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Giardia duodenalis is one of the commonest human parasites and has prevalences of 4–43% in low‐income countries and 1–7% in high‐income countries. It has the distinction of being the first parasitic protozoa to be described. This happened in 1681 when the pioneering microscopist Antoine van Leeuwenhoek observed it in a sample of his own diarrhoea. Currently, scientists divide G. duodenalis into eight genetic assemblages (A–H) but only two of these, A and B, infect us. In addition to humans, assemblages A and B both parasitise wild and domestic mammals. In some parts of America, the implication of beavers as reservoirs of infection has resulted in giardiasis gaining the popular moniker of ‘beaver fever’ (Tsui et al. 2018). However, the extent to which G. duodenalis is a zoonotic infection cycling between humans and other mammals is uncertain.

The trophozoite stage of G. duodenalis is pear‐shaped 12–15 μm in length and has four pairs of flagellae (Figure 3.6). Its ventral surface has a concave profile on which there are two depressions referred to as ‘adhesive discs’ or ‘suckers’ although they have a supportive function rather than being contractile. A pair of flagella located within the ‘ventral groove’ work as a ‘pump’ that removes fluid from underneath the adhesive discs and may facilitate the removal of nutrients from the underlying host mucosa. The oval‐shaped cyst stage is 8–12 μm in size and initially contains two nuclei but once they are mature, four nuclei are present along with several prominent axonemes (microtubules that constitute the core of the flagella): the flagellae and adhesive discs are broken down and stored as fragments during the cyst stage. Infected people shed huge numbers of cysts in their faeces – possibly as high as 1 × 10⁸ viable cysts per gram of faeces. Cyst shedding is intermittent, and laboratory confirmation of the diagnosis often requires the patient to produce several faecal samples. Transmission usually occurs through consuming the cysts in food and water, or through touching contaminated surfaces and then transferring the cysts to one’s mouth.

Figure 3.6 Life cycle of Giardia duodenalis. The trophozoite stage (T) normally infects the duodenum and upper section of the small intestine where it attaches to the gut lining. The cyst stage (C) is produced in huge, but intermittent, numbers and passed in the faeces. Transmission is via faecal‐oral contamination of the cysts. Drawings not to scale.

Giardia duodenalis normally resides in our duodenum and upper small intestine although sometimes our stomach, ileum, and colon become infected. The parasites attach to the surface epithelium and overlying mucus layer and although they may completely cover the surface of the gut, they do not invade the underlying tissues. Many people become non‐symptomatic carriers of the parasite, but some develop an acute form of enteritis, referred to as giardiasis, that manifests as profuse watery diarrhoea. The diarrhoea has a characteristic foul smell because the parasite interferes with the absorption of fats. If undiagnosed and untreated, the infection can become chronic. This is characterised by episodes of abdominal pain and defaecating loose, clay‐coloured stools that have a smell reminiscent of bad eggs. The consequence of a long‐term infection can be malnourishment due to malabsorption. It can also result in a deficiency in fat‐soluble vitamins, such as vitamin K, and hence associated metabolic disorders. Interestingly, some people who suffer giardiasis develop lactose intolerance, and this may persist even after the infection is cured. Parasite strain differences and our own immune status probably contribute to the reason G. duodenalis afflicts some of us more severely. In addition, Giardia spp. have complex interactions with the resident host gut microbiome that may lead to protection or exacerbation of an infection. For example, in mice, Giardia infection results in a dramatic shift in the balance of aerobic and anaerobic commensal bacteria (Barash et al. 2017). Whether the shift is a direct consequence of the waste products of Giardia metabolism or an indirect one resulting from the host’s immune response to the parasite is uncertain. Of course, it could also be a consequence of both factors. This interaction with the microbiome has led workers to investigate the possibility of using probiotics or prebiotics to either prevent infections or treat established infections. For example, supplementing the diet of mice with the prebiotic inulin reduces the severity of giardiasis (Shukla et al. 2016).

Giardia duodenalis is classed as a re‐emerging infection. This is mainly due to increased incidences in the developed regions of Australasia, North America, and Western Europe. Several factors contribute to these increases. The most obvious is that global travel is now cheap and accessible to many people in high‐income countries. Consequently, increasing numbers of them travel to countries with a high prevalence where they become infected. Furthermore, they often transfer the parasite to others on their return home. However, blaming other countries is sometimes unfair. For example, a study of giardiasis in Northwest England found that 75% were acquired within the United Kingdom (Minetti et al. 2015). In addition, apparent rises in the numbers of cases of giardiasis are sometimes a consequence of hospital laboratories introducing new, more sensitive diagnostic techniques (Minetti et al. 2016). Nevertheless, giardiasis is a frequent cause of diarrhoea outbreaks among young children in day care facilities, following contamination of domestic water supplies, and among people living in buildings with inadequate sanitation. Giardia duodenalis is also a sexually transmitted infection. It is reportedly common among men who have sex with men and those indulging in risky sexual practices such as oral–anal sex (Escobedo et al. 2014).