Occurrence: Worldwide, some herds free.
Age affected: Piglets pre-weaning, weaners, growers/ finishers.
Causes: Bacterium – Bordetella bronchiseptica; worse if atrophic rhinitis present.
Effects: Sneezing, nose bleed, tear staining, mild snout deformity, poor growth.
Occurrence: Worldwide, some herds free.
Bordetellosis is caused by Bordetella bronchiseptica, a small rod-shaped bacterium, which can be grown readily in the laboratory. It is resilient, surviving both drying and being in water for 3 weeks. It produces a number of structures which can adhere to cells of the respiratory tract including fimbriae, (hair-like projections), a filamentous material and an adhesive protein, pertactin. The bacteria also produce various toxins. A number of toxins damage cells-alpha haemolysin (destroys red blood cells), a cytotoxin destroys respiratory epithelium, a dermonecrotoxin destroys skin cells and an osteocytic toxin destroys bone cells. B. bronchiseptica infects non-immune young pigs by aerosol spread or contact. It colonises the ciliated epithelium which lines the respiratory tract by means of its adhesive organs. It rapidly reaches high numbers and then causes damage to the epithelium. The epithelium loses its cilia and its ability to move respiratory secretions, and become inflamed. The toxins diffuse into the tissue in the nasal region to produce a mild and reversible form of atrophic rhinitis by damaging the rapidly growing bones. The damage caused to the epithelium of the nose allows colonisation with Pasteurella multocida, the organism which causes progressive atrophic rhinitis. Damage to the lower respiratory tract allows the secretions, bacteria and inflammatory cells to pool and cause bronchopneumonia. Recovered animals carry the organism for weeks.
Infected pigs shed the organism by coughing and sneezing and also be contaminating drinkers and surfaces. Very high levels can be found in the air just after weaning and infection is by inhalation. The organism may survive in dust and can be spread from farm to farm in carrier pigs and on contaminated clothing and equipment. The organism can be found in rats, dogs and cats on farms, but the strains normally present in these species do not infect pigs readily. They may, however, carry infection between farms, even if rarely.
Outbreaks of sneezing occur in baby pigs from 1 week of age and this may be severe with snorting and sometimes bleeding. Tear staining is often present, and mucus may be seen on the nostrils, hanging from them or dropped on the pen floor. As the organism is present in most pig herds, these signs frequently suggest the presence of the organism. Occasionally signs of twisting of the snout may develop in uncomplicated infections but this and other persistent changes of atrophic rhinitis such as shortening of the upper jaw and complete turbinate atrophy are more common in progressive atrophic rhinitis. Pigs with the pneumonic form cough within 3-4 days of infection and develop mild fever (40˚C, 104˚F), inappetence and loss of condition and increased respiratory rates. Mortality can occur at this stage in uncomplicated infections and may reach 30%. Uncomplicated infections with B. bronchiseptica can cause reductions in the rate of daily live weight gain of 26-30% in conventional pigs. In complicated infections these figures could be exceeded in non-immune pigs but in immune pigs may be reduced as is the severity of the clinical signs. Sneezing amongst piglets may be the only finding in the litters of immune sows, and may also occur shortly after weaning and mixing. The present of B. bronchiseptica can be confirmed by laboratory isolation from cotton-tipped nasal swabs.
Post-mortem findings in affected pigs with uncomplicated B. bronchiseptica infection include inflammation of the lining of the nasal cavity, the presence of mucus, failure of the scroll bones to develop and occasional distortion of the nasal septum. Pus is present in the bronchi, and bronchopneumonia appears as areas of red, solid pneumonic lung in the cranial and middle lung lobes. These lesions heal by collapse and leave fissures in the lung which survive until slaughter. The bacteria can be seen adhering to surviving ciliated epithelium by microscopic examination. B. bronchiseptica can be isolated from the nasal cavity, trachea, bronchi and bronchial lymph nodes in early cases, but less easily in chronic cases. Its presence can be confirmed by tests for its DNA and antibody can be detected in recovered pigs.
B. bronchiseptica infection can be treated using tetracyclines, ampicillin, erythromycin, cloxacillin, enrofloxacin, streptomycin, sulphonamides such as sulphadimidine, and trimethoprim sulphonamide. Severely affected pigs may have to be injected and treatment continued by oral dosing of piglets with the same drug or medicating the water in weaned pigs. Treatment should be continued for at least 10 days and preferably for 2 weeks. Medication in feed over the period of risk (usually immediately after weaning and mixing) may be used to reduce or eliminate B. bronchiseptica infection. Trimethoprim sulphonamide, ampicillin, tylosin sulphonamide mixtures may all be used and all pigs in the airspace should be treated. Injection with trimethoprim sulphonamide given at 3 days, 10 days and 3 weeks of age prevents clinical signs of the disease and reduces shedding B. bronchiseptica. Sow vaccination can protect the offspring whilst sucking, but vaccination of the piglet at 7 and 28 days may be required to protect the weaned piglet. All-in, all-out housing and good ventilation reduce the severity of the disease. Bordetella infection has been eliminated from some herd using treatment programmes, but is frequently reintroduced as it can survive dried on clothing and in the nasal flora of dogs, rats and other species.
The antimicrobial treatments described here may be subject to national or professional guidelines on prescribing, so these should be consulted before starting a course of treatment.