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 Actinobaculumsuis, 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. 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.

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 . 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 defense mechanism. Oligosaccharides may also help detach some bound bacteria from the bladder wall. 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

1. On what stages of production is the urinary tract the most susceptible to infections?
2. What processes inhibit the growth of competitive microflora and turn increase inflammatory changes in the bladder mucosa?
3. What are the clinical sings of UTI?
4. What are the pathological changes during UTI?
5. Is it possible to diagnose UTI only by means of clinical sings?
6. What are the peculiarities of prevention and treatment of UTI?