Bacterial Pneumonia – StatPearls – NCBI Bookshelf

Continuing Education Activity

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 lung parenchyma that is more often, but not always, caused by infections. The many causes of pneumonia include bacteria, viruses, fungi, and parasites. This activity reviews the cause, pathophysiology, presentation, and diagnosis of bacterial pneumonia and highlights the interprofessional team’s role in the management of these patients.

Objectives:

• Identify the etiology of bacterial pneumonia.

• Recall the X-ray findings in a patient with bacterial pneumonia.

• Outline the treatment and management options available for bacterial pneumonia.

• Employ interprofessional team strategies for improving care coordination and communication to advance the management of patients affected by bacterial pneumonia and improve outcomes.

Access free multiple choice questions on this topic.

Introduction

The word “pneumonia” takes its origin 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 lungs’ parenchyma that is more often, but not always, caused by infections. The many causes of pneumonia include bacteria, viruses, fungi, and parasites. This article will focus on bacterial pneumonia, as it is the major cause of morbidity and mortality. 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 or within 48 hours of the hospital admission.

• HAP: The acute infection of lung tissue in a non-intubated patient that develops after 48 hours of hospitalization.

• 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 centers, outpatient clinics, or a patient with a history of hospitalization within the past three months.

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

Etiology

Community-acquired pneumonia can be caused by an extensive list of agents that include bacteria, viruses, fungi, and parasites, but this article will focus on bacterial pneumonia and its causes. Bacteria have classically been categorized into two divisions based on 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, Staphylococcus aureus, Group A streptococci, Moraxella catarrhalis, anaerobes, and aerobic gram-negative bacteria.

• Atypical pneumonia is mostly caused by Legionella, Mycoplasma pneumoniae, Chlamydia pneumoniae, and Chlamydia psittaci.

The most common cause 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. 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

In the United States, lower respiratory tract infections account for more morbidity and mortality than any other infection. [5] 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 a mortality rate of less than 1%, and 20% are treated as inpatients with a 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 in females and other Americans. However, the total number of deaths has been on the rise among females.[6] The incidence rates are higher at extremes of age; 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 were the eighth most common cause of death in the United States and the seventh most common cause of death in Canada. The mortality rate is variable among different regions, such as 7.3% for the United States and Canada, 9.1% for Europe, and 13.3% for Latin America.[7][8]

Pathophysiology

The lower respiratory tract is not sterile, and it always is exposed to environmental pathogens. Invasion and propagation of the above-mentioned bacteria into lung parenchyma at the alveolar level causes bacterial pneumonia. The body’s inflammatory response against it causes the clinical syndrome of pneumonia.

To prevent this proliferation of microorganisms, several host defenses work together in the 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 proliferating. In this setting, the alveolar macrophages kickoff the inflammatory response to strengthen the lower respiratory tract defenses. This inflammatory response is the main reason for the clinical manifestation of bacterial pneumonia. Cytokines are released in response to the inflammatory reaction and cause constitutional symptoms; for example, IL-1 (interleukin-1) and TNF (tumor necrosis factor) cause fever. Chemokine-like IL-8 (interleukin-8) and colony-stimulating factors like G-CSF (granulocyte colony-stimulating factor) promote chemotaxis and neutrophil 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.[9][10][11]

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: In this stage, the lobe becomes consolidated, firm, and liver-like. Microscopically, there are fibrin, 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 exudate-filled alveoli.

4. Resolution: After a week, it starts resolving as lymphatic drainage or a productive cough clears the exudate.

History and Physical

While taking the history, it is crucial to explore the patient’s potential exposures, risks of aspiration, host factors, and presenting symptoms.

Exposure: A detailed history of possible exposures should be sought as it can help in establishing the potential etiologies. The following are some associations of exposures and etiologies of bacterial pneumonia:

• Contaminated air-conditioning and water systems may cause Legionella pneumonia.

• Crowded places, such as jails, shelters, etc., expose a person to Streptococcus pneumonia, Mycobacteria, Mycoplasma, and Chlamydia.

• Exposures to several animals, such as cats, sheep, and cattle, may lead to infection with Coxiella burnetii

• Some birds, such as chickens, turkeys, and ducks, can expose a person to Chlamydia psittaci.

Risks of Aspiration: Patients with an increased risk of aspiration are more prone to develop pneumonia secondary to aspiration. Associated risks are:

Host mechanisms: It is of utmost importance to explore a detailed history to find clues towards the etiology of pneumonia. For instance, a history of asthma, COPD, smoking, and immunocompromised status can be indicative of H. influenzae infection. H influenza most commonly appears in the winter season. Similarly, social, sexual, medication, and family history can all be useful in determining the cause of illness.

Features in the history 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 significant 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.

