Outbreak of Acute Respiratory Febrile Illness Among College Students—Acapulco, Mexico, March 2001 FREE

MMWR. 2001;50:261-262

On March 30, 2001, CDC was notified by Pennsylvania Department of Health (PDH) of an acute respiratory febrile illness in 44 students from two colleges who traveled to Acapulco, Mexico, for spring break vacation during March 3-18. Within 7-14 days of their return from Acapulco, 21 students presented to health-care providers with illness characterized by fever, chills, dry cough, chest pain, and headache. Two students were hospitalized. On the basis of clinical symptoms and chest radiographs that revealed bilateral, nodular patchy infiltrates, acute pulmonary histoplasmosis was the suspected illness. While in Acapulco, most of the students stayed at the Calinda Beach Hotel and participated in group activities at other recreational locations.

All state health departments and selected travel agencies were notified to identify additional students who traveled to Acapulco during March and became ill. As of April 9, 37 colleges in 18 states* and the District of Columbia have reported 221 students who returned to the United States from Acapulco with an acute respiratory febrile illness. Ten students in six states were hospitalized.

A case is defined as an acute respiratory febrile illness characterized by fever for at least 3 days and one or more of the following symptoms: cough, shortness of breath, chest pain, or headache in a student who visited Acapulco during March 2001. Preliminary laboratory test results suggest histoplasmosis, an infection caused by Histoplasma capsulatum, a fungus that is present in soil in areas where the disease is endemic, and is acquired through inhalation. Gomori methenamine-silver stain of transbronchial and thoracic lymph node biopsy specimens from a hospitalized student revealed the presence of yeasts consistent with H. capsulatum. In addition, of specimens from 27 students in three states serologically tested for histoplasmosis using immunodiffusion and complement fixation tests, five were positive.¹ However, convalescent-phase serum specimens will be needed for confirmation. Testing continues for other possible causes (e.g., Mycoplasma, Legionella, and Chlamydia).

Pennsylvania Dept of Health. Council of State and Territorial Epidemiologists, Atlanta, Georgia. American College Health Association, Baltimore, Maryland. Mycotic Diseases Br, Respiratory Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases; and EIS officers, CDC.

CDC recommends that students who have traveled to Acapulco since March 1 seek medical care if they develop symptoms of fever and/or cough, shortness of breath, chest pain, or headache. Most cases of acute histoplasmosis in immunocompetent persons will not require treatment; however, persons with severe histoplasmosis can be treated with 200 mg of itraconazole, an antifungal medication, once daily for 6-12 weeks.² Physicians should notify state health departments of acute respiratory febrile illness among returning college students and other persons.

On April 3, PDH alerted other health departments of the outbreak through EPI-X (the Epidemic Information Exchange); on April 6, CDC issued a travelers' advisory at http://www.cdc.gov/travel/other/res-mexico-apr2001.htm. Information on histoplasmosis is available at http://www.cdc.gov/ncidod/dbmd/diseaseinfo. The Mexico Ministry of Health and CDC are conducting an investigation of the outbreak. Additional information is available from CDC, telephone (888) 688-2732. CDC's Mycotic Diseases Branch (MDB) is interested in receiving reports through state and local health departments of travelers to Acapulco since March who have become ill. MDB will test serum and lung tissue specimens for histoplasmosis received through state and local health departments.

References: 2 available

*Arizona, Connecticut, Delaware, Illinois, Indiana, Maryland, Massachusetts, Michigan, Missouri, New Jersey, New York, North Carolina, North Dakota, Ohio, Pennsylvania, Rhode Island, Texas, and Wisconsin.

MMWR. 2001;50:246-248

The Occupational Lead Poisoning Prevention Program (OLPPP) of the California Department of Health Services and a county health department investigated cases of lead poisoning in six furniture workers and their families in 1998. The investigation, initiated after a blood test of a worker's child revealed an elevated blood lead level (BLL), found that lead remaining in previously painted or coated stripped wood was carried from the workplace on clothes and shoes and was the source of the child's lead exposure and subsequent poisoning. Employers in industries in which workers restore or build using stripped wood should assess lead exposure and, when necessary, should establish a comprehensive lead safety program.

During a routine medical examination, the 18-month-old child of a worker received a BLL test at his mother's request. The result, 26 µg/dL, met the CDC-recommended criterion for a lead poisoning case requiring clinical management (i.e., BLLs ≥20 µg/dL).¹ A county public health nurse conducted a home visit and arranged blood testing of other family members. Laboratory tests revealed that the father, who worked for a company that refinished antique furniture, had a BLL of 46 µg/dL and his 4-month-old daughter a BLL of 24 µg/dL.

