Vous êtes sur la page 1sur 10

DERMATOPATHOLOGY

Demodicosis: A clinicopathological study


Chao-Kai Hsu, MD,a,b Mark Ming-Long Hsu, MD,a and Julia Yu-Yun Lee, MDa,c
Tainan, Taiwan
Background: Demodex mites are common commensal organisms of the pilosebaceous unit in human
beings and have been implicated in pityriasis folliculorum, rosacea-like demodicosis, and demodicosis
gravis.
Objective: We sought to describe the spectrum of clinicopathological findings and therapeutic responses of
demodicosis in Taiwanese patients.
Methods: We conducted a retrospective study to review clinicopathologic findings and therapeutic
responses of 34 cases of diagnosed demodicosis.
Results: Fifteen cases with positive results of potassium hydroxide examination, standardized skin
surface biopsy specimen, and/or skin biopsy specimen, and resolution of skin lesions after anti-Demodex
treatment were included for final analysis. Nineteen cases were excluded because of insufficient positive
data to make a definite diagnosis. There were 4 male and 11 female patients (age 1-64 years, mean age
38.7 years). The disease was recurrent or chronic with a duration ranging from 2 months to 5 years (mean
15.7 months). The skin lesions were acne rosacea-like (n = 8), perioral dermatitis-like (n = 5),
granulomatous rosacea-like (n = 1), and pityriasis folliculorum (n = 1). Skin biopsy was performed in 7
patients. Overall, the histopathology was characterized by: (1) dense perivascular and perifollicular
lymphohistiocytic infiltrates, often with abundant neutrophils and occasionally with multinucleated
histiocytes; (2) excessive Demodex mites in follicular infundibula; and (3) infundibular pustules
containing mites or mites in perifollicular inflammatory infiltrate. The skin lesions resolved after
treatment including systemic metronidazole, topical metronidazole, crotamiton, or gamma benzene
hexachloride.
Limitations: Small sample size and a fraction of patients without long-term follow-up are limitations.
Conclusion: Demodicosis should be considered in the differential diagnosis of recurrent or recalcitrant
rosacea-like, granulomatous rosacea-like, and perioral dermatitis-like eruptions of the face. Potassium
hydroxide examination, standardized skin surface biopsy, skin biopsy, or a combination of these are
essential to establish the diagnosis. ( J Am Acad Dermatol 2009;60:453-62.)
Key words: Demodex granuloma; demodicosis; pathology; perioral dermatitis; rosacea-like dermatitis.

emodicosis (or demodicidosis) is the


term applied to cutaneous diseases
caused by Demodex mites. D folliculorum and D brevis are common commensals of the
From the Departments of Dermatologya and Pathology,c College
of Medicine, University Hospital, and Institute of Clinical
Medicine,b National Cheng Kung University.
Funding sources: None.
Conflicts of interest: None declared.
Reprint requests: Julia Yu-Yun Lee, MD, Departments of
Dermatology and Pathology, National Cheng Kung University
College of Medicine and Hospital, 138 Sheng-Li Rd, Tainan,
Taiwan. E-mail: yylee@mail.ncku.edu.tw.
0190-9622/$36.00
2008 by the American Academy of Dermatology, Inc.
doi:10.1016/j.jaad.2008.10.058

pilosebaceous units in human beings.1,2 The face,


scalp, and upper aspect of the chest are the predilection
sites. D folliculorum is usually found in the follicular
infundibulum, and D brevis in sebaceous ducts and
meibomian glands. Demodex mites are thought to play
a pathogenic role when present in excessive number1,3-5 or penetrating into the dermis6,7 and have been
implicated in papulopustular rosacea,3,4 pityriasis folliculorum,5,8 rosacea-like demodicosis,9 demodicosis
gravis (granulomatous rosacea-like demodicosis),10
and blepharitis.11 However, there is no consensus as
to what degree these mites are contributing to these
skin lesions.
Demodicosis appears to be uncommon among
Taiwanese patients. We report a series of 15 cases of
453

Case No.

