Clinics in Dermatology (2015) 33, 420–428

Bacterial infections of the folds

(intertriginous areas)
Yalçın Tüzün, MD a,⁎, Ronni Wolf, MD b , Burhan Engin, MD a ,
Ayşegül Sevim Keçici, MD a , Zekayi Kutlubay, MD a
a
Department of Dermatology, Cerrahpaşa Medical Faculty, Istanbul University, 34098, Fatih, Istanbul, Turkey
b
Dermatology Unit, Kaplan Medical Center, Rehovot, Israel affiliated with the School of Medicine, Hebrew University and
Hadassah Medical Center, Jerusalem, Israel

Abstract The axillary, inguinal, post-auricular, and inframammary areas are considered skin folds,
where one skin layer touches another. Skin fold areas have a high moisture level and elevated
temperature, both of which increase the possibility of microorganism overgrowth. A massive amount of
bacteria live on the surface of the skin. Some are purely commensal; thus, only their overgrowth can
cause infections, most of which are minor. In some cases, colonization of pathogenic bacteria causes
more serious infections. This contribution reviews the bacterial infections of the skin fold areas.
© 2015 Elsevier Inc. All rights reserved.

Introduction bacteria that are usually regarded as nonpathogenic can

The resident microorganisms of the surface of the skin
and hair follicles may increase in number and cause minor
infections; nevertheless, pathogenic bacteria that are not
normally found on the surface of epidermis can potentially
cause serious infections.1 On some occasions, bacteria
colonize on the surface of the skin in large amounts and
over long periods of time. These bacteria are called
temporary residents of the skin surface. As an example of
this condition, skin of the facial area may be contaminated
through the nostrils or mouth by Staphylococcus aureus or
β-hemolytic streptococci, even though these organisms are
not members of normal resident flora.2 Similarly, if the skin
is damaged or an immunosuppressive condition exists,
⁎ Corresponding author.
E-mail address: yalcintuzun@yahoo.com (Y. Tüzün).
also cause opportunistic infections.
From the viewpoint of host defense mechanisms, the
nature and health of the epithelia, the ability of cells to
replicate, the interactions between normal floral microor-
ganisms and pathogens, and the cellular and humoral
immune factors (eg, diabetes mellitus, HIV infection) are
important in maintaining self-protection against microorgan-
isms. Compared with the normal skin surfaces, skin fold
areas, such as the axillary and inguinal regions, areas behind
the external ear, and inframammary areas have relatively
thinner epithelia. The effects of elevated temperature and
increased moisture can be seen in these areas. Low levels of
oxygen combined with high levels of humidity and
elevated temperatures make these areas more prone to
microorganism overgrowth.
The pH of the skin surface also plays a role in determining
the microbial inhabitants. It is usually acidic and is so named

http://dx.doi.org/10.1016/j.clindermatol.2015.04.003
0738-081X/© 2015 Elsevier Inc. All rights reserved.

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Bacterial infections of the folds (intertriginous areas)
the acid mantle. The pH value varies and is higher in the
intertriginous areas, such as the axillae and groin.3
Normal flora of the skin
Numerous methods can be used to obtain samples from
normal or infected skin. The best quantitative method is to
use an open-ended cylinder and scrub the surface of the skin
with a liquid substance. This method is useful for studying
changes in the number of organisms under different
environmental conditions but is very time consuming.4 The
number of organisms is increased by the duration of rubbing,
pressure exerted, and moistening the swab. Sticky tape
sampling may also provide semi-quantitative data. Material
for a full-thickness skin biopsy would be the best sample for
bacterial quantification, but in practice it is expensive and
invasive. The media used for isolation of the bacteria are also
important. In general, ordinary blood or serum agar for
aerobic organisms and solid Brewer’s thioglycollate medium
without indicator but with 1% Tween-80 for Propionibac-
terium acnes would be the best choice.5 Also there are newer
molecular genetic methods, with extraction of the DNA of
responsible microorganisms combined with processing and
amplification. Broad-range polymerase chain reaction
primers target highly conserved regions of bacteria and
provide amplification of the small subunit ribosomal RNA
gene sequences.6
In the case of normal bacterial flora, some variations exist
within subjects and even within the same subject over time.
