1472

2. Hull HF, Williams PJ, Oldfield F. Measles mortality and vaccine efficacy in rural WestAfrica Lancet 1983; i: 972-75.

3 Government of Zaire, Division of Statistics. Hospital morbidity and mortality reports,Kinshasa, 1975-1980.

4. Rolfe M. Measles immunization in the Zambian copperbelt: cause for concern. TransRoy Soc Trop Med Hyg 1982; 76: 529-30.

5 Government of Zaire, Division of Statistics. Hospital morbidity and mortality reports,Kinshasa 1975-1980.

6. Foster SO, Pifer JM. Mass measles control in West and Central Africa. Afr J Med Sci1971, 7: 151-58.

7. Grigsby ME, Adetosoye JIA. Measles epidemiology and control in western Nigeria. JNat Med Assoc 1973; 65: 378-85.

8. Foege WH. Measles vaccination in Africa. Sci Pub PAHO 1971; 226: 207-12.9. Greene R, Johnson M. Assessment of vaccination in Abidjan. Institut d’Hygiene,

Abidjan, 1979.10. Ministry of Health of Kenya and World Health Organization. Measles immunity in the

first year after birth and the optimum age for vaccination in Kenyan children. BullWHO 1977, 55: 21-31.

11. Expanded Programme for Immunization Programme Statement. Geneva: WHO,1976: 4.

12. World Health Organization. Weekly Epidemiol Rev 1979; 44: 337-3913. Guyer B, McBean M. The epidemiology and control of measles in Yaounde,

Cameroun, 1968-1975. Int J Epidemiol 1981; 10: 263-69.14. McBean AM, Hermann K, Foster SO, Gateff C. Evaluation of a mass measles

immunization campaign in Yaounde, Cameroon. Trans Roy Soc Trop Med Hyg1976; 70: 206-12.

15. Henderson RH, Davies H, Eddins DL, Foege WH. Assessment of vaccinationcoverage, vaccination scar rates, and smallpox scarring in five areas of West Africa.Bull WHO 1973; 48: 183-94.

16. Government of the United Republic of Cameroon Measles registry, Yaounde CentralHospital, 1975-1979.

17. U.S. Department of Health and Human Services/Public Health Service. Reportedmorbidity and mortality in the United States, annual summary 1981: 1982, 30:54-57.

18. Black FL. The role of herd immunity in control of measles. Yale J Biol Med 1982; 55:351-60.

Public Health

THE ARJENYATTAH EPIDEMICA Mass Phenomenon: Spread and Triggering

Factors

BARUCH MODANMOSHE TIROSH

EMIL WEISSENBERGCILLA ACKER

T. A. SWARTZCORINA COSTIN

ALEXANDER DONAGIMOSHE REVACH

GASTON VETTORAZZI

Chaim Sheba Medical Center, Tel Hashomer;Tel Aviv University Medical School; and

Ministry of Health, Jerusalem, Israel; andInternational Programme in Chemical Safety,

World Health Organisation, Geneva, Switzerland

Summary A massive epidemic of psychogenicaetiology occurred in three districts of the

West Bank over two weeks in March-April, 1983. It affected949 individuals, 727 (77%) of them adolescent females. Thesymptoms were not accompanied by positive physical signsor by laboratory findings. The epidemiological pattern waspathognomonic of that of a psychogenic disorder. The initialtrigger was probably the odour of H2S escaping from a faultylatrine in the schoolyard of the first affected school.

Subsequent spread of the disease was due to psychologicaland extra-medical factors, including publicity by the massmedia. Spread was stopped immediately after closure ofschools.

INTRODUCTION

EPIDEMICS of psychogenic disease are characterised by theoccurrence of symptoms that are not accompanied byfindings and by a consistent epidemiological pattern in whichby far most of the subjects are female.’-’6 The epidemicsreported have been limited to one place.During a period of 14 days in late March and early April,

1983, we witnessed, in the West Bank area, an extensiveepidemic similar in nature to those referred to above in sizeand in its spread throughout a number of communities. Theepidemic started in the village of Arrabah in the Jenin district,moved to the city of Jenin proper, and ended in the southerndistrict of Hebron, most notably in the village of Yattah. Itshortly became evident that, although we were dealing with asingle and well-defined epidemic the triggering factors variedbetween the main geographic areas affected. The followingclinico-epidemiological survey of this event refers to it as theArjenyattah epidemic, after AR(rabah), JEN(in), andYATTAH.