For unbeknownst reasons, the presence of rigors is more often indicative of pneumococcal pneumonia than other bacterial pathogens.[12]

The presence of a productive cough is the most common and significant presenting symptom. Some bacterial causes have particular manifestations, such as:

• S. pneumoniae – Rust-colored sputum

• Pseudomonas, Hemophilus – Green sputum

• Klebsiella – Red currant-jelly sputum

• Anaerobes – foul-smelling and bad-tasting sputum

Atypical pneumonia presents with pulmonary and extra-pulmonary manifestations, such as Legionella pneumonia, which often presents with altered mentation and gastrointestinal symptoms.

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

• Increased temperature (usually more than 38 C or 100.4 F)[13]

• Decreased temperature (less than 35 C or 95 F)

• Increased respiratory rate (more than 18 breaths/min)

• Increased heart rate (more than 100/min)

• Bradycardia (less than 60/min)

• Cyanosis

• Percussion sounds vary from flat to dull.

• Tactile fremitus

• Crackles, rales, and bronchial breath sounds are heard during auscultation.

• Tracheal deviation

• Lymphadenopathy

• Pleural rub

• Egophony

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

Some examination findings are specific for certain etiologies, such as:

• Bradycardia – Legionella

• Dental illnesses – Anaerobes

• Impaired gag reflex – Aspiration pneumonia

• Cutaneous nodules – Nocardiosis

• Bullous myringitis – Mycoplasma

Evaluation

The approach to evaluate and diagnose pneumonia depends on the clinical status, laboratory parameters, and radiological evaluation.[14]

• 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.[15]

  • Blood cultures should be obtained before administering antibiotics. Unfortunately, they are only positive in 40% of cases.

  • If good quality, sputum evaluation may reveal more than 25 WBC per low-power field and less than 10 squamous epithelial cells.

  • Some bacterial causes present with specific biochemical evidence, such as Legionella, may present with hyponatremia and microhematuria.

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 the risk for bacterial pneumonia, especially CAP. [17][18][19]

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 of these risk factors. For a score of 0-1, outpatient treatment is advised. If the total score is 2 or more, it indicates medical ward admission. If the total score is 3 or more, 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, macrolide or doxycycline can be used 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, therapy should be altered according to the culture-specific pathogen.

The patient also can benefit from smoking cessation, counseling, and vaccination for influenza and pneumococcus.

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

Distinguishing pneumonia from other pulmonary diseases can be a daunting task, particularly in patients with co-existing pulmonary pathology. The differential diagnoses are different for children and adults, as mentioned below:

Differential Diagnosis in Children

• Asthma or reactive airway disease

• Bronchiolitis

• Croup

• Respiratory distress syndrome

• Epiglottitis

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 infection

Prognosis

The prognosis of pneumonia depends on many factors, including age, comorbidities, and hospital setting (inpatient or outpatient). Generally, the prognosis is promising in otherwise healthy patients. Patients older than 60 years or younger than 4 years of age have a relatively poorer prognosis than young adults. If pneumonia is left untreated, the overall mortality may become 30%. Antibiotic resistance is very concerning due to the excessive and unjustified use of antibiotics. The Pneumonia Severity Index (PSI) may be utilized as a tool to establish a patient’s risk of mortality.

In a study conducted on etiologies of CAP, S. pneumoniae was found to be the cause of mortality in most patients; however, Pseudomonas, Staphylococcus aureus, and mixed etiologies had the highest mortality rates in those affected.[20]

Complications

The most common bacterial pneumonia complications are respiratory failure, sepsis, multiorgan failure, coagulopathy, and exacerbation of preexisting comorbidities. Other potential complications of bacterial pneumonia include:

• Lung fibrosis

• Destruction of lung parenchyma

• Necrotizing pneumonia

• Cavitation

• Empyema

• Pulmonary abscess

• Meningitis

• Death

Deterrence and Patient Education

Patients should be counseled to quit smoking, abstain from alcohol intoxication, and maintain dental hygiene. Furthermore, to prevent bacterial pneumonia, recommendations include:

• Vaccination against pneumococcus

• The annual vaccine against influenza

• Elderly and immunocompromised patients should be instructed to seek medical assistance as soon as they develop symptoms such as dyspnea, rigors, or fever.

Pearls and Other Issues

1. Most patients respond with improvement within 48 to 72 hours.

2. The chest X-ray findings lag behind clinical features and may take 6 to 12 weeks to clear.

3. If patients fail to improve within 72 hours, another cause should be suspected, antibiotic resistance or development of complications 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 administering 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 teach about antibiotic compliance and 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.[19][21] [Level 5] Only with open communication between the interprofessional team can the morbidity of pneumonia be lowered.

