Lower Respiratory Tract Infections
Return to Syllabus  

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:

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

 

Many microorganisms can cause pneumonia, but most cases are caused by bacteria. The most likely causes of pneumonia depend on various clinical and epidemiological factors. These factors include how the patient acquired the pneumonia (e.g., inhalation, aspiration), where the patient acquired the pneumonia [e.g., community-acquired pneumonia (CAP), health care-associated pneumonia (HCAP)], the age of the patient, the type of pneumonia the patient manifests (e.g., typical versus atypical (interstitial) pneumonia) and the immune status of the patient (i.e., immunocompromised versus immunocompetent). The clinical and epidemiologic factors mentioned above are used to determine the most likely causes of each individual case of pneumonia and have a significant affect on the antimicrobial agents used to empirically treat patients with pneumonia.

 

The emergence of multi-drug resistant (MDR) bacteria (e.g., methicillin resistant Staphylococcus aureus (MRSA), Pseudomonas aeruginosa, Acinetobacter, and MDR Enterobacteriaceae) has made the treatment of pneumonia more challenging. MDR bacterial pneumonias are more likely to occur in a health care setting (e.g., hospital, ICU, nursing home). This increase in MDR bacterial pneumonias has resulted in a revised classification of pneumonia. Currently, there are two categories of pneumonia; community-acquired pneumonia (CAP) and health care-associated pneumonia (HCAP). HCAP contains two subcategories; hospital-acquired pneumonia (HAP), and ventilator-associated pneumonia (VAP). The etiological agents and the chances of them being a MDR differ depending on the category of pneumonia and the risk factors a patient has. This also has a significant affect on the antimicrobial agents used to treat these patients.

 

 

Table LRI-1 Common Causes of CAP by Site of Care after Diagnosis

 

Hospitalized Patients

Outpatients

Non-ICU

ICU

Streptococcus pneumoniae, Mycoplasma pneumoniae, Haemophilus influenzae, Chlamydophila pneumoniae,       Respiratory viruses

S. pneumoniae, M. pneumoniae, C. pneumoniae, H. influenzae, Legionella sp., Respiratory viruses

S. pneumoniae, Staphylococcus aureus, Legionella sp., Gram-negative bacilli, H. influenzae

Respiratory viruses = Influenza A and B viruses, adenoviruses, respiratory syncytial viruses, parainfluenza viruses.

Note: The organisms are listed in descending order of frequency. ICU- intensive care unit


 

LRI-2 Common Causes of VAP and HAP

VAP Non-MDR

VAP MDR

HAP Non-MDR

HAP MDR

S. pneumoniae,  other Streptococcus sp.,    H. influenzae, MSSA, antibiotic sensitive Enterobacteriaceae (E. coli, Klebsiella pneumoniae, Proteus sp., Enterobacter sp., Serratia marcescens)

Pseudomonas aeruginosa, MRSA, Acinetobacter sp., antibiotic resistant Enterobacteriaceae (see VAP Non-MDR column), ESBL-positive strains of Klebsiella, Legionella pneumophila, Burkholderia cepacia, Aspergillus (note this one is a fungus)

Same as VAP Non-MDR

Non-MDR infections and anaerobic bacterial infections (Prevotella melaninogenicus, Fusobacterium nucleatum, Peptostreptococcus, Peptococcus, and other anaerobes) are more common in HAP than VAP

 

Same as VAP MDR, MDR infections are less frequent in HAP than in VAP.

MSSA- methicillin sensitive S. aureus, MRSA- methicillin resistant S. aureus, MDR- multidrug resistant, ESBL- extended spectrum beta-lactamase

 


Table LRI-3. 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-4. 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 atypical (interstitial) pneumonia

Mycoplasma pneumoniae, respiratory viruses†, Chlamydophila pneumoniae, Legionella sp.

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 A and B viruses, parainfluenza viruses, adenoviruses, and respiratory syncytial virus.


