Scarlet fever is a syndrome characterized by exudative pharyngitis, fever, and

scarlatiniform rash. It is most commonly caused by pyrogenic exotoxinproducing

group A Streptococcus, although staphylococcal infections can produce a
similar-appearing disease. The exact mechanism by which toxins produce the
symptomology is unclear. Compelling studies by Schlievert that the scarlatiniform
eruption could only be induced in mice that were previously sensitized against toxins,
suggests that a combination of a conventional delayed type and
superantigen-mediated processes are occurring.21 It should be noted that
streptococcal toxins, especially SPEA has areas of significant homology with collagen,
which could provide a mechanism for rare autoimmune sequelae of streptococcal
scarlet fever, including renal failure and rheumatic fever.22,23 It should be noted that
scarlet fever is no longer the major public health threat it was in the past; not only
because of antibiotic treatment but that most streptococcal isolates causing scarlet
fever express the less virulent SPEB and SPEC rather than SPEA.

STREPTOCOCCAL SCARLET FEVER

Streptococcal scarlet fever is a childhood disease, and is most common in winter and
early spring. It is estimated that up to 10% of childhood group A streptococcal
pharyngitis patients develop scarlet fever. Approximately 12 hours to 5 days after
exposure, an abrupt prodrome consisting of pharyngitis, headache, vomiting,
abdominal pain, and fever develops. The rash appears 1 to 2 days after onset of the
illness, first on the neck and then extending to the trunk and extremities, although
sparing the palms and soles. The exanthem texture is usually coarse like fine-grade
sandpaper, and the erythema blanches with pressure. The skin can be mildly pruritic,
but usually is not painful. A few days following generalization of the exanthem, it
becomes more intense around skinfolds and lines of confluent petechiae resulting
from increased capillary fragility (the Pastia sign) can be seen. The generalized
exanthem begins to fade 3 to 4 days after onset and a desquamative phase begins,
usually starting with the face. Peeling from the palms and fingers and sometimes soles
occurs approximately a week later and can last for as long as 1 month.

Oral findings of streptococcal scarlet fever include edematous, erythematous tonsils

sometimes covered with a yellow, gray, or white exudate and tender anterior cervical
lymphadenopathy is common. Petechiae and punctuate red macules are seen on the
soft palate and uvula (Forchheimer spots). A flushed face with circumoral pallor is
also commonly noted. The tongue in scarlet fever has characteristic changes. During
the first 2 days of the disease, the tongue has a white coat through which the red and
edematous papillae project (white strawberry tongue). After 2 days, the tongue
desquamates resulting in a red tongue with prominent papillae (red strawberry
tongue).

The diagnosis of scarlet fever is made by the characteristic clinical signs and
confirmed by rapid streptococcal test or throat culture. Scarlet fever usually follows a
benign course and any undue morbidity/mortality is likely to be from suppurative
complications, including peritonsillar abscess, sinusitis, pneumonia, and meningitis,
or from nonsuppurative complications associated with immune-related rheumatic
fever or glomerulonephritis. The risk of acute rheumatic fever following an untreated
group A streptococcal infection is estimated to be approximately 3% in epidemics,
and 0.3% in endemic scenarios. The risk of glomerulonephritis can be up to 15% after
infection with nephritogenic group A streptococcal strain. In addition to pharyngitis,
group A Streptococcus can cause scarlet fever–like eruptions from skin (often surgical
wounds) or uterine infections.

Treatment of scarlet fever is by antibiotics (penicillin or erythromycin for a 10-day

course) and supportive care. Fever usually abates within 12 to 24 hours after initiation
of antibiotic therapy. Recurrences are common.

