Dermatol Clin 24 (2006) 449–457

Pruritic Papular Eruption in HIV

Samantha Eisman, MBChB, MRCP
Division of Dermatology, Groote Schuur Hospital, Anzio Road, Observatory 7925, South Africa

Pruritic papular eruption (PPE) is character- Etiology

ized by chronic pruritus and symmetric papular
The pathophysiology of PPE is not completely
eruptions on the trunk and extremities with the
understood, and the cause remains difficult to
absence of other definable causes of itching in an
determine, because the clinical and histologic crite-
HIV-infected patient [1]. There is no clear consen-
ria are not fully agreed upon and are too limited in
sus on the etiology of PPE, the exact spectrum of
scope to provide any consensus as to the etiology of
the condition, the pathologic findings, or treat-
PPE. Some have suggested that PPE is a group of
ment. Nevertheless, it remains the most common
similar diseases with different etiologies [5].
cutaneous manifestation in HIV-infected patients,
An environmental factor, such as insect bites,
with a prevalence that varies between 11% and
has been suggested by some, first because of the
46% according to the geographic area [2–6].
apparent geographic restriction of the condition,
Reports of PPE began early in the course of
which commonly occurs in the tropics, and second
the HIV epidemic with cases from AfricadDem-
because of the involvement of extremities [6]. Res-
ocratic Republic of Congo [7], Rwanda [8],
neck and colleagues [10] believe that PPE is indeed
Uganda [9,10], Zambia [4], Mali [11], Tanzania
a reaction to arthropod bites. Most of their histo-
[12], Nigeria [13] and Togo [14]das well as Haiti
logic findings of early lesions of PPE support this
[6], Brazil [2,15], and Thailand [16]. It seems to
causation, suggesting that the term ‘‘arthropod-
be much less common in the developed countries
induced prurigo of HIV’’ would be a more appro-
of Europe and North America [3]. It is, however,
priate name for the condition. They propose that
the most common dermatologic disease associated
most, if not all, lesions of PPE do begin as an ar-
with HIV in South Florida [17,18]. More than half
thropod bite and that the diffuse distribution of
of HIV-infected patients in some countries may
the disease, on areas typically covered as well as
report the eruption as the initial manifestation
on exposed areas, can be explained by the ability
of their disease [3]; in a Haitian study [6], PPE
of many arthropods, including mosquitoes, to
was the presenting symptom in 79% of patients,
bite through clothing. They also propose that pa-
often appearing months before the diagnosis of
tients who have PPE may become hypersensitive
HIV. Others have reported PPE as an initial pre-
to arthropod antigens that they previously may
sentation in only 25% of cases [16]. In one study
have tolerated. A similar theory explaining this
a patient developed PPE 3 years before other clin-
hypersensitivity in HIV-infected patients has
ical signs of HIV infection [3]. The reported posi-
been proposed to explain the increase in drug hy-
tive predictive value for HIV infection is 82% to
persensitivity, noted with previously tolerated
87% [3], and PPE therefore has played a major
medications, as CD4 counts decline, thought per-
role in diagnosing HIV infection in countries
haps to be caused by polyclonal B-cell or T-cell
where serologic testing is not available or afford-
activation [19,20]. This concept of arthropod hy-
able [1].
persensitivity has been suggested before by Pen-
neys and colleagues [21] in patients who had
lesions and pruritus; in their study, five of seven
E-mail address: samanthak@telkomsa.net patients had increased antibodies to salivary
0733-8635/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.det.2006.06.005 derm.theclinics.com
450
antigens of a common local mosquito. They have
suggested that perhaps the pruritus represents
a form of chronic recall reaction to this antigen
in the setting of nonspecific B-cell activation.
Aires and colleagues [15] noted lower interleukin
(IL)-2 and g-interferon (IFN) in patients who
had PPE and also have suggested the potential
role of type 2 helper cell (Th2)-dominant humoral
immunity. Patients who have Th2 dominance may
be more predisposed to the development of ar-
thropod hypersensitivity leading to PPE. Th2 lym-
phocytes also produce IL-4 and IL-5, which
promote IgE production and eosinophil differenti-
ation [22] that may enhance the exaggerated im-
munologic phenomena in the skin.
