[Cryptosporidiosis, a cause of acute diarrhea: A review and retrospective study of cases in Rouen university hospital's pediatrics department]. / La cryptosporidiose, une cause de diarrhée aiguë : revue de la littérature et étude rétrospective des cas dans le département de pédiatrie du CHU de Rouen.

Cryptosporidium is the most important diarrhea-causing protozoan parasite, with severe health consequences for very young, malnourished children living in endemic areas and for immunocompromised individuals. Cryptosporidium is widely distributed and disease transmission can occur through person-to-person or animal-to-person contact, or contaminated food or water (drinking or swimming), leading to large outbreaks. The zoonotic Cryptosporidium parvum and the anthroponotic Cryptosporidium hominis are responsible for the majority of human cases. Specific therapy, primarily nitazoxanide, has some effect in healthy individuals, but drugs effectively preventing or controlling this disease in all clinical situations are not yet available. In France, as elsewhere in Europe, little epidemiological and molecular information is available regarding the burden of cryptosporidiosis in children. Cryptosporidium is usually not tested in all fecal samples submitted for routine parasitological examination and only tested on special request, primarily in immunocompromised patients. Between January 2007 and October 2014, out of a total of 5337 immunocompetent children with diarrhea in Rouen university hospital's pediatrics department, the prevalence of Cryptosporidium infection was 0.97 % (52 infected children). The median age of infected children was 3 years (range, 5 months to 11 years) and 80 % of the cases occurred between July and November. Thirty-six (69.2 %) and 16 (30.8 %) infections were due to C. parvum and C. hominis, respectively. The fact that the species C. parvum, mainly the IIaA15G2R1 subtype, was detected in most locally infected children suggests that cryptosporidiosis must primarily be considered as a zoonotic disease in Upper Normandy.

A penicillin- and metronidazole-resistant Clostridium botulinum strain responsible for an infant botulism case.

The clinical course of a case of infant botulism was characterized by several relapses despite therapy with amoxicillin and metronidazole. Botulism was confirmed by identification of botulinum toxin and Clostridium botulinum in stools. A C. botulinum A2 strain resistant to penicillins and with heterogeneous resistance to metronidazole was isolated from stool samples up to 110 days after onset. Antibiotic susceptibility was tested by disc agar diffusion and MICs were determined by Etest. Whole genome sequencing allowed detection of a gene cluster composed of blaCBP for a novel penicillinase, blaI for a regulator, and blaR1 for a membrane-bound penicillin receptor in the chromosome of the C. botulinum isolate. The purified recombinant penicillinase was assayed. Resistance to ß-lactams was in agreement with the kinetic parameters of the enzyme. In addition, the ß-lactamase gene cluster was found in three C. botulinum genomes in databanks and in two of 62 genomes of our collection, all the strains belonging to group I C. botulinum. This is the first report of a C. botulinum isolate resistant to penicillins. This stresses the importance of antibiotic susceptibility testing for adequate therapy of botulism.