**4. Incidence and burden of disease**

many domestic animals and wildlife [10], and the host-specific groups C–H. Among the latest ones, groups C and D infect dogs, cats, coyotes, and wolves [11]; group E infects cattle, sheep, goats, pigs, water buffaloes, and mouflons [12]; group F infects cats [12]; group G infects rats [12]; and group H infects marine animals [13]. This classification could be of great clinical value given that in addition to many genetic differences found, these genotypes exhibit several relevant biologic differences also. In example, genotype B seems to be more pathogenic than genotype A in humans, although they appear to grow slower [14]. Contradictory, the genetics of parasites of the genus *Giardia* is still poorly understood. Furthermore, recent evidence has cast doubt the classical view of an asexually replicating organism in favor of the occurrence of meiosis and genetic exchange. Such game breaker discovery demanded that the whole population genetics of *Giardia* should be reevaluated to take into account the effect of

Life cycle begins with the infection by the ingestion of the cyst. Then the excystation continues, which starts at the stomach triggered by the exposure of the cyst to the gastric acid, the presence of bile and trypsin in the duodenum and/or the alkaline, protease-rich milieu, duodenum [2]. Excystation ends at the proximal small intestine where the emerging parasites (excyzoites) quickly transform into trophozoites that attach to the intestinal epithelial cells using the adhesive disc. The adhesive disc is essential for attachment and appears to play a major role in the virulence of *Giardia* [15]. Several disc-associated proteins have been identified using proteomics [16], and it is clear that the disc is an advanced cytoskeletal structure [17]. At the jejunum, the trophozoites start to encyst forming the wall that enables the parasite to survive outside the host for several weeks in cold water. This process is triggered by a particular composition of biliary secretions, possibly by a deprivation of cholesterol [18]. Regulatory factors are encystation-specific transcription factors, chromatin remodeling enzymes, and posttranslational modifications, which vary their expression in correlation with the variation of antigens on the parasite surface [19]. Finally, trophozoites and cysts are released with the stool, with cysts continuing the transmission of the disease when ingested

Reservoir hosts include humans, as well as a variety of animals, including cats, dogs, dairy cattle, beavers, and other farm, wild, and domesticated animals such as horses, pigs, cows, chinchillas, alpacas, lemurs, sheep, guinea pigs, monkeys, goats, and rats [20]. However, among all these animal hosts, only beavers, dogs, and humans have been implicated as a source of infection in different waterborne epidemics and outbreaks of giardiasis in humans. Additionally, it is important to highlight the key role of "reverse zoonotic transmission" (zooanthroponotic) in the epidemiology of *Giardia* infections, which means that humans have been identified as the source of infection for beavers, muskrats, and coyotes in the Unites States and Canada [21–23], muskoxen in the Canadian arctic [24], nonhuman primates (gorillas) and painted dogs in Africa [25], marsupials in Australia, house mice in remote islands

[26], and marine mammals (seals) in various parts of the world [27].

recombination on *G. lamblia* species [14].

**3. Life cycle**

16 Current Topics in Giardiasis

by another host.

*G. lamblia* has been consistently reported as one of the most common pathogens worldwide [29]. Due to high endemicity among humans, and domestic and wildlife animals, it is considered of public health and veterinary health importance [12]. Symptomatic infections have been reported by millions in Asia, Africa, and Latin America by the World Health Organization, which have estimated that it causes 183 million (confidence interval of 95%, 130–262 million) cases of giardiasis [30].

Worldwide, the incidence of Giardiasis has been estimated in 2.8 × 108 cases per year [31]. However, several epidemiological studies have reported that such rates could be significantly underestimated, with giardiasis prevalence rates ranging from 10 to 20% of the general population [32], from 10 to 50% in developing countries [33, 34], and from 2 to 5% in developed countries [35, 36]. This could be explained by the large fraction of asymptomatic carriers, which regardless of the absence of symptoms also contribute to the transmission of the diseases.

Giardiasis is a ubiquitous disease so it occurred across broad epidemiological contexts and with a broad range of distributions. On one side, in most developed countries such as the United Kingdom [37] and Germany [8], *Giardia* is mostly reported as a rare disease affecting travelers. Furthermore, in the countries such as the Unites States, where *Giardia* is continually under surveillance, *Giardia* has higher incidences (incidence rate ratios, 1.2–1.5) in counties with higher private well reliance compared to counties with lower well reliance [38]. On the other side, in most developing countries, *Giardia* has been associated with poor health hygiene, poor toilet training, overcrowding, and low socioeconomic status [39]. Furthermore, due to the high prevalence of *Giardia* among children, and its higher exposure to dogs in poor setting, it is believed that *Giardia* has developed zoonotic transmission. This possibility has been reported concordantly by genotyping and molecular studies from Mexico [40], Jamaica [41], and Cambodia [42].

The high prevalence of *Giardia* among children raised a major concern about their long-term impacts, which currently have been well documented and reported as more worrisome due to the association between persistent *Giardia* and children's growth [43]. *Giardia* infections can be detected repetitively in over 40% of children suggesting that persistent infections are common and associated with a damage of the intestinal permeability, which—independently of diarrhea—can lead to stunted growth. In fact, according to the results from the MAL-ED birth cohort study, the persistence of *Giardia* before 6 months of age was associated with a −0.29 (95% CI, −0.53 to −0.05) deficit in weight-for-age z score and −0.29 (95% CI, −0.64 to 0.07) deficit in length-for-age *z* score at 2 years [44].
