Most common bacterial pneumonia: Bacterial Pneumonia – StatPearls – NCBI Bookshelf

27.12.197904.12.2021 by alexxlab

Содержание

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 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 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 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 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 the 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 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.[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:

Congestion: In this stage, pulmonary parenchyma is not fully consolidated, and microscopically, the alveoli have serous exudates, pathogens, few neutrophils, and macrophages.
Red hepatization: In this stage, the lobe becomes consolidated, firm, and liver-like. Microscopically, there is fibrin and serous exudate, pathogens, neutrophils, and macrophages. The capillaries are congested, and the alveolar walls are thickened.
Gray hepatization: The lobe is still liver-like in consistency but gray in color due to suppurative and exudate-filled alveoli.
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 productive cough is the most common and significant presenting symptom. Some bacterial causes have particular manifestation, 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 on 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.

Radiological Evaluation: It includes a 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.[16][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 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 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

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

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

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:

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:

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

Most patients respond with improvement within 48 to 72 hours.
The chest X-ray findings lag behind clinical features and may take 6 to 12 weeks to clear.
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 lead 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]

References

1.: 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]
2.: 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]
3.: Ashurst JV, Dawson A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Feb 5, 2021. Klebsiella Pneumonia. [PubMed: 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 Med J. 2018 Sep;39(9):878-885. [PMC free article: PMC6201010] [PubMed: 30251730]
5.: Mizgerd JP. Acute lower respiratory tract infection. N Engl J Med. 2008 Feb 14;358(7):716-27. [PMC free article: PMC2711392] [PubMed: 18272895]
6.: 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]
7.: 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]
8.: 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]
9.: 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]
10.: 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]
11.: 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]
13.: Claudius I, Baraff LJ. Pediatric emergencies associated with fever. Emerg Med Clin North Am. 2010 Feb;28(1):67-84, vii-viii. [PubMed: 19945599]
14.: 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]
15.: 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]
16.: Franquet T. Imaging of Community-acquired Pneumonia. J Thorac Imaging. 2018 Sep;33(5):282-294. [PubMed: 30036297]
17.: 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]
18.: 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]
19.: 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]
20.: 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]
21.: 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]
22.: 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]
23.: 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]

Bacterial Pneumonia – StatPearls – NCBI Bookshelf

Continuing Education Activity

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

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

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.

Epidemiology

Pathophysiology

Histopathology

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

Congestion: In this stage, pulmonary parenchyma is not fully consolidated, and microscopically, the alveoli have serous exudates, pathogens, few neutrophils, and macrophages.
Red hepatization: In this stage, the lobe becomes consolidated, firm, and liver-like. Microscopically, there is fibrin and serous exudate, pathogens, neutrophils, and macrophages. The capillaries are congested, and the alveolar walls are thickened.
Gray hepatization: The lobe is still liver-like in consistency but gray in color due to suppurative and exudate-filled alveoli.
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.

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:

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 productive cough is the most common and significant presenting symptom. Some bacterial causes have particular manifestation, 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.

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 on 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.

Radiological Evaluation: It includes a 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.[16][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

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 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

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

Complications

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:

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

Most patients respond with improvement within 48 to 72 hours.
The chest X-ray findings lag behind clinical features and may take 6 to 12 weeks to clear.
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.

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

Outcomes

References

1.: 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]
2.: 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]
3.: Ashurst JV, Dawson A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Feb 5, 2021. Klebsiella Pneumonia. [PubMed: 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 Med J. 2018 Sep;39(9):878-885. [PMC free article: PMC6201010] [PubMed: 30251730]
5.: Mizgerd JP. Acute lower respiratory tract infection. N Engl J Med. 2008 Feb 14;358(7):716-27. [PMC free article: PMC2711392] [PubMed: 18272895]
6.: 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]
7.: 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]
8.: 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]
9.: 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]
10.: 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]
11.: 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]
13.: Claudius I, Baraff LJ. Pediatric emergencies associated with fever. Emerg Med Clin North Am. 2010 Feb;28(1):67-84, vii-viii. [PubMed: 19945599]
14.: 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]
15.: 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]
16.: Franquet T. Imaging of Community-acquired Pneumonia. J Thorac Imaging. 2018 Sep;33(5):282-294. [PubMed: 30036297]
17.: 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]
18.: 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]
19.: 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]
20.: 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]
21.: 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]
22.: 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]
23.: 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]

Bacterial Pneumonia – StatPearls – NCBI Bookshelf

Continuing Education Activity

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

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

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.

Epidemiology

Pathophysiology

Histopathology

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

Congestion: In this stage, pulmonary parenchyma is not fully consolidated, and microscopically, the alveoli have serous exudates, pathogens, few neutrophils, and macrophages.
Red hepatization: In this stage, the lobe becomes consolidated, firm, and liver-like. Microscopically, there is fibrin and serous exudate, pathogens, neutrophils, and macrophages. The capillaries are congested, and the alveolar walls are thickened.
Gray hepatization: The lobe is still liver-like in consistency but gray in color due to suppurative and exudate-filled alveoli.
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.

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:

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 productive cough is the most common and significant presenting symptom. Some bacterial causes have particular manifestation, 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.

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 on 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.

Radiological Evaluation: It includes a 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.[16][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

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 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

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

Complications

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:

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

Most patients respond with improvement within 48 to 72 hours.
The chest X-ray findings lag behind clinical features and may take 6 to 12 weeks to clear.
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.

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

Outcomes

References

1.: 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]
2.: 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]
3.: Ashurst JV, Dawson A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Feb 5, 2021. Klebsiella Pneumonia. [PubMed: 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 Med J. 2018 Sep;39(9):878-885. [PMC free article: PMC6201010] [PubMed: 30251730]
5.: Mizgerd JP. Acute lower respiratory tract infection. N Engl J Med. 2008 Feb 14;358(7):716-27. [PMC free article: PMC2711392] [PubMed: 18272895]
6.: 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]
7.: 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]
8.: 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]
9.: 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]
10.: 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]
11.: 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]
13.: Claudius I, Baraff LJ. Pediatric emergencies associated with fever. Emerg Med Clin North Am. 2010 Feb;28(1):67-84, vii-viii. [PubMed: 19945599]
14.: 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]
15.: 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]
16.: Franquet T. Imaging of Community-acquired Pneumonia. J Thorac Imaging. 2018 Sep;33(5):282-294. [PubMed: 30036297]
17.: 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]
18.: 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]
19.: 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]
20.: 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]
21.: 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]
22.: 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]
23.: 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]

Typical Bacterial Pneumonia – StatPearls

Continuing Education Activity

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States. Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.” HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months. This activity reviews the evaluation and management of typical community-acquired pneumonia and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes.

