Sunday 11 December 2011

Legionnaires' Disease

View Strep or Sore Throat Slideshow Pictures Legionellosis is an infection that is caused by a bacterium.The bacterium thrives in the mist that is sprayed from air-conditioning ducts.The bacterium can infest an entire building.The illness takes two distinct forms: Legionnaires' disease and Pontiac fever.Legionnaires' disease is the more severe form and can be fatal.Pontiac fever is the far milder form of the illness.Symptoms of Legionnaires' disease include fever, chills, and a cough.At its worst, Legionnaires' disease can cause severe pneumonia and respiratory failure.Although antibiotics are effective for treatment, the most useful approach is prevention.

Legionellosis is an infection that is caused by the bacterium Legionella pneumophila. The disease has two distinct forms:




MedicineNet Doctors Pneumonia Pneumonia is inflammation of one or both lungs with consolidation. Pneumonia is frequently but not always due to infection. The infection may be bacterial, viral, fungal or parasitic. Symptoms may include fever, chills, cough with sputum production, chest pain, and shortness of breath.Diarrhea Diarrhea is a change is the frequency and looseness of bowel movements. Cramping, abdominal pain, and the sensation of rectal urgency are all symptoms of diarrhea. Absorbents and anti-motility medications are used to treat diarrhea.Headache Headaches can be divided into two categories: primary headaches and secondary headaches. Migraine headaches, tension headaches, and cluster headaches are considered primary headaches. Secondary headaches are caused by disease. Headache symptoms vary with the headache type. Over-the-counter pain relievers provide short-term relief for most headaches.Chronic Cough Chronic cough is a cough that does not go away and is generally a symptom of another disorder such as asthma, allergic rhinitis, sinus infection, cigarette smoking, GERD, postnasal drip, bronchitis, pneumonia, medications, and less frequently tumors or other lung disease. Treatment of chronic cough is dependant upon the cause.Fever Although a fever technically is any body temperature above the normal of 98.6 degrees F. (37 degrees C.), in practice a person is usually not considered to have a significant fever until the temperature is above 100.4 degrees F (38 degrees C.). Fever is part of the body's own disease-fighting arsenal: rising body temperatures apparently are capable of killing off many disease- producing organisms.ARDS (Acute Respiratory Distress Syndrome) Acute respiratory distress syndrome (ARDS) is a lung condition in which trauma to the lungs leads to inflammation of the lungs, accumulation of fluid in the alveolar air sacs, low blood oxygen, and respiratory distress. Causes of ARDS include: pneumonia, aspiration, severe blow to the chest, sepsis, severe injury with shock, drug overdose, and/or inflamed pancreas. Treatment for ARDS include extra oxygen, and/or medication.

Symptom Checker: Your Guide to Symptoms & Signs: Pinpoint Your Pain


Chronic Cough »

Chronic cough is a cough that persists. Chronic cough is not a disease in itself; rather it is a symptom of an underlying condition. Chronic cough is a common problem and the reason for many doctor visits.

Some common causes of chronic cough include asthma, allergic rhinitis, sinus problems (for example sinus infection), and esophageal reflux of stomach contents. In rare occasions, chronic cough may be the result of aspiration of foreign objects into the lungs (usually in children). It is very important to see a doctor who may order a chest X-ray if a chronic cough is present. The following are common causes of chronic coughing.

Cigarette smoking actually is the most common cause of chronic cough. Asthma is a disease of airways, resulting in difficulty breathing or wheezing often characterized by abnormal breathing...

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Cluster of travel-associated Legionnaires' disease in Lazise, Italy, July to August 2011

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How Legionnaires' bacteria proliferate, cause disease

ScienceDaily (Nov. 17, 2011) — A University of Louisville scientist has determined for the first time how the bacterium that causes Legionnaires' disease manipulates our cells to generate the amino acids it needs to grow and cause infection and inflammation in the lungs.

The results are published online on Nov. 17 in Science.

Yousef Abu Kwaik, Ph.D., the Bumgardner Endowed Professor in Molecular Pathogenesis of Microbial Infections at UofL, and his team believe their work could help lead to development of new antibiotics and vaccines.

"It is possible that the process we have identified presents a great target for new research in antibiotic and vaccine candidates, not only for Legionnaires' disease but in other bacteria that cause illness," he said.

According to the Centers for Disease Control and Prevention, Legionnaires' disease is a lung infection caused by the bacterium called Legionella. The bacterium got its name in 1976, when many people who went to a Philadelphia convention of the American Legion suffered from an outbreak of pneumonia of unknown causes that was later determined to be caused by the bacterium. Each year, between 8,000 and 18,000 people are hospitalized with Legionnaires' disease in the U.S. There is no vaccine currently available for it.

For two years, the researchers examined Legionella which is an intracellular bacterium that exists in amoebae in the water systems; it is transmitted to humans through inhalation of water droplets. Cooling towers and whirlpools are the major sources of transmission. The bacterium uses the amoeba's cellular process to "tag" proteins, causing them to degrade into their basic elements of amino acids. These amino acids are used by the bacteria as the main source of energy to grow and cause disease.

"The bacteria live on an 'Atkins diet' of low carbs and high protein, and they trick the host cell to provide that specialized diet," Abu Kwaik said.

The same process occurs in a host -- animal or human -- who inhales the bacterium and is diagnosed with Legionnaires' disease. However, the bacteria do not tag the proteins, but rather trick the host into tagging the proteins for degradation to generate the amino acids.

In the laboratory, Abu Kwaik and his team saw that by inactivating the bacterial virulence factor responsible for tricking the cell into tagging proteins for degradation in mice models, the pulmonary disease was totally prevented. This was totally due to disabling the bacteria from generating amino acids, he said.

