Transcript Document

Respiratory Tract Infections
Prof. M.Awad Tag Eldin
Infections Of The Respiratory Tract
Respiratory infections are mainly caused by
bacteria, viruses, or Mycoplasma pneumonia.
Rickettsial and fungal infections are relatively
uncommon and are largely confined to certain
geographical regions. Respiratory infections occur
at any age but are commonest6 in the young, the
elderly and the immunosuppressed. The clinical
features are determined by the causal organism, the
site of infection and whether the infection in acute or
chronic.
Acute Respiratory Infections
Acute infections predominantly involve
the upper respiratory tract, e.g. coryza,
the bronchial tree, e.g. acute bronchitis or
the lungs, e.g. pneumonia, lung abscess.
Acute Exacerbation of Chronic Bronchitis
 A sustained worsening of respiratory
symptoms that is acute in onset and
usually requires a patient to seek
medical help or alter treatment.
PNEUMONIA, DEFINITION
A syndrome caused by acute infection
characterized by clinical and/or
radiographic signs of consolidation of a
part or parts of one or both lungs.
PNEUMONIA,Etiology
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Bacterial.
Viral.
Bacteria-like& rickettsia-like.
Fungal& actinomycotic.
Parasitic.
Chemical.
Physical.
PNEUMONIA, Clinical Settings
 Community-acquired pneumonia
(CAP).
 Hospital-acquired pneumonia (HAP).
 Aspiration pneumonia.
 Pneumonia in ICH.
 Pneumonia in HIV.
LUNG ABSCESS AND EMPYEMA
Definition
A lung abscess is a localized area of pulmonary
suppuration and necrosis with a central cavity,
caused by infection with pyogenic organisms.
Bronchiectasis
Definition
Bronchiectasis is the term used to
described pathological dilation of the
bronchi. Secretions accumulate in the
bronchiectasisbronchi and chronic
infection causes persistent cough and
purulent sputum.
Egyptian Picture of RTIs
Prof. M.Awad Tag Eldin
Epidemiology of RTIs in Egypt
Acute Respiratory Tract Infections in developing
countries among children 5 years of age
 A large proportion of ARI is present as
pneumonia or bronchiolitis .
Dr Thamer.K.Yousif/MBCh.B/FICMS, DR.BAN A. Khaleq/MSC. Middle East Journal of family medicine. 2006, 14;3.
Acute Respiratory Tract Infections in developing
countries among children 5 years of age
 Incidence of ARI is almost the same all over
the world :
 5-7 episodes/ child/ years in urban areas
 3-5 episodes in rural areas.
Dr Thamer.K.Yousif/MBCh.B/FICMS, DR.BAN A. Khaleq/MSC. Middle East Journal of family medicine. 2006, 14;3.
Egyptian Data on Acute Febrile Illness
due to different pathogens
 Acute respiratory infections are the second
leading cause of death in Egyptian infants (1).
 For *55 months, 10,130 patients meeting
the case definition of #AFI had a clinical
evaluation, 1,005 (10%) patients had
positive blood cultures including :
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77 with Staphylococcus aureus
494 with ST infection
275 with Brucella
159 with other bacterial pathogens.
Am. J. Trop. Med. Hyg., 73(2), 2005, pp. 392-399
*Between March 1999 and October 2003
1.International Development Research Center, Egypt.
#Acute
Febrile Illness
Epidemiology of *MRSA in Egypt
*MRSA: Methicillin Resistant Staph. Aureus
Indexed in MedLine as: Euro Surveill 2006;11(7):164-7
Epidemiology of Penicillin &
Erythromycin-Resistant Strains
Indexed in MedLine as: Euro Surveill 2006;11(7):164-7
Group A Streptococcal Pharyngitis in
School-aged Children and Their Families
for 16 months
 The incidence of group A streptococcal Pharyngitis is
13% for school-aged children (5-12 years).
 In families who had a primary case, 43% had at
least 1 secondary case
 The incidence in adults is higher than expected.
Pediatrics. 2007 Nov ;120 (5):950-957 17974731
Acute Respiratory Tract Infections in developing
countries among children 5 years of age
Conclusion:
 In all countries ARI is a leading cause of
hospitalization and death.
 The WHO estimate that in 1990 ARI tragically
caused 13 million children die each year, 4.3
million children die from ARI, mostly pneumonia,
every year in developing countries.
 Antibiotics were the most common types of
medications used by cases before presenting to
hospital, which didn’t prevent children from
reaching the hospital indicating misusage of
antibiotics.
