Bladder infection after virus




















Bladder infections occur when bacteria like E. They can cause severe discomfort and a persistent urge to use the bathroom. Bladder infections are one of the most common types of urinary tract infections UTI and disproportionately affect women.

Women are also more susceptible to urinary tract infections during pregnancy and after menopause. When men experience urinary tract infections, they can be caused by a prostate infection or urethral obstruction. Cystitis is simply the medical term describing the inflammation of the bladder. This is most commonly due to a urinary tract infection, but can also occur from certain medications, radiation therapy, irritants, spermicidal jellies, or long-term catheter use.

Due to the variety of causes of cystitis, getting the proper diagnosis is essential to undergoing the correct treatment plan. Interstitial cystitis IC is commonly known as painful bladder syndrome and is defined by the presence of persistent pain, pressure, or discomfort localized in the bladder.

While there are no diagnostic tests to definitively test for interstitial cystitis, testing will be done to rule out other, more serious causes. Painful bladder syndrome is a chronic condition with no known cause. Talk to your doctor to learn more about how to manage discomfort and alleviate symptoms. Bladder infections are associated with a few tell-tale symptoms. If you notice any of the following signs or symptoms, see your doctor immediately :. If you have a urinary tract infection, also commonly referred to as bladder infection, you are certainly not alone.

According to Medscape , a leading online resource for physicians and healthcare professionals around the world, an estimated 25 to 40 percent of American women report having had at least one UTI. The same study also noted that this type of infection causes over 6 million physician visits every year. It is worth pointing out that a UTI is a type of bladder infection. And it is one that typically occurs when bacteria makes its way into the urethra.

The urethra is a tube that allows the movement of urine from the body into the bladder. Here is a notable fact about UTIs. While they can occur in both men and women, they are considerably more common among women. The long and short of it is that women have a much shorter urethra than men, which means that if bacteria were to develop, it does not need to travel as far to reach the bladder where it can cause a urinary tract infection. Moreover, women, particularly those who are of childbearing age, utilize some form of birth control that can further increase their chances of developing UTIs and other bladder infections.

And UTIs are no exception in this regard. For example, diaphragms, one of the more popular forms of birth control, have been shown to push infection-causing bacteria more in-depth into the bladder even if used correctly.

Of course, the reasons behind why UTIs are more prevalent among women compared to men do not end there as the following are also contributing factors:. And this is especially true when it comes to UTIs. According to the Centers for Disease Control and Prevention , an estimated 8 percent of UTIs among women occur while they are pregnant. Even when women are out of their childbearing years, they are still at a high risk of developing a UTI, according to most urologists. Further, studies show that most women produce less estrogen, the primary female sex hormone, after entering menopause.

This alteration, along with a decline in estrogen production , can significantly increase the chances of postmenopausal women developing a UTI.

Though the majority of bladder infections, including UTIs, impact the lives of women, we should recognize that a small percentage of men do develop them as well. And when they do, it is usually caused by an infected or enlarged prostate. However, they are also caused by mineral deposits that form in the bladder, commonly referred to as bladder stones.

In short, any urological condition that prevents the bladder from fully emptying can lead to the development of UTIs and other bladder infections in men. When it comes to bladder infections, which include UTIs, they impact everyone differently. While some women might find themselves struggling with a wide range of symptoms, others may not experience any symptoms at all. One study published by Harvard Health Publishing found that a small percentage of women, even though they may have large numbers of bacteria in their urine, never experience UTI-related symptoms.

This unique phenomenon that affects only a handful of women is known as asymptomatic bacteriuria. And it will usually go away on its own over time. However, in cases where a woman is pregnant, most physicians will recommend antimicrobial therapy to minimize the risk of pregnancy complications.

When it comes to UTIs and other bladder infections, they can affect any part of the urinary system. For reference, the urinary system includes the bladder, kidneys, ureters, and urethra. However, most individuals tend to develop infections in their lower urinary tract, which consists of the urethra and bladder. In any event, symptoms of a bladder infection, with a few exceptions, are the same for both men and women.

The following sections are dedicated to BKV-related syndromes affecting the urinary tract. Early-onset HC occurs typically during or within 48 h after the end of conditioning regimen, and it is the result of a direct toxic effect of drug metabolites and radiotherapy on the bladder mucosa. The concurrent presence of prohemorrhagic abnormalities of coagulation, severe thrombocytopenia and mucosal inflammation are predisposing factors for any type of HC.

The pathogenesis of BKV is not well understood as similarly high urine BKV loads are found in kidney transplant patients, most of whom do not develop cystitis or gross hematuria Funk et al. Rather, a sequence of events has been suggested, starting with subclinical urothelial damage by the conditioning regimen, high-level BKV replication leading to viral denudation of the pre-damaged regeneration-impaired urothelial lining and urinary leakage in the submucosa followed by hemorrhagic exacerbation with abundant inflammatory cell infiltrates following allogenic stem cell engraftment Bedi et al.

