Pneumonia

 Pneumonia is as an acute respiratory illness
associated with recently developed
radiological pulmonary shadowing, which
may be segmental, lobar or multilobar.
 Pneumonia is defined as inflammation of the
pulmonary parenchyma caused by an
infectious agent
 Pneumonitis reflects inflammation due to
both infection and noninfectious causes

 COSOLIDATION = Inflammatory induration
of a normally aerated lung due to the
presence of cellular exudative in alveoli’

Why the lung are vulnerable to
infectious agent?
(gas exchange function)

How the Microorganisms gain access to LRT?
1-The most common is by aspiration from the oropharynx
2-exposure to secretion from upper respiratory tract
3-Many pathogens are inhaled as contaminated droplets
4-Rarely, pneumonia occurs via hematogenous spread (e.g.,
from tricuspid endocarditis)
5-contiguous extension from an infected pleural or
mediastinal space.

pulmonary host defenses
1-Mechanical defenses
 hairs and turbinates of the nares
capture
larger inhaled particles
 The branching architecture of the
tracheobronchial tree traps microbes
on the airway lining, where
mucociliary clearance and local
antibacterial factors either clear or
kill the potential pathogen.

 gag reflex and the cough mechanism protection
from aspiration.
 the normal flora adhering to mucosal cells of the
oropharynx, whose components are remarkably
constant, prevents pathogenic bacteria from
binding and thereby decreases the risk of
pneumonia caused by these more virulent
bacteria.

2-Airway Secretions Airway epithelial cells secrete
a broad array of antimicrobial
 Lysozyme is secreted in abundant quantities in
human airways
 Antiprotases (α1-antitrypsin, α2-chymotrypsin,
and α2-macroglobulin) airway epithelial cell-
derived antiproteases (secretory leukocyte
protease inhibitor [SLPI] and elafin).
 cationic antimicrobial peptides β-defensin and
cathelicidin.

 When all barriers are overcome or when
microorganisms are small enough to be inhaled to
the alveolar level
 ALVEOLAR MACROPHAGES are a heterogeneous
population of phagocytes that constitute the first
line of defense against microbes that reach the
alveolus

 Most of the time, the body filters organisms.
 This keeps the lungs from becoming infected.
 But organisms sometimes enter the lungs and
cause infections.
This is more likely to occur when:
 immune system is weak.
 organism is very strong.
 body fails to filter the organisms.

 The host inflammatory response, rather than
the proliferation of microorganisms, triggers
the clinical syndrome of pneumonia

Risk Factors
 Advanced age
 chronic illnesses
 Cigarette smoking
 Dementia
 Malnutrition
 Previous episode of pneumonia
 Splenectomy

 Reduced host defences against
bacteria
 Reduced immune defences (e.g.
corticosteroid treatment, diabetes,
malignancy)
 Reduced cough reflex (e.g. post-
operative)
 Disordered mucociliary clearance (e.g.
anaesthetic agents)
 Bulbar or vocal cord palsy
Factors that predispose to
Pneumonia

 Aspiration of nasopharyngeal or gastric
secretions
 Immobility or reduced conscious level
 Vomiting, dysphagia, achalasia or severe
reflux
 Nasogastric intubation
 Bacteria introduced into lower respiratory
tract
 Endotracheal intubation/tracheostomy
 Infectedventilators/nebulisers/
bronchoscopes
 Dental or sinus infection
Factors that predispose to
Pneumonia

 The C/S fever or hypothermia, sweats, rigors,
or chills,
 pulmonary symptoms, such as cough,
sputum production, dyspnea, pleurisy, or
pulmonary lesions on CXR.
 NSS are loss of appetite, fatigue, and
confusion.
Approach to the Patient with
Pneumonia

 The diagnosis and management of
pneumonia has been complicated by
1- recognition of newer pathogens
2- expanded antimicrobial resistance
3-increased populations of
immunocompromised patients
4-by newer diagnostic tools and antimicrobial
agents.
Pneumonia?

 History -----clues
1-Exposure to contaminated air-conditioning cooling towers, recent travel
associated with a stay in a hotel--- Legionella pneumophila
2-Outbreak of pneumonia in shelters for homeless men, jails, military
training camps--- Streptococcus pneumoniae; Mycobacterium tuberculosis
3-Exposure to turkeys, chickens, ducks, or psittacine birds---C. psittaci
4-Travel almost anywhere -----Legionella species
Pneumonia?

Host factors
1-Diabetic ketoacidosis--- S. pneumoniae Staphylococcus aureus
2-Alcoholism ----S. pneumoniae Klebsiella pneumoniae S. aureus
3-COPD ---- S. pneumoniae, Haemophilus influenzae ,Moraxella
catarrhalis ,Pseudomonas aeruginosa (in the subset of patients
with advanced COPD)
4-Solid-organ transplant recipient (pneumonia occurring >3 mo
after transplant) ----S. pneumoniae ,H. influenza & P. jiroveci
5-Sickle cell disease ------S. pneumonia
6-HIV infection with CD4 cell count <200/Μl -------P. jiroveci
Pneumonia?

 Occupational history
Pneumonia in a healthcare worker who works
in a large city hospital with patients infected
with HIV -----M. tuberculosis
Welding ---------S. pneumoniae
Pneumonia?

