Pneumonia
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Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Alejandro Lemor, M.D. [3], Priyamvada Singh, M.D. [4], Philip Marcus, M.D., M.P.H.[5]
Synonyms and keywords: PNA
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Priyamvada Singh, M.D. [3], Alejandro Lemor, M.D. [4]
Overview
Pneumonia is an illness of the lungs and respiratory system in which the alveoli (microscopic air-filled sacs of the lung responsible for absorbing oxygen from the atmosphere) become inflamed and flooded with fluid. Pneumonia can result from a variety of causes, including infection with bacteria, viruses, fungi, parasites, and chemical or physical injury to the lungs. Typical symptoms associated with pneumonia include cough, chest pain, fever, and difficulty in breathing. Diagnostic tools include x-rays and an examination of the sputum. Treatment depends on the cause of pneumonia; bacterial pneumonia is treated with antibiotics. Pneumonia is a common illness which occurs in all age groups, and is a leading cause of death among the elderly and people who are chronically and terminally ill. Vaccines to prevent certain types of pneumonia are available. The prognosis depends on the type of pneumonia, the appropriate treatment, any complications, and the person’s underlying health.
Historical Perspective
Pneumonia has been recognized since ancient times. It was initally described by Hippocrates who recorded his observations of its symptoms and complications. Edwin Klebs was the first to identify bacteria in the lungs of patients who died from pneumonia in 1875. This discovery was soon-after substantiated by the works of Carl Friedländer and Albert Fränkel who were the first to identify Streptococcus pneumoniae as a causative agent. The introduction of the gram stain subsequently led to the discovery of other causative organisms. Despite being an important cause of mortality before the late twentieth century, the advent of antibiotics, modern surgical techniques, and vaccination drastically lowered the morbidity and mortality of pneumonia with the turn of the century.
Classification
Several pneumonia classification schemes have been described. The earliest classification was based on the anatomical distribution of the infectious process observed on autopsy and eventually on medical imaging. Advances in microbiology led to a classification based on etiologic group (bacterial, viral, fungal) despite difficulties often encountered in identifying the etiologic agent. With the advent of antibiotics and the rise in resistance, a classification scheme taking into account the setting in which the pneumonia was acquired was introduced to guide empiric therapy. Pneumonia was classified into community-acquired pneumonia (CAP), healthcare-associated pneumonia (HCAP), ventilator-associated pneumonia (VAP), and hospital-acquired pneumonia (HAP). Despite significant overlap, this classification is essential in selecting appropriate antimicrobial therapy.
Pathophysiology
Bacteria and fungi typically enter the lung with inhalation. Once inside the alveoli, these microbes travel into the spaces between the cells and also between adjacent alveoli through connecting pores. This invasion triggers the immune system response by sending white blood cells responsible for attacking microorganisms (neutrophils) to the lungs resulting in manifestations of pneumonia.
Causes
Pneumonia can result from a variety of causes including infection with bacteria, viruses, fungi, parasites, and chemical or physical injury to the lungs. The etiology will depend upon various factors such as age, immune status, geographical area, and comorbidities.
Epidemiology and Demographics
Pneumonia is a common illness in all parts of the world. It is a major cause of death among all age groups. Mortality from pneumonia generally decreases with age until late adulthood. Elderly individuals, however, are at particular risk for pneumonia and associated mortality. More cases of pneumonia occur during the winter months than during other times of the year. Pneumonia occurs more commonly in males than females, and more often in African Americans than Caucasians. People who are hospitalized for any reason are also at high risk for pneumonia. Following urinary tract infections, pneumonia is the second most common cause of nosocomial infections, and its prevalence is 15-20% of the total number.
Risk Factors
The risk factors for pneumonia include smoking, age, immuno-suppression, exposure to chemicals, underlying lung disease, and exposure to chemicals.
Diagnosis
Diagnostic Criteria
Community acquired pneumonia should be distinguished from healthcare-associated pneumonia as these diseases have different causative organism, prognosis, diagnostic, and treatment guidelines.
History and Symptoms
People with pneumonia often have a productive cough, fever, shaking chills, shortness of breath, pleuritic chest pain,hemoptysis, headaches, diaphoresis, and clammy skin. Other possible symptoms are loss of appetite, fatigue,blueness of the skin, nausea, vomiting, mood swings, andjoint pains or muscle aches. In elderly people manifestations of pneumonia may not be typical. They may develop a new or worsening confusion or may experience unsteadiness, leading to falls. Infants with pneumonia may have many of the symptoms above, but in many cases they are simply sleepy or have a decreased appetite.
Physical Examination
Physical examination may reveal fever or sometimes low body temperature, an increased respiratory rate, low blood pressure, a fast heart rate, or a low oxygen saturation, which is the amount of oxygen in the blood as indicated by either pulse oximetry or blood gas analysis. Patients who are struggling to breathe, who are confused, or who have cyanosis (blue-tinged skin) require immediate attention. Auscultation findings include lack of normal breath sounds, the presence of crackling sounds (rales), or increased loudness of whispered speech (whispered pectoriloquy) with areas of the lung that are stiff and full of fluid, called consolidation. Vital signs are useful in determining the severity of illness and have predictive values. However, a high degree of suspicion should be kept in elderly as the presentation could be subtle in them.
Laboratory Findings
Laboratory findings such as leukocytosis are helpful for the diagnosis of bacterial pneumonia or to assess the status of the patient. Sputum samples need to be collected from every patient and sent for gram staining and culture that need to be performed to determine the exact pathogen causing the pneumonia. Other tests include urine antigen test, PCR, C-reactive protein, and procalcitonin.
Chest X Ray
An important test for making a diagnosis of pneumonia is a chest x-ray. Chest x-rays can reveal areas of opacity (seen as white) which represent consolidation. Pneumonia is not always seen on x-rays, either because the disease is only in its initial stages, or because it involves a part of the lung not easily seen by x-ray.
CT
A chest CT scan is not routinely done in patients with pneumonia, but is a diagnostic test that may be useful when a chest x-ray is not conclusive. CT findings may include lobar consolidation, ground-glass opacities, pleural effusion, lymphadenopathy, and tree-in-bud appereance.
Other Imaging Findings
Bronchoscopy with bronchoalveolar lavage is useful to obtain samples for gram stain and culture in patients with certain conditions, such as immunocompromised patients, ICU admission or antibiotic failure.
Treatment
Medical Therapy
The treatment of pneumonia involves three critical decisions: firstly whether the patient truly has pneumonia, secondly what is the severity of the pneumonia, and lastly whether hospitalization is required for adequate management. Most cases of pneumonia can be treated without hospitalization. Typically, oral antibiotics, rest, fluids, and home care are sufficient for complete resolution. However, people with pneumonia who are having trouble breathing, comorbidities, and the elderly may need more advanced treatment. If the symptoms get worse, the pneumonia does not improve with home treatment, or complications occur, the person will often have to be hospitalized.
Prevention
There are several ways to prevent infectious pneumonia. Appropriately treating underlying illnesses (such as AIDS), smoking cessation, vaccination against pneumococcal, and influenza are the commonly used methods.
References
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Serge Korjian M.D., Priyamvada Singh, M.D. [3]
Overview
The pneumonia syndrome has been recognized since ancient times. It was initially described by Hippocrates who recorded his observations of its symptoms and complications. Edwin Klebs was the first to identify bacteria in the lungs of patients who died from pneumonia in 1875. This discovery was soon-after substantiated by the works of Carl Friedländer and Albert Fränkel who were the first to identify Streptococcus pneumoniae as a causative agent. The introduction of the gram stain subsequently led to the discovery of other causative organisms. Despite being an important cause of mortality before the late twentieth century, the advent of antibiotics, modern surgical techniques, and vaccination drastically lowered the morbidity and mortality of pneumonia with the turn of the century.
Historical Perspective
Discovery
- Pneumonia was first discovered by Hippocrates.
- In 1817, Dr. Simpson of United Kingdom was the first to report a case of pneumonia treated with blood letting.[1]
- In 1842, Dr. Edward Newfold of United Kingdom was the first to report a case of typhoid pneumonia.[2]
- In 1875, Dr. Edwin Klebs was the first to discover the association between bacteria and the development of pneumonia.
Landmark Events in the Development of Treatment Strategies
- In 1902, Dr. Wright discovered the pneumococcal vaccine as a preventative treatment of pneumonia.[3]
References
- ↑ “Case ofPneumonia, Where the Extent to Which Blood-Letting May Be Successfully Carried Is Fully Exemplified”. Med Chir J Rev. 4 (24): 460–463. 1817. PMC 5570882. PMID 29257545.
- ↑ Newbold E (1842). “Case of Typhoid Pneumonia”. Prov Med J Retrosp Med Sci. 4 (84): 87. PMC 2489819. PMID 21373079.
- ↑ Harris AB (1909). “Observations on the Therapeutic Value of the Pneumococcus Vaccine in the Treatment of Pneumonia and some of its Complications”. Br Med J. 1 (2530): 1530–5. PMC 2320626. PMID 20764553.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Priyamvada Singh, M.D. [3]
Overview
Bacteria and fungi typically enter the lung with inhalation. Once inside the alveoli, these microbes travel into the spaces between the cells and also between adjacent alveoli through connecting pores. This invasion triggers the immune system response by sending white blood cells responsible for attacking microorganisms (neutrophils) to the lungs resulting in manifestations of pneumonia.
Pathophysiology
Mode of Transmission
1. Inhalation of Aerosolized Droplets
- Inhalation of aerosolized droplets of 0.5 to 1 micrometer is the most common pathway of acquiring pneumonia.
- A few bacterial and viral infections are transmitted in this fashion.
- The lung can normally filter out particles between 0.5 to 2 micrometer by recruiting the alveolar macrophages.[1]
2. Microaspiration of Oropharyngeal Contents
- Aspiration of oropharyngeal contents containing pathogenic microorganisms is one of the mechanism of acquiring pneumonia.
- It most commonly occurs in normal persons during sleep, in unconscious persons due to gastroesopahegeal reflux or impaired gag reflex and cough reflex.[1]
3. Blood-Borne or Systemic Infection
- Microbial entered through circulation may also result in pulmonary infections.
- Blood-borne pneumonia is seen more commonly in intravenous drug users. Staphylococcus aureus causes pneumonia in this way.
- Gram negative bacteria typically account for pneumonia in immunocompromised individuals.
4. Trauma or Local Spread
- Pneumonia can occur after a pulmonary procedure or a penetrating trauma to the lungs.
- A local spread of a hepatic abscess can also lead to pneumonia.
Agent Specific Virulence Factors
Several strategies are evolved to evade host defence mechanisms and facilitate spreading before establishing an infection.