Objectives:

Explain the causes of
typical community-acquired pneumonia.
Describe the evaluation of a patient with typical community-acquired pneumonia.
Summarize the treatment options for typical community-acquired pneumonia.
Explore modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by typical community-acquired pneumonia.

Access free multiple choice questions on this topic.

Introduction

Pneumonia can be classified into 2 types based on how the infection is acquired:

Community-acquired pneumonia (CAP): Most common type
Nosocomial pneumonia

Hospital-acquired pneumonia (HAP)
Ventilator-associated pneumonia (VAP)
Healthcare-associated pneumonia (HCAP)

Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.”

HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months.

Etiology

Pneumonia occurs secondary to airborne infection which includes bacteria, virus, fungi, parasites, among others.

The typical bacteria which cause pneumonia are Streptococcus pneumoniae, Staphylococcus aureus, Group A Streptococcus, Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, anaerobes, and gram-negative organisms. These organisms can be easily cultured on standard media or seen on Gram stain, unlike atypical organisms.

Streptococcus pneumoniae is the most commonly identified bacterial cause of CAP in all age groups worldwide. Methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, and other Enterobacteriaceae are the predominant causes of HAP, VAP, and HCAP.

Although it is not necessary to have a predisposing condition to acquire pneumonia, having such factors makes a person more likely to develop the lung infection. Any condition or disease that impairs the host immune response, for example, older age (older than 65 years), immunosuppression, diabetes, cystic fibrosis, lung cancer, among others. Conditions which increase the risk of macro- or micro-aspiration include stroke, seizures, anesthesia, drug intoxication. Cigarette smoking, alcoholism, malnutrition, obstruction of bronchi from tumors are other common predisposing conditions.

Epidemiology

The overall rate of CAP is 5-7 per 1000 persons per year. The rate of CAP is higher in males and increases with increasing age. It is more commonly seen in winter months. The combination of Pneumonia and Influenza causes high mortality and was the eighth most common cause of death in the US and the seventh most common cause of death in Canada in 2005.

Pathophysiology

The pulmonary system and the airways are continuously exposed to particulate matter and environmental pathogens. The healthy airways normally contain some bacterial species and are not sterile. The most common mechanism through which the micro-organisms or pathogens reach the lung is known as micro-aspiration. Hematogenous spread and macro-aspiration are other mechanisms.

However, the pulmonary defense mechanisms such as cough reflex, mucociliary clearance system, immune response help maintain low levels of the microbiome. CAP occurs when there is a defect in normal host defense, or a virulent pathogen overwhelms the immune response or a large infectious microbial inoculum. The invasion and propagation of these virulent strains of bacteria in the lung parenchyma following micro-aspiration cause the host immune response to kick in leading to a cascade of inflammatory response causing pneumonia.

Alveolar macrophage is the predominant immune cell which responds to lower airway bacteria. However, a stronger immune response comes into play when an overwhelming virulent pathogen or a large inoculum causes these alveolar macrophages to recruit polymorphonuclear neutrophils(PMN) to phagocytose and engulf these bacteria. The alveolar macrophages release cytokines namely, tumor necrosis factor-alpha and interleukins. Interleukin-8 and granulocyte colony-stimulating factor promotes neutrophil chemotaxis and maturation. The leakage of the alveolar-capillary membrane due to cytokines can lead to a decrease in compliance and hence, dyspnea. Cytokines such as IL-1 and TNF can lead to constitutional symptoms such as fever. Bacterial pneumonia is a result of this inflammatory response. These cytokines are essential for the immunity but, the excess can lead to sepsis and multiorgan failure. The body tries to balance the deleterious effects of cytokines by attenuation of several inflammatory mechanisms by IL-10.

Microbial virulence factors and predisposing host conditions make a person more vulnerable to pneumonia.[3]

Histopathology

Based on the area of the lung involved, pneumonia can be classified histologically into lobular, lobar, bronchopneumonia, and interstitial. The major types of acute bacterial pneumonia include:

Bronchopneumonia: A descending infection started around bronchi and bronchioles, which then spreads locally into the lungs. Lower lobes are usually involved. Patchy areas of consolidation which represents neutrophil collection in the alveoli and bronchi.
Lobar pneumonia: Acute exudative inflammation of the entire lobe. Uniform consolidation with a complete or near complete consolidation of a lobe of a lung. Majority of these cases are caused by Streptococcus pneumoniae.

Lobar pneumonia has 4 classical stages of inflammatory response if left untreated, namely:

Congestion/consolidation in the first 24 hours in which the lungs are heavy, red, and, boggy. Microscopically characterized by vascular engorgement and intra-alveolar edema. Many bacteria and few neutrophils are present.
Red hepatization/early consolidation begins 2 to 3 days after consolidation and lasts for 2 to 4 days and named because of firm liver-like consistency. The affected lung is red-pink, dry, granular and, airless. Fibrin strands replace the edema fluid of the previous phase. Microscopically marked cellular exudate of neutrophils with some showing ingested bacteria, extravasation of erythrocytes, desquamated epithelial cells, and fibrin within the alveoli are seen. The alveolar septa become less prominent because of the exudate.
Grey hepatization/late consolidation occurs 2 to 3 days following red hepatization and lasts for 4 to 8 days. The lung appears gray with liver-like consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells, and hemosiderin. The macrophages begin to appear.
Resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally which liquefies the previous solid fibrinous content and eventually restores aeration. Macrophages are the predominant cells which contain engulfed neutrophils and debris.

Toxicokinetics

The most common cause of typical bacterial pneumonia worldwide is Pneumococcus. The polysaccharide capsule of Streptococcus pneumoniae inhibits the complement binding to the cell surface and hence, inhibits phagocytosis. Virulent pneumococcal proteins such as IgA1 protease, neuraminidase, pneumolysin, autolysin, and the surface protein A further help the organism to counteract the host immune response and allow it to cause infection in humans.

