Bacterial Pneumonia

Article Author:
Saud Bin Abdul Sattar
Article Editor:
Sandeep Sharma
12/12/2019 11:04:36 PM
PubMed Link:
Bacterial Pneumonia


The word "pneumonia" originates from the ancient Greek word "pneumon" which means "lung," so the word "pneumonia" becomes "lung disease." Medically it is an inflammation of one or both lung's parenchyma that is more often but not always caused by infections. The many causes of pneumonia include bacteria, viruses, fungi, and parasites. This article is about bacterial causes of pneumonia as it is the major cause of mortality and morbidity by pneumonia. According to the new classification of pneumonia, there are four categories: community-acquired (CAP), hospital-acquired (HAP), healthcare-associated (HCAP) and ventilator-associated pneumonia (VAP). [1][2][3]

Types of Bacterial Pneumonia

  • CAP: The acute infection of lung tissue in a patient who has acquired it from the community.
  • HAP: The acute infection of lung tissue that develops 48 hours or longer after the hospitalization of a non-intubated patient.
  • VAP: A type of nosocomial infection of lung tissue that usually develops 48 hours or longer after intubation for mechanical ventilation.
  • HCAP: The acute infection of lung tissue acquired from healthcare facilities such as nursing homes, dialysis centres, and outpatient clinics or a patient with hospitalization within the past 3 months (previously included in HAP but becomes a separate category after some cases presenting as outpatients with pneumonia have been found to be infected with multidrug-resistant (MDR) pathogens previously associated with HAP).

Some articles include both HAP and VAP under the category of HCAP, so defining HCAP is problematic and controversial.


Etiology of community-acquired pneumonia is an extensive list of agents that include bacteria, viruses, fungi, and parasites, but this article is about bacterial pneumonia and its causes. Bacteria have classically been categorized into two divisions on the basis of etiology, "typical" and "atypical" organisms. Typical organisms can be cultured on standard media or seen on Gram stain, but "atypical" organisms do not have such properties. [4]

  • Typical pneumonia refers to pneumonia caused by Streptococcus  pneumoniae, Haemophilus influenzae, S. aureus, Group A streptococci, Moraxella catarrhalis, anaerobes, and aerobic gram-negative bacteria.
  • Atypical pneumonia is mostly caused by Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae, and C. psittaci.

The most common causes of community-acquired pneumonia (CAP) is S. pneumoniae followed by Klebsiella pneumoniae, Haemophilus influenzae, and Pseudomonas aeruginosa. The most common causes of HCAP and HAP are MRSA (methicillin-resistant Staphylococcus aureus) and Pseudomonas aeruginosa respectively. The causative agents of VAP include both multi-drug resistant (MDR) agents (e.g., S. pneumoniae, other Strep spp, H. influenzae and MSSA) and non-MDR (e.g., P. aeruginosa, methicillin-resistant Staphylococcus aureus, Acinetobacter spp. and antibiotic-resistant Enterobacteriaceae) bacterial pathogens.


The incidence of CAP in the United States is more than 5 million per year; 80% of these new cases are treated as outpatients with the mortality rate of less than 1%, and 20% are treated as inpatients with the mortality rate of 12% to 40%. The incidence of CAP varies among different genders; for example, it is more common in males and African Americans than females and other Americans. The incidence rates are higher at extremes of age distribution range; the adult rate is usually 5.15 to 7.06 cases per 1000 persons per year, but in the population of age less than 4 years and greater than 60 years, the rate is more than 12 cases per 1000 persons. In 2005, influenza and pneumonia combined was the eighth most common cause of death in the United States and the seventh Most common cause of death in Canada. The mortality rate also is variable among different regions at  7.3% for the United States and Canada, 9.1% for Europe, and 13.3% for Latin America.[5][6]


The lower respiratory tract is not sterile, it always is exposed to environmental pathogens. Invasion and propagation of the above-mentioned bacteria into lung parenchyma at alveolar level causes bacterial pneumonia, and the body's inflammatory response against it causes the clinical syndrome of pneumonia. To prevent this proliferation of microorganisms there are a number of host defenses working together in lungs such as mechanical (e.g., hair in nostrils and mucus on nasopharynx and oropharynx) and chemical (e.g., proteins produced by alveolar epithelial cells like surfactant protein A and D, which have the intrinsic property of opsonizing bacteria). Another component of the pulmonary defense system is made up of immune cells such as alveolar macrophages, which work to engulf and kill proliferating bacteria, but once bacteria overcome the capacity of host defenses, they start proliferation. In this setting, the alveolar macrophages kickoff the inflammatory response to strengthen the lower respiratory tract defenses. This inflammatory response is the main culprit of clinical manifestation of bacterial pneumonia. Cytokines are released in response to the inflammatory reaction and cause the constitutional symptoms, for example, IL-1 (interleukin-1) and TNF (tumor necrosis factor) causes fever. Chemokine-like IL-8 (interleukin-8) and colony-stimulating factors like G-CSF (granulocyte colony-stimulating factor) promote chemotaxis and neutrophils maturation respectively, resulting in leukocytosis on serological lab and purulent secretions. These cytokines are responsible for the leakage of the alveolar-capillary membrane at the site of inflammation, causing a decrease in compliance and shortness of breath. Sometimes even erythrocytes cross this barrier and result in hemoptysis.[7][8][9]


