BACTERIAL INFECTION ON

RESPIRATION TRACT

Ike Irmawati P.A, MSi Med

Mikrobiologi FK Yarsi
 Infections of the Respiratory tract
• Most common entry point for
infections
• Upper respiratory tract
→nose, nasal cavity, sinuses,
mouth, throat (pharynx)
• Lower respiratory tract
→Trachea, bronchi,
bronchioles, & alveoli in
the lungs 2
 Upper & Lower Respiratory Tract
Infection

• Type microorganism:
- restricted to surface epithelium
- spread through body

• Two groups of microbes can distinguished :

“professional” & “secondary” invaders

3
 Protective Mechanisms

Normal flora : Commensal organisms

• Limited to the upper tract
• Mostly Gram positive or anaeorbic
• Microbial antagonist (competition)

4
 Protective Mechanisms
Clearance of particles & organisms from the
respiratory tract

For the upper respiratory tract :

❖ The mucociliary system →
in the nasopharynx

❖ The flushing action of

saliva → in the oropharynk

5
 Bacterial Infections
❖Specific areas of the upper respiratory
system can become infected → pharyngitis,
laryngitis, tonsillitis, sinusitis, & epiglotitis.

❖May be caused by several

bacteria and viruses, often in combination.
Streptococcal infection on
Respiratory Tract
 Streptococci
• Characters of Streptococci
– Gram positive cocci
– Φ 1µm
– Chains or pairs
– Usually capsulated
– Non motile
– Non spore forming
– Facultative anaerobes
– Require CO2
– Catalase negative
– Of these organism considered in this chapter:
S.pyogenes, S.pneumoniae, S .viridans
Classification of Streptococci

• Streptococci can be classified according to:

– Oxygen requirements
• Anaerobic (Peptostreptococcus)
• Aerobic or facultative anaerobic (Streptococcus)

– Serology (Lanciefield Classification)

– Hemolysis on Blood Agar

 Serology: Lanciefield Classification
Streptococci

Lanciefield classification

Group A Group B Group C Group D Other groups

S. pyogenes S. agalactiae S. equisimitis Enterococcus (E-U)

• Streptococci classified into many groups from A-K & H-V

• One or more species per group
• Classification based on C- carbohydrate antigen of cell wall
– Groupable streptococci
• A, B and D (more frequent)
• C, G and F (Less frequent)
– Non-groupable streptococci
• S. pneumoniae (pneumonia)
• viridans streptococci
– e.g. S. mutans
 Classification of Streptococci
Based on Hemolysis on Blood Agar

Hemolysis on BA
– -hemolysis
Partial hemolysis
Green discoloration around the colonies
non-groupable streptococci (S. pneumoniae & S.
viridans)
– -hemolysis
Complete hemolysis
Clear zone of hemolysis around the colonies
Group A & B (S. pyogenes & S. agalactiae)
– -hemolysis
No lysis
Group D (Enterococcus spp)
 Hemolysis on Blood agar

-hemolysis

-hemolysis

-hemolysis
Hemolysis patterns on blood agar

13
https://www.cdc.gov/streplab/groupa-strep/index.html
Figure . Cell surface structure of Streptococcus pyogenes
and secreted products involved in virulence.
S.pyogenes ❖Protein F & lipoteichoic acid : mediates Pharyngitis,pneumonia,
epithelial cell attachment & adhesion Rheumatic fever

❖M protein as antiphagositic
→The M protein has many antigenic
varieties and thus, different strain of
S.pyogenes cause repeat infections

❖Hyaluronic acid capsule, which acts to

camouflage the bacteria

❖Produce enzyme and hemolysins

→contribute tissue invasion and
destructions,i.e: streptolysin O,S,
streptokinase, DNAse B & hyaluronidase

❖Streptococcal Pyrogenic exotoxins that scarlet

stimulate macrophages and helper T cells fever,Streptococcal toxic
to release cytokines shock syndrome
 Pathogenesis S.pyogenes

Pathogenesis of group A streptococci

❖ Adherence to the epithelial cells;
>10 adhesion molecules
❖ invasion into the epithelial cells;
mediated by M protein and F protein
important for persistent infections and invasion into deep tissues
❖ avoiding opsonization and phagocytosis;
M protein, M-like proteins, and C5a peptidase
❖ producing enzymes and toxins
 Complication that result from S. pyogenes
infection (poststreptococcal disease)

– Rheumatic fever
▪ most commonly preceded by infection of the respiratory tract.
▪ Life threatening inflammatory disease that leads to damage of heart
valves muscle
▪ Inflammation of heart (pancarditis), joints, blood vessels, and
subcutaneous tissue. Results from cross reactivity of anti-M protein Ab
and the human heart tissue. This disease can be reactivated by recurrent
streptococcal infections

– Glomerulonephritis
Deposition of antibody-streptococcal Ag complexes in kidneys results in
damagee to glomeruli
https://www.cdc.gov/streplab/pneumococcus/index.html
 S. pneumoniae
Morphology and Physiology

▪ Gram-positive lancet-shaped diplococci

▪ alpha-hemolytic
▪ Growth is enhanced by 5-10% CO2
▪ These organism may harmlessly inhabit the upper
respiratory tract

