PATIENT’S PROFILE

Name: Carmelo Rolando

Address: Platero Mamerto Natividad, Nueva Ecija
Age: 56 years old
Religion: Catholic
Civil Status: Married
Admission date and time: November 22, 2017

I. PATIENT’S HISTORY

 History of present illness

PTB treatment completed (2015), no allergy

 Mechanism of trauma
Pt was at a farm when he suddenly collapsed

II. Physical Examination

 General Status: Disoriented

Vital Signs: T-36.9, RR-24, PR- 92, BP- 100/70

 Admission Diagnosis:
Community Acquired Pneumonia - Moderate Risk, T/C PTB abscess vs. Pulmonary New
Growth

ANATOMY AND PHYSIOLOGY

The lungs
The lungs are located in the chest and are part of the respiratory system.

The lungs take up most of the space inside the chest. The lungs are surrounded by the chest wall.
The chest wall is made up of the ribs and the muscles between the ribs. The lungs are separated
by the mediastinum, which contains the heart and other organs. Below the lungs is the
diaphragm, a thin muscle that separates the chest cavity from the abdomen.
Each lung is divided into lobes (sections):
 The left lung has 2 lobes. The heart sits in a groove (cardiac notch) in the lower lobe.
 The right lung has 3 lobes and is slightly larger than the left lung.
The windpipe (trachea) is the tube-shaped airway in the neck and chest. It divides into 2 tubes or
branches called the main bronchi. One bronchus goes to each lung. The area where each
bronchus enters the lung is called the hilum.
The pleura is a thin membrane that covers the lungs and lines the chest wall. It protects and
cushions the lungs and produces a fluid that acts like a lubricant so the lungs can move smoothly
in the chest cavity. The pleura is made up of 2 layers:
 inner (visceral) pleura – the layer next to the lung
 outer (parietal) pleura – the layer that lines the chest wall
The area between the 2 layers is called the pleural space.
Each of the main bronchi divides or branches into smaller bronchi (which have small glands and
cartilage in their walls). These smaller bronchi eventually divide into even smaller tubes called
bronchioles, which have no glands or cartilage. At the end of the bronchioles are millions of tiny
sacs called alveoli. Surrounding the alveoli are very tiny blood vessels (capillaries).
The bronchi are lined with cells that have very fine hair-like projections called cilia.
The lungs produce a mixture of fats and proteins called lung or pulmonary surfactant. The
surfactant coats the surfaces of the alveoli, making it easier for them to expand and deflate with
each breath.
Different groups of lymph nodes, which are part of the lymphatic system, drain fluid normally
produced in the lung:
 bronchial nodes – lymph nodes around the main bronchi
 hilar nodes – lymph nodes in the area where the windpipe divides into the main bronchi
 mediastinal nodes – lymph nodes along the windpipe in between the 2 lungs
 subcarinal mediastinal nodes – lymph nodes just below the windpipe where it divides into
the main bronchi
What the lungs do

The main functions of the lungs are to transfer oxygen from the air to the blood and to release
carbon dioxide from the blood to the air.
Air enters the mouth or nose and travels through the windpipe, bronchi and bronchioles to the
alveoli. The exchange of oxygen and carbon dioxide takes place in the alveoli:
 The alveoli absorb oxygen from the air and pass it into the blood, which circulates the
oxygen around the body.
 Carbon dioxide, which is a waste product of the body’s cells, passes from the blood into
the alveoli and is breathed out.
The lungs also play a role in the body’s defences against harmful substances in the air, such as
smoke, pollution, bacteria or viruses. These substances can pass through the nose and become
trapped in the lungs. The lungs produce a thick, slippery fluid (mucus), which can trap and partly
destroy these substances from the air. The cilia move rapidly to push the mucus up through the
bronchi, where it is removed by coughing or swallowing.

Community-Acquired Pneumonia
Definition

Pneumonia is an infection of the lung parenchyma. Community-acquired pneumonia refers to pneumonia

acquired outside of hospitals or extended-care facilities. Nursing home–acquired pneumonia refers to
infection acquired in an extended-care facility. Nosocomial pneumonia and hospital-acquired
pneumonia describe infections acquired in the hospital setting. The signs and symptoms of acute
pneumonia develop over hours to days, whereas the clinical presentation of chronic pneumonia often
evolves over weeks to months.