Indeed, conditioning involving cyclophosphamide, busulfan and total body irradiation has been implicated, and the pronounced toxic, inflammatory properties of cyclophosphamide and its metabolite acrolein are supported by clinical and experimental studies Romih et al. Adenovirus, JCV, citomegalovirus CMV and other infectious bacteria, parasite and non-infectious etiologies bleeding disorders with or without low platelet count, primary or metastatic neoplasia, vesical catheter or ureteric stenting may also cause hemorrhagic cystitis, and must be excluded for appropriate diagnosis and management Hirsch and Pergam, a , Hirsch and Pergam, b.

The severity of hematuria is commonly described as microscopic grade 1 ; macroscopic grade 2 ; macroscopic with clots grade 3 ; or macroscopic with clots and postrenal failure secondary to urinary tract obstruction grade 4. The first reports describing disease resembling polyomavirus-associated nephropathy PyVAN in kidney transplant patients, came as early as Coleman et al.

At that time, new and more potent immunosuppressive regimens were being taken into use, capable of decreasing the rejection rates at the expense of increased risk of opportunistic infections like BKV.

PyVAN rarely affects patients other than kidney transplant recipients, and so far only 26 cases of biopsy confirmed PyVAN, in native kidneys of other immunocompromised patients, have been reported Sharma et al. This clearly suggests that there must be risk factors associated with the allograft and not only with the suppressed immune status.

Prognostication is complicated by the many putative risk factors, including HLA-mismatch, donor gender female and age high , recipient of male gender, type and dose of immunosuppressive medication and transplantation events such as ureteric stents, steroid exposure and acute rejection Brennan et al.

The pathogenesis of PyVAN is characterized by high-level BKV replication in the renal-tubular epithelial cells of the transplanted kidney leading to cytopathogenic loss and thereby denudation of the epithelial monolayer in the allograft tubulus. As a consequence, the virus leaks into the tissue and bloodstream and inflammatory cells infiltrate the interstitium leading to tubular atrophy and interstitial fibrosis.

This reduces the graft function and increases the risk of graft loss. Of note, the urothelial cells may also play an important role in PyVAN. This is supported by histopathologic data revealing extensively infected urothelial cells in the bladder of patients with PyVAN.

In agreement with this, primary human urothelial cells from bladder were found to be very permissive to BKV infection. BKV was first identified in the urine of a renal transplantation recipient with the initials B. Sylvia Gardner in the kidney transplant patient from whom BKV was initially isolated, was suffering from ureteric stenosis Gardner et al.

Since then, there have been several reports on BKV-associated ureteric stenosis, usually in kidney transplant patients, both pediatric Rajpoot et al. The pathogenesis of ureteric stenosis is still not completely resolved. Coleman suggested in that high-dose steroids, given to kidney transplant patients post-transplantation, permitted reactivation of BKV Coleman et al.

The ureteric epithelium which was damaged by ischemia or inflammation supported infection and was replaced with granulation tissue. In a study of kidney transplanted cynomolgus monkeys receiving immunosuppression, a reactivation of a new polyomavirus called cynomolgus polyomavirus occurred in 12—57 monkeys Van Gorder et al. The virus was detected in the urothelium of graft ureters in association with inflammation and in the smooth muscle cells of the ureteric wall showing signs of apoptosis.

A significant incidence of late onset stenosis was seen. Apparently, ureteric stenosis is now less frequently reported, possibly due to better surgical techniques and a decline in the use of ureteral stents Hirsch, In renal transplant patients and more generally in those suffering from immune system impairments, human polyomaviruses can on rare occasions cause tubulo-interstitial nephritis.

Nevertheless, data regarding the ability of JCV to induce ureteral and bladder damage are very scarce Di Maida et al. The triggering mechanisms for JC virus reactivation are not well defined yet. It has recently been suggested that there is a higher risk of JC virus reactivation in immunocompromised patients and those treated with immunomodulatory drugs for chronic inflammatory disorders, hematological malignancies, or following organ transplantation Kartau et al.

However, drug specific causality is difficult to assess, since most patients receive multiple immunomodulatory medications concomitantly or sequentially, or present with several immunocompromising factors related to their underlying disease. At the level of the urinary tract, the association between patient immune status and JCV pathogenicity appears even more ambiguous, due to the limited available evidence. The central nervous system and kidney are considered as the reservoirs of JC virus infection, in which the virus can persist in latency after primary infection.

