Why infection prevention and control teams should be on Twitter!

Guest Blogger Infection Prevention and Control , ,

twitter birdie 2

Guest bloggers Fiona Reakes-Wells and Carolyn Dawson write…

“Are you going to twit that?” honorary IPC team member (my mother) asked one day when I took a picture. “Will I be famous?”.

Twitter, tweet, retweet, hashtag, Follow Friday (FF) are commonly used jargon you will find in your friendly “twictionary”, however these days they are also terms you will often hear used in your daily lives.  The small blue Twitter bird symbol is used by the media, advertising companies, universities, and even governmental departments for quick and concise information sharing with the masses.  However under its umbrella term of ‘social media’, Twitter is met with scepticism by some people, a frivolous exercise opening yourselves up to criticism and destroying professionalism.  But is this truly the case?

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Q-fever and lymphoma linked!

Andreas Voss (@AVIPNL) Q-fever , ,

Schermafbeelding 2015-10-08 om 15.04.38

Okay, the following is not strictly infection control, but it has to do with infections and it will have major impact on how people who were unfortunate enough to contract Q-fever will feel about their safety.   The pathway of chronic infections – interaction with IL-10 – immune-supression and cancer isn’t new, but to my knowledge mainly described in viruses. The Netherland had one of the largest outbreaks of Q-fever, leaving behind a sizable number of (chronic) Q-fever patients.  Many of these patients will be shellshocked by the increased chance of developing lymphoma. Consequently, research to cooperate (or dismiss) Raoult’s study is needed, to relief the patient population from uncertainty.

Bacterium that causes Q fever linked to non-Hodgkin lymphoma

AMERICAN SOCIETY OF HEMATOLOGY

(WASHINGTON, October, 13, 2015) -The bacterium that causes Q fever, an infectious disease that humans contract from animals, is associated with an increased risk of lymphoma, according to a study published online today in Blood, the Journal of the American Society of Hematology (ASH).

Q fever is caused by infection with Coxiella burnetii, a bacterium primarily transmitted through the excrement of cattle, sheep, and goats. Approximately 3 percent of healthy adults in the United States and 10-20 percent of those in high-risk occupations such as veterinarians and farmers have antibodies for C. burnetii, suggesting previous infection.1 Symptoms of Q fever vary from person to person and can be acute and resolve spontaneously, or chronic and persistent. Because some patients have been reported to also suffer from lymphoma, researchers believed that this type of cancer could be a risk factor for Q fever. However, the experience of one patient prompted doctors to consider the opposite – that the infection might actually cause the lymphoma.

“During a follow-up scan in a patient we had successfully treated for Q fever, we observed a tumor close to the location of the previous infection,” said senior study author Didier Raoult, MD, PhD, of Aix-Marseille University in Marseille, France. “The discovery that it was a lymphoma tumor containing C. burnetii encouraged us to consider that the infection might have contributed to the development of the cancer.”

In order to better understand the association between C. burnetii and lymphoma, Dr. Raoult and colleagues screened 1,468 patients treated at the French National Referral Center for Q Fever from 2004 to 2014. Investigators conducted imaging of patient tissue samples to identify seven people, including the initial patient, who developed lymphoma after C. burnetiiinfection (6 patients were diagnosed with diffuse large B-cell lymphoma and one with follicular lymphoma). Of all the Q fever patients included in the study, 440 presented a persistent infection concentrated to one area.

To determine if patients with Q fever have a higher risk of lymphoma than the general population, researchers compared the incidence of lymphoma in the Q fever registry to the incidence reported in France’s general population. Based on this analysis, researchers conclude that patients with Q fever are 25 times more likely to develop diffuse large B-cell lymphoma than those without the infection. In addition, the odds of lymphoma in patients with persistent concentrated infections are higher than those with other forms of Q fever.

