Can I Really Not Sleep With a Tampon in During My Period?


Let’s talk toxic shock syndrome.
tampon-at-night

You’ve probably heard a lot of alarming warnings about toxic shock syndrome (TSS), a rare but life-threatening complication of certain bacterial infections.

One of the most prevalent rumors is that sleeping with a tampon in during your period is practically a guarantee that you’ll wind up with TSS, so you should never do it unless you want to take that risk. But sleeping with a tampon in also happens to be way more convenient and significantly less messy than relying on a pad—so how concerned should you really be? Here, experts discuss the truth about tampons and toxic shock syndrome.

No doubt you’ve heard of TSS before, but you may be hazy on the details.

TSS is primarily caused by Staphylococcus aureus (staph) bacteria, but it can also be caused by a kind of Streptococcus (strep) bacteria, according to the Mayo Clinic. Clostridium sordellii can cause this infection as well, according to the Cleveland Clinic.

Your vagina has its own natural bacterial flora, and it can contain these bacteria without making you sick, G. Thomas Ruiz, M.D., an ob/gyn at MemorialCare Orange Coast Medical Center in Fountain Valley, Calif., tells SELF. But sometimes this bacteria can produce the toxins that lead to toxic shock syndrome, according to the Mayo Clinic.

Unfortunately, no one really knows the exact mechanism that links tampons to TSS, Mary Jane Minkin, M.D., a clinical professor of obstetrics and gynecology and reproductive sciences at Yale Medical School, tells SELF. One theory is that if you leave a tampon in for too long, these bacteria can flourish and become trapped, then enter your uterus through your cervix, according to the Cleveland Clinic.

This may be more likely if you use a really absorbent tampon when your period is too light to need one. Not only does this make it less likely that you’ll change it as often as you should, but the more absorbent a tampon is, the more it can dry out your vaginal mucosa, Lauren Streicher, M.D., an associate professor of clinical obstetrics and gynecology at Northwestern University Feinberg School of Medicine, tells SELF. This can increase the risk of tears in the vagina, which can allow bacteria to enter the body. The cuts don’t need to be big—even microscopic disruptions in your vaginal mucosa can be enough, Dr. Streicher says.

But TSS isn’t just associated with tampons. People can also develop TSS after getting a cut or burn on their skin, having recent surgery, using diaphragms or sponges, or having a viral infection like the flu or chickenpox, according to the Mayo Clinic.

While present-day tampons can cause TSS, the condition was most prevalent when women were using ultra-absorbent tampons that are no longer on the market.

Those tampons contained ingredients like polyester foam and carboxymethylcellulose, a thickening agent that enabled more expansion than other tampons did, according to the Centers for Disease Control and Prevention (CDC). This allowed women to keep ultra-absorbent tampons in for longer periods of time, but the longer wear allowed bacteria to colonize, Suzanne Fenske, M.D., assistant professor of obstetrics, gynecology, and reproductive sciences at Mount Sinai Health System, tells SELF.

Tampons with these ingredients were pulled from shelves after the spate of TSS cases, according to the CDC. Now, the Food and Drug Administration requires that manufacturers use a set system for measuring tampon absorbency so as not to get into dangerous territory. That doesn’t mean that the tampons on sale today can’t cause TSS, but that they’re much less likely to do so than higher-absorbency ones from decades ago.

The vast majority of people who leave a tampon in too long will be fine.

TSS isn’t as common as it once was, but there’s still a small risk of developing it. At its peak in 1980, incidence rates of TSS were 6 to 12 per 100,000 women between the ages of 12 and 49, according to the CDC. By 1986, that went down to 1 in 100,000 women between the ages of 15 and 44, and that’s still the approximate incidence today.

“The most common side effect [of using a tampon for too long] is a smelly vaginal odor,” Sherry A. Ross, M.D., an ob/gyn and women’s health expert at Providence Saint John’s Health Center in Santa Monica, Calif., and author of She-ology: The Definitive Guide to Women’s Intimate Health. Period., tells SELF.

It’s unclear why a few unlucky people develop TSS after leaving a tampon in for too long while so many others others don’t, Maura Quinlan, M.D., M.P.H., an assistant professor in the Department of Obstetrics and Gynecology at the Northwestern University Feinberg School of Medicine, tells SELF. “For some women, their immune system may not fight off the bacteria as well,” she says. But again, doctors really don’t know.