Prevalence

Despite a broad armamentarium of antimicrobials available to treat the disease, pneumonia remains the
seventh leading cause of death in the United States.1 In 2003, the age-adjusted death rate caused by
influenza and pneumonia was 20.3 per 100,000 persons.1 Estimates of the incidence of community-
acquired pneumonia range from 4 million to 5 million cases per year, with about 25% requiring
hospitalization.2 Nosocomial pneumonia is estimated to occur in 250,000 persons per year, representing
about 15% to 18% of all nosocomial infections.

Microbiology

Streptococcus pneumoniae remains the most commonly identified pathogen in community-acquired

pneumonia (Fig. 1). Other pathogens have been reported to cause pneumonia in the community, and their
order of importance depends on the location and population studied (Table 1). These include long-
recognized pathogens such as Haemophilus influenzae, Mycoplasma pneumoniae, and influenza A, along
with newer pathogens such as Legionella species and Chlamydophilia pneumoniae. Other common causes
in the immunocompetent patient include Moraxella catarrhalis, Mycobacterium tuberculosis, and
aspiration pneumonia. The causative agent of community-acquired pneumonia remains unidentified in
30% to 50% of cases.
Table 1: Identified Pathogens in Community-Acquired Pneumonia

Pathogen Cases (%)

Streptococcus pneumoniae 20-60

Haemophilus influenzae 3-10

Staphylococcus aureus 3-5

Gram-negative bacilli 3-10

Legionella species 2-8

Mycoplasma pneumoniae 1-6

Chlamydia pneumoniae 4-6

Viruses 2-15

Aspiration 6-10

Others 3-5

Previously seen mainly in extended-care facilities and acute-care hospitals, strains of methicillin-
resistant Staphylococcus aureus (MRSA) have emerged as prevalent pathogens in community
settings.6 Necrotizing pneumonia is a characteristically severe manifestation of these virulent strains.

A new human pathogen, severe acute respiratory syndrome (SARS)-associated coronavirus, emerged and
spread worldwide in the winter of 2002 to 2003. No cases have been identified since 2004. Influenza
continues to be a prevalent seasonal disease in the United States, causing considerable morbidity, loss of
productivity, and mortality. A strain of H5N1 influenza has spread rapidly through avian flocks in Asia
and Europe. Cases of transmission from birds to humans with severe disease have led to international
concern about a possible avian influenza pandemic.

Many pathogens listed as potential agents of bioterrorism are spread by the respiratory route. Among the
most likely candidates are Bacillus anthracis, Francisella tularensis, and Yersinia pestis. A more
extensive discussion of the agents of bioterrorism can be found elsewhere in this section (“Biologic
Weapons and the Primary Care Clinician”).

Nursing home–acquired pneumonias are often caused by community-acquired pathogens. However, there
is an increased influence of pathogens seen with relatively low frequency in the community, such as S.
aureus and gram-negative organisms.

Pathophysiology

Six mechanisms have been identified in the pathogenesis of pneumonia in immunocompetent adults
(Table 2). Inhalation of infectious particles is probably the most important pathogenetic mechanism in the
development of community-acquired pneumonia, with particular importance of pneumonia caused
by Legionella species and M. tuberculosis.
Mechanism Frequency

Inhalation of infectious particles Common

Aspiration of oropharyngeal or gastric contents Common

Hematogenous deposition Uncommon

Invasion from infection in contiguous structures Rare

Direct inoculation Less common

Reactivation More common in immunocompromised hosts

The aspiration of oropharyngeal or gastric contents is the most prevalent pathogenetic mechanism in
nosocomial pneumonia, with several contributing factors. Swallowing and epiglottic closure may be
impaired by neuromuscular disease, stroke, states of altered consciousness, or seizures. Endotracheal and
nasogastric tubes interfere with these anatomic defenses and provide a direct route of entry for pathogens.
Impaired lower esophageal sphincter function and nasogastric and gastrostomy tubes increase the risk of
aspiration of gastric contents. Fortunately, aspiration rarely leads to overt bacterial pneumonia.

Direct inoculation rarely occurs as a result of surgery or bronchoscopy but may play a role in the
development of pneumonia in patients supported with mechanical ventilation. Hematogenous deposition
of bacteria in the lungs is also uncommon but is responsible for some cases of pneumonia caused by S.
aureus, Pseudomonas aeruginosa, and Escherichia coli. The direct extension of infection to the lung from
contiguous areas, such as the pleural or subdiaphragmatic spaces, is rare.

