What is it the most common reason for community acquired pneumonia?

What is it the most common reason for community acquired pneumonia?

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This is a difficult question because there are many types of community-acquired pneumonia (CAP): typical acute, atypical acute and chronic. Most common microorganisms are also different among different groups: children, adults, elderly, immunocompromised and people at risk of different diseases.

Some options:

  • Streptococcus pneumoniae
  • Hemophilus influenzae
  • Escherichia coli
  • Klebsiella pneumoniae
  • Pseudomonas aeruginosa
  • bronchiectasis
  • Chlamydia pneumoniae

Not any virus, since they are present in only about 20% of diseases. Streptococcus pneumonia is probably a good choice.

What is the most common reason for community acquired pneumonia?

You are right in that there are several ways to split down CAP, and plenty of different pathogens to look at. But then we are looking for the most common. Pnumonia is most common in children and adults over the age of 75 (or 65 depending on who's counting). Luckily there are plenty of good reviews for both populations.

From the pediatric side we have Iroh Tam PY(1):

Pneumonia occurs more often in early childhood than at any other age, with the exception of adults older than 75 years, and kills more children than any other disease worldwide

As far as pathogens:

Streptococcus pneumoniae and Haemophilus influenzae type b (Hib) have been characterized as 2 bacteria predominately responsible for cases of fatal pneumonia in children. However, widespread introduction of Hib and pneumococcal conjugate vaccines has led to significant declines, especially of Hib, although Streptococcus pneumoniae is still the predominant bacteria isolated from bacterial CAP in children. There is increasing recognition of the prevalence of mixed bacterial and viral infections, which have been documented in 23% to 33% of cases of pneumonia.

Then we move to the geriatric side of things with Falcone et al (2):

Common pathogens include H. influenzae, enteric gram-negative bacilli, the atypical organisms, S. aureus, Pseudomonas aeruginosa, and M. catarrhalis, although the relative prevalence of each tends to vary among studies. Among elderly individuals with aspiration pneumonia, gram-negative bacilli are the predominate organisms (49 %), followed by anaerobic bacteria (16 %) and S. aureus (12 %).

Though I should note, having done them myself, getting accurate cultures is difficult, and viral levels a very likely to be under reported because of handling and skill.

For example, in different prospective studies in which the microbiologic etiology of CAP was systematically sought in the elderly, a definite or presumptive pathogen was often reported in <60 % of the patients. (2)

And again in children:

There are 2 main challenges in the diagnosis of CAP: the first is the definition of CAP, particularly in young children, in whom bacterial and viral infections can occur with similar frequencies, and in whom overdiagnosis of mild symptoms and signs may lead to unnecessary antibiotic use; the second is the identification of a causative pathogen, which is frequently impractical and inadequate in children, and in whom the failure to isolate an organism can result in unnecessary antibiotic use. (1)

Taking into account more global sources, I'm actually thinking Hib infection has dropped more due to vaccination than I gave it credit for, putting my bet on S. pneumoniae, and showing my regional experience may not be representative (3, 4, 5, 6).

(1) Iroh Tam PY. Approach to common bacterial infections: community-acquired pneumonia. Pediatr Clin North Am. 2013 Apr;60(2):437-53. doi: 10.1016/j.pcl.2012.12.009. Epub 2013 Jan 12

(2) Falcone M. et al. Pneumonia in frail older patients: an up to date. Intern Emerg Med. 2012 Oct;7(5):415-24. Epub 2012 Jun 12.

(3) Brown JS. Community-acquired pneumonia. Clin Med. 2012 Dec;12(6):538-43.

(4) Kurutepe S, Ecemiş T, Ozgen A, Biçmen C, Celik P, Aktoğu Özkan S, Sürücüoğlu S. [Investigation of bacterial etiology with conventional and multiplex PCR methods in adult patients with community-acquired pneumonia]. Mikrobiyol Bul. 2012 Oct;46(4):523-31.

(5) Tao LL, Hu BJ, He LX, Wei L, Xie HM, Wang BQ, Li HY, Chen XH, Zhou CM, Deng WW. Etiology and antimicrobial resistance of community-acquired pneumonia in adult patients in China. Chin Med J (Engl). 2012 Sep;125(17):2967-72.

(6) Capelastegui A, España PP, Bilbao A, Gamazo J, Medel F, Salgado J, Gorostiaga I, Lopez de Goicoechea MJ, Gorordo I, Esteban C, Altube L, Quintana JM; Poblational Study of Pneumonia (PSoP) Group. Etiology of community-acquired pneumonia in a population-based study: link between etiology and patients characteristics, process-of-care, clinical evolution and outcomes. BMC Infect Dis. 2012 Jun 12;12:134. doi: 10.1186/1471-2334-12-134.

Community-acquired pneumonia in adults

Pneumonia is a breathing (respiratory) condition in which there is an infection of the lung.

This article covers community-acquired pneumonia (CAP). This type of pneumonia is found in people who have not recently been in the hospital or another health care facility such as a nursing home or rehab facility. Pneumonia that affects people in health care facilities, such as hospitals, is called hospital-acquired pneumonia (or health care-associated pneumonia).

Causes of Community-Acquired Pneumonia

Many organisms cause community-acquired pneumonia, including bacteria, viruses, fungi, and parasites. In most cases, the specific microorganism causing the pneumonia is not identified. However, doctors can usually predict which microorganisms are most likely to be causing the pneumonia based on the person’s age and other factors, such as whether the person also has other diseases. The term community-acquired pneumonia is usually reserved for people who have pneumonia caused by one of the more common bacteria or viruses.

"Walking pneumonia" is a nonmedical term used to describe a mild case of community-acquired pneumonia that does not require bedrest or hospitalization. Some people even feel well enough to go to work and participate in other daily activities. The cause is often a viral lung infection or a bacterial infection with Mycoplasma pneumoniae or Chlamydophila pneumoniae.

Bacterial causes of pneumonia

The most common bacterial causes of community-acquired pneumonia are

Streptococcus pneumoniae

Haemophilus influenzae

Chlamydophila pneumoniae

Mycoplasma pneumoniae

Streptococcus pneumoniae (pneumococcus) causes about 900,000 cases of pneumonia in the United States each year. There are over 90 types of pneumococci, but most serious disease is caused by only a small number of types. Pneumococcal pneumonia can be very severe, particularly in young children and older people.

Haemophilus influenzae pneumonia may occur in adults but is more common among children. However, childhood infection has become much less common since children have been routinely vaccinated against H. influenzae. H. influenzae pneumonia is more common among adults who have underlying chronic lung disorders such as chronic obstructive pulmonary disease (COPD) and bronchiectasis.

