Molecular Study of Adenovirus Genotypes 40 and 41 in Children with Acute Gastroenteritis.

BACKGROUND: Adenovirus is a common virus associated with acute gastroenteritis in children. There are certain genotypes that are prevalent in these infections, such as genotypes 40 and 41. OBJECTIVE: The aim of the present study was to investigate the incidence of adenovirus genotypes 40 and 41 in children with acute gastroenteritis by polymerase chain reaction (PCR) and also to determine the possibility of Adenovirus co-infections with Rotavirus. METHODS: The study was a cross-sectional study that included 100 children with acute gastroenteritis. The children were subjected to full history taking and clinical examination. Stool samples from the patients were subjected to detection of adenovirus and rotavirus antigens by enzyme-linked immunosorbent assay (ELISA) and detection of adenovirus genotypes 40 and 41 by polymerase chain reaction (PCR). RESULTS: The most prevalent virus by the used methods was rotavirus antigen in the stool (35%). Adenovirus antigen detection was positive in 23% of the stool samples, with positive PCR for these samples in 22%. The ADv40 was detected in 13 samples, and ADv41 was detected in 9 samples. One positive sample by adenovirus antigen ELISA was negative by PCR for these genotypes. Mixed rotavirus and adenovirus by ELISA were detected in 7% of the children. In patients with positive adenovirus antigen by ELISA, the most common symptoms were vomiting (54.5%) and abdominal pain (45.5%). An insignificant difference between fever (P=0.94) and abdominal pain (P=0.63) was detected in children infected with adenovirus compared to patients infected with other organisms. The adenovirus was detected in 68.2% of children with acute gastroenteritis ≤ 24 months. Vomiting was significantly increased in children with adenovirus (54.5%) compared to children negative for adenovirus (23.1%-P=0.004, OR 4.0, 95%CI: 1.5-10.8). CONCLUSION: The study highlights the presence of adenovirus genotypes 40 and 41 in the stool of children with acute gastroenteritis. Combined rotavirus and adenovirus infections were detected in our study.

Molecular Detection of Sapovirus in Children Under Five Years with Acute Gastroenteritis in Mansoura, Egypt between January 2019 and February 2020.

Background: Sapovirus has emerged as a viral cause of acute gastroenteritis. However, there are insufficient data about the presence of this virus among children with acute gastroenteritis. The present study aimed to evaluate the presence of sapovirus in children with acute gastroenteritis by reverse transcriptase-polymerase chain reaction (RT-PCR). Methods: A cross-sectional study enrolled 100 children patients with acute gastroenteritis from outpatient clinics with excluded bacterial pathogens and parasitic infestation. A stool sample was collected from each child for laboratory examination. Each stool sample was subjected to study by direct microscopic examination, study for rotavirus by enzyme-linked immunoassay (ELISA) and the remaining sample was subjected to RNA extraction and RT- PCR for sapovirus. Results: The most frequently detected virus was rotavirus by ELISA (25%). RT-PCR detected sapovirus in 7% of the stool samples. The children with sapovirus were all from rural regions and presented mainly during the winter season in Egypt (42.9%). The main presenting symptoms were fever (71.4%) and vomiting (57.1%). None of the children with sapovirus had dehydration. Rotavirus was significantly associated with sapovirus infections in 5 patients (71.4%, P=0.01). There was an insignificant difference between symptoms of gastroenteritis in children with sapovirus and children with gastroenteritis without sapovirus as regards vomiting (P=0.7), fever (P=0.46), and abdominal pain (P=0.69). Conclusion: The present study highlights the emergence of sapovirus as a frequent pathogen associated with acute gastroenteritis in children. There is a need for a national survey program for the study of sapovirus among other pathogens associated with acute gastroenteritis for better management of such infection.

Kidney injury in infants and children with iron-deficiency anemia before and after iron treatment.

BACKGROUND: Our study aimed to investigate the effects of iron-deficiency anemia (IDA) on renal tubular functions before and after iron treatment for infants and children with IDA. We measured urinary levels of two kidney injury markers: neutrophil gelatinase-associated lipocalin (NGAL) and liver-type fatty acid-binding protein (L-FABP). MATERIAL AND METHODS: Thirty-six infants and children with IDA and 20 matched healthy controls were included. We assessed different laboratory parameters, estimated glomerular filtration rate, urinary levels of NGAL, and L-FABP. Urinary kidney injury markers were measured in IDA patients before and after 3 months of oral iron therapy. RESULTS: IDA patients had significantly higher urinary NGAL and L-FABP levels compared to their healthy controls. After 3 months of oral iron treatment, there was a significant improvement (decrease) in urinary NGAL and L-FABP in infants and children with IDA. Urinary markers returned to normal levels (healthy control levels) in children with IDA, but not for infants with IDA compared to their healthy controls. CONCLUSION: Subclinical kidney injury was found in infants and children with IDA. This injury was completely reversible in older children with IDA and partially reversible in infants with IDA after iron therapy. Higher urinary levels of kidney injury molecules in IDA infants after iron treatment are suggestive of more sensitivity of these infants to oxidative stress caused by iron therapy or may be due to the immaturity of the kidney and more damage caused by IDA which may require more time to recover.

