An overview of sexually transmitted diseases. Part III ... - Dermatology

The HIV epidemic has drastically altered the medical 

community’s approach to sexually transmitted 

diseases (STDs). For generations, multiple 

STDs occurred in individual patients. However, not 

until HIV did these infections interact so significantly 

with each other. Clinically, HIV can alter the presentation 

or treatments of other STDs as in, for example, a 

case of coexistent HIV and scabies. Conversely, an 

increasing recognition of the ways in which STDs influence 

HIV transmission has underscored the importance 

of early detection and treatment of all STDs. In 1998, 

the Centers for Disease Control and Prevention (CDC) 

published Guidelines for the Treatment of Sexually 

Transmitted Diseases, 1 and in addition the CDC published 

recommendations for the prevention of HIV 

through early detection and treatment of other STDs. 2 

From the Department of Dermatology at the University of Texas— 

Houston Health Science Center and St Joseph Hospital, 

Houston a ; the Department of Dermatology at the University of 

Texas—Southwestern Medical School and Veterans Affairs 

Hospital, Dallas b ; and the Departments of Dermatology, 

Microbiology & Immunology and Internal Medicine at the 

University of Texas Medical Branch, Galveston. c 

Reprint requests: Stephen K. Tyring, MD, PhD, Department of 

Dermatology, Route 1070, University of Texas Medical Branch, 

Galveston, TX 77555-1070. E-mail: styring@utmb.edu. 

16/2/105158 

doi:10.1067/mjd.2000.105158 

CONTINUING MEDICAL EDUCATION 

An overview of sexually transmitted diseases. 

Part III. Sexually transmitted diseases in 

HIV-infected patients 

Adam Czelusta, MD, a Angela Yen-Moore, MD, b Melody Van der Straten, MD, c 

Daniel Carrasco, MD, c and Stephen K. Tyring MD, PhD c Houston, Dallas, and Galveston, Texas 

The HIV epidemic has dramatically altered the field of sexually transmitted diseases (STDs). HIV infection 

is unique among sexually transmitted diseases because it can modify the clinical presentation and features 

of other STDs. Conversely, other STDs can affect the transmission of HIV. This review is the third part of a 

series that has provided a general overview of STDs. In this article, genital ulcer diseases (genital herpes, 

syphilis, chancroid, lymphogranuloma venereum, and granuloma inguinale), human papillomavirus 

infection (anogenital warts and subclinical infections), molluscum contagiosum, human herpesvirus 8 

infection, viral hepatitis, and ectoparasitic infestations (scabies and pediculosis pubis) are discussed as they 

occur in HIV-infected hosts. Additional features as they relate to HIV-infected patients, such as 

epidemiology and transmission, are discussed when applicable. 

Learning objective: At the conclusion of this learning activity, participants should improve their 

understanding of sexually transmitted diseases in the HIV-infected host. (J Am Acad Dermatol 2000;43:409-32.) 

Abbreviations used: 

ASIL: anal squamous intraepithelial lesion 

CDC: Centers for Disease Control and 

Prevention 

CSF: cerebrospinal fluid 

CSIL: cervical squamous intraepithelial lesion 

HAART: highly active antiretroviral therapy 

HBV: hepatitis B virus 

HCV: hepatitis C virus 

HHV: human herpesvirus 

HPV: human papillomavirus 

HSV: herpes simplex virus 

KS: Kaposi’s sarcoma 

MCV: molluscum contagiosum virus 

STD: sexually transmitted disease 

Given the predominantly cutaneous manifestations of 

many STDs, dermatologists are uniquely situated to 

diagnose and treat these diseases in HIV-infected 

patients. This article reviews the STDs that affect HIV 

patients, with particular emphasis on those issues most 

pertinent to dermatologists. 

GENITAL ULCER DISEASE 

Effect on HIV acquisition and transmission 

Each of the major genital ulcer diseases, genital 

herpes simplex virus (HSV) infections, syphilis, and 

409

410 Czelusta, Yen-Moore, and Tyring J AM ACAD DERMATOL 

SEPTEMBER 2000 

chancroid, have been associated with an increased 

risk of acquiring and transmitting HIV. One estimation 

suggests that STDs increase the overall risk of 

acquiring HIV about 3 to 5 times. 3 Cross-sectional 

studies performed in Nairobi, Kenya have consistently 

found that HIV seropositivity was more 

common in persons with either a history or clinical 

evidence of genital ulcer disease, 4-7 and one 

prospective study from this same region showed an 

increased risk of seroconversion in patients with 

genital ulcer disease. 8 Similarly, Telzak et al 9 found 

that 2.9% of men with genital ulcer disease turned 

HIV-positive, whereas only 1% of men without genital 

ulcer disease seroconverted. Clearly, a relationship 

between genital ulcer disease and HIV transmission 

exists; subsequently, prevention of genital ulcer 

disease should decrease transmission of HIV. A 

Tanzanian study showed that communities that 

improved their recognition and treatment of STDs 

saw a decrease in the incidence of HIV infection in 

their population. 10 This is the first documented 

intervention involving treatment of STDs that was 

associated with a decrease in HIV incidence in a 

defined population. Thus, through the early recognition 

and treatment of all STDs, including genital 

ulcer disease, HIV transmission can be reduced. 

Numerous studies have isolated HIV from genital 

ulcer exudates. 11-14 Mechanisms by which genital 

ulcer disease appear to facilitate HIV transmission 

have been suggested. Disruption of the genital 

mucosa is associated with the recruitment of inflammatory 

cells such as CD4 + T lymphocytes and 

macrophages. The presence of these cells can facilitate 

transmission of HIV virions from HIV-infected 

persons to uninfected persons or provide additional 

targets for HIV entry in HIV-negative persons who 

are being exposed to the virus. 14-17 

Studies implicating the specific agents of genital 

ulcer disease have focused mostly on genital herpes, 

syphilis, and chancroid. Several reports have shown an 

association between genital HSV lesions and the acquisition 

of HIV infection in the affected population. 

4,9,18-23 Keet et al 23 showed in a prospective 

cohort that pre-existing herpes simplex virus type 2 

(HSV-2) seropositivity was a predictor of HIV seroconversion. 

HIV virions have been shown in HSV ulcers, 24 

and in one study HIV RNA was isolated from herpetic 

lesions on 67% of the days that lesions were present. 13 

Similarly, arguments implicating syphilis and chancroid 

in the acquisition of HIV can be made. Two studies 

from Baltimore document strong associations 

between HIV seroconversion and either positive 

syphilis serology or a history of syphilis. 25,26 One 

cross-sectional study from Kenya found a similar association 

5 ; however, the difficulty in making this associ- 

ation statistically significant may reflect the difficulty 

in identifying cases of syphilis with active genital 

ulcers during the study. 8 An outbreak of chancroid in 

Jackson, Mississippi showed a strong association 

between this infection and HIV seropositivity, 27 and 

most of the ulcers in an aforementioned Kenyan 

study were due to chancroid and were associated 

with increased HIV seropositivity. 6 Lymphogranuloma 

venereum and granuloma inguinale are rare diseases, 

and, as such, they have not been extensively studied 

in relation to HIV transmission. Granuloma inguinale 

has been associated with a significant number of HIV 

infections, 28 and its eradication (in an effort to prevent 

HIV transmission) has been suggested. 29 

Clinical features and treatment 

Genital herpes. Genital herpes is the most common 

cause of genital ulceration worldwide, 30 and its 

association with HIV was noticed as early as 1981. 31 

Although genital herpes is most commonly caused 

by HSV-2, an increasing number of cases are suspected 

to be caused by HSV-1. 1,32 In HIV-infected 

patients, genital herpes can result in severe and atypical 

clinical presentations, and treatment may 

require increased doses of antiviral medications. 

Suppressive therapy for HSV appears to significantly 

improve survival in HIV-positive patients. 

