eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Hospital-Acquired Infections

Quoc V Nguyen, MD, Assistant Professor, Department of Pediatrics, New York State Health Department

Updated: Jan 14, 2009

Introduction

Background

Hospital-acquired infections (HAIs), also known as health-care–associated infections, encompass almost all clinically evident infections that do not originate from a patient's original admitting diagnosis. Within hours after admission, a patient's flora begins to acquire characteristics of the surrounding bacterial pool. Most infections that become clinically evident after 48 hours of hospitalization are considered hospital-acquired. Infections that occur after the patient's discharge from the hospital can be considered to have a nosocomial origin if the organisms were acquired during the hospital stay.

Pathophysiology

Within hours of admission, colonies of hospital strains of bacteria develop in the patient's skin, respiratory tract, and genitourinary tract. Risks factors for the invasion of colonizing pathogens can be categorized into 3 areas: iatrogenic, organizational, and patient-related.

• Iatrogenic risk factors include pathogens on the hands of medical personnel, invasive procedures (eg, intubation and extended ventilation, indwelling vascular lines, urine catheterization), and antibiotic use and prophylaxis.
• Organizational risk factors include contaminated air-conditioning systems, contaminated water systems, and staffing and physical layout of the facility (eg, nurse-to-patient ratio, open beds close together).
• Patient risk factors include the severity of illness, underlying immunocompromised state, and length of stay.

Frequency

United States

The National Nosocomial Infections Surveillance (NNIS) System of the Centers for Disease Control and Prevention (CDC) performed a survey from October 1986 to April 1998.¹ They ranked hospital wards according to their association with central-line bloodstream infections. The highest rates of infection occurred in the burn ICU, the neonatal ICU, and the pediatric ICU.

Nosocomial infections are estimated to occur in 5% of all acute-care hospitalizations; the incidence rate is 5 infections per 1,000 patient-days. Based on the 35 million patients admitted to 7,000 acute-care institutions in the United States, the incidence of HAIs is more than 2 million cases per year.² HAIs result in an additional 26,250 deaths (range 17,500-70,000) and an added expenditure in excess of $4.5 billion.

International

The impact of HAIs on the health care systems of developed countries is significant and is proportionate to that of the United States.

Mortality/Morbidity

Nosocomial infections are estimated to more than double the mortality and morbidity risks of any admitted patient and probably result in as many as 70,000 deaths per year in the United States. This is the equivalent of 350,000 years of life lost in the United States.

Sex

HAIs do not have a discernible sex predilection. However, in the neonatal period, low birth weight and male sex (male-to-female ratio is 1.7:1) are associated with an increased risk of HAIs.

Age

Among bacterial HAIs, bacteremias and surgical site infections were more common in infants younger than 2 months than in older children. However, urinary tract infections (UTIs) were reported more frequently in children older than 5 years than in younger children.

Clinical

History

• Nosocomial infections are caused by viral, bacterial, and fungal pathogens. These pathogens should be investigated in all febrile patients who are admitted for a nonfebrile illness.
• During their hospital stay, many patients acquire viral respiratory infections (eg, influenza, parainfluenza, respiratory syncytial viruses) in the winter, rotaviral infections in winter, and enteroviral infections in the summer. Viruses are the leading etiologies of nosocomial infections in pediatric patients (responsible for ≤14% of hospital-acquired infections [HAIs] with identifiable pathogens).
• Bacterial and fungal infections are less common. However, they are significantly associated with more morbidity and mortality. Most patients who are infected with nosocomial bacterial and fungal pathogens have a predisposition to infection caused by invasive supportive measures such as intubation and the placement of intravascular lines and urinary catheters. Fungal infections are more likely to arise from the patient's own flora; occasionally, they are caused by contaminated solutions (eg, those used in parenteral nutrition).

