LEGIONELLA, SPRINGTIME AND POTTING SOIL

B de Jong ()1, P Zucs1

1. European Centre for Disease Control and Prevention, Stockholm, Sweden

Citation: de Jong B, Zucs P. Legionella, springtime and potting soils. Euro Surveill. 2010;15(8):pii=19497. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19497

Date of submission: 25 February 2010

Legionnaires’ disease has been named after the outbreak in Philadelphia 1976 when a mysterious pneumonia affected a large number of members of the American Legion, a United States military veterans association, which held a gathering at a hotel [1]. Legionella, the bacterium causing the disease was identified several months after this outbreak for the first time. Today we know that there are about 50 different species of Legionella and that not all of them seem to be pathogenic to humans. The vast majority of reported cases are infected with L. pneumophila by inhalation of aerosols (water droplets) containing the bacteria, which is the route of infection for most Legionella cases. This is also described in an article by Joseph and Ricketts in this issue [2]. 

However, in some instances cases are infected by other Legionella species. A second paper in this issue describes a possible association between handling potting soil and infection with L. longbeachae [3]. As pointed out by the Scottish authors, this has long been well known and documented in Australia and New Zealand. In a soil survey performed in 1989 to 1990 in Australia, 33 (73%) of 45 potting soil samples tested positive for Legionella; 26 (79%) of the 33 contained L. longbeachae [4].
On their homepage, the Auckland Regional Public Health Service as well as the other public health services in Australia and New Zealand offers the following advice on how to minimise the risk of contracting legionellosis [5]:

• Take care when dealing with compost, potting mix and any form of soil or dirt. Read the warning labels on commercially available bags of compost and potting mix.
• To minimise risk, avoid stirring up dust, avoid inhaling dust, dampen the soil/compost before use, wear a dust mask that fits tightly over nose and mouth.

As the Scottish paper indicates, these recommendations may nowadays also be valid in Europe. Cases of L. longbeachae infections often appear as single cases and it could prove difficult to find a link with a commercial potting soil.
According to Steele et al., potting soils are made from different products [4].  In Australia, they tend to consist of composted waste products such as sawdust and hammer milled bark while in Europe peat moss is a major component. It is indicated that the use of different products emanating from wood could facilitate the occurrence of different Legionella bacteria in potting soil. In some parts of Europe, potting soils have bark soil as a component. However, studies from Switzerland have shown that Legionella spp. could also be present in potting soil containing peat moss [6].
Spring will soon come, and with the milder temperatures and increasing amounts of sunlight, gardeners all over Europe will start planting seeds and growing flowers and vegetables. These activities may involve contact with different potting soils and their dust, possibly giving rise to Legionnaires’ disease. In this light of spring, cases should not only be questioned about their travel history and contact with aerosols but also if they have had any contact with potting soils or done any gardening.  

Clinicians seeing patients with atypical pneumonia should be aware that the Legionella urinary antigen test is only valid for detection of Legionella pneumophila serogroup 1 and therefore other samples should be collected from the patient and submitted to the laboratory in order to be able to identify the causative agent.
In order to be able to estimate how many cases of Legionnaires’ disease in Europe are attributable to potting soil, more clinical samples and samples from incriminated potting soils should be cultured. Besides gaining new insight into the epidemiology of this serious disease, the source of each infection could be traced, thus reducing the risk of subsequent cases occurring.

References

1. Fraser DW, Tsai TR, Orenstein W, Parkin WE, Beecham HJ, Sharrar RG, et al. Legionnaires’ disease: description of an epidemic of pneumonia. N Engl J Med. 1977;297(22):1189-97.