 Physical exam. -----clues
1- foul-smelling sputum--- anaerobs
2-Bullous myringitis, Encephalitis & Erythema multiforme
M. pneumonia.
3-Absent gag reflex, altered level of consciousness, or a
recent seizure--Polymicrobial (oral aerobic and anaerobic
bacteria)
4- Cerebellar ataxia ----M. pneumonia& L. pneumophila
5- Erythema nodosum--- C. pneumonia M. tuberculosis
Pneumonia?

 No radiologic pattern provides a specific etiologic
diagnosis
 However, the radiographic pattern, combined with
clinical and epidemiologic information, may allow
narrowing of the diagnostic
 Several radiographic patterns may be helpful in
categorizing infectious and noninfectious causes:
 (1) airspace or alveolar pneumonia,
 (2) broncho- or lobular pneumonia
 (3) interstitial pneumonia, and
 (4) nodular infiltrates.

Interstitial
PneumoniaA
reticular or
reticulonodular
pattern of infiltration
is the radiographic
representation of
interstitial
inflammation—that
is, a
peribronchovascular
infiltrate.

Fine nodularity
present in both
lungs.

 Common and serious illness despite
antibiotics and vaccines
 Sixth leading cause of death and number one
infectious death in USA
 Overall incidence rate is 170 (per 10,000) and
increases with age, with an incidence of 280
for those 65 years of age or older
 Outpatient mortality 1- 5 % , inpatient
mortality may reach about 30% .25 %,
greater if an ICU admission is required

 Classic pneumonia evolves through a series of pathologic
changes.
 1- congestion the alveolar units are flooded by
proteinaceous exudate and by neutrophils and red blood
cells,and numerous pneumococci may be observed.
 2-As fibrin forms on the cut surface of the affected lobe, it
resembles liver and so this stage is known as red
hepatisation.
 3-As congestion resolves, the lung tissue becomes grey
(‘grey
hepatisation’), and ultimately, clearance and repair
mechanisms restore the normal architecture of the lung
 4-InVAP, respiratory bronchiolitis may precede the
development of a radiologically apparent infiltrate.

 1.Bronchopneumonia
affects the lungs in
patches around bronchi
 2.Lobar pneumonia is an
infection that only
involves a single lobe, or
section, of
a lung.
 3.Interstitial pneumonia
involves the areas in
between the alveoli

1-Community-acquired pneumonia
 Typical (i.e., classic) pneumonia
 Atypical pneumonia
 Aspiration pneumonia
2-Pneumonia in the elderly
 Community acquired
 Nursing home residents
3-Nosocomial pneumonia
 Hospital-acquired pneumonia (HAP)
 Ventilator-associated pneumonia (VAP)
 Healthcare-associated pneumonia (HCAP)

 Pneumonia that develops outside the hospital is considered community-
acquired pneumonia (CAP).
 Community-Acquired Pneumonia (CAP) is described as a lung infection,
acquired in the community, most commonly bacterial in nature, evidence
of consolidation of part or parts of one or both
 A clinical definition of pneumonia is two or more of the following
symptoms/physical findings:
1-productive cough, purulent sputum,
2-dyspnea or tachypnea (respiratory rate >20 breaths per minute),
3- rigors or chills,
4-pleuritic chest pain in conjunction with a new opacity on chest radiograph
Community-acquired
Pneumonia

 There are about five cases of CAP per 1000
persons per year in the U.S..
 The incidence increases with age.
 Annual all-cause mortality in CAP patients is
up to 28%.

 In 50% of cases, the etiologic organism responsible forCAP
cannot be identified.
 In the remaining cases, a variety of causative organisms have
been identified

Inpatient (ICU)(Inpatient Non-ICU)Outpatient
Streptococcus pneumoniae
Staphylococcus aureus
Legionella species
Gram-negative bacilli
H. influenza
Above organisms plus
Legionella species
Aspiration
Streptococcus
pneumoniae
Mycoplasma
pneumoniae
Haemophilus influenzae
Chlamydophila
pneumoniae
Respiratory viruses

 Influenza, RSVs:The most common viral pathogens,
but can be difficult to differentiate from bacterial
pneumonia.
 Parainfluenza, adenovirus, RSV Can cause
fatal/severe pneumonia in patients who are
immunocompromised, including stem cell and solid
organ transplant recipients.
 Coronaviruses: Responsible for severe acute
respiratory syndrome (SARS) (travel to China, Hong
Kong, Singapore; no cases reported since 2004) and
Middle East Respiratory Syndrome (MERS) (recent
travel to Arabian peninsula or neighboring countries).

Hantavirus:
o Can cause a severe respiratory illness.Associated
with travel to
southwestern U.S., causes an ARDS-like picture.
Varicella pneumonia:
o Most frequent complication of varicella infection in
healthy adults;
fatality rate 10–30%.

 CLINICAL FEATURES—Cough with or without sputum, dyspnea,
fever or hypothermia, chest pain, chills. Extrapulmonary
symptoms: headache, myalgia, and GI symptoms.
 PHYSICAL EXAM—Tachypnea, rales, egophony, increased
fremitus, and dullness to percussion. Pneumonia within 48 hours
of admission to hospital is considered CAP.
 IMAGING—CXR showing air space consolidation with air
bronchograms strongly suggests bacterial pneumonia. Interstitial
infiltrates are not seen with usual bacterial pneumonias. Studies
suggest that early CXRs lack sensitivity. In patients whose
presentation is suggestive of pneumonia, it may be reasonable to
start treatment and repeat imaging in 24–48 hours.

