The Role of the Primary Care Physician in Hospital Acquired Pneumonia (HAP)

More about the emergence “super bugs,” and ways to avoid them.

By Randy A. Schuck, DO

Hospital Acquired Pneumonia (HAP) is a relatively common occurrence in health care today. Unfortunately, so is the emergence of resistant bacteria strains that are the root cause of these infections. The emergence has been documented in the media, as well as in the medical journals.

More troubling than the emergence of resistance is the lack of new medications to treat these strains.

The primary care physician is the primary admitting physician, and therefore is often the one instituting medical treatment protocols. It is crucial that the primary care physician is able to recognize resistant pathogens and to institute appropriate treatment as rapidly as possible. Often the treatment for resistant pathogens is left up to Infectious Disease (ID) or Pulmonology Medicine (PM) specialists. Unfortunately, there can be a delay of treatment due to communication errors, or slow response to requested consults.

HAP is a direct product of patient time spent in a potentially infectious environment. According to the National Nosocomial Infection Surveillance (NNIS) group of the Centers for Disease Control and Prevention (CDC), the types of bacteria and the number of infections in the community versus the hospital setting directly correlates with the length of time in the hospital. Therefore, it is a primary concern to minimize the time spent in the hospital setting.

Length of stay issues are often discussed by the medical team, and the national average is trended by the Centers for Medicare & Medicaid Services (CMS). Often, physicians feel this statistic is only for the benefit of the hospital for reimbursement, but studies show length of stay also correlates with infection rates. The primary care physician can be the primary factor in reducing patient length of stay, and therefore, an important key in reducing the patient’s exposure time to resistant strains of bacteria.

Data Regarding HAP
Examination of the data from the NNIS group of the CDC from January 1989 through July 1998 documents Gram-positive organisms as the most common pathogens associated with Nosocomial infections in ICUs.(1) According to Fridkin, et al,(6) coagulase-negative staphylococci and Staphylococcus aureus were the two most common pathogens isolated from all Nosocomial infections(6) Fridkin, et al evaluated over 235,000 isolates in ICU patients.

Schaberg and Zervos report strains of methicillin-resistant Staphylococcus aureus (MRSA) with intermediated resistance to glycoproteins may signify the development of strains with higher level of resistance to vancomycin.(14) Glycoprotein-intermediate S. aureus (GISA) originally reported in 1996, is generally associated with previous MRSA infections, repeated and prolonged use of vancomycin and dialysis.(16)

With the prevalence of MRSA, the use of vancomycin has also increased. The increased use of vancomycin helps foster the growth of another resistant strain of bacteria found in the isolates from the ICU patients, Vancomycin-resistant enterococcus (VRE). Schaberg and Zervos explained that vancomycin resistance is carried on a plasmid, and can potentially spread beyond enterococci to staphylococci and streptococci.(14) The CDC reported the first case of vancomycin-resistant S. aureus (VRSA) infection in July 2002; the second case was reported in October 2002.(2) Although unrelated, both isolates contained the mecA and vanA genes, mediating oxacillin and vancomycin resistance respectively. According to the CDC, “the presence of the vanA in this VRSA suggests that the resistance determinate was acquired from a vancomycin-resistant enterococcus (VRE).”(2)

VRE is a highly infectious pathogen that is spread primarily by direct contact. Multiple studies have linked the lack of hand washing and cleaning of stethoscopes, to the VRE infection rate.(11) As the primary care physician and the attending physician leadership primarily sets the direction of the health care team, strict hand washing and cleansing of the stethoscopes between patients in all settings of the hospital, as well as in our private offices, would help decrease the rate of spread. Perhaps the implementation of the above guidelines and the reduced use of vancomycin could reduce the prevalence of VRE, and in turn, reduce the link between VRE and VRSA. It is our responsibility to safeguard our patients’ exposure, as well as reduce potentially resistant strains.

Therapies, Studies and Treatments
Kollef, et al,(10) identified a relationship between inadequate antimicrobial treatment and mortality. The cohort study was performed from July 1997 through March 1998, when 169 patients initially received inadequate anti­microbial therapy for an infection. This represented 26 percent of the 655 patients assessed to have either community-acquired or nosocomial infections. All-cause mortality was 52 percent in patients receiving inadequate antimicrobial therapy, versus 12 percent in those receiving adequate therapy (P<.001). In­fection-related mortality was 42 percent in patients receiving inade­quate therapy, versus 18 percent for those receiving adequate therapy.