Outcomes

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 leads to residual impairment in lung function. Other reported complications of pneumonia that occur in 1 to 5% of patients include lung abscess, empyema, and bronchiectasis.[22][23] [Level 5]

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

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Leung AK, Hon KL, Leong KF, Sergi CM. Measles: a disease often forgotten but not gone. Hong Kong Med J. 2018 Oct;24(5):512-520. [PubMed: 30245481]

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Grief SN, Loza JK. Guidelines for the Evaluation and Treatment of Pneumonia. Prim Care. 2018 Sep;45(3):485-503. [PMC free article: PMC7112285] [PubMed: 30115336]

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Ashurst JV, Dawson A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jan 30, 2023. Klebsiella Pneumonia. [PubMed: 30085546]

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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 Med J. 2018 Sep;39(9):878-885. [PMC free article: PMC6201010] [PubMed: 30251730]

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Mizgerd JP. Acute lower respiratory tract infection. N Engl J Med. 2008 Feb 14;358(7):716-27. [PMC free article: PMC2711392] [PubMed: 18272895]

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Kung HC, Hoyert DL, Xu J, Murphy SL. Deaths: final data for 2005. Natl Vital Stat Rep. 2008 Apr 24;56(10):1-120. [PubMed: 18512336]

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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 J Pediatr. 2018 Sep;61(9):291-300. [PMC free article: PMC6172518] [PubMed: 30274507]

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Lat I, Daley MJ, Shewale A, Pangrazzi MH, Hammond D, Olsen KM., DEFINE study group and the Discovery Research Network. A Multicenter, Prospective, Observational Study to Determine Predictive Factors for Multidrug-Resistant Pneumonia in Critically Ill Adults: The DEFINE Study. Pharmacotherapy. 2019 Mar;39(3):253-260. [PubMed: 30101412]

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Søndergaard MJ, Friis MB, Hansen DS, Jørgensen IM. Clinical manifestations in infants and children with Mycoplasma pneumoniae infection. PLoS One. 2018;13(4):e0195288. [PMC free article: PMC5919654] [PubMed: 29698412]

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Karakuzu Z, Iscimen R, Akalin H, Kelebek Girgin N, Kahveci F, Sinirtas M. Prognostic Risk Factors in Ventilator-Associated Pneumonia. Med Sci Monit. 2018 Mar 05;24:1321-1328. [PMC free article: PMC5848715] [PubMed: 29503436]

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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. Int J Med Microbiol. 2018 Mar;308(2):290-296. [PubMed: 29325882]

12.

van der Poll T, Opal SM. Pathogenesis, treatment, and prevention of pneumococcal pneumonia. Lancet. 2009 Oct 31;374(9700):1543-56. [PubMed: 19880020]

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Claudius I, Baraff LJ. Pediatric emergencies associated with fever. Emerg Med Clin North Am. 2010 Feb;28(1):67-84, vii-viii. [PubMed: 19945599]

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Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985 Oct;13(10):818-29. [PubMed: 3928249]

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Kang YA, Kwon SY, Yoon HI, Lee JH, Lee CT. Role of C-reactive protein and procalcitonin in differentiation of tuberculosis from bacterial community acquired pneumonia. Korean J Intern Med. 2009 Dec;24(4):337-42. [PMC free article: PMC2784977] [PubMed: 19949732]

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Franquet T. Imaging of Community-acquired Pneumonia. J Thorac Imaging. 2018 Sep;33(5):282-294. [PubMed: 30036297]

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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. J Glob Health. 2018 Dec;8(2):020806. [PMC free article: PMC6150611] [PubMed: 30254744]

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Hanretty AM, Gallagher JC. Shortened Courses of Antibiotics for Bacterial Infections: A Systematic Review of Randomized Controlled Trials. Pharmacotherapy. 2018 Jun;38(6):674-687. [PubMed: 29679383]

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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. , CAP group (community-acquired pneumonia) from the Infections in Emergencies – Sepsis Code working group. [Recommendations for the care of patients with community-acquired pneumonia in the Emergency Department]. Rev Esp Quimioter. 2018 Apr;31(2):186-202. [PMC free article: PMC6159381] [PubMed: 29619807]

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Cillóniz C, Ewig S, Polverino E, Marcos MA, Esquinas C, Gabarrús A, Mensa J, Torres A. Microbial aetiology of community-acquired pneumonia and its relation to severity. Thorax. 2011 Apr;66(4):340-6. [PubMed: 21257985]

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Coon ER, Maloney CG, Shen MW. Antibiotic and Diagnostic Discordance Between ED Physicians and Hospitalists for Pediatric Respiratory Illness. Hosp Pediatr. 2015 Mar;5(3):111-8. [PubMed: 25732983]

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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 Pulm Med. 2018 Aug 20;18(1):141. [PMC free article: PMC6102812] [PubMed: 30126392]

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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. J Int Med Res. 2018 Nov;46(11):4596-4604. [PMC free article: PMC6259400] [PubMed: 30027805]

Disclosure: Saud Bin Abdul Sattar declares no relevant financial relationships with ineligible companies.