MATERIALS AND METHODS

Personal data on each reported case which included age, schoolgrade, occupation, place of residence, disease onset, and hospitaladmission were obtained from the following sources: (a) admittancerecords at 15 local hospitals; (b) interviews of the school principals;(c) a specially designed home interview conducted in Arrabah andYattah by Arabic-speaking public health workers. The homeinterview data are reported on p 1474,17 as are the chemical andbiological tests of suspected substances and of our samples.

Clinical and laboratory examinations of severely ill patients weredone in three major Israeli medical centres.

RESULTS

Altogether, 949 individuals, including 727 schoolgirls,were affected. The events occurred in three waves (table r),with the well-known preponderance among females (table II).The attack rate among schoolchildren, all of them female,varied between 8 - 7% and 32 - 9% and was highest inadolescent girls (table III).The epidemic started shortly after classes began on the

morning of March 21 at the Arrabah Girls’ School, when a17-year-old student from grade lOB presented with

dyspnoea, dizziness, and abdominal pains. During the

following 85 min, until the morning schoolbreak, similarcomplaints were described by 10 other girls. Some of the girlsreported an odour of rotten eggs coming from a latrine in thesoutheast area of the schoolyard. No complaints were

recorded during the schoolbreak, but during the next 2 hours15 more girls were affected and by the end of the second day, atotal of 61 schoolgirls and 5 adults were referred to thehospital. Attack rates by geography of school buildingshowed rates of 30 40/0, 14 7%, and 2 - ° 601o for the upper,lower, and right wing classes, respectively. Highest rateswere observed in 3 upper floor classes nearest the latrine fromwhich most of the odour was reported, and lowest rates inwing most distant from the latrine.5-6 days later, on March 26 and 27, 246 persons had

similar symptoms; they were the female students and staff insix schools in the town of Jenin and two neighbouringvillages. On the evening of March 27, 64 residents in aneastern neighbourhood in Jenin, primarily young adult

females, were admitted to the local hospital with similarsymptoms after reports of thick smoke being expelled from arapidly passing car.The third wave was considerably more massive and

occurred simultaneously in the districts of Tulkarem andHebron and centered around the girls’ school in the village ofYattah. The condition spread very rapidly, with more than90% of the students becoming affected within 2 h. A moredetailed description of the Yattah event is also given on p1474. 4 cases were reported among Israeli soldiers in thearea.

The main complaints were headache, dizziness, abdominal

1473

TABLE I-SUMMARY OF THE SEQUENCE OF THE EVENTS

TABLE II-AGE AND SEX DISTRIBUTION OF AFFECTED INDIVIDUALS

TABLE m-ATTACK RATE BY SCHOOL AND AGE

TABLE IV- FREQUENCY OF SYMPTOMS* IN ARRABAH SCHOOL AND

JENIN STREET EVENTS

*As recorded on the admission charts of the patients.

pains, and blurred vision (table IV). The symptomsexperienced by the Arrabah schoolgirls were more severe andlonger lasting than were those experienced by the residents ofJenin and its neighbouring villages. Approximately 27 - 3% ofthe patients were admitted more than once and about 4%three times or more. Only palliative treatment was given.11 % did not need drugs or other supporting therapy duringtheir hospital stay.Closure of schools on April 4 interrupted the chain of

events and put a halt to the epidemic.

DISCUSSION

The differential diagnosis of an event of this kind includes(1) a foodborne or waterborne infection, (2) air, water, or dust-borne chemical pollution, (3) an allergic reaction, (4) theeffect of noxious physical factors, and (5) epidemic hysteria.Only after all physical, chemical, and biological factors

have been ruled out can a diagnosis of mass hysteria be made.The more neutral term mass phenomenon seems preferableto mass hysteria, since the lay connotation of hysteria mayencourage spread of the disease, especially when the mediagives widespread publicity to the epidemic.As shown by Landrigan et al17 none of the organic factors

listed above was responsible for the epidemic. The number ofcomplaints, the paucity of physical signs and laboratory data,and the epidemiological pattern were typical of other

epidemics.3-7,13-I6 But the Arjenyattah epidemic differedfrom the others in (a) the rapid succession of a number ofschool events in a very short time, (b) its high"transmissibility" to the community, as expressed by theJenin Street event, and (c) the succession of triggermechanisms operating at different phases of the outbreak.The factor that triggered and maintained the outbreakdiffered for the various phases of the epidemic.Phase one consisted of two parts, both taking place at the

