Adolescent Health Care: A Practical Guide

Chapter 67

Other Sexually Transmitted Diseases Including Genital Ulcers, Pediculosis, Scabies, and Molluscum

Wendi G. Ehrman

  1. Susan Jay

Lawrence S. Neinstein

Chancroid, lymphogranuloma venereum (LGV), and granuloma inguinale constitute the classic minor ulcerative sexually transmitted diseases. All three of these diseases are uncommon but should be considered in the differential diagnosis of genital ulcers. In the United States, the most common causative agent of genital ulcers is the herpes simplex virus (HSV) followed by Treponema pallidum or syphilis. Approximately 3% to 10% of these patients will have more than one of these conditions present. In addition, there is an increased risk of human immunodeficiency virus (HIV) infection associated with these ulcerative infections.

Chancroid

Chancroid is a genital ulcer infection caused by the gram-negative coccobacillus, Haemophilus ducreyi. Although uncommon in the United States, it is endemic in some areas of the country. Discrete outbreaks have been associated with poverty, urban prostitution, and illicit drug use. Chancroid is more commonly found in developing countries, with the highest prevalence in southern, central, and eastern Africa. Chancroid is a known risk factor for HIV and an enhancer of disease transmission. In addition, as many as 10% of patients with chancroid acquired in the United States are coinfected with T. pallidum or HSV. This number is estimated to be even higher for those case acquired outside the United States.

Epidemiology

  1. Incidence: Chancroid was endemic in most parts of the world well into the 20th century. Since then, it has been disappearing in developing countries because of programs targeting increased condom use among commercial sex workers, and improved antibiotics. Despite increased eradication efforts worldwide, there is still an estimated rate of 7 million cases/year. Although outbreaks have occurred sporadically, the incidence of chancroid in the United States has steadily declined from a peak of 5,001 cases in 1988 to 17 cases in 2005. The incidence rate peaked in 1988 at 2.04 per 100,000 and has dropped to <0.01 per 100,000 in 2005. Given that chancroid is difficult to culture, often not considered, and usually diagnosed on the basis of morphological features alone, it is probably significantly under diagnosed.
  2. Race: The incidence is increased in African-American and Hispanic patients.
  3. Ratio of males-to-females is typically >10:1 in outbreaks.

Clinical Manifestations

  1. Incubation period: Three to 10 days
  2. Presentation: Chancroid presents as a tender inflammatory papule on the genitalia. It is thought to inoculate through microabrasions on the genital skin, which occur during sexual intercourse. Within 1 to 2 days, the papule becomes pustular, eroded and then ulcerates into an extremely painful, shallow lesion. The characteristic ulcer is soft, friable, and nonindurated with ragged undermined margins, a granulomatous base, and a foul-smelling yellow or gray, necrotic purulent exudate. Multiple lesions may be present, especially in females. Lesions have been known to remain pustular (“dwarf chancroid”), coalesce to form giant or serpiginous ulcers or resemble folliculitis or a pyogenic infection. Within 1 to 23 weeks, painful unilateral inguinal lymphadenitis known as a bubo, develops in 40% to 50% of patients. Twenty-five percent of these patients will have progression of the lymphadenitis into a suppurative bubo, which may rupture and ulcerate if not aspirated and drained. If this occurs, the patient can develop autoinoculation with bilateral opposing ulcers, known as kissing lesions. Large inguinal abscesses can occur, leading to significant destruction of skin and soft tissue.

Although males usually present with ulcer or inguinal pain, females may be asymptomatic or develop nontender ulcers along with dysuria, dyspareunia, vaginal discharge, pain with defecation, and rectal bleeding.

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Superinfection of ulcers with anaerobes can also occur leading to further ulceration and destruction of genital tissue. Fever and malaise may occur but are rare.

  1. Location
  2. In males: Prepuce, coronal sulcus, and frenulum
  3. In females: Vulva, clitoris, cervix, and perianal region
  4. Extragenital sites (rare): Breasts, thighs, fingers, and mouth; has not been shown to spread to distant sites
  5. Pregnancy: There have been no reports of adverse effects on pregnancy outcome or on the fetus.
  6. HIV-infected patients: Studies on HIV-seropositive males suggest that this group has increased numbers of genital ulcers that may heal slower and require longer courses of therapy.

Differential Diagnosis

Chancroid may be confused with or coexist with herpes genitalis, primary syphilis, LGV traumatic lesions, Behçet syndrome, or fixed drug eruptions. Among adolescents, the most common etiology of genital ulcers would be herpes, followed by nonspecific trauma, syphilis, and chancroid.

  1. Herpetic lesions initially present as vesicles, are usually very painful, more superficial, more numerous, and are surrounded by a narrower zone of erythema. Adenopathy is usually bilatera Constitutional symptoms and lymphadenopathy may occur in first-time infections. Culture or antigen test for HSV should be performed.
  2. Syphilitic ulcers are nonpainful and have indurated borders. Dark-field examination and serological examination are needed for confirmation.
  3. Lesions associated with LGV are nonpainful and adenopathy develops after the lesions have healed.