The possible role of JC virus in urinary tract involvement has only recently been recognized. Based on laboratory findings and PCR studies, several authors have long considered BK virus as the only polyomavirus eventually affecting the kidneys and urinary tract. Indeed, although genomic sequences of both JCV and BKV DNA have been detected by PCR in renal biopsies of transplanted patients, combined immunohistochemical and molecular biology studies suggested that renal impairment was secondary to the replication of BK virus, whereas JC virus was usually present as a co-infecting agent in a latent, non-replicative phase Boldorini et al.

As such, JC virus has long been considered unable to elicit pathological effects. Nickeleit et al. Conversely, Boldorini et al. JC virus-related nephropathy is now recognized as a rare cause of nephropathy in transplant recipients Wiegley et al. Ureteral and bladder involvement is more rarely reported in different types of immunosuppressed patients Cavallo et al.

As the initial presentation of PyVAN is insidious, it is strongly recommended to screen kidney transplant patients regularly for early diagnosis Hirsch, Screening should be performed at least every 3 months the first 2 years after transplantation and then annually until the fifth year of post-transplantation.

Alternatively, cytological examination of urine in search of decoy cells Mackenzie et al. No specific anti-viral therapy has been developed to treat PyVAN. Thus, early treatment before the development of irreversible histopathological damage are important to ensure a favorable prognosis. Currently, the AST guideline recommends two strategies Hirsch et al. In addition, several medical treatments have been tried, including intravenous immunoglobulin Piburn and Al-Akash, , cidofovir Kuten et al.

The drug is taken up via the organic anion transporters OAT1 , which are mainly expressed on the basolateral side of renal tubular epithelial cells. Cidofovir is nephrotoxic and has less potent anti-BKV activity than the other therapies. Intravenous immunoglobulin through osmotic injury causes vacuolation in proximal tubular epithelial cells, in turn leading to acute kidney injury Levy and Pusey, Fluoroquinolones are synthetic broadspectrum antimicrobial agents targeting the bacterial enzymes topoisomerase II and IV and are also suggested to interfere with the helicase activity of BKV LTag Ali et al.

Critical aspects of Fluoroquinolone in this setting are related to their gastrointestinal and central nervous system side effects, given the lack of significant effects on BKV replication and hemorrhagic cystitis severity, and the selection of antibiotic resistance Walker, None of these treatments have sufficient clinical data supporting their use as standard practices.

PyVAN sometimes accompanies acute rejection; these cases are difficult to treat. Due to the lack of effective anti-viral drugs, the main therapeutic strategy is to reduce immunosuppression; at the same time, clinicians must pay attention to the risk of allograft rejection. Therapy for PyVHC is purely supportive, involving symptom relief by analgesia, hyperhydration to increase diuresis and continuous bladder irrigation to prevent clot formation and urinary tract obstruction Hirsch et al.

Moreover, lost platelets and erythrocytes are substituted. Other treatments of PyVHC aim at repair and regeneration of the urothelial mucosa through hyperbaric oxygen therapy or by topical application of fibrin glue. Finally, topical applications to the damaged bladder mucosa to achieve hemostasis through cystoscopy have been reported in single-center retrospective series of 35 patients.

Similarly, several compounds to reduce bleeding have been used in case studies and small series, e. As the understanding regarding the pathogenesis of PyVHC is evolving, new potential therapeutic targets are expected to emerge. Recently, Schneidewind et al. Such culture methods will highlight the interactions between BKV and human urothelial cells which might unveil the unknown nuances associated with BKV pathogenesis.

Furthermore, they might facilitate the in vitro testing of antiviral drugs against new potential therapeutic targets Schneidewind et al. In a recent experimental study, a novel 3D cell culture approach was used to study BKV pathogenesis and potential new therapeutic targets. Although tocilizumab an anti-IL-6 antibody did not yield significant results in this study, its role in the treatment of BKV infection will need detailed further exploration, as IL-6 is an important component of the STAT3 pathway Schneidewind et al.

Likewise, it may be expected that further experimental studies focussed on the STAT3 pathway in BKV infection might unveil more potential therapeutic targets. Polyomavirus BK persistently infects the majority of people at an early age, usually without causing disease. Pathological consequences appear mainly in immunodeficient individuals, an expanding patient group due to transplantations, use of immunosuppressive therapy and the increasing average age of the population.

Safe and effective antiviral treatment of BKV diseases is still lacking and for patients with PyVAN, the only treatment strategy with documented effect is reduction of immunosuppressive therapy. Screening of asymptomatic HSCT patients at risk remains an area of investigation and is presently not recommended, as pre-emptive therapy is not established DII. Specific antiviral prophylaxis is not available and fluoroquinolones are not recommended. PyVHC treatment is based on the best supportive therapy, such as hyperhydration, bladder irrigation, platelet transfusions as needed to reduce bleeding, and pain treatment, particularly when using myeloablative conditioning based on cyclophosphamide, busulfan and total body irradiation.

