[Neisseria meningitidis invasive infections in children in Tunis: about 79 cases]. / Les infections invasives a Neisseria meningitidis chez l'enfant a Tunis : a propos de 79 cas.

We conducted a retrospective study of meningococcal invasive diseases (MID) contracted in children in Tunis between January 1997 and January 2006. The purpose of this study is to specify the clinical, epidemiological, therapeutic and evolutionary features of these infections and to determine antimicrobial susceptibility and the antigenic formula of N. meningitidis isolates. During the study period, we have collected 79 cases of MID arising in children aged 3 days to 11 years. The majority of children's were less than of 4 years (57.3%). We note a frequency of the MID in winter and in spring. The most frequent clinical shape was meningitis (53%). Twenty one patients (26.6%) had a fulminant meningococcal disease. In our series, the rate of lethality was equal to 17.7%. Among the 46 meningococcal isolates, the most frequent serogroup was the B (73%) followed by C and A. A high heterogeneousness of the antigenic formulae was observed The most frequent phenotype was NT: NST for the group B isolates and 4:P1.13 for the group C ones. N meningitidis with reduced susceptibility to penicillin and to amoxicillin account for 54% and 10% of all isolates respectively. The cefotaxim and the rifampin were uniformly active.

Thrombosis in congenital deficiencies of AT III, protein C or protein S: a study of 44 children.

Congenital deficiency in coagulation inhibitors is a cause of hereditary thrombotic disease. The severity of symptoms is variable and depends on the type of deficit. In this paper, 44 children suffering from deep venous thrombosis, with a mean age of 5 years, were studied. A search for Lupus anticoagulant (LA) and coagulation inhibitor deficiency showed: 3/44 cases (6.8%) had protein S deficiency, 2/44 cases (4.5%) had protein C deficiency, 1/44 cases (2.3%) had deficiencies in both protein C and S; no cases of AT III deficiency and LA was positive in 2/44 cases (4.5%). Only 1 case of APC resistance out of 13 studied was found. Four family studies were performed and confirmed the congenital origin of the disorder.