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Aim: This study was aimed to determine the virulent genes and antibiotic resistance patterns among circulating diarrheagenic Escherichia coli (DEC) pathotypes in a tertiary care health center in east of Nigeria. Materials and Methods: Diarrheal stool samples were obtained from 80 children under 5 years and E. coli was isolated and identified using standard biochemical and molecular methods. Multiplex polymerase chain reaction (PCR) was used to detect eight virulent genes of DEC. Disk diffusion method was used to determine the antibiotic susceptibility of DEC. Results: DEC infection was observed in 54 (68%) children among which ial gene for enteroinvasive E. coli (EIEC) (40% [n=22]) was commonly detected followed by eltA/eltB for enterotoxigenic E. coli (ETEC) (30% [n=16]), pCVD for enteroaggregative E. coli (EAEC) (20% [n=11]), and eaeA/bfpA for typical enteropathogenic E. coli (EPEC) (10% [n=5]). The DEC isolates phenotypically exhibited resistance for ampicillin (AMP) (44 [81%]), followed by ciprofloxacin (CIP)/ levofloxacin (LEV) (28 [52%]), cefoxitin (FOX) (11 [20%]), and amoxicillin-clavulanic acid (AMC) (6 [11%]). About 60% isolates of stable toxins-ETEC were resistant to AMC, CIP, and LEV while all the labile toxin-ETEC exhibited resistance to AMP. About 60% (n=6) resistance were seen in EAEC against ampicillin, AMC, FOX, CIP, and LEV. In EIEC, all the isolates (n=22) were resistant to AMP while 50% (n=11) were resistant to both CIP and LEV. All EPEC (n=5) were resistant to AMP, FOX, CIP, and LEV. Conclusion: High frequency of virulent ial and eltA/eltB genes for EIEC and ETEC, respectively, suggests that they are the primary etiological agents of diarrhea in children among DEC pathotypes. Resistance of DEC to more than two classes of antibiotics indicate possible emergence of multidrug resistance.

Nitric oxide maintains the integrity of the gastric epithelium and is also elevated in diarrheal disease condition. Nitric oxide synthase isoforms (NOS) are responsible for production of nitric oxide (NO) in physiological and pathophysiological circumstances. Zinc supplementation has been used as part of treatment of infants and children with diarrheal illnesses in most developing nations. The aim of this study was to establish the effect of zinc-fortification on fecal nitric oxide and colonal inducible nitric oxide synthase gene in enterotoxigenic E. coli (ETEC) induced zinc-deficient diarrhea. Albino rats were grouped into normal fed (NF), zinc deficient (ZD) and zinc fortified (ZF) groups with control, LT-ETEC induced and ST-ETEC induced diarrheal sub-groups. Nitric oxide concentrations were determined in feces using griess reaction system while reverse transcription polymerase chain reaction with GAPDH gene as internal reference was used to monitor the presence of colonal inducible NOS gene. The amount of stool output was significantly (p ˂ 0.05) increased in normal fed and zinc deficient LT [661 ± 2.00], [760 ± 2.22] and ST-induced [772 ± 2.00], [886 ± 2.12] groups when compared with the control [555 ± 3.03], [600 ± 3.11] groups, respectively. Fecal nitric oxide significantly increased in LT [82.09 ± 1.30], [132.24 ± 2.24] and ST-ETEC [68.81 ± 2.30], [88.21 ± 1.14] induced groups in NF and ZD rats when compared with controls [54.27 ± 1.23], [66.86 ± 2.01], respectively. When compared with both NF and ZD rats, fecal NO decreased significantly in ZF rats in both LT [48.06 ± 0.96] and ST-induced [45.48 ± 0.60] groups. The colonal inducible nitric oxide synthase gene was not detected in NF, ZD and ZF rats. Zinc deficiency increased both stool output and fecal nitric oxide in ETEC induced diarrhea, while zinc-fortification reduced stool output and restores fecal nitric oxide. This suggests that zinc and nitric oxide play a role in mediating pathological conditions in ETEC-induced diarrhea of which inducible nitric oxide synthase may not be involved.

Selenium nanoparticles (SeNPs) and metformin (Met) elicit individually protective effects against testicular oxidative injury in diabetic rats. However, the combined effects of both compounds have not been investigated. We investigated the effects of SeNPs and Met individual/co-treatment on testicular oxidative injury in diabetic rats. Diabetes was induced by a single intraperitoneal administration of streptozotocin (STZ-40 mg/kg bwt). The rats were equally divided into 6 groups: Group one—non-diabetic; group two—diabetic untreated; and group six—non-diabetic received citrate buffer (2 mL/kg bwt), while group three, four, and five received SeNPs (0.1 mg/kg bwt), Met (50 mg/kg bwt), and SeNPs/Met combined respectively, for 42 days. Results revealed that SeNPs, as well as Met treatment significantly (p