Clinically, HIV-infected patients may experience 

an increased number and size of lesions in both primary 

and reactivated HSV infections as compared 

with HIV-uninfected patients. 31,33,34 The vesicles and 

ulcers are more painful and heal slower than those 

experienced by an immunocompetent host. 35 As 

CD4 cell counts drop and immunosuppression worsens, 

recurrent outbreaks increase in frequency and 

severity. 36,37 Chronic HSV-2 ulcers of more than 1 

month in duration are an AIDS-defining illness in 

HIV-infected patients. 38,39 

Atypical HSV presentations occur relatively often 

in HIV-infected patients. Particularly severe lesions 

have been reported on patients’ lower backs, buttocks, 

or perianal regions, and these lesions may 

expand to 20 cm in diameter (Fig 1). 31,40 Such ulcers 

commonly become impetiginized and require intensive 

long-term therapy. 31 Several case reports 

describe HSV-2 presenting as hyperkeratotic verrucous 

lesions resembling condyloma in severely 

immunocompromised patients. 41-44 These masses 

can become large 41,43 and may represent concurrent 

HSV and cytomegalovirus infection. 44 A recent 

report describes a patient with a pseudotumor of the 

tongue that was discovered to be an atypical recurrence 

of HSV-2. 45 HSV may also cause esophagitis, 

hepatitis, pneumonitis, or life-threatening disseminated 

infections in AIDS patients. 46

J AM ACAD DERMATOL 

VOLUME 43, NUMBER 3 

Acyclovir, valacyclovir, and famciclovir are recognized 

by the CDC as appropriate therapies for primary 

or recurrent genital herpes in the HIV-infected 

patient. 1 As in the immunocompetent patient, therapy 

should start as soon as possible, preferably during 

the prodromal period. Therapy is then continued 

until clinical resolution is obtained. 1 For acyclovir 

and famciclovir, increased dosages above those recommended 

for immunocompetent persons may be 

required. For example, whereas the recommended 

oral dose of acyclovir is either 400 mg 3 times per 

day or 200 mg 5 times per day, regimens of 400 mg 

given 5 times per day have been useful in immunocompromised 

patients. 1 Likewise, famciclovir 250 

mg twice daily is recommended for suppression of 

genital herpes in the immunocompetent person, but 

500 mg twice daily has been effective in decreasing 

both the rate of recurrences and the rate of subclinical 

shedding among HIV-seropositive persons. 47 

When given at doses of 8 g per day to markedly 

immunocompromised persons for suppression of 

cytomegalovirus infections, valacyclovir was associated 

with either thrombotic thrombocytopenic purpura 

or the hemolytic uremic syndrome. 1,48,49 However, no 

cause-and-effect relationship was ascertained. When 

taken as a dose of 500 mg twice daily, valacyclovir 

appeared safe and effective for the suppression of 

genital HSV in HIV-seropositive persons and was 

superior to acyclovir 400 mg twice daily. 50 Therefore 

acyclovir, valacyclovir, and famciclovir all appear useful 

for treatment and suppression of HSV in immunocompromised 

persons. 47-55 

Interestingly, acyclovir treatment of HSV infections 

in HIV-positive patients may offer a significant 

survival benefit. Eight randomized controlled trials, 

combined in a meta-analysis, showed that patients 

treated with acyclovir had a significant survival 

advantage compared with those who went untreated. 

51 Two multicenter clinical trials noted that 

patients given acyclovir and zidovudine lived longer 

than those given only zidovudine. 56,57 These studies 

suggest that long-term suppressive acyclovir therapy 

prolongs survival in AIDS patients with extensive histories 

of HSV infections. 

The mechanism by which this occurs is unclear. 

Studies demonstrate that acute or reactivated HSV 

infection may stimulate HIV replication. 58-60 

Furthermore, Mole et al 61 documented increased 

plasma HIV viral loads in HIV patients experiencing 

an outbreak of HSV. By reducing or attenuating 

the occurrences of HSV outbreaks, acyclovir therapy 

may help reduce these deleterious effects of 

the infections. Clearly, further investigation 

regarding this issue is required, as evidenced by 

the study of Gallant et al, 62 which found no asso- 

Czelusta, Yen-Moore, and Tyring 411 

Fig 1. HIV-positive patient. Large suprapubic ulcer due to 

HSV type 2. 

ciation between survival and acyclovir use in HIVinfected 

patients. 

A preliminary report from the CDC noted that 

6.4% of HSV isolates from 140 HIV-positive patients 

were resistant to acyclovir compared with less than 

1% of isolates from immunocompetent persons. 63 

Typically, resistance to acyclovir is also associated 

with resistance to the other thymidine kinase 

inhibitors. Resistance rates before the advent of 

these medicines appear similar to those currently 

seen in the population. Resistance does not appear 

to be increased or induced by long-term suppressive 

therapy with these medications. 64 In contrast, the 

increased HSV acyclovir-resistance rates seen in HIVpositive 

patients may reflect the increased replication 

of HSV in these patients; therefore resistance 

may actually be reduced by long-term suppressive 

thymidine kinase inhibitor therapy. 65 

Resistance to acyclovir may be mediated by mutations 

in either the HSV thymidine kinase or HSV 

DNA polymerase genes with decreased substrate 

affinity or by decreased or absent production of the



Fig 2. HIV-positive patient. Primary syphilis: perianal 

chancres. 

HSV thymidine kinase. 66 If resistance is suspected, 

HSV cultures and susceptibility testing are indicated. 

As such, the virus remains susceptible to foscarnet 

(which competitively blocks the pyrophosphate 

binding site of viral DNA polymerase) and cidofovir 

(which is a nucleotide analogue not dependent on 

viral thymidine kinase). 67 In cases of acyclovir resistance, 

intravenous foscarnet, 40 mg/kg of body 

weight every 8 hours, or topical cidofovir 1% applied 

to the lesions daily is suggested therapy from the 

CDC. 1 

Foscarnet resistance has been reported, and this 

may make cidofovir the most viable option. 68,69 

Regardless, these two medicines have important 

potential side effects. Foscarnet is nephrotoxic and 

can produce severe hypocalcemia, and in a phase I/II 

trial, topical cidofovir gel in concentrations of 3% 

and 5% was associated with local toxicity and delayed 

healing. 70 

Syphilis. The interactions between syphilis and 

HIV gained widespread attention after a 1987 case 

series described HIV-infected patients whose syphilis 

infection was either refractory to appropriate thera- 

pies or displayed a rapid progression from primary 

syphilis to neurosyphilis. 71 Since this report, many 

investigators have studied the atypical features of 

syphilis in the setting of HIV disease, but the significance 

of these features remains unclear. Syphilis in 

the HIV patient appears to progress more rapidly 

through the clinical stages of syphilis, often will have 

an atypical clinical presentation, may have a refractory 

course after appropriate intramuscular penicillin, 

and may lead to unusual serologic test results (Fig 2). 

Numerous reports describe an accelerated progression 

through the syphilitic stages in HIV patients. 71-74 

This progression may be related to level of immunosuppression; 

one study described HIV-infected 

patients initially presenting to physicians with undiagnosed 

secondary syphilis when their CD4 cell counts 

were less than 500 cells/mm 3 . 75 Others reported an 

association between accelerated ulcerating syphilis 

(malignant syphilis) and advancing HIV disease. 76,77 

An association between advancing HIV disease and 

progression to neurosyphilis has also been noted. 76 In 

contradiction to these findings, Dowell et al 78 found 

no association between HIV stage and syphilitic progression 

or relapse after treatment. 

Although the clinical presentation is commonly the 

same in the HIV-infected host as it is in the otherwise 

healthy host, unusual features may be seen. The primary 

stage of syphilis may consist of multiple or more 

extensive chancres in the HIV patient. 79 Secondary 

syphilis affecting the immunocompetent host can present 

in a multitude of fashions, and likewise, the HIV 

patient can exhibit a wide range of cutaneous manifestations 

in this stage. Several reports document that 

patients with HIV are more likely to progress to neurosyphilis 

in the first 2 years after diagnosis, often 

despite appropriate therapy. 71-73,80-85 Unusual manifestations 

of neurosyphilis 86 have been documented 

in HIV-infected patients, as have unusual gummatous 

lesions. 87 Furthermore, rapidly developing cases of 

ocular syphilis 82,88,89 and syphilitic aortitis 90 have been 

reported in the HIV-infected population. Encephalitis 

and arteritis are other potential atypical presentations 

of syphilis in the HIV-infected host. 

For most people with coinfections of HIV and 

syphilis, laboratory tests can be interpreted as they 

would in an immunocompetent person. 1 However, 

atypical serologic responses in HIV-infected patients 

with syphilis do occur. Most reports involve falsepositive 

responses to the two nontreponemal 

screening tests: the rapid plasma reagin card test and 

the Venereal Disease Research Laboratory (VDRL) 

test. This sort of false-positive test is termed a “biologic 

false positive.” Several studies document an 

increased rate of biologic false positives in HIVinfected 

patients when compared with controls. 91-93



In addition, one study noted an increased rate of biologic 

false-positive findings among those HIV 

patients who acquired their disease through intravenous 

drug abuse and in those who were coinfected 

with the hepatitis B virus (HBV), as compared 

with homosexual HIV-positive controls. 94 Other 


Fig 3. HIV-positive patient. Biopsy-confirmed, seronegative secondary syphilis. 

