eMedicine Specialties > Pulmonology > Infectious Lung Diseases

Pneumonia, Bacterial

Author: Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital
Contributor Information and Disclosures

Updated: Feb 12, 2007

Introduction

Background

Medical practitioners have known of pneumonia since ancient times. Hippocrates indoctrinated his students about "peripneumonia," which, for the ancient healers, had a connotation of an acute illness either with pain in the side or with severe dyspnea. The term acquired a more punctilious meaning as the study of morbid anatomy and physical diagnosis progressed over the last few centuries. Morgagni contributed the concept of solidification of the lung. Laennec, the father of pulmonary medicine, described pathological stages of the disease and showed how to diagnose them using auscultation.

Rokitansky's graphic narration helped distinguish lobar from lobular or bronchial pneumonia. Pasteur discovered Streptococcus pneumoniae in 1880, and before long, this organism was proved to be a cause of lobar pneumonia. The contemporary physicians of the 19th century were well aware of lobar pneumonia. Coope described lobar pneumonia as that "which consists of a series of changes by which the spongy pulmonary tissue is rapidly converted into a solid mass, returning afterwards, in cases that recover, to its normal condition." The modern physician, who is more adept with the x-ray viewing box than the autopsy room, has acquired sufficient familiarity with this common malady as knowledge and wisdom has been acquired over the centuries.

Pneumonia is defined as inflammation and consolidation of the lung tissue due to an infectious agent. Pneumonia that develops outside the hospital setting is considered community-acquired pneumonia. Pneumonia developing 72 hours or more after admission to the hospital is termed nosocomial or hospital-acquired pneumonia. Community-acquired pneumonia is caused most commonly by bacteria that traditionally have been divided into 2 groups, typical and atypical. Typical organisms include S pneumoniae (pneumococcus) and Haemophilus and Staphylococcus species. Atypical refers to pneumonia caused by Legionella, Mycoplasma, and Chlamydia species.

The most common atypical pneumonias are caused by 3 zoonotic pathogens, Chlamydia psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever), and 3 nonzoonotic pathogens, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Legionella pneumoniae. These atypical community-acquired pneumonias (CAPs) often cause systemic manifestations and are helpful in clinically differentiating from typical CAPs by the pattern of extrapulmonary organ involvement, which is characteristic for each atypical CAP. While zoonotic pneumonias may be eliminated from diagnostic consideration with a negative contact history, the atypical pneumonias are infrequent (approximately 15% of CAPs are atypical), difficult to diagnose, and unresponsive to beta-lactam therapy.

A definitive laboratory diagnosis of Legionella is usually based on investigations such as direct fluorescent antibody (DFA) or indirect fluorescent antibody (IFA). Antibiotics used against Legionella include macrolides, doxycycline, rifampin, quinolones, and telithromycin. Treatment is usually continued for 2 weeks although morbidity and mortality is high.

Pathophysiology

Pathogenesis of typical pneumonia

S pneumoniae generally resides in the nasopharynx and is carried asymptomatically in approximately 50% of healthy individuals. Invasive disease may occur upon acquisition of a new epithelium serotype. A strong association exists with viral illnesses, such as influenza. Viral infections increase pneumococcal attachment to the receptors on activated respiratory epithelium. Once aerosolized from the nasopharynx to the alveolus, pneumococci infect type II alveolar cells. The pneumonic lesion progresses as pneumococci multiply in the alveolus and invade alveolar epithelium. Pneumococci spread from alveolus to alveolus through the pores of Kohn, thereby producing inflammation and consolidation along lobar compartments.

A recent multivariate analysis showed an independent association between pneumococcal CAP and alcoholism. Current alcohol abuse was associated with severe CAP. No significant differences were found in mortality, antibiotic resistance of S pneumoniae, and other etiologies.

