These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university Do Not Forget To Visit Our Pages On Facebook on the following Links: https://www.facebook.com/groups/569435236444761/ AND https://www.facebook.com/groups/690331650977113/

1. Hamdi Turkey- chest physicanHamdi Turkey- chest physican
Community acquired pneumonia
(CAP)

2. Pneumonias- classification
Nosocomial Pneumonias

3. Sir William Osler
Sir William Osler, known as
"the father of modern
medicine," appreciated the
morbidity and mortality of
pneumonia, describing it as
the "captain of the men of
death" in 1918, as it had
overtaken tuberculosis as
one of the leading causes of
death in his time.
Sir William Osler, known as
"the father of modern
medicine," appreciated the
morbidity and mortality of
pneumonia, describing it as
the "captain of the men of
death" in 1918, as it had
overtaken tuberculosis as
one of the leading causes of
death in his time.

4. Pneumonia classification

5. Community acquired pneumonia
(CAP)
An acute infection of the pulmonary parenchyma that isAn acute infection of the pulmonary parenchyma that is
associated with some symptoms of acute infection,associated with some symptoms of acute infection,
accompanied by the presence of an acute infiltrate on aaccompanied by the presence of an acute infiltrate on a
chest radiograph, or auscultatory findings consistentchest radiograph, or auscultatory findings consistent
with pneumonia, in a patient not hospitalized or residingwith pneumonia, in a patient not hospitalized or residing
in a long term care facility forin a long term care facility for >> 14 days before onset of14 days before onset of
symptoms.symptoms.
An acute infection of the pulmonary parenchyma that isAn acute infection of the pulmonary parenchyma that is
associated with some symptoms of acute infection,associated with some symptoms of acute infection,
accompanied by the presence of an acute infiltrate on aaccompanied by the presence of an acute infiltrate on a
chest radiograph, or auscultatory findings consistentchest radiograph, or auscultatory findings consistent
with pneumonia, in a patient not hospitalized or residingwith pneumonia, in a patient not hospitalized or residing
in a long term care facility forin a long term care facility for >> 14 days before onset of14 days before onset of
symptoms.symptoms.

6. CAP - Why do we care about it?
5.6 million cases annually5.6 million cases annually
1.1 million require hospitalization1.1 million require hospitalization
Mortality rate =12% in-hospital; nearMortality rate =12% in-hospital; near
40% in ICU patients40% in ICU patients
5.6 million cases annually5.6 million cases annually
1.1 million require hospitalization1.1 million require hospitalization
Mortality rate =12% in-hospital; nearMortality rate =12% in-hospital; near
40% in ICU patients40% in ICU patients

7. Clinical presentations
Sudden onset of CAP
High fever, shaking chills
Pleuritic chest pain, SOB
Productive cough
Rusty sputum, blood tinge
Poor general condition
High mortality up to 20% in
patients with bacteremia
S.pneumoniae causative
Sudden onset of CAP
High fever, shaking chills
Pleuritic chest pain, SOB
Productive cough
Rusty sputum, blood tinge
Poor general condition
High mortality up to 20% in
patients with bacteremia
S.pneumoniae causative
Gradual & insidious onset
Low grade fever
Dry cough, No blood tinge
Good GC – Walking CAP
Low mortality 1-2%; except in
cases of Legionellosis
Mycoplasma, Chlamydiae,
Legionella, Ricketessiae,
Viruses are causative
Gradual & insidious onset
Low grade fever
Dry cough, No blood tinge
Good GC – Walking CAP
Low mortality 1-2%; except in
cases of Legionellosis
Mycoplasma, Chlamydiae,
Legionella, Ricketessiae,
Viruses are causative
TypicalTypicalTypicalTypical AtypicalAtypicalAtypicalAtypical

8. Pathogenesis
CAPCAP
InhalationInhalation
AspirationAspiration
HematogenousHematogenous

9. AgeAge
Obesity; Exercise isObesity; Exercise is
protectiveprotective
SmokingSmoking
Asthma, COPDAsthma, COPD
Immuno-suppression,Immuno-suppression,
HIVHIV
Institutionalization, OldInstitutionalization, Old
age homes etcage homes etc
DementiaDementia
AgeAge
Obesity; Exercise isObesity; Exercise is
protectiveprotective
SmokingSmoking
Asthma, COPDAsthma, COPD
Immuno-suppression,Immuno-suppression,
HIVHIV
Institutionalization, OldInstitutionalization, Old
age homes etcage homes etc
DementiaDementia
CAP- risk factorsCAP- risk factors

10. Organism specific risk factors
CAP: alcoholism, asthma, immunosuppression, institutionalization, age of 70Y versus 60–69 Y
Pneumococcus : dementia, seizure, heart failure, CVA, alcoholism, smoking, COPD, HIV
CA-MRSA: Native Americans, homeless youths, men who have sex with men, prison inmates,
military recruits, children in day-care centers, and athletes such as wrestlers
Enterobacteriaceae: recently hospitalization and/or antibiotic therapy, comorbidities such as
alcoholism, heart failure, renal failure
P. aeruginosa : as above, severe structural lung disease
Legionella: diabetes, hematologic malignancy, cancer, severe renal disease, HIV infection,
smoking, male gender, a recent hotel stay or ship cruise
CAP: alcoholism, asthma, immunosuppression, institutionalization, age of 70Y versus 60–69 Y
Pneumococcus : dementia, seizure, heart failure, CVA, alcoholism, smoking, COPD, HIV
CA-MRSA: Native Americans, homeless youths, men who have sex with men, prison inmates,
military recruits, children in day-care centers, and athletes such as wrestlers
Enterobacteriaceae: recently hospitalization and/or antibiotic therapy, comorbidities such as
alcoholism, heart failure, renal failure
P. aeruginosa : as above, severe structural lung disease
Legionella: diabetes, hematologic malignancy, cancer, severe renal disease, HIV infection,
smoking, male gender, a recent hotel stay or ship cruise