Arrabah School. The first, occurring before the schoolbreak,was triggered off by an unpleasant odour from a nearbyschool latrine. The second part started during the schoolrecess and was triggered off by rumours spread by the friendsof the affected girls. These rumours led to a highly"contagious" process and mass involvement of close to 50additional cases.Phase two affected mainly six schools in Jenin and two

neighbouring villages and some of the residents in the area.Information spread by the mass media and local rumoursstrongly contributed to the propagation of the disease in theschools, after a latent period of about 4-5 days. Part of thisphase was a self-limited one occurring in an isolated

neighbourhood in Jenin and it was triggered off by a passingcar emitting smoke from probably a faulty exhaust pipe; itoccurred against a framework of consistent rumours aboutnoxious factors.The final phase was more disseminated, the predominant

triggering factors being rumours spread continuously by the

1474

media and superimposed, to a certain extent, by local

pressure.The epidemic ended abruptly when "vector" contact was

eliminated by closure of the schools.The correct management of a mass phenomenon requires,

besides its prompt identification, a calm and authoritativeapproach to the affected population. Firm and immediatereassurance, based on a positive diagnosis should dispel fearand a point of the utmost importance is the use of the massmedia to counter rumours about deliberate or incidentalintoxication.We thank the following for their help: Dr Y. Adler, Mr Y. Arad, Dr A. Avni,

Mr A. Eisenberg, Dr F. Liff, Dr I. Sever, Dr J. Shemeir, Dr I. Skolnick, andMrs M. Zmn.

Correspondence should be addressed to B. M., Chaim Sheba MedicalCenter, Tel Hashomer, Israel.

REFERENCES

1. Colligan MJ, Murphy LR. Mass psychogenic illness in organizations an overview. JOccup Psych 1979; 52: 77-90.

2. Acheson ED. The clinical syndrome variously called ’benign myalgicencephalomyelitis’, ’Iceland disease’, and ’epidemic neuromyasthenia’. Am J Med1959; 26: 569-95

3 Moss PD, McEvedy CP An epidemic of overbreathing among schoolgirls. Br Med J1966; ii. 1295-300

4. McEvedy CP, Griffith A, Hall T. Two school epidemics. Br Med J. 1977; ii: 1300-025. Knight JA, Friedman TI, Sulianti J. Epidemic hysteria: a field study. Am J Pub Hlth

1965; 55: 858-65.6. Levine RJ, Sexton DJ, Romm FJ, Wood BT, Kaiser J. Outbreak of psychosomatic

illness at a rural elementary school. Lancet 1974; ii: 1500-03.7. Levine RJ. Epidemic faintness and syncope in a school marching band JAMA 1977;

238: 2373-76.8. Murphy LR, Colligan MJ. Mass psychogenic illness in a shoe factory a case report Int

Arch Occup Environ Hlth 1979; 44: 133-389. Colligan MJ, Urtes M-A, Wisseman C, Rosensteel RE, Anania TL, Hornung RW. An

investigation of apparent mass psychogenic illness in an electronics plant. J BehavMed 1970; 2: 297-309.

10. McEvedy CP, Beard AW. Royal Free epidemic of 1955: a reconsideration. Br Med J1970, i: 7-11.

1 1 Shelokov A, Habel K, Verder E, Welsh W. Epidemic neuromyasthenia: an outbreak ofpoliomyelitislike illness in student nurses. N Engl J Med 1957; 257: 345-55

12. Parish JG Early oubreaks of ’epidemic neuromyasthenia’. Postgrad Med J. 1978; 54:711-17.

13. Small CW, Nicholi AM. Mass hysteria among schoolchildren. Early loss as a

predisposing factor. Arch Gen Psychiatry 1982; 39: 721-24.14. Moffat MEK. Epidemic hysteria in a Montreal train station Pediatrics 1982; 70:

308-10.

15. Mohr PD, Bond MJ. A chronic epidemic of hysterical blackouts in a comprehensiveschool. Brit Med J 1982; 284: 961-62.

16. Small GW, Borus JF. Outbreak of illness in a school chorus: toxic poisoning or masshysteria. N Engl J Med 1983; 308: 632-35.

