Genus: Bordetella
There are 3 important species of Bordetella:
B. pertussis is the causative agent of a highly infectious disease which is called pertussis
(whooping cough).
B. parapertussis can cause a disease similar to whooping cough, but ofter subclinical of
mild.
B. bronchisepica is important in canines, infrequently is responsible for chronuic RTI in
human
Bordetella pertussis:
With toluidine blue stain, bipolar metachromatic granules can be demonstrated.
A capsule is present which can be stained by safranin O stain.
Culture:
Because it is a fastidious m.o., it requires enriched media for its cultivation which are:
1. For primary isolation; Bordet-Gengou (potato-blood-glycerol agar). The medium contains
20-30 % sheep blood cells and penicillin -G or methicillin to make more selective.
2. Buffered charcoal yeast extract agar (BCYE)
3. Blood Charcoal Agar (BCA) ( inhibits respiratory flora).
4. Lowe-Regan agar which is similar to BCA, but contains a half strength of charcoal.
5. Charcoal and cephalexin.
Cultural requirments:
This m.o. Is a strict aerobe, best grow at 35-37 C .
Growth (cultural) characteristics:
The colonies have iridescence and surrounded by narrow zones of haemolysis.
Biochemically;
the m.o. can ferment glucose with acid, but no gas production. Also, these m.o. do not
require neither X nor V factors.
Variations of B. pertussis:
This m.o. has 4 phases:
1. Phase - I :The m.o. are capsulated, haemolytic, pertussis toxin-producing
2. Phase II & III : Are intermediate phases between I & IV.
3. Phase IV: Opposit to phase I (i.e., all charactrestics are opposit).
The shift from phase I to IV is related phenotypic modulation (enviromental).
Antigenic structure and biologically active substances:
1. Capsule (K-Ag) which is mainly present in phase I and is a virulent factor.
2. Pertussis Toxin which is a major virulent factor and has the following effects:
A. It gives a prolonged immunity because it is an immunogenic factor.
B. It causes anaphylactic –like reaction due to histamine sensitization.
C. It is responsible for the characteristic paroxysmal cough that is followed by deep
inspiration .
D. It causes hypoglycaemia (enhances insulin secretion).
E. It reduces the migratory and phagocytic activity of macrophages and neutrophils.
F. It can increase the release of both B and T cells from the bone marrow, and lymphiod
tissues , However, they remain in the blood causing an absolute lymphocytosis
3. Filamentous haemagglutinin that mediates adhesion to ciliated epithelial cells.
4. Leucocytes promoting factor that promote lymphocytosis.
5. Lethal toxin that causes local necrosis.
6. Tracheal cytotoxin which affects the activity of epith. and cilia of respiratory tract.
7. Adenylate cyclase complex that can impair phagocytosis.
Pathogenesis and pathology:
A. Transmission of the m.o. occurs via the respiratory tract from patients and carriers.
B. There are two stages in the pathogenesis of the m.o.:
1. Colonization Stage:
1. During this stage
2. the m.o. adher to the epithelial cells of
the trachea and bronchi ,
3. multiply locally and interfer with the
ciliary functions.
4. The m.o. do not invade to the blood.
2. Toxaemic Stage:
The m.o. start to liberate the toxins and
biologically active substances .
Clinical picture of pertussis:
The incubation peroid of pertussis is about 2 weeks.
There are two stages in pertussis that are parallel to the two stages of the pathogenicity
stages of B. pertussis:
1. Catarrhal stage:
a) This stage coincides with the colonization stage of the causative m.o.
b) about 10 days
c) the patient suffers from flu-like illness with sneezing and mild cough.
d) During this stage the patient is very infectious because spraying huge numbers of m.o.
through the respiratory tract.
2. Paroxysmal stage:
1. This stages coincides with toxaemic phase of the pathogenicity of the m.o.
2. the patients suffer from the characteristic cough (whooping) which may be associated
with vomiting .
3. The patients may have cyanosis and convulsion.
4. Secondary infections may also occur.
5. Obstruction of the bronchioles with mucous blugs may lead to the collapse of lung
tissues (ateletasis).
6. during this stage the toxic effects of pertussis toxin are manifested as absolute
lymphocytosis or hypoglycaemia.
7. Fatal encephalitis may occur in depilitated
Diagnostic laboratory tests:
1. Specimens
2. Direct fluorescent antibody
(FA) test to examine
nasopharyngeal swab
specimens with sensitivity of
50%.
3. Cultures: CAN BE
IDENTIFIED BY agglutination
test with specific antisera.
4. PCR It is the most sensitive
method for the diagnosis of
pertussis .
5. Serology: Serological tests
are of limited value because
specifIC antibodies rise does
not occur until the third week
of illness.
Immunity:
1. Recovery from pertussis
or adequate vaccination
is followed by immunity.
2. Second infections may
occur, but are mild
,reinfection occuring
years later in adults may
be severe.
3. The first defence against
infection is the antibody
that prevents attachment
of B. pertussis .
Treatment:
1. Antimicrobial drugs:
a) erythromycin promotes
the elemination of the
m.o. and may have
prophylactic value.
b) Treatment during the
paroxysmal stage rarely
alters the clinical course.
2. Oxygen inhalation and
sedation may prevent anoxic
damage to the brain.
Prevention:
1. Vaccination (part of DTP)
2. New acellular vaccine of 5 antigens is also available.
3. Prophylactic erythromycin for 5 days is given for unimmunized infants or heavly exposed
adults.