2
1285 be tried. Although the jet nebuliser used contains a filter designed to remove most of the pentamidine from exhaled gases, improper use of the nebuliser may lead to release of pentamidine into the environment, precipitating acute bronchospasm in bystanders. Clinicians should be aware of this potential adverse effect, especially in individuals with a history of hypersensitive airways. Aerosol pentamidine should be administered only in well-ventilated rooms. Further toxicity testing and specific guidelines for handling aerosol pentamidine are indicated, as Dr McDiarmid and Dr Jacobson- Kram (Oct 7, p 863) have noted. Department of Medicine, VA Hospital and University of Missouri Hospital and Clinics, Columbia, Missouri 65212, USA DONALD C. DOLL 1. Girard PM, Landman R, Gaudebout C, et al. Prevention of Pneumocystis carinii pneumonia relapse by pentamidine aerosol in zidovudine-treated AIDS patients. Lancet 1989; i: 1348-53. DIABETES MELLITUS, AIDS, AND NIGHT SWEATS SIR,-Dr Swai and colleagues (Oct 21, p 976) describe patients with diabetes mellitus who were misdiagnosed as having AIDS. We have had a further such experience. An 18-year-old man presented in September, 1989, with a 4 week history of weight loss, polyuria, and polydipsia in mild diabetic ketoacidosis. He was rehydrated and put on twice-daily insulin (’Actraphane HM’). 8 weeks after starting on insulin he contacted our clinic with concerns about his HIV serology. For about 4 weeks he had been experiencing sweats every night. These were drenching, often requiring a change of bed clothes, and were associated with tiredness and occasionally a headache in the morning. His insulin dose remained unchanged. Through media education programmes he knew that night sweats could be a symptom of AIDS, and he consulted four primary care physicians. He was heterosexual and in no high-risk groups for HIV infection but he became preoccupied by the belief that he had AIDS. This resulted in significant social problems, but he eventually consented to an HIV test. Before the test result became available he contacted our clinic when the night sweats and morning symptoms were recognised to represent nocturnal hypoglycaemia. These symptoms responded to a reduction in his evening dose of insulin. He was HIV seronegative, as expected. Night sweats are a common symptom of nocturnal hypoglycaemia, as well as of AIDS. This patient had falling insulin requirements after starting treatment for his diabetes, as is commonly seen. Failure to reduce his insulin dose in this setting produced the nocturnal hypoglycaemia, night sweats, and fear that he had AIDS. The failure of early recognition of his night sweats as a symptom of hypoglycaemia by the patient and by the primary care physicians contributed to his extreme anxiety about HIV infection, with significant personal and family distress. Department of Endocrinology and Diabetes, Royal Perth Hospital, Perth, Western Australia 6001 PETER L. SILBERT ANAL AND CERVICAL INTRAEPITHELIAL NEOPLASIA SIR,-Mr Scholefield and colleagues (Sept 30, p 765) prospectively evaluate an endoscope in the examination of the anal canal for the detection of premalignant conditions, and, by their finding of an association between anal and cervical intraepithelial neoplasia, implicate the human papillomavirus (HPV). In an analysis of 16 patients with invasive and squamous cell carcinoma (SCC) treated over eight years we have shown an association between anal SCC and previous cervical intraepithelial neoplasia (CIN III) or invasive cervical carcinoma (p<0’001, Fisher’s exact test) in 3 women (mean age 42 years). None of these women had a history of clinical manifestations of anogenital HPV infection. DNA hybridisation was done on stored specimens for each of these patients. No lesion was seen to contain HPV 6/11, but all showed active HPV 16 infection. HPV 16 was also identified in an area of Bowen’s disease excised from the inner thigh of 1 of these patients. We are doing DNA hybridisation on a 4th patient, aged 42, who was