Still, it’s important to learn the signs of TSS so that, if it ever does happen to you or someone close to you, you can get help as soon as possible.

Common TSS symptoms include a sudden high fever, low blood pressure, vomiting or diarrhea, a rash that looks like a sunburn, confusion, muscle aches, seizures, and headaches, according to the Mayo Clinic.

If you suspect that you have TSS, get to the emergency room immediately—the condition can progress quickly, Dr. Quinlan says. There’s no one test for TSS, but doctors will likely take blood and urine samples to test for a staph or strep infection, according to the Mayo Clinic.

While doctors try to figure out the source of the infection, you’ll be treated with antibiotics, receive medication to stabilize your blood pressure if it’s low, get fluids to treat dehydration, and have other care based on how your illness is presenting. In very serious cases, surgery can be necessary to remove dead tissue that resulted from the infection.

Bottom line: TSS is scary, but you can sleep with a tampon in as long as you don’t push the eight-hour limit.

It’s also important to use the lowest-absorbency tampon possible to lower the odds that you’ll develop TSS, Dr. Minkin says. The less absorbent your tampon, the less likely you’ll leave it in for too long, and the less likely it’ll sap your vaginal mucosa of too much moisture. The guidelines are there for a reason—if you want to be as safe as possible, follow them.

Dr. Ruiz recommends putting in a new tampon right before you go to sleep and changing it as soon as you get up. Even better if you can manage it when you get up to pee in the middle of the night, he says, but it’s not a requirement—if you’d rather tumble back into bed and deal with it in the morning, feel free. And if you’d prefer to avoid the whole question of sleeping with a tampon in altogether, you may want to try something like a menstrual cup instead. These reusable products are typically made of medical-grade silicone, collect blood rather than absorbing it, and can be used safely for up to 12 hours—more than enough time to hit snooze and still be completely in the clear.

Antibiotics resistance could kill 10 million a year by 2050


A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050

A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050

London (AFP) – A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050.

The Review on Antimicrobial Resistance said surgeries that have become widespread and low-risk thanks to antibiotics, such as caesarean sections, could become more dangerous without urgent action.

The review announced by British Prime Minister David Cameron was led by Jim O’Neill, former chief economist at US investment bank Goldman Sachs, and included British senior public health experts.

It found the region with the highest number of deaths attributable to antimicrobial resistance would be Asia with 4.7 million, followed by Africa with 4.1 million, while there would be 390,000 in Europe and 317,000 in the United States.

For comparison, the review estimated that the second-biggest killer, cancer, would account for 8.2 million deaths a year by 2050.

“The damaging effects of antimicrobial resistance are already manifesting themselves across the world,” the report said.

“Antimicrobial-resistant infections currently claim at least 50,000 lives each year across Europe and the US alone,” it added.

The calculations were based on existing studies by the think tank Rand Europe and the consultancy KPMG.

It warned drug resistance was not “a distant and abstract risk” and called for “a major intervention to avert what threatens to be a devastating burden on the world’s healthcare systems”.

The review emphasised the economic advantage of investment in tackling the problem early.

It said that three types of bacteria — the Klebsiella pneumonia, Escherichia coli (E. coli) and Staphylococcus aureus — were already showing signs of resistance to medicine.

Treatment of HIV, malaria and tuberculosis were broader public health issues in which resistance “is a concern”, the report said.

In the United States, antibiotic-resistant infections are associated with 23,000 deaths and two million illnesses each year.

The economic costs annually are as high as $20 billion (16 billion euros) in excess direct health care costs and $35 billion (28 billion euros) in lost productivity.

Staph Nasal Carriage: A Link With Lupus?


The skin microbiome now implicated in disease pathogenesis.

Nasal carriage of Staphylococcus aureus was associated with a distinct disease phenotype among patients with systemic lupus erythematosus, Italian researchers found.

At the time of enrollment into a lupus cohort, renal involvement was more common among S. aureus carriers than noncarriers (11.6% vs 3%, P=0.0009), while joint involvement was less frequent (11.1% vs 21.2%, P=0.02), according to Cristiano Alessandri, MD, of Sapienza Universita di Roma in Rome, and colleagues.

 The carriers also had higher prevalence of several lupus-associated autoantibodies such as anti-double stranded (ds) DNA (77.7% vs 39.4%, P<0.0001), the researchers reported online in Arthritis Research & Therapy.