- Influenza virus possesses neuraminidases for cleavage of sialic acid residues on the cell surface and viral proteins, which prevent aggregation and facilitate propagation of viral particles.
- Chlamydophila pneumoniae induces complete abortion of cilia motions which assists colonization at the respiratory epithelium.[2]
- Mycoplasma pneumoniae produces a virulence factor with ADP-ribosylating activity which is responsible for airway cellular damage and mucociliary dysfunction.[3]
- Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis produce proteases that split mucosal IgA.
- Streptococcus pneumoniae possesses pneumolysin that aid the bacteria during colonization, by facilitating adherence to the host,[4] during invasion by damaging host cells,[5] and during infection by interfering with the host immune response.[6]
Host Factors
- The lungs can normally filter out large droplets of aerosols.
- Smaller droplets of the size of 0.5 to 2 micrometer are deposited on the alveoli and then engulfed by alevolar macrophages.
- These macrophages release cytokines and chemokines, which also includes tumor necrosis factor-alpha, interleukin-8 and LTB4.
- The neutrophils are recruited by these cells to eliminate these microorganisms.[7][8]
1. Diminished Mucociliary Clearance
- The cilia lining the respiratory epithelium serve to move secreted mucus containing trapped foreign particles including pathogens towards the oropharynx for either expectoration or swallowing.
- Elevated incidence of pneumonia in patients with genetic defects affecting mucociliary clearance such as primary ciliary dyskinesia suggests its role in the pathogenesis of community-acquired pneumonia.
2. Impaired Cough Reflex
- Cough, together with mucociliary clearance, prevent pathogens from entering the lower respiratory tract.
- Cough suppression or cough reflex inhibition seen in patients with cerebrovascular accidents and drug overdosages is associated with an enhanced risk for aspiration pneumonia.
- Another relation to cough is genetic polymorphisms in the angiotensin-converting enzyme (ACE) gene.
- The role of cough in preventing pneumonia may be explained by a higher risk for developing pneumonia in homozygotes carrying deletion/deletion (DD) genotype who are found to have lower levels of bradykinin and tachykinins such as substance P.[9][10]
3. Defective Immune System
- Pathogen-associated molecular patterns (PAMPs) are initially recognized by Toll-like receptors (TLRs) and other pattern-recognition receptors (PRRs) of the innate immune system.
- Effectors in the acquired immune system are involved in elimination of microorganisms and generation of immunological memory.
- Other components in the immune system such as complement system, cytokines, and collectins, also mediate the defense against microorganisms causing pneumonia.
Microscopic Pathology

Microbial PathogenesisVirulence FactorsSeveral mechanisms have evolved to evade host defense mechanisms and facilitate microbial spread to establish an infection.
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References
- ↑ 1.0 1.1 Wunderink, RG.; Waterer, GW. (2004). “Community-acquired pneumonia: pathophysiology and host factors with focus on possible new approaches to management of lower respiratory tract infections”. Infect Dis Clin North Am. 18 (4): 743–59, vii. doi:10.1016/j.idc.2004.07.004. PMID 15555822. Unknown parameter
|month=ignored (help) - ↑ 2.0 2.1 Shemer-Avni, Y.; Lieberman, D. (1995). “Chlamydia pneumoniae-induced ciliostasis in ciliated bronchial epithelial cells”. J Infect Dis. 171 (5): 1274–8. PMID 7751703. Unknown parameter
|month=ignored (help) - ↑ 3.0 3.1 Kannan, TR.; Baseman, JB. (2006). “ADP-ribosylating and vacuolating cytotoxin of Mycoplasma pneumoniae represents unique virulence determinant among bacterial pathogens”. Proc Natl Acad Sci U S A. 103 (17): 6724–9. doi:10.1073/pnas.0510644103. PMID 16617115. Unknown parameter
|month=ignored (help) - ↑ Rubins, JB (December 1998). “Pneumolysin in pneumococcal adherence and colonization”. Microbial pathogenesis. 25 (6): 337–42. doi:10.1006/mpat.1998.0239. PMID 9895272. Unknown parameter
|coauthors=ignored (help) - ↑ Rubins, JB (January 1998). “Pneumolysin: a multifunctional pneumococcal virulence factor”. The Journal of laboratory and clinical medicine. 131 (1): 21–7. PMID 9452123. Unknown parameter
|coauthors=ignored (help) - ↑ Cockeran, R (June 2002). “The role of pneumolysin in the pathogenesis of Streptococcus pneumoniae infection”. Current Opinion in Infectious Diseases. 15 (3): 235–9. PMID 12015456. Unknown parameter
|coauthors=ignored (help) - ↑ Strieter, RM.; Belperio, JA.; Keane, MP. (2003). “Host innate defenses in the lung: the role of cytokines”. Curr Opin Infect Dis. 16 (3): 193–8. doi:10.1097/01.qco.0000073766.11390.0e. PMID 12821807. Unknown parameter
|month=ignored (help) - ↑ Mason, CM.; Nelson, S. (2005). “Pulmonary host defenses and factors predisposing to lung infection”. Clin Chest Med. 26 (1): 11–7. doi:10.1016/j.ccm.2004.10.018. PMID 15802161. Unknown parameter
|month=ignored (help) - ↑ Morimoto, S.; Okaishi, K.; Onishi, M.; Katsuya, T.; Yang, J.; Okuro, M.; Sakurai, S.; Onishi, T.; Ogihara, T. (2002). “Deletion allele of the angiotensin-converting enzyme gene as a risk factor for pneumonia in elderly patients”. Am J Med. 112 (2): 89–94. PMID 11835945. Unknown parameter
|month=ignored (help) - ↑ Rigat, B.; Hubert, C.; Alhenc-Gelas, F.; Cambien, F.; Corvol, P.; Soubrier, F. (1990). “An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels”. J Clin Invest. 86 (4): 1343–6. doi:10.1172/JCI114844. PMID 1976655. Unknown parameter
|month=ignored (help) - ↑ Rubins, JB (December 1998). “Pneumolysin in pneumococcal adherence and colonization”. Microbial pathogenesis. 25 (6): 337–42. doi:10.1006/mpat.1998.0239. PMID 9895272. Unknown parameter
|coauthors=ignored (help) - ↑ Rubins, JB (January 1998). “Pneumolysin: a multifunctional pneumococcal virulence factor”. The Journal of laboratory and clinical medicine. 131 (1): 21–7. PMID 9452123. Unknown parameter
|coauthors=ignored (help) - ↑ Cockeran, R (June 2002). “The role of pneumolysin in the pathogenesis of Streptococcus pneumoniae infection”. Current Opinion in Infectious Diseases. 15 (3): 235–9. PMID 12015456. Unknown parameter
|coauthors=ignored (help)
Causes
Caused by pathogen: Bacterial | Viral | Fungal
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Priyamvada Singh, M.D. [3]; Alejandro Lemor, M.D. [4]; Ogheneochuko Ajari, MB.BS, MS [5]
Overview
Pneumonia can result from a variety of causes, including infection with bacteria, viruses, fungi, parasites, and chemical or physical injury to the lungs. The etiology will depend upon various factors such as age, immune status, geographical area, and comorbidities.
Causes
Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
Common Causes
- Cryptococcus neoformans
- Flu
- Histoplasmosis
- Hospital-acquired pneumonia
- Mycoplasma pneumonia
- Pneumocystis jiroveci
- Respiratory syncytial virus
- Rhinovirus
- Streptococcus pneumoniae
Causes by Pathogen
Infants
Source of Infection
- Aerosol
- Aspiration of amniotic fluid
- Blood-borne infection across the placenta
Newborn
- Most common cause is Streptococcus agalactiae (Group B Streptococcus)
- GBS causes at least 50% of cases of CAP in the first week of life.[1]
- Other bacterial causes in the newborn period include Listeria monocytogenes and tuberculosis
- Viral causes like herpes simplex virus (most common) adenovirus, mumps, and enterovirus
Children
- For the most part, children older than one month are at risk for the same microorganisms as adults.
- However, children less than five years are much less likely to have pneumonia caused by mycoplasma pneumoniae, chlamydophila pneumoniae, or legionella pneumophila.
- In contrast, older children and teenagers are more likely to acquire mycoplasma pneumoniae and chlamydophila pneumoniae than adults.[2]
- A unique cause of CAP in this group is chlamydia trachomatis, which is acquired during birth but does not cause pneumonia until 2-4 weeks later.
- Common viruses include respiratory syncytial virus (RSV), metapneumovirus, adenovirus, parainfluenza, influenza, and rhinovirus.
- RSV in particular is a common source of illness and hospitalization.[3]
- Fungi and parasites are not typically encountered in otherwise healthy infants, though maternally-derived syphilis can be a cause of CAP in this age group.
Microbiological Etiology
| Typical Bacteria | Atypical Bacteria | Viruses |
|---|---|---|
| Outpatient | Inpatient (non-ICU) | Inpatient (ICU) |
|---|---|---|
Community Acquired Pneumonia
| Outpatient | Inpatient (non-ICU) | Inpatient (ICU) |
|---|---|---|
Common Causes by Age Group
| Age Group | Neonates | Children | Adults |
|---|---|---|---|
| Bacteria |
Typical Bacteria
Atypical Bacteria | ||
| Virus |
- Newborn infants, children, and adults are at risk for different spectrums of disease causing microorganisms.
- In addition, adults with chronic illnesses, who live in certain parts of the world, who reside in nursing homes, who have recently been treated with antibiotics, or who are alcoholics are at risk for unique infections.
Infants and Newborns
- GBS causes at least 50% of cases of CAP in the first week of life.[6]
- Other bacterial causes in the newborn period include Listeria monocytogenes and Mycobacterium tuberculosis.
- Viral causes like herpes simplex virus (most common), adenovirus, mumps, and enterovirus.
Children
- For the most part, children older than one month are at risk for the same microorganisms as adults.
- Children less than five years are much less likely to have pneumonia caused by Mycoplasma pneumoniae, Chlamydophila pneumoniae, or Legionella pneumophila.[7]
- In contrast, older children and teenagers are more likely to acquire Mycoplasma pneumoniae and Chlamydophila pneumoniae than adults.[7]
- A unique cause of CAP in this group is Chlamydia trachomatis, which is acquired during birth but does not cause pneumonia until 2-4 weeks later.
- Common viruses include respiratory syncytial virus (RSV), metapneumovirus, adenovirus, parainfluenza, influenza, and rhinovirus.
- RSV in particular is a common source of illness and hospitalization.[8]
- Fungi and parasites are not typically encountered in otherwise healthy infants, though maternally-derived syphilis can be a cause of CAP in this age group.
