Wednesday, January 30, 2013

 

Infections Succumbs to Blue Light


Infections Succumbs to Blue Light

January 2013

Blue light can selectively eradicate Pseudomonas aeruginosa infections of the skin and soft tissues, while preserving the outermost layer of skin, according to a proof-of-principle study led by Michael R. Hamblin of the Massachusetts General Hospital, and the Harvard Medical School in Boston. The research is published online ahead of print in the journal Antimicrobial Agents and Chemotherapy.

"Blue light is a potential non-toxic, non-antibiotic approach for treating skin and soft tissue infections, especially those caused by antibiotic resistant pathogens," says Hamblin.

In the study, animal models were infected with P. aeruginosa. All of the animals in the group treated with blue light survived, while in the control, 82 percent (9 out of 11) of the animals died.

Skin and soft tissue infections are the second most common bacterial infections encountered in clinical practice, and represent the most common infection presentation—more than 3 percent—in patients visiting emergency departments, says Hamblin. The prevalence of skin and soft tissue infections among hospitalized patients is 10 percent, with approximately 14.2 million ambulatory care visits every year and an annual associated medical cost of almost $24 billion (equivalent to $76 for every American), says Hamblin.

Treatment of skin and soft tissue infections has been significantly complicated by the explosion of antibiotic resistance, which may bring an end to what medical scientists refer to as the antibiotic era, says Hamblin. "Microbes replicate very rapidly, and a mutation that helps a microbe survive in the presence of an antibiotic drug will quickly predominate throughout the microbial population. Recently, a dangerous new enzyme, NDM-1, that makes some bacteria resistant to almost all antibiotics available has been found in the United States. Many physicians are concerned that several infections soon may be untreatable."

Besides harming public health, antibiotic resistance boosts health care costs. "Treating resistant skin and soft tissue infections often requires the use of more expensive, or more toxic drugs, and can result in longer hospital stays for infected patients," says Hamblin.
Reference: Dai T, Gupta A, et al.  2013. Blue light rescues mice from potentially fatal Pseudomonas aeruginosa burn infection: efficacy, safety, and mechanism of action. Antim. Agents Chemother. Published ahead of print Dec. 21, 2012 ,doi:10.1128/AAC.01652-12)

Infection Control Today

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# posted by Pat O'Connor @ 9:46 AM

Tuesday, December 25, 2012

 

Infectious arthritis caused by bacteria requires quick treatment


Infectious arthritis caused by bacteria requires quick treatment
By DR. KOMOROFF Universal Uclick 
Published: 12/24/2012  2:21 AM 
Last Modified: 12/24/2012  3:54 AM

 Dear Doctor K: I saw my doctor for pain and inflammation in my knee. He said I have arthritis caused by a bacterial infection. Could this be true? 

 Dear Reader: Wear and tear on a joint is the main cause of the most common type of arthritis, osteoarthritis. In rheumatoid arthritis and juvenile idiopathic arthritis, an overactive immune system causes joint inflammation. 

 But joints also can become infected with bacteria and fungi. These microbes may directly infect the joint, for example, through a puncture wound or major injury. But more often, the infection spreads to a joint by traveling through the bloodstream from somewhere else in the body. Once the microbe reaches the joint, it can multiply. The immune system recognizes the invading foreigner and tries to wipe it out. The infection and the immune response cause warmth, pain, stiffness and swelling. 

 Several types of bacteria can cause arthritis. The diagnosis of infectious arthritis is made by removing fluid from the joint through a needle. The microbe causing the infection can usually be identified in that fluid. 

 Once diagnosed, you'll immediately begin antibiotic treatment. This should eliminate the infection and help prevent permanent joint damage if begun early enough. If your infection is advanced, or if joint damage has already occurred, you may need to be hospitalized. 

 At the hospital, your affected joint can be drained. Sometimes fluid is repeatedly removed with a needle and syringe. In other cases, a surgeon needs to open the joint and place a drain in it to let the joint fluid constantly leak out of the body. You can also receive antibiotics intravenously if necessary. If your joint is seriously damaged, you may need surgery to remove damaged tissue and reconstruct the joint. 

 Often you need to briefly immobilize your affected joint while recovering from the infection. But it's best to become active again as soon as you are able.

TulsaWorld





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# posted by Pat O'Connor @ 6:06 AM

Saturday, September 01, 2012

 

Diagnostic methods in sepsis: the need of speed.


Diagnostic methods in sepsis: the need of speed.


August 2012

Coelho FR, Martins JO.

Source

Laboratory Specialist, Instituto de Química, Universidade de São Paulo, São Paulo, SP, Brazil.

Abstract


Keywords: Sepsis, methods, cytokines.

OBJECTIVE:

Sepsis is a common condition encountered in hospital environments. There is no effective treatment for sepsis, and it remains an important cause of death at intensive care units. This study aimed to discuss some methods that are available in clinics, and tests that have been recently developed for the diagnosis of sepsis.

METHODS:

A systematic review was performed through the analysis of the following descriptors: sepsis, diagnostic methods, biological markers, and cytokines.

RESULTS:

The deleterious effects of sepsis are caused by an imbalance between the invasiveness of the pathogen and the ability of the host to mount an effective immune response. Consequently, the host's immune surveillance fails to eliminate the pathogen, allowing it to spread. Moreover, there is a pro-inflammatory mediator release, inappropriate activation of the coagulation and complement cascades, leading to dysfunction of multiple organs and systems. The difficulty achieve total recovery of the patient is explainable. There is an increased incidence of sepsis worldwide due to factors such as aging population, larger number of surgeries, and number of microorganisms resistant to existing antibiotics.