“In recent years there has been growing interest in the possible role of the microbiome in the development and course of disease. Of note, the gut microbiome has been widely investigated in autoimmune diseases, such as type 1 diabetes, inflammatory bowel diseases, rheumatoid arthritis, and spondyloarthropathies,” Alessandri and colleagues wrote.

Less is known, however, about the skin microbiome, which acts as the primary barrier against pathogenic insults and, when out of balance, could be associated with disease.

The commensal S. aureus can be found intermittently in the anterior nares in approximately one-third of the population. Its presence has been associated with atopic dermatitis, and studies have considered a possible association with other skin disorders such as acne vulgaris and rosacea.

In addition, a study in patients with rheumatoid arthritis found carriage rates of 50% compared with 33% in controls, and another study found an association between carriage and disease development and relapse in granulomatosis with polyangiitis.

 The pathogenesis of lupus — a highly heterogeneous disease — is believed to have both genetic and environmental influences, with infection being a prominent environmental factor.

Therefore, to investigate the possibility that S. aureus nasal colonization could have an association with lupus, Alessandri and colleagues enrolled 84 patients from their clinic along with 154 healthy blood donors as controls.

Most of the lupus patients were women. Mean age was 41 and mean disease duration was almost 12 years. Involvement of the joints was present in 68%, of the skin in 69%, and of the kidney in 37%.

All had antinuclear antibodies present, 82% had anti-ds-DNA, 29% had anti-SSA antibodies, 12% had anti-SSB, and 16% had anti-Sm antibodies. Twenty of the patients also had other autoimmune diseases such as antiphospholipid syndrome or Sjogren’s syndrome in addition to their lupus.

A total of 21.4% of patients with lupus were found to be carriers of S. aureus, which was similar to the rate of 28.6% among healthy controls, and all cases were methicillin-sensitive.

Along with high rates of renal involvement, carriers more often had lupus skin manifestations compared with noncarriers (22.1% vs 15.1%), although this was not a significant difference.

And in addition to high rates of anti-ds-DNA antibodies, S. aureus carriers also had greater prevalence of these autoantibodies compared with noncarriers:

  • Anti-Sm: 22.2% vs 9.1% (P=0.01)
  • Anti-SSA: 44.4% vs 21.1%, (P=0.0008)
  • Anti-SSB: 16.6% vs 6.1%, (P=0.03)
  • Anti-RNP: 16.6% vs 6.1%, (P=0.03)

“Carriers had a significantly higher prevalence of anti-SSA and anti-SSB antibodies, which are associated with cutaneous involvement. In addition, anti-ds-DNA and anti-Sm antibodies, which are associated with renal involvement, were present in S. aureus-positive patients,” the authors noted.

In contrast, complement levels were lower among noncarriers. Low C3 levels were seen in 29.7% of noncarriers compared with 16.6% of carriers (P=0.01), while C4 levels were low in 32.8% of noncarriers compared with 22.2% of carriers (P=0.03).

Persistently high disease activity was noted in the year before enrollment among carriers, although this was not statistically significant (27.7% vs 17.2%).

Significantly more carriers were receiving steroid treatment (83.3% vs 65.1%, P=0.01), but there was no difference in weekly prednisone dose (40.2 mg vs 49.1 mg).

“It should be considered that glucocorticoid treatment could determine skin abnormalities. In particular, permeability barrier homeostasis and stratum corneum integrity and cohesion could be modified by glucocorticoid treatment,” the researchers explained.

They also offered potential explanations for why carriage of S. aureus might contribute to lupus pathogenesis, stating that its presence “seems to induce an inflammatory response by exposing staphylococcal superantigen, molecular mimicry, causing increased toll-like receptor signaling in leukocytes, and inducing neutrophil extracellular traps.”

Carriage also could lead to T-cell activation, they suggested. “Data from the literature demonstrated that staphylococcal enterotoxins could bind directly the major histocompatibility complex class II of antigen-presenting cells. The presentation to T cells leads to massive nonspecific activation of the immune system, by stimulating around 20% of the naive T-cell population.”

A limitation of the study was the use of morphological evaluation for S. aureusidentification. In addition, it cannot be determined whether the association of carriage with the distinct disease phenotype “is an epiphenomenon rather than a causal factor.”