Similarly, different anatomic localizations of the skin also
differ in bacterial concentrations. Dry skin leads to a low
level of colonization, whereas moist areas, such as skin folds
and areas with more sebaceous glands, contain large amounts
of bacteria.7
The resident aerobic flora consists of gram-positive cocci
of Staphylococcus species, Micrococcus species, and a
variety of gram-positive rods, the coryneforms or diphthe-
roids. These coryneform organisms are mainly Corynebac-
terium species. The most important gram-negative residents
are Acinetobacter species. Propionibacterium species are
the main anaerobic residents and are mostly found from the
deepest part of the infrainfundibulum up to the entrance of
the acroinfundibulum of the hair follicles.8 Streptococci may
be found as transients on perioral skin or other sites before
the onset of impetigo. Staphylococcus saccharolyticus is an
anaerobic Staphylococcus organism and a member of the
normal flora. Coagulase-positive species S aureus, however,
is not a normal flora member but can frequently be found in
the anterior nares and perineal skin. Healthy axillary skin and
toe clefts in shoe-wearing populations may also contain
coagulase-positive species S aureus.
Environmental factors may also contribute to the
composition of normal flora. Lack of proper hygiene and
bathing do not increase the bacterial count. As the
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421
temperature and humidity increase, the number of microor-
ganisms also increases. The effects of increased hydration
have been studied by covering the skin with plastic film.
Occlusive topical products may be a risk factor for skin
infections.9 The total flora increases greatly; in the early
stages, coagulase-negative staphylococci and micrococci
predominate, but later lipophilic coryneforms increase in
number. Pseudomonas aeruginosa is commonly isolated
from moist areas and in high-humidity atmospheres.10
Certain areas of the skin have specific floras that differ from
those at other sites, quantitatively or qualitatively. The
common organisms of the nasal vestibule are coagulase-
negative staphylococci, micrococci, coryneforms, and Strep-
tococcus pyogenes. The axillary region has a very high level of
bacterial colonization, mostly staphylococci, micrococci, and
coryneforms. Some individuals have a mainly coccal flora,
whereas others mostly have aerobic coryneforms.11 Propio-
nibacterium acnes is usually present and P avidum is often
found as Acinetobacter spp. The fourth toe cleft is often
macerated in individuals who wear shoes for prolonged
periods. In such conditions, large number of bacteria, mainly
general residents of the flora and also Gram-negative
organisms are found. The toe web is also an important area
for Brevibacterium and Acinetobacter species.12 Coagulase-
negative staphylococci, micrococci, and aerobic coryneforms
can be found in the perineum and groin regions.13
Function of the normal flora
The normal flora of the skin has several functions, the
most important of which is to defend against pathogenic
bacteria. Normal flora produce lipases and esterases that
break down triglycerides into free fatty acids, resulting in a
lower skin surface pH; such an acidic environment inhibits
the growth of pathogens.14 Apocrine sweat is sterile and
odorless when secreted. The odor develops due to bacterial
secretions, mainly aerobic corynebacteria. Deodorants are
effective largely through their antibacterial activity.15
Bacterial infections
The ability of bacteria to adhere to the skin surface
depends on many factors. On wet surfaces, the hydropho-
bic nature of bacterial walls promotes sticking of the
bacteria to skin. There is a tendency of the skin to stay
moist and wet in the fold areas. As a result, a greater
number of bacteria can adhere to the skin surface on these
fold areas, and overgrowth of these bacteria can easily
cause infections. In addition, outer surface proteins called
adhesins promote adhesion. 16 An example of bacterial
adhesin is lipoteichoic acid, which is found in both
staphylococci and streptococci.
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Subcutaneous tissue infections: Cellulitis
and erysipelas
Cellulitis is an acute inflammation of subcutaneous tissue,
mostly due to bacterial agents. Erysipelas, on the other hand,
is the bacterial infection of the dermis and upper subcuta-
neous tissue characterized by a well-defined edge due to
more superficial involvement. These two entities cannot be
fully distinguished from each other and may exist in the same
patient at the same time. Although many bacteria are present
in affected tissue, it is almost impossible to isolate them. In a
study of 50 patients, only 26% had positive results after
microbiologic examination.17 Immunofluorescence may also
show streptococcal group antigens in biopsy specimens.18
Cellulitis and erysipelas are predominantly caused by group
A streptococci, whereas rarely groups G, C, and B organisms
can also play a role. In adults, group B streptococci may
cause pelvic erysipelas, especially after surgery.19 In
cellulitis, as opposed to erysipelas, S aureus is occasionally
found.20 Cellulitis of the lower extremities and inguinal
region can be also caused by Aeromonas hydrophila,
especially if there is a history of contaminated water or soil
exposure. Marine organism Vibrio alginolyticus is also
another causative agent.21,22 P aeruginosa may cause
gangrenous cellulitis and ecthyma gangrenosum.