Physical

In addition to the presence of systemic signs and symptoms of infection (eg, fever, tachycardia, tachypnea, skin rash, general malaise), the source of HAIs may be suggested by the instrumentation used in various procedures. For example, an endotracheal tube may be associated with sinusitis, otitis, tracheitis and pneumonia; an intravascular catheter may be the source of phlebitis or line infection; and a Foley catheter may be associated with a candidal UTI.

Causes

• Among 6,290 pediatric ICU patients surveyed between 1992 and 1997, the incidence of nosocomial invasive bacterial and fungal infections were as follows:³
  • Bloodstream infections - 28%
  • Ventilator-associated pneumonia - 21%
  • Urinary tract infection (UTI) - 15%
  • Lower respiratory infection - 12%
  • Gastrointestinal, skin, soft tissue, and cardiovascular infections - 10%
  • Surgical-site infections - 7%
  • Ear, nose, and throat infections - 7%
• Nosocomial etiologies in bloodstream infections
  • Coagulase-negative staphylococci - 40%
  • Enterococci - 11.2%
  • Fungi - 9.65%
  • Staphylococcus aureus - 9.3%
  • Enterobacter species - 6.2%
  • Pseudomonads - 4.9%
  • Acinetobacter baumannii with substantial antimicrobial resistance - Reported with increasing frequency
• Nosocomial etiologies in UTI
  • Gram-negative enterics - 50%
  • Fungi - 25%
  • Enterococci - 10%
• Nosocomial etiologies in surgical-site infections
  • S aureus - 20%
  • Pseudomonads - 16%
  • Coagulase-negative staphylococci - 15%
  • Enterococci, fungi, Enterobacter species, and Escherichia coli - Less than 10% each
• Nosocomial etiologies in fever
  • Viral infections are most common causes of nosocomial fevers.
  • Phlebitis is the second most common cause of nosocomial fevers in the hospitalized child.
  • Clostridium difficile colitis is also a cause of nonsocomial fevers.

Differential Diagnoses

Other Problems to Be Considered

Rotavirus infection
Sepsis
Streptococcal infection, group D (enterococcus)

Workup

Laboratory Studies

A detailed physical examination and review of systems most likely reveal the involved organs or systems. Investigation should focus on these abnormal areas. Studies should center on infections in the bloodstream, UTI, and pneumonia, unless an obvious source (eg, surgical-site infection) is readily identified.

• Bloodstream infections
  • Obtaining quantitative blood cultures with samples from the intravenous line and peripheral vein is recommended to aid in differential diagnosis of line-associated bacteremia. Because of the small volume of blood that is vacuum aspirated into quantitative sample tubes, a regular blood culture is recommended, as this sample may grow the pathogen in cases involving low-inoculum bacteremia.
  • Fungal cultures should be obtained if fungal infection is suspected. The laboratory should incubate cultures longer for fungus detection than for other pathogens.
  • In immunocompromised patients, special studies are occasionally requested, such as cultures for nocardia and atypical mycobacteria, cytomegalovirus, and cytomegalovirus antigenemia detection.
• Pneumonia
  • Radiography, oxygenation, and hemodynamic status determination are required in the evaluation of nosocomial pneumonia.
  • Examination of the sputum, endotracheal aspiration material, and pleural effusion fluid with Gram staining and culturing may be useful.
  • Rapid diagnostic testing may be useful in specific cases. Examples include the direct fluorescent antibody test for Legionella organisms or for organisms that cause pertussis; immunofluorescence tests for influenza, respiratory syncytial virus, which is transmitted by contact, and Pneumocystis jiroveci; and modified acid-fast stains for mycobacteria. 
• Urinary tract infection
  • UTIs are expected in patients who require indwelling urinary catheters.
  • Efforts should be made to differentiate colonization, cystitis, and frank pyelonephritis using urinalysis, urine Gram staining, and culturing.
  • Early removal of the urinary catheter is always helpful in the treatment of catheter-associated UTI. 
• Colitis
  • A stool Gram stain should be performed to detect WBCs.
  • Tests for C difficile toxins are useful in the workup for nosocomial fevers and loose stool. (Rotavirus spreads among susceptible infants during local epidemics in cold months. In infants, colonization with C difficile often does not cause problems.)
• Other laboratory studies
  • Obtaining general viral cultures from the throat and rectum can be helpful in management.
  • Acute and convalescent titers against viral agents can also be helpful.
  • The antigen for Legionella pneumophila serotype 1 can be detected in the urine.
  • Several versions of the nucleic acid amplification test (NAAT) are available to test for specific pathogens in most clinical samples. NAATs have been developed for a wide variety of infectious pathogens and permit rapid diagnoses. 