Genetic mutations causing an active efflux of drug and eventually resistance have led to an increase in drug-resistant Streptococcus Pneumoniae (DRSP) over the last few years.

Alteration in penicillin-binding protein has increased the penicillin resistance and an increased rate of penicillin-resistant S. pneumoniae. Penicillin resistance occurs due to failure to bind to the microbe cell wall.[1][2]

History and Physical

The signs and symptoms vary according to disease severity. The common symptoms of bacterial pneumonia include fever, cough, sputum production (may or may not be present). The color and quality of sputum provide the clue to microbiological etiology. Bacterial pneumonia mostly presents with mucopurulent sputum.

Pleuritic chest pain due to localized inflammation of pleura can be seen with any kind of pneumonia but, is more common with lobar pneumonia. Constitutional symptoms such as fatigue, headache, myalgia, and arthralgias can also be seen.

Severe pneumonia can lead to dyspnea and shortness of breath. In severe cases, confusion, sepsis, and multi-organ failure can also manifest.

Tachypnea, increased vocal fremitus, egophony (E to A changes), dullness to percussion are the major clinical signs depending on the degree of consolidation and presence/absence of pleural effusion. Chest auscultation reveals crackles, rales, bronchial breath sounds.

The respiratory rate closely correlates with the degree of oxygenation and, therefore essential in determining the severity. Hypoxia is seen in severe pneumonia, which leads to hyperventilation.

Evaluation

To start with the evaluation of any pneumonia, clinical suspicion based on careful patient history and physical exam should always be followed by chest radiography which is the most important initial test.

Chest x-ray not only shows the presence of the disease and demonstrates pulmonary infiltrate, but also provides the clue to the diagnosis whether its lobar, interstitial, unilateral or bilateral. Typical bacterial pneumonia is usually lobar pneumonia with para-pneumonic pleural effusions. However, a chest x-ray cannot reliably differentiate bacterial from a non-bacterial cause. When the labs and clinical features are positive, a positive chest radiograph is considered a gold standard for diagnosis of pneumonia. Although computed tomography (CT) is a more reliable and accurate test, its use is limited due to relatively high radiation exposure and high cost. It can sometimes be done with high clinical syndrome favoring pneumonia with a negative chest x-ray. In a hospitalized patient with high clinical suspicion and negative radiograph, empiric presumptive antibiotic treatment should be started followed by a repeat chest x-ray after 24 to 48 hours.

Complete blood count (CBC) with differentials, inflammatory biomarkers ESR and acute phase reactants are indicated to confirm the evidence of inflammation and assess severity. Leukocytosis with a leftward shift is a major blood test abnormality whereas leukopenia can occur and points towards poor prognosis.

Sputum Gram stain and culture should be done next if lobar pneumonia is suspected. The most specific diagnostic test for lobar pneumonia is sputum culture. It is very important to identify the cause for the proper treatment.

It is preferable to test for influenza during the winter months as the combination of influenza and pneumonia is fatal.

CURB-65 and pneumonia severity index help in the stratification of the patients and to determine if the patient needs hospitalization for treatment.

Routine diagnostic tests are optional for outpatients with pneumonia, but hospitalized patients should undergo sputum culture, blood culture, and/or urine antigen testing preferably before the institution of antibiotic therapy.

Thoracocentesis, bronchoscopy, pleural biopsy, or pleural fluid culture are invasive tests and are carried out very occasionally.

An open lung biopsy is the ultimate specific diagnostic test.[6]

Treatment / Management

The treatment depends on the severity of the disease. It is important to determine whether the patient needs to be treated inpatient or as an outpatient. CURB-65 pneumonia severity score or expanded CURB-65 can be used to stratify patients. One point for each factor which includes:

Confusion
Uremia (BUN greater than 20 mg/dL
Respiratory rate greater than 30 per minute
Hypotension (SBP less than 90 and DBP less than 60)
Age older than more than 65 years

Patients with comorbid conditions such as renal disease, liver disease, cancer, chronic lung disease usually do better with inpatient treatment with IV medications.

A CURB-65 score of greater than or equal to 2 is an indication for hospitalization. A score of greater than or equal to 4 is an indication for intensive care unit (ICU) admission and more intense therapy.

Depending on the clinical response, the therapy is indicated for 5 to 7 days. A favorable clinical response is the resolution of tachypnea, tachycardia, hypotension; absence of fever for more than 48 hours. In case of delayed response, the therapy should be extended.

Empiric therapy recommended for the following:

Outpatient/non-hospitalized patient management: Empiric therapy is almost always successful and usually testing is not required. In patients with no comorbidity, monotherapy with macrolides, such as azithromycin and clarithromycin are the first choice. Alternatively, newer fluoroquinolones like levofloxacin, moxifloxacin, or gemifloxacin can be used. The therapy is targeted against mycoplasma and chlamydia pneumoniae which are the common causes of less severe CAP. Patients with comorbid conditions (chronic lung or heart disease, diabetes, smoking, HIV, among others) do well with newer fluoroquinolones alone or with a combination of beta-lactam and a macrolide.
Inpatient non-ICU management: The recommended therapy includes newer fluoroquinolones alone or a combination of beta-lactam/second or third-generation cephalosporin and a macrolide.
Inpatient ICU management: The recommended therapy is a combination of macrolide/newer fluoroquinolone and a beta-lactam. Ampicillin-sulbactam or ertapenem can be used in patients with risk of aspiration. If there is a risk of Pseudomonas infection, a combination of anti-pseudomonal beta-lactam with anti-pseudomonal fluoroquinolone is indicated. For MRSA, vancomycin or linezolid should be added. In case of complications such as empyema, chest tube drainage is required. Surgical decortication is needed in case of multiple loculations.

All hospitalized patients who test positive for influenza virus must be treated with oseltamivir irrespective of the onset of illness.

