Brachyspira pilosicoli and Porcine Intestinal Spirochetosis in Weaned Pigs
Introduction
Porcine intestinal spirochetosis (PIS) is an enteric disease of weaned pigs caused by the anaerobic spirochete Brachyspira pilosicoli. The condition is characterized by mild to moderate diarrhea, reduced growth rates, and colitis in pigs typically between 4 and 16 weeks of age. B. pilosicoli colonizes the large intestine, attaching to the apical surface of colonic enterocytes via one cell end, a phenomenon termed "false brush border." This organism is distinct from Brachyspira hyodysenteriae, the agent of swine dysentery, and from other Brachyspira species such as B. intermedia and B. murdochii. Understanding the biology, pathogenesis, and control of B. pilosicoli is essential for managing enteric health in post-weaning pigs.
Etiology
Brachyspira pilosicoli is a Gram-negative, anaerobic, helically shaped spirochete belonging to the family Brachyspiraceae. The bacterium measures 6 to 10 micrometers in length and 0.3 to 0.4 micrometers in diameter, with 8 to 12 periplasmic flagella per cell. It is weakly beta-hemolytic on blood agar, a key feature differentiating it from the strongly hemolytic B. hyodysenteriae. B. pilosicoli is oxidase-negative, catalase-negative, and indole-negative. It ferments a limited range of carbohydrates, producing acetic acid and succinic acid as major end products.
The organism possesses a unique mechanism of attachment: it inserts one cell tip into the intercellular junction of colonic epithelial cells, leading to effacement of microvilli and formation of an adherent layer of spirochetes on the mucosal surface. This attachment is mediated by outer membrane proteins and lipooligosaccharides. B. pilosicoli also produces a hemolysin and a beta-lactamase enzyme, contributing to tissue damage and antimicrobial resistance.
Epidemiology
Brachyspira pilosicoli is distributed worldwide in swine herds. Prevalence varies by region and management system, with higher rates reported in continuous-flow operations compared to all-in/all-out systems. The organism is shed in feces of infected pigs and can survive in slurry, water, and contaminated environments for several weeks under cool, moist conditions. Transmission occurs via the fecal-oral route, often through contaminated boots, equipment, or feed.
Weaned pigs are the most susceptible age group. Maternal antibodies from sows may provide partial protection, but waning immunity after weaning, combined with stressors such as diet change, transport, and mixing, predisposes pigs to clinical disease. Coinfections with other enteric pathogens, including Lawsonia intracellularis (causing porcine proliferative enteropathy), Escherichia coli, Salmonella spp., and Trichuris suis, can exacerbate clinical signs and complicate diagnosis.
Clinical Signs
The hallmark of porcine intestinal spirochetosis is mild to moderate diarrhea in weaned pigs. Feces are pasty to watery, often greenish or gray, and may contain mucus but rarely blood. Affected pigs exhibit reduced feed intake, decreased weight gain, and uneven body condition within a group. Rectal temperature remains normal or mildly elevated. In most cases, the disease is self-limiting within 7 to 14 days, but chronic or recurrent diarrhea can occur in herds with poor biosecurity.
Severe disease is uncommon but may develop in pigs with concurrent infections or immunosuppression. Mortality is low, but morbidity can reach 30% to 50% in affected groups. The economic impact stems from reduced growth performance, increased days to market, and costs associated with treatment and control measures.
Pathology
Gross lesions are confined to the cecum and colon. The colonic mucosa appears thickened, edematous, and hyperemic, with a roughened, granular surface. In chronic cases, a fibrinous exudate may be present. The mesenteric lymph nodes are often enlarged.
Histopathological examination reveals a characteristic "false brush border" composed of a dense layer of spirochetes attached to the apical surface of colonic enterocytes. The attached spirochetes are oriented perpendicular to the epithelial surface, with one end inserted into the intercellular space. Microvilli are effaced, and enterocytes may show vacuolation, attenuation, and occasional necrosis. The lamina propria contains increased numbers of lymphocytes, plasma cells, and macrophages. Crypt hyperplasia and goblet cell depletion are common findings.
Diagnostics
A definitive diagnosis of Brachyspira pilosicoli infection requires laboratory confirmation. The following methods are used:
Culture and Isolation
Fecal samples or colonic scrapings are plated on selective media such as trypticase soy agar containing 5% sheep blood, spectinomycin (400 micrograms per milliliter), and colistin (25 micrograms per milliliter). Plates are incubated anaerobically at 37 degrees Celsius for 3 to 7 days. B. pilosicoli appears as a weak zone of beta-hemolysis. Identification is confirmed by biochemical tests (indole negative, hippurate hydrolysis positive) or by species-specific polymerase chain reaction (PCR).
Polymerase Chain Reaction
PCR assays targeting the 16S rRNA gene or the nox gene (NADH oxidase) are highly sensitive and specific for B. pilosicoli. Real-time PCR allows quantification of bacterial load and can differentiate B. pilosicoli from other Brachyspira species. PCR can be performed directly on fecal samples, reducing turnaround time compared to culture.
