Severe infection including disseminated herpes zoster triggered by subclinical Cushing's disease: a case report.

BACKGROUND: Subclinical Cushing's disease (SCD) is defined by corticotroph adenoma-induced mild hypercortisolism without typical physical features of Cushing's disease. Infection is an important complication associated with mortality in Cushing's disease, while no reports on infection in SCD are available. To make clinicians aware of the risk of infection in SCD, we report a case of SCD with disseminated herpes zoster (DHZ) with the mortal outcome. CASE PRESENTATION: An 83-year-old Japanese woman was diagnosed with SCD, treated with cabergoline in the outpatient. She was hospitalized for acute pyelonephritis, and her fever gradually resolved with antibiotics. However, herpes zoster appeared on her chest, and the eruptions rapidly spread over the body. She suddenly went into cardiopulmonary arrest and died. Autopsy demonstrated adrenocorticotropic hormone-positive pituitary adenoma, renal abscess, and DHZ. CONCLUSIONS: As immunosuppression caused by SCD may be one of the triggers of severe infection, the patients with SCD should be assessed not only for the metabolic but also for the immunodeficient status.

[Microbial associations defecting in children with chronic pyelonephritis].

AIM: To study rate of detection of bacteria and viruses from different taxonomic groups and their associations in children with pyelonephritis. MATERIALS AND METHODS: Two hundred seventy-four patients aged 5-10 years divided on two groups were studied: 1st group--240 children with chronic secondary pyelonephritis, 2nd group--children with nephrectomy due to terminal stage of renal obstructive process. Qualitative and quantitative composition of bacterial flora in urine and renal biopsy samples was studied by bacteriological methods as well as presence of viruses (HSVI, HSVII, CMV, EBV, HPV) by means of PCR. RESULTS: In group 1, 72.2% of children had bacterial mixed infection with associations of coagulase-negative staphylococci, Escherichia, peptococci, and Mycoplasma. Herpesviruses and human papillomaviruses were detected in 50.0% of cases. In group 2, bacterial flora was isolated from preoperative urine in diagnostically-significant titer in 91.2% of cases, whereas in urine obtained from the same patients during operation the microorganisms were detected in 38.2% of cases with predominance of Mycoplasma and Ureaplasma. Bacteriological tests of renal biopsy samples yielded bacteria in 29.5% of cases. Studied viruses were detected in preoperative and intraoperative urine as well as in renal biopsy samples in 52.9%, 44.1%, and 58.8% of cases, respectively. In 32.4% of patients viruses were detected in biopsy samples but not in intraoperative renal pelvis' urine. There was no difference in HPV and CMV detection rate in the nephrectomy group. CONCLUSION: Bacterial-viral mixed infection is encountered in children with obstructive pyelonephritis and this should be taken into account during diagnostics and treatment of this condition.

[Type 1 and type 2 interferon inductor (cycloferon) in therapy of children with pyelonephritis associated with herpes viruses].

The clinical and laboratory efficacy of the treatment of children with pyelonephritis with addition of cycloferon, an inductor of early interferon of types 1 and 2, to the main therapy was studied. The mechanism of the cycloferon action was described. The clinical and laboratory remission within a year was observed in 64.3% of the patients treated with addition of cycloferon vs. 47.1% of the patients under the main therapy without the cycloferon addition. The number of the relapses lowered to 7.1% vs. 20.6% of the episodes in the control group. The minimal risk of the disease exacerbation (0.37) in the patients treated with cycloferon and the relative risk of the unfavourable outcomes among the patients under the therapy with addition of cycloferon (0.5967< or =1) were determined.

Isolated Neurogenic Bladder Associated With Human T-Lymphotropic Virus Type 1 Infection in a Renal Transplant Patient From Central Australia: A Case Report.

BACKGROUND: Human T-lymphotropic virus type 1 (HTLV-1) is endemic amongst the Aborigines of the Northern Territory of Australia. HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) has been associated with this infection. In general population, isolated neurogenic bladder dysfunction in HTLV-1-infected individuals without HAM/TSP has been reported, and the HTLV-1 proviral load has been found to be higher in such patients compared with asymptomatic carriers. In solid organ transplantation, few cases of HAM/TSP have been reported worldwide, but not an isolated neurogenic bladder. CASE: A 50-year-old indigenous women from Alice Springs with end stage renal disease secondary to diabetic nephropathy with no prior history of bladder dysfunction received a cadaveric renal allograft following which she developed recurrent urinary tract infections. The recipient was seropositive for HTLV-1 infection. HTLV-1 status of donor was not checked. Urodynamic studies revealed stress incontinence and detrusor overactivity without urethral intrinsic sphincter deficiency. She had no features of myelopathy. There was elevation of the serum and cerebrospinal fluid HTLV-1 proviral load. The magnetic resonance imaging myelogram was normal. Pyelonephritis was diagnosed based on clinical features, positive cultures, and renal allograft biopsy. Continuous suprapubic catheter drainage helped preventing further episodes of allograft pyelonephritis in spite of chronic colonization of the urinary tract. CONCLUSION: Isolated bladder dysfunction is a rare manifestation of HTLV-1 infection and is probably associated with high proviral loads. This may adversely affect renal allograft and patient outcomes.