 LABORATORY TESTS
1- Leukocytosis with a left shift; white blood cell count
can be depressed in severe shock or normal in the
elderly. Leukopenia portends a poor prognosis.
2-Sputum cultures optional for outpatients with CAP
since they do very well with empiric treatment.
3-Per IDSA/ATS 2007 guidelines, investigation for
specific pathogens should be done when such
pathogens are suspected based on clinical and
epidemiologic clues, and the results of such an
investigation would change management .
Diagnosis

 LABORATORYTESTS
4-Routine serologic testing for Legionella, Streptococcus
pneumoniae, and C.pneumoniae is not recommended.
5-Blood cultures are positive in < 10% of patients but are
recommended in those ill enough to be hospitalized. Most
common isolate is S. pneumoniae.
6-Procalcitonin (precursor of calcitonin) is elevated in
bacterial infections but decreased in viral infections; a low
level (< 0.1 μg) favors a decision to avoid or stop antibiotics;
use as an adjunct to clinical judgment.
7-Bronchoscopy (BAL, brushing, washing, protected
specimen brushing) usually not done unless the pneumonia
is severe, or refractory to antibiotic therapy.
Diagnosis

 Many classification systems exist .
 Objective scores should not be used as the sole
determinant for hospitalization.
 Reasons to admit low risk patients:
complications of pneumonia, exacerbation of
underlying diseases, inability to take oral
medications.
 IDSA/ATS guidelines recommend direct
admission to ICU when 3 minor criteria or 1
major criterion for severe CAP are met

 The appropriate treatment depends on the disease severity
 Outpatient Macrolide (azithromycin, clarithromycin) or
doxycycline
 Alternative: Anti-PNM FQ
 If risk factors for drug resistance: FQ or anti-PNM BL (high-dose
amoxicillin, amoxicillin–clavulanate, cefpodoxime) + macrolide
 Note
1-May need to reserve FQ to prevent FQ-resistant strains
2-Duration: Minimum of 5 days

 Inpatient,non-ICU FQ (IV or oral) alone or
 Anti-PNM BL (cefotaxime, ceftriaxone, ampicillin–sulbactam) +
macrolide
If concern forCA-MRSA, add vancomycin or linezolid If structural
lung disease, cover PSD
Note
 Duration: 5–7 days for typical organisms
 10–14 days for atypical except Legionella (21 days);
 convert to oral from IV therapy when patient improving
clinically.

 Inpatient, ICU IV BL (piperacillin–tazobactam, imipenem,
meropenem, cefepime) + either an FQ (IV or oral) or a macrolide
 If concern for CA-MRSA, add vancomycin or linezolid
 If suspecting PSD or resistant pathogens:
1-BL above plus anti-PSD FQ or
2-BL + AG + azithromycin or
3-BL + AG + anti-PNM FQ
 When covering PSD, use combination treatment to prevent
inappropriate initial therapy
 Duration: As for inpatient non ICU but longer if extrapulmonary
infection

 Risk factors for drug resistant pathogens:
1- Age > 65
2-Alcoholism
3-Significant medical comorbidities (COPD, liver/kidney
diseases, cancer, DM, chronic heart disease,
immunosuppression)
4- Recent (3–6 months) history of β-lactam, macrolide, or
FQ use

 ASPIRATION PNEUMONIA—Per IDSA/ATS
guidelines, anaerobic coverage is indicated in those
with suspecting A.P.
1- β-lactam/β-lactamase inhibitor
2-Penicillin plus metronidazole (50% failure rate with
monotherapy)
3- Clindamycin

 Some clinical improvement generally is seen within
48–72 hours of initiating antibiotic therapy; if no
improvement within 72 hours, the patient is
considered to be a non responder (6–15% of
hospitalized patients).
 The median defervescence time is 3 days. Other
symptoms may take up to a month to resolve,
especially when age > 50 years, severe pneumonia,
and comorbid conditions present.
 Antibiotic changes prior to 72 hours should be
considered in only patients who are deteriorating or
have new culture data/epidemiologic history.

1- Inadequate or delayed host response.
2- Ineffective antibiotic coverage (TB, fungi,
Nocardia, Actinomyces, resistant pathogens).
4- Complications of initial infection: Consider
chest CT and thoracentesis to evaluate for
effusions, abscess, airway obstruction, and
empyema.

 A 60-year-old man with history of insulin dependent
diabetes mellitus, hypertension, chronic obstructive
pulmonary disease, current everyday smoking history (one
pack per day), and recent bout of influenza was admitted
to the hospital or acute respiratory failure secondary to
community-acquired pneumonia. Sputum and blood
cultures grew methicillin sensitive staphylococcus aureus.
He was given 7 days of nafcillin but failed to improve. He
was persistently febrile and his leukocytosis did not
improve.Repeat cultures showed Staphylococcus aureus
in sputum and blood.
 Below was his sequential chest CT scans, 1 week apart.