found to have an area of invasive SCC within a patch of anal Bowen’s disease; four years earlier she had been treated for cervical carcinoma. Although this is a small and retrospective series, the results suggest that sexually active women with previous cervical intraepithelial neoplasia are at risk of multifocal anogenital malignancy, both intraepithelial and invasive. Thus, with the evidence from Scholefield and colleagues’ study, we advocate screening the whole anogenital area in women with CIN III and evidence of HPV 16 infection. Our findings also suggest that the anal intraepithelial neoplasia III that Scholefield et al found requires careful follow-up-if not immediate treatment. Department of Surgery, City Hospital, Nottingham NG5 1PB; and Departments of Pathology and Surgery, Leicester Royal Infirmary, Leicester ANTHONY R. DIXON HOWARD PRINGLE DAVID F. L. WATKIN DIAGNOSIS OF BACTERIAL MENINGITIS SIR,-The letters by Dr Burans and others ( July 15, p 158) and by Dr Girgis and colleagues (Oct 28, p 1039), comparing methods of diagnosis of bacterial meningitis, are interesting but both lack essential information. The clinical state of the patients and the duration of symptoms affect the success or failure of the methods used. It is not safe to assume that the state of the patients from whom specimens come is comparable. For example, about 30 years ago a world famous laboratory in the United States reported that a high proportion of cases of tuberculous meningitis had been diagnosed by direct microscopy of the cerebrospinal fluid. I was due to visit the laboratory and hoped to learn their technique, which would improve our results. I found, however, that the techniques on the two sides of the Atlantic were almost identical but that the US patients were usually admitted in coma whereas in our National Health Service hospital in the UK it was rare to have to attempt a diagnosis at such an advanced stage of the disease. Anyone contemplating changing diagnostic methods because of reports of superior results needs to bear in mind, when clinical information is omitted, that the specimens themselves may not be comparable (quite apart from differences in reagents and techniques and in the presence or absence of antibiotic treatment). This important information is often omitted, probably because laboratory-based authors are unaware of it. Department of Microbiology, University College Hospital, London WC1 E. JOAN STOKES LISTERIA MONOCYTOGENES AND PATE SIR,-Although listeriosis remains a rare disease the incidence has doubled in the past seven years in England and Wales. Whilst this increase may reflect greater awareness of the importance of listeriosis and better reporting, it is thought to be a real one. 1 Listeriosis can be food-borne,2,3 and epidemiological data implicate a variety of foodstuffs in outbreaks,4,5 though only a minority have been microbiologically confirmed.6,7 Sporadic cases of listeriosis have also been attributed to food8,9 but ascribing a source is often difficult because of the variable incubation period before clinical symptoms and the unavailability of food samples for analysis at the time of onset of illness. It has been suggested that some sporadic cases may be related, but their association remains unrecognised in the absence of unusual circumstances.1o Besides being found in myriad locations in the environment Listeria monocytogenes has been identified in various foods, including milk, cream, meat and meat products, salad vegetables, and soft cheeses. Pate is another potential source. We examined fourteen varieties of pate, produced by several manufacturers and purchased from different shops, but primarily two branches of a supermarket. Samples were obtained from delicatessen counters and from unopened packs in refrigerators. Most of the products sampled were imported. Of the 73 pates examined 37 contained L monocytogenes, 7 with counts of 10 000 or more/g (table). No other Listeria species was isolated. 25 were serovar 4b, 16 were 4b(X), and 1 was 1/2; 5 samples

