Article Update

Sunday, October 4, 2020




Health care–associated pneumonia (HCAP) refers to pneumonia in patients who have had contact with the health care environment before developing pneumonia and thus may be at risk of being colonized and infected with potentially drug-resistant pathogens. This group includes patients who have been in the hospital for at least 2 days in the past 90 days, those coming from a nursing home or extended care facility, those getting hemodialysis or home wound care, and those exposed to a family member harboring drug-resistant pathogens. Because many of these patients are at risk for infection with multidrug-resistant (MDR) gram- negative and gram-positive organisms, these patients do not have CAP, but are now defined as having HCAP. Clinical risk factors for MDR pathogens include severe pneumonia, poor functional status, recent antibiotic therapy (within the past 3 months), recent hospitalization, and immune suppression (including corticosteroid therapy).

It is important to recognize patients with HCAP because some may have a more complex spectrum of etiologic agents than those with community-acquired pneumonia (CAP), including a higher mortality rate, longer length of stay, higher frequency of aspiration, and more frequent receipt of incorrect empiric antibiotic therapy. In this regard, patients with HCAP are similar to those with hospital-acquired pneumonia (HAP).



In critically ill patients, pneumonia is the second most common intensive care unit (ICU)–acquired infection and the one that is most likely to lead to mortality. By definition, HAP occurs after the patient has been in the hospital for at least 48 hours and can occur in patients who are intubated and mechanically ventilated or in those who are not. If the patient has been intubated for at least 48 hours and then develops pneumonia, it is termed ventilator-associated pneumonia (VAP).

HAP occurs with increased frequency in any patient population with impaired immune function (either as a result of serious underlying illness or because of therapy-associated immune dysfunction) and increased exposure of the lower respiratory tract to bacteria (via aspiration with or without an endotracheal tube in place). VAP is present in 20% to 50% of mechanically ventilated patients, depending on the diagnostic criteria that are used and the risk factors in the patient population being considered. The risk of pneumonia increases with the duration of mechanical ventilation. Up to 40% of VAP is early onset (in the first 5 days of hospitalization).

In addition to mechanical ventilation, other risk factors for nosocomial pneumonia include age older than 60 years, malnutrition (serum albumin <2.2 g/dL), acute lung injury (acute respiratory distress syndrome), coma, burns, recent abdominal or thoracic surgery, multiple organ failure, transfusion of more than 4 U of blood, transport from the ICU, prior antibiotic therapy, elevation of gastric pH (by antacids or histamine-type 2 blocking agents), large volume aspiration, use of a nasogastric tube (rather than a tube placed in the jejunum or a tube inserted through the mouth), use of inadequate endotracheal tube cuff pressure (allowing aspiration of oral secretions into the lower respiratory tract), prolonged sedation and paralysis, maintaining patients in the supine position in bed, use of total parenteral nutrition feeding rather than enteral feeding, and repeated reintubation.

The mortality rate for patients with HAP can be as high as 50% to 70% in mechanically ventilated patients. In addition, the odds ratio for mortality in patients who acquire VAP compared with those who do not is nearly twofold, and the presence of VAP can prolong length of stay by at least 6 to 7 days. The greatest contributors to attributable mortality of VAP are use of an inappropriate antibiotic therapy (one that is not active against the identified etiologic pathogens), the presence of certain high-risk drug-resistant organisms (e.g., Pseudomonas aeruginosa, Acinetobacter spp., or Staphylococcus aureus), and the development of illness in a medical (rather than surgical) patient. Other mortality risk factors for HAP include coma on admission, creatinine level above 1.5 mg/dL, transfer from another ward to the ICU, bilateral radiographic abnormalities, age older than 60 years, an ultimately fatal underlying condition, shock, prior antibiotic therapy, pneumonia being a superinfection, multiple system organ failure, and an increasing APACHE (Acute Physiology and Chronic Health Evaluation) score during pneumonia therapy.