Question 1: Which o the following antibiotics would
need to be initiated?
A. Cefepime
B. Linezolid
C.Vancomycin
D. Meropenem
E. Ceftazidime

Question 1: Which of the following antibiotics would
need to be initiated?
A. Cefepime
B. Linezolid
C.Vancomycin
D. Meropenem
E. Ceftazidime
the patient has necrotizing pneumonia from M.sensitive S.producing
panton-valentine leukocidin (PVL) endotoxin. Previously thought
to be restricted to MRSA, PVL forms pores in membranes of infected
cells. Monotherapy might eradicate the bacteria but has no efect on
the endotoxin. Linezolid can eradicate the bacteria and the endotoxin.
Other options includes dual regimen of penicillin or vancomycin with
clindamycin or rifampin. Antibiotic duration is from 4 to 8 weeks. If

Question 2: What other organism is closely related
with this disease?
A. Adenovirus
B. Influenza
C. Cryptococcus
D. Pseudomonas
E. Klebsiella

Question 3: What risk factor is associated with this
disease in this patient?
A. Diabetes mellitus
B. Smoking history
C. Hypertension
D. Influenza
E. Age

Question 3: What risk actor is associated with this
disease in this patient?
A. Diabetes mellitus
B. Smoking history
C. Hypertension
D. Influenza
E. Age

A 21-year-old woman with no known medical history or prior
hospitalization was presented to the emergency department
with complaints of shortness of breath,cough, and fevers for 3
days.
On physical examination,her vital signs showed blood pressure
of 120/80 mmHg, heart rate o 110/min, respiratory rate of
18/min,temperature 38.1ºC, and oxygen saturation 95% on
room air. She had rhonchi in the LLLF and chest radiography
revealed LLLC.
Laboratory evaluation showed white blood cell count
14,000/m/μL with a left shift , hemoglobin 14 g/dL,
platelets300,000/μL, sodium 145 mEq/L, potassium 4 mEq/L,
chloride 101 mEq/L, bicarbonate 28 mEq/L, blood urea
nitrogen 16 mg/dL, creatinine 0.6 mg/dL, glucose
100 mg/dL. She received a dose of ceftriaxone and
azithromycin in the emergency department.

• Question 1: What level of care should this
patient receive?
A. Outpatient management
B. Medical/surgical floor
C. telemetry floor
D. Intensive care unit
E. One dose of antibiotics in the emergency
department

• Question 2: What antibiotics should she be treated
with?
A. Ceftriaxone 1 g intramuscularly once a day
B. Azithromycin and ceftriaxone for at least 3 days and
then continue to de-escalate if patient improves
C. Vancomycin and cefepime for at least 3 days and then
continue to de-escalate if patient improves
D. Hold antibiotics until further tests such as Legionella
urine antigen and strep urine antigen
E. Azithromycin 500 mg PO daily followed by 250 mg PO
daily for 4 additional days

• Question 3: What is the accurate association
between antibiotic and cause oF resistance?
A. Vancomycin–gyrase
B. Moxifloxacin–topoisomerase IV
C. Levofloxacin–topoisomerase IV and gyrase
D. Azithromycin–gyrase
E. Cefepime–oxacillin mediated

• Question 3: What is the accurate association
between antibiotic and cause o resistance?
A. Vancomycin–gyrase
B. Moxifloxacin–topoisomerase IV
C. Levofloxacin–topoisomerase IV and gyrase
D. Azithromycin–gyrase
E. Cefepime–oxacillin mediated

• Hospital acquired pneumonia is defined as
pneumonia occurring 48 hours or more after
admission to a hospital.
• Ventilator-acquired pneumonia is defined as
pneumonia occurring more than 48–72 hours after
endotracheal intubation (ATS/IDSA 2005)

• Health care–associated pneumonia (HCAP):
• Non hospitalized patients exposed to a health care
setting (home IV therapy, wound care, IV
chemotherapy in the past 30 days)
• Resident of nursing home or long-term care facility
or Hemodialysis clinic in the past 30 days
• Recent hospitalization for 2 or more days in the last
90 days

• Primary route of infection is through
microaspiration of colonized organisms of the
oropharyngeal or GI tract.
• Efforts to prevent microaspiration of contaminated
secretions (e.g., improved endotracheal tube
technology, various decontamination techniques)
have had limited success.

• Risk factors for developing VAP
1-Endotracheal intubation 2-Enteral feeding
3-Oversedation 4-Reintubation
5-Supine positioning
• Similarly, HCAP and HAP are also caused by micro
aspiration.
• The differences between HCAP/HAP and VAP are
simply based on the location of the patient and the
timing of onset of infection.

• Factors predisposing to hospital-acquired pneumonia
• Reduced host defences against bacteria
1-Reduced immune defences (e.g. corticosteroid treatment,
diabetes, malignancy)
2- Reduced cough reflex (e.g. post-operative)
3-Disordered mucociliary clearance (e.g. anaesthetic agents)
4- Bulbar or vocal cord palsy
• Aspiration of nasopharyngeal or gastric secretions
1- Immobility or reduced conscious level
2- Vomiting, dysphagia (N.B. stroke disease), achalasia or
severe reflux
3- Nasogastric intubation

• Factors predisposing to hospital-acquired pneumonia
• Bacteria introduced into lower respiratory tract
1- Endotracheal intubation/tracheostomy
2- Infected ventilators/nebulisers/bronchoscopes
3-Dental or sinus infection
• Bacteraemia
1- Abdominal sepsis
2- IV cannula infection
3-Infected emboli

• Microbiology
• Common pathogens are aerobic gram-negative bacilli (E.
coli, Klebsiella, Enterobacter, Pseudomonas aeruginosa
[PSDA], Acinetobacter) and grampositive cocci
(Staphylococcus, Streptococcus).

