Epidemiologic Notes and Reports

The first reported common-source outbreak of Leptospira interrogans serotype grippotyphosa in the United States occurred in Tennessee in August 1975.

Seven children, 4 males and 3 females ranging in age from 11-16 years, had onset of illness in the period August 1-10, characterized by fever (7), headache (7), nausea and/ or vomiting (6), chills (5), myalgias (4) and abdominal pain (1). Five of the 7 were hospitalized; diagnoses included acute viral gastroenteritis (2), shigellosis (1), aseptic meningitis (1), and fever of unknown origin (1). The patient with the latter diagnosis underwent laparotomy because of suspected appendicitis. Another patient was treated as an outpatient for gastroenteritis, and 1 did not consult a physician. The median duration of illness was 14 days and the mean hospital stay of the hospitalized patients was 6.6 days. Laboratory findings on the 5 hospitalized patients included either minimal pyuria (6-8 white blood cells per high power field) or proteinuria (trace to 1+) in 4 individuals and mildly elevated SGOT levels (range 93-131 IU/ml) in 3.

A specimen of cerebrospinal fluid which was obtained on admission from the patient with aseptic meningitis had a protein of 48mg%, glucose of 60mg%, and 180 white blood cells (WBC)/mm3 (predominantly lymphocytes). The total peripheral blood WBC counts were in the normal range for all 5 patients (4,800-10,400/mm3), but there was a definite shift to the left in 3.

All 7 patients had serologic evidence of recent infection with Leptospira interrogans serotype grippotyphosa. Urine for culture was obtained from 6 patients 16 to 25 days after onset of illness; all were negative for leptospires.

All 7 patients had swum in a local creek in the month preceding their illness. No other common source could be identified. A case-control study showed a definite association between acquiring leptospirosis and swimming in the creek. A questionnaire and serologic survey of 91 other people who had swum in the creek during the summer of 1975 failed to detect any additional cases.

Samples of the creek water taken for culture and for animal inoculation 4 weeks after the outbreak did not yield the organism. Serum specimens were obtained from 50 cattle in 5 of 7 herds pastured along the creek, but serologic testing did not implicate any herd. Wildlife was also

considered as a possible source of contamination. Limited trapping was unsuccessful; no wild animals were obtained for testing.

Reported by WW Prine, Jr, MD, Clarkesville; PF Wright, MD, Vanderbilt University; EP Cutter, MD, Montgomery County Health Dept; J Holt, RN, Stewart County Health Dept; RH Hutcheson, Jr, MD, State Epidemiologist, Tennessee Dept of Public Health; Field Services Div, and Bacterial Zoonoses Branch, Bacterial Diseases Div, Bur of Epidemiology, CDC.

Editorial Note: Because of the prominent gastrointestinal illness and because of failure to incriminate a bacterial pathogen, the outbreak was initially believed to have a viral etiology. Leptospirosis was considered only after the initial epidemiologic investigation incriminated swimming in the stream as the only common factor shared by all 7 patients. Common-source leptospirosis outbreaks due to grippotyphosa have been frequently reported in Europe (1). Although prominent gastrointestinal illness can occur with infection by other serotypes, abdominal forms of the disease are considered to be particularly common with grippotyphosa infections (1).

Reference

1. Alston JM, Broom JC: Leptospirosis in Man and Animals. Edinburgh and London, E&S Livingstone Ltd., 1958, pp 150-155

With this issue the Morbidity and Mortality Weekly Report (MMWR) adopts a new format. In addition to the graphic changes, issues are now dated according to the release date; week-ending dates are still given on the tables, however. In addition, Table I, formerly entitled "Cases of Specified Notifiable Diseases: United States," has been moved permanently to the inside front page and renamed "Summary-Cases of Specified Notifiable Diseases: United States." Table II, "Notifiable Diseases of Low Frequency," appears on the same page. Circulation and editorial information, formerly displayed on the back page, now appears below Table IV.

U.S.MAIL

lication No. (CDC) 76-8017

421S

POSTAGE AND FEES PAID U.S. DEPARTMENT OF HEV

HEW 399

Epidemiologic Notes and Reports

In November 1975, symptoms and signs of lead toxicity were seen in workers in a secondary lead smelter in Memphis, Tennessee. Evidence of excessive lead absorption was also found in 50 of 102 workers' children, the parent's contaminated clothing apparently being the source of exposure. Seven children required hospitalization and chelation therapy. In January 1976, the plant was temporarily closed and efforts begun to reduce exposure to workers and their families.