Dr Thamer.K.Yousif/MBCh.B/FICMS, DR.BAN A. Khaleq/ MSC. Middle East Journal of family medicine. 2006, 14;3.
Lower Respiratory Tract
Infections
1. Bronchitis
Types of Bronchitis
 Acute bronchitis usually comes on quickly and
gets better after 2 to 3 weeks.
 Approximately 90% of these infections
are viral in origin.
 Most cases of acute bronchitis are viral or
noninfectious.
 Secondary bacterial infection of acute bronchitis
SBIAB by such bacterial pathogens as
Streptococcus pneumoniae or Haemophilus
influenzae may occur.
Types of Bronchitis
 Chronic bronchitis is defined as a condition
characterized by cough and sputum
production on most days during 3
consecutive months for >2 successive years.
 Chronic bronchitis has a very high incidence in smokers
and it is also known as “the smokers’ disease”.
 Acute exacerbation of chronic bronchitis
(AECB) is characterized by increased cough,
sputum production, and dyspnea, in addition
to development of sputum purulence.
Etiology of Bronchitis
 Non-infectious bronchitis
 Due to prolonged exposure to chemicals, cigarette
smoke and pollutants.
 Allergens (pollen, dust particles) are also triggers
of non-infectious bronchitis.
 Infectious bronchitis
 Involves infection with microorganisms and its
usually more intense.
 Common infectious agents are bacteria, viruses,
mycoplasmas and fungal organisms.
Triggering factors for Acute Bronchitis
 Smoke.
 Certain dusts or fumes may develop
occupational bronchitis.
 Gastro esophageal reflux disease (GERD).
 Low resistance, This may result from
another acute illness, such as a cold, or from
a chronic condition that compromises your
immune system.
Diagnosis of Bronchitis
 Cold-like symptoms (runny nose, sneezing, and
dry cough).
 Cough soon becomes deep and painful
accompanied by wheezing with a greenish-yellow
sputum.
 Fever of up to 39°C is common.
 Shortness of breath
 Chest radiography may be necessary to
exclude pneumonia.
 A sputum culture may be performed, especially
if green or bloody.
Treatment of Bronchitis
 Non-Pharmacological Treatment:
 Plenty of fluids, having rest, and avoiding smoking are
useful.
 Pharmacological Treatment:
 Cough with sputum should not be treated because it helps
remove mucus and other harmful materials from the lungs.
 Analgesics and antipyretics can also be useful.
 Acute bacterial bronchitis and Secondary bacterial infection
of acute bronchitis can be treated with Antibiotics.
Meta-Analysis of the Benefits
of Antibiotics in AECB
Favors Placebo
Favors Antibiotic
Elmes et al. 1957
Berry et al. 1960
Fear, Edwards. 1962
Elmes et al. 1965
Petersen et al. 1967
Pines et al. 1972
Nicotra et al. 1982
Anthonisen et al. 1987
Jorgensen et al. 1992
Overall
–1.0
–0.5
0
0.5
Effect Size
Saint S et al. JAMA. 1995;274:1131-1132.
1.0
1.5
Treatment of Bronchitis
 The ideal antibiotic for AECB must:
 Be active against the likely pathogens
 Be resistant to destruction by bacterial betalactamases
 Have high concentrations in lung parenchyma
against target organisms
 Have a bacterial killing mechanism that does not
increase airway inflammation.
Treatment of Bronchitis in Egyptian
Outpatient Clinic
 Antibiotics were used in
 50% of cases with bronchitis and wheezy
bronchitis
 3.5% of cases of the common cold.
 Amoxicillin was the most commonly used
antibiotic in Pharyngitis, tonsillitis and
wheezy bronchitis.
 The duration of antibiotic therapy was < 7
days in 82.6% of cases of tonsilitis and 60%
of pneumonia.
A. Zaki, M. Abdel-Fattah, A. Bassili, M. Arafa and R. Bedwani. Eastern Mediterranean Health Journal Volume 5, Issue 2, 1999, Page 320-327
2. Community Acquired
Pneumonia
Community Acquired Pneumonia
(CAP)
 CAP is a disease in which individuals who
have not recently been hospitalized develop
an infection of the lungs (pneumonia).
 CAP often causes problems like breathing,
fever, chest pains, and cough.
 CAP occurs because the areas of the lung
which absorb oxygen (alveoli) from the
atmosphere become filled with fluid and
cannot work effectively.
Resistance for Antibiotics
Epidemiology of CAP
 It is a major cause of death among all age
groups.
 WHO estimates that 1 in 3 newborn infant
deaths are due to pneumonia with over
2,000,000 worldwide deaths a year.
 More cases of CAP occur during winter
months than during other times of the year.
Symptoms of CAP
 Breathing problems
 Cough with greenish or yellow sputum