CONCLUSION: The search for new diagnostic markers associated with increased risk of sepsis development and molecules that can be correlated to certain steps of sepsis is becoming necessary. This would allow for earlier diagnosis, facilitate patient prognosis characterization, and prediction of possible evolution of each case. All other markers are regrettably constrained to research units.

SciELO Brazil

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# posted by Pat O'Connor @ 8:57 AM

Friday, July 06, 2007

 

Clostridium difficile: changing epidemiology and new treatment options.

Clostridium difficile: changing epidemiology and new treatment options.

Curr Opin Infect Dis. 2007 Aug

Kuijper EJ, van Dissel JT, Wilcox MH.
aDepartment of Medical Microbiology, Leiden University Medical Center, Leiden, the Netherlands bInfectious Diseases, Leiden University Medical Center, Leiden, the Netherlands cDepartment of Medical Microbiology, Leeds Teaching Hospitals and University of Leeds, Leeds, UK.

PURPOSE OF REVIEW: The review summarizes changes in the epidemiology and treatment of Clostridium difficile-associated disease.

RECENT FINDINGS: Recent outbreaks of Clostridrium difficile-associated diarrhoea with increased severity, high relapse rate and significant mortality, have been related to the emergence of a new, hypervirulent C. difficile strain in north America, Japan and Europe. Definitions have been proposed by the European Centre for Disease Prevention and Control to identify severe cases of Clostridrium difficile-associated diarrhoea and to differentiate community-acquired cases from nosocomial-acquired cases. The emerging strain is referred to as North American pulsed-field type 1 and polymerase chain reaction ribotype 027. The emerging strain has also been detected in calf diarrhoea and ground meat samples in Canada.

Attempts to prevent outbreaks caused by type 027 should focus on controlling the overall use of antibiotics, and high-risk antibiotics such as cephalosporins, clindamycin and fluoroquinolones. Several new antibiotic and non-antibiotic alternatives have become available; there is currently no place for probiotic treatments. Patients who suffer multiple relapses of C. difficile-associated diarrhoea present a major therapeutic challenge.

SUMMARY: The early recognition of Clostridrium difficile-associated diarrhoea caused by NAP1/027 is necessary to start rapid treatment, to prevent complications, and to prevent further spread of the bacterium.

Lippincott, Williams & Wilkins

A portrait of the geographic dissemination of the Clostridium difficile North American pulsed-field type 1 strain and the epidemiology of C. difficile-associated disease in Québec.

Clin Infect Dis. 2007 * Full Text Article

Hubert B, Loo VG, Bourgault AM, Poirier L, Dascal A, Fortin E, Dionne M, Lorange M.
Institut National de Santé Publique du Québec, Québec, Canada. bruno.hubert@chu-bordeaux.fr

BACKGROUND: An increase in the incidence and severity of Clostridium difficile-associated disease in Québec and the United States has been associated with a hypervirulent strain referred to as North American pulsed-field type 1 (NAP1)/027.

METHODS: In 2005, a prospective study was conducted in 88 Québec hospitals, and 478 consecutive nosocomial isolates of C. difficile were obtained. The isolates were subjected to pulsed-field gel electrophoresis (PFGE) typing, antimicrobial susceptibility testing, and detection of binary toxin genes and tcdC gene deletion. Data on patient age and occurrence of complications were collected.

RESULTS: PFGE typing of 478 isolates of C. difficile yielded 61 PFGE profiles. Pulsovars A (57%), B (10%), and B1 (8%) were predominant. The PFGE profile of pulsovar A was identical to that of strain NAP1. It showed 67% relatedness with 15 other PFGE patterns, among which 11 had both binary toxin genes and a partial tcdC deletion but different antibiotic susceptibility profiles. Pulsovars B and B1 were identical to strain NAP2/ribotype 001. In hospitals showing a predominant clonal A or B-B1 PFGE pattern, incidence of C. difficile-associated disease was 2 and 1.3 times higher, respectively, than in hospitals without any predominant clonal PFGE pattern. Severe disease was twice as frequent among patients with strains possessing binary toxin genes and tcdC deletion than among patients with strains lacking these virulence factors.

CONCLUSIONS: This study helped to quantify the impact of strain NAP1 on the incidence and severity of C. difficile-associated disease in Québec in 2005. The identification of the geographic dissemination of this predominant strain may help to focus regional infection-control efforts.

University of Chicago Press * Full Text Article

Implications of the changing face of Clostridium difficile disease for health care practitioners.

Am J Infect Control. 2007 May

McFarland LV, Beneda HW, Clarridge JE, Raugi GJ.

From the Department of Health Services Research and Development, Veterans Administration Puget Sound Health Care System, Seattle, WA 98101, USA. Lynne.McFarland@va.gov

Recent reported outbreaks of Clostridium difficile-associated disease in Canada have changed the profile of C difficile infections.

Historically, C difficile disease was thought of mainly as a nosocomial disease associated with broad-spectrum antibiotics, and the disease was usually not life threatening. The emergence of an epidemic strain, BI/NAP1/027, which produces a binary toxin in addition to the 2 classic C difficile toxins A and B and is resistant to some fluoroquinolones, was associated with large numbers of cases with high rates of mortality.

Recently, C difficile has been reported more frequently in nonhospital-based settings, such as community-acquired cases. The C difficile disease is also being reported in populations once considered of low risk (children and young healthy women). In addition, poor response to metronidazole treatment is increasing. Faced with an increasing incidence of C difficile infections and the changing profile of patients who become infected, this paper will reexamine the current concepts on the epidemiology and treatment of C difficile-associated disease, present new hypotheses for risk factors, examine the role of spores in the transmission of C difficile, and provide recommendations that may enhance infection control practices.

Elsevier

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# posted by Pat O'Connor @ 4:23 AM

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