Scrub typhus: A rare cause of secondary nephrotic syndrome.

Scrub typhus is an important etiological agent in acute febrile illness in the post-monsoon season in tropical countries. It leads to dreaded complications if left untreated. Acute kidney injury is one such complication. Malaria, syphilis, and HIV have been associated with secondary nephrotic syndrome in pediatric age group. Scrub typhus has been reported only once with nephrotic syndrome. We report a case of scrub typhus-associated nephrotic syndrome with acute kidney injury in a five-year-old female with uneventful outcome.

"Polymorphisms in folate metabolism genes as maternal risk factor for neural tube defects: an updated meta-analysis".

Epidemiological studies have evaluated the association between maternal methylenetetrahydrofolate reductase (MTHFR) C677T, A1298C and methionine synthase reductase (MTRR) A66G polymorphisms and risk of neural tube defects (NTDs) in offspring. However, the results from the published studies on the association between these three polymorphisms and NTD risk are conflicting. To derive a clearer picture of association between these three maternal polymorphisms and risk of NTD, we performed meta-analysis. A comprehensive search was conducted to identify all case-control studies of maternal MTHFR and MTRR polymorphisms and NTD risk. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. Overall, we found that maternal MTHFR C677T polymorphism (OR(TvsC) =1.20; 95% CI = 1.13-1.28) and MTRR A66G polymorphism (OR(GvsA) = 1.21; 95% CI = 0.98-1.49) were risk factors for producing offspring with NTD but maternal MTHFR A1298C polymorphism (OR(CvsA) = 0.91; 95% CI = 0.78-1.07) was not associated with NTD risk. However, in stratified analysis by geographical regions, we found that the maternal C677T polymorphism was significantly associated with the risk of NTD in Asian (OR(TvsC) = 1.43; 95% CI: 1.05-1.94), European (OR(TvsC) = 1.13; 95% CI: 1.04-1.24) and American (OR(TvsC) = 1.26; 95% CI: 1.13-1.41) populations. In conclusion, present meta-analysis supports that the maternal MTHFR C677T and MTRR A66G are polymorphisms contributory to risk for NTD.

Acid exposure induces multiplication of Salmonella enterica serovar Typhi.

Salmonella enterica serovar Typhi faces several environmental stresses while going through the stomach (acidic pH) to the small intestine (basic pH) and intracellularly in macrophages (acidic pH) in humans. The acidic pH followed by alkaline pH in the small intestine might be responsible for expression of certain stress-induced genes, resulting in not only better survival but also induction of multiplication and invasion of the bacterium in the small intestine. Based on this hypothesis, we developed a process wherein we exposed the blood, urine, and stool specimens from 90 acute typhoid fever patients and 36 chronic typhoid carriers to acidic pH to see the effect on isolation rate of S. Typhi. About 5 g of freshly passed unpreserved stool, a centrifuged deposit of 15 ml of urine, and 5 ml of blood clot were subjected to 5 ml of Luria-Bertani (LB) broth (pH 3.5) for 20 min, followed by enrichment in bile broth-selenite F broth. When the combined isolation from all 3 specimens, i.e., blood, urine, and stool, after acid exposure was considered, a total of 77.7% of the acute typhoid patients were observed to be positive for the isolation of the S. Typhi serotype, compared to 8.8% by the conventional method. Similarly, 42% (15/36) of chronic carriers yielded positive for S. Typhi growth after acid exposure, compared to 5.5% (2/36) by the conventional method. It therefore can be concluded that acid shock triggers the multiplication of the bacteria, resulting in better isolation rates from blood clot, stool, and urine specimens.

Clinical, biochemical and outcome profile of dengue fever in hospitalised children in Eastern Uttar Pradesh, India.

Dengue fever is an important cause of acute febrile illness in the postmonsoon season in India. This study was done to record the incidence of dengue in admitted patients with acute febrile illness in a hospital setting. The study also intends to record the clinical, biochemical and outcome profile of paediatric dengue cases admitted in tertiary centres in Eastern Uttar Pradesh, India. It was a prospective case record analysis at a tertiary care research hospital in Eastern Uttar Pradesh. The study recruited fifty-53 children (<18 years) with serology-proven diagnosis of dengue disease. Disease was confirmed by doing Ns1Ag, IgM antibody test by ELISA method. Six hundred children were screened and 53 met the inclusion criteria. The incidence of dengue disease in hospitalised acute febrile illness was 8.8%. There were thirty-one males. The mean age of presentation of the study population was 9.32 ± 5 years with a range of 0.25 - 17 years. Fever (94%), nausea and vomiting (59 %), abdominal pain (55%), persistent vomiting (49%), thrombocytopenia (<100,000 [66%]), and petechiae and purpura (43%) were the important clinical manifestations. Six required intensive care monitoring. There was only one death. Dengue fever is an important cause of acute febrile illness in children. Case fatality rate can be minimised with proper World Health Organisation classification and protocol-based management of cases.

