Lower Respiratory Tract Infections
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LOWER RESPIRATORY TRACT INFECTIONS.

General Goal: To know how to diagnose pneumonia.

Specific Educational Objectives: The student should be able to:

1. describe how one determines a person has pneumonia. Know the common causes pneumonia based on a person's age, where or how they acquire the pneumonia, and based on when signs and symptoms of pneumonia begin (acute, subacute, chronic).

2. describe the differences between typical and atypical pneumonia.

3. know why on examination of a smear of sputum the laboratory will reject some samples as saliva and not sputum.

4. if necessary know how to get a definitive diagnosis.

5. describe how some pneumonias can be prevented.

Reading: Mosby's Color Atlas and Text of Infectious Diseases by Christopher P. Conlon and David R. Snydman. pp. 67-76.

Lecture: Dr. Neal R. Chamberlain

References:

OVERVIEW

Lower respiratory tract infections cause disease in the alveolar sacs, and the resulting infections are called pneumonia. This section of the handout will discuss the various types of pneumonia (i.e., typical, interstitial, chronic, and fungal pneumonia) and the agents that cause them.

PNEUMONIA

Pneumonia is an infection of the alveoli or the walls of the alveolar sacs. Diagnosis of pneumonia is relatively straightforward; however, since so many microorganisms can cause pneumonia, determining the cause of a patient’s pneumonia can be very difficult.

Etiology

Numerous microorganisms can cause pneumonia, but most cases are caused by bacteria. The common causes of pneumonia are dependent on the immune status of the patient, the location where the patient acquired the pneumonia, the age of the patient, and the type of pneumonia the patient manifests (e.g., typical versus interstitial pneumonia). The clinical and epidemiologic factors are used to determine the most likely cause of each individual case of pneumonia. Table LRI-1 lists causes of pneumonia by age of the patient; Table LRI-2 lists the causes of pneumonia according to the location where the disease was acquired and the immune status of the patient; Table LRI-3 lists causes of pneumonia acquired from unusual exposure; and Table LRI-4 lists causes of pneumonia by time of onset and where acquired; and Table LRI-5 lists the most common cause of various types of pneumonia diagnosed in the U.S.

Table LRI-1. Common Causes of Pneumonia Listed by Patient Age
Age	Most Likely Organisms
Neonatal (0–1 month)	Escherichia coli, Streptococcus agalactiae (group B)
Infants (1–6 months)	Chlamydia trachomatis, respiratory syncytial virus
Children (6 months–5 years)	Respiratory syncytial virus, parainfluenza viruses
Children (5–15 years)	Mycoplasma pneumoniae, influenza virus type A
Young adults (16–30 years)	Mycoplasma pneumoniae, Streptococcus pneumoniae
Older adults	Streptococcus pneumoniae, Haemophilus influenzae

Table LRI-2. Pneumonia Listed by Location Where Disease Was Acquired or by the Immune Status of the Patient and the Causes of that Pneumonia
Location or Patient’s Immune Status	Most Common Causes		Infrequent Causes
Community acquired typical pneumonia	Streptococcus pneumoniae, Haemophilus influenzae, Klebsiella pneumoniae		Staphylococcus, Moraxella catarrhalis, Neisseria meningitidis
Nosocomial pneumonia typical pneumonia	Gram-negative aerobic bacilli (Enterobacter, Klebsiella, Acinetobacter, Pseudomonas), Staphylococcus aureus, anaerobic bacteria, standard bacteria*		Legionella, Streptococcus pneumoniae
Community acquired primary interstitial pneumonia	Mycoplasma pneumoniae, respiratory viruses†, influenza virus, Chlamydophila pneumoniae, Legionella sp.		Adenovirus, Chlamydophila psittaci, Chlamydia trachomatis, primary tuberculosis, acute fungal pneumonias
Hematogenous pneumonia	Staphylococcus, Streptococcus		Gram-negative aerobic bacilli
Opportunistic pneumonia occurring in immunocompromised host		Standard bacteria, Pneumocystis jirovecii,* Cytomegalovirus, herpes simplex virus, Nocardia, opportunistic fungi (e.g., Candida, Phycomycetes mucor, Aspergillus)		Legionella, Listeria, Histoplasma, Coccidioides
Pneumonia acquired by environmental exposure		Histoplasma capsulatum, Coccidioides immitis, Chlamydophila psittaci, Mycobacterium tuberculosis		Burkholderia mallei, Burkholderia pseudomallei Coxiella burnetii, Yersinia pestis, Pasteurella multocida, Paracoccidioides
Aspiration pneumonia		Prevotella melaninogenicus, Fusobacterium nucleatum, Peptostreptococcus, Peptococcus, and other anaerobes, Staphylococcus, Gram-negative aerobic bacilli

