Background: We identified a cluster of LP cases in January 2009. Our 953 bed hospital does not provide care for transplant patients and had not previously identified a problem with healthcare-associated legionellosis (HCAL).
Objective: We describe our outbreak investigation and control measures.
Methods: We defined HCAL as lab-confirmed legionellosis in a patient hospitalized ≥10 days continuously prior to onset of illness (definite HCAL) or 2-9 days before onset (possible HCAL).
Results: Between 2006 and 2008, there were 11 laboratory confirmed cases of LP: 9 were community-acquired; there were no definite and 2 possible HCAL cases (1 in 2006, 1 in 11/08).
Between 1/21 and 1/30/09, 4 positive LP urine Ag tests were reported. We identified 3 patients and 1 HCW with HCAL (1 definite, 3 possible). The possible HCAL case from 11/08 was also considered part of this outbreak. All 5 LP cases had underlying disease and had been exposed to 1 of 2 vertically contiguous wards (X and Y) with a common air-handler dedicated to these areas. No other common exposures were identified.
Immediate measures included closure of wards X and Y, environmental cultures, surveillance for healthcare-associated pneumonia in patients and HCWs, and review of plumbing/HVAC records.
Initial cultures (n=250) were positive from 100% hot and ≥ 40% cold water samples from wards X and Y, but also from 4 “control” wards located in the main hospital. Cooling towers, hydrotherapy, water from the adjacent building, and ice machines were negative. Plumbing changes in 10/08 after the failure of a water heater in the main hospital included cross-connections between galvanized pipes (> 50 yrs old) and copper pipes (15 yrs old). Excessively high water pressures were documented in some areas due to problems with recirculation.
The finding of widespread LP contamination led to immediate cessation of potable water use. We then installed 0.2 micron water filters on all showers and faucets in the main hospital to allow resumption of normal water use pending remediation. System upgrades included installation of tankless water heaters and 2 chlorine dioxide (ClO2) water treatment systems, removal of cross-connections, and rebalancing of the hot water system.
The frequency and median concentration of LP in hot water samples decreased significantly from 3/09 to 5/09 (58% pos.[ median >100 cfu/ml] vs 11% pos. [median 15 cfu/ml]).
No further cases of HCAL were identified after January 2009.
Conclusions: An outbreak of LP occurred after plumbing changes which disturbed hot water recirculation and connected older galvanized pipes with newer plumbing. Higher water pressures on wards X and Y may have contributed to the association of HCAL with those areas. Employing point of use water filters was instrumental to our ability to continue to provide safe patient care while addressing this significant water contamination.