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The Research Review
by Kenny Navarro

Drug resistant bacteria in the prehospital environment

While working in an infectious environment, taking precautions is key

By Kenny Navarro

Introduction

Antibiotic-resistant bacteria are widespread and their numbers are growing. In 1974, only 2% of staph bacteria tested in United States hospitals were drug resistant (Panlilio et al., 1992). By 2008, that number increased to about 59% (Talan et al., 2011).

Antibiotic resistance among bacteria may be innate or acquired (Aldrin et al., 2013). Acquired resistance results from exposure to less than lethal antibiotic doses, as in cases where a patient stops taking prescribed antibiotics before the infection is over.

Future antibiotic exposure eradicates susceptible bacteria thereby allowing proliferation of the resistant strain, which can then spread from the treated individual to others in the surrounding environment (Livermore, 2003).

A number of multi-drug resistant organisms (MDRO) represent a threat to EMS professionals and their patients (Shlaes et al., 1997). It is beyond the scope of this article to review or even name each of those pathogens.

However, the predominant drug resistant pathogen responsible for most purulent skins and soft-tissue infections is methicillin-resistant Staphylococcus aureus, known simply as MRSA (Talan et al., 2011).

Drug resistance

Multi-drug resistance first appeared in nosocomial infections. Nosocomial infections result from pathogen exposure within the healthcare environment, which includes EMS personnel and the patient care compartment of the ambulance.

Epidemiologists can often trace these infections back to improper infection-control procedures including inadequate hand-washing techniques, inadequate cleaning of the patient care environment, or inadequate decontamination of patient care equipment. Researchers estimate that 85% of all MRSA infections began with a nosocomial exposure (Naimi et al., 2003).

In just one example, despite the best infection control efforts, a burn victim in a Southern California hospital transmitted MRSA to 34 other patients resulting in the deaths of half of them (Locksley et al., 1982).

In the 1990s, a disturbing trend emerged as individuals in the community without the traditional risk factors began developing MRSA infections (Herold et al., 1998; Lindenmayer, Schoenfeld, O'Grady, & Carney, 1998; Maguire, Arthur, Boustead, Dwyer, & Currie, 1996). Further investigation revealed a genetically different strain of Staph from the one causing problems in the healthcare community.

Epidemiologists differentiate these strains through the use the terms community-acquired MRSA (CA-MRSA) or hospital-acquired MRSA (HA-MRSA) (Kilbane & Reynolds, 2008). CA-MRSA tends to be more virulent than HA-MRSA as it carries genes for the production of a leukotoxin associated with tissue necrosis (Appelbaum, 2007; Chua, Laurent, Coombs, Grayson, & Howden, 2011; Naimi et al., 2003; Voyich et al., 2006).

Some groups are at higher risk for community-acquired infections than others. These include athletes, children in day care centers, military recruits, prisoners, IV drug abusers, patients in extended care facilities, and anyone who comes into contact with recently hospitalized people, especially ICU or surgical patients.

It is possible, however that people with no apparent risk factors can still develop significant infections. Within a two-year period in the mid-west, four children between the ages of 1 and 13 years without any identifiable risk factors died from MRSA infections (Centers for Disease Control and Prevention, 1999).

EMS studies

Researchers in Indiana swabbed the nasal cavities of EMS personnel from a hospital-based agency and students in an EMT training program (Miramonti et al., 2013). Overall, about 5% of the personnel tested positive for the presence of MRSA. This was about five times the prevalence found among the public (Kuehnert et al., 2006).

The researchers could not demonstrate a statistically significant difference between student and provider colonization rates although paramedics appear to have colonization rates twice that of EMT-Basics.

Researchers tested 21 ambulances in an urban ambulance fleet for the presence of MRSA (Roline, Crumpecker, & Dunn, 2007). The research staff swabbed various areas inside the ambulance including the steering wheel, the cot handrail, the cot cushion, the work area to the right of the patient, and the tip of the hard tonsil suction.