Fig 4. Photomicrograph of biopsy specimen of secondary syphilis shows dense lichenoid infiltrate 

with abundant plasma cells and histiocytes. 

abnormalities reported in serologic tests involve 

delayed titer responses after treatment of syphilis in 

HIV-infected patients. Typically, a patient’s biologic 

titers are expected to drop 4-fold after treatment. In 

HIV-infected patients, studies have documented 

both a normal serologic titer response after syphilis



Table I. Recommended management for syphilis in HIV-infected patients 1 

Stage Treatment Follow-up 

Primary, secondary, or early latent 2.4 × 10 6 U intramuscular benzathine Clinical and serologic exams at 3, 6, 9, 12, 

syphilis penicillin G once and 24 mo 

Late latent syphilis or syphilis of 2.4 × 10 6 U of intramuscular Clinical and serologic exams at 6, 12, 18, 

unknown duration benzathine penicillin G weekly for and 24 mo 

3 wk 

Neurosyphilis or ocular syphilis* 3-4 × 10 6 U of intravenous aqueous If CSF pleocytosis was initially present, 

crystalline penicillin G every 4 h for CSF exams every 6 mo (for up to 2 yr) 

10-14 days (or) intramuscular until this parameter returns to normal 

procaine penicillin 2.4 × 10 6 U daily 

and oral probenicid 500 mg 4 times 

per day for 10-14 days 

*Some experts recommend the addition of a single intramuscular dose of 2.4 × 10 6 U of benzathine penicillin G to the conclusion of therapy 

in cases of neurosyphilis. 

treatment 75,95,96 and a delayed serologic titer 

response after syphilis treatment. 79,97-99 Finally, 

other reports describe cases of seronegative syphilis, 

accelerated loss of antibody reactivity after treatment, 

antibody production to decreased numbers of 

treponemal antigens, and the return of titers to nonreactive 

as immunosuppression advances (Fig 

3). 100-105 When serologic tests are inconsistent with 

clinical suspicion, other tests are indicated, such as 

lesional biopsy (Fig 4), dark-field microscopy, or 

direct fluorescent antibody staining of lesion material. 

1 Still, the histologic features of a biopsied lesion 

may be altered in HIV-infected patients. 106 

Progression to neurosyphilis despite appropriate 

therapy 71-73,80-85 has prompted some experts to recommend 

regular cerebrospinal fluid (CSF) examinations 

in HIV-infected patients when they are first 

diagnosed with either primary or secondary syphilis 1 

in addition to current recommendations for CSF 

examinations in HIV-infected patients with late latent 

syphilis. * These experts recommend modification of 

treatment based on the CSF laboratory results. 

However, the CSF results in this population may be 

difficult to interpret, given the fact that HIV-positive 

patients have high rates of CSF abnormalities without 

syphilis infection. 1 

General treatment guidelines as recommended 

by the CDC are outlined in Table I. In the management 

of patients with primary, secondary, or early 

latent syphilis, some specialists recommend supple- 

*Early latent syphilis is defined as those asymptomatic patients 

with titers suggestive of a current syphilis infection who, within 

the past year, acquired syphilis as reflected either by a documented 

seroconversion, indisputable symptoms of primary or 

secondary syphilis, or a sex partner who had primary, secondary, 

or early latent syphilis in the past year. Almost all other patients 

have either late latent syphilis or syphilis of unknown duration. 

mental antibiotic therapy in addition to that listed, 

and some experts recommend a CSF examination at 

6 months after therapy in this group. 1 Those patients 

in this group who do not respond to treatment but 

whose CSF findings remain normal are treated with 

intramuscular benzathine penicillin G 2.4 × 10 6 U 

weekly for 3 weeks. 1 

If during the follow-up of any patient with late 

latent syphilis or syphilis of unknown duration, he or 

she develops symptoms or a rise in antibody titers, 

then CSF should be examined and retreatment 

administered appropriately. 1 In any HIV-infected 

patient with syphilis of any stage, penicillin desensitization 

is recommended if the patient is allergic to 

penicillin. 1 The management of syphilis in the HIVinfected 

host is a complex issue in which further 

study is clearly necessary. 

Chancroid. Chancroid is the most common cause 

of genital ulceration in Africa, 107 and outbreaks have 

been reported in Europe, Canada, and the United 

States. 108,109 Men are most commonly affected, and 

the typical clinical presentation is single or multiple 

soft-edged ulcers that are accompanied by inguinal 

adenopathy in 40% to 70% of cases. 110 Although relatively 

few studies have evaluated chancroid in HIVpositive 

patients, the clinical presentation appears to 

have only minor differences from HIV-negative 

patients, and the rate of treatment failures may be 

slightly increased in HIV-positive patients. 111-115 

Ulcer size was consistently unaffected by HIV 

serostatus in all studies surveyed. 111-114 The only differences 

reported include a longer ulcer duration 

113,114 and a greater number of ulcers at initial 

presentation 113 in HIV-positive patients. Nonetheless, 

atypical presentations can occur as evidenced 

by an HIV-positive patient from New York who had 

chancroid that presented as a chronic penile ulcer



Fig 5. HIV-positive patient. Chancroid with typical “kissing” ulcers. 

accompanied by the development of ulcers on his 

legs and digits 115 (Fig 5). 

Two studies that evaluated histologic features of 

punch biopsy specimens from chancroid ulcers 

found that specimens from HIV-negative and -positive 

patients had no notable differences. 114,116 As in 

the immunocompetent host, diagnosis of chancroid 

in the HIV-positive patient is ideally made by culture 

of the causative organism, Haemophilus ducreyi, or, 

if this is not possible, by the presence of a clinical 

presentation typical of chancroid (ie, genital ulcers, 

usually painful, often multiple, with ragged edges 

and a base covered by a necrotic, yellow-gray exudate), 

and negative laboratory evaluations for both 

Treponema pallidum and HSV. 1 

Several clinical trials report the efficacy of antibiotic 

therapy for chancroid on the basis of their subjects’ 

HIV serostatus. 112-114,117-120 Studies of a single 

quinolone (fleroxacin) dose demonstrated that HIVpositive 

patients are cured of chancroid less frequently 

with these treatments than are HIV-negative 

patients. 117,118 However, despite the apparent consistent 

difference in response rates, none of these studies 

achieved statistical significance in this comparison. 

One study actually extended the quinolone therapy of 

HIV-negative patients to 5 days and compared it with 

single-dose therapy in HIV-positive patients. 112 Again, 

while the HIV-positive patients were cured at a lower 

rate than the HIV-negative patients, the difference was 

not statistically significant. Single-dose ceftriaxone and 

single-dose azithromycin demonstrate statistically sig- 


nificant failure rates in treating HIV-positive patients 

with chancroid when compared with HIV-negative 

patients. 119,120 Similarly, 7-day erythromycin therapy 

has shown significantly lower rates of curing chancroid 

infections in HIV-infected patients at 1 and 2 weeks 

after starting therapy, 113,114,120 but when these 

patients are observed to 3 weeks, the cure rates are 

not significantly different between HIV-positive and 

-negative patients. 114 Current CDC recommendations 

for treatment of chancroid in immunocompetent and 

HIV-infected patients are the same: oral azithromycin 

1 g in a single dose, intramuscular ceftriaxone 250 mg 

in a single dose, oral ciprofloxacin 500 mg twice daily 

for 3 days, or oral erythromycin base 500 mg 4 times 

daily for 7 days. 1 In addition, the CDC notes that HIVpositive 

patients may require longer courses of therapy 

than those listed and that any of the regimens may 

fail. For this reason, close follow-up of HIV-positive 

chancroid patients with chancroid is essential. 

Granuloma inguinale. Granuloma inguinale, 

caused by Calymmatobacterium granulomatis, is 

endemic to the Caribbean, South America, South 

Africa, Southeast India, Papua New Guinea, and 

among the Aborigines in central Australia, 121 but it is 

extremely rare in North America. 122 It typically 

involves the genitalia with a chronic, destructive, 

beefy red, nontender granulomatous ulcer, and diagnosis 

is made in both HIV-positive and HIV-negative 

patients by visualizing characteristic intracytoplasmic 

Donovan bodies on microscopic evaluation of either 

tissue smears or biopsy specimens. 123 Few data are



Table II. Recommended therapy for granuloma inguinale and lymphogranuloma venereum 1 

Infection Recommended therapy Alternative therapy 

Granuloma inguinale* Oral trimethoprim-sulfamethoxazole Oral ciprofloxacin 750 mg twice daily (or) 

double-strength tablet twice daily oral erythromycin base 500 mg 4 times 

(or) oral doxycycline 100 mg twice daily until lesions heal or for at least 3 wk 

daily until lesions heal or for at least 

3 wk 

Lymphogranuloma venereum Aspiration or incision and drainage of Aspiration or incision and drainage of 

buboes if necessary and oral buboes if necessary and oral erythromycin 

doxycycline 100 mg twice daily for 3 wk base 500 mg 4 times daily for 3 wk 

*Gentamicin (1 mg/kg intravenously every 8 h) should be strongly considered in HIV-positive patients. 

available about the effects of HIV infection on this 

disease, but it appears that HIV-positive patients 

have ulcers that persist for a longer duration and 

may require more intensive antibiotic therapy as 

compared with HIV-negative patients. 124 A prospective 

case-control study of 50 patients (21 HIV-positive 

and 29 HIV-negative) in India demonstrated 

that, while the ulcer size and clinical presentations of 

HIV-positive and HIV-negative patients with granuloma 

inguinale were not significantly different, the 

mean duration to complete ulcer healing was significantly 

longer in HIV-positive patients (25.7 vs 16.8 

days) and associated with greater tissue destruction. 