The nurse contacted OLPPP, the state program that provides follow-up for occupational lead poisoning cases. An OLPPP industrial hygienist interviewed the employer who described the process for repairing and restoring wood furniture. Before arriving at the shop, the furniture was chemically stripped of all paint or coatings and was believed to be free of lead. Four carpenters made necessary repairs using power tools such as saws and planers. In an adjacent outdoor courtyard, two refinishers smoothed the wood using manual and power sanders, washed the furniture, and applied wax. Workers routinely ate and drank in work areas, wore no protective equipment, and returned home in work clothes and shoes.

OLPPP instructed the employer to provide BLL and zinc protoporphyrin testing for the six workers and encouraged testing through the county of six family members who might have been affected by lead toxicity. All six workers had elevated BLLs: the two refinishers had BLLs of 29 and 54 µg/dL, and the four carpenters had BLLs of 46, 46, 47, and 56 µg/dL. The Occupational Safety and Health Administration lead regulation requires employees with BLLs ≥40 µg/dL to receive a medical examination, additional laboratory testing, and follow-up.² Five of the six family members, aged 7-12 years, did not have elevated BLLs; however, a 7-month-old infant, whose father's BLL was >40 µg/dL, had a BLL of 16 µg/dL; it was 15 µg/dL on retesting 30 days later.

OLPPP recommended that the employer establish a comprehensive lead safety program that included exposure monitoring, good hygiene practices, medical examinations, protective clothing, respiratory protection, safe dust clean-up methods, and training. The employer arranged personal exposure monitoring and surface wipe sampling for lead and implemented workplace improvements, including a respiratory protection program; use of HEPA vacuum-attached power sanders; use of a high-efficiency toxic dust HEPA vacuum; daily clean uniforms; separate storage lockers, changing area with showers, and lunch room; warning signs; safety training addressing take-home lead; and a lead medical surveillance program. Workers' BLLs declined after these steps were taken, and the average BLL decreased 15 µg/dL in approximately 3 months.

The nurse advised the affected families on cleaning residences and vehicles. At the residence of the index case, a wipe sample taken on a carpet where the worker played with his children showed a lead surface concentration of 30 µg/ft². After steam cleaning the carpet, the level was 14 µg/ft². This lead level on interior floors is below 40 µg/ft², the threshold level the Environmental Protection Agency has determined to be harmful.³ In addition to the take-home lead contamination, the investigation identified deteriorated lead paint, which the landlord remediated. When the 4-month-old infant's BLL remained elevated several months later, more thorough testing of painted surfaces was performed, and the landlord was required to remediate additional lead painted surfaces. The infant's BLL then decreased steadily.

B Materna, PhD, Occupational Lead Poisoning Prevention Program, California Dept of Health Svcs. Div of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, CDC.

Exposure to lead in paints and coatings is a known health risk, and recommendations have been made to prevent exposure.^4,5 This investigation revealed that wood chemically stripped of lead-containing coatings can retain harmful amounts of lead. The process of alkaline stripping can cause lead to migrate from the paint layer into the pores of the wood substrate.⁶ Although the wood appears uncoated, sufficient airborne lead dust is released while using power and hand tools to cause surface contamination and elevated BLLs in workers.⁷

Employers in industries that sand or otherwise disturb lead-impregnated stripped wood (e.g., furniture refinishing and construction) may be unaware of the risk for lead exposure and therefore may not be taking adequate precautions. Public health agencies that address lead issues should send hazard alerts to trade associations and employers in the affected industries. The incident in this report illustrates that industries that handle chemically stripped wood need to comply with lead safety measures, including exposure assessment and control, provision of work clothing and shoes, good hygiene and workplace housekeeping practices, employee training, and medical surveillance. This incident also underscores that a thorough investigation of a childhood lead poisoning case should consider the occupations of adults in the household. Where take-home lead is suspected, BLL tests of the adults can help to confirm workplace exposure. Follow-up at the work-site, including screening of other workers and their young children, can identify others at risk.

References: 7 available

MMWR. 2001;50:265-268

West Nile virus (WNV), a mosquitoborne arbovirus identified in New York in 1999, has become enzootic in the northeastern United States, affecting humans, birds, horses, and other mammals. Although no human WNV infection was identified in Connecticut or New Jersey in 1999, 62 persons with WNV illness, including seven deaths, were detected in New York City (NYC) and nearby New York counties.¹ In 2000, these jurisdictions implemented active surveillance (AS) and enhanced passive surveillance (EPS)* to detect human illness; 21 persons were identified with acute WNV infection (14 in New York, six in New Jersey, and one in Connecticut), including two deaths (one each in New York and New Jersey).² This report summarizes the human WNV surveillance systems in Connecticut, New Jersey, New York, and NYC and recommends EPS for hospitalized patients with encephalitis of unknown etiology for the continental United States.

