PNEUMONIA

I. Definition
- Pneumonia is an infection of the pulmonary parenchyma.
 Classification:
1. Community Acquired Pneumonia (CAP)
2. Hospital-acquired (HAP)
3. Ventilator-associated (VAP)
4. Health Care Associated pneumonia (HCAP)- cause: MDR pathogen associated w/ HAP.
II. Risks:
 Kindly See Table 121-1 Risk Factors of Pathogen Resistant to Usual Therapy of CAP.

III. Pathophysiology
1. Microorganisms gain access to the lower respiratory tract via aspiration while unconsciously
asleep or via hematogenous spread (e.g., from tricuspid endocarditis) or by contiguous
extension from an infected pleural or mediastinal space.
2. The hairs and turbinates of the nares capture larger inhaled particles before they reach the
lower respiratory tract.
3. The branching architecture of the tracheobronchial tree traps microbes on the airway lining.
4. Mucociliary clearance and local antibacterial factors either clear or kill the potential pathogen
trapped in tracheobronchial tree.
5. Patient gag and cough reflexes offer critical protection from aspiration.
6. Normal flora adhering to mucosal cells of the oropharynx prevents pathogenic bacteria from
binding and thereby decreases the risk of pneumonia.
7. Barriers are overcome and small microorganisms are inhaled to the alveolar level.
8. Resident alveolar macrophages clears and kills pathogens.
9. Pathogens are eliminated via either the mucociliary elevator or the lymphatics.
  In Pneumonia Cases:
1. Resident alveolar macrophages are exceeded by the pathogens.
2. Alveolar macrophages initiate the inflammatory response to bolster lower respiratory tract
defenses.
3. The host inflammatory response triggers the clinical syndrome of pneumonia.
4. Inflammatory mediators released by macrophages and the newly recruited neutrophils create
an alveolar capillary leak equivalent to that seen in acute respiratory distress syndrome.
5. Erythrocytes cross the alveolar–capillary membrane and causes hemoptysis.
6. Pathogens appear to interfere with the hypoxemic vasoconstriction that can result severe
hypoxemia.
7. Increased respiratory drive in the systemic inflammatory response syndrome leads to
respiratory alkalosis.
8. Decreased compliance due to capillary leak, hypoxemia, increased respiratory drive, increased
secretions, and occasionally infection-related bronchospasm all lead to dyspnea.
9. Continuous reductions in lung volume and compliance and the intrapulmonary shunting of
blood may cause respiratory failure and death.
 Inflammatory Mediators:
1. Interleukin 1 and tumor necrosis factor: results in fever.
2. Chemokines ( Interleukin 8 and Granulocyte colony-stimulating factor): stimulate the
release of neutrophils. Producing both peripheral leukocytosis and increased purulent
secretions.

IV. Pathology
1. Edema - Initial phase
2. Red hepatization phase- Second stage, erythrocytes, neutrophil influx and bacteria are occasionally
seen in pathologic specimens collected during this phase.
3. Gray hepatization- Third Stage, lysed and degraded erythrocytes, neutrophil is the predominant cell,
fibrin deposition is abundant, and bacteria have disappeared.
4. Resolution Phase- Final stage, the macrophage reappears as the dominant cell type in the alveolar
space, and the debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory
response.

V. COMMUNITY ACQUIRED PNEUMONIA

• ETIOLOGY: bacteria, fungi, viruses, and protozoa.
➢ Newly identified pathogens: metapneumoviruses, the coronaviruses responsible for severe
acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), and
community-acquired strains of MRSA
➢ Most common: Streptococcus pneumoniae
➢ MRSA-primary etiologic agent of CAP
➢ Other: must also be considered in light of the patient’s risk factors and severity of illness.
➢ Typical: S. pneumoniae, Haemophilus influenzae, and (in selected patients) S. aureus and
gram-negative bacilli such as Klebsiella pneumoniae and Pseudomonas aeruginosa.
➢ Atypical: (cannot be cultured on standard media or seen on Gram’s stain AND intrinsically
resistant to all β-lactam agents and must be treated with a macrolide, a fluoroquinolone, or a
tetracycline.) Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella species as
well as respiratory viruses such as influenza viruses, adenoviruses, human metapneumovirus,
and respiratory syncytial viruses.
➢ MOST COMMON CAUSES:
 Kindly See Table 121-2 Microbial Causes of CAP by Site of Care.

• EPIDEMIOLOGY:
 Kindly See Table 121-3 Epidemiologic Factors Suggesting Possible Causes of CAP.

