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Journal ofContinuingEducation

Official publication of the American Medical Technologists

January 2013Volume 15 ■ Number 1

TOPICSISSUES

TOPICSISSUES&&

✒ Combatting an Emerging Bacterium

✒ Discovering Medical Nemesis

✒ The Laboratory and Tight GlycemicControl

✒ Update on Kingella kingae:Pathogenesis,Identification, andTreatment

✒ Infectious Mononucleosis:A Brief Review

Inside This IssueInside This Issue

For additional Information:Contact AMT: 10700 West Higgins Road, Suite 150Rosemont, IL 60018Phone 847/823-5169 • Fax: 847/823-0458E-mail: [email protected] Website: www.americanmedtech.org

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AMT 75th Educational Program & National Meeting • July 8–12, 2013

PITTSBURGH, PENNSYLVANIA

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Omni William Penn Hotel530 William Penn Place, Pittsburgh, PA 15219Phone (412) 281-7100Website: http://www.omnihotels.com/

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o know Pittsburgh, you have to see it for yourself. Come and see a city that has had a remarkable environmental renaissance, a top-10 city for certified green building space, a city ripe with natural and cultural amenities. • Pittsburgh International Airport is nation’s third largest airport.

• In a statement to the New York Times, Prince Phillip said that Pittsburgh is the only city he has ever seen that has an entrance. The first glimpse of the Golden Triangle upon exiting the Fort Pitt Tunnel, on the way in from the airport, is absolutely incredible!

• There are 50 museums located in and around the Pittsburgh area.• Pittsburgh, the “City of Champions,” is a sports fan’s paradise with a new football

stadium and new baseball park.• Located just a short drive from Pittsburgh is one of the most famous private

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Contents2 AMTIE President’s Report

4 Article 393Combatting an Emerging BacteriumMatthew T. Patton

6 Questions for Article 393

10 Article 394Discovering Medical NemesisSol Goldenberg


14 Article 395The Laboratory and Tight Glycemic ControlDavid Plaut and Deena Davis


17 Fast Facts

18 Article 396Update on Kingella kingae: Pathogenesis, Identification, and TreatmentEleanor Powell and Joel Mortensen


26 Article 397Infectious Mononucleosis: A Brief ReviewGerard P. Boe


30 AMT Directory

32 Abstracts From the Current Literature

Journal of Continuing Education Topics & Issues (ISSN 1522-8606) is published in January, April, and August under the sponsor-ship of the American Medical Technologists, 10700 W. Higgins Rd., Suite 150, Rosemont, Illinois 60018. Copyright 2013 by Amer-ican Medical Technologists. Subscriptions include three issues of Journal of CE Topics & Issues and four issues of AMT Events:$50.00/year + $10 postage for foreign countries. Members may not deduct subscription price from dues.Postmaster: Please send change of address to AMT, 10700 W. Higgins Rd., Suite 150, Rosemont, Illinois 60018.Moving? Be sure AMT publications move with you. Send your new address and old mailing label from an AMT publication to AMT six weeks before you move.Cover photo: Linoleic photomicrograph, © Eric Clark, National High Magnetic Field Laboratory, Florida State University, Tallahassee.

EditorGerard P. Boe, PhD

Associate EditorDiane Powell

Business OfficeAmerican Medical Technologists10700 W. Higgins Rd., Suite 150Rosemont, IL 60018847-823-5169e-mail address: [email protected] Site: http://www.americanmedtech.org

Journal ofContinuingEducationJanuary 2013

Volume 15 ■ Number 1

TOPICSISSUES&

2 January 2013 • Continuing Education Topics & Issues

Amer ican Medica l Technolog is ts Inst i tu te for Excel lence (AMTIE)

PRESIDENT’S REPORTGreetings! I hope each of you had a joyous holiday season with your family and

friends. The big tree has come down but the rest of the decora-tions are staying up for a while. It is a season, not a day, and Ilike the decorations, and love the feeling of sharing, and giving.

Events for your consideration:

• The national AMT meeting is the week of July 8th in Pitts-burgh, PA.

• Two openings will be available on the AMTIE Board. Theterms of Marty Hinkel and Kay Fergason will expire. Martyis eligible for re-election, but Kay has reached her term lim-its and will not be running again. Please consider runningfor a position on the AMTIE Board. The AMTIE Board is awonderful opportunity to solicit donations and give scholar-ships to members and students. A nomination form can be downloaded from theAMT website. The form must be completed and received by the AMT home officeby April 1, 2013, in order to be printed in the AMT publication AMT Events. Thedeadline for declaring candidacy is July 8th at 10 am.

• Please consider donating to the Chester B. Dziekonski Memorial Fund when youpay your dues. Money donated is tax deductible. Monies contributed are for twocontinuing education/continued competency grants of $500. Grants are awarded atthe national convention .

• Did you have fun during the AMTIE fund raiser last year in San Antonio? An-other fun surprise is planned for you in Pittsburgh. Taffy Durfee has agreed tohead up a silent auction. Georgia AMT member Peggy Oiler has suggested thatmembers donate their custom crafts for this event. Many members seem to be ex-cited about this fund-raiser and willing to show off their talents. I already knowsomething I want to bid on. If you would like to participate and donate to theauction, please send Taffy a message at [email protected]. We will againhave the 50/50 raffle.

• The deadline for applications for the scholarships is April 1, 2013. If you are con-tinuing your educational quest in one of the allied health careers that are certifiedby AMT or you know a high school student who plans to attend an AMT certifi-cate program, go to the AMT website and download an application. There areseparate applications for AMT members and students. The scholarships includeone AMT member scholarship of $2,500, three AMT member scholarships of$1,500, and five student scholarships of $500.

As an AMT member, you have the opportunity to participate at the state societylevel and on the national level. Your efforts are appreciated!

You are the “Pride of the Profession.”

Best regards,

Linda

Linda Jones, MT,AMTIE President

Continuing Education Topics & Issues • January 2013 3

April 1 is the filing deadline for applications and supportingdocuments in the AMTIE 2013 undergraduate/graduate scholar-ship program and for grants to high school graduates pursuingmedical technology, medical assisting, dental assisting, or phle-botomy studies.

Up to three $1,500 AMT Member Scholarships may beawarded annually. Applicants must be members in good stand-ing with AMT and enrolled in a college or university accreditedby a regional accrediting commission. The course of study shouldbe concerned with the disciplines certified by AMT. Scholarshiprecipients will be selected by the AMT Institute of Excellenceand scholarship committee based on financial need, career goals,and previous scholastic record.

Up to five $500 Student Scholarships are awarded annuallyand available to high school graduates interested in pursuingmedical technology, medical assisting, dental assisting, or phle-

botomy studies. Applicants must be enrolled or planning to en-roll in a school accredited by an accrediting agency recognizedby the U.S. Dept. of Education, or enrolled or planning to enrollin college, university, or junior college medical technology,medical assisting, dental assisting, or phlebotomy studies.Scholarship recipients will be selected by AMTIE Board ofTrustees based primarily on need; taken into consideration areindividual goals and motivation, school grades, participation inextracurricular activities, work experience, and personal refer-ences.

All scholarships will be awarded during the 2013 AMT Na-tional Convention in Pittsburgh, PA, July 8–12.

For information and to receive an application, visitwww.americanmedtech.org

Application deadline is April 1, 2013.

2013 AMTIE Scholarships

Be paid to write a feature or technical article! Whether you have something to say about anunusual laboratory procedure, research findings, theory — or just have some thoughts about yourrole as a professional, AMT encourages you to “put pen to paper” and share your expertise orwisdom.

Topics should be related to the medical technologist, medical assistant, dental assistant, orphlebotomist disciplines, allied health instruction, or lab consulting. Practical knowledge,research, techniques, scientific studies, and management are all possible areas for exploration.Or articles on solutions to personnel problems, or any day-to-day experiences as a professionalin the fields mentioned above would also be welcomed.

Papers must be original, never-before-published works, typed and double-spaced, and at least1,500 words in length. Technical or scientific articles must include a bibliography. Mail articlesto: [email protected], or AMT Events, 10700 W. Higgins Rd., Suite 150,Rosemont, IL 60018. All articles become the property of American Medical Technologists,which reserves publication rights.

If your article is selected for publication by the AMT Editorial Advisory Board, you will benotified and a stipend will be paid if you are a first time writer for AMT publications.

NOTE: This program is open to AMT members only.

A Great Opportunity!

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Gain Monetary Reward!


It's often said war comes with a price. In this case,one of the costs of war was the acquisition and ulti-mately the introduction of what some fear couldcause widespread infection and death.

It's multidrug resistant Acinetobacter baumanniiand it was introduced into North America by troopsreturning from the Middle East in Canadian soldiersinjured and requiring mechanical ventilation as a partof the medical treatment.1 The ventilators were popu-lated with the organism that was passed along to thepatients. In addition, soldiers acquired skin infectionsas a result of chafing with secondary infections.1,2

Already, tens of thousands of hospital patients havedied from a result of infection.3

Jason Tetro, microbiologist and Coordinator forEmerging Pathogens Research Centre and Centre forResearch on Environmental Microbiology in Ottawa,Canada, said, “A. baumannii is ubiquitous in soil andsurface water and can be carried on the skin by nor-mal healthy individuals without any clinical conse-quences.”

“However, the bacterium is opportunistic and caninfect individuals who have compromised immunesystems. The rise in such individuals is primarily thereason for the increase in the case rate of these infec-tions. As with any bacterium, an increased prevalenceeventually leads to increased antibiotic resistance,” heexplained.4,5

Amesh Adalja, MD, FACP, clinical assistant pro-fessor at the University of Pittsburgh (PA) MedicalCenter said, “A. baumannii is on the rise for severalreasons, the most important being the proportion ofpatients in hospitals who transition from hospital tonursing home and long-term care facility and backseveral times. He said these patients serve almost asvectors for the bacterium and introduce it into hospi-tal settings which can then foster nosocomial spreadthrough lax infection control practices.”

The New MRSA?The similarities for the potential of widespread in-

fection sound strikingly and alarmingly familiar toMethicillin-resistant Staphylococcus aureus (MRSA).According to the Centers for Disease Control and

Prevention, MRSA is a type of staph bacteria resis-tant to treatment with a certain group of antibioticscalled beta-lactams, including methicillin, oxacillin,penicillin and amoxicillin.

“The most ominous issue with A. baumannii issome strains are multi-drug resistant. We have no newdrugs to combat it and, in some cases, there is nothinga physician can do to treat this infection,” explainedDr. Adalja.