2. Joseph CA, Ricketts KD, on behalf of the European Working Group for Legionella Infections. Legionnaires’ disease in Europe 2007–2008. Euro Surveill. 2010;15(8):pii=19493. Available from: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19493


3. Pravinkumar SJ, Edwards G, Lindsay D, Redmond S, Stirling J, House R, et al. A cluster of Legionnaires’ disease caused by Legionella longbeachae linked to potting compost in Scotland, 2008-2009. Euro Surveill. 2010;15(8):pii=19496. Available from: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19496


4. Steele TW, Moore CV, Sangster N. Distribution of Legionella longbeachae serogroup 1 and other Legionella in potting soils in Australia. Appl Environ Microbiol. 1990;56(10):2984-8.


5. Fact Sheet – Legionellosis. New Zealand: Auckland Regional Public Health Service (ARPHS). Available from: www.arphs.govt.nz/notifiable/downloads/legionellosis.pdf


6. Casati S, Giora-Martinoni A, Gaia V. Commercial potting soils as an alternative infections source of Legionella pneumophila and other Legionella species in Switerland. Clin Microbiol Infect. 2009;15(6):571-5.

Drug-Resistant Acinetobacter Infection Triples in U.S. Hospitals

Cases of a type of drug-resistant bacteria especially common among Iraqi war veterans have tripled in U.S. hospitals, researchers reported on Wednesday.
They found a 300% increase in cases of Acinetobacter that are resistant to imipenem.
"The findings are troubling because they suggest this bacteria is becoming resistant to nearly everything in our arsenal," said Ramanan Laxminarayan of Resources for the Future, a think-tank examining the issue.
He and his colleagues reported on drug-resistant Acinetobacter in Infection Control and Hospital Epidemiology. Their data came from 300 hospitals around the United States.
"There is a lot of attention on MRSA, but less on infections caused by bacteria like Acinetobacter for which there are fewer drugs in the development pipeline," Laxminarayan said.
Infection Control and Hospital Epidemiology 2009.

26 deaths for every 100,000 cases of swine flu


(Research: Mortality from pandemic A/H1N1 2009 influenza in England: public health surveillance study)

http://www.bmj.com/cgi/doi/10.1136/bmj.b5213

New data, published today on bmj.com, reveal that there were 26 deaths out of every 100,000 cases of swine flu in England (a fatality rate of 0.026%). The authors conclude that “the first influenza pandemic of the 21 st century is considerably less lethal than was feared in advance.” However, they emphasise that this is not a justification for public health inaction when death, serious illness and admission to hospital can be prevented.

This paper will be published on bmj.com at 15:00 hrs UK time, Thursday 10 December, to coincide with the Department of Health’s weekly H1N1 update, hosted by the Chief Medical Officer for England , Sir Liam Donaldson.

After the pandemic was announced, from June 2009 the Department of Health in England compelled all primary care trusts and acute hospitals to collate data on individuals who were believed to have died from swine flu. Today’s study is the first analysis of this material and includes all known deaths in England from swine flu up until 8 November 2009. The research, which was carried out by Sir Liam Donaldson’s research team, reveals that two thirds of the patients who died (66.7%) from swine flu would now be eligible for vaccination. The authors say that this demonstrates the importance of getting high risk groups vaccinated. Donaldson and his team also argue that there is a case for extending the vaccination programme to the wider population given that a substantial minority (38%) of deaths occurred in non-high risk groups.

While the over 65’s had less chance of contracting swine flu, the study reveals that this group were more likely to die from the disease if they developed it. The authors argue that perhaps older people were less likely to become infected with swine flu because they had already been exposed to similar strains and that “without this previous exposure, the pandemic might have caused many more deaths in this age group.” The researchers say their fatality rate estimate compares well with the other three 20th century influenza pandemics – the rate for the 1918 Spanish flu was 2-3% and subsequent pandemics (1957-8 and 1967-8) had rates of around 0.2%.

Donaldson argues that “improvements in nutritional status, housing and health care availability might explain some of the apparent decrease in case fatality from one pandemic to the next” and that “since the most recent pandemic there have been major advances in intensive care medicine.” The authors conclude that “many more patients may have died in England without the ready availability of critical care support, including mechanical ventilation.”