Reactivation of pathogens can take place in the setting of deficits of cell-mediated immunity. Pathogens
such as Pneumocystis jiroveci, Mycobacterium tuberculosis, and cytomegalovirus can remain latent for
many years after exposure, with flares of active disease occurring in the presence of immune compromise.
Reactivation tuberculosis occasionally occurs in immunocompetent hosts.

Once bacteria reach the tracheobronchial tree, defects in local pulmonary defenses can make infection
more likely. The cough reflex can be impaired by stroke, neuromuscular disease, sedatives, or poor
nutrition. Mucociliary transport is depressed with the aging process, tobacco smoking, dehydration,
morphine, atropine, prior infection with influenza virus, and chronic bronchitis. Anatomic changes such
as emphysema, bronchiectasis, and obstructive mass lesions prevent the clearance of microbes.
Inflammatory cells drawn to infected areas of the pulmonary tree release proteolytic enzymes, altering the
bronchial epithelium and ciliary clearance mechanisms and stimulating the production of excess mucus.
Community-acquired MRSA strains contain Panton-Valentine leukocidin, a toxin that creates holes in
neutrophil cell membranes, releasing chemotactic and inflammatory factors.

A blunted cellular and humoral immune response can also increase the risk of pneumonia. For example,
granulocyte chemotaxis is reduced with aging, diabetes mellitus, malnutrition, hypothermia,
hypophosphatemia, and corticosteroids. Granulocytopenia may be caused by cytotoxic chemotherapy.
Alveolar macrophages are rendered dysfunctional by corticosteroids, cytokines, viral illnesses, and
malnutrition. Diminished antibody production or function can accompany hematologic malignancies such
as multiple myeloma or chronic lymphocytic leukemia.

History and Physical Examination

Because the clinical syndromes characterizing pneumonic infections caused by various agents often
overlap one another and because interobserver variability regarding physical findings of pneumonia is
high, the diagnosis of pneumonia can be challenging. A diligent history (Table 3) and physical
examination can help narrow the differential diagnosis. In general, typical bacterial pathogens such as S.
pneumoniae, H. influenzae, and the enteric gram-negative organisms usually manifest acutely with high
fever, chills, tachypnea, tachycardia, and productive cough. Examination findings are localized to a
specific lung zone and can include rales, rhonchi, bronchial breath sounds, dullness, increased fremitus,
and egophony. In contrast, atypical pathogens such as Mycoplasma, Chlamydophilia, and viruses can
manifest in a subacute fashion with fever, nonproductive cough, constitutional symptoms, and absent or
diffuse findings on lung examination. Rapid progression of disease to respiratory failure can be seen in
severe pneumococcal or Legionella pneumonia. Influenza may be complicated by bacterial pneumonia
caused by S. aureus or S. pneumoniae.

Table 3: Microbiologic Differential Diagnosis of Pneumonia: Historical Features

History Associated Organisms

Alcoholism Streptococcus pneumoniae, oral anaerobes, Mycobacterium tuberculosis

Chronic obstructive lung S. pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Legionella spp.
disease (COPD)

Exposure to bat or bird Histoplasma capsulatum

droppings, construction
sites, caves

Exposure to birds Chlamydia psittaci

Exposure to rabbits Francisella tularensis

HIV infection “Typical” bacterial pathogens, M. tuberculosis, Pneumocystis jiroveci,

cytomegalovirus, Cryptococcusspp., Histoplasma spp., Coccidioides spp.

Travel to desert, Coccidioides spp., Hantavirus (Sin Nombre virus)

southwest United States

Farm exposure Coxiella burnetii (animals), Aspergillus spp. (barns, hay)

Postinfluenza S. pneumoniae, S. aureus, Streptococcus pyogenes, H. influenzae

Aspiration Mixed aerobic, anaerobic

Marijuana smoking Aspergillus spp.

Anatomic abnormality of Pseudomonas aeruginosa, Burkholderia cepacia, S. aureus

lung parenchyma, e.g.,
bronchiectasis, cystic
fibrosis

Injection drug use S. aureus, anaerobes, M. tuberculosis, and S. pneumoniae

Obstruction of large Anaerobes, S. pneumoniae, H. influenzae, S. aureus

airway

Incarceration M. tuberculosis

Neutropenia Aspergillus spp., Zygomycetes

Asplenia S. pneumoniae, H. influenzae

SARS manifests with high fever and myalgia for 3 to 7 days, followed by a nonproductive cough and
progressive hypoxemia, with progression to mechanical ventilation in 20% of cases. This can be
distinguished from other viral infections by the higher fever and lack of conjunctivitis, sneezing,
rhinorrhea, and pharyngitis. Inhalation anthrax can manifest with flulike symptoms of myalgia, fatigue,
and fever before rapidly progressing to respiratory distress, mediastinitis, meningitis, sepsis, and death.

