When the urinary tract, which is usually sterile, is colonized by bacteria it results in an infection which is most often sub-clinical. A variety of endogenous and opportunistic microbes such as E. coli, Streptococcus sp., Staphylococcus epidermidis, Klebsiella sp., Pseudomonas sp., Aeromonas sp., Bacteroides sp. are natural inhabitants of the lower urinary tract and are able to cause non specific UTI. However, they may open the door to invasion by Actinobaculum suis, which is gram-positive, fimbriated etiologic agent of specific UTI. UTI includes cystitis (inflammation of urinary bladder) and pyelonephritis (inflammation of kidneys). The microbiological ecosystem of urinary tract of sows changes spontaneously during production events but the largest changes are caused by antimicrobial treatments.
UTIs are among the most frequent bacterial infections in the herd but are not often diagnosed. They are often environmental in origin and the fecal flora obtains access to the urinary tract more easily in females than males. Under intensive confinement conditions the sows’ vulvas are often placed in direct contact with feces (SMITH, 1990). The dog-sitting position helps to force fecal material into the vagina. When the animal’s immunity is poor and the infection pressure high, bacteria can cause disease. The incidence of UTI in confinement operations increases with age, going from 18% in young sows to 38% in old sows, and is a predominant cause of death in pigs over one year of age.
UTIs are more common during lactation. The lactating sow concentrates urine in an effort to conserve water, leading to higher specific gravity, and she urinates less and less frequently. This ultimately leads to higher bacterial loads as there is less urine available for flushing the urinary tract. UTI also predisposes the sow to post-partum dysgalatia syndrome (PPDS) of which MMA is considered to be a particular form. Ascending
invasion of the uterus by pathogens is possible at farrowing, and the mammary glands can also be affected due to contamination of the resting area. There are several reports of identical O and K serotypes of E. coli being found in bladder, uterus and udder indicating that the micro-organisms underlying these infections are often the same (DEE, 1992). Biksi 2000 reports a strong epidemiological association between urocystitis and
Table 1: Normal bacterial flora of the female lower urogenital tract (BIKSI, 2000)
* Potential urinary tract pathogens
A thin mucus layer, glycosaminoglycan (GAG or mucin), on the bladder epithelium covers the mucosa and binds with water to form a barrier to prevent urinary constituents from coming in contact with urothelium (DEE, 1992). This layer prevents adherence of bacteria by covering possible receptor sites. Secretion of the GAG layer is under the influence of estrogen and progesterone. A defective layer can be observed in animals with urinary tract infection (WENDT, 1998; LIEBHOLD et al., 1995). In cases of significant bacteriuria, the rapid and massive appearance of goblet cells and the ensuing excessive mucus production can be interpreted as a non-specific local defence mechanism (LIEBHOLD et al., 1995). Oligosaccharides may also help detach some bound bacteria from the bladder wall (DEE, 1992). The bladder mucosa is known to have antibacterial activity due to several non-specific factors such as high osmolality, urea concentration and low urine pH. In addition, the presence of immunoglobulins such as IgG, IgA and secretory IgA in the urine and exfoliation of epithelial cells bound with bacteria aids in bacterial clearance (WENDT, 1998).
It is assumed that most pathogenic agents ascend through the urethra, favored by its wide and short conformation in sows. This ascension is also enhanced by relaxation of the sphincter muscle in late pregnancy and postpartum, and the relaxation of ligaments pre-partum due to the effects of corticosteroids. Weakening of the muscle sphincter vesicae in late pregnancy and post partum, constipation, traumas to the urethra and bladder at parturition, abnormal colonization of bacteria of the sinus urogenitalis and genital organs and incomplete closure of the vulva can also predispose sows to UTIs. Other environmental and management
factors can also contribute, such as assistance at farrowing, retained placenta or fluids, dirty or poorly sanitized farrowing crates and poor water flow rates or quality which leads to reduced water intake in sows, and ultimately reduced urination.
A. suis is a commensal organism of the porcine urogenital tract, is fimbriated, and the short, wide urethra of the sow enhances accessibility to the bladder where the alkalinity of the environment increases because the bacteria are able to cause cleavage of urea into ammonia with the urease enzyme. The elevated pH, increased from a normal range of 6.0-7.5 to 8.0-9.0 enhances bacterial proliferation and causes an inflammatory reaction
of the mucosal surface, inhibiting the growth of competitive microflora and promoting the precipitation of urinary salts and crystals, which in turn increase inflammatory changes in the bladder mucosa and provides a nest for bacterial growth and protection from antibiotics and host defence mechanisms.
Dietary electrolyte balance, acid-base balance (ACB), is also a critical point to determine urine pH and thus bacterial proliferation in the urinary tract of the sow. Another consequence is a major mobilization of calcium from bones leading to a higher rate in the blood (DEROCHEY, 2000).
With the majority of UTIs, clinical signs are absent. However, sows with significant bacteriuria are more often seen in the dogsitting position, have inferior body condition, longer wean-to-service interval, lower fertility rates and tend to wean small litters. There may be unusual vulvar discharges, (see Table 2) with small to moderate discharge at the end of urination more frequent in older sows.
Table 2: Types of vulvar discharges in female pigs.