Nonetheless, further investigation into the skin microbiome in lupus is warranted, they concluded.

Drug Resistance Forecasts May Inform Drug Design


  • Drug Resistance Forecasts May Inform Drug Design

    Attempting to emulate the ability of chess grandmasters to think multiple moves ahead, scientists are learning to anticipate the most likely move–countermove scenarios that give rise to drug resistance. For example, scientists at Duke University and the University of Connecticut have developed a computational approach that can predict resistance mechanisms, including previously unidentified mutations—that pathogens might use to defeat new drugs. The scientists point out that their approach can be used long before new drugs are tested on patients.

    The scientists used their approach to evaluate a potential treatment for methicillin-resistantStaphylococcus aureus (MRSA) infections. Encouraged by the accuracy of their resistance forecasts in this work with Staphylococcus aureus, the scientists plan to broaden their efforts by evaluating drug resistance mutations that may occur in Escherichia coli and Enterococcus. Looking even farther ahead, the scientists say that their approach could help forecast drug resistance mutations in diseases such as cancer, HIV, and influenza. In these diseases, the scientist note, raising resistant cells or strains in the lab is more difficult to do than with bacteria.

    The scientists presented their results December 31 in the Proceedings of the National Academy of Sciences, in an article entitled, “Protein design algorithms predict viable resistance to an experimental antifolate.”

    “In this study, a structure-based protein design algorithm (K* in the OSPREY suite) was used to prospectively identify single-nucleotide polymorphisms that confer resistance to an experimental inhibitor effective against dihydrofolate reductase (DHFR) from Staphylococcus aureus,” wrote the authors. “Four of the top-ranked mutations in DHFR were found to be catalytically competent and resistant to the inhibitor. Selection of resistant bacteria in vitro revealed that two of the predicted mutations arise in the background of a compensatory mutation.”

    Essentially, the researchers used their algorithm to identify DNA changes in bacteria that would alter a drug’s protein target, an enzyme the bacteria need to build DNA. The researchers were particularly interested in DNA changes that would disguise the target from an experimental drug while allowing it to retain its biological function. Such changes would be expected to enhance antibiotic resistance.
    “We wanted to find out what countermoves the bacteria are likely to employ against these novel compounds. Will they be the same old mutations we’ve seen before, or might the bacteria do new things instead?” said study co-author Bruce Donald, a professor of computer science and biochemistry at Duke.

    From a ranked list of possible mutations, the researchers zeroed in on four single nucleotide polymorphisms, or SNPs. Though none of the mutations they identified had been reported previously, experiments with live bacteria in the lab showed that the researchers’ predictions were right.
    When the scientists treated MRSA with the new drugs and sequenced the bacteria that survived, more than half of the surviving colonies carried the predicted mutation that conferred the greatest resistance—a tiny change that reduced the drug’s effectiveness by 58-fold.

    The accurate forecast encouraged the researchers that their approach could be used to enable preemptive strategies in drug design, giving drug developers a head start on the next line of compounds that could remain effective despite resistance mutations. The model could also be expanded to anticipate a microbe’s response more than one move ahead, Donald said: “We might even be able to coax a pathogen into developing mutations that enable it to evade one drug, but that then make it particularly susceptible to a second drug, like a one-two punch.”

Researchers have developed an artificial spleen that cleans up blood infections


A new device can clean up blood infections and remove “everything from E. coli to Ebola”.

PicMonkey_Collage-web

Top images show the magnetic nanobeads binding to Escherichia coli (left) and Staphylococcus aureus(right)  in the blood. Bottom images show the artificial biospleen set up.

Scientists from the US have developed a new, high-tech device that can clear infections from blood – even those caused by unknown pathogens.

The technology was inspired by our own spleen, and, as Sara Reardon reports for Nature News, it can rid the blood of “everything from Escherichia coli to Ebola”.

Blood infections are extremely difficult to treat and can lead to sepsis – an extreme immune response that can be fatal. More than half of the time, doctors don’t know what causes these blood infections, and they have to rely on broad-scale antibiotics in an attempt to treat the original infection, Reardon explains. This isn’t always effective, and can lead to antibiotic resistance.

But this new artificial “biospleen”, developed by a team of researchers led by Donald Ingber from Harvard University’s Wyss Institute for Biologically Inspired Engineering in Boston, promises to filter the blood and get rid of these infections more effectively.