Age, y/sex

Clinical picture

Diagnosis at
presentation

Duration

KOH
examination/SSSB

Pathology

Acne rosacea-like

Demodicosis

1y

Positive

ND

2
3

38/F
27/F

Acne rosacea-like
Acne rosacea-like

Demodex folliculitis
Demodex folliculitis

6 mo
6 mo

Positive
Positive

ND
ND

18/F

Acne rosacea-like

Demodicosis

6 mo

ND

1/F

Acne rosacea-like

2 mo

ND

64/M

1y

Positive

ND

60/F

Perioral
dermatitis-like
Acne rosacea-like
(nose only)

Demodicosis vs
impetigo
Acne rosacea
Rosacea

3y

Positive

ND

28/F

Positive

ND

34/M

Rosacea with
steroid rosacea
Demodicosis vs
perioral
dermatitis

2y

Pityriasis
folliculorum
Acne rosacea-like

3 mo

Positive

Demodex
folliculitis

10

44/F

Acne rosacea-like
(severe)

Extensive
demodicosis vs
fungal infection

2 mo

Positive

Demodex
folliculitis

11

42/F

Perioral
dermatitis-like

2y

Positive

Demodex
folliculitis

12

24/F

Perioral dermatitis-like

Eosinophilic
folliculitis vs
rosacea
Demodex folliculitis

5y

Positive

13

52/M

Perioral dermatitis-like
(right eyelids only)

Demodicosis

1y

Demodex
folliculitis
Demodex
folliculitis

MN 250 mg tid 3 wk;


MNG bid 3 wk
MN 250 mg tid 1 wk
MN 250 mg tid 3 wk;
MNG bid 3 wk

MN 250 mg tid 3 wk;


MNG bid 3 wk
Crotamiton 10% qd 1 wk
MN 500 mg bid 1 wk,
500 mg bid 3 wk
Crotamiton 10% qd 1 wk
(minimal effect),
switched to MNG
bid 1 wk
MNG 1 wk (minimal effect),
switched to g-BHC 2 wk
Doxycycline
250 mg 3 wk,
prednisolone 10
mg bid tapered in 3
wk; g-BHC 2 wk
MN 250 mg
tid 3 wk, prednisolone
10 mg bid tapered in 3
wk; MNG bid 3 wk
MNG bid 2 wk

MN 500 mg tid 2 wk;


g-BHC 2 wk
MN 250 mg tid 1 wk

CR
CR
CR; two
relapses
(at 40 and
47 mo)
CR

Follow-up
duration

2 wk
15 mo
82 mo

2 mo

CR

ND

CR

3 wk

CR

ND

CR

3 mo

CR; one
relapse
at 2 mo

10 mo

CR

6 wk

CR

ND

CR

3 mo

CR

ND

MARCH 2009

53/M

Outcome

J AM ACAD DERMATOL

Treatment

454 Hsu, Hsu, and Lee

Table I. Clinicopathological data of 15 patients with demodicidosis

J AM ACAD DERMATOL

Hsu, Hsu, and Lee 455

BHC, Benzene hexachloride 1%; bid, twice per day; CR, complete resolution of skin lesions; F, female; KOH, potassium hydroxide; M, male; MN, metronidazole; MNG, metronidazole gel 0.75%; ND: not
done; qd, once a day; SSSB: standardized skin surface biopsy; tid, three times per day.
*KOH examination revealed presence of Demodex mites with unspecified number.
y
Case reported separately.12

7 wk
CR
Demodex
granuloma
ND
6 mo
48/F
15y

Granulomatous
rosacea-like
(whole face, neck, and
upper aspect of chest)

Granulomatous
rosacea

ND
47/F
14

Perioral dermatitis-like,
steroid rosacea

Granulomatous
rosacea vs
perioral dermatitis

2y

Demodex
folliculitis

MN 250 mg tid 3 wk;


tacrolimus 0.03% bid 5 wk,
changed to pimecrolimus
1% 11 wk
MN 500 mg tid tapered in 3
wk, prednisolone 5 mg tid
tapered in 3 wk; MNG
bid 8 wk

CR

7 mo

VOLUME 60, NUMBER 3

demodicosis in which the diagnosis was confirmed


based on the clinicopathological findings and therapeutic responses.

METHODS
In this retrospective study, we searched our
department database (July 1990-June 2007) for
cases with clinical or pathologic diagnosis or tentative diagnosis of demodicosis (or demodicidosis)
or Demodex folliculitis by the Crux Integrated
System, a database system developed in our department. The clinical picture, the initial clinical
diagnosis at the time of the first visit, the pathologic
slides, and the response to therapy were reviewed.
Microscopic examination of mites was done either
by potassium hydroxide (KOH) examination of
skin scrapings or by cyanoacrylate glue standardized skin surface biopsy (SSSB). The result was
considered positive when there were more than 5
mites either in one follicle or in one low-power
field by scraping or in 1-cm2 area by SSSB.3,4
Pathological findings, including the pattern of inflammation, presence of infundibular pustules containing mites, and density of infundibular Demodex
mites and inflammatory cells were analyzed. The
density of inflammatory cells or mites was graded
using an arbitrary scale of 1 to 41 in increasing
density.