Disclosure: Sandeep Sharma declares no relevant financial relationships with ineligible companies.

Bacterial Pneumonia – StatPearls – NCBI Bookshelf

Continuing Education Activity

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 lung parenchyma that is more often, but not always, caused by infections. The many causes of pneumonia include bacteria, viruses, fungi, and parasites. This activity reviews the cause, pathophysiology, presentation, and diagnosis of bacterial pneumonia and highlights the interprofessional team’s role in the management of these patients.

Objectives:

• Identify the etiology of bacterial pneumonia.

• Recall the X-ray findings in a patient with bacterial pneumonia.

• Outline the treatment and management options available for bacterial pneumonia.

• Employ interprofessional team strategies for improving care coordination and communication to advance the management of patients affected by bacterial pneumonia and improve outcomes.

Access free multiple choice questions on this topic.

Introduction

The word “pneumonia” takes its origin 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 lungs’ parenchyma that is more often, but not always, caused by infections. The many causes of pneumonia include bacteria, viruses, fungi, and parasites. This article will focus on bacterial pneumonia, as it is the major cause of morbidity and mortality. 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 or within 48 hours of the hospital admission.

• HAP: The acute infection of lung tissue in a non-intubated patient that develops after 48 hours of hospitalization.

• 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 centers, outpatient clinics, or a patient with a history of hospitalization within the past three months.

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

Etiology

Community-acquired pneumonia can be caused by an extensive list of agents that include bacteria, viruses, fungi, and parasites, but this article will focus on bacterial pneumonia and its causes. Bacteria have classically been categorized into two divisions based on 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, Staphylococcus aureus, Group A streptococci, Moraxella catarrhalis, anaerobes, and aerobic gram-negative bacteria.

• Atypical pneumonia is mostly caused by Legionella, Mycoplasma pneumoniae, Chlamydia pneumoniae, and Chlamydia psittaci.

The most common cause 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. 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

In the United States, lower respiratory tract infections account for more morbidity and mortality than any other infection. [5] 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 a mortality rate of less than 1%, and 20% are treated as inpatients with a 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 in females and other Americans. However, the total number of deaths has been on the rise among females.[6] The incidence rates are higher at extremes of age; 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 were the eighth most common cause of death in the United States and the seventh most common cause of death in Canada. The mortality rate is variable among different regions, such as 7.3% for the United States and Canada, 9.1% for Europe, and 13.3% for Latin America.[7][8]

Pathophysiology

The lower respiratory tract is not sterile, and it always is exposed to environmental pathogens. Invasion and propagation of the above-mentioned bacteria into lung parenchyma at the alveolar level causes bacterial pneumonia. The body’s inflammatory response against it causes the clinical syndrome of pneumonia.

To prevent this proliferation of microorganisms, several host defenses work together in the 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 proliferating. In this setting, the alveolar macrophages kickoff the inflammatory response to strengthen the lower respiratory tract defenses. This inflammatory response is the main reason for the clinical manifestation of bacterial pneumonia. Cytokines are released in response to the inflammatory reaction and cause constitutional symptoms; for example, IL-1 (interleukin-1) and TNF (tumor necrosis factor) cause fever. Chemokine-like IL-8 (interleukin-8) and colony-stimulating factors like G-CSF (granulocyte colony-stimulating factor) promote chemotaxis and neutrophil 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.[9][10][11]

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: In this stage, the lobe becomes consolidated, firm, and liver-like. Microscopically, there are fibrin, 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 exudate-filled alveoli.

4. Resolution: After a week, it starts resolving as lymphatic drainage or a productive cough clears the exudate.

History and Physical

While taking the history, it is crucial to explore the patient’s potential exposures, risks of aspiration, host factors, and presenting symptoms.

Exposure: A detailed history of possible exposures should be sought as it can help in establishing the potential etiologies. The following are some associations of exposures and etiologies of bacterial pneumonia:

• Contaminated air-conditioning and water systems may cause Legionella pneumonia.

• Crowded places, such as jails, shelters, etc., expose a person to Streptococcus pneumonia, Mycobacteria, Mycoplasma, and Chlamydia.

• Exposures to several animals, such as cats, sheep, and cattle, may lead to infection with Coxiella burnetii

• Some birds, such as chickens, turkeys, and ducks, can expose a person to Chlamydia psittaci.

Risks of Aspiration: Patients with an increased risk of aspiration are more prone to develop pneumonia secondary to aspiration. Associated risks are:

Host mechanisms: It is of utmost importance to explore a detailed history to find clues towards the etiology of pneumonia. For instance, a history of asthma, COPD, smoking, and immunocompromised status can be indicative of H. influenzae infection. H influenza most commonly appears in the winter season. Similarly, social, sexual, medication, and family history can all be useful in determining the cause of illness.

