The presence of human Giardia in several animals suggests a zoonotic transmission. We studied G. Intestinalis isolates obtained from: children with diarrhea (n=6), asymptomatic children (n=7), axenic cultures (n=7) and dogs (n=11). The sequence corresponding to 16 S rRNA was amplified by PCR, sequenced and compared with genotypes A, B and Dog sequences reported in the Gene Bank database. Results show that 9/20 (45%) of children isolates belonged to genotype A and 11/20 (55%) showed some variable sites, allowing classification in three arbitrary clusters: A1, A2 and A3. In addition 7/11 (63%) of dog isolates were genotype A, including those dogs that lived in the same locality as the children lived, while 4/11 (37%) belonged to an arbitrary A4 cluster living in a different locality. In this study, genotype A was associated with samples from children and dogs, and, therefore, we could infer zoonotic transmission as a way of getting the disease.

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Giardia intestinalis can develop resistance to albendazole, although the molecular mechanism is not understood. The aim of this study was to investigate the differences and permanent mutation in the beta-giardin gene of G. intestinalis strains: sensitive, resistant, or recovered-resistance to albendazole. The beta-giardin gene was amplified by nested polymerase chain reaction. The IC(50) values varied from 0.29 to 0.38 microg/mL for strains sensitive to albendazole. For resistant strains, the IC(50) range was 1.31-2.12 microg/mL. Recovered-sensitivity albendazole strains' IC(50) values were 0.33-0.49 microg/mL, and for strains with recovered-resistance, the IC(50) was 1.42-2.74 microg/mL. beta-giardin amplicon (720 bp) was sequenced and analysis sequence revealed several amino acid mutations from resistant and recovered-sensitive strains of G. intestinalis. Most of the mutations were located in the ROD domain of beta-giardin with a change from the sequence "TIARERA" in sensitive strains instead "IDRPRE" in resistant strains. A comparative sequence analysis in resistant, recovered-sensitive, and resistant-recovered strains revealed permanent mutation. This is the first report of combinatorial serine-proline-arginine repeats in the ROD domain of beta-giardin, whereas such repeats have been reported previously in the HEAD domain of SF-assemblin proteins. This is the first time that the resistance to albendazole correlates with genetics but it is not necessarily caused by mutations in the beta-giardin gene of G. intestinalis.

Agarose gel electrophoresis of gdh gene fragments, amplified by Multiplex, was used to classify the assemblage of 24 Giardia isolates obtained from axenic cultures, children's stools, and feces of puppies from different dog breeds. Isolates were compared with seven reference strains of Giardia intestinalis. The results showed that 22/24 isolates (91%) belonged to assemblage A and could be further subclassified as assemblage A1 (18/22, 81%) and assemblage A2 (4/22, 19%). One sample revealed a mixture of A1/A2 genotypes, and another was assemblage G, indicating mixed infections by different strains in the same host, and an association with the assemblage reported in animals. The procedure described is useful to determine the Giardia genotype that parasitizes each host to conduct epidemiological studies assessing the close association between human- and animal-infecting strains and to monitor the adaptability of animal strains to humans.

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