The age of the patient can play an important role in disease presentation. Older patients often have
humoral and cellular immunodeficiencies as a result of underlying diseases, immunosuppressive
medications, and the aging process. They are more commonly institutionalized with anatomic problems
that inhibit the pulmonary clearance of pathogens. The presentation is often more subtle than in younger
adults, with more-advanced disease and sepsis, despite minimal fever and sputum production.

Extrapulmonary physical findings can provide clues to the diagnosis. Poor dentition and foul-smelling
sputum can indicate the presence of a lung abscess with an anaerobic component. Bullous myringitis can
accompany infection with M. pneumoniae. An absent gag reflex or altered sensorium raises the question
of aspiration. Encephalitis can complicate pneumonia caused by M. pneumoniae or Legionella
pneumophila. Cutaneous manifestations of infection can include erythema multiforme (M. pneumoniae),
erythema nodosum (C. pneumoniae and M. tuberculosis), or ecthyma gangrenosum (P. aeruginosa).

Diagnostic and treatment considerations

Radiography

A cornerstone of diagnosis is the chest x-ray, which is recommended for diagnosis in every circumstance
and usually reveals an infiltrate (Fig. 2) at presentation. However, this finding may be absent in the
dehydrated patient. Also, the radiographic manifestations of chronic diseases such as congestive heart
failure, chronic obstructive pulmonary disease (COPD), and malignancy can obscure the infiltrate of
pneumonia.

Although radiographic patterns are usually nonspecific, they can suggest a microbiologic differential
diagnosis (Table 4).

Table 4: Radiographic Patterns of Common Etiologic Agents

Chest Radiographic Pattern Pathogen

Focal; large pleural effusion Usually bacteria

Cavitary Bacterial abscess, fungi, acid-fast bacilli, Nocardia

Miliary Acid-fast bacilli, fungi

Rapid progression/multifocal Legionella spp., Pneumococcus, Staphylococcus

Interstitial Viruses, Pneumocystis jiroveci, Mycoplasma, Chlamydia psittaci

Mediastinal widening without infiltrate Inhalation anthrax

Risk Factor Point Value

Age

Men Age (in yr)

Women Age (in yr) −10

Nursing home resident +10

Comorbid Illnesses

Neoplastic disease +30

Liver disease +20

Kidney disease +10

Cerebrovascular disease +10

Congestive heart failure +10

Physical Findings

Altered mentation +20

Tachypnea (>30 breaths/min) +20

Systolic hypotension (<90 mm Hg) +20

Body temperature (<35° or >40° C) +15

Heart rate >125 beats/min +10

Laboratory and Radiographic Findings

Blood pH (arterial) <7.35 +30

Hypoxemia (arterial Pao2<60 mm Hg or O2 saturation <90%) +10

Serum urea nitrogen (BUN) >30 mg/dL +20

Na <130 mEq/L +20

Blood sugar >250 mg/dL +10

Anemia (hematocrit <30%) +10

Pleural effusion 10
 All others were evaluated with the laboratory tests listed in Table 5 and assigned to risk classes by point
totals (Table 6). Those in classes I and II are considered excellent candidates for outpatient oral therapy,
assuming no hemodynamic instability, no chronic oxygen dependence, immunocompetence, and the
ability to ingest, absorb, and adhere to an oral regimen. Patients in risk class III may be considered for
outpatient or brief inpatient therapy, depending on clinical judgment. Patients in risk classes IV and V are
recommended for hospital admission. Ultimately, each decision to admit must be individualized.

Table 6: Pneumonia Severity Index: Risk of 30-Day Mortality By Point Total

Risk Class Point Score Mortality (%)

I No points assigned 0.1

II <70 0.6

III 71-90 2.8

IV 91-130 8.2

V >130 29.2

A slightly less complex scheme is the CRB-65. In this algorithm, patients are felt better served by
hospitalization if they they meet more than of the following criteria: confusion, respiratory rate greater
than 30 breaths per minute, blood pressure less than 90 mm Hg systolic or 60 mm Hg diastolic, or age
older than 65 years.9

Diagnostic Testing

When the patient is not severely ill (ie outpatient treatment or not severely ill in the inpatient setting) and
has few risk factors, the consensus guidelines of the Infectious Diseases Society of America (IDSA) and
American Thoracic Society (ATS)10 suggest empirical therapy without extensive laboratory evaluation
(Box 1). When identification of a pathogen might change therapy, further studies are indicated (see Box
1). The value of such studies is not uniformly agreed on (see later, “National Guidelines”). However,
pathogen identification has important implications for the breadth of therapeutic antibiotic spectrum,
development of resistance, and epidemiology.

