In
spite of the development of new anti-infective agents, community acquired
pneumonia (CAP) remains challenge, since the disease is still the cause
of considerable morbidity and mortality worldwide placing a major burden
on health services. CAP is the most serious of the respiratory infections,
and may develop rapidly into a severe disease requiring hospitalisation.
Bacteremic cases can have a mortality rate of 5 to 15 % with the elderly,
the young, the Immunocompromised and those with severe underlying disease
being at particular risk. Initial treatment of the disease is invariably
empiric.
History:
· Patients with CAP due to typical bacterial pathogens present
with a variety of pulmonary symptoms.
· Patients with CAP due to atypical pathogens present with a
variety of pulmonary symptoms and a variety of extrapulmonary symptoms.
· Typically, patients with bacterial CAP present with variable
degrees of fever, usually with a productive cough and often with pleuritic
chest pain.
· Clinical presentation in patients with CAP due to atypical
pathogens usually is less acute than those with typical bacterial pathogens.
· CAP due to atypical pathogens may have one or more extrapulmonary
features, a clue to their presence.
· Patients with Legionella infections may have a productive or
nonproductive cough. In contrast, patients with pneumonia due to Mycoplasma
pneumoniae or Chlamydia pneumoniae usually present with a nonproductive
cough.
· With the exception of Legionella infections, chest pain is
usually not a feature of nonzoonotic atypical pathogens causing CAP.
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Examination:
· With typical bacterial-associated CAP, abnormal physical findings
are confined to the chest.
· Rales are heard on auscultation of the chest over the involved
lobe or segment. If consolidation is present, an increase in tactile
fremitus, bronchial breathing and E to A change may be present.
· Patients with a pleural effusion (usually due to Haemophilus
influenzae) have signs of a pleural effusion if it is large enough to
be detected on physical examination.
· Patients with a pleural effusion have decreased tactile fremitus
and dullness on chest percussion.
· Purulent sputum is characteristic of pneumonia caused by typical
bacterial pathogens and usually is not a feature of atypical pathogens,
with the exception of Legionnaires disease.
· Blood-tinged sputum may be found with pneumococcal infections,
Klebsiella pneumonia, or Legionella pneumonia.
· Atypical pneumonias that may present with signs of consolidation
are Legionella pneumonia, Q fever, and psittacosis.
· Consolidation is not a feature of pneumonia caused by Mycoplasma
pneumoniae or Chlamydia pneumoniae.
· Pleural effusion in a patient with CAP and extrapulmonary manifestations
should suggest the presence of Legionella species. Pleural effusion
with an appropriate epidemiologic history, eg, contact with a rabbit
or deer, may suggest the presence of tularemia.
· Severe CAP
Severe CAP is caused by the same spectrum of
pathogens as mild or moderately severe CAP.
Severity of CAP is determined by the pre-existing
function of the heart, lungs, and spleen.
Host factors, not different or more virulent
pathogens, make CAP mild or severe.
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Bacteriology:
In recent years, a number of other organisms have been recognised as
having pathogen potential in respiratory infections. These include the
atypical organisms, Chlamydia, Pneumoniae, Mycoplasma pneumoniae and
Legionella Pneumophilia, none of which are sensitive to Beta-Lactam
antibiotics. All three species are obligate intracellular pathogens.
Beta-lactam does not penetrate mammalian cells to any great extent.
In addition, Chlamydia and Mycoplasma lack cell walls, the target of
Beta-lactam. The importance of some of the atypical organisms in CAP
is not always clearer; reports on their incidence vary. This is probably
influenced at least partly by the relative difficulty in isolating them
from affected patients.
The season, age of the patient and geographical area can also clearly affect their incidence. However they can occur in conjunction with other pathogens.
•Typical bacterial pathogens causing CAP are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis
In patients with chronic bronchitis who develop CAP requiring hospitalization, M catarrhalis is particularly common.
S pneumoniae remains the most common agent responsible for CAP.
•Importantly, Staphylococcus aureus, Klebsiella pneumoniae, and Pseudomonas aeruginosa are not causes of CAP in normal hosts.
S aureus causes CAP in the setting of postviral influenza.
K pneumoniae occurs primarily in chronic alcoholics.
P aeruginosa is a cause of CAP in patients with bronchiectasis or cystic fibrosis.
Other gram-negative pathogens rarely cause CAP.
Aspiration pneumonia is caused by the aspiration of oropharyngeal secretions into the lung.
The extent of aspiration and lobar distribution of the infiltrates depends upon the patient's position at the time of aspiration.
Nearly all cases of CAP are due to a single pathogen. Exceptions certainly occur, but they are rare.
Aspiration pneumonia is the only form of CAP due to multiple pathogens.
· Atypical pathogens
•Atypical pneumonias can be divided into zoonotic and nonzoonotic atypical pathogens.