Diagnosis

There are currently no easily accessed, highly sensitive tests available to diagnose chancroid. Oftentimes, the diagnosis is difficult because it is based on clinical findings and on the exclusion of HSV, syphilis, LGV, and granuloma inguinale. Accuracy rates from clinical diagnosis alone range from 33% to 80%. The “gold standard” for diagnosis has been culture. However H. ducreyi is a fastidious organism that requires special media and specialized laboratory conditions that are not widely available. To assist with diagnosis, all individuals with genital ulcers should receive serological testing for syphilis and if possible, a dark-field examination or direct immunofluorescence for T. pallidum, a culture and an antigen test for HSV, in addition to a culture for H. ducreyi. Diagnostic options include the following:

  1. Microscopy: Direct examination of gram-stained ulcer material or aspirate from an infected lymph node (bubo) may be suggestive if large numbers of gram-negative coccobacilli are seen. Material is collected on a calcium alginate or cotton-tipped swab from the ulcer base and carefully rolled in one direction onto a glass slide for gram staining. The bacteria typically arrange themselves in parallel short chains, described as “schools of fish” and tend to occur close to polymorphonuclear leukocytes. This technique has poor sensitivity and specificity and may be misleading due to the polymicrobial flora often present in genital ulcers. As a result, it should not be used alone for diagnosis.
  2. Culture: Culture material may be obtained from genital ulcers or buboes, although intact buboes tend to be sterile. Laboratories should be informed as soon as possible to prepare for the specimens. Compared with newer diagnostic techniques such as multiplex polymerase chain reaction (M-PCR), the sensitivity of culture is 35% to 75% and specificity is 94% to 100%.
  3. Immunodiagnostic DNA probes and DNA amplification tests (M-PCR) are being investigated but are not routinely available in the United States. However, testing can be performed by commercial labs that have developed their own polymerase chain reaction (PCR) test. Sensitivity ranges from 56% to 100%.
  4. Center for Disease Control and Prevention (CDC) criteria for “probable” chancroid diagnosis are as follows:
  5. One or more painful genital ulcers.
  6. No evidence of T. pallidumon dark-field examination of ulcer exudate or by a serological test for syphilis performed at least 7 days after onset of ulcers.
  7. The clinical presentation, appearance of the genital ulcers, and, if present, regional lymphadenopathy are typical for chancroid.
  8. A negative result on HSV test performed on ulcer exudates.
  9. The combination of a painful ulcer with tender inguinal adenopathy is suggestive of chancroid, and when accompanied by suppurative inguinal adenopathy it is almost pathognomonic.

Treatment

  1. CDC recommended pharmacotherapy
  2. Azithromycin 1 g orally in a single dose
  3. Ceftriaxone 250 mg intramuscularly (IM) in a single dose
  4. Ciprofloxacin 500 mg orally twice daily for 3 days

Note: Ciprofloxacin is contraindicated for pregnant and lactating women, children, and adolescents younger than 18 years.

  1. Erythromycin base 500 mg orally three times a day for 7 days.
  2. Worldwide, several isolates with intermediate resistance to either ciprofloxacin or erythromycin have been reported.
  3. Treatment of buboes: Aspiration of fluctuant buboes provides symptomatic relief and can prevent spontaneous rupture. Alternatively, incision and drainage of buboes along with wound packing can avoid the need for frequent reaspirations.
  4. HIV and syphilis testing should be performed at the time of diagnosis and repeated in 3 months if initially negative. In addition, patients should be tested for other sexually transmitted diseases such as gonorrhea, chlamydia, and hepatitis B.
  5. Follow-up: Follow-up with infected individuals should occur within 3 to 7 days of initiation of therapy and should continue weekly until resolution of signs and symptoms. There should be subjective improvement within 3 days and objective improvement within 7 days. If there is no improvement, the practitioner must consider whether the diagnosis is correct, there is a coinfection with another sexually transmitted disease (STD), the individual is infected with HIV, treatment compliance is poor, or there is resistance to the prescribed antimicrobial. Large ulcers may require more than 2 weeks

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to resolve, and fluctuant lymphadenopathy heals even more slowly than ulcers. Healing may also occur more slowly if the ulcers are under the foreskin of an uncircumcised male patient. Adenopathy may progress to fluctuation despite successful therapy and does not represent treatment failure. Patients need to be told that there should be no sexual activity while clinical disease is present.

  1. Sexual partners: Treatment should be initiated when sexual contact has occurred within 10 days preceding the onset of symptoms in the infected patient, regardless of whether symptoms are present in the partners.
  2. HIV-infected patients: Treatment failures have occurred and these individuals may require longer courses of therapy. The 7-day erythromycin regimen may be better unless very close follow-up is possible.

Lymphogranuloma Venereum

LGV is a systemic, sexually transmitted disease that remains rare in the United States. Although uncommon in most of the industrialized world, LGV is endemic in parts of Africa, India, South America, and the Caribbean. Recent outbreaks of LGV have been reported in the Netherlands and parts of Europe among men who have sex with other men, especially those who were HIV positive. In early 2005, there were already four confirmed cases reported in a similar population in New York City.

Etiology

LGV is caused by the obligate intracellular organism Chlamydia trachomatis. Chlamydia has 18 serological variants (serovars) associated with disease. Serovars L1, L2, and L3 are more invasive and cause LGV whereas serovars B and D through K are associated with nongonococcal urethritis and cervicitis.

