Updated: Jun 27, 2008
Nursing home–acquired pneumonia (NHAP) is defined as pneumonia occurring in a resident of a chronic care facility or nursing home. NHAP is one of the most common infectious diseases in chronic care facilities and is a significant cause of mortality and morbidity among residents of such facilities. NHAP more closely resembles community-acquired pneumonia (CAP) than nosocomial pneumonia (NP).
NP occurs when the pathogen is distributed in a hospital setting, resulting in a subsequent infection. Aerobic gram-negative bacilli, including Pseudomonas aeruginosa, cause NPs. Staphylococcus aureus (eg, methicillin-susceptible S aureus [MSSA] and methicillin-resistant S aureus [MRSA]) infection is not a significant cause of CAP, NP, or NHAP. The presence of P aeruginosa and other aerobic gram-negative bacilli defines the NP group. Because NHAP is caused by CAP-associated pathogens and not NP-associated pathogens, NHAP is considered diagnostically and therapeutically synonymous to CAP. Patients with NHAP have the same length of hospital stay as patients with CAP. Physicians, therefore, approach the treatment strategy for NHAP and CAP in a similar way and with similar empiric antibiotic coverage.
Table 1. Comparison of Characteristics of Nursing Home–Acquired Pneumonia, Community-Acquired Pneumonia, and Nosocomial Pneumonia
Type of Pneumonia | Most Common Pathogens | Uncommon Pathogens | Appearance on Chest Radiograph | Length of Stay (Days) |
NHAP | Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis | Legionella Chlamydia pneumoniae 1 | Focal sequential/lobar ± consolidation ± pleural effusion No cavitation | 7-10 |
CAP | S pneumoniae H influenzae M catarrhalis | Legionella Mycoplasma | Focal sequential/lobar ± consolidation ± pleural effusion No cavitation | 7-10 |
NP | P aeruginosa Klebsiella Escherichia coli | Serratia | Necrotizing pneumonia and cavitation with P aeruginosa and Klebsiella Bilateral infiltrates without cavitation or pleural effusion | 10-21 |
The pathophysiology of NHAP is the same as the pathophysiology of CAP. NHAP may result when a patient aspirates oropharyngeal contents into one or more lung segments or lobes. NHAP may also occur if a distant focus of infection hematogenously disseminates to the lungs.
Aspiration pneumonia, whether community-acquired or acquired in a nursing home, results microbiologically from aspirated anaerobic oropharyngeal flora. Hundreds of species of oropharyngeal anaerobes may be cultured from patients with aspiration pneumonia. However, oropharyngeal anaerobes are not like Bacteroides fragilis, which is the primary anaerobe below the diaphragm and is sensitive to nearly all antibiotics. Patients with CAP or NHAP do not require specific anti– B fragilis coverage. In aspiration pneumonia, the location of the lung lesion is related to the position of the patient at the time of aspiration. Because most patients are supine when they aspirate, most lung infiltrates observed on chest radiographs and most aspiration pneumonia occur in segments of the right lung.
If aspiration occurs when patients are lying on their right side, the pulmonary infiltrates most likely involve the right upper lobe. If patients are lying on their left side, the most likely location of the infiltrates is the left upper lobe. If patients are supine and the aspiration is massive, bilateral infiltrates involving multiple lung segments or lobes are possible and may produce a radiologic appearance indistinguishable from left ventricular failure or acute respiratory distress syndrome.
Table 2. Radiographic Patterns in Aspiration Pneumonia
Patient Position at Aspiration | Chest Radiograph Lobar Involvement |
Supine | Right lower lobe (ie, superior or posterior segment) or bilateral infiltrates (ie, all lobes) |
Right side down | Right upper lobe (ie, axillary segment) |
Left side down | Left upper lobe (ie, axillary segment) |
Prone | Right middle lobe (ie, lingula) |
Sitting upright | Right lower lobe (ie, basilar segments) |
Hematogenously acquired pneumonia is not common among patients with CAP or NHAP. Hematogenously acquired pneumonia presents with bilateral symmetrical perihilar infiltrates, as opposed to the localized segmental or lobar distribution characteristic of pneumonia acquired via primary inhalation.
The degree of impaired lung function resulting from NHAP depends on the extent of aspiration and the patient's preexisting physiologic and anatomic lung function. The histologic changes in lung parenchyma resulting from NHAP are the same as those observed resulting from CAP (ie, no cavitation, necrosis, or blood vessel invasion). As with CAP, resolving NHAP restores the lung function that existed prior to acquiring pneumonia.