The device’s power lies in a special, magnetic-nanobead filter. To create the filter, the scientists took magnetic nanobeads and coated them with a modified version of a protein called mannose-binding lectin (MBL). This protein is found in humans and it binds to sugar molecules on the surface of more than 90 different bacteria, viruses and fungi – including the toxins that dead bacteria release, which can trigger sepsis.

As a patient’s blood passes through the biospleen, these MBL-coated magnetic nanobeads bind to the majority of pathogens. A magnet in the artificial spleen then pulls the beads and the bacteria and viruses they’re attached to out of the blood, leaving the blood purified and ready to be pumped back into the patient.

The device has now been tested on rats infected with either E. coli or Staphylococcus aureus. Five hours after infection, 89% of the rats whose blood had been filtered through the biospleen were still alive, compared to only 14% of those who were not treated. Impressively, the scientists found that the device had removed more than 90% of the bacteria from the rats’ blood. Theresults are published in Nature Medicine.

“The rats whose blood had been filtered also had less inflammation in their lungs and other organs, suggesting they would be less prone to sepsis,” writes Reardon.

The team then tested the biospleen on five litres of blood, which is the volume in the average human, and found that within five hours, the device could remove most pathogens.

Reardon explains at Nature News: “That degree of efficacy is probably enough to control an infection, Ingber says. Once the biospleen has removed most pathogens from the blood, antibiotics and the immune system can fight off remaining traces of infection — such as pathogens lodged in the organs, he says.”

The biospleen could also be used to treat viral infections such as HIV and Ebola, according to Ingber, and testing as now begun in pigs.

Nigel Klein, an infection and immunity expert at University College London in the UK, told Reardon that he expects the biospleen could be trialled in humans within a couple of years.

First case of infection with vancomycin-resistant Staphylococcus aureus in Europe.


Although vancomycin is often prescribed for the treatment of meticillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant S aureus (VRSA) infections remain rare, with only few cases confirmed worldwide—mostly in the USA.1Here, we report the isolation and preliminary characterisation of the first VRSA strain in Europe isolated from a patient in Portugal.

A 74-year-old woman with diabetes mellitus, chronic renal failure requiring haemodialysis, and peripheral vascular disease conditioning critical limb ischaemia underwent endovascular revascularisation and amputation of two gangrenous toes. Previous cultures of the wound amputation site revealed Pseudomonas aeruginosa and vancomycin-susceptible MRSA, for which she was treated with vancomycin and amikacin. In May, 2013, a meticillin-resistant VRSA strain was isolated from pus of the toe amputation wound. The minimum inhibitory concentrations for vancomycin and teicoplanin were >256 μg/mL and 24 μg/mL, respectively. Vitek 2 and MicroScan systems both detected VRSA. MALDI-TOF analyses confirmed the identification of S aureus. Vancomycin-resistant Enterococcus faecalis (VRE) and P aeruginosa were also isolated from the same wound.

The strain was sequence type ST105, SCCmec type II, and harboured the mecA and vanA genes, the latter was also identified in the VRE. The genetic background of the strain is similar to that of VRSA isolated in the USA.2 However, we have not identified an epidemiological link with the USA of the patient or health-care providers, and the concomitant isolation of VRE suggests a possible source for the vanA gene,3 supporting an independent acquisition of the vancomycin-resistance determinant. The VRSA was resistant to erythromycin, clindamycin, gentamicin, and ciprofloxacin, and susceptible to co-trimoxazole, tetracycline, tygecycline, linezolid, daptomycin, quinupristin/dalfopristin, fusidic acid, cloramphenicol, rifampicin, and mupirocin.

Precautions were reinforced. The patient is clinically well, and is being treated with daptomycin, rifampicin, and amikacin, and aggressive wound care. An epidemiological investigation is ongoing, but so far transmission of VRSA from this patient to contacts at home, other patients or health-care workers from the dialysis unit was not detected.

The identification of VRSA is particularly worrying since Portugal is a country with one of the highest prevalences of MRSA and VRE in Europe.4

In all cases of VRSA detected so far there was no spread of the strain. However, the potential sustained use of vancomycin, and the circulation of strains capable of receiving elements carrying vancomycin-resistance determinants5 raise the possibility of further selection of VRSA. To prevent the emergence and dissemination of these strains, adherence to infection control recommendations, antibiotic stewardship, and surveillance are essential.