From a purely infection control perspective, Tetrosaid healthcare practitioners may very well be staringdown the barrel of the next strong, drug-resistant out-break. “Hospitals are unfortunately the new breedingground for infections and as MRSA started in healthcare facilities, so can be said for A. baumannii,” hewarns. “Also, as MRSA became increasingly com-munity-acquired, the same is occurring with A. baumannii albeit at a slower rate.” He said theproblem for both these bacteria lies in the number ofimmunocompromised individuals who cannot co-exist with the opportunistic organisms and prevent in-fection.

Adalja is concerned, but not panicked. “I think inspecific patient segments it could be akin to MRSA.However, I do not think this organism possesses theattributes necessary to cause a widespread epidemicin otherwise healthy individuals (unlike MRSA),” henoted. “A. baumannii infections principally occur infrail, elderly, chronically hospitalized individuals re-flecting the predilection of this bacterium for a com-promised host,” he said.

There are exceptions. In fact, some of those in-clude military personnel with wounds. “But for themost part, A. baumannii would have trouble sustain-ing an epidemic in the general population. In the hos-pital — especially ICUs — it is considered on parwith MRSA,” Dr. Adalja noted.

Strict Infection ControlTetro said that, for the most part, all healthcare

practitioners should be aware of the bacterium as apotential cause of illness.

“[Healthcare practitioners] especially need to un-derstand the clinical symptomology of this infection,

Article 393 0.5 Clock Hour

Matthew T. Pattonis a freelance writerbased in Atlanta.Visit his website atwww.matthewtpat-ton.com.

Combatting an EmergingBacteriumCould a new drug-resistant “superstrain” be lying in wait?

Matthew T. Patton


which can range from UTIs to wound infection tobloodstream infections to meningitis,” he said. In theevent they notice any possible change in a patient's con-dition relating to these clinical impacts, they should beready to explore the potential etiology of this bacteri-um.

Moreover, should A. baumannii be identified, Tetrosaid an immediate identification of any antibiotic resis-tance is necessary “such that proper stewardship can beperformed.” Finally, any evidence of infection shouldbe reported to the local health authorities for tracking.

Sheryl A. Whitlock, MA, MT(ASCP)BB, laboratorycoordinator at the University of Delaware StudentHealth Services in Newark along with Kevin E. Whit-lock, MT(ASCP)CM, a medical student at the Philadel-phia (PA) College of Osteopathic Medicine, stress theincrease in antimicrobial resistance may be related tooveruse of antibiotics.

“Multidrug resistant organisms have developed andpresent a new public health hazard related to, but notexclusively caused by, extensive use of antibiotics. Theunnecessary use of antibiotics has been addressed in themedical community extensively, but in some casesmight be shutting the barn door after the horse is out,”explained Sheryl A. Whitlock.

“In addition to overuse of antibiotic agents, somepatients who always want antibiotics do not finish acourse and then allow the microorganisms to ‘changetheir colors’ and develop a resistance to the previously

susceptible antibiotic,” Kevin E. Whitlock noted. “Mi-croorganisms require complete extermination and whenthis does not happen, the few remaining organisms maybecome resistant.”

Dr. Adalja asserted laboratory professionals andother healthcare workers will have to remain vigilantfor the presence of this bacteria and, when it is present,abide by strict infection control procedures includingvigorously monitoring hand hygiene, donning appro-priate gloves and gowns and ensuring proper antimi-crobial therapy is initiated. He also stressed healthcarepractitioners can decrease the impact of the bacteriumsimply by ensuring 100 percent compliance with estab-lished infection control guidelines.

References1. Peleg AY, Seifert H, Paterson DL. Acinetobacter baumannii:

Emergence of a successful pathogen. Clin Micro Rev. Availableat: http://cmr.asm.org/content/21/3/538.full. Last accessed May2, 2012.

2. Tien H, Battad A, Bryce E, et al. Multi-drug resistant Acineto-bacter infections in critically injured Canadian forces soldiers.BMC Infectious Diseases 2007, 7:95.

3. Pollack A. Rising threat of infections unfazed by antibiotics. NewYork Times. Available at: http://www.nytimes.com/2010/02/27/business/27germ.html. Last accessed April 28, 2012.

4. Acinetobactor baumannii. Available at: www.acinetobacter.org.Last accessed April 27, 2012.

5. The Invisible Enemy. Available at: www.wired.com/wired/archive/15.02/enemy.html. Last accessed April 30, 2012.

CAREER OPPORTUNITY

in Tonopah, Nevada, has openings for a Full Time

Medical Technologist Supervisor/ManagerRequirements: ASCP or AMT certified, strong blood banking experience and

a Nevada General Supervisor License. Previous Supervisor experience preferred. Excellent employment package offered including benefits. Relocation costs covered where applicable.

Interested candidates should send their resume with cover letter to:Human Resources, [email protected] or fax 775-482-2480.

Call 775-482-6233 HR Dept. with questions. NRMC is an equal opportunities employer


1. A. baumannii has origins in:A. daycare populationsB. troops returning home from the Middle

EastC. well waterD. veterinary clinics

2. Acinetobactor baumannii can be carried onthe skin by normal healthy individualswithout any clinical consequences.

A. TrueB. False

3. A. baumannii is on the rise because of:A. understaffed facilities, particularly

healthcare practitioner to patient ratios.B. inappropriate use of medical

equipment.C. the proportion of patients in hospitals

that transition from hospital to nursinghome and long-term care facility andback several times.

D. decreased antimicrobial resistance.

4. MRSA is a type of staph bacteria resistant totreatment with certain group of antibioticsincluding:

A. fluvastatin sodium.B. acetaminophen and oxycodone.C. lisinopril, moexipril, and perindopril.D. methicillin, oxacillin, penicillin and

amoxicillin.

5. A. baumannii infections principally occur instrong, irregularly hospitalized elderlyindividuals.

A. TrueB. False

6. Which of the following is not typical ofA. baumannii?

A. UTIs B. wound infection C. bloodstream infectionsD. myocardial infarction

7. Multidrug resistant organisms have developedand present a new public health hazard relatedto, but not exclusively caused by:

A. extensive use of antibiotics.B. increased allergies to latex gloves.C. handwashing techniques.D. compromised hosts.

8. Patients who do not complete a prescribedcourse of antibiotics typically pose a risk totheir own healthcare.

A. TrueB. False

9. Which of the following can best help curb thespread of multidrug resistant organisms?

A. innovative laboratory methodsB. vigorous hand hygieneC. discontinued use of ventilatorsD. patient discharge data

10. What approach can best help reduce theimpact of A. baumannii?

A. increased use of antibioticsB. increased staffing in long-term care

facilitiesC. ensuring 100 percent compliance with

established infection control guidelinesD. frequent communication with the

Centers for Disease Control and otherreporting agencies

Questions for STEP ParticipantsAMT strongly encourages you to submit your answers online so that the CE credits can be auto-

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Article 3930.5 Clock Hour

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Almost 30 years ago, Ivan Illich wrote a bookon Medical Nemesis, which suggested that med-ical care can do more physical and social harmthan good. He described it as “social Iatrogene-sis” suggesting that medical damage to an indi-vidual can occur by a sociopolitical mode. Hesuggested that medical bureaucracy creates ill-health by increasing stress, by multiplying dis-abling dependence, by generating new painfulneeds, by lowering the levels of tolerance for dis-comfort or pain and by abolishing even the rightto self-care.

Three years ago, Shannon Brown wrote a bookentitled “Overtreated: How much Medicine is Mak-ing Us Sicker and Poorer.” This impressed Dr. VikaiSaini, a Harvard cardiologist and president ofThe Lown Foundation, to set up a conference atCambridge, Massachusetts, and invited 130prominent doctors from USA, Canada and theUK. The purpose of the conference was to ex-plore the problem of over-investigation and over-treatment of patients. U.S.A.'s per capita spend-ing was rising sharply, faster than lifeexpectancy. The conference concluded that thereasons for this ever increasing cost of medicalcare were due to:

1) Fear of malpractice lawsuits2) Supply driven demand3) Knowledge gaps4) Biased research5) Profit seeking6) Patient demand7) Financial conflicts of guideline writers8) Failure to inform the patient of potential

harm9) The way US doctors are paid by fee of

service.Participants poured out examples of overuse

of screening tests and imaging technology aswell as an epidemic of doubtful benefit surgery.Tonsillectomies went up by 74% from 1996 to

2006. Cancer screening for the over-75-years agegroup and increasing rates of percutaneous coro-nary interventions also increased dramatically.

There was general agreement that guidelinesshould be written by those who are free of con-flicts of interest, reduce hospital stay and reformtort law. There was some disagreement that theAffordable Care Act would reduce hospital costs.

Each culture has its own characteristic per-ception of disease and its preferred method ofhealing. Cost is irrelevant in achieving goodhealth and longevity. Some doctors think that apatient refuses invasive treatment because he orshe is in denial. In her work on palliative care,Diane Meier said it was not the patient who wasin denial but the doctor.

Is the U.S.A’s Problem Unique?Having worked on both sides of the pond, I feel

I am able to judge the pros and cons of our med-ical industry. The UK is insulated against need-less over-testing, over-treating and over- diagnos-ing. However, medical practice in the UK isgoverned by the National Institute for Health andClinical Excellence (NICE), which offers evi-dence-based medical care. The National Screen-ing Committee provides clinical recommenda-tions of what screening is effective and useful.Medical care is governed by politics. The presentcoalition government in the UK intends to bringin “value based” medical care in 2014 rather thanfollowing the recommendations of NICE. Med-ical care in the UK is becoming too expensiveand the NHS of which the UK prides itself maydisintegrate into community health care unitscontrolled by bureaucrats. The judge determineswhat is legal and who is guilty. The priest de-clares what is holy and who has sinned. Thephysician decides what is a symptom and who issick. He is a moral entrepreneur, charged with in-quisitorial powers to discover certain wrongs to

Article 394 .5 Clock Hour

Solomon Golden-berg, M.Sc., FRCP(LOND), RMA(AMT), previously afamily physician inLondon, U.K., nowwith Citimed,Miami, FL.

Discovering Medical Nemesis*Sol Goldenberg

*Author Note: Nemesis was the goddess of controversy in Greek mythology.



be righted. The medicalization of a budget is theshare taken out of a person's yearly income tospend under doctor's orders.

ObamaCare — Basic FactsThe official name for “ObamaCare” is the Patient

Protection and the Affordable Care Act. It is a billthat was signed on March 23, 2010, by PresidentBarack Obama. It is intended to reform the healthcare industry. The basic facts are as follows:

1) The Affordable Care Act requires insuranceplans to cover preventative services.

2) It stops insurance companies from droppingUS citizens when they are sick.