A variety of classification schemes for HAP are available that divide patients into categories based on the likelihood of specific pathogens. If the patient has earlyonset infection (within the first 5 days of hospitalization) and no risk factors for MDR pathogens (recent hospitalization, recent antibiotic therapy, the presence of HCAP), then the patient is likely to be infected with a group of “core pathogens.” These include nonresistant gram-negative organisms (Escherichia coli, Klebsiella spp., Enterobacter spp., Serratia marcescens, and Proteus spp.), methicillin-sensitive S. aureus, and pneumococcus. On the other hand, if the patient has late-onset infection (day 5 or later) or any of the risk factors for MDR pathogens, then in addition to the core pathogens, the patient is also at risk for infection with MDR gram–negative organisms such as P. aeruginosa, Acinetobacter spp., and extended-spectrum beta-lactamase (ESBL) producers such as Klebsiella and Enterobacter spp. or MDR gram-positive organisms such as methicillin-resistant S. aureus (MRSA).

The diagnosis of HAP, particularly VAP, is controversial because the clinical diagnostic criteria are sensitive but not specific for infection. These include the finding of a new or progressive lung infiltrate plus at least two of the following: temperature below 36.0˚C or above 38.3˚C, leukocyte count above 10,000/mm3 or below 5000/mm3, and purulent sputum. Another common clinical finding in patients with pneumonia is worsening oxygenation. All of these findings are not specific for pneumonia, so they are supplemented by microbiologic testing to define both the presence of pneumonia and the etiologic pathogen. Although some studies have suggested that clinical management can be improved if therapy decisions are guided by quantitative culture data, not all studies have confirmed this finding, and quantitative cultures are not routinely used to establish the diagnosis of HAP and VAP.

Therapy is initially empiric based on the likely etiologic pathogens and is generally done with a single agent if only the core pathogens are expected, although a broad-spectrum multidrug regimen is used if MDR pathogens are likely. After culture data become available, therapy is focused on the organism(s) identified.



When a patient develops HAP or VAP, there is a high likelihood that the etiologic agent will be antibiotic resistant. In fact, in patients with VAP the frequency may exceed 50% if the patient has been in the hospital for at least 7 days and has a history of prior antibiotic use. Drug-resistant organisms are not intrinsically more virulent than sensitive pathogens, but because their presence is often not anticipated, the initial therapy may be incorrect, and this factor contributes to the excess mortality associated with these organisms when they cause VAP.



Patients with VAP are most commonly infected by gram-negative organisms, including P. aeruginosa, Acinetobacter baumannii. K. pneumoniae, and extended-spectrum-lactamase (ESBL)–producing Enterobacteriaceae. All of these organisms can be antibiotic resistant, making therapy difficult. P. aeruginosa is the most common of these organisms causing VAP, but A. baumannii is occurring with increasing frequency, and many hospitals have epidemics of ESBL-producing Enterobacteriaceae and carbapenemase-producing K. pneumoniae, making the challenges presented by these bacteria quite daunting.

P. aeruginosa is an especially virulent organism because of its production of destructive exoenzymes and its resistance to a wide range of antibiotics. Patients often have upper respiratory tract (oropharynx) colonization before colonization and infection of the lung, but primary lower respiratory tract colonization can also occur. In the ICU, nosocomial pneumonia is the biggest concern, but this organism can also lead to ventilator-associated tracheobronchitis, an infection in the airway that may later progress to pneumonia. The organism is also involved in chronic airways infections such as bronchiectasis, with or without associated cystic fibrosis. P. aeruginosa is such a prevalent nosocomial pathogen because it can grow in virtually any environment, and it produces a wide range of virulence factors that allow it to infect nearly any body site. In addition, the organism can form a biofilm on an endotracheal tube and persist despite antibiotics and host defense mechanisms. When a critical number of bacteria are present, they can coordinate their growth in a biofilm and overcome host defenses through quorum sensing, which is promoted by the release of signaling substances.




This organism has been discussed above as a cause of CAP. The strain of MRSA causing nosocomial pneumonia is different, is more antibiotic-resistant than the community-acquired strain, and is more prone to causing lung infection. Unlike community-acquired MRSA, it is not a clonal disease, and bacterial virulence factors are not as widely present. Important clinical risk factors for MRSA as a nosocomial pneumonia pathogen are acute neurologic illness, hemodialysis, heart disease, and solid organ transplantation. Most pneumonias are not accompanied by bacteremia, but when they are, endocarditis should be assumed to be present, and patients may develop metastatic infection in the brain, bones, and solid organs, and prolonged therapy (4-6 weeks) is needed.

Share with your friends

Give us your opinion

Note: Only a member of this blog may post a comment.

This is just an example, you can fill it later with your own note.