Adults
The causes of CAP in adults are outlined in the following categories:
Viruses
- Viruses account for about 20% cases of CAP.
- Common viruses are influenza, parainfluenza, respiratory syncytial virus, metapneumovirus, and adenovirus.
- Less common viruses include chicken pox, SARS, avian flu, and hantavirus.[9]
Streptococcus pneumoniae
- Streptococcus pneumoniae is the most common cause of community-acquired pneumonia.
- Aspiration pneumonia is most commonly caused by anaerobic organisms.
- Prior to the development of antibiotics and vaccination, it was a leading cause of death.
- Traditionally, it was highly sensitive to penicillin, but during the 1970s resistance to multiple antibiotics began to develop.
- Current strains of drug resistant Streptococcus pneumoniae (DRSP) are common, accounting for twenty percent of all streptococcal infections.
- Risk factors for DRSP in adults include being older than 65, having exposure to children in day care, alcoholism, other severe underlying disease, or recent treatment with antibiotics; individuals exposed to these risk factors should initially be treated with antibiotics effective against DRSP.[10]
Atypical Organisms
- Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila are often grouped as atypical pneumonia. Community-acquired pneumonia caused by these agents present insidiously, with a non-productive cough and prominent extra-pulmonary complaints, such as myalgias and diarrhea (lack the typical pneumonia symptoms of fever, cough, and sputum).
- Mycoplasma pneumoniae is often referred to as “walking pneumonia.” It is transmitted via respiratory droplets and is common among healthy individuals in close contact with one another in settings such as dormitories or military barracks.
- Atypical organisms are more difficult to grow and respond to different antibiotics; they were discovered more recently than the typical bacteria discovered in the early twentieth century.
Haemophilus influenzae
- Haemophilus influenzae used to be a common bacterial cause of CAP.
- First discovered in 1892, it was initially believed to be the cause of influenza because it commonly causes CAP in people who have suffered recent lung damage from viral pneumonia.
Enteric Gram-Negative Bacteria
- Enteric bacteria such as Escherichia coli and Klebsiella pneumoniae may cause commnity-acquired penumonia.
- Risk factors in adults for infection include: living in a nursing home, serious heart and lung disease, and recent antibiotic use; these individuals should initially be treated with antibiotics effective against enteric Gram-negative bacteria.
Pseudomonas aeruginosa
- Pseudomonas aeruginosa is an uncommon cause of CAP, but it is a particularly difficult bacteria to treat.
- Individuals who are malnourished, have bronchiectasis, are on corticosteroids, or have recently had strong antibiotics for a week or more, should initially be treated with antibiotics effective against Pseudomonas aeruginosa.[11]
Special Situations
- Coccidioides spp. are common in southwestern area of the United States.
- Anaerobic infection is common in alcoholics. Pneumococcal pneumonia remains the most common cause of CAP in alcoholics.
- Psittacosis (caused by Chlamydophila psittaci) should be considered in the patient with exposure to birds or bird droppings.
- Anaerobes are common in patients with poor dental hygiene and a suspected large volume of aspiration.
- Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Legionella species are the common causes of community acquired pneumonia in those with chronic obstructive pulmonary disorders and smokers.
- Streptococcus pneumoniae, Gram-negative bacilli, Haemophilus influenzae, Staphylococcus aureus, anaerobes, and Chlamydophila pneumoniae are more common in nursing home residents.
- Streptococcus pneumoniae, Haemophilus influenzae, and Mycobacterium tuberculosis are common pathogens in early stages of HIV, whereas, Pneumocystis jiroveci, Histoplasma, and Cryptococcus are commonly seen in late stages HIV.
- In patients with structural lung disease such as bronchiectasis and cystic fibrosis, Pseudomonas aeruginosa, Burkholderia cepacia, and Staphylococcus aureus are the common pathogens involved.
Aspiration Pneumonia
- Incompetent swallowing mechanism, as can be found in neurological disease (a common cause being strokes) or while a person is intoxicated.
- Iatrogenic causes such as general anaesthesia for an operation. Patients are therefore instructed to be nil per os (NPO) for at least four hours before surgery.
- Whether aspiration pneumonia represents a true bacterial infection or a chemical inflammatory process remains the subject of significant controversy.
Hospital Acquired Pneumonia
The causes of hospital acquired pneumonia are as follows:[8]
Aerobic Gram Negative Pathogens
- Commonly polymicrobial
- Common microbial agents include:
Gram-Positive Pathogens
- Staphylococcus aureus
- Methicillin resistant staphylococcus aureus (common in patients with diabetes mellitus, head trauma, and in ICU)
Elderly Population
- S. aureus
- Enteric gram-negative rods
- Streptococcus pneumoniae
- Pseudomonas
Ventilator-associated Pneumonia (VAP)
- The microbiologic flora responsible for VAP is different from that of the more common community-acquired pneumonia (CAP). In particular, viruses and fungi are uncommon causes in people who do not have underlying immune deficiencies.
- Though any microorganism that causes CAP can cause VAP, there are several bacteria which are particularly important causes of VAP because of their resistance to commonly used antibiotics. These bacteria are referred to as multidrug resistant (MDR).
- VAP has been classified into either early-onset pneumonia (EOP), if pneumonia develops within 96 hours of the patient’s admission to an ICU or intubation for mechanical ventilation, and late-onset pneumonia (LOP), if pneumonia develops after 96 hours of the patient’s admission to an ICU or intubation for mechanical ventilation. [9]
- This categorization can be helpful to clinicians in initiating empiric antimicrobial therapy for cases of pneumonia, when the results of microbiologic diagnostic testing are not yet available.
- EOP has been associated usually with non-multi-antimicrobial-resistant microorganisms such as Escherichia coli, Klebsiella spp., Proteus spp., S. pneumoniae, H. influenzae, and oxacillin-sensitive S. aureus.
- On the other hand, LOP has been associated with Pseudomonas aeruginosa, oxacillin-resistant S. aureus, and Acinetobacter spp (strains that are usually multi-antibiotic-resistant).
The following is a list of the most MDR common pathogens associated with ventilator-associated pneumonia:
- Pseudomonas aeruginosa is the most common MDR gram-negative bacterium causing VAP. Pseudomonas has natural resistance to many antibiotics and has been known to acquire resistance to every antibiotic except for polymixin B. Resistance is typically acquired through upregulation or mutation of a variety of efflux pumps which pump antbiotics out of the cell. Resistance may also occur through loss of an outer membrane porin channel (OprD).
- Klebsiella pneumoniae has natural resistance to some beta-lactam antibiotics such as ampicillin. Resistance to cephalosporins and aztreonam may arise through induction of a plasmid-based extended spectrum beta-lactamase (ESBL) or plasmid-based ampC-type enzyme.
- Serratia marcescens has an ampC gene which can be induced by exposure to antibiotics such as cephalosporins. Thus, culture sensitivities may initially indicate appropriate treatment which fails due to bacterial response.
- Enterobacter as a group also have an inducible ampC gene. Enterobacter may also develop resistance by acquiring plasmids.
- Citrobacter also has an inducible ampC gene.
- Stenotrophomonas maltophilia often colonizes people who have endotracheal tubes or tracheostomies but can also cause pneumonia. It is often resistant to a wide array of antibiotics but is usually sensitive to co-trimoxazole.
- Acinetobacter are becoming more common and may be resistant to carbapenems such as imipenem and meropenem.
- Burkholderia cepacia is an important organism in people with cystic fibrosis and is often resistant to multiple antibiotics.
- Methicillin-resistant Staphylococcus aureus is an increasing cause of VAP. As many as fifty percent of Staphylococcus aureus isolates in the intensive care setting are resistant to methicillin. Resistance is conferred by the mecA gene.
Aspiration Pneumonia Causes
- Incompetent swallowing mechanism, such as in neurological disease (a common cause being strokes) or while a person is intoxicated.
- Iatrogenic causes such as general anaesthesia for an operation. Patients are therefore instructed to be nil per os (NPO) for at least four hours before surgery.
- Whether aspiration pneumonia represents a true bacterial infection or a chemical inflammatory process remains the subject of significant controversy.
Drug Side Effect
- Blinatumomab
- Belimumab
- Boceprevir
- Ceritinib
- Dornase Alfa
- Enfuvirtide
- ethanolamine oleate
- Felbamate
- Iloperidone
- interferon alfacon-1
- Pegylated interferon alfa-2b
Causes in Aphabetical Order
Causes by Organ System
References
- ↑ Webber S, Wilkinson AR, Lindsell D, Hope PL, Dobson SR, Isaacs D (1990). “Neonatal pneumonia”. Arch Dis Child. 65 (2): 207–11. PMC 1792235. PMID 2107797.
- ↑ Wubbel L, Muniz L, Ahmed A, Trujillo M, Carubelli C, McCoig C; et al. (1999). “Etiology and treatment of community-acquired pneumonia in ambulatory children”. Pediatr Infect Dis J. 18 (2): 98–104. PMID 10048679.
- ↑ Abzug MJ, Beam AC, Gyorkos EA, Levin MJ (1990). “Viral pneumonia in the first month of life”. Pediatr Infect Dis J. 9 (12): 881–5. PMID 2177540.
- ↑ 4.0 4.1 Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, Dowell SF, File TM, Musher DM, Niederman MS, Torres A, Whitney CG (2007). “Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults”. Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 44 Suppl 2: S27–72. doi:10.1086/511159. PMID 17278083. Retrieved 2012-09-06. Unknown parameter
|month=ignored (help) - ↑ 5.0 5.1 Wong, KK.; Fistek, M.; Watkins, RR. (2013). “Community-acquired pneumonia caused by Yersinia enterocolitica in an immunocompetent patient”. J Med Microbiol. 62 (Pt 4): 650–1. doi:10.1099/jmm.0.053488-0. PMID 23242642. Unknown parameter
|month=ignored (help) - ↑ 6.0 6.1 Oh, YJ.; Song, SH.; Baik, SH.; Lee, HH.; Han, IM.; Oh, DH. (2013). “A case of fulminant community-acquired Acinetobacter baumannii pneumonia in Korea”. Korean J Intern Med. 28 (4): 486–90. doi:10.3904/kjim.2013.28.4.486. PMID 23864808. Unknown parameter
|month=ignored (help) - ↑ Shachor-Meyouhas, Y.; Arad-Cohen, N.; Zaidman, I.; Gefen, A.; Kassis, I. (2012). “[Legionella pneumonia in a child with leukemia]”. Harefuah. 151 (8): 479–82, 496. PMID 23350295. Unknown parameter
|month=ignored (help) - ↑ “Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia”. American Journal of Respiratory and Critical Care Medicine. 171 (4): 388–416. 2005. doi:10.1164/rccm.200405-644ST. PMID 15699079. Retrieved 2012-09-12. Unknown parameter
|month=ignored (help) - ↑ “CDC GUIDELINES FOR PREVENTING HEALTH-CARE-ASSOCIATED PNEUMONIA, 2003” (PDF).