Upon further imaging of the patient samples, investigators observed that Q fever patients with lymphoma demonstrate overproduction of the critical anti-inflammatory pathway interleukin-10 (IL-10), suggesting that suppression of the immune system may have allowed the lymphoma cells to evade immune detection and multiply.

“As we continue to learn more about the association between C. burnetii and lymphoma, these results should encourage clinicians to survey high-risk patients as early as possible for potential cancer,” said Dr. Raoult. “Ultimately, this early diagnosis and treatment would improve outcomes for Q fever patients who subsequently develop lymphoma, particularly those with B-cell non-Hodgkin lymphoma.”

Guidelines to control multidrug-resistant Gram-negative bacteria: an ‘evidence-free zone’

Jon Otter (@jonotter) MDR-GNR , , , , ,

citation needed

I recently had a review published in CMI comparing EU guidelines for controlling multidrug-resistant Gram-negative bacteria (MDR-GNB). I included the following guidelines in my review: ECCMID 2014, Irish MDRO, PHE CPE, HPS CPE, ECDC systematic review on CPE (not strictly a guideline, but did include some recommendations). A couple of important points arise:

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I’ll take the tube.. out!

Martin Kiernan (@emrsa15) CAUTI , ,

file6971249324663A few papers on the use of urinary catheters have caught my eye recently. It’s a subject close to my heart and was the subject of my eponymous lecture at the Infection Prevention 2013 meeting in London, available online for insomniacs via the excellent Webber Training Teleclass recording The slides are here. Despite these devices being second to peripheral cannulation in the ‘most’ used devices’ awards annually (and a clear winner in the ‘most overused’ section), the evidence base is somewhat thin. Are they inserted well? Possibly (and indeed probably) not. Do they only get inserted appropriately and are they speedily removed? Um… maybe not. Continue reading →

Spread the word, not the MDROs!

Guest Blogger Epidemiology , ,

xdro registry

Guest blogger, Rita Bos (bio below) writes:

This month, while randomly searching Pubmed with the subject MDRO (I know, a rather bizarre hobby), I came across a French study on MDRO information in patient transfer letters. In this paper, which was published in the French journal “Médecine et maladies infectieuses” Lefebvre et al (of the Infection Control Unit of the Dijon University Hospital, Dijon, France) investigated the proportion of transfer letters that contained information of infection or colonization with MDR bacteria.

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Molecular diagnostics for C. difficile infection: too much of a good thing?

Jon Otter (@jonotter) C. difficile , , , ,

A study in JAMA Internal Medicine suggests that we may be ‘overdiagnosising’ C. difficile in this era of molecular diagnostics. The researchers from California grouped the 1416 patients tested for C. difficile into three groups: Tox+/PCR+ (9%), Tox-/PCR+ (11%), and Tox-/PCR+ (79%) (see Figure). Perhaps unsurprisingly, compared with Tox+/PCR+ cases, Tox-/PCR+ cases had lower bacterial load, less prior antibiotic exposure, less faecal inflammation, a shorter duration of diarrhoea, were less likely to suffer complications, and were less likely to die within 30 days. Perhaps even more importantly, patients with Tox-/PCR+ were pretty much identical to patients with Tox-/PCR- specimens in all of these metrics. In short: these patients had C. difficile in their gut, but they did not have C. difficile infection. The key message here is that we should not be treating patients who are C. difficile “positive” by molecular tests only.

