Monthly Archives: July 2011

The largest outbreak of Legionnaires’ Disease may be due to insufficient heating of hot water

Insufficient heating of the hot-water system in Miami Valley Hospital’s new 12-story addition was the primary reason for the largest outbreak of Legionnaires’ disease in Ohio since 2004, according to the hospital.


The outbreak of Legionnaires’ disease at the hospital in February and March highlights an unintended result of plumbing codes that could put vulnerable populations like hospital patients at risk.


In certain cases, an outbreak of Legionnaires’ disease can be an “unfortunate consequence of something that’s intended to protect public health,” said Dr. Lauri Hicks, a medical epidemiologist with the Centers for Disease Control and Prevention.


In an exclusive interview this week with the Dayton Daily News, hospital officials announced the cause of the outbreak, which sickened 11 patients and may have contributed to the death of one of those patients.


Prior to occupancy of the $135 million patient tower on Dec. 28, a construction team made sure the water that supplied showers and faucets was heated to no more than 120 degrees Fahrenheit, as required by the Ohio Plumbing Code, hospital officials said.


Hospital officials said they had planned to heat the water to 130 to 140 degrees, but were told to lower the water temperature to comply with code requirements, which are intended to prevent scalding.


“When the codes recommended a certain water temperature, those codes didn’t contemplate a vulnerable population” and its susceptibility to waterborne bacteria such as Legionella, said Jennifer Theibert, the hospital’s risk-management director. The acutely ill are more susceptible to contracting Legionnaires’ disease than the general population.


State codes like Ohio’s that require hospitals to keep water temperatures at 120 degrees are “irresponsible,” said Tim Keane, who was hired by Miami Valley Hospital after it detected its first cases of Legionnaires’ disease in late February.


“One of the primary drivers of Legionella in health care are codes,” Keane said.


Such codes aim to minimize the risk of scalding by requiring caps on water temperatures. But Keane claims the risk of hot water systems becoming colonized with Legionella bacteria is far greater than those associated with scalding.


Legionella bacteria begin to die at 108 degrees Fahrenheit, according to the CDC. But not all of those bacteria die at that temperature, and water typically begins to cool as it moves away from the heating source, the CDC’s Hicks said. In large buildings, the temperature can drop as much as 10 to 20 degrees in some parts of the hot water plumbing system. Consequently, “bacteria may be thriving in the pipes near the shower head, but not in the hot water heater itself,” Hicks said.


Miami Valley Hospital is now heating water in the entire hospital to 140 degrees, and has the ability to mix hot and cold water at faucets and other points where people come in contact with the water to reduce scalding risks.


The hospital also has installed a hyperchlorination system to “make sure this never happens to us again,” said Barbara Johnson, the hospital’s chief operating officer.


Reduced water flow in parts of the new addition’s plumbing system also contributed to the outbreak.


Legionella is found in most water sources, but is usually contracted by breathing in mist from water that contains high concentrations of the bacteria. Legionnaires’ disease is not contagious.


The hospital spent about $61,000 to eradicate Legionella from the hot water system. It declined to release both its report on the outbreak and a white paper summarizing what it’s learned.


The hospital has received inquiries about the outbreak from attorneys representing patients who had Legionnaires’ disease, but no legal action has been taken against the hospital, Theibert said.


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New Strategy Used By Legionnaires Disease Bacteria

Purdue associate professor of biological sciences Zhao-Qing Luo, foreground, and graduate student Yunhao Tan identified a new way in which bacteria modify healthy cells during infection. Shown on the computer screen are cells infected with a mutant strain of the bacteria Legionella pneumophila used in their research. (Purdue University photo/Mark Simons)

Purdue University biologists identified a new way in which bacteria hijack healthy cells during infection, which could provide a target for new antibiotics.

Zhao-Qing Luo, the associate professor of biological sciences who led the study, said the team discovered a new enzyme used by the bacterium Legionella pneumophila – which causes Legionnaires’ disease – to control its host cell in order to take up residence.

“Legionnaires’ disease is a severe form of pneumonia, and this finding could lead to the design of a new therapy that saves lives,” Luo says. “At the same time it also provides great insight into a general mechanism of both bacterial infection and cell signaling events in higher organisms including humans.”

Successful infection by Legionella pneumophila requires the delivery of hundreds of proteins into the host cells that alter various functions to turn the naturally hostile environment into one tailor-made for bacterial replication. These proteins tap into existing communication processes within the cells in which an external signal, such as a hormone, triggers a cascade of slight modifications to proteins that eventually turns on a gene that changes the cell’s behavior, he said.

“Pathogens are successful because they know how information in our cells is relayed and they amplify some signals and block others in order to evade the immune system and keep the cell from defending itself,” Luo says. “Despite our understanding of this, we do not know much about how the proteins delivered by the bacteria accomplish this – how they work. This time we were able to pinpoint an enzyme and see how it disrupted and manipulated a specific signaling pathway in order to create a better environment for itself.”

The signaling pathway involved was only recently identified, and the discovery by Luo and graduate student Yunhao Tan also provides a key insight into its process. A paper detailing their National Institutes of Health-funded work is published online in the current issue of the journal Nature.

The signaling pathway involves a new form of protein modification called AMPylation in order to relay instructions to change cell behavior and has been found to be used by almost all organisms, Luo said.

The bacterial enzyme discovered by the Purdue team, named SidD, reverses or stops the AMPylation process, he said.

“It had not been known before if the AMPylation signaling process was reversible or if it was regulated by specific enzymes,” Luo says. “Now we know that it is, and we have a more complete picture that will allow us to use it as a scientific tool to learn more about complex cellular processes. By being able to turn the signaling on and off, we can control different activities and detect mechanisms we wouldn’t see under normal physiological conditions.”

The bacterium affects the host cell’s functions differently during different phases of the infection process, tapping into signaling pathways to turn on and off certain natural cellular activities. SidD stops the AMPylation process four hours after the start of infection in order to reverse an earlier modification that would be detrimental to the cell if left in place, he said.

“During its process of infection, the bacteria can trigger reactions that can lead to the death of the host cell,” Luo says. “Of course this is not in the best interest of the bacteria because it would no longer be able to replicate and continue infection, so it has evolved mechanisms to neutralize such reactions and keep the host cell alive.”

Luo said further investigation of the structure and function of the SidD enzyme is needed to better understand its role in the infection process and its involvement in other cellular processes.

“The more we can learn about an infectious agent, the better equipped we will be to design a therapy to fight it,” he says. “Before a new antibiotic therapy can be created, we must understand the enzyme enough to find chemicals to inhibit its activity. Further, because the bacteria have coevolved with us for millions of years, they provide some of the best tools for us to understand the intricacy of cellular processes.”

Luo plans to further study SidD and investigate other proteins used by Legionella pneumophila bacteria.