 Fever that may be accompanied with sweating,
chills, and uncontrollable shaking
 Chest pain
 Less common symptoms include:
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Bloody cough
Headaches (including migraine)
Loss of appetite & excessive fatigue
Blueness of the skin (cyanosis)
Nausea, vomiting & diarrhea
joint pain (arthralgia) & muscle aches (myalgia)
Symptoms of CAP
 Older people might experience different
manifestations of pneumonia :
 New or worsening confusion
 Hypothermia
 Falls
 Additional symptoms for infants could
include:
 Being overly sleepy
 Yellowing of the skin (jaundice)
 Difficulties in feeding
Diagnosis of CAP
 Hypotension
 Tachycardia
 Changes in the amount of oxygen in the
blood.
 Rales in breath
 Increased vibration of the chest when
speaking.
 X-rays, and blood tests of blood and sputum
are commonly used.
Distribution of Pathogens in CAP
H influenzae
4.9%
H parainfluenzae
1.9%
M pneumoniae
15%
M Catarrhalis
1.1%
S aureus
1.1%
C pneumoniae
12%
C pneumoniae +
M pneumoniae
2.1%
S pneumoniae
5.9%
Unknown
51.6%
Bartlett JG, Mundy LM. N Engl J Med. 1995;333:1618; American Thoracic Society. Am J Respir Crit Care Med. 2001;163:1730’ Hall MJ, Owings,
MF. 2000 National Hospital Discharge Survey. NCHS. 2002:1; National Vital Statistics Report. 2001;49:14. Marrie TJ et al. Resp Med. 2005;
99:60-65.
Micro organisms causing CAP
 In Adults;
 Viruses cause 20% of CAP cases;
 Influenza,
 Parainfluenza,
 Respiratory syncytial virus,
 Metapneumovirus,
 Adenovirus.
Micro organisms causing CAP
 In Children > 5 years and teenagers;
 Are more likely to acquire
Mycoplasma pneumonia and
Chlamydophila pneumonia than adults
& children < 5 years of age.
Treatment of CAP
 *ATS & **BCTS, established guidelines for the
management of adults with CAP which divided
individuals with CAP into four categories:
1.Healthy outpatients without risk factors
2.Outpatients with underlying illness and/or risk
factors
3.Hospitalized individuals not at risk for Pseudomonas
4.Individuals requiring intensive care at risk for
Pseudomonas
Complications of CAP
 Severe complications can result from CAP,
including:
 Sepsis
 Respiratory failure
 Pleural effusion and empyema
 Abscess
ANTIOBITICS
REVOLUTION
1- Introduction to Antibiotics
1.1 Development of Antibiotics
Synthetic era arrived around
1900 and involved The development
First era started from
of various dyes To treat bacterial
1600 to 1900 and involved
infections as pyocyanas
The use of Cinchona bark in the
produced by
Treatment of malaria
Pseudomonas aeruginosa
Miracle era which arrived
when Alexander Fleming
Discovered Penicillin in 1929
and apparently recognized by
Flory and his team in 1940
1- Introduction to Antibiotics
(Cont)
1.2 Antibiotic Resistance
There are four types of antimicrobial resistance
Inherent (Natural) Resistance:
Bacteria may be inherently resistant to an antibiotic by establishing a barrier
against the antibiotic or lacking a transport system
Acquired Resistance:
Bacteria can develop resistance to antibiotics which results from changes in
the bacterial genome either by mutation and selection or exchange of genes
between strains and species
Vertical evolution
A spontaneous mutation in the bacterial chromosome which imparts
resistance to a member of bacterial population
Horizontal evolution:
The acquisition of genes for resistance from another organism e.g. a
streptomycete has a gene for resistance to streptomycin (its own antibiotic),
but somehow that gene escape and gets into E-Coli or Shigella
1- Introduction to Antibiotics
(Cont)
1.3 Quantitative Susceptibility
The minimum inhibitory concentration (MIC) is defined as the
minimum concentration required to inhibit 50% of a bacterial
population.
MIC however, doesn’t represent an absolute value and the
true MIC is somewhere between the lowest test concentration
that inhibits the organism growth and the next lower test
concentration
The following table gives an indication of MIC values of a
selected range of antibiotics against four reference strains.
Acceptable quality control ranges of MICs (ug/ml) for
reference strains (NCCLS, 1991)
Antibiotic
S. aureus E. faecalis E. coli
P. aeruginosa
Amikacin
1-4
64-256
0.5-4
0.5-8
Azithromycin
0.28-1
-
-
-
Cefaclor
1-4
>32
1-4
-
Cefazolin
0.25-1
>16
1-4
-
Cefuroxime
0.5-2
-
2-8
-
Chloramephenicol
2-8
4-16
2-8
-