* Standard bacteria refer to the bacteria that commonly cause community-acquired pneumonias. † Respiratory viruses include influenza, parainfluenza, and respiratory syncytial virus.

Table LRI-3. Disease, Causative Agent, and Environmental Source of the Patient’s Disease
Disease	Causative Agent	Source
Psittacosis (parrot fever)	Chlamydophila psittaci	Infected birds
Q fever	Coxiella burnetii	Contact with placenta of cattle, sheep, and goats; consumption of unpasteurized milk
Histoplasmosis	Histoplasma capsulatum	Soil contaminated by starling, chicken, and batexcreta (Ohio and Mississippi river valleys)
Coccidioidomycosis	Coccidioides immitis or Coccidioides posadasii	Soil in Southwestern United States
Cryptococcosis	Cryptococcus neoformans	Pigeon excreta and debris
Plague	Yersinia pestis	Contact with wild prairie dogs and infected pets; flea bites; person to person
Melioidosis	Burkholderia pseudomallei	Soil
Tularemia	Francisella tularensis	Ticks and deerflies; following aerosolization of dead infected animal carcasses by lawn mowers and string weed cutters

Table LRI-4. Causes of Pneumonia by Time of Onset, Where Acquired and Transmission
Time of onset	Location pneumonia was acquired	Transmission	Causative agents
Acute	Community acquired	Person-to-person	Streptococcus pneumoniae, Mycoplasma pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Klebsiella pneumoniae, Neisseria meningitidis, Moraxella catarrhalis, influenza virus, Streptococcus pyogenes
Acute	Community acquired	Animal or environmental exposure	Legionella, Francisella tularensis, Coxiella burnetii, Chlamydophila psittaci, Yersinia pestis (plague), Bacillus anthracis (anthrax), Burkholderia pseudomallei (melioidosis), Pasteurella multocida (pasteurellosis)
Acute	Community acquired	Person to person in infants and young children	Chlamydia trachomatis (an afebrile pneumonia), respiratory syncytial virus and other respiratory viruses, Streptococcus agalactiae (Group B), S aureus, Cytomegalovirus, S pneumoniae, H influenza
Acute	Nosocomial pneumonia	Person to person	Enterobacteriaceae, Pseudomonas aeruginosa, Acinetobacter calcoaceticus, S aureus
Subacute interstitial	Community acquired	Person to person	Mycoplasma pneumoniae, influenza virus
Subacute	Nosocomial or community acquired	Aspiration	Mixed anaerobic and aerobic gram-negative enteric bacteria, are usually polymicrobial
Subacute or chronic	Nosocomial or community acquired	Person to person or aspiration in the immunocompromised	Pneumocystis jiroveci, cytomegalovirus, atypical mycobacterium (e.g., Mycobacterium kansasii), Nocardia, Aspergillus, Phycomycetes mucor, Candida albicans
Chronic	Community acquired	Person to person	Mycobacterium tuberculosis, most common cause of chronic pneumonia. Blastomyces dermatitides (most common of cause of fungal pneumonia), Histoplasma capsulatum, Coccidioides immitis, Coccidioides posadasii, Cryptococcus neoformans