Urolithiasis associated with experimental lymphocytic choriomeningitis virus inoculation in Lewis rats.

A high frequency of struvite urolithiasis, hydronephrosis, and other urinary tract lesions developed in a group of Lewis rats inoculated intracranially with lymphocytic choriomeningitis virus (LCMV). Initially, clinically ill rats were referred to necropsy: 30 rats over 3 years. These rats had high frequency of urolithiasis (8/30, 27%), hydronephrosis (12/30, 40%), cystitis (9/30, 30%), transitional cell carcinoma (4/30, 13%), and pyelonephritis (19/30, 63%). Lesions were more common in LCMV-inoculated rats. After this trend was noted, all rats on this protocol were necropsied as part of a cohort study (n = 144). Although the apparent frequency of disease was lower due to increased sampling, there still was a high number of urolithiasis (9/144, 6%) and hydronephrosis (40/144, 28%) cases. All cases of urolithiasis developed in rats inoculated with LCMV (9/44, 20%), as did most cases of hydronephrosis (31/44, 70%). Although sham-injected and uninoculated control rats also had high frequency of hydronephrosis (6/57 [11%] and 3/43 [7%], respectively), LCMV-inoculated rats had a significantly higher frequency of disease than did sham inoculated (P < 0.0001) and uninoculated (P < 0.0001) controls. These results suggest that Lewis rats may be predisposed to developing lesions of the urinary tract, and that intracranial inoculation of rats with LCMV augments this tendency, leading to formation of struvite calculi and associated urinary tract disease.

Adenovirus-induced obstructive uropathy with acute renal failure in an immunodeficient child.

Viral infections represent severe complications in immunodeficient patients, associated with significant morbidity and mortality. We report a case of a bone marrow-transplanted adolescent with hemorrhagic cystitis 4 weeks after transplant, associated with renal failure because of obstructive pyelonephritis. Diagnostic workup finally revealed adenovirus infection. A double-J stent was inserted with spontaneous favorable evolution thereafter. Adenovirus infection in an immunocompromised patient can cause hemorrhagic cystitis without specific symptoms and might evolve toward obstructive pyelonephritis because of tubular necrosis. Diagnosis is made by urine culture and/or blood polymerase chain reaction. In case of fatal dissemination, diagnosis might only be revealed on autopsy.

Acute graft pyelonephritis following renal transplantation.

BACKGROUND: Urinary tract infection is the most common form of bacterial infection encountered in a renal transplant recipient. Studies explaining the long-term consequences of acute graft pyelonephritis (AGPN) are few. METHODS: A total of 1022 consecutive renal allograft recipients were studied retrospectively over a period of 10 years for evidence of AGPN. These patients were classified into two groups according to the presence or absence of at least one AGPN episode. Only culture-proven infections were included in the study. RESULT: Of the 1022 renal transplant recipients, 169 patients (16.5%) developed AGPN. In the multivariate analysis with stepwise logistic regression, significant associations were observed between AGPN and placement of ureteric stent (odds ratio [OR]=4.6), urological malformations of native kidney (OR=2.1), cytomegalovirus (CMV) disease (OR=2.0), mycophenolate mofetil (MMF)-based regimen (OR=1.9), and acute rejection episodes (OR=1.5). However, age>40 years, female gender, induction therapy, anti-CD3 treatment, and hyperglycemia did not show such an association. In comparison with the non-AGPN group, these patients had a lower graft and patient survival (though it did not attain statistical significance). In the multivariate analysis using the Cox model for the entire study population, AGPN did not independently contribute to poor graft or patient survival. CONCLUSION: AGPN in the renal transplant setting is an ominous event, as these patients are also more prone to develop bacteremia, acute rejection, and CMV disease, which could then lead to poor graft and patient survival. Its association with MMF needs further clarification.

Adenovirus pyelonephritis in a pediatric renal transplant patient.

Gross hematuria, graft pain, and rising serum creatinine are classic signs of acute rejection, obstruction, or bacterial pyelonephritis for patients with renal transplants. This presentation often prompts percutaneous renal allograft biopsy. If subsequent evaluation fails to show evidence of acute rejection, obstruction, or bacterial infection, viral etiologies should be considered. We report a 14-year-old Hispanic female with a living-related renal transplant who had gross hematuria, graft tenderness, and increased serum creatinine, but did not have evidence of acute rejection, obstruction, or bacterial pyelonephritis. To our knowledge, this is the first report of adenovirus pyelonephritis in a transplanted kidney of a pediatric patient, with isolation of adenovirus in the urine and in the allograft using immunocytochemical techniques.