Epidemiology

  1. Frequency: There were 42 known cases in the United States in 2000. This prevalence may be falsely low because of underreporting and misdiagnosis. LGV has not been nationally notifiable since 1995.
  2. Age: Peak incidence is from 15 to 40 years of age.
  3. Sex: Male to female predominance as high as a 5:1 ratio. A higher prevalence is seen among men who have sex with other men.

Clinical Manifestations

  1. Incubation period: Three to 30 days (usually 7 to 12 days)
  2. LGV occurs in three separate stages:
  3. Primary stage: The primary lesion of LGV starts out as a small, painless, papule or pustule at the site of inoculation that can erode into an asymptomatic herpetiform ulcer. Although these lesions can be multiple and deeply erosive, they often heal within a week without scarring and may go unnoticed. Primary lesions are typically found on the penis, urethral glans, and scrotum on the male; and on the vulva, vaginal wall, fourchette, and cervix in females. Rectal lesions can occur in both sexes from receptive anal intercourse and can be associated with diarrhea, rectal discharge, and tenesmus. Mucopurulent cervicitis and urethritis may also occur. Females usually have primary involvement of the rectum, vagina, and cervix.
  4. Secondary stage or inguinal stage: This stage typically occurs 2 to 6 weeks after the appearance of the primary lesion and involves painful inflammation and infection of the inguinal and femoral lymph nodes. Inguinal adenopathy is unilateral in 70% of cases. Although most men present during this stage, only 20% to 30% of women develop inguinal adenopathy. The “groove” sign is the result of enlarged inguinal nodes above Poupart ligament and femoral nodes below it and is said to be “pathognomonic” for LG Deep pelvic nodes may be involved in females, leading to lower abdominal or back pain. Infected macrophages drain the regional lymph nodes, typically producing unilateral enlargement, infection, and necrotic abscesses. Nodes can become matted and fluctuant. This produces the characteristic bubo. The skin overlying the bubo often becomes attached to the underlying lymph nodes and takes on a characteristic deep reddish blue color (“blue balls”). The buboes may rupture in one third of patients, or develop into hard nonsuppurative masses. Most of these buboes will eventually heal, however, some will develop into sinus tracts. Bubonic relapse can occur in 20% of untreated cases. Constitutional symptoms may occur with the inguinal buboes and be associated with systemic spread of chlamydia leading to arthritis, hepatitis, and pneumonitis. Rarer systemic complications include cardiac involvement, aseptic meningitis, and ocular inflammatory disease.
  5. Tertiary stage or genitoanorectal syndrome: Uncommon but occurs more often in females who were asymptomatic during previous stages of the disease and in homosexual males typically due to receptive anal intercourse. Patients initially develop proctocolitis with symptoms of anal pruritus, rectal discharge, rectal pain, tenesmus, and fever. Later manifestations include perirectal abscesses, rectovaginal and anorectal fistulas, rectal strictures, and rectal stenosis. Chronic inflammation can lead to hyperplasia of intestinal and perirectal lymphatics or “lymphorrhoids.” In addition, chronic untreated LGV can lead to a process of repetitive scarring and fistulous tract formation in the genital region. Potential complications from this include elephantiasis of the genitals 1 to 20 years after onset (rare), esthiomene (enlargement, induration, ulceration, and destruction of the vulva), and infertility.

Differential Diagnosis

  1. Genital inguinal lesion
  2. Syphilis
  3. Herpes simplex
  4. Chancroid
  5. Granuloma inguinale
  6. Pyogenic infection
  7. Cat-scratch fever
  8. Rectal fistulas
  9. Inflammatory bowel disease
  10. Chronic rectal infections: Gonorrhea, amebiasis, tuberculosis
  11. Granuloma inguinale

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Diagnosis

The diagnosis of LGV has often been made based on clinical findings, due to lack of available laboratory services for identifying the organism, difficulty in culturing the organism, and the cross-reactivity of serology between several serotypes. For a laboratory diagnosis of LGV, the infective agent must first be identified as C. trachomatis and then the LGV serotype of C. trachomatis determined. Available laboratory services can be located at www.cdc.gov/std/lgv-labs.htm.

Tests for identification of C. trachomatis are as follows:

  1. Culture and culture typing: Not a widely available test. Chlamydiamay be isolated from ulcer material or from a node aspirate. The recovery rate is less than 30% and culture is not highly specific for LGV.
  2. NAAT (nucleic acid amplification tests): Not U.S. Food and Drug Administration (FDA) cleared for use with rectal specimens, although some laboratories are able to use this test after meeting Clinical Laboratory Improvement Amendments (CLIA) guidelines. Also not specific for LGV.
  3. Tests for serotyping LGV are as follows:
  4. Complement fixation: Titers ≥1:64 along with clinical correlation are consistent with a diagnosis of LGV infection. A fourfold increase in titer also supports the diagnosis of LGV. However, titers can also be positive after chlamydial urethritis, psittacosis, or trachoma, although they are rarely higher than 1:16. Disease severity does not correlate with antibody titers.
  5. The microimmunofluorescence test is more sensitive and specific than complement fixation but is not routinely available. A high titer (typically >1:128 but can vary by laboratory) is consistent with a diagnosis of LGV. Immunofluorescence techniques are usually applied to lymph node aspirates and may not be applicable in proctitis presentations.
  6. Genotyping is not widely available.