Once the exact cause is determined, specific therapy should be initiated.[3][4][5]

Differential Diagnosis

Asthma or reactive airway disease
Viral Pneumonia
Pneumonia, Fungal
Pneumonia, Atypical bacterial
Lung Abscess
Bronchiectasis
Bronchiolitis
Asthma
Acute and Chronic Bronchitis
Atelectasis
Croup
Respiratory distress syndrome
Aspiration of a foreign body[6][7]

Complications

Pleural effusion
Empyema
Lung Abscess
Septicemia
Bacteremia

Enhancing Healthcare Team Outcomes

Pneumonia is a common infectious lung disease. It requires interprofessional care and the involvement of more than one subspecialty. This patient-centered approach involving a physician with a team of other health professionals, physiotherapists, respiratory therapists, nurses, pharmacists, and support groups working together for the patient plays an important role in improving the quality of care in pneumonia patients. It not only decreases the hospital admission rates but also positively affect the disease outcome. For healthy patients, the outcomes after treatment are excellent but in the elderly and those with comorbidities, the outcomes are guarded.

Figure

Lung Abscess, CT Scan, Computer Tomography, Thick-walled cavitary lesion in the right lung is an abscess, Diffuse ground glass infiltrates that are present in both lungs represent pneumonia. Contributed by Wikimedia Commons, Yale Rosen (CC by 2.0) https://creativecommons.org/licenses/by/2.0/ (more…)

Figure

Combination of two x-rays, A represents a normal healthy Chest x-ray, B represents a Chest X-ray documenting Q fever pneumonia, Pathology. Contributed by Wikimedia Commons (Public Domain)

Figure

Lung X-ray of patient showing infection with pneumocystis carinii, Pneumonia. Contributed by The National Institutes of Health (NIH)

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Streptococcus Pneumoniae example antibiogram. Contributed by Zachary Sandman, BA

References

1.: Yamaguchi M, Minamide Y, Terao Y, Isoda R, Ogawa T, Yokota S, Hamada S, Kawabata S. Nrc of Streptococcus pneumoniae suppresses capsule expression and enhances anti-phagocytosis. Biochem Biophys Res Commun. 2009 Dec 04;390(1):155-60. [PubMed: 19799870]
2.: Cools F, Torfs E, Vanhoutte B, de Macedo MB, Bonofiglio L, Mollerach M, Maes L, Caljon G, Delputte P, Cappoen D, Cos P. Streptococcus pneumoniae galU gene mutation has a direct effect on biofilm growth, adherence and phagocytosis in vitro and pathogenicity in vivo. Pathog Dis. 2018 Oct 01;76(7) [PubMed: 30215741]
3.: Segreti J, House HR, Siegel RE. Principles of antibiotic treatment of community-acquired pneumonia in the outpatient setting. Am J Med. 2005 Jul;118 Suppl 7A:21S-28S. [PubMed: 15993674]
4.: Pineda L, El Solh AA. Severe community-acquired pneumonia: approach to therapy. Expert Opin Pharmacother. 2007 Apr;8(5):593-606. [PubMed: 17376015]
5.: Liu JL, Xu F, Zhou H, Wu XJ, Shi LX, Lu RQ, Farcomeni A, Venditti M, Zhao YL, Luo SY, Dong XJ, Falcone M. Corrigendum: Expanded CURB-65: a new score system predicts severity of community-acquired pneumonia with superior efficiency. Sci Rep. 2018 Aug 09;8:47005. [PMC free article: PMC6083369] [PubMed: 30091425]
6.: Hauswaldt J, Blaschke S. [Dyspnea]. Internist (Berl). 2017 Sep;58(9):925-936. [PubMed: 28608125]
7.: Berliner D, Schneider N, Welte T, Bauersachs J. The Differential Diagnosis of Dyspnea. Dtsch Arztebl Int. 2016 Dec 09;113(49):834-845. [PMC free article: PMC5247680] [PubMed: 28098068]

Typical Bacterial Pneumonia – StatPearls

Continuing Education Activity

Objectives:

Explain the causes of
typical community-acquired pneumonia.
Describe the evaluation of a patient with typical community-acquired pneumonia.
Summarize the treatment options for typical community-acquired pneumonia.
Explore modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by typical community-acquired pneumonia.

Access free multiple choice questions on this topic.

Introduction

Pneumonia can be classified into 2 types based on how the infection is acquired:

Community-acquired pneumonia (CAP): Most common type
Nosocomial pneumonia

Hospital-acquired pneumonia (HAP)
Ventilator-associated pneumonia (VAP)
Healthcare-associated pneumonia (HCAP)

Etiology

Pneumonia occurs secondary to airborne infection which includes bacteria, virus, fungi, parasites, among others.

Epidemiology

Pathophysiology

Microbial virulence factors and predisposing host conditions make a person more vulnerable to pneumonia.[3]

Histopathology

Based on the area of the lung involved, pneumonia can be classified histologically into lobular, lobar, bronchopneumonia, and interstitial. The major types of acute bacterial pneumonia include:

Bronchopneumonia: A descending infection started around bronchi and bronchioles, which then spreads locally into the lungs. Lower lobes are usually involved. Patchy areas of consolidation which represents neutrophil collection in the alveoli and bronchi.
Lobar pneumonia: Acute exudative inflammation of the entire lobe. Uniform consolidation with a complete or near complete consolidation of a lobe of a lung. Majority of these cases are caused by Streptococcus pneumoniae.

Lobar pneumonia has 4 classical stages of inflammatory response if left untreated, namely:

Congestion/consolidation in the first 24 hours in which the lungs are heavy, red, and, boggy. Microscopically characterized by vascular engorgement and intra-alveolar edema. Many bacteria and few neutrophils are present.
Red hepatization/early consolidation begins 2 to 3 days after consolidation and lasts for 2 to 4 days and named because of firm liver-like consistency. The affected lung is red-pink, dry, granular and, airless. Fibrin strands replace the edema fluid of the previous phase. Microscopically marked cellular exudate of neutrophils with some showing ingested bacteria, extravasation of erythrocytes, desquamated epithelial cells, and fibrin within the alveoli are seen. The alveolar septa become less prominent because of the exudate.
Grey hepatization/late consolidation occurs 2 to 3 days following red hepatization and lasts for 4 to 8 days. The lung appears gray with liver-like consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells, and hemosiderin. The macrophages begin to appear.
Resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally which liquefies the previous solid fibrinous content and eventually restores aeration. Macrophages are the predominant cells which contain engulfed neutrophils and debris.

Toxicokinetics

Genetic mutations causing an active efflux of drug and eventually resistance have led to an increase in drug-resistant Streptococcus Pneumoniae (DRSP) over the last few years.

History and Physical

Severe pneumonia can lead to dyspnea and shortness of breath. In severe cases, confusion, sepsis, and multi-organ failure can also manifest.