JM-C has received research grants and honoraria for serving on the speakers bureaus of Pfizer, Novartis and Gilead. MR has received honoraria for serving on speakers bureau of Pfizer. The other authors declare that they have no conflicts of interest.

Source: Lancet

Panton-Valentine leucocidin and pneumonia.


Laura Shallcross and colleagues1 concluded on the basis of their meta-analyses that individuals with pneumonia were less likely to be infected with a Panton-Valentine leucocidin (PVL)-positive Staphylococcus aureus strain than are those with skin and soft-tissue infection. While PVL-positive strain might have a lesser propensity to cause pneumonia compared with skin and soft-tissue infection, these meta-analyses cannot be used to make any inference regarding whether or not PVL contributes to the pathogenesis and outcomes of pneumonia. Such inference could be made on the basis of comparison of outcomes in patients with PVL-positive pneumonia versus those with PVL-negative pneumonia. However, Shallcross and colleagues did not do a meta-analysis on outcomes of PVL-positive and PVL-negative pneumonia, but instead provide qualitative summary of pneumonia outcomes from seven studies that used different study designs and cannot be combined. Gillet and colleagues’ study2 addressing this issue was unfortunately excluded from their systematic review.1 Gillet and colleagues’ study showed that median survival was 4 days in patients with PVL-positive pneumonia compared with 25 days in patients with PVL-negative pneumonia, although overall mortality rates were not different between groups at 60 days after hospital admission.2 The rapidly fatal course of infection caused by the PVL-positive strains was associated with acute respiratory distress syndrome and characterised by severe hypoxaemia, leucopenia, haemoptysis, alveolar haemorrhage, and necrosis.2

An animal model is needed to investigate molecular mechanisms by which PVL induces the rapidly fatal course of haemorrhagic necrotising pneumonia. In this regard, Shallcross and colleagues’ review1 failed to identify another study3 that elucidated mechanisms by which PVL rapidly induces severe hypoxaemia, leucopenia, lung necrosis, pulmonary oedema, alveolar haemorrhage, haemoptysis, and death in a rabbit model of necrotising pneumonia. This rabbit model showed that PVL causes lung inflammation by activating and recruiting neutrophils into the lungs and then lysing them to release granule enzymes and reactive oxygen metabolites that damage the lungs.3 In contrast with the fact that rodent and monkey neutrophils are resistant to cytotoxic effects of PVL,3—5 the similar susceptibilities of rabbit and human neutrophils to PVL indicate that the rabbit model of necrotising pneumonia could be used for preclinical development and evaluation of anti-PVL therapeutic approaches. Ultimately, the question of whether or not PVL has a role in disease severity could be settled by a clinical trial testing efficacy of anti-PVL therapy (eg, specific monoclonal antibody that neutralises PVL) in protecting against rapidly progressive necrotising pneumonia in human beings.

References

1 Shallcross LJ, Fragaszy E, Johnson AM, Hayward AC. The role of the Panton-Valentine leucocidin toxin in staphylococcal disease: a systematic review and meta-analysis. Lancet Infect Dis 2013; 13: 43-54. Summary | Full Text | PDF(390KB) |CrossRef | PubMed

2 Gillet Y, Issartel B, Vanhems P, et al. Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Lancet 2002; 359: 753-759. Summary | Full Text | PDF(2631KB) | CrossRef | PubMed

3 Diep BA, Chan L, Tattevin P, et al. Polymorphonuclear leukocytes mediate Staphylococcus aureus Panton-Valentine leukocidin-induced lung inflammation and injury. Proc Natl Acad Sci USA 2010; 107: 5587-5592. PubMed

4 Loffler B, Hussain M, Grundmeier M, et al. Staphylococcus aureus panton-valentine leukocidin is a very potent cytotoxic factor for human neutrophils. PLoS Pathogens 2010; 6: e1000715. CrossRef | PubMed

5 Spaan AN, Henry T, van Rooijen WJ, et al. The staphylococcal toxin Panton-Valentine leukocidin targets human c5a receptors. Cell Host Microbe 2013; 13: 584-594. CrossRef | PubMed

Source: Lancet

 

Effectiveness of a bundled intervention of decolonization and prophylaxis to decrease Gram positive surgical site infections after cardiac or orthopedic surgery: systematic review and meta-analysis.


