BORDETELLAE PERTUSSIS

BY

ASLAM MATANIAFACULTY OF MEDICINE

GROUP-3

B. pertussis

B. parapertussis

B. bronchosepticus

B. pertussis

B. parapertussis

B. bronchosepticus

Bordetella species of clinical importance

Bordetella species of clinical importance

BORDETELLA PERTUSSIS

Minute Gram negative coccobacilli

With toluidine blue stain bipolar metachromatic granules can be seenCapsule is present

Culture characterstics

Obligate Aerobe.Fastidious.

Complex medium.

• “Bordet – Gengou –

– Potato Blood glycerol

Agar” that contain pencillin G

• charcoal agar with 10 % blood

• The plates are incubated at 35–37°C for 3–7 days aerobically in a moist environment

• Small faintly staining g- identified.B .pertussis is non motile

Growth Characteristics

• strict aerobe• it is oxidase and catalase positive• but nitrate, citrate, and urea negative

• The results of which are useful for differentiating among the other species of bordetellae

• It does not require X and V factors on subculture

The bvg locusControls expression of virulence factorsEncodes BvgA, BvgS

bvgS responds to environmental signals, and bvgA is a transcriptional activator of the virulence genes

Antigenic Structure• 1.Filamentous haemaggutinin:

• Present on bacillary surface.

• Facilitates adhesion of bacilli to ciliated

columnar epithelium of respiratory tract.

• Promotes secondary infection

• 2. Pertussis toxin:• Pertussis toxin is expressed on the surface,

secreted into the surrounding medium• Posses Biochemical and Biological activity

of producing lymphocytosis producing factor causes Lymphocytosis

• Acts as Histamine sensitizing factor• inhibits G protein coupling that regulates an

adenylate cyclase-mediated conversion of ATP to cyclic AMP

3. Invasive Adenylate cyclase:•Responsible for hemolysis on blood agar.• Activated by bvg system

4. Lethal toxin: Inflammation & Necrosis.5. Tracheal cytotoxin:

•Not regulated by bvg

•Inhibit DNA synthesis in ciliary muscles and

cause paralysis of ciliary esclator

Pathogenesis: • An acute, highly contagious respiratory

pediatric disease. Source is patient in early stage Droplets, contaminated fomites. Incubation period is1 – 2 weeks. Onset is insidious.

• The organism adheres to and multiplies rapidly on the epithelial surface of the trachea and bronchi and interferes with ciliary action.

• The blood is not invaded. • The bacteria liberate the toxins and

substances that irritate surface cells, causing coughing and marked lymphocytosis.

• Later, there may be necrosis of parts of the epithelium

• This causing whooping cough in children

Clinical Findings• 1. “catarrhal stage” -mild coughing and

sneezing and large number of droplets are release and infectious

• 2. paroxysmal” stage – cough develops its explosive character

• This leads to rapid exhaustion and may be associated with vomiting, cyanosis, and convulsions.

• WBC count is high

Diagnostic Laboratory Tests

• A) Specimens-A saline nasal wash is the preferred specimen.

• Cough plate method• B. Direct Fluorescent Antibody Test-The

fluorescent antibody (FA) reagent can be used to examine nasopharyngeal swab specimens

• C. Culture• D. Polymerase Chain Reaction• E. Serology

Treatment

• Erythromycin for 14

– days.

• Cough suppressants.

• Corticosteroids.

• Vaccination is there for

Prevention of disease