This is a case of a 74 year old woman who was diagnosed with
Community Acquired Pneumonia.
Pneumonia is an inflammation or infection of the lungs most commonlycaused by a bacteria or virus. Pneumonia can also be caused by inhaling vomitor other foreign substances. In all cases, the lungs' air sacs fill with pus , mucous,and other liquids and cannot function properly. This means oxygen cannot reachthe blood and the cells of the body.Most pneumonias are caused by bacterial infections.The most commoninfectious cause of pneumonia in the United States is the bacteria Streptococcuspneumoniae. Bacterial pneumonia can attack anyone. The most common causeof bacterial pneumonia in adults is a bacteria called Streptococcus pneumoniaeor Pneumococcus. Pneumococcal pneumonia occurs only in the lobar form.An increasing number of viruses are being identified as the cause of respiratoryinfection. Half of all pneumonias are believed to be of viral origin. Most viralpneumonias are patchy and the body usually fights them off without help frommedications or other treatments.Pneumococcus can affect more than the lungs. The bacteria can also causeserious infections of the covering of the brain (meningitis), the bloodstream, andother parts of the body.
develops in people with limited or no contactwith medical institutions or settings. The most commonly identified pathogensareStreptococcus pneumoniae, Haemophilus influenzae, and atypical organisms(ie, Chlamydia pneumoniae,Mycoplasma pneumoniae, Legionella sp). Symptomsand signs are fever, cough, pleuritic chest pain, dyspnea, tachypnea, andtachycardia. Diagnosis is based on clinical presentation and chest x-ray.Treatment is with empirically chosen antibiotics. Prognosis is excellent for relatively young or healthy patients, but many pneumonias, especially whencaused by S. pneumoniae or influenza virus, are fatal in older, sicker patients.
II. PATIENT PROFILE
Community-acquired pneumonia (CAP) is one of the most common infectious diseases and is an important cause of mortality and morbidity worldwide. Typical bacterial pathogens that cause CAP include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis (see images below). However, with the advent of novel diagnostic technologies, viral respiratory tract infections are being identified as common etiologies of CAP. The most common viral pathogens recovered from hospitalized patients admitted with CAP include human rhinovirus and influenza. 
Presentation and pathogens in typical community-acquired pneumonia
The term “typical” CAP refers to a bacterial pneumonia caused by pathogens such as S pneumoniae, H influenzae, and M catarrhalis. Patients with typical CAP classically present with fever, a productive cough with purulent sputum, dyspnea, and pleuritic chest pain. Characteristic pulmonary findings on physical examination include the following:
Rales heard over the involved lobe or segment
Increased tactile fremitus, bronchial breath sounds, and egophony may be present if consolidation has occurred.
Decreased tactile fremitus and dullness on chest percussion may result from parapneumonic effusion or empyema.
Epidemiologic data may provide clues to the specific pathogen causing CAP, as follows:
The most common overall pathogen is S pneumoniae
Underlying chronic obstructive pulmonary disease (COPD)  : H influenzae or M catarrhalis
Recent influenza infection  : Staphylococcus aureus
Alcoholic patient presenting with “currant jelly” sputum : Klebsiella pneumoniae 
Atypical community-acquired pneumonia
The clinical presentation of so-called “atypical” CAP is often subacute and frequently indolent. In addition, patients with atypical CAP may present with more subtle pulmonary findings, nonlobar infiltrates on radiography, and various extrapulmonary manifestations (eg, diarrhea, otalgia). Atypical CAP pathogens include the following:
Chlamydophila ( Chlamydia) pneumoniae
Legionnaires disease ( Legionella pneumophila)
Respiratory viruses, including the following:
Influenza A and B
Respiratory syncytial virus
Adenovirus 4 and 7
Other rare viral pneumonias include the following:
Coronavirus (MERS-CoV, SARS)
Herpes simplex virus
Human herpesvirus 6
Psittacosis ( Chlamydophila psittaci)
Q fever ( Coxiella burnetii)
Tularemia ( Francisella tularensis)Endemic fungi (causing subacute or chronic pneumonia), as follows:
Cryptococcus neoformans neoformans and neoformans gattii
Mycobacteria: Mycobacteria tuberculosis and nontuberculous mycobacteria (uncommon)
Extrapulmonary signs and symptoms seen in some forms of atypical CAP may include the following:
Rash (Horder spots in psittacosis; erythema multiforme in Mycoplasma pneumonia)
While historical clues and physical examination findings may suggest a causative pathogen, the clinical signs and symptoms of CAP are not sufficiently specific to reliably differentiate the exact etiologic agent.  Therefore, additional testing remains necessary to identify the pathogen and to optimize therapy in CAP.
Standard diagnostic studies for CAP include the following:
Sputum Gram stain and/or culture
Other laboratory tests
Depending on the perceived severity of illness and suspected etiology, additional workup may be warranted, including the following:
Complete blood cell (CBC) count with differential
Serum sodium level
Serum blood urea nitrogen (BUN) and creatinine levels
Serum transaminase levels
Serum phosphorus level
Lactic acid level
Creatine phosphokinase (CPK)
C-reactive protein (CRP)
Lactate dehydrogenase (LDH)
Cold agglutinin titers
Urinary antigen testing for Legionella species and S pneumoniae
Serologic studies for M pneumoniae, C pneumoniae, Bordetella pertussis, C burnetii
Molecular diagnostics, ie, polymerase chain reaction (PCR) testing
Obtain chest radiographs in all patients with suspected CAP to evaluate for an infiltrate compatible with the presentation of CAP and to help exclude conditions that may mimic CAP (ie, lung cancer, pulmonary emboli). [5, 6] Patients who present very early with CAP may have negative findings on chest radiography. In these patients, repeat chest radiography within 24 hours may be beneficial. CT scanning may also be necessary in immunocompromised patients who present with symptoms that suggest CAP in whom chest radiography findings are negative. Serial chest radiography can be used to observe the progression of CAP; however, radiographic improvement may lag behind clinical improvement.
