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Control and Treatment
Bordetellosis most negatively effects young turkey poultry flocks, with clinical signs normally seen at 2-6 weeks of age. In outbreak flocks, the morbidity can be high (80-100%), but mortality is usually low (<10%). However, the severity of disease can be exacerbated by adverse environmental conditions (low temperature, high ammonia and dust, low humidity) and secondary bacterial infections; increasing mortality up to 40% or 60%. It is uncommon to see outbreaks in breeder flocks, but up to 20% morbidity with no mortality is reported. Generally, the most common comorbidity associated with increased severity of disease and mortality is secondary infection with E. coli.  B. avium is thought to decrease clearance of secondary organisms in the trachea which allow them to set up infection. Most turkey poults with B.avium infection without secondary complications will recover from bordetellosis in 4-6 weeks, and resistance is formed at 5-6 weeks.

Bordetellosis, turkey coryza, or rhintracheitis, is highly transmissible. Small backyard turkey flocks a mile from large commercial farms have shown isolated infections of B. avium. Transmission is by direct contact between birds, or aerosol droplets that contaminate water or litter. B. avium survival and transmission in the environment is highly regulated by temperature and humidity. It can survive in the environment less than 2 days at higher temperatures (40°C), up to a month with low temperature (10°C) and humidity (32-58%), and up to 6 months in feed, water and damp litter. Good bio-security protocols, thorough cleaning, and excellent husbandry practices are the best methods for controlling outbreaks. Optimal temperature, humidity, and control of ammonia and dust are critical to reduce B.avium growth in the environment and reduce irritants to the tracheal epithelium. Most common disinfectants used do kill B. avium. Thorough cleaning includes removal of litter and other fomites between flocks, disinfection of the barn and flushing of water lines with disinfectants, and fumigation with methyl-bromide or formaldehyde. Foot baths, using on farm-clothing, controlling traffic between barns, preventing contact with wildlife, and showers between sites also reduces transmission between farms. For infected flocks, increasing ventilation and reaching optimal temperature are key. It has been reported that niacin or 0.016% oxy-halogen added to water lines given early in life reduces the severity of bordetellosis.

Antibiotic treatment is not considered effective for B. avium infections, and there is conflict in evidence for susceptibility. The mechanism of resistance in some strains of B. avium have been recorded. This includes antibacterial resistance genes encoded on plasmids (pRAM resistance genes to tetracycline and 2 sulfonamides) and lack of a penicillin binding protein 3 (PBP3) which drugs bind to to inhibit cell wall synthesis. Plasmid conjugation between B. avium isolates also occurs. The difficulty with characterizing antibiotic resistance and susceptibility in B. avium strains is most strains will appear sensitive in vitro, but in reality has a much different outcome in vivo. Most isolate strains of B. avium have resistance to a number of antibiotics. Resistance has been elucidated to aztreonam, ampicillin, tetracycline, cephalosporins, penicillins, sulbactams, sulfonamides, streptomycin, carbapenem, imipenem, fluoroquinolones, chloramphenicol, gentamycin, cefoperazon, cefepime, cetazidime, piperacillin and amikacin. However, some susceptibility has also been shown to ampicillin, amoxicillin, penicillin, ceftiofur, enrofloxacin, norfloxacin, ciprofloxacin, erythromycin, florfenicol, and co-trimoxazole. Isolates are believed to be sensitive in vitro but not in vivo due to the inability of the drug to reach therapeutic doses within the tracheal epithelium of turkeys where bacteria dwell.

Two vaccines are available for poultry against B. avium bordetellosis: a temperature sensitive mutant live strain of B.avium and a bacterin isolate vaccine. Bacterins are administered to breeder hens to induce maternal IgG to pass onto their progeny, providing maternal immunity up to 4 weeks in poults. The mutant live-strain is administered to poults twice; at hatchery and then at 2-3 weeks of age. However, vaccines are not known to be very efficacious, and may only protect against severe clinical signs, or delay onset of disease, not stop the spread of infection. Most significant immunity in turkey poults is likely going to be acquired humoral immunity. Vaccinations are considered if there is recurrence in outbreaks of bordetellosis.