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Management of well people found positive by screening.-Such people should be informed of a positive result andcounselled about the personal precautions set out above.Seropositive people should inform their doctors and

dentists before any blood sampling, dental, or surgicalprocedures. An appointment with the local AIDS

counselling service can then be arranged.

Community Management of HTL V-III-infected PeopleDomiciliary nursing guidelines have been set out by the

DHSS. When treating anti-HTLV-III-positive people,dentists should take the same precautions as they would toprevent the spread of hepatitis B.

Hospital InpatientsIt is normal practice to isolate in a single room any patient

with an undiagnosed infection. However, precautions to thelevel of single-room isolation, or special admission policies,are not indicated for HTLV-III-infected people, includingthose with AIDS, unless (i) a particular superinfectionrequires special isolation precautions; (ii) protective isolationis judged necessary; (iii) there are difficulties in maintainingstandards of hygiene, such as profuse diarrhoea, faecal incon-tinence, uncontrolled bleeding, or altered behaviour

secondary to central nervous system involvement; (iv) theseverity or terminal nature of the illness necessitates care in asingle room.

Laboratory SafetyAdvice is set out in the Advisory Committee on Dangerous

Pathogens interim guidelines. A revision is in preparation.Precautions for the taking of blood samples from antibody-positive patients are set out in the DHSS AIDS booklet 2, andare also available from the Public Health Laboratory Service,Colindale.

This prevention programme can only operateefficiently with cooperation from the general public,and medical workers can contribute not only bybecoming knowledgeable about the practices that carrymost risk but also by developing a positive andunderstanding approach to people whose way of lifemay be different from their own.

OUTBREAKS OF SHINGLES

THE relation between varicella (chickenpox) and herpeszoster (shingles) was suspected on clinical grounds for manyyears before the in-vitro studies of Weller in the 1950s, 1,2 andmolecular analyses3 have now confirmed that the vesiculareruptions are two manifestations of infection by a singlehuman herpes virus-varicella-zoster virus (VZV). Thegenerally accepted theory of the pathophysiology of the twoconditions is that postulated by Hope-Simpson4-namely,that primary infection with VZV produces varicella and thatthe virus then persists in the sensory nerve ganglia in a latentstate before recrudescence as zoster when the host’s

immunity has waned. The fundamental validity of this theory

1. Weller TH, Coons AH. Fluorescent antibody studies with agents of varicella andherpes zoster propagated in vitro Proc Soc Exp Biol Med 1954; 86: 789-94.

2 Weller TH, Witton HM, Bell EJ. The etiologic agents of varicella and herpes zoster:isolation, propagation, and cultural characteristics in vitro. J Exp Med 1958; 108:843-68.

3. Hyman RW. Structure and function of the varicella-zoster virus genome. In. NahmiasAJ, Dowdle WR, Schinazi RF, eds. The human herpes viruses: and

interdisciplinary prespective. New York. Elsevier: 1981: 63-71.4. Hope-Simpson RE The nature of herpes zoster a long-term study and new hypothesis.

Proc Roy Soc Med 1965; 58: 9-20.

has been shown by the finding ofVZV antigens5 and nucleicacids6,7 in trigeminal ganglia obtained post mortem fromthose dying with shingles and from normal persons with ahistory of varicella. e

The DNA of VZV can be broken into fragments withrestriction endonucleases and, by means of several suchenzymes, individual strains of the virus can be

distinguished. In this way the viruses obtained from

epidemiologically related cases of varicella have been shownto be identical and those from unrelated cases to be different. 8In addition, Straus et a19 showed that, in an individual

patient, the viruses isolated from an initial attack of varicellaand from subsequent shingles lesions were identical strains,’thus seeming to prove the Hope-Simpson hypothesis.The concept that shingles is always due to recrudescence of

latent virus has, however, been challenged on severaloccasions by epidemiological studies suggesting that, in bothimmunocompromised"-" and normal" persons, herpeszoster was occasionally temporally related to exposure toVZV. These reports were sometimes open to question eitherbecause of the atypical nature of the zosterlo,m or because ofinadequate statistical analysis; but the same can not be said ofthe paper by Dr Palmer and his colleagues on p 1108 of thisissue. These workers describe the occurrence over a three-month period of 7 cases of shingles among a group of 101 staffworking in one department of a large office complex- anincidence strikingly greater than that in the rest of theworkforce or other controls. Most of the cases were in normalindividuals with a history of previous VZV infection. If, asthis paper suggests, a chain of transmission can link cases of

zoster, then it is far from clear by what mechanism freshexposure to.VZV might produce the disease, although therewould obviously be a prerequisite for reinfection with thevirus.