Histopathology
Colonic tissue sections stained with hematoxylin and eosin or with silver stains (e.g., Warthin-Starry) demonstrate the attached spirochetes. Immunohistochemistry using monoclonal antibodies against B. pilosicoli can provide specific visualization.
Serology
Enzyme-linked immunosorbent assays (ELISAs) for detection of antibodies against B. pilosicoli are available for research and herd-level surveillance. Serology is less useful for individual diagnosis due to delayed antibody response and cross-reactivity with other Brachyspira species.
Differential Diagnosis
Porcine intestinal spirochetosis must be differentiated from swine dysentery (B. hyodysenteriae), porcine proliferative enteropathy (L. intracellularis), salmonellosis, colibacillosis, and whipworm infection (T. suis). Coinfections are common, and diagnostic panels that include multiple pathogens are recommended.
flowchart TD
A[Fecal sample or colonic scraping], > B{Selective culture on blood agar with spectinomycin/colistin}
B, > C[Anaerobic incubation 3-7 days]
C, > D{Weak beta-hemolysis?}
D, >|Yes| E[Biochemical tests: indole -, hippurate +]
D, >|No| F[Consider other Brachyspira spp.]
E, > G[PCR confirmation: 16S rRNA or nox gene]
G, > H[Positive: B. pilosicoli]
G, > I[Negative: re-evaluate]
A, > J[Direct fecal PCR]
J, > K[Quantitative or qualitative result]
K, > H
A, > L[Histopathology of colon]
L, > M[Silver stain or IHC]
M, > N[Attached spirochetes: false brush border]
N, > H
Treatment
Antimicrobial therapy is indicated for clinically affected pigs and for groups with high morbidity. The following antimicrobials have demonstrated efficacy against B. pilosicoli in vitro and in vivo:
- Tiamulin (water-soluble or in-feed) at 8.8 milligrams per kilogram body weight for 5 to 7 days.
- Valnemulin (in-feed) at 75 to 125 parts per million for 7 to 10 days.
- Lincomycin (water-soluble) at 11 milligrams per kilogram for 5 to 7 days.
- Doxycycline (in-feed) at 10 milligrams per kilogram for 7 days.
Antimicrobial susceptibility testing is recommended due to emerging resistance. B. pilosicoli has shown reduced susceptibility to tylosin and tiamulin in some regions. Beta-lactamase production confers resistance to penicillins and cephalosporins. Treatment failures may occur with suboptimal dosing, reinfection from the environment, or concurrent infections.
Supportive care includes electrolyte solutions for dehydrated pigs and provision of highly digestible feed. Probiotics and organic acids have been used as adjuncts but lack robust evidence for efficacy.
Control
Control of porcine intestinal spirochetosis relies on a combination of management practices, biosecurity, and strategic antimicrobial use.
Biosecurity
All-in/all-out production by room or barn reduces pathogen build-up. Thorough cleaning and disinfection of pens between groups is essential. B. pilosicoli is susceptible to common disinfectants including quaternary ammonium compounds, chlorhexidine, and peroxygen compounds. Footbaths and dedicated boots for each room help prevent mechanical transmission.
Management
Minimizing stress at weaning is critical. Gradual diet transitions, adequate feeder space, and optimal environmental temperature reduce susceptibility. Avoiding overcrowding and maintaining good ventilation lower the risk of fecal-oral spread.
Vaccination
No commercial vaccine is currently available for B. pilosicoli. Autogenous bacterins have been used in some herds but with variable results. Research into subunit vaccines targeting outer membrane proteins is ongoing.
Antimicrobial Stewardship
Given the risk of antimicrobial resistance, metaphylactic use should be based on confirmed diagnosis and susceptibility data. Targeted treatment of affected pens rather than whole-herd medication is preferred when feasible.
Conclusion
Brachyspira pilosicoli is a significant cause of diarrhea and reduced performance in weaned pigs worldwide. Accurate diagnosis requires laboratory confirmation through culture, PCR, or histopathology. Treatment with tiamulin or valnemulin is effective, but resistance is a growing concern. Control depends on rigorous biosecurity, stress reduction, and prudent antimicrobial use. Integration of these measures within a herd health program is essential for minimizing the economic impact of porcine intestinal spirochetosis.
References
- Taylor DJ, Trott DJ. Brachyspira pilosicoli. In: Zimmerman JJ, Karriker LA, Ramirez A, Schwartz KJ, Stevenson GW, editors. Diseases of Swine. 10th ed. Ames, IA: Wiley-Blackwell; 2012. p. 683-694.
- Hampson DJ, La T, Phillips ND. Brachyspira and other intestinal spirochetes. In: Gyles CL, Prescott JF, Songer JG, Thoen CO, editors. Pathogenesis of Bacterial Infections in Animals. 4th ed. Ames, IA: Blackwell Publishing; 2010. p. 559-574.