The process was then reversed, and the disease became evident when the mice, infected by the disabled bacteria, were injected with amino acids to compensate for the inability of the altered bacteria.

"Bacteria need to live on high protein and amino acids as sources of nutrition and energy in order to replicate in a host. This is what causes pulmonary disease," Abu Kwaik said. "No one has known how they generate sufficient sources of nutrients from the host to proliferate. Our work is the first to identify this process for any bacteria that cause disease."

He added that the type of host infected does not appear to affect the process. "Whether in a single-cell amoeba or a multi-cellular mammal, Legionella seems to know what to do; the process is the same, and is highly conserved through evolution. By interfering with the bacterium's sources of nutrients, we can stop it from thriving and causing disease."

Examining nutrient sources for organisms with the goal of stopping them from acquiring nutrients is a relatively new arena of basic research that deserves further study, he said. "We went after the basics -- the food and energy source -- which are prerequisite for the bacteria to grow and cause disease. It is not a process that is well understood yet, but by first discovering how an organism gets nutrients by tricking the host into degrading proteins, and then interfering with that process, we can, in effect, starve it to death and prevent or treat the disease."

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The above story is reprinted from materials provided by University of Louisville.

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Journal Reference:

Christopher T. D. Price, Tasneem Al-Quadan, Marina Santic, Ilan Rosenshine, and Yousef Abu Kwaik. Host Proteasomal Degradation Generates Amino Acids Essential for Intracellular Bacterial Growth. Science, 17 November 2011 DOI: 10.1126/science.1212868

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.


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Correction for O'Connor et al., Minimization of the Legionella pneumophila genome reveals chromosomal regions involved in host range expansion [Correction]

MICROBIOLOGY Correction for “Minimization of the Legionella pneumophila genome reveals chromosomal regions involved in host …


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Legionella secreted effectors and innate immune responses

Legionella secreted effectors and innate immune responses - Luo - 2011 - Cellular Microbiology - Wiley Online LibrarySkip to Main Content

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PUBLICATIONSBROWSE BY SUBJECTRESOURCESABOUT US LOGIN Enter e-mail address Enter password REMEMBER ME NOT REGISTERED ?FORGOTTEN PASSWORD ?INSTITUTIONAL LOGIN > Home > Microbiology & Virology > Microbiology & Virology > Journal Home > Early View > Abstract JOURNAL TOOLS Get New Content Alerts Get RSS feed Save to My Profile Get Sample Copy Recommend to Your Librarian JOURNAL MENUJournal HomeFIND ISSUESCurrent IssueAll Issues FIND ARTICLES Early ViewAccepted Articles GET ACCESS Subscribe / Renew FOR CONTRIBUTORS Author GuidelinesSubmit an Article ABOUT THIS JOURNAL NewsOverviewEditorial BoardPermissionsAdvertiseContact SPECIAL FEATURES Virology Virtual Special IssueFaculty of 1000PostersWiley Job NetworkParasitology Virtual Special Issue You have free access to this contentLegionella secreted effectors and innate immune responsesZhao-Qing LuoArticle first published online: 10 NOV 2011

DOI: 10.1111/j.1462-5822.2011.01713.x

© 2011 Blackwell Publishing Ltd

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How to CiteLuo, Z.-Q. (2011), Legionella secreted effectors and innate immune responses. Cellular Microbiology. doi: 10.1111/j.1462-5822.2011.01713.x

Author Information

Department of Biological Sciences, Purdue University, 915 West State Street, West Lafayette, IN 47907, USA

*Correspondence: Zhao-Qing Luo,

*Correspondence: E-mail luoz@purdue.edu; Tel. (+1) 765 496 6697; Fax (+1) 765 494 0876.

Publication HistoryArticle first published online: 10 NOV 2011Accepted manuscript online: 11 OCT 2011 03:50AM ESTReceived 1 August, 2011; revised 3 October, 2011; accepted 5 October, 2011. SEARCH Search Scope All contentPublication titlesIn this journalIn this issue Search String Advanced >Saved Searches > SEARCH BY CITATION Volume: Issue: Page: ARTICLE TOOLSGet PDF (300K)Save to My ProfileE-mail Link to this ArticleExport Citation for this ArticleGet Citation AlertsRequest Permissions AbstractArticleReferencesCited By View Full Article (HTML) Get PDF (300K) Summary

Legionella pneumophila is a facultative intracellular pathogen capable of replicating in a wide spectrum of cells. Successful infection by Legionella requires the Dot/Icm type IV secretion system, which translocates a large number of effector proteins into infected cells. By co-opting numerous host cellular processes, these proteins function to establish a specialized organelle that allows bacterial survival and proliferation. Even within the vacuole, L. pneumophila triggers robust immune responses. Recent studies reveal that a subset of Legionella effectors directly target some basic components of the host innate immunity systems such as phagosome maturation. Others play essential roles in engaging the host innate immune surveillance system. This review will highlight recent progress in our understanding of these interactions and discuss implications for the study of the immune detection mechanisms.