Pediatric Renal Rickets at a Tertiary Center.

We report clinical and etiological profile of 19 children (10 males) with renal rickets managed in the years 2021-2022. Median (IQR) age of presentation was 60 (18-96) months. The commonest cause was renal tubular acidosis (n=8). Genetic analysis revealed the diagnosis in 83% subjects (5 out of 6 tested).

Use of urine with nested PCR targeting the flagellin gene (fliC) for diagnosis of typhoid fever.

This study was planned to evaluate the efficacy of the use of nested PCR with a large volume of easily available urine as an effort to devise a test that can meet the levels necessary to be considered a gold standard for the diagnosis of typhoid fever. A total of 60 subjects with suspected cases of typhoid fever and 20 apparently healthy control subjects were included in the study. The study period extended from March 2010 to June 2011. Blood, urine, and stool specimens were collected from the participating individuals. Nested PCR was done targeting the flagellin gene (fliC) of Salmonella enterica subspecies enterica serotype Typhi. Specimens in all three categories could be collected from 22 of the subjects with suspected cases of typhoid fever; 21 of the 22 urine samples (95.4%) yielded a desired amplicon of 343 bp, whereas none of the urine samples collected from the 20 control subjects (0%) yielded the amplicon. The analyses of blood and stool samples were found to be inferior to urine sample analysis in sensitivity, with detection rates of 90.9% and 68.1%, respectively. Culture isolation was observed to display very poor sensitivity (31.8%). A large volume of urine may be the ideal specimen for PCR-based detection of typhoid fever.

Molecular Study of Childhood Steroid-Resistant Nephrotic Syndrome: A Hospital-Based Study.

Steroid-resistant nephrotic syndrome (SRNS) patients with genetic mutations most commonly have histology of focal segmental glomerulosclerosis (FSGS) and do not respond to immunosuppressive drugs. We report the molecular screening results of 18 pediatric SRNS cases presented to our nephrology clinic. Three pathogenic variants have been detected, two previously reported and one novel variant. The reported pathogenic variants have been detected in NPHS1 and NPHS2 genes. A novel pathogenic variant has been detected in the inverted formin 2 gene ( INF2 ) gene. We did not detect any variant of the WT1 gene. There were 13 males. Mean age of study participants at enrollment was 69 months. There were 12 cases of primary SRNS. The mean duration from onset of symptoms to SRNS diagnosis was 13 months. FSGS and minimal change disease (MCD) were present in the same number of cases. The response rate (complete or partial) to immunosuppressive drugs was seen in only one patient in the genetic SRNS group ( n = 3), while the response rate in nongenetic cases ( n = 15) was 80%. Two nonresponders in the genetic SRNS group had FSGS for histopathology and pathogenic variants (NPHS2 and INF2). The other three nonresponders in the nongenetic SRNS group had both FSGS ( n = 1) and MCD ( n = 2) histopathology. There were two deaths in the study cohort of the nongenetic SRNS group. This study highlights the screening of the SRNS cohort by a panel of extended genes rather focussing on the three most common genes ( NPHS1 , NPHS2 , and WT1 ). This further confirms the molecular etiology of SRNS in three cases and extends the list of pathogenic variants of genetic SRNS in the North Indian population. This is the first study in the eastern part of Uttar Pradesh in India.

Mechanism of CaM kinase IV activation during hypoxia in neuronal nuclei of the cerebral cortex of newborn piglets: the role of Src kinase.