124 A retrospective study of pregnant women 

with granuloma inguinale demonstrated no difference 

in pregnancy outcome between HIV-negative 

and HIV-positive patients. 125 Although extragenital 

dissemination of granuloma inguinale has been 

reported in association with HIV infection, 126 most 

case reports note the failure of traditional antibiotic 

treatments. 127-129 In one case, a patient who did not 

respond to therapy or relapsed after treatment with 

doxycycline, tetracycline, erythromycin, cephalexin, 

ceftriaxone, and trimethoprim-sulfamethoxazole 

finally responded to a combination of trimethoprimsulfamethoxazole 

and ofloxacin. 129 

Currently the CDC recommends the same treatments 

for granuloma inguinale in HIV-negative and 

HIV-positive patients (Table II) with the note that 

gentamicin (1 mg/kg administered intravenously 

every 8 hours) should be strongly considered in HIVpositive 

patients. 1 Although granuloma inguinale is a 

relatively rare infection, O’Farell, Windsor, and 

Becker 28 have recommended a unified public health 

effort for its eradication based on its ease of treatment 

and strong association with HIV transmission. 

LYMPHOGRANULOMA VENEREUM 

Lymphogranuloma venereum, caused by the L 1 , 

L 2 , and L 3 immunotypes of Chlamydia trachomatis, 

may present clinically as primary (papule), secondary 

(inguinal), and tertiary (rectal) lesions. 130,131 

Lymphogranuloma venereum occurs most frequently 

in tropical countries and is rare in the United 

States. 132 In both HIV-positive and HIV-negative 

patients, diagnosis is made by a combination of clinical 

presentation and high chlamydial complement 

fixation antibody titers (≥ 1:64). No studies have 

been performed on patients with concomitant HIV 

infection and lymphogranuloma venereum, and 

remarkably little anecdotal evidence regarding clinical 

features and treatment has been published. 

Retrospective analysis of 27 cases of lymphogranuloma 

venereum seen in a Paris hospital found 6 

cases of concomitant HIV and lymphogranuloma 

venereum infection. HIV appeared to have no effect 

on the clinical presentation in each of these 6 

cases. 133 Similarly, Heaton et al 134 reported a case in 

which an HIV-positive pregnant woman had uncomplicated 

lymphogranuloma venereum. 

Nonetheless, an atypical presentation of 

Parinaud’s oculoglandular syndrome (unilateral follicular 

conjunctivitis followed by enlargement of 

preauricular lymph nodes) with associated inguinal 

lymphadenopathy due to Chlamydia trachomatis 

immunotype L 2 has been reported. This patient 

responded well to surgical management, topical 

(ocular) cefazolin and gentamicin, and oral tetracycline. 

135 The CDC recommends the same treatments 

for lymphogranuloma venereum in HIV-negative and 

HIV-positive patients (see Table II), with the note 

that disease duration may be prolonged in HIV-positive 

patients. 1 

HUMAN PAPILLOMAVIRUS 

Subclinical genital human papillomavirus 

infections 

Subclinical genital human papillomavirus (HPV) 

can affect the cervix, vagina, vulva, penis, anus, or 

any other genital skin. 136 The same types can also



Fig 6. HIV-positive patient. Oral condyloma acuminatum (ie, HPV type 6). 

infect the oral epithelium (Fig 6). The association 

between certain HPV types (eg, HPV types 16, 18, 31, 

and 45) and the development of dysplastic lesions in 

the cervix is well known. 137 The dysplastic lesion, 

termed a cervical squamous intraepithelial lesion 

(CSIL), occurs in the transformation zone along the 

squamocolumnar junction near the cervical os. CSIL 

is a precursor to cervical cancer. Similarly, the anal 

canal has a squamocolumnar junction and transformation 

zone that is affected by HPV infections. 

Specifically, the anal squamous intraepithelial lesion 

(ASIL) and invasive anal cancer appear to be associated 

with HPV infections, most notably HPV type 16 

infections. 138-141 

Genital HPV infections occur more commonly in 

HIV-infected men and women when compared with 

age-matched healthy control populations. 140,142-145 

The lesions are more frequently diffuse, dysplastic, 

and subclinical in HIV patients, whereas control populations 

more commonly have condylomatous 

lesions and less commonly have subclinical and dysplastic 

lesions. 146 In addition, HIV-positive patients 

tend to be infected with more HPV types than control 

populations. 144,147-149 As CD4 cell count decreases, 

shedding of HPV and extent of disease appear to 

increase. 150,151 

Given these clinical features, HPV replication and 

disease progression appear to be potentiated by HIV 

infections. 150,151 The mechanism behind this phenomena 

is unclear. HIV appears to influence gene 

transcription in HPV. 152,153 This may lead to a defect 

in the host’s local immune defenses and, when 


accompanied by the systemic immunosuppression 

of HIV infection, may explain the increased severity 

of HPV infections observed in this setting. 

Regardless of the exact mechanism, it is clear that 

HIV-infected persons have higher rates of cervical, 

anal, and other genital cancers (Figs 7 and 8). Those 

persons most at risk are women with a history of 

abnormal Papanicolaou (pap) smears and men or 

women who participate in receptive anal intercourse 

or have a history of anal condyloma. Not surprisingly, 

anal cancer is currently the fourth most common 

reportable cancer among HIV-positive men 154 and is 

about 7 times more common in homosexual men 

with HIV than those who are HIV seronegative. 

Likewise, cervical cancer in an HIV patient is an 

AIDS-defining illness. 38 

Clinically, full genital examinations in HIV-positive 

patients are extremely important. In women, the 

CDC recommends two pap smears and pelvic examinations 

during the first year after a diagnosis of HIV. 1 

If the results are normal, yearly pap smears and 

pelvic examinations are indicated thereafter. 1 

Abnormal results should be managed in consultation 

with a gynecologist, and current CDC recommendations 

regarding this issue are listed in the “Interim 

Guidelines for Management of Abnormal Cervical 

Cytology.” 155 Some research suggests that pap 

smears are an insensitive method to screen for cervical 

cancer in AIDS patients. 156 Subsequently, some 

experts support colposcopy as a regular screening 

tool in patients when they are initially diagnosed 

with HIV. 156 Nonetheless, a more recent study con-



Fig 7. HIV-positive patient. Adenocarcinoma of the anus. 

(Courtesy of Axel Hoke, MD, Novato, Calif.) 

tradicts these arguments by finding that pap smears 

are adequately sensitive in HIV-infected patients. 157 

The CDC specifically states that colposcopy is not 

indicated as a regular screening tool for women with 

HIV. 1 

There is no established method of screening for 

anal disease in HIV patients. Certainly inspection of 

the anal region is an important part of the evaluation. 

Often, dysplastic lesions are highlighted in 

white after the application of acetic acid. Moreover, 

ASIL may present as Bowen’s disease of the perianal 

region. 151 This usually presents as pigmented 

papules or plaques. Condylomata acuminata may 

harbor dysplastic lesions, and anal cancer frequently 

originates from epithelium external to the anal 

verge. Anal cancer may present with perirectal bleeding, 

constipation, or tenesmus, and occasionally 

perirectal induration or erythema. For these reasons, 

external inspection is an important tool in the 

screening for anal disease in HIV-infected patients. 

Palefsky 151 supports an ASIL screening process 

that would test only the persons at highest risk for 

Fig 8. HIV-positive patient. Verrucous carcinoma of the 

penis. 

ASIL in whom treatment would be most appropriate. 

Specifically, the group would include HIV-positive 

men with a history of receptive anal intercourse who 

might benefit from aggressive treatment of premalignant 

lesions. Excluded from this group would be 

HIV-infected patients with a poor prognosis, as 

determined by either CD4 cell counts or HIV plasma 

RNA levels. In addition, HIV-negative men who participate 

in receptive anal intercourse or have a history 

of perianal or intra-anal condylomas may represent 

an appropriate group for screening. Palefsky 

recognizes that similar risk groups in women might 

be appropriate for screening but admits that too few 

studies have evaluated ASIL in women for sound scientific 

recommendations regarding this population. 

Anogenital warts 

In the immunocompetent host anogenital warts 

are most commonly caused by HPV types 6 and 11. 

Studies have demonstrated that when compared 

with normal hosts, HIV-infected patients’ anogenital 

warts more frequently represent infections with mul



tiple HPV types, including oncogenic types. 146,158-60 

Clinically, although HIV patients may have the same 

condylomas as normal persons, they may also have 

more extensive or even disseminated condylomas 

that may be relatively refractory to treatment. 