RESULTS
In all, 34 cases were retrieved from the database
originally. Nineteen of them were excluded because
of the lack of clinical photographs or follow-up
information, incomplete clinical or pathological
evaluation, or poor response to anti-Demodex therapy. The remaining 15 cases showed good responses
to antiacarid therapy. Based on the clinical presentations, positive histopathological and/or KOH examination, and positive response to anti-Demodex
therapy, these 15 cases were concluded to be
demodicosis. The clinicopathological findings are
summarized in Table I. Case 15, a patient with
granulomatous rosacea-like demodicosis, has been
described previously.12
Of the 15 confirmed patients, 4 were male and 11
were female (age range 1-64 years, mean age 38.7
years). The disease duration at presentation ranged
from 2 months to 5 years (mean 15.7 months). Three
patients had history of malignancy, buccal cancer,
colon cancer, and nasopharyngeal carcinoma, one
each, and were not receiving chemotherapy at presentation. Clinically, the lesions consisted of many
erythematous papulopustules, dome-shaped papules, or tiny follicular papules on the face and/or

456 Hsu, Hsu, and Lee

J AM ACAD DERMATOL
MARCH 2009

Fig 1. Perioral dermatitis-like demodicosis (case 9; D07-0936). A, Many erythematous


papulopustules were present on chin and left cheek of 34-year-old man for 3 months. B,
Rash resolved after 2 weeks of treatment. C, Histologically, there is dense perifollicular and
perivascular lymphohistiocytic infiltrate with abundant neutrophils and plasma cells in dermis.
D, At least 5 Demodex mites are packed inside neutrophil-infiltrated infundibulum. (C and D,
Hematoxylin-eosin stain; original magnifications: C, 320; D, 3100.)

neck area with a predilection for the perioral area


and cheeks. Based on the morphology and distributions of the lesions, the clinical picture was classified
into 4 types as follows. Eight patients had acne
rosacea-like rash with erythematous papulopustular
lesions involving multiple areas of the face (Figs
1 and 2). Five patients manifested as perioral dermatitis-like rash with papulopustular lesion limited
to the perioral areas (4 patients) or eyelids (one
patient) (Figs 3 to 5). One patient (case 15) presented
with granulomatous rosacea-like eruption consisting
of discrete erythematous dome-shaped papules
without obvious pustules on the entire face, neck,
and upper aspect of chest (Fig 6). One patient (case
8) had pityriasis folliculorum with numerous tiny
follicular plugs and scales and a faint background
erythema accompanied by itching and burning sensations (Fig 7). KOH examination or SSSB was
performed in 11 patients; 10 showed positive results
(Fig 7). Demodicosis was diagnosed or suggested
at presentation in 9 patients; other diagnoses
were impetigo, acne rosacea, perioral dermatitis,
eosinophilic folliculitis, and granulomatous rosacea
(Table I).

Skin biopsy was performed in 7 patients (cases 9


to 15). In cases 9 to 14, the biopsy specimens were
taken from papulopustular lesions, and case 15 from
a dome-shaped papule. Multiple step sections were
examined. The main pathologic findings are summarized in Table II. Multiple Demodex mites were
found in dilated infundibula (cases 9 to 15); mites
were found also within infundibular pustules (cases
11 to 14) (Figs 1, 3, and 5). The dermis showed a
moderate to dense perivascular and perifollicular
lymphohistiocytic infiltrate with various amounts of
neutrophils. The suppurative infiltrate in case 10 was
associated with a ruptured hair follicle. Numerous
plasma cells were present in two specimens (cases 9
and 12). Multinucleated histiocytes without obvious
foreign body giant cells were present in two specimens (cases 14 and 15), and were more numerous in
case 15 where two Demodex mites were found
within the inflammatory infiltrate surrounding an
apparent intact infundibulum (Fig 6). Cases 9 to 14
showed features of Demodex folliculitis, which differed from the Demodex granuloma in case 15 by
lacking an obvious granulomatous component in the
inflammatory infiltrate.

