Is swine dysentery making a comeback?
Tuesday, May 31, 2011
Considered eradicated in the 1900s, this old nemesis is back in parts of North America, but treatment and control is possible with the right combination of measures
by S. ERNEST SANFORD
Swine dysentery is an old nemesis that we thought we had eradicated in the 1990s, but apparently not so. Over the last two or three years, there have been increasing reports of outbreaks from several parts of the U.S. Midwest and Southeast, and also some parts of Canada.
Swine dysentery (SD) is a severe intestinal bacterial disease causing bloody diarrhea (bloody scours) primarily in grow-finish pigs, although any age or size of pigs can be affected. SD occurs worldwide.
Etiology of Swine Dysentery
SD is caused by the bacterium Brachyspira hyodysenteriae. (This organism had many different previous names including Vibrio coli, Treponema hyodysenteriae and Serpulina hyodysenteriae). Infection is restricted to the large intestines (colon and cecum). A closely related bacterium, B. pilosicoli, causes a milder, non-bloody diarrhea that somewhat resembles SD.
Prior to the 1970s, Vibrio coli, the cause of dysentery in humans, had been thought to be also the etiological agent of SD giving rise to an earlier named vibrionic dysentery prior to the 1970s. To further complicate matters, there have been new Brachyspira spp.
identified in recent years that resemble B. hyodysenteriae culturally and produce varying degrees of bloody diarrhea similar to SD. Included among these new Brachyspira spp. are B. murdochii, B. suanatina and B. "novel" (not yet named). The last was identified by Dr. John Harding at the Western College of Veterinary Medicine, University of Saskatchewan, who was also involved in first identifying porcine circovirus.
Furthermore, the University of Minnesota Veterinary Diagnostic Laboratory reports that 70 per cent of Brachyspira spp. isolates from SD-like cases since 2006 have been "untypable." More intense diagnostic work reported at the annual meeting of the American Association of Swine Veterinarians in March 2011 revealed that 56 of 79 of these "untypables" were B. murdochii, four were B. innocens and 19 were of two "new" Brachyspira spp. All of these isolates were from clinical SD-like cases.
Transmission of B. hyodysenteriae is via the fecal-oral route. Asymptomatic carrier pigs are a common mode of herd-to-herd transmission, although rodents and dogs can harbour and transmit the organism for up to 180 and 90 days, respectively. Birds, flies and fomites (inanimate objects or substances) are also means whereby the organism can be moved mechanically between and within herds.
The incubation period of SD is variable, but clinical disease is usually evident within 10-14 days of exposure to the causative organism, although outbreaks have been reported from two days to three months after initial exposure. Other factors contributing to outbreaks include overcrowding, change of feed, shipping, extreme changes in environmental temperatures and other stresses. Large financial losses can occur due to mortality, reduced growth rate, poor feed conversion and antibiotic treatment costs.
Clinical signs. The first signs of SD are of pigs with messy, mucoid diarrhea which quickly becomes bloody. Affected pigs become dehydrated and gaunt with hollow flanks and lose body condition rapidly. In untreated cases, morbidity is high and mortality approaches 50 per cent.
A similar but much less severe condition, spirochaetal colitis, caused by the related organism, B. pilosicoli, produces a mild diarrhea with mucus but no blood.
Diagnosis. Diagnosis of SD can be made from a combination of the clinical signs and gross post mortem lesions, which are restricted to the large intestines and consist of fibrin, mucus and necrotic debris mixed with blood on the surface of the colon and cecum.
To confirm the diagnosis, however, it is necessary to identify the causative bacterium, B. hyodysenteriae, associated with the intestinal lesions, and to rule out other spirochaetes, some of which can produce lesions that mimic those of B. hyodysenteriae.
Bacteriological culture is the old standard, but polymerase chain reaction (PCR) is now a quick, reliable means of both confirming B. hyodysenteriae and differentiating it from other nonpathogenic Brachyspira that inhabit the gut.
SD must be differentiated from other enteric diseases of grow-finish pigs, including ileitis, whipworms, gastric ulcer and the aforementioned spirochaetal colitis (B. pilosicoli). Differentiation from all of these other diseases, except whipworm infestation, is assisted by the fact that they are not restricted to the large intestines. Severe whipworm infestation can readily mimic SD and the worms are not usually visible until late (three to four weeks after initial infestation) in the course of the disease.
Fortunately, whipworm infestations in our pigs are extremely rare to nonexistent today as virtually all of them are reared indoors and have no access to whipworm eggs to start an infestation. Although the other diseases are not restricted to the large intestines, dual and multiple infections can and do occur, so a diagnostic workup by the herd veterinarian is still necessary to rule out other infections.
Treatment and control. Preventing B. hyodysenteriae from entering a herd is paramount. The first focus is making sure that replacement stock comes from sources that are free of SD. Instituting a quarantine period of 30-60 days before entry into the breeding herd represents an additional barrier against introducing the disease.
Several antibiotics are licensed for treatment and control of SD with lincomycin, tiamulin and tylosin seemingly being the most effective. Aggressive treatment, usually starting with water medication with one of the above antibiotics, is needed at the earliest signs of SD. This is followed by in-feed medication for at least three weeks with the same or another of the anti-SD antibiotics. Severely affected animals have to be injected immediately with the same antibiotics prior to or concurrent with water medication.
As mentioned before, SD was believed to have been eradicated from most Canadian and U.S. herds by the mid-1990s. This was accomplished by the introduction of systematic techniques to eliminate B. hyodysenteriae. Intensive medication accompanied by thorough clean-up and disinfection were the methods of choice prior to the introduction of SEW (Segregated Early Wean) and multi-site and/or all-in/all-out production systems.
To accomplish this, every pig in the herd must be treated with therapeutic levels of one of the anti-SD antibiotics, lincomycin, tiamulin or tylosin. Any debilitated animals must be removed from the herd since they will likely not be eating and hence will not have been treated and will become a source of shedding of the organism if allowed to remain in the herd. With the advent of SEW programs, pigs weaned at less than three weeks of age and taken to an off-site nursery and finisher remain free of B. hyodysenteriae and can become the source of restocking with SD-free animals. The original herd can then be marketed and the premises cleaned and disinfected.
Complete depopulation and repopulation with clean stock after cleanup and disinfection is best done during the warm (summer) months and conclusively eliminates SD. BP
S. Ernest Sanford, DVM, Dip. Path., Diplomate ACVP, is a swine specialist with Boehringer Ingelheim Vetmedica (Canada) in Burlington. Email: ernest.sanford@boehringer-ingelheim.com