Furthermore, HIV-infected patients’ condylomas are 

associated with a significant risk of transformation 

into squamous cell carcinoma. 

Proper diagnosis is essential in these cases. 

Usually, anogenital warts are diagnosed by clinical 

acumen, but in HIV-infected patients biopsy should 

be considered before therapy so that appropriate 

diagnosis of dysplastic changes or squamous cell 

cancer can be ascertained early in the disease management 

process. 1,158 Treatment options available to 

the HIV-infected host do not differ from those available 

to the immunocompetent host and are discussed 

by Brown, Tyring, and Yen-Moore 161 in part II 

of this series on sexually transmitted diseases. Some 

clinicians advocate treatment by excision and electrodesiccation 

because of the poor response and frequent 

recurrences after topical treatments 162 and 

the association between HPV and cancer in this population. 

158,163 

Notwithstanding, some studies have evaluated 

nonsurgical treatment modalities for genital warts 

in the immunocompromised host. Podophyllotoxin 

has been studied for genital warts in HIV-positive 

Tanzanian patients, 164 but given the association of 

HPV in HIV-infected patients with squamous cell 

cancer, this therapy may be inappropriate for this 

population. 165 Interferon has been studied in this 

population, 166,167 as has imiquimod. 168 Although 

both have some efficacy in treating HPV infection in 

HIV patients, neither appears to be effective as 

monotherapy in completely clearing clinical lesions 

from the most severely immunocompromised 

patients. Use of imiquimod as adjunctive therapy 

after surgical or cytodestructive treatment of 

condyloma acuminatum does appear effective in 

HIV-seropositive and in other immunocompromised 

patients in terms of significant delays or prevention 

of recurrences. Cidofovir gel has been 

studied in a phase I/II trial of HIV-positive patients 

with condylomata acuminata and appears safe and 

potentially effective in this population. 169 Finally, 

Orlando et al 170 recently reported that relapse 

rates of condyloma in HIV-infected patients 

decreased with improved treatment of their underlying 

HIV infection with antiretroviral medication. 

Successful treatment of condylomas thus appears 

easier when a person’s underlying HIV infection is 

better controlled. Clearly, treatment of HPV infections 

in HIV-infected patients is an issue that 

deserves further study. 


MOLLUSCUM CONTAGIOSUM 

The association between HIV infection and molluscum 

contagiosum was first noticed in 1983 

through an autopsy study of 10 patients with 

AIDS. 171 Many reports of severe and atypical infections 

have surfaced, and in AIDS patients, the prevalence 

of molluscum contagiosum lesions ranges 

from 5% to 18%. 172-176 Dann and Tabibian 177 document 

molluscum contagiosum as one of the 3 most 

common reasons nondermatologists referred HIVinfected 

patients to a university-based immunosuppression 

skin clinic. 

In HIV-infected patients, molluscum contagiosum 

manifests itself most commonly when immune function 

has been dramatically reduced. Several studies 

document that molluscum contagiosum infection is 

a clinical sign of marked HIV progression and very 

low CD4 cell counts. 176,178-181 Specifically, when the 

CD4 cell count drops below 200/mm 3 , the incidence 

of molluscum contagiosum appears to increase dramatically. 

182 The unfortunate clinical correlate with 

this finding is that AIDS patients in whom molluscum 

contagiosum occurs have a poor prognosis, 

with a median survival time of 12 months in one 

study. 176 The presence of mollusca, however, does 

not appear to be an independent prognostic indicator 

after accounting for immunosuppression. 

Considerable debate remains as to whether the 

disease is caused by the reactivation of latent virus or 

whether it represents a recently acquired infection 

complicating patients’ progressive immunosuppression. 

The molluscum contagiosum virus commonly 

infects the general population. In an Australian study 

incorporating both HIV-positive and HIV-negative 

patients, 23% of the studied population had antibodies 

consistent with either a current or previous 

infection. 183 As the age of the studied population 

increased, so did the frequency of molluscum contagiosum 

antibodies. 183 These findings were believed 

to support the theory that mollusca in AIDS patients 

reflect the reactivation of a latent infection. 184 

However, other studies contradict this supposition. 

Molecular research demonstrates that molluscum 

contagiosum viruses can be divided into two 

major types (designated MCV-1 and MCV-2) based 

upon restriction fragment cleavage patterns of the 

viruses’ genome. 185 Although it is not yet clear what 

clinical implications these types may have, the ratio 

of MCV-1 to MCV-2 in one Japanese population was 

found to be 13:1. 186 MCV-1 occurred in highest frequency 

in children and adult women, whereas MCV- 

2 occurred more frequently in adult men and 

patients with HIV. 186 This study was consistent with 

an earlier Australian study that showed HIV-positive 

patients were significantly more likely to be infected



Fig 9. HIV-positive patient. Molluscum contagiosum. 

by the MCV-2 virus than control patients. 187 The 

presence of MCV-2 in these patients may suggest 

that HIV-positive patients are manifesting an adult 

acquired infection because young and healthy 

patients are more commonly infected with MCV-1. 187 

Clinically, molluscum contagiosum in HIV-positive 

persons appears to be transmitted in both sexual and 

nonsexual patterns. Lesions in healthy, sexually 

active adults commonly occur on the lower 

abdomen, inner thighs, and genitalia. HIV-infected 

patients may have lesions with this distribution, but 

lesions on the face and neck are more common (Fig 

9). In one study of mostly homosexual HIV-positive 

men, 14 of 27 patients had lesions on the face and 

neck, whereas only 7 patients had lesions in locations 

associated with sexual transmission. 188 

Ophthalmologists have described many cases of 

complicated eyelid mollusca in HIV-infected 

patients. 189,190 The lesions can become quite large 

(up to 2 cm) 191 and numerous (numbering up to the 

hundreds). 192 They are prone to autoinoculation, 

and in male patients, shaving the beard area has 

been reported to cause particularly severe infec- 

tions, with lesions encompassing their entire 

face. 184,193,194 Certainly, numerous lesions on a 

patient who is not yet diagnosed with HIV disease 

should prompt discussion of an HIV test. 195 

Atypical molluscum contagiosum is common in 

HIV patients. Lesions may resemble comedones, 

abscesses, furuncles, condylomas, syringomas, keratoacanthomas, 

basal cell carcinomas, ecthyma, a 

sebaceous nevus of Jadassohn, and a cutaneous 

horn. 196-201 Importantly, disseminated fungal infections, 

specifically cryptococcosis, 202,203 Penicillium 

marneffei infection, and histoplasmosis, 204 are 

reported to clinically mimic molluscum contagiosum 

and should be included in the differential diagnosis 

for these patients. 

Because of the atypical nature of mollusca in the 

HIV-positive patient, diagnosis is in large part dependent 

on biopsy. Studies evaluating the microscopic 

and ultrastructural (electron microscopic) features 

of mollusca identified no major differences between 

samples taken from healthy patients as compared 

with patients with AIDS. 184,205 One possible exception 

to this might be that AIDS patients are less likely 

to have the inflammation and lymphocytic infiltrates 

associated with mollusca regression in their 

tissue. Interestingly, Smith et al 206 noted ultrastructural 

evidence for the presence of viral particles in 

“immunocompetent” skin adjacent to mollusca in 

HIV-infected patients. This was thought to help 

explain the high recurrence rates of lesions after 

treatment. 206,207 

Molluscum contagiosum in HIV-positive patients 

is notoriously difficult to treat, 208 and unlike otherwise 

healthy hosts, there is no evidence that lesions 

spontaneously resolve. Most available evidence 

regarding the management of molluscum contagiosum 

in HIV-infected patients is anecdotal. Some 

potential treatment modalities are listed in Table III. 

Perhaps the most widely used methods are curettage 

209 and cryosurgery. Tretinoin may serve as a 

helpful adjunct to any locally destructive therapy 

through daily applications. 192 Although this medicine 

does appear to diminish the appearance of new 

lesions and help eliminate old lesions, its use is 

limited by local irritation. Nonetheless, some 

researchers have reported success in AIDS patients 

by using nightly tretinoin as an adjunct to cantharidin 

(applied for up to 24 hours) on body and 

facial lesions followed by curettage for recalcitrant 

lesions. 192 One study using trichloroacetic acid peels 

yielded an average reduction in molluscum contagiosum 

lesion counts of 40.5% in 7 HIV-seropositive 

patients. 210 Intralesional 211 and systemic interferon 

212 have been used with minimal to moderate success 

in treating AIDS patients with mollusca.



Imiquimod has been studied in AIDS patients and 

certainly deserves consideration as a potential therapy. 

