BORDETELLABordetella organisms are small, gram-negative coccobacillicapsulated ,metachromatic granules in bipolarstaining,which are strict aerobes.Most important human pathogen in this genus is B.pertussis, the organism which causes whooping cough.Bordetella occurs worldwide and is strictly a humanpathogen. The disease is spread via the respiratory routeand the organism is non-invasive.
Two other species of Bordetella are also clinicallyrelevant. B. parapertussis can cause a mild pharyngitis.Bordetella bronchiseptica is usually an animalpathogen (i. e. kennel cough in dogs). It is rarely a cause of human disease, but can causebroncho-pulmonary symptoms in severelyimmunosuppressed individuals.
Bordetella pertussisMorphologyIt is an extremely small; slow growing, strictly aerobic,Gram negative, capsulated, non-motile cocobacillus(short rod). Compared to other Bordetella species, B. pertussis doesnot grow on common laboratory media. Selected mediainclude Bordet-Gengou medium.
PathogenesisIn addition to the attachment and growth onciliated cells, the organism produces anumber of exotoxins which contribute to thesymptoms.
Colonization is mediated by filamentoushemagglutinin, and the pertussis toxin.1. Filamentous hemagglutinins: are not exotoxins. They are filament associated lipo-oligo-saccharides which are involved in the binding of the organism to ciliated epithelial cells.
2. Pertussis toxin (pertussigen): It is an AB-typeexotoxins(A-enzymatic active moiety,B-bindingcomponent) with 6 subunits (A: subunit 1; B:subunit 2-5 complex) which is the major cause ofthe abnormal cough. The toxin is both secreted into the extracellularfluid and cell bound. Subunits S2 and S3 functionas adhesins, and bind the bacteria to host cells. Systemically it causes lymphocytosis, enhancedinsulin secretions, increased IgE synthesis,increased histamine production and endotoxinsensitivity.
Pertussis is primarily a toxin mediated disease.Localized damage and systemic symptoms arecaused by the production of various toxins.3.Adenylate cyclase toxin: exotoxin acts locallyto inhibit phagocyte and NK cell functions. It alsohelps the organism initiate infection.4. Dermonecrotic (heat-labile) toxin: causesinflammation and local necrosis adjacent to siteswhere B. pertussis is located. It is also a very strong vasoconstrictor and causesextravasation of leukocytes. In association withtracheal cytotoxin, it causes necrosis of the trachealtissue.
5. Tracheal cytotoxin: a peptidoglycan-likemolecule which binds to ciliated epithelialcells, preventing the ciliated cells frombeating (ciliostasis). The destruction of these cells contributes tothe symptoms of pertussis. The extrusion ofciliated cells leads to mucous plugs resultingin pulmonary obstructions and atelectasis.
6. Lipopolysaccharide (LPS): Like LPS (endotoxin) ofother Gram-negative bacteria, it is pyrogenic, mitogenic,and can activate and induce tumor necrosis factorproduction in macrophages.It also causes the induction of a number of cytokines andother inflammatory products ( TNF, IL1, IL6,prostaglandins, etc.) and generates complement-activationproducts.
7.Pertactin-is an outer membrane proteinAg in all virulent strains.Ab to pertactin can seen in infected andimmunized children.Included in acellular vaccine
Epidemiology:Most of the patients with whooping coughare less than a year old, although olderchildren may also get the disease and theincidence among adults has decreaseddisproportionately in recent years.
PathogenicityThe organism, contained in aerosol droplets, gains access viainhalation and colonizes the cilia of the mammalian respiratoryepitheliumThe incubation period is 7 to 10 days -3 stages-Catarrhal,Paroxymal,Convalescent1. Mild symptoms of rhinitis, mild Dry irritatng cough and sneezingoccur (catarrhal stage) which last 1-2 weeks. During the catarrhal stage, the propagation of the organismincreasingly compromises ciliary function resulting in the increasedfrequency and intensity of symptoms.At this stage the organism can be recovered in large numbers frompharyngeal cultures, and the severity and duration of the disease canbe reduced by antimicrobial treatment. The patient is highly
After 2 weeks the disease progresses to the paroxysmalstage, characterized by gradually increasing prolonged andparoxysmal coughing that often ends in a characteristicinspiratory gasp (whoop).long inrush of air in to emptylungs The cough recurs at variable intervals; often every few minutes andinterferes with oral intake.The swallowed mucus may inducevomiting, resulting in severe dehydration and weight loss. Hypoxia during prolonged attacks may lead to seizure, hypoxicencephalopathy or coma. During the paroxysmal stage, B. pertussis can rarely berecovered, and antimicrobial agents have no effect on the progress ofthe disease.This stage of the disease is mediated by a variety of soluble toxins
The cough episodes gradually decreaseafter 2 to 4 weeks and the patientrecovery can take 3-16 weeks(convalescent stage).
ComplicationsVIOLENT COUGH(Subconjuctival hemorrhage)Respiratory(broncho pneumonia)Neurological(epilepsy,paralysis,blindness,deafness)LIMITED IN RESPIRATORY INFECTION NO BLOOD STREAMINFECTION
Lab Diagnosis:Symptoms are characteristic.Laboratory diagnosis is made by obtainingnasopharyngeal secretionsPernasal swab,West ‘s Post nasal swab)Cough plate methodPrimary cultures are obtained on Bordet-Gengou medium with incubation for 10-14 days.small transparent hemolytic colonies on bloodagar.
Direct fluorescent antibody testing onnasopharyngeal specimens a good diagnostictool. PCR if available is highly sensitive andspecific.Slide agglutination with specific antibodiesis also used but less specificSerologically B. pertussis can bedistinguished from B. parapertussis and B.bronchiseptica.
Prevention and treatment:Erythromycin is the antibiotic of choice.Antibiotic treatment during the catarrhal stage mayameliorate the disease. However, antibiotic treatment oncethe paroxysmal stage has begun may have no apparent effecon the course of the disease.Immunisation with killed B pertussis vaccine(alumadsorbed)Usually combination-DPT-3 DOSE intervels of 4-6weeks,before 6 months,followed by booster at 1 yrAcellular vaccine consisting of filamentous hemagglutininsand detoxified pertussigen. These components are combinedwith diphtheria and tetanus toxoids in the DTaP vaccine.