STAPHYLOCOCCAL SCARLET FEVER

Staphylococcal scarlet fever, also known as scarlatiniform erythroderma/rash, was

first described in 1927 and until recently was considered to be a milder or abortive
form of SSSS.21 Patients usually develop a generalized erythroderma with a
roughened, sandpaper-like texture. The exanthem of staphylococcal scarlet fever
tends to be more tender than corresponding streptococcal scarlet fever. Systemic signs,
including malaise and fever, are invariably present. Within a few days of initiation of
rash, thick flakes develop and the entire skin desquamates over the next week. Unlike
generalized SSSS, the scarlatiniform eruption is not associated with the formation of
bullae or superficial exfoliation and can be very difficult to differentiate from other
infectious erythrodermal causes, such as TSS and streptococcal scarlet fever. Scarlet
fever induced by staphylococci differs from streptococcalmediated disease by the lack
of pharyngitis. A study by Wang and colleagues examined the clinical characteristics
and toxin(s) detected from 20 children with staphylococcal scarlet fever.23 They
found that all of the patient’s staphylococcal infections arose from the skin; 16 of 20
cases from furuncles/carbuncles; 2 each from abscesses or wound infections. All of
the S. aureusstrains expressed SEB. Of note, SEB shows significant protein sequence
homology with SPEA, a known exotoxin associated with streptococcal scarlet fever.
Yet other studies have implicated other staphylococcal enterotoxins.24 One
explanation for this heterogeneity of toxins associated with this disorder is that the
diagnosis is made upon clinical grounds. It is possible that staphylococcal scarlet
fever represents an incomplete form of TSS, in which toxins spread from the skin and
thus activating the skin-associated lymphoid tissue rather than mucosal-associated
lymphoid tissue. Because most cases of streptococcal scarlet fever arise from a
pharyngitis, the lack of pharyngitis in a patient with characteristic rash and other
clinical signs of scarlet fever should alert the clinician to look for a localized nidus of
infection (eg, furuncle) that could be cultured to establish the diagnosis.

DIFFERENTIAL DIAGNOSIS

The diagnosis of scarlet fever is made upon clinical grounds with supporting positive
bacterial cultures. The differential diagnosis of scarlet fever would include other
toxin-mediated disorders, including SSSS. Although Kawasaki syndrome has many
similar clinical findings, including mucosal involvement (eg, strawberry tongue), and
swelling of extremities and desquamation of palms and soles during convalescence,
Kawasaki syndrome differs in that the course of fever is prolonged and cultures would
be expected to be negative. Atypical drug hypersensitivity reactions can have some
cutaneous but less likely mucosal features and there is usually a history of an
offending drug and peripheral eosinophilia. Scarlet fever from group A Streptococcus
can usually be differentiated from that induced by S. aureus as the usual nidus of
infection in streptococcal scarlet fever is from a pharyngitis whereas the
staphylococcal variant usually has its infectious nidus in the skin.

TREATMENT AND PROGNOSIS

The treatment of scarlet fever includes antibiotics to eradicate the offending bacteria.
If the localized nidus of infection is an abscess or furuncle/carbuncle, then this should
be drained. Acute rheumatic fever or glomerulonephritis are not associated with
staphylococcal scarlet fever. For situations in which more systemic signs resembling
TSS are becoming apparent, then the treatment could resemble TSS (see above)

Phythriasis Vesicolor

Malassezia species are normal ¢ora of human skin.

Malassezia species can produce a variety of clinical presentations including

pityriasis (tinea) versicolor, Malassezia folliculitis, seborrheic dermatitis, and neonatal
cephalic pustulosis. Rarely, Malassezia species have been implicated in systemic
infections, including catheter-related fungemia.

The diagnosis can be made via potassium hydroxide (KOH) preparation or skin
biopsy. The organism is not typically cultured for this purpose as it requires special
growing conditions (additional lipid).

Malassezia skin infections generally respond readily to topical treatments,

including azole antifungals and selenium sulfide–based preparations. More extensive
cases or those with folliculitis may require systemic antifungals.

Malassezia infections tend to have high recurrence rates and may require
prophylactic treatment to prevent further episodes