213 Crude podophyllin extract might be a poor 

choice in an HIV-infected patient, given the predisposition 

for the development of cancer in these 

patients and podophyllin’s link to the mutagens 

quercetin and kaempherol. 165 Cidofovir is a 

nucleotide analog that is used most commonly for 

the treatment of cytomegalovirus retinitis in AIDS 

patients. 214 Because of its activity against DNA viruses, 

it may be effective as either an intravenous or topical 

therapy for recalcitrant mollusca. A recent case 

report describes resolution of extensive facial lesions 

in 3 AIDS patients after beginning either intravenous 

or topical cidofovir therapy. 215 The authors of this 

report point out that the patients’ improvement 

most closely correlates with the use of cidofovir, but 

that it is impossible to exclude the possible immune 

system–enhancing effects of antiretroviral therapy. 

At least 3 case reports describe the reduction in 

number of patients’ extensive mollusca after beginning 

potent combination antiretroviral treatment. 

190,216,217 In one early case, a patient improved 

after initiation of zidovudine, 190 and in a more recent 

case, a patient improved after starting ritonavir. 216 

This highlights an important point: every attempt 

should be made to optimize treatment of the HIV 

infection in patients afflicted with molluscum contagiosum 

because this will make treatment of the molluscum 

contagiosum infection more feasible. 218 

HUMAN HERPESVIRUS 8 

Human herpesvirus 8 (HHV-8), formerly known 

as Kaposi’s sarcoma–associated herpesvirus, was 

originally identified in Kaposi’s sarcoma (KS) from 

AIDS patients. 221 It has been linked with all other 

forms of KS as well. 222-226 HHV-8 is also associated 

with a rare type of non-Hodgkin’s lymphoma, 

termed primary effusion lymphoma, 227,228 and with 

the plasma cell variant of Castleman’s disease. 229,230 

Furthermore, patients with HIV-associated KS are at 

a significantly greater risk for the development of 

non-Hodgkin’s lymphoma than their unaffected 

counterparts. 231-234 Schwartz 235 discussed the major 

issues relating to KS in a comprehensive review, and 

a similar discussion would be inappropriate here. 

Although the biology of HHV-8 is not entirely understood, 

it appears to be a sexually transmitted infection 

in the United States and Western Europe. 

Most cases of AIDS-associated KS have appeared 

in men who participated in promiscuous homosexual 

activities or had a history of STDs. 236-244 

Furthermore, homosexual men whose partners live 

in areas of high HHV-8 prevalence, such as San 

Francisco or New York City, appear to be at an 


Table III. Treatment modalities for molluscum 

contagiosum 

Surgical 

Curettage 192,209 

Electrodesiccation 192,218 

Cryotherapy 219 

Laser surgery 220 

Cytodestructive 

Cantharadin 192 

Iodine 192,218 

Lactic acid 207 

Phenol 192,207 

Salicylic acid 207 

Silver nitrate 192 

Tretinoin 192 

Trichloroacetic acid 210 

Chemotherapeutic/antiviral 

Cidofovir 215 

Interferon 211,212 

Imiquimod 213 

increased risk of acquiring the virus. Those persons 

who acquired HIV nonsexually (eg, hemophiliacs or 

intravenous drug abusers) have much lower rates of 

KS than those people who contracted HIV from 

homosexual or bisexual contacts. 

Many studies have focused on shedding of HHV-8 

into semen with variable results. Most studies were 

unable to detect HHV-8 in either the semen of 

healthy patients or HIV patients, 245-249 and detection 

of HHV-8 in the semen of patients with KS proved 

similarly difficult. However, two controversial studies 

reported high rates of HHV-8 in the semen of 

healthy patients. 250,251 Oral secretions in patients 

with KS appear to consistently shed HHV-8 virions. 

252,253 Other suggested, but less investigated 

methods of transmission, include oral-anal contacts 

or exposure to feces. 254-256 Further investigation 

regarding this virus, its transmission, and its relationship 

to HIV is indicated. 

KS was originally described in HIV-seronegative 

persons (ie, classic KS). This form usually presents as 

purple plaques or papules on the lower extremities 

of elderly men of Mediterranean and/or Jewish 

decent. Patients with classic KS may die with this sarcoma 

but rarely die from it. In HIV-positive persons, 

however, a much wider variety of lesions (eg, patches, 

plaques, papules, nodules, ulcers) may appear 

anywhere on the skin or mucous membranes (Fig 

10). Visceral involvement of KS is common in HIVseropositive 

persons and is associated with significant 

morbidity and mortality. KS has been much less 

common in the past 3 years since the availability of 

highly active antiretroviral therapy (HAART), which



suggests that the development or resolution of KS is 

tightly linked to immune system control of HHV-8. 

HEPATITIS B VIRUS AND HEPATITIS C 

VIRUS 

Both hepatitis B virus and hepatitis C virus (HBV 

and HCV, respectively) commonly coinfect HIVseropositive 

persons. Sexual transmission of HBV, 

however, appears to be more frequent than with HCV. 

Discussion of the cutaneous manifestations of those 

viruses as well as their treatment and prophylaxis can 

be found in part II of this 3-part STD review. 161 

The relationship between hepatitis C infection 

and sporadic porphyria cutanea tarda in the 

immunocompetent host is well documented. 257,258 

Similarly, sporadic porphyria cutanea tarda can occur 

in the HIV-positive patient in association with HCV 

infection. 259-262 Some reports evaluate the potential 

of HIV infection as an independent cofactor in the 

development of porphyria cutanea tarda. 262-265 One 

recent report describes a case in which an HCV- and 

HIV-infected man whose porphyria cutanea tarda 

subsided 18 months after starting HAART for HIV 

infection. 259 Regardless, any patients presenting with 

porphria cutanea tarda should be evaluated for both 

HCV and HIV infection. 

ECTOPARASITIC INFESTATIONS 

Scabies 

Scabies occurs commonly in young adults who 

acquire it through sexual contact. In 1848, Danielssen 

Fig 10. HIV-positive patient. Kaposi’s sarcoma. 

and Boeck first described a particularly contagious 

and fulminant form of scabies in Norwegian patients 

immunosuppressed as a consequence of Hansen’s 

disease. These patients’ infestations were characterized 

by thick, friable plaques. This form of scabies, 

Norwegian or crusted scabies, has emerged as yet 

another harbinger of HIV infection. Published reports 

of atypical and crusted scabies infestations in association 

with HIV infection have become increasingly frequent 

since the first such report in 1986. 266-298 

The defining clinical features of scabies in the 

HIV-positive patient are often determined by the 

degree of immunocompromise. 299 The typical presentation 

of a person infested with scabies (papules 

and burrows in the axillae, groin, or digital web 

spaces associated with complaints of nocturnal pruritus) 

occurs in HIV-infected patients with relatively 

normal immune function. However, as patients 

become progressively more immunosuppressed, the 

more contagious and fulminant forms of scabies 

become apparent. 267-269,271,272,282 This conversion 

from ordinary scabies to more severe and unusual 

infestations has been documented in individual 

patients who experience declines in their CD4 cell 

counts to below 200/mm 3 . 266,272,274,285 Still, as noted 

by Portu et al, 295 although low CD4 cell counts may 

be more commonly associated with the severe and 

unusual forms of scabies, these fulminant infections 

can occur in early stages of HIV disease. 

These severe and unusual forms of scabies can be 

divided into two overlapping and broad categories:



papular (also known as atypical or exaggerated) scabies 

and crusted (also known as Norwegian or 

hyperkeratotic) scabies. 285,299,300 The papular forms 

are characterized by generalized papules, each of 

which is topped by a scabietic burrow, which may be 

scaly. Patients complain of severe pruritus with this 

form. 266,273,277,285 The crusted forms are characterized 

by thick, friable, white-gray plaques, which may 

also be diffuse, but are commonly localized to individual 

body regions including the scalp, face, back, 

buttocks, nails, and feet (Fig 11). The plaques are 

often associated with fissuring that may be mild to 

severe. 267-272 Furthermore, as a patient’s lesions 

become crusted, they tend to become less pruritic. 

The distinction between papular and crusted scabies 

is not mutually exclusive, and some reports document 

patients with lesions characteristic of both 

forms. 270,284 

Infestations may be mistaken for eczema, psoriasis, 

contact dermatitis, drug reactions, seborrheic 

dermatitis, Darier’s disease, or dermatophytosis. 

Scabies must be suspected in any HIV-infected person 

with an atypical or pruritic rash. Similarly, young 

patients with HIV risk factors in whom papular or 

crusted scabies develops without an apparent underlying 

cause should be suspected of having HIV infection. 

Skin scrapings are often diagnostic in crusted 

or papular scabies and may be taken from any nonexcoriated 

region or from underneath the nails; however, 

if scrapings are negative and clinical suspicion 

remains, a skin biopsy can be very helpful. 285,299,300 

It must be noted that a key feature of crusted scabies 

infestations in the HIV-infected patient is an 

exceptionally high mite burden. Whereas an immunocompetent 

host is estimated to have 10 to 15 live 

female mites during an infestation, 301 individual 

crusts in crusted scabies may harbor thousands of 

mites. Furthermore, although the scabies mite has a 

limited life span (



reinfected from other untreated personal contacts or 

from improper cleaning of bedding and clothing. 