View Full Article (HTML) Get PDF (300K) More content like this Find more content: like this article Find more content written by:Zhao-Qing Luo ABOUT USHELPCONTACT USAGENTSADVERTISERSMEDIAPRIVACYTERMS & CONDITIONSSITE MAP

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Saturday 10 December 2011

Tumor Necrosis Factor-alpha (TNFα) Blockers: Label Change - Boxed Warning Updated for Risk of Infection from Legionella and Listeria

including Remicade (infliximab), Enbrel (etanercept), Humira (adalimumab), Cimzia (certolizumab pegol), and Simponi (golimumab)

AUDIENCE: Rheumatology, Gastroenterology, Oncology

ISSUE: FDA notified healthcare professionals that the Boxed Warning for the entire class of Tumor Necrosis Factor-alpha (TNFa) blockers has been updated to include the risk of infection from two bacterial pathogens, Legionella and Listeria. In addition, the Boxed Warning and Warnings and Precautions sections of the labels for all of the TNFa blockers have been revised so that they contain consistent information about the risk for serious infections and the associated disease-causing pathogens.

Patients treated with TNFa blockers are at increased risk for developing serious infections involving multiple organ systems and sites that may lead to hospitalization or death due to bacterial, mycobacterial, fungal, viral, parasitic, and other opportunistic pathogens.

BACKGROUND: The class of TNFa blockers are used to treat Crohn's disease, ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, plaque psoriasis, and/or juvenile idiopathic arthritis.

RECOMMENDATION: The risks and the benefits of TNFa blockers should be considered prior to initiating therapy in patients with chronic or recurrent infection and patients with underlying conditions that may predispose them to infection. See the Drug Safety Communication for a listing of recommendations for healthcare professionals and patients, as well as a data summary.

Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA's MedWatch Safety Information and Adverse Event Reporting Program:

Complete and submit the report Online: www.fda.gov/MedWatch/report.htm
Download form or call 1-800-332-1088 to request a reporting form, then complete and return to the address on the pre-addressed form, or submit by fax to 1-800-FDA-0178
Read the MedWatch safety alert, including a link to the FDA Drug Safety Communication, at:

http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm270977.htm

Posted: September 2011



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Disease cases in Britain linked to travel

Published: Oct. 7, 2011 at 6:27 PM

LONDON, Oct. 7 (UPI) -- Nine cases of Legionnaire's disease in Britain have been linked to travel to the Greek island of Corfu since August, health authorities say.

The Health Protection Agency advising people to be aware of the symptoms of Legionnaire's disease -- which can lead to pneumonia and is sometimes fatal -- if they are traveling to the island, the BBC reported Friday.

"We are concerned that U.K. residents traveling to Corfu should be aware of this potential risk, however we are not suggesting that people change their holiday plans," Nick Phin of the Legionnaire's disease department at the HPA said.

The HPA cannot rule out a U.K. source of the infections and is still investigating, he said.

Symptoms may not appear until two weeks after infection and generally start as a "flu-like" illness, the HPA said, but the disease can be treated with antibiotics.


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Recovery of Legionella species from water samples using an internal method based on ISO 11731: suggestions for revision and implementation

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The htpAB operon of Legionella pneumophila cannot be deleted in the presence of the groE chaperonin operon of Escherichia coli

Gheyath K. Nasrallah,a Elizabeth Gagnon,a,* Dennis J. Orton,a,† Rafael A. Garduñoa,b aDepartment of Microbiology and Immunology, Dalhousie University, Sir Charles Tupper Medical Building, 7th Floor, 5850 College Street, Halifax, NS B3H 1X5, Canada.

bDepartment of Medicine — Division of Infectious Diseases, Dalhousie University, Dickson Building, 1276 South Park Street, Halifax, NS B3H 2Y9, Canada.

*Present address: Department of Microbiology and Immunology, The University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC V6T 1Z4, Canada

†Present address: Department of Pathology, Dalhousie University, Sir Charles Tupper Medical Building, NS B3H 1X5, Canada

Published on the web 27 October 2011.

Canadian Journal of Microbiology, 2011, 57:(11) 943-952, 10.1139/w11-086

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Pittsburgh pneumonia agent: direct isolation from human lung tissue. J. Infect. Dis. 141(6): 727-732 .Sadosky AB, Wiater LA, Shuman HA. 1993. Identification of Legionella pneumophila genes required for growth within and killing of human macrophages. Infect. Immun. 61(12): 5361-5373 .Sambrook, J., and Russell, D.W. 2001. Molecular cloning: a laboratory manual. 3rd ed. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, N.Y. Sandegren L, Andersson DI. 2009. Bacterial gene amplification: implications for the evolution of antibiotic resistance. Nat. Rev. Microbiol. 7(8): 578-588 .Sigler PB, Xu Z, Rye HS, Burston SG, Fenton WA, Horwich AL. 1998. Structure and function in GroEL-mediated protein folding. Annu. Rev. Biochem. 67(1): 581-608 .Singh B, Gupta RS. 2009. Conserved inserts in the Hsp60 (GroEL) and Hsp70 (DnaK) proteins are essential for cellular growth. Mol. Genet. Genomics 281(4): 361-373 .Taylor JS, Raes J. 2004. Duplication and divergence: the evolution of new genes and old ideas. Annu. Rev. Genet. 38(1): 615-643 .Towbin H, Staehelin T, Gordon J. 1979. Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications. Proc. Natl. Acad. Sci. U.S.A. 76(9): 4350-4354 .Viswanathan, V.K., and Cianciotto, N.P. 2001. Electroporation of Legionella species. In Electro-transformation of bacteria. Edited by N. Eynard and J. Teissie. Springer-Verlag Publications, Heidelberg, Germany. pp. 203–211. Young RA, Elliott TJ. 1989. Stress proteins, infection, and immune surveillance. Cell 59(1): 5-8 .Zhang J. 2003. Evolution by gene duplication: an update. Trends Ecol. Evol. 18(6): 292-298 .

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Legionella - Every Infection Preventionist's Dream—Or Is It?