Malassezia (formerly known as Pityrosporum) are lipophilic dimorphic fungi that have been
implicated in several skin conditions: pityriasis (tinea) versicolor, and Malassezia folliculitis.
These organisms also have been identified at increased rates in inflammatory conditions including
seborrheic dermatitis and atopic dermatitis, although their role in these conditions is less clear and
thought to be more an exacerbating factor rather than a true infection.28 There are currently 14
species in the genus Malassezia, of which 11 have been detected as commensals on human skin.29
Colonization tends to occur by the age of 3 to 6 months, with earlier colonization in the neonatal
phase associated with length of neonatal intensive care unit stays.30Higher rates of Malassezia
skin infections are seen in tropical climates and at the ages of peak sebum production (adolescence
to young adulthood).31 In pityriasis versicolor and Malassezia folliculitis, Malassezia globosa is
the most commonly isolated species,32,33 with Malassezia restricta and Malassezia sympodialis
also frequently isolated from Malassezia folliculitis.34These fungi also have been found to play a
role in internal infections, with Malassezia (most frequently M. restricta and M. globosa) isolated
from the sinuses of both healthy controls and patients with chronic rhinosinusitis.35 Malassezia
species also are implicated in urinary tract infections, meningitis, pneumonia, and nosocomial
bloodstream infections.36,37Cather-related fungemia has been reported in neonates (most
commonly by Malassezia pachydermatis, particularly preterm infants receiving parenteral lipid
infusions and those with prolonged vascular catheterization.38 Malassezia fungemias also have
been described in a series of immunocompromised older children and adults (with leukemias,
solid tumors, diabetes, and severe combined immunodeficiency) with indwelling catheters, none
of whom were receiving lipid infusions.39

CLINICAL FEATURES

CUTANEOUS FINDINGS
Pityriasis versicolor is a superficial Malassezia infection most commonly seen in adolescents and
young adults. This condition is also known as tinea versicolor, but this nomenclature may be
misleading as other tinea presentations are caused by dermatophytes rather than yeast. This
condition manifests with asymptomatic to mildly pruritic patches and thin plaques with overlying
fine scale favoring the neck, chest and back, upper arms, and, less commonly, the scalp, abdomen,
and groin areas (Fig. 161-11). The name “versicolor” alludes to the spectrum of skin color
changes that may be seen including hypopigmentation and hyperpigmentation, as well as
erythematous to salmon-colored skin lesions (Fig. 161-12).

Malassezia folliculitis presents as follicularly based erythematous monomorphic papules and

pustules on the face, trunk, and upper arms (Fig. 161-13A). In contrast to acne vulgaris,
comedones are a not a feature, and Malassezia folliculitis tends to spare the centrofacial areas.33
The lesions are often, but not always, pruritic. The condition is frequently diagnosed as
misdiagnosed as acne vulgaris, and may even appear concurrently with acne.

ETIOLOGY AND PHATOGENESIS

Malassezia are normal flora of human skin, and rely upon hydrolysis of their human
host sebum triglycerides as they lack a fatty acid synthase to allow endogenous
production of C14-C16 saturated fatty acids.28,40. The free fatty acids thereby
produced are believed to provoke inflammation in the skin of the host, as evidenced
by the presence of a perivascular inflammatory infiltrate on histopathology.31 In
pityriasis versicolor, the organism is able to transition to its pathogenic mycelial form
and invade the stratum corneum. The pigmentary alterations produced in the skin are
believed to be achieved via several mechanisms. The hypopigmentation seen
especially in darker-skinned patients is thought to be a result of the production of
azelaic acid, a dicarboxylic acid that inhibits of tyrosinase (an enzyme that catalyzes a
key step in melanin synthesis) and also may be directly cytotoxic to melanocytes,41
while hyperpigmented lesions have been attributed to increased melanosomes and
thickening of the stratum corneum.42

RISK FACTORS
Tropical climates and heavy sweating are associated with increased rates of both pityriasis
versicolor and Malassezia folliculitis. In addition, immunosuppression, oral antibiotics, and
corticosteroids also are reported risk factors for Malassezia folliculitis.43 There has not been a
consistent gender predilection reported.

Diagnosis

SUPPORTIVE STUDIES
Pityriasis versicolor is often diagnosed visually based on its fairly distinctive morphology.
Dermoscopy has been recommended as an ancillary tool in making the diagnosis of pityriasis
versicolor as it highlights the fine scaling that may not always be readily visible to the naked
eye.44 In both pityriasis versicolor and Malassezia folliculitis, illumination with a Wood lamp
may reveal yellow-green fluorescence

KOH preparation can be a particularly useful in-clinic diagnostic test for pityriasis versicolor or
Malassezia folliculitis and it will reveal short hyphae and yeast forms (the “ziti and meatballs”
sign; Fig. 161-15). Although a superficial scraping of skin scales is adequate in pityriasis
versicolor, the use of a comedone extractor or a needle to puncture an intact pustule is
recommended to obtain a specimen in cases of Malassezia folliculitis where the yeast is
situated deeper within the follicle.34,45 Staining with calcofluor white or May- Grunwald-
Giemsa stain may improve visualization