Erythema, swelling, increased heat, and tenderness are the
main clinical characteristics of the inflammation. In
erysipelas, the edge of the lesion is well demarcated and
raised from the surface, whereas in cellulitis it is diffuse.3 In
erysipelas, blistering and hemorrhaging into the blisters can
be seen. In severe cases, bullae and dermal necrosis can
develop and may progress to fasciitis or myositis.23 In the
past, erysipelas was usually limited to the face. Today the
most common site for erysipelas is the leg; when there is a
wound on the leg, an ulcer or interdigital fungal or bacterial
infections can be responsible as a port of entry. There is
slower spread and less edema in the legs, but lymphangitis
and lymphadenopathy are often found.
Recurrent streptococcal cellulitis can be due to lymphatic
damage. It can cause further lymphedema. 24 Venous
insufficiency often causes recurrent erysipelas of the leg.
Both lymphangitis and lymphadenopathy, together with
systemic symptoms such as fever and malaise, are frequent.
Specimens for microbiologic examination for bacteria
should be taken from vesicle fluid or the surface of the ulcer
as well as from blood cultures. If a specimen is to be taken for
skin biopsy, the fascia should not be penetrated. These
specimens still would most likely fail to show the causative
agent. Serologic studies may show evidence of streptococcal
or staphylococcal infection.25
If the case is mild, oral treatment can be sufficient. But if
systemic involvement with fever and septicemia is present,
full-dosage intramuscular or intravenous antibiotics are
necessary.26 Prompt antibiotic therapy is essential and yields
dramatic response. Flucloxacillin with bactericidal effect on
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Y. Tüzün et al.
both streptococci and staphylococci can be given as an oral
monotherapy. In more severe forms, a combination of
flucloxacillin and benzylpenicillin is preferred. Anticoagu-
lant therapy is also given if there is accompanying
thrombophlebitis.27
Furuncle
Furuncles are very common, especially under conditions of
poor hygiene or decreased immune status. A furuncle is an
acute and necrotic infection of hair follicles with S aureus. It is
most common in adolescence and during early adulthood,
especially in men (Figure 1). The surface defense mechanisms
of the skin may be disturbed, leading to the proliferation of
staphylococci. Mechanical damage to the skin, especially in
the fold areas, may cause the lesions to spread upward.
Malnutrition, diabetes mellitus, and immunodeficiency are
possible predisposing factors, although most patients with
furuncles are otherwise healthy. Furuncles can be found on all
hair-bearing body sites. The nuchal area, face, axillary region,
buttocks, arms, and legs are the main sites.
A furuncle is an abscess of a vellus-type hair follicle. The
abscess formation is followed by necrosis and destruction of
the follicle. A small follicular papule first appears in an
inguinal fold area and then becomes pustular and necrotic. It is
left on the site of the lesion after the discharge of a violaceous
macule. The lesions may be single or multiple, and mild
systemic symptoms may accompany them. The buttocks and
the anogenital region can also be affected.28 Staphylococcal
folliculitis, halogen eruptions, and hidradenitis lesions must
also be considered in the differential diagnosis.
Treatment of furuncles is relatively easy, but the major
problem with furuncles is their frequent recurrence.29
Furuncles should be treated systemically with flucloxacillin
or other penicillinase-resistant antibiotics, in combination
with a topical antibacterial agent.30 Nasal and perineal
Fig. 1 A patient with furuncles localized in the axillary region.