J AM ACAD DERMATOL
VOLUME 60, NUMBER 3

Hsu, Hsu, and Lee 457

Fig 2. Severe acne rosacea-like demodicosis (case 10; D07-0066). A, Numerous papulopustules were present over entire face in 44-year-old woman for 2 months. B, Rash resolved after 3
weeks of systemic and topical metronidazole and low-dose prednisolone.

The disease was recurrent or chronic persistent in


most patients with poor responses to prior treatments, but resolved completely after a short course
of treatments that included topical metronidazole gel
0.75% (8 patients), topical gamma benzene hexachloride cream 1% (3 patients) and crotamiton 10%
(two patients), and oral metronidazole (250 mg three
times per day) for 1 to 3 weeks (10 patients) (Table I).
A short course of low-dose oral prednisolone was
given in 3 patients to reduce inflammation.

DISCUSSION
We described the clinical and pathologic findings
of 15 cases of demodicosis, the first series in Taiwan.
In our series, the mean age was 38.7 years with a
female predominance. In the report by Forton et al,13
the mean age was 49 years with male:female ratio of
2:5. Children are rarely affected by demodicosis.1
Our series included a 1-year-old child. Some studies
showed that immunocompromised hosts, such as
patients with AIDS14,15 and leukemia,15,16 are more
prone to Demodex infestation. In our study, no
patient was immunocompromised.
Ayres and Ayres5 initially described two clinical
forms of Demodex infestation in human beings:
pityriasis folliculorum and rosacea-like demodicosis.
Since then, Demodex has been implicated in various
dermatoses, including papulopustular rosacea,3

demodicosis gravis (granulomatous rosacea-like


demodicosis),1,17 pustular folliculitis,18,19 perioral
dermatitis,20 Demodex abscesses,21 and blepharitis.11,22 The clinical manifestations in our series
were consistent with acne rosacea-like in 8 patients,
perioral dermatitis-like in 5, granulomatous rosacealike in one, and pityriasis folliculorum in one.
Interestingly, pityriasis folliculorum seems to be
very uncommon in our experience. It is possible
that this variant had been underdiagnosed because
of the subtlety of the lesions and our staffs lack of
familiarity with this variant. On the other hand, the
climate in Taiwan is relatively hot and humid, and
does not require frequent use of facial skin care
products with high oil contents.
Three histopathological variants of demodicosis
have been described.23 Rosacea-like demodicosis is
characterized by presence of Demodex mites in
infundibula with a primarily perifollicular infiltrate
of mononuclear cells that occasionally assumed a
granulomatous pattern.1,24 In our series, 6 cases with
papulopustular lesions and one case with granuloma-like lesion were examined. They all showed
moderate to dense perivascular and perifollicular
lymphohistiocytic infiltrates with variable amounts
of neutrophils. More importantly, multiple mites
were present within infundibular pustules or inflamed infundibula, findings supporting the pathogenic role of this organism.

458 Hsu, Hsu, and Lee

J AM ACAD DERMATOL
MARCH 2009

Fig 3. Perioral dermatitis-like demodicosis (case 11; D051078). A, Many small erythematous papulopustules were
present on chin of 42-year-old woman for 2 years. B,
Histologically, there is pustule next to follicular orifice and
dense perifollicular and perivascular lymphohistiocytic
infiltrate with neutrophils in dermis. Note that infundibulum is packed with many mites. (Hematoxylin-eosin stain;
original magnification: 340.)

Fig 4. Perioral dermatitis-like demodicosis (case 12;


D07-0344). A, Multiple erythematous papulopustules
were present around mouth of 24-year-old woman for
5 years. B, Histologically, there is dense perifollicular and
perivascular lymphohistiocytic infiltrate with large, partially destroyed infundibular pustule containing multiple
mites. (Hematoxylin-eosin stain; original magnification:
340.)