The present study aims to investigate the mechanism of CaM kinase IV activation during hypoxia and tests the hypothesis that hypoxia-induced increased activity of CaM kinase IV is due to Src kinase mediated increased tyrosine phosphorylation of calmodulin and CaM kinase IV in neuronal nuclei of the cerebral cortex of newborn piglets. Piglets were divided into normoxic (Nx, n = 5), hypoxic (Hx, F(i)O(2) of 0.07 for 1 h, n = 5) and hypoxic-pretreated with Src kinase inhibitor PP2 (Hx-Srci, n = 5) groups. Src inhibitor was administered (1.0 mg/kg, I.V.) 30 min prior to hypoxia. Neuronal nuclei were isolated and purified, and tyrosine phosphorylation of calmodulin (Tyr(99)) and CaM kinase IV determined by Western blot using anti-phospho-(pTyr(99))-calmodulin, anti-pTyrosine and anti-CaM kinase IV antibodies. The activity of CaM kinase IV and its consequence the phosphorylation of CREB protein at Ser(133) were determined. Hypoxia resulted in increased tyrosine phosphorylation of calmodulin at Tyr(99), tyrosine phosphorylation of CaM kinase IV, activity of CaM kinase IV and phosphorylation of CREB protein at Ser(133). The data show that administration of Src kinase inhibitor PP2 prevented the hypoxia-induced increased tyrosine phosphorylation of calmodulin (Tyr(99)) and tyrosine phosphorylation of CaM.kinase IV as well as the activity of CaM kinase IV and CREB phosphorylation at Ser(133). We conclude that the mechanism of hypoxia-induced increased activation of CaM kinase IV is mediated by Src kinase-dependent tyrosine phosphorylation of the enzyme and its activator calmodulin. We propose that Tyr(99) phosphorylated calmodulin, as compared to non-phosphorylated, binds with a higher affinity at the calmodulin binding site (rich in basic amino acids) of CaM kinase IV leading to increased activation of CaM kinase IV. Similarly, tyrosine phosphorylated CaM kinase IV binds its substrate with a higher affinity and thus increased tyrosine phosphorylation leads to increased activation of CaM kinase IV resulting in increased CREB phosphorylation that triggers increased transcription of proapoptotic proteins that initiate hypoxic neuronal death.

Clinical Profile and Outcome of COVID-19 Among Immunocompromised Children.

This retrospective study describes the clinical profile, risk of infection and outcome of coronavirus disease-19 in immuno-compromised children. It was found that children on immuno-suppressant medication has 2.89 times increased risk of infection (P=0.01). Disease manifestation was asymptomatic (P=0.01) or mild with predominant gastrointestinal symptoms (P=0.02) without alteration in immunosuppressive treatment regime.

Steroid Sensitive Nephrotic Syndrome: Revised Guidelines.

JUSTIFICATION: Steroid sensitive nephrotic syndrome (SSNS) is one of the most common chronic kidney diseases in children. These guidelines update the existing Indian Society of Pediatric Nephrology recommendations on its management. OBJECTIVE: To frame revised guidelines on diagnosis, evaluation, management and supportive care of patients with the illness. PROCESS: The guidelines combine evidence-based recommendations and expert opinion. Formulation of key questions was followed by review of literature and evaluation of evidence by experts in two face-to-face meetings. RECOMMENDATIONS: The initial statements provide advice for evaluation at onset and follow up and indications for kidney biopsy. Subsequent statements provide recommendations for management of the first episode of illness and of disease relapses. Recommendations on the use of immunosuppressive strategies in patients with frequent relapses and steroid dependence are accompanied by suggestions for step-wise approach and plan of monitoring. Guidance is also provided regarding the management of common complications including edema, hypovolemia and serious infections. Advice on immunization and transition of care is given. The revised guideline is intended to improve the management and outcomes of patients with SSNS, and provide directions for future research.

Thyroid function in patients with idiopathic nephrotic syndrome.

BACKGROUND: Albumin is the major protein excreted in urine in patients with nephrotic syndrome (NS). However, low-molecular-weight proteins including some binding proteins are also excreted. Thyroid hormone and its binding globulins are excreted in urine in excess in nephrotic syndrome. Therefore, it has been postulated that patients with nephrotic syndrome may show hypothyroidism, subclinical or overt. METHODS: In this prospective observational study, patients of idiopathic nephrotic syndrome aged 1-40 years of both gender were included. Serum T3, T4 and TSH were assayed at diagnosis and repeated at 12 weeks or at remission whichever was earlier. Renal biopsy was performed as required. RESULTS: Among 100 patients taken for analysis (42 children, 58 adult), 30 cases were of first episode, 40 were of frequent relapse/steroid-dependent NS, and 30 patients had steroid-resistant NS (SRNS). Three (3%) cases had overt hypothyroidism and 18 (18%) patients had subclinical hypothyroidism. Most hypothyroid cases belonged to SRNS subgroup. Mean Serum T3, T4 and TSH values showed significant improvement in remission in comparison to nephrosis state (P < 0.01). Serum TSH had significant positive correlation (r = 0.391, P < 0.01) with 24-h proteinuria and negative correlation with serum albumin (r = - 0.303, P < 0.01) in nephrosis. CONCLUSION: Hypothyroidism is common among nephrotic syndrome patients especially in SRNS subgroup. Therefore, routine screening is recommended in steroid-resistant nephrotic syndrome patients.