Almost fifty percent of the swabbed ambulances tested positive for the presence of MRSA.

In another study, researchers tested fifty stethoscopes used by EMS personnel in an urban service (Merlin et al., 2009). During the test, researchers asked EMS personnel to complete a questionnaire identifying the last time someone disinfected the stethoscope.

Sixteen of the fifty stethoscopes, or approximately 32% tested positive for the presence of MRSA. One-third of the EMS personnel could not pinpoint the time when someone last cleaned their stethoscopes.

Researchers in New Jersey compared nosocomial infection rates between in-patients who arrived at a level-one trauma center by paramedic-staffed ambulance with patients who arrived by other means (Alter & Merlin, 2011). Although the community-acquired infection rate was not significantly different between the two groups, the rate of nosocomial infections was greater in the group of admitted patients who arrived by ambulance compared to those who arrived by other means.

The results of this study do not suggest that paramedic transport causes higher infection rates but it does suggest that patients transported by ambulance are at a higher risk for nosocomial infection once admitted to the hospital. EMS agencies must at least consider the possibility that inadequate or ignored infection control procedures in the field may allow colonization during transport.

The role of the provider

You play an important role in stopping the spread of MRSA and other pathogens. Most experts agree that proper hand washing is the single most effective way of preventing the spread of infection (Fridkin & Raynes, 1999) as the hands appear to be the main source of cross transmission for nosocomial infections (Hardy, Hawkey, Gao, & Oppenheim, 2004).

Many healthcare providers do not wash their hands as often or as effectively as they should (Karabey, Ay, Derbentli, Nakipoglu, & Esen, 2002; Pittet, Mourouga, & Perneger, 1999). Medical personnel could significantly reduce the rate of resistant organism colonization by increasing hand hygiene compliance (Pittet et al., 2000; Sebille, Cheveret, & Valleron, 1997).

In the field, use commercial waterless hand cleaners. However, after arrival at the hospital, wash your hands as soon as possible after transferring patient care to the emergency department staff.

Wear disposable, single-use gloves for all patient contact and change them when moving from one patient to another or when they become heavily soiled. It is important to remember, however that wearing gloves is not a substitute for proper hand washing.

You should take additional measures of protection such as wearing a gown when caring for a patient with a known MRSA contamination. The eyes, nose, and mouth are common portals of entry for infectious agents.

If the patient is producing respiratory droplets, you should wear a facemask and eye protection. It is also a good idea to put a facemask on the patient to prevent the spread of bacteria into the patient care environment.

After delivering the patient to the hospital, you must properly decontaminate the patient care compartment. Wipe all surfaces with a commercial disinfectant and allow it air dry.

Staphylococci can survive for at least a day on common medical materials with some viability even after 56 to 90 days on polyester and polyethylene plastics (Duckworth & Jordens, 1990; Lacey, Barr, Barr, & Inglis, 1986; Mortimer, Wolinsky, Gonzaga, & Rammelkamp, 1966).

One of the most important equipment decontamination practices is to clean surfaces with soap and water before disinfection (Rutala, 1996). Cleaning removes the foreign material from the objects while disinfection removes the microorganisms.

Before disinfecting, clean all equipment that came into contact with the patient or your gloves with soap and water. This includes the stethoscope, blood pressure cuff, ECG monitor cable, stretcher, and clipboard.

The disinfectant should be a commercial solution or a 1:10 concentration of household bleach and water (Goodman & Cone, 2001).

Drug resistant bacteria pose a risk for all EMS providers, their families, and their patients. Some groups of patients are at an increased risk from this pathogen. EMS personnel and their equipment are a source of exposure and contamination.

Once infected, eradication of MRSA is very difficult and complicated. Pre-hospital care providers must protect themselves by using standard precautions, washing their hands often and especially between patient contacts, thoroughly cleaning and disinfecting all equipment and patient care surfaces with an appropriate disinfectant, and carefully disposing of contaminated materials such as pus, blood, or urine.