Chlamydophila pneumoniae is the second most common cause of lung infections in healthy people aged 5 to 35 years. C. pneumoniae is commonly responsible for outbreaks of respiratory infection within families, in college dormitories, and in military training camps. It causes a pneumonia that is rarely severe and infrequently requires hospitalization. Chlamydia psittaci pneumonia (psittacosis) is a rare infection caused by a different strain of chlamydia and occurs in people who own or are often exposed to birds.

Mycoplasma pneumoniae causes infection very similar to that caused by C. pneumoniae. M. pneumoniae pneumonia is more common among older children and adults younger than 40, especially those living in crowded environments, such as schools, college dormitories, and military barracks. Although the illness is rarely severe, symptoms can last for weeks or even months.

Legionella pneumophila causes pneumonia and flu-like symptoms sometimes called Legionnaires’ disease. It accounts for about 1 to 8% of all pneumonias and about 4% of fatal pneumonias acquired in hospitals. Legionella bacteria live in water, and outbreaks have occurred primarily in hotels and hospitals when the organism has spread through the air conditioning systems or water supplies, such as showers. No cases have been identified in which one person directly infected another.

Staphylococcus aureus causes pneumonia that is resistant to some types of antibiotics. This bacteria is known as community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA), and it can cause severe pneumonia, primarily in young adults. Since the year 2000, the number of cases of community-acquired pneumonia caused by S. aureus has increased, but the infection is still uncommon.

Pseudomonas aeruginosa is an especially common cause of pneumonia in people with cystic fibrosis and other lung diseases and in those with an impaired immune system.

Community-Acquired Viral Pneumonia

Pneumonia is the fourth leading cause of death in the world, accounting for about 5% of deaths annually. Over the last decade, community-acquired viral infections of the lung have captured media and public attention after pandemic outbreaks of the severe acute respiratory syndrome (SARS) coronavirus of 2002-2003, the avian influenza A (H5N1) virus of 2005, the influenza A (H1N1) virus of 2009, and the Middle East Respiratory Syndrome coronavirus (MERS-CoV) of 2012. These pandemics demonstrated the capacity of respiratory viruses to cause worldwide epidemics with high attack rates, morbidity, and mortality.

In clinical studies of community-acquired pneumonia (CAP) utilizing polymerase chain reaction (PCR) techniques and serological testing, respiratory viruses are detected in up to 50% of young children and 10-30% of adults. The highest incidence rates are found in children younger than age five, adults older than 75, and immunocompromised hosts. Recently, there has been a trend towards increased identification of viral pathogens in community-acquired lung infections, probably because of improved vaccination against bacterial pathogens (Haemophilus influenza type B and S. pneumoniae), increased numbers of immunocompromised hosts, and improved diagnostic assays, such as rapid viral antigen and PCR techniques. All clinicians should have a high index of suspicion for viral infections of the lung in order to initiate antiviral therapy promptly and implement adequate infection control measures to prevent community and nosocomial spread.


Viral infections of the lung can present with acute tracheobronchitis, bronchiolitis, bronchopneumonia, and pneumonia. These infections are difficult to distinguish from bacterial etiologies. Acute respiratory failure requiring mechanical ventilation, acute respiratory distress syndrome (ARDS), and diffuse alveolar hemorrhage were reported during the pandemic SARS and influenza A (H5N1) and (H1N1) infections.

The most commonly isolated viruses in childhood pneumonia requiring hospitalization are respiratory syncytial virus (RSV, 28%), rhinovirus (27%), human metapneumovirus (HMPV, 13%), adenovirus (11%), influenza viruses (7%), parainfluenza (7%), and coronavirus (5%). In adult CAP, viruses are isolated at a lower rate of 10-29%, and the most common viruses among adults requiring hospitalization are rhinovirus (9%), influenza viruses (6%), human metapneumovirus (4%), RSV (3%), parainfluenza (2%), and coronavirus (2%). See Table I for details.

Table I.

Viruses associated with community-acquired pneumonia in children and adults

Are you sure your patient has community-acquired viral pneumonia? What should you expect to find?

The symptoms and signs of community-acquired viral pneumonia are indistinguishable from those of bacterial lung infections and include cough, dyspnea, sputum production, and pleurisy. In children under five years of age, upper airway symptoms of rhinorrhea and congestion, low-grade fever, wheezing, and prominent intercostal retractions are highly suggestive of viral lung infection. Recent studies in adults suggest that patients with viral pneumonia have less sputum production, chest pain, and rigors than bacterial pneumonia patients. Other key clinical features that suggest a viral etiology are a seasonal pattern with RSV in late fall and winter, rhinovirus in the fall and spring, and influenza in the winter.

Beware: there are other diseases that can mimic community-acquired viral pneumonia:

Bacterial pneumonia is typically indistinguishable from viral community-acquired pneumonia, as both processes present with cough, dyspnea, fever, and pleurisy. This confusion may delay establishment of proper droplet and respiratory isolation for contagious viral pathogens. Viral pneumonias are more common in older patients with cardiac co-morbidities, who usually complain less of chest pain or rigors. Systemic symptoms, such as sore throat, rhinorrhea, myalgias, headaches, nausea, vomiting, and diarrhea, are more common in viral pneumonia, particularly seasonal influenza. Patients with viral pneumonia also have lower peripheral white blood cell counts, procalcitonin levels, and C-reactive protein levels. Finally, a recent study demonstrates that patients with viral pneumonia have higher creatinine kinase levels, lower platelet counts, and an increased frequency of alveolar-interstitial infiltrates compared to patients with bacterial pneumonia.

How and/or why did the patient develop community-acquired viral pneumonia?

The epidemiology of community-acquired viral infections of the lung is characterized by a seasonal pattern or pandemic events associated with high attack rates and person-to-person transmission. Upper and lower respiratory tract infections from RSV occur in the late fall and winter, rhinovirus in the fall and spring, and influenza in the winter. Another important epidemiological clue is the patient’s home environment. For example, rhinoviruses have caused outbreaks of severe and even fatal pneumonia in elderly nursing home residents, and adenovirus pneumonia outbreaks have occurred in military recruits housed in barracks.

During pandemic viral infections, a history of recent travel to an endemic area is an important epidemiological clue. The severe acute respiratory syndrome (SARS) coronavirus pandemic of 2002-2003 originated in a province of China and spread rapidly, causing severe pneumonia in 8,000 patients and 774 deaths in 26 countries and five continents. This virus infects people who are engaged in the commercial trade of exotic animals.

The pandemic influenza of 2003-2004 was caused by a highly virulent H5N1 avian influenza virus that was first detected in Thailand and spread worldwide, resulting in 450 human infections and a high case mortality of approximately 60%. In the spring of 2009, a novel influenza A (H1N1) infection originated in Mexico with high attack rates (17%) and a low case fatality rate of less than 0.5%. By March 2010, virtually all countries reported cases, resulting in more than 18,500 deaths from laboratory-confirmed cases worldwide. Eighty percent of the global mortality from H1N1 occurred in people under age 65.

