Lobar  Pneumonia

"hospital acquired" and "community acquired " pneumonia.? 

Community-acquired pneumonia.

The most common organisms are

• Streptococcus pneumoniae (30%)

• Hemophilus influenzae (10%)

• Mycoplasma pneumoniae (10%) 

• Chlamydia pneumoniae (8%)

• influenza virus (7%)

• Legionella species (3%) 

• In up to 40% cases, no pathogen is identified

• gram negative Enterobacteriaceae (3%)

• Chlamydia psittaci (1%)

• Moraxella catarrhalis (0.5%)

• other pathogens (8-10%)

Host factors 

Healthy adults have intact pulmonary clearance mechanisms that remove aspirated secretions.

Damaged clearance mechanisms 

• smoking

• chronic bronchitis 

• asthma

• viral respiratory infections

 Systemic defects 

• malnourished persons

• alcoholics

• residents of nursing home

• patients with heart disease

• diabetes mellitus

• liver disease

• kidney disease 

• HIV infection. 

Inability to mount an antibody response

• lymphoma

• myeloma

• cancer 

• splenectomy

Pathogenesis of pneumococcal pneumonia

S. pneumoniae lives in the nasopharynx, and can be cultured in 5-10% healthy adults, 20-40% children. Nearly all infants are colonized at some point in the first two years of life. In epidemics involving a closed population, 5-10% of all persons carry the epidemic strain.

• Aspiration of respiratory secretions containing pneumococci is generally followed by cough and epiglottic reflexes, mucociliary action and phagocytosis. 

• If these defenses are impaired, pneumococci multiply in alveoli. 

• If there is sufficient level of circulating antibody to the capsular polysaccharide, the infections is controlled. If not Serous edema fluid is poured out, which interferes with gas exchange and facilitates spread. 

• By the fourth day, neutrophils predominate and the alveoli consolidate. 

• This process usually affects a single lobe in the lung. 

• Bacteremia results from multiplication of the organisms. 

• Destruction of pneumococci occurs when anticapsular antibody is formed pneumococci are phagocytosed. Granulocytes are replaced by macrophages, and resolution of the lesion occurs. 

• Damage to the lung is uncommon, and recovery is associated with complete resolution of the pathologic changes.

The major virulence factor is the

• pneumococcal capsule, which prevents phagocytosis by PMN’s. 

• Antibody to the capsule confers immunity. 

• Pneumolysin is toxic to pulmonary cells and causes cell lysis. 

• Other factors include pneumococcal protein A (Psp A), adhesins, alpha protease, and neuraminidase.

Diagnosis 

• Gram stain: The diagnosis is suggested by the demonstration of large numbers of PMN’s and gram-positive diplococci in a gram stained sputum specimen.
• Sputum culture: The diagnosis is confirmed by identification of Streptococcus pneumoniae in sputum culture. Sputum cultures, however, may be contaminated with mouth flora and should be collected very carefully. The primary disadvantage is the confusion that results from contamination of the sputum with oropharyngeal flora and excessive contamination with saliva. 
• Blood cultures will grow S. pneumoniae in 20-30% cases. When positive, blood cultures are highly significant.

S. pneumoniae are gram positive diplococci which produce alpha hemolytic colonies on blood agar. It is distinguished from viridans streptococcus by susceptibility to Optochin and by bile solubility.

Therapeutic strategy

• Penicillin has been the standard drug to treat pneumonococcal pneumonia. Procaine penicillin G, amoxicillin, cefazolin, and erythromycin are effective. 

• Trimethoprim-sulfamethoxazole should be avoided as up to 20% isolated from day care centers are resistant. 

• In penicillin – allergic patients, erythromycin is an alternative.

• The emergence of penicillin resistant strains is of great concern . Where the incidence of resistance of high, Ceftriaxone or erythromycin are the agents of choice. 

• At LUMC, the incidence of resistance is approximately 20%.

The length of treatment will vary with the severity of illness and the presence of underlying disease. 

• Generally, 7-10 days of antibiotic should be sufficient.

• Pneumococci are no longer detected in the sputum within several hours of the first dose of penicillin. 

• Dramatic symptomatic improvement in 24 hours

• The lack of lung destruction and complete resolution of pathologic changes on recovery, coupled with the dramatic response to penicillin, allow for a relatively short duration of treatment.

Pneumococcal resistance to penicillin

• Penicillin acts by binding to and blocking the action of cell membrane enzymes (PBP’s) responsible for cell wall synthesis. 

• Alteration of penicillin – binding proteins requires high concentrations of penicillin to saturate them, and leads to resistance. 

• Intermediate resistance to penicillin is defined as an MIC between 0.1 and 1 microgram. These isolates may be treated with ceftriaxone, erythromycin or increased doses of penicillin.

• High-level resistance occurs when MIC is > 2 microgram. These isolates should be treated with vancomycin.

Complications of Pneumococcal pneumonia

• In the pre-antibiotic era, empyema was the most common complication, and still occurs in 25% cases. 
• Bacteremia
• Meningitis
• Septic arthritis
• Endocarditis 
• Purulent pericarditis 

Prevention 

Pneumococcal vaccine containing capsular polysaccharide from the 23 serotypes that most commonly cause infection is available.

• Vaccination is recommended for individuals with chronic pulmonary or cardiovascular disease, diabetes, alcoholism, cirrhosis, chronic renal insufficiency, CSF leak and everyone above the age of 65. 

• In addition, immunocompromised patients with lymphoma, Hodgkin's, myeloma, organ transplantation, splenic dysfunction and HIV infection should be vaccinated.

• Vaccination once in 5 years