11. Pathophysiology
 Pneumonia results from the proliferation of microbial
pathogens at the alveolar level and the host's response to
those pathogens
 Microorganisms gain access to the lower respiratory tract
in several ways: »»»»»»»»»»»»»»»»»»
• The most common is by aspiration from the oropharynx
• Many pathogens are inhaled as contaminated droplets
• pneumonia occurs via hematogenous spread
• contiguous extension from an infected pleural or
mediastinal space
 Pneumonia results from the proliferation of microbial
pathogens at the alveolar level and the host's response to
those pathogens
 Microorganisms gain access to the lower respiratory tract
in several ways: »»»»»»»»»»»»»»»»»»
• The most common is by aspiration from the oropharynx
• Many pathogens are inhaled as contaminated droplets
• pneumonia occurs via hematogenous spread
• contiguous extension from an infected pleural or
mediastinal space

12. Pathophysiology
 Mechanical factors are critically important in host defense:
 hairs and turbinates of the nares catch larger inhaled particles
 branching architecture of the tracheobronchial tree traps
particles on the airway lining
 mucociliary clearance and local antibacterial factors either
clear or kill the potential pathogen
 gag reflex and the cough mechanism
 normal flora adhering to mucosal cells of the oropharynx
 resident alveolar macrophages
 Only when the capacity of the alveolar macrophages to ingest
or kill the microorganisms is exceeded does clinical pneumonia
become manifest »»»»»»»»»»»» the alveolar
macrophages initiate the inflammatory response to bolster
lower respiratory tract defenses
 Mechanical factors are critically important in host defense:
 hairs and turbinates of the nares catch larger inhaled particles
 branching architecture of the tracheobronchial tree traps
particles on the airway lining
 mucociliary clearance and local antibacterial factors either
clear or kill the potential pathogen
 gag reflex and the cough mechanism
 normal flora adhering to mucosal cells of the oropharynx
 resident alveolar macrophages
 Only when the capacity of the alveolar macrophages to ingest
or kill the microorganisms is exceeded does clinical pneumonia
become manifest »»»»»»»»»»»» the alveolar
macrophages initiate the inflammatory response to bolster
lower respiratory tract defenses

13. Pathophysiology
 The host inflammatory response, rather than the proliferation of
microorganisms, triggers the clinical syndrome of pneumonia
 The release of inflammatory mediators, such as IL-1 and TNF
»»»»»»»»»»»» fever
 Chemokines, such as IL-8 and GCSF, stimulate the release of
neutrophils and their attraction to the lung »»»»»»»»»»»
peripheral leukocytosis and increased purulent secretions
 Even erythrocytes can cross the alveolar-capillary membrane,
with consequent hemoptysis
 The capillary leak results in a radiographic infiltrate and rales
detectable on auscultation
 hypoxemia results from alveolar filling
 The host inflammatory response, rather than the proliferation of
microorganisms, triggers the clinical syndrome of pneumonia
 The release of inflammatory mediators, such as IL-1 and TNF
»»»»»»»»»»»» fever
 Chemokines, such as IL-8 and GCSF, stimulate the release of
neutrophils and their attraction to the lung »»»»»»»»»»»
peripheral leukocytosis and increased purulent secretions
 Even erythrocytes can cross the alveolar-capillary membrane,
with consequent hemoptysis
 The capillary leak results in a radiographic infiltrate and rales
detectable on auscultation
 hypoxemia results from alveolar filling

14. Pathophysiology
 some bacterial pathogens appear to interfere with the hypoxic
vasoconstriction that would normally occur with fluid-filled
alveoli, and this interference can result in severe hypoxemia
 Increased respiratory drive in the SIRS leads to respiratory
alkalosis
 Dyspnea due to :
Decreased compliance due to capillary leak
Hypoxemia
Increased respiratory drive
Increased secretions
Infection-related bronchospasm
 Dyspnea due to :
Decreased compliance due to capillary leak
Hypoxemia
Increased respiratory drive
Increased secretions
Infection-related bronchospasm

15. Pathology
The initial phase »»»»»»»» edema
presence of a proteinaceous exudate—and often of bacteria—in the
alveoli
This phase is rarely evident in clinical or autopsy specimens because
it is so rapidly followed by a red hepatization
The second stage »»»»»»»»» red hepatization
• presence of erythrocytes in the cellular intraalveolar exudate
• neutrophils are also present and are important from the standpoint
of host defense
• Bacteria are occasionally seen in cultures of alveolar specimens
The initial phase »»»»»»»» edema
presence of a proteinaceous exudate—and often of bacteria—in the
alveoli
This phase is rarely evident in clinical or autopsy specimens because
it is so rapidly followed by a red hepatization
The second stage »»»»»»»»» red hepatization
• presence of erythrocytes in the cellular intraalveolar exudate
• neutrophils are also present and are important from the standpoint
of host defense
• Bacteria are occasionally seen in cultures of alveolar specimens

16. Pathology (2)
The third phase »»»»»»»»gray hepatization
no new erythrocytes are extravasating, and those already present have
been lysed and degraded
The neutrophil is the predominant cell
fibrin deposition is abundant
bacteria have disappeared
This phase corresponds with successful containment of the infection
and improvement in gas exchange
The final phase »»»»»»»»» resolution
the macrophage is the dominant cell type in the alveolar space
the debris of neutrophils, bacteria, and fibrin has been cleared, as has
the inflammatory response

17. CAP – The Pathogens InvolvedCAP – The Pathogens Involved

18. CAP – Age wise IncidenceCAP – Age wise Incidence

19. CAP – Age wise MortalityCAP – Age wise Mortality

20. Etiology
 The extensive list of potential etiologic agents in CAP
includes bacteria, fungi, viruses, and protozoa
 Newly identified pathogens include hantaviruses,
metapneumoviruses, the coronavirus (SARS, MERS,
and community-acquired strains of MRSA)
 Most cases of CAP are caused by relatively few
pathogens
 Streptococcus pneumoniae is most common
 other organisms must also be considered in light of the
patient's risk factors and severity of illness
 it is most useful to think of the potential causes as
either "typical" or "atypical" organisms