The respiratory rate closely correlates with the degree of oxygenation and, therefore essential in determining the severity. Hypoxia is seen in severe pneumonia, which leads to hyperventilation.

Evaluation

It is preferable to test for influenza during the winter months as the combination of influenza and pneumonia is fatal.

CURB-65 and pneumonia severity index help in the stratification of the patients and to determine if the patient needs hospitalization for treatment.

Thoracocentesis, bronchoscopy, pleural biopsy, or pleural fluid culture are invasive tests and are carried out very occasionally.

An open lung biopsy is the ultimate specific diagnostic test.[6]

Treatment / Management

Confusion
Uremia (BUN greater than 20 mg/dL
Respiratory rate greater than 30 per minute
Hypotension (SBP less than 90 and DBP less than 60)
Age older than more than 65 years

Patients with comorbid conditions such as renal disease, liver disease, cancer, chronic lung disease usually do better with inpatient treatment with IV medications.

Empiric therapy recommended for the following:

Outpatient/non-hospitalized patient management: Empiric therapy is almost always successful and usually testing is not required. In patients with no comorbidity, monotherapy with macrolides, such as azithromycin and clarithromycin are the first choice. Alternatively, newer fluoroquinolones like levofloxacin, moxifloxacin, or gemifloxacin can be used. The therapy is targeted against mycoplasma and chlamydia pneumoniae which are the common causes of less severe CAP. Patients with comorbid conditions (chronic lung or heart disease, diabetes, smoking, HIV, among others) do well with newer fluoroquinolones alone or with a combination of beta-lactam and a macrolide.
Inpatient non-ICU management: The recommended therapy includes newer fluoroquinolones alone or a combination of beta-lactam/second or third-generation cephalosporin and a macrolide.
Inpatient ICU management: The recommended therapy is a combination of macrolide/newer fluoroquinolone and a beta-lactam. Ampicillin-sulbactam or ertapenem can be used in patients with risk of aspiration. If there is a risk of Pseudomonas infection, a combination of anti-pseudomonal beta-lactam with anti-pseudomonal fluoroquinolone is indicated. For MRSA, vancomycin or linezolid should be added. In case of complications such as empyema, chest tube drainage is required. Surgical decortication is needed in case of multiple loculations.

All hospitalized patients who test positive for influenza virus must be treated with oseltamivir irrespective of the onset of illness.

Once the exact cause is determined, specific therapy should be initiated.[3][4][5]

Differential Diagnosis

Asthma or reactive airway disease
Viral Pneumonia
Pneumonia, Fungal
Pneumonia, Atypical bacterial
Lung Abscess
Bronchiectasis
Bronchiolitis
Asthma
Acute and Chronic Bronchitis
Atelectasis
Croup
Respiratory distress syndrome
Aspiration of a foreign body[6][7]

Complications

Pleural effusion
Empyema
Lung Abscess
Septicemia
Bacteremia

Enhancing Healthcare Team Outcomes

Figure

Combination of two x-rays, A represents a normal healthy Chest x-ray, B represents a Chest X-ray documenting Q fever pneumonia, Pathology. Contributed by Wikimedia Commons (Public Domain)

Figure

Lung X-ray of patient showing infection with pneumocystis carinii, Pneumonia. Contributed by The National Institutes of Health (NIH)

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Streptococcus Pneumoniae example antibiogram. Contributed by Zachary Sandman, BA

References

1.: Yamaguchi M, Minamide Y, Terao Y, Isoda R, Ogawa T, Yokota S, Hamada S, Kawabata S. Nrc of Streptococcus pneumoniae suppresses capsule expression and enhances anti-phagocytosis. Biochem Biophys Res Commun. 2009 Dec 04;390(1):155-60. [PubMed: 19799870]
2.: Cools F, Torfs E, Vanhoutte B, de Macedo MB, Bonofiglio L, Mollerach M, Maes L, Caljon G, Delputte P, Cappoen D, Cos P. Streptococcus pneumoniae galU gene mutation has a direct effect on biofilm growth, adherence and phagocytosis in vitro and pathogenicity in vivo. Pathog Dis. 2018 Oct 01;76(7) [PubMed: 30215741]
3.: Segreti J, House HR, Siegel RE. Principles of antibiotic treatment of community-acquired pneumonia in the outpatient setting. Am J Med. 2005 Jul;118 Suppl 7A:21S-28S. [PubMed: 15993674]
4.: Pineda L, El Solh AA. Severe community-acquired pneumonia: approach to therapy. Expert Opin Pharmacother. 2007 Apr;8(5):593-606. [PubMed: 17376015]
5.: Liu JL, Xu F, Zhou H, Wu XJ, Shi LX, Lu RQ, Farcomeni A, Venditti M, Zhao YL, Luo SY, Dong XJ, Falcone M. Corrigendum: Expanded CURB-65: a new score system predicts severity of community-acquired pneumonia with superior efficiency. Sci Rep. 2018 Aug 09;8:47005. [PMC free article: PMC6083369] [PubMed: 30091425]
6.: Hauswaldt J, Blaschke S. [Dyspnea]. Internist (Berl). 2017 Sep;58(9):925-936. [PubMed: 28608125]
7.: Berliner D, Schneider N, Welte T, Bauersachs J. The Differential Diagnosis of Dyspnea. Dtsch Arztebl Int. 2016 Dec 09;113(49):834-845. [PMC free article: PMC5247680] [PubMed: 28098068]

Viral vs. Bacterial Pneumonia: Understanding the Difference

Having pneumonia can be frightening because this illness directly impacts one vital function — our breathing. For those who are at high risk of getting pneumonia and the complications that may accompany it, it is very important to make an accurate diagnosis.

According to the World Health Organization’s most current statistical data, pneumonia is one of the leading causes of death in children — responsible for 18% of all deaths in children under age five. Many of these outcomes can be prevented with global measures that increase access to immunizations, adequate pre and post-natal care for mother and baby, sufficient nutrition, and clean water.¹

The two most common causes of pneumonia are from viral pathogens or bacterial pathogens. Some types of bacterial pneumonia can be prevented with vaccines, such as the aggressive bacteria Strep. Pneumoniae, prevented with the pneumococcal vaccine. Despite increasing vaccine availability globally, the persistence of Strep pneumonia infections remains. At the same time, vaccine utilization remains stagnant.