3) It does not replace private insurance,Medicare or Medicaid.

4) It aims to improve community health carecenters to provide improved health care forthose who cannot afford private health care.

5) ObamaCare puts a cap on insurance compa-nies raising premiums starting in 2013 andinto 2014. The insurance companies will haveto justify rate hikes to the state and post themto their websites.

6) Starting in October, 2013, insurance compa-nies will compete via a health insurance ex-change pool to decrease insurance premiumsfor all Americans.

7) Americans will buy affordable health carecoverage on the “ObamaCare” health insur-ance exchanges.

8) American employers with 25 but less than 50employees may receive tax breaks of up to35% of the cost of their employees’ insur-ance premiums. Employers with more than50 employees must insure their workers orpay a tax (like the current state run unem-ployment and workers compensationprograms).

9) Only 3% of small businesses will have to paythe additional 0.9% ObamaCare Medicare taxincrease. This tax is only paid on profitable in-come over $250K.

10) If the citizen chooses not to purchase health-care through the Online Health Insurance Ex-change, they can still buy private insurance,get insurance through work or Medicare/Medicaid. Those who choose to not partici-pate will pay a penalty tax.

11) ObamaCare expects to cut $716 billion ofwaste from Medicare and cut reimbursementsto private Medicare Advantage plans and rein-vest it into Obama's health care reform.

12) 19 million Americans will receive tax creditsto help pay for healthcare.

13) By 2019, 17 million Americans below thepoverty line will be eligible for Medicaid dueto expansion of the program.

14) Over 20.4 million women will gain access tonew women’s health care preventative ser-vices and better access to wellness visits andfree preventative care on all insurance plans.

Where is ObamaCare Heading?Whether one is a Republican or Democrat, the

nation has voted that ObamaCare is here to stay.From a politician’s perspective, this is a politicaldream come true. From a patient’s point of view,this is nowhere near the ”free for all” medical careof the British National Health Service system. Isthe patient's autonomy safeguarded? Is there a bal-ance of the needs and the demands of the patient?Can we afford the high standard of medical carewe have in the USA without capping the paymentsmade by the high malpractice awards? From theprofession’s perspective, does it limit the extensiveinvestigation and treatments offered to patientsand, therefore, reduce their income and threatenjobs of ancillary staff? The purpose of any healthcare is to restore function and maintain autonomy.The innovative practitioner should therefore de-velop new ways of maintaining a good patient-pro-fessional relationship without risking the patient'srights to healthcare and thus leading to social ia-trogenesis.

References:Godlee,Fiona, editor BMJ ”Overtreatment, over here,” BMJ 2012;

345 : e6684Lenzer,Jeaune “Unnecessary profit driven healthcare to blame.” BMJ

2012;345: e6230Obamacare Facts 2012 - Internet


1. Which of these terms is NOT synonymouswith MEDICAL NEMESIS?

A. Social IatrogenesisB. Medical DependenceC. Medical bureaucracy does not create ill

healthD. Overtreatment can cause more harm

2. Which of the following is NOT a cause ofovertreatment?

A. Fee for service medical careB. Supply driven demandC. People are more sick than they used to

beD. Fear of malpractice lawsuits

3. Over treatment and over investigation isdependent on good insurance or ability to pay

A. TrueB. False

4. Under the Affordable Care Act 2010insurance companies will compete for healthinsurance by

A. January 2013B. October 2013C. January 2014D. January 2015

5. Medicaid will be available for 17 millionAmericans below the poverty line by 2014

A. True B. False

6. How will Obamacare affect MEDICARE?A. Increase by $455 billionB. Will be cut by $716 billionC. Would not be affectedD. Will run out of funds by 2019

7. The free for all British National HealthSystem is becoming very expensive

A. TrueB. False

8. How many Americans will receive tax creditsto help pay for health care?

A. 8 MillionB. 19 MillionC. 24 MillionD. 32 Million

9. What does the author think will NOT keepcosts of medical health care down?

A. Cap malpractice awardsB. Follow strict guidelines of testing and

treatmentC. Agree to patient’s request for over

investigation. D. Develop guidelines for necessary

investigation and treatment

10. How does Obamacare affect women’s healthA. Offer women less access to preventative

health careB. Offer women less planned parenthood

servicesC. Offer women less counseling for plastic

surgeryD. Offer women less access to better

health care.




Article 394 .5 Clock HourArticle 394 .5 Clock Hour


As the people who perform a number, if not all,the glucoses run in our institutions, we have animportant role to play in Tight Glycemic Control(TCG). Over the past several years, the idea ofmaintaining a patient’s glucose within a rathernarrow range has been proposed and arguedagainst. It appears that at least some, if not much,of the argument is the definition of TGC. Thiscould be in large part due to the method for mea-suring glucose on which the limits for TGC areset. For example, if the lower limit is set at 110or 120 mg/dL, this could be due to the instrumentused and/or the sample — whole blood or serum.

Let’s consider some of the research that hasbeen done on this topic and see how the labora-tory can assist the clinicians who are dependenton us for providing the important data.

One of the early studies was done in Leuven,Belgium. “Leuven I” was the study that launchedmany of the current TGC protocols; in the ICU,TGC has been endorsed by a number of profes-sional societies and is currently an emergingstandard of care worldwide. Nevertheless, afternearly six years, there has been a lack of confir-matory evidence in the critical care literature,and conversely, a number of studies that argueagainst TGC due to higher mortality. In 2004, the1,600-patient “before and after” study performedby an ICU team and reported as the Stamford(Connecticut) Study provided data confirmingthe benefit of TGC in a mixed medical-surgicalpopulation. “Leuven II,” undertaken in a medicalICU setting, emerged five years after the first Bel-gian study, detailing more modest benefits of in-tensive insulin therapy.

How does one explain the divergent results ofdifferent interventional trials regarding TGC andmortality? Leuven I and the Stamford studieswere strongly positive; Leuven II was positivewhen considering only a targeted group of pa-tients with ICU stays of longer than three days

but negative in the intention-to-treat analysis ofthe entire group. Moreover, the results of two tri-als have cast more doubt about the efficacy ofTGC. The European investigators of the Efficacyof Volume Substitution and Insulin Therapy inSevere Sepsis trial performed a multicenter, ran-domized, prospective study of intensive vs. “con-ventional” glycemic control and two differentfluid resuscitation strategies in a two-by-two de-sign. The trial was closed prematurely becauseof a nearly six-fold increase in severe hypo-glycemia among the patients in the intensivelytreated group. The Glucontrol Trial, another mul-ticenter European study of TGC in medical-sur-gical ICUs, was halted due to protocol violationsand an unacceptable rate of hypoglycemia in theintensively treated group.

These two trials share one important parame-ter with Leuven II — a high rate of severe hypo-glycemia (SH) [usually defined as blood glucose<40 mg/dL] and therefore might not be deemedindictments of TGC but rather as examples offailed trials. The rates of SH among the conven-tionally and intensively treated patients in Leu-ven II were 3.1% and 18.7%, respectively. In con-trast, the corresponding rates in Leuven I were0.8% and 5.1%, and the rate of SH in the Stamfordstudy did not change with implementation ofTGC. The Leuven II authors stated that “(statisti-cal) analysis identified hypoglycemia as an inde-pendent risk factor for death. Hence, it is possi-ble that hypoglycemia induced by intensiveinsulin therapy may have reduced a portion ofthe potential benefit.” Indeed, even a singleepisode of SH conferred an increased risk ofmortality in an analysis of the 5,365 patient co-hort from the Stamford study.

Why was the rate of hypoglycemia so differentin the two Leuven studies? One important differ-ence between Leuven I and Leuven II concernsthe method of glycemic monitoring. The first

David Plaut, Plano,TX, Consultant,AMT’s BookReviewer, andfrequent speaker atAMT regionalmeetings and nationalconventions; Deena DavisPOC Coordinator,Bozeman-DeaconessHospital, Bozeman,MT

The Laboratory and TightGlycemic ControlDavid Plaut and Deena Davis



study relied exclusively on arterial blood gas ana-lyzers, while the second study used arterial bloodin an unspecified smaller number of patients, withthe remainder of samples obtained from capillaryblood and measured on bedside glucometers. An-other difference is the patient population. The pa-tients in the medical ICU had much higherAPACHE (acute physiology and chronic healthevaluation) II scores and a higher prevalence ofsepsis on admission, risk factors for the develop-ment of SH, than did the surgical ICU patients.

Consider the role the laboratory plays in helpingto achieve any TGC goal. In the case of blood glu-cose, four glucose measurement methods areused:

• hand-held devices (POCT) • paper or plastic sticks to test a drop of blood • blood gas analyzers • laboratory analyzers in core laboratories Each method is subject to specific challenges

and limitations that can affect the overall systemperformance. Weber and Neeser point out severalsalient facts concerning the identification and doc-umentation of the type of the sample. They arguethat fasting glucose values in venous blood are5–10% lower than in arterial samples, while capil-lary samples show 5–15% higher values comparedto venous blood samples. Similarly, venous or cap-illary plasma samples are showing 10–15% highervalues compared to whole blood hemolysate. Aswas pointed out at the beginning of this article,these difference can easily cause the variation inthe low limit for glucose control. Lastly, as we arewell-aware, hand-held instruments for measuringglucose have not always been found without sig-nificant error and variation.

Krinsley points out that the avoidance of hypo-glycemia requires several key components. TheICU culture must accept protocol-driven care; a

glycemic target should be chosen that can beachieved safely; the strengths and weaknesses ofthe different available glucose monitoring tech-nologies must be understood; and finally, clini-cians need to have access to actionable, real-timedata, not just relating to glucose control, but ide-ally also to relevant outcomes such as severity-ad-justed mortality and measures of morbidity andresource utilization.

References1. Clin Ther. 2005 Oct;27(10):1489-99.Monitoring glycemic con-

trol: the cornerstone of diabetes care.LeRoith D, Smith DO.2. Int J Obes Relat Metab Disord. 2004 Sep;28 Suppl 2:S8-13.In-

tensive insulin regimens: evidence for benefit. Bretzel RG.3. Endocr Pract. 2006 Jan-Feb;12 Suppl 1:34-41.Insights from the

diabetes control and complications trial/epidemiology of diabetesinterventions and complications study on the use of intensiveglycemic treatment to reduce the risk of complications of type 1diabetes. Genuth S see also Int J Obes Relat Metab Disord. 2004Sep;28 Suppl 2:S8-13.Intensive insulin regimens: evidence forbenefit.Bretzel RG.