Clarithromycin
0.12-0.5
-
-
-
Erythromycin
0.12-0.5
1-4
-
-
Gentamycin
0.12-1
4-16
0.25-1
0.25-4
Ofloxacin
0.12-1
1-4
0.015-0.12
1-8
Penicillin G
0.25-1
1-4
-
-
Tetracycline
0.25-1
8-32
1-4
8-32
Vancomycin
0.5-2
1-4
-
-
2- Classification of Antibiotics
The most common methods classifies the antibiotics according to
their chemical structure, as generally they will show similar
patterns of activity, effectiveness, toxicity and allergic potential.
1- Penicillins
2- Cephalosporins
3- Tetracyclines
4- Quinolones
5- Sulphonamides
6- Aminoglycosides
7- Imidazoles
8- Glycopeptides
9- Macrolides
10- Linezolid
2- Classification of Antibiotics
(Cont)
1- Penicillins
Natural penicillin: penicillin G and penicillin V potassium
Penicillinaze-resistant penicillins: cloxacillin, methicillin & oxacillin
Aminopenicillins: amoxicillin, ampicillin & bacampicillin
Extended-spectrum penicillin: pipracillin, carbenicillin & mezlocillin
Mechanism: Inhibit bacterial cell wall synthesis
Coverage: gm +/- ve, Streptococcus, Enterococcus &
Staphylococcus species.
Adverse effects: Urticaria, pruritis, nausea, vomiting,
diarrhea and abdominal pain.
2- Classification of Antibiotics
(Cont)
2- Cephalosporins
1st , 2nd , 3rd and 4th generations
Mechanism: They act by inhibiting mucopeptide
synthesis in the bacterial cell wall (similar to penicillins)
which leads to the destruction of the bacteria
Coverage : They are divided into groups according their
antimicrobial activity (will be discussed later)
Side Effects: Similar to penicillins
2- Classification of Antibiotics
(Cont)
3- Tetracyclines
Tetracycline, Minocycline, Doxycycline, Lymecycline
Mechanism: Inhibit bacterial protein synthesis
Coverage : gm –ve, +ve, protozoa, Mycoplasma,
Rickettsia, Chlamydia, syphilis and Lyme disease
Side effects: Strong affinity to Calcium, discoloration of
permanent teeth, pseudomembranous colitis and
gastric upsets.
2- Classification of Antibiotics
(Cont)
4- Quinolones
Norfloxacin, Ciprofloxacin, Ofloxacin, Enoxacin
Mechanism: Inhibit bacterial DNA synthesis
Coverage: First oral antibiotics effective against
gm –ve bacteria and some gm +ve bacteria
Therapeutic uses: Lower Respiratory Tract infections
Bone and joint infections and urinary tract infections
Side Effects: headache, fatigue, nausea, increased liver
Function and integumentary rash
Respiratory Quinolone
The Quinolone class of antimicrobial
agents has generated considerable
interest since its discovery >40 years
ago. Substantial progress has been made
in our understanding of the molecular
mechanisms of the action of Quinolones
against pathogenic bacteria, the
induction of resistance to Quinolones in
these organisms, and the potential of
each Quinolone compound to induce
toxicity in treated patients.
The prolific development of the
Quinolones began in 1962, when
Lesher et al. made the accidental
discovery of Nalidixic Acid as a byproduct of the synthesis of the
Antimalarial Compound Chloroquine.
 Date
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Quinolone
1960–1969 Nalidixic acid
1970–1975 Cinoxacin
1975–1985 Norfloxacin
1985–1990 Ciprofloxacin, Ofloxacin
1990–1995 Temafloxacin, Sparfloxacin
1995–2000 Grepafloxacin, Levofloxacin, Trovafloxacin
2000–2005 Moxifloxacin, possibly Gemifloxacin and
Garenoxacin in 2003 or later
Proposed classification of
Fluoroquinolones
Urinary agents (1960–1985)
 Nalidixic acid
 Cinoxacin
 Enoxacin
 Norfloxacin
activity against common
Enterobacteriaceae, short serum
half-lives, renal elimination
main use in UTI
Gram-negative systemic agents (1985–1995)
 Ciprofloxacin
 Ofloxacin
 Levofloxacin
wide activity against Gram-negatives,including P.
aeruginosa, marginal activity against Grampositives,
longer serum half-lives
widely used against tissue-based and urinary
infections
Broad spectrum systemic agents (1990–
2000)
 Temafloxacin
 Clinafloxacin
 Trovafloxacin
wide activity against Gramnegatives,including P. aeruginosa for
some agents, and Gram-positives, for
some agents
long serum half-lives,
some activity against anaerobes
widely used against a broad range of
tissue based infections
Respiratory agents (1995 onwards)
 Levofloxacin
 Sparfloxacin
 Grepafloxacin
 Moxifloxacin
 Gatifloxacin
 Gemifloxacin
 Garenoxacin
wide activity against Enterobacteriaceae,
active against Gram-positives, especially S.
pneumoniae,