Demodicosis gravis resembles severe granulomatous rosacea clinically, and is characterized pathologically by dermal granulomas with central
caseation necrosis and mite remnants phagocytized
by foreign-body giant cells.10 In a series of 53 cases
of granulomatous rosacea, intact or fragmented
Demodex mites in granulomas were observed in 10
specimens.25 In demodectic mange of the dog, the
histopathology shows disruption of the follicle with
Demodex mites lying free within inflammatory infiltrates.6 Clinically the rash in our case 15 mimicked
granulomatous rosacea, and it differed from acne
rosacea-like or perioral dermatitis-like cases in the
current series by lacking obvious pustules.
Histopathologically, it showed intact mites within
the suppurative and granulomatous inflammatory
infiltrate outside an apparent intact follicle. Similar
findings were reported in case of Demodex
granuloma.6
Pityriasis folliculorum is characterized by follicular hyperkeratosis filled with Demodex mites and a
perivascular and diffuse dermal lymphocytic infiltrate without granuloma formation.5,8 No biopsy was

performed in the only case of pityriasis folliculorum


in our series. However, a large number of Demodex
mites were found in a single extracted follicular plug
(Fig 7).
Overall, the histopathology in our series was
characterized by: (1) dense perivascular and perifollicular lymphohistiocytic infiltrates, often with
abundant neutrophils and occasionally with multinucleated histiocytes; (2) excessive Demodex mites
in follicular infundibula; and (3) infundibular pustules containing mites or mites in perifollicular
inflammatory infiltrate. In cases 9 to 14, no obvious
granulomatous component in the perifollicular
inflammatory infiltrate was present, and the changes
were interpreted as Demodex folliculitis. In contrast,
the presence of obvious granulomatous component
in case 15 qualified it as a Demodex granuloma. The
granuloma, however, was not associated with caseation necrosis. Instead, it showed focal suppuration
around the extruded intact mites. This reaction
pattern may represent an early stage of granulomatous demodicosis. Based on our observation and
those of others,1,26,27 the variation in the clinical

J AM ACAD DERMATOL
VOLUME 60, NUMBER 3

manifestation and histopathology of demodicosis


may depend on the degree of Demodex infestation,
duration of the disease, hosts age and general
health, and evolutional stage of individual lesions.
The causal relationship of Demodex mites in
various forms of demodicosis remains controversial.
Only a small number of people develop skin lesions
despite a very common presence of these mites in
human skin. The rate of Demodex mite infestation in
healthy skin increases with age in general population,28 up to 100% in elderly people.26,29 However,
the density in normal-appearing skin is generally
low.30 Aylesworth and Vance26 found Demodex
mites in 10% of all skin biopsy specimens and in
12% of all follicles in a study of consecutive skin
biopsy specimens, and the prevalence rate increased
with age. In a study by Vollmer,27 Demodex mites
were found in 42% of 388 follicles with inflammation,
but only in 10% of noninflamed follicles. Overall,
83% of the follicles with mites showed inflammation
in that series. Granulomatous reaction to extrafollicular Demodex has also been observed in granulomatous rosacea-like skin lesions25,31 and in rosacea-like
demodicosis.9 In the latter, up to 10 or 15 mites were
found in the affected follicles.32 It has been suggested
that an increasing density of mites correlates with an
increasing perifollicular inflammation and clinical
manifestation.3 A density of more than 5 mites/follicle
or 5 mites/cm2 of SSSB specimen has been considered
to be pathogenic.2,3 Symptoms may develop when
the follicles become heavily infested, or when the
mites penetrate into the dermal tissue.5
The density of Demodex mites can be studied by
KOH preparations of follicular plugs, skin scrapings, and SSSB specimens.18,30,33 In our series, the
examination was performed in 11 patients, and
only one had a negative result (3 mites/follicle).
Forton and Song34 found that when the first SSSB
specimen was negative, a subsequent SSSB specimen from the same site had yielded more than 5
mites/cm2. Therefore, a second SSSB should be
performed at the same site to avoid a false-negative
result.34
Several pathogenic mechanisms have been proposed for demodicosis, including: (1) blockage of
hair follicles and sebaceous ducts by the mites or
the reactive hyperkeratosis; (2) stimulation of the
hosts humoral and cell-mediated immune reactions
by the mites and their waste products; (3) a foreign
body granulomatous reaction to the mites chitinous skeleton; and (4) a vector role for bacteria.1,4,35
Recently, Lacey et al36 reported that antigenic
proteins related to Bacillus oleronius isolated from
D folliculorum mites are capable of stimulating
an inflammatory response in patients with

Hsu, Hsu, and Lee 459

Fig 5. Perioral dermatitis-like demodicosis (case 13; D070148). A, Multiple erythematous papulopustules were
present over right periorbital area of 52-year-old man
for 1 year. B, Histologically, more than 5 Demodex mites
are found in pustule within partially destroyed infundibulum. (Hematoxylin-eosin stain; original magnification:
3100.)