The Connecticut Department of Public Health (CTDPH) implemented EPS statewide during April 1-October 31, and AS in two southwestern counties during July 1–October 31. Surveillance criteria included all hospitalized patients with encephalitis, meningo-encephalitis, or Guillain-Barre syndrome (GBS) with fever; in August, criteria were expanded to include hospitalized aseptic meningitis patients aged ≥18 years. EPS consisted of monthly mailings to physicians and all acute-care hospitals to solicit reports of patients meeting surveillance criteria. In counties participating in AS, infection-control practitioners (ICPs) were asked to review emergency department and hospital admissions and report patients meeting surveillance criteria. ICPs were contacted weekly by CTDPH staff for follow-up on all reported patients. Serum and cerebrospinal fluid (CSF) specimens from all reported patients were tested for WNV-reactive IgM by enzyme-linked immunosorbent assays (ELISA) at the CTDPH laboratory.

During April 1–October 31, 235 patients were tested: 46 (20%) with encephalitis or meningoencephalitis, 44 (19%) with aseptic meningitis, and one (<1%) with GBS; 144 (61%) patients did not meet surveillance criteria but were tested at their physicians' requests. Of these 235 patients, one mildly symptomatic outpatient tested positive for WNV. Tested patients were not categorized by surveillance method.

The New Jersey Department of Health and Senior Services implemented EPS statewide during June 1-November 30, and AS in six counties near NYC during July 15–October 31. Surveillance criteria included all patients hospitalized for viral encephalitis, meningoencephalitis, or GBS and patients aged ≥17 years with aseptic meningitis. For EPS, public health staff distributed WNV fact sheets, surveillance criteria, and reporting instructions to health-care providers. For AS, ICPs in six counties reviewed emergency department and hospital admissions, surveyed physicians, and provided weekly fax reports of patients meeting surveillance criteria. ICPs and physicians were contacted weekly for follow-up on all reported patients. Serum and CSF specimens from patients who met the surveillance criteria were tested for WNV-reactive IgM and IgG by ELISA at the state's Public Health and Environmental Laboratory.

Of 55 patients tested, 18 (33%) had encephalitis, 15 (27%) had meningoencephalitis, 19 (35%) had aseptic meningitis, and three (6%) had GBS. Six patients had laboratory evidence of WNV infection; five (83%) were identified through EPS and one (17%) through AS.

The New York City Department of Health (NYCDOH) implemented EPS citywide during May 1–November 25, active physician-based surveillance (APS) during June 1–September 30, and active laboratory-based surveillance (ALS) during July 1–September 30. Surveillance criteria included all hospitalized patients with encephalitis, meningo-encephalitis, or GBS with fever or altered mental status and patients aged ≥17 years with aseptic meningitis. For EPS, public health staff provided surveillance criteria and laboratory testing information to health-care providers through medical rounds, biweekly alerts, and a special issue of the NYCDOH's medical bulletin. APS was conducted at 18 sentinel sites; infectious disease and critical-care specialists and neurologists and chief medical residents were contacted biweekly for reports of patients meeting surveillance criteria. Twelve sites participated in ALS; hospital microbiology laboratories submitted CSF specimen results with parameters suggesting viral etiology for testing on a weekly basis. APS and ALS sites were selected initially on the basis of 1999 WNV activity; additional sites were added during the season as increasing WNV activity in birds and mosquitoes was detected in Staten Island and south Brooklyn. All serum and CSF specimens were tested for WNV-reactive IgM by ELISA at the NYC Public Health Laboratory.

Of 512 patients tested, 205 (40%) had encephalitis or meningoencephalitis, 236 (46%) aseptic meningitis, 22 (4%) GBS, 41 (8%) other diagnoses, and eight (2%) unknown diagnoses; 56 (11%) did not meet surveillance criteria but were tested at their physicians' request. Fourteen NYC residents had WNV infection diagnosed; 11 (79%) infections were detected at APS hospitals and three (21%) at hospitals where only EPS was conducted. Two patients with WNV infection reported by physicians were identified simultaneously through ALS.

During May 1–October 31, the New York State Department of Health (NYSDOH) and local units conducted EPS statewide and AS in counties with WNV activity in humans, birds, mosquitoes, or horses in 1999 or 2000; in April, NYSDOH implemented commercial laboratory surveillance. Surveillance criteria included all patients with viral encephalitis or meningoencephalitis and patients aged ≥2 years with aseptic meningitis. EPS included distributing alerts that encouraged physician reporting and specimen submission instructions to all local health units. Suggested activities for local health units conducting AS included weekly contact with medical staff at sentinel acute-care hospitals about patients meeting surveillance criteria. Commercial laboratories licensed by NYSDOH to perform arbovirus testing participated in surveillance by reporting patients who tested positive for antibodies to arboviral panels. Serum and CSF specimens from reported patients were tested for WNV infection at the New York Wadsworth Laboratory; testing included WNV-reactive IgM and IgG by ELISA, polymerase chain reaction, and plaque-reduction neutralization.