▪ Pneumococcal infections → spread from person to person

via droplets/aerosols
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3685878/
 S. pneumoniae
Pathogenesis and Immunity
Pneumococci produce disease →ability to multiply in the tissues
(invasiveness).
40-70% of humans are at sometimes carrier of virulent pneumococci.
→ host defense mechanisms: ciliated cells of respiratory tract and spleen
The normal respiratory tract has natural resistance to the pneumococcus.
Loss of natural resistance may be due to:
1. Abnormalities of the respiratory tract (e.g. viral RT infections)
2. Alcohol or drug intoxication; abnormal circulatory dynamics.
3. Patients undergone renal transplant; chronic renal diseases.
4. Malnutrition, general debility, sickle cell anemia, hyposplenism
or splenectomy, nephrosis or complement deficiency.
5. Young children and the elderly.
Pneumonia: Common Invasion Strategy
• As bacteria enter the lower respiratory
tract, the initiation of pneumonia requires
escape from mucous defenses and
bacterial migration into the alveolus.

• Adherence of bacteria to the alveolar

epithelium → replication → initiation of
host damage responses lead to the classic
evolution of lobar pneumonia.
• The interaction of secreted products and cell
surface-anchored bacterial components with the
alveolar epithelium and innate immune defenses
drives this process.
• The pore-forming toxin pneumolysin and
hydrogen peroxide released in copious amounts
by the bacteria disrupt the alveolar epithelium
and edema fluid accumulates in the alveolar
space
 Clinical diseases

Sudden onset with fever, chills and sharp

chest pain. Bloody, rusty sputum. Empyema is
a rare but significant complication.

Complications caused by spreading of

pneumococci to other organs: sinusitis,
meningitis, endocarditis, septic arthritis,
middle ear infection.
 Prevention
• The widespread use of pneumococcal
conjugate vaccines (PCVs) has reduced
invasive disease of sero-types with the
capsular polysaccharide (CPS) types that
are included in the vaccine
 Streptococcus viridans
• Alpha hemolytic or nonhemolytic
• Non-groupable
• S.viridans colonizes in the oropharynx, GI tract, urinary tract, and
rareli on skin surface.
• Generally considered to be of low virulence
• Production of extracellular complex polysacarides (such as glucans
& dextrans) enhance attachment to host cell surface,
such as cardiac endothelial cells & tooth surface → dental caries
• Disease:
❖ Sub acut bacterial endocarditis (particularly patients with previosly
damaged heart valves)
❖ Intra abdominal infection
❖ caries dentis
 Diagnosis of streptococcal
disease

Clinical diagnosis
Depend on signs &
symtoms Antigen detection
Streptococcal test
disease
Antibody detection
Laboratory methode
diagnosis
Culture

Identification
 Laboratory diagnosis S. pyogenes
• Antigen detection methode:
✓ Antigen detection tests: commercial kits for rapid detection of
group A streptococcal antigen from throat swabs, using latex
agglutination,coagglutination & Elisa tecnology.
→Latex agglutination able to detect Capsuler pollysacharide
antigen of pneumococcus
• Serological test/antibody detection methode:
✓ ASO titration for respiratory infections.
✓ Anti-DNase B and antihyaluronidase titration for skin infections.
✓ Antistreptokinase; anti-M type-specific antibodies.
• Culture: Specimens are cultured on blood agar plates in air.
• Identification
 Laboratory diagnosis S. pneumoniae

Examination of sputum
Stained smears of sputum: a rapid diagnosis.
Quellung test with multivalent anticapsular antibodies.
Culture
Specimen: sputum, aspirates from sinus or middle ear, CSF.
cultured on blood agar plate in 5-10% CO2.
Identification: bile solubility, optochin sensitivity, etc. for
differentiation from other a-hemolytic streptococci.
Additional biochemical, serologic or molecular diagnostic tests
for a definitive identification.
Antigen detection: detect capsular polysaccharide in body
fluids.
 Outline of differentiation between Gram-
Positive cocci

18.05.09 36
Differentiation between -hemolytic Streptococci

Hemolysis Bacitracin CAMP test

sensitivity
S. pyogenes  Susceptible Negative

S. agalactiae  Resistant Positive

Differentiation between -hemolytic Streptococci

Hemolysis Optochin Bile Inulin

sensitivity solubility Fermentation
S. pneumoniae  Sensitive (≥ Soluble ferment
14 mm)

S. viridans  Resistant Insoluble Not Ferment

(≤13 mm)
 Prevention and Control
Most streptococci are normal flora of the human body
Source of S. pyogenes and S. agalactiae is a person harboring these
organisms (carrier).
Control:
1. Prompt eradication of streptococci from early infections.
2. Prophylactic antibiotic treatment for rheumatic fever
patients.
3. Eradication of S. pyogenes from carriers.
4. Dust control, ventilation, air filtration, UV irradiation and
aerosol mists are of doubtful efficacy.
5. Intrapartum penicillin to mother at risk of giving birth to an
infant with invasive group B disease.
 Reference
• Baley & Scott’s. 2007. Diagnostic Microbiology.
Twelfth edition. Mosby Elseiver.
• Goering RV, Dockrell, Zuckerman M, Chiodini PL.
2019. Mims Medical Microbiology and Immunology.
Sixth Edition. Elsevier. China. Page 189-213.
• Todar online textbook