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Update on Legionnaires' cluster in UK travellers returning from Corfu

The Health Protection Agency (HPA) has issued an update on the Legionnaire’s cluster – three further cases have now been confirmed, which brings the total to 12 confirmed cases in people who have travelled to Corfu since August.  Another three possible cases with travel history to Corfu are currently under investigation.

Laboratory tests have identified three different subtypes of Legionnella from the patients’ samples, suggesting that one common source is unlikely. In addition, detailed questioning of the people who became unwell has also failed to reveal a common source.

The HPA is continuing to advise people going on holiday to Corfu to be aware of the signs and symptoms of Legionnaires’ disease – please see the link below for details.  A briefing note was recently issued to GPs asking them to be alert to returning travellers from Corfu with relevant symptoms. 


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Friday 9 December 2011

How Legionnaires' bacteria cause disease

Published: Nov. 18, 2011 at 11:05 PM

LOUISVILLE, Ky., Nov. 18 (UPI) -- A bacterium that causes Legionnaires' disease manipulates cells to generate amino acids it needs to grow and infect the lungs, U.S. researchers say.

Yousef Abu Kwaik of the University of Louisville and his team said their work could help lead to development of new antibiotics and vaccines for the disease.

"It is possible that the process we have identified presents a great target for new research in antibiotic and vaccine candidates, not only for Legionnaires' disease but in other bacteria that cause illness," Abu Kwaik said in a statement.

For two years, the researchers examined Legionella, which is an intercellular bacterium that exists in amoebae in the water systems; it is transmitted to humans through inhalation of water droplets. Cooling towers and whirlpools are the major sources of transmission.

The study, published in the journal Science, said the bacterium uses the amoeba's cellular process to "tag" proteins, causing them to degrade into their basic elements of amino acids, which are used by the bacteria as the main source of energy to grow and cause disease.

"The bacteria live on an 'Atkins diet' of low carbs and high protein and they trick the host cell to provide that specialized diet," Abu Kwaik said.


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[Interdisciplinary management of a large Legionella outbreak in Germany].

Landratsamt Alb-Donau-Kreis, Alb-Donau-Kreis, Deutschland.

Between December 2009 and the end of January 2010, the largest hitherto known outbreak of Legionella in Germany took place in the cities of Ulm and Neu-Ulm. Of a total of 64 patients involved, 60 patients had to be hospitalized, and 5 patients died from the infection. This event was caused by a wet cooling tower of a large air conditioning system in the city center of Ulm. The search for the source of the Legionella emission was extremely difficult, since these plants are neither notifiable nor subject to authorization in Germany. We report about the search for the source and the measures to control the outbreak. We also discuss communication and coordination during these investigations. Regulatory measures as proposed by the World Health Organization (WHO) and the European Network for Legionellosis (EWGLI) and already implemented in numerous other European countries would be desirable to prevent such outbreaks in the future.


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Detection of Legionella by quantitative-Polymerase Chain Reaction (qPCR) for monitoring and risk assessment

Open Access Research article Louise H Krojgaard, Karen A Krogfelt, Hans-Jorgen Albrechtsen and Soren A Uldum

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BMC Microbiology 2011, 11:254 doi:10.1186/1471-2180-11-254

Published: 21 November 2011

Background Culture and quantitative polymerase chain reaction (qPCR) assays for the detection of Legionella were compared on samples from a residential area before and after two interventions. A total of 84 samples were collected from shower hoses and taps as first flush samples and at constant temperature. Samples were grouped according to the origin of the sample, a) circulation water b) water from empty apartments c) water from shower hoses. The aims were to investigate the usefulness of qPCR compared to culture for monitoring remedial actions for elimination of Legionella bacteria and as a tool for risk assessment.

In water collected from the apartments Legionella spp were detected by qPCR in the concentration range from LOQ to 9.6*105GU/L while L. pneumophila were detected in a range from LOQ to 6.8 *105 GU/L. By culturing, the legionellae were detected in the range from below detection limit (> 10 CFU/L) to 1.6 * 106 CFU/L. In circulating water and in first flush water from shower hoses, culture and qPCR showed the same tendencies. The overall correlation between the bacteria number detected by culture and the two developed qPCR assays (L. spp and L. pneumophila) was relatively poor (r2 =0.31 for culture and Legionella spp. assay, r2 = 0.20 for culture and L. pneumophila assay).

Detection by qPCR was suitable for monitoring changes in the concentration of Legionella but the precise determination of bacteria is difficult. Risk assessment by qPCR only on samples without any background information regarding treatment, timing, etc is dubious. However, the rapid detection by qPCR of high concentrations of Legionella - especially Legionella pneumophila - is valuable as an indicator of risk, although it may be false positive compared to culture results. On the other hand, the detection of a low number of bacteria by qPCR is a strong indication for the absence of risk.


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Identification of Legionella pneumophila serogroups and other Legionella species by mip gene sequencing

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PCR methods for the rapid detection and identification of four pathogenic Legionella spp. and two Legionella pneumophila subspecies based on the gene amplification of gyrB

Guangpeng Zhou, Boyang Cao, Yan Dou, Yanwei Liu and Lu Feng, et al.

