Bacterial Pneumonia

Article Author:
Saud Bin Abdul Sattar
Article Editor:
Sandeep Sharma
Updated:
2/11/2019 8:56:52 PM
PubMed Link:
Bacterial Pneumonia

Introduction

The word "pneumonia" originates from the ancient Greek word "pneumon" which means "lung," so the word "penumonia" 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

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.

Epidemiology

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]

Pathophysiology

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]

Histopathology

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.

Evaluation

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.
  • 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]

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.

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.

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

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.

Complications

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.

Enhancing Healthcare Team Outcomes

The management of a pneumonia is multidisciplinary. 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 discontinuation of smoking and abstaining from alcohol. Further, patients should be encouraged to get the appropriate influenza and pneumococcal vaccines. Finally, it is important to educate the patient on compliance with antibiotics if they want a complete resolution of the infectious process.[13][14] (Level V)

Outcomes

In healthy people, the outcome after a 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 a pneumonia is left untreated, it carries a 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)


References

[1] Leung AK,Hon KL,Leong KF,Sergi CM, Measles: a disease often forgotten but not gone. Hong Kong medical journal = Xianggang yi xue za zhi. 2018 Sep 24     [PubMed PMID: 30245481]
[2] Grief SN,Loza JK, Guidelines for the Evaluation and Treatment of Pneumonia. Primary care. 2018 Sep     [PubMed PMID: 30115336]
[3] Ashurst JV,Dawson A, Pneumonia, Klebsiella null. 2018 Jan     [PubMed PMID: 30085546]
[4] Calik S,Ari A,Bilgir O,Cetintepe T,Yis R,Sonmez U,Tosun S, The relationship between mortality and microbiological parameters in febrile neutropenic patients with hematological malignancies. Saudi medical journal. 2018 Sep     [PubMed PMID: 30251730]
[5] Shin EJ,Kim Y,Jeong JY,Jung YM,Lee MH,Chung EH, The changes of prevalence and etiology of pediatric pneumonia from National Emergency Department Information System in Korea, between 2007 and 2014. Korean journal of pediatrics. 2018 Sep     [PubMed PMID: 30274507]
[6] Lat I,Daley MJ,Shewale A,Pangrazzi MH,Hammond D,Olsen KM, A Multicenter, Prospective, Observational Study to Determine Predictive Factors for Multidrug-Resistant Pneumonia in Critically Ill Adults: The DEFINE Study. Pharmacotherapy. 2018 Aug 12     [PubMed PMID: 30101412]
[7] Søndergaard MJ,Friis MB,Hansen DS,Jørgensen IM, Clinical manifestations in infants and children with Mycoplasma pneumoniae infection. PloS one. 2018     [PubMed PMID: 29698412]
[8] Karakuzu Z,Iscimen R,Akalin H,Kelebek Girgin N,Kahveci F,Sinirtas M, Prognostic Risk Factors in Ventilator-Associated Pneumonia. Medical science monitor : international medical journal of experimental and clinical research. 2018 Mar 5     [PubMed PMID: 29503436]
[9] Phillips-Houlbracq M,Ricard JD,Foucrier A,Yoder-Himes D,Gaudry S,Bex J,Messika J,Margetis D,Chatel J,Dobrindt U,Denamur E,Roux D, Pathophysiology of Escherichia coli pneumonia: Respective contribution of pathogenicity islands to virulence. International journal of medical microbiology : IJMM. 2018 Mar     [PubMed PMID: 29325882]
[10] Franquet T, Imaging of Community-acquired Pneumonia. Journal of thoracic imaging. 2018 Sep     [PubMed PMID: 30036297]
[11] Ayede AI,Kirolos A,Fowobaje KR,Williams LJ,Bakare AA,Oyewole OB,Olorunfemi OB,Kuna O,Iwuala NT,Oguntoye A,Kusoro SO,Okunlola ME,Qazi SA,Nair H,Falade AG,Campbell H, A prospective validation study in South-West Nigeria on caregiver report of childhood pneumonia and antibiotic treatment using Demographic and Health Survey (DHS) and Multiple Indicator Cluster Survey (MICS) questions. Journal of global health. 2018 Dec     [PubMed PMID: 30254744]
[12] Hanretty AM,Gallagher JC, Shortened Courses of Antibiotics for Bacterial Infections: A Systematic Review of Randomized Controlled Trials. Pharmacotherapy. 2018 Jun     [PubMed PMID: 29679383]
[13] Julián-Jiménez A,Adán Valero I,Beteta López A,Cano Martín LM,Fernández Rodríguez O,Rubio Díaz R,Sepúlveda Berrocal MA,González Del Castillo J,Candel González FJ, [Recommendations for the care of patients with community-acquired pneumonia in the Emergency Department]. Revista espanola de quimioterapia : publicacion oficial de la Sociedad Espanola de Quimioterapia. 2018 Apr     [PubMed PMID: 29619807]
[14] Coon ER,Maloney CG,Shen MW, Antibiotic and Diagnostic Discordance Between ED Physicians and Hospitalists for Pediatric Respiratory Illness. Hospital pediatrics. 2015 Mar     [PubMed PMID: 25732983]
[15] Bickenbach J,Schöneis D,Marx G,Marx N,Lemmen S,Dreher M, Impact of multidrug-resistant bacteria on outcome in patients with prolonged weaning. BMC pulmonary medicine. 2018 Aug 20     [PubMed PMID: 30126392]
[16] Luan Y,Sun Y,Duan S,Zhao P,Bao Z, Pathogenic bacterial profile and drug resistance analysis of community-acquired pneumonia in older outpatients with fever. The Journal of international medical research. 2018 Jan 1     [PubMed PMID: 30027805]