Defi nition and nomenclature

Tinea corporis is ringworm of the glabrous skin. The clinical manifestations

result from invasion and proliferation of the causal fungi
in the stratum corneum. Terminal hair in the affected parts may be
invaded. By defi nition, it includes lesions of the trunk and limbs,
excluding ringworm of specialized sites such as the scalp, feet and
groins, which are considered later.
Synonyms and inclusions
• Ringworm of the body
• Tinea circinata
Pathophysiology
Natural infection is acquired by the deposition of viable arthrospores
or hyphae on the surface of the susceptible individual. The source
of infection is usually an active lesion on an animal or on another
human, although fomite transmission is known to occur, and infection
from soil is a well‐established if unusual occurrence. In young
children infected with Trichophyton rubrum and Epidermophyton
fl occosum , half of the infections may come from their parents. In
geriatric wards, epidemics may occur [ 1 ]. Spread from existing
localized infection (e.g. feet, groins, scalp and nails) is not uncommon.
Invasion of the skin at the site of infection is followed by
centrifugal spread through the horny layer of the epidermis. After
this period of establishment (incubation), which lasts 1–3 weeks,
the tissue responses to infection become evident. The characteristic
annular appearance of many ringworm infections results from
the elimination of the fungus from the centre of the lesion, and the
subsequent resolution of the infl ammatory host response at that
site. This area usually becomes resistant to reinfection, although a
second wave of centrifugal spread from the original site may occur
with the formation of concentric erythematous infl ammatory rings.
However, many lesions lack any tendency to central clearing. The
natural history is variable. Some infl ammatory cases of animal

infection resolve spontaneously in a few months, while a typical

case of T. rubrum tinea corporis may persist for years.

Causative organisms
For any part of the world, the causes of tinea corporis can be
assessed by reference to the prevailing dermatophyte fl ora in the
region [ 1–3 ]. All known dermatophytes can produce lesions of the
glabrous skin. A comprehensive list of causal species thus corresponds
to a complete list of dermatophytes. The most common are
T. rubrum and zoophilic dermatophytes such as Microsporum canis .
Some species have predilections for particular parts of the body;
for example, M. audouinii , classically a cause of tinea capitis, and
T. rubrum , which most commonly causes tinea pedis, can and on
many occasions do cause tinea corporis [ 4,5 ].
Environmental factors
Tinea corporis can occur in any climate although it is commoner
in the tropics.
Clinical features
Presentation
The site of infection is typically on exposed skin, unless the infection
represents an extension from a pre‐existing infection. In such
cases, infection may spread from the scalp, down the neck on to the
upper trunk, or from the groins on to the buttocks and lower trunk.
Characteristic lesions are circular, usually sharply marginated
with a raised edge (Figure 32.21 ). Single lesions occur, or there may
be multiple plaques. The latter may remain discrete or become confl
uent. This clinical pattern is often modifi ed in patients with defects
in cellular immune responses [ 6 ]. The degree of infl ammation is
very variable. This feature depends not only on the species of the
fungus and the immune status of the host, but it is also roughly
proportional to the extent of follicular invasion; thus, tinea corporis
is generally less infl ammatory than tinea capitis or tinea barbae. In
infl ammatory lesions, pustules or vesicles may dominate and even
in mild infections close observation may reveal one or two small
pustules. Rarely, frank bullae have been reported as an extreme
expression of infl ammatory change. In less infl ammatory infections,

scaling is a common but not constant fi nding. Central resolution,

which is a common but not invariable feature of tinea corporis,
is perhaps more frequent in infl ammatory lesions, but it is by no
means confi ned to them. The process is often incomplete, and the
central skin may show postinfl ammatory pigmentation, a change of
texture or residual erythematous dermal nodules.
Clinical variants
Lesions of the glabrous skin caused by M. canis are not rare. They are
as common in adults as in children, and are characteristically annular.
M. audouinii or T. tonsurans produce short‐lived lesions of tinea
corporis in some cases of scalp infection [ 7 ]. T. verrucosum from cattle,
T. erinacei from hedgehogs, T. mentagrophytes from small rodents in
general, and M. persicolor from voles, are all likely to cause infl ammatory
lesions of exposed skin. Although classically a cause of kerion, T.
verrucosum can lead to extensive annular lesions of the upper trunk,
especially in children [ 8 ]. These often start around the neck.
The ubiquitous anthropophilic species T. rubrum may invade
the buttocks and lower back, as well as more distant sites of the
trunk as an extension from tinea cruris. Similar patterns are seen
occasionally with E. fl occosum and T. megninii (now recognized as
a member of the T. rubrum complex). In infants, ringworm is rare,
but the moist conditions of the perineal area may predispose to E.
fl occosum or T. rubrum infections [ 1 ].
Tinea corporis resulting from T. rubrum is often particularly
extensive, and the infl ammatory margin diffi cult to distinguish
[ 9 ]. T. rubrum may cause typical lesions with raised margins on
the legs and usually extending from the feet, but rather psoriasiform
lichenifi ed plaques without central clearing may also occur,
and a variety of vasculitis‐like lesions are recognized. The perifollicular
granulomatous papules are classic (Figure 32.22 ),