Imaging Studies

• Special imaging techniques (eg, ultrasonography, CT scanning, MRI) may be helpful in evaluating obscure-site infections.

Treatment

Medical Care

Symptomatic treatment of shock, hypoventilation, and other complications should be provided, along with the administration of empiric broad-spectrum antimicrobials, antifungals, and antivirals.

Infections caused by methicillin-resistant Staphylococcus aureus (MRSA) are not worse than those caused by susceptible S aureus. MRSA requires treatment with different families of antibiotics. Although the pathogenicity does not generally differ from that of susceptible strains of S aureus, MRSA strains that carry the loci for Panton-Valentine leukocidin can be hypervirulent and can cause lymphopenia, rapid tissue necrosis, and severe sepsis.

• Bloodstream infections
• Line removal should be considered if the line is suspected in the cause of sepsis.
• Broad-spectrum antibiotics should be selected according to the local epidemiologic patterns of microbial susceptibility.
• Antifungals (eg, fluconazole, caspofungin, voriconazole, amphotericin B) are added to empiric antibiotics in some cases.
• Antivirals (eg, ganciclovir, acyclovir) could be used in the treatment of suspected disseminated viral infections.
• Pneumonia
• Change nasotracheal tubes to orotracheal tubes, if feasible.
• Broad-spectrum antibiotics are administered with guidance from the results of rapid examination of the sputum, endotracheal suction material, and bronchial lavage wash.
• Macrolide antibiotics are indicated in legionellosis.
• Antivirals (neuraminidase inhibitors for both influenza A and influenza B) are used if viral pneumonia is suspected. Since the 2005-2006 influenza season, the CDC has not recommended amantadine and rimantadine because of resistance. Laboratory testing by the CDC on the predominant strain of influenza (H3N2) currently circulating in the United States shows that it is resistant to these drug.
• Indications for the use of neuraminidase inhibitors in children have been defined for oseltamivir phosphate (approved for treatment and prophylaxis in children >1 y) and zanamivir (approved for treatment in children ≥7 y and for prophylaxis in children ≥5 y).
• Anti-influenza therapy has been used to treat symptomatic patients and patients with immunodeficiency or chronic lung diseases to limit morbidity and mortality.
• Oseltamivir (Tamiflu) resistance has emerged in the United States during the 2008-2009 influenza season.
• The CDC has issued revised interim recommendations for antiviral treatment and prophylaxis of influenza. Preliminary data from a limited number of states indicate a high prevalence of influenza A (H1N1) virus strains resistant to oseltamivir (Tamiflu). Because of this, zanamivir (Relenza) is recommended as the initial choice for antiviral prophylaxis or treatment when influenza A infection or exposure is suspected. A second-line alternative is a combination of oseltamivir plus rimantadine, rather than oseltamivir alone. Local influenza surveillance data and laboratory testing can assist the physician regarding antiviral agent choice.
• Influenza A viruses, including 2 subtypes (H1N1 and H3N2), and influenza B viruses currently circulate worldwide; the prevalence of each can vary among communities and within a single community over the course of an influenza season. In the United States, 4 prescription antiviral medications (oseltamivir, zanamivir, amantadine, rimantadine) are approved for treatment and chemoprophylaxis of influenza. Since January 2006, the neuraminidase inhibitors (oseltamivir, zanamivir) have been the only recommended influenza antiviral drugs because of widespread resistance to the adamantanes (amantadine, rimantadine) among influenza A (H3N2) virus strains. The neuraminidase inhibitors have activity against influenza A and B viruses, whereas the adamantanes have activity against only influenza A viruses.
• In 2007-2008, a significant increase in the prevalence of oseltamivir resistance was reported among influenza A (H1N1) viruses worldwide. During the 2007-2008 influenza season, 10.9% of H1N1 viruses tested in the United States were resistant to oseltamivir. Complete recommendations are available from the CDC.
• Overall, the most cost-effective prevention measure is seasonal vaccination against influenza A and B. The 2007-2008 vaccine strains consist of A/Solomon Island/3/2006 (H1N1)–like, A/Wisconsin/67/2005 (H3N2)–like, and B/Malaysia/2506/2004–like antigens.
• Urinary tract infection
• Indwelling catheters should be removed, if feasible.
• Empiric antibiotic and antifungal therapy is based on the preliminary results of urinalysis and urine Gram staining.
• Surgical-site infections: These should be managed with a combination of surgical care and aggressive antibiotic therapy guided by the results of deep-tissue Gram staining and culturing. Fasciitis is of special concern because it is associated with mucoid group A streptococci and high morbidity and mortality rates.
• C difficile colitis: Management of C difficile colitis includes the discontinuation of the offending antibiotics and the use of oral metronidazole or vancomycin. Macrobiotics may be beneficial.

