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

Jules Bordet Belgian physician - bacteriologist ( ) - 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)

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

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

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

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

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

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 ) fever, depression cough bronchopneumonia –adult: join to distemper bronchopneumonia cat sneezing disease secondary infection (calici virus, infectious rhinotracheitis)

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

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).

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!

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%)

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

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)

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

oculonasal discharge, conjunctivitis beak-breathing

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

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

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

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

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