Features in the history 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 significant 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.

For unbeknownst reasons, the presence of rigors is more often indicative of pneumococcal pneumonia than other bacterial pathogens.[12]

The presence of a productive cough is the most common and significant presenting symptom. Some bacterial causes have particular manifestations, such as:

• S. pneumoniae – Rust-colored sputum

• Pseudomonas, Hemophilus – Green sputum

• Klebsiella – Red currant-jelly sputum

• Anaerobes – foul-smelling and bad-tasting sputum

Atypical pneumonia presents with pulmonary and extra-pulmonary manifestations, such as Legionella pneumonia, which often presents with altered mentation and gastrointestinal symptoms.

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

• Increased temperature (usually more than 38 C or 100.4 F)[13]

• Decreased temperature (less than 35 C or 95 F)

• Increased respiratory rate (more than 18 breaths/min)

• Increased heart rate (more than 100/min)

• Bradycardia (less than 60/min)

• Cyanosis

• Percussion sounds vary from flat to dull.

• Tactile fremitus

• Crackles, rales, and bronchial breath sounds are heard during auscultation.

• Tracheal deviation

• Lymphadenopathy

• Pleural rub

• Egophony

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

Some examination findings are specific for certain etiologies, such as:

• Bradycardia – Legionella

• Dental illnesses – Anaerobes

• Impaired gag reflex – Aspiration pneumonia

• Cutaneous nodules – Nocardiosis

• Bullous myringitis – Mycoplasma

Evaluation

The approach to evaluate and diagnose pneumonia depends on the clinical status, laboratory parameters, and radiological evaluation. [14]

• 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.[15]

  • Blood cultures should be obtained before administering antibiotics. Unfortunately, they are only positive in 40% of cases.

  • If good quality, sputum evaluation may reveal more than 25 WBC per low-power field and less than 10 squamous epithelial cells.

  • Some bacterial causes present with specific biochemical evidence, such as Legionella, may present with hyponatremia and microhematuria.

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 the risk for bacterial pneumonia, especially CAP.[17][18][19]

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 of these risk factors. For a score of 0-1, outpatient treatment is advised. If the total score is 2 or more, it indicates medical ward admission. If the total score is 3 or more, 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, macrolide or doxycycline can be used 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, therapy should be altered according to the culture-specific pathogen.

The patient also can benefit from smoking cessation, counseling, and vaccination for influenza and pneumococcus.

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

Distinguishing pneumonia from other pulmonary diseases can be a daunting task, particularly in patients with co-existing pulmonary pathology. The differential diagnoses are different for children and adults, as mentioned below:

Differential Diagnosis in Children

• Asthma or reactive airway disease

• Bronchiolitis

• Croup

• Respiratory distress syndrome

• Epiglottitis

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 infection

Prognosis

The prognosis of pneumonia depends on many factors, including age, comorbidities, and hospital setting (inpatient or outpatient). Generally, the prognosis is promising in otherwise healthy patients. Patients older than 60 years or younger than 4 years of age have a relatively poorer prognosis than young adults. If pneumonia is left untreated, the overall mortality may become 30%. Antibiotic resistance is very concerning due to the excessive and unjustified use of antibiotics. The Pneumonia Severity Index (PSI) may be utilized as a tool to establish a patient’s risk of mortality.

In a study conducted on etiologies of CAP, S. pneumoniae was found to be the cause of mortality in most patients; however, Pseudomonas, Staphylococcus aureus, and mixed etiologies had the highest mortality rates in those affected.[20]

Complications

The most common bacterial pneumonia complications are respiratory failure, sepsis, multiorgan failure, coagulopathy, and exacerbation of preexisting comorbidities. Other potential complications of bacterial pneumonia include:

• Lung fibrosis

• Destruction of lung parenchyma

• Necrotizing pneumonia

• Cavitation

• Empyema

• Pulmonary abscess

• Meningitis

• Death

Deterrence and Patient Education

Patients should be counseled to quit smoking, abstain from alcohol intoxication, and maintain dental hygiene. Furthermore, to prevent bacterial pneumonia, recommendations include:

• Vaccination against pneumococcus

• The annual vaccine against influenza

• Elderly and immunocompromised patients should be instructed to seek medical assistance as soon as they develop symptoms such as dyspnea, rigors, or fever.

Pearls and Other Issues

1. Most patients respond with improvement within 48 to 72 hours.

2. The chest X-ray findings lag behind clinical features and may take 6 to 12 weeks to clear.

3. If patients fail to improve within 72 hours, another cause should be suspected, antibiotic resistance or development of complications 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 administering 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 teach about antibiotic compliance and 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.[19][21] [Level 5] Only with open communication between the interprofessional team can the morbidity of pneumonia be lowered.