In the fall of 2012, Middle East Respiratory Syndrome coronavirus (MERS-CoV) emerged in Saudi Arabia, producing ARDS and acute kidney injury in two patients. Since 2012, 1879 laboratory-confirmed cases have been reported, primarily in the Arabian Peninsula but with several cases reported from North Africa, Europe, Asia, and North America. MERS-CoV should be suspected in patients with either pneumonia or ARDS and contact with a confirmed MERS-CoV case or recent travel to the Middle East.

Which individuals are at greatest risk of developing community-acquired viral pneumonia?

Patients at higher risk for viral infections of the lung include children under age five and adults older than 75. Infants younger than six months are at particularly high risk for RSV and parainfluenza infection. In elderly patients, frail condition or the presence of congestive heart failure and/or pulmonary disease pose greater risk. Pregnant women are susceptible to pneumonia from varicella and pandemic influenza A (H1N1) with higher virulence and mortality. Other risk factors for viral pneumonia include HIV infection, cancer, radiation, chemotherapy, malnutrition, skin breakdown, and burns.

What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

Laboratory studies may suggest the diagnosis of viral pneumonia, but they are not diagnostic. Viral pneumonia patients have lower peripheral white blood cell and neutrophil count compared to those with bacterial pneumonia. For patients with a clinical diagnosis of pneumonia, a procalcitonin level of < 0.1 mcg/L is suggestive of a viral etiology, while a level > 0.25 mcg/L suggests bacterial infection. CRP is less sensitive for bacterial pneumonia than procalcitonin, but a CRP level >40 has a sensitivity of roughly 70% for bacterial pneumonia.

What imaging studies will be helpful in making or excluding the diagnosis of community-acquired viral pneumonia?

The community-acquired pneumonia guidelines published by the Infectious Disease Society of America and American Thoracic Society recommend obtaining a CXR in all patients with suspected pneumonia to document the presence of pulmonary infiltrates. Bilateral interstitial infiltrates are highly suggestive of a viral pneumonia, but alveolar infiltrates are seen in about half of infected children.

Multilobar infiltrates are reported in approximately half of patients with confirmed viral infection. Chest CT commonly demonstrates multifocal ground-glass opacities or consolidation and centrilobular nodules following a “tree-in-bud” pattern. These CT findings are non-specific, so routine chest CT scanning is not recommended for evaluation of the etiology of pneumonia.

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of community-acquired viral pneumonia?

Non-invasive pulmonary diagnostic studies, such as pulmonary function tests and cardiopulmonary exercise testing, are not helpful in diagnosing or differentiating the community-acquired viral infections of the lung.

What diagnostic procedures will be helpful in making or excluding the diagnosis of community-acquired viral pneumonia?

Diagnostic confirmation of viral infections of the lung requires the detection of viruses or viral antigens in upper or lower respiratory tract samples via culture, direct immunofluorescence, or PCR to viral antigens. Higher yields are obtained with the use of nasopharyngeal aspirates in children and nasopharyngeal swabs in adults. When these procedures are performed, the nasal swabs should enter the nares and advance to a depth of at least 2 cm. Suitable samples may be obtained from throat swabs, tracheal aspirates, and sputum cultures. Bronchoalveolar lavage, which is more difficult to obtain, typically has a lower antigen or viral particle burden because of low-level viral shedding at the peripheral lung. However, H1N1 was found to have a predilection for the lower respiratory tract, so if clinical suspicion is high, a tracheal aspirate, sputum culture, or bronchoalveolar lavage may be necessary to detect the virus.

Because viral cultures typically take between 3-14 days for results, many medical centers have respiratory viral panels that utilize direct fluorescent antigen detection assays to diagnose common viral pathogens more quickly. Serologic testing may confirm a diagnosis of a recent viral infection if there is a four-fold increase in titer from acute to convalescent viral-specific antibodies.

Recently, PCR-based methods have revolutionized the rapid diagnosis of viral infections by simultaneously testing for a large number of common respiratory viruses with a single specimen. This technique, which can rapidly identify viral infection with less than a 24-hour turnaround, is quickly becoming the test of choice. With the use of PCR, recent microbiological studies have demonstrated that almost a third of adult CAPs have an identified viral pathogen. The clinician must remember that a positive viral PCR is suggestive of viral infection however, because respiratory viruses can be present in the nasopharynx without causing illness, positive viral PCR results may overestimate the actual incidence of viral pneumonia. During the pandemic influenza outbreaks with H1N1 and H5N1, viral RNA detection by reverse-transcriptase-PCR had the highest diagnostic yield. In fact, commercial influenza antigen assays had low sensitivity and were unable to distinguish between influenza A subtypes.

What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of community-acquired viral pneumonia?

There are no cytologic or genetic studies that can assist in the diagnosis of community-acquired viral lung infections. Lung biopsy specimens are rarely obtained during episodes of viral pneumonia. Post-mortem examination typically reveals interstitial pneumonitis with lymphocytic infiltration. RSV typically invades bronchial and alveolar epithelial cells with alveolar macrophages and inflammation with CD3-lymphocytes inflammation in a bronchocentric pattern.

Some viruses, such as adenovirus and human metapneumovirus, demonstrate histological evidence of a hemorrhagic pneumonia. Patients who died from SARS coronavirus, influenza A (H5N1), influenza A (H1N1), or MERS-CoV infection demonstrated a diffuse alveolar damage pattern with pneumocyte desquamation, hyaline membranes, and interstitial edema.

If you decide the patient has community-acquired viral pneumonia, how should the patient be managed?

Patients with viral pneumonia should be triaged for admission based on CAP mortality prediction scores, such as PORT, CURB-65, IDSA-ATS criteria, and SMART-COP. In one study that compared the available prediction scores for intubation and mortality in pneumonia, the IDSA-ATS criteria had the highest sensitivity (74%) for predicting intubation or death, while CURB-65 had the best specificity (80%). Please note that these prediction scores were validated for bacterial pneumonia rather than viral etiologies.

When clinicians suspect a viral pneumonia, respiratory and droplet isolation is strongly recommended. It is important that visitors and hospital personnel wear disposable gloves, masks, and gowns, especially when entering the rooms of patients with RSV. Most experts recommend treating with antibiotics, since bacterial co-infection or superinfection is not easily excluded.

The treatment of viral pneumonia is primarily supportive with oxygen therapy, adjuvant antibacterial antibiotics, and non-invasive or invasive ventilation (if required). Patients with viral pneumonia who develop ARDS should be managed with lung protective ventilation strategies and conservative fluid management similar to patients with ARDS from other causes. The use of antiviral therapy for viral pneumonia is limited and discussed in the section below. Table II lists a few antiviral agents available for specific treatment of viral pneumonias:

Table II.

