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  1. 1. Bordetella pertussis Made by : khloud A.elbaset khloud511@ya
  2. 2. Pertussis toxin Classification : Domain: Prokaryotes Kingdom:Bacteria Class:Betaproteobacteria Order:Burkholderiaceae Genus: Bordetella Species: B. pertussis
  3. 3.  Nomenclature:Bordetella pertussis (B. Pertussis) is a small,coccobacillus. Coccobacillus are rod-shaped bacteria. Cocco comes from "cocci"meaning spherical shaped and bacilluscomes from "bacilli" meaning elongated. B.pertussis, like most pathogenic bacteria, isGram-negative.It is an encapsulated immotile aerobe thatdoes not make spores.Protein exotoxin forming bacteria
  4. 4. Types:Eight species in the Bordetella genus:Three species in this genus are known to bepathogenic to humans. B. pertussis and B.parapertussis are very similar species. B. bronchiseptica causes respiratory diseasein various mammals and occasionally inhumans. The human pathology of the remaining fivespecies is relatively unknown. B. avium andB. hinzii, are known to cause respiratorydisease.
  5. 5. Areas of infection : - Mouth - Nose - Throat.Risk groups:- Unvaccinated children (especially infants)- Adolescents whose immunity has waned.- Adults whose immunity has waned.
  6. 6. Transmission;- Direct contact with droplets from coughing orsneezing by an infected person- Can continue to transmit the bacteria threeweeks after coughing spells have stopped- Can be carried by individuals who areimmune and transmitted to those who arenot.NOTE: It cannot survive in the environment; itmust reside in a host either in small groups orsingly. It grows at an optimal temperature of 35-
  7. 7. Cell and toxin Structure:Its cell structure : consists of an outermembrane, an inner membrane and aperiplasmic space with a thin peptidoglycanlayer in between. On its outer membrane,Bordetella pertussis has unusuallipoopolysaccharides (LPS), endotoxins.Toxin structure :Pertussis toxin is a 105 kDa protein composedof six subunits: S1, S2, S3, (2)S4, and S5.And adenylate cyclase toxin, filamentoushemagglutinin,
  8. 8.  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 acommon cold: runny nose, sneezing, mildcough, and low-grade fever.
  9. 9. Mechanism of pathogenesis:The disease pertussis has two stages:1.Colonization(the attachment to and growthon ciliated cells)2.Toxemic (organism produces a number ofexotoxins which contribute to thesesymptoms.)
  10. 10. 1.The two most important colonizationfactors are the filamentous hemagglutinin(FHA) and the pertussis toxin (PTx). Filamentous hemagglutinin is a large (220kDa) protein that forms filamentousstructures on the cell surface. FHA bindsto galactose residues on a sulfatedglycolipid .
  11. 11. the pertussis toxin (PTx), is also involved inadherence to the tracheal epithelium.Pertussis toxin is a 105 kDa proteincomposed of six subunits: S1, S2, S3,(2)S4, and S5.. Some components of thecell-bound toxin (S2 and S3) function asadhesins, and appear to bind the bacteriato host cells.S2 binds specifically to a glycolipid calledlactosylceramide, which is found primarilyon the ciliated epithelial cells. S3 binds toa glycoprotein found mainly on phagocyticcells.
  12. 12. Toxicity :Mainly through elevating the cAMP level , resultin disrupting cell function.Pertussis toxin:The A subunit gains enzymatic activity andtransfers the ADP ribosyl moiety of NAD to themembrane-bound regulatory protein Gi thatnormally inhibits the eukaryotic adenylatecyclase. The Gi protein is inactivated andcannot perform its normal function to inhibitadenylate cyclase.The intracellular levels of cAMP increase.
  13. 13. Increased intracellular cAMP affects normalbiological signaling. The toxin causes severalsystemic effects, among which is anincreased release of insulin, causinghypoglycemia.The role of the toxin in whooping cough is notknown.It inhibits the early recruitment of neutrophilsand macrophages, and interferes with theearly chemokine production and the inhibitionof the neutrophil chemotaxis.
  14. 14. Adenylate cyclase toxin:This exotoxin penetrates the host cells, isactivated by calmodulin and catalyzes theconversion of ATP to cAMP. Likepertussigen, it also inhibits phagocyte andNK cell functions.the cAMP increase caused by this toxin isshort-lived.
  15. 15. Tracheal cytotoxin:This is a peptidoglycan-like molecule(monomer) which binds to ciliated epithelialcells, thus interfering with ciliary movement.In higher concentrations, it causes ciliatedepithelial cell extrusion and destruction. Thedestruction of these cells contributes topertussis.
  16. 16. Dermonecrotic (heat-labile) toxinDermonecrotic toxin is a very strongvaso-constrictor and causes ischemiaand extravasation of leukocytes and,in association with tracheal cytotoxin,causes necrosis of the tracheal tissue
  17. 17. Diagnosis:Symptoms are characteristic. Laboratorydiagnosis is made by obtaining anasopharyngeal aspirate and primary cultureon Bordet-Gengou medium (potato-glycerol-blood agar).Prevention and treatment:A killed whole bacterial vaccine is normallyadministered as DPT combination.Erythromycin is the current drug of choice.