As mentioned, PPE is far more prevalent in
Africa and Southeast Asia than in the developed
countries of North America and Europe. It has
been proposed that this increased prevalence may
be caused by different arthropod antigens that may
be more likely to cause this reaction in Africa and
Asia [10]. Palungwachira and colleagues [23] sug-
gest that PPE is the commonest dermatosis in Thai-
land because of the high prevalence of mosquitoes.
Host factors also may be an important consider-
ation predisposing certain populations to this con-
dition. In the southern United States, eosinophilia
and rashes were more prevalent in HIV-infected pa-
tients of African American descent [24].
Liautaud and colleagues [6], however, found
that the histology of lesions did not support in-
sect-bite reactions. Family members and friends
did not have similar lesions, as would be expected
were insect bites the cause. These investigators
concluded that PPE may be a generalized hyper-
sensitivity reaction to insect saliva in which, as
with papular urticaria, only a few bites can cause
crops of lesions to erupt in previously affected sites.
Despite the advanced level of immunosuppres-
sion associated with PPE, there has been no
evidence implicating an infectious agent. James
and Redfield [25] initially postulated that the pru-
ritic papular eruption that occurs in HIV is a result
of an abnormal host-cellular immune response to
an infective process, whereas Duvic [26] stated
that this eruption is most likely caused by a variety
of infective agents, namely scabies, Demodex folli-
culorum, or Staphylococcus aureus. Although infec-
tion may be a concurrent phenomenon, if it is the
cause of the primary pathology, lesions usually re-
spond to appropriate anti-infective treatment. Pa-
tients diagnosed as having PPE have been treated
with protracted courses of antibiotics without any
improvement [6]. Liautaud and colleagues [6] also
EISMAN
found no evidence that PPE represents an opportu-
nistic cutaneous infection or scabies.
Many HIV-infected patients take several med-
ications. The histology and clinical findings of PPE
may be compatible with a drug eruption, but no
single drug has been implicated [3,6,17], and PPE
can be found in patients taking no medication.
Some believe that, as in eosinophilic folliculitis
(EF), the etiology is associated with the piloseba-
ceous unit, because inflammatory cells may local-
ize and invade the hair follicle [27]. In 28 patients
who had PPE, Hevia and colleagues [17] noted
follicular spongiosis in 46%, folliculitis in 25%,
and perifollicular mononuclear cell infiltrate in
87%. Resneck and colleagues [10], however,
found no infiltrates centered around hair follicles,
arrector pili muscles, or the sebaceous glands.
Kinloch-de Loes and colleagues [28] found cir-
culating antibodies to bullous pemphigoid antigen
in 75% of patients who had PPE, and up to 30%
meet the diagnostic criteria on histology, Western
blotting, immunofluorescence, and immunoelec-
tron microscopy, suggesting that an autoimmune
skin reaction may account for or be related to
the distressing pruritus of PPE.
Perhaps PPE must be considered as a conse-
quence of primary HIV infection of the skin [6].
The possibility of immune dysregulation is sup-
ported by data showing that, in the late stages
of HIV infection, there is an elevated eosinophil
count that in most cases correlates with skin dis-
eases such as EF, atopic dermatitis, and prurigo
nodularis [24]. There also is evidence that PPE
may occur in non–HIV-infected patients who
have a syndrome of idiopathic CD4-positive lym-
phocytopenia, suggesting that immune dysregula-
tion is of paramount importance [29]. The
effectiveness of antiretroviral therapy for PPE
also may provide additional information on the
immunologic basis of this disease [10].
Clinical findings
PPE is characterized by multiple discrete skin-
colored papules that often are excoriated. These
papules typically are symmetrical and are found
on the extremities, face, and trunk with sparing of
the mucous membranes, palms, soles, and digital
web spaces (Fig. 1) [5]. Colebunders and col-
leagues [3] found that in 95% of patients lesions
are found on the arms and legs. On the arms,
lesions are specifically localized on the extensor
surface and on the dorsum of the hands. Less
commonly, lesions may be erythematous or
 PRURITIC PAPULAR ERUPTION IN HIV 451

Fig. 1. Multiple firm excoriated and erythematous papules (A) on the back and arms and (B) on the torso on a back-
ground of older lesions revealing postinflammatory hyperpigmentation.