Antiviral Agents with Potential Benefits in Viral Pneumonia

Seasonal influenza: When started within 48 hours from onset of influenza symptoms, the neuraminidase inhibitors, oseltamivir (Tamiflu) and zanamivir (Relenza), decrease the duration of influenza by 0.5 to 2.5 days. If patients are hospitalized, the recommendation is to utilize these agents even in patients presenting late with symptoms for more than 48 hours. The use of high-dose corticosteroids is not recommended and has been associated with increased mortality and longer viral shedding in patients suffering with H7N9 influenza pneumonia.

Respiratory syncytial virus (RSV): Inhaled ribavirin has been utilized for the treatment of children and immunocompromised hosts with modest benefits. Its use requires supervised nebulization in a closed room to prevent spread of RSV to hospital personnel and because of its teratogenicity. An IV formulation has been studied for severe disease and oral formulations have been used as well. RSV hyperimmune globulin and monoclonal antibody preparations are used for severe infection in recipients of bone marrow and solid organ transplants. Corticosteroids are ineffective.

Varicella pneumonia: Prevention with prophylactic doses of oral acyclovir or varicella zoster immunoglobulin should be considered for patients at high risk for progression to pneumonia, such as pregnant women, AIDS patients, organ transplant patients, and other immunocompromised hosts. Confirmed or suspected cases of varicella pneumonia should be treated with IV acyclovir 10 mg/kg three times a day for seven to ten days.

Cytomegalovirus (CMV) pneumonia: CMV, a herpes virus, may cause severe infection in recipients of solid organ and stem cell transplants and in patients with AIDS. CMV usually occurs 6-12 weeks after solid organ or stem cell transplantation, and it occurs commonly in patients with advanced AIDS who have low CD4 counts. This infection carries a high mortality rate, and prophylaxis with ganciclovir or valganciclovir in combination with CMV hyperimmune globulin (CMV-IVIG) is commonly utilized. Treatment of active CMV pneumonitis usually consists of ganciclovir and immune globulin.

Coronavirus-associated SARS: This pandemic was treated with ribavirin based on its broad-spectrum antiviral action against DNA and RNA viruses, despite lack of in vitro virucidal activity. High-dose methylprednisolone was utilized for modulation of the inflammatory immune response with some anecdotal success. In vitro and animal models suggest that interferon beta, pegylated interferon alfa, and chloroquine may be therapeutic alternatives for SARS, and clinical studies are warranted. Other agents tested include IV immunoglobulin and combined lopinavir and ritonavir.

Pandemic influenza H5N1: Avian influenza A (H5N1) should be treated with oseltamivir (Tamiflu) and antibacterial antibiotics. Resistance to amantidine has been reported, and its use is not recommended. Adjuvant corticosteroids are not beneficial and may be associated with increased mortality, as demonstrated during the last pandemic.

Pandemic influenza H1N1: The most recent swine-origin influenza A (H1N1) infection was treated with the neuraminidase inhibitors, oral oseltamivir (Tamiflu) and inhaled zanamivir (Relenza). This influenza A was resistant to amantidine and rimantidine. For hospitalized patients, the preferred agent is IV zanamivir, which may be obtained via a compassionate-use request. Recently, IV peramivir was approved by the FDA for the treatment of acute influenza in patients 18 years or older and was utilized for treatment of critically-ill influenza A H1N1 patients in the U.S. Varying doses and duration of empiric corticosteroids were used in up to 69% of patients during the pandemic with no clear benefit.

Middle East respiratory syndrome coronavirus (MERS-CoV): Antiviral agents are not routinely recommended for the treatment of MERS-CoV. Retrospective observational reports of combination treatment with ribavirin and pegylated interferon alpha have shown inconsistent results. Adjunct corticosteroids are not recommended and may increase mortality. Mycophenolate demonstrates in vitro activity but was not effective in animal models. The utility of convalescent plasma and monoclonal antibodies is under investigation.

Side effects of antiviral therapy: Each antiviral agent has its own side effect profile. Ribavirin nebulization, which may precipitate bronchospasm and respiratory compromise, is also a teratogenic drug. IV ribavirin has been associated with mild hemolytic anemia. The neuraminidase inhibitors, oseltamivir (Tamiflu) and zanamivir (Relenza) are associated with a less than 5% rate of reported side effects: diarrhea, nausea, sinusitis, nasal symptoms, headache, and dizziness.

Inhaled zanamivir, a neuramidase inhibitor used in seasonal influenza, may precipitate bronchospasm and should be used with caution in patients with reactive airway disease. IV acyclovir may cause seizures, leukopenia, thrombocytopenia, and renal impairment. Ganciclovir and valganciclovir are associated with bone marrow suppression, nephrotoxicity, pancreatitis, and gastrointestinal symptoms.

What is the prognosis for patients managed in the recommended ways?

Although the prognosis for viral pneumonia including seasonal influenza is generally good, viral infections may cause significant morbidity and mortality in immunocompromised patients and in patients older than 65. Recent pandemics with SARS-associated coronavirus, MERS, and avian and swine origin influenza A highlighted the virulence of newly identified viral strains that originate from animal viruses. The case fatality rate for MERS-CoV is approximately 36%, while SARS-associated coronavirus led to 774 deaths and a case fatality rate of about 10%. The case fatality rate for avian origin influenza virus is very high, ranging from 27% for H7N9 to 50% for H5N1. In contrast, case fatality rates for swine origin influenza A (H1N1) and seasonal influenza are much lower at 0.5% and 0.1%, respectively.

What other considerations exist for patients with community-acquired viral pneumonia?

A patient suffering from a community-acquired viral infection must be placed in respiratory and droplet isolation to avoid spread to close contacts and hospital personnel. Hand-washing is essential to prevent person-to-person transmission. Annual influenza vaccination is essential for the prevention of seasonal influenza and associated pandemics.

For suspected pandemic influenza or MERS-CoV, it is essential that the patient is rapidly triaged and isolated with standard, contact, and airborne precautions. Expert infectious disease consultation is recommended.