In the most recent 2020 textbook update from Biomedical Science, scientists state, “Diagnosis [of pneumonia] still remains challenging for medical providers. Because bacterial pneumonia can be treated with antibiotics, it is important to be able to differentiate between viral and bacterial pneumonia.²

What are the main differences between bacterial and viral pneumonia?

Common symptoms of pneumonia include³

cough
fever
difficulty breathing
increased breathing rate

When a patient presents with these symptoms, the next step is to examine the lungs with a stethoscope. With pneumonia, decreased breath sounds, wheezing, or crackles on listening to the lungs, are all indications that can help point towards a diagnosis. The next step is to order a radiograph or X-ray if pneumonia is suspected.

The radiograph still remains the reference standard for a medical diagnosis of pneumonia, and also helps to differentiate between bacterial and viral pneumonia. However, a combination of clinical symptoms, exam findings, and imaging is the best way to uncover the most likely culprit.^3,4

Classic Viral Pneumonia

Often viral cases of pneumonia begin as congestion and cough with or without fever in the first few days. When a doctor listens to the lungs and finds breathing sounds are not clear on either side of the chest, a viral cause over bacterial is even more highly suspected. Viruses affect both sides of the lungs by producing a more homogeneous inflammatory reaction that causes increased cellular debris and mucus where previously open lung pockets were present. An X-ray is likely to demonstrate a more “diffuse” involvement of the lungs.^3,4

Classic Bacterial Pneumonia

When a provider hears lung sounds that seem normal on one side but absent on the other, bacterial pneumonia is more likely. Bacteria tend to aggressively attack one lobe or section of the lungs causing a specific area of inflammation to take over the cells that were filled with air. An X-ray will show one white condensed area or opacity with the other areas of the lung visualized as having normal air exchange.⁵

While the process of combining the presence of respiratory symptoms with an abnormal exam and X-ray helps to delineate the cause of pneumonia, the only gold standard test to confirm the presence of a specific pathogen is a culture (a sample of respiratory mucous secretions or blood that is analyzed in the lab for the presence of a virus or bacteria). If a culture grows one particular microorganism, you know the exact cause.

Critical Role of Pneumococcal Vaccine in Preventing Pneumonia

In children aged three months to four years, the most common type of bacterial pneumonia is Strep. pneumoniae. In children greater than age four, it remains in the top three most common types. The pneumococcal vaccine series, started at two months of age, significantly reduces the rates of bacterial pneumonia from Strep. Pneumoniae. The vaccine is usually administered during wellness or prevention visits and cannot be given to a child with a fever. This emphasizes the need for healthcare access globally.⁶

With global vaccination rates currently plateauing, the challenges of diagnosing and treating community acquired pneumonia are even more pertinent for prevention of severe respiratory illness. Vaccine uptake challenges can be overcome with global measures to increase the access and use of vaccines. Addressing vaccine use and providing education about common pneumonia symptoms can aid in early diagnosis of pneumonia and lower the rate of severe respiratory illness and prolonged hospitalization.

References

World Health Organization Health Topics. Immunization, Vaccines and Biologicals: National programs and systems on improving vaccination demand and addressing hesitancy. 17 June 2020 update.
Popovsky EY, Florin TA. Community-Acquired Pneumonia in Childhood. Reference Module in Biomedical Sciences. 2020;B978-0-08-102723-3.00013-5. doi:10.1016/B978-0-08-102723-3.00013-5
Shah SN, Bachur RG, Simel DL, Neuman MI. Does This Child Have Pneumonia?: The Rational Clinical Examination Systematic Review [published correction appears in JAMA. 2017 Oct 3;318(13):1284].JAMA. 2017;318(5):462-471. doi:10.1001/jama.2017.9039
Hunton R. Updated concepts in the diagnosis and management of community-acquired pneumonia. JAAPA. 2019;32(10):18-23. doi:10.1097/01.JAA.0000580528.33851.0c
Reynolds JH, McDonald G, Alton H, Gordon SB. Pneumonia in the immunocompetent patient.Br J Radiol. 2010;83(996):998-1009. doi:10.1259/bjr/31200593
Alicino C, Paganino C, Orsi A, et al. The impact of 10-valent and 13-valent pneumococcal conjugate vaccines on hospitalization for pneumonia in children: A systematic review and meta-analysis. Vaccine. 2017;35(43):5776-5785. doi:10.1016/j.vaccine.2017.09.005

Pneumonia | Pneumonia Symptoms | Signs of Pneumonia

What is pneumonia?

Pneumonia is an infection in one or both of the lungs. It causes the air sacs of the lungs to fill up with fluid or pus. It can range from mild to severe, depending on the type of germ causing the infection, your age, and your overall health.

What causes pneumonia?

Bacterial, viral, and fungal infections can cause pneumonia.

Bacteria are the most common cause. Bacterial pneumonia can occur on its own. It can also develop after you’ve had certain viral infections such as a cold or the flu. Several different types of bacteria can cause pneumonia, including:

Viruses that infect the respiratory tract may cause pneumonia. Viral pneumonia is often mild and goes away on its own within a few weeks. But sometimes it is serious enough that you need to get treatment in a hospital. If you have viral pneumonia, you are at risk of also getting bacterial pneumonia. The different viruses that can cause pneumonia include:

Fungal pneumonia is more common in people who have chronic health problems or weakened immune systems. Some of the types include:

Who is at risk for pneumonia?

Anyone can get pneumonia, but certain factors can increase your risk:

Age; the risk is higher for children who are age 2 and under and adults age 65 and older
Exposure to certain chemicals, pollutants, or toxic fumes
Lifestyle habits, such as smoking, heavy alcohol use, and malnourishment
Being in a hospital, especially if you are in the ICU. Being sedated and/or on a ventilator raises the risk even more.
Having a lung disease
Having a weakened immune system
Have trouble coughing or swallowing, from a stroke or other condition
Recently being sick with a cold or the flu

What are the symptoms of pneumonia?

The symptoms of pneumonia can range from mild to severe and include:

The symptoms can vary for different groups. Newborns and infants may not show any signs of the infection. Others may vomit and have a fever and cough. They might seem sick, with no energy, or be restless.