Differentiating Pneumonia from other Diseases
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Priyamvada Singh, M.D. [3] Syed Hassan A. Kazmi BSc, MD [4]

Overview
Pneumonia should be differentiated from other conditions that cause cough, fever, shortness of breath and tachypnea, such as asthma, COPD, CHF, cancer, GERD, pulmonary emboli.
Differentiating Pneumonia from other Diseases
| Disease | Findings |
|---|---|
| Acute bronchitis | No infiltrates seen on the chest X-ray. |
| Asthma | Past medical history, no infiltrates seen on chest X-ray. |
| Bronchiolitis obliterans | Should be suspected in patients with pneumonia who do not respond to antibiotics treatment. |
| Congestive heart failure | Bilateral pulmonary edema, shortness of breath. |
| COPD | Past medical history, no infiltrates on chest X-ray, fever is uncommon. |
| Empyema | CXR showing features of pleural effusion, inflammatory markers on thoracocentesis. |
| Endocarditis | Finding of septic pulmonary emboli |
| Gastroesophageal reflux disease (GERD) | Normal chest X-ray, symptoms are worse during night and associated with meals. |
| Lung abscess | Chest X-ray shows signs of lung abscess. |
| Lung cancer | Weight loss, clear sputum. CT scan and biopsy are helpful in ruling out malignancy. |
| Pertussis | Productive cough for weeks, nasopharyngeal aspirate aids in diagnosis. |
| Pulmonary embolus | A high degree of suspicion should be kept for pulmonary embolus. Chest X-ray may be normal. |
| Sinusitis | Sinus tenderness, post nasal drip. |
| Vasculitis | Systemic manifestations of collagen vascular disease may be seen. |
Differential diagnosis
| Causes of
Lung Cavities |
Differentiating Features | Differentiating Radiological Findings | Diagnosis Confirmation |
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Table 1: Differentiating psittacosis from other diseases
| Clinical feature | Cough | Sputum | Dyspnea | Sore throat | Headache | Confusion | Diarrhea | Chest radiograph changes | Hyponatremia | Leukopenia | Abnormal Liver function tests | Treatment |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Psittacosis | ++ | – | + | – | +++ | + | Minimal |
|
– | + | – | Doxycycline |
| C.pneumoniae pneumonia | + | + | + | +++ | ++ | + | – |
|
– | – | – | Doxycycline, Azithromycin |
| M. pneumoniae pneumonia | ++ | ++ | ++ | – | – | – | – |
|
– | – | + | Doxycycline |
| L. Pneumophila infection | + | +++ | +++ | – | + | ++ | + | Often Multifocal | ++ | + | ++ | Doxycycline |
| Influenza | ++ | ++ | ++ | ++ | ++ | +/- | +/- |
|
– | – | – | zanamivir, oseltamivir, |
| Endocarditis | ++ | ++ | + | – | – | – | – |
bases bilaterally |
– | +/- | +/- | Vancomycin |
| Coxiella burnetii infection | ++ | – | + | +/- | – | +/- | Minimal |
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– | +/- | =/- | Doxycycline |
| Leptospirosis | ++ | + | ++ | + | + | ++ | – |
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+++ | Doxycycline, azithromycin, amoxicillin | ||
| Brucellosis | ++ | – | + | – | ++ | + | – |
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-/+ | +/- | +/- | Doxycycline, rifampin |
Key;
+, occurs in some cases
++, occurs in many cases,
+++, occurs frequently
Pnemonia must be differentiated from other diseases that cause atypical pneumonia such as Q fever and legionella pneumonia:
| Disease | Prominent clinical features | Lab findings | Chest X-ray |
|---|---|---|---|
| Q fever |
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| Mycoplasma pneumonia |
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| Legionellosis |
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| Chlamydia pneumonia |
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Other differentials
Pneumonia should be differentiated from other diseases presenting with cough, fever, shortness of breath and tachypnea. The differentials include the following:[18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37]
| Diseases | Diagnostic tests | Physical Examination | Symptoms | Past medical history | Other Findings | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| CT scan and MRI | EKG | Chest X-ray | Tachypnea | Tachycardia | Fever | Chest Pain | Hemoptysis | Dyspnea on Exertion | Wheezing | Chest Tenderness | Nasalopharyngeal Ulceration | Carotid Bruit | |||
| Pulmonary embolism |
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✔ | ✔ | ✔ (Low grade) | ✔ | ✔ (In case of massive PE) | ✔ | – | – | – | – |
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| Congestive heart failure |
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✔ | ✔ | ✔ | – | – | ✔ | – | – | – | – |
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| Percarditis |
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✔ | ✔ | ✔ (Low grade) | ✔ (Relieved by sitting up and leaning forward) | – | ✔ | – | – | – | – |
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| Pneumonia |
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✔ | ✔ | ✔ | ✔ | – | ✔ | ✔ | – | – | – |
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| Vasculitis |
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✔ | ✔ | ✔ | ✔ | ✔ | ✔ | – | ✔ | ✔ | ✔ |
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| Chronic obstructive pulmonary disease (COPD) |
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✔ | ✔ | – | – | – | ✔ | ✔ | – | – | – |
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References
- ↑ Schiele F, Muller J, Colinet E, Siest G, Arzoglou P, Brettschneider H; et al. (1992). “Interlaboratory study of the IFCC method for alanine aminotransferase performed with use of a partly purified reference material”. Clin Chem. 38 (12): 2365–71. PMID 1458569.
- ↑ Castro-Guardiola A, Armengou-Arxé A, Viejo-Rodríguez A, Peñarroja-Matutano G, Garcia-Bragado F (2000). “Differential diagnosis between community-acquired pneumonia and non-pneumonia diseases of the chest in the emergency ward”. Eur J Intern Med. 11 (6): 334–339. PMID 11113658.
- ↑ Ahnsjö, Sven (1935). “Contribution to the Differential Diagnosis of Pneumonia in Childhood”. Acta Paediatrica. 17 (3): 439–446. doi:10.1111/j.1651-2227.1935.tb07697.x. ISSN 0803-5253.
- ↑ 4.0 4.1 Chaudhuri MR (1973). “Primary pulmonary cavitating carcinomas”. Thorax. 28 (3): 354–66. PMC 470041. PMID 4353362.
- ↑ Mouroux J, Padovani B, Elkaïm D, Richelme H (1996). “Should cavitated bronchopulmonary cancers be considered a separate entity?”. Ann. Thorac. Surg. 61 (2): 530–2. doi:10.1016/0003-4975(95)00973-6. PMID 8572761.
- ↑ Onn A, Choe DH, Herbst RS, Correa AM, Munden RF, Truong MT, Vaporciyan AA, Isobe T, Gilcrease MZ, Marom EM (2005). “Tumor cavitation in stage I non-small cell lung cancer: epidermal growth factor receptor expression and prediction of poor outcome”. Radiology. 237 (1): 342–7. doi:10.1148/radiol.2371041650. PMID 16183941.
- ↑ 7.0 7.1 Langford CA, Hoffman GS (1999). “Rare diseases.3: Wegener’s granulomatosis”. Thorax. 54 (7): 629–37. PMC 1745525. PMID 10377211.
- ↑ Lee KS, Kim TS, Fujimoto K, Moriya H, Watanabe H, Tateishi U, Ashizawa K, Johkoh T, Kim EA, Kwon OJ (2003). “Thoracic manifestation of Wegener’s granulomatosis: CT findings in 30 patients”. Eur Radiol. 13 (1): 43–51. doi:10.1007/s00330-002-1422-2. PMID 12541109.
- ↑ Baughman RP, Teirstein AS, Judson MA, Rossman MD, Yeager H, Bresnitz EA, DePalo L, Hunninghake G, Iannuzzi MC, Johns CJ, McLennan G, Moller DR, Newman LS, Rabin DL, Rose C, Rybicki B, Weinberger SE, Terrin ML, Knatterud GL, Cherniak R (2001). “Clinical characteristics of patients in a case control study of sarcoidosis”. Am. J. Respir. Crit. Care Med. 164 (10 Pt 1): 1885–9. doi:10.1164/ajrccm.164.10.2104046. PMID 11734441.
- ↑ Brauner MW, Grenier P, Mompoint D, Lenoir S, de Crémoux H (1989). “Pulmonary sarcoidosis: evaluation with high-resolution CT”. Radiology. 172 (2): 467–71. doi:10.1148/radiology.172.2.2748828. PMID 2748828.
- ↑ Murphy J, Schnyder P, Herold C, Flower C (1998). “Bronchiolitis obliterans organising pneumonia simulating bronchial carcinoma”. Eur Radiol. 8 (7): 1165–9. doi:10.1007/s003300050527. PMID 9724431.
- ↑ 12.0 12.1 Al-Ghanem S, Al-Jahdali H, Bamefleh H, Khan AN (2008). “Bronchiolitis obliterans organizing pneumonia: pathogenesis, clinical features, imaging and therapy review”. Ann Thorac Med. 3 (2): 67–75. doi:10.4103/1817-1737.39641. PMC 2700454. PMID 19561910.
- ↑ Cordier JF, Loire R, Brune J (1989). “Idiopathic bronchiolitis obliterans organizing pneumonia. Definition of characteristic clinical profiles in a series of 16 patients”. Chest. 96 (5): 999–1004. PMID 2805873.
- ↑ Lee KS, Kullnig P, Hartman TE, Müller NL (1994). “Cryptogenic organizing pneumonia: CT findings in 43 patients”. AJR Am J Roentgenol. 162 (3): 543–6. doi:10.2214/ajr.162.3.8109493. PMID 8109493.
- ↑ Suri HS, Yi ES, Nowakowski GS, Vassallo R (2012). “Pulmonary langerhans cell histiocytosis”. Orphanet J Rare Dis. 7: 16. doi:10.1186/1750-1172-7-16. PMC 3342091. PMID 22429393.
- ↑ Moore AD, Godwin JD, Müller NL, Naidich DP, Hammar SP, Buschman DL, Takasugi JE, de Carvalho CR (1989). “Pulmonary histiocytosis X: comparison of radiographic and CT findings”. Radiology. 172 (1): 249–54. doi:10.1148/radiology.172.1.2787035. PMID 2787035.
- ↑ 17.0 17.1 17.2 17.3 Irfan M, Farooqi J, Hasan R (2013). “Community-acquired pneumonia”. Curr Opin Pulm Med. 19 (3): 198–208. doi:10.1097/MCP.0b013e32835f1d12. PMID 23422417.