Applied Microbiology and Biotechnology, 2011, Volume 91, Number 3, Pages 777-787

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Legionella pneumophila DNA in serum samples during Legionnaires’ disease in relation to C-reactive protein levels

F. L. van de Veerdonk, C. P. C. de Jager, J. J. A. Schellekens, C. J. J. Huijsmans and F. Beaumont, et al.

European Journal of Clinical Microbiology & Infectious Diseases, 2009, Volume 28, Number 4, Pages 371-376

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LAMP-based method for a rapid identification of Legionella spp. and Legionella pneumophila

Xi Lu, Zi-Yao Mo, Hong-Bo Zhao, He Yan and Lei Shi

Applied Microbiology and Biotechnology, 2011, Volume 92, Number 1, Pages 179-187

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Profiling of environmental Legionella pneumophila strains by randomly amplified polymorphic DNA method isolated from geographically nearby buildings

Zuhal Zeybek, Irfan Türetgen, Ayten Kimiran Erdem, Gönül Filoglu and Aysin Çotuk

Environmental Monitoring and Assessment, 2009, Volume 149, Numbers 1-4, Pages 323-327

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Anin vitro evaluation of the interactions ofLegionella pneumophila serogroups 2 to 14 strains with other bacteria in the same habitat

Ayten Kimiran Erdem and Aysegül Yazici

Annals of Microbiology, 2008, Volume 58, Number 3, Pages 395-401

Reference Work Entry

Legionella Species and Legionnaires’ Disease

Paul Edelstein and Nicholas Cianciotto

2006, The Prokaryotes, PART 3, SECTION 3.3, Pages 988-1033

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Screening-level assays for potentially human-infectious environmental Legionella spp.

Helen Y. Buse, Abby Brehm, Jorge W. Santo Domingo and Nicholas J. Ashbolt

The Journal of Microbiology, 2011, Volume 49, Number 2, Pages 200-207

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Online First™ Efficacy of Colloidal Silver-Hydrogen Peroxide and 2-Bromo-2-nitroporopane-1,3-diol Compounds Against Different Serogroups of Legionella pneumophila Strains

N. O. Sanli-Yurudu, A. Kimiran-Erdem, E. O. Arslan-Aydogdu, Z. Zeybek and S. Gurun

Indian Journal of Microbiology, Online First™, 28 June 2011


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UofL researcher determines how Legionnaires' bacteria proliferate, cause disease

[ Back to EurekAlert! ] Public release date: 17-Nov-2011
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Contact: Jill Scoggins
jill.scoggins@louisville.edu
502-852-7461
University of Louisville

LOUISVILLE, Ky. ? A University of Louisville scientist has determined for the first time how the bacterium that causes Legionnaires' disease manipulates our cells to generate the amino acids it needs to grow and cause infection and inflammation in the lungs. The results are published online today (Nov. 17) in "Science."

Yousef Abu Kwaik, Ph.D., the Bumgardner Endowed Professor in Molecular Pathogenesis of Microbial Infections at UofL, and his team believe their work could help lead to development of new antibiotics and vaccines.

"It is possible that the process we have identified presents a great target for new research in antibiotic and vaccine candidates, not only for Legionnaires' disease but in other bacteria that cause illness," he said.

According to the Centers for Disease Control and Prevention, Legionnaires' disease is a lung infection caused by the bacterium called Legionella. The bacterium got its name in 1976, when many people who went to a Philadelphia convention of the American Legion suffered from an outbreak of pneumonia of unknown causes that was later determined to be caused by the bacterium. Each year, between 8,000 and 18,000 people are hospitalized with Legionnaires' disease in the U.S. There is no vaccine currently available for it.

For two years, the researchers examined Legionella which is an intercellular bacterium that exists in amoebae in the water systems; it is transmitted to humans through inhalation of water droplets. Cooling towers and whirlpools are the major sources of transmission. The bacterium uses the amoeba's cellular process to "tag" proteins, causing them to degrade into their basic elements of amino acids. These amino acids are used by the bacteria as the main source of energy to grow and cause disease.

"The bacteria live on an 'Atkins diet' of low carbs and high protein, and they trick the host cell to provide that specialized diet," Abu Kwaik said.

The same process occurs in a host ? animal or human ? who inhales the bacterium and is diagnosed with Legionnaires' disease. However, the bacteria do not tag the proteins, but rather trick the host into tagging the proteins for degradation to generate the amino acids.

In the laboratory, Abu Kwaik and his team saw that by inactivating the bacterial virulence factor responsible for tricking the cell into tagging proteins for degradation in mice models, the pulmonary disease was totally prevented. This was totally due to disabling the bacteria from generating amino acids, he said.

The process was then reversed, and the disease became evident when the mice, infected by the disabled bacteria, were injected with amino acids to compensate for the inability of the altered bacteria.

"Bacteria need to live on high protein and amino acids as sources of nutrition and energy in order to replicate in a host. This is what causes pulmonary disease," Abu Kwaik said. "No one has known how they generate sufficient sources of nutrients from the host to proliferate. Our work is the first to identify this process for any bacteria that cause disease."

He added that the type of host infected does not appear to affect the process. "Whether in a single-cell amoeba or a multi-cellular mammal, Legionella seems to know what to do; the process is the same, and is highly conserved through evolution. By interfering with the bacterium's sources of nutrients, we can stop it from thriving and causing disease."

Examining nutrient sources for organisms with the goal of stopping them from acquiring nutrients is a relatively new arena of basic research that deserves further study, he said. "We went after the basics ? the food and energy source ? which are prerequisite for the bacteria to grow and cause disease. It is not a process that is well understood yet, but by first discovering how an organism gets nutrients by tricking the host into degrading proteins, and then interfering with that process, we can, in effect, starve it to death and prevent or treat the disease."

With Abu Kwaik, authors of the paper are Christopher T.D. Price, Ph.D. and Tasneem Al-Quadan, a doctoral student, in UofL's Department of Microbiology and Immunology; Marina Santic, Ph.D., of the University of Rijeka, Croatia; and Ilan Rosenshine, Ph.D., of the Hebrew University Medical School in Jerusalem, Israel.

