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Association of pandemic H1N1 influenza and pityriasis rosea - a case report.

Byline: Vijay Zawar and Antonio Chuh


Pityriasis rosea (PR) is an inflammatory papulosquamous disease of unknown etiology.

Different viral infections have been implicated as causative agents for PR. We herein report an adult male patient who clinically manifested as pityriasis rosea (PR) during an episode of infection caused by pandemic H1N1 influenza virus in whom the clinical progression and regression of both the diseases were in tandem.


Pityriasis rosea of Gibert polymerase chain reaction seasonal influenza viral exanthem viral rash.


The H1N1 influenza pandemic in 2009 involved more than 399000 laboratory- confirmed cases from 192 countries.1 After the pandemic H1N1 viruses are still circulating in many parts of the world and it is likely that the novel H1N1 now known as A(H1N1)pdm09 is becoming seasonal influenza.2-4

Pityriasis rosea (PR) is suspected to be caused by various viruses. However a single definite viral cause has not been identified. We report here a case of PR suspected to be associated with H1N1 Influenza virus infection.

Case Report

A 31-year-old man was being managed by a physician for acute onset of flu-like illness and fever. His brother was diagnosed as having pandemic influenza A 2009 one week ago and was hospitalised for severe acute respiratory distress. The patient developed a mildly pruritic generalised skin eruption five days after onset of fever and was referred to us.

Before the onset of his skin eruption the patient received oral paracetamol and diphenhydramine for two days. He had taken the same medications previously with no history of adverse reactions or drug allergy. His drug history before onset of the rash was unremarkable otherwise. His past health was good. He did not have clinical influenza over the past three years. He had not been vaccinated against pandemic H1N1 influenza or seasonal influenza.

Our examination revealed a large scaly oval plaque of about 3 cm X 1.5 cm at his right scapular area. Further history taking revealed that such occurred on day three of the fever. Numerous oval-shaped scaly plaques were noted on trunk and proximal aspects of four extremities. The lesions were oriented along the lines of skin cleavage. Collarette scales were evident on some of the lesions (Figure 1).

His external genitalia mucous membranes palms soles axillae and groins were uninvolved. His throat was inflammed. Chest was slightly congested. There was no generalised lymphadenopathy.

His blood counts revealed marginal

lymphocytosis (lymphocytes 7.4 X 10 /L

neutrophils 47% lymphocytes 49% monocytes 3% eosinophils 0% and basophils

1%). Blood glucose liver function tests renal function tests and electrolytes were normal. ASOT was not elevated. VDRL and HIV antibodies were negative. Urinalysis revealed no abnormality. Chest X-ray was normal. Serum sample collected more than 14 days after onset of illness was positive against pandemic influenza H1N1 2009 at a titre of

1:80 (reference range: less than 1:40) by haemagglutination inhibition assay. Skin scrapings for potassium hydroxide smear revealed no evidence of dermatophytosis.

Our clinical diagnosis was PR. The patient was closely observed on an out-patient basis by us and by his physician. Oseltamivir was not prescribed. We prescribed topical white petrolatum and oral cetirizine 10 mg once daily for five days. We noted almost complete regression of his scaly lesions two weeks later. Some post-inflammatory hypopigmentation was noted. He was systemically well then.


Our patient represents the third reported case of suspected association of PR and pandemic H1N1 infection. For this patient the diagnosis of H1N1 infection was established based on the epidemiological link and serology. We did not perform PCR on his nasopharyngeal secretions and skin biopsy. We did not arrange for PCR for other

viruses (such as herpesviruses) on his plasma peripheral blood mononuclear cells and skin biopsy specimen. Serological examinations for viruses other than H1N1 were also not performed. Therefore the possibility of having co-infection(s) as the true culprit of PR could not be excluded.

A possible association of PR with viruses causing upper respiratory tract infections is not a novel idea. A report in 1981 indicated that

out of 11 patients with PR six (55%) gave a history of antecedent upper respiratory illness. However when examined for antibodies against influenza A influenza B parainfluenza I parainfluenza II and parainfluenza III viruses from paired acute and convalescent sera no significant rise in antibody titre was noted.5

If viruses causing respiratory tract infections are associated with PR a seasonal variation or variations associated with flu epidemics would be expected. However previous reports do not document such variations.6-16 We have previously reported a meta-analysis on 1379 patients with PR in vastly different

geographical locations. No seasonal variation or correlation with flu epidemics was found.17

However seasonal influenza differs from pandemic influenza as the latter may be associated with a more prolonged virus replication and thus a more intense stimulation to the immune system. Thus PR may only be a consequence of pandemic influenza but not seasonal influenza.

As for pandemic (H1A1) 2009 influenza specifically a four-year-old-girl with PR and H1N1 influenza occurring in June 2009 was reported in Saudi Arabia.18 The clinical features were conclusive with PR and lesional skin biopsy features were compatible with PR. The H1N1 was confirmed by PCR on the nasopharyngeal wash. However PCR was not performed on the skin biopsy specimen owing to lack of such facilities. As a result the authors admitted that the evidence was inconclusive whether the H1N1 infection is the sole cause of PR or whether H1N1 infection is just a trigger for endogenous reactivation of other viruses which then caused PR.18

Subsequently in 2010 a six-year-old girl in Korea was reported to have a herald patch followed by the concomitant occurrence of flu symptoms and generalised PR rash four days later.19 PCR was positive for H1N1 on her nasopharyngeal secretion but not on her skin biopsy specimen. The authors believed that the time sequence is supportive of reactivation of H1N1 directly causing PR as the appearance of the herald patch was within the incubation period of H1N1 and there was no evidence of other viral infections. They attributed the failure of detecting H1N1 DNA by PCR on the skin biopsy specimen to the delay of specimen collection (17 days after onset of herald patch).19 Nevertheless one should note that viruses can cause skin rash either by direct invasion or immune-mediated mechanisms and viruses are only present in lesions in the former.

However other investigators argued that virology studies (such as those for human herpesvirus 6 and 7) have not been performed.20 Moreover the concept that H1N1 can remain latent and then subsequently reactivated was unsubstantiated such being applicable to the herpesviruses only.20 These arguments seem to be in line with previous findings of ours2122 and possibly other investigators.

It is never easy to attribute causal relationships between a viral infection and a skin eruption based on DNA/mRNA sequence-based investigation findings. This is particular so if PCR is positive in only one of the specimens. In a systematic review23 we have applied the guidelines according to Fredericks and Relman24 to assess such associations. We believe that such and other guidelines should be consulted and the entire virological picture be assessed collectively before attributing causal relationships of viral infections and skin rashes.

In conclusion based on the two previous case reports and the one presented here we hypothesise that pandemic influenza may trigger PR in certain predisposed individuals either directly or via reactivation of another latent virus. Further studies are worthwhile to improve our understanding and management of this intriguing disease.


The authors thankfully acknowledge expert inputs in preparing this manuscript from Prof Paul KS Chan MD FRCPath Department of Microbiology The Chinese University of Hong Kong.


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Author:Zawar, Vijay; Chuh, Antonio
Publication:Journal of Pakistan Association of Dermatologists
Date:Mar 31, 2014
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