21. Etiology
Typical bacterial pathogens includes : S. pneumoniae,
Haemophilus influenzae, S. aureus , gram-negative bacilli such
as Klebsiella pneumoniae and Pseudomonas aeruginosa
Atypical organisms include : Mycoplasma pneumoniae,
Chlamydophila pneumoniae, Legionella spp, respiratory viruses
such as influenza viruses, adenoviruses, RSVs
The atypical organisms cannot be cultured on standard
media, nor can they be seen on Gram's stain
are intrinsically resistant to all -lactam agents and must be
treated with macrolide, fluoroquinolone, tetracycline
Data suggest that a virus may be responsible in up to 18% of
cases of CAP
In the ~10–15% of CAP cases that are polymicrobial
Typical bacterial pathogens includes : S. pneumoniae,
Haemophilus influenzae, S. aureus , gram-negative bacilli such
as Klebsiella pneumoniae and Pseudomonas aeruginosa
Atypical organisms include : Mycoplasma pneumoniae,
Chlamydophila pneumoniae, Legionella spp, respiratory viruses
such as influenza viruses, adenoviruses, RSVs
The atypical organisms cannot be cultured on standard
media, nor can they be seen on Gram's stain
are intrinsically resistant to all -lactam agents and must be
treated with macrolide, fluoroquinolone, tetracycline
Data suggest that a virus may be responsible in up to 18% of
cases of CAP
In the ~10–15% of CAP cases that are polymicrobial

22. S. aureus pneumonia is well known to complicate influenza
infection. Recently, however, MRSA strains have been reported as
primary causes of CAP. While this entity is still relatively
uncommon, clinicians must be aware of its potentially serious
consequences, such as necrotizing pneumonia. Two important
developments have led to this problem: the spread of MRSA from
the hospital setting to the community and the emergence of
genetically distinct strains of MRSA in the community. These novel
CA-MRSA strains have infected healthy individuals who have had no
association with health care
Unfortunately, despite a careful history and physical examination as
well as routine radiographic studies, it is usually impossible to
predict the pathogen in a case of CAP with any degree of certainty;
in more than half of cases, a specific etiology is never determined.
Nevertheless, it is important to consider epidemiologic and risk
factors that might suggest certain pathogens

23. Influenza A and B viruses, adenoviruses,
respiratory syncytial viruses, parainfluenza viruses
Anaerobes play a significant role only when an
episode of aspiration has occurred days to weeks
before presentation for pneumonia. combination of
an unprotected airway (alcohol or drug overdose or
a seizure disorder) and significant gingivitis
constitutes the major risk factor. Anaerobic
pneumonias are often complicated by abscess
formation and significant empyemas or
parapneumonic effusions

24. First case of deadly MERS-coronavirus
confirmed in Yemen
Hamdi Turkey

25. Recent studies support the premise that camels serve as the
primary source of the MERS CoV infecting humans and that other‐
livestock are not involved. Although bats may have been the
ultimate reservoir of the progenitor virus, epidemiologically it
seems much more likely that camels would be the source of
infection for humans. The evidence for this includes the frequency
with which virus has recently been found in camels to which human
cases have been exposed, the serological data that indicate
widespread transmission in camels, the similarity of the camel‐
derived virus to human derived virus collected in the same area, and‐
the frequency of either direct or indirect contact between camels
and humans in the region.
Recent studies support the premise that camels serve as the
primary source of the MERS CoV infecting humans and that other‐
livestock are not involved. Although bats may have been the
ultimate reservoir of the progenitor virus, epidemiologically it
seems much more likely that camels would be the source of
infection for humans. The evidence for this includes the frequency
with which virus has recently been found in camels to which human
cases have been exposed, the serological data that indicate
widespread transmission in camels, the similarity of the camel‐
derived virus to human derived virus collected in the same area, and‐
the frequency of either direct or indirect contact between camels
and humans in the region.

26. Microbial causes of CAP by site of care
Outpatient
Hospitalized
Non ICU
hospitalized
ICU
S. pneumoniae
Mycoplasma
pneumoniae
Haemophilus
influenzae
Chlamydophila
pneumoniae
Respiratory
viruses
S. pneumoniae
Mycoplasma
pneumoniae
Chlamydophila
pneumoniae
Haemophilus
influenzae
Legionella spp
Respiratory
viruses
S. pneumoniae
S. aureus
Legionella spp
Gram negative
organisms
Haemophilus
influenzae

27. Distribution of potential etiologies of
CAP

28. Epidemiological factors suggesting
the cause of CAP

29. “I nearly die of double bronchial pneumonia at the
age of five”
“I nearly die of double bronchial pneumonia at the
age of five”
–Roger Moore

30. Diagnosis
When confronted with possible CAP, the physician must ask two
questions:
Is this pneumonia? »»»»»»»»»» answered by clinical and
radiographic methods
what is the etiology? »»»»»»»» requires the aid of laboratory
techniques
When confronted with possible CAP, the physician must ask two
questions:
Is this pneumonia? »»»»»»»»»» answered by clinical and
radiographic methods
what is the etiology? »»»»»»»» requires the aid of laboratory
techniques

31. Clinical symptoms of acute infectious pneumonia
Cough
 either nonproductive or productive of mucoid,
purulent, or blood-tinged sputum
Dyspnea
 patient may be able to speak in full sentences or
may be very short of breath
Chest pain
 If the pleura is involved, the patient may
experience pleuritic chest pain
Constitutio
nal symptoms
 fever, tachycardia, chills and/or sweats
GI
symptoms
 Up to 20% of patients may have GI symptoms such
as nausea, vomiting, and/or diarrhea
Other
symptoms
 fatigue, headache, myalgias, and arthralgias
 CAP can vary from indolent to fulminant in
presentation and from mild to fatal in severity
 CAP can vary from indolent to fulminant in
presentation and from mild to fatal in severity

