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Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
Bordetella mahadi ppt
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Bordetella mahadi ppt

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  • 1. 4/15/20131BordettelaSharq Elneil CollegeSchool of Medical LaboratorySciencesDepartment of MicrobiologyMedical Bacteriology course U.Mahadi Hassan MahmoudBsc, Msc, MIBMS Microbiology
  • 2. 4/15/20132In 1906, Jules Bordet and OctaveGengou (another famous Belgianbacteriologist : 1875-1957) discoveredthe microbe that causes whoopingcough (Bordet-Gengou bacillus orBordetella pertussis).Medically Important spp the genus contains threemedially important speciesB. pertussisB. parapertussisB. bronchoseptica
  • 3. 4/15/20133General propertiesMorphology and culturalcharacteristicsSmall gram negative coccobacilliB. parapertussis and B.bronchoseptica both grow onsheep BA (SBA) in 1-2 daysBordetella pertussis
  • 4. 4/15/20134B. pertussis for initial isolation(The best clinical specimen is anasopharyngeal swab.) theorganism requires special mediawith additional nutrients forgrowth and absorbents to removetoxic substances found incomplex media such as fatty acidsand sulfides.Borget-Gengou media – containsglycerol, potato infusion, albumin(binds fatty acids), and up to 50%defibrinated SRBCsCharcoal agar supplemented with10% horse blood with or withoutcephalexin.May take 3-7 days for growth andcolonies are smooth, raised, andglistening (phase 1 colonies).They are also hemolytic and producetoxin.
  • 5. 4/15/20135Upon extensive subculturing, the coloniesbecome rough (they progress throughphases 2, 3, and finally 4) and can now begrown on SBA.They are now less virulent due to loss ofcapsule, hemolytic activity, and toxinproduction.These changes, however, are reversible.The organisms are strict aerobes andgrow best at 35-370 C. No growth on Mac for B. pertussis,others are variableOxidase test is variableVirulence factors (B. pertussis)Pili for attachmentPertactin, an outer membrane proteinalso acts as an adhesionFilamentous hemagglutinin – is foundon the cell surface of and is alsosecreted. It attaches to cilia by binding to exposedlactose receptors.
  • 6. 4/15/20136Pertussis toxinHas one A subunit (toxic part),plus four different kinds of Bsubunits (involved in binding).Structure of pertussis toxinA subunitB subunits
  • 7. 4/15/20137Activation of pertussis toxinTrachael cytotoxin – is related to theB.pertussis peptidoglycan.When this is incubated with cells inculture, the cells are destroyed, so itmight contribute to the killing andsloughing off of ciliated cells in therespiratory tract.Lipooligosaccharide associated with thesurface of the bacteria and has potentendotoxin activity.
  • 8. 4/15/20138PathogenesisRespiratory droplet exposureEnter respiratory tractAttach to ciliated epithelial cellsEndotoxin inhibits cilia clearanceReplication on outside of respiratorycellsCells eventually die and release toxinThree stages of WhoopingCoughCatarrhal stageFirst stage as bacteria just start to die andrelease toxinMild cold symptoms, coughing, sneezingChild is not that sick so parent thinks theyhave a common cold and don’t isolate fromother childrenThis is the MOST contagious stage sincemany bacteria still alive in respiratory
  • 9. 4/15/20139Paroxysmal stageMaximum cell death and toxin releaseSevere Cough40 – 50 cough spells/day, 20-30 coughs ina row with no chance to breathCoughing causes stomach upset and vomitingMucous build-up in LungsAir blockage can in rare cases lead to deathSecondary pneumonia is biggest threat Caused by other bacterial pathogensH. influenzae, S. aureus, S. pneumoniaeConvalescent stageCoughing spells diminishslowlydecrease in number of spellsand severityPossible CNS complications insome children. Thepathogenesis is not clear
  • 10. 4/15/201310Clinical significanceB. pertussis – causes whooping coughAcquired by inhalation of dropletscontaining the organismThe organism attaches to the ciliated cellsof the respiratory tract.During an incubation period of 1-2 weeks,the organism multiplies and starts to liberateits toxins.Next the catarrhal stage occurs - thepatient has a mild cough and sneezingwhereby large numbers of organisms arespread through the respiratory secretions. This last ~ 2 weeks.Next is the paroxysmal stage thatlasts 4-6 weeks.The patient has rapid, consecutivecoughs with a rapid intake of airbetween the coughs (has a whoopingsound).The ciliary action of the respiratorytract has been compromised, mucoushas accumulated, and the patient istrying to cough up the mucousaccumulations.The coughs are strong enough to breakribs!