Surgical Care

• Surgical debridement is an integral part of management of surgical-site infections or superinfected decubitus ulcers. Tissue sample should be processed using appropriate stains and cultures to identify the pathogen and its susceptibility.

Consultations

• Many patients with nosocomial infections require expert care from an ICU team.
• Infectious disease specialists, burn care specialists, and surgical teams are usually involved in the care of these complicated cases.

Medication

Pharmacologic treatment depends on the underlying etiology.

Follow-up

Patient Education

• For excellent patient education resources, visit eMedicine's Yeast and Fungal Infections Center. Also, see eMedicine's patient education article Candidiasis (Yeast Infection).

Miscellaneous

Medicolegal Pitfalls

• Outbreaks of nosocomial invasive infections may become the subject of adverse publicity and legal suits against institutions and medical personnel.
• Many states have adopted educational courses that emphasize infection control, as well as strict enforcement and reporting of violation of hand-washing codes. Many hospitals have reorganized the physical layout of hand-washing stations and have adopted patient cohorting to prevent the spreading of pathogens. They have also restricted or rotated the administration of many antibiotics that are used to combat nosocomial infections.

Special Concerns

• Bacterial agents: Multiple-resistant organisms, such as vancomycin-resistant enterococci, glycopeptide-resistant S aureus, and inducible or extended-spectrum beta-lactamase gram-negative organisms, are a constant threat.
• Viral agents: The rapid spread of respiratory syncytial virus among pediatric patients during an epidemic poses a threat to susceptible children who require hospitalization during winter months.

References

1. National Nosocomial Infections Surveillance (NNIS) System. National Nosocomial Infections Surveillance (NNIS) System report, data summary from October 1986-April 1998, issued June 1998. Am J Infect Control. Oct 1998;26(5):522-33. [Medline].

2. Wenzel R, Edmond MD. The impact of Hospital Acquired Blood Stream Infections. Emerg Inf Dis. Mar-Apr 2001;7(174).

3. Richards MJ, Edwards JR, Culver DH, Gaynes RP. Nosocomial infections in pediatric intensive care units in the United States. National Nosocomial Infections Surveillance System. Pediatrics. Apr 1999;103(4):e39. [Medline].