32. Clinical signs of CAP
General
examination
 Tachypnea, hypotension and shock in severe cases
 Tachycardia
 Fever, herpis labilais, bulbous maryngitis, erythema
multiforme
Inspection  Use of accessory muscles of respiration
Palpation  increased tactile focal fremitus
Percussion  Dullness to percussion over the involved area
Auscultatio
n
 Bronchial breathing, egophony, whispering peqtriloqy, increased
vocal resonance , fne crakles ( early) coarse crackers during
resolution , pleural friction rub

33.  The clinical presentation may not be so obvious in the
elderly who may initially display new-onset or
worsening confusion and few other manifestations.
 The clinical presentation may not be so obvious in the
elderly who may initially display new-onset or
worsening confusion and few other manifestations.

34. Hx, PE, CXRHx, PE, CXRHx, PE, CXRHx, PE, CXR
Infiltrate or clinicalInfiltrate or clinical
evidence of CAPevidence of CAP
Infiltrate or clinicalInfiltrate or clinical
evidence of CAPevidence of CAP
No infiltrateNo infiltrateNo infiltrateNo infiltrate
Alternate diagnosisAlternate diagnosisAlternate diagnosisAlternate diagnosis Evaluate the need forEvaluate the need for
hospital admissionhospital admission
Evaluate the need forEvaluate the need for
hospital admissionhospital admission
PORT, CURB-65, PSIPORT, CURB-65, PSIPORT, CURB-65, PSIPORT, CURB-65, PSI
Out patientOut patientOut patientOut patient Inpatient(ward)Inpatient(ward)Inpatient(ward)Inpatient(ward) Inpatient ( ICU)Inpatient ( ICU)Inpatient ( ICU)Inpatient ( ICU)
CAP – Evaluation of a PatientCAP – Evaluation of a PatientCAP – Evaluation of a PatientCAP – Evaluation of a Patient

35. Radiological classification of
pneumonia
Lobar pneumonia: homogenous opacity
involving a lobe or multi-lobular (streptococcal
pneumonia )
Bronchopneumonia: patchy air-space opacities
(staphylococcal pneumonia)
Interstitial pneumonia: reticular opacities ( viral
pneumonias, atypical pneumonias)
Lobar pneumonia: homogenous opacity
involving a lobe or multi-lobular (streptococcal
pneumonia )
Bronchopneumonia: patchy air-space opacities
(staphylococcal pneumonia)
Interstitial pneumonia: reticular opacities ( viral
pneumonias, atypical pneumonias)

36. Diagnosis

37. CAP – Laboratory TestsCAP – Laboratory Tests
• CXR – PA & lateral
• CBC with Differential
• BUN and Creatinine
• FBG, PPBG
• Liver enzymes
• Serum electrolytes
• Gram stain of sputum
• Culture of sputum
• Pre Rx. blood cultures
• Oxygen saturation
• CXR – PA & lateral
• CBC with Differential
• BUN and Creatinine
• FBG, PPBG
• Liver enzymes
• Serum electrolytes
• Gram stain of sputum
• Culture of sputum
• Pre Rx. blood cultures
• Oxygen saturation

38. Value of CXR
• Usually needed to establish diagnosis
• It is a prognostic indicator
• To rule out other disorders
• May help in etiological diagnosis
• Usually needed to establish diagnosis
• It is a prognostic indicator
• To rule out other disorders
• May help in etiological diagnosis

39. CXR
Lobar pneumonia. Pneumococcal pneumonia involving the entire
left lower lobe. A, Posteroanterior view. B, Lateral view.
Lobar pneumonia. Pneumococcal pneumonia involving the entire
left lower lobe. A, Posteroanterior view. B, Lateral view.

40. Diagnosis
Diagnosis depends on a good thorough history, physical
examination and CXR
For cases managed on an outpatient basis, the clinical and
radiologic assessment is usually all that is done before treatment
is started since most laboratory test results are not available
soon enough to influence initial management
In certain cases, however (influenza virus infection), the
availability of rapid point-of-care diagnostic tests and access to
specific drugs for treatment and prevention can be very
important.
In hospitalized severe cases a more laboratory tests should be
performed including: sputum examination, CBC, blood culture,
serological tests and urinary antigen testing.
Diagnosis depends on a good thorough history, physical
examination and CXR
For cases managed on an outpatient basis, the clinical and
radiologic assessment is usually all that is done before treatment
is started since most laboratory test results are not available
soon enough to influence initial management
In certain cases, however (influenza virus infection), the
availability of rapid point-of-care diagnostic tests and access to
specific drugs for treatment and prevention can be very
important.
In hospitalized severe cases a more laboratory tests should be
performed including: sputum examination, CBC, blood culture,
serological tests and urinary antigen testing.

41. Diagnosis
 The etiology of pneumonia usually cannot be determined on the basis of clinical
presentation
 Except for the 2% of CAP patients who are admitted to the ICU, no data exist to
show that treatment directed at a specific pathogen is statistically superior to
empirical therapy.
 The benefits of establishing a microbial etiology can therefore be questioned,
particularly in light of the cost of diagnostic testing.
 a number of reasons can be advanced for attempting an etiologic diagnosis:
 Identification of an unexpected pathogen allows narrowing of the initial empirical
regimen, which decreases antibiotic selection pressure and may lessen the risk of
resistance
 Pathogens with important public safety implications, such as TB and influenza
virus
 without culture and susceptibility data, trends in resistance cannot be followed
accurately
 The etiology of pneumonia usually cannot be determined on the basis of clinical
presentation
 Except for the 2% of CAP patients who are admitted to the ICU, no data exist to
show that treatment directed at a specific pathogen is statistically superior to
empirical therapy.
 The benefits of establishing a microbial etiology can therefore be questioned,
particularly in light of the cost of diagnostic testing.
 a number of reasons can be advanced for attempting an etiologic diagnosis:
 Identification of an unexpected pathogen allows narrowing of the initial empirical
regimen, which decreases antibiotic selection pressure and may lessen the risk of
resistance
 Pathogens with important public safety implications, such as TB and influenza
virus
 without culture and susceptibility data, trends in resistance cannot be followed
accurately