Antiviral treatment with intravenous cidofovir is controversial due to the absence of randomized controlled studies. Until the availability of safe and effective antivirals, the use of cidofovir may be an option although there is uncertainty of efficacy, the best dose schedule and the need to balance any benefit against its renal side effects.

Non-specific measures aimed at speeding the healing process of the damaged urothelial lining such as hyperbaric oxygen therapy or urologic fibrin glue application have been successful in a limited number of uncontrolled studies.

No recommendation is possible for several other treatments such as the administration of intravesical sodium hyaluronate, intravenous FXIII concentrate, leflunomide, estrogens, mesenchymal cells and cellular immune therapy because these treatments have only been used sporadically in a very limited number of patients or are still experimental.

These evidence-based recommendations are applicable for both pediatric and adult patients. In conclusion, despite much progress in understanding the pathogenesis, epidemiology and risk factors of PyVHC, this complication still represents a disabling unmet clinical need with limited prophylactic and therapeutic options. To overcome this deficiency will require novel antiviral treatment approaches supported by proper clinical trials. BKV PCR-based search is performed every 3 months in the first year post-transplantation, every 6 months in the second year, and annually thereafter.

The search for SV40 on renal tissue is also performed in order to quantify the renal injury. Our strategy in case of clinically significant BKV infection is based on three progressive steps:. They are known to cause upper respiratory, gastrointestinal, and conjunctival infections in healthy people and children; however, their pathogenicity is altered by the immunologic status of the host, and in immunocompromised patients, ADV can affect many other systems Ison, Types 1—51 were identified by serotyping, whereas types 52—67 were identified by genomic sequencing and bioinformatic analysis.

As the assay for ADV detection covers only a proportion of the currently known virus types, the occurrence of ADV infection of the urinary tract may have been underestimated. In addition, ADV has been identified as the causative agent of various diseases, including acute upper respiratory inflammation, pneumonia, pharynx conjunctivitis, gastroenteritis, hepatitis, and myocarditis Echavarria, Normally, ADV causes asymptomatic infection of lymphoepithelial tissues, but in the immunocompromised patient, they can reactivate the latent infection or cause de novo infection.

The adenoviral infections are more common in stem cell transplantation and solid organ transplantations. ADV are ubiquitous infectious agents that cause significant morbidity and even loss of life, particularly in select groups of at-risk individuals. Troubling outbreaks of ADV infection occur far too frequently, and these can also affect otherwise healthy individuals not normally at risk for serious infection. History of solid organ or bone marrow transplantation and use of immunosuppressants aids in diagnosis because ADV cystitis occurs almost exclusively in immunocompromised patients.

Most cases of ADV-related hemorrhagic cystitis occur within 12 months of transplantation Hofland et al. The adenoviral infection can often coexist with Aspergillosis and CMV in immunocompromised patients, and broad cultures should be obtained.

A urine bacteriological culture, urine cytology, and the presence of urine ADV and BKV DNA were examined in those with a diagnosis of urinary tract infection based on symptoms of macrohematuria and dysuria i. ADV DNA in the urine and blood is detected using a qualitative polymerase chain reaction assay Lion, for ADV types 1—6, 8, 19, and 37; types 7 and 11 were also included because of hemorrhagic cystitis. Your kidneys, located in the rear portion of your upper abdomen, produce urine by filtering waste and fluid from your blood.

A urinary tract infection UTI is an infection in any part of your urinary system — your kidneys, ureters, bladder and urethra. Most infections involve the lower urinary tract — the bladder and the urethra. Women are at greater risk of developing a UTI than are men. Infection limited to your bladder can be painful and annoying. However, serious consequences can occur if a UTI spreads to your kidneys. Doctors typically treat urinary tract infections with antibiotics. But you can take steps to reduce your chances of getting a UTI in the first place.

Urinary tract infections don't always cause signs and symptoms, but when they do they may include:. UTIs may be overlooked or mistaken for other conditions in older adults. Each type of UTI may result in more-specific signs and symptoms, depending on which part of your urinary tract is infected. Contact your doctor if you have signs and symptoms of a UTI. Urinary tract infections typically occur when bacteria enter the urinary tract through the urethra and begin to multiply in the bladder.

Although the urinary system is designed to keep out such microscopic invaders, these defenses sometimes fail. When that happens, bacteria may take hold and grow into a full-blown infection in the urinary tract.

The most common UTIs occur mainly in women and affect the bladder and urethra. Infection of the bladder cystitis. However, sometimes other bacteria are responsible.



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