Fever of Unknown Origin in Children: A 6 year- Experience in a Tertiary Pediatric Egyptian Hospital.

BACKGROUND: Fever of unknown origin (FUO) is among the most conditions which poses challenge in diagnosis. The presence of information on regional patterns of FUO will shorten the time for diagnosis and reduces health services costs. There are almost no previous studies describing the etiology of FUO in children of Egypt or nearby countries. AIM OF THE STUDY: To determine different causes of FUO and the possible diagnostic procedures. METHODS: Data of patients with FUO, presented to the Infectious Diseases Unit of Mansoura University Children Hospital, were retrospectively collected in a 6 year-period from May 2006 to May 2011. The study included children with a fever of 38.3° C or more documented by a health care provider and for which the cause could not be identified after 3 weeks of evaluation as an outpatient or after a week of evaluation in hospital. Patients were then categorized into 5 groups. RESULTS: 127 patients met the diagnostic criteria. Infectious diseases were the commonest causes of FUO in 46 cases (36.22%) followed by the miscellaneous causes in 38 cases (29.9%). Meanwhile, collagen vascular diseases and malignancy were diagnosed in 13 cases (10.2%) and 10 cases (7.87%) respectively. While, 20 cases (15.75%) remained undiagnosed. CONCLUSIONS: Infectious diseases are the commonest cause of FUO. The delay in diagnosis was due to atypical presentations or inappropriate use of antibiotic prior to the referral. Non infectious causes, malignancy and collagen or vascular disorders were diagnosed in rest of the patients. However, about 15% of our patients remained undiagnosed. The diagnosis was established by non-invasive means in more than two-third of the cases.

HLA-DQB1* alleles and genetic susceptibility to type 1 diabetes mellitus.

AIM: To determine human leukocyte antigen (HLA)-DQB1 allele association with susceptibility to type 1 diabetes (T1D) and to clinical and laboratory findings. METHODS: This study was conducted on 85 unrelated Egyptian children with T1D recruited consecutively from the Pediatric Diabetes Endocrinology outpatients Clinic; Mansoura University Children's Hospital, Egypt. Patient mean follow up period was 2.5 years. Patients were subdivided according to level of HbA1c (optimal/suboptimal control < 8.5% and poor control ≥ 8.5%). The control group consisted of 113 unrelated age- and sex-matched healthy subjects without T1D or other autoimmune diseases. Genomic DNA extraction was done for all subjects using a DNA isolation kit. HLA-Class II-DQB1 allele typing was carried out with a polymerase chain reaction-sequence-specific oligonucleotide probe using a INNO-LiPA HLA-DQB1 update kit. RESULTS: Significant differences were detected between Egyptian patients with T1D and control groups in the frequencies of DQB1*02 [44.4% vs 18.6%, corrected P value (Pc) < 0.001] and DQB1*03 (41.2% vs 24.4%, Pc < 0.001). Significant differences were also observed between control groups and T1D patients in the frequencies of DQB1*05 (14.6% vs 7.2%, P = 0.029) and DQB1*06 (34.1% vs 7.2%, P < 0.001). However, after correction for multiple comparisons, the significance was retained for HLA-DQB1*06 (Pc < 0.001) but lost for HLA-DQB1*05. HLA-DQB1*0201, *0202, *030201 were positively associated with T1D (Pc = 0.014, Pc < 0.001, and Pc < 0.001 respectively), while HLA-DQB1*060101 was negatively associated (Pc < 0.001) with the condition. Although the HLA-DQB1 alleles 030101 and 050101 were significantly higher in controls (P = 0.016, P = 0.025 respectively), both of them lost statistical significance after correction of P value. The frequency of the HLA-DQB1 genotypes 02/02, 02/03, and 03/03 was higher in T1D patients, and the frequency of the genotypes 03/06, 05/06, and 06/06 was higher in controls, these differences being statistically significant before correction. After correction, the genotypes 02/02, 02/03 in T1D, and the genotypes 03/06, 06/06 in controls were still significant (Pc = 0.01, Pc < 0.001, Pc < 0.001, and Pc = 0.04, respectively). Non-significant associations were found between the frequency HLA-DQB1 alleles and genotypes in T1D in relation to the grade of diabetic control, Microalbuminuria, age, gender, age of presentation, weight, height, frequency of diabetic ketoacidosis (P = 0.42), serum cholesterol, and fasting and post-prandial level of C-peptide (P = 0.83, P = 0.9, respectively). CONCLUSION: The Current work suggests that HLA-DQB1 alleles *030201, *0202, *0201, and genotypes 02/03, 02/02 may be susceptibility risk factors for development of T1D in Egyptian children, while the HLA-DQB1*060101 allele, and 03/06, 06/06 genotypes may be protective factors. HLA-DQB1 alleles and genotypes do not contribute to microalbuminuria or grade of diabetic control.