42. Sputum examination- gram stain
and culture
 a sputum sample must have >25 neutrophils and <10 squamous
epithelial cells per low-power field
 sensitivity / specificity of the sputum Gram's stain and culture are
highly variable »»»»»»»»» in cases of proven bacteremic
pneumococcal infection the yield of positive cultures from sputum
samples is 50%
 Some patients, particularly elderly individuals, may not be able to
produce an appropriate expectorated sputum sample.
 The inability to produce sputum can be a consequence of
dehydration, and the correction of this condition may result in
increased sputum production and a more obvious infiltrate on
radiography
 For patients admitted to the ICU and intubated, a deep-suction
aspirate or BAL sample
 a sputum sample must have >25 neutrophils and <10 squamous
epithelial cells per low-power field
 sensitivity / specificity of the sputum Gram's stain and culture are
highly variable »»»»»»»»» in cases of proven bacteremic
pneumococcal infection the yield of positive cultures from sputum
samples is 50%
 Some patients, particularly elderly individuals, may not be able to
produce an appropriate expectorated sputum sample.
 The inability to produce sputum can be a consequence of
dehydration, and the correction of this condition may result in
increased sputum production and a more obvious infiltrate on
radiography
 For patients admitted to the ICU and intubated, a deep-suction
aspirate or BAL sample

43. Good sputum samples is obtained only from 39%
83% show only one predominant organism
Good sputum samples is obtained only from 39%
83% show only one predominant organism
CAP – Gram’s Stain of SputumCAP – Gram’s Stain of SputumCAP – Gram’s Stain of SputumCAP – Gram’s Stain of Sputum

45. Blood culture
1) The yield from blood cultures, even those obtained before antibiotic therapy, is
disappointingly low
 Only ~5–14% of cultures of blood from patients hospitalized with CAP are positive
 the most frequently isolated pathogen is S. Pneumoniae
2) Since recommended empirical regimens all provide pneumococcal coverage, a
blood culture positive for this pathogen has little effect on clinical outcome
************* susceptibility data may allow a switch from a broader-spectrum
regimen to penicillin in appropriate cases
 Because of 1) the low yield and 2) the lack of significant impact on outcome, blood
cultures are no longer considered for all hospitalized patients.
 CAP patients should have blood cultured :
 neutropenia secondary to pneumonia
 Asplenia
 complement deficiencies
 chronic liver disease
 severe CAP

46. Pathogens Retrieved from Blood CulturePathogens Retrieved from Blood Culture

47. Antigen detection tests
 Two commercially available tests detect
a) pneumococcal
b) certain Legionella antigens in urine
 The test for Legionella pneumophila detects only serogroup 1, but this serogroup
accounts for most CAP cases of Legionnaires' disease
a) The sensitivity and specificity of the Legionella urine antigen test are as high as 90%
and 99%
 The pneumococcal urine antigen test is also quite sensitive and specific 80% and >90%
 false-positive results can be obtained with samples from colonized children,but the
test is reliable
 Both tests can detect antigen even after the initiation of appropriate antibiotic
therapy and after weeks of illness
a) Other antigen tests include a rapid test for influenza virus and direct fluorescent
antibody tests for influenza virus and RSV
b) the test for RSV is only poorly sensitive

48. PCR
PCR tests are available for a
number of pathogens,
including :
 L. Pneumophila
 Mycobacteria
a multiplex PCR can detect
the nucleic acid of
 Legionella spp.
 M. Pneumoniae
 C. pneumoniae
PCR tests are available for a
number of pathogens,
including :
 L. Pneumophila
 Mycobacteria
a multiplex PCR can detect
the nucleic acid of
 Legionella spp.
 M. Pneumoniae
 C. pneumoniae

49. Serology
 A fourfold rise in specific IgM antibody titer between
acute- and convalescent-phase serum samples is
generally considered diagnostic of infection with the
pathogen in question
 Recently, however, they have fallen out of favor
because of the time required to obtain a final result
for the convalescent-phase sample
 A fourfold rise in specific IgM antibody titer between
acute- and convalescent-phase serum samples is
generally considered diagnostic of infection with the
pathogen in question
 Recently, however, they have fallen out of favor
because of the time required to obtain a final result
for the convalescent-phase sample

50. Management

51. Assessment of severity
 Site of Care
 cost of inpatient management exceeds that of
outpatient treatment by a factor of 20
 There are currently two sets of criteria:
 Pneumonia Severity Index (PSI), a prognostic model
used to identify patients at low risk of dying
 the CURB-65 criteria, a severity-of-illness score
 The PSI is less practical in a busy emergency-room
setting because of the need to assess 20 variables
 Site of Care
 cost of inpatient management exceeds that of
outpatient treatment by a factor of 20
 There are currently two sets of criteria:
 Pneumonia Severity Index (PSI), a prognostic model
used to identify patients at low risk of dying
 the CURB-65 criteria, a severity-of-illness score
 The PSI is less practical in a busy emergency-room
setting because of the need to assess 20 variables

