Download An overview of sexually transmitted diseases. Part III

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, PhDc 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.)
T
he 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,
Houstona; the Department of Dermatology at the University of
Texas—Southwestern Medical School and Veterans Affairs
Hospital, Dallasb; 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: [email protected].
16/2/105158
doi:10.1067/mjd.2000.105158
Abbreviations used:
ASIL:
CDC:
anal squamous intraepithelial lesion
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
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 al9 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 al23 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 association5; however, the difficulty in making this associ-
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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 large41,43 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
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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 al61 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
412 Czelusta, Yen-Moore, and Tyring
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-
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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/mm3.75 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 al78 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 neurosyphilis86 have been documented
in HIV-infected patients, as have unusual gummatous
lesions.87 Furthermore, rapidly developing cases of
ocular syphilis82,88,89 and syphilitic aortitis90 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
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Czelusta, Yen-Moore, and Tyring 413
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.
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
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
414 Czelusta, Yen-Moore, and Tyring
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Table I. Recommended management for syphilis in HIV-infected patients1
Stage
Primary, secondary, or early latent
syphilis
Late latent syphilis or syphilis of
unknown duration
Neurosyphilis or ocular syphilis*
Treatment
Follow-up
2.4 × 106 U intramuscular benzathine
penicillin G once
2.4 × 106 U of intramuscular
benzathine penicillin G weekly for
3 wk
3-4 × 106 U of intravenous aqueous
crystalline penicillin G every 4 h for
10-14 days (or) intramuscular
procaine penicillin 2.4 × 106 U daily
and oral probenicid 500 mg 4 times
per day for 10-14 days
Clinical and serologic exams at 3, 6, 9, 12,
and 24 mo
Clinical and serologic exams at 6, 12, 18,
and 24 mo
If CSF pleocytosis was initially present,
CSF exams every 6 mo (for up to 2 yr)
until this parameter returns to normal
*Some experts recommend the addition of a single intramuscular dose of 2.4 × 106 U of benzathine penicillin G to the conclusion of therapy
in cases of neurosyphilis.
treatment75,95,96 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
therapy71-73,80-85 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 syphilis1
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 × 106 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 duration113,114 and a greater number of ulcers at initial
presentation113 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
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Fig 5. HIV-positive patient. Chancroid with typical “kissing” ulcers.
accompanied by the development of ulcers on his
legs and digits115 (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
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Table II. Recommended therapy for granuloma inguinale and lymphogranuloma venereum1
Infection
Granuloma inguinale*
Lymphogranuloma venereum
Recommended therapy
Alternative therapy
Oral trimethoprim-sulfamethoxazole
double-strength tablet twice daily
(or) oral doxycycline 100 mg twice
daily until lesions heal or for at least
3 wk
Aspiration or incision and drainage of
buboes if necessary and oral
doxycycline 100 mg twice daily for 3 wk
Oral ciprofloxacin 750 mg twice daily (or)
oral erythromycin base 500 mg 4 times
daily until lesions heal or for at least 3 wk
Aspiration or incision and drainage of
buboes if necessary and oral erythromycin
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
Becker28 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 L1,
L2, and L3 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 al134 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 L2 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
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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 men154 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-
418 Czelusta, Yen-Moore, and Tyring
J AM ACAD DERMATOL
SEPTEMBER 2000
Fig 7. HIV-positive patient. Adenocarcinoma of the anus.
(Courtesy of Axel Hoke, MD, Novato, Calif.)
Fig 8. HIV-positive patient. Verrucous carcinoma of the
penis.
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.
Palefsky151 supports an ASIL screening process
that would test only the persons at highest risk for
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-
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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-Moore161 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 treatments162 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 al170 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.
Czelusta, Yen-Moore, and Tyring 419
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 Tabibian177 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/mm3, 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 MCV2 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
420 Czelusta, Yen-Moore, and Tyring
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-
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SEPTEMBER 2000
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 al206 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 curettage209 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 Intralesional211 and systemic interferon212 have been used with minimal to moderate success in treating AIDS patients with mollusca.
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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 Schwartz235 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
Czelusta, Yen-Moore, and Tyring 421
Table III. Treatment modalities for molluscum
contagiosum
Surgical
Curettage192,209
Electrodesiccation192,218
Cryotherapy219
Laser surgery220
Cytodestructive
Cantharadin192
Iodine192,218
Lactic acid207
Phenol192,207
Salicylic acid207
Silver nitrate192
Tretinoin192
Trichloroacetic acid210
Chemotherapeutic/antiviral
Cidofovir215
Interferon211,212
Imiquimod213
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
422 Czelusta, Yen-Moore, and Tyring
J AM ACAD DERMATOL
SEPTEMBER 2000
Fig 10. HIV-positive patient. Kaposi’s sarcoma.
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
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/mm3.266,272,274,285 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:
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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 (<30 minutes) off an ordinary
human host, a shed crust that is filled with mites can
serve as a food supply and protection, sustaining
organisms for up to 1 week.302 For this reason, scabies
in HIV-infected patients can be particularly contagious. Numerous reports have documented nosocomial transmission from infected patients to other
patients and hospital staff.272,274,275,279,292,295 One
case reported 72 infested contacts (health care workers and inpatients) after admission of an HIV-infected
man with undiagnosed crusted scabies.295 A question
that often arises in these situations concerns the possibility of spreading HIV through transmitted mites.