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Community-Acquired Pneumonia in Adults: Diagnosis and Management

Community-acquired pneumonia is a leading cause of death. Risk factors include older age and medical comorbidities. Diagnosis is suggested by a history of cough, dyspnea, pleuritic pain, or acute functional or cognitive decline, with abnormal vital signs (e.g., fever, tachycardia) and lung examination findings. Diagnosis should be confirmed by chest radiography or ultrasonography. Validated prediction scores for pneumonia severity can guide the decision between outpatient and inpatient therapy. Using procalcitonin as a biomarker for severe infection may further assist with risk stratification. Most outpatients with community-acquired pneumonia do not require microbiologic testing of sputum or blood and can be treated empirically with a macrolide, doxycycline, or a respiratory fluoroquinolone. Patients requiring hospitalization should be treated with a fluoroquinolone or a combination of beta-lactam plus macrolide antibiotics. Patients with severe infection requiring admission to the intensive care unit require dual antibiotic therapy including a third-generation cephalosporin plus a macrolide alone or in combination with a fluoroquinolone. Treatment options for patients with risk factors for Pseudomonas species include administration of an antipseudomonal antibiotic and an aminoglycoside, plus azithromycin or a fluoroquinolone. Patients with risk factors for methicillin-resistant Staphylococcus aureus should be given vancomycin or linezolid, or ceftaroline in resistant cases. Administration of corticosteroids within 36 hours of hospital admission for patients with severe community-acquired pneumonia decreases the risk of adult respiratory distress syndrome and length of treatment. The 23-valent pneumococcal polysaccharide and 13-valent pneumococcal conjugate vaccinations are both recommended for adults 65 years and older to decrease the risk of invasive pneumococcal disease, including pneumonia.

Together, influenza and pneumonia are the eighth leading cause of mortality among adults in the United States and result in more than 60,000 deaths annually.1 – 4 Community-acquired pneumonia (CAP) disproportionately affects persons who are very young or very old, with an annual incidence of 9.2 to 33 per 1,000 person-years.1 , 5 Out of an estimated 878,000 adults 45 years and older who were hospitalized with a primary diagnosis of CAP in 2010, 71% were 65 years or older, and 10% to 20% required admission to the intensive care unit (ICU).1 , 2 , 6 , 7 Pneumococcal pneumonia alone was responsible for 866,000 outpatient visits in 2004.8 In the United States, annual health care costs associated with CAP range from $10.6 to $17 billion and are expected to grow as the proportion of older persons increases.1 , 2 , 4 Inpatient care accounts for more than 90% of pneumonia-related health expenditure.2 , 3 , 5


For patients with severe community-acquired pneumonia, corticosteroids decrease the risk of adult respiratory distress syndrome and modestly reduce intensive care unit and hospital stays, duration of intravenous antibiotic treatment, and time to clinical stability without increasing major adverse events.

Adults 65 years and older should routinely receive the 13-valent pneumococcal conjugate vaccine (PCV13 Prevnar 13) and the 23-valent pneumococcal polysaccharide vaccine (PPSV23 Pneumovax 23), preferably PCV13 first followed by PPSV23 in 12 months.

Levofloxacin in the treatment of community-acquired pneumonia

Levofloxacin is a fluoroquinolone that has a broad spectrum of activity against several causative bacterial pathogens of community-acquired pneumonia (CAP). The efficacy and tolerability of levofloxacin 500 mg once daily for 10 days in patients with CAP are well established. Furthermore, a high-dose (750 mg), short-course (5 days) of once-daily levofloxacin has been approved for use in the USA in the treatment of CAP, acute bacterial sinusitis, acute pyelonephritis and complicated urinary tract infections. Levofloxacin can be used as a monotherapy in patients with CAP, however, levofloxacin combination therapy with anti-pseudomonal beta-lactam (or aminoglycoside) should be considered if Pseudomonas aeruginosa is the causative pathogen of the respiratory infection. The high-dose, short-course levofloxacin regimen maximizes its concentration-dependent antibacterial activity, decreases the potential for drug resistance and has better patient compliance. Oral levofloxacin is rapidly absorbed and is bioequivalent to the intravenous formulation and the patients can switch between these formulations, which results in more options with respect to the therapeutic regimens. Furthermore, levofloxacin is generally well tolerated, has good tissue penetration and adequate concentrations can be maintained at the site of infections.

Manage CAP at home:

  • Breathe warm, moist air. This helps loosen mucus. Loosely place a warm, wet washcloth over your nose and mouth. A room humidifier may also help make the air moist.
  • Drink liquids as directed. Ask your healthcare provider how much liquid to drink each day and which liquids to drink. Liquids help make mucus thin and easier to get out of your body.
  • Gently tap your chest. This helps loosen mucus so it is easier to cough. Lie with your head lower than your chest several times a day and tap your chest.
  • Get plenty of rest. Rest helps your body heal.

Health Risk Factors

Pneumonia can affect anyone at any age, but the two age groups at the highest risk both for contracting it and for having more severe cases are children under age 2 and adults over age 65.

Other risk factors include:

  • Being in the hospital: Because your immune system is already weakened, your risk of developing pneumonia is higher if you're hospitalized in the ICU.   Your risk is even higher if you're on a ventilator to help you breathe.
  • Having a chronic disease: If you have COPD, asthma, heart disease, bronchiectasis, cystic fibrosis, diabetes, celiac disease, or sickle cell disease, your risk of contracting pneumonia is higher than that of the general population.  
  • Having a suppressed immune system: If you have HIV or AIDS, have had an organ or bone marrow transplant, are receiving chemotherapy or long-term steroids, or have an autoimmune disorder, you're at higher risk for pneumonia.
  • Difficulty swallowing: If you have a hard time swallowing due to a condition like Parkinson's disease or because of a stroke, you're at a higher risk of aspirating food, drink, saliva, or vomit and, thus, developing aspiration pneumonia.  
  • Reduced consciousness: Whether you're sedated, prone to generalized seizures, or have had anesthesia, these episodes of reduced consciousness can contribute to aspiration pneumonia.
  • Difficulty coughing: Not being able to cough properly or often enough can lead to pneumonia.

8 things you should know about pneumonia

Pneumonia is an infection that causes the air sacs in the lungs to fill up with fluid or pus, which makes it harder to breathe. The most common symptoms are cough that may be dry or produce phlegm, fever, chills and fatigue. Other symptoms may include nausea, vomiting, diarrhea, and pain in the chest. and shortness of breath. Signs that indicate a more severe infection are shortness of breath, confusion, decreased urination and lightheadedness. In the U.S., pneumonia accounts for 1.3 visits to the Emergency Department, and 50,000 deaths annually.

With the COVID-19 pandemic continuing to affect people around the world, pneumonia has become an even larger health concern. Some people infected with the COVID-19 have no symptoms, while others may experience fever, body ache, dry cough, fatigue, chills, headache, sore throat, loss of appetite, and loss of smell.

The more severe symptoms of COV-19, such as high fever, severe cough, and shortness of breath, usually mean significant lung involvement. The lungs can be damaged by overwhelming COVID-19 viral infection, severe inflammation, and/or a secondary bacterial pneumonia. COVID-19 can lead to long lasting lung damage.