papulopustular rosacea. Akilov and Mumcuoglu37


showed that an increasing density of the mites was
associated with an increasing trend of apoptosis in
lymphocytes. This could result in local immunosuppression, allowing the mites to survive in the
host.
With regard to the terminology of the disease,
both demodicosis and demodicidosis have been
used with the latter being more commonly used in
the older dermatologic literature. Demodicidosis
with the suffix id is analogous to tuberculid or
bacterid, and implies a state of hypersensitivity or
allergic reaction to substances of the pathogen.
Therefore, demodicidosis does not reflect the
current view on the pathogenesis of this dermatosis,
and demodicosis would be a preferred term.
Various regimens have been used to treat demodicosis, including systemic metronidazole and ivermectin as well as topical metronidazole, salicylic
acid, gamma benzene hexachloride, sublimed
sulfur, permethrin, crotamiton, and benzyl benzoate.1,38,39 Among these, metronidazole 2%, sublimed
sulfur 10%, permethrin 1%, and lindane 1% did not
show any acaricidal activity, whereas the efficacy of

460 Hsu, Hsu, and Lee

J AM ACAD DERMATOL
MARCH 2009

Fig 6. Granulomatous rosacea-like demodicosis (case 15; D05-0959). A, Many discrete dull red
papules with no obvious pustules were present on face of 48-year-old woman for 6 months. B,
Histopathological examination reveals dense perifollicular lymphohistiocytic infiltrate with
multinucleated histiocytes and neutrophils. Note presence of two mites (arrow) within
suppurative (asterisk) and granulomatous infiltrate around apparently intact follicle plugged
by keratin and inflammatory cells. Inset, Close-up view of mite and granulomatous infiltrate.
(Hematoxylin-eosin stain; original magnification: 340.)

Fig 7. Pityriasis folliculorum (case 8). A, Numerous tiny


follicular plugs with faint erythematous background were
present for 2 years on both cheeks of 28-year-old woman.
B, Potassium hydroxide examination revealed 7 Demodex
mites (arrows) from one follicle (low-power field).

crotamiton 10% once a day was confirmed by


SSSB.40 Demodex can survive in the presence of as
much as 1 mg/mL of metronidazole, a concentration

that cannot be achieved in vivo.41 It has been


proposed that metronidazole may act on the mite
via one or more of its active metabolites formed in
vivo.1 In the current series, the skin lesions resolved
rapidly after systemic and/or topical metronidazole
therapy in most patients, and after topical crotamiton or gamma benzene hexachloride treatment in a
few patients. Of the patients who had follow-up
longer than 10 months, two had relapses but
responded again to antiacarid treatments. One of
our patients (case 14) was treated initially with
0.03% tacrolimus because of the clinical diagnosis of
perioral dermatitis and steroid rosacea. Oral metronidazole was added when the skin biopsy specimen
revealed Demodex folliculitis. The lesions responded to the combination therapy. It should be
noted that there are reports of demodicosis induced
by tacrolimus/pimecrolimus.42,43
In summary, we described the clinicopathologic
findings of 15 cases with confirmed diagnosis of
demodicosis based on the clinicopathological correlation and positive responses to antiacarid therapy. Our patients often had a long history of
papulopustular or acne rosacea-like eruptions on
the face with poor response to nonantiacarid treatments before the correct diagnosis was rendered.
Demodicosis should be considered in the differential diagnosis of recurrent or recalcitrant facial
eruptions, including rosacea-like, granulomatous
rosacea-like, and perioral dermatitis-like dermatitis,
steroid rosacea, and eosinophilic folliculitis. KOH

J AM ACAD DERMATOL

Hsu, Hsu, and Lee 461

VOLUME 60, NUMBER 3

Table II. Pathological features of demodicosis in 7 patients


Case
No.