4. Clin Cornerstone. 2003;5(2):56-63.Insulin therapy for the criti-cally ill patient.Van den Berghe G. and Endocr Pract. 2011 Dec2:1-19. [Epub ahead of print]. See also: Adapting to the NewConsensus Guidelines for Managing Hyperglycemia During Crit-ical Illness: The Updated Yale Insulin Infusion Protocol. Shetty S,Inzucchi SE, Goldberg PA, et al.

5. Chest. 2010 Mar;137(3):544-51. Epub 2009 Dec 16.Toward un-derstanding tight glycemic control in the ICU: a systematic re-view and metaanalysis. Marik PE, Preiser JC.

6. stat.kuleuven.be/consulting/Show%20cases/LDP.pdf7. Crit Care. 2008;12(1):R29. Epub 2008 Feb 29.Intensive insulin

therapy and mortality in critically ill patients. Treggiari MM,Karir V,Yanez ND, et al.

8. J Emerg Trauma Shock. 2011 Jul;4(3):359-64.Tight blood glu-cose control in trauma patients: Who really benefits? ErikssonEA, Christianson DA, Vanderkolk WE, et al.

9. J Thorac Cardiovasc Surg. 2011 Feb;141(2):543-51. Epub 2010Dec 15.Superiority of moderate control of hyperglycemia to tightcontrol in patients undergoing coronary artery bypass grafting.Bhamidipati CM, LaPar DJ, Stukenborg GJ, et al.

10. Overdiagnosed : making people sick in the pursuit of health.Welch, H. G. Boston, Mass. Beacon Press, c2011.

11 J Diabetes Sci Technol. 2011 May 1;5(3):755-67.Intensive insulintherapy in critically ill hospitalized patients: making it safe and ef-fective. Klonoff DC.


1. What does TGC stand for?A. Today’s glucose calibratorB. Tight glycemic controlC. Tight glycemic calibrationD. Terrific glucose control

2. Where was one of the earliest studies of TGCperformed?

A. John’s HopkinsB. LeuvenC. Loma LindaD. Los Alamos

3. TGC is maintained by employing which of thefollowing therapies?

A. Intensive glucose therapyB. Strict dietary requirements managed by a

nutritionistC. Intensive insulin therapyD. Continuous glucose montoring

4. What study confirmed the benefit of TGC in amedical-surgical population?

A. Leuven IB. Leuven IIC. The Stanford StudyD. The Stamford (Connecticut Study)

5. What is the generally accepted definition ofSevere Hypoglycemia?

A. Blood Glucose <40 mg/dlB. Blood Glucose <50 mg/dlC. Blood Glucose <60 mg/dlD. Blood Glucose <70 mg/dL

6. What three trials all resulted in an unacceptablyhigh rate of Severe Hypoglycemia in thestudies’ patients?

A. Leuven I, Leuven II and StamfordB. Efficacy of Volume Substitution and

Insulin Therapy in Severe Sepsis trial,Leuven I and the Glucontrol trial

C Efficacy of Volume Substitution andInsulin Therapy in Severe Sepsis trial, theGlucontrol trial and Leuven II

D. Efficacy of Volume Substitution andInsulin Therapy in Severe Sepsis trial, theGlucontrol and Stamford

7. What methodology did Leuven I use to monitorblood glucose in its patients?

A. Fingerstick bedside glucometersB. Arterial blood gas analyzersC. Laboratory analyzers in core laboratoriesD. Plastic sticks to test blood drop

8. Which sample type yields a higher glucosevalue?

A. Whole bloodB. PlasmaC. UrineD. Serum

9. What is the key point in avoiding hypoglycemiain the ICU culture?

A. Accept protocol driven careB. A glycemic target should be chosen that

can be achieved safelyC. Strengths and weaknesses of the different

available glucose monitoring technologiesmust be understood

D. All of the above

10. TGC was found to result in moreA. Normal glucose levels in more patientsB. A greater hunger in patientsC. A lesser hunger in patientsD. Hypoglycemia in more patients






Thalassemias

There is a group of disorders which are all dif-ferent and inherited and called thalassemias. Es-sentially, they are defined by a decreased or ab-sent production of a specific globin chain.

Hemoglobin moleculeA hemoglobin molecule is made up of two

alpha chains and two other chains, either beta,gamma, or delta. Normal adult hemoglobin isHemoglobin A, consisting of two alpha chainsand two beta chains. This is about 97% of nor-mal hemoglobin. A small percentage of hemo-globin A2 and hemoglobin F is also present inthe population, Hemoglobin F is predominatelyin fetuses and newborns.

The thalassemias are classified by a decreaseor absent production of a specific globulinchain. Thus we see that beta thalassemia is themost common form of thalassemia and is iden-tified by a decrease or absence of beta chains.Alpha thalassemia is a reduction or absence ofalpha chains ..

The inheritance of any type of thalassemiamay be homozygous or heterozygous. Depend-ing on the state of inheritance, the disorder isthen known as beta thalassemia minor or tha-lassemia major.

References: Bank ,A. “The Thalassemia Syndromes”, Blood 51:369

(March,1978). Lee, G. Richard et. al. Wintrobe's Clinical Hematology, 10th ed.

Philadelphia: Lea and Febiger, 1999.

Submitted by Gerard P. Boe., Ph.D.

We welcome reader submissions for future“Fast Facts.” Send them to the AMT Office, atten-tion Journal Editor.

Fast Facts


Kingella kingae was initially isolated byElizabeth O. King in 1960 during her tenure at theCenter for Disease Control10. She sent two strainsto Bovre and Henriksen at the University of Oslo,Norway, asking if they thought the new isolatewas a member of the genus Moraxella and, if so, ifit was a member of an existing species. She diedbefore the species could be fully described, butK. kingae is now recognized as an important pe-diatric pathogen. Improvements in culture andidentification methods have led to K. kingaebeing detected more frequently. It is now knownto be the leading cause of pediatric osteoarticu-lar infections (OAI), infection of bone or joint, forwhich a causative agent has been determined4.

Though a cause of endocarditis, bacteremia,and lower respiratory infection, K. kingae is mostcommonly seen as a causative agent of OAI. Itsrole in endocarditis led to K. kingae being includ-ed in the HACEK (Haemophilus, Aggregatibacter,Cardiobacterium, Eikenella, and Kingella) groupingof organisms. As Kingella’s growing importanceis recognized, it is critical to understand theorganism’s presentation, pathogenesis, epidemi-ology, identification, and treatment.

TaxonomyBovre and Henriksen initially reported on

Kingella kingae in 1968. They named it Moraxellakingii, as it had a similar appearance to otherMoraxella species and was isolated from similarbody sites10. Further study showed that unlikeother Moraxella species, M. kingae was catalasenegative. Attempts to transform Moraxellaspecies with DNA from M. kingae were unsuc-cessful, suggesting that the two were not closelyrelated. Analysis of fatty acid compositionshowed that M. kingae was most related to mem-bers of the family Neisseriaceae, though it wasdistinct from previously identified members ofthat family13.

After further study, Bovre and Henriksen re-named the species Kingella kingae and placed itin the family Neisseriaceae, which also containsthe genus Neisseria and the genus Eikenella.Three other species of the genus Kingella havesince been discovered: Kingella oralis, Kingelladenitrificans, and Kingella potus (Table 1). Analysisof 16S RNA sequencing suggests that K. kingae,K. oralis, and K. potus are very closely related,while K. denitrificans is more closely related toEikenella corrodens 6, 19.

Clinical Significance and DiseaseKingella kingae has been implicated in a variety

of diseases, including osteoarticular infections(OAI), septic arthritis, lower respiratory tract in-fections, meningitis, endocarditis, and afocalbacteremia38. The use of automated blood cul-ture instruments for blood and other body fluids(like joint fluid, beginning in 1992) has increasedthe ability to detect K. kingae38. This has led to anincreased appreciation for the role of K. kingae indisease.

In a 2007 French study, Sylvia Chometon andcolleagues found that K. kingae is now the lead-ing cause of osteoarticular infections in chil-dren4. This study used three different methodsto detect K. kingae: automated blood culturemachines to culture joint fluid, PCR with uni-versal 16S primers on culture negative samples,and Kingella-specific PCR and sequencing oncultures negative after universal PCR. The useof these three techniques led to a high rateKingella kingae detection. Causative agents weredetermined for 86 of 131 samples. Of these, 39(45%) were positive for Kingella kingae. Staphy-lococcus aureus, the most common causativeagent when only automated culture resultswere considered, was found in only 29% of sam-ples, even when S. aureus specific 16S sequenc-ing was added.

Eleanor Powell,B.S., Department ofPathology and Lab-oratory Medicine,Cincinnati Chil-dren's HospitalMedical Center;and Division of Di-gestive Disease,University ofCincinnati Collegeof Medicine,Cincinnati, OH;Joel E. Mortensen,Ph.D. Dept. ofPathology and Lab-oratory Medicine,Cincinnati Chil-dren’s HospitalMedical Center

Update on Kingella kingae:Pathogenesis, Identification,and TreatmentEleanor Powell and Joel Mortensen

Article 396 1.5 Clock Hour


A second study found that K. kingae is secondonly to S. aureus as the leading cause of OAI (33).36.5% of positive cultures were positive for S. aureus, while 22.2% were positive for K. kingae.Only automated culture allowed detection ofK. kingae. Unlike the previous study, only solid cul-ture media and automated joint fluid culture wereused to detect pathogens. It is likely that somecases of K. kingae were not identified, as no PCRwas performed on culture negative samples. Takentogether, these studies show that K. kingae is theleading cause of OAI and that automated bloodculture machines are necessary to effectively iden-tify K. kingae from joint fluid.

Though skeletal infections comprise most casesof invasive K. kingae infection, other disease pre-sentations are also common. In one study of pa-tients in an Israeli hospital, 69.4% of K. kingae in-fections were skeletal infections, 29.7% werebacteremia, and 4.1% were lower respiratory in-fections36. All cases were in patients under fouryears of age, except for one adult who hadK. kingae endocarditis. K. kingae endocarditis is rel-atively rare and typically occurs in children withpre-existing heart conditions9.

The source of invasive K. kingae infections islikely colonization of the oropharynx37. In onestudy, blood samples and throat swabs were col-

lected from three patients with invasive K. kingaeinfections. K. kingae was isolated from all bloodand throat specimens. Pulse field gel elec-trophoresis and random amplified polymorphicDNA PCR were performed on each isolate. For allthree patients, the patterns seen for the blood iso-late were identical to the throat isolate and distinctfrom other, non-related strains. This suggests thatK. kingae involved in invasive infections originatesfrom normal oropharyngeal colonization byK. kingae. Though colonization appears to be thesource of invasive K. kingae, colonization is notconsidered a health risk. In healthy colonized chil-dren, the probability of developing K. kingae OAI isless than one percent2.