but erythema induratum‐like plaques sometimes occur with an

almost haemorrhagic appearance.
Tinea imbricata (Tokelau) resulting from T. concentricum , an
anthropophilic dermatophyte found in southern Asia, the islands
of the South Pacifi c and in Guatemala, southern Mexico and Brazil,
causes a distinctive infection [ 12 ]. It seems to affect mainly the
native peoples of these areas, and although susceptibility may be
inherited as an autosomal recessive character [ 13 ], it occurs in both
sexes and at all ages. Occasional cases may be seen elsewhere in
travellers from these regions [ 14 ]. The infection begins as a scaling
ring; centrifugal spread follows, but within the area of central
clearing a second wave of scaling soon arises. The process is
repeated to give numerous concentric rings (Figure 32.23 ) and, as
the natural history is normally prolonged, the whole body may
become affected. Pruritus is intense and may lead to lichenifi cation.
Hypopigmentation may accompany the lesions [ 15 ].
Atypical deep forms of tinea corporis occur. There are some reports
of extensive and persistent cases of tinea corporis, in which dermal
or subcutaneous involvement has been a feature [ 16,17 ]. Occasionally,
a specifi c defect of immune function has been detected, such
as a missing plasma factor. In other patients, depression of cellular
immune responses is associated with the presence of a serum factor,
possibly circulating antigen or immune complexes [ 6,18 ]. Such cases
may present with dermal nodules, abscesses or draining sinuses
[ 19 ]. A few particularly unusual dermatophyte infections with invasion
of bone, central nervous system and lymph nodes have been
reported [ 16,20 ]; some are associated with CARD9 mutations.
Differential diagnosis
Although tinea corporis can masquerade as any of a vast
number of skin diseases, in practice the diagnosis is usually

straightforward. The characteristic lesions seen with infection

resulting from M. canis are easily diagnosed, but atypical infections
caused by dermatophytes can, on occasion, cause great
diffi culty. Indeed, the possibility that any red, scaly rash on the
body is a fungus infection should be considered, because lesions
produced by fungi are so variable. Seborrhoeic dermatitis often
causes diffi culty, but the condition is symmetrical and there is
often associated seborrhoeic dermatitis of the scalp and perhaps
intertrigo in the body folds. Psoriasis can lead to confusion in
those cases in which the distribution is not quite typical. Its presence
on the knees, elbows and scalp, and associated psoriasis of
the nails, particularly if pitting is present, is helpful. Patches of
impetigo are often confused, particularly when dermatophytosis
is of the circinate type. Growth of staphylococci from a skin
swab does not, of course, exclude tinea. Lichenifi cation of a patch
of tinea (e.g. of the leg) can mimic lichen simplex. Nummular
eczema is a common source of error. The plaques of papulovesicles
tend to occur symmetrically on the limbs. Pityriasis rosea
is also symmetrical and characteristically confi ned to the trunk
and proximal parts of the limbs, but the herald patch, if seen, is
almost impossible to differentiate from ringworm without microscopic
examination of scales. Candidosis, tertiary syphilis and
pityriasis versicolor should be excluded.
Disease course and prognosis
Spontaneous resolution can occur but is uncommon.
Management
Localized tinea corporis, especially of recent origin, commonly
responds to topical therapy applied twice daily, usually for
about a month. Topical terbinafi ne often works in a shorter
time period (e.g. 2 weeks). In more widespread infections of
recent onset, oral terbinafi ne or itraconazole will generally be
preferred, and may be expected to clear the condition in about
2–3 weeks, depending on the dosage used. With griseofulvin,
much longer term treatment is needed – up to several months
with extensive infections. With T. concentricum , treatment failures
may occur with griseofulvin. Both terbinafi ne and itraconazole
are effective in tinea imbricata, but the most appropriate
regimen is not clear.