Here are other important facts you should know about pneumonia:,

  1. Pneumonia can be a bacterial, viral, or fungal infection. Any of these organisms on their own cause pneumonia. Bacterial pneumonia can also complicate a viral illness like the flu. Many viruses can cause pneumonia. Most cases of viral pneumonia are relatively mild, but some can cause severe symptoms, such as severe acute respiratory system (SARS) coronavirus and the more recent SARS-CoV-2 (COVID-19). The most common cause of bacterial pneumonia is Strep pneumoniae (often called pneumococcal pneumonia).
  2. Both the young and the old are at risk. Young children and older adults (over age 65) are at the highest risk of getting pneumonia, and of having complications from it. About one million adults receive care in a hospital for pneumonia and, around the world, it is the leading cause of hospitalization and death in children under 5 years old.
  3. Vaccines are available to help prevent pneumococcal pneumonia. The PCV13 vaccine for children younger than two and those over age two who have preexisting health conditions helps protect against 13 types of pneumococcal bacteria, while the PPSV23 vaccine for older adults protects against 23 types. Yet, about one-third of adults aged 65 and older have not been vaccinated.
  4. Pneumonia can be spread from person to person, but it can also be caused by other factors. Like other contagious respiratory illnesses, the viruses and bacteria that cause pneumonia can spread when an infected person coughs or sneezes, releasing germ-filled droplets into the air. The illness that results can range from mild to severe.
  5. Doctors divide pneumonia into two main types. Doctors use term health-care associated pneumonia (HCAP) if the person who develops the lung infection has had been hospitalized, has stayed in a long-term care facility like a nursing home or has been on dialysis within the last three months. Otherwise, the designation is usually community acquired pneumonia (CAP).
  6. The initial treatment of pneumonia depends on whether it is HCAP or CAP and whether the person has a normal vs. a compromised immune system. It's important to begin treatment for pneumonia as soon as the diagnosis is made. Because the specific cause cannot be determined immediately, doctors almost always prescribe antibiotics initially to cover bacterial infections.

For CAP that does not require hospitalization, doctors typically prescribe a single or a combination of two different oral antibiotics, such as amoxicillin with or without azithromycin or doxycycline. Patients with CAP who require hospitalization almost always receive two different antibiotics. Most people with HCAP pneumonia or compromised immune systems generally need treatment in the hospital with intravenous (IV) antibiotics.

3: Community-acquired pneumonia

Community-acquired pneumonia is caused by a range of organisms, most commonly Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae and respiratory viruses.

Chest x-ray is required for diagnosis.

A risk score based on patient age, coexisting illness, physical signs and results of investigations can aid management decisions.

Patients at low risk can usually be managed with oral antibiotics at home, while those at higher risk should be further assessed, and may need admission to hospital and intravenous therapy.

For S. pneumoniae infection, amoxycillin is the recommended oral drug, while benzylpenicillin is recommended for intravenous use all patients should also receive a tetracycline (eg, doxycycline) or macrolide (eg, roxithromycin) as part of initial therapy.

Flucloxacillin or dicloxacillin should be added if staphylococcal pneumonia is suspected, and gentamicin or other specific therapy if gram-negative pneumonia is suspected a third-generation cephalosporin plus intravenous erythromycin is recommended as initial therapy for severe cases.

Infections that require special therapy should be considered (eg, tuberculosis, melioidosis, Legionella, Acinetobacter baumanii and Pneumocystis carinii infection).

Few infections generate as much controversy as community-acquired pneumonia. Reasons for this include the range of possible pathogens, difficulty in determining which pathogen to target when choosing an antibiotic, the variety of available antibiotics and increasing antibiotic resistance. In this article, we have tried to balance the needs of the individual patient with the need to control healthcare costs and antibiotic resistance. Our recommendations are restricted to the management of adults.

Community-acquired pneumonia (CAP) is commonly defined as an acute infection of the lower respiratory tract occurring in a patient who has not resided in a hospital or healthcare facility in the previous 14 days.1 Current approaches to the empirical management of CAP emphasise the type of patient ("community" or "hospital"), rather than the type of symptoms ("typical" or "atypical").

We lack detailed information on the incidence of CAP in Australia, but in the United States CAP requiring hospital admission occurs in about 258 per 100 000 population per year, rising to 962 per 100 000 among those aged 65 years or over.1 Mortality rates in recent years appear to have increased. Mortality averages 14%, but is less than 1% for those not requiring admission to hospital.1

Although inhalation and micro-aspiration constantly deliver potential pathogens, the respiratory tract below the larynx is normally sterile. Sterility is maintained by host defence systems, which include innate and acquired immunity and the mucociliary transport system. Factors that perturb these systems or predispose to aspiration increase the risk of pneumonia.

In community studies in Finland, the rate of CAP increased for each year of age over 50 years other risk factors were alcoholism, asthma, immunosuppression, and institutionalisation.1 In the United States, studies of risk factors for infection with Streptococcus pneumoniae have implicated dementia, seizure disorders, smoking, heart failure, stroke and chronic obstructive pulmonary disease.2 In Australia, Indigenous people have an increased risk of admission to hospital with CAP3 , 4 and of pneumococcal pneumonia5 (Box 1). Studies in Victoria have shown that pneumococcal pneumonia is common in active elderly people, not only in the sick and infirm.6

Many pathogens can cause CAP. A South Australian study of 106 adults admitted to hospital with CAP in 1987–1988 found that the most common cause was S. pneumoniae ("pneumococcus") (42%), followed by respiratory viruses (18%), Haemophilus influenzae (9%), Mycoplasma pneumoniae and enteric gram-negative bacteria (8% each), Chlamydia psittaci (5%), Staphylococcus aureus , Legionella spp. and Mycobacterium tuberculosis (3% each). 7 More recent overseas studies have shown that S. pneumoniae is still the most common pathogen overall, followed possibly by M. pneumoniae and Chlamydia pneumoniae .1 , 2 In ambulatory care, the proportion of patients with pathogens such as M. pneumoniae and C. pneumoniae that do not respond to penicillin, amoxycillin or cephalosporins may approach 50%. 8

Race, geographic location, lifestyle and country of origin influence the expected aetiology of CAP. For example, pneumococcal pneumonia occurs at high rates in Indigenous Australians, while Burkholderia pseudomallei (melioidosis) and Acinetobacter baumanii are important causes of CAP in people in tropical Australia,9 , 10 as is tuberculosis in people born overseas. HIV infection should be considered in patients with recurrent pneumococcal pneumonia. Pneumocystis carinii infection may be the cause of an unusually prolonged dry cough in a patient with HIV risk factors.

