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The term pityriasis rosea (PR) was first used by Gibert in 1860 and means pink (rosea) scales (pityriasis). Historically, PR has been considered to be caused by an infectious agent, given (1) the resemblance of the rash to known viral exanthems, (2) rare recurrences of PR that suggest lifelong immunity after one episode, (3) occurrence of seasonal variation in some studies, (4) clustering in some communities, and (5) the appearance of flu-like symptoms in a subset of patients. The best scientific evidence suggesting that PR is a viral exanthem associated with reactivation of either HHV-7 or HHV-6 (and sometimes with both viruses) is strong. Despite these findings, there is still controversy over the role of HHV-7 and HHV-6 in the etiology of PR, because a number of studies with “negative” results have failed to support a causative role for HHV-7 and HHV-6 in this disease.
Correct interpretation of the recent viral literature on PR also requires proper understanding of the biology of HHV-7 and HHV-6. It is important to note that the concept that PR represents a reactive viral exanthem containing few infected cells within skin lesions and viral reactivation within circulating blood CD4+ T cells is perfectly analogous to that of the disease roseola, which is well accepted to be caused by primary infection with either HHV-6 or HHV-7 . In classic PR, patients usually describe the onset of a single truncal skin lesion followed several days to weeks later by the onset of numerous smaller lesions on the trunk.
In approximately 20 percent of patients, the clinical picture diverges from the classic one described earlier.
The morphology of the secondary lesions may be atypical, and in these cases, the diagnosis of PR can be more challenging. In rare cases enanthema may occur with hemorrhagic macules and patches, bullae on the tongue and cheeks, or lesions that resemble aphthous ulcers. In cases of classic PR, most patients do not require skin biopsies because the diagnosis is straightforward on clinical grounds and the histologic findings are nonspecific. In older lesions, the perivascular infiltrate is often both superficial and deep, with less spongiosis and more pronounced acanthosis.
Secondary syphilis may present with slightly scaly lesions and can mimic papular PR with no primary plaque. PR is a common acute, self-limited skin eruption that typically begins as a single thin oval scaly plaque on the trunk (“herald patch”) and is typically asymptomatic. Although PR is usually considered to be more common in the spring and fall months in temperate zones, seasonal variation has not been borne out in studies performed in other parts of the world. Numerous studies over the past 50 years have explored various pathogens as possible causes of PR. In fact, the most definitive and compelling study on herpesviruses and PR was by Broccolo and colleagues in 2005. Whereas the studies with positive results have used the most sensitive, specific, and calibrated techniques for virologic studies and reports have been published in high-quality journals, the studies with negative results either used laboratory methods that were not particularly sensitive, calibrated, or quantifiable, or focused on peripheral blood mononuclear cells rather than cell-free plasma or serum. HHV-7 and HHV-6 are closely related ?-herpesviruses, and the clinical diseases and biology associated with this group of herpesviruses are not as well studied as those of the ?-herpesviruses (herpes simplex virus 1 and 2, varicella-zoster virus) and the ?-herpesviruses (Epstein-Barr virus and Kaposi sarcoma-associated herpesvirus).
Pruritus is severe in 25 percent of patients with uncomplicated PR, slight to moderate in 50 percent, and absent in 25 percent. The primary plaque may be missing or present as double or multiple lesions , often close together.