Mechanism of post-translational modification by tyrosine phosphorylation of apoptotic proteins during hypoxia in the cerebral cortex of newborn piglets.

The present study aims to investigate the mechanism of phosphorylation of apoptotic proteins and tests the hypothesis that the hypoxia-induced increased tyrosine phosphorylation of apoptotic proteins Bcl-2 and Bcl-xl is Ca(2+)-influx-dependent. Piglets were divided in normoxic (Nx, n = 5), hypoxic (Hx, n = 5) and hypoxic-pretreated with clonidine (Clo + Hx, n = 4) groups. Hypoxic animals were exposed to an FiO(2) of 0.06 for 1 h. Clonidine (12.5 microg/kg, IV) was administered to piglets 30 min prior to hypoxia. Hypoxia was confirmed by ATP and phosphocreatinine (PCr) levels. Cytosol was isolated and separated by 12% SDS-PAGE and probed with tyrosine phosphorylated (p) -Bax, Bad, Bcl-2 and Bcl-xl antibodies and bands were detected. The ATP levels (micromol/g brain) in the Nx, Hx, Clo + Hx were 4.3 +/- 1.0 (P < 0.05 vs. Hx, Clo-Hx), 0.9 +/- 0.8 and 1.5 +/- 0.3, respectively. The PCr levels in the Nx, Hx, Clo + Hx were 2.7 +/- 0.7 (P < 0.05 vs. Hx, Clo-Hx), 0.9 +/- 0.2 and 0.9 +/- 0.9, respectively. Ca(2+)-influx (pmoles/mg protein) was 4.96 +/- 0.94 in Nx, 11.11 +/- 2.38 in Hx, and 6.23 +/- 2.07 in Clo + Hx (P < 0.05 Nx vs. Hx and Hx vs. Clo + Hx). p-Bcl-2 density was 21.1 +/- 1.1 Nx, 58.9 +/- 9.6 Hx and 29.5 +/- 6.4 Clo + Hx (P < 0.05 vs. Hx). p-Bcl-xl density was 29.6 +/- 1.5 Nx, 50.6 +/- 7.4 Hx and 32.1 +/- 0.1 Clo + Hx (P < 0.05 vs. Hx). p-Bax density was 38.6 +/- 16.2 Nx, 46.1 +/- 5.5 Hx and 41.6 +/- 1.9 Clo + Hx groups (P = NS). p-Bad was 66.7 +/- 12.8 Nx, 71.2 +/- 6.8 Hx and 78.7 +/- 22.5 Clo + Hx groups (P = NS). Results showed that clonidine administration prior to hypoxia prevents the hypoxia-induced increased nuclear Ca(2+)-influx and increased phosphorylation of Bcl-2 and Bcl-xl while phosphorylation of Bad and Bax was not altered. We conclude that post-translational modification of anti-apoptotic proteins Bcl-2 and Bcl-xl during hypoxia is nuclear Ca(2+)-influx-dependent. We propose that blockade of nuclear Ca(2+)-influx that prevents phosphorylation of antiapoptotic proteins may become a neuroprotective strategy.

Mechanism of increased tyrosine (Tyr(99)) phosphorylation of calmodulin during hypoxia in the cerebral cortex of newborn piglets: the role of nNOS-derived nitric oxide.

