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Between August 13 and December 15, 1987, a cluster of 20 cases of HenochSchönlein Purpura (HSP) involving children under 10 years of age was identified in Connecticut. In contrast, eight cases had been identified in the state during the first 7 months of the year. HSP is a vasculitis that involves the skin and other organ systems and primarily affects children.

The cluster was initially noted by a Hartford pediatric nephrologist who was consulted regarding eight children, four of whom became ill over a 2-week period. The Connecticut Department of Health Services then identified other cases by calling approximately 100 practicing pediatricians and members of all nine hospital pediatric departments in Hartford County. In addition, selected pediatric group practices and all teaching hospitals with pediatric or family practice training programs throughout the state were contacted.

Ten cases were identified in Hartford County, where case finding was the most intensive. Six of the ten patients lived in the city of Hartford and had onset of symptoms between October 15 and November 25 (attack rate for the city of Hartford, 2.9/10,000 children under 10 years of age). The other four lived in surrounding towns (0.5/10,000 children). Hispanic children accounted for five cases in Hartford County and had an attack rate more than five times that of either black or white children (Hispanic children, 4.0/10,000; black children, 0.8/10,000; white children, 0.5/10,000). The ten cases outside of Hartford County involved eight white and two Asian children. No confirmed cases were found in Bridgeport, a city with a demographic composition similar to Hartford's.

All 20 children had a rash characteristic of HSP. Sixteen children developed arthritis, 16 had abdominal pain, and at least five had microscopic hematuria. Ten children were hospitalized. None died or developed serious complications.

To increase case finding, a letter requesting reports of all cases seen since January 1, 1987, has been sent to all pediatricians and all family practitioners in the state. A statewide case-control study to identify risk factors for acquiring the illness is under way.

Reported by: M Rasoulpour, MD, Hartford Hospital, Hartford; M Cartter, MD, N Tolentino, MSPH,
P Mshar, JL Hadler, MD, MPH, State Epidemiologist, Connecticut Dept of Health Svcs.
Epidemiology Office, Div of Viral Diseases, Center for Infectious Diseases; Div of Field Svcs,
Epidemiology Program Office, CDC.

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES/PUBLIC HEALTH SERVICE

BAT MAR 23 1999

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Editorial Note: HSP is identified by a characteristic rash most prominent on the buttocks and legs and is often associated with arthritis of the knee or ankle, abdominal cramping, or hematuria (1). As in this outbreak, the prognosis for the disease is generally good. However, a small percentage of children develop chronic glomerulonephritis (1,2). The number of children in the United States with renal failure resulting from HSP is unknown; however, it has been estimated that HSP is the cause of renal failure for 15% of the children on dialysis in Europe (3).

Because HSP is not generally a reportable disease, the incidence of the disease in the United States is unknown. Series of cases in the literature indicate seasonal changes in the incidence; the largest number of cases usually occur in the winter (2,4). An extensive search of the literature did not reveal any previous reports of clusters of HSP or of a predilection for Hispanic or urban children. The etiology of HSP is unknown; however, it is believed to be caused by an immunologic response to a variety of different stimuli (5). In individual cases, it has been linked to foods (6), medicines (7), toxins (8), insect bites (9), and various infectious agents (10-13). Approximately two-thirds of the children in three large clusters of HSP reported symptoms of an upper respiratory infection during the month before onset (1,2,4). However, no agent was implicated as a cause of the symptoms.

State health departments are requested to notify the Epidemiology Office, Division of Viral Diseases, Center for Infectious Diseases, CDC, of any clusters of HSP. Investigation of clusters may identify agents responsible for causing HSP and may ultimately help in formulating strategies for prevention.

References

1. Allen DM, Diamond LK, Howell DA. Anaphylactoid purpura in children (Schönlein-Henoch syndrome): review with a follow-up of the renal complications. AMA J Dis Child 1960; 99:833-54.

2. Sterky G, Thilen A. A study on the onset and prognosis of acute vascular purpura (the Schoenlein-Henoch syndrome) in children. Acta Paediat (Upps) 1960;49:217-29.

3. Meadow R. Schönlein-Henoch syndrome. Arch Dis Child 1979;54:822-4.

4. Bywaters EG, Isdale I, Kempton JJ. Schönlein-Henoch purpura: evidence for a group A B-haemolytic streptococcal aetiology. Q J Med 1957;102:161-75.