It was long assumed that the immunity to VZV thatdevelops after primary infection would prevent further

exogenous infections. There is, however, now good evidencethat reinfection does occur even though most of thesereinfections are subclinical and can only be detected

serologically.15-17 A substantial proportion of individualswith evidence of previous immunity to VZV show a rise inlevels of IgG, IgA, and, rather surprisingly, IgM whenintimately exposed to cases of VZV infection. 15 Clinical

expression of this fresh exogenous infection is well described

5. Esiri MM, Tomlinson AH. Herpes zoster: demonstration of virus in trigeminal nerveand ganglion by immunofluorescence and electron microscopy. J Neurol Sci 1972;15: 35-48.

6. Hyman RW, Ecker JR, Tenser RB. Varicella-zoster virus RNA in human trigeminalganglia. Lancet 1983; ii: 814-16.

7. Gilden DH, Vafai A, Shtram Y, Becker Y, Devlin M, Wellish M. Varicella-zoster virusDNA in human sensory ganglia. Nature 1983; 306: 478-80.

8. Straus SE, Hay J, Smith H, Owens J. Genome differences among varicella-zoster virusisolates. J Gen Virol 1983; 64: 1031-41.

9. Straus SE, Reinhold W, Smith HA, Ruyechan WT, Henderson DK, Blaese RM, HayJ. Endonuclease analysis of viral DNA from varicella and subsequent zosterinfections in the same patient. N Engl J Med 1984; 311: 1362-64.

10. Schimpff S, Serpick A, Stoler B, et al. Varicella-zoster infection in patients with cancer.Ann Intern Med 1972; 76: 241-54.

11. Morens DM, Bregman DJ, West M, et al An outbreak of varicella-zoster infectionamong cancer patients. Ann Intern Med 1980; 93: 414-19.

12. Sokal JE, Firat D. Varicella-zoster infection in Hodgkin’s disease. Am J Med 1965; 39:452-63.

13. Rado JP, Tako J, Geder L, Jeney E. Herpes zoster house epidemic in steroid-treatedpatients; a clinical and viral study. Arch Intern Med 1965; 116: 329-35.

14. Thomas M, Robertson WJ Dermal transmission of virus as a cause of shingles. Lancet1971; ii: 1349-50.

15. Arvin AM, Koropchak CM, Wittek AE. Immunologic evidence of reinfection withvaricella-zoster virus. J Infect Dis 1983; 148: 200-05.

16. Gershon A, Steinberg S, Borkowsky W, Lennette D. IgM to varicella-zoster virus:demonstration in patients with and without clinical zoster. Pediat Infect Dis 1982; 1:164-67.

17 Brunell PA, Gershon AA, Uduman SA, Steinberg S. Varicella-zoster immunoglobulinsduring varicella, latency, and zoster. J Infect Dis 1975; 132: 49-54.

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in immunocompromised patients’ 0, 11 but seems to be rare inimmunocompetent individuals, in whom it has only latelybeen recorded. 18 In most of the cases so far described, andcertainly in those studied in detail, the clinical disease hastaken the form of a disseminated chickenpox rash which, atleast in patients "immune" as a result of the live varicellavaccine, was due to the exogenous wild virus strain. 18The site of natural VZV inoculation has not been proven

but there is much circumstantial evidence pointing to therespiratory mucosa.19 It is difficult to envisage how freshrespiratory implantation ofVZV could be expressed as zoster.If this were to occur then one might expect some cases ofprimary VZV infection to be manifest as shingles-aphenomenon that has not yet been recorded. By restrictionendonuclease analysis of the DNA of viruses isolated fromapparently related cases of shingles it should be possible todetermine whether they are identical and to settle once andfor all whether zoster can be contracted by fresh exposure.Another explanation for the finding of clusters of shingles

cases is that reinfection with VZV could reactivate latentvirus already in the sensory ganglia. The factors that controlthe latency of the virus are not completely understoodl9 but itis clear that humoral immunity per se is not of paramountimportance. Shingles normally develops despite the presenceof specific immunoglobulins and the disease is not more likelyto develop in patients with agammaglobulinaemia. Cell-mediated immunity is obviously more important in that thefrequency of shingles is inversely related to the level ofspecific VZV-induced lymphocyte proliferation, which hasbeen shown to be low in the immunocompromisedlo and todecrease with age.21,22 It has been suggested that the defencesthat are responsible for preventing recrudescent VZVinfection are reliant on continual boosts of immunityconsequent upon subclinical reinfections or reactivation oflatent virus.’9 How then could re-exposure to VZV inducereactivation of latent virus? A clue might be obtained from thework of Gershon and Steinberg,23 who showed that in vitrothe inactivation of VZV by primed lymphocytes could beblocked by the addition of antibody; it is possible, therefore,that the humoral response induced by reinfection couldinterfere with the cellular defences that keep the latent virusin check. Thus, despite the epidemiological evidence foroutbreaks of shingles, there is still much to be explained andthe final answer to the vexing question will probably comefrom studies of viral latency. Until then there will remain"believers" and "non-believers".