- ↑ Brenes-Salazar JA (2014). “Westermark’s and Palla’s signs in acute and chronic pulmonary embolism: Still valid in the current computed tomography era”. J Emerg Trauma Shock. 7 (1): 57–8. doi:10.4103/0974-2700.125645. PMC 3912657. PMID 24550636.
- ↑ “CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis | RadioGraphics”.
- ↑ Bĕlohlávek J, Dytrych V, Linhart A (2013). “Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism”. Exp Clin Cardiol. 18 (2): 129–38. PMC 3718593. PMID 23940438.
- ↑ “Pulmonary Embolism: Symptoms – National Library of Medicine – PubMed Health”.
- ↑ Ramani GV, Uber PA, Mehra MR (2010). “Chronic heart failure: contemporary diagnosis and management”. Mayo Clin. Proc. 85 (2): 180–95. doi:10.4065/mcp.2009.0494. PMC 2813829. PMID 20118395.
- ↑ Blinderman CD, Homel P, Billings JA, Portenoy RK, Tennstedt SL (2008). “Symptom distress and quality of life in patients with advanced congestive heart failure”. J Pain Symptom Manage. 35 (6): 594–603. doi:10.1016/j.jpainsymman.2007.06.007. PMC 2662445. PMID 18215495.
- ↑ Hawkins NM, Petrie MC, Jhund PS, Chalmers GW, Dunn FG, McMurray JJ (2009). “Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology”. Eur. J. Heart Fail. 11 (2): 130–9. doi:10.1093/eurjhf/hfn013. PMC 2639415. PMID 19168510.
- ↑ Takasugi JE, Godwin JD (1998). “Radiology of chronic obstructive pulmonary disease”. Radiol. Clin. North Am. 36 (1): 29–55. PMID 9465867.
- ↑ Wedzicha JA, Donaldson GC (2003). “Exacerbations of chronic obstructive pulmonary disease”. Respir Care. 48 (12): 1204–13, discussion 1213–5. PMID 14651761.
- ↑ Nakawah MO, Hawkins C, Barbandi F (2013). “Asthma, chronic obstructive pulmonary disease (COPD), and the overlap syndrome”. J Am Board Fam Med. 26 (4): 470–7. doi:10.3122/jabfm.2013.04.120256. PMID 23833163.
- ↑ Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, Oh JK (2010). “Pericardial disease: diagnosis and management”. Mayo Clin. Proc. 85 (6): 572–93. doi:10.4065/mcp.2010.0046. PMC 2878263. PMID 20511488.
- ↑ Bogaert J, Francone M (2013). “Pericardial disease: value of CT and MR imaging”. Radiology. 267 (2): 340–56. doi:10.1148/radiol.13121059. PMID 23610095.
- ↑ Gharib AM, Stern EJ (2001). “Radiology of pneumonia”. Med. Clin. North Am. 85 (6): 1461–91, x. PMID 11680112.
- ↑ Schmidt WA (2013). “Imaging in vasculitis”. Best Pract Res Clin Rheumatol. 27 (1): 107–18. doi:10.1016/j.berh.2013.01.001. PMID 23507061.
- ↑ Suresh E (2006). “Diagnostic approach to patients with suspected vasculitis”. Postgrad Med J. 82 (970): 483–8. doi:10.1136/pgmj.2005.042648. PMC 2585712. PMID 16891436.
- ↑ Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW (1975). “The electrocardiogram in acute pulmonary embolism”. Prog Cardiovasc Dis. 17 (4): 247–57. PMID 123074.
- ↑ Warnier MJ, Rutten FH, Numans ME, Kors JA, Tan HL, de Boer A, Hoes AW, De Bruin ML (2013). “Electrocardiographic characteristics of patients with chronic obstructive pulmonary disease”. COPD. 10 (1): 62–71. doi:10.3109/15412555.2012.727918. PMID 23413894.
- ↑ Stein PD, Matta F, Ekkah M, Saleh T, Janjua M, Patel YR, Khadra H (2012). “Electrocardiogram in pneumonia”. Am. J. Cardiol. 110 (12): 1836–40. doi:10.1016/j.amjcard.2012.08.019. PMID 23000104.
- ↑ Hazebroek MR, Kemna MJ, Schalla S, Sanders-van Wijk S, Gerretsen SC, Dennert R, Merken J, Kuznetsova T, Staessen JA, Brunner-La Rocca HP, van Paassen P, Cohen Tervaert JW, Heymans S (2015). “Prevalence and prognostic relevance of cardiac involvement in ANCA-associated vasculitis: eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis”. Int. J. Cardiol. 199: 170–9. doi:10.1016/j.ijcard.2015.06.087. PMID 26209947.
- ↑ Dennert RM, van Paassen P, Schalla S, Kuznetsova T, Alzand BS, Staessen JA, Velthuis S, Crijns HJ, Tervaert JW, Heymans S (2010). “Cardiac involvement in Churg-Strauss syndrome”. Arthritis Rheum. 62 (2): 627–34. doi:10.1002/art.27263. PMID 20112390.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Priyamvada Singh, M.D. [3]; Alejandro Lemor, M.D. [4]
Overview
Pneumonia is a common illness in all parts of the world. It is a major cause of death among all age groups. Mortality from pneumonia generally decreases with age until late adulthood. Elderly individuals, however, are at particular risk for pneumonia and associated mortality. More cases of pneumonia occur during the winter months than during other times of the year. Pneumonia occurs more commonly in males than females, and more often in African Americans than caucasians. People who are hospitalized for any reason are also at high risk for pneumonia. Following urinary tract infections, pneumonia is the second most common cause of nosocomial infections, and its prevalence is 15-20% of the total number.
Epidemiology and Demographics
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United States of America
- It is the seventh most common cause of death in the United States
- It causes around 500,000 hospitalizations and 65,000 deaths annually.
International
- It is a common illness in all parts of the world, but countries like India, China, Pakistan, Bangladesh, Indonesia and Nigeria have high rates of childhood pneumonia.[2]
Age
- The incidence is higher in children and elderly.
- In children, the majority of deaths occur in the newborn period, with over two million worldwide deaths a year.
- In fact, the WHO estimates that one in three newborn infant deaths are due to pneumonia.
- Mortality decreases with age until late adulthood; elderly individuals are particularly at risk for CAP and associated mortality.
Seasonal
- More common during winter months than during other times of the year.
Gender
- CAP occurs more commonly in males than females
Race
- More common in African Americans than caucasians.
Mortality
- Patients hospitalized with pneumonia have a mortality rate of 12-14%.
Special Considerations
- Individuals with underlying illnesses such as Alzheimer’s disease, cystic fibrosis, emphysema, tobacco smoking, alcoholism, or immune system problems are at increased risk for pneumonia.[6]
| Country | Predicted no. of new cases (millions) | Estimated incidence(e/cy) |
|---|---|---|
| India | 43.0 | 0.37 |
| China | 21.1 | 0.22 |
| Pakistan | 9.8 | 0.41 |
| Bangladesh | 6.4 | 0.41 |
| Nigeria | 6.1 | 0.34 |
| Indonesia | 6.0 | 0.28 |
| Ethiopia | 3.9 | 0.35 |
| Democratic Republic of the Congo | 3.9 | 0.39 |
| Viet Nam | 2.9 | 0.35 |
| Philippines | 2.7 | 0.27 |
| Sudan | 2.0 | 0.48 |
| Afghanistan | 2.0 | 0.45 |
| United Republic of Tanzania | 1.9 | 0.33 |
| Myanmar | 1.8 | 0.43 |
| Brazil | 1.8 | 0.11 |
| Table adapted from WHO [3] | ||
Community Acquired Pneumonia
![]() Graph obtained from CDC [4] |
- As many as 400,000 hospitalizations from pneumococcal pneumonia are estimated to occur annually in the United States. Pneumococci accounts for about 30% of adult community-acquired pneumonia. [5]
- In 2012, 59.9% of adults 65 years and older received a pneumococcal vaccination.[6]
- In 2010, the number of discharges for patient admitted with pneumonia in hospitals in the US was 1.1 million patients. The average length of stay for pneumonia patients admitted to hospitals was 5.2 days.[6]
- An increasing rate of CAP is seen with age. Approximately 5 to 6 cases of pneumonia per 1000 persons are observed among adults. A pronounced seasonal effect on the number of patients presenting to the emergency department is also noted. During the winter months, there is an approximately 50% rise in the number of cases compared to the summer months.[7]
- Streptococcus pneumoniae is the leading cause of pneumonia worldwide.[8]
Mortality
- About 3.5 million deaths yearly have been attributed to lower respiratory tract infections (LRTI). LTRIs are the third most common cause of overall death and the leading cause of death from infectious diseases worldwide.[9]
- Pneumonia is the ninth leading cause of death in the United States.
- The number of deaths in the US in 2011 attributed to pneumonia was 52,294. [6]
- Pneumonia mortality rate was 16.8 deaths per 100,000 in the US in 2011. [6]
- A higher mortality rate is seen in invasive diseases, nursing home patients and severe bacteremia.
- More than 40 % mortality rate is seen in ICU admitted patients.
- The percentage of hospital inpatient deaths from pneumonia in the US 2006 was 3.4%. [10]
Age
- Individuals older than 85 years of age are at a particularly high risk of developing CAP that can reach an annual rate of 5-10%.[11]
- Individuals younger than 3 years and older than 65 years of age are more likely to be hospitalized with severe symptoms and complications.
Gender
- The risk of CAP is similar in males and females.
Incidence of Community–Acquired Pneumonia in 2010 in Children 0–4 Years of Age in 192 Countries[12]
▸ Click on the following regions to expand the data.
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Hospital Acquired Pneumonia
- Pneumonia has accounted for approximately 20% of all hospital-associated infections and 27% and 24% of all infections acquired in the medical intensive-care unit (ICU) and coronary care unit, respectively. [13]
Incidence
- The incidence of HAP is 5-15 cases per 1 000 hospital admissions. [14]
- The incidence of VAP is 6 to 20 times more than in patients without mechanical support.
| Age | Females | Males |
|---|---|---|
| 18-44 years | 5% | 4% |
| 45-64 years | 14% | 13% |
| ≥ 65 years | 34% | 30% |
| Total | 53% | 47% |
| Table adapted from 2009–2011 National Medicare Patient Safety Monitoring System [15] | ||
Mortality
- HAP and VAP are nosocomial infections with a high mortality in contrast with other nosocomial infections.
- This higher mortality rate is associated with MDR pathogens.
Age
- HAP is more commonly reported in patients > 65 years, probably due to the fact that this age population is more commonly hospitalized.
