Emma is a four-year old spayed yellow Labrador Retriever. She was brought to you after her owner noticed that she was having difficulty urinating for the past three days. The owner normally walks Emma twice a day on a leash, but, "In the past three or four days, she's been demanding to go out more and more often." He's noticed that she's apparently been experiencing some pain on urination ("...she whines...") and despite the frequency of her walks, "...she doesn't seem to produce as much as usual."

Emma isn't dehydrated, her owner says she's been drinking normally, and her bladder seems full on palpation, but not terribly hard.  Emma is afebrile, her pulse rate is normal, as is her respiration.  You decide to express her bladder to obtain a urine sample and she lets out a yelp as you do so. The urine is light pink and has a strong odor.  You submit the urine to a technician to be analyzed.

A dipstick test and sediment examination reveal the presence of bacteria and white blood cells (leukocytes). You have a culture plate prepared, to be sure of what you're dealing with, but you've got your diagnosis.


Emma has case of bacterial cystitis, an inflammation of the urinary bladder caused by infection.  Females are more often affected than males, because bacteria find it easier to ascend the female's shorter urethra. The most common cause in canines is bacterial infection from the lower urinary tract.  Since E. coli is the most common cause, you're not surprised when the culture results come back positive for it, but by then you have already put Emma on a course of ampicillin at 11 mg/kg every 8 hours for a week.

Ordinary urination and certain antibacterial properties of urine itself normally prevent bacteria from ascending to the bladder, and cystitis is usually secondary to another condition that allows the infection to take hold. Incomplete emptying of the bladder, congenital diverticula in the bladder, diabetes mellitus, and trauma due to urolithiasis or catheterization are some pretty typical ways this happens. (Cystitis can also be due to non-bacterial causes: presence of drug metabolites or toxins in the urine, difficult parturition, or irritation from urolithiasis).

Incomplete emptying and congenital diverticula both provide reservoirs that aren't regularly emptied and thus become havens for bacteria and a place to replicate and establish an infection.  Diabetes mellitus overwhelms the glomerular filtration system of the nephron that normally retains glucose and results in a concentrated glucosuria:  this provides bacteria with an abundant source of energy and promotes high bacterial growth.  Finally, urolithiasis and catheterization cause mechanical trauma and break down the protective barrier that the bladder epithelium provides, allowing easier attachment and invasion.

Regardless of the initiating cause, the most common signs of cystits include dysuria, stranguria, hematuria, and pain upon urination.  Inflammation in the bladder is like inflammation anywhere else: there will be redness, heat, pain, and swelling.  Microscopically, there will be hyperremia, local edema and swelling, and intracellular swelling associated with the insult.


At left is a cystoscopic image of a urinary bladder with bacterial cystitis. The mucosal lining is inflamed and patchy areas of sub-mucosal hyperremia can be seen. This sort of test wasn't needed in Emma's case, but it shows pretty well how the symptoms she'd experienced could occur. If the inflammation continues and erosion of the mucosa occurred, blood in the urine is an obvious consequence. At right you can see how the transitional epithelium of the urinary bladder has become swollen; the epithelium along the free border has many cells with large, clear vacuoles in the cytoplasm. These cells appear to have an increased cytoplasm-to-nucleus ratio and they seem to crowd their neighboring cells. Notice the congested blood vessels in the sub-epithelial CT. One of the early events in the inflammatory response is increased blood flow; these vessels are congested (hyperremic) and in some cases actually leaking blood into the intersitital spaces (hemorrhage).

This higher-magnification view of the same region of the sample shows that many transitional cells are swollen and are distended with clear fluid. Cells closest to basement membrane stain purple and appear less distorted than those which are at the perimeter. The difference in staining may be due to a difference in pH indicative of cell necrosis at the perimeter.

This epithelium has suffered damage that compromises its ability to maintain fluid homeostasis. If unchecked, this influx will impede the normal function of the cells, in this case, maintenance of the mucosal barrier. If the stress lasts long enough, many cells will stretch till they burst. By observing the sediment from a urine sample you can determine if this has happened. Some cells may go beyond mere injury, and actually die. This typically occurs at the most distant reaches of the epithelial layer, where cells are farthest from their blood supply. Hydrostatic pressure, anoxia bacterial irritation are causing this pathology. Those bacteria which can thrive in the urinary bladder are typically capable of elaborating urease, an enzyme that breaks down urea, changing the local pH to provide a more hospitable environment. While this is hospitable for the bugs, it's irritating to the bladder epithelium which is adapted to the normal urine pH, and damage results.

This view shows that there isn't only damage to the epithelium, but also to the underlying tissues. The transitional epithelium's major function is to act as a barrier to keep urine, bacteria, and any other irritant or contaminant from reaching the inner compartment: here the barrier has been breached, the epithelial cells can't maintain the tight junctions that create an effective shield. The submucosa and muscularis are showing signs of edema, hyperemia, and hemorrhage in response to the insult. You can see clear regions of fluid infiltration at the level of the basement membrane (edema), great numbers of red cells in the local vasculature (hyperemia), and leakage of blood outside the vessels.

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