LABORATORY TESTING
Culture is not generally used to confirm Malasseziainfection because of the organism’s lipid
requirement, which makes culture more logistically challenging—a layer of olive oil must be
added or special growth media such as modified Dixon are required—and this is complicated
further by slightly different growth requirements among different species.31

PATHOLOGY
Histopathology demonstrates Malassezia yeast forms; in pityriasis versicolor, they may be seen
within the stratum corneum, while in Malassezia folliculitis they are found within dilated
infundibula of plugged follicles in association with keratin debris (see Fig. 161-13B).46A
perivascular inflammatory infiltrate of lymphocytes, histiocytes, and neutrophils may be seen,
which is typically mild unless the follicle has ruptured. A periodic acid–Schiff stain will highlight
the organism.

CLINICAL COURSE
AND PROGNOSIS
Superficial Malassezia infections are generally innocuous, and although most will respond readily
to appropriate antifungal therapy, recurrence is common, particularly in those individuals with
strong risk factors. Preterm neonates, immunosuppressed patients, and patients on parenteral lipid
infusions are at higher risk of disseminated infection, as discussed above.
summarizes the management of cutaneous Malassezia infections. For pityriasis versicolor,
first-line treatments are topical and include shampoos (pyrithione zinc or selenium sulfide),
propylene glycol in aqueous solution, and azole antifungal creams (ketoconazole is the most
studied).45 For particularly extensive involvement or disease refractory to topicals, oral antifungal
medications, including fluconazole (300 mg for 2 doses 7 days apart) or itraconazole (200 mg
daily for 7 days), are effective; however, fluconazole may be preferable because of its more
variable bioavailability.45,47 Ketoconazole, once a mainstay of treatment, is no longer
recommended as on May 19, 2016, the U.S. Food and Drug Administration issued a statement
warning against the use of oral ketoconazole for skin and nail fungal infections because of risk of
liver damage and adrenal dysfunction.48 Despite a complete mycologic cure, pigmentary changes
(particularly hypopigmented patches) may take many months to resolve and patients should be
counseled about appropriate expectations.

Given the high propensity for recurrence, prophylactic long-term treatment may be warranted
in some patients; options include either periodic use of topical selenium sulfide shampoo or
ketoconazole 2% shampoo, or itraconazole 200 mg twice daily 1 day per month for 6 months.49

For Malassezia folliculitis, given the presence of the fungus deep within the hair follicle,
monotherapy with topical antifungals is of less reliable efficacy. The addition of a keratolytic such
as propylene glycol may improve the efficacy of topical antifungal treatment.45Ultimately, many
patients may require systemic treatment, with itraconazole being the best-studied treatment (200
mg daily for 1 to 3 weeks)

TINEA KORPORIS

Tinea corporis refers to any dermatophytosis of glabrous skin except palms, soles, and the groin.
EPIDEMIOLOGY
Tinea corporis may be transmitted directly from infected humans or animals, via fomites, or it
may occur via autoinoculation from reservoirs of dermatophyte colonization on the feet.74
Children are more likely to contract zoophilic pathogens, especially M. canis, from dogs or cats.
Occlusive clothing and a humid climate are associated with more frequent and severe
eruptions.75Wearing of occlusive clothing, frequent skin-to-skin contact, and minor traumas, such
as the mat burns in competitive wrestling, create an environment in which dermatophytes flourish.
“Tinea corporis gladiatorum” is caused most commonly by T. tonsurans, and it occurs most
frequently on the head, neck, and arms.

CLINICAL FINDINGS
Table 160-12 summarizes the subtypes and most common causes of tinea corporis.

The classic presentation is that of an annular (“ringworm”-like; Fig. 160-9A) or serpiginous

plaque with scale across the entire active erythematous border. The border, which may be
vesicular, advances centrifugally. The center of the plaque is usually scaly but may exhibit
complete clearance. Whereas concentric vesicular rings suggest tinea incognito (often caused by T.
rubrum), the erythematous concentric rings of tinea imbricata demonstrate little to no vesiculation.
T. rubrum infections may also present as large, confluent, polycyclic (Fig. 160-9B) or
psoriasiform (Fig. 160-9C) plaques, especially in immunosuppressed individuals.