acneform with pustules. They do not form conflu-
ent plaques and may or may not be follicular [3].
Initially, lesions often resemble papular urticaria
[29], and pruritus, generally the only symptom
experienced, commences with lesion appearance.
Because of this pruritus, most patients scratch to
the point of extensive excoriations, with subsequent
postinflammatory hyperpigmentation (Fig. 2) and,
with time, formation of prurigo-like nodules and
scarring (Fig. 3). The course tends to be chronic
and waxes and wanes [17], but new lesions often
appear daily.
Pathology
Numerous authors have reported the patho-
logic findings in PPE with much inconsistency.
Resneck and colleagues [10] noted that in early
PPE, findings resembled arthropod bites, showing
dense superficial and deep perivascular and inter-
stitial infiltrate of lymphocytes and eosinophils of-
ten extending into the subcutis and associated
with epidermal hyperplasia and in some cases
a punctum. Hevia and colleagues [17] found a su-
perficial and mid-dermal mixed perivascular and
perifollicular infiltrate of lymphocytes and eosino-
phils with variable degrees of follicular damage.
Rosatelli and colleagues [30] noted an increase in
CD8-positive T lymphocytes, mast cells, macro-
phages, and eosinophils in lesional skin when com-
pared with healthy skin and suggested that PPE
better justifies their description than EF. The num-
ber of CD8-positive lymphocytes in the lesion was
noted to be higher than in healthy skin, suggesting
that their presence does not simply represent spill-
over from peripheral blood. These increased
CD8-positive cells may be responsible for the pro-
duction of cytokines, explaining the increased mac-
rophages, mast cells, and eosinophils. Ramos and
colleagues [31] found a predominantly perivascular
dermal lymphohistiocytic inflammatory infiltrate.
Langerhans cells were distributed normally in the
epidermis and were seen among the cellular
components of dermal infiltrates. The density of

Fig. 2. Concentration of lesions on the extremities of the (A) the lower legs and (B) arm showing postinflammatory
hyperpigmentation at the site of old papules.
452
Fig. 3. (A and B) Lesions on the upper extremities becoming more nodular with chronic scratching.
CD8-positive lymphocytes was elevated, and the
density of CD4-positive cells was reduced in dermal
infiltrates. The predominant cytokine in the lesion
was IL-5. Electron microscopy did not reveal
HIV or other infectious agents. Pardo and col-
leagues [32] reported a predominance of T lympho-
cytes in PPE but, in contrast to Rosatelli and
colleagues [30] and Ramos and colleagues [31]
noted a 2:1 ratio of CD4-positive to CD8-positive
cells. Others have shown hyperkeratosis, acantho-
sis, focal dyskeratosis, and necrotic cells in the epi-
dermis and dermal fibrosis with proliferation of
factor XIIIa- positive dermal dendrocytes, the der-
mal infiltrate containing lymphocytes, plasma cells,
eosinophils, and mast cells [29].
Cultures from pustules and skin biopsies are
universally negative for bacteria, fungi, and
mycobacteria. Hevia and colleagues [17] noted
Demodex mites were found in biopsies from 2 of
28 patients, whereas Pityrosporum orbiculare was
not observed in any case.
Hematologic and immunologic findings
There is no clear consensus as to the laboratory
findings in PPE. Sanchez and colleagues [33]
looked at 41 patients who had PPE and found
that 80% of patients had a CD4 T-cell count be-
low 100 /mm3, 77% had elevated IgE, and 55%
had elevated eosinophils. Boonchai and colleagues
[16] noted that the majority of their patients
EISMAN
(75%) who had PPE had a CD4 cell count below
50/mm3, suggesting that PPE should be regarded
as a cutaneous marker for advanced HIV infec-
tion. Pardo and colleagues [32] detected increased
levels of IgG and IgE in patients but no change in
IgM or IgA. All patients had a decrease in CD4-
positive T-cell counts and an elevation of CD8-
positive T cells. The investigators saw no other
significant changes in T and B cells or T-cell sub-
sets. Hevia and colleagues [17] noted an elevated
mean serum IgE versus controls in 28 patients.