52. ConfusionConfusion
UreaUrea
Respiratory rate > 30Respiratory rate > 30
BP ( systolic BP < 90 mmHg, diastolic BP < 60)BP ( systolic BP < 90 mmHg, diastolic BP < 60)
Age > 65Age > 65
( give one point for each feature present)( give one point for each feature present)
ConfusionConfusion
UreaUrea
Respiratory rate > 30Respiratory rate > 30
BP ( systolic BP < 90 mmHg, diastolic BP < 60)BP ( systolic BP < 90 mmHg, diastolic BP < 60)
Age > 65Age > 65
( give one point for each feature present)( give one point for each feature present)
CURB-65 score Severity Where to treat
0 Low Home
1 Low Home
2 Moderate Hospital
3-5 Severe
Hospital assess for
ICU admission
CURB-65 scoreCURB-65 score

53. PORT Scoring –PORT Scoring –
PSIPSI
Pneumonia Patient
Outcomes Research Team

54. < 70< 70Predictor absentPredictor absent 71-9071-90
90-13090-130 > 130> 130
Mortality 0.1-0.4Mortality 0.1-0.4
Out patientOut patientOut patientOut patient
MortalityMortality
0.6-0.70.6-0.7
Out patientOut patientOut patientOut patient
MortalityMortality
0.9-2.60.9-2.6
BriefBrief
hospitalizationhospitalization
BriefBrief
hospitalizationhospitalization
MortalityMortality
8.5-9.38.5-9.3
InpatientInpatientInpatientInpatient
MortalityMortality
27-31.127-31.1
Inpatient-ICUInpatient-ICUInpatient-ICUInpatient-ICU

55. Who Should be Hospitalized?Who Should be Hospitalized?
Class I and IIClass I and II Usually do not require hospitalizationUsually do not require hospitalization
Class IIIClass III May require brief hospitalizationMay require brief hospitalization
Class IV and VClass IV and V Usually do require hospitalizationUsually do require hospitalization
Class I and IIClass I and II Usually do not require hospitalizationUsually do not require hospitalization
Class IIIClass III May require brief hospitalizationMay require brief hospitalization
Class IV and VClass IV and V Usually do require hospitalizationUsually do require hospitalization
Severity of CAP with poor prognosisSeverity of CAP with poor prognosis
RR > 30; PaORR > 30; PaO22/FiO2 < 250, or PO/FiO2 < 250, or PO22 < 60 on room air< 60 on room air
Need for mechanical ventilationNeed for mechanical ventilation
Multi lobar involvementMulti lobar involvement
HypotensionHypotension
Need for vasopressorsNeed for vasopressors
•
OliguriaOliguria
Altered mental statusAltered mental status
Severity of CAP with poor prognosisSeverity of CAP with poor prognosis
RR > 30; PaORR > 30; PaO22/FiO2 < 250, or PO/FiO2 < 250, or PO22 < 60 on room air< 60 on room air
Need for mechanical ventilationNeed for mechanical ventilation
Multi lobar involvementMulti lobar involvement
HypotensionHypotension
Need for vasopressorsNeed for vasopressors
•
OliguriaOliguria
Altered mental statusAltered mental status

56. CAP – Criteria for ICU AdmissionCAP – Criteria for ICU Admission
Major criteriaMajor criteria
Invasive mechanical ventilation requiredInvasive mechanical ventilation required
Septic shock with the need of vasopressorsSeptic shock with the need of vasopressors
Minor criteria (least 3)Minor criteria (least 3)
Confusion/disorientationConfusion/disorientation
Blood urea nitrogen ≥ 20 mg%Blood urea nitrogen ≥ 20 mg%
Respiratory rate ≥ 30 / min; Core temperature < 36ºCRespiratory rate ≥ 30 / min; Core temperature < 36ºC
Severe hypotension; PaO2/FiO2 ratio ≤ 250Severe hypotension; PaO2/FiO2 ratio ≤ 250
Multi-lobar infiltratesMulti-lobar infiltrates
WBC < 4000 cells; Platelets <100,000WBC < 4000 cells; Platelets <100,000
Major criteriaMajor criteria
Invasive mechanical ventilation requiredInvasive mechanical ventilation required
Septic shock with the need of vasopressorsSeptic shock with the need of vasopressors
Minor criteria (least 3)Minor criteria (least 3)
Confusion/disorientationConfusion/disorientation
Blood urea nitrogen ≥ 20 mg%Blood urea nitrogen ≥ 20 mg%
Respiratory rate ≥ 30 / min; Core temperature < 36ºCRespiratory rate ≥ 30 / min; Core temperature < 36ºC
Severe hypotension; PaO2/FiO2 ratio ≤ 250Severe hypotension; PaO2/FiO2 ratio ≤ 250
Multi-lobar infiltratesMulti-lobar infiltrates
WBC < 4000 cells; Platelets <100,000WBC < 4000 cells; Platelets <100,000

57. New Treatment ParadigmNew Treatment Paradigm
Hit hard and early with appropriate
antibiotic(s)
Hit hard and early with appropriate
antibiotic(s)
Short Rx. Duration; De-escalate where possibleShort Rx. Duration; De-escalate where possible

58. Risk assessment approachRisk assessment approach
Early Antibiotic selectionEarly Antibiotic selection
Change treatment driven by local surveillanceChange treatment driven by local surveillance
Hit hard and hit earlyHit hard and hit early
As short a duration as possibleAs short a duration as possible
De-escalate when and where possibleDe-escalate when and where possible
Risk assessment approachRisk assessment approach
Early Antibiotic selectionEarly Antibiotic selection
Change treatment driven by local surveillanceChange treatment driven by local surveillance
Hit hard and hit earlyHit hard and hit early
As short a duration as possibleAs short a duration as possible
De-escalate when and where possibleDe-escalate when and where possible
CAP Treatment ConsensusCAP Treatment ConsensusCAP Treatment ConsensusCAP Treatment Consensus