Clinical picture

Perioral dermatitis-like

10

Acne rosacea-like

11

Perioral dermatitis-like

12

Perioral dermatitis-like

13

Perioral dermatitis-like

14

Perioral dermatitis-like

15

Granulomatous
rosacea-like

Histologic
pattern diagnosis

Density
of mites

Folliculitis with
early pustule
Disrupted infundibulum
with nodular suppurative
infiltrate
Folliculitis with
infundibular pustule
Dense diffuse
lymphohistiocytic
infiltrate with
infundibular pustule
Folliculitis with
infundibular pustule
Folliculitis with
infundibular pustule
Suppurative granulomatous
infiltrate with
extrafollicular mites

31

N 31

N 21L/H 21P 21

11

Disrupted

N 41L/H 21

41

Pustule containing
mites
Disrupted, pustule
containing mites

N 11L/H 21

21

31
31
21

Changes in
infundibulum

Disrupted, pustule
containing mites
Pustule containing
mites
Intact, with
hyperkeratosis,
inflammatory cells

Dermal infiltrate

N 11L/H 21P 21

N 21L/H 21
N 21L/H 21MNH 11
N 21L/H 31MNH 21

Density of inflammatory cells or mites in infundibula are graded using arbitrary scale of 1 to 41 in increasing density.
L/H, Lymphocyte/histiocyte; MNH, multinucleated histiocyte; N, neutrophil; P, plasma cell.

examination, SSSB, skin biopsy, or a combination


of these are essential to establish the correct
diagnosis.
REFERENCES
1. Baima B, Sticherling M. Demodicidosis revisited. Acta Derm
Venereol 2002;82:3-6.
2. Erbagci Z, Ozgoztasi O. The significance of Demodex folliculorum density in rosacea. Int J Dermatol 1998;37:421-5.
3. Forton F, Seys B. Density of Demodex folliculorum in rosacea: a
case-control study using standardized skin-surface biopsy. Br J
Dermatol 1993;128:650-9.
4. Bonnar E, Eustace P, Powell FC. The Demodex mite population
in rosacea. J Am Acad Dermatol 1993;28:443-8.
5. Ayres S Jr, Ayres S III. Demodectic eruptions (demodicidosis) in the human: 30 years experience with 2 commonly
unrecognized entities; pityriasis folliculorum (Demodex) and
acne rosacea (Demodex type). Arch Dermatol 1961;83:
816-27.
6. Ecker RI, Winkelmann RK. Demodex granuloma. Arch Dermatol
1979;115:343-4.
7. Hoekzema R, Hulsebosch HJ, Bos JD. Demodicidosis or rosacea: what did we treat? Br J Dermatol 1995;133:294-9.
8. Dominey A, Tschen J, Rosen T, Batres E, Stern JK. Pityriasis
folliculorum revisited. J Am Acad Dermatol 1989;21:81-4.
9. Ayres S Jr, Mihan R. Rosacea-like demodicidosis involving the
eyelids: a case report. Arch Dermatol 1967;95:63-6.
10. De Dulanto F, Camacho-Martinez F. Demodicidosis gravis.
[French]. Ann Dermatol Venereol 1979;106:699-704.
11. Post CF, Juhlin E. Demodex folliculorum and blepharitis. Arch
Dermatol 1963;88:298-302.
12. Lee JY, Hsu CK. Granulomatous rosacea-like demodicidosis.
Dermatol Online J 2007;13:9.
13. Forton F, Germaux MA, Brasseur T, De Liever A, Laporte M,
Mathys C, et al. Demodicosis and rosacea: epidemiology and

14.

15.

16.
17.

18.

19.

20.

21.

22.
23.

24.

significance in daily dermatologic practice. J Am Acad


Dermatol 2005;52:74-87.
Dominey A, Rosen T, Tschen J. Papulonodular demodicidosis
associated with acquired immunodeficiency syndrome. J Am
Acad Dermatol 1989;20:197-201.
Ashack RJ, Frost ML, Norins AL. Papular pruritic eruption of
Demodex folliculitis in patients with acquired immunodeficiency syndrome. J Am Acad Dermatol 1989;21:306-7.
Sahn EE, Sheridan DM. Demodicidosis in a child with leukemia.
J Am Acad Dermatol 1992;27:799-801.
Helm KF, Menz J, Gibson LE, Dicken CH. A clinical and
histopathologic study of granulomatous rosacea. J Am Acad
Dermatol 1991;25:1038-43.
Karincaoglu Y, Bayram N, Aycan O, Esrefoglu M. The clinical
importance of Demodex folliculorum presenting with nonspecific facial signs and symptoms. J Dermatol 2004;31:618-26.
Purcell SM, Hayes TJ, Dixon SL. Pustular folliculitis associated
with Demodex folliculorum. J Am Acad Dermatol 1986;15:
1159-62.
Dolenc-Voljc M, Pohar M, Lunder T. Density of Demodex
folliculorum in perioral dermatitis. Acta Derm Venereol 2005;
85:211-5.
Schaller M, Sander CA, Plewig G. Demodex abscesses: clinical
and therapeutic challenges. J Am Acad Dermatol 2003;
49(Suppl):S272-4.
Smith S, McCulloch C. Demodex folliculorum palpebrarum. Can
J Ophthalmol 1969;4:3-15.
Loffreda MD. Inflammatory diseases of hair follicles, sweat
glands, and cartilage. In: Elder DE, Elenitsas R, Johnson BL Jr,
Murphy GF, editors. Levers histopathology of the skin. Philadelphia: Lippincott: Williams and Wilkins; 2005. pp. 469-512.
Georgala S, Katoulis AC, Kylafis GD, Koumantaki-Mathioudaki E,
Georgala C, Aroni K. Increased density of Demodex folliculorum
and evidence of delayed hypersensitivity reaction in subjects
with papulopustular rosacea. J Eur Acad Dermatol Venereol
2001;15:441-4.