Resneck and colleagues [10] noted that increase
in rash severity was associated with a decrease in
CD4 cell count and a higher peripheral eosinophil
count. Rosatelli and colleagues [30] also noted an
eosinophilia and high serum IgE. Aires and
colleagues [15] looked at cytokine profiles in pa-
tients who had HIV and found high IL-2, IL-12,
and g-IFN levels in those with and without
PPE, probably explaining the protection against
immunosuppression. In those who had PPE how-
ever, lower IL-2 and g-IFN levels were thought to
explain why PPE may be an indicator of an early
phase of immunosuppression. (IL-2 has a negative
correlation with peripheral CD4-positive lympho-
cytes). IL-5 was increased in patients who had
HIV compared with the HIV-negative group [34]
but did not differ when comparing HIV-positive
patients with and without PPE [3]. As mentioned,
Kinloch-de Loes and colleagues [28] found that
75% of patients who had PPE had circulating bul-
lous pemphigoid autoantibodies, and up to 30%
 PRURITIC PAPULAR ERUPTION IN HIV
met the diagnostic criteria for this condition on
histology, Western blotting, immunofluorescence,
and immunoelectron microscopy.
Differential diagnosis
There is an extensive clinical differential di-
agnosis of PPE (Fig. 4), probably reflecting
changes in lesions with time and alterations from
prolonged scratching caused by typically pro-
tracted disease. Histology, therefore, can be an
important tool in differentiating PPE from the
many other processes that can mimic it.
One of the more difficult distinctions to make
is with EF (Table 1). Some investigators hypothe-
size that PPE and EF are part of the same disease
spectrum [5]. This can cause confusion in inter-
preting the literature, because the two terms often
are used interchangeably. Others regard EF as
a subset of PPE accounting for 25% to 50% of
cases [35]. EF predominantly involves the fore-
head, eyelids, cheeks, neck, postauricular areas,
upper arms, and trunk, characteristically above
the nipple line [36]. Lesions appear as excoriated
or edematous papules. Pustules are not, as in
PPE, the predominant lesion, and the disease is
more common in men; only seven cases in women
have been described [37]. Interestingly, EF can
develop 3 to 6 months after the initiation of anti-
retroviral therapy, regardless of the regimen [37].
Hematologic examination in patients who have
EF may reveal elevated IgE levels and peripheral
eosinophilia. CD4 cell counts are usually less
than 300/mL. Histology for this condition is diag-
nostic, revealing follicular spongiosis and follicu-
locentric inflammatory infiltrate involving the
ITCHY PAPULAR AND PUSTULAR ERUPTION IN HIV
Pustules not predominant
1. EXCLUDE
2.CONSIDER
nodular prurigo
papular atopic dermatitis
drug eruption
papular granuloma annulare
Eosinophilic folliculitis papular syphilis
psoriasis
-neck,forehead, seborrheic dermatitis
papular mucinosis
cheeks, trunk
photodermatitis
-edematous papules
-excoriations
-histology specific
a.Scabies-(scraping)
b.Demodicidiosis- (scraping)
c.Papular Urticaria/ Arthropod Bites-
(history/season/location/pets home)
Fig. 4. A clinical approach to an HIV-positive patient who has an itchy papular or pustular eruption.
453
outer root sheaths of hair follicles. This infiltrate
is rich in eosinophils, with variable involvement
by lymphocytes, histiocytes, mast cells, and neu-
trophils. Flame figures and eosinophilic abscesses
may be seen [36,38]. A simple method of diagnos-
ing this condition entails preparing a smear from
an intact papule or pustule and staining with
Wright’s stain to reveal a prominence of eosino-
phils [39]. The cytokine profiles of PPE and EF
also differ [15,40]. EF is thought to be caused by
an inflammatory response directed either at the
follicle or the skin flora antigens in the late stages
of HIV infection, when immune response shifts
from a Th1- to a Th2-dominant cytokine profile
with increased secretion of IL-4 and IL-5 known
to promote eosinophilia [41]. There are no studies
to support a best-practices standard of treatment
for EF [42]. Multiple treatment modalities have
been suggested, including antihistamines, metro-
nidazole, itraconazole, long-term application of
permethrin, ivermectin, oral isotretinoin, ultravio-
let B (UVB) phototherapy, potent topical steroids,
low-dose prednisone (10–20 mg/d), dapsone,
0.1% topical tacrolimus ointment, and antiretro-
viral therapy [37,42,43].