The present study aims to investigate the mechanism of calmodulin modification during hypoxia and tests the hypothesis that hypoxia-induced increase in Tyr(99) phosphorylation of calmodulin in the cerebral cortex of newborn piglets is mediated by NO derived from nNOS. Fifteen piglets were divided into normoxic (Nx, n = 5), hypoxic (Hx, F(i)O(2) of 0.07 for 1 h, n = 5) and hypoxic-pretreated with nNOSi (Hx-nNOSi, n = 5) groups. nNOS inhibitor I (selectivity >2,500 vs. eNOS and >500 vs. iNOS) was administered (0.4 mg/kg, I.V.) 30 min prior to hypoxia. Cortical membranes were isolated and tyrosine phosphorylation (Tyr(99) and total) of calmodulin determined by Western blot using anti-phospho-(pTyr(99))-calmodulin and anti-pTyr antibodies. Protein bands were detected by enhanced chemiluminescence, analyzed by densitometry and expressed as absorbance. The pTyr(99) calmodulin (ODxmm(2)) was 78.55 +/- 10.76 in Nx, 165.05 +/- 12.26 in Hx (P < 0.05 vs. Nx) and 96.97 +/- 13.18 in Hx-nNOSi (P < 0.05 vs. Hx, P = NS vs. Nx). Expression of total tyrosine phosphorylated calmodulin was 69.24 +/- 13.69 in Nx, 156.17 +/- 16.34 in Hx (P < 0.05 vs. Nx) and 74.18 +/- 3.9 in Hx-nNOSi (P < 0.05 vs. Hx, P = NS vs. Nx). The data show that administration of nNOS inhibitor prevented the hypoxia-induced increased Tyr(99) phosphorylation of calmodulin. Total tyrosine phosphorylation of calmodulin was similar to Tyr(99) phosphorylation. We conclude that the mechanism of hypoxia-induced modification (Tyr(99) phosphorylation) of calmodulin is mediated by NO derived from nNOS. We speculate that Tyr(99) phosphorylated calmodulin, as compared to non-phosphorylated, binds with a higher affinity at the calmodulin binding site of nNOS leading to increased activation of nNOS and increased generation of NO.

Hypoxia-induced activation of epidermal growth factor receptor (EGFR) kinase in the cerebral cortex of newborn piglets: the role of nitric oxide.

The present study aims to investigate the mechanism of EGFR kinase activation during hypoxia and tests the hypothesis that hypoxia-induced increased activation of EGFR kinase in the cerebral cortical membrane fraction of newborn piglets is mediated by nitric oxide (NO) derived from neuronal nitric oxide synthase (nNOS). Fifteen newborn piglets were divided into normoxic (Nx, n = 5), hypoxic (Hx, n = 5) and hypoxic-treated with nNOS inhibitor (Hx-nNOSi, n = 5). Hypoxia was induced by an FiO2 of 0.07 for 60 min. nNOS inhibitor I (selectivity >2,500 vs. endothelial NOS, eNOS, and >500 vs. inducible NOS, iNOS) was administered (0.4 mg/kg, i. v.) 30 min prior to hypoxia. EGFR kinase tyrosine phosphorylation at Tyr1173, an index of activation of EGFR kinase, was determined by Western blot analysis using an anti-phospho (pTyr(1173))-EGFR kinase antibody. Protein bands were analyzed by imaging densitometry and expressed as absorbance (OD x mm(2)). EGFR kinase activity was determined radiochemically using immunopurified enzyme. EGFR kinase activity was expressed as pmols/mg protein/hr. Density of phosphor (pTyr(1173))-EGFR kinase (OD x mm(2)) was 60.2 +/- 9.8 in Nx, 177.0 +/- 26.9 in Hx (P < 0.05 vs. Nx) and 79.9 +/- 15.7 in Hx-nNOSi (P < 0.05 vs. Hx, P = NS vs. Nx). Activity of EGFR kinase (pmoles/mg protein/hr) was 4,603 +/- 155 in Nx, 8,493 +/- 427 in Hx (P < 0.05 vs. Nx) and 4,516 +/- 104 in Hx-nNOSi (P < 0.05 vs. Hx, P = NS vs. Nx). Pretreatment with nNOS inhibitor prevented the hypoxia-induced increased phosphorylation and increased activity of EGFR kinase. We conclude that the mechanism of hypoxia-induced increased activation of EGFR kinase is mediated by nNOS-derived NO.

Proptosis of eyeball in children with medial rectus cysticercosis: report of 2 cases.

PURPOSE: To report 2 children with medial rectus cysticercosis presenting as proptosis of eyeball. METHODS: Case report. RESULTS: In orbital cysticercosis, extraocular muscle cysticercosis is the most common type. Two children, a 12-year-old girl and an 8 year-old boy, presented with proptosis and pain in the left eye. Both were diagnosed with medial rectus cysticercosis based on computed tomographic scan and serologic report and treated with oral albendazole and prednisolone without any residual ocular motility restriction. CONCLUSIONS: We report 2 cases of medial rectus muscle enlargement caused by cysticercosis; describe its clinical importance, diagnosis, and treatment; and present a review of the literature.

Spectrum of Lysosomal Storage Disorders at Tertiary Centre: Retrospective Case-Record Analysis.