Treatment

Owing to the difficulty confirming LGV by diagnostic testing, patients with a clinical syndrome consistent with LGV, including proctocolitis or genital ulcer disease with lymphadenopathy, should be treated for LGV.

  1. CDC recommended pharmacotherapy
  2. Doxycycline 100 mg orally twice daily for 21 days
  3. CDC alternative regimens
  4. Erythromycin 500 mg orally four times a day for 21 days
  5. Azithromycin 1 g orally weekly for 3 weeks (suggested by some specialists but clinical data lacking)
  6. Surgical intervention: Occasionally, aspiration of a fluctuant node or incision and drainage of an abscess is required for prevention of ulcer formation or relief of inguinal pain. The late complications of LGV may necessitate surgical repair after antibiotic treatment is complete.
  7. Follow-up: Patients should be monitored clinically until signs and symptoms have resolved.
  8. Sex partners: Sexual contacts within 60 days before onset of symptoms should be examined, tested for urethral or cervical chlamydial infection, and treated. In the absence of symptoms, contacts should be treated with azithromycin 1 g oral single dose or doxycycline 100 mg orally twice daily for 7 days.
  9. Pregnancy and lactation: Erythromycin should be used to treat pregnant and lactating women. Azithromycin may be an alternative, although published safety and efficacy data are lacking.
  10. HIV infection: HIV-infected adolescents should be treated with the same regimens as for noninfected HIV adolescents although prolonged treatment may be necessary.

Granuloma Inguinale

Granuloma inguinale, also known as Donovanosis, is a rare STD in the United States but should be considered in the differential diagnosis of chronic progressive genital ulcers. It is endemic in certain tropical, subtropical, and developing areas of the world and is often associated with impoverished communities.

Etiology

Granuloma inguinale is caused by Calymmatobacterium granulomatis, a nonmotile, obligate intracellular, encapsulated, gram-negative coccobacillus.

Epidemiology

  1. Incidence: Indigenous granuloma inguinale is no longer present in the United States or most other developed countries. Cases that occur in the United States are uncommon and imported. At present this disease is not notifiable in the United States and only eight cases were reported to the CDC in 1997. Granuloma inguinale is considered endemic in Papua, New Guinea, South-East India, South Africa, central Australia, Brazil, and the Caribbean.
  2. Sex: Higher prevalence in males.
  3. Age: Most cases occurs between the ages of 20 and 40 years.
  4. Transmission: Primarily through sexual contact, most commonly from a person with an active infection but possibly also from a person with asymptomatic rectal infection. Transmission may also occur during vaginal childbirth, and young children can acquire infection through infected secretions. Autoinoculation can lead to spread of the disease. Granuloma inguinale is thought to be only mildly contagious, requiring several exposures for clinical disease.

Clinical Manifestations

  1. Incubation period: Eight to 80 days
  2. Granuloma inguinale has a variety of presentations and atypical lesions, which makes identification a challenge.
  3. Ulcerovegetative or ulcerogranulomatous forms: Most common form; produces large, extensive, nonindurated ulcerations with beefy-red, friable granulation tissue.
  4. Nodular form: Consists of soft red nodules or plaques that erode to form ulcerations.
  5. Hypertrophic or verrucous form: Consists of dry vegetative masses with raised irregular edges that resemble a walnut or condylomata acuminata.

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  1. Necrotic form: Less common, foul-smelling, deep ulcer that produces rapid and extensive tissue destruction. Unlike most lesions of granuloma inguinale, it is often painful.
  2. Sclerotic or cicatricial form: Rare; consists of dry, nonbleeding ulcers that expand into plaques with band-like scarring. Lymphedema can occur due to constriction.
  3. True inguinal lymphadenopathy does not occur with granuloma inguinale unless bacterial superinfection develops. However, subcutaneous granulomas near the inguinal nodes (pseudobuboes) can result in inguinal enlargement.
  4. Location: Lesions are typically localized without constitutional symptoms. The genital area is involved in 90% of cases and inguinal area in 10%. Extragenital lesions occur in 6% of cases secondary to autoinoculation of primary genital lesions.
  5. Males: Coronal sulcus, prepuce, frenulum, glans penis, and anus. More common in uncircumcised males with poor genital hygiene.
  6. Females: Labia minora and fourchette; can infect the cervix and upper genital tract mimicking cervical cancer.
  7. Extragenital sites: Oropharynx, neck, nose, larynx, and chest.
  8. Hematogenous dissemination is rare and associated with a grave prognosis. Dissemination to the abdominal cavity and organs, lung, bone, and female reproductive organs has occurred and is usually associated with cervical infection related to trauma during pregnancy.

Differential Diagnosis

The disease in its early stages may be confused with syphilis, herpes simplex, chancroid, or carcinoma of the penis if tissue destruction or necrosis is present.