Majocchi granuloma is a superficial and subcutaneous dermatophytic infection involving deeper

portions of the hair follicles, presenting as scaly, follicular papules and nodules that coalesce in an
annular arrangement (Fig. 160-10). It is most commonly caused by T. rubrum, T. interdigitale, and
M. canis. Majocchi granuloma is observed on the legs of women who become inoculated after
shaving or who apply topical corticosteroids to the involved area, thereby facilitating infection. It
also has been increasingly observed among immunocompromised patients.

ETIOLOGY AND PATHOGENESIS

Although any dermatophyte can cause tinea corporis, it is caused most commonly caused by T.
rubrum, which is also the most likely candidate in cases withconcomitant follicular
involvement.69 E. floccosum, T. interdigitale (anthropophilic and zoophilic strains), M. canis, and
T. tonsurans are also common pathogens.1Tinea imbricata, caused by T. concentricum, is limited
geographically to areas of the Far East, South Pacific, and South and Central America.

DIAGNOSIS
Table 160-4 outlines common laboratory dermatophyte identification methods and Table 160-6
outlines the colony and microscopic morphology features of the most common dermatophytes.

DIFFERENTIAL DIAGNOSIS
Table 160-17 summarizes the differential diagnosis of tinea corporis.

MANAGEMENT
Table 160-9 outlines the treatment of tinea corporis, Table 160-10 lists oral antifungal agents, and
Table 160-11 lists topical antifungal agents.

For isolated plaques on the glabrous skin, topical allylamines (eg, terbinafine), imidazoles (eg,
clotrimazole)tolnaftate, butenafine, and ciclopirox are effective. Most are applied twice daily for 2
to 4 weeks. Oral antifungal agents are reserved for widespread or more inflammatory eruptions.

TINEA KRURIS

Tinea cruris is a dermatophytosis of the groin, genitalia, pubic area, and perineal and perianal skin.
The designation is a misnomer, because in Latin, “cruris” means “of the leg.” It is the second-most
common type of dermatophytosis worldwide.

EPIDEMIOLOGY
Much like tinea corporis, tinea cruris spreads via direct contact or fomites, and is exacerbated by
occlusion and humidity. Autoinfection from distant reservoirs of T. rubrum or T. interdigitale on
the feet, for example, is common.74 Tinea cruris is 3 times more common in men, and adults are
affected more often than children.

CLINICAL FINDINGS
Tinea cruris presents classically as a well-marginated annular plaque with a scaly raised border
that extends from the inguinal fold to the inner thigh, often bilaterally. Presentation with
erythematous, scaly patches with papules and vesicles involving the inner thighs is also common
but perhaps less obvious. Pruritus is common, as is pain when plaques are macerated or
secondarily infected. Plaques in tinea cruris caused by E. floccosum are more likely to
demonstrate central clearing with involvement of the genitocrural crease and medial upper thigh.
In contrast, plaques in tinea cruris caused by T. rubrum coalesce with extension to the pubic,
perianal, buttock, and lower abdominal areas (Fig. 160-11). Genitalia (including the scrotum) are
infrequently affected and may be useful to distinguish from other conditions such as inverse
psoriasis.

ETIOLOGY AND PATHOGENESIS

Most tinea cruris is caused by T. rubrum and E. floccosum, the latter being most often responsible
for epidemics.63T. interdigitale and T. verrucosum are implicated less often.

DIAGNOSIS
Table 160-4 outlines common laboratory dermatophyte identification methods and Table 160-6
outlines the colony and microscopic morphology features of the most common dermatophytes.

DIFFERENTIAL DIAGNOSIS
Table 160-18 summarizes the differential diagnosis of tine cruris.

MANAGEMENT
Medical treatment of tinea cruris is the same as that for tinea corporis, which is discussed
earlier.In addition to medical treatment, it also may be helpful to correct any underlying moisture
issues in the affected area (with use of loose-fitted clothing and regular application of
barrier-protective zinc-containing cream) or other areas of infection (eg, tinea pedis). If tinea pedis
is present, in addition to medical treatment targeting the feet, one might also recommend the
patient apply socks before underwear so as to prevent autoinoculation of the area