Demodex folliculorum can inhabit hair follicles
commensally in immunocompetent humans but
with altered immunity can elicit an inflammatory
response similar to that seen with scabies. Because
the clinical appearance of these two conditions
can be almost identical to PPE, a scraping or his-
tologic specimen can help differentiate it from
PPE. In demodex follicultis (demodicidosis),
the mite can be visualized, and a spongiotic infun-
dibular folliculitis may be present. With scabies,
mites, feces, or eggs are deposited within the
Pustules predominant
1 AND 2 UNLIKELY swab
infective non-infective
PRURITIC PAPULAR ERUPTION
-hyperpigmented & skin colored
urticated papules
-diffuse and symmetrical
-extremities common
-prurigo-like nodules, excoriarions
and scarring 1.bacterial folliculitis
-chronic course
2.Pityrosporum ovale
1.acne-
vulgaris
steroid-induced
2.rosacea
Table 1

Differential diagnosis of pruritic papular eruption: summary of clinical characteristics
Pruritic papular eruption
Clinical findings Skin-colored papules
Excoriations
Pustules rare
Postinflammatory
hyperpigmentation
Prurigo-like nodules
Scarring
Distribution Symmetrical
Extremities, face, trunk
Rare on palms, soles, digital
web spaces
Histopathology Dermal perivasuclar and
interstitial lymphocytes,
eosinophils
Epidermal hyperplasia
Eosinophilic folliculitis
Edematous papules
Pustules not predominant
Forehead, eyelids, cheeks,
neck, postauricular,
upper arms and trunk
Follicular spongiosis
Folliculocentric infiltrate
rich in eosinophils
Flames figures
Demodex folliculorum
Rosacea-like
Erythematous papules with
background erythema
Head, neck
Spongiotic, infundibular
folliculitis
Scabies
Pauples/plaques with crust
or excoriations
Burrows
Vesicles nodules
Eczematous
Hands, wrists, interdigital,
ankles, ears face, scalp
Scabies mite feces or eggs
in epidermis
Eosinophils in reticular
dermis
454
Folliculitis: bacterial (B)
Pityrosporum (P)
Pustules predominate
Follicular pattern
Periofollicular papules
B: head, neck. upper trunk,
axillae, groin, buttocks
P: back, chest, shoulders
B: Staphylococcus aureus:
suppurative folliculitis,
gram stain
P: yeast forms

EISMAN
Follicular damage? Eosinophilic abscesses
Investigations [ IgE [ IgE Skin scraping Skin scraping Skin swab
Eosinophilia Eosinophilia PCR from scale P: KOH yeast forms
CD4 ! 100/mL CD4 ! 300/mL
[ CD8 T cells
[ IgG ?
Antibodies to bullous pem-
phigoid antigen?
Treatment Potent topical steroids Potent topical steroids Lindane Lindane B: intranasal mupirocin
Emollients Antihistamines Crotamiton Crotamiton ointment
Antipruritic lotions Prednisone Permethrin Permethrin Topical benzoyl peroxide
Antifungal creams Metronidazole Oral/topical metro nidazole Malathion Topical or oral antibiotics
Antiscabies therapy Itraconazole Ivermectin Sulphur ointment Antibacterial washes
Anitihistamines Permethrin/ivermectin Ivermectin P: topical antifungals
Oral antibiotics Isotretinoin Selenium sulphide shampoo
Pentoxifylline Dapsone 50% propylene glycol in
Anti-retrovirals UVB water
UVB phototherapy 1% tacrolimus ointment Fluconazole
Itraconazole
Abbreviations: KOH, potassium hydroxide; PCR, polymerase chain reaction.
 PRURITIC PAPULAR ERUPTION IN HIV
epidermis [10]. Treatment with 1% lindane or
10% crotamiton lotion [44] has proven efficacious
for demodex, as have long-term application of
permethrin and oral ivermectin.
Papular urticaria or arthropod bite reactions
may be indistinguishable clinically from PPE and
can be excluded more easily by a history of pets at
home, seasonal variation, or location of lesions. If
severe, some authors treat this resistant state with
systemic corticosteroids, which, although effica-
cious, may be problematic with long-term use in
an HIV-infected patient [29].