The CDC recommendation for HIV-infected 

patients with crusted or papular scabies is for “consultation 

with an expert.” 1 Five percent permethrin 

cream is the best topical agent currently available for 

treatment of crusted or papular scabies. 300 Although 

topical lindane preparations have been used frequently 

in published reports, this medicine has the 

potential for serious neurotoxicity. In crusted scabies, 

deep fissures often enhance the systemic absorption 

of lindane resulting in potentially high serum concentrations 

of the neurotoxin. Furthermore, many HIVpositive 

patients have AIDS-related neurologic 

changes, which may predispose them to any neurotoxic 

effects. At least one death in an HIV-infected 

patient with scabies has been attributed to lindane. 290 

For these reasons, permethrin is the preferred treatment 

in HIV-positive patients. 300 

Taplin and Meinking, 300 among others, have recommended 

ivermectin as an oral alternative to topical 

therapies for the treatment of scabies. Several 

studies 302-305 document the safety and efficacy of 

ivermectin in the treatment of scabies, including one 

such study that evaluated the medicine’s effects on 

HIV-positive patients who were taking multiple medications 

including antiretrovirals and antifungals. 305 

However, no reports have directly compared the efficacy 

of ivermectin with the currently recommended 

regimens (permethrin or lindane), and it is not yet 

approved by the FDA for this purpose. 

In the treatment of crusted scabies, it is also clear 

that patients benefit from keratolytic agents (eg, 6% 

salicylic acid) or, if possible, manual debridement. 

This serves to decrease the patient’s mite load and to 

facilitate the penetration of topical medications. 

Some researchers support combined topical permethrin, 

keratolytics, and oral ivermectin as a potential 

regimen in the management of these patients. 298,300 

It is believed that the combination of topical therapy 

and oral therapy maximizes the penetration of antiscabietic 

medications into the crusts. Therapy for 

the infestation in crusted or papular scabies needs to 

be persistent because the high mite burdens in these 

patients are difficult to eradicate. Special attention 

should be paid to the head and neck as well as 

underneath the fingernail. Skin scrapings should be 

collected often, and treatment continued until 

repeated scrapings yield no mites. Permethrin treatments 

may be needed 2 to 3 times per week for up 

to 6 weeks to eradicate the menace. 

A unique complication that accompanies crusted 

scabies is bacteremia. This is seen when the 

patients have severe fissuring associated with their 

crusts and has led to the patients’ death on several 

occasions. Streptococcal, 268 staphylococcal, 271 and 

Pseudomonas spp 274,284 have caused bacteremia in 

patients with crusted scabies, and antibiotic prophylaxis 

appropriate to the bacterial flora profile of 

the hospital is highly recommended in these cases 

to avoid this complication. 283,288,299,300 

Pediculosis pubis 

Very little has been written about the effect that 

HIV infection has on infestation with Phthirus pubis. 

It appears that the ectoparasite behaves the same 

clinically regardless of HIV serostatus. The CDC recommends 

the same treatment for HIV-positive 

patients with pediculosis pubis as it does HIV-negative 

patients. 1 Permethrin 1% cream rinse applied for 

10 minutes, lindane 1% shampoo applied for 4 minutes, 

or pyrethrins with piperonyl butoxide applied 

for 10 minutes are all appropriate therapies when 

accompanied by appropriate decontamination of 

bedding and clothing. Pediculosis of the eyes should 

be treated with an occlusive ophthalmic ointment 

twice daily for 10 days. 

In summary, STDs may enhance both the acquisition 

and the transmission of HIV. This relationship is 

especially true of STDs causing genital ulcers. STDs 

in HIV-seropositive persons may differ qualitatively 

or quantitatively, or both, in both clinical and laboratory 

parameters from STDs in immuncompetent 

persons. Such measures as education, which may 

lead to early recognition of the signs and symptoms 

of STDs, have the potential to positively affect the 

HIV epidemic. Therefore enhanced efforts should be 

devoted to the prevention and treatment of STDs. 

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to lindane in an HIV-seropositive patient: an old medication’s 

new problem. J Fam Pract 1995;40:291-6. 

291. Corbett EL, Crossley I, Holton J, Levell N, Miller RF, De Cock KM. 

Crusted (Norwegian) scabies in a specialist HIV unit: successful 

use of ivermectin and failure to prevent nosocomial transmission. 

Genitourin Med 1996;72:115-7. 

292. Nandwani R, Pozniak AL, Fuller LC, Wade J. Crusted 

(Norwegian) scabies in a specialist HIV unit. Genitourin Med 

1996;72:453. 

293. DelGuidice P, Carles M, Couppie P, Bernard E, Lacour JP, Marty P, 

et al. Successful treatment of crusted (Norwegian) scabies 

with ivermectin in two patients with human immunodeficiency 

virus infection. Br J Dermatol 1996;135:494-5. 

294. Valks R, Buezo GF, Dauden E. Scabies and leukocytoclastic vasculitis 

in an HIV-seropositive man. Int J Dermatol 1996;35:605-6. 

295. Portu JJ, Santamaria JM, Zubero Z, Almeida-Llamas MV, 

Aldamiz-Etxebarria San Sebastian M, Gutierrez R. Atypical scabies 

in HIV-positive patients. J Am Acad Dermatol 1996; 

34:915-7. 

296. Farrell AM, Ross JS, Bunker CB, Staughton RCD. Crusted scabies 

with scalp involvement in HIV-1 infection. Br J Dermatol 1998; 

138:192-3. 

297. Bitman LM, Rabinowitz AD. Hyperkeratotic plantar plaques in 

an HIV-positive patient. Arch Dermatol 1998;134:1019,1022-3. 

298. Guggisberg D, de Viragh PA, Constantin C, Panizzon RG. 

Norwegian scabies in a patient with acquired immunodeficiency 

syndrome. Dermatology 1998;197:306-8. 

299. Orkin M. Scabies in AIDS. Semin Dermatol 1993;12:9-14. 

300. Taplin D, Meinking TL. Treatment of HIV-related scabies with 

emphasis on the efficacy of ivermectin. Semin Cutan Med 

Surg 1997;16:235-40. 

301. Mellanby K. Scabies in 1976. R Soc Health J 1977;97:32-6. 

302. Currie BJ, Maguire GP, Wood YK. Ivermectin and crusted 

(Norwegian) scabies. Med J Aust 1995;163:559-60. 

303. Glaziou P, Cartel JL, Alzieu P, Briot C, Moulia-Pelat JP, Martin PM. 

Comparison of ivermectin and benzyl benzoate for treatment 

of scabies. Trop Med Parasitol 1993;44:331-2. 

304. Marty P, Gari-Toussaint M, Le-Fichoux Y, Gaxotte P. Efficacy of 

ivermectin in the treatment of an epidemic of sarcoptic scabies. 

Ann Trop Med Parasitol 1994;88:453. 

305. Meinking TL, Taplin D, Hermida J, Pardo R, Kerdel FA. The treatment 

of scabies with ivermectin. N Engl J Med 1995;333:26-30.

Directions for questions 1-16: Give single best response. 

1. A patient with AIDS comes to your clinic with her first 

case of genital herpes. A good estimate of the likelihood 

that her infection will be resistant to acyclovir is 

a. less than 1% 

b. 3% 

c. 6% 

d. 12% 

e. 24% 

2. A patient comes to your clinic with AIDS and a history 

of anal warts. Each of the following is true except 

a. patients with AIDS generally have more human 

papillomavirus (HPV) subtypes present in their 

infections. 

b. as his CD4 cell counts drop, this patient will shed 

more HPV virions. 

c. concurrent HIV and anal HPV infections increase 

this patient’s risk for anorectal carcinoma. 

d. optimizing his antiretroviral medications may 

make management of any anal wart recurrences 

more feasible. 

d. acetic acid is not a useful diagnostic tool for recognizing 

anal squamous intraepithelial lesions in this 

patient. 

3. Kaposi’s sarcoma (KS) 

a. is not associated with human herpesvirus type 8 in 

HIV-infected patients 

b. is associated with an increased risk for non- 

Hodgkin’s lymphoma in HIV-infected patients 

c. occurs most commonly among people who 

acquired HIV through intravenous drug abuse 

d. occurs at similar rates for HIV-infected patients in 

all US cities 

e. does not follow the epidemiologic patterns of an 

infectious disease 

4. The best approximation for the number of scabies 

mites on an HIV-infected patient with crusted scabies 

is 

a. fewer than 5 

b. 5-10 

c. 10-20 

d. 20-50 

e. more than 50 

5. In the treatment of AIDS patients with crusted scabies, 

which of the following medications has been 

CME examination 

Identification No. 800-109 

Instructions for Category I CME credit appear in the front advertising section. See last page of Contents for page number. 