active against atypical bacteria, variable activity
against anaerobes, long serum half-life
main use in respiratory tract infection
2- Classification of Antibiotics
(Cont)
6- Aminoglycosides
Gentamycin, Neomycin, Streptomycin, Tobramycin
and Amikacin
Mechanism: Irreversible binding of 50S ribosomal
protein synthesis
Coverage : Most Broad gm – ve as Pseudomonas spp,
E. coli, Proteus spp, Klebsiella spp and some gm +ve
Side effects: Ototoxicity and nephrotoxicity are the
Most significant side effects
2- Classification of Antibiotics
(Cont)
5- Sulphonamides
Co-trimoxazole, Trimethoprim, sulfadiazine,
sulfamethiazole, sulphamethoxazole and sulfisoxazole
Mechanism: Blocks bacterial cell metabolism by
inhibiting enzymes
Coverage : Most gm + ve and some gm – ve because of resistance
Therapeutic use: Are used only in very specific situations, including
treatment of urinary tract infection, in meningococcal strains, & as
prophylactic for rheumatic fever
Side-effects : may include disruption of the gastrointestinal tract
and hypersensitivity.
2- Classification of Antibiotics
(Cont)
7- Imidazoles
Metronidazole
Mechanism: Inhibit bacterial DNA synthesis
Coverage and effects:
- Anaerobic gm-ve bacilli, including most Bacteroides
species, Fusobacterium and Veillonella; anaerobic gm-ve
cocci including Clostridium, Eubacterium, Peptococcus
and Peptostreptococcus.
-Metallic taste in mouth, nausea, upper abdominal pain or
headaches sometimes occur after usual therapeutic doses
2- Classification of Antibiotics
(Cont)
8- Glycopeptides
Vancomycin, Bacitracin
Mechanism: Inhibit bacterial cell wall synthesis
Coverage and effects:
- Broad gm + ve
- Resistance is very rare
- In most cases does not contribute to renal failure
- Should be given every six hours as it is concentration
Dependant
- POOR LUNG PENETRATION
2- Classification of Antibiotics
(Cont)
9- Macrolides
Erythromycin, Azithromycin, Clarithormycin
Mechanism: Inhibit bacterial protein synthesis.
It reversibly bind 50S ribosome, and block peptide
elongation
Coverage : gm +/- ve, Streptococcus pyogenes,
haemophilus Influenza, Syphilis, Lyme disease,
Gonorrhea, Chlamydia And Mycoplasma
Side effects: Nausea, vomiting, diarrhea and
hepatoxicity
2- Classification of Antibiotics
(Cont)
10- Linezolid
Zyvox
Mechanism: Inhibit bacterial protein synthesis
Coverage : Bacteriostatic for VREF infections, S.
aureus. Bactericidal for Strep pneumo, Strep
pyogenes.
Side effects Potential interaction with adrenergic
and serotonergic agents
3- Cephalosporins Antibiotics
Cephalosporins are semisynthetic derivatives from a
fungus, they are structurally and pharmacologically
related to Penicillins
They are divided into four groups according to their
antimicrobial activity
1st Generation Cephalosporins: include molecules with the greatest
activity against Gram positive bacteria
2nd Generation Cephalosporins: Molecules with the greatest
activity against Gram negative bacteria
3rd Generation Cephalosporins: against Pseudomonas aeruginosa
4th Generation Cephalosporins: against anaerobic bacteria
4- Efficacy of Antibiotics
Evaluating antibacterial efficacy using pharmacokinetics and
pharmacodynamics
Pharmacokinetics (PK)
- serum concentration profile
- penetration to site of infection
Pharmacodynamics (PD)
susceptibility – MIC (potency)
concentration- vs. time-dependent killing
persistent (post-antibiotic) effects (PAE)
Conclusions: antibacterial choice for
empiric use in RTI
Most clinical studies do not show clinical differences
between agents
PK/PD parameters correlate with bacteriological and
clinical outcome in animal models and in humans
PK/PD parameters can be used to select agents with
maximum potential for bacterial eradication
Currently available agents vary significantly in
achieving PK/PD parameters necessary for bacterial
eradication
•
•
•
•
PNEUMONIA,CAP,TREATMENT
 A respiratory quinolone or a cephalosporin
plus either a macrolide or a provides
optimal coverage.
 Take into consideration: side-effect
profiles, resistance potential,
pharmacokinetics, and cost of individual
agents.
ATS/evidence-based
American Thoracic Society
 Outpatient treatment
 Cardiopulmonary disease ±
modifying factors: ß-lactam
(eg, cefuroxime, high-dose
amoxicillin,
amoxicillin/clavulanate) +
(macrolide or doxycycline)
or antipneumococcal
fluoroquinolone.
Hospital treatment