Box 1: Diagnostic Testing for Community-Acquired Pneumonia

All patients with suspected pneumonia

 Chest radiography
 Complete blood count
 Complete metabolic profile
 Blood gases or pulse oximetry

Severely ill or immunocompromised patients, patients with anatomic lung disease

 Sputum Gram stain and culture

 Blood cultures: two sets before antibiotics
 Legionella serology, urinary antigen, direct fluorescent antibody testing
 Pneumococcal urinary antigen testing

Inpatients with appropriate history or physical findings

 HIV serology
 Mycoplasma serology
 Chlamydia serology
 Fungal serology
 SARS-associated coronavirus serology or PCR
 Stains or cultures for fungi, mycobacteria, Pneumocystis jiroveci
 Analysis or cultures of pleural or cerebrospinal fluid
 Nasopharyngeal swab for viral direct fluorescent antibody or other rapid technique
 Tuberculin skin testing

Deteriorating patient without definitive diagnosis of cause

 Bronchoscopy (bronchoalveolar lavage, protected catheter, transbronchial biopsy)

 Thoracoscopic or open-lung biopsy
 Radiographically guided transthoracic aspirate
 Legionella, Chlamydia, Mycoplasma serology
 Fungal serology
 Evaluation for congestive heart failure, pulmonary embolus, neoplasm, connective tissue disease

A Gram-stained sputum specimen can help focus empirical therapy. Unfortunately, sputum is often
difficult to obtain from older patients because of a weak cough, obtundation, and dehydration. Nebulized
saline treatments might help mobilize secretions. Nasotracheal suctioning can sample the lower
respiratory tract directly but risks oropharyngeal contamination. A sputum specimen reflects lower
respiratory secretions when more than 25 white blood cells (WBCs) and fewer than 10 epithelial cells are
seen in a low-powered microscopic field.11 Empirical therapy based on a predominant organism in such a
specimen is likely to contain appropriate coverage.12

Other stains, such as the acid-fast stain for mycobacteria, modified acid-fast stain for Nocardia, or
toluidine blue and Gomori's methenamine silver stains should be used when directed by the history or
clinical presentation. Direct fluorescent antibody (DFA) staining of sputum, bronchoalveolar lavage fluid,
or pleural fluid can help identify Legionella species. Similarly, DFA testing of nasopharyngeal specimens
provides rapid diagnosis of influenza types A and B, as well as other common respiratory viruses such as
respiratory syncytial virus, adenovirus, and parainfluenza virus. In an outbreak setting, DFA and other
rapid techniques can assist in decision making for therapy and infection control.

The sputum culture remains a controversial tool but is useful to help tailor therapy when the patient is
severely ill, has a history of structural lung disease or alcohol abuse, has pleural effusion, or has evidence
of pneumococcal or Legionella infection. Culture is particularly helpful for identifying organisms of
epidemiologic significance, either for patterns of transmission or resistance. Expectorated morning
sputum specimens should be sent for mycobacterial culture when the history is suggestive.

Blood cultures can also shed light on a pathogen, and samples should be drawn in severely ill or
immunocompromised patients (see later, “Outcomes”). Pleural or cerebrospinal fluid should be sampled
when infections in these spaces are suspected.
When these procedures fail to yield a microbiologic diagnosis and when the patient does not respond to
empirical antibiotic therapy, more-invasive diagnostic techniques may be indicated. Fiberoptic
bronchoscopy allows the use of several techniques for the diagnosis of pneumonia. Bronchoalveolar
lavage with saline can obtain deep respiratory specimens for the gamut of stains and cultures mentioned
earlier. Transbronchial biopsy of lung parenchyma can reveal alveolar or interstitial pneumonitis, viral
inclusion bodies, and fungal or mycobacterial elements. The protected brush catheter is used to
distinguish quantitatively between tracheobronchial colonizers and pneumonic pathogens.