Questions 1-31, Czelusta A, Yen-Moore A, Tyring SK. J Am Acad Dermatol 2000;43:409-32. 

documented as a potential cause of severe neurologic 

side effects in case reports? 

a. Lindane 

b. Permethrin 

c. Mebendazole 

d. Metronidazole 

e. Ivermectin 

6. The most likely mechanisms by which herpes simplex 

virus (HSV) mediates resistance to thymidine kinase 

inhibitors includes each of the following except 

a. production of viral thymidine kinase with decreased 

substrate affinity 

b. production of viral DNA polymerase with decreased 

substrate affinity 

c. decreased production of viral thymidine kinase 

d. absence of viral thymidine kinase production 

e. altered transport of thymidine kinase inhibitors 

into infected cells 

7. An HIV-infected patient who is allergic to penicillin 

comes to your clinic with early latent syphilis. Which 

of the following antibiotics is the most appropriate 

therapy? 

a. Intramuscular benzathine penicillin G 

b. Oral ciprofloxacin 

c. Oral erythromycin 

d. Intravenous vancomycin 

e. Intramuscular ceftriaxone 

8. Chancroid in HIV-positive patients 

a. is commonly atypical in its clinical presentation 

b. presents with larger ulcers than those seen in HIVnegative 

patients 

c. has distinct histologic differences from HIV-negative 

patients on microscopic examination 

d. increases the risk of HIV transmission to sexual 

partners 

e. cannot be cured by the same antibiotic regimens 

that are recommended for immunocompetent 

patients 

9. A patient with advanced AIDS presents with a facial 

molluscum contagiosum. Which of the following 

should he be told about the lesion? 

a. Shaving his face will help improve skin cleanliness 

and decrease the likelihood of new lesions developing. 

b. Optimization of his antiretroviral medications will 

not help in the care of this lesion. 

433

434 CME examination J AM ACAD DERMATOL 


c. Crude podophyllin resin is the safest therapeutic 

modality for the removal of this lesion. 

d. This infection is unlikely to resolve spontaneously. 

e. Carbon dioxide laser therapy is the most efficacious 

modality for treating this lesion. 

10. Each of the following statements regarding syphilis in 

the HIV-infected host is true except 

a. Clinical presentation is usually the same in HIVinfected 

persons as it is in HIV-negative hosts. 

b. Several studies document increased rates of falsepositive 

fluorescent treponemal antibody absorption 

assays. 

c. A patient’s progression through the various stages 

of syphilis may be faster if he is HIV infected. 

d. HIV-infected patients may progress to neurosyphilis 

despite treatment with recommended 

antibiotic regimens. 

e. Histologic examination of tissue specimens may be 

helpful in cases in which the results of HIV-infected 

patients’ serologic tests are not consistent with 

their dermatologists’ clinical suspicions. 

11. Which of the following statements is false? 

a. Patients with genital herpes are at increased risk of 

acquiring HIV from their HIV-positive partners. 

b. Antiviral control of HSV has no impact on a 

patient’s response to antiretroviral drugs. 

c. Treatment of genital herpes in HIV-positive persons 

may require increased doses of acyclovir or 

famciclovir. 

d. A person with both HSV and HIV infections has an 

increased risk of transmitting HIV relative to an 

HSV-negative person with HIV. 

e. Taking famciclovir daily reduces both symptomatic 

and asymptomatic HSV viral shedding in HIV-positive 

persons. 

12. Which of the following is the most common cause of 

genital ulcer disease worldwide? 

a. HIV 

b. Chancroid 

c. Herpes 

d. Lymphogranuloma venereum 

e. Granuloma inguinale 

13. Which of the following drugs is most likely to benefit 

a patient with acyclovir-resistant herpes? 

a. Cidofovir 

b. Famciclovir 

c. Valacyclovir 

d. Penciclovir 

e. Zidovudine 

14. Which of the following is least likely to mimic molluscum 

contagiosum in an HIV-positive person? 

a. Cryptococcus 

b. Penicillium marneffei 

c. Histoplasmosis 

d. Condyloma acuminatum 

e. Granuloma inguinale 

15. Which of the following statements is false? 

a. Anal cancer is the most common reportable cancer 

among HIV-positive men. 

b. Anal cancer is 7 times more common in homosexual 

men with HIV than those who are HIV seronegative. 

c. Cervical cancer in an HIV-infected patient is an 

AIDS-defining illness. 

d. Condyloma acuminatum in an HIV-positive person 

may contain dysplastic foci. 

e. Crude podophyllin resin contains mutagens. 

16. What effect has highly active antiretroviral therapy 

had on KS? 

a. KS is more treatment resistant. 

b. KS is less prevalent. 

c. KS is more frequently seen in HIV-positive women. 

d. KS is more frequently seen in hemophiliacs 

e. KS is more likely to be the immediate cause of 

death in HIV-positive persons. 

Directions for questions 17-21: For each numbered item, 

choose the appropriate lettered item. 

a. Hepatitis C virus 

b. Human papillomavirus type 16 

c. Chancroid 

d. Molluscum contagiosum virus 1 

e. Molluscum contagiosum virus 2 

17. Children 

18. Porphyria cutanea tarda 

19. Anal cancer 

20. Genital ulcers in Africa 

21. Facial papules in HIV-positive adults 

Directions for question 22: Give single best response. 

22. Which of the following statements is true? 

a. Scabies are proven to transmit HIV. 

b. KS in HIV-negative persons is not associated with 

human herpesvirus type 8. 

c. High recurrence rates of molluscum contagiosum 

are usually due to reinfection. 

d. HIV can frequently be found in herpetic ulcers of 

HIV-positive persons. 

e. Acyclovir has direct antiretroviral activity. 

Directions for questions 23-27: For each numbered item, 

choose the appropriate lettered item. 

a. Foscarnet 

b. Cidofovir 

c. Famciclovir 

d. Imiquimod 

e. Azithromycin 

23. May be useful topical therapy for warts and molluscum 

contagiosum (also available in a topical formulation) 

24. Requires thymidine kinase for activation



25. Approved by the Centers for Disease Control and 

Prevention (CDC) in intravenous form for acyclovirresistant 

herpes 

26. Nucleotide analog 

27. Recommended by the CDC for therapy of chancroid 

in HIV-positive persons 

Directions for questions 28-31: Give single best response. 

28. What is the approximate relative increase in risk of 

HIV transmission from having a sexually transmitted 

disease? 

a. 1- to 2-fold 

b. 3- to 5-fold 

c. 6- to 10-fold 

d. 11- to 20-fold 

e. 21- to 50-fold 

29. Which statement is false regarding herpetic ulcers in 

HIV-positive persons? 

a. Hyperkeratotic verrucous lesions may resemble 

condyloma acuminatum. 

b. Higher doses of antiherpes agents may be required. 

c. Ulcers may be coinfected with cytomegalovirus. 

d. Therapy may prevent visceral spread of HSV. 

e. Foscarnet therapy has the same safety profile as 

acyclovir. 

AVAILABILITY OF JOURNAL BACK ISSUES 

CME examination 435 

30. Which statement is true regarding scabies in HIV-positive 

persons? 

a. Mites are difficult to detect. 

b. Crusted lesions are more pruritic than papular 

lesions. 

c. Papular and crusted lesions are not mutually exclusive. 

d. Crusted scabies is clearly distinguishable clinically 

from eczema. 

e. Plaques of crusted scabies rarely fissure. 

31. Which statement is false regarding granuloma 

inguinale in HIV-positive persons? 

a. It is strongly associated with HIV transmission. 

b. CDC-recommended treatment of granuloma 

inguinale is different than in HIV-negative persons. 

c. The mean duration of ulcer healing may be longer 

in HIV-positive persons. 

d. Greater tissue destruction may be seen in HIV-positive 

persons. 

e. Extragenital dissemination has been reported in 

HIV-positive persons. 

As a service to our subscribers, copies of back issues of the Journal of the American Academy of 

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(313)761-4700.

1. c 

2. e 

3. b 

4. e 

5. a 

6. e 

7. a 

8. d 

9. d 

10. b 

11. b 

12. c 

13. a 

14. e 

15. a 

16. b 

436 

Answers to CME examination 

Identification No. 800-109 

September 2000 issue of the Journal of the American Academy of Dermatology 

Questions 1-31, Czelusta A, Yen-Moore A, Tyring SK. J Am Acad Dermatol 2000;43:409-32. 

17. d 

18. a 

19. b 

20. c 

21. e 

22. d 

23. d 

24. c 

25. a 

26. b 

27. e 

28. b 

29. e 

30. c 

31. b 

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