Contacts:
Liam Donaldson, Chief Medical Officer for England, Department of Health, Richmond House, London, UK 
Tel (via Kate Pike or Peter Graham): +44 (0)20 7210 5703
Out of hours: +44 (0)7050 073 581 (DH duty press officer)

Chikungunya fever: an old disease re-emerges

The new era of globalization and environmental change has witnessed the arrival of many new and re-emerging diseases which create new challenges for policy makers and researchers working on infectious diseases. Massive urbanization has facilitated the spread of contagious diseases in human populations due to faster travel over greater distances and worldwide trade. Although more affluent countries are better-equipped to manage the spread and treatment of infectious diseases, it has become increasingly clear that they still face major challenges when dealing with diseases whose boundaries have been expanding due to warmer and wetter weather. A good example of such an abrupt increase in the incidence of disease are infections caused by arboviruses, whose expansion to new geographic areas has been facilitated by the establishment of new vectors. The Chikungunya outbreaks in late 2005 represent a fine example of how a virus originally from Africa and mosquitoes originally from Asia can meet in the Indian Ocean and contribute to re-emergence of a disease, and then spread to other parts of the world.

Chikungunya fever - Re-emergence of an old disease. Lisa F.P. Ng, David M. Ojcius. Microbes and Infection, Volume 11, Issues 14-15, December 2009, Pages 1163-1164

Lipid Factors From Common Bacteria Could Trigger Multiple Sclerosis

Current research suggests that a common oral bacterium may exacerbate autoimmune disease. The related report by Nichols et al, “Unique Lipids from a Common Human Bacterium Represent a New Class of TLR2 Ligands Capable of Enhancing Autoimmunity,” appears in the December 2009 issue of The American Journal of Pathology.

Multiple sclerosis (MS), a disease where the immune system attacks the brain and spinal cord, affects nearly 1 in 700 people in the United States. Patients with multiple sclerosis have a variety of neurological symptoms, including muscle weakness, difficulty in moving, and difficulty in speech.

Porphyromas gingivalis, a common oral bacterium in humans, produces a unique type of lipid, phosphorylated dihydroceramides (DHCs), which enhance inflammatory responses. These lipids are also likely produced by bacteria found in other parts of the body including the gastrointestinal tract. To determine if these lipids accentuate immune-mediated damage in autoimmune disease, researchers led by Robert B. Clark and Frank C. Nichols of the University of Connecticut Health Center administered phosphorylated DHCs in a mouse model of MS. The severity of disease was significantly enhanced by the addition of these lipids in a manner that was dependent on activation of the immune system. These data suggest that phosphorylated DHCs from bacteria commonly found in humans may trigger or increase the severity of autoimmune diseases such as multiple sclerosis.

The authors state that “while it is clear that the immune system in most individuals has the potential to attack self-tissues, the “tipping” factors that initiate and propagate autoimmune diseases such as multiple sclerosis in only a subset of individuals remain unknown. Overall, [their] results represent the first description that phosphorylated DHCs derived from common human bacteria are capable of enhancing autoimmune disease.” Thus, these lipids may function as “tipping” factors, playing a previously unrecognized role in initiating or exacerbating human autoimmune diseases. In future studies, Dr. Clark and colleagues plan to characterize the effects of phosphorylated DHCs on specific cells of the immune system and to identify how and where these lipids are deposited in tissues throughout the body. In addition to the role of these lipids in triggering and worsening MS, the authors believe that phosphorylated DHCs may have the potential to serve both as new markers of MS disease activity and as new targets for therapeutic intervention.

Nichols FC, Housley W, O’Conor C, Manning T, Wu S, Clark RB: Unique Lipids from a Common Human Bacterium Represent a New Class of TLR2 Ligands Capable of Enhancing Autoimmunity. Am J Pathol 175: 2430-2438.This work was supported by grants from the National MS Society (RG4070-A-6) (RBC) and the Patterson Trust Foundation (FN). There is a provisional patent application pending for the use of bacterial phosphorylated dihydroceramides. This application pertains to Dr. Frank Nichols and Dr. Robert B. Clark.