NHAP is one of the most common causes of infection in chronic care facilities and is one the most significant infection-related causes of mortality and morbidity in such facilities.
NHAP is a common cause of infection in chronic care facilities.
Pleural Effusion
Pulmonary Embolism
Most patients from chronic care facilities who are transferred to acute care hospitals do not have nursing home–acquired pneumonia (NHAP). The most common causes of diagnostic confusion in patients with NHAP are noninfectious cardiac and pulmonary disorders.
CHF is the most common disorder that resembles NHAP in the chronic care facility setting. CHF may represent an exacerbation of preexisting CHF, resulting in increasing shortness of breath for the patient, which mimics the presentation of NHAP.
The clinical presentation of patients in nursing homes who develop asymptomatic acute myocardial infarctions may also mimic the clinical presentation of patients with NHAP. Myocardial infarction may be associated with fever, shortness of breath, and chest pain; all are signs that mimic NHAP.
Many elderly patients are unable to raise sputum, making the absence of a productive cough an inadequate determination to differentiate NHAP and CHF.
Preexisting lung disease, pulmonary emboli, and bronchogenic malignancies mimic NHAP. Collagen vascular diseases affecting the lungs, pulmonary drug reactions, and pulmonary hemorrhage may also mimic NHAP.
Chest radiography is the best study for diagnosing NHAP. Patients with NHAP have a segmental or lobar distribution of infiltrates, as seen on chest radiographs. Patients with CHF have a redistribution of vasculature to the upper lobes, usually accompanied by cardiomegaly. Verify cardiomegaly by physical examination. If CHF is present, it usually is accompanied by an S3 gallop rhythm.
Preexisting chest radiographs may reveal previous interstitial lung disease that may mimic the appearance of NHAP. Chest radiography is the primary tool for ruling out the mimics of pneumonia and any new or preexisting lung disorders.
Fever that is equal to or greater than 102°F and accompanied by pulmonary symptoms suggests NHAP, especially when accompanied by a productive cough. However, in elderly patients who are the usual residents of chronic care facilities, the febrile response may be blunted. Therefore, the absence of fever or the presence of a low-grade fever is unhelpful in differentiating NHAP from its mimics.
Pleural effusions occasionally cause diagnostic confusion in the diagnosis of pneumonia. Bacterial pneumonias, particularly infections with S pneumoniae and H influenzae, may be accompanied by pleural effusion. However, pleural effusions without associated infiltrates are not pneumonia. Bilateral pleural effusion rarely, if ever, results from an infectious etiology. The presence of bilateral pleural effusions with unilateral or bilateral pulmonary infiltrates suggests a noninfectious etiology, and the workup should be designed accordingly.Findings include local polymorphonuclear neutrophil infiltration of infected lung areas without cavitation, necrosis, or blood vessel invasion.
If the physician suspects nursing home–acquired pneumonia (NHAP) and the mimics of pneumonia can be ruled out, early appropriate empiric therapy is the critical component of medical management. Promptly instituting empiric antimicrobial therapy significantly decreases the likelihood of mortality and morbidity associated with NHAP and community-acquired pneumonia (CAP). Direct antimicrobial coverage against the most likely pathogens (ie, S pneumoniae, H influenzae, M catarrhalis, C pneumoniae).
The goals of pharmacotherapy are to reduce morbidity, to eradicate the infection, and to prevent complications.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the clinical setting.
Second-generation quinolone. Acts by interfering with DNA gyrase in bacterial cells. For pseudomonal infections and infections resulting from multi-drug–resistant gram-negative organisms. Highly active against gram-negative and gram-positive organisms, including highly penicillin-resistant S pneumoniae.
500 mg PO/IV qd for 7-14 d
<18 years: Not recommended
>18 years: Administer as in adults
Administer antacids 1-2 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins.