Abstract

Objective To evaluate studies assessing the effectiveness of a bundle of nasal decolonization and glycopeptide prophylaxis for preventing surgical site infections caused by Gram positive bacteria among patients undergoing cardiac operations or total joint replacement procedures.

Design Systematic review and meta-analysis.

Data sources PubMed (1995 to 2011), the Cochrane database of systematic reviews, CINAHL, Embase, and clinicaltrials.gov were searched to identify relevant studies. Pertinent journals and conference abstracts were hand searched. Study authors were contacted if more data were needed.

Eligibility criteria Randomized controlled trials, quasi-experimental studies, and cohort studies that assessed nasal decolonization or glycopeptide prophylaxis, or both, for preventing Gram positive surgical site infections compared with standard care.

Participants Patients undergoing cardiac operations or total joint replacement procedures.

Data extraction and study appraisal Two authors independently extracted data from each paper and a random effects model was used to obtain summary estimates. Risk of bias was assessed using the Downs and Black or the Cochrane scales. Heterogeneity was assessed using the Cochran Q and I2 statistics.

Results 39 studies were included. Pooled effects of 17 studies showed that nasal decolonization had a significantly protective effect against surgical site infections associated with Staphylococcus aureus (pooled relative risk 0.39, 95% confidence interval 0.31 to 0.50) when all patients underwent decolonization (0.40, 0.29 to 0.55) and when only S aureus carriers underwent decolonization (0.36, 0.22 to 0.57). Pooled effects of 15 prophylaxis studies showed that glycopeptide prophylaxis was significantly protective against surgical site infections related to methicillin (meticillin) resistant S aureus (MRSA) compared with prophylaxis using β lactam antibiotics (0.40, 0.20 to 0.80), and a non-significant risk factor for methicillin susceptible S aureus infections (1.47, 0.91 to 2.38). Seven studies assessed a bundle including decolonization and glycopeptide prophylaxis for only patients colonized with MRSA and found a significantly protective effect against surgical site infections with Gram positive bacteria (0.41, 0.30 to 0.56).

Conclusions Surgical programs that implement a bundled intervention including both nasal decolonization and glycopeptide prophylaxis for MRSA carriers may decrease rates of surgical site infections caused by S aureus or other Gram positive bacteria.

Discussion

Although multiple studies have assessed the efficacy of interventions to prevent surgical site infections caused by Gram positive bacteria, these interventions are not uniformly applied to surgical patients. Our results showed that nasal decolonization was associated with decreased rates of Gram positive surgical site infections andStaphylococcus aureus surgical site infections among patients undergoing cardiac or orthopedic surgical procedures. However, these results remained statistically significant for S aureus surgical site infections, though not all Gram positive surgical site infections, when the meta-analysis was limited to randomized controlled trials. Additionally, a bundle that included nasal decolonization and glycopeptide prophylaxis for patients who carried methicillin (meticillin) resistant S aureus (MRSA) was associated with significantly decreased rates of surgical site infections caused by Gram positive bacteria and by S aureus.

We also found that routine use of prophylactic glycopeptides protected against MRSA infections but not against all Gram positive surgical site infections. Additionally, dual prophylaxis with a glycopeptide and another antimicrobial agent seemed to be more protective against Gram positive surgical site infections than prophylaxis with glycopeptides alone. This finding is consistent with studies of methicillin susceptible S aureus (MSSA) bacteremia, which found that vancomycin is less effective than a β lactam antibiotic for treating MSSA infections.63 64 These results are similar to the conclusions of a recent review article, which stated that vancomycin is not recommended for preoperative prophylaxis but may be considered as a component of an MRSA bundle to prevent surgical site infections.65

Our meta-analyses were the first to assess a bundle that included nasal decolonization and targeted glycopeptide prophylaxis for MRSA carriers. Other meta-analyses have assessed nasal decolonization or glycopeptide prophylaxis alone,66 67 68 and our results confirm the findings of the previous studies and extend these by including the results of recent studies. Future meta-analyses should assess other outcomes associated with these interventions. These outcomes could include duration of hospital stay since one group of researchers found that the mean duration of hospital stay was significantly shorter in those randomized to mupirocin and chorhexidine gluconate rather than to placebo.27 Future meta-analyses should also confirm our preliminary findings that these interventions do not open a niche for pathogens other than S aureusto fill, and should also analyze other patient populations such as those requiring trauma surgery to determine if these findings are generalizable to other surgical specialties.