References

Aldrin, M., Raastad, R., Tvete, I. F., Berild, D., Frigessi, A., Leegaard, T., Monnet, D. L., Walberg, M., & Müller, F. (2013). Antibiotic resistance in hospitals: a ward-specific random effect model in a low antibiotic consumption environment. Statistics in Medicine, 32(8), 1407–1418. doi:10.1002/sim.5636

Alter, S. M., & Merlin, M. A. (2011). Nosocomial and community-acquired infection rates of patients treated by prehospital advanced life support compared with other admitted patients. American Journal of Emergency Medicine, 29(1), 57–64. doi:10.1016/j.ajem.2009.07.020

Appelbaum, P. C. (2007). Microbiology of antibiotic resistance in Staphylococcus aureus. Clinical Infectious Diseases, 45(Suppl 3), S165–70. doi:10.1086/519474

Centers for Disease Control and Prevention. (1999, Aug 20). Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus—Minnesota and North Dakota, 1997-1999. Morbidity and Mortality Weekly Report, 48(32), 707-710.

Chua, K., Laurent, F., Coombs, G., Grayson, M. L., & Howden, B. P. (2011). Antimicrobial resistance: Not community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA)! A clinician's guide to community MRSA – Its evolving antimicrobial resistance and implications for therapy. Clinical Infectious Diseases, 52(1), 99–114. doi:10.1093/cid/ciq067

Duckworth, G. J., & Jordens, J. Z. (1990). Adherence and survival properties of an epidemic methicillin resistant strain of Stapylococcus aureus compared with those of methicillin sensitive strains. Journal of Medical Microbiology, 32(3), 195-200.

Fridkin, S. K., & Raynes, R. P. (1999). Antimicrobial resistance in intensive care units. Clinics in Chest Medicine, 20(2), 303-316. doi:10.1016/S0272-5231(05)70143-X

Goodman, C. S., & Cone, D. C. (2001). Emergency medical services equipment hygiene practices. Prehospital Emergency Care, 5(2), 169-173.

Hardy, K. J., Hawkey, P. M., Gao, F., & Oppenheim, B. A. (2004). Methicillin resistant Staphylococcus aureus in the critically ill. British Journal of Anaesthesia, 92(1), 121-130. doi:10.1093/bja/aeh008

Herold, B. C., Immergluck, L. C., Maranan, M. C., Lauderdale, D. S., Gaskin, R. E., Boyle-Vavra, S., Leitch, C. D., & Daum, R. S. (1998). Community-acquired methicillin-resistant Staphylococcus aureus in children with no identified predisposing risk. Journal of the American Medical Association, 279(8), 593–598. doi:10.1001/jama.279.8.593

Karabey, S., Ay, P., Derbentli, S., Nakipoglu, Y., Esen, F. (2002). Hand washing frequencies in an intensive care unit. Journal of Hospital Infections, 50(1), 36-41. doi:10.1053/jhin.2001.1132

Kilbane, B. J., & Reynolds, S. L. (2008). Emergency department management of community-acquired methicillin-resistant Staphylococcus aureus. Pediatric Emergency Care, 24(2), 109-114. doi:10.1097/PEC.0b013e318163df51.

Kuehnert, M. J., Kruszon-Moran, D., Hill, H. A., McQuillan, G., McAllister, S. K., Fosheim, G., McDougal, L. K., Chaitram, J., Jensen, B., Fridkin, S. K., Killgore, G., & Tenover, F. C. (2006). Prevalence of Staphylococcus aureus nasal colonization in the United States, 2001–2002. Journal of Infectious Disease, 193(2), 172–179. doi:10.1086/499632

Lacey, R. W., Barr, K. W., Barr, V. E., & Inglis, T. J. (1986). Properties of methicillin resistant Stapylococcus aureus colonising patients in a burns unit. Journal of Hospital Infection, 7(2), 137-148. doi:10.1016/0195-6701(86)90056-3

Lindenmayer, J. M., Schoenfeld, S., O'Grady, R., & Carney, J. K. (1998). Methicillin-resistant Staphylococcus aureus in a high school wrestling team and the surrounding community. Archives of Internal Medicine, 158(8), 895–899.