Other Kingella species have also been implicat-ed in disease. K. denitrificans has been identified asthe causative agent in cases of infective endo-carditis, both on native valves11, 12, 26 and prostheticvalves17. It has also been isolated from cases ofgranulomatous disease in an AIDS patient21, amni-otic fluid from a woman with chorioamnionitis20,pus from empyema in a patient with lung cancer22,and a retropharyngeal abscess in a patient onmethotrexate23. K. oralis is commonly found in den-tal plaque and other oral sites3. It is unclear ifK. oralis plays a pathogenic role or merely colo-nizes these areas. K. potus has been isolated as the

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Table 1. Kingella species


causative agent of a wound infection from a bitefrom a kinkajou, a South American mammal (19).

Pathogenic MechanismsThe process through which colonization of the

oropharynx leads to invasive Kingella kingae in-fection is not fully understood. Several potentialcontributing factors have been proposed. In onestudy, 80% of patients with invasive K. kingae infections also had a concurrent respiratory orgastrointestinal illness7. Due to the high fre-quency of co-infections, it has been hypothe-sized that viral infections disrupt the respira-tory epithelium, allowing K. kingae to enter thebloodstream32. From the bloodstream, K. kingaecan reach other areas of infection, like jointsand the endocardium.

Kingella kingae also produces a cytotoxic RTXtoxin16. In vitro studies have shown that the or-ganism is cytotoxic to conjunctiva cells, type IIpneumocytes, laryngeal cells, synovial cells,and macrophage-like cells, but only when theRTX toxin is present16. It is possible that pro-duction of the RTX toxin allows K. kingae to dis-rupt the laryngeal epithelium and enter thebloodstream, causing invasive disease. TheRTX toxin’s cytotoxicity to synovial cells mayalso help explain how Kingella kingae causesseptic arthritis.

The production of a type IV pilus allows adher-ence of K. kingae to respiratory epithelium, pro-moting colonization14. In vitro assays show thatpilus expression is required for K. kingae adher-ence to laryngeal cells, type II pneumocytes, andsynovial cells. This suggests that pilus expressionmay be involved both in colonization of theoropharynx and infection of joint synovia in OAI14.Pili expression has been shown to correspond toboth site of isolation and colony morphology15.Clinical isolates from the respiratory tract andbloodstream are usually piliated, and thesecolonies form either spreading/corroding or non-spreading/non-corroding colonies, but not domedcolonies. In contrast, isolates from sites of invasiveinfection, like joint fluid and the endocardium, areless likely to have pili and are more likely to formdomed colonies. This suggests that there is a se-lective disadvantage on the expression of pili in in-vasive infection, though this is not yet fully under-stood15. K. denitrificans also produces a type IVpillus28.

Epidemiology and Routes ofTransmission

When considering the prevalence of Kingellakingae, it is necessary to consider both the preva-lence of colonization and the incidence of invasiveinfection. Colonization rates vary with age.K. kingae is usually acquired beginning around sixmonths of age, with colonization rates peaking be-tween twelve and twenty four months of age. With-in this age group, 9-12% of children are colo-nized2, 38. K. kingae is transmitted by droplettransmission from colonized children27. Childrenthat are frequently around other children, likethose who attend day care, have higher rates ofcolonization31.

Similarly, rates of K. kingae invasive infection arehighest in the first two years. One study of an Is-raeli pediatric hospital found the incidence ofK. kingae invasive infection to be 21.2 cases per100,000 population in the first year of life and 22.6cases cases per 100,000 population in the secondyear36. These rates then fell quickly with an inci-dence of 4.8 cases per 100,00 population in thethird year and 1.4 cases per 100,000 population inthe fourth year. Children under the age of four ac-count for 98.6% of invasive infections36. Infectionsoccurred at an average rate of 12 cases per 100,000emergency department visits and did not changesignificantly during the study period7.

While rare, two outbreaks of Kingella kingae havebeen reported in the literature to date18, 34. One out-break occurred in southern Israel, while the otheroccurred in Minnesota. Each outbreak involved asingle day care center from which three childrendeveloped osteomyelitis. In the Minnesota out-break, all three affected children were in the samedaycare classroom. K. kingae carriage rates in thisclassroom were 45%, much higher than the aver-age 9-12%18. In the Israeli outbreak, the daycarecenter the affected children attended had a car-riage rate of 33.3%. In both outbreaks, the strainisolated from the affected patients and carriers at-tending the same day care center had similar bandpatterns when undergoing pulse field gel elec-trophoresis18, 34. This suggests that the same strainwas spread among the children harboringK. kingae. Furthermore, strains were isolated fromother day care centers in the same areas. Whensubjected to pulse field gel electrophoresis, thesestrains had similar patterns within each day carecenter, but not between centers. This suggests thata unique strain had spread among each individual


day care center. It also may suggest that certainK. kingae strains are more prone to invasive infec-tions than others, as children in other day care cen-ters did not develop osteomyelitis34.

Laboratory Identification K. kingae are Gram-negative bacilli with flat ends

in pairs or short chains, though they may resist de-colorizing or decolorize unevenly1, 27, 30 (Table 2).They are non-motile, facultative anaerobic bacte-ria capable of fermenting glucose and maltose8.K. kingae are oxidase positive, indole negative, ure-ase negative, and catalase negative. Biochemicalcharacteristics that identify K. kingae from othermembers of family Neisseriacea are summarized inTable 2. Defining characteristics of K. kingae fromother Kingella species are summarized in Table 3.

Reliable detection of K. kingae requires the useof automated blood culture machines33. Joint fluidcan be incubated in a BACTEC aerobic blood cul-ture bottle or other similar bottle. When thepathogen is Kingella, automated blood culture ma-chines recognize growth after 2-4 days of incuba-tion10. Positive culture bottles can then be sub-cultured onto blood or chocolate agar. Selectivemedia can also be used. Thayer-Martin agar ormedia containing clindamycin or vancomycin may

be helpful in isolating Kingella, as these agars se-lect against other common oropharyngeal flora27.Direct inoculation of solid media with synovialfluid during surgery has also been successful in isolating K. kingae from patients withosteomyelitis10.

Once isolated, K. kingae can be identified usingany of several common laboratory systems. Twocommercially available tests, Remel RapID NH andAPI NH strips, use dehydrated substrates to per-form biochemical tests on isolated organisms.These can be read after 4-5 hours of incubation.

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Table 2. Biochemical differentiation between Kingella kingae and other species in family Neisseriaceae

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Automated systems may also be used to identifyK. kingae. VITEK 2 NH identification cards and theVITEK 2 system use similar colormetric tests toidentify K. kingae, though varying levels of accura-cy have been reported24, 25. Additionally, matrix as-sisted laser desorption/ionization (MALDI) time offlight (TOF) mass spectrometry (MS) has recentlybeen successfully used to identify Kingella kingae5,Powell, manuscript in preparation).

Culture-independent methods have also been de-veloped to identify K. kingae, especially from cul-ture-negative samples4. Both universal and specificPCR have been employed. Universal PCR involvesamplifying 16S ribosomal genes, sequencing thePCR product, and searching a database of knownsequences to identify the bacteria from which thegene was isolated. Specific PCR involves the useof primers that amplify 16S ribosomal genes ofK. kingae only. If any product results from the PCR,the sample is positive for K. kingae. Both methodshave improved the detection rate for K. kingae inculture negative samples.

Antibiotic SusceptibilityK. kingae is generally susceptible to beta-lactams

and cephlosporins4, 7, 35. These drugs are most com-monly used to treat invasive K. kingae infections.Several studies have also found them to be sus-ceptible to aminoglycocides, macrolides, chloram-phenicol, fluroquinolones, tetracylcines, colistin,and rifampin. Occasional resistance has been seento gentamicin, amikacin, trimethoprim-sul-famethoxazole, tobramycin, and oxacillin. Resis-tance patterns previously reported in literature aresummarized in Table 4.

Recent testing in our laboratory on patient iso-lates, laboratory stock strains, and ATCC strain23331 showed similar results. Antibiotic suscepti-bility testing was performed using E-test strips oncation-adjusted Mueller-Henton agar with 5%sheep blood. Results were compared to standardspublished. Results are summarized in Table 5. Allisolates were susceptible to ampicillin, ceftriax-one, ciprofloxacin, and meropenem. Four of 13 iso-lates were resistant to trimethoprim-sulfamethox-azole. Clindomyacin was tested, and all isolateshad minimum inhibitory drug concentrations be-tween 1.5 and 16 �g/mL (Mean: 4.61 �g/mL). Stan-dards have not been established for minimum in-hibitory concentration interpretation ofclindamycin with K. kingae, but relatively high min-imum inhibitory concentrations suggest clin-damycin may not be appropriate for use againstK. kingae. Similar resistance patterns were seenwith K. denitrificans and K. oralis, though only oneisolate of each was tested.

ConclusionKingella kingae is now recognized as an emerg-

ing fastidious pediatric pathogen, although it islikely still under-detected. The advent of blood cul-ture instruments for culturing synovial fluid hasled to increased rates of detection, but many caseslikely still go undetected when PCR is not em-ployed4. Development of standard K. kingae specif-ic PCR assays would increase the detection rate ofK. kingae and decrease the number of cases of OAIfor which no cause can be determined. It is still un-clear how K. kingae moves from the oropharynx tothe bloodstream, but there is evidence for a rolefor the RTX toxin and viral co-infection. Furtherresearch may further elucidate this process, iden-tifying potential targets for decreasing the inci-dence of systemic K. kingae infection.

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References1. Bergey, D. H., and J. G. Holt. 1993. Bergey's manual of determi-

native bacteriology, 9th ed. Williams & Wilkins, Baltimore.2. Ceroni, D., V. Dubois-Ferriere, R. Anderson, C. Combescure, L.

Lamah, A. Cherkaoui, and J. Schrenzel. 2012. Small Risk of Os-teoarticular Infections in Children with Asymptomatic Oropha-ryngeal Carriage of Kingella kingae. The Pediatric infectious dis-ease journal.

3. Chen, C. 1996. Distribution of a newly described species, Kingel-la oralis, in the human oral cavity. Oral microbiology and im-munology 11:425-427.

4. Chometon, S.,Y. Benito, M. Chaker, S. Boisset, C. Ploton, J. Be-rard, F. Vandenesch, and A. M. Freydiere. 2007. Specific real-time polymerase chain reaction places Kingella kingae as themost common cause of osteoarticular infections in young chil-dren. The Pediatric infectious disease journal 26:377-381.