462 Hsu, Hsu, and Lee

25. Grosshans EM, Kremer M, Maleville J. Demodex folliculorum


and the histogenesis of granulomatous rosacea. [German].
Hautarzt 1974;25:166-77.
26. Aylesworth R, Vance JC. Demodex folliculorum and Demodex
brevis in cutaneous biopsies. J Am Acad Dermatol 1982;7:583-9.
27. Vollmer RT. Demodex-associated folliculitis. Am J Dermatopathol 1996;18:589-91.
28. Andrews JR. The prevalence of hair follicle mites in Caucasian
New Zealanders. N Z Med J 1982;95:451-3.
29. Boge-Rasmussen T, Christensen JD, Gluud B, Kristensen G, Norn
MS. Demodex folliculorum hominis (Simon): incidence in a normomaterial and in patients under systemic treatment with erythromycin or glucocorticoid. Acta Derm Venereol 1982;62:454-6.
30. Plewig G, Kligman AM. The role of Demodex. Berlin: SpringerVerlag; 2000. p. 507-12.
31. Mehregan AH, Hashimoto K. Pinkus guide to dermatohistopathology. New York: Appleton and Lange; 1991. pp. 260-2.
32. Ayres S Jr, Mihan R. Demodex granuloma. Arch Dermatol 1979;
115:1285-6.
33. Ayres S Jr. Rosacea and rosacea-like demodicidosis. Int J
Dermatol 1987;26:198-9.
34. Forton F, Song M. Limitations of standardized skin surface
biopsy in measurement of the density of Demodex folliculorum: a case report. Br J Dermatol 1998;139:697-700.

J AM ACAD DERMATOL
MARCH 2009

35. Rufli T, Buchner SA. T-cell subsets in acne rosacea lesions and
the possible role of Demodex folliculorum. Dermatologica
1984;169:1-5.
36. Lacey N, Delaney S, Kavanagh K, Powell FC. Mite-related
bacterial antigens stimulate inflammatory cells in rosacea. Br J
Dermatol 2007;157:474-81.
37. Akilov OE, Mumcuoglu KY. Immune response in demodicosis.
J Eur Acad Dermatol Venereol 2004;18:440-4.
38. Forstinger C, Kittler H, Binder M. Treatment of rosacea-like
demodicidosis with oral ivermectin and topical permethrin
cream. J Am Acad Dermatol 1999;41:775-7.
39. Shelley WB, Shelley ED, Burmeister V. Unilateral demodectic
rosacea. J Am Acad Dermatol 1989;20:915-7.
40. Forton F, Seys B, Marchal JL, Song AM. Demodex folliculorum
and topical treatment: acaricidal action evaluated by standardized skin surface biopsy. Br J Dermatol 1998;138:461-6.
41. Persi A, Rebora A. Metronidazole and Demodex folliculorum.
Acta Derm Venereol 1981;61:182-3.
42. Lubbe J, Stucky L, Saurat JH. Rosaceiform dermatitis with
follicular Demodex after treatment of facial atopic dermatitis
with 1% pimecrolimus cream. Dermatology 2003;207:204-5.
43. Antille C, Saurat JH, Lubbe J. Induction of rosaceiform
dermatitis during treatment of facial inflammatory dermatoses
with tacrolimus ointment. Arch Dermatol 2004;140:457-60.

Vous aimerez peut-être aussi