 

 

Table LRI-5. 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 bat excreta (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-6. 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 immuno-compromised

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-7. 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

Atypical (interstitial)

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 seen in material taken from lung

Fungal

Coccidioides immitis or Coccidioides posadasii

Spherule seen in material taken from lung

 

Fungal

Histoplasma capsulatum

Yeast cells usually in PMNs or monocytes in material taken from lung;

When grown in vitro at room temperature the organism produces hyphae and tuberculate macroconidia.

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 and auscultatory findings that may include abnormal breath sounds, dullness to percussion, wheezes, and crackles (rales). One exception regarding fever is a neonate who diagnosed with afebrile Chlamydia trachomatis pneumonia.

 

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-8).

 

Atypical pneumonia (interstitial 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-8).


 

Table URI-8. Comparison of Typical and Atypical (Interstitial) Pneumonias

Feature

Typical Pneumonia

Atypical (Interstitial) 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 may be seen on chest radiographs if the patient has M. tuberculosis pneumonia.

 

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.

 

Symptoms of HCAP are like those mentioned above; fever, leukocytosis, increase in respiratory secretions, pulmonary consolidations on physical examination, along with a new or changing radiographic infiltrate or consolidation. Other signs and symptoms may include tachycardia, tachypnea, worsening oxygenation, and increased minute ventilation (Tidal volume x Respiratory rate = minute ventilation; normal 5-8 L/minute).

 

Radiograph interpretation in a patient with VAP may be difficult in that they may have abnormal chest radiographs even before the pneumonia begins.

 

Some causes of pneumonia that result in unique signs and symptoms

Epidemiology

 

 

Pathogenesis

The microbiota of the lower respiratory tract rarely, if ever, cause pneumonia. Usually, a patient with pneumonia has inhaled or aspirated a pathogenic organism or a new bacterial strain of an organism already dwelling in the lungs. The two most common means of acquiring a lower respiratory tract infection is by inhalation and aspiration. Pathogenic organisms and different strains of bacteria in the microbiota of the lung 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. PMN’s are important in elimination of organisms after an infection and pneumonia has begun.

 

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.

  1. 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.
  2. 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.
  3. 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.

 

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.

 

VAP- The endotracheal tube bypasses most of the host defenses that prevent aspiration of organisms into the lungs. In critically ill patients the oropharyngeal flora is replaced by pathogenic bacteria. Factors important in causing this change in the oropharyngeal flora are: antibiotic selection pressure, cross-infection from other infected/colonized patients, contaminated equipment, and malnutrition. Due to factors yet to be identified in around one third of patients that are mechanically ventilated the lower respiratory tract defenses are overwhelmed and allow pathogenic bacteria to infect the lungs. In severely ill patients that are mechanically ventilated it appears that they go through a period of immunosuppression after admission to the ICU. Recent studies suggest that hyperglycemia maybe be one factor causing this immunosuppression. Keeping the patients’ blood sugar close to normal with exogenous insulin may be beneficial. More frequent transfusions with leukocyte-depleted RBC’s may also positively affect the immune response of patients on a mechanical ventilator.

Diagnosis

Patients with CAP and HCAP

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 an atypical (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,

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-7, and TablesLRI-8 and LRI-9).

Table LRI-9. 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-10) 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 don’t 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-10. 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

 

Patient with VAP

Diagnosis of these patients can be difficult because:

 

There is still much debate concerning how to determine if a mechanically ventilated patient has VAP. There are now two approaches: the quantitative culture approach and the clinical approach.

 

Quantitative culture approach tries to discriminate between bacterial colonization and true bacterial infection by determining the bacterial burden. The respiratory tree can be sampled at various points; endotracheal aspirates and bronchoscopy. A quantitative endotracheal aspirate would be positive for bacterial colonization if the colony forming units (CFU) were less than 106 CFU/ml. If greater than 106 CFU/ml then the patient would have a VAP. If a bronchoscope was used to get a protected brush specimen to sample further down in the lungs then a CFU less than 103 CFU/ml would indicate the patient is only colonized. However, if the CFU from the protect brush specimen were greater than 103 CFU/ml then the patient has VAP. One important point to remember is that these samples should be obtained BEFORE antibiotic therapy has begun. If not false negative samples are more likely. The cultures can then also be used to identify the pathogen and determine its sensitivity to antimicrobial agents.