 Risk factors: alcoholism, asthma, immunosuppression, institutionalization, and an age of

≥70 years
 In the elderly: decreased cough and gag reflexes as well as reduced antibody
and Toll-like receptor responses
 Pneumococcal pneumonia: dementia, seizure disorders, heart failure, cerebrovascular disease,
alcoholism, tobacco smoking, chronic obstructive pulmonary disease (COPD), and HIV infection.
 CA-MRSA pneumonia: patients with skin colonization or infection with CA-MRSA.
 Enterobacteriaceae: patients who have recently been hospitalized and/or received antibiotic
therapy or who have comorbidities such as alcoholism, heart failure, or renal failure.
 P. aeruginosa: is patients with severe structural lung disease, such as bronchiectasis, cystic
fibrosis, or severe COPD.
 Legionella infection: include diabetes, hematologic malignancy, cancer, severe renal
disease, HIV infection, smoking, male gender, and a recent hotel stay or ship cruise.
• CLINICAL MANIFESTATION:
1. Fever, Chills, Sweat
2. Tachycardia
3. Productive/ Nonproductive Cough
4. Sputum: Mucoid/ Purulent/ Blood tinged
5. Gross hemoptysis – seen in CA-MRSA Pneumonia
6. Pleuritic Chest Pain
7. Nausea, Vomiting, Diarrhea
8. Fatigue, Headache, Myalgia

• PHYSICAL EXAM
1. Increase Respiratory Rate
2. Increase/ Decrease Tactile fermitus
3. Percussion: Dull to Flat : Consolidation / Pleural Fluid
4. Crackles
5. Pleural Friction Rub
6. Septic Shock- Seen in Severe CAP
7. Confusion- Seen in Severe CAP
8. Early Organ Failure- Seen in Severe CAP

• DIFFERENTIAL DIAGNOSIS
1. Acute/ Chronic Bronchitis
2. Heart Failure
3. Pulmonary Embolism
4. Hypersensitivity Pneumonitis/ Radiation Pneumonitis

• CLINICAL DIAGNOSIS
1. Chest Xray
 Severe : Cavitation and Multilobar Involvement.
 S. aureus : Pneumatoceles
 TB: Upper lobe cavitating lessions
2. CT Scan
 Indication for post obstructive pneumonia caused by foreign body or cavitary disease.
3. Gram Staining
 To Identify : S. pneumoniae, S. aureus, Gram (-) Bacteria
4. Sputum Culture
 > 25 Neutrophils
 <10 squamous epithelial cells per Lower Power Field.
5. Blood Culture
 No longer considered test.
6. Urinary Antigen Test
 Identify : Pneumococcal Antigen
: Legionella Antigen- Serogroup I
 7. PCR
 Nasopharyngeal Swabs: Standard for diagnosis of viral infections.
 Identify: 1. Legionella spp.
2. M. pneumoniae
3. C. pneumoniae
4. Mycobacteria
8. Serology
 (+) four fold rise in IgM antibody Titer
 Identify: Coxiella burnetii
9. Biomarkers
 CRP – Identify treatment failure or worsening disease.
 PCT- Identify Bacteria vs Virus
- Less Antibiotic Failure
- Decrease Mortality Rate

• TREATMENT CRITERIAS
1. Pneumonia Severity Index (PSI)
 Identify Patient Risk of Dying.
 Determine Patient Need for ICU.
 Result Interpretation:
o Class 1 - 0.10% Mortality Risk
o Class 2 – 0.60% Mortality Risk
o Class 3 - 2.8 % Mortality Risk
o Class 4 – 8.2 % Mortality Risk
o Class 5 – 29.2% Mortality Risk
2. CURB – 65
 Determine Severity of Illness.
 Deermine Patient need for ICU.
• ANTIBIOTIC RESISTANCE
o Main Pathogen: S. pneumoniae and CA-MRSA
A. Penicillin Resistance
1. Minimal Inh. Concentration for Penicillin:
 Susceptible: < 2mcg/mL
 Intermediate: > 2-4 mcg/mL
 Resistant: > 8mcg/ mL
2. Risk Factors for Penicillin Resistant:
 Age: < 2 yrs old or > 65 yrs old
 Recent Hospitalization
 HIV Infection
B. Macrolide Resistance
1. Mechanism of Macrolide Resistance:
 Target site modification by ribosomal methylation of 23s rRNA.
 Efflux mechanism by the mef gene- low resistance effect.
C. Flouroquinolone Resistance
1. Flouroquinolones eg. Ciprofloxacin and Levoflixacin.
2. Resistant Pathogens are: MRSA/ CA-MRSA/ Enterobacter Spp.

• MANAGEMENT
1. If Suspected Increase CA-MRSA Risk for Infection.
 Add Linizolid or Vancomycin to Initial Regimen.
 Vancomycin has poor penetration to epithelial lining fluid.
 Vancomycin has no effect on toxin production relative to Linizolid.
2. Adjuctive Therapies:
 Adequate Hydration
 O2 Therapy
 Vassopressors or Assisted Ventilation
3. If Patient shows failure to Improve.
 Evaluate for 3 days
 Proceed CT or Bronchoscopy
o Common Cause of Failure:
a. Wrong Drug, Dose, Frequency of Administration
b. Drug Resistant Pathogen
c. CAP associated with TB/ Fungi/ CA-MRSA
d. Patient acquired nosocomial infections
 4. Kindly see Table 121-5 Empirical Treatment of CAP.