59. Antibiotics of choice for CAPAntibiotics of choice for CAPAntibiotics of choice for CAPAntibiotics of choice for CAP

65. Empiric Treatment – OutpatientEmpiric Treatment – Outpatient
Healthy and no risk factors for DRHealthy and no risk factors for DR S.pneumoniaeS.pneumoniae
1. Macrolide or Doxycycline1. Macrolide or Doxycycline
Presence of co-morbidities, use of antimicrobialsPresence of co-morbidities, use of antimicrobials
within the previous 3 months, and regions with awithin the previous 3 months, and regions with a
high rate (>25%) of infection with Macrolidehigh rate (>25%) of infection with Macrolide
resistantresistant S. pneumoniaeS. pneumoniae
1. Respiratory FQ – Levoflox, Gemiflox or Moxiflox1. Respiratory FQ – Levoflox, Gemiflox or Moxiflox
2. Beta-lactam (High dose Amoxicillin, Amoxicillin-2. Beta-lactam (High dose Amoxicillin, Amoxicillin-
Clavulanate is preferred; Ceftriaxone, Cefpodoxime,Clavulanate is preferred; Ceftriaxone, Cefpodoxime,
Cefuroxime)Cefuroxime) plus a Macrolideplus a Macrolide or Doxycyclineor Doxycycline
Healthy and no risk factors for DRHealthy and no risk factors for DR S.pneumoniaeS.pneumoniae
1. Macrolide or Doxycycline1. Macrolide or Doxycycline
Presence of co-morbidities, use of antimicrobialsPresence of co-morbidities, use of antimicrobials
within the previous 3 months, and regions with awithin the previous 3 months, and regions with a
high rate (>25%) of infection with Macrolidehigh rate (>25%) of infection with Macrolide
resistantresistant S. pneumoniaeS. pneumoniae
1. Respiratory FQ – Levoflox, Gemiflox or Moxiflox1. Respiratory FQ – Levoflox, Gemiflox or Moxiflox
2. Beta-lactam (High dose Amoxicillin, Amoxicillin-2. Beta-lactam (High dose Amoxicillin, Amoxicillin-
Clavulanate is preferred; Ceftriaxone, Cefpodoxime,Clavulanate is preferred; Ceftriaxone, Cefpodoxime,
Cefuroxime)Cefuroxime) plus a Macrolideplus a Macrolide or Doxycyclineor Doxycycline

66. 1.1. A Respiratory Fluoroquinolone (FQ) LevoA Respiratory Fluoroquinolone (FQ) Levo oror
2.2. A Beta-lactamA Beta-lactam plusplus a Macrolide (or Doxycycline)a Macrolide (or Doxycycline)
(Here Beta-lactam agents are 3 Generation(Here Beta-lactam agents are 3 Generation
Cefotaxime, Ceftriaxone, Amoxiclav)Cefotaxime, Ceftriaxone, Amoxiclav)
3.3. If Penicillin-allergic Respiratory FQ orIf Penicillin-allergic Respiratory FQ or
Ertapenem is another optionErtapenem is another option
1.1. A Respiratory Fluoroquinolone (FQ) LevoA Respiratory Fluoroquinolone (FQ) Levo oror
2.2. A Beta-lactamA Beta-lactam plusplus a Macrolide (or Doxycycline)a Macrolide (or Doxycycline)
(Here Beta-lactam agents are 3 Generation(Here Beta-lactam agents are 3 Generation
Cefotaxime, Ceftriaxone, Amoxiclav)Cefotaxime, Ceftriaxone, Amoxiclav)
3.3. If Penicillin-allergic Respiratory FQ orIf Penicillin-allergic Respiratory FQ or
Ertapenem is another optionErtapenem is another option
Empiric Treatment – Inpatient – Non ICUEmpiric Treatment – Inpatient – Non ICUEmpiric Treatment – Inpatient – Non ICUEmpiric Treatment – Inpatient – Non ICU

67. Empiric Treatment: Inpatient inEmpiric Treatment: Inpatient in
ICUICU
1.1. A Beta-lactam (Cefotaxime, Ceftriaxone,A Beta-lactam (Cefotaxime, Ceftriaxone,
or Ampicillin-Sulbactam)or Ampicillin-Sulbactam) plusplus
eithereither AzithromycinAzithromycin oror FluoroquinoloneFluoroquinolone
2.2. For penicillin-allergic patients, a respiratoryFor penicillin-allergic patients, a respiratory
Fluoroquinolone and AztreonamFluoroquinolone and Aztreonam
1.1. A Beta-lactam (Cefotaxime, Ceftriaxone,A Beta-lactam (Cefotaxime, Ceftriaxone,
or Ampicillin-Sulbactam)or Ampicillin-Sulbactam) plusplus
eithereither AzithromycinAzithromycin oror FluoroquinoloneFluoroquinolone
2.2. For penicillin-allergic patients, a respiratoryFor penicillin-allergic patients, a respiratory
Fluoroquinolone and AztreonamFluoroquinolone and Aztreonam

68. Empiric Rx. – SuspectedEmpiric Rx. – Suspected
PseudomonasPseudomonas
1.1. Piperacillin-Tazobactam, Cefepime, CarbapenumsPiperacillin-Tazobactam, Cefepime, Carbapenums
(Imipenem, or Meropenem)(Imipenem, or Meropenem) plus eitherplus either Cipro or LevoCipro or Levo
2.2. Above Beta-lactamAbove Beta-lactam ++ AminoglycosideAminoglycoside ++ AzithromycinAzithromycin
3.3. Above Beta-lactamAbove Beta-lactam ++ AminoglycosideAminoglycoside ++ anan
antipseudomonal and antipneumococcal FQantipseudomonal and antipneumococcal FQ
4.4. If Penicillin allergic - Aztreonam for the Beta-lactamIf Penicillin allergic - Aztreonam for the Beta-lactam
1.1. Piperacillin-Tazobactam, Cefepime, CarbapenumsPiperacillin-Tazobactam, Cefepime, Carbapenums
(Imipenem, or Meropenem)(Imipenem, or Meropenem) plus eitherplus either Cipro or LevoCipro or Levo
2.2. Above Beta-lactamAbove Beta-lactam ++ AminoglycosideAminoglycoside ++ AzithromycinAzithromycin
3.3. Above Beta-lactamAbove Beta-lactam ++ AminoglycosideAminoglycoside ++ anan
antipseudomonal and antipneumococcal FQantipseudomonal and antipneumococcal FQ
4.4. If Penicillin allergic - Aztreonam for the Beta-lactamIf Penicillin allergic - Aztreonam for the Beta-lactam

