Pityriasis

Pityriasis (Tinea) Versicolor

• A mild chronic infection of the skin caused by Malassezia yeasts, and characterized by discrete or confluent, scaly, discolored or hypopigmented areas mainly on the upper trunk. 
• Caused by a lipophilic yeast species, Malassezia furfur, belonging to the genus Malassezia. 

Risk factors for the development of P. versicolor 

• Hot, humid climate : The disease is more common in summers and in tropical countries.
• Malnutrition states and in diseases like Cushing’s syndrome or in patients taking corticosteroids.
• Pregnancy
• Genetic predisposition

Pityriasis versicolor

Diagnosis of fungal infections 

• Clinical features
• KOH examination

Fungal hyphae in dermatophytes

“Spaghetti & meat ball” appearance in P.versicolor.

• Fungal culture- SDA

Management of Pityriasis

May be treated with many therapeutic agents, but these regimens should be continued for several weeks to ensure cure. 

• Topical: 

Selenium sulfide suspension.

Ketoconazole 2 % shampoo, for bath twice weekly.

Zinc pyrithione containing shampoos are also effective.

Topical antifungal and keratolytic creams/ointments.

• Systemic: may be used in severe infections.

Oral Ketoconazole, 200 mg daily for 5 to 10 days OR 400 mg monthly for 4 to 15 months has a 90-95 % cure rate.

Oral Itraconazole, 200 mg daily for 5 to 7 days.

Oral Fluconazole, single dose of 400 mg may be used.

• Preventive measures like keeping the skin dry and maintenance of hygiene aids in preventing recurrences. 

Pityriasis Rosea

Pityriasis denotes fine scales, and rosea is colored or pink.

• Pityriasis rosea (PR) is a common benign papulosquamous disease that was originally described by Camille Melchior Gibert in 1860. 

• PR can have a number of clinical variations. 

• Its diagnosis is important because it may resemble secondary syphilis.

Pathophysiology

• PR has often been considered to be a viral exanthem. 

• Its clinical presentation supports this concept. 

• PR has been linked to upper respiratory infections, it can cluster within families and close contacts, and it has an increased incidence in individuals who are immunocompromised. 

• As with viral exanthems, the incidence may increase in the fall and the spring. 

• A single outbreak tends to elicit lifelong immunity.

• Immunologic data suggest a viral etiology. Increased amounts of CD4 T cells and Langhans cells are present in the dermis; this observation may indicate viral antigen processing and presentation. 

• Also, anti-immunoglobulin M (IgM) to keratinocytes has been found in patients with PR; this finding may be associated with the exanthem phase of the presumed viral infection.

• Despite these tendencies, no single virus has been proven to cause the disease. 

• A number of viruses have been studied for a link to PR. 

• Serology and polymerase chain reaction for viral DNA has been negative for Epstein-Barr virus, parvovirus B19, and cytomegalovirus in patients diagnosed with PR.

• Human herpesvirus (HHV)–7 viral is demonstrated DNA in both the lesions and the plasma in patients with PR. 

• In addition, a separate study found HHV-7 DNA in lymphocytes.

• Polymerase chain reaction has shown both HHV-7 and HHV-6 DNA in a variety of tissues and secretions from patients with PR. 

• In the same study, in situ hybridization of lesional lymphocytes showed both HHV-7 and HHV-6 mRNA. 

• However, herpesvirus like particles were not seen via electron microscopy. Follow-up studies have not confirmed a herpes etiology, and because HHV-7 is frequently found in healthy individuals, its etiologic role is controversial

Causes

• PR may represent a viral exanthem (and at times enanthem).

• PR-like drug eruptions may be difficult to distinguish from non–drug-induced cases. Medication-induced eruptions have been reported with captopril, metronidazole, isotretinoin, penicillamine, levamisole, bismuth, gold, barbiturates, ketotifen, clonidine, aspirin, and omeprazole.
• Certain vaccinations, such as the BCG vaccine or the diphtheria vaccine, have been reported to cause similar eruptions. 

• Lesions are also thought to be increased in individuals with high stress levels.

Frequency

International

Worldwide, PR has been estimated to account for 2% of dermatologic outpatient visits. 

The disease is more common in the spring and the fall in temperate climate zones. 

However, it may be more frequent in the summer in some other regions, and it favors the hot, dry season in Australia, India, and Malaysia.

Mortality/Morbidity

PR is a benign self-limited disease associated with mild morbidity with rash and occasional pruritus.

Race

No racial predominance is reported. 

More intensely pigmented Africans tend to have more widespread disease. 

The lesions in African Americans may lack a rose color, and they may appear darker than the surrounding skin.

Sex

PR is more common in women than in men. 

Age

PR commonly develops in children and young adults, although any age group can be affected. 

Most patients are aged 10-35 years.

History

• The history should include questions about close contacts with similar eruptions. 
• This finding is uncommon because most cases of PR are sporadic, as PR is thought to reflect a weakly contagious disease. 
• A history of medication intake should be obtained because several medications have been shown to cause a similar exanthem.

• The disease typically begins with a solitary macule that heralds the eruption (called the herald spot/patch), which is usually a salmon-colored macule. 

• This initial lesion enlarges over a few days to become a patch with a  collarette of fine scale just inside the well-demarcated border. 

