Giardia lamblia (syn. intestinalis, duodenalis) - Intestinal Parasites

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Chapter: Pharmaceutical Microbiology : Protozoa

Giardia duodenalis (syn lamblia and intestinalis) is the causative agent of giardiasis, a severe diarrhoeal disease. The incidence of Giardia infection worldwide ranges from 1.5% to 20% but is probably significantly higher in countries where standards of hygiene are poor.


Giardia lamblia (syn. intestinalis, duodenalis)

 

Giardia duodenalis (syn lamblia and intestinalis) is the causative agent of giardiasis, a severe diarrhoeal disease. The incidence of Giardia infection worldwide ranges from 1.5% to 20% but is probably significantly higher in countries where standards of hygiene are poor. The most common route of spread is via the faecal–oral route, although spread can also occur through ingestion of contaminated water and these modes of transmission are particularly prevalent in institutions, nurseries and daycare centres. Recent outbreaks and epidemics in the UK, USA and eastern Europe have been caused by drinking contaminated water from community water supplies or directly from rivers and streams. Many animals harbour Giardia species that are indistinguishable from the human infective types. There is now clear evidence from genotyping studies (see section 6.1.2) that the G. duodenalis species is made up of a number of genetically distinct groups which may represent species. This has raised the question of the existence of animal reservoirs of Giardia. Recent findings of Giardia infected animals in watersheds from which humans acquired giardiasis, and the successful interspecies transfer of these organisms, suggests that human giardiasis can be acquired by zoonotic transfer, however it is not clear if the major route of transfer is from animal to human or from human to animal. More recently, it has been recognized that Giardia infection may be transmitted by sexual activity, particularly among homosexual men.

 

This organism exhibits only two life cycle forms: the vegetative binucleate trophozoite (10–20 μm long × 2 –3 μm wide) (Figure 6.2d) and the transmissible quadranucleate cyst (10–12 μm long × 1–3 μm wide). Trophozoites have four pairs of flagella and an adhesive disc, which is thought to help adhesion to the intestinal epithelium. Division in trophozoites is by longitudinal fission.

 

It was long believed that Giardia was a non-pathogenic commensal. However, we now know that Giardia can produce disease ranging from a self limiting diarrhoea to

 

severe chronic syndrome. Immune competent individuals with giardiasis may exhibit some or all of the following signs and symptoms: diarrhoea or loose, foul  smelling stools; steatorrhoea (fatty diarrhoea); malaise; abdominal cramps; excessive flatulence; fatigue and weight loss. Infected individuals with an immune deficiency or protein-calorie malnutrition may develop a more severe disease and will exhibit symptoms such as interference with the absorption of fat and fat-soluble vitamins, retarded growth, weight loss, or a coeliac disease like syndrome.

 

Giardia infection is initiated by ingestion of viable cysts (Figure 6.6), the infective dose of which can be as low as one cyst, although infection initiated by 10–100

viable cysts is more likely. As the cysts pass through the stomach the low pH and elevated CO2 induce excystation (cyst–trophozoite transformation). From each cyst two complete trophozoites emerge and these rapidly undergo division then attach to the duodenal and jejunal epithelium. Once attached, they will undergo division, and 4–7 days later they will detach and begin to round up and form cysts (encystment). This process is thought to be induced in response to bile. The first cysts are found in faeces after 7–10 days.

 

The underlying pathology of giardiasis is not fully understood. The trophozoites do not invade the mucosa, and although their presence may have some physical effects on the surface it is more likely that some of the pathology is caused by inflammation of the mucosal cells of the small intestine causing an increased turnover rate of intestinal mucosal epithelium. The immature replacement cells have less functional surface area and less digestive and absorptive ability. This would account for the microscopic changes seen in infected epithelia. It has been suggested that other mechanisms may exist, e.g. toxin production, but to date no such molecule has been observed.

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