5. British Medical Association. Henoch-Schönlein purpura. Br Med J 1977;1:190-1.

6. Ackroyd JF. Allergic purpura, including purpura due to foods, drugs and infections. Am J Med 1953;14:605-32.

7. Beeching NJ, Gruer LD, Findlay CD, Geddes AM. A case of Henoch-Schönlein purpura syndrome following oral ampicillin. J Antimicrob Chemother 1982;10:479-82.

8. Duell PB, Morton WE. Henoch-Schönlein purpura following thiram exposure. Arch Intern Med 1987;147:778-9.

9. Burke DM, Jellinek HL. Nearly fatal case of Schoenlein-Henoch syndrome following insect bite. AMA Am J Dis Child 1954;88:772-4.

10. Sussman M, Jones JH, Almeida JD, Lachmann PJ. Deficiency of the second component of complement associated with anaphylactoid purpura and presence of mycoplasma in the serum. Clin Exp Immunol 1973;14:531-9.

11. Gower RG, Sausker WF, Kohler PF, Thorne GE, McIntosh RM. Small vessel vasculitis caused by hepatitis B virus immune complexes: small vessel vasculitis and HBSAG. J Allergy Clin Immunol 1978;62:222-8.

12. Lefrere JJ, Courouce AM, Soulier JP, et al. Henoch-Schönlein purpura and human parvovirus infection [Letter]. Pediatrics 1986;78:183-4.

13. Bull PW, Scott JT, Breathnach SM. Henoch-Schönlein purpura associated with Legionnaires' disease. Br Med J 1987;294:220.

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During the period June-October 1987, Puerto Rico experienced an islandwide epidemic of acute hemorrhagic conjunctivitis (AHC). The public health surveillance system for conjunctivitis identified 31,772 cases; a peak of 13,347 cases was reported in September. By December 1987, the number of reported cases was returning to the background level. Further review of the surveillance data revealed an earlier islandwide outbreak of 18,500 cases of AHC from December 1986 to February 1987 (Figure 1).

Laboratory evidence indicates that Coxsackie virus A24 variant (CA24v) was responsible for the most recent epidemic. In September, CA24v was isolated from 17 of 22 cultures of eye swabs from acutely ill patients. Also in September, 13 of 17 patients with conjunctivitis seroconverted to CA24v. In addition, laboratory studies suggest that CA24v had been responsible for the earlier outbreak. Three of seven serum samples obtained from convalescent patients with onset of AHC during the period December 1986-February 1987 yielded antibodies to CA24v. None of the ten controls had antibodies to CA24v.

During the epidemic, the Puerto Rico Department of Health began a campaign to control AHC transmission. They disseminated information emphasizing the importance of good handwashing practices and of not sharing towels or medications. The health department also recommended that symptomatic children be excluded from school.

Reported by: D Guzman, MD, T Rosa, E Robles, E Rosado, J Villanueva, JD Jimenez, MD, JV Rullan, MD, Commonwealth Epidemiologist, Puerto Rico Dept of Health. Dengue Br, Div of Vector-Borne Viral Diseases; Respiratory and Enterovirus Br, Epidemiology Office, Div of Viral Diseases, Center for Infectious Diseases, CDC.

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Conjunctivitis - Continued

Editorial Note: Epidemics of AHC usually occur in tropical climates, are explosive in nature, and primarily affect low-socioeconomic areas. They ordinarily spread rapidly to the majority of a community within a few months (1). Transmission is usually person to person or through contact with fomites (e.g., contaminated towels). AHC epidemics in the tropics have been caused by CA24v, enterovirus 70 (EV70), and adenovirus 11 (Ad11). AHC that is caused by CA24v has an incubation period of 1 to 2 days and causes mild to severe symptoms of excessive tearing, redness, foreign body sensation, and palpebral swelling. Both eyes are usually affected, and some patients have subconjunctival hemorrhage and palpebral folliculitis. Recovery is most often complete within 7 days (1,2). AHC caused by EV70 has clinical and epidemiologic characteristics similar to those of CA24v-induced AHC; however, the percentage of patients with subconjunctival hemorrhage is usually higher. EV70-induced

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TABLE II. Notifiable diseases of low frequency, United States

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*Four of the 61 reported cases for this week were imported from a foreign country or can be directly traceable to a known internationally imported case within two generations.

TABLE III. Cases of specified notifiable diseases, United States, weeks ending
February 27, 1988 and February 28, 1987 (8th Week)

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