5. Couturier, M. R., E. Mehinovic, A. C. Croft, and M. A. Fisher.2011. Identification of HACEK clinical isolates by matrix-assist-ed laser desorption ionization-time of flight mass spectrometry.Journal of clinical microbiology 49:1104-1106.

6. Dewhirst, F. E., C. K. Chen, B. J. Paster, and J. J. Zambon. 1993.Phylogeny of species in the family Neisseriaceae isolated fromhuman dental plaque and description of Kingella oralis sp. nov[corrected]. International journal of systematic bacteriology43:490-499.

7. Dubnov-Raz, G., O. Scheuerman, G. Chodick, Y. Finkelstein, Z.Samra, and B. Z. Garty. 2008. Invasive Kingella kingae infectionsin children: clinical and laboratory characteristics. Pediatrics122:1305-1309.

8. Eriquez, L. A., and N. E. Hodinka. 1983. Development of a testsystem for rapid differentiation of Neisseria and Haemophilusspp. Journal of clinical microbiology 18:1032-1039.

9. Feder, H. M., Jr., J. C. Roberts, J. C. Salazar, H. B. Leopold, andO. Toro-Salazar. 2003. HACEK endocarditis in infants and chil-dren: two cases and a literature review. The Pediatric infectiousdisease journal 22:557-562.

10. Gene, A., J. J. Garcia-Garcia, P. Sala, M. Sierra, and R. Huguet.2004. Enhanced culture detection of Kingella kingae, a pathogenof increasing clinical importance in pediatrics. The Pediatric in-fectious disease journal 23:886-888.

11. Goldman, I. S., P. D. Ellner, E. L. Francke, G. J. Garvey, and N.Squilla. 1980. Infective endocarditis due to Kingella denitrificans.Annals of internal medicine 93:152-153.

12. Hassan, I. J., and L. Hayek. 1993. Endocarditis caused by Kingel-la denitrificans. The Journal of infection 27:291-295.

13. Henriksen, S. D., and K. Bovre. 1976. Transfer of Moraxellakingae Henriksen and Bovre to the Genus Kingella gen. nov. inthe Family Neisseriaceae. International journal of systematic bac-teriology 26:447-450.

14. Kehl-Fie, T. E., S. E. Miller, and J. W. St Geme, 3rd. 2008.Kingella kingae expresses type IV pili that mediate adherence torespiratory epithelial and synovial cells. Journal of bacteriology190:7157-7163.

15. Kehl-Fie, T. E., E. A. Porsch, P. Yagupsky, E. A. Grass, C. Obert,D. K. Benjamin, Jr., and J. W. St Geme, 3rd. 2010. Examinationof type IV pilus expression and pilus-associated phenotypes inKingella kingae clinical isolates. Infection and immunity78:1692-1699.

16. Kehl-Fie, T. E., and J. W. St Geme, 3rd. 2007. Identification andcharacterization of an RTX toxin in the emerging pathogenKingella kingae. Journal of bacteriology 189:430-436.

17. Khan, J. A., S. Sharp, K. R. Mann, and J. Brewer. 1986. Kingelladenitrificans prosthetic endocarditis. The American journal of themedical sciences 291:187-189.

18. Kiang, K. M., F. Ogunmodede, B. A. Juni, D. J. Boxrud, A. Glen-nen, J. M. Bartkus, E. A. Cebelinski, K. Harriman, S. Koop, R.Faville, R. Danila, and R. Lynfield. 2005. Outbreak of os-teomyelitis/septic arthritis caused by Kingella kingae among childcare center attendees. Pediatrics 116:e206-213.

19. Lawson, P. A., H. Malnick, M. D. Collins, J. J. Shah, M. A. Chat-taway, R. Bendall, and J. W. Hartley. 2005. Description of Kingel-la potus sp. nov., an organism isolated from a wound caused by ananimal bite. Journal of clinical microbiology 43:3526-3529.

20. Maccato, M., W. McLean, G. Riddle, and S. Faro. 1991. Isola-tion of Kingella denitrificans from amniotic fluid in a womanwith chorioamnionitis. A case report. The Journal of reproduc-tive medicine 36:685-687.

21. Minamoto, G. Y., and E. M. Sordillo. 1992. Kingella denitrificansas a cause of granulomatous disease in a patient with AIDS. Clin-ical infectious diseases : an official publication of the InfectiousDiseases Society of America 15:1052-1053.

22. Molina, R., T. Baro, J. Torne, R. Miralles, J. Gutierrez, J. F. Sol-sona, and C. Alia. 1988. Empyema caused by Kingella denitrifi-cans and Peptostreptococcus spp. in a patient with bronchogeniccarcinoma. The European respiratory journal : official journal ofthe European Society for Clinical Respiratory Physiology 1:870-871.

23. Rajanna, D. M., J. Manickavasagam, L. Jewes, and R. Capper.2011. Retropharyngeal abscess from an unusual organism-Kingella denitrificans-in a patient on low-dose methotrexate. Ear,nose, & throat journal 90:E15-17.

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Table 5. Antibiotic susceptibility in Kingella species isolates


24. Rennie, R. P., C. Brosnikoff, S. Shokoples, L. B. Reller, S. Mir-rett, W. Janda, K. Ristow, and A. Krilcich. 2008. Multicenter eval-uation of the new Vitek 2 Neisseria-Haemophilus identificationcard. Journal of clinical microbiology 46:2681-2685.

25. Sonksen, U. W., J. J. Christensen, L. Nielsen, A. Hesselbjerg, D.S. Hansen, and B. Bruun. 2010. Fastidious Gram-Negatives:Identification by the Vitek 2 Neisseria-Haemophilus Card and byPartial 16S rRNA Gene Sequencing Analysis. The open microbi-ology journal 4:123-131.

26. Swann, R. A., and B. Holmes. 1984. Infective endocarditis causedby Kingella denitrificans. Journal of clinical pathology 37:1384-1387.

27. Versalovic, J., and American Society for Microbiology. 2011.Manual of clinical microbiology, 10th ed. ASM Press, Washing-ton, DC.

28. Weir, S., and C. F. Marrs. 1992. Identification of type 4 pili inKingella denitrificans. Infection and immunity 60:3437-3441.

29. Yagupsky, P. 2012. Antibiotic susceptibility of Kingella kingaeisolates from children with skeletal system infections. The Pedi-atric infectious disease journal 31:212.

30. Yagupsky, P. 2004. Kingella kingae: from medical rarity to anemerging paediatric pathogen. The Lancet infectious diseases4:358-367.

31. Yagupsky, P., and R. Dagan. 1997. Kingella kingae: an emergingcause of invasive infections in young children. Clinical infectiousdiseases : an official publication of the Infectious Diseases Soci-ety of America 24:860-866.

32. Yagupsky, P., R. Dagan, C. B. Howard, M. Einhorn, I. Kassis, andA. Simu. 1993. Clinical features and epidemiology of invasiveKingella kingae infections in southern Israel. Pediatrics 92:800-804.

33. Yagupsky, P., R. Dagan, C. W. Howard, M. Einhorn, I. Kassis,and A. Simu. 1992. High prevalence of Kingella kingae in jointfluid from children with septic arthritis revealed by the BACTECblood culture system. Journal of clinical microbiology 30:1278-1281.

34. Yagupsky, P., Y. Erlich, S. Ariela, R. Trefler, and N. Porat. 2006.Outbreak of Kingella kingae skeletal system infections in chil-dren in daycare. The Pediatric infectious disease journal 25:526-532.

35. Yagupsky, P., O. Katz, and N. Peled. 2001. Antibiotic suscepti-bility of Kingella kingae isolates from respiratory carriers and pa-tients with invasive infections. The Journal of antimicrobialchemotherapy 47:191-193.

36. Yagupsky, P., N. Peled, and O. Katz. 2002. Epidemiological fea-tures of invasive Kingella kingae infections and respiratory car-riage of the organism. Journal of clinical microbiology 40:4180-4184.

37. Yagupsky, P., N. Porat, and E. Pinco. 2009. Pharyngeal coloniza-tion by Kingella kingae in children with invasive disease. The Pe-diatric infectious disease journal 28:155-157.

38. Yagupsky, P., E. Porsch, and J. W. St Geme, 3rd. 2011. Kingellakingae: an emerging pathogen in young children. Pediatrics127:557-565.


1. Kingella kingae is most often associated withwhich of the following clinical diseases?

A. Infectious endocarditisB. Osteoarticular infections C. PneumoniaD. Bacteremia

2. Which of the following is the most likelysource for invasive K. kingae infections?

A. Oropharyngeal colonizationB. Skin lesions over jointsC. Exposure to contaminated blood

productsD. Airborne bacteria

3. In which age group are K. kingae infectionsmost common?

A. 0-4 yearsB. 4-10 yearsC. 10-18 yearsD. adults

4. Which characteristic of K. kingae isINCORRECT?

A. Gram-negativeB. Oxidase positiveC. Indole negativeD. Catalase positive

5. Which technology has been successfullyapplied to the identification of K. kingae inthe routine clinical laboratory?

A. VITEK 2B. 16S sequencingC. MALDI-TOFD. All of the above

6. K. kingae is in what family?A. PasterellaceaeB. NeisseriaceaeC. CardiobacteriaceaeD. Enterobacteriaceae

7. In addition to K. kingae, which of thefollowing lists include the other species in thegenus Kingella?

A. K. oralis, K. potus and K. denitrificans B. K. corrodans, K. potus and

K. denitrificans C. K. mitis, K. proteus and K. denitrificansD. K. oralis, K. potus and

K. decarboxylatus

8. What risk factor has been identified forinvasive K. kingae infection?

A. Concurrent respiratory or GI infectionsB. Extended stay in the hospitalC. Exposure to infected waterD. Antibiotic treatment

9. In what population have K. kingae outbreaksbeen observed?

A. Returning veterans of foreign warsB. Chronically ill childrenC. Children attending daycareD. No outbreaks have been observed.

10. To which class of antibiotics has resistancenot been seen in K. kingae?

A. AminoglycosidesB. SulfonamidesC. Beta-lactamsD. Cephalosporins






In an article entitled “Mononuclear Leukocyto-sis in Reaction to Acute Infection (infectiousmononucleosis),” which appeared in the Bulletinof the John Hopkins Hospital in 1920, the authorsdescribed the clinical characteristics of thecausative organism of the disease.

Since the 1800s, infectious mononucleosis hadbeen recognized as a clinical syndrome of fever,adenopathy and pharyngitis. But it wasn't untilthe late 1960s that the association between in-fectious mononucleosis and the Epstein-BarrVirus (EBV) was described.