Nodular prurigo can resemble the chronic
lesions of PPE and is resistant to most forms of
therapy. Phototherapy and intralesional steroid in-
jections may prove useful, as may thalidomide [45].
In bacterial folliculitis and pityrosporal follic-
ulitis, pustules are the predominant lesions. A
swab of the pus for bacterial culture or a biopsy
for histology can confirm the diagnosis. Staphylo-
coccus aureus folliculitis (suppurative folliculitis)
is a common cutaneous infection in HIV-infected
patients, in part because of the high staphylococ-
cal nasal carriage rate in these patients, which has
been found to be twice that of controls [46].
Pustules rather than papules also are the pre-
dominant lesion in acne and rosacea, and these
conditions tend not to be as itchy as PPE. Papular
atopic dermatitis, drug eruptions, papular muci-
nosis [47], papular granuloma annulare, papular
syphilis, psoriasis, onchocerciasis, photodermati-
tis, viral exanthems, drug eruptions, and papulo-
necrotic, tuberculid, and seborrheic dermatitis
also need to be considered in the differential.
Treatment
Treatment for PPE remains notoriously diffi-
cult. Pruritus often is severe and unresponsive to
traditional antipruritic measures. No formal stud-
ies have been reported, and treatment successes or
failures are purely anecdotal. Treatments have
included potent topical corticosteroids, used alone
or in combination with oral antihistamines; oral
antibiotics; emollients; antipruritic lotions; anti-
fungal creams; and antiscabies treatments [5,17].
These therapies have had variable success based
on anecdotal reports.
Ishii and colleagues [48] demonstrated UVB
phototherapy to be effective in the treatment of
PPE. Pardo and colleagues [32] performed a pro-
spective study of UVB in eight patients with the
condition. After 4 weeks of UVB therapy given
three times weekly, seven of the eight patients
455
had improvement in pruritus; the eighth patient,
despite ongoing pruritus, had a moderate decrease
in the number of papules. The mean time to recur-
rence was 8 weeks. The mechanism by which UVB
relieves the pruritus in PPE is unknown. UVB is
a potent immunomodulatory agent [49,50] and
in PPE most likely acts locally, modifying local
immune cell networks rather than having an effect
on systemic immune status, because skin improve-
ment was seen only at the treated sites. Contro-
versy exists, however, because UVB has been
found to enhance the transcription of HIV in vitro
and in vivo, raising concerns about its safety when
used in HIV-infected patients [51,52]. Subsequent
studies, however, have not found enhanced HIV
transcription to be of clinical significance [53].
Berman and colleagues [54] found that treat-
ment with pentoxifylline, a known inhibitor of tu-
mor necrosis factor-a production, 400 mg three
times daily for 8 weeks, successfully and signifi-
cantly decreased the pruritus in 10 of 11 patients
who had PPE. Patients had detectable levels of se-
rum tumor necrosis factor-a or IL-4 at baseline
and had undetectable levels at the end of the
study, but testing may not have detected tissue
levels. A potential confounding issue is that these
patients were all receiving antiretroviral therapy
at the time of commencing pentoxifylline treat-
ment, but they had been receiving a constant
dose regimen before the study, and no changes
were made during the study period. Some patients
also continued UVB therapy that they had been
receiving before the study at the same dose and
frequency of treatment.
Resneck and colleagues [10] present anecdotal
reports of PPE improving with the initiation of
antiretroviral medication. Some researchers, in
fact, have suggested the PPE be added to the list
of conditions qualifying patients for therapy.
Summary
Interpreting the literature on PPE is difficult.
There is no consensus on clinical or histologic
criteria for diagnosis, etiology, or treatment. The
problem remains that ‘‘PPE’’ is used by some as
a broad umbrella term for any itchy papular
eruption in an HIV-positive patient rather than,
perhaps more appropriately, as a separate and
distinct disease entity. Many authors do not define
and distinguish PPE, and therefore it is difficult to
ascertain what they mean by the term ‘‘PPE.’’
Nevertheless, PPE has a major impact on the
quality of life of the affected patient, both from
456 EISMAN
a medical and a cosmetic point of view, subjecting
patients to HIV-related stigma in their communi-
ties. Perhaps a consensus as to what constitutes
the disease may help in recognizing this condition
as a marker of advanced HIV infection and
allowing better treatment of this recalcitrant and
distressing condition.
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