Diagnosis

  1. Granuloma inguinale is usually diagnosed by identification of intracytoplasmic inclusion bodies known as Donovan bodieswithin histiocytes of granulation tissue smears or biopsy specimens. Tissue smears are obtained by firmly rolling a cotton swab across the base of a nonbleeding ulcer and then rolling the swab across a slide. “Crush biopsies” are obtained by removing a piece of tissue from the advancing surface of the ulcer and “crushing” or smearing the resultant specimen between two slides. Giemsa or Wright's stain is then used to identify the dark-staining, safety pin–shaped Donovan bodies. Histological examination of biopsy specimens can also be used for diagnosis.
  2. PCR tests and serological tests using immunofluorescence have been developed but remain mostly available on a research basis.
  3. Isolation of C. granulomatisis extremely difficult and has not been available although several research labs have reported successful culture of the organism.
  4. Lesions should be cultured for H. ducreyito exclude chancroid (pseudogranuloma inguinale). Granuloma inguinale is frequently misdiagnosed as carcinoma, which can be excluded by histological examination of tissue or by response of the lesion to antibiotics.

Treatment

  1. CDC recommended regimens: All treatments should be given for a minimum of 3 weeks and until all lesions have completely healed.
  2. Doxycycline 100 mg orally twice a day for a minimum of
  3. 3 weeks or until all lesions healed
  4. Alternative regimens
  5. Azithromycin 1 g orally per week for a minimum of 3 weeks
  6. Ciprofloxacin 750 mg orally twice a day for a minimum of 3 weeks (not used in children younger than 18 years).
  7. Erythromycin base 500 mg orally four times a day for a minimum of 3 weeks
  8. Trimethoprim-sulfamethoxazole, one double strength tablet orally twice a day for a minimum of 3 weeks or until all lesions healed
  9. Resistance: An aminoglycoside such as gentamycin 1 mg/kg IV every 8 hours may be added to any of the regimens if lesions are not responding within the first few days of treatment.
  10. Pregnancy: Erythromycin should be used in pregnant and lactating women with consideration for adding a parental aminoglycoside such as gentamycin. Azithromycin is an alternative, although published data is currently not available.
  11. HIV: Treatment is the same as in HIV-negative patients although consideration should be given to the addition of an aminoglycoside.
  12. Follow-up: Patients should be followed up until complete resolution of clinical signs and symptoms. If therapy is effective, partial healing of the ulcer should be seen within 7 days. Prolonged therapy is required for granulation and reepithelialization of ulcers. Relapses can occur in 6 to 18 months after treatment especially if antibiotics are stopped prematurely. As with other genital ulcer diseases, patients should be tested for other sexually transmitted diseases such as gonorrhea, chlamydia, herpes, syphilis, HIV, and hepatitis B.
  13. Sexual partners: Sexual partners should be examined and offered treatment if they had contact with the patient during the 60 days before the onset of symptoms or if they are clinically symptomatic. The value of empirical antibiotic therapy in patients without clinical signs or symptoms is unknown.

Pediculosis and Scabies

Scabies and pediculosis are ubiquitous and highly contagious parasitic skin infections that have been present since antiquity and are distributed worldwide. Infections occur both in individuals and in clusters such as school children, homeless people, hospital staff, and immunocompromised persons. Difficulties in management have returned scabies and pediculosis to the limelight.

Pediculosis Pubis

Etiology

Pediculosis pubis is caused by the pubic or crab louse, Pthirus pubis, an obligate human parasite. It is a wingless

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insect 1 to 3 mm in length with three sets of legs; two that are clawed and one that is shortened and vestigial. The hook-like claws and opposing thumb provide a grasp on the pubic and auxiliary hair. Serrations on its first set of claws also allow it to cling to flat, hairless surfaces. The lice are able to move around the skin surface at approximately 10 cm/day.

Epidemiology

  1. Transmission: Pubic lice infestations are most
  2. common among adolescents and young adults. Transmission occurs as a result of close bodily contact, chiefly through sexual contact. Condoms do not prevent transmission and frequently infestations coexist with other STDs. Pubic lice can potentially be transmitted by infected clothing, towels, and bedding. Lice have also been found on eyelashes of younger children and may be an indicator for sexual abuse. At present there is no evidence linking ectoparasites to transmission of HIV.
  3. Life cycle: The parasite spends its life on skin and feeds on blood. It dies in approximately 24 hours off its human host. The female pubic louse lays approximately three to four eggs/day, which are attached to hair shafts as nits. The nits hatch in 6 to 10 days into nymphs that mature into adult lice within 10 to 14 days. Adult life expectancy is believed to be approximately 1 month.

Clinical Manifestations

  1. Symptoms occur 2 weeks or more after contact at which point the infection is usually well established. Pruritus, the main symptom, is related to the louse bite and is probably a hypersensitivity reaction. Secondary infections can occur from scratching. In addition, symptoms occur more rapidly if the patient experienced a prior infestation.
  2. Common areas of infection: Pubic hair, hairs of abdomen, chest, thighs, axilla, and perianal area. Occasionally, eyebrows and lashes are involved in young children and beards in males.
  3. After prolonged infestation, small blue spots called maculae caeruleaemay appear on thighs and abdomen. These are uncommon but specific for pubic lice. They represent feeding sites of the louse.
  4. Coexisting STDs are common in adolescents infested with pubic lice. One study showed that infested teens were twice as likely to have concurrent chlamydia or gonorrhea than noninfested teens (Pierzchalski et al., 2002).