Aspiration pneumonia is an important variant of community-acquired pneumonia that occurs particularly in elderly people and those with conditions such as bulbar weakness, laryngectomy or stroke. Pulmonary segments that are lowermost at the moment of aspiration are involved. The most common causative organisms identified in recent studies were S. aureus , H. influenzae and gram-negative aerobes. Contrary to standard teaching, no anaerobes were found.11 , 12

CAP should be considered when a patient presents with two or more of the following symptoms:

change in sputum colour if there is a chronic cough

However, many patients who satisfy these criteria do not have pneumonia, and failure to distinguish pneumonia from acute bronchitis is an important reason for overuse of antibiotics.1 , 2 Furthermore, CAP can present with fever without localising features, and some patients may have no fever (eg, elderly patients may present only with a sudden change in functional status).

Thus, if pneumonia is being considered, a chest x-ray is needed. No set of decision rules is as yet superior to clinical judgement when deciding whom to x-ray.13 Physical signs of consolidation are suggestive but are often not found at presentation. Nevertheless, some clinical signs, such as confusion, should be specifically noted because of their prognostic value14 , 15 (see Risk stratification ).

This is the cardinal investigation. In the appropriate setting, a new area of consolidation on chest x-ray makes the diagnosis, but x-ray is a poor guide to the likely pathogen. Other causes of a new lung infiltrate on chest x-ray include atelectasis, non-infective pneumonitis, haemorrhage and cardiac failure. Occasionally, the chest x-ray initially appears normal (eg, in the first few hours of S. pneumoniae pneumonia and early in HIV-related P. carinii pneumonia) (Box 2).

There is debate about the value of sputum samples in diagnosis of CAP. Oral flora rather than the offending pathogen may dominate a sputum Gram stain and culture. Nevertheless, we believe that an attempt should be made to obtain a sputum sample before beginning antibiotic therapy, as this is sometimes the best opportunity to identify pathogens that need special treatment. Microscopy and culture for M. tuberculosis should be requested if the patient was born overseas.

All patients with CAP being assessed in emergency departments or admitted to hospital should have oximetry, measurement of serum electrolytes and urea levels, and a full blood count to assist in assessing severity. Blood gas measurement is also recommended, as it provides prognostic information (pH and Pa o 2 ) and may identify patients with ventilatory failure or chronic hypercapnia (Pa co 2 ). If the patient has known or suspected diabetes mellitus, measurement of blood glucose also assists in assessing severity.

Blood cultures are the most specific diagnostic test for the causative organism, but are positive in only around 10% of patients admitted to hospital with CAP.1 The more severe the pneumonia, the more likely blood cultures are to be positive.16 We recommend that blood be cultured from all patients, except those well enough to be managed at home with oral antibiotics.

The Legionella urinary antigen test is rapid, reliable and has a high degree of sensitivity and specificity.17 It should be performed in all patients with CAP, except perhaps those with low enough risk to be managed at home with empirical oral therapy (see Risk stratification ). However, the test detects only Legionella pneumophila serogroup 1, which accounts for only half of all cases of Legionella pneumonia.

Viral immunofluorescence testing of a nasopharyngeal aspirate is rapid and useful if it detects influenza or respiratory syncytial virus. Virus detection does not preclude a secondary bacterial invader.

Serological diagnosis requires acute and convalescent serum samples and is therefore not useful in acute management of CAP. Some laboratories offer acute serodiagnosis for M. pneumoniae , but these tests may lack specificity.18

Even after extensive investigations, the microbial cause of CAP is revealed in only about half of all patients.1 , 2 New diagnostic tests are under development. The most promising are rapid screens that can be performed on throat swabs, using polymerase chain reaction.

CAP is common, and many patients will recover with a simple oral antibiotic regimen, or even without antibiotics. However, a small proportion are at significant risk of death. Questions to be considered after radiological confirmation of CAP are:

Where should the patient be managed?

Which antibiotics should be used?

Risk-stratification systems can help answer these questions. One approach is to refer to a list of mortality risk factors (Box 3). A New Zealand study found that patients with CAP who had at least two key features on admission (diastolic blood pressure ≤ 60 mmHg, respiratory rate ≥ 30 per minute, serum urea level > 7 mmol/L, or confusion) were 36 times more likely to die than those without these features.15

In the United States, a prospectively validated severity prediction score is increasingly used — the Pneumonia Severity Index (PSI).19 , 20 The method of scoring this index is shown in Box 4, and risk of death in different PSI risk classes in Box 5. The rule was derived in patients aged over 18 years who were HIV-antibody negative and had not been in hospital during the previous seven days, although they included nursing home residents. Strictly, the PSI score identifies predictors of mortality and was not originally designed to triage patients or guide prescribing. However, high PSI scores correlate with admission to hospital and an intensive care unit, and there is limited evidence that the score correctly identifies patients who can be safely managed in the community with oral antibiotics.20

A suggested protocol for determining patient risk and management using the PSI score is shown in Box 6. We recommend that all but the lowest-risk patients (PSI risk class I) be further assessed. Whenever practicable, this assessment should be in an emergency department with rapid access to laboratory results. To apply the PSI algorithm, blood pH must be estimated while pulse oximetry measurement of O 2 saturation can substitute for p o 2 , until recently there has been no alternative to arterial blood gas measurement to assess pH. A recent Australian study showed that pH obtained by rapid analysis of a venous blood sample is a good approximation of arterial blood pH.21 Therefore, if arterial blood gas cannot be measured, O 2 saturation plus venous blood pH could be substituted.

Risk-stratification systems, such as the PSI score, should not replace good clinical judgement. For example, a homeless low-risk patient should not be sent "home" on oral antibiotics, and a patient who is vomiting should not be treated with oral therapy. In addition, the original description of the PSI score contained the important caveat that all patients with hypoxia in room air (O 2 saturation < 90% or p o 2 < 60 mmHg) or unusual comorbidities not specifically scored (eg, severe neuromuscular disease) should be admitted to hospital, regardless of PSI score.19

In Australia, some organisms that cause CAP are increasingly resistant to antibiotics. However, laboratory resistance does not automatically correlate with treatment failure. For example, although about 20% of clinical isolates of S. pneumoniae now have reduced susceptibility to penicillin,22 most of this resistance is "intermediate", meaning that CAP is likely to respond to oral amoxycillin or parenteral benzylpenicillin. Clinical failure of penicillins in respiratory infection caused by S. pneumoniae is unlikely unless the penicillin minimum inhibitory concentration exceeds 4 mg/L (high-level resistance).23 Such strains are still rare in Australia. In contrast, treatment has failed in cases of meningitis caused by S. pneumoniae with intermediate resistance,24 because of the additional problem of drug penetration to the cerebrospinal fluid. Third-generation cephalosporins may also fail against these strains. S. pneumoniae may also be resistant to trimethoprim–sulfamethoxazole (42% of clinical isolates), tetracyclines (15%) and erythromycin (11%).25

Resistance to amoxycillin is steadily increasing in H. influenzae and is currently about 25%. Resistance of Mycoplasma , Chlamydia and Legionella species to their drugs of choice is rare.