With cardiopulmonary disease
± modifying factors: ß-lactam
(eg, cefotaxime, ceftriaxone,
ampicillin/sulbactam, highdose ampicillin, IV) +
(macrolide or doxycycline, IV
or oral) or
antipneumococcal
fluoroquinolone (IV)
IDSA/evidence-based
Infectious Diseases Society of America
Outpatient treatment


Macrolide, doxycycline, or
antipneumococcal
fluoroquinolone
(alternative: ß-lactam (eg,
amoxycillin/clavulanate,
cefuroxime), but these
agents not active against
atypical pathogens)
For older patients with
comorbidities, the
fluoroquinolone may be
a preferred choice
Hospital treatment

Extended-spectrum
cephalosporin + macrolide
or ß-lactam/ß-lactamase
inhibitor + macrolide or
fluoroquinolone
Canadian Infectious Diseases
Society/Canadian Thoracic
Society/evidence-based
Outpatient
treatment


Without modifying
factors: macrolide or
doxycycline
With modifying factors
and COPD (no recent
antibiotics or oral
steroids): macrolide
(eg, azithromycin or
clarithromycin).
Hospital treatment

Nursing home resident
or suspected S
pneumoniae, Legionella
pneumophila, or C
pneumoniae:
respiratory
fluoroquinolone or ßlactam (eg,
cephalosporin) +
macrolide
Canadian Infectious Diseases
Society/Canadian Thoracic
Society/evidence-based
Outpatient treatment
 Recent antibiotics or oral steroids, H influenzae
or Gram-negative pathogen suspected:
respiratory fluoroquinolone or ß-lactam (eg,
amoxicillin/clavulanate or second generation
cephalosporin) – macrolide cephalosporin +
macrolide
Canadian Infectious Diseases
Society/Canadian Thoracic
Society/evidence-based
Outpatient treatment
 Suspected macroaspiration pneumonia
(anaerobes): ß-lactam (eg,
amoxicillin/clavulanate) ± macrolide or
respiratory fluoroquinolone +
(clindamycin or metronidazole)
Canadian Infectious Diseases
Society/Canadian Thoracic
Society/evidence-based
Outpatient treatment

Suspected home resident with
suspected S pneumoniae, enteric
gram-negative or H influenzae:
respiratory fluoroquinolone or ßlactam (amoxicillin/clavulanate or
second-generation cephalosporin) +
macrolide.
Canadian Infectious Diseases
Society/Canadian Thoracic
Society/evidence-based
Outpatient treatment
 Nursing home resident with
suspected S pneumoniae, enteric
Gram-negative or H influenzae:
respiratory fluoroquinolone or ßlactam (eg, amoxicillin/clavulanate
or second-generation
cephalosporin) + macrolide
British Thoracic Society/evidence-based
Outpatient treatment

