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Outbreak of Pharyngoconjunctival Fever at a Summer Camp -- North Carolina, 1991

On July 19, 1991, the Communicable Disease Section of the North Carolina Department of Environment, Health, and Natural Resources (DEHNR) was notified that an outbreak of acute upper respiratory illness had occurred in campers and counselors at a 4-week summer camp. Manifestations of the illness included pharyngitis, cough, fever to 104 F (40 C), headache, myalgia, malaise, and conjunctivitis. On August 2, the DEHNR was notified of a similar outbreak during a second 4-week session at the camp. The epidemiologic investigation, initiated by the DEHNR on August 7, identified the cause as pharyngoconjunctival fever (PCF) associated with infection with adenovirus type 3. This report summarizes findings from the investigation.

The first camp session (June 16-July 12) was attended by 768 boys aged 7-16 years and 300 counselors aged 17-22 years. On July 12, first-session campers returned home, but counselors remained at the camp for the second session (July 14-August 9), which 800 boys attended. Approximately 700 persons swam each day in a 1-acre, manmade pond that had a maximum depth of 10 feet. Well water was continuously pumped into the pond at multiple sites through pipes located one foot below the surface of the water; the water overflowed, through a spillway, into an adjacent river. An automatic chlorination system treated the water before it entered the pond. The pond water was turbid, and plants grew in the bottom of the pond.

During the first session, 226 persons (175 campers and 51 staff members (i.e., counselors, administrative staff, and infirmary personnel)) visited the camp infirmary because of onset of symptoms of upper respiratory illness. During the second session, 369 campers and 86 staff members visited the infirmary with the same upper respiratory manifestations noted during the first session.

A convenience sample of 181 campers from the second session and 40 staff members at the camp was interviewed. A case of PCF was defined as two of four symptoms -- sore throat, fever, cough, and red eyes -- lasting more than 1 day. The attack rate for those surveyed was 112 (52%) (88 campers (Figure 1) and 24 staff members) of 216; duration of illness was unknown for five persons.

Every camper swam at least once during the 4 weeks; 158 (90%) of 175 swam one or more times per day. The attack rate for campers who swam daily (74 (48%) of 153) did not differ significantly from that for campers who swam less than once per week (11 (65%) of 17 (relative risk (RR)=0.8; 95% confidence interval (CI)=0.5-1.3)). The attack rate for staff who swam was higher than that for staff who did not swim (10 (77%) of 13 versus 13 (54%) of 24 (RR=1.4; 95% CI=0.9-2.3)) and increased with increased frequency of swimming. The attack rate for nonswimmers was 54% (13 of 24); for infrequent swimmers (i.e., those who swam once per week or less), was 75% (six of eight); and for frequent swimmers (i.e., those who swam three or more times per week), was 80% (four of five). Of the 221 campers and staff members interviewed, 75 (41 campers and 34 staff members) reported whether they had shared a towel with another person. Towel sharing increased the risk for illness (11 of 12 who shared versus 31 of 63 who did not (RR=1.9; 95% CI=1.4-2.5)).

Of viral cultures (nasopharyngeal and throat swabs) obtained from 25 ill persons, 19 grew adenovirus serotype 3. Convalescent geometric mean titers (GMT) to adenovirus for persons with cases during sessions one and two (GMT 14 and GMT 28, respectively) were each significantly higher (p less than 0.01) than the GMT of persons not meeting the case definition (GMT 6). Bacterial analysis of grab samples of water obtained from the pond yielded 80 colonies per 100 cc of fecal coliforms, 200 colonies per 100 cc of enterococcus, and 9000 colonies per 100 cc of staphylococcus. A concentrated sample of pond water drawn approximately 6 feet below the surface yielded adenovirus serotype 3. Residual chlorine was not detectable.

One week after the end of the second session the pond was drained, and most counselors left. No further outbreaks were reported following the second session; however, all subsequent sessions during the summer and fall were of maximum 1-week duration.

Reported by: NS McMillan, SA Martin, MD; MD Sobsey, PhD, DA Wait, MS, Univ of North Carolina School of Public Health, Chapel Hill; Virology/Serology Section, Virology Culture Section, North Carolina Laboratory of Public Health; RA Meriwether, MD, JN MacCormack, MD, State Epidemiologist, North Carolina Dept of Environment, Health, and Natural Resources. Respiratory and Enterovirus Br, National Center for Infectious Diseases; Div of Field Epidemiology, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: The illness described in this outbreak is consistent with PCF, a syndrome caused by adenovirus (especially serotypes 3 and 7) (1). As in previous reports (2,3), three routes (person to person, fomites, and water contact) probably transmitted virus in this outbreak.

Because of the turbidity of water in soil-bottom reservoirs, chlorination is ineffective. Turbid water contains organic molecules (e.g., humic and fulvic acids from plant decay) that react with chlorine, generating trihalomethanes (THM), especially chloroform (4,5); THM molecules have no antiviral activity (5). Viruses may attach or embed in suspended particles in turbid water (5,6), and these virus-containing particles precipitate into the sediment on the bottom where they may remain viable in the cooler temperatures. The virus containing particles may become resuspended when the water is agitated by swimmers (6,7). Natural bodies of water may have inherent virucidal properties possibly related to certain species of bacteria (6,8). Consequently, chlorination of natural waters may actually slow elimination of virus from the water (6,8).

Outbreaks of both bacterial and viral diseases have been linked to swimming in streams and reservoirs. Although North Carolina monitors the microbiologic quality of streams and reservoirs, it does not regulate swimming in these waters; furthermore, there are no uniformly accepted microbiologic standards for swimming in streams and reservoirs. Regulation of swimming in these streams and reservoirs could be based on a variety of parameters such as swimmer density, water turbidity, or bacterial counts (e.g., fecal coliforms, fecal streptococcus, or staphylococcus).


  1. Monto AS. Acute respiratory infections. In: Last JM, ed. Maxcy-Rosenau preventive medicine and public health. 12th ed. East Norwalk, Connecticut: Appleton-Century-Crofts, 1986:147-54.

  2. Bell JA, Rowe WP, Engler JI, Parrott RH, Huebner RJ. Pharyngoconjunctival fever: epidemiological studies of a recently recognized disease entity. JAMA 1955;157:1083-92.

  3. Sprague JB, Hierholzer JC, Currier RW II, Hattwick MAW, Smith MD. Epidemic keratoconjunctivitis: a severe industrial outbreak due to adenovirus type 8. N Engl J Med 1973;289:1341-6.

  4. Craun GF. Chemical drinking water contaminants and disease. In: Craun GF, ed. Waterborne diseases in the United States. Boca Raton, Florida: CRC Press, Inc, 1986:43-69.

  5. LeChevallier MW, Evans TM, Seidler RJ. Effect of turbidity on chlorination efficiency and bacterial persistence in drinking water. Appl Environ Microbiol 1981;42:159-67.

  6. Katzenelson E. Survival of viruses. In: Berg G, ed. Indicators of viruses in water and food. Ann Arbor, Michigan: Ann Arbor Science Publishers, 1978:39-50.

  7. Seyfried PL, Tobin RS, Brown NE, Ness PF. A prospective study of swimming-related illness. II. Morbidity and the microbiological quality of water. Am J Public Health 1985;75:1071-5.

  8. Berg G. Microbiology -- detection, occurrence, and removal of viruses. J Water Pollut Control Fed 1975;47:1587-95.

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