Gender
- There is no predominance in gender, although some data reports a higher incidence among females.
Ventilator-associated Pneumonia
- VAP occurs in up to 25% of all people who require mechanical ventilation.
- VAP can develop at any time during ventilation, but occurs more often in the first few days after intubation.
- This is because the intubation process itself contributes to the development of VAP.
- VAP occurring early after intubation typically involves fewer resistant organisms and is thus associated with a more favorable outcome.
- Because respiratory failure requiring mechanical ventilation is itself associated with a high mortality, determination of the exact contribution of VAP to mortality has been difficult.
- As of 2006, estimates range from 33% to 50% death in patients who develop VAP.
- Mortality is more likely when VAP is associated with certain microorganisms (Pseudomonas, Acinetobacter), blood stream infections, and ineffective initial antibiotics.
- VAP is especially common in people who have acute respiratory distress syndrome (ARDS).
References
- ↑ “Pneumococcal Disease – Epidemiology and Prevention of Vaccine-Preventable Diseases”.
- ↑ Rudan I, Boschi-Pinto C, Biloglav Z, Mulholland K, Campbell H (2008). “Epidemiology and etiology of childhood pneumonia”. Bull World Health Organ. 86 (5): 408–16. PMC 2647437. PMID 18545744.
- ↑ http://www.who.int/bulletin/volumes/86/5/07-048769-table-T2.html
- ↑ “CDC Early Release of Selected Estimates Based on Data From the 2012 National Health Interview Survey – Receipt of pneumococcal vaccination” (PDF).
- ↑ “CDC Pneumococcal Disease – Clinical Features”.
- ↑ 6.0 6.1 6.2 6.3 “CDC Pneumonia FastStats”.
- ↑ Marrie, TJ.; Huang, JQ. (2005). “Epidemiology of community-acquired pneumonia in Edmonton, Alberta: an emergency department-based study”. Can Respir J. 12 (3): 139–42. PMID 15875065. Unknown parameter
|month=ignored (help) - ↑ Miniño, AM.; Murphy, SL.; Xu, J.; Kochanek, KD. (2011). “Deaths: final data for 2008”. Natl Vital Stat Rep. 59 (10): 1–126. PMID 22808755. Unknown parameter
|month=ignored (help) - ↑ “WHO”. Text ” The top 10 causes of death ” ignored (help)
- ↑ http://www.cdc.gov/nchs/data/series/sr_13/sr13_168.pdf
- ↑ Jackson ML, Neuzil KM, Thompson WW, Shay DK, Yu O, Hanson CA; et al. (2004). “The burden of community-acquired pneumonia in seniors: results of a population-based study”. Clin Infect Dis. 39 (11): 1642–50. doi:10.1086/425615. PMID 15578365.
- ↑ Rudan I, O’Brien KL, Nair H, Liu L, Theodoratou E, Qazi S; et al. (2013). “Epidemiology and etiology of childhood pneumonia in 2010: estimates of incidence, severe morbidity, mortality, underlying risk factors and causative pathogens for 192 countries”. J Glob Health. 3 (1): 010401. doi:10.7189/jogh.03.010401. PMC 3700032. PMID 23826505.
- ↑ Magill, Shelley S.; Edwards, Jonathan R.; Bamberg, Wendy; Beldavs, Zintars G.; Dumyati, Ghinwa; Kainer, Marion A.; Lynfield, Ruth; Maloney, Meghan; McAllister-Hollod, Laura; Nadle, Joelle; Ray, Susan M.; Thompson, Deborah L.; Wilson, Lucy E.; Fridkin, Scott K. (2014). “Multistate Point-Prevalence Survey of Health Care–Associated Infections”. New England Journal of Medicine. 370 (13): 1198–1208. doi:10.1056/NEJMoa1306801. ISSN 0028-4793.
- ↑ “Guidelines for the Management of Adults with Hospital-acquired, Ventilator-associated, and Healthcare-associated Pneumonia”. American Journal of Respiratory and Critical Care Medicine. 171 (4): 388–416. 2005. doi:10.1164/rccm.200405-644ST. ISSN 1073-449X.
- ↑ Eckenrode, Sheila; Bakullari, Anila; Metersky, Mark L.; Wang, Yun; Pandolfi, Michelle M.; Galusha, Deron; Jaser, Lisa; Eldridge, Noel (2014). “The Association between Age, Sex, and Hospital-Acquired Infection Rates: Results from the 2009–2011 National Medicare Patient Safety Monitoring System”. Infection Control and Hospital Epidemiology. 35 (S3): S3–S9. doi:10.1086/677831. ISSN 0899-823X.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Priyamvada Singh, M.D. [3]Philip Marcus, M.D., M.P.H.[4]
Overview
The risk factors for pneumonia include: smoking, age>65, immuno-suppression, exposure to chemicals, and underlying lung disease.
Risk Factors
Airway Obstruction
- When part of the airway (bronchi) leading to the alveoli is obstructed, the lung is not able to clear fluid when it accumulates. This can lead to infection of the fluid resulting in community-acquired pneumonia (CAP).
- One cause of obstruction, especially in young children, is inhalation of a foreign object such as a marble or toy. The object is lodged in the small airways and pneumonia can form in the trapped areas of lung.
- Another cause of obstruction is lung cancer, which can grow into the airways blocking the flow of air.
Lung Disease
- Smoking, and diseases such as emphysema, result in more frequent and severe bouts of CAP.
- In children, recurrent episodes of CAP may be the first clue to diseases such as cystic fibrosis or pulmonary sequestration.
Immune Compromise
- People who have immune system problems are more likely to get CAP.
- Risk factors for increased mortality from community acquired pneumonia are: active malignancy, immuno-suppression, neurological disease, congestive heart failure, coronary artery disease, and diabetes mellitus
- People who have AIDS are much more likely to develop CAP. Pneumonia could be the first manifestation of an underlying undiagnosed HIV. It is thus recommended by the Center for Disease Control (CDC) that all patients aged 13 to 64 in a medical setting regardless of known risk factors be screened for HIV. The American College of Physicians and HIV Medicine Association recommends expanding screening for HIV from age 13 to 75 [1], [2].
- Other immune problems range from severe immune deficiencies of childhood such as Wiskott-Aldrich syndrome to less severe deficiencies such as common variable immunodeficiency.[5]
- Elderly people are affected with increased incidence and severity of community acquired pneumonia. It is the fifth most common cause of death among individuals who are > 65 years of age, and fourth in individuals who are 85 years or older. The clinical picture in elderly could be subtle and could present only as delirium without any fever, cough or sputum. Therefore, a high index of suspicion should be kept in these groups of people.
Community Acquired Pneumonia
The following are risk factors related to specific causative pathogens in community-acquired pneumonia:
Exposure to Animals
| Animals | Most Common Pathogens |
|---|---|
| Bat or bird droppings | Histoplasma capsulatum |
| Birds | Chlamydophila psittaci |
| Rabbits | Francisella tularensis |
| Farm animals or parturient cats | Coxiella burnetti (Q fever) |
| Table adapted from IDSA/ATS Guidelines for CAP in Adults [3] | |
Travel
| Condition | Most Common Pathogens |
|---|---|
| Hotel or cruise ship stay | Legionella spp |
| Travel to southwestern US | Coccidioides spp, Hantavirus |
| Travel to southeast or east Asia | Burkholderia pseudomallei, avian influenza, SARS |
| Table adapted from IDSA/ATS Guidelines for CAP in Adults [3] | |
Obstruction
- Airway obstruction may cause fluid accumulation in the lungs and result in CAP if the fluids become infected.
- One cause of obstruction, especially in young children, is inhalation of a foreign object such as a marble or toy. The object is lodged in the small airways and pneumonia can form in the trapped areas of lung.
- Another cause of obstruction is lung cancer, which can grow into the airways blocking the flow of air.
Lung Disease
- In children, recurrent episodes of CAP may be the first clue to diseases such as cystic fibrosis or pulmonary sequestration.
- Previous episode of pneumonia or chronic bronchitis
Immune Problems
- People who have immune disorders are more likely to acquire CAP.
- Risk factors for increased mortality from community-acquired pneumonia are: active malignancy, immunosuppression, neurological disease, congestive heart failure, coronary artery disease, and diabetes mellitus.
- People who have AIDS are much more likely to develop CAP. Pneumonia could be the first manifestation of an underlying undiagnosed HIV. It is, thus, recommended by the Center for Disease Control (CDC) that all patients aged 13 to 64 in a medical setting, regardless of known risk factors, be screened for HIV. The American College of Physicians and HIV Medicine Association recommends expanding screening for HIV from age 13 to 75 [1], [2].
- Other immune problems range from severe immune deficiencies from childhood, such as Wiskott-Aldrich syndrome, to less severe deficiencies, such as common variable immunodeficiency.[6]
- Elderly people are affected with increased incidence and severity of community-acquired pneumonia. It is the fifth most common cause of death amongst individuals who are greater than 65 years of age, and it is the fourth most common cause of death in individuals who are 85 years or older. The clinical picture in elderly could be subtle and it could be present only as delirium without any fever, cough or sputum. Therefore, a high index of suspicion should be kept in these groups of people.
- Immotile cilia syndrome
- Kartagener’s syndrome (ciliary dysfunction, situs inversus, sinusitis, bronchiectasis)
- Young’s syndrome (azoospermia, sinusitis, pneumonia)
Other Risk Factors
A few other conditions may lead to pneumonia due to altered pulmonary defense mechanisms.[4]
- Dysphagia due to esophageal lesions and motility problems
- HIV infection (especially for pneumococcal pneumonia)
Drugs
Acid-Suppressing Drugs
- Usage of H2 blockers, proton pump inhibitors, and antacids may increase the pH and, as a result, may increase the risk of pneumonia.[5][6][7]
- A similiar study showed increase risk of pneumonia after starting PPI, especially within the first 48 hours.[5][6][7] However, the association between PPI and CAP may be cofounded.[8]
Antipsychotic Drugs
- A case control study has shown a significant correlation between the use of antipsychotic drugs and community-acquired pneumonia. A 60 percent increase in the rate of pneumonia can be seen in elderly patients who utilize antipsychotic medications.[9]
- The use of atypical antipsychotics was associated with an increases risk of community-acquired pneumonia.
ACE Inhibitors
- A randomized trial has shown that ACE inhibitors reduce the risk of pneumonia.[10]
Hospital Acquired Pneumonia
| Major risk factors for hospital-acquired pneumonia |
|---|
|
|
|
|
|
|
|
|
|
|
|
|
|
| Table adapted from CDC[11] |
The following are major points for risk factors of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia:[12]
| “ |
Major Points and Recommendations for Modifiable Risk FactorsGeneral Prophylaxis
Intubation and Mechanical Ventilation
Aspiration, Body Position, and Enteral Feeding
Modulation of Colonization: Oral Antiseptics and Antibiotics
|
” |
For Level of evidence and classes click here.