• Risk factors for MDR pathogens:
1-Recent antibiotics within last 90 days
2- Current hospitalization of 5 days or more
3- High frequency of antibiotic resistance in the community or
hospital unit
4- Immunosuppression
5- Risk factors for HCAP (see above), although some studies
report that it may be an over generalization to consider all
HCAP patients to be at risk for MDR pathogens

• Risk factors for MRSA pathogens:
1- hospitalization for more than 48 hours
2- any hospitalization for 2 or more days in the preceding 3
months
3- individuals residing in nursing homes or extended care
facilities, chronic dialysis unit
4- home infusion therapy
5- home wound care
6-family member with a multidrug-resistant infection

The organisms implicated in early-onset HAP
(occurring within 4–5 days of admission) are
similar to those involved in CAP
Late onset HAP is associated with a different
range of pathogens to CAP, with more Gram-
negative bacteria (e.g.
Escherichia, Pseudomonas, Klebsiella species and
Acinetobacter baumannii), Staph. aureus
(including the meticillin resistant type (MRSA))

The diagnosis should be considered in any hospitalised
or ventilated patient who develops purulent sputum (or
endotracheal secretions), new radiological infiltrates, an
otherwise unexplained increase in oxygen requirement,
a core temperature of more than 38.3°C, and a leucocytosis
or leucopenia.

1-Obtain blood cultures, and thoracentesis, if possible.
2-Obtain lower respiratory tract samples via
tracheobronchial aspiration through endotracheal tube or
bronchoscopically via BAL or protected specimen brush
(PSB).
3-Quantitative culture is significant if the value exceeds
1,000,000 colony forming units (CFU)/mL for
tracheobronchial aspiration, 10,000 CFU/mL for BAL, or
1000 CFU/mL for samples obtained by PSB.
4-Consider lower thresholds if risk of missing aVAP exceeds
risk of unnecessary treatment.

1-aspiration pneumonitis
2-pulmonary infarction,
3-ARDS
4-pulmonary hemorrhage/contusion
5-infiltrative tumor
6- radiation pneumonitis
7- pulmonary drug toxicity
8- cryptogenic organizing pneumonia.

• The principles of management are similar to those for
CAP, focusing on adequate oxygenation,
• Appropriate fluid balance and antibiotics.
• The choice of empirical antibiotic therapy is
considerably more challenging, given the diversity of
pathogens and the potential for drug resistance.

• In early-onset HAP, patients who have received no
previous Abs can be treated with co-amoxiclav or
cefuroxime
• If the patient has received a course of recent ABs, then
piperacillin/tazobactam or a 3rd generation cephalosporin
should be considered.
• In late-onset HAP, the choice of ABs must cover the Gram-
negative bacteria , Staph. aureus (including MRSA) and
anaerobes

NotesAntibioticsScenario
If concern for resistant GNB
based on
institutional data, can start
piperacillin–
tazobactam, cefepime, or
anti-PSD
carbapenem as monotherapy
Ceftriaxone 2 g IV daily; or ampicillin–
sulbactam 3 g IV q6h; or levofloxacin 750
mg IV daily; or moxifloxacin 400 mg IV
daily;. or ertapenem 1 g IV daily
No known
MDR risk
factors

NotesAntibioticsScenario
No conclusive evidence to support
combination therapy for gram-
negative
pathogens such as PSD but
commonly
done since MDR pathogens that
may be
resistant to one antibiotic may be
susceptible to the other
Anti-PSD FQ is preferred if
Legionella is
likely
AG can be stopped in 5–7 days in
those
who respond
Colistin may be appropriate if
highly
resistant PSD species,
Acinetobacter
species, Enterobacteriaceae
family are suspected or
established
Cefepime (2 g q8h) or ceftazidime (2 g
q8h), or
Imipenem, meropenem, or doripenem,
or
Piperacillin–tazobactam
AND
Anti-PSD FQ, or
AG, or
Colistin
AND if suspecting MRSA:
Linezolid (600 mg q12h IV or oral), or
Vancomycin (15–20 mg/kg IV q8-12h
with target trough 15–20 mg/L)
Known MDR
risk factors

Physiotherapy is important to aid expectoration in
the immobile and elderly, and nutritional support is
often required.

Whereas antimicrobials are often needed to treat a
suspected or definitive case of HAP orVAP, much effort has
been directed toward prevention of HAP andVAP. One
approach has been the use of a ventilator bundle.

• The ventilator bundle has been shown to decrease the
risk ofVAP as well as other potential complications
related to mechanical ventilation
Assess for readiness to extubate Assess level of
consciousness by lightening or stopping sedation1-Daily SAT/SBT
spontaneous awakening trial;SBT =
spontaneous breathing trial
2-Elevate HOB to 30-45% Reduce theVAP risk by reducing the risk of aspiration
Contraindications/precautions include:
• Severe hypotension
• Unstable spine
• Pelvic fracture
• Intra-aortic balloon pump
• Morbid obesity
• Prone position

3-Oral care ReduceVAP risk by decreasing oropharyngeal colonization
4-Stress ulcer prophylaxis
5-DVT/PE prophylaxis

Patients immunocompromised by drugs or disease(particularly HIV)
are at high risk of pulmonary infection.
The majority of cases are caused by the same pathogens that cause
pneumonia in non-immunocompromised individuals, but in patients
with more profound immunosuppression, unusual organisms or
those normally considered to be of low virulence or non-pathogenic
may become ‘opportunistic’ pathogens
Therefore, the possibility of Gram-negative bacteria, especially
Pseudomonas aeruginosa,viral agents, fungi, mycobacteria, and less
common organisms such as Nocardia asteroides has to be
considered.
Infection is often due to more than one organism.