Tamoxifen (TAM) is used in breast cancer chemotherapy since its approval by the Food and Drug Administration in 1977. However, TAM therapy is accompanied with hepatotoxicity - a source of worry to clinicians. Oxidative stress and inflammation are the major implicated mechanisms contributing to TAM hepatotoxicity. In this study, we explored whether zinc (Zn) supplementation could prevent TAM-induced hepatotoxicity in female Wistar rats. Rats were subjected to oral pretreatment of Zn (100 mg/kg body weight (b.w.)/day) for 14 days against hepatic toxicity induced by single intraperitoneal administration of TAM (50 mg/kg b.w.) on day 13. TAM markedly elevated serum liver enzymes, whereas total protein and albumin considerably reduced. TAM caused prominent depletion of hepatic-reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity. Also, TAM significantly increased malondialdehyde (MDA) level. Further, it raised liver levels of tumor necrosis factor-α (TNF-α), interleukin-1β, (IL-1β), interleukin-6 (IL-6), and nitric oxide (NO) confirmed by the liver histopathological alterations. The mechanistic inflammatory expression of inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-ĸB), and expression of caspase-3 protein prominently increased. Zinc supplementation significantly modulated serum liver function markers, antioxidant enzymes, and GSH and MDA levels. Zinc downregulated the expression of cytokines, NO, iNOS, NF-ĸB and caspase-3, and ameliorated histopathological changes. Zinc protects against TAM-induced hepatotoxicity; it may serve as an adjuvant supplement for female patients undergoing TAM chemotherapy.

Background: Acute gastroenteritis is a common infectious disease with a high rate of morbidity and mortality in children below five years of age. Appropriate empirical treatment is therefore vital for reducing the incidence of the disease. Objective: This study aimed at determining the trends in the empirical treatment of hospitalized children with acute gastroenteritis. Method: The study involved the data analysis of 88 medical folders of children who were diagnosed with gastroenteritis from January to February 2020 (a period of gastroenteritis yearly outbreak) in Mile 4 Hospital Abakaliki, Ebonyi State, Nigeria. Socio-demographic data and administered antibiotics data were collected. Result: Out of the 88 children, a total of 54 (61%) children were males, while 34 (39%) were females. The ages of the children ranged between 1-51 months, while the mean age was seen at 14 months. About 58 (66%) were diagnosed with acute gastroenteritis alone, with children aged 7-12 months recording higher numbers [25 (28%)]. Severe dehydration was seen as the most common morbidity of children with acute gastroenteritis. The guardians/parents of these children stayed at home for an average of 3 days (1-6 days) before visiting the hospital. The children were treated for an average of 5 days (2-9 days) in the hospital. The most singly used antibiotics was ciprofloxacin [31 (35%)] followed by a combination of ciprofloxacin and ceftriaxone [21 (24%)]. About 12 (14%) of the children were treated using a single dose of the antimalarial drug while 10 (11%) were treated in double combination therapy. The lowest duration in hospitalization (4 days) was seen in the use of a single dose regimen, while the highest hospitalization time (6 days) was seen in the use of a triple dose regimen. Conclusion: The best empirical treatment of acute gastroenteritis may involve the use of ciprofloxacin alone and its combination with ceftriaxone. The severity of gastroenteritis may also be exacerbated with malaria.

Purpose To determine the effect of zinc deficiency on fecal protein, electrolyte, and short-chain fatty acid levels in both heat-stable (ST) and heat-labile (LT) enterotoxigenic Escherichia coli (ETEC)-induced diarrhea in rats. Methods Albino rats, weighing 100 to 150 g, were divided into 2 groups, with 15 animals each: non-zinc and zinc-deficient. These two groups were sub-divided into three sub-groups with five rats each: control (saline); LT-ETEC; and ST-ETEC. Sodium phytate (30 mmol/L) was added to the animals’ water to induce zinc deficiency, while diarrhea was induced using 5×109 ETEC cells/mL. Fecal protein levels were estimated using the Bradford method, while sodium and potassium levels were determined using atomic absorption spectrophotometry. Short-chain fatty acids were measured using gas chromatography-mass spectrometry. Results Among the non-zinc and zinc-deficient groups, there were significant increases (p=0.04), (p=0.03) in fecal protein concentrations (mg/mL) in the LT-ETEC- (4.50±0.33), (6.50±0.26) and ST-ETEC- (3.85±0.19), (5.98±0.32) induced groups compared to the control groups (2.60±0.52), (3.50±0.11) respectively. Fecal sodium and potassium levels (mg/L) were significantly (p=0.029) increased in non-zinc-deficient rats induced with LT-ETEC (9.35±0.95, 1.05±0.48), and ST-ETEC (9.96±1.02, 1.21±0.45) compared with the control group (8.07±0.44, 0.47±0.17) but the increase were not statistically significant (p=0.059) in the zinc deficient rat groups. Fecal acetate and propionate levels (mg/g) significantly (p=0.032) increased when induced with LT-ETEC and ST-ETEC in non-zinc and zinc-deficient groups compared with the control groups. Conclusion Zinc deficiency among rats with ETEC-induced diarrhea elevated fecal protein loss but may not have an effect on fecal sodium, potassium and short-chain fatty acid levels.

