Abstract. Gnathostomiasis was first described in Mexico in 1970, and endemic areas have been spreading in six states of this country. In Culiacan, Sinaloa, 300 cases of cutaneous larva migrans were recorded between January 1992 and December 1995. In addition, a Gnathostoma larva was surgically removed from the eye of one patient. Cutaneous lesions were observed mainly on the face, neck, arms, and legs. About 70% of the patients showed eosinophilia. A skin biopsy was carried out on 35 patients and the parasite was identified in histopathologic sections of 12 of these patients. In four patients, the larva migrated out spontaneously from the skin. An enzyme-linked immunosorbent assay using a crude somatic extract of adult Gnathostoma doloresi worms showed that 93% of the patients were seropositive, confirming the reliability of clinical diagnosis. A total of 14 advanced third-stage Gnathostoma larvae were found in four species of ichthyophagous birds captured on dams and dikes near the city of Culiacan. Scanning electron micrographs of human and bird larvae showed that they were morphologically indistinguishable from G. spinigerum. We conclude that the life cycle of Gnathostoma has been established in Sinaloa, and has become a serious public health issue for residents.Gnathostomiasis is one of the important food-borne parasitic zoonoses caused by infection with larvae of the spirurid nematode, genus Gnathostoma, with the disease being characterized principally as cutaneous larva migrans. 1 Among 12 distinctive species, only G. spinigerum had been considered as the causative species of human gnathostomiasis until the recent discovery of human cases infected with G. hispidum, G. doloresi, and G. nipponicum in Japan. [2][3][4][5][6][7][8] The life cycle of Gnathostoma is essentially identical within the genus, with only slight variations in the secondary, paratenic, and definitive hosts. Eggs are released from adult worms that live in the stomach or esophagus wall of the definitive hosts (cats, dogs, and other wild mammals). After being hatched from eggs in fresh water, the first-stage larvae are ingested by copepods where they molt twice to become the early third-stage larva (L 3 ). They then develop into the advanced L 3 in fish and amphibians, the second intermediate hosts. They are then disseminated into a wide range of paratenic hosts such as large carnivorous fishes, reptiles, and birds along the food chain.Infection in humans occurs when the second intermediate/ paratenic hosts contaminated with the L 3 are ingested. The disease is endemic mainly in Japan and Thailand, where people prefer to eat raw freshwater fish as a delicacy. 2, 3, 9 Sporadic cases have also been described in other Asian countries. 2,3,9 In America, native cases were first found in Mexico and later in Ecuador. 10,11 Subsequently, a large number of patients with cutaneous migratory swellings were identified in the states of Oaxaca and Veracruz in Mexico. 12 Endemic areas in Mexico have spread to the states of Guerrero, Nayarit, Tamaulipas, a...

We have analyzed 97 CF unrelated Mexican families for mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Our initial screening for 12 selected CFTR mutations led to mutation detection in 56.66% of the tested chromosomes. In patients with at least one unknown mutation after preliminary screening, an extensive analysis of the CFTR gene by single stranded conformation polymorphism (SSCP) or by multiplex heteroduplex (mHET) analysis was performed. A total of 34 different mutations representing 74.58% of the CF chromosomes were identified, including five novel CFTR mutations: W1098C, P750L, 846delT, 4160insGGGG and 297-1G-->A. The level of detection of the CF mutations in Mexico is still lower than that observed in other populations with a relatively low frequency of the deltaF508 mutation, mainly from southern Europe. The CFTR gene analysis described here clearly demonstrated the high heterogeneity of our CF population, which could be explained by the complex ethnic composition of the Mexican population, in particular by the strong impact of the genetic pool from southern European countries.

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Our data support the association between the TT genotype and susceptibility to LL in this Mexican population.