These typically include fever, cough and breathlessness, but are
influenced by the degree of immunosuppression;
The speed of onset tends to be less rapid in patients with
opportunistic organisms such as P. jirovecii and mycobacterial
infections than with bacterial infections
In P. jirovecii pneumonia, symptoms of cough and breathlessness can
be present for several days or weeks before the onset of systemic
symptoms or the appearance of X-ray abnormalities..

Invasive investigations, such as bronchoscopy, BAL, transbronchial
biopsy or surgical lung biopsy, are often impractical, as many patients
are too ill to undergo these safely.
However induced sputum offers a relatively safe method of
obtaining microbiological samples
HRCT is useful in differentiating the likely cause:
1-Focal unilateral airspace opacification--- mycobacteria or Nocardia.
2- Bilateral opacification--- P. jirovecii , fungi, viruses and unusual
bacteria
3- Cavitation------- N. asteroides, mycobacteria and fungi.
4-The presence of a ‘halo sign’ may suggest Aspergillus
5-Pleural effusions suggest a pyogenic bacterial infection and are
uncommon in P. jirovecii pneumonia.

treatment should be based on the identified causative organism but,
this is frequently unknown and BS AB is required, such as a third-
generation cephalosporin or a quinolone, plus an antistaphylococcal
antibiotic, or an antipseudomonal penicillin plus an aminoglycoside.

Trimethoprim-sulfamethoxazole remains the treatment of choice.
Unfortunately, side effects are common at the high doses required for
PJP infection.
Clindamycin plus primaquine is a reasonable alternative that is better
tolerated
Steroids are useful in moderate to severe PJP.
Its used for PJP patients who are hypoxic (PaO2 < 70 mm Hg).
Steroids reduce the rate of worsening respiratory failure and death by
as much as 50% in some series.
They are most effective when given within 72 hours of onset of disease.
used in a dose /prednisolone 20 mg twice daily, 40 mg once daily for
five days, or 20 mg once daily for 11 days.

Epidemiology
More than 140 NTM have been identified, at least 40 of which are
associated with human lung infection. It is difficult to determine the
epidemiology of NTM, as reporting is not mandatory, but it appears
that the incidence and prevalence are increasing.

Transmission
NTM is present everywhere in the environment and can be found in
natural and drinking water, biofilms, soil, and aerosols.
Human-to-human transmission has never been documented.
Risk factors for disease include impaired host immunity, impaired
lung immunity, and host demographics.

NTM pulmonary disease can present in diverse ways including
TB-like cavitary disease
Bronchiectasis
Hypersensitivity-like lung disease
Esophageal dysmotility
NTM in AIDS most commonly causes disseminated disease that
presents with nonspecific symptoms such as fever, night sweats,
diarrhea, abdominal pain, and lymphadenopathy. In such patients,
Mycobacterium avium complex (MAC) is the most frequent isolate.

Clinical, radiographic, and microbiologic criteria must be met to
make a diagnosis of NTM infection.
Clinical criteria include pulmonary symptoms and exclusion of
other diagnoses, and radiographic criteria include nodular or
cavitary opacities on chest radiograph or bronchiectasis with small
nodules on chest CT.

Slowly growing NTM that cause human disease include MAC,
Mycobacterium kansasii, and Mycobacterium xenopi.

There are three manifestations of pulmonary disease due to MAC—
nodular/bronchiectatic disease, cavitary disease, and advanced or
previously treated disease.
Recommended duration of treatment is 12 months after documented
sputum culture negativity; treatment involves a macrolide,
ethambutol, and rifamycins.
Preventive therapy for MAC is recommended for all HIV patients
with CD4+ < 50; azithromycin 1200 mg weekly is the preferred
agent.

Tap water is the major reservoir, and there is no recommended
prophylaxis for disseminated disease.
Recommended regimen for treating pulmonary M. kansasii disease is
three agents for 12 months of negative sputum cultures: rifampin (600
mg/day), isoniazid (300 mg/day), and ethambutol (15 mg/kg/day).

Survives in hot water systems and natural hot water reservoirs
Rarely isolated in the U.S., but often isolated in Canada, UK, and
Europe
Overall mortality is high
A number of accepted treatment regimens include clarithromycin,
rifampin, and ethambutol isoniazid for 12 months

Fulminant, rapidly progressive form of the disease has been seen in
patients with gastroesophageal disorders and cystic fibrosis.
Typically resistant to most of the medications used to treatTB, and
therapy usually consists of IV agents such as imipenem or cefoxitin plus
amikacin
Therapy should be continued for at least 2–4 months, although cure
with medical therapy alone may be difficult to achieve

NTM is present everywhere in the environment, so complete
avoidance is difficult.
Transmission of NTM disease in the health care setting has most
frequently been linked to tap water exposure.
it is recommended that tap water not be used in various nosocomial
settings. Potent disinfectants have been unsuccessful in eradicating
these organisms.
Prophylaxis should be given to adults with AIDS with CD4 counts < 50;
azithromycin and clarithromycin have proven efficacy.