Older adults and people who have serious illnesses or weak immune systems may have fewer and milder symptoms. They may even have a lower than normal temperature. Older adults who have pneumonia sometimes have sudden changes in mental awareness.

What other problems can pneumonia cause?

Sometimes pneumonia can cause serious complications such as:

Bacteremia, which happens when the bacteria move into the bloodstream. It is serious and can lead to septic shock.
Lung abscesses, which are collections of pus in cavities of the lungs
Pleural disorders, which are conditions that affect the pleura. The pleura is the tissue that covers the outside of the lungs and lines the inside of your chest cavity.
Kidney failure
Respiratory failure

How is pneumonia diagnosed?

Sometimes pneumonia can be hard to diagnose. This is because it can cause some of the same symptoms as a cold or the flu. It may take time for you to realize that you have a more serious condition.

Your health care provider may use many tools to make a diagnosis:

A medical history, which includes asking about your symptoms
A physical exam, including listening to your lungs with a stethoscope
Various tests, such as
- A chest x-ray
- Blood tests such as a complete blood count (CBC) to see if your immune system is actively fighting an infection
- A Blood culture to find out whether you have a bacterial infection that has spread to your bloodstream

If you are in the hospital, have serious symptoms, are older, or have other health problems, you may also have more tests, such as:

Sputum test, which checks for bacteria in a sample of your sputum (spit) or phlegm (slimy substance from deep in your lungs).
Chest CT scan to see how much of your lungs is affected. It may also show if you have complications such as lung abscesses or pleural effusions.
Pleural fluid culture, which checks for bacteria in a fluid sample that was taken from the pleural space
Pulse oximetry or blood oxygen level test, to check how much oxygen is in your blood
Bronchoscopy, a procedure used to look inside your lungs’ airways

What are the treatments for pneumonia?

Treatment for pneumonia depends on the type of pneumonia, which germ is causing it, and how severe it is:

Antibiotics treat bacterial pneumonia and some types of fungal pneumonia. They do not work for viral pneumonia.
In some cases, your provider may prescribe antiviral medicines for viral pneumonia
Antifungal medicines treat other types of fungal pneumonia

You may need to be treated in a hospital if your symptoms are severe or if you are at risk for complications. While there, you may get additional treatments. For example, if your blood oxygen level is low, you may receive oxygen therapy.

It may take time to recover from pneumonia. Some people feel better within a week. For other people, it can take a month or more.

Can pneumonia be prevented?

Vaccines can help prevent pneumonia caused by pneumococcal bacteria or the flu virus. Having good hygiene, not smoking, and having a healthy lifestyle may also help prevent pneumonia.

NIH: National Heart, Lung, and Blood Institute

90,000 Bacterial pneumonia. Help – RIA Novosti, 17.04.2009

Frequency of the disease: 236.2 cases per 100 thousand adolescents 15-17 years old, 522.8 cases per 100 thousand people under 14 years old. The frequency of community-acquired pneumonia is 1200 cases per 100 thousand of the population per year, hospital pneumonia is 800 cases per 100 thousand hospitalizations per year.

The prevailing age of patients is younger than 20 and older than 60 years.

Pathogens of bacterial pneumonia: Streptococcus pneumoniae (30-50% of cases), Haemophilus influenzae (10-20% of cases), atypical pathogens – Chlamidophila pneumoniae, Mycoplasma pneumoniae, Legionella pneumophila (8-25% of cases).Typical, but rare (3-5% of cases) include Staphylococcus aureus, Klebsiella pneumoniae (rarely other enterobacteria), Moraxella catarrhalis (Branhamella catarrhalis). Community-acquired pneumonia is most often caused by pneumococci (their sensitivity to penicillin is significantly reduced in many countries), in very rare cases – by Pseudomonas aeruginosa.

Among the risk factors are recent acute respiratory viral infections, renal failure, cardiovascular diseases, chronic obstructive pulmonary disease, immunodeficiency states, and dysbiosis.Risk factors for hospital pneumonia – artificial ventilation, early postoperative period, dysbiosis. Risk factors for aspiration pneumonia are impaired consciousness, seizures, central nervous system diseases, anesthesia, reflux esophagitis.

Ways of infection – aspiration of oropharyngeal secretions, inhalation of aerosol containing microorganisms, spread of the causative agent from the extrapulmonary focus of infection (for example, with endocarditis, with septic thrombophlebitis), direct spread of infection from neighboring affected organs (for example, with liver abscess) or as a result of injury and chest infections.

Symptoms of bacterial pneumonia – cough with mucopurulent (sometimes “rusty”) sputum, chest pain when breathing (with concomitant pleurisy), shortness of breath, weakness, fatigue, night sweats.

The basis of treatment is antibiotic therapy. It begins from the moment the diagnosis is made, but after the collection of material for bacterioscopic and bacteriological studies of sputum.

The patient is also supposed to have a complete diet with a sufficient protein content and a high content of vitamins A, C, group B, restriction of carbohydrates to 200-250 g per day, table salt to 4-6 g per day, an increase in the proportion of dairy products, the introduction of a sufficient amount of liquid (1500-1700 ml per day), saturation of the diet with foods rich in vitamin P (chokeberry, rose hips, black currants, lemon).Fruit and vegetable juices are recommended. Food is given in crushed and liquid form, food intake 6-7 times a day.

The course and prognosis of bacterial pneumonia depend on the pathogen, the patient’s age, the time of initiation of treatment, the adequacy of the initial therapy, the state of the immune system, and concomitant diseases. Mortality from community-acquired pneumonia: 1-3% – among young, previously healthy people, 15-30% – in older age groups with concomitant diseases.

Viral pneumonia: symptoms, diagnosis and treatment

Viral pneumonia

Viruses are considered the second cause of pneumonia after bacteria: according to statistics, they are responsible for 13-50% of cases (1).Over the past decade, the prevalence of viral pneumonia has increased significantly, and with the onset of the coronavirus pandemic, the number of cases has increased many times. What are the symptoms of the disease and what treatment is prescribed in such a situation?

How does the disease develop?

Lung inflammation is a disease in which, as a result of an infectious process, damage to small air sacs, alveoli, occurs. They fill with fluid or pus, because of this, their function is impaired, which makes it difficult to transfer oxygen to organs and tissues.Most often, the viral form of the disease occurs in people with low immune defenses, therefore it is most common in childhood and old age, when the immune response is reduced (2).