4. Dancer SJ. Mopping up hospital infection. J Hosp Infect. Oct 1999;43(2):85-100. [Medline].

5. Davey P, Brown E, Fenelon L, et al. Interventions to improve antibiotic prescribing practices for hospital inpatients. In: Cochrane Database of Systematic Reviews. John Wiley & Sons, Ltd; 2005.

6. Deville JG, Adler S, Azimi PH, et al. Linezolid versus vancomycin in the treatment of known or suspected resistant gram-positive infections in neonates. Pediatr Infect Dis J. Sep 2003;22(9 Suppl):S158-63. [Medline].

7. Garner JS. Guideline for isolation precautions in hospitals. The Hospital Infection Control Practices Advisory Committee [published erratum appears in Infect Control Hosp Epidemiol 1996 Apr;17(4):214]. Infect Control Hosp Epidemiol. Jan 1996;17(1):53-80. [Medline].

8. McKibben L, Horan T, Tokars JI, et al. Guidance on public reporting of healthcare-associated infections: recommendations of the Healthcare Infection Control Practices Advisory Committee. Am J Infect Control. May 2005;33(4):217-26. [Medline].

9. Moellering RC Jr. Vancomycin-resistant enterococci. Clin Infect Dis. May 1998;26(5):1196-9. [Medline].

10. Rice LB, Shlaes DM. Vancomycin resistance in the enterococcus. Relevance in pediatrics. Pediatr Clin North Am. Jun 1995;42(3):601-18. [Medline].

11. Scott PT, Petersen K, Fishbain J. Acinetobacter baumannii Infections Among Patients at Military Medical Facilities Treating Injured US Service Members, 2002-2004. MMWR. 2004;53:1063-1066.

12. Siegel JD, Rhinehart E, Jackson M, Chiarello L. Management of Multidrug-Resistant Organisms in Health Care Settings, 2006. Atlanta, GA: Healthcare Infection Control Practices Advisory Committee; 2006. 1-74.

13. Standfast SJ, Michelsen PB, Baltch AL. A prevalence survey of infections in a combined acute and long-term care hospital. Infect Control. Apr 1984;5(4):177-84. [Medline].

14. Steed CJ. Common infections acquired in the hospital: the nurse's role in prevention. Nurs Clin North Am. Jun 1999;34(2):443-61. [Medline].

15. Tablan OC, Anderson LJ, Besser R, Bridges C, Hajjeh R. MMWR Recommendations and Reports: Guidelines for Preventing Health Care-Associated Pneumonia. Atlanta, GA: CDC; March 26, 2004. 1-36.

16. Weinstein JW, Mazon D, Pantelick E. A decade of prevalence surveys in a tertiary-care center: trends in nosocomial infection rates, device utilization, and patient acuity. Infect Control Hosp Epidemiol. Aug 1999;20(8):543-8. [Medline].

17. Witte W, Braulke C, Cuny C, et al. Emergence of methicillin-resistant Staphylococcus aureus with Panton-Valentine leukocidin genes in central Europe. Eur J Clin Microbiol Infect Dis. Jan 2005;24(1):1-5. [Medline].

Keywords

hospital-acquired infections, health care–acquired infections, nosocomial infection, vancomycin-resistant enterococcus, VRE, methicillin-resistant Staphylococcus aureus, MRSA, Pseudomonas, candidiasis, Legionella, respiratory syncytial virus, thrush, Clostridium difficile, viral respiratory infections, influenza, parainfluenza, sinusitis, otitis, tracheitis, phlebitis, line infection, bloodstream infection, ventilator-associated pneumonia, urinary tract infection, UTI, surgical-site infection, coagulase-negative staphylococci, enterococci, fungi, , pseudomonads,

Contributor Information and Disclosures

Author

Quoc V Nguyen, MD, Assistant Professor, Department of Pediatrics, New York State Health Department
Disclosure: Nothing to disclose.

Medical Editor

David Jaimovich, MD, Chief Medical Officer, Joint Commission International and Joint Commission Resources
David Jaimovich, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
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Managing Editor

Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University
Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

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