Pathologically, lobar pneumonia is the acute exudative inflammation of a lung lobe. It has the following four advanced stages if left untreated:

  1. Congestion: In this stage, pulmonary parenchyma is not fully consolidated, and microscopically, the alveoli have serous exudates, pathogens, few neutrophils, and macrophages.
  2. Red hepatization: Here the lobe is now consolidated, firm, and liver-like. Microscopically, there is an addition of fibrin along with serous exudate, pathogens, neutrophils, and macrophages. The capillaries are congested, and the alveolar walls are thickened.
  3. Gray hepatization: The lobe is still liver-like in consistency but gray in color due to suppurative and exudative filled alveoli.
  4. Resolution: After a week, it starts resolving as lymphatic drainage or a productive cough clear the exudate.

History and Physical

The history findings of bacterial pneumonia may vary from indolent to fulminant. Clinical manifestation includes both constitutional findings and findings due to damage to the lung and related tissue. The following are major history findings:

  • Fever with tachycardia and/or chills and sweats.
  • The cough may be either nonproductive or productive with mucoid, purulent or blood-tinged sputum.
  • Pleuritic chest pain, if the pleura is involved.
  • Shortness of breath with normal daily routine work.
  • Other symptoms include fatigue, headache, myalgia, and arthralgia.

Physical findings also vary from patient to patient and mainly depend on the severity of lung consolidation and existence or nonexistence of pleural effusion. The following are major clinical findings:

  • Increased respiratory rate.
  • Percussion sounds vary from flat to dull.
  • Tactile fremitus.
  • Crackles, rales, and bronchial breath sounds are heard on auscultation.

Confusion manifests earlier in older patients. A critically ill patient may present with sepsis or multi-organ failure.


The approach to evaluate and diagnose pneumonia depends on different modalities but primarily it is like a tripod stand which has 3 legs which are summed up as:

  • Clinical Evaluation: It includes taking a careful patient history and performing a thorough physical examination to judge the clinical signs and symptoms mentioned above.
  • Laboratory Evaluation: This includes lab values such as complete blood count with differentials, inflammatory biomarkers like ESR and C-reactive protein, blood cultures, sputum analysis or Gram staining and/or urine antigen testing or polymerase chain reaction for nucleic acid detection of certain bacteria.
  • An arterial blood gas may reveal hypoxia and respiratory acidosis
  • Pulse oximetry of less than 92% indicates severe hypoxia and elevated CRP predicts a serious infection.
  • Blood cultures should be obtained before administering antibiotics. Unfortunately, they are only positive in 40% of cases
  • Sputum evaluation if good quality may reveal more than 25 WBC per low power field and less than 10 squamous epithelial cells
  • Radiological Evaluation:  It includes chest x-ray as an initial imaging test and the finding of pulmonary infiltrates on plain film is considered as a gold standard for diagnosis when the lab and clinical features are supportive.[10][2]
  • The chest x-ray may reveal a consolidation or parapneumonic effusion.
  • Chest CT is done for complex cases where the cause is not known.
  • Bronchoalveolar lavage is done in patients who are intubated and can provide samples for culture.

Treatment / Management

In all patients with bacterial pneumonia, empirical therapy should be started as soon as possible. The first step in treatment is a risk assessment to know whether the patient should be treated in an outpatient or inpatient setting. Cardiopulmonary conditions, age, and severity of symptoms affect risk for bacterial pneumonia, especially CAP.[11][12][13]

An expanded CURB-65 or CURB-65 pneumonia severity score can be used for risk quantification. It includes C = Confusion, U = Uremia (BUN greater than 20 mg/dL), R = Respiratory rate (greater than 30 per min), B = B.P (BP less than 90/60 mmHg) and age greater than 65 years. One point is scored for each previously mentioned risk factor. If the total of the score is 2 or more than 2, it indicates hospital admission. If the total is 4 or more than 4, it indicates ICU admission. Recommended therapy for different settings are as follows:

  • Outpatient Setting: For patients having comorbid conditions ( e.g., diabetes, malignancy, etc.) the regimen is "fluoroquinolone" or "beta-lactams + macrolide." For patients with no comorbid conditions, we can use "macrolide" or "doxycycline" empirically. Testing is usually not performed as the empiric regimen is almost always successful.
  • Inpatient Setting (non-ICU): Recommended therapy is fluoroquinolone or macrolide + beta-lactam.
  • Inpatient setting (ICU): Recommended therapy is beta-lactam + macrolide or beta-lactam + fluoroquinolone.
  • MRSA: Vancomycin or linezolid can be added.

After getting a culture-positive lab result, therapies should be directed to the culture-specific pathogen.

The patient also can benefit from smoking cessation counseling and influenza and pneumococcal vaccination.

All patients treated at home should be scheduled for a follow-up visit within 2 days to assess any complication of pneumonia.

The role of corticosteroids remains controversial and may be used in patients who remain hypotensive with presumed adrenal insufficiency.

Other measures:

  • Hydration
  • Chest physical therapy
  • Monitoring with pulse oximetry
  • Upright positioning
  • Respiratory therapy with bronchodilators
  • Mechanical support if patients are in respiratory distress
  • Nutrition
  • Early mobilization

Differential Diagnosis

Differential Diagnosis in Children

  • Asthma or reactive airway disease
  • Bronchiolitis
  • Croup
  • Respiratory distress syndrome

Differential Diagnosis in Adults

  • Acute and chronic bronchitis
  • Aspiration of a foreign body
  • Asthma
  • Atelectasis
  • Bronchiectasis
  • Bronchiolitis
  • Chronic obstructive pulmonary disease
  • Fungal
  • Lung abscess
  • Pneumocystis jiroveci pneumonia
  • Respiratory failure
  • Viral


Prognosis of pneumonia depends on many factors including age, comorbidities, and hospital setting (inpatient or outpatient). Patients older than 60 years or younger than 4 years of age have a relatively poorer prognosis than young adults. Antibiotic resistance, very concerning due to the enhancement of antibiotic regimens, and infectious diseases, especially those like bacterial pneumonia, can be easily cured.


The most common complications of bacterial pneumonia are respiratory failure, sepsis, multiorgan failure, coagulopathy, and exacerbation of preexisting comorbidities. Three distinct complications are metastatic infections, lung abscess, and complicated pleural effusion.

Deterrence and Patient Education

To prevent bacterial pneumonia, recommendations include:

  • Vaccination against pneumococcus
  • Annual vaccine against H influenza

Pearls and Other Issues

  1. Most patients respond with improvement within 48-72 hours.
  2. The chest x-ray findings lag behind clinical features and may take 6-12 weeks to clear
  3. If patients fail to improve within 72 hours, another cause should be suspected, antibiotic resistance or development of complication like empyema

Enhancing Healthcare Team Outcomes

The management of pneumonia requires an interprofessional team. The reason is that most patients are managed as outpatients but if not properly treated, the morbidity and mortality are high.

Besides the administration of antibiotics, these patients often require chest physical therapy, a dietary consult, physical therapy to help regain muscle mass and a dental consult. The key is to educate the patient on the discontinuation of smoking and abstaining from alcohol.

Patients need to be referred to a dietitian to ensure that they are eating healthy.

Further, the clinicians should encourage patients to get appropriate influenza and pneumococcal vaccines. The pharmacist should not only teach about antibiotic compliance but ensure that the patient is prescribed the right antibiotics aimed at the target organism. An infectious disease specialty-trained pharmacist is particularly helpful in assisting the team with difficult antibiotic treatment choices. Nursing can counsel on the appropriate dosing and administration of medications and answer patient questions, as well as charting treatment progress, and reporting any issues to the clinician managing the case.

Finally, it is important to educate the patient to follow up with clinicians if they want a complete resolution of the infectious process.[13][14] (Level V) Only with open communication between the interprofessional team can the morbidity of pneumonia be lowered.


In healthy people, the outcome after bacterial pneumonia is excellent. However, in people with advanced age, lung disease, immunosuppression, infection with aggressive gram-negative organisms (Klebsiella) and other comorbidities, the outcomes are usually poor. When pneumonia is left untreated, it carries mortality in excess of 25%. Pneumonia can also lead to extensive lung damage and lead to residual impairment in lung function. Other reported complications of pneumonia that occur in 1-5% of patients include lung abscess, empyema, and bronchiectasis.[15][16] (Level V)


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