Of 589 patients tested, 230 (39%) had encephalitis or meningoencephalitis, 191 (32%) had aseptic meningitis, 89 (15%) did not meet surveillance criteria, and 79 (13%) were missing data to determine clinical status. Tested patients were not categorized by surveillance method. Commercial laboratory surveillance identified four patients who had flavivirus antibodies; investigation by local health units for travel and vaccination history and additional WNV testing indicated that none had a current or nontravel-related flavivirus infection. No human WNV infection was identified in New York outside of NYC.

M Cartter, MD, D Mayo, PhD, R Nelson, DVM, L Wilcox, MPH, J Hadler, MD, State Epidemiologist, Connecticut Dept of Public Health. F Sorhage, VMD, B Wolf, MS, E Bresnitz, MD, State Epidemiologist, New Jersey Dept of Health and Senior Svcs. J Greenko, MPH, J Kellachan, MPH, B Edwin, I Poshni, PhD, M Layton, MD, New York City Dept of Health; G Johnson, G Lukacik, B Wallace, MD, C Huang, PhD, L Kramer, PhD, S Wong, PhD, P Smith, MD, State Epidemiologist, New York State Dept of Health. Arbovirus Diseases Br, Div of Vector Borne Infectious Diseases, National Center for Infectious Diseases; State Br, Div of Applied Public Health Training, Epidemiology Program Office; and EIS officers, CDC.

In 2000, public health jurisdictions used active and passive surveillance approaches based on staff and laboratory resources and degree of WNV activity identified by bird, mosquito, and mammalian surveillance. AS fostered ongoing communication between health departments and health-care providers but had variable yield. Eleven of 14 WNV-confirmed patients from NYC but only one of six in New Jersey were identified at AS hospitals. AS could have identified a higher proportion of WNV illnesses in NYC because the location of AS coincided with the epicenter of the outbreak (Staten Island). In comparison with AS, EPS was less labor intensive for health-care providers and health department staff, and intense public awareness of WNV in the northeast United States may have improved EPS effectiveness, resulting in increased reporting. However, EPS did not provide direct education about WNV to health-care providers, and in the absence of media and public interest, EPS may have missed reports of suspect illnesses. To plan future surveillance strategies, jurisdictions should evaluate the costs and yields of active and passive WNV surveillance efforts in upcoming transmission seasons.

All jurisdictions focused surveillance on severe WNV manifestations. Serologic studies suggest that approximately one in 150 infected persons develop neurologic disease requiring hospitalization.^2- 3 By monitoring patients with severe disease, the number of infected persons can be estimated; however, jurisdictions with few nonhospitalized human WNV infections may not be identified. Surveillance among patients with mild and nonspecific symptoms (e.g., fever and headache) probably would exhaust laboratory and staff resources.

Most states did not conduct WNV testing on pediatric patients with meningitis in summer months because they most likely represented enteroviral infections.⁴ In addition, most 1999 human infections were identified in older hospitalized patients. Therefore, studies during outbreaks should be considered to determine the spectrum of clinical illness and the extent to which children are affected.

In 2001, EPS for hospitalized patients with encephalitis of unknown etiology is recommended for the continental United States.⁵ All suspect WNV illnesses should be screened by testing CSF and appropriately timed acute and convalescent serum specimens for IgM ELISA antibody. Appropriately timed acute and convalescent serum samples should be tested for a four-fold or greater rise in WNV-specific neutralizing antibody. With the availability of commercial laboratory testing for WNV, jurisdictions are encouraged to identify patients with commercial laboratory reports indicative of recent WNV infection and to verify these results by viral-specific neutralizing antibody testing. Monitoring of milder illnesses (e.g., aseptic meningitis or GBS) depends on jurisdictions' resources and should be a lower priority. AS should be considered in areas with known WNV activity on the basis of bird and mosquito surveillance data. Jurisdictions in the northeastern, central, and western United States should begin human surveillance by June 2001 or earlier if other surveillance activities, such as avian mortality surveillance, demonstrate WNV activity. WNV could circulate throughout the year in some areas, especially the Gulf States; therefore, human surveillance should be considered year round in southern states. Because the ELISA and hemagglutination-inhibition test can be cross-reactive between WNV, St. Louis encephalitis, yellow fever, dengue, and Powassan viruses, patients who test positive for antibodies to these viruses should be tested for specific neutralizing antibody.

*AS = Health department-initiated contact with health-care providers to solicit reports; EPS = passive surveillance (i.e., health-care provider-initiated reports) enhanced by general alerts to key health-care personnel (e.g., primary-care providers, infectious disease physicians, and hospital infection-control personnel).