Lysosomal storage disorders (LSDs) are relatively common slow progressive inborn error of metabolism encountered by clinicians. This work intends to highlight the more common LSDs, their clinical presentation, outcome, and mutation (wherever feasible) collected from the genetic clinic at tertiary care center in Eastern Uttar Pradesh. The data for analysis were collected retrospectively from genetic records from a follow-up clinic. All cases < 18 years of age were analyzed. Cases with LSDs with confirmed enzyme results were enrolled in this study. Clinical profile, screening test results, and outcome were collected. There were 32 cases including 27 males and 5 females in this cohort: 8 Gaucher disease (GD) patient and 24 non-GD patients. GD (type 1) is the commonest LSD in GD group. Anemia, thrombocytopenia, splenomegaly, and hepatomegaly were the consistent finding in patients with GD (type 1). L483P mutation was reported in two GD patients. One GD patient is on enzyme replacement therapy for 2 years and is currently doing well. The commonest disorders in non-GD were mucopolysaccharidosis (MPS) ( n = 11), metachromatic leukodystrophy ( n = 4), I-cell disease ( n = 3), Niemann-Pick A/B ( n = 3). MPS-II is the commonest MPS among non-GD group.

Ultrafiltered biopulping strategy for the production of good quality pulp and paper from sugarcane bagasse.

This research was carried out with an objective to examine the efficacy of ultrafiltered xylano-pectinolytic enzymes in pulping of sugarcane bagasse. Maximum biopulping was achieved with enzyme dose of xylanase (175 IU / g bagasse) and pectinase (75 IU / g bagasse) at treatment period of 180 min. The temperature, pH, and bagasse to liquid ratio for biopulping experiments were kept constant at 55o C, 8.5, and 1:10 (g/ml), respectively. The ultrafiltered biopulping improved chemical pulping, resulted in 25.11%, 9.17% increase in brightness, unscreened pulp production and 11.81, 59.50, and 49.14% decrease in total solids, rejections. and kappa number, respectively. The bagasse biopulping also resulted in 15% decrease of alkali load to attain similar kappa number and optical properties as obtained under 100% alkali dosage. Ultrafiltered biopulped-unbleached samples showed significant increase in breaking length (13.55%), burst index (40.21%), tear index (19.04%), double fold (42.5%), Gurley porosity (28.21%) and viscosity (13.37%) in comparison with non-enzymatically treated control pulp samples. In comparison with non biotreated-bleached pulp samples, ultrafiltered biopulped-bleached samples also resulted in higher burst index (56.80%), breaking length (17.38%), double fold (39.58%), tear index (3.38%), viscosity (30.68%), and Gurley porosity (52.50%). This environmentally sustainable ultrafiltered biopulping approach for sugarcane bagasse has the potential to decrease the demand of chemicals, ultimately pollution along with enhance the quality of paper.

Eco-friendly pulping of wheat straw using crude xylano-pectinolytic concoction for manufacturing good quality paper.

In this study, suitability of xylano-pectinolytic enzymes in pulping of wheat straw has been explored. The suitable biopulping conditions were optimized, with xylanase dose of 400 and pectinase dose of 120 IU/g wheat straw, 1:10 (g/ml) material to liquid ratio, 55 °C temperature, 3 h treatment time, 0.75% Tween 80 and pH 8.5. Enzymatic pretreatment efficiently increased the pulpability of wheat straw, generated pulp with higher yield, lower kappa number (15.67%) and rejections (59.65%) in comparison with chemical pulp. The brightness of pretreated wheat straw pulp with enzyme was 16.04% higher than that of the non-enzyme treated wheat straw pulp. The biopulping resulted in 12% reduction of pulping chemicals along with more residual alkali content, in order to achieve similar optical and chemical properties as obtained by 100% chemically treated pulp. Physical properties of pulp also improved after enzymatic pretreatment, increasing burst index (26.50%), tear index (18.22%) and breaking length (5.56%). The enzyme plus chemical (88% pulping chemicals) treated pulp showed improvement in brightness and whiteness, with reduction in yellowness at all bleaching stages. In comparison with chemically bleached pulp, biopulp with reduced alkali dose (88%) had higher breaking length (6.63%), double fold number (51.28%), tear index (2.83%), burst index (24.31%), along with increased viscosity (6.12%) and Gurley porosity (27.50%). These results clearly suggest that biopulping of wheat straw with xylano-pectinolytic enzymes can reduce chemical loading during soda-anthraquinone pulping and also improve the quality of paper. This is the first report demonstrating the biopulping of wheat straw using crude xylano-pectinolytic enzymes.