  • 11. 4/15/201311Other symptoms due to the activity of thereleased toxins include:Increased peripheral lymphocytes due toa blocking of homing of lymphocytes tothe spleen and lymph nodes.Metabolic alteration such as increasedinsulin release and the resultinghypoglycemiaIncreased capillary permeability andincreased susceptibility to histamine,serotonin, and endotoxin shockFinally there is a convalescent stageduring which symptoms graduallysubside.This can last for months.B. pertussis rarely spreads to other sites,but a lot of damage may occur, such asCNS dysfunction which occurs in ~10 %of the cases and is due to an unknowncause.Secondary infections such as pneumoniaand otitis media are common.
  • 12. 4/15/201312B. pertussis pathogenesisB. parapertussis – causesa mild form of whoopingcoughB. bronchosepticaWidespread in animals whereit causes kennel cough.Occasionally causesrespiratory or woundinfections in humans.
  • 13. 4/15/20131325Specimens: Pernasal swab from Naso pharyngealsecretion.Microscope: B-Pertusis issmall-Non Motile –capsulated G-VeCoccobacilli – Non sporing.Lab Diagnosis:
  • 14. 4/15/20131427Culture: B-Pertusis, when culture oncharcoal cephatexin blood Agar(CCBA) or Bordet – Gengoupencillin. It is strike O2 incubation (35 – 37Co)for 3 days produce mucoid – grayish– white colonies with shiny surfaceand high convex shape (bisectedpearl) or (mercury drop)appearance28Biochemical: we can differential betweenspecies of B-Pertusis by manytest e.g (Motility – Urea –Oxidase – catalase – pigment– Producing – Growth onblood agar.
  • 15. 4/15/20131529B.Pertusis: Non Motile – catalase +ve –oxidase +ve urea –ve.  can not grow on blood agar. not produce pigment. It differ from Haemophilusinfluenzae in its continuedviability at low temp. (00 – 10C0).30Serology:B.Pertusis has three major Ags(Serotype)Type 1,2/type 1,2,3/ type 1,3B. Pertusis can be detected by:Slide agglutinating.Immunofluorescentmicroscopes.Complement Fixation.ELISA.
  • 16. 4/15/20131631B. Parapertusis:Oxidase –ve - grow rapidy on bloodAgarUrea +ve - Produce brown Pigment inN. AgarNon Motile - it can grow on blood AgarB. Bronchiseptica:Motile - it can grow in blood Agar.Urea +ve - oxidase +veBordetella bronchisepticaLeifson flagella stain
  • 17. 4/15/20131733Antimicrobial Sensitivity:Erythromycin –only effective inearly stages of the disease beforethe toxin(s) have been released chloramphenicol.Tetracycline.Vaccination Vaccination (DPT – diphtheria, pertussis,tetanus) CNS toxicity was major stumbling block Blamed on whole cell pertussis prep in the DPT vaccine Many parents avoided vaccine and apathy led to widespread outbreaks New genetic engineered noncellular preparationshave helped to alleviate fear in parents However, only effective in 80-85% of children Therefore, we still need to give antibiotics tocontacts
  • 18. 4/15/201318Any Questions?

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