69. Strategies for Prevention of CAPStrategies for Prevention of CAP
•Cessation smokingCessation smoking
•Influenza Vaccine (Flu shot – Oct through Feb)Influenza Vaccine (Flu shot – Oct through Feb)
It offers 90% protection and reduces mortality by 80%It offers 90% protection and reduces mortality by 80%
•Pneumococcal Vaccine (Pneumonia shot)Pneumococcal Vaccine (Pneumonia shot)
It protects against 23 types of PneumococciIt protects against 23 types of Pneumococci
70% of us have Pneumococci in our RT70% of us have Pneumococci in our RT
It is not 100% protective but reduces mortalityIt is not 100% protective but reduces mortality
Age 19-64 with co morbidity of high for pneumoniaAge 19-64 with co morbidity of high for pneumonia
Above 65 all must get it even without high riskAbove 65 all must get it even without high risk
•Starting first dose of antibiotic with in 4 h & OStarting first dose of antibiotic with in 4 h & O22 statusstatus

70. Switch to Oral TherapySwitch to Oral Therapy
Four criteriaFour criteria
Improvement in cough, dyspnea & clinical signsImprovement in cough, dyspnea & clinical signs
Afebrile on two occasions 8 h apartAfebrile on two occasions 8 h apart
WBC decreasing towards normalWBC decreasing towards normal
Functioning GI tract with adequate oral intakeFunctioning GI tract with adequate oral intake
If overall clinical picture is otherwise favorable,If overall clinical picture is otherwise favorable,
hemodynamically stable; can switch to oral therapyhemodynamically stable; can switch to oral therapy
while still febrile.while still febrile.
Four criteriaFour criteria
Improvement in cough, dyspnea & clinical signsImprovement in cough, dyspnea & clinical signs
Afebrile on two occasions 8 h apartAfebrile on two occasions 8 h apart
WBC decreasing towards normalWBC decreasing towards normal
Functioning GI tract with adequate oral intakeFunctioning GI tract with adequate oral intake
If overall clinical picture is otherwise favorable,If overall clinical picture is otherwise favorable,
hemodynamically stable; can switch to oral therapyhemodynamically stable; can switch to oral therapy
while still febrile.while still febrile.

71. CAP- complications
Hypotension and septic shockHypotension and septic shock
3-5% Pleural effusion; Clear fluid + pus cells3-5% Pleural effusion; Clear fluid + pus cells
1% Empyema thoracis pus in the pleural space1% Empyema thoracis pus in the pleural space
Lung abscess – destruction of lungLung abscess – destruction of lung
Single (aspiration) anaerobes,Single (aspiration) anaerobes, PseudomonasPseudomonas
Multiple (metastatic)Multiple (metastatic) Staphylococcus aureusStaphylococcus aureus
Septicemia – Brain abscess, Liver AbscessSepticemia – Brain abscess, Liver Abscess
Multiple Pyemic AbscessesMultiple Pyemic Abscesses
Hypotension and septic shockHypotension and septic shock
3-5% Pleural effusion; Clear fluid + pus cells3-5% Pleural effusion; Clear fluid + pus cells
1% Empyema thoracis pus in the pleural space1% Empyema thoracis pus in the pleural space
Lung abscess – destruction of lungLung abscess – destruction of lung
Single (aspiration) anaerobes,Single (aspiration) anaerobes, PseudomonasPseudomonas
Multiple (metastatic)Multiple (metastatic) Staphylococcus aureusStaphylococcus aureus
Septicemia – Brain abscess, Liver AbscessSepticemia – Brain abscess, Liver Abscess
Multiple Pyemic AbscessesMultiple Pyemic Abscesses

72. CAP – So How Best to Win theCAP – So How Best to Win the
War?War?
Early antibiotic administration within 4-6 hoursEarly antibiotic administration within 4-6 hours
Empiric antibiotic Rx. as per guidelines (IDSA / ATS)Empiric antibiotic Rx. as per guidelines (IDSA / ATS)
PORT – PSI scoring and Classification of casesPORT – PSI scoring and Classification of cases
Early hospitalization in Class IV and VEarly hospitalization in Class IV and V
Change Abx. as per pathogen & sensitivity patternChange Abx. as per pathogen & sensitivity pattern
Decrease smoking cessation - advice / counselingDecrease smoking cessation - advice / counseling
Arterial oxygenation assessment in the first 24 hArterial oxygenation assessment in the first 24 h
Blood culture collection in the first 24 h prior to Abx.Blood culture collection in the first 24 h prior to Abx.
Pneumococcal & Influenza vaccination; SmokingPneumococcal & Influenza vaccination; Smoking XX
Early antibiotic administration within 4-6 hoursEarly antibiotic administration within 4-6 hours
Empiric antibiotic Rx. as per guidelines (IDSA / ATS)Empiric antibiotic Rx. as per guidelines (IDSA / ATS)
PORT – PSI scoring and Classification of casesPORT – PSI scoring and Classification of cases
Early hospitalization in Class IV and VEarly hospitalization in Class IV and V
Change Abx. as per pathogen & sensitivity patternChange Abx. as per pathogen & sensitivity pattern
Decrease smoking cessation - advice / counselingDecrease smoking cessation - advice / counseling
Arterial oxygenation assessment in the first 24 hArterial oxygenation assessment in the first 24 h
Blood culture collection in the first 24 h prior to Abx.Blood culture collection in the first 24 h prior to Abx.
Pneumococcal & Influenza vaccination; SmokingPneumococcal & Influenza vaccination; Smoking XX