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Reflections from Infection Prevention 2015 Part III: Thinking outside the box

Jon Otter (@jonotter) Conferences , , , , , , ,

think outside the box

For the third and final installment of my blog-report from Infection Prevention 2015, I thought I’d cover some of the more innovative approaches in and around the IPC sphere:

Part I: Beating the bugs

Part II: Improving the systems

Part III: Thinking outside the box

New technology to improve hand and environmental hygiene

I for one am pretty sick of seeing unrealistically high levels of hand hygiene compliance being reported from peer-to-peer manual auditing approaches. One way to get more realistic compliance data is through automated approaches to hand hygiene compliance, reviewed here by Drs Dawson (Warwick) and Mackrill (Imperial College London), who also presented their findings at the conference, and by another group here. Drs Dawson and Mackrill considered issues around product usage, self-reporting, direct observation, perceptions of technology (often viewed, unhelpfully, as a ‘silver bullet’), and staff perceptions of need and benefit. They divided the technology into those that monitored product usage, surveillance systems that monitored individual performance, and systems that monitored both product usage and individual performance. Although automated surveillance systems will always be imperfect and involve a degree of inference, would you rather monitor the 5 moments sporadically / badly or have robust measurements of a smaller number of moments? Automated surveillance methods will not replace manual audits – at least for now – but it’s time to take a long hard look at what is available.

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Reflections from Infection Prevention 2015 Part II: Improving the systems

Jon Otter (@jonotter) Conferences , , , , ,

Swiss_cheese_model_of_accident_causation

Welcome to the second installment of my blog-report from Infection Prevention 2015, focused on improving the systems around the delivery of safe healthcare, and infection prevention and control:

Part I: Beating the bugs

Part II: Improving the systems

Part III: Thinking outside the box

The economics of HCAI is going to become increasingly important as the NHS – and healthcare systems worldwide – continue to “seek efficiency savings” (aka demand more for less). So the overview of HCAI economics from Dr Nick Graves (QUT, Australia) was timely. I find it remarkable that we are still so reliant on the 2000 Plowman report to gauge the cost of HCAI – surely there must be a more sophisticated approach? There is something rather uncomfortable about setting an ‘acceptable’ level of HCAI, or putting a £ value that we would be prepared pay to save a life, but this is exactly what we have to do to manage the demands of scarcity. Dr Graves presented some useful worked examples to illustrate his point, around coated catheters, hip replacements, hand hygiene improvement, and MRSA screening. In most cases, there comes a point where a health benefit is too expensive to ‘purchase’, which is an uncomfortable but very real choice across all areas of healthcare (e.g. cancer drugs).

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Reflections from Infection Prevention 2015 Part I: Beating the bugs

Jon Otter (@jonotter) Conferences , , , ,

time person of the year

Infection Prevention 2015, the annual conference of IPS, was held in Liverpool this year. I’m delighted to say that the abstracts from the submitted science are published Open Access in the Journal of Infection Prevention. This first instalment of my report will be “bug-focussed”, followed by another two on different themes:

Part I: Beating the bugs

Part II: Improving the systems

Part III: Thinking outside the box

Opening lectures

The conference kicked off with fellow ‘Reflections’ blogger Prof Andreas Voss. By Andreas’ own admission, he was given a curve-ball of a title: ‘CRE, VRE, C. difficle or MRSA: what should be the priority of infection prevention?’ [No idea where that could have come from…] Andreas developed a framework for grading the priority of our microbial threats, accounting for transmissibility, virulence, antibiotic resistance, at-risk patients, feasibility of decolonisation, cost, and impact of uncontrolled spread. And the result? Any and all microbes that cause HCAI should be a priority of infection prevention. Even those that seem to have less clinical impact (such as VRE) are good indicators of system failure. If we focus too much on one threat, we risk losing sight of the bigger picture.

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What is the fitness cost of mupirocin resistance?

Guest Blogger MRSA , ,

Jon posted a blog last week on mupirocin resistance in MRSA. This week, guest blogger Dr Gwen Knight (bio below) writes about a companion paper also published in the Journal of Antimicrobial Chemotherapy, which models mupirocin resistance…

It is a truth universally acknowledged, that acquiring most mechanisms of drug resistance incurs a fitness cost to the host bacterium. Determining the size of this cost and the impact that this cost will have on the spread of drug resistance is difficult. Is a 10% reduction in growth rate in the laboratory enough to stop resistance spreading in a hospital?

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