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Bacterial infections of the folds (intertriginous areas)
carriage of S aureus should also be eliminated to prevent
recurrence.31
Streptococcal intertrigo
Mechanical intertrigo is colonized mostly by many
organisms, including bacteria and fungi. Hemolytic strepto-
cocci may cause crusting and fissuring in the flexural areas,
especially under moist environment conditions.32 Fissuring
is also characteristically seen during the course of infective
eczematoid dermatitis of the ears. It is important to
distinguish fungal causes of intertriginous eczemas, partic-
ularly where there are satellite papules and pustules. Another
differential diagnosis can be flexural psoriasis that may
involve many scales. Topical antibiotherapy is effective but
recurrences are common.33
Scarlet fever
Scarlet fever is an acute infection caused by pyrogenic
exotoxin producing strains of S pyogenes; otherwise, the
disease is similar to an ordinary streptococcal pharyngitis. It
is most commonly observed during childhood, especially in
winter. After an incubation period of 2 to 5 days, there is an
acute follicular or membranous tonsillitis with painful
lymphadenopathy. The eruption becomes prominent on the
second day. The erythematous lesions typically start from the
antecubital and popliteal fossa, as well as the groin region,
and progress to diffuse involvement of whole body parts.
Transverse red streaks in the skin folds due to capillary
fragility are known as Pastia’s lines. In the severe toxic form
of scarlet fever, the eruption is very intense and may be
purpuric.8
Erythrasma
Erythrasma is a chronic, superficial infection of the skin
caused by aerobic coryneform bacteria, usually known as
Corynebacterium minutissimum. For a long period of time,
erythrasma was thought to be caused by an actinomycete,
namely Nocardia minutissima. It is now very well known
that coryneforms are the responsible agents, based on the
gram-positive rods and filaments found in the scales of
erythrasma lesions.3 The causative agent is C minutissimum
but there seems to be more than one species. These
coryneform bacteria are normally found on skin flora,
especially in larger fold areas such as the axillary region,
inguinal area, and toe clefts. Warmth and humidity are the
ideal predisposing factors. Erythrasma has a special
importance in diabetic patients, as it can be the presenting
sign of diabetes.34
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Erythrasma can occur at any age but is more commonly
observed among the adult population, with incidence
increasing by age. The incidence of erythrasma is higher in
closed populations such as hospitals, mental institutions, or
prisons. The most common form is the one seen in the toe cleft,
whereas infections of the axilla and groin are relatively rare.35
Erythrasma affecting the axillae, inframammary folds, and
large areas of the trunk, as well as the groin area, is more
common in obese, middle-aged African-American women.36
Based on Wood’s light examination technique, the most
common location of erythrasma is the toe clefts; however,
according to clinical findings, the most-affected areas are
mainly fold areas, the groin, axillae, and the intergluteal and
submammary regions (Figure 2).37 In the groin region, both
thighs can be affected, particularly the areas in contact with the
scrotal skin. In rare cases, the glans penis and prepuce skin can
be involved. Typical clinical lesions of erythrasma are irregular
red patches with sharp borders. With time, these lesions
become brownish. New lesions have a smooth texture,
whereas older lesions tend to be hard and scaly. In generalized
erythrasma, these red-brown patches may cover wide surfaces
of the trunk and extremities. As the temperature and humidity
of the air increase, lichenification may be obvious due to
chronic irritation, especially in the groin area. A rare form,
perianal erythrasma, may also cause chronic pruritus ani.38
Toe cleft involvement is usually asymptomatic but there can
also be mild scaling, fissuring, or maceration. In some rare
cases, C minutissimum has been associated with systemic
disease, such as recurrent abscesses or endocarditis.35
A coral-red fluorescent appearance with Wood’s light
examination is due to the presence of coproporphyrin III. This
appearance is typical of erythrasma but it does not necessarily
show active infection. The fluorescence may persist even after
eradication of the bacteria, which can be attributable to the
thickness of the horny layer. In the groin and axillary regions,
acanthosis nigricans may also cause a brilliant pink color, probably
due to heavy colonization with fluorescent coryneforms.39
Fig. 2 Irregular red patches with sharp borders shown on axilla.
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424
Tinea versicolor is the most confusing disease in the
differential diagnosis of erythrasma. It is more commonly
seen on the upper part of the trunk. Tinea cruris also mimics
erythrasma in the inguinal area but appears with satellite
lesions and vesiculation in most cases. In tinea pedis in the
toe clefts, the best way to differentiate erythrasma is by
Wood’s light examination; however, most patients have both
tinea and erythrasma. 40,41 Erythrasma usually persists
without treatment, with recurrent attacks.