For patients at low risk (risk class I and many patients in classes II and III, corresponding to PSI score < 90), management with oral antibiotic therapy in the community is probably appropriate, provided they are not hypoxic and their social circumstances are suitable. Regular review is essential. We recommend a combination of amoxycillin and either roxithromycin or doxycycline (the latter should be avoided in pregnancy).

Amoxycillin is aimed at S. pneumoniae , as this is still the single most likely pathogen, and is preferable to penicillin as absorption and dosing frequency are more favourable. Doxycycline and roxithromycin are usually effective against other potential pathogens not covered by amoxycillin, which are common in ambulatory patients. Resistance of S. pneumoniae to these agents is more likely to be clinically significant than resistance to penicillin or amoxycillin. We believe that pneumococcal resistance to roxithromycin and doxycycline is now too common in Australia to recommend use of one of these agents alone for CAP. In this respect, our recommendations differ from those of the 11th version of Therapeutic guidelines: antibiotic .26

In patients with penicillin allergy, oral cephalexin or cefaclor should probably not be used, as their coverage of S. pneumoniae with reduced penicillin susceptibility is suboptimal. Sole reliance on a macrolide or tetracycline is also not recommended for the reasons above. An option for these patients is a combination of either oral cefuroxime axetil or outpatient intravenous ceftriaxone (which can be given once daily) with oral roxithromycin or doxycycline. Another option is single-agent therapy with one of the new fluoroquinolones — moxifloxacin or gatifloxacin — as these agents are effective against all common pathogens. However, they are not yet available on the Pharmaceutical Benefits Scheme, are expensive compared with standard oral therapy, and their overuse could generate resistance to valuable reserve agents, such as ciprofloxacin.

Patients at higher risk (PSI risk class IV and some patients in other classes) require intravenous therapy. Intravenous benzylpenicillin plus oral roxithromycin or doxycycline still provide excellent cover for almost all pathogens, except S. aureus and gram-negative organisms (case report, Box 7). Flucloxacillin or dicloxacillin should be added if staphylococcal pneumonia is suspected (ie, recent influenza, sputum Gram stain shows gram-positive cocci resembling staphylococci, or blood or sputum cultures yield S. aureus ). Similarly, gram-negative rods in the sputum or blood should prompt immediate addition of an aminoglycoside or extended-spectrum cephalosporin.

For patients at highest risk of death (PSI risk class V), early broad-spectrum parenteral therapy is essential. Failure to include antibiotics effective against the pathogen in the initial regimen worsens prognosis.1

Intravenous erythromycin plus ceftriaxone or cefotaxime has been recommended for severe CAP by Therapeutic guidelines: antibiotic for several years. In contrast, the 11th (2000) version recommends intravenous erythromycin plus penicillin and gentamicin, with the previous regimen reserved for patients with penicillin allergy.24 A recent non-randomised comparison in Australia suggested that the two regimens may be equivalent,27 but a properly powered, randomised study is required to settle the issue.28 Until better evidence is available, we continue to recommend intravenous erythromycin plus either ceftriaxone or cefotaxime in these very unwell patients. It is also necessary to consider carefully the possibility of specific pathogens which may require additional therapy (eg, S. aureus , Pseudomonas spp., other gram-negative organisms and P. carinii ).

Patients in tropical Australia, particularly those with more severe pneumonia, may be infected with B. pseudomallei (melioidosis) or A. baumannii and thus may require different initial empirical therapy. Patients with CAP in risk classes III or IV who also have risk factors for these infections (eg, diabetes, chronic airways disease, high alcohol intake or renal disease) should receive initial therapy with regimens that include intravenous gentamicin plus ceftriaxone (2 g for adults). All patients in risk class V should receive regimens that include intravenous gentamicin plus meropenem, if available. The regimen needs to be further refined if one of these pathogens is identified.24 [This paragraph corrected on 5 August 2002- click here for previous wording]

For patients with hypoxaemia, continuous oxygen therapy should be provided with the aim of maintaining O 2 saturation over 95% (or 90% in those with chronic hypercapnia). Patients with asthma or chronic obstructive pulmonary disease require optimisation of their bronchodilator therapy. Adequate hydration is also important, but care should be taken in older patients to avoid fluid overload, which may worsen gas exchange. Specific therapy for cardiac failure may be required. Occasionally, patients with severe pneumonia develop acute renal failure, which may require temporary dialysis. Changes in renal function should be kept in mind when selecting antibiotics and antibiotic doses.

Patients with chest pain require pain control to facilitate coughing and clearance of secretions, but routine chest physiotherapy is probably not useful unless secretions are copious. Adequate humidification of inspired air and suctioning of the large airways in patients with reduced consciousness or poor cough may also be useful.

Patients need to be monitored clinically to ensure that their condition improves on treatment. Daily review for the first few days is recommended. Improvement on chest x-ray is often slow and should not be used to monitor initial response to treatment. Improved sense of well-being, reduced temperature and reduced respiratory rate are expected in most patients in 24 to 72 hours, but may take longer if pneumonia is severe. 14 Failure to improve should prompt review of the case. Antibiotic failure itself is not usually the reason.

If the patient's condition does not improve, the following should be considered:

Is the diagnosis correct? (Results of diagnostic tests should be rechecked.)

Is the patient taking the antibiotics?

Would hospital admission and intravenous therapy now be appropriate?

Is there a complication (eg, effusion or empyema)?

Is there obstruction (eg, bronchial carcinoma or a foreign body)?

Is the pathogen S. aureus , Pseudomonas spp. or other gram-negative rod, which may not respond to standard empirical regimens?

Could the patient have HIV infection?

Should the patient be referred to a specialist (eg, for diagnostic bronchoscopy)?

Annual influenza vaccination and five-yearly pneumococcal vaccination are recommended for people with risk factors and all those aged over 65 years.29 For Indigenous people, who have much higher rates of CAP than the non-Indigenous population, regular influenza and pneumococcal vaccination is recommended from the age of 50.29

Legionnaire's disease, tuberculosis and psittacosis are notifiable diseases. Suspected cases should be reported immediately to local public health authorities so that public health measures can be taken.

Certain patient, clinical and laboratory features at presentation are independently associated with risk of death from community-acquired pneumonia14 , 19 (E3 2 ).

These features can be used to generate a pneumonia severity index which correlates with risk of death, need for hospital admission, length of hospital stay and need for intensive care19 (E3 2 ).

The pneumonia severity index can be used with caution to guide decisions about where and how to manage patients20 (E3 3 ).


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