References
- ↑ 1.0 1.1 “Summaries for patients. Screening for HIV infection in health care settings: a guidance statement from the American College of Physicians and HIV Medicine Association”. Annals of Internal Medicine. 150 (2): I–44. 2009. PMID 19047021. Retrieved 2012-09-04. Unknown parameter
|month=ignored (help) - ↑ 2.0 2.1 Qaseem A, Snow V, Shekelle P, Hopkins R, Owens DK (2009). “Screening for HIV in health care settings: a guidance statement from the American College of Physicians and HIV Medicine Association”. Annals of Internal Medicine. 150 (2): 125–31. PMID 19047022. Retrieved 2012-09-04. Unknown parameter
|month=ignored (help) - ↑ 3.0 3.1 3.2 Mandell, L. A.; Wunderink, R. G.; Anzueto, A.; Bartlett, J. G.; Campbell, G. D.; Dean, N. C.; Dowell, S. F.; File, T. M.; Musher, D. M.; Niederman, M. S.; Torres, A.; Whitney, C. G. (2007). “Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines on the Management of Community-Acquired Pneumonia in Adults”. Clinical Infectious Diseases. 44 (Supplement 2): S27–S72. doi:10.1086/511159. ISSN 1058-4838.
- ↑ Almirall, J.; Bolíbar, I.; Balanzó, X.; González, CA. (1999). “Risk factors for community-acquired pneumonia in adults: a population-based case-control study”. Eur Respir J. 13 (2): 349–55. PMID 10065680. Unknown parameter
|month=ignored (help) - ↑ 5.0 5.1 Laheij, RJ.; Sturkenboom, MC.; Hassing, RJ.; Dieleman, J.; Stricker, BH.; Jansen, JB. (2004). “Risk of community-acquired pneumonia and use of gastric acid-suppressive drugs”. JAMA. 292 (16): 1955–60. doi:10.1001/jama.292.16.1955. PMID 15507580. Unknown parameter
|month=ignored (help) - ↑ 6.0 6.1 Gulmez, SE.; Holm, A.; Frederiksen, H.; Jensen, TG.; Pedersen, C.; Hallas, J. (2007). “Use of proton pump inhibitors and the risk of community-acquired pneumonia: a population-based case-control study”. Arch Intern Med. 167 (9): 950–5. doi:10.1001/archinte.167.9.950. PMID 17502537. Unknown parameter
|month=ignored (help) - ↑ 7.0 7.1 Hermos, JA.; Young, MM.; Fonda, JR.; Gagnon, DR.; Fiore, LD.; Lawler, EV. (2012). “Risk of community-acquired pneumonia in veteran patients to whom proton pump inhibitors were dispensed”. Clin Infect Dis. 54 (1): 33–42. doi:10.1093/cid/cir767. PMID 22100573. Unknown parameter
|month=ignored (help) - ↑ Jena, AB.; Sun, E.; Goldman, DP. (2013). “Confounding in the association of proton pump inhibitor use with risk of community-acquired pneumonia”. J Gen Intern Med. 28 (2): 223–30. doi:10.1007/s11606-012-2211-5. PMID 22956446. Unknown parameter
|month=ignored (help) - ↑ Knol, W.; van Marum, RJ.; Jansen, PA.; Souverein, PC.; Schobben, AF.; Egberts, AC. (2008). “Antipsychotic drug use and risk of pneumonia in elderly people”. J Am Geriatr Soc. 56 (4): 661–6. doi:10.1111/j.1532-5415.2007.01625.x. PMID 18266664. Unknown parameter
|month=ignored (help) - ↑ Caldeira, D.; Alarcão, J.; Vaz-Carneiro, A.; Costa, J. (2012). “Risk of pneumonia associated with use of angiotensin converting enzyme inhibitors and angiotensin receptor blockers: systematic review and meta-analysis”. BMJ. 345: e4260. PMID 22786934.
- ↑ “CDC GUIDELINES FOR PREVENTING HEALTH-CARE-ASSOCIATED PNEUMONIA, 2003” (PDF).
- ↑ “Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia”. American Journal of Respiratory and Critical Care Medicine. 171 (4): 388–416. 2005. doi:10.1164/rccm.200405-644ST. PMID 15699079. Retrieved 2012-09-13. Unknown parameter
|month=ignored (help)
Natural History, Complications and Prognosis
Prognosis Predictor Scores: CURB-65 | Pneumonia Severity Index | Criteria for Severe Community-Acquired Pneumonia
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Priyamvada Singh, M.D. [3]
Overview
Pneumonia is an infection of the lungs that can cause mild to severe illness in people of all ages. The incubation period is between 1 and 3 days and symptoms include fever, cough, chest pain, dyspnea and tachypnea. Complications of pneumonia include sepsis, respiratory failure, pleural effusion, empyema, and lung abscess. Most types of pneumonia can be completely cured with the appropriate medical therapy and mortality rates can be 1%, depending on the age and comorbidities.
Natural History
- Pneumococcal pneumonia is the most common clinical presentation of pneumococcal disease among adults, although pneumonia without bacteremia or empyema is not considered to be “invasive” disease. [1]
- The incubation period of pneumococcal pneumonia is short, about 1 to 3 days. [1]
- Symptoms generally include an abrupt onset of fever and chills or rigors. [1]
- Typically there is a single rigor, and repeated shaking chills are uncommon. [1]
- Other common symptoms include pleuritic chest pain, cough productive of mucopurulent, rusty sputum, dyspnea, tachypnea, hypoxia, tachycardia, malaise, and weakness. Nausea, vomiting, and headaches occur less frequently.[1]
- Transmission of streptococcus pneumonia occurs as a result of direct person-to-person contact via respiratory droplets and by autoinoculation in persons carrying the bacteria in their upper respiratory tract. [1]
- The pneumococcal serotypes most often responsible for causing infection are those most frequently found in carriers.[1]
Complications
Despite appropriate antibiotic therapy, severe complications can result from CAP, including:
Sepsis
- Sepsis can occur when microorganisms enter the blood stream and the immune system responds.
- Sepsis most often occurs with bacterial pneumonia
- Streptococcus pneumoniae is the most common cause.
- Individuals with sepsis require hospitalization in an intensive care unit. They often require medications and intravenous fluids to keep their blood pressure from going too low. Sepsis can cause liver, kidney, and heart damage among other things.
Respiratory Failure
- If enough of the lung is involved, it may not be possible for a person to breathe enough to live without support.
- Non-invasive machines such as a bilevel positive airway pressure machine may be used.
- Otherwise, placement of a breathing tube into the mouth may be necessary. A ventilator may also be used to help the person breathe.
Pleural Effusion and Empyema
- Occasionally, microorganisms from the lung will cause fluid to form in the space surrounding the lung, called the pleural cavity.
- If the microorganisms themselves are present, the fluid collection is often called an empyema.
- If pleural fluid is present in a person with CAP, the fluid should be collected with a needle (thoracentesis) and examined.
- Depending on the result of the examination, complete drainage of the fluid may be necessary, often with a chest tube. If the fluid is not drained, bacteria can continue to cause illness because antibiotics do not penetrate well into the pleural cavity.
Abscess
- Rarely, microorganisms in the lung will form a pocket of fluid and bacteria called an abscess.
- Abscesses can be seen on an x-ray as a cavity within the lung. Abscesses typically occur in aspiration pneumonia and most often contain a mixture of anaerobic bacteria.
- Usually antibiotics are able to fully treat abscesses, but sometimes they must be drained by a surgeon or radiologist.
Sometimes pneumonia can lead to additional complications. Complications are more frequently associated with bacterial pneumonia than with viral pneumonia. The most important complications include:
Respiratory and Circulatory Failure
- Because pneumonia affects the lungs, often people with pneumonia have difficulty breathing, and it may not be possible for them to breathe well enough to stay alive without support.
- Non-invasive breathing assistance may be helpful, such as with a bilevel positive airway pressure machine.
- In other cases, placement of an endotracheal tube (breathing tube) may be necessary, and a ventilator may be used to help the person breathe.
- Pneumonia can also cause respiratory failure by triggering acute respiratory distress syndrome (ARDS), which results from a combination of infection and inflammatory response.
- The lungs quickly fill with fluid and become very stiff. This stiffness, combined with severe difficulties extracting oxygen due to the alveolar fluid, creates a need for mechanical ventilation.
- Sepsis and septic shock are potential complications of pneumonia.
- Sepsis occurs when microorganisms enter the bloodstream and the immune systemresponds by secreting cytokines.
- Sepsis most often occurs with bacterial pneumonia; Streptococcus pneumoniae is the most common cause.
- Individuals with sepsis or septic shock need hospitalization in an intensive care unit.
- They often require intravenous fluids and medications to help keep their blood pressure from dropping too low.
- Sepsis can cause liver, kidney, and heart damage, among other problems, and it often causes death.
Prognosis
- Individuals who are treated for CAP outside of the hospital have a mortality rate less than 1%.
- Fever typically responds in the first two days of therapy and other symptoms resolve in the first week.
- The x-ray, however, may remain abnormal for at least a month, even when CAP has been successfully treated.
- Among individuals who require hospitalization, the mortality rate averages 12% overall, but it is as much as 40% in people who have bloodstream infections or require intensive care.[4]
- When CAP does not respond as expected, there are several possible causes.
- A complication of CAP may have occurred or a previously unknown health problem may be playing a role.
- Additional causes include inappropriate antibiotics for the causative organism (ie DRSP), a previously unsuspected microorganism (such as tuberculosis), or a condition which mimics CAP (such as Wegener’s granulomatosis).
- Additional testing may be performed and may include additional radiologic imaging (such as a computed tomography scan) or a procedure such as a bronchoscopy or lung biopsy.
Prognosis and Mortality
- With treatment, most types of bacterial pneumonia can be cured within one to two weeks.
- Viral pneumonia may last longer, and mycoplasmal pneumonia may take four to six weeks to resolve completely.
- The eventual outcome of an episode of pneumonia depends on how ill the person is when he or she is first diagnosed.
- In the United States, about one of every twenty people with pneumococcal pneumonia will die.[2]
- In cases where the pneumonia progresses to blood poisoning (bacteremia), one of every five will die. The death rate (or mortality) also depends on the underlying cause of the pneumonia. Pneumonia caused by Mycoplasma, for instance, is associated with little mortality. However, about half of the people who develop methicillin-resistant Staphylococcus aureus (MRSA) pneumonia while on a ventilator will die.[3]
- In regions of the world without advanced health care systems, pneumonia is even deadlier.