Macules may occur and lack scaling, papules may be follicular, and typical plaques may be absent or resemble psoriasis .
Typical histopathologic features include focal parakeratosis, a reduced or absent granular cell layer, mild acanthosis, mild spongiosis, papillary dermal edema, a perivascular and superficial dermal interstitial infiltrate of lymphocytes and histiocytes, and focal extravasation of erythrocytes . However, leukocytosis, neutrophilia, basophilia, lymphocytosis, and slight increases in erythrocyte sedimentation rate and levels of total protein, ?1- and ?2-globulins, and albumin have been reported. Mucosal lesions and lymphadenopathy may occur in both PR and syphilis, but as with involvement of the palms and soles, these findings are much more common in the latter. The disease duration normally varies between 4 and 10 weeks, with the first few weeks associated with the most new inflammatory skin lesions and the greatest likelihood of flu-like symptoms.
The initial lesion is followed several days to weeks later by the appearance of numerous similar-appearing smaller lesions located along the lines of cleavage of the trunk (a so-called Christmas tree pattern). Complete understanding of the role of HHV-7 and HHV-6 in the pathogenesis of PR is lacking at this time.
In a minority of patients, flu-like symptoms have been reported, including general malaise, headache, nausea, loss of appetite, fever, and arthralgias. The primary plaque may be the sole manifestation of the disease or only one of two lesions . The palms and soles are involved at times, and the clinical picture in these patients may simulate a widespread eczematous eruption.
Lymphadenopathy may occur in patients with PR, especially early in the course of the disease and in association with flu-like symptoms. These include arsenic, barbiturates, bismuth, captopril, clonidine, gold, interferon-?, isotretinoin, ketotifen, labetalol, organic mercurials, methoxypromazine, metronidazole, omeprazole, D-penicillamine, salvarsan, sulfasalazine, terbinafine, and tripelene amine hydrochloride. PR most commonly occurs in teenagers and young adults, and is most likely a viral exanthem associated with reactivation of human herpesvirus 7 (HHV-7) and sometimes HHV-6.
PR most commonly occurs between the ages of 10 and 35 years.8 It is rare in both the very young (defined as less than 2 years) and the elderly (defined as older than 65 years). Beginning with a study by Drago and colleagues in 1997,2 most recent PR etiologic and pathogenetic studies have been focused on two ubiquitous HHVs, HHV-7 and HHV-6.
Taken together, these data strongly suggest that PR is a viral exanthem associated with systemic reactivation of HHV-7 and, to a lesser extent, HHV-6. The primary plaque is usually located on the trunk in areas covered by clothes, but sometimes it is on the neck or proximal extremities. Tinea corporis may resemble PR, especially when PR occurs as only a primary plaque or when it is localized to the groin area. Of note, a more recent addition to this list is imatinib,21 a drug used in the treatment of chronic myeloid leukemia. As with other skin diseases, this occurs more commonly in individuals with darker skin color, with hyperpigmentation predominating.
Recurrences of PR are rare, which suggests lasting immunity after an initial episode of PR.

Critical evaluation of the medical and scientific literature on PR reveals neither credible nor reproducible evidence that PR is associated with any pathogen other than HHV-7 and HHV-6. Patients are viremic, which may explain associated flu-like symptoms in some patients, and they generally do not have infected epithelial cells or large viral loads within skin lesions, which explains the difficulty in detecting these viruses by electron microscopy and by non-nested polymerase chain reaction testing. As well, the characteristic distribution of lesions and differences in lesional and non-lesional skin are unexplained.
Scaling will be at the periphery of the plaques in tinea corporis as opposed to inside the periphery of plaques in PR. Drug-induced PR may be of the classic type, but it often shows atypical features, a protracted course, large lesions, subsequent marked hyperpigmentation, and transformation to lichenoid dermatitis.
Treatment with ultraviolet light phototherapy may also worsen post-inflammatory hyperpigmentation and should be used with caution. Although patients were blinded to the type of treatment they received, the trial was limited in that the investigators were not blinded and the patients were not randomly assigned to one of the two treatment groups. One study suggests that administration of high-dose acyclovir for 1 week hastens recovery from PR. These cells are the likely source of cell-free viral DNA found in plasma or serum samples of patients with PR. The site of the primary lesion does not differ in males and females. months, but the secondary eruption typically occurs within 2 weeks of the appearance of the primary plaque.
Localized forms of disease may involve certain body regions such as the scalp, axillae, vulva, and groin (see eFigs.
They are also the likely source of the scattered perivascular and perifollicular virus-positive cells observed within some lesions of PR.
The lesions of nummular dermatitis are usually round, not oval, and pinpoint papules and vesicles are more prominent than in PR.
Several years ago, erythromycin was reported to be of benefit to patients with PR, but clinical experience and a more recent report showing no efficacy of azithromycin in PR have not confirmed this initial result.23 Some patients with PR may benefit from phototherapy,24 although this should be used with caution given that it can increase the risk of post-inflammatory hyperpigmentation after disease resolution .
The secondary eruption occurs in crops at intervals of a few days and reaches its maximum in approximately 10 days. Guttate psoriasis may cause difficulties in diagnosing PR when only a few lesions are present, when lesions follow lines of cleavage, and when the disease course is chronic. The symmetric eruption is localized mainly to the trunk and adjacent regions of the neck and proximal extremities . The most pronounced lesions extend over the abdomen and anterior surface of the chest as well as over the back . Two main types of secondary lesions occur: (1) small plaques resembling the primary plaque in miniature aligned with their long axes along lines of cleavage and distributed in a Christmas tree pattern, and (2) small, red, usually non-scaly papules that gradually increase in number and spread peripherally.

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