Diagnosis

Diagnosis of pubic lice is made by direct visualization of lice or nits (eggs) on the hair shafts. Lice appear as tiny, tan to grayish-white oval insects. Nits can be seen as small yellowish-white, glistening oval kernels attached to hair shafts.

Treatment

Pubic lice do not transmit systemic disease. Treatment is mainly for symptomatic relief and prevention of reinfestation and transmission. Topical treatments are more effective when applied to dry hair. Most treatments are toxic to the nervous system of the pubic louse. Embryos may survive initial treatment, requiring a second course of the treatments listed in the subsequent text in 7 to 10 days:

  1. CDC recommended regimens
  2. Permethrin 1% creme rinse (Nix) applied to affected area and washed off after 10 minutes. Treatment of choice because of low toxicity, high cure rate, and possible ovicidal activity.
  3. Pyrethrins and piperonyl butoxide (nonprescription RID, R & C Lice treatment, Clear, Pronto) applied to the affected area and washed off after 10 minutes.
  4. Alternative regimens
  5. Malathion lotion 0.5% (Ovide) applied for 8 to 12 hours then rinsed off in hot water. Reapply in 7 to 9 days if live lice are still present. Used for resistant infestations in adults because of odor and flammability, and toxicity if ingested. Approved for use only in those aged 6 years and older.
  6. Ivermectin at a single dose of 250 µg/kg repeated in 2 weeks (not ovicidal). This drug should not be used on anyone weighing <15 kg, or in pregnant or breast-feeding women. There is some potential for neurotoxicity, so this drug should be used with caution. It may be particularly useful in people who have more than one parasitic infection.
  7. Lindane 1% shampoo applied for no longer than 4 minutes and then thoroughly washed off.

Note: Not recommended for pregnant or lactating women and children <2 years, anyone with a seizure disorder, or anyone with inflamed or traumatized skin. Should be used only for treatment failures or inability to tolerate other treatment regimens. Has potential for central nervous system toxicity.

  1. Clothing or bed linen coming in contact with the patient within the last 2 days should be machine washed at 130°F to 140°F and machine dried (hot cycle for 20 minutes) or dry cleaned. Clothing that cannot be decontaminated as above should be bagged for at least 72 hours. Fumigation is not necessary.
  2. Residual nits should be removed with a fine comb. For nits that are difficult to remove, a solution of vinegar and water can be used to loosen them.
  3. Sexual contacts within the last month should be treated. Sexual contact should be avoided until both patient and partner are treated and reevaluated for persistence of the infestation.
  4. Pregnancy: Use permethrin or pyrethrins with piperonyl butoxide.
  5. HIV infection: Use the same therapy as for a noninfected adolescent.
  6. Pediculosis of eyelashes: Treat with application of occlusive ophthalmic ointment to the eyelid margins two times a day for 10 days. This smothers the lice and nits. Do not apply lindane or other medications to the eyes. Oral sulfamethoxazole/trimethoprim for 10 days has reportedly been effective but is not FDA approved for this use.

Scabies

Scabies is a highly contagious, ectoparasitic infection. It is one of the most widespread infestations in the world, with approximately 300 million cases of scabies worldwide each year.

Etiology

Scabies is caused by a small mite, Sarcoptes scabiei var. hominis. The adult mite has a rounded body, has four pairs

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of legs, and measures 400 µm in length. This parasite is host-specific for humans.

Epidemiology

  1. Transmission: The mite is transmitted by prolonged skin-to-skin contact. Sexual transmission is common, as is nonsexual spread in family groups. Transmission can occur before the patient is symptomatic and throughout the infestation as long as it remains untreated. Scabies is frequently found in institutional settings and epidemics are associated with poverty, overcrowding, sexual promiscuity, travel, waning immunity, and other factors.
  2. Life cycle: The impregnated female mite burrows into the skin where she lays between 10 and 25 eggs in a 1-cm-long tunnel. Egg-laying is completed in 4 to 5 weeks, and the adult female dies within the burrow. After 3 to 5 days the eggs hatch, and the larvae return to the skin surface to mature in 10 to 17 days. Only 10% of eggs become adults. The average infected host has 3 to 50 adult female mites. Away from the host, human mites have been shown to survive up to 24 to 96 hours.
  3. Age: In underdeveloped countries, scabies has the highest prevalence in preschool children and adolescents. In developed nations, the prevalence is similar in all ages.

Clinical Manifestations

  1. Incubation: Symptoms occur 3 to 6 weeks after first exposure and 1 to 4 days after reexposure.
  2. Lesions: Scabies is an intensely pruritic, papular eruption associated with eczematous lesions and areas of excoriation. Pruritus is often worse at night or after a hot bath and is caused by a cell-mediated immune reaction to the mite and its by-products. The burrows, if seen, appear as short wavy lines a few millimeters to 1 cm in length.
  3. Involved areas: Skin lesions are typically seen in between finger webs, on the flexor surfaces of the wrists, in the axillary folds, on the nipples, waist and umbilicus, buttocks, thighs, knees, and ankles. In males, the penis and scrotum are often involved. Scabies usually spares the face, neck, and scalp except in children.
  4. Crusted or Norwegian scabies: This is a rare and aggressive form of scabies most often associated with immunodeficient, debilitated, or malnourished patients. Crusted scabies is characterized by a hyperinfestation of the mite with a concomitant inflammatory and hyperkeratotic reaction. The numerous scaling lesions are heavily infested with mites and more contagious than typical scabies. Treatment failures occur frequently and septicemia is a common complication.
  5. Differential diagnosis: The lesions can become secondarily infected and eczematized and therefore confused with eczema, atopic or contact dermatitis, or impetigo. Papulovesicular lesions may be confused with papular urticaria, chicken pox, drug eruptions, folliculitis, insect bites, or dermatitis herpetiformis.