Ljungan Virus: a Zoonotic Human Pathogen?

Ljungan virus (LV), a picornavirus, was discovered in the Swedish vole population after six clustered deaths from myocarditis were noted in orienteers between 1989 and 1992. Four of five sera from the orienteer patients had detectable antibodies against one of the LV isolates. Researchers tracked data about the population density of Swedish voles carrying LV and compared them to various disease incidences in humans in northern Sweden. Both animal and human data support the possibility that LV causes or contributes to diabetes, fetal death, fetal malformations, and sudden infant death syndrome. Current research has raised the question of the importance of this newly recognized zoonotic pathogen within rodent vectors. Evidence indicates that it would be prudent to consider LV infection in clinical practice, and LV will no doubt be the subject of upcoming intensive research.

Ljungan Virus: an Emerging Zoonosis? Anna Greene McDonald. Clinical Microbiology Newsletter, Volume 31, Issue 23, 1 December 2009, Pages 177-182

MRSA Strain on the Rise in Hospitals

Study Shows Community-Associated MRSA Is Spreading in Health Care Facilities. By Bill Hendrick, WebMD Health News.

A potentially dangerous and rapidly spreading strain of the "superbug" MRSA poses a much greater public health threat than previously thought, new research shows.

Community-associated MRSA (CA-MRSA) is spreading in hospitals and other health care facilities, according to a study in the December issue of Emerging Infectious Diseases. The CA-MRSA strain of superbug can be picked up in fitness centers, schools, and other public places, and is increasing the already significant burden of MRSA (methicillin-resistant Staphylococcus aureus) in hospitals, the researchers report. CA-MRSA and hospital-associated MRSA (HA-MRSA) are bacteria resistant to most common antibiotics.

HA-MRSA infections occur mostly in hospitals and other health care settings, including dialysis centers and nursing homes, and often strike mostly older adults, people having invasive medical procedures, and people with weakened immune systems. CA-MRSA is a leading cause of serious skin and soft tissue infections, entering the body through scrapes and cuts, the researchers say.

The study, which analyzed data from more than 300 microbiology labs across the U.S., found a sevenfold increase in the proportion of CA-MRSA in outpatients between 1999 and 2006. This community-associated strain is making its way into hospitals, the researchers say, increasing threats to patient safety because patients and their doctors move back and forth between inpatient and outpatient units of hospitals. "This emerging epidemic of community-associated MRSA strains appears to add to the already high MRSA burden in hospitals," Ramanan Laxminarayan, PhD, MPH, a senior fellow at Extending the Cure, a project at the Resources for the Future think tank in Washington, D.C., says in a news release. This major increase in CA-MRSA, the researchers say, has become a major concern.

Over the length of the study, the scientists report finding that the proportion of MRSA had increased more than 90% among outpatients with staph, and now accounts for more than 50% of all Staphyloccus aureus infections. This was due, the findings suggest, almost entirely to an increase in CA-MRSA strains. Similar increases in inpatients suggest these strains are spreading rapidly into hospitals. "MRSA has generally been a significant problem only in hospitals," says Eili Klein, MA, the lead author of the report and also a researcher at Resources for the Future. "But the findings from this study suggest there is a significant reservoir in the community as well." This suggests that the increased cases of CA-MRSA are causing that bug to spread from the community into hospitals, Klein says.

Hospitals need to take steps to stop this by stepping up infection control procedures, the researchers say, adding that the best way to contain MRSA and other superbugs is through surveillance and regular efforts aimed at infection control. "Community-associated methicillin-resistant Staphylococcus aureus has become a major problem in U.S. hospitals already dealing with high levels of hospital-associated MRSA," the researchers write. They conclude that "more rapid diagnostic methods are urgently needed to better aid physicians" in fighting MRSA.

SOURCES: News release, Emerging Infectious Diseases, Burness Communications. 

Klein, E. Emerging Infection Diseases, December 2009; vol 15.