Cystic echinococcosis (CE) or hydatidosis, caused by the larval stage (metacestode) of the tapeworm Echinococcus granulosus (Cestoda: Taeniidae) has a global distribution and is one of the most important zoonotic diseases in the world.1,2 The adult worm infects the small intestine of a wild or domestic Canidae as the definitive host. Human and livestock become infected after ingestion of food contaminated by parasite eggs that after ingestion harbor the hydatid cysts in the liver, lungs, and other internal organs as the intermediate host.

In fact, with a few rare exceptions, human is an aberrant host, because the parasite life cycle cannot be completed.3 Clinical signs of the condition are generally manifested as pressure on surrounding tissues as a result of pressures exerted by this space-occupying lesion. Cyst rupturing and spillage of the contents may create anaphylactic shock and secondary CE.

Hydatidosis is endemic in some parts of China, Middle East, North Africa, and South America.4 Iran is an important endemic region of CE where there are various species of the intermediate host for E. granulosus.5 Several studies have reported that hydatid cysts are routinely found in sheep, camels, cattle, and goats in a wide distribution across Iran.6–9 Adult worms have been recovered from dogs, wolves, and jackals in different geographical areas.7,10–14 Human CE cases are also routinely documented in medical centers in different parts of Iran, and the rate of human infection is 0.61–2/1,000,000 people in various regions.7,15 Serological studies on humans showed seroprevalence of CE within 1.2–21.4% of the population in different parts of the country.7 A recent study reported that the total annual cost of CE in Iran is US$232.25 million, with the cost of the disease conjectured to be about 0.03% of the country's gross domestic product.16

There is a high level of genetic variation within E. granulosus. During recent decades, based on mitochondrial and nuclear genetic markers, a number of variants have been described within the E. granulosus species.17 These strains/genotypes vary in host range, pathogenicity, maturation patterns of the parasite, epidemiology and sensitivity to chemotherapeutic agents, and prevention and control strategies of hydatid disease.18 To date, 10 genotypes (G1–G10) have been identified for E. granulosus. These genotypes consist of two sheep strains (G1 and G2), two bovid strains (G3 and G5), a horse strain (G4), a camel strain (G6), two pig strains (G7 and G9), and two cervid strains (G8 and G10).17,19,20 However, some of these distinct strains were originally defined many years ago as separate species or subspecies. Consequently, a taxonomic reappraisal relying mainly on mitochondrial data has proposed that E. granulosus species splits to four valid species including: 1) E. granulosus sensu stricto (G1–G3 complex), 2) E. equines (G4), 3) E. ortleppi (G5), and 4) E. canadensis (G6–G10).17,21,22 Moreover, E. felidis (lion strain) is closely related to E. granulosus sensu stricto and is placed within the E. granulosus complex.23 Recently, based on more complex data containing nuclear sequences and the epidemiological aspects, it was recommended that genotypes G6–G10 should be broken into two distinct species including E. canadensis (G8 and G10 genotypes) and E. intermedius (G6/G7 genotypes).24 The validity of the G9 genotype has been controversial.24,25 All genotypes except G4 and G10 have been reported to infect humans. Most human CE cases in the world have been found to be infected with the G1 genotype of E. granulosus.1,26

Several molecular epidemiological studies have been performed on E. granulosus isolates in Iran using sequence data of mitochondrial and nuclear genes. Overall, four different genotypes of E. granulosus (genotype G1, G3, and G6) have been reported from different livestock27–36 and dogs (genotype G1, G2, and G3)37 from Iran. To date, only a few human isolates of E. granulosus have been genetically characterized in Iran that indicated G1, G3, and G6 genotypes (Table 1). In each endemic area, the molecular identification of the occurring genotypes in human CE has significant impacts on control strategies. Therefore, the current study was conducted to determine E. granulosus genotypes of the causative agents of CE using a high number of human isolates from Iran. The study used partial sequencing of the mitochondrial cytochrome c oxidase subunit I (CO1) gene using formalin-fixed paraffin-embedded (FFPE) tissues as a DNA source.