Diagnosis

  1. Diagnosis is often made on the basis of the body distribution of lesions along with a history of intense itching and similar symptoms in family members or sexual partners. Definitive diagnosis requires microscopic identification of mites, eggs, or feces from skin scrapings of papules or burrows. Burrows are virtually pathognomonic for human scabies but are often difficult to demonstrate.
  2. Isolation of mite: Best results are obtained by using a no. 15 scalpel blade to scrape the leading edge of an intact burrow or affected area under fingernails. Visibility of burrows can be enhanced with application of mineral oil, immersion oil, saline, or ink to the skin. Scrapings are transferred to a cover slide under oil or saline and examined under low power for the presence of eggs, feces, or the mite. Alternately, punch or shave biopsies of inflamed lesions may also be used with varying results.

Treatment

  1. CDC recommended regimens
  2. Permethrin cream (Elimite) 5% applied to all areas of the body from the neck down and washed off after 8 to 14 hours. Application should include the area beneath the fingernails and skin folds. The cream can be applied at bedtime and removed by bathing the next morning.
  3. Ivermectin 200 µg/kg orally, repeated in 2 weeks.

Note: Ivermectin is not recommended for pregnant or lactating women or children weighing <15 kg. Use may be considered in epidemics, especially if topical scabicides have failed.

  1. Alternative regimens
  2. Lindane (1%) (Kwell) 1 oz of lotion or 30 g of cream applied thinly to all areas of the body from the neck down and washed off thoroughly after 8 hours. Application should include web spaces of digits and under fingernails. Lindane should not be applied immediately after a shower or bath because this may increase unnecessary systemic absorption.

Note: Lindane should not be used by pregnant or lactating women, children <2 years of age, or by those with seizure disorders or with extensive dermatitis. Lindane is not recommended as first-line therapy because of toxicity. It should only be used as an alternative if the patient cannot tolerate other therapies or if other therapies have failed.

Both aplastic anemia and seizures (when used after a bath or by patients with extensive dermatitis) have been reported with use. Lindane resistance has been reported in the United States.

  1. Crotamiton 10% (Eurax) applied for 24 hours once daily for 2 consecutive days followed by bathing 48 hours after the final application. Appears to work better as an antipyretic agent but associated with higher treatment failures, irritation, and allergic reactions. Crotamiton is no longer included by the CDC in their 2006 recommendations.
  2. Other agents used in the past with mixed results include benzyl benzoate, malathion, and sulfur 5% to 10% precipitated in ointment.
  3. The patient should not be contagious after 24 hours of treatment.
  4. Bedding and clothing worn during the 4 days preceding treatment should be machine washed, machine dried using hot cycle, dry cleaned, or removed from body contact and set aside in a sealed plastic bag for at least 72 hours. Fumigation of living areas is not necessary.
  5. Follow-up: Pruritus may persist for up to 2 weeks after treatment. Symptoms persisting longer can be due to a number of factors including resistance to medication, incorrect scabicidal application, poor skin penetration in crusted scabies, reinfection, or other allergies.

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Consideration can be given to re-treatment with a different regimen after 1 to 2 weeks, although some specialists recommend this only with the confirmation of live mites.

  1. Sex partners and household contacts: Prophylactic treatment is recommend for sex partners, as well as close personal or household contacts within the last month.
  2. Pregnant women: Pregnant or lactating women should use permethrin or crotamiton regimens.
  3. Oral antipruritics such as hydroxyzine (Atarax), or topical corticosteroids can be used to relieve itching.
  4. HIV infection: HIV-infected individuals should use the same treatment as those HIV-negative. Infected individuals are at increased risk for Norwegian scabies, a disseminated infection that should be managed in consultation with a specialist.
  5. Crusted scabies: This is a difficult to treat infection that may require combined treatment with Ivermectin and topical scabicides and keratolytic therapy or multiple doses of Ivermectin. Ivermectin is not FDA licensed for this use.

Molluscum Contagiosum

Etiology

Molluscum contagiosum is a self-limited, benign, viral skin disease caused by a large DNA poxvirus. It has a worldwide distribution and appears particularly prevalent in warm, humid climates.

Epidemiology

Humans appear to be the only known host of the virus. Transmission occurs by direct person-to-person contact, fomites, or autoinoculation. Transmission has also been associated with swimming pools. Among adolescents, sexual contact is believed to be the most common form of transmission. The incubation period is variable and appears to be from 2 weeks up to 6 months.