DAY HOSPITALS FOR PSYCHIATRIC CARE

THE first psychiatric day hospital was opened in the USSRin the 1930s and the first in the United Kingdom by DrJoshua Bierer in 1946.1 Since then there has been a hugeexpansion of day facilities for psychiatric patients. In many

18. Gershon AA, Steinberg SP, Gelb L and the National Institute of Allergy and InfectiousDiseases Collaborative Varicella Vaccine Study Group. Clinical reinfection withvaricella-zoster virus. J Infect Dis 1984; 149: 137-42

19. Weller TH. Varicella and herpes zoster. N Engl J Med 1983; 309: 1362-68, 1434-40.20. Arvin AM, Pollard RB, Rasmussen LE, Merrigan TC. Cellular and humoral immunity

in the pathogenesis of recurrent herpes viral infections in patients with lymphoma.J Clin Invest 1980; 65: 869-78.

21. Miller AE. Selective decline in cellular immune response to varicella-zoster in the

elderly. Neurology (Minneap) 1980; 30: 582-87.22. Burke BL, Steele RW, Beard OW, Wood JS, Cain TD, Marmer DJ. Immune responses

to varicella-zoster in the aged. Arch Intern Med 1982; 142: 291-93.23. Gershon AA, Steinberg SP. Cell-mediated immunity to varicella-zoster virus measured

by virus inactivation: mechanism and blocking of the reaction by specific antibody.Infect Immun 1979; 25: 164-69.

1. Bierer J The day hospital. London. Lewis, 1951.

places this was part of a systematic development of extra-hospital care; in other areas, day hospitals simply emerged.When fashions determine progress, mistakes will be made,and it is only lately that studies have been carried out toanswer the many questions that both planners and clinicianshave about this apparently healthy and vigorous limb of thepsychiatric services.The psychiatric day hospitals cater for the three main

groups with different needs. One of the motives for setting uppsychiatric day hospitals was to provide an alternative tohospital admission. This requires a well-staffed unit that isprepared to accept a wide range of patients and includeseveral treatment programmes that can be run

simultaneously. Most of the evidence suggests that this use ofday hospitals is beneficial. In studies in which patients wererandomly allocated to day-patient or inpatient care, eitherimmediately or within four weeks of admission, day care hasproved to be a feasible alternative to standard inpatienttreatment.2-5 Patients seem to prefer day-care to inpatienttreatment’ and to remain well for longer after day care,although definite evidence for this claim is still lacking. Notall inpatients are suitable for day care. Severely psychoticpatients seldom comply with treatment and are not

sufficiently independent to live outside hospital at night.Inpatients with neurotic disorder, adjustment reactions, andpersonality disorders are more suitable and, when selectedcarefully, do well.A second group of day hospitals cares for patients with

predominantly neurotic and minor personality disorders whoare not handicapped enough to be considered for inpatientcare. With such patients day care is thought of as supplyingmore intensive treatment programmes than can be offered in

outpatient clinics. Most of this treatment is of a psycho-therapeutic nature but it may also involve behaviour therapy.The evidence for efficacy in this group is limited. Taken as agroup such patients do not improve any more than whentreated in outpatient clinics.7 Behaviour therapy is now seento be most effective when conducted in the patient’s naturalenvironment, so any formal sessions in hospitals and clinicsshould be combined with homework practice.8 It is a littleartificial to place patients in day hospitals for this treatment.The last group of psychiatric day patients is the largest but

tends to be forgotten. These are chronic patients, mainly withschizophrenia, who attend day centres rather than dayhospitals. Such centres have fewer staff than day hospitalsand are often seen as supportive rather than therapeutic.9Whilst day centres are undoubtedly valuable, there are no

comparisons of this type of care with the equivalent serviceprovided outside the hospital structure. Many day centres arenow run by social services personnel and have little or nodirect medical input. In the UK this trend has been promotedby the Department of Health and Social Security, whose

2. Zwerling I, Wilder JF. An evaluation of the applicability of the day hospital intreatment of acutely disturbed patients. Isr Ann Psychiatr Rel Dis 1964; 2: 165-85.

3. Herz MI, Endicott J, Spitzer RL, Mesnikoff A. Day versus in-patient hospitalisation, acontrolled study Am J Psychiatry 1971; 127: 1371-82.

4. Hirsch SR, Platt S, Knights A, Wayman A. Shortening hospital stay for psychiatriccare: effects on patients and their families. Br Med J 1979; i: 442-46.

5. Dick P, Cameron L, Cohen D, Barlow N, Ince A. Day and full-time psychiatrictreatment: a controlled comparison. Br J Psychiatry 1985; 147: 246-50.

6. Dick P, Ince A, Barlow M. Day treatment: suitability and referral procedures. Br JPsychiatry 1985; 147: 250-53.

7. Tyrer PJ, Remington M. Controlled comparison of day-hospital and outpatienttreatment for neurotic disorders. Lancet 1979; i: 1014-16

8. Mathews A, Gelder MG, Johnson DW Agoraphobia: nature and treatment. LondonTavistock, 1981.

9. Gath DH, Hassall C, Cross KW. Whither psychiatric day care? A study of day patientsin Birmingham. Br Med J 1973; i: 94-98.