Pathogenesis of atypical infection

After aspiration or inhalation, the atypical organisms attach to the respiratory epithelial cells by a variety of mechanisms. The presence of pili on the surface of Legionella species facilitates attachment. Once adhered, the organisms cause injury to the epithelial cells and their associated cilia. Many of the pathogenetic mechanisms may be immune-mediated rather than due to direct injury by the bacteria. A host defense is mounted via cell-mediated and humoral immunity. Infection caused by atypical organisms often spreads beyond the lobar boundaries and frequently is bilateral.

Pathogenesis of nosocomial pneumonia

Aspiration plays a central role in the pathogenesis of nosocomial pneumonia. Approximately 45% of healthy subjects aspirate during sleep, and an even higher proportion of severely ill patients aspirate routinely. Depending on the number and virulence of the pathogenic organisms reaching the lower respiratory tract and on the host defense factors, pneumonia may develop. The oropharynx of hospitalized patients may become colonized with aerobic gram-negative bacteria within a few days of admission. Therefore, nosocomial pneumonia is caused predominantly by the gram-negative bacilli. However, the incidence of Staphylococcus aureus lower respiratory tract infection is increasingly common in the hospitalized and institutionalized patient and must now be considered a possible pathogen for nosocomial pneumonia.

Frequency

United States

Community-acquired pneumonia remains a common illness. Approximately 4.5 million cases of community-acquired pneumonia occur annually, and 20% result in hospitalization. Estimates of incidence of nosocomial pneumonia range from 4-7 episodes per 1000 hospitalizations. Approximately 25% of patients in intensive care units (ICUs) develop pneumonia. Overall incidence of community-acquired pneumonia is reported to be 170 cases per 100,000 persons. With advancing age, the incidence increases from 94 cases per 100,000 persons in patients aged 44 years to 280 cases per 100,000 persons in those older than 65 years. Pneumonia as a cause of hospitalization increased from 36 to 48 cases per 100,000 persons between 1984 and 1995.

Mortality/Morbidity

Pneumonia is the sixth leading cause of death in the United States and is the most common infectious cause of death. The mortality rate is reported to be 1% in the outpatient setting but may increase to up to 25% in those requiring hospital admission. In a patient with preexisting respiratory disease, onset of bacterial pneumonia may result in deterioration of respiratory status, leading to respiratory failure and death.

• Nosocomial pneumonia is the leading cause of death among hospital-acquired infections. Recent studies have shown that nosocomial pneumonia causes excessive risk of death, and the mortality rates range from 20-50%.
• Although less common in the antibiotic era, bacterial pneumonia may lead to bronchiectasis. However, lower respiratory infection with pneumococci, staphylococci, and Klebsiella species may result in bronchiectasis, especially if treatment is delayed. The damaged alveoli and small- to medium-sized airways are replaced by dilated saccules that are filled with purulent material. Ongoing chronic inflammation may gradually destroy the surrounding lung tissue.
• In patients with community-acquired pneumonia, daily activities were restricted for 24.8 days per 100 persons. Lost days of work were 8.9 days per 100 adult employees. The annual cost to treat patients with community-acquired pneumonia in the United States was 9.7 billion dollars in 1994; 92% of these costs were secondary to hospitalization. A substantial difference in cost exists between inpatient and outpatient therapy for pneumonia (US $7517 vs $264).

Sex

Incidence is greater in males than in females.

Age

Advanced age increases the incidence of pneumonia and the mortality from pneumonia.

• Elderly persons have weaker immune responses, higher risk of aspiration, and other comorbidities.
• In a 20-year US study, the mortality rate from pneumococcal pneumonia with bacteremia was 20.3%, overall. However, a higher mortality rate (37.7%) occurred in elderly patients.

Clinical

History

Clinical presentation in patients with pneumonia varies from a mildly ill ambulatory patient to a critically ill patient with respiratory failure or septic shock.