The work was funded by a grant from the National Institute of Allergy and Infectious Diseases.

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Researcher Determines How Legionnaires' Bacteria Proliferate, Cause Disease

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Respiratory / Asthma
Article Date: 21 Nov 2011 - 0:00 PST

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A University of Louisville scientist has determined for the first time how the bacterium that causes Legionnaires' disease manipulates our cells to generate the amino acids it needs to grow and cause infection and inflammation in the lungs. The results are published online in Science.

Yousef Abu Kwaik, Ph.D., the Bumgardner Endowed Professor in Molecular Pathogenesis of Microbial Infections at UofL, and his team believe their work could help lead to development of new antibiotics and vaccines.

"It is possible that the process we have identified presents a great target for new research in antibiotic and vaccine candidates, not only for Legionnaires' disease but in other bacteria that cause illness," he said.

According to the Centers for Disease Control and Prevention, Legionnaires' disease is a lung infection caused by the bacterium called Legionella. The bacterium got its name in 1976, when many people who went to a Philadelphia convention of the American Legion suffered from an outbreak of pneumonia of unknown causes that was later determined to be caused by the bacterium. Each year, between 8,000 and 18,000 people are hospitalized with Legionnaires' disease in the U.S. There is no vaccine currently available for it.

For two years, the researchers examined Legionella which is an intercellular bacterium that exists in amoebae in the water systems; it is transmitted to humans through inhalation of water droplets. Cooling towers and whirlpools are the major sources of transmission. The bacterium uses the amoeba's cellular process to "tag" proteins, causing them to degrade into their basic elements of amino acids. These amino acids are used by the bacteria as the main source of energy to grow and cause disease.

"The bacteria live on an 'Atkins diet' of low carbs and high protein, and they trick the host cell to provide that specialized diet," Abu Kwaik said.

The same process occurs in a host - animal or human - who inhales the bacterium and is diagnosed with Legionnaires' disease. However, the bacteria do not tag the proteins, but rather trick the host into tagging the proteins for degradation to generate the amino acids.

In the laboratory, Abu Kwaik and his team saw that by inactivating the bacterial virulence factor responsible for tricking the cell into tagging proteins for degradation in mice models, the pulmonary disease was totally prevented. This was totally due to disabling the bacteria from generating amino acids, he said.

The process was then reversed, and the disease became evident when the mice, infected by the disabled bacteria, were injected with amino acids to compensate for the inability of the altered bacteria.

"Bacteria need to live on high protein and amino acids as sources of nutrition and energy in order to replicate in a host. This is what causes pulmonary disease," Abu Kwaik said. "No one has known how they generate sufficient sources of nutrients from the host to proliferate. Our work is the first to identify this process for any bacteria that cause disease."

He added that the type of host infected does not appear to affect the process. "Whether in a single-cell amoeba or a multi-cellular mammal, Legionella seems to know what to do; the process is the same, and is highly conserved through evolution. By interfering with the bacterium's sources of nutrients, we can stop it from thriving and causing disease."

Examining nutrient sources for organisms with the goal of stopping them from acquiring nutrients is a relatively new arena of basic research that deserves further study, he said. "We went after the basics - the food and energy source - which are prerequisite for the bacteria to grow and cause disease. It is not a process that is well understood yet, but by first discovering how an organism gets nutrients by tricking the host into degrading proteins, and then interfering with that process, we can, in effect, starve it to death and prevent or treat the disease."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject. With Abu Kwaik, authors of the paper are Christopher T.D. Price, Ph.D. and Tasneem Al-Quadan, a doctoral student, in UofL’s Department of Microbiology and Immunology; Marina Santic, Ph.D., of the University of Rijeka, Croatia; and Ilan Rosenshine, Ph.D., of the Hebrew University Medical School in Jerusalem, Israel.
The work was funded by a grant from the National Institute of Allergy and Infectious Diseases.
University of Louisville Please use one of the following formats to cite this article in your essay, paper or report:

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Thursday 8 December 2011

Biofilms in drinking water and their role as reservoir for pathogens.

Biofilm Centre, University of Duisburg-Essen, Universitätsstraße 5, D-45141 Essen, Germany.

Most microorganisms on Earth live in various aggregates which are generally termed "biofilms". They are ubiquitous and represent the most successful form of life. They are the active agent in biofiltration and the carriers of the self-cleaning potential in soils, sediments and water. They are also common on surfaces in technical systems where they sometimes cause biofouling. In recent years it has become evident that biofilms in drinking water distribution networks can become transient or long-term habitats for hygienically relevant microorganisms. Important categories of these organisms include faecal indicator bacteria (e.g., Escherichia coli), obligate bacterial pathogens of faecal origin (e.g., Campylobacter spp.) opportunistic bacteria of environmental origin (e.g., Legionella spp., Pseudomonas aeruginosa), enteric viruses (e.g., adenoviruses, rotaviruses, noroviruses) and parasitic protozoa (e.g., Cryptosporidium parvum). These organisms can attach to preexisting biofilms, where they become integrated and survive for days to weeks or even longer, depending on the biology and ecology of the organism and the environmental conditions. There are indications that at least a part of the biofilm populations of pathogenic bacteria persists in a viable but non-culturable (VBNC) state and remains unnoticed by the methods appointed to their detection. Thus, biofilms in drinking water systems can serve as an environmental reservoir for pathogenic microorganisms and represent a potential source of water contamination, resulting in a potential health risk for humans if left unnoticed.

Copyright © 2011 Elsevier GmbH. All rights reserved.