Depending on the age of the patient, his general condition, concomitant pathologies, viral pneumonia can proceed in different forms: from mild, not causing much concern, to severe, life-threatening. So, with weakened immunity, respiratory failure and other serious complications can develop, which require intensive treatment and a long recovery period (1).

Not all respiratory viruses can cause inflammation in the lower respiratory tract. The most common infectious agents in the lungs are:

influenza A and B viruses;
respiratory syncytial virus;
adenovirus;
parainfluenza virus.

Viral pneumonia is considered the most frequent complication of the new coronavirus infection COVID-19: according to some reports, it is detected in more than 91% of cases (3).In addition, the inflammatory process in the lower respiratory tract can develop when infected with other coronaviruses, enteroviruses, Epstein-Barr virus, cytomegalovirus, measles virus, herpes, and so on (2).

Who is at high risk?

There are so-called risk factors that increase the likelihood of developing pneumonia of viral origin. Among them:

Age – the disease often occurs in children, especially young children, and the elderly, and the reason for this is the physiological age-related suppression of the immune response.
Pregnancy – during pregnancy, the immune response also decreases, which is associated with a rather high prevalence of viral pneumonia in expectant mothers. Their disease can be most difficult and be accompanied by complications from both the woman and the child, who may also experience respiratory failure.
Low immune response, which can be the result of chemotherapy or radiation therapy for malignant neoplasms, the use of drugs that suppress the immune response, which are used in some severe chronic diseases, after organ transplantation.
Comorbidities and conditions – trauma, burns, uncontrolled diabetes mellitus, unbalanced diet, adverse environmental influences, and so on.

How does the infection occur?

Most often, viruses enter the respiratory tract by inhalation of viral particles spread by a sick person by coughing or sneezing. The new coronavirus SARS-CoV-2, the causative agent of COVID-19, uses special receptors to enter the cell, which are located in the nasopharynx and in the lower respiratory tract of our body – receptors for the antiotensin-converting enzyme ACE2 (4).

It is known that SARS-CoV-2 has a special spike that binds closely to ACE2 receptors, after which the virus begins to actively multiply. Due to the vital activity of the virus, the cell walls become more permeable to liquid, and its transport is enhanced. As a result, fluid accumulates in the alveoli and gas exchange is disrupted (4).

Symptoms and Diagnostics

The classic manifestations of the disease are practically indistinguishable from the symptoms of bacterial pneumonia.These include:

cough; 90 046
shortness of breath;
fever;
chest pain;
Muscle pain, headache;
sweating;
decreased appetite;
fatigue.

In the form of inflammation caused by infection with a new coronavirus infection, the symptoms can vary greatly from erased in mild cases to pronounced, with symptoms of respiratory failure, a drop in the level of oxygen in the blood during a severe course of the disease.

Diagnosing viral pneumonia can be difficult. The clinical picture is very similar to the course of an acute respiratory viral infection, bacterial forms of pneumonia. In addition, in elderly people and patients with weakened immunity, the disease can be atypical, practically asymptomatic, which makes it even more difficult to make a diagnosis.

With pneumonia associated with coronavirus infection, the symptoms may be the same as with illness caused by other viruses.Just like with influenza, herpes virus, with COVID-19, lung damage can be accompanied by fever (89-98% of cases), dry cough (in 76-82% of patients), muscle pain (in 11-44% of cases) , fatigue (6).

As a rule, the diagnosis is established on the basis of data of x-ray, ultrasound and / or computed tomography of the lungs. In case of inflammation against the background of a new coronavirus infection, radiographs show bilateral thickening areas in the affected area, and on computed tomograms – changes like “ground glass” (7).

In addition, pneumonia associated with infection with SARS-CoV-2 is confirmed by the detection of viral RNA by polymerase chain reaction in a swab from the nose, nasopharynx or oropharynx (7).

Laboratory tests also help to distinguish a viral infection from a bacterial infection – a complete blood count, blood tests for C-reactive protein, procalcitonin, the level of which increases when infected with bacteria (5,6).

Complications and prognosis of the disease

In people with a normal immune response, the disease is usually mild and does not have serious consequences.However, in some cases, complications are possible.

Secondary bacterial infections are common – pathogenic bacteria, usually pneumococci, Staphylococcus aureus, streptococci, Haemophilus influenzae, join the viruses. In such cases, combined treatment is required, including antibiotics.

One of the common complications is the formation of scar tissue (fibrosis) in the lungs. In addition, with COVID-19, the likelihood of bleeding disorders increases, which can lead to the development of thrombosis.Blood clots clog vessels in various organs, which can lead to pulmonary embolism, deep vein thrombosis, myocardial infarction, stroke, and other serious complications (7).

How to treat?

The treatment regimen may vary depending on which virus is causing the disease. If pneumonia occurs against the background of influenza, the doctor prescribes antiviral drugs that are active against the influenza virus. They block an enzyme that is involved in the multiplication of influenza viruses, thus stopping infection (8).

Unfortunately, there is no proven effective antiviral drug that is active against the vast majority of respiratory viruses that can cause pneumonia. To date, there is no evidence of the effectiveness of any drugs in COVID-19. Therefore, treatment is prescribed on the basis of clinical experience in the management of patients with atypical pneumonia (8).

Antiviral drugs, interferon drugs, and symptomatic drugs aimed at relieving symptoms and preventing complications may be included in the therapy regimen.These include antipyretics, pain relievers, and, if necessary, agents that facilitate the passage of sputum, including in inhalation form, and other drugs (8).

In the presence of bronchospasm, bronchodilators may be recommended to widen the airway and make breathing easier. They are often used by inhalation, through a nebulizer, which allows the drug to be delivered directly to where it is needed – into the alveoli. However, we must not forget that all medications for viral pneumonia are prescribed by a doctor.Self-medication can be dire and should not be used (8).

Page not found |

404.Page not found

Monthly archive

MonTueWedThuFtSaSun

6789101112

13141516171819

20212223242526

2728293031

3031

15161718192021

25262728293031

123

45678910

17181920212223

2728293031

1234

567891011

891011121314

11121314151617

28293031

1234

12345

6789101112

567891011

12131415161718

19202122232425

3456789

17181920212223

24252627282930

12345

13141516171819

20212223242526

2728293031

15161718192021

22232425262728

2930