A more substantial amount of lung tissue may be obtained for culture and histologic examination by
thoracoscopic or open lung biopsy. Because these procedures can carry considerable morbidity, they are
usually reserved for the deteriorating patient with a pneumonia that defies diagnosis by less-invasive
techniques.

Serologic Testing

Often relegated to retrospective or epidemiologic interest because of delays in testing or reporting,

serologic testing for such pathogens as Legionella species, Mycoplasma species, and C.
pneumoniae should include sera drawn in the acute and convalescent phases for comparison. A fourfold
increase in the immunoglobulin G (IgG) titer suggests recent infection with these organisms. An IgM
microimmunofluorescence titer of more than 1:16 is considered diagnostic of C. pneumoniae infection.
Infection with SARS-associated coronavirus is most often diagnosed by antibody testing and polymerase
chain reaction (PCR) testing.

A sensitive enzyme immunoassay has been developed for the detection of L. pneumophila type 1 antigen
in urine. Because the antigen persists for up to 1 year after infection, it is difficult to differentiate between
past and current infections when using this assay.

A urinary assay is also available for detecting S. pneumoniae cell wall polysaccharide. This assay may
offer some advantage for the rapid diagnosis of pneumococcal pneumonia in culture-proven or unknown
cases, but assay specificity is an ongoing question.

Molecular Techniques

Powerful molecular techniques are now being applied to the early diagnosis of pneumonia. DNA probes
have been used to detect Legionella species, M. pneumoniae, and M. tuberculosis in sputum. These
probes have excellent sensitivity and specificity but can yield false-positive results. The PCR assay has
been used for the early detection of various pathogens that are difficult or slow to culture from sputum
specimens, including atypical bacteria, viruses (e.g., influenza), and mycobacteria. Given the large
percentage of pneumonia cases for which no microbial cause is identified, it is likely that molecular tools
will eventually be applied to the identification and antimicrobial susceptibility testing of almost all
causative agents of pneumonia.

Summary

 The patient's history can help narrow the microbial differential diagnosis.
 The chest radiograph is the cornerstone of diagnosis.
 The sputum Gram stain and culture are controversial, but they are still useful for targeting
antimicrobial therapy when the patient is severely ill or immunocompromised.
 Serologic testing is slow and therefore often not useful for real-time diagnosis.
 Molecular methods are playing an increasing role in identifying difficult-to-culture pathogens.
 The pneumonia severity index uses history, examination, chest radiograph, and initial laboratory
test results to identify low-risk patients for outpatient treatment.
Antimicrobial Treatment

Community-Acquired Pneumonia

Antibiotic therapy for community-acquired pneumonia should always be selected with patient
characteristics, place of acquisition, and severity of disease in mind. With concerns about antimicrobial
overuse, health care costs, and bacterial resistance increasing, many experts believe that therapy should
always follow confirmation of the diagnosis of pneumonia and should always be accompanied by a
diligent effort to identify a causative agent (see later, “National Guidelines”). When a specific pathogen is
identified, pathogen-specific therapy can be used (Table 7).

Table 7: Pathogen-Specific Therapy for Community-Acquired Pneumonia in Adults

Organism Primary Therapy

Streptococcus pneumoniae, penicillin- Penicillin G; amoxicillin

susceptible

S. pneumoniae, penicillin-resistant Cefotaxime, ceftriaxone, fluoroquinolone, vancomycin,

others, based on susceptibility studies

Haemophilus influenzae Second- or third-generation cephalosporin, doxycycline,

beta-lactam or beta-lactamase inhibitor, azithromycin, TMP-
SMX

Moraxella catarrhalis Second- or third-generation cephalosporin, TMP-SMX

macrolide, beta-lactam or beta-lactamase inhibitor

Legionella spp. Macrolide, tetracycline, fluoroquinolone alone

Mycoplasma pneumoniae Doxycycline, macrolide

Chlamydia pneumoniae Doxycycline, macrolide

Anaerobes Beta-lactam or beta-lactamase inhibitor, clindamycin

Enteric gram-negative bacilli Third-generation cephalosporin ± aminoglycoside;

carbapenem

Pseudomonas aeruginosa Aminoglycoside + ticarcillin, piperacillin, mezlocillin,

ceftazidime, cefepime, aztreonam, or carbapenem

Staphylococcus aureus, methicillin- Nafcillin or oxacillin

susceptible

S. aureus, methicillin-resistant Vancomycin or linezolid

Bacillus anthracis Ciprofloxacin or doxycycline + two of the following:

rifampin, vancomycin, penicillin, ampicillin,
chloramphenicol, imipenem, clindamycin, clarithromycin

Influenza A, within 48 hr of symptom Amantidine, rimantadine, oseltamivir, zanamivir

onset or immunocompromised host

Influenza B, within 48 hr of symptom Oseltamivir, zanamivir

onset or immunocompromised host
*
For community-acquired methicillin-resistant S. aureus, some clinicians add agents that inhibit toxin
production, such as clindamycin, when susceptibility patterns allow..