To reduce the chance of inadequate therapy, Evans, et al,(5) designed a study to develop a computerized antibiotic consultant to assist physicians in the selection of the appropriate antimicrobial therapy. The study design used two-stage random-selection studies to compare antibiotics suggested by the computer antibiotic consultant with the 482 associate antibiotic susceptibility results and the concurrent antibiotics ordered by physicians (PCP and ID consultants).

The results clearly showed that if the pathogen was matched to appropriate therapy, all phases of the admission were improved. The computer matched the antimicrobial sensitivities, which allowed the appropriate therapy. This reduced the variability of personal choice of antibiotic selection by the personal choice of the physician, which appeared to be the leading cause of inappropriate therapy.

Singh, et al(15) designed a study to evaluate the outcomes of short-course antimicrobial therapy, based on the premise of de-escalation of antibiotics, and the establishment of time lines to start potent broad spectrum antibiotics early and their removal if certain criteria were not met within 72 hours. The study proposed that patients with the clinical pulmonary infection score (CPIS) less than or equal to 6 (implying a low likelihood of pneumonia) would be randomized to receive either standard therapy (choice and duration of antibiotics at the discretion of the physicians) or ciprofloxacin monotherapy with reevaluated at Day Three.

Antimicrobial resistance and/or super infections were documented in 14 percent (five of 37) of the patients in the experimental (short-course) group and 38 percent (14 of 37) of the patients in the standard (control) group (P=.017). The emergence of the super infection and antibiotic resistance was so striking in the standard (control) therapy group that the Institutional Review Board (IRB) recommended termination of the study due to ethical reasons.

Both of these studies showed physicians were often using inappropriate antimicrobial therapies. It is the suggestion of the authors (Singh and Evans) to reduce variability of selection of antibiotics, as well as removing antibiotics as early as possible, especially when it is determined that the patient didn’t need antibiotics. According to the study by Singh, the removal of antibiotics did not lead to resistance of bacteria, or super infections.

The role of the primary care physician in the determination of therapy begins in the Emergency Department (ED). Multiple studies have shown the delay in starting of antibiotic therapy increases morbidity and mortality.(7, 10) It is the responsibility of the primary care physician to ensure continuity of appropriate antibiotic therapy instituted in the ED prior to transfer to the hospital ward. The Emergency physician is ultimately responsible for the treatment of the patient in the ED, but the primary care physician can assure initiation of antibiotics are met when admission is requested by the ED physician.

Appropriate antibiotics based on the type of patient, i.e. nursing home patient or recently discharged patients with suspected pneumonia, should be considered HAP and treated with aggressive antimicrobial therapy and de-escalated in 72 hours if the initial diagnosis is ruled out by subsequent testing.

Summary
The primary care physician is considered the gatekeeper in many Health Maintenance Organization (HMO) models, but usually not within the hospital setting. The attending physician may consult sub-specialists to determine appropriate antimicrobial treatments in HAP. This may lead to delay in treatment due to communication difficulties, or slow response by the consultants. There are multiple studies available to demonstrate the inappropriate use of antibiotics by sub-specialists, and the availability of treatment tools to correct the inappropriate choice.

The delay of onset of antibiotics has been demonstrated to increase morbidity and mortality. The primary care physician can institute antibiotics upon admission and consult a specialist if treatment appears inappropriate. Usually, the primary care physician has taken care of the patient prior to admission, and knows the history of the patient. The primary care physician can direct the ED physician with appropriate information to determine the risk scale of the patient (i.e. prior admissions, prior MRSA infections, nursing home patient).

The primary care physician should lead the health care team in decision making to minimize length of stay, thus reducing the exposure of the patient to resistant strains of bacteria. The primary care physician should minimize the length of time the patient is within the ICU by utilizing the ICU only when necessary. Washing hands and stethoscope between patients is a most effective measure that may guard against inadvertent transmission of infection.

Ultimately, the primary care physician’s goal should be to keep the patient out the hospital, and out of HAP’s way.


