syphilis contracted during late pregnancy may involve bones, teeth (see “Oral Manifestations”), eyes, cranial nerves, viscera, skin, and mucous membranes. A classic triad of congenital syphilis known as Hutchinson’s triad includes interstitial keratitis of the cornea, eighth nerve deafness, and dental abnormalities, including Hutchinson’s incisors (Figure 13-6) and mulberry molars.


FIGURE 13-6 Congenital syphilis: Hutchinson’s teeth.

Laboratory Findings

T. pallidum has never been cultured successfully on any type of medium; therefore, the definitive diagnosis of syphilis is made from a positive darkfield microscopic examination or on the basis of direct immunofluorescent antibody tests on fresh lesion exudates. Darkfield examination yields consistently positive findings only during primary and early secondary stages. Definitive diagnosis of oral lesions by this method is difficult, because other species of Treponema are indigenous to the oral cavity.

Syphilis typically is diagnosed by a two-step process involving a nonspecific (screening) antibody test, followed by a treponeme-specific test. Screening antibody tests of blood also are known as serologic tests for syphilis (STS). These tests are of two basic types, indirect and direct, and are differentiated by the types of antibodies they measure.

Screening Serologic Tests for Syphilis: Nontreponemal Tests—VDRL and RPR

Standard screening tests for syphilis consist of the Venereal Disease Research Laboratory (VDRL) slide test, the rapid plasma reagin (RPR) test, and the automated reagin test (ART). These indirect, nontreponemal serologic tests are designed to detect the presence of an antibody-like substance called reagin that is produced when T. pallidum reacts with various body tissues. They are equally valid. A disadvantage of reaginic tests is the occasional biologic false-positive result that can occur.

Nontreponemal tests produce titers (reported quantitatively as serologic dilutions [e.g., 1 : 2, 1 : 4, 1 : 8]) that usually correlate with disease activity. Results are consistently positive and the highest titers are obtained between 3 and 8 weeks after the appearance of the primary chancre. In primary syphilis, nontreponemal tests usually revert to negative within 12 months after successful treatment. In secondary syphilis, up to 24 months may be required for the patient to become seronegative. Occasionally, a patient will remain seropositive for life, or will test positive in the presence of an associated infection or condition (false-positive). With tertiary syphilis, many patients remain seropositive fo/>

Only gold members can continue reading. Log In or Register to continue

Jan 4, 2015 | Posted by in General Dentistry | Comments Off on 13: Sexually Transmitted Diseases
Premium Wordpress Themes by UFO Themes