Table LRI-5. Common Causes of Types of Pneumonia and Important Laboratory Findings
Type of pneumonia	Most Common Cause	Important Laboratory Findings
Typical	Streptococcus pneumoniae	Gram-positive diplococcus (lancet-shaped diplococcus), alpha hemolytic sensitive to Optochin antibiotic
Interstitial (atypical)	Mycoplasma pneumoniae	No cell wall and cannot be Gram stained; fried-egg appearance on growth medium
Chronic	Mycobacterium tuberculosis	Acid-fast positive rod-shaped
Fungal	Blastomyces dermatitidis	Broad-based budding yeast
Aspiration (community acquired)	Oral anaerobes or Streptococcus pneumoniae	Anaerobes can include Prevotella, Peptostreptococcus, Bacteroides, Fusobacterium
Aspiration (hospital acquired)	Oral anaerobes, gram-negative enterics, or Staphylococcus aureus	Anaerobes same as above; gram-negative enterics can include Klebsiella pneumoniae and Escherichia coli

Manifestations

Many patients who are diagnosed with pneumonia mention having previous flu-like symptoms or an upper respiratory tract infection. A patient with pneumonia will frequently continue to have symptoms of upper respiratory tract infection and develop respiratory symptoms that are indicative of a lower respiratory tract infection—cough, dyspnea, sputum production, and tachycardia. Pneumonia is even more likely to be the diagnosis if the patient also has a fever (an exception is neonates who are diagnosed with afebrile Chlamydia trachomatis pneumonia) and auscultatory findings that may include abnormal breath sounds, dullness to percussion, wheezes, and crackles (rales).

Pneumonias can be classified based on how rapid the pneumonia manifests. Acute onset pneumonias develop within 24–48 hours and are common in patients with typical pneumonia. The patient’s only complaint may be an upper respiratory infection but manifestations of typical pneumonia rapidly develop—high fever, shaking chills, dyspnea, tachycardia, productive cough with purulent sputum production, toxic facies, and consolidations in the lungs as seen on chest radiographs (Table LRI-6).

Interstitial pneumonia (atypical pneumonia) has a subacute onset; it may take several days to 1 week before the patient develops signs and symptoms of pneumonia—low-grade fever, chills, paroxysmal cough with mucoid sputum or no sputum production, well-appearing facies, and infiltrates in the lungs as seen on chest radiographs (Table LRI-6).

Table URI-6. Comparison of Typical and Interstitial (Atypical) Pneumonias
Feature	Typical Pneumonia	Interstitial (Atypical) Pneumonia
Onset	Sudden	Gradual
Rigors	Single chill	“Chilliness”
Facies	“Toxic”	Well
Cough	Productive	Nonproductive: paroxysmal
Sputum	Purulent (bloody)	Mucoid
Temperature	103–104°F	< 103°F
Pleurisy	Frequent	Rare
Consolidation	Frequent	Rare
Gram stain (sputum)	Neutrophils	Mononuclear cells
White blood cell count and differential count	> 15,000/mm3 with left shift	> 15,000/mm3
Chest radiograph	Defined density, lobar pneumonia	Nondefined infiltrate or interstitial pneumonia
Most common cause	Streptococcus pneumoniae	Mycoplasma pneumoniae

Chronic pneumonias can take several weeks to 1 month for symptoms to fully develop. Patients usually present with a history of night sweats, low-grade fever, significant weight loss, productive cough with purulent sputum production, and dyspnea; coin lesions (Ghon focus) in the lungs are seen on chest radiographs.

Symptoms of aspiration pneumonia are similar to other acute onset pneumonias, except patients experience recurrent chills rather than a shaking chill, and consolidations in the dependent lung segments are seen on chest radiographs. About one half of patients with aspiration pneumonia will produce foul-smelling sputum.