Animals that experience late or no diagnosis frequently experience weight loss and reduced productivity secondary to end-stage renal disease, resulting in premature removal from the breeding herd.
The pathology of UTIs usually comprises thickening and inflammation of the cystic mucosa, microscopically prominent goblet cell proliferation in the whole uroepithelial layer leading to necrosis inside possibly both ureters and kidneys as inflammation increases.
Complications may lead to hemorrhagic kidneys with pus and excess mucus and blood in the pelvis, ureters dilated and filled with pus and the bladder wall grossly thickened inflamed and covered with excess mucus (see picture 1, 2 and 3).
Picture1: E. coli Cystitis in a five year old sow in the third month of pregnancy. Note the intensely reddened mucosa and pools of pus. The normal mucosa of the lower urinary tract is smooth, grayish white and glistening resulting from acute cystitis (SMITH, 1990).
Picture 2: Pyelonephritis in sow, caused by A. Suis, note the inflamed pelvis and the massively dilated ureter (SMITH,1990).
It is very difficult diagnose UTIs with a clinical examination. Bacteriology is complicated by contamination of bacteria normally present in the vagina and distal part of urethra. However, distinction between infections can be based on the number of bacteria in the urine and urine reagent sticks can be used to determine urine parameters such as pH, blood, nitrites and leukocytes. Cytology can provide information to differentiate between pyelonephritis, cystitis and bacteriuria. Also, specific gravity measurements may provide valuable information if sows have sufficient access to water.
Even though UTIs are often asymptomatic bacteriuria events with temporary deterioration to cystitis and spontaneous remission, without therapy the infection may progress upwardly to involve ureters and then kidneys. Broad spectrum antibiotics (tetracyclines, trimethoprim sulphas, fluorquinolones) are often needed cephalosporins, penicillin, ampicillin and amoxicillin have the propensity to be excreted by the kidneys and are effective in alkaline conditions, but not against E. coli. Sulphonamides are nephrotoxic and are inactivated by pus and necrotic debris.
Picture 3: Inflamation of bladder and ureter.
Table 3: Sensivity test to antibiotics for sow urine problems against E.coli, Year 2000-04 (BUSSE, 2006)
I would like to stress that the use of specific drugs could be significantly reduced by keeping the pH of the urine inside the physiological range of 6.0 – 7.5. Recovery is sometimes possible by simply increasing access to water which leads to a natural washing and correction of the urine pH. In the case of UTIs, prevention is better than therapy and water consumption by the sow can be easily checked. Group antibiotic treatments, which are routinely provided from 2 to 5 times a year in sow units should be reduced to the absolute necessity. Instead, the acidification of sow feed, and ultimately their urine, with specific products is recommended. Particular attention should also be paid to the hygiene of farrowing and gestating crates, use of hygienic mating procedures (AI), washing of sows when transferring between facilities and minimization of sedentary behavior.
A close relationship exists between the urinary pH value and the acid-base balance (ACB) of the diet (Urine pH = 3*10-6 x ACB2+ 0.003 x ACB + 6.19). Cations (Ca, Mg, Na, K) are effective in increasing the ACB while anions (P, Cl) having acidifying effects. Adding urine acidifying substances leads to a more appropriate anion-cation balance and helps maintain a healthy urinary tract.
Almond, G.W., et al., (2006) IPVS, Urine Abnormalities in Lactating Sows. Almond, G.W., Pork Checkoff, An Assessment of Urinary Tract Infections in Sows.
Arboleda, Nilo, et al.,The Prevalence of Sub-Clinical Urogenital Tract Infection in Sows.
DTW. Deutsche tierärztliche Wochenschrift
Biksi, I., (2002) Some aspects of urogenital tract diseases of female breeding swine.
Szent István Egyetem Állatorvostudományi Doktori Iskola, Budapest.
Busse, FWB., (2006) IPVS, Correlations between the infection of urogenital tract and MMA and steps again the infection
Dee SA, (1992) Porcine urogenital disease. Vet Clin North Am Food Anim Pract.
De Rouchey, J.M., et al., (2000) Effects of dietary elctrolyte balance on sow and litter performance, blood chemistry, and urine chemistry in lactating sows.
Krag, L., et al., (2006) IPVS, Aetiology of pyelonephritis in slaughtered sows.
Liebhold, M., (1995) et al., The Veterinary Record, by BVA,Clinical, and light and electron microscopical findings in sows with cystitis.
Martineau, GP., et al., (2006) IPVS, Urinary infection in sows: fact or fiction? Case study (France) with controls (Belgium).
Martineau, GP., 1 et al., Histopatological lesions of the kidney in cull sows from farms free from clinical urinary tract infections
Mauch, C., (2004) et al., The influence of prepartum bacteriuria on the reproductive performance of the sow. Deutsche Tierärztliche Wochenschrift.
Muirhead, M.R, Alexander, T.J.L., (1997) Managing pig health and the treatment of disease, 5M Enterprises Ltd., ISBN 0953015009.
Eich, K.O., (1984) Manuale di patologia suina.
Salle, E., et al., (2006) IPVS, The evolution of urinary tract infections in pregnant sows
Wendt M., (1998) 15th IPVS, Urinary system disorders of pigs.