Fifty-three (68%) of 78 workers tested had blood lead levels 60ug/100ml, the range considered by the National Institute for Occupational Safety and Health (NIOSH) to represent unacceptable lead absorption posing a risk to health (1). Thirty workers (36%) had 2 or more symptoms of lead poisoning, including abdominal pain, gastrointestinal dysfunction, muscular weakness, tremor, anorexia, joint pains, and fatigue. Peripheral neuropathy, indicated by weakness of wrist extensors, was seen in 10 workers. Anemia, defined as a hemoglobin level below 14gm/100ml, was seen in 11 workers. Anemic workers had significantly higher blood lead and erythrocyte protoporphyrin (EP) levels than nonanemic workers, thus identifying the anemia as lead-related (2). Elevations in blood urea nitrogen (BUN) above 20mg/100ml were seen in 6 employees (range, 2240mg/100ml).

Arsenic levels in urine were elevated (>100μg/liter when corrected to a specific gravity of 1.024) in 10 of 72 workers. Highest levels were seen in workers in the casting area where arsenic is added to molten lead

Fifty of 102 (49%) smelter workers' children had lead levels 30μg/100ml.* Seven of these 50 were hospitalized for chelation therapy because of lead levels >80μg/100ml and/or EP levels 190μg/100ml. Two infant children of smelter employees, both 4-month-old boys, had blood lead levels of 50 and 52μg/100ml, with EP values of 92 and 185μg/100ml, respectively.

*A lead level >30ug/100ml in children is indicative of excessive absorption; a lead level >80ug/100ml or an EP level 190ug/100ml blood represents excessive absorption which necessitates immediate medical attention (3).

This frequency of elevated blood lead levels differs strikingly from levels in children elsewhere in the Memphis area, as determined by the Memphis-Shelby County Health Department's Childhood Lead Screening Program. In the census tract adjacent to the smelter, 13 (6%) of 228 children 1-5 years old had blood lead levels 30ug/100ml. In another socioeconomically similar industrial area of Memphis having no lead production facility, 38 (12%) of 307 children had lead levels >30ug/100ml.

Reported by G Lovejoy, MD, TA Taylor, Memphis-Shelby County Health Dept; M Frank, RH Hutcheson, Jr, MD, State Epidemiologist, Div of Communicable Disease Control, and R Wolle, Occupational and Radiological Div, Tennessee Dept of Public Health; Div of Technical Services and Div of Surveillance, Hazard Evaluation and Field Studies, NIOSH; Field Services Div, and Cancer and Birth Defects Div, Bur of Epidemiology, CDC.

Editorial Note: Members of workers' families associated with industries other than those dealing with lead have been known to become ill following exposure to toxic materials transported from factory to home on work clothing. Asbestosis (4), berylliosis (5), and chloracne (6) are examples of other occupational diseases transmitted in this fashion.

Such reports emphasize the importance of improved work practices and engineering controls not only in safeguarding worker health, but also in shielding families of workers from contact with toxic industrial materials.

References

1. Occupational exposure to lead: Proposed rulemaking. Federal Register 40:45934, Oct 3, 1975

2. Piomelli S, Davidow B, Guinne UF, et al: The FEP (free erythrocyte prophyrins) test: A screening micromethod for lead poisoning. Pediatrics 51:254-259, 1973

3. Center for Disease Control: Increased lead absorption and lead poisoning in young children, 1975

4. Anderson HA, Selikoff IJ, Lilis R, et al: Asbestos-related disease from household exposure to occupational dusts. Presented at the American Conference of Chest Physicians. New Orleans, Oct 2-4, 1974

5. Eisenbud M, Wanta RC, Dustan C, et al: Non-occupational berylliosis. J Ind Hyg Toxicol 31:282-294, 1949

6. Jensen NE, Sneddon IB, Walter AE: Chloracne: Three cases. Proc R Soc Med 65:687-688, 1972

Current Trends

Zoster Immune Globulin (ZIG), prepared from the plasma of healthy donors convalescing from herpes zoster, is again available for release. ZIG is an investigational drug (IND) and is only released when patients meet 5 criteria (Table 1).

A doctor who desires ZIG for his patient must contact one of the ZIG Consultants physicians located in different areas of the country cooperating with CDC on ZIG distribution - or the immunization division, CDC. If the pa tient meets the established criteria, and the physician and patient agree to comply with the conditions of the IND protocol, ZIG is released.

ZIG is currently in short supply and donors of Zoster Immune Plasma are needed. Anyone with knowledge of potential donors should contact:

Center for Disease Control

Attention: Dr. Robert Ellis

Building 1, Room B-237

Atlanta, Georgia 30333

(404) 633-3311, ext 3356

*Delayed Reports: TB: Mo. 6 (1975), delete 2 (1976); N. Car. delete 1; GC: Nebr. delete 8, Nev. 24, Guam 8; Syphilis: Nev. 1.