Infectious Mononucleosis is also calledPfeiffer's Disease and Filatov's Disease namedfor two researchers who described the syn-drome as an infectious process, the first by Fi-latov in 1887, and later, independently by Pfeif-fer in 1889.

It is easily transmitted orally and is so oftencalled the “kissing disease.” It is said to be morecommon among adolescents and young adults.The Epstein-Barr virus (EBV) is a member of theHerpes virus family which is said to infect almosteveryone at some point in their lives. EBV oftencauses no symptoms but it can cause mononu-cleosis.

Classic Symptoms The very basic symptoms are sore throat, fa-

tigue, pharyngeal inflammation, vomiting, loss ofappetite and petechiae. Infectious mononucleo-sis occurs with the viral infection of Epstein-Barrvirus. The virus is spread by saliva and has an in-cubation period of from four to seven weeks. Thesymptoms usually persist for two to three weeksbut the feeling of malaise and fatigue may lastlonger. The most commonly used diagnostic cri-terion is the presence of 50% or more lympho-cytes with at least 10% atypical lymphocytes(large, irregular nuclei). The atypical lympho-cytes resembled monocytes when they were first

discovered, and thereafter the term mononucle-osis, was used.

General Description of Leukocytes inInfectious Mononucleosis

In infectious mononucleosis, the total whitecell count is variable, but is usually increasedover the normal. There is a relative and an ab-solute increase in the cells of the lymphocytic se-ries. Usually this lymphocytosis is greater than60 percent.

The feature of this lymphocytosis is the vari-ability of the cells as compared with the unifor-mity of the cell types in leukemia.

Neutrophils are relatively decreased with a slightshift to the left. The eosonophils, however, tend tobe slightly increased while Basophils, typical lym-phocytes and typical monocytes are also present.

Case Studies # 1 - Peripheral blood (Wright's stain)

A teen-aged Caucasian boy was in good healthwhen he suddenly developed a sore throat, fever,and generalized enlargement of the lymph nodes.Three days after the onset of the illness, the WBCcount was 10,000, with 85 percent lymphocytes.One week later, the WBC count was 37,000 with85 percent lymphocytes, 3 percent monocytes,11 percent segmented neutrophils and 1 percenteosinophils.

Clinical Diagnosis: Infectious mononucleosis Photos contain atypical lymphocytes in infec-

tious mononucleosis. The cytoplasm of the larger

Gerard P. Boe, Ph.D.,CLC(AMT),MT(AMT), ExecutiveDirector of AMTIE,Editor of AMT Jour-nal of Continuing Ed-ucation Topics & Is-sues, and Chair, AMTC L C E v a l u a t i o nCommittee

Infectious Mononucleosis: ABrief ReviewGerard P. Boe



cell is blue and contains small red granules. Redblood cells indent the margins of the larger cell.

#2 Peripheral blood (Wright's stain )

This 3-yr old boy reported with generalized en-largement of the lymph nodes and spleen.

His WBC count was 19,000, with 72 per cent lym-phocytes.

Clinical Diagnosis: Infectious mononucleosis. Photos show the cytoplasm of the cell is bluish

gray and granular and has a small but definite vac-uole. The nucleus has “brain- like” convolutions.

#3 Peripheral blood (Wright's stain)

This 20 year old white male had a severe sorethroat and a low grade fever. The mucous mem-brane of his nasopharynx was inflamed and hem-orrhagic. His cervical lymph nodes were enlarged.

Clinical diagnosis: Infectious mononucleosis. Photos show small and large lymphocyte and

monocyte in infectious mononucleosis. Alsoshown are a monocyte and atypical early cell of in-fectious mononucleosis.

#4 Peripheral blood (Wright's stain)

The initial findings in this 30-year old manwere fever, headache, sore throat, and enlarge-ment of lymph nodes. The patient was in bedfor approximately ten days, and for one monththereafter, he felt weak. His heterophile agglu-

tination titer was 1:128 and his WBC count was12,500.

Photos show lymphocytes with multiple chro-mophobic areas in their cytoplasm. Notice the vari-ability of the atypical cells versus the uniformity ofthe normal cells.

Differential Diagnosis There are two disorders in patients with primary

infection which should be closely evaluated versusIM. They are acute cytomegalovirus infection andToxoplasma gondii infections. Because the clinicalsigns of the above mentioned tests are very simi-lar, it is often difficult to tell between EBV monoand the cytomegalovirus infection. It is not alwayshelpful, or possible, to distinguish between EBVmononucleosis, but in pregnant women, the testshould be completed because of the consequencesfor the fetus.

In patients with a primary EBV IM infection, thedemonstration of heterophile is diagnostic. Onepoint of information here is the fact that the origi-nal Paul-Bunnell test has been replaced with rapidqualitative agglutination or ELISA tests.The testsdetect 80-85% of IM. A negative test should simplyimply the absence of significant IM-specific het-erophile antibodies. Heterophile antibodies appearin 60% of patients with IM within the first and sec-ond weeks, and in 80-90% by the first month.

References Bruu A. , Hjetland R, Holter E, et al : Evaluation of 12 commerial

Tests for detection of Epstein-Barr virus specific and heterophileantibodies, J.Clin Micobiol 7:451-456,2000

Murray PR, Baron, EJ, Jorgensen, JH et.al, editors: Manual of clinicalmicrobiology, Washington, DC 20003, American Society for Mi-crobiology. Wu, Alan HB, editor

Tietz Clinical Guide to Laboratory Tests, 4th edition, W.B. SaundersCompany


1. The connection of the Epstein-Barr virus toinfectious mononucleosis was described asearly as 1887.

A. TrueB. False

2. EBV has an incubation period from four toseven weeks.

A. TrueB. False

3. One of the most commonly used diagnosticcriteria is the Presence of 50% or more oflymphocytes.

A. TrueB. False

4. It is often difficult to identify IM cellsbecause there is little variability whencompared to the uniformity of cell types inLeukemia.

A. TrueB. False

5. Heterophile antibodies are not necessarilydiagnostic of EBV mononucleosis.

A. TrueB. False

6. EB mononucleosis is called "the kissingvirus" because so many teenagers get it.

A. TrueB. False

7. Sore throat, fatigue, and pharyngealinflammation are considered some of thebasic symptoms.

A. TrueB. False

8. The lymphocytosis in this disease is usuallygreater than 60% .

A. TrueB. False

9. There is an absolute as well as relativeincrease in lymphocytes in the disease.

A. TrueB. False

10. Atypical lymphocytes are primarily identifiedby their large, irregular nuclei.

A. TrueB. False






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CredentialsJeff Lavender, MT, ChairJeannie Hobson, RMA, RPT, CMAS,

AHIJanet Crigler, MTCecil Hunt, MTMarilyn Johnson-Gilliam, RMAChristopher Seay, MT

Future Planning/MembershipMary Midkiff, MT, ChairTaffy Durfee, MT, Co-ChairEdna Anderson, MTNancy Barrow, MTAlicia Gregorio, MTJosephine Harden, MTDebra Janeczko, RMAJeffrey Lavender, MTLucy Leyva, RPTBrett Merkle, RMAFrancine Oran, RMAAnn Roby, COLTLinda Witte, RMACarol Yankovich, MTChristopher Damon, JD (ex-officio)Kathy Cilia, MT (ex-officio)

ProctoringEverett Bloodworth, MT, ChairAll State Society Proctor ChairsKathy Cilia (ex-officio)

NominatingLouise Isbell, RMAMelissa Martin, RMAKim Meshell, RMA, RPT, AHISueollen Schobert, MLTDave McCullouth, MT

NominatingAlternatesCharles Baker, MTLeann Bart, RMAVernell Boyd, MTJohn Sherer, MTBarbara Ware, MT

ConventionPeggy Oiler, MT, ChairJanet Crigler, MTGloria Culla, MTLynn Dunlop, MLTCarla Filles, RPTHeather Herring, MT, RMAMarty Hinkel, MTAlicia Houston, MLTJerry Hudgins, MTElizabeth Sarchet, MLTLia Kaye Spears, MTDiane Powell, CMP (ex-officio)

Scientific/SpeakersKay Fergason, MT, ChairMichelle Jenkins, MT, Vice ChairJeri Bond, RMA, AHIDon Bouchelle, MTClara Boykin, MTTereyo Cop, MTSujana De Almeida, RMAArlene DeCarli, MTRoxanne Erskine, MTHattie Gallon, MTLt. Calvina Glover, MTSolomon Goldberg, RMAPatty Harris, MTVern Hein, MTPam Kriegel, MTDorothy Marks, MTMelissa Martin, RMANaomi Melvin, MTFred Morley, MTJean Palmer, RMA, AHIPatricia Poitier-Sands, RMADelores “Lola” Rosalis, RMAMimi Roush, MTAlberta Smith, RMA, AHISieglinde Wildie, MLTFelicia Williams, MTDiane Powell, CMP (ex-officio)

MentorBarbara Ware, MT, ChairTera Benefiel, MTNathalie Dixon, MTBetty Geary, MTAlice Macomber, AHI, RPTJuanita Stocke, MTAudrienne Whitley, MTVirgil Marchand, RMA

Student ActivitiesJulie Hardcastle, MT, ChairIvette Rivera, RMA, AHI, Vice ChairVanessa Austin, AHI, RMALisa Marie Bromley, RMANorman Frankel, PhD

Jamie Horn, RMA, RPTElizabeth Hurd, MTAmber Huskinson, MLTKarina Ibarra, RMA, RPTAlaine Johnson, RMA, AHICynthia Jones, MTKody Karas, RPTGrant Lambert, MTFred Morley, MTShannon Newman, MTRikki Packer, RMAChris Pontious, RMAFaith Robeson, MA StudentOzzie Skinner, MTLeonila Sumarsono, RMA, RPTLynette Thomson, MTNicole Weiss, RMA, RPTKathy Cilia, MT (ex-officio)

PublicationsNancy Gabi, RMA, ChairMaria Chevy-Newham, MTCarole Fecteau, MTMaria Guzman, MTKen Hawker, MTTeresita Hacuman, AHIKim Meshell, RMA, RPT, AHIRobin Miliner, MTDonna Nelson, RMASuellen Schobert, MLTEdith Tefft, MTKaye Tschop, MTDiane Powell, CMP (ex-officio)

Armed ServicesCalvina Jordan, MT, ChairSarah Hanaway, MLTGerald Simi, MLT, AHIRandy Swopes, MTFelicia Williams, MTViviana Vera, RMAChristopher Damon, JD (ex-officio)

CLC Evaluation CommitteeGerard P. Boe, PhD, ChairAnn Bachman, CLCJoel E. Mortensen, PhDAnn M. Steele, PhDDianne B. Zielinski, PhDChristopher A. Damon, J.D.