1 g IV q24h
Neonates >7 days: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants and children: 100 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d
Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Gallbladder sludge (eg, pseudobiliary lithiasis) may require cholecystectomy; associated with non-C difficile diarrhea; adjust dose in renal impairment; caution in breastfeeding women and allergy to penicillin
Second-generation long-acting tetracycline. More active than tetracycline against many pathogens, especially S pneumoniae and Legionella. Different adverse effect profile and pharmacokinetics compared to tetracycline. Inhibits protein synthesis, thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
100-200 mg PO/IV q12h
<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO/IV in 1-2 divided doses; not to exceed 200 mg/d
Bioavailability decreases minimally with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Unsafe in pregnancy
Rarely, if ever, causes photosensitivity, but may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Fourth-generation cephalosporin with good gram-negative coverage. Similar to third-generation cephalosporins but has better gram-positive coverage.
2 g IV q12h
50 mg/kg IV q8h; not to exceed 2 g
Probenecid at high dose decreases cefepime clearance; aminoglycosides increase nephrotoxic potential of cefepime
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
Adjust dose in severe renal insufficiency; prolonged use of cefepime may predispose patients to superinfection
Troy CJ, Peeling RW, Ellis AG, et al. Chlamydia pneumoniae as a new source of infectious outbreaks in nursing homes. JAMA. Apr 16 1997;277(15):1214-8. [Medline].
Beck-Sague C, Villarino E, Giuliano D, et al. Infectious diseases and death among nursing home residents: results of surveillance in 13 nursing homes. Infect Control Hosp Epidemiol. Jul 1994;15(7):494-6. [Medline].
Bobba RK, Bollu M, Arsura EL. Antibiotic use in nursing home-acquired pneumonia. J Am Geriatr Soc. Nov 2007;55(11):1893-4; author reply 1894-5. [Medline].
Bonoan JT, Cunha BA. S. aureus as a cause of community-acquired pneumonia in patients with diabetes mellitus. Infectious Disease Practice. 1999;8:319-321.
Buehrens PE. Effectiveness of oral antibiotic treatment in nursing-home acquired pneumonia. J Am Geriatr Soc. Dec 1995;43(12):1443; author reply 1443-4. [Medline].
Chan Carusone SB, Walter SD, Brazil K, et al. Pneumonia and lower respiratory infections in nursing home residents: predictors of hospitalization and mortality. J Am Geriatr Soc. Mar 2007;55(3):414-9. [Medline].
Crossley KB, Thurn JR. Nursing home-acquired pneumonia. Semin Respir Infect. Mar 1989;4(1):64-72. [Medline].
Cunha BA. Antibiotic Essentials. 7th ed. Royal Oak, Mich: Physicians Press; 2008.
Cunha BA. Penicillin resistant streptococcal pneumoniae nursing home acquired pneumonia. Emerg Med. 2001;33:25-7.
Cunha BA. Cunha BA (ed). Pneumonia Essentials. 2nd ed. Royal Oak, MI: Physicians Press; 2008.
Cunha BA. Pneumonia in the elderly. Drugs Today (Barc). Nov 2000;36(11):785-91. [Medline].
Degelau J, Guay D, Straub K, et al. Effectiveness of oral antibiotic treatment in nursing home-acquired pneumonia. J Am Geriatr Soc. Mar 1995;43(3):245-51. [Medline].
El Solh AA, Pietrantoni C, Bhat A, et al. Indicators of potentially drug-resistant bacteria in severe nursing home-acquired pneumonia. Clin Infect Dis. Aug 15 2004;39(4):474-80. [Medline].
Fried TR, Gillick MR, Lipsitz LA. Whether to transfer? Factors associated with hospitalization and outcome of elderly long-term care patients with pneumonia. J Gen Intern Med. May 1995;10(5):246-50. [Medline].
Garb JL, Brown RB, Garb JR, et al. Differences in etiology of pneumonias in nursing home and community patients. JAMA. Nov 10 1978;240(20):2169-72. [Medline].
Levinson ME. Pneumonias. In: Isselbacher KJ, Braunwald E, Wilson JD, eds. Harrison's Principles of Internal Medicine. 3rd ed. 1998:1437-39.
Loeb M. Epidemiology of community- and nursing home-acquired pneumonia in older adults. Expert Rev Anti Infect Ther. Apr 2005;3(2):263-70. [Medline].
Marrie TJ. Pneumonia in the elderly. Curr Opin Pulm Med. May 1996;2(3):192-7. [Medline].
Marrie TJ, Blanchard W. A comparison of nursing home-acquired pneumonia patients with patients with community-acquired pneumonia and nursing home patients without pneumonia. J Am Geriatr Soc. Jan 1997;45(1):50-5. [Medline].