- Limited access to clinics and hospitals, limited access to x-rays, limited antibiotic choices, and inability to treat underlying conditions inevitably leads to higher rates of death from pneumonia.
Clinical Prediction Rules
- Clinical prediction rules have been developed to more objectively prognosticate outcomes in pneumonia.
- These rules can be helpful in deciding whether or not to hospitalize the person.
- Pneumonia severity index[4] –online calculator
- CURB-65 score, which takes into account the severity of symptoms, any underlying diseases, and age.[5]
Community Acquired Pneumonia
Natural History
- Pneumococcal pneumonia is the most common clinical presentation of pneumococcal disease amongst adults, although pneumonia without bacteremia or empyema is not considered to be “invasive” disease. [1]
- The incubation period of pneumococcal pneumonia is short, about 1 to 3 days. [1]
- Symptoms generally include an abrupt onset of fever and chills or rigors. [1]
- Typically there is a single rigor; repeated shaking chills are uncommon. [1]
- Other common symptoms include: pleuritic chest pain, cough productive of mucopurulent, rusty sputum, dyspnea, tachypnea, hypoxia, tachycardia, malaise, and weakness. Nausea, vomiting, and headaches occur less frequently.[1]
- Transmission of Streptococcus pneumoniae occurs as a result of direct person-to-person contact via respiratory droplets and by autoinoculation in persons carrying the bacteria in their upper respiratory tract. [1]
Causes
- The pneumococcal serotypes most often responsible for causing infection are those that are most frequently found in carriers.[1]
- Pneumococcal pneumonia is the most common clinical presentation of pneumococcal disease amongst adults, although pneumonia without bacteremia or empyema is not considered to be “invasive” disease. [1]
- The incubation period of pneumococcal pneumonia is short, about 1 to 3 days. [1]
- Symptoms generally include an abrupt onset of fever and chills or rigors. [1]
- Typically there is a single rigor; repeated shaking chills are uncommon. [1]
- Other common symptoms include: pleuritic chest pain, cough productive of mucopurulent, rusty sputum, dyspnea, tachypnea, hypoxia, tachycardia, malaise, and weakness. Nausea, vomiting, and headaches occur less frequently.[1]
- Transmission of Streptococcus pneumoniae occurs as a result of direct person-to-person contact via respiratory droplets and by autoinoculation in persons carrying the bacteria in their upper respiratory tract. [1]
- The pneumococcal serotypes most often responsible for causing infection are those that are most frequently found in carriers.[1]
Complications
Pleural Effusion and Empyema
- Community-acquired pneumonia may be complicated by parapneumonic pleural effusions. Thoracentesis and pleural fluid analysis should be performed.
- Empyema may occur if there is local formation of pus in the pleural cavity; this requires drainage in addition to antibiotic therapy.
Abscess
- Intraparenchymal abscesses (with or without loculation) may be seen in aspiration pneumonia. They are often primarily anaerobic or polymicrobial.
Sepsis and Septic Shock
- Sepsis most often occurs with bacterial pneumonia, with Streptococcus pneumoniae as the most common etiology.
Respiratory Failure
- Patients at the opposite ends of the age spectrum are at a high risk of respiratory failure.
- Non-invasive maneuvers, such as a bilevel positive airway pressure (BI-PAP) machine, may be used for respiratory support. Otherwise, intubation with mechanical ventilation may be required.
- Pneumonia may be complicated by acute respiratory distress syndrome (ARDS), which results from a combination of infection and inflammatory response.
Prognosis and Mortality
- With treatment, most types of bacterial pneumonia can be cured within one to two weeks.
- Viral pneumonia may last longer, and mycoplasmal pneumonia may take four to six weeks to resolve completely.
- The eventual outcome of an episode of pneumonia depends on how ill the person is when he or she is first diagnosed.
- In the United States, about one out of every twenty people with pneumococcal pneumonia will die.[6]
- In cases where pneumonia progresses to blood poisoning (bacteremia), one of every five will die.
- The death rate (or mortality) also depends on the underlying cause of the pneumonia.
- Pneumonia caused by Mycoplasma, for instance, is associated with little mortality. However, about half of the people who develop methicillin-resistant Staphylococcus aureus (MRSA) pneumonia while on a ventilator will die.[3]
- In regions of the world without advanced health care systems, pneumonia is even deadlier.
- Limited access to clinics and hospitals, x-rays, antibiotic choices, and inability to treat underlying conditions will inevitably lead to higher rates of death from pneumonia.
- Individuals who are treated for CAP outside of the hospital have a mortality rate of less than 1%.
- Fever typically responds in the first two days of therapy and other symptoms resolve in the first week.
- The CXR, however, may remain abnormal for at least a month, even when CAP has been successfully treated.
- Amongst individuals who require hospitalization, the mortality rate averages 12% overall, but it is as much as 40% in people who have bloodstream infections or require intensive care.[5]
- When CAP does not respond as expected, there are several possible causes.
- A complication of CAP may have occurred or a previously unknown health problem may be playing a role.
- Additional causes include: inappropriate antibiotics for the causative organism (such as drug resistant Streptococcus pneumoniae, a previously unsuspected microorganism (such as tuberculosis), or a condition which mimics CAP (such as Wegener’s granulomatosis).
- Additional testing may be performed and may include radiologic imaging (such as a computed tomography scan) or a procedure such as a bronchoscopy or lung biopsy.
Hospital Acquired Pneumonia
Natural History
- The natural course of hospital-acquired pneumonia will depend on several factors, such as the causative pathogen, the host immune status and the choice of antibiotic therapy.
- By definition, hospital-acquired pneumonia occurs 48 hours or more since hospital admission; and ventilator-associated pneumonia occurs 48 to 72 hours after the patient was intubated. [7]
- Physicians should suspect of hospital-acquired pneumonia in hospitalized patients that develop fever (> 38° C), productive cough and/or leukocytosis associated with a new chest X-ray infiltration.
- Empirical antibiotic therapy should be started in case of high suspicion, as it has shown improvement of patient survival.
Complications
Despite appropriate antibiotic therapy, severe complications can result from HAP, including:
Sepsis
- Sepsis can occur when microorganisms enter the blood stream and the immune system responds.
- Sepsis most often occurs with bacterial pneumonia
- Streptococcus pneumoniae is the most common cause.
- Individuals with sepsis require hospitalization in an intensive care unit. They often require medications and intravenous fluids to keep their blood pressure from going too low. Sepsis can cause liver, kidney, and heart damage among other things.
Respiratory Failure
- If enough of the lung is involved, it may not be possible for a person to breathe enough to live without support.
- Non-invasive machines such as a bilevel positive airway pressure machine may be used.
- Otherwise, placement of a breathing tube into the mouth may be necessary and a ventilator may be used to help the person breathe.
Pleural Effusion and Empyema
- Occasionally, microorganisms from the lung will cause fluid to form in the space surrounding the lung, called the pleural cavity.
- If the microorganisms themselves are present, the fluid collection is often called an empyema.
- If pleural fluid is present in a person with CAP, the fluid should be collected with a needle (thoracentesis) and examined.
- Depending on the result of the examination, complete drainage of the fluid may be necessary, often with a chest tube. If the fluid is not drained, bacteria can continue to cause illness because antibiotics do not penetrate well into the pleural cavity.
Abscess
- Rarely, microorganisms in the lung will form a pocket of fluid and bacteria called an abscess.
- Abscesses can be seen on an x-ray as a cavity within the lung. Abscesses typically occur in aspiration pneumonia and most often contain a mixture of anaerobic bacteria.
- Usually antibiotics are able to fully treat abscesses, but sometimes they must be drained by a surgeon or radiologist.
Prognosis
With treatment, most types of bacterial pneumonia can be cured within one to two weeks. Viral pneumonia may last longer, and mycoplasmal pneumonia may take four to six weeks to resolve completely. The eventual outcome of an episode of pneumonia depends on how ill the person is when he or she is first diagnosed.
In the United States, about one of every twenty people with pneumococcal pneumonia will die.[8] In cases where the pneumonia progresses to blood poisoning (bacteremia), one of every five will die. The death rate (or mortality) also depends on the underlying cause of the pneumonia. Pneumonia caused by Mycoplasma, for instance, is associated with little mortality. However, about half of the people who develop methicillin-resistantStaphylococcus aureus (MRSA) pneumonia while on a ventilator will die.[3] In regions of the world without advanced health care systems, pneumonia is even deadlier.
- Fever typically responds in the first two days of therapy and other symptoms resolve in the first week.
- The x-ray, however, may remain abnormal for at least a month, even when HAP has been successfully treated.
- When HAP does not respond as expected, there are several possible causes.
- A complication of HAP may have occurred or a previously unknown health problem may be playing a role.
- Additional causes include inappropriate antibiotics for the causative organism (ie DRSP), a previously unsuspected microorganism (such as tuberculosis), or a condition which mimics HAP (such as Wegener’s granulomatosis).
- Additional testing may be performed and may include additional radiologic imaging (such as a computed tomography scan) or a procedure such as a bronchoscopy or lung biopsy.
Clinical Prediction Rules
Clinical prediction rules have been developed to more objectively prognosticate outcomes in Hospital-acquired pneumonia. Pneumonia severity index[4] –online calculator
- CURB-65 score, which takes into account the severity of symptoms, any underlying diseases, and age[5] –online calculator
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 “CDC Pneumococcal Disease Clinical Features”.
- ↑ http://www.kidshealth.org/parent/infections/bacterial_viral/pneumonia.html
- ↑ 3.0 3.1 3.2 Combes A, Luyt CE, Fagon JY, Wollf M, Trouillet JL, Gibert C, Chastre J; PNEUMA Trial Group. Impact of methicillin resistance on outcome of Staphylococcus aureus ventilator-associated pneumonia. Am J Respir Crit Care Med. 2004 Oct 1;170(7):786-92. PMID 15242840
- ↑ 4.0 4.1 Fine MJ, Auble TE, Yealy DM, Hanusa BH, Weissfeld LA, Singer DE, Coley CM, Marrie TJ, Kapoor WN. A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med. 1997 Jan 23;336(4):243–250. PMID 8995086
- ↑ 5.0 5.1 Lim WS, van der Eerden MM, Laing R; et al. (2003). “Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study”. Thorax. 58 (5): 377–82. PMID 12728155.
- ↑ http://www.kidshealth.org/parent/infections/bacterial_viral/pneumonia.html
- ↑ “http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient_Care/PDF_Library/HAP.pdf” (PDF). External link in
|title=(help) - ↑ http://www.kidshealth.org/parent/infections/bacterial_viral/pneumonia.html
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