Some causes of pneumonia that result in unique signs and symptoms

Legionnaire’s diseasecaused by Legionella sp. can result in pneumonia with relative bradycardia, abdominal pain, vomiting, diarrhea, hematuria, mental confusion, abnormal results on liver and renal function tests, and increases in serum creatinine phosphokinase levels.
Psittacosisdue to Chlamydophila psittaci (formerly known as Chlamydia psittaci) can result in pneumonia with relative bradycardia, epistaxis, Horder spots, splenomegaly, and a normal or low leukocyte count. This disease is associated with caretakers of psittacine birds.
Q fever due to Coxiella burnetii can cause pneumonia with relative bradycardia, tender hepatomegaly, endocarditis, and abnormal liver function tests. Q fever is associated with farmers who have recently birthed livestock.
Erythema nodosum and hilar adenopathy can be seen in patients with pneumonia due to fungi like Histoplasma capsulatum (endemic in the Ohio and Mississippi river valleys) and Coccidioides immitis and Coccidioides posadasii (These two species are dimorphic fungi endemic to the Western Hemisphere. They can be found in the soil in certain arid regions in the southwestern United States, and in Mexico, Central America, and South America. These 2 species are morphologically identical but genetically and epidemiologically distinct. C. immitis is found only in California's San Joaquin valley region. C posadasii can be found in the desert of the southwest United States, Mexico, and South America).
Fungal pneumonia is most often caused by Blastomyces dermatitidis in the United States. It can also produce rough verrucous skin lesions. This fungus is endemic in the Southeastern United States.

Epidemiology

Two to three million cases of pneumonia are reported each year in the United States.
Patients with pneumonia are responsible for over 10 million patient visits, 500,000 hospitalizations, and 45,000 deaths annually. Together, influenza and pneumonia are the eight leading cause of death in the U.S (in 2006; 56,326 deaths).
The patient with pneumonia usually has had a previous viral upper respiratory tract infection.
Inhalation and aspiration are the two most common means of acquiring an infectious pneumonia. Aspiration pneumonia is an endogenous infection.
Pneumonia is more common during the winter months and in persons older than 65 years of age.
Elderly patients are more likely to be hospitalized and die following onset of pneumonia.
The following conditions predispose persons to aspiration pneumonia: an altered level of consciousness, alcoholism, seizures, anesthesia, central nervous system disorders, trauma, dysphagia, esophageal disorders, and nasogastric tubes.

Pathogenesis

There are no resident bacteria in the lower respiratory tract. The two most common means of acquiring a lower respiratory tract infection is by inhalation and aspiration. Organisms that enter the alveoli are eliminated by alveolar macrophages. Alveolar macrophages are the most important means of eliminating organisms that get in the alveoli after escaping the defense mechanisms in the upper respiratory tract and the respiratory airways.

Once a microorganism enters the alveoli, it can be opsonized by IgG in the fluid lining the alveoli and then be ingested by the macrophage via their Fc receptors.

If there is no specific antibody to the organism present, the macrophage can still phagocytize the invader using receptors that bind C-reactive protein or complement or by receptors to pathogen-associated molecular patterns (PAMPs). Mannan, lipopolysaccharide, lipoteichoic acid, N–formylated methionine-containing peptides, muramyl peptides, and peptidoglycan are all examples of PAMPs, which the alveolar macrophage can use to phagocytize bacterial invaders.
When the microorganism is phagocytized, the macrophage will destroy the organism, if possible, and present microbial antigens on the surface to awaiting B and T cells.
Once activated, the B and T cells can produce more antibody and activate macrophages. Macrophages simultaneously release factors that help carry polymorphonuclear leukocytes (PMNs) from the bloodstream and initiate an inflammatory response. PMNs, antibodies, and complement components are useful in destroying the “invaders.”

Many bacteria that cause pneumonia can initially survive in the alveoli due to the following defense mechanisms.

Capsule (e.g., S pneumoniae, H influenzae) production prevents phagocytosis by the alveolar macrophage.
Viruses and Chlamydia invade host cells before the alveolar macrophages can phagocytize them.
M tuberculosis can survive in alveolar macrophages even after being phagocytized.