• The character of sputum produced may suggest a particular pathogen.
  • Patients with pneumococcal pneumonia may produce bloody or rust-colored sputum. Infections with Pseudomonas, Haemophilus, and pneumococcal species are known to expectorate green sputum.
  • Anaerobic infections characteristically produce foul-smelling and bad-tasting sputum. Currant-jelly sputum suggests pneumonia from Klebsiella or pneumococcal species.
• Patients may report rigors or shaking chills.
• Patients may complain of other nonspecific symptoms, which include headaches, malaise, nausea, vomiting, and diarrhea. These symptoms may suggest infection with Legionella, Chlamydia, or Mycoplasma species.
• Malaise, myalgias, and exertional dyspnea may be observed.
• Pleuritic chest pain or abdominal pain secondary to pleuritis is a common feature of pneumococcal infection, but these may occur in other bacterial pneumonias.
• A meticulous past medical history and history of environmental, occupational, and recreational exposures should be obtained. This history should include whether the patient has recently traveled or had contact with animals that might serve as a source of an infectious agent.
  • Legionella pneumophila: Patients may report exposure to contaminated air-conditioning cooling towers, exposure to a grocery store mist machine, or a visit or recent stay in a hospital with a contaminated water system.
  • Coccidioides immitis: Pneumonia may develop after travel to the southwestern United States and after exposure to a wind or rain storm in an endemic area.
  • S pneumoniae, Mycobacterium tuberculosis, Mycoplasma, and Chlamydia pneumonia: Patients may report exposure to overcrowded institutions such as jails, shelters for homeless persons, or military training camps.
  • Blastomyces dermatitidis: Patients may have traveled to the midwestern United States or the Canadian Shield.
  • Histoplasma capsulatum: Infection can result from exposure to contaminated bat caves or from excavation in endemic areas.
  • Coxiella burnetii: This is related to exposure to infected parturient cats, cattle, sheep, or goats.
  • Chlamydia psittaci: Patients may report exposure to turkeys, chickens, ducks, or psittacine birds.
• Travel history
  • Burkholderia (Pseudomonas) pseudomallei (melioidosis): This infection may result from travel to Thailand or other countries in Southeast Asia.
  • M tuberculosis: Pneumonia may develop in immigrants from Asia or Africa.
• Occupational history
  • Pneumonia may develop in a health care worker who works with patients infected with HIV in a large city.
  • M tuberculosis may be a causative agent.
• Host factors
  • Evaluation of host factors often provides a clue to the bacterial diagnosis.
  • Diabetic ketoacidosis may lead to S pneumoniae or S aureus infection.
  • Alcoholism may indicate Klebsiella pneumoniae infection.
  • Chronic obstructive lung disease may lead to Haemophilus influenzae or Moraxella catarrhalis infection.
  • In patients who have received solid organ transplants, pneumonia from S pneumoniae may occur more than 3 months after the transplant. Other organisms include Legionella species, Pneumocystis carinii, and cytomegalovirus.
  • Sickle cell disease may indicate S pneumoniae or H influenzae infection.
  • HIV infection (CD4 cell count >200/μ L) may lead to Cryptococcus neoformans, M tuberculosis, or Rhodococcus equi infection. A CD4 cell count of fewer than 200/μ L may indicate Mycobacterium avium-intracellulare infection or Pneumocystis pneumonia.

Physical

Physical examination findings vary depending on the type of organisms, severity of pneumonia, coexisting host factors, and presence of complications.

• The common findings of consolidation are as follows:
  • Fever or hypothermia (temperature >38.5°C or <36°C)
  • Tachypnea (respiratory rate >18 breaths per min)
  • Tachycardia or bradycardia
  • Central cyanosis
  • Dullness to percussion over pneumonic consolidation
  • Decreased intensity of breath sounds
  • Rales or crackles
  • Egophony upon auscultation
  • Whispering pectoriloquy
  • Pleural friction rub
  • Altered mental status
• Physical examination findings that may indicate the etiology of pneumonia are as follows:
  • Periodontal disease with foul-smelling sputum - Anaerobes, possible mixed aerobic-anaerobic infection
  • Bullous myringitis -Mycoplasma pneumoniae
  • Absent gag reflex, altered level of consciousness, recent seizure - Polymicrobial (aerobic and anaerobic), possible macroaspiration or microaspiration
  • Encephalitis -M pneumoniae, C burnetii, L pneumophila
  • Cerebellar ataxia, erythema multiforme, erythema nodosum -Chlamydia pneumoniae, M tuberculosis
  • Erythema gangrenosum -Pseudomonas aeruginosa, Serratia marcescens
  • Cutaneous nodules (abscesses and CNS findings) -Nocardia species