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Page 1: LISTERIA MONOCYTOGENES AND PATE

1285

be tried. Although the jet nebuliser used contains a filter designed toremove most of the pentamidine from exhaled gases, improper useof the nebuliser may lead to release of pentamidine into theenvironment, precipitating acute bronchospasm in bystanders.Clinicians should be aware of this potential adverse effect, especiallyin individuals with a history of hypersensitive airways. Aerosolpentamidine should be administered only in well-ventilated rooms.Further toxicity testing and specific guidelines for handling aerosolpentamidine are indicated, as Dr McDiarmid and Dr Jacobson-Kram (Oct 7, p 863) have noted.

Department of Medicine,VA Hospital and University of Missouri

Hospital and Clinics,Columbia, Missouri 65212, USA DONALD C. DOLL

1. Girard PM, Landman R, Gaudebout C, et al. Prevention of Pneumocystis cariniipneumonia relapse by pentamidine aerosol in zidovudine-treated AIDS patients.Lancet 1989; i: 1348-53.

DIABETES MELLITUS, AIDS, AND NIGHT SWEATS

SIR,-Dr Swai and colleagues (Oct 21, p 976) describe patientswith diabetes mellitus who were misdiagnosed as having AIDS. Wehave had a further such experience.An 18-year-old man presented in September, 1989, with a 4 week

history of weight loss, polyuria, and polydipsia in mild diabeticketoacidosis. He was rehydrated and put on twice-daily insulin(’Actraphane HM’). 8 weeks after starting on insulin he contactedour clinic with concerns about his HIV serology. For about 4 weekshe had been experiencing sweats every night. These were

drenching, often requiring a change of bed clothes, and wereassociated with tiredness and occasionally a headache in the

morning. His insulin dose remained unchanged. Through mediaeducation programmes he knew that night sweats could be asymptom of AIDS, and he consulted four primary care physicians.He was heterosexual and in no high-risk groups for HIV infectionbut he became preoccupied by the belief that he had AIDS. Thisresulted in significant social problems, but he eventually consentedto an HIV test. Before the test result became available he contactedour clinic when the night sweats and morning symptoms wererecognised to represent nocturnal hypoglycaemia. These symptomsresponded to a reduction in his evening dose of insulin. He was HIVseronegative, as expected.Night sweats are a common symptom of nocturnal

hypoglycaemia, as well as of AIDS. This patient had falling insulinrequirements after starting treatment for his diabetes, as is

commonly seen. Failure to reduce his insulin dose in this settingproduced the nocturnal hypoglycaemia, night sweats, and fear thathe had AIDS. The failure of early recognition of his night sweats asa symptom of hypoglycaemia by the patient and by the primary carephysicians contributed to his extreme anxiety about HIV infection,with significant personal and family distress.

Department of Endocrinology and Diabetes,Royal Perth Hospital,Perth, Western Australia 6001 PETER L. SILBERT

ANAL AND CERVICAL INTRAEPITHELIALNEOPLASIA

SIR,-Mr Scholefield and colleagues (Sept 30, p 765)prospectively evaluate an endoscope in the examination of the analcanal for the detection of premalignant conditions, and, by theirfinding of an association between anal and cervical intraepithelialneoplasia, implicate the human papillomavirus (HPV).

In an analysis of 16 patients with invasive and squamous cellcarcinoma (SCC) treated over eight years we have shown anassociation between anal SCC and previous cervical intraepithelialneoplasia (CIN III) or invasive cervical carcinoma (p<0’001,Fisher’s exact test) in 3 women (mean age 42 years). None of thesewomen had a history of clinical manifestations of anogenital HPVinfection. DNA hybridisation was done on stored specimens foreach of these patients. No lesion was seen to contain HPV 6/11, butall showed active HPV 16 infection. HPV 16 was also identified inan area of Bowen’s disease excised from the inner thigh of 1 of these

patients. We are doing DNA hybridisation on a 4th patient, aged 42,who was found to have an area of invasive SCC within a patch ofanal Bowen’s disease; four years earlier she had been treated forcervical carcinoma.

Although this is a small and retrospective series, the resultssuggest that sexually active women with previous cervical

intraepithelial neoplasia are at risk of multifocal anogenitalmalignancy, both intraepithelial and invasive. Thus, with theevidence from Scholefield and colleagues’ study, we advocatescreening the whole anogenital area in women with CIN III andevidence of HPV 16 infection. Our findings also suggest that theanal intraepithelial neoplasia III that Scholefield et al found

requires careful follow-up-if not immediate treatment.

Department of Surgery,City Hospital, Nottingham NG5 1PB;and Departments of Pathology and Surgery,

Leicester Royal Infirmary, Leicester

ANTHONY R. DIXONHOWARD PRINGLEDAVID F. L. WATKIN

DIAGNOSIS OF BACTERIAL MENINGITIS

SIR,-The letters by Dr Burans and others ( July 15, p 158) andby Dr Girgis and colleagues (Oct 28, p 1039), comparing methods ofdiagnosis of bacterial meningitis, are interesting but both lackessential information. The clinical state of the patients and theduration of symptoms affect the success or failure of the methodsused. It is not safe to assume that the state of the patients from whomspecimens come is comparable. For example, about 30 years ago aworld famous laboratory in the United States reported that a highproportion of cases of tuberculous meningitis had been diagnosedby direct microscopy of the cerebrospinal fluid. I was due to visit thelaboratory and hoped to learn their technique, which wouldimprove our results. I found, however, that the techniques on thetwo sides of the Atlantic were almost identical but that the US

patients were usually admitted in coma whereas in our NationalHealth Service hospital in the UK it was rare to have to attempt adiagnosis at such an advanced stage of the disease. Anyonecontemplating changing diagnostic methods because of reports ofsuperior results needs to bear in mind, when clinical information isomitted, that the specimens themselves may not be comparable(quite apart from differences in reagents and techniques and in thepresence or absence of antibiotic treatment). This importantinformation is often omitted, probably because laboratory-basedauthors are unaware of it.