(ex-officio)

Career Education Advisory CommitteeBradley Moore, ChairJanice DonnellyJudith Dry, RDASandy OckTammy RennerMarylou de-Roma-RagazaJanet Sesser, RMAJohn Smith, Ed.D.Christopher A. Damon, J.D.

(ex-officio)Kathy Cilia (ex-officio)

DIRECTORYSTATE SOCIETY PRESIDENTS

2013 COMMITTEES

ALABAMA Rikki Packer, RMA, Virginia Col, 17634 DaileyLane, Foley, AL 36535, email: [email protected] Fred Morley, MT, 5700 East El Camino Quinto,Apache Junction, AZ 85119, email: [email protected] Tonda Ellis, CMLA, RPT, 1160 Midway Rd.,Monticello, AR 71655, email: [email protected] Sheryl Rounsivill, RMA, RPT, CMAS, AHI,2078 S. Hayston, Fresno, CA 93702, email: [email protected] – (See Rocky Mountain)CONNECTICUT – (See Tri-State)DC/DELAWARE/MARYLAND Robin Miliner, MT, 9695Halstead Ave., Laurel, MD 20723, email: [email protected] Kay Fergason, MT, 3712 Arava Dr., Green CoveSprings, FL 32043, e-mail: [email protected] Marvin Matthews, MT, 5565 La Fleur Trail,Lithonia, GA 30038, email: [email protected] Minelva B. Manuel, RMA, 98-410 Koauka LP Unit 10F, Aiea, HI 96701 e-mail: [email protected] Nancy Gabl, RMA, AHI, 1768 Coach Drive,Naperville, IL 60565, email: [email protected] L.E. Vern Hein, MT, 6060 E. 141st Ave.,Crown Point IN 46307-9254IOWA Beverly Christiansen, RMA, 1096 Grouse Ave.,Hampton, IA 50441, email: [email protected]/NEBRASKA (CENTRAL PLAINS) Tera Benefiel,MT, 622 S. McPherson Ave., Burrton, KS 67020, email: [email protected] Christina Huff, RPT, RMA, 597 Morehead Rd.,Bowling Green, KY 42101, email: huffcggclinic.comLOUISIANA Zenaida Maraggun, MT, 1602 Amour Drive,Leesville, LA 71446, email: [email protected]

MASSACHUSETTS – (See Tri-State)MAINE/NEW HAMPSHIRE Susan Constable, MT, 257 Heywood Rd., Winslow, ME 04901, email: [email protected] Sieglinde Wildie, MLT, 25 Rural St., Port Huron,MI 48060MINNESOTA Edith Tefft, MT, 317 Frenn Ave., Red Wing,MN 55066, email: [email protected] Cecil Hunt, MT, 4040 Colton Dr., Olive Branch,MS 38654, email: [email protected] Alberta Smith, RMA, AHI, 1997 Ridgeway,Arnold, MO 63010, email: [email protected] Juanita Stocke, MT, 1812 Cambridge Hills Ct.,Reno, NV 89523, email: [email protected] JERSEY Elizabeth Suarez, RMA, Lincoln Tech Inst, 3Silvercolt Dr., Colts Neck, NJ 07722, email: [email protected] MEXICO Virgil E. Marchand, RMA, Pima Med Inst,3501 Santa Teresa NW, Albuquerque, NM 87120-3627,email: [email protected] YORK Camille McIntyre, MT, 4401 Matilda Ave., Bronx,NY 10470, email: [email protected] CAROLINA Jerry Johnson, MT, 1296 Reeves MillRd., Mt. Airy, NC 27030, email: [email protected] Christopher Williams, RMA,AHI, 6637 Hubbard Dr.,Huber Heights, OH 45424-3534, email: [email protected] Kimberly Digby, MLT, 2013 Brighton Ave.,Oklahoma City, OK 73120, email: [email protected] Marilyn Albertsen, MT, 88515 Hwy. 202, Astoria,OR 97103, email: [email protected]

PENNSYLVANIA John A. Rudnick, MT, 501 Locust St.,Greensburg, PA 15601RHODE ISLAND – (See Tri-State)ROCKY MOUNTAIN (Colorado, Wyoming)Jennifer Dillard, RMA, 16324 E. 107th Pl., Commerce City, CO80022, email: [email protected] CAROLINA Peggy McCutcheon, MT, 941 McCutchen Rd., Cades, SC 29518, email: [email protected] Jerry T. Hudgins, MT, 221 Windsor Park Ln.,Hendersonville, TN 37075, email: [email protected] Taffy K. Durfee, MT, PO Box 432, Iola, TX 77861,email: [email protected] (Connecticut, Massachusetts, Rhode Island)Phyllis Nordby, RMA, Porter & Chester Inst., 166 Davis St.,Oakville, CT 06779, Email: [email protected] Michelle Tew, RMA, 1158 Lafayette Drive, Salt LakeCity, UT 84116, email: [email protected] Don Bouchelle, MT, 5001 7th Rd. South T-1,Arlington, VA 22204-2556, email: [email protected] STATE/IDAHO/MONTANA (NORTHWEST)Jo Abraham, RMA, 25032 SE 384th St., Enumclaw, WA98022, email: [email protected] VIRGINIA Tonya Brown, MT, 333 Baldwin St.,Fairmont, WV 26554, email: [email protected] Julie Lent, MT, 610 Fremont St., Algoma, WI54201, email: [email protected] – (See Rocky Mountain)CARIBBEAN ASSN. (CASMET) Grant Lambert, AHI, PO Box 2293, Lagoon Rd., St. George’s, Grenada, WestIndies, email: [email protected]


ABSTRACTS FROM THE CURRENT LITERATURE

None of us can read all the medical literature, even that that pertains particularly to medical technology.Presented below are short abstracts from current literature presented with the hope that they will answersome of your questions and lead you to a better understanding of what is happening. You are encouragedto send copies of articles you have found in journals or on the Internet to AMT and we will abstract them foran upcoming issue. We encourage and welcome future contributors from readers of this journal. Pleasesend your abstracts to Editor, Journal of Continuing Education Topics & Issues, 10700 W. Higgins Rd., Suite150, Rosemont, IL 60018.

The following abstracts were contributed by David Plaut, Plano, TX, who is AMT’s book reviewer and a frequent speaker at AMT annual conventions.

Your hospital librarian or your public librarian can help obtain copies of the full text of these articles.

A retrospective study of risk factors for poor outcomes in methicillin-resistantstaphylococcus aureus (MRSA) infection in surgical patients. J Orthop Surg Res. 2011May 23;6(1):25. Eseonu KC, Middleton SO, Eseonu CC.

Since its isolation, Methicillin-resistant Staphlococcus aureus (MRSA) has become a major cause of hospi-tal acquired infection (HAl), adverse patient outcome and overall resource utilization. This is a retrospectivestudy of the rates and outcomes of MRSA infection in orthopedic trauma at the Royal Infirmary of Edinburgh.This study found significant associations between adverse patient outcome (persistent deep infection, os-teomyelitis, the necessity for revision surgery, amputation and mortality) and the following patient variables:Length of inpatient stay, immuno-compromise, pre-admission residence in an institutional setting (such as aresidential nursing home) and the number of antibiotics used in patient care. Despite 63% of all infectionssampled resulting from proximal femoral fractures, no association between patient outcome and site of infec-tion or diagnosis was found. Somewhat surprisingly, the relationship between age and outcome of infectionwas not proved to be significant, contradicting previous studies suggesting a statistical association. Antibioticprophylaxis, previously identified as a factor in reducing overall incidence of MRSA infection, was not found tobe significantly associated with outcome. Early identification of high-risk patients as identified by this studycould lead to more judicious use of therapeutic antibiotics and reductions in adverse outcome, as well as so-cioeconomic cost. These results could assist in more accurate risk stratification based on a evidence basedevaluation of the significance of the risk factors investigated.

MRSA prevalence in European healthcare settings: a review. BMC Infect Dis. 2011 May20;11(1):138. Dulon M, Haamann F, Peters C.

During the past two decades, methicillin-resistant Staphylococcus aureus (MRSA) has become increas-ingly common as a source of nosocomial infections. Most studies of MRSA surveillance were performed dur-ing outbreaks, so that results are not applicable to settings in which MRSA is endemic. This paper gives anoverview of MRSA prevalence in hospitals and other healthcare institutions in non-outbreak situations in West-ern Europe. Thirty-one observational studies were included in the review. Four of the studies were of goodquality. Surveillance screening of MRSA was performed in long-term care (11 studies) and acute care (20studies). Prevalence rates varied over a wide range, from less than 1% to greater than 20%. Prevalence in theacute care and long-term care settings was comparable. The prevalence of MRSA was expressed in variousways -- the percentage of MRSA among patients (range between 1% and 24%), the percentage of MRSAamong S. aureus isolates (range between 5% and 54%), and as the prevalence density (range between 0.4and 4 MRSA cases per 1,000 patient days). The screening policy differed with respect to time points (on ad-mission or during hospital stay), selection criteria (all admissions or patients at high risk for MRSA) andanatomical sampling sites. This review underlines the methodological differences between studies of MRSAsurveillance. For comparisons between different healthcare settings, surveillance methods and outcome cal-culations should be standardized.

Methicillin-resistant Staphylococcus aureus in long-term-care facilities. Clin MicrobiolInfect. 2009 Dec; 15 Suppl 7: 26-30. Manzur A, Gudiol F.

Owing to a high prevalence of methicillin-resistant Staphylococcus aureus (MRSA) among residents, long-term-care facilities (LTCFs) have become substantial reservoirs of this microorganism. Few data on the natur-al history of MRSA colonization in this setting are available. The cumulative incidence appears to be approxi-mately 20% per year, and more than half of carriers have persistent colonization. Several host-related factors-- such as antibiotic use, invasive devices, and poor infection control practices -- increase the risk of coloniza-tion. Clinical experience suggests that subsequent MRSA infections are neither frequent nor severe while col-onized residents are living in an LTCF; however, when admitted to an acute-care center, colonized individualsmay spread MRSA to other patients and may develop severe infections. Therefore, the epidemiological im-pact of the high prevalence of MRSA in these centers is more relevant than the clinical impact of this coloniza-tion for an individual resident. Standard precautions should be applied as routine infection control measuresfor all residents of LTCFs, whereas barrier precautions, cohorting, decolonization and other measures shouldbe undertaken only for controlling outbreaks of MRSA infection.

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