Livermore, D. M. (2003). Bacterial resistance: origins, epidemiology, and impact. Clinical Infectious Diseases, 36(Suppl 1), S11–S23. doi:10.1086/344654

Locksley, R. M., Cohen, M. L., Quinn, T. C., Tompkins, L. S., Coyle, M. B., Kirihara, J. M., & Counts, G. W. (1982). Multiply antibiotic-resistant Staphylococcus aureus: introduction, transmission, and evolution of nosocomial infection. Annals of Internal Medicine, 97(3), 317-324. doi:10.7326/0003-4819-97-3-317

Maguire, G. P., Arthur, A. D., Boustead, P. J, Dwyer, B., & Currie, B. J. (1996). Emerging epidemic of community-acquired methicillin-resistant Staphylococcus aureus infection in the Northern Territory. Medical Journal of Australia, 164(12), 721–723.

Merlin, M. A., Wong, M. L., Pryor, P. W., Rynn, K., Marques-Baptista, A., Perritt, R., Stanescu, C. G., & Fallon, T. (2009). Prevalence of methicillin-resistant Staphylococcus aureus on the stethoscopes of emergency medical services providers. Prehospital Emergency Care, 13(1), 71-74. doi:10.1080/10903120802471972

Miramonti, C., Rinkle, J. A., Iden, S., Lincoln, J., Huffman, G., Riddell, E., & Kozak, M. A. (2013). The prevalence of methicillin-resistant staphylococcus aureus among out-of-hospital care providers and emergency medical technician students. Prehospital Emergency Care, 17(1), 73–77. doi:10.3109/10903127.2012.717169

Mortimer, E. A., Wolinsky, E., Gonzaga, A. J., & Rammelkamp, C. H. (1966). Role of airborne transmission in Staphylococcal infections. British Medical Journal, 1(5483), 318-322.

Naimi, T. S., LeDell, K. H., Como-Sabetti, K., Borchardt, S. M., Boxrud, D. J., Etienne, J., Johnson, S. K., Vandenesch, F., Fridkin, S., O'Boyle, C., Danila, R. N., & Lynfield, R. (2003). Comparison of community- and health care-associated methicillin-resistant staphylococcus aureus infection. Journal of the American Medical Association, 290(22), 2976–2984. doi:10.1001/jama.290.22.2976

Panlilio, A. L., Culver, D. H., Gaynes, R. P., Banerjee, S., Henderson, T. S., Tolson, J. S., & Martone, W. J. (1992). Methicillin-resistant staphylococcus aureus in U.S. hospitals, 1975-1991. Infection Control and Hospital Epidemiology, 13(10), 582-586.

Pittet, D., Hugonnet, S., Harbarth, S., Mourouga, P., Sauvan, V., Touveneau, S., & Perneger, T. V. (2000). Effectiveness of a hospital-wide programme to improve compliance with hand hygiene. Lancet, 356(9238), 1307-1312. doi:10.1016/S0140-6736(00)02814-2

Pittet, D., Mourouga, P., Perneger, T. V. (1999). Compliance with handwashing in a teaching hospital. Annals of Internal Medicine, 130(2), 126-130

Roline, C. E., Crumpecker, C., & Dunn, T. M. (2007). Can methicillin-resistant staphylococcus aureus be found in an ambulance fleet? Prehospital Emergency Care, 11(2), 241–244. doi:10.1080/10903120701205125

Rutala, W. A. (1996). Association for professionals in infection control guidelines for selection and use of disinfectants. American Journal of Infection Control, 24(4), 313-342. doi:10.1016/S0196-6553(96)90065-6

Sebille, V., Cheveret, S., & Valleron, A. J. (1997). Modeling the spread of resistant nosocomial pathogens in an intensive-care unit. Infection Control and Hospital Epidemiology, 18(2), 84-92. doi:10.2307/30142395