Department of Microbiology,University College Hospital,London WC1 E. JOAN STOKES

LISTERIA MONOCYTOGENES AND PATE

SIR,-Although listeriosis remains a rare disease the incidencehas doubled in the past seven years in England and Wales. Whilstthis increase may reflect greater awareness of the importance oflisteriosis and better reporting, it is thought to be a real one. 1Listeriosis can be food-borne,2,3 and epidemiological data implicatea variety of foodstuffs in outbreaks,4,5 though only a minority havebeen microbiologically confirmed.6,7 Sporadic cases of listeriosishave also been attributed to food8,9 but ascribing a source is oftendifficult because of the variable incubation period before clinicalsymptoms and the unavailability of food samples for analysis at thetime of onset of illness. It has been suggested that some sporadiccases may be related, but their association remains unrecognised inthe absence of unusual circumstances.1o Besides being found inmyriad locations in the environment Listeria monocytogenes hasbeen identified in various foods, including milk, cream, meat andmeat products, salad vegetables, and soft cheeses. Pate is anotherpotential source.We examined fourteen varieties of pate, produced by several

manufacturers and purchased from different shops, but primarilytwo branches of a supermarket. Samples were obtained fromdelicatessen counters and from unopened packs in refrigerators.Most of the products sampled were imported.Of the 73 pates examined 37 contained L monocytogenes, 7 with

counts of 10 000 or more/g (table). No other Listeria species wasisolated. 25 were serovar 4b, 16 were 4b(X), and 1 was 1/2; 5 samples

Page 2: LISTERIA MONOCYTOGENES AND PATE

1286

INCIDENCE AND COUNTS OF LISTERIA MONOCYTOGENES (/g)ISOLA’I’1?17 FROM DISPLAYED AND STORED PA’I’E

yielded two serotypes. More than one brand and variety were foundto contain L monocytogenes.

Cross-contamination between pates on the same display countercould not be excluded though the isolation of L monocytogenes fromunopened stored pate does suggest that the pate itself could be thesource of the bacterium. The high counts obtained from pate weresimilar to those found in some soft cheese." The predominantserotype from soft cheese was 1/2, however. Serotype 4b, the mostfrequent serotype in the pate, is responsible for about 80% ofhuman infections, and in 1987 was responsible for a

disproportionate increase in listeriosis.1 The isolation of serovar4b(X) is interesting because this serovar was responsible for acluster of cases of listeriosis in 1987 for which no source was

epidemiologically implicated.’"Pate may now be added to the list of potential sources of

L monocytogenes.

We thank Dr J. McLauchlin (Central Public Health Laboratory) forserotyping, and colleagues in the Rhymney Valley and Taff-Ely DistrictCouncil environmental health departments for the samples.

Public Health Laboratory,University Hospital of Wales,Cardiff CF4 4XW

I. J. MORRISC. D. RIBEIRO

1. Hall SM, Crofts N, Gilbert RJ, Pini PN, Taylor AG, McLauchlin J. Epidermiology oflisteriosis, England and Wales. Lancet 1988; ii: 502-03.

2. WHO Working Party. Foodborne listeriosis Bull World Health Org 1988, 66: 421-28.3. Gill P. Is listeriosis often a food-borne illness? J Infect 1988; 17: 7-28.4. Schwartz B, Broome CV, Brown GR, et al. Association of sporadic listeriosis with

consumption of uncooked hot dogs and undercooked chicken Lancet 1988; ii:779-82

5. McLauchlin J, Audurier A, Taylor AG. Aspects of the epidemiology of humanListeria monocytogenes infections in Britain 1967-1984; the use of serotyping andphage typing. J Med Microbiol 1986; 22: 367-77.

6. James SM, Fannin SL, Agee BA, et al. Listeriosis outbreak associated with Mexicanstyle cheese. MMWR 1985; 34: 357-59.

7. Linnan MJ, Mascola L, Lou DX, et al. Epidemic listeriosis associated with Mexicanstyle cheese. N Engl J Med 1988; 319: 823-28.

