Human schistosomiasis: clinical perspective: review

The clinical manifestations of schistosomiasis pass by acute, sub acute and chronic stages that mirror the immune response to infection. The later includes in succession innate, TH1 and TH2 adaptive stages, with an ultimate establishment of concomitant immunity. Some patients may also develop late complications, or suffer the sequelae of co-infection with other parasites, bacteria or viruses. Acute manifestations are species-independent; occur during the early stages of invasion and migration, where infection-naivety and the host's racial and genetic setting play a major role. Sub acute manifestations occur after maturity of the parasite and settlement in target organs. They are related to the formation of granulomata around eggs or dead worms, primarily in the lower urinary tract with Schistosoma haematobium, and the colon and rectum with Schistosoma mansoni, Schistosoma japonicum, Schistosoma intercalatum and Schistosoma mekongi infection. Secondary manifestations during this stage may occur in the kidneys, liver, lungs or other ectopic sites. Chronic morbidity is attributed to the healing of granulomata by fibrosis and calcification at the sites of oval entrapment, deposition of schistosomal antigen-antibody complexes in the renal glomeruli or the development of secondary amyloidosis. Malignancy may complicate the chronic lesions in the urinary bladder or colon. Co-infection with salmonella or hepatitis viruses B or C may confound the clinical picture of schistosomiasis, while the latter may have a negative impact on the course of other co-infections as malaria, leishmaniasis and HIV. Prevention of schistosomiasis is basically geared around education and periodic mass treatment, an effective vaccine being still experimental. Praziquantel is the drug of choice in the treatment of active infection by any species, with a cure rate of 80%. Other antischistosomal drugs include metrifonate for S. haematobium, oxamniquine for S. mansoni and Artemether and, possibly, Mirazid for both. Surgical treatment may be needed for fibrotic lesions

Urinary Schistosomiasis: review

In this review, the clinical manifestations of urinary schistosomiasis are displayed from a pathogenetic perspective. According to the prevailing host's immune response profile, urinary schistosomiasis may be broadly categorized into cell-mediated and immune-complex-mediated disorders. The former, usually due to Schistosoma haematobium infection, are attributed to the formation of granulomata along the entire urinary tract. As they heal with excessive fibrosis, they may lead to strictures, calcifications and urodynamic abnormalities. The main impact is lower urinary, the site of heaviest ovi-position. Secondary bacterial or viral infection is common, any may be incriminated in secondary stone formation of the development of bladder malignancy. Immune-complex mediated lesions are usually associated with hepatosplenic schistosomiasis due to Schistosoma mansoni infection. Circulating complexes composed of schistosomal gut antigens and different classes of immunoglobulins deposit in the kidneys leading to several patterns of glomerular pathology. The latter have been categorized under six classes based on the histological and immunofluorescence profile. These classes have been linked to respective clinical manifestations and depend on the stage of evolution of the host's immune response, extent of associated hepatic fibrosis and co-infection with salmonella or hepatitis C. Secondary amyloidosis develops in 15% of such patients, representing a critical impairment of macrophage function. The wide clinicopathological spectrum of urinary schistosomiasis mirrors the evolution of the host's immune response according to chronicity of infection, bacterial or viral co-infection and, in the case of glomerulonephritis, to the extent of hepatic co-morbidity

Non invasive assessment of renal failure: comparison between the different available techniques to discriminate different causes of acute renal failure [ARF] from chronic renal failure [CRF] with normal kidney size

Forty-one uremic cases presenting to the emergency of nephrology section and 10 normal control subjects [N] were assessed clinically and biochemically [serum levels of urea, creatinine, uric acid, sodium, potassium, calcium and phosphorus and estimation of FENa] by abdominal ultrasonography, color Doppler of renal arteries and static [DMSA] and dynamic [DTPA] renal scintigraphy. Clinical assessment, follow up and/or renal biopsy showed that uremic cases had ARF due to acute tubular necrosis [ATN] in 16, obstructive uropathy[OBST] in 12 and CRF in 13. ATN showed very high FENa [17.7 +/- 10.5% vs 0.69 +/- 0.19, 13.4 +/- 12.9 and 10.1 +/- 5.6 in ATN, N, OBST and CRF cases, respectively], normal DTPA perfusion with poor DTPA accumulation, flat renogram with very long T1/2 and very high resistivity indices of intrarenal arteries measured by D. OBST showed pelvic caliectasis by US, impaired DMSA uptake, impaired DTPA perfusion with fair DTPA accumulation, rising renogram during the excretory phase with very long T1/2 and very high resistivity indices of intrarenal arteries measured by D. CRF had very high resistivity indices, impaired DTPA perfusion and accumulation with poor excretion, flat renogram with very long T1/2 and very high resistivity indices of intrarenal arteries measured by D. Follow up of ATN and OBST cases showed incomplete normalization of US, D and [DTPA] renal scintigraphy in spite of clinical and chemical recovery. The study concluded that the most reliable noninvasive tool in discriminating cases presenting acutely with uremia is radioisotopic static [DMSA] and dynamic [DTPA] renal scintigraphy. Moreover, clinical, biochemical, ultrasonographic and Doppler studies are neither specific nor sensitive tools in such field. Also, the kidneys did not usually recover completely after ARE