A 72-year-old man is evaluated for fever in the hospital after being on
mechanical ventilation for 1 week for hypoxic respiratory failure due
to influenza. After an initial period of improvement, his level of
purulent sputum production has increased over the past 24 hours,
and over the previous 48 hours it has been necessary to increase his
FIO2 to maintain his oxygenation.
His only medication is oseltamivir delivered by orogastric tube.
On physical examination, temperature is 38.3 °C (100.9 °F), blood
pressure is 110/60 mm Hg, pulse rate is 115/min, and respiration rate
is 18/min (ventilator set rate is 14/min).
Pulmonary examination reveals diffuse crackles.

Laboratory studies reveal a leukocyte count of 18,000/μL (18 × 109/L),
increased from 12,500/μL (12.5 × 109/L) 2 days ago.
Chest radiograph shows worsening pulmonary infiltrates.
Which of the following is the most appropriate next step in
management?
A- Begin empiric ceftriaxone and azithromycin
B -Chest physiotherapy
C -Deep sampling of the lower respiratory tract
D-Substitute zanamivir for oseltamivir

All of the following are associated with an increase risk
of MRSA S.aureus as a cause of HCAP EXCEPT
A.Antibiotic therapy in the preceding 3 months
B. Chronic dialysis
C. Home wound care
D. Hospitalization for more than 2 days in the preceding
3 months
E. Nursing home residence

All of the following are associated with an increase risk
of MRSA S.aureus as a cause of HCAP EXCEPT
A-Antibiotic therapy in the preceding 3 months
B. Chronic dialysis
C. Home wound care
D. Hospitalization for more than 2 days in the preceding
3 months
E. Nursing home residence

Many noninfectious conditions cause patients to present
with a syndrome consistent with acute or subacute
pneumonia
Cryptogenic organizing pneumonia
acute interstitial pneumonia,
Eosinophilic pneumonia
and other interstitial pneumonias .
Are uncommon conditions that almost always are initially
misdiagnosed as community-acquired pneumonia.

Pulmonary hemorrhage and vasculitis may also cause
pulmonary infiltrates and fever. In ANCA-associated
granulomatous vasculitis, these infiltrates may also be
associated with cavitary lesions.
Pulmonary embolus with infarction can cause pleuritic chest pain and
pulmonary infiltrates, with sputum that contains neutrophils but few or
no bacteria.
Pulmonary edema is the most common noninfectious cause of a
community-acquired pneumonia-like syndrome in middle-aged and
older patients.
Dx ----BNP

Patients with lung cancer commonly present with fever and
a pulmonary infiltrate, which sometimes is attributed to a
postobstructive pneumonia.
Acute respiratory distress syndrome in response to a serious
nonpulmonary infection is often indistinguishable from pneumonia
because it commonly presents with fever, lung crackles, an elevated
WBC count, and pulmonary infiltrates.

Aspiration is a relatively common event that is typically well
tolerated. Numerous studies indicate that virtually all
healthy persons aspirate, but that this is usually
inconsequential.
In one study, airway protective mechanisms were challenged by
placing contrast material in the mouths of sleeping patients.The
following morning, most patients had radiographic evidence of
aspiration, defined as contrast material seen on imaging of the lungs,
but no evidence of a disease process

dye markers placed in the stomach of postoperative
patients has later been aspirated from the tracheobronchial
tree, indicating aspiration of gastric contents during general
anesthesia in 7% to 16%.
The conclusion is that aspiration is relatively common but usually
resolves spontaneously

Inoculum
• Acid breathing
• Pulmonary Sequelae
• Chemical
pneumonitis
Clinical Features
Therapy
• SOB, PR ;RR,BT
cyanosis,
• bronchospasm
• CXR infiltrates in one
or both lower lobes
• Hypoxemia
Therapy
Supplemental oxygen,
bronchodilators,
mechanical
ventilation as needed

Inoculum
• Oropharyngeal
bacteria
• Pulmonary Squeal
• Bacterial infection
Clinical Features
• Usually insidious
onset Cough, fever,
purulent sputum
• Radiographic infiltrate
in dependent
pulmonary segment or
lobe ± cavitation
Therapy
Antibiotics

Inoculum
• Inert fluids
• Mechanical
obstruction
• Reflex airway closure
Clinical Features
• Acute dyspnea,
cyanosis ± apnea
• Pulmonary edema
Therapy
Tracheal suctioning,
supplemental
oxygen, mechanical
ventilation as needed

Inoculum
• Particulates
• Mechanical
obstruction
Clinical Features
• Dependent on level of
obstruction, ranging
from acute apnea and
rapid death
• to irritating chronic
cough ± recurrent
superimposed
infections
Therapy
Extraction of matter
Antibiotics for infection

INTRODUCTION Fungi---------------- rarely cause
respiratory tract infection

Systemic factors
• Diabetes mellitus
• Chronic alcoholism
• HIV
• Radiotherapy
• Corticosteroids and
other
immunosuppressant
medication
Local factors
• Tissue damage by
suppuration or necrosis
• Alteration of normal
bacterial flora by
antibiotic therapy

