Bordetella pertussis is a small, Gram-negative coccobacillus bacterium that causes whooping cough (pertussis). It produces several toxins, including pertussis toxin and adenylate cyclase toxin, which increase intracellular cAMP levels and disrupt cell signaling. Pertussis toxin also inhibits the immune response. B. pertussis colonizes the respiratory tract and causes a severe cough that often ends in a "whooping" sound. Whooping cough is highly contagious and prevents by vaccination.

1. Bordetella pertussis
Made by :
khloud A.elbaset
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2. Pertussis toxin
 Classification :
 Domain: Prokaryotes
Kingdom:Bacteria
Class:Betaproteobacteria
Order:Burkholderiaceae
Genus: Bordetella
Species: B. pertussis

3.  Nomenclature:
Bordetella pertussis (B. Pertussis) is a small,
coccobacillus. Coccobacillus are rod-
shaped bacteria. Cocco comes from "cocci"
meaning spherical shaped and bacillus
comes from "bacilli" meaning elongated. B.
pertussis, like most pathogenic bacteria, is
Gram-negative.
It is an encapsulated immotile aerobe that
does not make spores.
Protein exotoxin forming bacteria

4. Types:
Eight species in the Bordetella genus:
Three species in this genus are known to be
pathogenic to humans. B. pertussis and B.
parapertussis are very similar species.
B. bronchiseptica causes respiratory disease
in various mammals and occasionally in
humans.
The human pathology of the remaining five
species is relatively unknown. B. avium and
B. hinzii, are known to cause respiratory
disease.

5. Areas of infection :
- Mouth
- Nose
- Throat.
Risk groups:
- Unvaccinated children (especially infants)
- Adolescents whose immunity has waned.
- Adults whose immunity has waned.

6. Transmission;
- Direct contact with droplets from coughing or
sneezing by an infected person
- Can continue to transmit the bacteria three
weeks after coughing spells have stopped
- Can be carried by individuals who are
immune and transmitted to those who are
not.
NOTE:
It cannot survive in the environment; it
must reside in a host either in small groups or
singly.
It grows at an optimal temperature of 35-

7. Cell and toxin Structure:
Its cell structure : consists of an outer
membrane, an inner membrane and a
periplasmic space with a thin peptidoglycan
layer in between. On its outer membrane,
Bordetella pertussis has unusual
lipoopolysaccharides (LPS), endotoxins.
Toxin structure :
Pertussis toxin is a 105 kDa protein composed
of six subunits: S1, S2, S3, (2)S4, and S5.
And adenylate cyclase toxin, filamentous
hemagglutinin,

10.  Pathology: Humans are its only host.
Pertussis is a severe, highly contagious
respiratory disease characterized by
outbursts of coughing followed by “whooping”
sound during breathing in. Often vomiting
takes place with discharge of sticky mucus.
Symptoms :
The symptoms of pertussis are similar to a
common cold: runny nose, sneezing, mild
cough, and low-grade fever.

11. Mechanism of pathogenesis:
The disease pertussis has two stages:
1.Colonization(the attachment to and growth
on ciliated cells)
2.Toxemic (organism produces a number of
exotoxins which contribute to these
symptoms.)

12. 1.The two most important colonization
factors are the filamentous hemagglutinin
(FHA) and the pertussis toxin (PTx).
Filamentous hemagglutinin is a large (220
kDa) protein that forms filamentous
structures on the cell surface. FHA binds
to galactose residues on a sulfated
glycolipid .

13. the pertussis toxin (PTx), is also involved in
adherence to the tracheal epithelium.
Pertussis toxin is a 105 kDa protein
composed of six subunits: S1, S2, S3,
(2)S4, and S5.. Some components of the
cell-bound toxin (S2 and S3) function as
adhesins, and appear to bind the bacteria
to host cells.
S2 binds specifically to a glycolipid called
lactosylceramide, which is found primarily
on the ciliated epithelial cells. S3 binds to
a glycoprotein found mainly on phagocytic
cells.

14. Toxicity :
Mainly through elevating the cAMP level , result
in disrupting cell function.
Pertussis toxin:
The A subunit gains enzymatic activity and
transfers the ADP ribosyl moiety of NAD to the
membrane-bound regulatory protein Gi that
normally inhibits the eukaryotic adenylate
cyclase. The Gi protein is inactivated and
cannot perform its normal function to inhibit
adenylate cyclase.
The intracellular levels of cAMP increase.

17. Increased intracellular cAMP affects normal
biological signaling. The toxin causes several
systemic effects, among which is an
increased release of insulin, causing
hypoglycemia.
The role of the toxin in whooping cough is not
known.
It inhibits the early recruitment of neutrophils
and macrophages, and interferes with the
early chemokine production and the inhibition
of the neutrophil chemotaxis.

18. Adenylate cyclase toxin:
This exotoxin penetrates the host cells, is
activated by calmodulin and catalyzes the
conversion of ATP to cAMP. Like
pertussigen, it also inhibits phagocyte and
NK cell functions.
the cAMP increase caused by this toxin is
short-lived.

19. Tracheal cytotoxin:
This is a peptidoglycan-like molecule
(monomer) which binds to ciliated epithelial
cells, thus interfering with ciliary movement.
In higher concentrations, it causes ciliated
epithelial cell extrusion and destruction. The
destruction of these cells contributes to
pertussis.

20. Dermonecrotic (heat-labile) toxin
Dermonecrotic toxin is a very strong
vaso-constrictor and causes ischemia
and extravasation of leukocytes and,
in association with tracheal cytotoxin,
causes necrosis of the tracheal tissue

22. Diagnosis:
Symptoms are characteristic. Laboratory
diagnosis is made by obtaining a
nasopharyngeal aspirate and primary culture
on Bordet-Gengou medium (potato-glycerol-
blood agar).
Prevention and treatment:
A killed whole bacterial vaccine is normally
administered as DPT combination.
Erythromycin is the current drug of choice.