Causes

Causes of bacterial pneumonia can be categorized as extrinsic and intrinsic.

• Extrinsic factors include infection with respiratory pathogens. Exposure to pulmonary irritants or direct pulmonary injury causes noninfectious pneumonitis.
  • Infectious agents responsible for bacterial pneumonias include S pneumoniae and H influenzae; Klebsiella, Staphylococcus, and Legionella species; and gram-negative organisms.
  • Aspiration and inhalation of aerosols containing the bacterial pathogen are the most common modes of infection. Some bacteria, such as Staphylococcus species, may spread to the lungs hematogenously.
• Intrinsic factors are related to the host's immune response, the presence of comorbidities, and other risk factors:
  • Loss of protective reflexes allows aspiration of oropharyngeal flora into the lung. Aspiration is facilitated by altered mental status from intoxication, deranged metabolic states, neurological causes (eg, stroke), and endotracheal intubation.
  • Local lung pathologies (eg, tumors, chronic obstructive pulmonary disease [COPD], bronchiectasis) are predisposing factors for bacterial pneumonia. Smoking impairs the host's defense to infection by a variety of mechanisms.
• S pneumoniae is the most common cause of bacterial pneumonia.
• Pneumonia from H influenzae often is associated with debilitating conditions such as asthma, COPD, smoking, and a compromised immune system.
• K pneumoniae may cause a severe necrotizing lobar pneumonia in patients with chronic alcoholism, diabetes, or COPD.
• S aureus pneumonia is observed in those who abuse intravenous drugs. S aureus generally occurs in hospitalized patients and patients with prosthetic devices; it spreads hematogenously to the lungs from contaminated local sites. This pathogen also is an important cause of pneumonia following infection with influenza A.
• L pneumophila infections occur either sporadically or as local outbreaks.
  • An outbreak in 1976 affected more than 180 members of the American Legion staying at the same hotel in Philadelphia for an annual convention. Twenty-nine of these legionnaires died. The organism was identified in 1977 and named Legionella.
  • Legionella is known to colonize the water condensed from air-conditioning systems and the water supply of institutions.
  • L pneumophila has 2 distinct clinical presentations. The first, Pontiac fever, is an immune-mediated reaction after exposure to the organism. Pontiac fever presents as a viral-like syndrome with malaise, fever and chills, myalgias, and headache. This disease resolves spontaneously. The second Legionella pneumonia is a severe and aggressive pneumonia associated with a mortality rate of up to 75% if treatment is delayed. Elderly and debilitated persons; those who smoke; and individuals with COPD, alcoholism, immunodeficiency, and trauma all are predisposed to Legionella infection.
  • Legionella pneumonia has associated GI symptoms, including anorexia, nausea, vomiting, and diarrhea, in 50% of patients.
• Gram-negative pneumonias are observed in individuals who are infirm, immunocompromised, and hospitalized. Causative organisms include Escherichia coli and Pseudomonas, Enterobacter, and Serratia species. Residents of chronic care facilities are at risk for gram-negative pneumonia.
• Aspiration pneumonia is observed in individuals with altered sensorium (eg, seizures, alcohol intoxication, drug intoxication) or CNS impairment (eg, stroke) causing a reduced gag reflex. The stomach or oropharyngeal contents are aspirated. The causative organisms include M catarrhalis and Bacteroides, Peptostreptococcus, and Fusobacterium species.

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