Nonsevere disease: ßlactam (eg, amoxicillin) or
macrolide (for patients
with ß-lactam intolerance)
Hospital treatment

Nonsevere disease with
nonclinical factors for
admission: ß-lactam
(amoxicillin) or
macrolideNonsevere
disease: ß-lactam
(amoxicillin, oral, or
ampicillin or
benzylpenicillin, IV) +
macrolide (oral or IV) or
antipneumococcal
fluoroquinolone
(levofloxacin, oral or
IV)
Spanish Respiratory Society/Spanish
Society of Chemotherapy/Questionably
evidence-based
Hospital treatment
Outpatient treatment


Mild disease, typical clinical
presentation: ß-lactam
(high-dose amoxicillin) or
new-generation
fluoroquinolone or macrolide
(controlled prescribing due
to resistance)
Mild disease, atypical
clinical presentation:
macrolide or newgeneration fluoroquinolone

ß-lactam (eg,
amoxicillin/clavulanate,
ceftriaxone, cefotaxime,
IV) ± (macrolide or
quinolone [eg,
ciprofloxacin, oral or
IV]) or new-generation
quinolone (oral or IV)
French Society of Infectious
Diseases/Questionably evidence-based
Outpatient treatment

Ambulatory with mild
disease, no comorbidity:
ß-lactam (eg, high-dose
amoxicillin) or
antipneumococcal
fluoroquinolone (in
patients with ß-lactam
intolerance). For patients
< 40 yr old with an
atypical clinical picture:
macrolide
Hospital treatment

Well-defined CAP: highdose ß-lactam (eg,
amoxicillin/clavulanate or
ceftriaxone, IV)Welldefined CAP: high-dose ßlactam
(amoxicillin/clavulanate or
ceftriaxone, IV)
French Society of Infectious
Diseases/Questionably evidence-based
Outpatient treatment
Hospital treatment
Ambulatory patients with
comorbidity, not
immediately at risk:
 Well-defined CAP: highdose ß-lactam (eg,
amoxicillin/clavulanate
or ceftriaxone, IV)
 Suspected atypical
pathogens: high-dose ßlactam/ß-lactamase
inhibitor + macrolide or
ß-lactam (eg,
amoxicillin) + ofloxacin
or ß-lactam (eg,
ceftriaxone, IV/IM) +
macrolide or new
fluoroquinolone
Ambulatory patients with
comorbidity, not
immediately at risk:
 Well-defined CAP: highdose ß-lactam
(amoxicillin/clavulanate
or ceftriaxone, IV)
 Suspected atypical
pathogens: high-dose ßlactam/ß-lactamase
inhibitor + macrolide or
ß-lactam (eg,
amoxicillin) + ofloxacin
or ß-lactam (eg,
ceftriaxone, IV/IM) +
macrolide or new
fluoroquinolone
German Respiratory Association/Paul
Ehrlich Society for
Chemotherapy/Questionably evidencebased
Outpatient treatment

Younger patients (< 65 yr)
without comorbidity: ß-lactams
(eg, aminopenicillins/ß-lactamase
inhibitors, cephalosporins),
macrolides, antipneumococcal
fluoroquinolones (eg,
levofloxacin); doxycyline only in
special cases.
German Respiratory Association/Paul
Ehrlich Society for
Chemotherapy/Questionably evidencebased
Outpatient treatment
 Elderly patients and/or
patients with
comorbidity: ß-lactams
(eg, aminopenicillins/ßlactamase inhibitors,
cephalosporins [eg,
cefuroxime,
cefotaxime]) or
antipneumococcal
fluoroquinolone
(levofloxacin)
Hospital treatment

Severe pneumonia in elderly
patients with comorbidity: ßlactams (eg,
acylaminopenicillins/ßlactamase inhibitors,
cephalosporins [eg,
cefotaxime, ceftriaxone]) +
(macrolide or
antipneumococcal
fluoroquinolones [eg,
levofloxacin]) or ß-lactam
(carbapenem) + macrolide or
fluoroquinolone (eg,
ciprofloxacin) + clindamycin
Thank You