If the organisms survive in the alveoli, microbial growth can cause tissue injury, which stimulates the host to mount an inflammatory response. Tissue injury can occur due to exotoxins produced by a bacterium, cell lysis caused by a virus, or death of alveolar macrophages and dumping of their lysosomal contents in the alveoli due to growth of an organism in the phagocyte. Vascular permeability increases, and PMNs arrive at the area with many of the serum components, attempting to contain and eliminate the organisms. While the microorganisms are damaging the alveoli, other alveolar macrophages are being recruited to the area of inflammation. Lymphoid tissue associated with the lungs (mediastinal lymph nodes) becomes enlarged following activation of the B and T lymphocytes. Chest radiographs may show evidence of mediastinal lymph node enlargement in the patient with pneumonia.

The accumulation of microorganisms, immune cells, and serum components can cause the alveoli to fill and spread to other alveoli that are in close proximity. This inflammatory response is described as an opacity or a consolidation seen on a chest radiograph, and is often seen in patients with pneumonia caused by S pneumoniae—this type of pneumonia is called typical or lobar pneumonia. The inflammatory response to the infection and the microorganisms produce factors that allow the microorganisms to leave the lung and exert systemic effects such as fever. Examples of microbial factors that can have systemic effects include endotoxin from gram-negative bacteria resulting in fever and septic shock, and cell wall components of gram-positive bacteria that can lead to fever and septic shock.

Organisms such as M pneumoniae and the influenza virus initially do not cause a large amount of fluid to accumulate in the alveoli. However, following infection with these organisms, inflammation of the interstitial spaces (walls of the alveoli) occurs, resulting in interstitial or atypical pneumonia. Chest radiographs of patients with this type of pneumonia show fine granular diffuse infiltrates.

Other organisms such as Staphylococcus aureus, gram-negative rod-shaped bacteria, and anaerobic bacteria produce abscesses or microabscesses. In these infections the immune system can wall off the organisms and produce localized abscesses or microabscesses that usually show well-defined circular lesions with necrotic translucent centers on chest radiographs.

Diagnosis

Patients with pneumonia may present with chest discomfort, cough (productive or nonproductive paroxysmal cough), rigors (patients with typical pneumonia) or chills (patients with interstitial pneumonia), shortness of breath, and fever. Physical examination may reveal increases in respiratory rate and heart rate and dullness to percussion over affected regions of the lungs and rales.

Chest radiographs showing new consolidations or infiltrates are definitive in helping to establish a diagnosis of pneumonia. When alveolar sacs fill with inflammatory cells and fluid, the chest radiograph will show consolidated well-defined densities that are unilateral (inhalation or aspiration pneumonia), bilateral (hematogenous spread to lungs), localized, or uniform. When a chest radiograph shows inflammation and thickening of the alveolar septa that surround the alveoli, rather than a filling of the alveolar sacs with inflammatory material, the diagnosis is more likely to be interstitial pneumonia.

Some organisms form abscesses in the lung (e.g., Staphylococcus aureus, Enterobacteriaceae, Pseudomonas aeruginosa, and anaerobic organisms) and in such cases, a chest radiograph is useful in revealing abscess formation. If present, certain classic radiologic patterns may be of diagnostic value; for example,

Klebsiella pneumoniae infection causing an upper lobar consolidation can result in a bowing fissure (“bulging fissure” sign).

Staphylococcus aureus infections of the lung can cause multiple bilateral nodular infiltrates with central cavitation. In children, the chest radiograph may show ill-defined, thin walled cavities (“pneumatoceles”), bronchopleural fistulas, and empyema.

Pseudomonas aeruginosa infections can result in microabscesses, which may coalesce into large abscesses.

Gram-negative rod infections (e.g., Klebsiella, Proteus, E coli) often cause lung necrosis.

Mycobacterium tuberculosis pneumonia can cause coin lesions.

Consolidations in the dependent lung segments may indicate aspiration pneumonia.

To identify the specific pathogen that is causing the pneumonia, clinical and epidemiologic data must be considered to limit the number of possible causes of the pneumonia (see Tables LRI-1 through LRI-4, and TablesLRI-6 and LRI-7).