Aspergillosis is the collective term used to describe all disease entities
caused by any one of ~50 pathogenic and allergenic species of
Aspergillus.
Only those species that grow at 37°C can cause invasive infection,
although some species without this ability can cause allergic syndromes
A. fumigatus is responsible for most cases of invasive aspergillosis, almost
all cases of chronic aspergillosis, and most allergic syndromes.
A.flavus --sinus infections, cutaneous infections, and keratitis
A. niger can cause invasive infection and causes external otitis.
A. terreus causes only invasive disease, usually with a poor prognosis.
A. nidulans occasionally causes invasive infection--- chronic granulomatous disease

Pulmonary aspergillosis may be classified .
Saprophytic
or
colonizing
invasive
allergic

Invasive aspergillosis occurs in patients with acquired or
primary defects in neutrophil function.
IA is classified as acute and subacute, with courses of ≤1
month and 1–3 months, respectively.
in recent years, even up to 41% of the cases of IA were
diagnosed in non neutropenic patients,especially in patients
with COPD, chronic liver disease,
More than 80% of cases of IA involve the lungs.
HIV Patients may develop IPA when CD4 count falls less than
50 cells/cumm

HRCT characteristically shows macronodules(usually ≥ 1 cm), which
may be surrounded by a ‘halo’ of low attenuation if captured early (<
5 days).
Culture or histopathological evidence of Aspergillus in diseased
tissues provides a definitive diagnosis, but the majority
of patients are too ill for invasive tests such as bronchoscopy
or lung biopsy.
Other investigations include detection of Aspergillus cell wall
components (galactomannan and β-1,3-glucan) in blood or BAL fluid
and Aspergillus DNA by PCR.

“Halo” sign in
angioinvasive
aspergillosis.CT
scan
of patient with
fever and
prolonged
neutropenia
during therapy
for
hematopoietic
malignancy
demonstrates a
macronodule
(N) surrounded
by a halo of
ground-glass
opacity (*).
N

“Air-crescent
sign in AIA.
CT -patient with
hematologic
malignancy
after recovery
from profound
neutropenia
demonstrates a
cavitary
macronodule
with an air
crescent
(arrows) at 10 to
1 o’clock
outlining a
central necrotic
sequestrum (S).
N S

IPA carries a high mortality rate, especially if treatment is delayed.
The treatment of choice is voriconazole.
Second-line agents include liposomal amphotericin, caspofungin or posaconazole
Response may be assessed clinically, radiologically and serologically (by estimation
of the circulating galactomannan level).
Posaconazole (200 mg 3 times daily) or itraconazole (200 mg/day) may
be prescribed for primary prophylaxis,
patients with a history of definite or probable IPA should be
considered for secondary prophylaxis before further
immunosuppression.

The fungal ball produces a tumour-like opacity on X-ray, distinguished
from a carcinoma by the presence of a crescent of air between the
fungal ball and the upper wall of the cavity. HRCT is more sensitive
Elevated serum precipitins to A. fumigatus are found in virtually all
patients.
Sputum microscopy typically demonstrates scanty hyphal fragments
and is usually positive on culture.
Less than half exhibit skin hypersensitivity to extracts of A. fumigatus.
Other filamentous fungi can cause intracavitary mycetoma and are
identified by culture.

Asymptomatic cases do not require treatment.
Specific antifungal therapy is of no value and steroids may predispose
to invasion.
Aspergillomas complicated by haemoptysis should be excised
surgically.
In those unfit for surgery, palliative procedures range from local
instillation of amphotericin B to bronchial artery embolisation.
The latter may be used to control haemoptysis prior to
definitive surgery.

Chronic pulmonary aspergillosis (CPA) is an indolent non-invasive
complication of chronic lung disease, such as COPD, tuberculosis,
opportunistic mycobacterial disease or fibrotic lung disease.
Radiological features include thick walled cavities (predominantlyapical), pulmonary
infiltrates, pleural thickening and, later, fibrosis.
The terms chronic necrotising (CNPA), cavitary (‘complex aspergilloma’) and
fibrosing pulmonary aspergillosis have been applied, depending on the predominant
features.
There is overlap between CNPA and ‘subacute’ and ‘semi-invasive’
aspergillosis

Subacute aspergillosis is increasingly recognised in intensive care
patients, especially those with COPD.
The diagnosis is made by a combination of radiological
examination,histopathology,
isolation of fungus from the respiratory tract and detection of
Aspergillus IgG in serum.
Treatment usually involves prolonged indefinite courses of
itraconazole or voriconazole, but cure is unusual.

Mucormycosis may present with a pulmonary syndrome(
indistinguishable clinically from acute IPA.
Diagnosis relies on histopathology (where available) and/or culture of
the organism from diseased tissue.
The principles of treatment are as for other forms of mucormycosis:
correction of predisposing factors, antifungal therapy with high-dose
liposomal amphotericin or posaconazole, and surgical débridement.

1-Fungal infections are associated with considerable
morbidity and mortality even when appropriately treated.
2-Delays in therapy can negatively impact outcomes and
increase health-care costs.
3-Several challenges exist in identifying patients at risk of
these infections and in achieving an accurate diagnosis.
Furthermore, antifungal pharmacotherapy has become very
complex with the introduction of new agents, susceptibility
testing, andTDM(theraputic drug monitoring)

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