17. Landrigan PJ, Miller B. Epidemic acute illness. Lancet 1983; ii: 1474-76.

THE ARJENYATTAH EPIDEMICHome Interview Data and Toxicological Aspects

PHILIP J. LANDRIGAN BESS MILLER

National Institute for Occupational Safety and Healthand Center for Infectious Diseases, Centers for Disease Control,

Georgia, Atlanta, USA

Summary In 1983, 949 cases of acute non-fatal illnessconsisting of headache, dizziness, blurred

vision, abdominal pain, myalgia, and fainting occurred in theWest Bank. Physical examination and biochemical tests wereotherwise normal. There was no common exposure to food,drink, or agricultural chemicals among those affected. Notoxins were consistently present in patients’ blood or urine.Hydrogen sulphide gas was detected in low concentrations(40 parts per billion) at the site of the first outbreak. No otherenvironmental toxins were found. The illness was thus of

psychological origin and possibly triggered by the smell ofhydrogen sulphide.

INTRODUCTION

THE major diagnostic challenge posed by epidemics ofnon-fatal illness as discussed on p 1472’ is to determine whethersuch illness is of toxic or psychological origin.2,3 Radioannouncements and newspaper reports suggested that a

neurotoxin was widely suspected of having been the cause ofthe epidemic which occurred in March and April, 1983, inthe West Bank.4,5 However, clinical, epidemiological, andtoxicological studies suggested that the illness was

psychological in origin.

METHODS

Clinical and EpidemiologicalWe assessed the clinical and epidemiological features of the illness

by interviewing and examining patients with acute andrecrudescent symptoms in two of the more severely affectedvillages-at Arrabah in northern West Bank, where the firstcases had occurred, and at Yattah in the south, patients wereinterviewed and examined in hospital 2-12 days after onset ofillness. This exercise preceded the home interview survey. Thehome interviews at Arrabah began 18 days after onset of illness, andat Yattah 8 days after onset. Patients as well as unaffected

comparison subjects of the same age, ethnic background, and sex

residing in the same village were invited to participate. Both casesand comparison subjects were interviewed individually by Arabic-speaking, female interpreters using a standard questionnaire aboutsociodemographic status; clinical features of illness; antecedentexposures to food, water, and agricultural chemicals; and generalstate of health. Questions were derived from survey instrumentsdeveloped previously by the Centers for Disease Control. Duringthe interviews, venous blood samples were obtained from

approximately 10 patients and 10 comparison subjects at eachvillage for toxicological screening. Additional serum, urine, andwhole blood samples for toxicological analysis were obtained fromacutely ill patients admitted to Mukassad Hospital, Jerusalem, andfrom patients evaluated at Bir Zeit University.

ToxicologicalSerum samples were examined toxicologically at the Centers for

Disease Control (CDC), Atlanta, Georgia. Evaluations began withheadspace analysis to detect volatile organic compounds. Sampleswere heated to 37° C in a closed container, and the headspace gaseswere analysed by gas chromatography/mass spectroscopy (GC/MS)as well as by gas chromatography/electron capture detection

(GC/ECD). Samples were also subjected to high-pressure liquidchromatography (HPLC) to detect water-soluble compounds.Additionally, samples were extracted with hexane/ethyl ether, andthe extracts were analysed by (1) GC coupled with flame

photometric detection (FPD); (2) GC with flame ionisationdetection (FID); (3) GC/ECD; and (4) GC/MS. Urine samples wereacid hydrolysed and extracted; the resulting derivatives were

analysed by capillary GC/ECD. Whole blood samples were

screened for inorganic toxins by inductively-coupled argon plasmaatomic emission spectroscopy; results were compared with datafrom composite whole blood samples which were prepared at theCDC from stored specimens collected in the Hispanic Health andNutrition Evaluation Survey (HHANES), a survey of a

representative sample of the US Hispanic population.

Environmental

To evaluate possible exposures to environmental toxins, air

samples collected at outbreak sites were analysed, by methodsdescribed previously, for carbon monoxide, hydrogen sulphide(H2S), sulphur dioxide, total hydrocarbon content, oxides ofnitrogen, and methane. Also, for each location, a broad spectrum ofpotentially toxic gases was sought by the use of continuous infraredspectroscopy, scanning over wavelengths from 2 - 5 to 14-5 5 lim,Samples were obtained of environmental materials regarded by

local residents as possible sources of illness. These included yellowpowder from schoolyards, water, dust, dirt, schoolroom curtains,empty cola cans, powder from a glass jar found in a schoolyard, and