1. Diseases caused by Bordetella species Lecture on Epidemiology, 2012.03.01. L. Makrai, SZIU-FVS, Department of Microbiology and Infectious Diseases

2. Jules Bordet Belgian physician - bacteriologist (1870-1961) - he worked at the Pasteur Institute in Paris and studied phagocytosis and complement-system - in 1906 he isolated the causative agent of whooping cough (B. pertussis)

3. General features of Bordetella species upper respiratory tract short Gram-negative rods not fastidious, obligate aerobes grow on MacConkey agar (colourless colonies) flagella +, capsule +, fimbria + catalase +, oxidase + cytotoxin production –Tracheal toxin: inhibits ciliary action, kills ciliated cells –Dermonecrotoxic toxin:Induces skin necrosis, impairs osteogenesis –Osteotoxin:toxic for osteoblasts

4. B. pertussis – whooping cough B. parapertussis – mild form of whooping cough + pneumonia of lambs B. bronchiseptica – pigatrophic rhinitis – dogsCanine infectious tracheobronchitis – kittenspneumonia – horsesrespiratory infections – rabbits upper respiratory infections – lab. rodentsbronchopneumonia B. avium– turkeyCoryza

5. Diseases caused by B. bronchiseptica Occurence: worldwide –Primary –Secondary (mixed infections) Epidemiology: –maintained by carrier animals –predisposing factors: - overcrowded rearing - high NH 3 and humidity - cold environment - coinfections

6. Swine bordetellosis Toxin producing strains, young piglets (till 8 weeks of age) –Rhinitis (inflammation of nasal mucosa, atrophy of nasal turbinate cartilage) Sneezing Serous-mucous nasal discharge –Bronchopneumonia: day old piglets, fever, serous or purulent nasal discharge, dyspnoe

7. Pneumonia caused by B. bronchiseptica (piglet) (arrow: emphysema) Vetési-Dobos-Kovács

8. Diseases of dogs and cats caused by B. bronchiseptica dog –young: „kennel-cough” (canine infectious tracheobronchitis) (Canine Adenov-1-2, C Parainfluenzav-2, C Distemperv., C Herpesv-1, Reov. 1-2-3) fever, depression cough bronchopneumonia –adult: join to distemper bronchopneumonia cat sneezing disease secondary infection (calici virus, infectious rhinotracheitis)

9. Turkey coryza Highly contagious upper respiratory tract infection of 2-6 weeks old poults (and broilers) with high morbidity Bordetella avium

10. Distribution Natural hosts of B. a.: turkey and other avian species Widespread in major turkey producing regions (USA, Canada, Australia, Germany, Great Britain, France, Israel, South Africa).

11. Etiology B. avium Cytotoxin production: - ciliostatic (epithelial degeneration of trachea) - dermonecrotoxin (softening of the cartilaginous rings of trachea) Virulent strains can haemagglutinate guinea pig RBC B. avium can survive in the litter for 1-6 month!

12. Epidemiology Naturally occuring infection is recognized in turkeys 2-6 weeks old (older turkeys and breeder flocks may also develop clinical disease) Highly contagious! Infection is spread through direct contact with infected poults (litter, water) high morbidity (80-100%), low mortality (less than 10%)

13. Pathogenesis I. Infection: by inhalation, perorally colonize airways generally restricted to airways (rarely septicaemia) cytotoxine: inhibition of cilia, epithelium degeneration Cilia associated bacterial colonies, progressive loss of ciliated epithelium

14. Pathogenesis II. Predisposing factors: –overcrowding –incomplete feed and water supply –high NH 3 and humidity –cold environment –coinfections: Mycoplasma, E. coli, Pasteurella, O. rhinotracheale, A. paragallinarum, Chlamydophila, viruses (TRT)

15. Clinical signs Incubation period: 7-10 days (when susceptible poults are exposed to infected poults by closed direct contact) –reduced activity –decreased consumption of feed and water –stunted growth –sneezing –excessive lacrimation –clear oculonasal discharge –beak-breathing –altered vocalization –mucus accumulates in the nares with swelling in the submaxillary sinuses –older turkeys: dry cough signs begin to subside after a course of 2-4 weeks

16. oculonasal discharge, conjunctivitis beak-breathing

17. Pathological findings Nasal and tracheal exsudates: initially: serous, later: tenacious and mucoid Tracheal lesions: softening and distorsion of the cartilaginous rings, dorsal-ventral compression and fibrinomucoid luminal exsudate EM: Cilia associated bacterial colonies, progressive loss of ciliated epithelium

18. Diagnosis based on clinical signs + gross pathological lesions isolation and identification of B. a. from tracheal mucosa (swab sample – MacConkey agar – early in the course of infection – pure cultures can be obtained from the trachea) Virulent isolates agglutinate guinea-pig RBC-s! Serology:- Microagglutination test - ELISA

19. Differential diagnosis Mycoplasmosis Chlamydophilosis Respiratory cryptosporidiosis Newcastle disease Adenovirus Influenzavirus Pneumovirus (TRT)

20. Treatment Broad spectrum ABs (tetracyclines, penicillins) early in the course of the disease In most cases: minimal clinical improvement Remain carriers

21. Control, Prevention Vaccines: - modified lived vaccines (live temp. sensitive mutant of B. a.) – immunization: 3 weeks of age: colonize the nasal mucosa - prevent the disease, but not the infection - whole cell killed and adjuvated bacterins for vaccination of breeder hens Thorough cleaning and disinfection of turkey houses