•Zoonotic atypical pathogens causing CAP include Chlamydia psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever).
1). Contact with the appropriate vector is required in order for these zoonotic pathogens to cause CAP.
2). The appropriate epidemiological questions for patients with Q fever include recent close contact with a parturient cat or sheep.
3). Patients who are suspected of having psittacosis have a history of recent close contact with psittacine birds.
4). Patients with tularemia have a history of recent close contact with deer or rabbits or have recently been bitten by a tick or deer fly.
•Nonzoonotic atypical pneumonias are caused by Legionella species, M pneumoniae, or C pneumoniae.
•The pattern of extrapulmonary findings, not individual findings, allows the clinician to differentiate between typical and atypical pneumonias.
•Typical bacterial pneumonias have few, if any, extrapulmonary findings. Each atypical pathogen has its own distribution pattern of extrapulmonary organ involvement, which permits an accurate and rapid presumptive clinical diagnosis
Penicillins have been the mainstays of therapy of CAP for many years,
since traditionally it had excellent activity against the major pathogens,
Streptococcus Pneumonia and Haemophilus influenzae. However, recent
years have shown an insidious reduction in susceptibility to Beta-Lactams
of these organisms; Beta-Lactamase production is widespread, among strains
of H. influenzae and strains of S.Pneumonia with reduced in vitro susceptible
to penicillins occurring world-wlde. Resistance in the pneumococcus
is the result of change in the Penicillin binding proteins, thus affecting
a wide variety of Beta-lactams. The majority of strains have diminished
susceptibility to penicillin G and to Amoxycillin. Beta-Lactam production
is also common in strains of staphylococcus aureus and Moraxella Catarrhalis.
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Imaging
Studies:
· Order chest x-ray in all patients
suspected of having CAP.
•Obtain chest x-ray to rule
out mimics of CAP and to confirm the presence of an infiltrate compatible
with CAP.
•Patients presenting very early
with CAP may have a negative chest x-ray. In these cases, repeat the
chest x-ray within 24 hours.
• Chest x-ray assists with
the differentiation of viral pneumonias from nonviral pneumonias. Viral
pneumonias have few or no infiltrates on chest x-ray but, when present,
are almost always bilateral, perihilar, symmetrical, interstitial infiltrates.
Bacterial pneumonias have predominantly a focal segmental or lobar distribution.
• In contrast, typical or atypical
pathogens produce a lobar or segmental pattern on chest x-ray, with
or without consolidation or pleural effusion.
• Chest x-ray should be negative
in patients with asthma and without CAP. Chest x-ray is also negative
in patients with chronic bronchitis.
•The infiltrates seen with
CHF appear as increased interstitial markings and vascular redistribution
to the upper lobes. Usually, cardiomegaly is present in patients with
preexisting heart failure.
•Patients presenting with acute
heart failure, eg, acute myocardial infarction without preexisting CHF,
often have normal cardiac silhouettes, bilateral, symmetrical moist
rales, and a S3 gallop rhythm present on auscultation.
• Rapid cavitation is not a
feature of CAP. Aspiration pneumonitis may develop cavitation one week
after aspiration. Findings of cavitation will not be present on the
initial chest x-ray in patients with CAP due to aspiration.
Chest X Ray AP&lateral views showing pneumonic consolidation in Rt Lower lobe
· Serial chest x-rays can be used to
follow the progression of CAP.
•Rapidly progressive asymmetrical
infiltrates suggest the possibility of Legionnaire's disease.
• Chest x-rays take a little
time to worsen and a long time to improve. Clinical resolution occurs
long before radiologic resolution.
 |
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| Chest X ray showing right middle lobe pneumonia | X ray chest -Lat view -Rt middle lobe consolidation |
•Obtain a CT scan of the chest
when one suspects an underlying bronchogenic carcinoma or if any abnormalities
exist not consistent with the diagnosis of pneumonia only.
CT
Scan showing Lower Lobe pneumoniic consolidation
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Procedures:
1). Transtracheal aspiration (TTA) is a potentially hazardous procedure
and offers no additional diagnostic information in patients with CAP.
2). Transthoracic fine needle aspiration (TFNA) of the infiltrate can
be performed and is less hazardous than TTA; however, TFNA offers no
additional information beyond that obtainable by other available diagnostic
measures. TFNA is most useful to assess for the cause of noninfectious-associated
infiltrates that are not responding to antibiotic treatment.
Histologic Findings: Lung sections
with typical bacterial pneumonias show the progression from red hepatization
to white hepatization during the resolution process. The lung is repaired
after bacterial pneumonia is complete and the infectious process resolves.