Fimbriated E.coli urinary tract infection in Egyptian children

The issue of E. coli [UTI] in children has received considerable attension over the past two decades, in view of its potential of inducing renal scarring and subsequent functional problems in later life. In this study 56 children with [UTI] were subjected to detailed bacteriological studies, ultrasonographic assessment and whenever applicable, radiological and functional evaluation. E. coli was the commonest organism isolated from their urins, constituting 41.7% of single brands and 75% of mixed infections. 80.8% of E. coli infections involved the upper UT, thereby constituting 58.3% of the total organisms isolated from those patients. 88.5% of patients with E. coli pyelonephritis were P - blood group positive and in 67% the organism was P-fimbriated, as indicated by the Gal-Gal test. The prevalence of P-fimbriated organisms was lower in recurrent infections. Ultrasonographic assessment in patients with E. coli pyelonephritis showed normal findings in 50%, focal scarring in 34.6%, stones in 7.6% and bladder neck obstruction in 3.8%. Only 22.2% of patients with focal scarring had Gal-Gal positive E. coli infection. It is concluded that at P-fimbriated E. coli are virulent organisms that do not require organic UT lesions to cause pyelonephritis in P-blood group positive patients, known to have specific receptors for P-fimbriae

Endemic cytomegalovirus [cmv] infection and renal transplantation in Egypt: a multi-center retrospective study

CMV is highly endemic in this country, its incidence in potential transplant recipients, i.e. Dialysis population is notoriously increased, being reported as 70%. The influence of such high of infection on the course and outcome of renal transplantation in this country is not precisely defined. In attempt to highlight this issue, data on 60 consecutive patients who had received renal allograft in 3 transplant centers were retrospectively analysed. Evidence of previous CMV infection [+ve I[g]G antibodies] was found in 71.2% of recipients and 68.3% of donors. This had no influence on patient [90%] nor on graft [88%] survival at six months. Subsequently, CMV +ve recipients fared progressively worse, with a patient survival of 82% at 1 year. 73% at 2 years and 49% at 3 years, compared to a steady 88% for CMV -ve recipients throughout the whole follow-up period. Graft survival showed a similar trend, being 77%, 65% and 49% at 1, 2 and 3 years respectively. The corresponding figure for CMV -ve recipients stabilised at 74% all through, without any appreciable difference in age, sex original disease, number of HLA mismatches, or immunosuppression. Over the period of follow-up of three years, acute rejection episodes were encountered in 41.9% of CMV +ve recipients, compared to 29.4% in CMV -ve patients [P< 0.05]. Acute rejection followed clinical overt CMV reactivation/ reinfection. There was no significant difference in the mean serum creatinine between the two groups of recipients throughout the study period. Four mortalities were directly attributed to CMV disease including peumonitis and cerebritis [2 cases each]. Two patients developed CMV- related glomeruopathy, presenting as membranous nepropathy in one progressive graft failure in another. CMV and HBV were found to have an additive deleterious effect on the outcome of both patients and graft. Recipients with positive CMV and HB[s]A[b] had lower patient survival [91% at six months, 73% at two years] and graft survival [91% at six months, 63% at six months, 73% at two years] and graft survival [91% at six months, 63% at two years] than the other group with CMV +ve HBV -ve viral status. There was a significantly higher rate of acute rejections [63.6% and 35% respectively, p< 0.01] a significantly higher mean serum creatinine a two years in the former group [3.68 mg/dl and 2.06 mg/dl respectively, P< 0.05]. To conclude, this study has show a distinctly deleterious effect of previous CMV infection on transplant recipients in Egypt. This is expressed by increase morbidity and higher rate of acute rejection, as well as lower patient and graft survival later than six months following transplantation. The associated Hepatitis B virus infection has an additive deleterious effect on the outcome of the renal allografts