Scrapings from lesions show bacteria and fine filaments,
with Gram or Giemsa stain. Culture is usually not necessary
if the clinical appearance is typical and and results of Wood’s
light examination are positive. Tissue culture medium 199
with 20% calf serum and 2% agar is the best medium for
cultivating fluorescent red colonies.8
Erythrasma responds well to most topical treatments with
azole antifungals such as clotrimazole and miconazole.42,43
The duration of the therapy varies depending on the extent of
the lesions and response but in most cases does not exceed 2
weeks.44 In more serious involvements, erythromycin is a
better choice, with topical fusidic acid or oral tetracyclines
alone. A 1-g single dose of clarithromycin can also clear the
infection successfully. Use of long-term antiseptic soaps
with povidone-iodine or drying powders can be used for
recurrence, which can be common in patients with
erythrasma.45,46 Photodynamic therapy using the porphyrin
produced by the causative organisms is also another
treatment option.47
Trichomycosis axillaris
Trichomycosis axillaris is a superficial infection of
axillary and pubic hairs. It is characterized by the formation
of yellow, black, or red granular nodules on the hair shaft.
Although the term trichomycosis is still used for the
nomination of the disease, it is not caused by fungal
microorganisms. Electron microscopic images allow bacte-
rial clusters to be easily distinguished within and between the
cuticular cells and sometimes inside the cortical area.48
Many different species of aerobic corynebacteria may cause
the disease; this reflects the various types of coryneform
bacteria in the normal flora of the axillary region. 49
Pathogenic bacteria produce different types of pigments
and eventually form nodules with multiple colors. Environ-
mental factors have a direct effect on the color diversity of
these nodules. In this context, nodules of different colors
may have been caused by the same strain of bacteria exposed
to different environmental conditions.50
Trichomycosis can be seen in both temperate and tropical
climates. Hyperhidrosis and improper hygiene are two
predisposing factors. There are no sexual or racial differ-
ences; however, the disease seems to be more prevalent
among men in some series, which can be attributable to the
lack of axillary hair in most women.51
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Trichomycosis is usually asymptomatic. The different-
colored nodules are sparsely distributed on the hair shaft,
with a firm or soft texture, sometimes solitary or sometimes
diffusely invading the hair. With diffuse nodular involve-
ment of the hair shaft, the hair may be brittle and easily
broken. The skin of the axillary region is completely normal,
but the sweat may be yellow, black, or red according to the
color of the nodules, which can also stain clothing. The most
common type is yellow, whereas the least common is black.
The characteristic foul acidic smell can be noticed both in the
axillary region and on the clothing.52
Trichomycosis can be mistaken for pediculosis, especially
when it presents in the pubic region. Microscopic confirma-
tion can be helpful in differentiating the two conditions.
Gram-positive bacilli can be seen by potassium hydroxide
preparation. For cultivating the microorganisms, 70%
alcohol is used to sterilize the hair. After this procedure,
blood agar can be used. With ultrastructural studies, a
glucan-like structure is observed, which enables bacteria to
adhere to the hair shafts.53
Treatment of trichomycosis axillaris is fairly easy.
Shaving the affected hairs and the application of antimicro-
bial ointment is usually sufficient. Aluminum chloride is also
helpful for decreasing perspiration and accelerating the
healing process.
Acinetobacter infection
Acinetobacter species are found as members of the
normal skin flora in the axillary and groin regions together
with toe webs in about 20% of otherwise healthy subjects.
These bacteria usually act as opportunistic pathogens and can
cause a wide range of infections, from minor erythema of the
folds to septicemia, meningitis, osteomyelitis, synovitis,
burn sepsis, and wound infections.54
Pseudomonas infections
There are many species of Pseudomonas, most of which
cause various infections throughout the world. P aeruginosa
is the most common species that causes both skin and
visceral infections. P aeruginosa is an aerobic, gram-
negative rod and a transient member of the skin flora mainly
in the anogenital region, axillae, between the toe webs, and
behind the external ear. It increases in number in areas of
burns, ulcers, or other areas of moist skin.55 It is mainly a
nosocomial pathogen and a serious problem in dermatology
practice as ointment containers can also be contaminated
with Pseudomonas. Systemic infections are mostly seen in
immunosuppressed patients. Repeated application of topical
antibiotics against the gram-positive floral members leads to
proliferation of the Pseudomonas group of bacteria.