Marrie TJ, Slayter KL. Nursing home-acquired pneumonia. Treatment options. Drugs Aging. May 1996;8(5):338-48. [Medline].
McCue JD. Pneumonia in the elderly. Special considerations in a special population. Postgrad Med. Oct 1993;94(5):39-40, 43-6, 51. [Medline].
Medina-Walpole AM, Katz PR. Nursing home-acquired pneumonia. J Am Geriatr Soc. Aug 1999;47(8):1005-15. [Medline].
Meehan TP, Chua-Reyes JM, Tate J, et al. Process of care performance, patient characteristics, and outcomes in elderly patients hospitalized with community-acquired or nursing home-acquired pneumonia. Chest. May 2000;117(5):1378-85. [Medline].
Mehr DR, Zweig SC, Kruse RL, et al. Mortality from lower respiratory infection in nursing home residents. A pilot prospective community-based study. J Fam Pract. Oct 1998;47(4):298-304. [Medline].
Minnaganti VR, Patel PJ, Cunha BA. Nursing home-acquired pneumonia: Community-acquired or nosocomial?. Infectious Disease Practice. 2000;24:20-23.
Muder RR. Management of nursing home-acquired pneumonia: unresolved issues and priorities for future investigation. J Am Geriatr Soc. Jan 2000;48(1):95-6. [Medline].
Muder RR. Pneumonia in residents of long-term care facilities: epidemiology, etiology, management, and prevention. Am J Med. Oct 1998;105(4):319-30. [Medline].
Mylotte JM, Goodnough S, Gould M. Pneumonia versus aspiration pneumonitis in nursing home residents: prospective application of a clinical algorithm. J Am Geriatr Soc. May 2005;53(5):755-61. [Medline].
Mylotte JM, Naughton B, Saludades C, et al. Validation and application of the pneumonia prognosis index to nursing home residents with pneumonia. J Am Geriatr Soc. Dec 1998;46(12):1538-44. [Medline].
[Best Evidence] Paladino JA, Eubanks DA, Adelman MH, et al. Once-daily cefepime versus ceftriaxone for nursing home-acquired pneumonia. J Am Geriatr Soc. May 2007;55(5):651-7. [Medline].
Phillips SL, Branaman-Phillips J. The use of intramuscular cefoperazone versus intramuscular ceftriaxone in patients with nursing home-acquired pneumonia. J Am Geriatr Soc. Oct 1993;41(10):1071-4. [Medline].
Quagliarello V, Ginter S, Han L, et al. Modifiable risk factors for nursing home-acquired pneumonia. Clin Infect Dis. Jan 1 2005;40(1):1-6. [Medline].
Ramirez JA. Switch therapy in community-acquired pneumonia. Diagn Microbiol Infect Dis. May-Jun 1995;22(1-2):219-23. [Medline].
Ruiz-Gonzalez A, Falguera M, Nogues A, et al. Is Streptococcus pneumoniae the leading cause of pneumonia of unknown etiology? A microbiologic study of lung aspirates in consecutive patients with community-acquired pneumonia. Am J Med. Apr 1999;106(4):385-90. [Medline].
Thompson RS, Hall NK, Szpiech M. Hospitalization and mortality rates for nursing home-acquired pneumonia. J Fam Pract. Apr 1999;48(4):291-3. [Medline].
Verghese A, Berk SL. Bacterial pneumonia in the elderly. Medicine (Baltimore). Sep 1983;62(5):271-85. [Medline].
Volicer L, Hurley AC. Risk factors for pneumonia in nursing home residents. J Am Geriatr Soc. Dec 1995;43(12):1443-4. [Medline].
Zimmer JG, Hall WJ. Nursing home-acquired pneumonia: avoiding the hospital. J Am Geriatr Soc. Mar 1997;45(3):380-1. [Medline].
nursing home–acquired pneumonia, NHAP, pneumonia in chronic care facilities, Streptococcus pneumoniae, S pneumoniae, Haemophilus influenzae, H influenzae, Moraxella catarrhalis, M catarrhalis, Legionella, Chlamydia pneumoniae, C pneumoniae, aspiration pneumonia, chronic bronchitis, CNS disease, esophageal disease, decreased gag reflex, community-acquired pneumonia, CAP, nosocomial pneumonia, NP
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Wesley W Emmons, MD, FACP, Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE
Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
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Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.