Table LRI-7. Pneumonia Patient’s Condition or Circumstance and the Most Common Causative Agents
Condition or Circumstance	Common causative agents
Cystic fibrosis	Pseudomonas aeruginosa or Staphylococcus aureus
Alchohol abuser	Klebsiella pneumoniae or oral anaerobic bacteria (e.g., Prevotella, Bacteroides, Peptostreptococcus, Fusobacterium)
Nursing home resident with underlying cardiopulmonary disease; recent antibiotic therapy; or multiple medical comorbidities	Enteric gram-negative bacteria (Enterobacter, Klebsiella pneumoniae, Escherichia coli)
Chronic obstructive pulmonary disease; alcohol abuser; elderly	Haemophilus influenzae and Klebsiella pneumoniae
Intravenous drug user	Staphylococcus aureus
Elderly; recent influenza virus infection	Staphylococcus aureus
Military recruits at basic training camp; college students living in dormitories	Neisseria meningitidis

Gram stain and appearance (Table LRI-8) of sputum from a patient with suspected pneumonia can be helpful in presumptive determination of the cause of the pneumonia. Some pathogens Gram stain poorly or do not Gram stain, and if pneumonia is caused by one of the suspected pathogens, Dieterle silver stain (Legionella sp.), acid fast stain (Mycobacteria), or Gomori methenamine silver stain (fungi and Pneumocystis) should be ordered.

Table LRI-8. Sputum Appearance and Most Likely Cause or Type of Pneumonia
Sputum Appearance	Most Likely Cause or Type of Pneumonia
Purulent	Typical pneumonia
Mucoid	Interstitial pneumonia
Rust color	Streptococcus pneumoniae
Green color	Pseudomonas aeruginosa or Haemophilus influenzae
Thick currant jelly-like	Klebsiella pneumoniae
Large amount of blood	Cavitary tuberculosis and lung abscess
Foul smelling	Anaerobic bacterial pneumonia

Additional laboratory tests that can aid in establishing a definitive diagnosis

Culture of the sputum.

Culture of blood samples for bacteria, fungi, or viruses.

Serology to detect antibodies produced against the pathogen or as a result of infection with the pathogen (e.g., cold agglutinins for Mycoplasma pneumoniae; detection of antibodies to the capsule of Streptococcus pneumoniae).

Antigen tests to detect certain antigens produced by the pathogen (e.g., polysaccharide testing for Streptococcus pneumoniae and Haemophilus influenzae).

Skin tests to detect delayed-type hypersensitivity reactions to certain pathogens (e.g., Mycobacterium tuberculosis: Mantoux test, Blastomyces dermatitidis, Histoplasma capsulatum, Coccidiodes immitis).

Polymerase chain reaction (PCR) performed on sputum samples to rapidly determine the cause of the pneumonia (e.g., tuberculosis).

Urinalysis for Legionella antigens.

Treatment and Prevention

Because most cases of pneumonias are caused by bacteria, treatment usually involves antibiotic therapy. Tables LRI-9 and LRI-10 list empiric treatment regimens for patients with pneumonia. In about one half of pneumonia patients, the etiologic agent can be determined and if the agent is known, more definitive therapy can be initiated.

Table LRI-9. Treatment of Pneumonia in Pediatric Patients by age or condition and Causative Agent
Patient age or condition	Causative agent	Empiric therapy
Neonatal pneumonia (birth to 1 month)	Streptococcus agalactiae, Escherichia coli and other coliforms, Listeria, Staphylococcus aureus, Chlamydia trachomatis, Treponema pallidum	Ampicillin + gentamicin ± cefotaxime; add vancomycin methicillin-resistant S aureus; if Chlamydia infection, treat with erythromycin
Infants (1–3 months)	Chlamydia trachomatis, Streptococcus pneumoniae	Erythromycin or azithromycin *S pneumoniae:* ampicillin
Children (4 months–5 years)	Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae	Outpatient: Amoxicillin Inpatient: Ampicillin intravenous Inpatient ICU: Cefotaxime If Mycoplasma is likely use clarithromycin or azithromycin.
Children (5–15 years)	Mycoplasma pneumoniae, Chlamydophila pneumoniae, S pneumoniae (uncommon)	Outpatient: Clarithromycin or azithromycin Inpatient: Ceftriaxone + azithromycin
Children with cystic fibrosis	Staphylococcus aureus early in disease, Pseudomonas aeruginosa later in disease	For S aureus: methicillin sensitive strains: oxacillin/nafcillin; methicillin-resistant strains: vancomycin For P aeruginosa: tobramycin + ticarcillin or piperacillin or tobramycin + ceftazine