Cyclophosphamide is an alkylating anticancer agent with strong efficacy; however, its clinical use is constrained because of its off-target multiple organ toxicity, and one of them is testicular injury. We assayed to explore whether garlic oil (GO) could prevent cyclophosphamide (CYP)-induced testicular oxidative stress and hormonal deficit in male rats. Rats were pretreated with GO for 21 days before a single injection of CP (50 mg/kg, ip). The total phenol and flavonoids of GO were estimated as well as its antioxidant capacity using DPPH and FRAP assays. CYP induced prominent depression in testicular activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and reduced glutathione (GSH) level, whereas levels of malondialdehyde (MDA) markedly increased and confirmed by histopathological alterations. Serum levels of testosterone, FSH and LH were considerably reduced. Interestingly, the GO supplementation attenuated the biochemical changes in the testis, enhanced the hormone levels and alleviated the histological injury. The IC50 of GO in DPPH assay was comparable to that of standard. GO is capable of protecting the testis from CYP toxicity via its antioxidant property. The findings suggest GO beneficial effects in male cancer patients undergoing CYP chemotherapy. Keywords: Garlic oil, Cyclophosphamide, Testosterone, Supplementation, Antioxidant

Background:Research studies that holistically investigated the effect of administration of Virgin Coconut Oil (VCO) on diabetic humans or animals are limited in literature.Objective:To investigate the effect of administration of VCO on lipid profile, markers of hepatic and renal dysfunction, and hepatic and renal antioxidant activities of alloxan induced diabetic rats.Methods:Twenty-four male albino rats were used, and they were divided into four groups of six rats each. Group 1 (Normal Control, NC) received distilled water (1 mL/kg); Group 2 (VCO Control) received VCO (5 mL/kg); Group 3 (Diabetic Control, DC) received distilled water (1 mL/kg); Group 4 (Test Group, TG) received 5 ml/kg of VCO.Results:There were no significant differences in blood glucose, body weights, relative liver weights, relative kidney weights, hepatic and renal Superoxide Dismutase (SOD) activities, Malondialdehyde (MDA), albumin, aspartate Amino Transaminase (AST), alanine Amino Transaminase (ALT), Alkaline Phosphatase (ALP), urea, creatinine, uric acid, total cholesterol, triacylglycerol, Very Low Density Lipoprotein cholesterol (VLDL) and Low Density Lipoprotein cholesterol (LDL) concentrations; significant increases in renal Glutathione (GSH), hepatic catalase, Glutathione Peroxidase (GPx) and GSH but significant reduction in renal GPx and catalase activities of VCO control group compared with NC group. There were significant increases in blood glucose, relative liver and kidney weights, hepatic GPx, hepatic and renal MDA concentration, ALP, AST, ALT, urea, creatinine, uric acid, triacylglycerol, total cholesterol, LDL and VLDL concentrations; and significant decreases in body weight, hepatic SOD and GSH activities and albumin concentration but no significant difference in hepatic catalase activity of DC group compared with NC group. Administration of VCO to diabetic rats positively modulated these parameters compared with the diabetic control.Conclusion:The study showed the potentials of VCO in the management of hyperlipidemia, renal and hepatic dysfunctions imposed by hyperglycemia and by oxidative stress in diabetic rats.

This study was aimed to investigate the effect of enterotoxigenic E. coli (ETEC)-induced diarrhea on fecal nitric oxide (NO) and intestinal inducible nitric oxide synthase (iNOS) expression in rats. E. coli isolates were gotten from infants diarrheal samples. Multiplex polymerase chain reaction (PCR) was used to detect the presence of eltA gene for heat-stable (ST) enterotoxigenic E. coli and eltB for heat-labile (LT) enterotoxigenic E. coli. Disk diffusion method was used to determine the antibiotic susceptibility of the organisms. Biofilm formation was detected by thiazoylblue tetrazolium bromide dye in a 96-well plate. Fecal NO was measured using standard griess reaction system. Reverse transcription PCR was used to investigate the expression of iNOS expression. Although none of the ETECs isolated in this study belonged to the classic serotype, serogroup O6 and O8 were found to be associated with ETECs. Among the three ETECs, two were found to be multidrug resistant. The biofilm production abilities of all the ETECs were found to exist between weak and moderate biofilm producers. Fecal NO was found to be elevated in both LT and ST-induced diarrheal groups but there was no corresponding intestinal iNOS expression. This suggests that the elevated NO could be as a result of up-regulation of constitutive NOS rather than iNOS.