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Scald risk in social housing can be reduced through thermostatic control system without increasing Legionella risk: a cluster randomised trial

An international peer-reviewed journal for health professionals and researchers covering conception to adolescence rssArch Dis Child 2011;96:1097-1102 doi:10.1136/archdischild-2011-300606 P Edwards1, MA Durand2, M Hollister3, J Green2, S Lutchmun4, A Kessel5, I Roberts1

1Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, London, UK
2Faculty of Public Health and Policy, London School of Hygiene & Tropical Medicine, London, UK
3Department of Housing & Adult Social Care, London Borough of Camden, London, UK
4Public Health Department, NHS Camden, St Pancras Hospital, London, UK
5Department of Social and Environmental Health Research, London School of Hygiene & Tropical Medicine, London, UK Correspondence to Dr Phil Edwards, NPHIR, Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, Keppel Street, London WC1E 7HT, UK; phil.edwards{at}LSHTM.ac.ukContributors PE, IR, JG, MAD, MH, SL and AK designed the study. MAD managed the data collection and fieldwork. PE conducted the data analyses. PE, MAD, IR and JG interpreted the results. PE and MAD wrote the first draft of the manuscript. IR, JG, AK, SL and MH commented on the draft and contributed to the final manuscript.

Accepted 10 August 2011 Published Online First 20 September 2011 Objective To quantify the effects of a thermostatic control system in social (public) housing on the prevalence of dangerous (>60°C) water temperatures and on fuel consumption.

Design Pair-matched double-blind cluster randomised controlled trial.

Setting Social housing in a deprived inner-London borough.

Participants 150 households recruited as clusters from 22 social housing estates. Four small estates were combined into two clusters (resulting in a total of 10 pairs of clusters).

Intervention Social housing estate boiler houses were randomised to a thermostatic control sterilisation programme (heating water to 65°C during 00:00–06:00 h and to 50°C from 06:00 to 00:00 h daily) or to standard control (constant temperature 65°C).

Main outcome measures Water temperature over 60°C (‘dangerous’) after running taps for 1 min and daily fuel consumption (cubic feet of gas).

Results 10 clusters (80 households) were allocated to the sterilisation programme and 10 clusters (70 households) to control, of which 73 and 67 households, respectively, were analysed. Prevalence of dangerous (>60°C) hot water temperatures at 1 min was significantly reduced with the sterilisation programme (mean of cluster prevalence 1% in sterilisation programme group vs 34% in control group; absolute difference 33%, 95% CI 12% to 54%; p=0.006). Prevalence of high (>55°C) hot water temperatures at 1 min was significantly reduced (31% sterilisation vs 59% control; absolute difference 28%, 95% CI 9% to 47%; p=0.009). Gas consumption per day reduced more in the control group than in the sterilisation programme group, although not statistically significantly (p=0.125).

Conclusions The thermostatic control with daily sterilisation was effective in capping hot water temperatures and therefore reduced scald risk. Although expected to save energy, fuel consumption was increased relative to the control group.

Funding This work was undertaken by the London School of Hygiene & Tropical Medicine who received funding from Camden Primary Care Trust (PCT). AK was Director of Public Health at Camden PCT at inception of the study and assisted with study design and writing of the report. He is currently employed by the Health Protection Agency as Director of Public Health Strategy. The views expressed in the paper are those of the authors and do not necessarily represent those of Camden PCT or the Health Protection Agency. Camden PCT had no role in data collection, data analysis, or data interpretation.

Competing interests None.

Ethics approval Ethical approval for the study was obtained from the London School of Hygiene & Tropical Medicine Research Ethics Committee.

Provenance and peer review Not commissioned; externally peer reviewed.


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Tsunami lung

Book Chapter

On the Studies of the Disaster Recovery and the Business Continuity Planning for Private Sector Caused by Great East Japan Earthquake

Koji Okuda, Masakazu Ohashi and Mayumi Hori

Communications in Computer and Information Science, 1, Volume 219, ENTERprise Information Systems, Part 1, Pages 14-21

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Nobuo Mimura, Kazuya Yasuhara, Seiki Kawagoe, Hiromune Yokoki and So Kazama

Mitigation and Adaptation Strategies for Global Change, 2011, Volume 16, Number 7, Pages 803-818

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Erratum to: Damage from the Great East Japan Earthquake and Tsunami - A quick report

Nobuo Mimura, Kazuya Yasuhara, Seiki Kawagoe, Hiromune Yokoki and So Kazama

Mitigation and Adaptation Strategies for Global Change, 2011, Volume 16, Number 8, Pages 943-945

Book Chapter

On the Studies of the Disaster Recovery for the Restoration of Local Communities and Local Governments from the Great East Japan Earthquake

Noriko Kurata, Masakazu Ohashi and Mayumi Hori

Communications in Computer and Information Science, 1, Volume 219, ENTERprise Information Systems, Part 1, Pages 22-33

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The Great East Japan Earthquake: Tohoku University Hospital’s efforts and lessons learned

Susumu Satomi

Surgery Today, 2011, Volume 41, Number 9, Pages 1171-1181

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Masaaki Hosomi

Clean Technologies and Environmental Policy, 2011, Volume 13, Number 3, Pages 415-416

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Open Access Attenuating posttraumatic distress with omega-3 polyunsaturated fatty acids among disaster medical assistance team members after the Great East Japan Earthquake: The APOP randomized controlled trial

Yutaka Matsuoka, Daisuke Nishi, Naoki Nakaya, Toshimasa Sone and Kei Hamazaki, et al.