Multiple scoring systems are available to assess the severity of CAP and to assist in deciding whether a patient should be hospitalized or admitted to the intensive care unit (ICU). The CURB-65 (confusion, uremia, respiratory rate, low blood pressure, age >65 years) and the Pneumonia Severity Index (PSI) are currently recommended by the 2007 Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines.  Patients with CURB-65 scores of 2 or more or PSI class IV-V may necessitate hospitalization or more intensive in-home services. ICU is recommended for any patient who requires mechanical ventilation or vasopressors. ICU admission should also be considered in patients with 3 or more minor risk factors, including respiratory rate of 30 or more, PaO2/FiO2<250, multilobar infiltrates, confusion, uremia, leukopenia, thrombocytopenia, hypothermia, and hypotension requiring aggressive fluid resuscitation.
Proposed scoring systems may also be helpful in certain populations to predict the severity of CAP. The SMART-COP score emphasizes the ability to predict the need for ventilator or vasopressor support and includes systolic blood pressure, multilobar infiltrates, serum albumin levels, respiratory rate, tachycardia, confusion, oxygenation, and pH level. The A-DROP (age, dehydration, respiratory failure, orientation, systolic blood pressure) is also a severity score. Recently, an expanded CURB-65 has been shown to improve prediction of 30-day mortality. It includes LDH, thrombocytopenia, and serum albumin, along with the traditional CURB-65, and has been shown to have better prediction accuracy. 
Adequate antimicrobial therapy for CAP includes coverage for S pneumoniae and atypical bacterial pathogens. Outpatient treatment for CAP in patients with no comorbidities and no risk factors for drug-resistant S pneumoniae frequently includes the following: 
A macrolide (azithromycin, clarithromycin, or erythromycin)
Treatment in patients with comorbidities such as chronic heart, lung, liver, or renal disease; diabetes mellitus; alcoholism; malignancy; asplenia; immunosuppression; prior antibiotics within 90 days; or other risk factors for drug-resistant infection includes the following:
Respiratory fluoroquinolones (moxifloxacin, levofloxacin)
Beta-lactam (high-dose amoxicillin 1 g 3 times/day) or amoxicillin/clavulanate (2 g twice daily), or ceftriaxone, cefpodoxime, or cefuroxime (500 mg twice daily) plus a macrolide or doxycycline
In regions with high rates of macrolide-resistant S pneumoniae, consider a nonmacrolide alternative.
For hospitalized patients, therapy consists of the following:
Beta-lactams (ceftriaxone or cefotaxime) plus a macrolide or
Recent studies have suggested that a beta-lactam alone may be noninferior to a beta-lactam/macrolide combination or fluoroquinolone therapy in hospitalized patients. 
Therapy in ICU patients includes the following:
Beta-lactam (ceftriaxone, cefotaxime, or ampicillin/sulbactam) plus either a macrolide or respiratory fluoroquinolone
For patients with penicillin allergy, a respiratory fluoroquinolone and aztreonam
If Pseudomonas is suspected, therapy is as follows:
Anti-pneumococcal and anti-pseudomonal beta-lactam (piperacillin/tazobactam, cefepime, carbapenem [imipenem, meropenem, or doripenem]) plus ciprofloxacin or levofloxacin or
Beta-lactam (as above) plus aminoglycoside and azithromycin or aminoglycoside and fluoroquinolone
For patients with penicillin allergy, aztreonam instead of the beta-lactam in the regimen listed above
If methicillin-resistant S aureus (MRSA) is suspected, vancomycin, linezolid, or ceftaroline should be added.
Rapid initiation of therapy is important for improved outcomes in CAP, although blanket measures to hasten treatment are not without potential negative consequences. Quality-improvement efforts aimed at the administration of antibiotics within a certain time period have contributed to increased inappropriate antibiotic use and increased incidence of Clostridium difficile colitis. Nevertheless, in patients with signs of severe CAP or sepsis, antibiotics should be given within the first hour of hypotension onset to reduce mortality.  Cultures of respiratory specimens, blood, and pleural fluid; PCR of respiratory samples; or antigen tests should be used to target therapy whenever possible. Inpatient CAP therapy usually consists of intravenous antibiotics followed by transition to an oral course of therapy. [11, 12, 13, 14] Patients who are severely ill or who are unable to tolerate or absorb oral medications may require a longer duration of parenteral therapy before switching to an oral antibiotic. 
Mild to moderately ill patients with CAP may be treated entirely via the oral route, on either an inpatient or outpatient basis. The duration of therapy for uncomplicated CAP is usually 5-7 days. [7, 10] Patients should be afebrile for 48-72 hours and have no signs of instability before antibiotic therapy is stopped. The duration of therapy may need to be increased if the initial empiric therapy has no activity against the specific pathogen.
Immunocompromised hosts who present with CAP are treated in the same manner as otherwise healthy hosts but may require a longer duration of therapy. Investigations into pathogens associated with compromised hosts may need to be pursued.