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Bacterial infections of the folds (intertriginous areas)
Prolonged maceration can also cause Pseudomonas infection
in otherwise healthy individuals. P cepacia leads
to infections in toe webs, especially in the military
population, whose feet are continuously in a moist
environment.56
Tropical immersion foot is a distinct clinical entity,
mostly located on toe webs. The predisposing factor is
usually the inhibition of the gram-positive flora or
dermatophytes by maceration or prolonged antibiotic
usage. There are areas of maceration and erosions, with
sharp margins. These lesions have a green fluorescent
appearance under Wood’s light examination due to
pyocyanin. 3 Blue-green discoloration of underwear offers
a clue to groin infections with these organisms. Also in
cases of Pseudomonas septicemia, skin lesions can
rarely be seen. Formation of bullae may occur particularly
in moist areas, such as the axillae, perineum, and
the buttocks, which can lead to ecthyma gangrenosum
lesions.
Cultures from skin lesions or blood can be helpful in
diagnosing Pseudomonas infection. If the lesions are
superficial, treatment outcome is usually good. Acetic
acid, potassium permanganate wet dressings, silver sulfadi-
azine, or povidone can be helpful.57 In case of severe
infection with systemic involvement, ceftazidime, pipera-
cillin, gentamicin, and amikacin combinations may be
necessary.58
Granuloma inguinale
Granuloma inguinale is a chronic granulomatous infec-
tion of the genitalia and surrounding skin caused by Ca-
lymmatobacterium granulomatis. The disease is especially
common in the tropics and subtropics, mainly in Africa and
South America. Young adults who are sexually active are the
most affected, with more frequent infection in homosexual
men.59 C granulomatis is a small, pleomorphic, gram-
negative bacillary bacteria.
The incubation period for granuloma inguinale can be
between 9 and 50 days. First, there is a firm papulonodular
lesion, which evolves into a sharply defined ulcer. The lesion
can be deep and rapidly extending but is usually painless
without lypmhadenopathies. The ulcer can show a serpigi-
nous pattern in the groin region and other flexures, in
addition to extending into the pubis and perineum. The
lymph nodes in the groin area are enlarged with granuloma-
tous infiltration and later necrosis. The lesions may persist
for years, with remissions and recurrences.60
Smears may be taken for diagnosis in the hope of finding
Donovan bodies. Azithromycin, tetracyclines, erythromycin,
streptomycin, gentamicin, and chloramphenicol are all
effective. Routine treatment is azithromycin 500 mg four
times per day for 10 to 20 days.61
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Lymphogranuloma venereum
Lymphogranuloma venereum is caused by Chlamydia
trachomatis types L1, L2, and L3. The only natural host is
humans. The disease is very common in tropical regions and
is transmitted sexually.62
Lymphogranuloma venereum develops as a small papule
on the genital region after an average incubation period of 10
days. One to 4 weeks after the primary infection, regional
lymph nodes enlarge; this is called “inguinal syndrome.”3
Inguinal adenitis is unilateral in 60% of cases. 63 The
lymphatic glands are hard and rather painful. Later, small
areas of fluctuation and chronic sinuses are formed. The
lymphatic glands divide the inguinal fold region into two
groups; this is called the “groove sign.” Genital lymphedema
may develop weeks or years after the infection and may
cause elephantiasis.64 The disease can resolve completely
within 6 to 8 weeks, even in untreated cases. Rarely,
lymphatic obstruction and possible edema may develop.