BMC Psychiatry, 2011, Volume 11, Number 1, 132

Book Chapter

Submarine Mass Movements and Their Consequences

Yasuhiro Yamada, Kiichiro Kawamura, Ken Ikehara, Yujiro Ogawa and Roger Urgeles, et al.

Advances in Natural and Technological Hazards Research, 1, Volume 31, Submarine Mass Movements and Their Consequences, Pages 1-12

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Community-acquired versus nosocomial Legionella pneumonia: Lessons learned from an epidemiologic investigation

Epidemiologically, the peak incidence of legionella community-acquired pneumonia (CAP) is in the summer/fall, but cases may occur anytime during the year. The peak age incidence of Legionnaire’s disease is in the elderly population, but Legionella CAP occurs in all age groups. The incubation period for Legionnaire’s disease is 2 to 10 days. Typically, legionella CAP occurs sporadically. Clinical presentation of Legionnaire’s disease is independent of legionella species and Legionella nosocomial pneumonia (NP) is indistinguishable clinically from legionella CAP. (Source: American Journal of Infection Control)

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Saturday 3 December 2011

Non-chemotactic influence of CXCL7 on human phagocytes. Modulation of antimicrobial activity against L. pneumophila.

Authors: González-Cortés C, Diez-Tascón C, Guerra-Laso JM, González-Cocaño MC, Rivero-Lezcano OM Abstract We have investigated the role of CXCL7 in the immune response of human phagocytes against the intracellular bacteria Mycobacterium tuberculosis and Legionella pneumophila. We have observed that polymorphonuclear neutrophil (PMN) chemotaxis induced by the supernatants of infected monocyte derived macrophages (MDM) may be attributed to CXCL8 rather than CXCL7, although both chemokines are present in large quantities. We have also found that CXCL7 is present not only in the supernatants of MDM, but also in the supernatants of PMN of some, but not all, individuals. Western blot analysis revealed that, in both MDM and PMN supernatants appeared two bands with molecular weights c...

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How Legionnaires' bacteria proliferate, cause disease

Scientist have determined for the first time how the bacterium that causes Legionnaires' disease manipulates our cells to generate the amino acids it needs to grow and cause infection and inflammation in the lungs. (Source: ScienceDaily Headlines)

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Population variation in NAIP functional copy number confers increased cell death upon Legionella pneumophila infection.

Authors: Boniotto M, Tailleux L, Lomma M, Gicquel B, Buchrieser C, Garcia S, Quintana-Murci L Abstract The NAIP gene encodes an intracellular innate immunity receptor that senses flagellin. The genomic region containing NAIP presents a complex genomic organization and includes various NAIP paralogs. Here, we assessed the degree of copy number variation of the complete NAIP gene (NAIPFull) in various human populations and studied the functional impact of such variation on host cell fate using Legionella pneumophila as an infection model. We determined that African populations have a NAIPFull duplication at a higher frequency than Europeans and Asians, with an increased transcription of the gene. In addition, we demonstrated that a higher amount of the NAIPFull protein dramatically i...

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Detection of Legionella by quantitative-Polymerase Chain Reaction (qPCR) for monitoring and risk assessment

Conclusion:Detection by qPCR was suitable for monitoring changes in the concentration of Legionella but the precise determination of bacteria is difficult. Risk assessment by qPCR only on samples without any background information regarding treatment, timing, etc is dubious. However, the rapid detection by qPCR of high concentrations of Legionella - especially Legionella pneumophila - is valuable as an indicator of risk, although it may be false positive compared to culture results. On the other hand, the detection of a low number of bacteria by qPCR is a strong indication for the absence of risk. (Source: BMC Microbiology - Latest articles)

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How Legionnaires' bacteria cause disease

LOUISVILLE, Ky., Nov. 18 (UPI) -- A bacterium that causes Legionnaires' disease manipulates cells to generate amino acids it needs to grow and infect the lungs, U.S. researchers say. (Source: Health News - UPI.com)

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Friday 2 December 2011

UofL researcher determines how Legionnaires' bacteria proliferate, cause disease

(University of Louisville) A University of Louisville scientist has determined for the first time how the bacterium that causes Legionnaires' disease manipulates our cells to generate the amino acids it needs to grow and cause infection and inflammation in the lungs. The results are published online today (Nov. 17) in Science. (Source: EurekAlert! - Medicine and Health)

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Legionella pneumophila urinary antigen subtyping using monoclonal antibodies as a tool for epidemiological investigations

Abstract  Legionnaires’ disease is diagnosed predominantly by urinary antigen detection, and patient isolates are rarely available. The lipopolysaccharide (LPS) epitope pattern of isolates detected by monoclonal antibodies is an accepted marker for the phenotyping of L. pneumophila serogroup 1 strains into monoclonal subgroups. L. pneumophila LPS is the dominant antigen in patients’ urinary specimens. By using commercially available microtiter wells coated with rabbit anti-Legionella serogroup 1 IgG as the catching antibody, LPS components in urine specimens were bound and detected separately by corresponding monoclonal antibodies of the Dresden Panel. The subtyping of LPS on urinary antigen molecules by using enzyme-linked immunosorbent assay (ELISA) allows deducing of ...

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Researcher Determines How Legionnaires' Bacteria Proliferate, Cause Disease

A University of Louisville scientist has determined for the first time how the bacterium that causes Legionnaires' disease manipulates our cells to generate the amino acids it needs to grow and cause infection and inflammation in the lungs. The results are published online in Science. Yousef Abu Kwaik, Ph.D., the Bumgardner Endowed Professor in Molecular Pathogenesis of Microbial Infections at UofL, and his team believe their work could help lead to development of new antibiotics and vaccines... (Source: Health News from Medical News Today)

View the original article here