Multiple Sclerosis (MS) is a chronic disease of the central nervous system where the immune system mistakenly attacks the myelin sheath protecting nerve fibers. This damage disrupts the electrical signals traveling between the brain and the body, leading to a wide range of neurological symptoms. A urinary tract infection (UTI) is a common and often serious complication for individuals with MS. UTIs reduce quality of life and can trigger a temporary worsening of existing MS symptoms, sometimes called a pseudo-exacerbation. This heightened susceptibility is primarily rooted in the neurological damage from MS that directly affects bladder function.
MS Damage and Bladder Control
The primary reason MS patients experience bladder issues is demyelination that creates lesions on the nerve pathways regulating urination in the brain and spinal cord. The brain and bladder must communicate seamlessly to coordinate storing and emptying urine. When this communication is interrupted, it results in a neurogenic bladder, which affects up to 85% of people with MS. Lesions can cause the detrusor muscle to contract involuntarily and prematurely, leading to detrusor overactivity, urinary frequency, urgency, and sometimes urge incontinence. Conversely, nerve damage can interfere with the signaling that tells the detrusor muscle to contract fully or the sphincter muscles to relax during urination.
This lack of coordination between the bladder muscle and the sphincter is known as detrusor-sphincter dyssynergia. The result is that the bladder cannot empty properly, leading to urinary retention. This incomplete emptying sets the stage for bacterial overgrowth and subsequent infection. The type of bladder dysfunction experienced, whether overactive or underactive, depends on the location of the lesions.
Incomplete Emptying and Bacterial Growth
Urinary retention, the inability to fully empty the bladder, is the most significant factor in UTI development. When the bladder fails to contract effectively or the sphincter fails to relax completely, residual urine remains in the bladder after voiding. This retained urine creates a pool of stagnant fluid. Normal urination acts as a flushing mechanism, washing away bacteria. When this natural defense fails, the residual urine provides a warm, nutrient-rich environment where bacteria can multiply unimpeded. The most common culprit is Escherichia coli (E. coli), which originates in the bowel.
The prolonged presence of bacteria allows them to adhere to the bladder wall, making them difficult to dislodge. In severe cases of retention, increased pressure can cause urine to back up into the ureters and toward the kidneys. This backward flow, called vesicoureteral reflux, can lead to pyelonephritis, a serious kidney infection.
Secondary Factors Increasing UTI Risk
Factors beyond direct neurological damage also contribute to the high frequency of UTIs in the MS population. Reduced mobility and impaired dexterity, which are common MS symptoms, make maintaining proper personal hygiene difficult. Simple actions like wiping become challenging, increasing the likelihood of bacteria migrating from the anal area to the urethra.
Many individuals with MS rely on assistive devices to manage bladder dysfunction, which introduces an external risk for infection. The use of catheters, such as intermittent self-catheterization or indwelling catheters, provides a direct pathway for bacteria to enter the bladder. Even with meticulous technique, any foreign body can become a site for bacterial colonization and biofilm formation.
Some people with MS restrict fluid intake to avoid the frequent and urgent need to urinate or to minimize the need to find an accessible restroom. This reduced hydration results in less dilute urine and less frequent flushing of the urinary tract. Less frequent urine flow concentrates the bacteria, undermining the body’s natural defense mechanism against infection.