VZV Foundation - A Decade Of Leadership In The Fight Against VZV Infections

	Oral Presentation Abstracts: 1B [1B] ZOSTER ASSOCIATED PAIN IN HEALTHY AND IMMUNOCOMPROMISED SUBJECTS FOLLOWING SHINGLES *J. Breuer (1), K. Hawrami (1), L. Batty(1), M. Leedham Green(1), R. Johnson (2), J. Gallagher (3), F. Scott (1) (1) Dept of Medical Microbiology, BLT & Queen Mary College, London E1 1BB (2) Dept of Anaesthetics, Bristol Royal Infirmary, Bristol (3) Dept of Anaesthetic, Barts London Trust, London Patients with active zoster presenting to general practitioners in East London, were recruited. The diagnosis was confirmed by immunofluorescence, PCR and culture of vesicle fluid. Demographic data was collected and the level of prodromal and presenting pain measured using questionnaires, visual analogue scales and McGill questionnaires. Anxiety and depression were measured by the Hospital Anxiety and Depression scoring system. Pain and anxiety were reassessed at 6, 12, 26 and 52 weeks following presentation. A blood sample was taken at baseline and at each visit. PBMCs were separated and tested for the presence of viral DNA. Thirty three patients with immunosuppression (steroids 21, HIV 1, chemotherapy/cancer 10, ESRF 1) who had been followed for one year were identified. Nested immunocompetant controls matched for age, gender and ethnic origin were identified from within the cohort. All the immunocompromised patients and the majority of the immunocompetant patients had received antiviral therapy. The two groups were compared for level of pain at presentation (VAS), the presence of VZV DNA in PBMCs at presentation and the duration of pain over time. The distribution of pain scores at presentation was similar in the immunocompromised and immunocompetant patients. Immunocompromised patients were more likely to be viraemic at presentation 24/31(77%) versus 57% (16/28) but the difference was not significant. A higher percentage of immunocompromised patients continued to have ZAP up to 12 months after rash onset and the differences were significant (p<0.05). Immunocompromised patients with viraemia were twice or more times as likely to have prolonged pain lasting three months or more than immunocompetant patients with viraemia. The implications of these data for our understanding of the pathogenesis of ZAP and the possible strategies for its prevention and management will be discussed. Corresponding Author: Dr Judy Breuer, MB BS MD FRCPath., Reader in Virology, Department of Medical Microbiology, Queen Mary College, ARC Bldg, 36, Ashfield St E1 1BB, United Kingdom

Oral Presentation Abstracts: 1B

[1B]

ZOSTER ASSOCIATED PAIN IN HEALTHY AND IMMUNOCOMPROMISED SUBJECTS FOLLOWING SHINGLES

*J. Breuer (1), K. Hawrami (1), L. Batty(1), M. Leedham Green(1), R. Johnson (2),
J. Gallagher (3), F. Scott (1)
(1) Dept of Medical Microbiology, BLT & Queen Mary College, London E1 1BB
(2) Dept of Anaesthetics, Bristol Royal Infirmary, Bristol
(3) Dept of Anaesthetic, Barts London Trust, London

Patients with active zoster presenting to general practitioners in East London, were recruited. The diagnosis was confirmed by immunofluorescence, PCR and culture of vesicle fluid. Demographic data was collected and the level of prodromal and presenting pain measured using questionnaires, visual analogue scales and McGill questionnaires. Anxiety and depression were measured by the Hospital Anxiety and Depression scoring system. Pain and anxiety were reassessed at 6, 12, 26 and 52 weeks following presentation. A blood sample was taken at baseline and at each visit. PBMCs were
separated and tested for the presence of viral DNA.
Thirty three patients with immunosuppression (steroids 21, HIV 1, chemotherapy/cancer 10, ESRF 1) who had been followed for one year were identified. Nested immunocompetant controls matched for age, gender and ethnic origin were identified from within the cohort. All the immunocompromised patients and the majority of the immunocompetant patients had received antiviral therapy. The two groups were compared for level of pain at presentation (VAS), the presence of VZV DNA in PBMCs at presentation and the duration of pain over time.
The distribution of pain scores at presentation was similar in the immunocompromised and immunocompetant patients. Immunocompromised patients were more likely to be viraemic at presentation 24/31(77%) versus 57% (16/28) but the difference was not significant. A higher percentage of immunocompromised patients continued to have ZAP up to 12 months after rash onset and the differences were significant (p<0.05).
Immunocompromised patients with viraemia were twice or more times as likely to have prolonged pain lasting three months or more than immunocompetant patients with viraemia.
The implications of these data for our understanding of the pathogenesis of ZAP and the possible strategies for its prevention and management will be discussed.

Corresponding Author: Dr Judy Breuer, MB BS MD FRCPath., Reader in Virology, Department of Medical Microbiology, Queen Mary College, ARC Bldg, 36, Ashfield St E1 1BB, United Kingdom