BackgroundCompared to developed countries, the use of antimicrobials in Egypt is less regulated and is available over the counter without the need for prescriptions. The impact of such policy on antimicrobial resistance has not been studied. This study aimed to determine the prevalence of early and late onset sepsis, and the frequency of antimicrobial resistance in a major referral neonatal intensive care unit (NICU).MethodsThe study included all neonates admitted to the NICU over a 12-month period. Prospectively collected clinical and laboratory data were retrieved, including blood cultures and endotracheal aspirate cultures if performed.ResultsA total of 953 neonates were admitted, of them 314 neonates were diagnosed with sepsis; 123 with early onset sepsis (EOS) and 191 with late onset sepsis (LOS). A total of 388 blood cultures were obtained, with 166 positive results. Total endotracheal aspirate samples were 127; of them 79 were culture-positive. The most frequently isolated organisms in blood were Klebsiella pneumoniae (42%) and Coagulase negative staphylococcus (19%) whereas in endotracheal cultures were Klebsiella pneumoniae (41%) and Pseudomonas aeruginosa (19%). Gram negative organisms were most resistant to ampicillins (100%), cephalosporins (93%–100%) and piperacillin-tazobactam (99%) with less resistance to aminoglycosides (36%–52%). Gram positive isolates were least resistant to vancomycin (18%). Multidrug resistance was detected in 92 (38%) cultures, mainly among gram negative isolates (78/92).ConclusionsAntibiotic resistance constitutes a challenge to the management of neonatal sepsis in Egypt. Resistance was predominant in both early and late onset sepsis. This study supports the need to implement policies that prohibits the non-prescription community use of antibiotics.

Alloimmunization to RBCs' antigens is a frequent finding among Egyptian transfusion-dependent thalassemic patients, with the majority of patients being transfused with blood matched for ABO and D antigens only. Absence of phenotypically matched donors, except for a limited number of patients, may have contributed to this problem.

The relationship between chronic hemolysis with subsequent iron overload, inflammation, and premature atherosclerosis has been documented in hemolytic anemias, particularly β-thalassemia. However, no such relationship has been established in sickle cell disease (SCD). We sought to evaluate SCD as a risk factor for early vascular insult by measuring carotid intima-media thickness (CIMT) and plasma chitotriosidase and to assess the role of the latter as a potential quantitative indicator of vascular inflammation and atherogenesis. Thirty SCD pediatric patients (3-18 years) and 30 matched controls were enrolled. Full clinical history, with hematological and biochemical parameters, was evaluated. CIMT and chitotriosidase activity were also assessed for all study participants. CIMT values were significantly higher in SCD patients (median 0.42; range 0.32-0.6 mm) compared to controls (0.36; 0.34-0.45 mm), P = 0.03. CIMT correlated positively with age (r = 0.460, P = 0.011), and total number of vascular incidents necessitating hospital admission (r = 0.439, P = 0.015). Similarly, chitotriosidase activity was significantly higher among SCD patients (median 59.6; range 7.3-512 nmol/ml plasma/h) compared to controls (32.7; 6.8-63.1 nmol/ml plasma/h), P < 0.001, and showed a positive correlation with serum ferritin (r = 0.517, P = 0.003) and CIMT (r = 0.535, P = 0.002). SCD children are at risk of developing premature atherogenic changes. Plasma chitotriosidase and CIMT may represent useful predictors of these changes.

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D uck virus hepatitis (DVH) is a highly fatal viral infection of young ducklings usually less than 3weeks of age. characterized by rapid onset of high morbidity and mortality (up to 95%) associated with hepatitis and enlarged hemorrhagic liver (Tseng and Tsai, 2007). DVH, is a non-enveloped, small RNA virus and has icosahedral symmetry which is categorized into three types I, II and III. According to (OIE, 2017), DVH type I can be caused by at least three different genotypes of duck hepatitis A virus (DHAV) which belongs to family Picornaviridae. The most pathogenic and widespread one is DHAV type 1 (DHAV-1) which was originally discovered in 1945 in the United States (Levine and Hofstad, 1945) and now it is globally distributed among duck-raising countries with a devastating economic impact. DVH accounts for more than 80% of mortality in ducklings less than 21 days old

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