When a pathogen is yet to be identified, empirical therapy is instituted. A number of expert panels have
recommended empirical pneumonia therapy, most prominently IDSA and ATS

Table 8: Empirical Antimicrobial Therapy for Community-Acquired Pneumonia In Immunocompetent

Adults

Patient, Setting Common Pathogens Empirical Therapy

Outpatients

<60 yr Streptococcus Macrolide or doxycycline

No comorbid diseases
pneumoniae
Mycoplasma pneumoniae
Chlamydia pneumoniae
Haemophilus influenzae
Viruses

>65 yr or with comorbid S. pneumoniae (drug- Macrolide or doxycycline fluoroquinolone*

disease or antibiotic resistant) Beta-lactam¶ and macrolide
therapy within last 3 mo M. pneumoniae
C. pneumoniae
H. influenzae
Viruses
Gram-negative bacilli†
S. aureus †

Inpatients

Not severely ill S. pneumoniae Macrolide and cefotaxime or ceftriaxone, or

H. influenzae beta-lactam or beta-lactamase inhibitor¶;
Polymicrobial fluoroquinolone‡ alone
Anaerobes
S. aureus
C. pneumoniae Viruses

Severely ill S. pneumoniae § Azithromycin, or fluoroquinolone‡ and

Legionella spp. cefotaxime, ceftriaxone, or beta-lactam or
Gram-negative bacilli beta-lactamase inhibitor¶
M. pneumoniae If P. aeruginosa possible—IV macrolide or
Viruses fluoroquinolone and aminoglycoside IV, or
S. aureus antipseudomonal quinolone and
antipseudomonal beta-lactam
If MRSA possible, add vancomycin or
linezolid

*
In the outpatient setting, many authorities prefer to reserve fluoroquinolones (levofloxacin, gatifloxacin,
moxifloxacin, gemifloxacin) for patients with comorbid diseases or risk factors.
†
In most cases, patients with pneumonias caused by these organisms should be hospitalized.
‡
Levofloxacin, gatifloxacin, moxifloxacin.
§
Critically ill patients in areas with significant rates of high-level pneumococcal resistance and a
suggestive sputum Gram stain should receive vancomycin or a newer quinolone pending microbiologic
diagnosis.
¶
Piperacillin-tazobactam or ampicillin-sulbactam.
¶Cefpodoxime, cefuroxime, high-dose amoxicillin, amoxicillin-clavulanate, or parenteral ceftriaxone
followed by oral cefpodoxime. **Cefotaxime, ceftriaxone, ampicillin-sulbactam, or high-dose ampicillin
Adapted from Mandell LA, Wunderink RG, Anzueto A, et al; Infectious Diseases Society of America;
American Thoracic Society. Infectious Diseases Society of America/American Thoracic Society
Aspiration Pneumonia

Clindamycin is preferred over penicillin for the treatment of community-acquired aspiration pneumonia
because of its superiority for treating oral anaerobes such as Bacteroides melaninogenicus. Amoxicillin-
clavulanic acid also provides excellent coverage in this setting. When large-volume aspiration is
documented in the hospital, a beta-lactam–beta-lactamase inhibitor combination or the combination of
clindamycin and an antipseudomonal agent should be used.

Other Considerations
Anthrax

Suspected or proven inhalation anthrax should be treated with ciprofloxacin or doxycycline and two other
agents (see Table 7). Clinical experience has suggested that rifampin may be an important agent in
empirical regimens.

Duration of Therapy

Although few data specifically address the duration of therapy, many cases of pneumonia are adequately
treated with 10 to 14 days of antibiotics. Longer courses may be required for certain organisms that cause
tissue necrosis, (e.g., Legionella spp., S. aureus, Pseudomonas aeruginosa), organisms that live
intracellularly (e.g., C. pneumoniae), or comorbidities that compromise local (COPD) or systemic
(hematologic malignancy) immunity.