Shlaes, D. M., Gerding, D. N., John, J. F., Jr., Craig, W. A., Bornstein, D. L., Duncan, R. A., Eckman, M. R., Farrer, W. E., Greene, W. H., Lorian, V., Levy, S., McGowan, J. E. Jr., Paul, S. M., Ruskin, J., Tenover, F. C., & Watanakunakorn, C. (1997). Society for healthcare epidemiology of America and infectious diseases society of America joint committee on the prevention of antimicrobial resistance: Guidelines for the prevention of antimicrobial resistance in hospitals. Infection Control and Hospital Epidemiology, 18(4), 275-291. doi:10.2307/30141215

Talan, D. A., Krishnadasan, A., Gorwitz, R. J., Fosheim, G. E., Limbago, B., Albrecht, V., & Moran, G. J. (2011). Comparison of staphylococcus aureus from skin and soft-tissue infections in US emergency department patients, 2004 and 2008. Clinical Infectious Diseases, 53(2), 144–149. doi:10.1093/cid/cir308

Voyich, J. M., Otto, M., Mathema, B., Braughton, K. R., Whitney, A. R., Welty, D., Long, R. D., Dorward, D. W., Gardner, D. J., Lina, G., Kreiswirth, B. N., & DeLeo, F. R. (2006). Is Panton-Valentine leukocidin the major virulence determinant in community-associated methicillin-resistant Staphylococcus aureus disease? Journal of Infectious Disease, 194(12), 1761–1770. doi:10.1086/509506

The author has no financial interest, arrangement, or direct affiliation with any corporation that has a direct interest in the subject matter of this presentation, including manufacturer(s) of any products or provider(s) of services mentioned.

Send correspondence concerning this article to Kenneth W. Navarro, The University of Texas Southwestern School of Health Professions, 5323 Harry Hines Blvd, MC 9134, Dallas, Texas 75390-9134. E-mail: kenneth.navarro@utsouthwestern.edu