Outcomes

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 leads to residual impairment in lung function. Other reported complications of pneumonia that occur in 1 to 5% of patients include lung abscess, empyema, and bronchiectasis.[22][23] [Level 5]

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

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Leung AK, Hon KL, Leong KF, Sergi CM. Measles: a disease often forgotten but not gone. Hong Kong Med J. 2018 Oct;24(5):512-520. [PubMed: 30245481]

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Ashurst JV, Dawson A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jan 30, 2023. Klebsiella Pneumonia. [PubMed: 30085546]

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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 Med J. 2018 Sep;39(9):878-885. [PMC free article: PMC6201010] [PubMed: 30251730]

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Mizgerd JP. Acute lower respiratory tract infection. N Engl J Med. 2008 Feb 14;358(7):716-27. [PMC free article: PMC2711392] [PubMed: 18272895]

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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 J Pediatr. 2018 Sep;61(9):291-300. [PMC free article: PMC6172518] [PubMed: 30274507]

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Lat I, Daley MJ, Shewale A, Pangrazzi MH, Hammond D, Olsen KM., DEFINE study group and the Discovery Research Network. A Multicenter, Prospective, Observational Study to Determine Predictive Factors for Multidrug-Resistant Pneumonia in Critically Ill Adults: The DEFINE Study. Pharmacotherapy. 2019 Mar;39(3):253-260. [PubMed: 30101412]

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Søndergaard MJ, Friis MB, Hansen DS, Jørgensen IM. Clinical manifestations in infants and children with Mycoplasma pneumoniae infection. PLoS One. 2018;13(4):e0195288. [PMC free article: PMC5919654] [PubMed: 29698412]

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Karakuzu Z, Iscimen R, Akalin H, Kelebek Girgin N, Kahveci F, Sinirtas M. Prognostic Risk Factors in Ventilator-Associated Pneumonia. Med Sci Monit. 2018 Mar 05;24:1321-1328. [PMC free article: PMC5848715] [PubMed: 29503436]

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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. Int J Med Microbiol. 2018 Mar;308(2):290-296. [PubMed: 29325882]

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van der Poll T, Opal SM. Pathogenesis, treatment, and prevention of pneumococcal pneumonia. Lancet. 2009 Oct 31;374(9700):1543-56. [PubMed: 19880020]

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Claudius I, Baraff LJ. Pediatric emergencies associated with fever. Emerg Med Clin North Am. 2010 Feb;28(1):67-84, vii-viii. [PubMed: 19945599]

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Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985 Oct;13(10):818-29. [PubMed: 3928249]

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Kang YA, Kwon SY, Yoon HI, Lee JH, Lee CT. Role of C-reactive protein and procalcitonin in differentiation of tuberculosis from bacterial community acquired pneumonia. Korean J Intern Med. 2009 Dec;24(4):337-42. [PMC free article: PMC2784977] [PubMed: 19949732]

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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. J Glob Health. 2018 Dec;8(2):020806. [PMC free article: PMC6150611] [PubMed: 30254744]

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Hanretty AM, Gallagher JC. Shortened Courses of Antibiotics for Bacterial Infections: A Systematic Review of Randomized Controlled Trials. Pharmacotherapy. 2018 Jun;38(6):674-687. [PubMed: 29679383]

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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. , CAP group (community-acquired pneumonia) from the Infections in Emergencies – Sepsis Code working group. [Recommendations for the care of patients with community-acquired pneumonia in the Emergency Department]. Rev Esp Quimioter. 2018 Apr;31(2):186-202. [PMC free article: PMC6159381] [PubMed: 29619807]

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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 Pulm Med. 2018 Aug 20;18(1):141. [PMC free article: PMC6102812] [PubMed: 30126392]

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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. J Int Med Res. 2018 Nov;46(11):4596-4604. [PMC free article: PMC6259400] [PubMed: 30027805]

Disclosure: Saud Bin Abdul Sattar declares no relevant financial relationships with ineligible companies.

Disclosure: Sandeep Sharma declares no relevant financial relationships with ineligible companies.

Pneumonia | MyPathologyReport.ca

Katerina Baranova, MD, and Matthew J. Cecchini, MD, FRCPC
May 26, 2022

What is pneumonia?

Pneumonia is an infection of the lungs caused by microorganisms such as viruses, bacteria, or fungi. Most cases of pneumonia begin when infectious particles that are inhaled through the nose and mouth enter the airways into the lungs. Pneumonia can affect one or both lungs at the same time. The disease can affect only part of the affected lung or the whole.

What are the symptoms of pneumonia?

The most common symptoms of pneumonia include cough, fever, chills, mucus, and difficulty breathing. Other less common symptoms include confusion, chest pain, blue lips and nails, and loss of appetite. Pneumonia, like other infections, is worse in older people and people with weakened immune systems.

What are the types of pneumonia?

There are many types of pneumonia, but most are caused by bacteria or viruses. Less common types are caused by a fungus. The most common types of pneumonia will be explained in the following sections.