Diagnosis can be proven by serologic analysis of anti-
Chlamydia antibody or molecular techniques. Doxycycline
treatment for at least 14 days is very inexpensive and
effective for lymphogranuloma venereum. Azithromycin and
erythromycin are other alternatives.63
Hidradenitis suppurativa
Hidradenitis suppurativa is a chronic inflammatory
disease of apocrine sweat glands that frequently leads to
secondary bacterial infection of fold areas, particularly the
inguinal, anogenital, and axillary regions. Mild hidradenitis
suppurativa can also be a painful and distressing condition
during attacks, but moderate to severe cases alter the
patient’s lifestyle, with physical and psychological distur-
bance. Although the pathogenesis of hidradenitis suppurativa
remains unclear, cytokine tumor necrosis factor alpha is
thought to be a key mediator of inflammation in active
disease. Inflammatory changes at the beginning of the
process are sometimes attributable to pyogenic bacterial
infection. These bacterial infections can also have a role in
disease progression in addition to scar formation.65 Bacterial
infection exists during almost all stages of the disease, but
sinus formation especially is closely related to the presence
of bacteria;66 however, microbiologic cultures are not always
positive. In most patients, though transient, partial or
complete response to antibiotic treatments is another proof
of bacterial involvement in the disease process.67 Purulent
disease and abscesses can be observed due to S aureus and
anaerobic streptococci. Microaerophilic streptococci and
Bacteroides species are also isolated from the lesions of
hidradenitis.68 Apocrine glands extend below the dermis and
reach subcutaneous tissue; thus, the bacterial infection also
breaks through the gland. Fully developed disease consists of
induration, obliteration of appendages, tissue distortion, and
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426
formation of epithelialized sinuses. Apart from bacteria,
hormonal factors also play major role.69,70 A genetic study
also showed an autosomal dominant inheritance pattern.71
In the early stages of the disease, there seem to be keratin
plugs in the apocrine gland follicles. Inflammatory changes
with many leukocytes may accompany the infection inside
and around the apocrine glands. Coccus bacteria are also
observed within the glands and in the dermis. When the
disease progresses to the suppurative phase, subcutaneous
tissues are also affected, with involvement of chronic
inflammatory cells, histiocytes, and keratinous debris.72
Hidradenitis suppurativa usually occurs in otherwise
healthy adolescents and adults. It rarely may begin before
puberty. The onset of hidradenitis suppurativa ranges from
11 to 50 years. The disease affects approximately 1% of the
general population72; African Americans have a slightly
increased incidence, possibly due to relatively greater
density of the apocrine glands72; Hidradenitis suppurativa
occurs primarily in skin containing apocrine glands. The
axillae and the genital, pubic, inguinal, and perianal areas;
the buttocks; and upper thighs are the main sites of
involvement.73 The breasts, the neck, the posterior aspect
of the ears and the adjacent scalp, and the back are also
affected. Different places may be affected with various stages
of the disease at the same time. Comedones and pustules may
accompany the firm and subcutaneous nodules, which may
be painful and tender for a long time. Multiple open
comedones and so-called bridged comedones are the
hallmark findings of hidradenitis suppurativa; and they
frequently progress to multiple abscesses and sinus tract
formations. Indurated plaques are signs of extension of
inflammation to the subcutaneous tissue. These firm nodules
soften over time and coalesce to form chronic sinuses with
serous discharge and eventually rupture to yield exudate,
blood, and pus. The disease has a typical course with
remissions and relapses. If there is marked purulation due to
bacteria, systemic symptoms such as fever can also be
seen.74,75
Hidradenitis suppurativa has many complications, such as
formation of fistulas to the urethra, bladder, and rectum;
secondary anemia; hypoproteinemia; and amyloidosis due to
chronic inflammation. Squamous cell carcinoma is also a
rare complication at the site of chronic involvement.74
Differential diagnosis of the disease includes scroful-
oderma, actinomycosis, granuloma inguinale, or lympho-
granuloma venereum. Crohn’s disease can also show similar
clinical findings.
Hidradenitis suppurativa has a major negative impact on
one’s quality of life, but unfortunately the treatment options are
not satisfying. As bacterial infections are major causative and
exacerbating factors, use of antiseptic agents can be helpful.
Acute episodes can benefit from systemic and local anti-
biotherapies. A combination of erythromycin and metronida-
zole is a good first choice in most patients. Clindamycin and
minocycline can also be tried.76,77 The lesions in most patients
improve with these treatments, but the potential relapse rate
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Y. Tüzün et al.
does not change with these treatments. Long-term use of
tetracyclines is another approach. Acute exacerbations may
also be controlled with systemic corticosteroids with a dose of
60 mg of prednisolone.78 Retinoids, such as isotretinoin,
etretinate, or acitretin, are also successful agents for second-line
therapy choices. New biologic agents, such as infliximab,
etanercept, and adalimumab, also may be useful. In refractory
cases, surgery is an option.79
Miscellaneous infections
Vincent’s organisms, Pseudomonas aeruginosa, and a
wide variety of gram-negative organisms are commonly
found in the groin region. Intertrigo of the crural region
caused by Pseudomonas species may be called the “blue
underpants sign.”80 Regardless of its low prevalence,
gangrenous ecthyma of infants may affect the inguinocrural
area, usually following operations for inguinal hernia.81
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