Clinical Manifestations

  1. Location: The lesions commonly occur on the face, trunk, and extremities. In sexually active adolescents, the lesions are commonly seen on the genital and pubic areas, and inner thighs.
  2. Appearance: Lesions are smooth, firm, flesh-colored, dome-shaped papules that can become soft, waxy or pearly gray, and semitranslucent with central umbilication. Immunocompetent hosts typically have less than 20 lesions that grow up to 5 mm in diameter over a period of a couple weeks. HIV-positive and immunocompromised patients may develop hundreds of lesions that may present in clusters. Additionally, HIV-positive patients can present with “giant molluscum” up to 15 mm in diameter that are difficult to eradicate and are easier spread.
  3. Symptoms: The lesions are usually asymptomatic; however, approximately 10% of patients will have an encircling eczematoid reaction.

Differential Diagnosis

  1. Condylomata acuminata
  2. Vulvar syringoma
  3. Squamous or basal cell carcinoma
  4. Juvenile xanthogranulomas
  5. Lichen nitidus

Diagnosis

  1. The clinical appearance is usually diagnostic.
  2. Wright or Giemsa staining of the caseous material found within the core will reveal intracytoplasmic inclusion bodies known as molluscum bodies. Poxvirus can be identified by electron microscopy of these core cells.

Treatment

Owing to the benign nature and self-limiting course of molluscum, nontreatment is an option for nongenital lesions. Individual lesions may resolve in 2 to 6 months but untreated infections can last as long as 5 years. However, autoinoculation can spread the disease and sexually active individuals are at risk of further transmitting the disease. Immunocompromised individuals are also at greater risk of secondary inflammation and bacterial infection. Treatment options include both mechanical and chemical means applied by either the provider or patient:

  1. Mechanical ablation: All are considered safe in pregnancy.
  2. Curettage or needle extraction of the central molluscum core with/without a local anesthetic such as EMLA. Cauterization of the lesion base with electrodesiccation or application of trichloroacetic acid (TCA) or podophyllin to the base may be of added benefit. Works best when there are only a few lesions.
  3. Cryotherapy through application of liquid nitrogen to the lesions and surrounding area for 5 to 10 seconds. Treatment may need to be repeated in 2- to 4-week intervals. Blistering and scarring are potential side effects.
  4. Electrodesiccation using high frequency electrical current may be used along with a local anesthetic.
  5. Pulse dye laser may be an option for recalcitrant lesions. Laser treatment has been associated with transient hyperpigmentation and development of new lesions after eradication of the old ones.
  6. Duct tape occlusion therapy has been used successfully over a course of months.
  7. Chemical cytotoxic agents:
  8. Podophyllin (25%) applied to individual lesions by a health care provider and washed off 1 to 4 hours later. Treatments are given weekly for 4 to 6 weeks and may be associated with significant irritation. Best used when limited number of nonfacial lesions are present. As an alternative, patients can self-apply podofilox twice daily for 3 consecutive days followed by 4 days without treatment, in 4 to 6 cycles. May be associated with pain, irritation, and mild scarring and has a low efficacy and potential toxicity. Not approved for use in pregnancy.
  9. TCA (80%–90%) applied by a health care provider to the lesion(s) once a week for 4 to 6 weeks. May result in mild pain, irritation, and scarring. Safe in pregnancy.

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  1. Cantharidin (0.7%–0.9%) carefully applied by a health care provider to lesions, and washed off within 2 to 6 hours. May be repeated in 2 to 4 weeks. Not FDA approved or recommended for face or genitalia use, secondary to significant blistering.
  2. Topical 0.5% tretinoin cream or gel applied to lesions daily for 2 to 3 months. Local irritation and dryness are side effects. No controlled clinical trials have been done and it is not recommended in pregnancy.
  3. Immunomodulators

Topical 5% imiquimod applied overnight three times per week and washed off in the morning, for 4 to 12 weeks. Currently not FDA approved for this use. May be associated with mild pain and erythema. Not for use in pregnancy.

  1. HIV/immunosuppressed patients

Molluscum contagiosum is considered an opportunistic infection in HIV disease and a marker for advanced infection. HIV-infected individuals have high treatment failure rates for almost all standard therapies for molluscum. Imiquimod (5%) may have some benefit, and experimental treatments utilizing the antiviral drug cidofovir (topically or intralesionally) and α-interferon (intralesionally) may be of benefit.

Follow-up

  1. Patients should be told to watch for the development of new lesions after several weeks that may have been incubating at the time of the initial treatment.
  2. Patients should refrain from sharing clothing or towels with others.
  3. Swimming in pools should be discouraged.
  4. Partners should be examined and treated for lesions, although the benefits of this are unknown.

Web Sites

For Teenagers and Parents

http://www.cdc.gov/ncidod/dpd/parasiticpathways/insects.htm. Centers for Disease Control and Prevention (CDC) handouts/information on scabies and public lice.

http://www.ashastd.org. American Social Health Association handout on STDs.

http://www.urologychannel.com/std/index.shtml. Information on sexually transmitted diseases.

For Health Professionals

http://www.cdc.gov/std/lgv. CDC website on diagnosing and testing for LGV.

References And Additional Readings

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Brown TJ, Yen-Moore A, Tyring SK. An overview of sexually transmitted diseases: part II. J Am Acad Dermatol 1999; 41:5.

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O'Farrell N. Donovanosis. Sex Transm infect 2002;78:452.

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