Bacterial pneumonia

This type of pneumonia starts when bacteria enter the lungs and alveoli, usually from the nose or mouth. Bacteria can also enter the lungs from other parts of the body through the blood. Bacteria in the alveoli will grow in the air space until they are detected by the body’s immune system, which tries to remove the bacteria from the body. To help with this process, the small capillaries surrounding the alveoli open up, increasing blood flow to the lungs. This allows more inflammatory cells including neutrophils to reach the lungs. Pathologists describe this process as acute inflammation. The green or yellow sputum produced when a person with pneumonia coughs is made up of millions of neutrophils and remnants of damaged tissue and dead bacteria. This is a sign that there is active inflammation in the lungs.

Although neutrophils are essential for killing and removing bacteria in the lungs, they can also damage the pneumocytes that line the alveoli. The combination of damaged pneumocytes with extra blood flow can lead to air spaces filling with fluid. This process is called edema. Because the fluid prevents air from entering the alveoli, a person with pneumonia may have difficulty breathing. When an x-ray or CT scan is performed, areas of the lung with infection and swelling are described as showing “consolidation”.

Once your immune system has the infection under control, specialized immune cells called macrophages will move in to clear out dead bacteria and damaged tissue. At the same time, the edematous fluid will organize itself in the air spaces and become firmer. These areas of the lung will appear gray or white on an X-ray or CT scan.

Bacterial pneumonia can be divided into lobar and bronchopneumonia. In lobar pneumonia, the bacteria have spread to cover most of a lobe of one lung. In bronchopneumonia, bacteria spread through small air spaces, affecting parts of more than one lobe of the lung. Because of this, the areas of the lung affected by bronchopneumonia are usually located near the airways.

Types of bacteria that commonly cause pneumonia include:

• Streptococcus
• Staphylococcus
• Klebsiella
• Pseudomonas
• Legionella
• Mycoplasma

Viral pneumonia

This type of pneumonia starts when viral particles enter the body, usually through the nose or mouth. The virus enters the lungs, where it infects pneumocytes or other cells in the alveoli and airways.

Viruses use specialized proteins found on their surface to attach to other proteins on the surface of lung cells. For example, SARS-CoV-2, the virus that causes Covid-19. uses a protein on its surface to attach to an angiotensin-converting enzyme 2 (ACE2) protein on lung cells. Once a virus attaches to a cell, it enters the inside of the cell, where it uses the cell’s machinery to make new copies of the virus.

Pneumocytes infected with the virus may become damaged and die. The body responds to this injury by replacing thin type 1 pneumocytes with thicker, stronger type 2 pneumocytes. Damaged pneumocytes also release signals that tell specialized virus-fighting immune cells called lymphocytes to come to the lungs. As with bacterial pneumonia, fluid fills the air spaces, making it difficult for a person with pneumonia to breathe.

Pathologists use the term hyaline membranes to describe the thick pink bands of tissue on the inner surface of the alveoli. These hyaline membranes are often found in association with type 2 pneumocytes and fluid filling the air spaces and alveolar walls. People with pneumonia have difficulty breathing because the thickened alveolar walls make it difficult for oxygen to be exchanged between the lungs and the blood. Viral pneumonia-related changes will also appear more gray or white on an x-ray or CT scan because the alveoli have less air than usual in these areas.

Types of viruses that commonly cause pneumonia include:

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
• Influenza
• parainfluenza
• measles
• respiratory syncytial virus
• Cytomegaly virus
• adenovirus
• Herpes simplex virus
• Varicella zoster virus

How do pathologists diagnose pneumonia?

A pathologist can make a diagnosis of pneumonia by examining a sample of lung tissue under a microscope. A procedure in which only a small sample of tissue is removed is called a biopsy. The amount of tissue sent for microscopic examination will depend on the type of biopsy performed.

Common types of biopsy include:

• Transbronchial biopsy : A small sample of tissue is removed using forceps that are inserted through the bronchial wall into the lung.
• Cryobiopsy : A larger tissue sample is obtained by freezing a small area of ​​the lung with a tube and removing the frozen tissue from the body.
• Endobronchial biopsy : Several small tissue samples are removed using forceps to obtain tissue from inside the airways or airway walls.
• Wedge biopsy : A large piece of lung is removed by the surgeon in the operating room.

Most of the changes associated with pneumonia can be seen when tissue is stained with a combination of dyes called hematoxylin and eosin (H&E). However, to determine the type of pneumonia, your pathologist may order special stains such as Gram, Grocott (GMS), and PAS stains. Another type of test called immunohistochemistry can be ordered to look for specific types of viruses. However, the exact cause can only be determined after a tissue sample is sent to a microbiology laboratory, which has special tools to detect viruses, bacteria, and fungi.