Nasal decolonization protected against S aureus surgical site infections when all patients were decolonized and when only S aureus carriers were decolonized. Routine nasal decolonization of all surgical patients may be easier to implement and more cost effective than using cultures or polymerase chain reaction testing to screen patients preoperatively.69 None the less, it may be prudent to reserve mupirocin decolonization for patients who carry S aureus to prevent widespread mupirocin resistance.70Similarly, it may be prudent to do further research on targeted prophylaxis with vancomycin before including this bundle in clinical practice. Of note, the pooled relative risks assessing Gram positive surgical site infections were identical for both the decolonization studies and the bundle studies. Thus high quality studies such as cluster randomized trials are still needed to determine whether adding glycopeptide prophylaxis to nasal decolonization will further decrease the incidence of Gram positive surgical site infections.

In our sensitivity analyses we found that nasal decolonization was associated with a 1% risk difference and the bundle was associated with a 0.5% risk difference in Gram positive surgical site infections. Although these differences seem small, they are clinically significant considering that cardiac and orthopedic operations are common and surgical site infections are associated with considerable morbidity. Each year, approximately 300 000 cardiac operations and approximately 900 000 total joint arthroplasties are done in the United States alone.71 Thus these interventions could prevent 6000 to 12 000 surgical site infections per year in the United States and even more worldwide.

Limitations of this study

Our study has some limitations. Firstly, meta-analyses are only as valid as the studies that contribute to the pooled risk ratio. We included many studies that were simple before and after quasi-experimental studies. Additionally, none of the included studies adjusted statistically for potential confounders, thus confounding may be problem, especially among the observational studies. To mitigate this limitation, we performed subset analyses on the results of only randomized controlled trials. Secondly, we did not include studies that did not report or could not provide specific data on Gram positive infections, thus we may have excluded important decolonization and prophylaxis studies. However, nine of 15 contacted investigators submitted additional data for inclusion in the analyses. Thirdly, studies of the association between interventions and Gram positive surgical site infections were heterogeneous, and thus some of the meta-analysis results should be interpreted with caution. Once these studies were stratified by potential sources of heterogeneity, the stratified subsets were homogeneous. For example, nasal decolonization aims to decrease the incidence of endogenous S aureus surgical site infections. The association between nasal decolonization and Gram positive surgical site infections may have been different for studies in which S aureus caused most Gram positive surgical site infections compared with studies in which surgical site infections due to other Gram positive pathogens were common. Thus we limited heterogeneity by doing subset analyses that separated studies focusing on S aureus surgical site infections from those focusing on all Gram positive surgical site infections.

Conclusion

Surgical site infections caused by Gram positive bacteria may be prevented by decolonizing patients who carry S aureus in their nares and potentially by adding a glycopeptide to the usual prophylaxis using β lactam antibiotics for MRSA carriers. High quality randomized controlled trials or cluster randomized trials should be performed to further assess this bundle.

What is already known on this topic

  • Surgical site infections (SSIs) are potentially preventable adverse events of cardiac and orthopedic operations
  • SSIs significantly increase hospital length of stay, readmission rates, healthcare costs, and mortality rates
  • Clinicians and researchers have debated whether nasal decolonization or glycopeptide antibiotic prophylaxis reduce SSIs caused by Gram positive bacteria
  • Among patients undergoing cardiac or orthopedic surgery:
  • Nasal decolonization with mupirocin ointment was protective against Gram positive SSIs
  • Preoperative prophylaxis with anti-methicillin (meticillin) resistant Staphylococcus aureus (MRSA) antibiotics when given to all patients was not protective against Gram positive SSIs
  • A bundle that included nasal decolonization and anti-MRSA prophylaxis for MRSA carriers was significantly protective against Gram positive SSIs

What this study adds

 

  • Among patients undergoing cardiac or orthopedic surgery:
  • Nasal decolonization with mupirocin ointment was protective against Gram positive SSIs
  • Preoperative prophylaxis with anti-methicillin (meticillin) resistant Staphylococcus aureus (MRSA) antibiotics when given to all patients was not protective against Gram positive SSIs
  • A bundle that included nasal decolonization and anti-MRSA prophylaxis for MRSA carriers was significantly protective against Gram positive SSIs

Source: BMJ

 

 

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