No cases have documented such a phenomena.
Corbett et al291 reported a case from London in which
14 of 16 exposed hospital staff members became
symptomatic for scabies after working with a crusted
Czelusta, Yen-Moore, and Tyring 423
Fig 11. HIV-positive patient. Norwegian (crusted) scabies.
scabies patient while wearing gloves and plastic
aprons to minimize skin-to-skin contact.291 This event
prompted the hospital to distinguish between crusted and ordinary scabies in their infection control
guidelines. Additional precautions were taken with
patients who had crusted scabies to include full
gowns rather than aprons, prophylactic medical treatment of staff members inadvertently exposed to skinto-skin contact, and regular damp dustings of the
patient’s room to decrease environmental mites. With
these changes, the hospital has since admitted and
treated patients with crusted scabies without nosocomial transmission.291
The CDC treatment recommendations for ordinary scabies in the HIV-infected patient is the same
as for HIV-negative patients: 5% permethrin cream
applied from the neck down (many clinicians also
treat the head) and washed off after 8 to 14 hours
accompanied by treatment of close personal and
household contacts and appropriate decontamination of bedding and clothing.1 Treatments may be
repeated if the patient remains symptomatic. If
repeated treatments fail, the patient may be getting
424 Czelusta, Yen-Moore, and Tyring
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
studies302-305 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
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SEPTEMBER 2000
occasions. Streptococcal,268 staphylococcal,271 and
Pseudomonas spp274,284 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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274. Sirera J, Ruis F, Romeu J, Llibre J, Ribera M, Soriano V, et al.
Hospital outbreak of scabies stemming from two AIDS
patients with Norwegian scabies. Lancet 1990;335:1227.
275. Rostami G, Sorg TB. Nosocomial outbreak of scabies associated with Norwegian scabies in an AIDS patient. Int J STD AIDS
1990;1:209-10.
276. Jessurun J, Romo-Garcia J, Lopez-Denis O, Olvera-Rabiela JE.
Crusted scabies in a patient with the acquired immunodeficiency syndrome. Virchows Archiv A Pathol Anat 1990;416:
461-3.
277. Squires J. Scabies: an unusual presentation in a patient with
AIDS. Clin Cases Dermatol 1990;2:5-9.
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278. Inserra DW, Bickley LK. Crusted scabies in acquired immunodeficiency syndrome. Int J Dermatol 1990;29:287-9.
279. Moss VA, Salisbury J. Scabies in an AIDS hospice unit. Br J Clin
Pract 1991;45:35-6.
280. Waldman BA. Crusted (Norwegian) scabies in an HIV-infected
man. Clin Cases Dermatol 1991;3:6-9.
281. Wlotzke U, Thiele B, Wolff HH, Meigel W. Norwegian scabies in
a patient with AIDS. Hautarzt 1992;43:717-20.
282. Donabedian H, Khazan U. Norwegian scabies in a patient with
AIDS. Clin Infect Dis 1992;14:162-4.
283. Hulbert TV, Larsen RA. Hyperkeratotic (Norwegian) scabies
with gram-negative bacteremia as the initial presentation of
AIDS. Clin Infect Dis 1992;14:1164-5.
284. Skinner SM, DeVillez RL. Sepsis associated with Norwegian
scabies in a patient with acquired immunodeficiency syndrome. Cutis 1992;50:213-6.
285. Funkhouser ME, Omohundro C, Ross A, Berger TG.
Management of scabies in patients with human immunodeficiency virus disease. Arch Dermatol 1993;129:911-3.
286. Mollison LC, Lo STH, Marning G. HTLV-1 and scabies in
Australian Aborigines. Lancet 1993;341:1281-2.
287. Spach DH, Fritsche TR. Images in clinical medicine: Norwegian
scabies in a patient with AIDS. N Engl J Med 1994;331:777.
288. Schlesinger I, Oelrich DM, Tyring SK. Crusted (Norwegian) scabies in patients with AIDS: the range of clinical presentations.
South Med J 1994;87:352-6.
289. Suarez Fernandez R, Rodriguez FM, Lopez Bran E, Nunez
Alonso C, Sanchez De Paz F, Sanchez Yus E. Norwegian scabies
in a patient with AIDS: report of a case. Cutis 1995;56:57-60.
290. Solomon HA, Haut SR, Carr EM, Shalita AR. Neurotoxic reaction
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.
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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
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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.
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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.
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 nonHodgkin’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
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
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
J AM ACAD DERMATOL
SEPTEMBER 2000
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
CME examination 435
J AM ACAD DERMATOL
VOLUME 43, NUMBER 3
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.
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.
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(313)761-4700.
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.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
c
e
b
e
a
e
a
d
d
b
b
c
a
e
a
b
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
d
a
b
c
e
d
d
c
a
b
e
b
e
c
b
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