Other Helpful Resources

Centers for Disease Control and Prevention

World Health Organization

Radiopedia – Pneumonia

Bacterial Pneumonia

Pneumonia (pneumonia) is an infectious disease that affects the lung tissue (alveoli). Fungi, viruses and bacteria can cause pathology. Bacterial pneumonia should be treated under medical supervision. The “Health Clinic” employs experienced specialists, has the most modern diagnostic base (ultrasound, CT, MRI), and the patient can undergo all the necessary diagnostics and get a doctor’s consultation without leaving the clinic.

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What is bacterial pneumonia?

Bacterial pneumonia is a lung disease caused by bacteria that enter the respiratory system. The inflammatory process develops when very aggressive bacteria get inside, which can resist the resistance of the body.

Species

The classification of bacterial pneumonia is based on the types of pathogen:

• pneumococcal;
• streptococcal;
• staphylococcal;
• meningococcal;
• pneumonia caused by Haemophilus influenzae, Legionella, Pseudomonas aeruginosa and so on.

According to the course and clinic, bacterial pneumonia is divided into:

• focal (bronchopneumonia) – inflammation affects some areas of the lungs and adjacent bronchi;
• lobar (croupous) – the entire lung lobe will be included in the inflammatory process. In most cases, the lower parts of the lung are affected.

Pneumonia can be:

• one-sided;
• double-sided;
• if the pleural cavity is affected, they speak of pleuropneumonia.

According to pathogenetics, bacterial pneumonia can be:

• out-of-hospital;
• hospital – the infection develops 2-3 days after the patient’s admission to the hospital.

The course of bacterial pneumonia can be:

• light;
• medium;
• severe course.

You can learn more about the disease and its treatment by calling the clinic: +7 (495) 628-22-05

Causes

The bacteria that cause pneumonia are part of the respiratory tract, that is, it is an opportunistic microflora. When the immune system is working well, these bacteria do not harm the body in any way. With a weakened immune system, they become dangerous.

Risk factors:

• influenza, SARS;
• smoking and other bad habits;
• beriberi;
• overwork and stress;
• over 70 years of age;
• unfavorable ecological situation;
• COPD;
• diabetes;
• sinusitis;
• cardiac pathologies.

Symptoms and signs

Typical manifestations of bacterial pneumonia are:

• increased body temperature;
• sweating, chills;
• cough with copious greenish sputum;
• pain in sternum, especially on deep breathing;
• weakness, headache, myalgia;
• pallor;
• low blood pressure, rapid pulse;
• shortness of breath, rapid breathing, wheezing.

Diagnostics

The doctor examines the patient, learns about the symptoms, and then prescribes laboratory tests of blood, urine, sputum.

Of the instrumental diagnostic procedures use:

• radiography;
• CT;
• MRI.

All procedures can be performed in our clinic, which is equipped with the latest generation of diagnostic equipment.

In order to make an appointment with a doctor or any type of diagnostics, choose the method convenient for you:

– Call the clinic: +7 (495) 628-22-05,
– Request a call back,
– Write or call via online chat, in the right corner of the page,
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Which doctor treats?

Bacterial pneumonia is treated by a pulmonologist or therapist. The Health Clinic is attended by specialists who will help develop the right treatment.

Methods of treatment

With a mild form of the course of the disease, treatment is carried out at home under the supervision of a doctor, severe forms are a reason for the patient to be hospitalized.

The patient is shown bed rest, plenty of fluids, the main treatment is antibiotics. Only a doctor can select a drug, based on the results of the tests. As a rule, penicillins, macrolides or cephalosporins are prescribed. These are broad spectrum antibiotics. In some cases, the doctor selects narrowly targeted drugs. Medicines are taken orally or intramuscularly. In severe cases, intravenous injections are indicated.

As an addition appoint:

• antipyretics;
• vitamins;
• expectorants;
• short courses of hormone therapy;
• oxygen therapy.

Results

With timely and competent treatment, the prognosis is favorable.

Rehabilitation and lifestyle restoration

After the patient’s condition begins to improve, the doctor adds:

• massage;
• physiotherapy;
• LFK;
• breathing exercises;
• recommends sanatorium rehabilitation.

Bacterial pneumonia lifestyle

The recommended lifestyle for bacterial pneumonia is as follows:

• healthy eating;
• a sufficient amount of protein food;
• adequate drinking regimen;
• inclusion of vegetables and fruits in the diet;
• introduction to the diet of fatty acids Omega-3 – found in fatty fish, nuts, vegetable oils;
• exclusion of smoking and alcohol.

As a preventive measure, it is recommended to strengthen the immune system and maintain a healthy lifestyle. Without treatment, bacterial pneumonia can lead to dangerous complications – chronic bronchitis, bronchial asthma, pulmonary infarction, pleurisy, pyopneumothorax, respiratory failure.

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