Randy A. Schuck, DO, is in practice in St. Petersburg, Florida.

References:

  1. Centers for Disease Control and Prevention. National Nosocomial Infections Surveillance (NNIS) System report, data summary from January 1990 – May 1999, issued June 1999. American Journal of Infection Control; 27: 520-532.
  2. Centers for Disease Control and Prevention. “Staphylococcus aureus Resistant to Vancomycin – United States, 2002.” Morbidity & Mortality Weekly Report 2002; 51: 565-567.
  3. Centers for Disease Control and Prevention. “Public health dispatch: Vancomycin-resistant Staphylococcus aureus – Pennsylvania, 2002.” Morbidity & Mortality Weekly Report 2002; 51: 902.
  4. Division of Healthcare Quality Promotion, Centers for Disease Control and Prevention Web site. Issues in Healthcare Settings, MRSA page, MRSA Prevalence Slide. Available at: http://www.cdc.gov/ncidod/hip/Aresist/mrsa.htm. Accessed February 29, 2004.
  5. Evans, R.S., Pestotnik, S.L., Classen, D.C., et al. “A Computer-Assisted Management Program for Antibiotics and Other Anti-Infective Agents.” New England Journal of Medicine, 1998: 338: 232-238.
  6. Fridkin, S.K., Welbel, S.F., Weinstein, R.A. “Magnitude and Prevention of Nosocomial Infections in the Intensive Care Unit.” Infectious Disease Clinics of North America, 1997; 11: 479-496.
  7. Heyland, D.K.,  Cook, D.J., Griffith, L., Keenan, S.P., Brun-Buisson, C., for the Canadian Critical Care Trials Group. “The Attributable Morbidity and Mortality of Ventilator-Associated Pneumonia in the Critically Ill Patient.” American Journal of Respiratory and Critical Care Medicine 1999; 159: 1249-1256.
  8. Hiramatsu, K., Hanaki, H., Ino, T., Yabata, K., Oguri, T., Tenover, F.C. “Methicillin-Resistant Staphylococcus aureus Clinical Strain with Reduced Vancomycin Susceptibility” (letter). Journal of Antimicrobiology Chemotherapy 1997; 40: 135-136.
  9. Jones, R.N., Low, D.E., Pfaller, M.A. “Epidemiologic Trends in Nonsocomial and Community-Acquired Infections due to Antibiotic-Resistant Gram-Positive Bacteria: The Role of Streptogramins and Other Newer Compounds.” Diagnostic Microbiol Infectious Diseases 1999; 33: 101-112.
  10. Kollef, M.H., Serman, G., Ward, S., Fraser, V.J. “Inadequate Antimicrobial Treatment of Infections: A Risk Factor for Hospital Mortality Among Critically Ill Patients.” Chest 1999; 115: 462-474.
  11. Martone, W.J. “Spread of Vanomycin-Resistant Enterococci: Why did it Happen in the U.S.?” Infection Control and Hospital Epidemiology 1998; 19: 539-545.
  12. Moellering, R.C. “Vancomycin-Resistant Enterococci.” Clinical Infectious Diseases 1998; 26: 1196-1199.
  13. Rubin, R.J., Harrington, C.A., Poon, A., Dietrich, K., Greene, J.A., Moiduddin, A. “The Economic Impact of Staphylococcus aureus Infection in New York City Hospitals.” Emerging Infectious Diseases 1999; 5: 9-17.
  14. Schaberg, D.R., Zervos, M.J. “Intergeneric and Interspecies Gene Exchange in Gram-Positive Cocci.” Antimicrobiological Agents Chemotherapy 1986; 30: 817-822.
  15. Singh, N., Rogers, P., Atwood, C.W., Wagener, M.M., Yu, V.L. “Short-Course Empiric Antibiotic Therapy for Patients with Pulmonary Infiltrates in the Intensive Care Unit.” American Journal of Respiratory and Critical Care Medicine 2000; 162: 505-511.
  16. Smith, T.L., Pearson, M.L., Wilcox, K.R., et al, for the Glycopeptide-Intermediate Staphylococcus aureus Working Group. “Emergence of Vancomycin Resistance in Staphylococcus aureus.” New England Journal of Medicine 1999; 340: 493-501.