Oral and Switch Therapies

The use of oral or switch therapies offers potential reductions in duration of stay, antibiotic administration
costs, complications of venous access, and disruption of families and careers. Many antibiotics are well
absorbed from the gastrointestinal tract, suggesting the possibility of effective fully oral treatment.
Because well-controlled, risk-stratified data comparing oral and intravenous therapies are few,
appropriate patient populations and treatment settings for full-course oral therapy have yet to be fully
defined. Better data exist for the use of IV to oral switch therapies for the stable patient who has good
gastrointestinal and swallowing function and adequate social support.

Failure to Respond to Initial Therapy

Worsening of clinical status despite adequate antibiotic therapy should trigger a reassessment of the
original clinical impression. First, the diagnosis of infection must be questioned. Entities such as cancers,
pulmonary edema, pulmonary embolus, pulmonary hemorrhage, connective tissue diseases, or drug
toxicity can mimic the clinical and radiographic appearance of pneumonia. Organisms with inherent (e.g.,
fungi, mycobacterial, P. jiroveci) or acquired (Pseudomonas aeruginosa) resistance to drugs commonly
used in pneumonia therapy must also be considered. A secondary infection, such as postinfluenza
staphylococcal pneumonia, might prove resistant to initial therapy. The patient might fail to respond for
reasons of poor adherence, poor drug absorption, or drug interaction. Finally, immunodeficiency (e.g.,
HIV, hematologic malignancy) or anatomic derangement (e.g., COPD, bronchiectasis, neoplasm) can
alter the clinical course of pneumonia and treatment.

Discharge Criteria

Criteria for hospital discharge in community-acquired pneumonia are based on common sense.
Candidates for discharge should have no more than one of the following poor prognostic indicators:
temperature higher than 37.8° C, pulse higher than 100 beats/min, respiratory rate higher than 24/min,
systolic blood pressure lower than 90 mm Hg, oxygen saturation lower than 90%, and inability to
maintain oral intake.

Summary

 Antibiotic therapy for community-acquired pneumonia should always be selected with patient
characteristics, place of acquisition, severity of disease, and local resistance patterns in mind.
 Antimicrobial therapy should be narrowed whenever a pathogen is identified.
 Most pneumonias, with some exceptions, can be cured with 10 to 14 days of antibiotic therapy.
 Switching to oral therapy is possible and desirable once the patient stabilizes.
 Failure to respond to initial therapy should raise questions of diagnosis, treatment adherence, and
antimicrobial resistance.

Prevention

Immunization against influenza and increasingly resistant pneumococci can play a critical role in
preventing pneumonia, particularly in immunocompromised and older adults. The influenza vaccine is
formulated and administered annually. The Centers for Disease Control and Prevention (CDC)
recommends that vaccines be offered to persons older than 50 years, residents of extended-care facilities,
and patients who have chronic heart and lung disorders, chronic metabolic diseases (including diabetes
mellitus), renal dysfunction, hemoglobinopathies, or immunosuppression.

The pneumococcal vaccine has been shown to be 60% to 70% effective in immunocompetent patients.
Side effects are rarely serious and consist of local pain and erythema, which occur in up to 50% of
recipients. The CDC recommends that vaccines be offered to all persons 65 years of age or older, those at
increased risk for illness and death from pneumococcal disease because of chronic illness, those with
functional or anatomic asplenia, and immunocompromised persons. Patients who are immunosuppressed
by chronic disease or treatment might not have sustained titers of protective antibody and should be
considered for revaccination after 6 years.

Residual immunity against Bordetella pertussis wanes over time, leading to transmission from older
adults to other adults and infants. Because secondary bacterial pneumonia occurs in a significant number
of cases of pertussis, the ACIP (Advisory Committee on Immunization Practices) has recommended that
the tetanus-diphtheria-acellular pertussis (Tdap) vaccine replace the tetanus-diphtheria (Td) vaccine in the
adult immunization schedule.

The emergence of SARS, with significant spread in hospitals, forced an extensive reassessment of
respiratory infection control in many institutions. Measures to prevent the spread of SARS-associated
coronavirus include close attention to cough hygiene, hand hygiene, contact precautions, and respiratory
droplet precautions.
 Wesleyan University – Philippines

Cabanatuan City

College of Nursing and Allied Medical Sciences

A Case Study Submitted

To the faculty of the College of Nursing
And Allied Medical Sciences

By:

John Kennedy Crisolo

BSN 3 BLOCK 1

S.Y. 2017-2018

1ST Semester