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· noninfectious conditions can also present as pneumonia and include: CHF, pulmonary infiltrates with eosinophilia, pulmonary hemorrhage, TB, Goodpasture's syndrome, pulmonary embolism, neoplastic disease, radiation injury, inhalation injury, pulmonary contusion, bronchiolitis obliterans with organizing pneumonia (BOOP), Wegener's granulomatosis, collagen-vascular disorders (including rheumatoid lung disease, SLE, scleroderma), amyloidosis, sarcoidosis, interstitial pneumonitis (e.g., farmers, bird breeders), and drug reactions (e.g., hydrochlorothiazide, asbestos, silicosis, etc.)
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Treatment:
1). Hospitalize patients with CAP who are moderately-to-severely ill.
Factors that predict risk for increased mortality in patients with CAP
have been studied and include older age, significant comorbidities,
increased respiratory rate, hypotension, fever, multilobar involvement,
anemia and hypoxia, to name a few.
2). Patients with severe CAP require admission to an intensive care
unit; oxygen and/or ventilatory support may be required.
3). Because the severity of CAP is frequently due to underlying severe
cardiopulmonary disease, direct medical efforts at supporting cardiopulmonary
function while treating the patient with antibiotics for CAP.
4). Patients admitted with severe CAP and hypotension or shock often
are hypotensive because of an acute pulmonary or cardiac insult such
as pulmonary embolism or acute myocardial infarction.
5).If no acute cardiopulmonary explanation can be found, eg, exacerbation
of severe underlying lung disease or exacerbation of preexisting CHF,
it is likely that the patient with shock has diminished or absent splenic
function.
•There are many underlying
conditions associated with diminished splenic function that may present
as severe CAP.
• Patients with an abdominal
scar resulting from abdominal trauma or lymphoma staging are obvious
manifestations of possible asplenia.
•Hyposplenism may be inferred
from the presence of Howell-Jolly bodies in the peripheral blood smear
in a patient presenting with CAP who is in shock. The first step in
treating a patient in shock is effective intravascular volume replacement.
If aggressive intravascular replacement is inadequate, then pressors
may be added. Do not administer pressors before adequate volume replacement
because effective intracirculating intravascular volume will decrease
and the blood pressure will drop further.
· Penicillin-resistant pneumococcal
pneumonia
1). The overuse of beta-lactam and macrolide antibiotics has probably
caused a gradual increase in the S pneumoniae minimal inhibitory concentration
(MIC). This relative increase in the MIC, ie, intermediate resistance
or relative resistance, can be overcome by using full recommended doses
of beta-lactams.
2). Treatment for most cases of penicillin-resistant S pneumoniae is
penicillin. Most strains have increased MICs but are still susceptible
and not clinically resistant to penicillin.
3). Penicillin resistance is classified according to MICs. Breakpoints
are as follows:
•
Sensitive: equal to or less than 0.6 mcg/ml.
•
Intermediate resistance: .1-1 mcg/ml
•
Highly resistant: equal to or greater than 2 mcg/ml
•
Fortunately, few highly penicillin-resistant pneumococci exist, eg,
MIC equal to or greater than 2 mcg/ml.
•
Strains of pneumococci that are highly resistant to penicillin may be
treated with levofloxacin, the only quinolone indicated for the treatment
of highly penicillin-resistant S pneumoniae. Alternatively, vancomycin,
clindamycin or linezolid may be used.
•
The use of non-cell wall active agents against S pneumoniae, eg, doxycycline
or levofloxacin, should decrease penicillin resistance among pneumococci.
•
The widespread use of macrolides, eg, trimethoprim-sulfamethoxazole
(TMP-SMX) and tetracycline (not doxycycline), has been associated with
H influenzae resistance.
•
Most oral cephalosporins, except cefprozil, have been associated with
increased S pneumoniae resistance.
•
Worldwide, the unrestricted use of levofloxacin since 1993 has not resulted
in any increase in S pneumoniae resistance though one study in Canada
showed an increase in fluoroquinolone resistance in its pneumococcal
isolates from 1993 to 1998.
· IV to Oral regimen switch programs
1). Most patients admitted to the hospital with CAP are treated with
empiric IV antibiotic therapy. After 48 hours, unless these patients
are acutely ill in the ICU or are unable to absorb medication for the
GI tract, patients may be switched to equivalent oral therapy to complete
a 2-week course of therapy.
2). Candidate agents for IV to PO switch programs have the same spectrum
as IV agents do, excellent bioavailability, few side effects, low-resistance
potential and relatively low cost. Ideal agents for IV to PO switch
programs include levofloxacin and doxycycline.
3). Other agents that may be used if S pneumoniae is not the etiologic
agent include azithromycin or clarithromycin.
Outpatient
Treatment of Community - Acquired Pneumonia
Inpatient Treatment of Community - Acquired Pneumonia
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Complications determining the precise etiology of CAP is still problematical,
and in many studies, even with invasive respiratory methods, samples
collected show no positive identification of a pathogen. It is clear
however, from many studies that even though atypical pathogen may be
more prevalent than had been recognised earlier the major bacterial
pathogen is the pneumococcus.