ICU, intensive care unit.

Table LRI-10. Treatment of Pneumonia in Adults by Causative Agent and Patient Characteristics
Patient Characteristics	Causative Agent	Empiric Therapy
Viral pneumonia in adults	Influenza virus, parainfluenza, adenovirus, RSV, hantavirus	For influenza A and B: zanamivir or oseltamivir
Community acquired; not hospitalized	No comorbidity: Mycoplasma pneumoniae, Chlamydophila pneumoniae, viral, Streptococcus pneumoniae Smokers: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis Postviral bronchitis: Streptococcus pneumonia, Staphylococcus aureus (rare) Alcoholic stupor: Streptococcus pneumoniae, Klebsiella pneumoniae and other coliforms, anaerobes (aspiration) IV drug abuse: Staphylococcus aureus Airway obstruction: Anaerobes	Azithromycin or clarithromycin or fluoroquinolones with enhanced activity against S pneumoniae (moxifloxacin > gatifloxacin > sparfloxacin > levofloxacin)
Community acquired; hospitalized	No comorbidity	Cephalexin + erythromycin or azithromycin or fluoroquinolones with enhanced activity against S pneumoniae
Hospital acquired (nosocomial)	Poststroke aspiration: Streptococcus pneumoniae, anaerobes Water colonization: Legionella sp. Organ failure: Coliforms Mechanical ventilation: Coliforms, Pseudomonas aeruginosa, Staphylococcus aureus; Steroid use: Yeast, Pneumocystis jiroveci	To cover coliforms, S pneumoniae, and anaerobes: Imipenem or meropenem or piperacillin Pneumocystis jiroveci pneumonia can be treated with trimethoprim/ sulfamethoxazole Yeast infections can be treated with amphotericin B
Aspiration pneumonia and lung abscess	Bacteroides, Peptostreptococcus, Fusobacterium	Clindamycin
Chronic pneumonia with fever, night sweats, and weight loss	Mycobacterium tuberculosis, coccidioidomycosis, histoplasmosis	Pulmonary tuberculosis: isoniazid + rifampin + pyrazinamide Primary pneumonia due in coccidioidomycosis and histoplasmosis treatment is not usually recommended; if symptoms do not resolve within several weeks to 2 months, treat with itraconazole; for severe disease, treat with amphotericin B

There are two vaccines that can be given to adults to help prevent pneumonia. The S pneumoniae vaccine contains 23 capsular types of the bacterial capsule and is used in persons older than age 65. The influenza vaccine should be given yearly to all persons older than age 65 to help prevent viral pneumonia or secondary bacterial pneumonia that may occur following infection with the influenza virus. Chemoprophylaxis to prevent influenza infections is helpful in preventing secondary bacterial pneumonia.

The conjugated S pneumoniae heptavalent vaccine is important in preventing infection with this organism in young children. The conjugated H influenzae type b (Hib) vaccine prevents childhood infections with H influenzae. Respiratory syncytial virus infections can be prevented in premature infants, neutropenic infants, or in infants with various comorbidities with a periodic injection of respiratory syncytial virus immune globulin or humanized mouse monoclonal antibody (palivizumab). Annual immunization of children with the influenza vaccine prevents influenza infections in vaccinated children and appears to prevent spread of the virus to close contacts that may be at high risk for adverse outcomes following this viral infection.