About the author

Kenny Navarro is an Assistant Professor in the Emergency Medicine Education Department at the University of Texas Southwestern Medical Center at Dallas. He coordinates all continuing education activities and assists in medical oversight for BioTel, a multi-jurisdictional EMS system composed of 14 fire/rescue agencies and more than 1,500 paramedics. Mr. Navarro serves as a Content Consultant for the AHA ACLS Project Team for Guidelines 2010 and served on two education subcommittees for NIH-funded research projects, as the Coordinator for the National EMS Education Standards Project, and as an expert writer for the National EMS Education Standards Implementation Team. Send correspondence concerning any articles in this section to Kenneth W. Navarro, The University of Texas Southwestern Medical School at Dallas, 6300 Harry Hines Blvd, MC 9134, Dallas, Texas 75390-9134, or e-mail kenny.navarro@ems1.com.
Comments
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Charles Edward Weber Charles Edward Weber Tuesday, February 25, 2014 12:22:24 AM Because of your interest in infection, you may find the article below similar to this reference [1] useful. Heating the area of an infection up as hot as one can stand with an infrared lamp usually works beautifully for infections in the body near the surface. I am not certain that this works for gram positive bacteria. It is possible that it does not because they do not produce a fever in alligators [2]. However, heating Mycobacterium ulcerans to 40 degrees centigrade cures an infection [9]. DISCUSSION I propose that fever evolved because bacteria grow poorly at elevated temperatures, and that the immune system evolved to become more active at elevated temperatures in order to take advantage of this bacterial weakness. The immune system is markedly stimulated by a rise in temperature. This may be a response arising through interleuken-1 [3]. This phenomenon has been demonstrated for interleukin–1 and interleukin-2 in post operative hypothermia [4]. Heat also stimulates tumor necrosis factor [5]. The above could be the reason why the ability to create a fever arose [6]. Doubling time of pneumococcal meningitis in rabbits is markedly increased at fever temperature, and that bacteria did not grow at all at 41 degrees centigrade in either soy broth or cerebral fluid [7], so it seems that the efficacy of body temperature effectiveness is dependent on more than enhancement of the immune system. It is conceivable in view of their results that rather than the fever evolving in order to enhance an innate characteristic of the immune system, the fever evolved to take advantage of an innate ineffectiveness of most bacteria at high temperatures and the immune system then evolved to be most effective during a fever. I have often cured a cold within a couple hours with an infrared heat lamp directed to my nose and it has been advantageous for me against other infections near the surface of the body such as sore throats and infected skin damage. It is probably necessary to start the temperature treatment early in the disease for viruses, because that is the case for rabies in mice [8]. Also it is possible that its efficacy is not on the virus so much as on the secondary infections in the case of nose colds. It is necessary to protect the eyes when applied near them though, because I have reason to believe their optical characteristics can change from a high temperature. I have cured abscessed teeth that were not cured by anacardic acids in raw cashew nuts [ http://charles_w.tripod.com/tooth.html ] and were very slow to respond to amoxicillin by heating the jaw with an infrared lamp in conjunction with the amoxicillin. It is possible that a laser directed on the tooth would work better and should be tried. It is very desirable to get rid of an infection first even if a root canal operation is desired, in my opinion, and certainly imperative if a root canal operation is financially or tactically impossible. Development of a device that heated the tooth up directly to the correct temperature should be very advantageous, at least for the few gram negative tooth infections. I have cured quite a few other kinds of infections in the last couple of years as well with artificial fever. CONCLUSION It would be desirable to perform experiments to determine whether this is a universal phenomenon or not for gram negative bacteria, because they produce many bad diseases near the surface of the body and this procedure would usually be practical and inexpensive as applied by patients. It would also be desirable to know for sure if gram positive infections can be cured. REFERENCES [1] Weber CE 2007 Creation of a local fever using an infrared lamp to cure a tooth abscess. Medical Hypotheses 68; 458. [2] Merchant M, Williams S, Trosclair PL 3rd, Elsey RM, Mills K. 2007 Febrile response to infection in the American alligator (Alligator mississippiensis). Comp Biochem Physiol A Mol Integr Physiol. 2007 Dec;148(4):921-5.. [3] Hanson DE, Murphy PA, Silicano R, Shin HS. The effect of temperature on the activation of thymocytes by interleukin I & II. Journal of Immunol. 1983; 130: 216, [4] Beilin B, Shavit Y, Razumovsky J, Wolloch Y, Zeidel A, Bessler H. Effects of Mild Perioperative Hypothermia on Cellular Immune Responses. Anesthesiology. 1998; 89(5):1133-1140, [5] Zellner M, Hergovics N, Roth E, Jilma B, Spittler A, Oehler R. Human monocyte stimulation by experimental whole body hyperthermia. Wien. Klin. Wochenschr. 2002 Feb 15; 114(3): 73-75. [6] Kluger MJ. The evolution and adabtive value of fever. American Sci. 1978; 66: 38-43. [7] Small PM, Täuber MG, Hackbarth CJ, Sande MA. Influence of body temperature on bacterial growth rates in experimental pneumococcal meningitis in rabbits. Infect Immun. 1986 May; 52(2): 484–487. [8] Bell JF, and Moore GJ. Effects of High Ambient Temperature on Various Stages of Rabies Virus Infection in Mice. Infect Immun. 1974 September; 10(3): 510–515. [9] Meyers WM Shelly WM Conner DH Heat treatment of Mycobacterium ulcerans infections without surgical incision. The American Journal of Tropical Medicine and Hygeine.1974 23(5); 924-929. Sincerely, Charles Weber PS Dr. Rastmanesh, a nutritionist from Iran, would like to secure a position in an English speaking university because of religious or possibly political problems. He has an impressive CV. If you know of an opening I will send you his CV. It would be a travesty to leave that fine scientist in that criminal country after he has gotten rid of rheumatoid arthritis for us.

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