• COMPLICATIONS
1. Most Common Complications:
 MI
 CHF
 Arrythmia
2. Complications seen in Severe CAP.
 Respiratory Failure
 Shock
 Multiorgan Failure
 Coagulopathy
 Exacerbation of Comorbid Illnesses.
3. Note Worthy Complications:
 Pleural Effusion- Seen in Aspiration Pneumonia
 Lung Abcess- Common cause are CA-MRSA/ P. aeruginosa/ S. pneumoniae
 Metastatic Infection – Brain abcess or Endocarditis
• FOLLOW UP GUIDELINE

 2-4 Days: Observe for Fever & Leukocytosis, heals after 2-4 Days.
 4-12 Weeks: Test for Chest Xray and observe abnormalities.
 4-6 Weeks: Test for Chest Xray if there is relapse.
: Neoplasm if in the same location.

• PROGNOSIS OF CAP
1. Factors : Patient’s age, comorbidities, and site of treatment (inpatient or outpatient).
2. Younger Patients: 2 weeks Recovery
3. Older Patients: > 2 weeks Recovery
4. Outpatient: <5% Mortality Rate
5. Inpatient: 2-40% Mortality Rate

• PREVENTION OF CAP
 The main preventive measure is vaccination.
1. Pneumococcal Polysaccharide Vaccine (PPSV23)
 Contains capsular material from 23 pneumococcal serotypes.
2. Protein Conjugate Pneumococcal Vaccine (PCV13)
 Contains capsular polysaccharide from 13 of the most common pneumococcal
pathogens affecting children.
 Produces T cell–dependent antigens that result in long-term immunologic memory.
 Followed by the replacement of vaccine serotypes with nonvaccine serotypes
(serotypes 19A and 35B) after introduction of the original 7-valent conjugate vaccine.
 Recommended for the elderly and for younger immuno-compromised patients.
3. Influenza vaccine
 Available in an inactivated or recombinant form.
 Live attenuated influenza vaccine or “nasal spray” vaccine is no longer recommended.
 Patients at risk from complications should be vaccinated immediately and given
chemoprophylaxis with either Oseltamivir or Zanamivir for 2 weeks, until vaccine-
induced antibody levels are sufficiently high.

VI. VENTILATOR-ASSOCIATED PNEUMONIA

 The greatest difference between VAP and HAP is the return to dependence on expectorated
sputum for a microbiologic diagnosis of HAP, which is further complicated by frequent
colonization by pathogens in patients with HAP.

A. Etiology
 Potential etiologic agents of VAP include both MDR and non-MDR bacterial pathogens
 Non-MDR:
a) Streptococcus pneumoniae -Other Streptococcus spp.
b) Haemophilus influenzae
c) Methicillin-sensitive Staphylococcus aureus (MSSA)
d) Antibiotic-sensitive Enterobacteriaceae
(E.coli, K.pneumoniae, Enterobacter spp., Serratia Marcescens)
 MDR:
a) P. aeruginosa
 b) MSSA -Acinetobacter spp.
c) Antibiotic-resistant Enterobacteriaceae
(ESBL-positive strains, Carbapenem-resistant strains)
d) Legionella pneumophila -Burkholderia cepacia
e) Aspergillus spp.
 Most hospitals have problems with Pseudomonas aeruginosa
and MRSA.
 The most obvious risk factor is the endotracheal tube, which bypasses the normal mechanical
factors preventing aspiration.
 Risk factors for MDR pathogens: -prior IV antibiotic use within 90 days.
a) Septic shock at time of VAP -ARDS preceding VAP
b) ≥5 days of hospitalization prior to occurrence of VAP
c) Acute renal replacement therapy prior to VAP onset
B. Pathogenesis
 Common pathogenic mechanisms include:
1. Oropharyngeal colonization with pathogenic bacteria
2. Cross-infection from other colonized patients
3. Large-volume aspiration
4. Microaspiration around endotracheal tube
5. Altered defenses respiratory host defenses

 Kindly See Table 121-7 Pathogenic Mechanism and Prevention Strategy of VAP.
C. Clinical Manifestations
 The clinical manifestations are generally the same in VAP as in all other forms of pneumonia:
a) Fever
b) Leukocytosis
c) Increase in respiratory secretions
d) Pulmonary consolidation on PE
e) A new or changing radiographic infiltrate
 Other Clinical Features:
a) Tachypnea
b) Tachycardia,
c) Worsening oxygenation
d) Increased minute ventilation

D. Treatment