8. Azadian BS, Finnerty GT, Pearson AD Cheese-home listeria meningitis in

immunocompetent panent Lancet 1989; i: 322-23.9. Kerr KG, Dealler SF, Lacey RW. Materno-fetal listeriosis from cook-chill and

refrigerated food. Lancet 1988; ii: 1133.10. McLauchlin J, Crofts N, Campbell DM. A possible outbreak of listeriosis caused by

an unusual strain of Listeria monocytogenes. J Infect 1989, 18: 179-87.11. Pini PN, Gilbert RJ. The occurrence in the UK of Listeria sp in raw chickens and soft

cheeses. Int J Food Microbiol 1988; 6: 317-26

MARITAL STATUS OF WOMEN WHO SMOKE

SIR,-More attention should be given to the variations in

smoking habits within the population.’ Smoking is responsible forabout 100 000 deaths per year in England and Wales, so statisticsabout its prevalence in subgroups of the population, by age, sex, andso on, are important. Recent reviews2,3 neglect one importantfactor-namely, marital status.The General Household Survey has collected statistics on

smoking by marital status since 1972 and publishes tables every twoyears, most recently for 1986. However, these reports focus onsocioeconomic variation, and have made no further comment onmarital status distribution of smoking since the first report in 1972;only with publication of the 1984 and 1986 reports have statistics onsmoking by age and marital status been widely available.The table shows rates of current cigarette smoking by marital

status for men and women, for 1972, 1984, and 1986, indirectlystandardised using the cigarette smoking rates among all men orwomen respectively in 1972 as the standard. The effects of

AGE-STANDARDISED CURRENT CIGARETTE SMOKING RATES PER

100 IN GREAT’BRITAIN

Source: General Household Survey Reports

non-comparability of the data collected at these different times (datafor ages 15 and over in 1972 compared with 16 and over in the lateryears, and the inclusion of cohabitees with married in 1986) will bequite small, though as a consequence both legally married men andwomen may in fact smoke least in 1986. Smoking prevalence hasdecreased over the period for both men and women, but for bothsexes the category of widowed/divorced/separated stands out aspersistently having the highest prevalence of cigarette smoking, andthe gap between them and the single/married is increasing,especially for women.We are concened that so little attention is paid to this differential,

particularly in view of the evidence of extensive effects of maritaldissolution upon health status.4 Although marital status is a morefluid and changeable state than socioeconomic position, largegroups of people are placed at higher risk of disease on account ofassociated smoking behaviour for considerable periods of time. Theexplanations for these persistent differences may well be complex,and the patterns do not, for instance, resemble marital status

differences in alcohol consumption.s Nevertheless, the first barrierto changing behaviour is a poor understanding of its variation.6

Department of Community Medicineand General Practice,

Radcliffe Infirmary,Oxford OX2 6HE

MIKE MURPHY

JILL DAWSONRAY FITZPATRICK

1. Jacobson B, Amos A, Aghi M Women and smoking world no tobacco day a challengefor women’s health. Lancet 1989; i: 1193-94

2. OPCS monitor SS 88/1 Cigarette smoking 1972-1986. London. OPCS, 19883. Wald N, et al. UK smoking statistics Oxford. Oxford University Press, 1988.4. Riessman C, Gerstel N Marital dissolution and health: do males or females have

greater nsk? Soc Sci Med 1988; 20: 627-35.5. General Household Survey 1984. (OPCS senes GHS no 14) London: HMSO, 19866 Marsh A, Matheson J Smoking attitudes and behaviour an enquiry carried out on

behalf of the Department of Health and Social Security. London. HMSO, 1983

MIGRAINE AFTER BONE-MARROWTRANSPLANTATION

SIR,-Migraine was first proposed as a disorder of blood in 1978’and there has been considerable though not universal support forthe hypothesis that platelets mediate migraine.2,3 We report a youngman in whom severe classical migraine first developed afterbone-marrow transplantation; the donor was his mother, who hadlongstanding migraine.The patient, aged 24, was diagnosed as having acute

lymphoblastic leukaemia in 1983. He went into remission withdifficulty and maintenance chemotherapy was tolerated poorly.Investigation of the family revealed a complete phenotypic match atHLA A, B, and DR loci with his mother, and a transplant was donein 1984. This was successful and he has had no evidence ofrecurrence of leukaemia. He has, however, had acute and chronicgraft-versus-host disease affecting skin, mucous membranes, andlungs which has partly responded to immunosuppression withsteroids, cyclosporin, and thalidomide. He also had

hypogammaglobulinaemia. Within a month of the transplant severeand incapacitating migraine developed, occurring every few weeks,though he had never had headaches of any type previously. Attacksinclude headache, vomiting, teichopsia, hemianopia and

paraesthesia to either side, and dysphasia. These episodes were notclearly precipitated by any dietary or other identifiable factor. His