 

Clinical approach uses a Clinical Pulmonary Infection Score (CPIS) to determine if a patient is more likely to have VAP. The clinical criteria used are weighted and added together to produce a final score. A maximum score is 12 when the tracheal aspirate data arrives. A score of 6 or greater indicates the patient has VAP. Clinical criteria used are fever, leukocytosis, oxygenation, chest radiograph, and tracheal aspirates. It is not important for you to memorize this scoring procedure for the exam!

 

Some medical facilities utilize both approaches for diagnosis of VAP. The clinical approach is used to quickly determine if a protected brush specimen should be used to do quantitative cultures.

 

Treatment and Prevention

Except for patients with CAP admitted to the ICU no data exists to show that treatment directed to a specific pathogen is statistically superior to empirical therapy. Therefore, most CAP patients are treated empirically (see below for CAP and HCAP). Because most cases of pneumonias are caused by bacteria, treatment usually involves antibiotic therapy. 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.

 

CAP

 

HCAP (includes HAP and VAP)

 

*Risk factors include: hospitalization for ≥48 hours, hospitalization for ≥2 days in the prior 3 months, residence in an extended-care or nursing home facility, antibiotic therapy in preceding 3 months, chronic dialysis, home infusion therapy, home wound care, or family member with MDR infection.

 

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 13-valent conjugate 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.

 

Exciting new research: After reading this handout you hopefully, realize that many respiratory diseases are due to viruses. Even pneumonia can be caused by viral pathogens. If the respiratory infection is due to a bacterial pathogen then early treatment with antibiotic will improve your patients’ outcomes.

 

Determining if a respiratory infection like pneumonia is due to a bacterium is still an educated guess. It is highly likely that pneumonia, in most of the patients you see, will be due to bacteria. However, what if the pneumonia occurs during the Influenza season? Viral pneumonia is more common during this time. The chances increase that a patient will have viral pneumonia. In later stages of viral pneumonia opacities in the chest radiograph can look a lot more like a consolidation than an infiltrate. It would be great if there were some blood test that could help the clinician decide whether the respiratory infection they were observing was bacterial, viral, or something else entirely.

 

Recent research using a blood test to detect levels of procalcitonin (PCT) maybe the test we are looking for to determine if a person’s respiratory tract infection is due to a bacterium. Further work has shown that PCT levels are helpful in determining how long to give a person with respiratory tract infections antimicrobial therapy.

 

Others have shown that PCT levels increase in the bloodstream during bacterial infections but do not go up during nonbacterial infection nor do they increase during nonspecific inflammatory reactions. PCT levels decrease when antimicrobial therapy has caused a favorable patient response. Thus, PCT levels have the potential to be used as a marker to decide if an antibacterial agent should be used and to determine the duration of treatment in a patient with a bacterial infection.

 

PCT is a precursor peptide of the hormone calcitonin and it is released in response to bacterial toxins and proinflammatory host mediators (e.g., interleukin 1b, interleukin 6) that are produced during a bacterial infection. The more severe the bacterial infection the higher the PCT levels in the blood. PCT levels increase within 6-12 h of the start of the bacterial infection and PCT levels decrease by half daily following effective control of the bacterial infection with the hosts’ immune system and/or antimicrobial agents. PCT levels are not increased by cytokines produced during a viral infection (e.g., interferon).

 

An algorithm using PCT levels to detect and treat bacterial infections of the respiratory tree has been developed for potential use in clinics and hospitals.

 

Send comments and email to Dr. Chamberlain, nchamberlain@atsu.edu
Revised 8/21/14
©2014 Neal R. Chamberlain, Ph.D., All rights reserved.