• Within the next 1-2 weeks, a generalized exanthem usually appears, although it may occur from hours to months after the herald patch.

•  This secondary phase consists of bilateral and symmetric macules with a  collarette of scale oriented with their long axes along cleavage lines. 

• This phase tends to resolve over the next 6 weeks, but variability is common. 

• Pruritus is common, usually of mild-to-moderate severity, and it occurs in 75% of patients

Physical examination

• The herald patch is usually a single pink patch, 2-10 cm in diameter, on the neck or the trunk with a fine collarette scale . It is observed in more than 50% of patients, and it may occur as multiple lesions or in atypical locations. 
• About 1-2 weeks after the herald patch is seen, the generalized eruption appears, although it has been known to occur from hours to 3 months later. It consists of salmon-colored macules or patches, 0.5-1.5 cm in diameter, with a collarette scale, often described as having a cigarette paper–like appearance. The long axes of the lesions are oriented in a parallel fashion along cleavage lines, giving the classic Christmas tree pattern . These secondary lesions most commonly occur on the trunk, the abdomen, the back, and the proximal upper extremities. 
• Pruritus occurs in 75% of patients and is severe in 25%. 
• Lymphadenopathy is uncommon, but, when present, it is usually observed in African Americans

• Atypical PR occurs in 20% of patients. 

These variations can be separated into changes in the lesions and/or their distribution. 

Photosensitivity may occur. Photoexacerbated and photoprotected forms have been documented, although photosensitivity is not a classic manifestation of the disease. 

Lesions may be localized to single areas, such as the abdomen, the groin, the axilla, the distal extremities, the palms, and the soles.

• An inverse PR may be seen. This form manifests as lesions on the face and the distal extremities, and it is more common in children than in adults. The herald patch may be the only manifestation of the disease. 
• A unilateral variant- lesions do not cross the midline. 
• Drug-induced cases are frequently observed without the herald patch.

• Variations in lesion morphology

Atypical, large patches tend to be fewer in number. They may coalesce to form a variant known as pityriasis circinata et marginata of Vidal. The primary lesions may be papules, vesicles, pustules, or urticarial or purpuric plaques. PR may first be evident with widespread, intensely pruritic papulovesicles in an unusual distribution, such as on the neck and the scalp. 

Papular PR tends to have scaling papules in the normal distribution; this form is more common in children than in adults. 

Erythema multiforme–like plaques may be evident. 

Purpuric PR is seen in both adults and children, and it follows the usual presentation of the disease

• Oral involvement may occur as punctate hemorrhages, ulcers, papulovesicles, bullae, or erythematous plaques. 

Lab Studies

• One must be careful to rule out syphilis. 

A screening rapid plasma reagin (RPR) test or a VDRL test should be ordered for appropriate individuals. 

One should be aware of the prozone phenomenon seen in secondary syphilis and request titration of the RPR test. 

An HIV test should also be considered in these patients.

• Other laboratory tests are usually normal and, therefore, unhelpful. 

• Changes in the white blood cell count and differential, as well as increases in erythrocyte sedimentation rate, total serum protein level, globulin level, and albumin level, are rarely reported

Histologic Findings

• A biopsy specimen is helpful to confirm the diagnosis, especially in atypical cases. 

• It shows superficial perivascular dermatitis . 

• Focal parakeratosis in mounds, hyperplasia, and focal spongiosis are observed in the epidermis. 

• The epidermis may show exocytosis of lymphocytes, variable spongiosis, mild acanthosis, and a thinned granular layer.

• In the dermis, extravasated red blood cells are a helpful finding along with a perivascular infiltrate of lymphocytes, histiocytes, and eosinophils. A number of monocytes are also commonly present. 

• The herald patch has similar features but has a deeper infiltrate and more acanthosis owing to its chronicity. 

• Such variations as dyskeratotic cells in the epidermis, multinuclear giant cells, and focal acantholytic dysfunction have been observed. 

• These features may closely resemble erythema annulare centrifugum, guttate psoriasis, superficial gyrate erythema, and small plaque parapsoriasis.

Medical Care

• The most important part of treating patients with PR is reassurance that the rash will resolve.

• Relief of pruritus is helpful and can be accomplished by using topical steroids, oral antihistamines, topical menthol-phenol lotions, and oatmeal baths. Systemic steroids are not recommended. Although they suppress pruritus, systemic steroids do not shorten the overall disease; in fact, they may prolong or exacerbate the disease. 

• Ultraviolet B (UV-B) light therapy, starting at 80% of the minimum erythrogenic dose, may rapidly relieve pruritus in resistant cases. 

• If itching is not controlled, the dose of UV-B light should be increased by 20% until symptoms decrease. 

• Decreased lesion severity with UV-B light therapy. 

• There is possibility of post inflammatory pigmentation with light therapy. 

• For vesicular PR, 20 mg of dapsone twice a day. 
• High-dose acyclovir (800 mg qid) may help shorten disease, especially if instituted early in the disease course

Further Outpatient Care

• Generally, the disease resolves within 12 weeks. 

• Most cases do not recur, but some patients may develop PR more than once. In cases where the diagnosis is in doubt or if the disease persists past this period, further evaluation is advised. 

• Persistent PR of more than a 3-month duration is classified as pityriasis lichenoides chronica