4/15/20131BordettelaSharq Elneil CollegeSchool of Medical LaboratorySciencesDepartment of MicrobiologyMedical Bacteriolo...
4/15/20132In 1906, Jules Bordet and OctaveGengou (another famous Belgianbacteriologist : 1875-1957) discoveredthe microb...
4/15/20133General propertiesMorphology and culturalcharacteristicsSmall gram negative coccobacilliB. parapertussis an...
4/15/20134B. pertussis for initial isolation(The best clinical specimen is anasopharyngeal swab.) theorganism requires ...
4/15/20135Upon extensive subculturing, the coloniesbecome rough (they progress throughphases 2, 3, and finally 4) and c...
4/15/20136Pertussis toxinHas one A subunit (toxic part),plus four different kinds of Bsubunits (involved in binding).St...
4/15/20137Activation of pertussis toxinTrachael cytotoxin – is related to theB.pertussis peptidoglycan.When this is in...
4/15/20138PathogenesisRespiratory droplet exposureEnter respiratory tractAttach to ciliated epithelial cellsEndotoxi...
4/15/20139Paroxysmal stageMaximum cell death and toxin releaseSevere Cough40 – 50 cough spells/day, 20-30 coughs ina ...
4/15/201310Clinical significanceB. pertussis – causes whooping coughAcquired by inhalation of dropletscontaining the ...
4/15/201311Other symptoms due to the activity of thereleased toxins include:Increased peripheral lymphocytes due toa b...
4/15/201312B. pertussis pathogenesisB. parapertussis – causesa mild form of whoopingcoughB. bronchosepticaWidespread ...
4/15/20131325Specimens: Pernasal swab from Naso pharyngealsecretion.Microscope: B-Pertusis issmall-Non Motile –capsul...
4/15/20131427Culture: B-Pertusis, when culture oncharcoal cephatexin blood Agar(CCBA) or Bordet – Gengoupencillin. It...
4/15/20131529B.Pertusis: Non Motile – catalase +ve –oxidase +ve urea –ve.  can not grow on blood agar. not produce ...
4/15/20131631B. Parapertusis:Oxidase –ve - grow rapidy on bloodAgarUrea +ve - Produce brown Pigment inN. AgarNon Moti...
4/15/20131733Antimicrobial Sensitivity:Erythromycin –only effective inearly stages of the disease beforethe toxin(s) ha...
4/15/201318Any Questions?
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Bordetella mahadi ppt

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Bordetella mahadi ppt

  1. 1. 4/15/20131BordettelaSharq Elneil CollegeSchool of Medical LaboratorySciencesDepartment of MicrobiologyMedical Bacteriology course U.Mahadi Hassan MahmoudBsc, Msc, MIBMS Microbiology
  2. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 18. 4/15/201318Any Questions?

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