Giardiasis

Giardiasis is an intestinal infection caused by Giardia lamblia (also termed Giardia duodenalis or Giardia intestinalis), a flagellated protozoan parasite. It is one of the commonest identifiable causes of parasitic gastrointestinal disease worldwide.

Infective cysts from contaminated water or food spread the infection by the faecal oral route. Direct person to person transmission occurs in settings of close contact. Contaminated water includes inadequately treated recreational and drinking water, a recognised and important route even in resource rich settings.

It produces a spectrum from asymptomatic carriage through to significant diarrhoeal illness with malabsorption. It is particularly relevant in returning travellers and in specific higher risk exposure settings.

Pathophysiology and risk factors

• After ingestion of cysts and excystation within the small intestine, trophozoites attach to the duodenal and jejunal mucosa via a specialised ventral adhesive disc. They do not invade the mucosa.
• Disease reflects direct mechanical interference with nutrient absorption across the affected mucosal surface and, in more significant infection, associated villous blunting.
• Travel to endemic regions is a risk factor, given the organism's global distribution and association with inadequate water treatment infrastructure.
• Recreational freshwater exposure is a risk factor, particularly swimming in lakes and rivers, where the organism survives standard levels of chlorination more resiliently than many bacterial pathogens.
• Childcare settings carry risk through close contact transmission, particularly among young children.
• Men who have sex with men are at risk through a recognised sexual transmission route.

• A substantial proportion of infections are asymptomatic, particularly in populations with repeated prior exposure and some acquired partial immunity.
• Symptomatic disease presents after an incubation period of one to three weeks with watery, foul smelling diarrhoea, abdominal bloating, cramping and flatulence.
• Characteristically there is prominent belching with a sulphurous taste, together with anorexia and, in more prolonged infection, weight loss.
• Steatorrhoea, reflecting fat malabsorption from the affected proximal small intestinal mucosa, occurs in more significant infection. Blood and mucus in the stool are characteristically absent, which distinguishes giardiasis from several bacterial and invasive protozoal causes of infectious diarrhoea.
• Chronic or relapsing infection occurs in a proportion of untreated or inadequately treated cases. It can produce prolonged malabsorption with weight loss and, particularly in children, growth impairment.
• Occasionally secondary lactose intolerance follows, reflecting brush border enzyme disruption from chronic mucosal changes.
• Clinical suspicion is supported by a relevant exposure history (travel to an endemic region, recreational freshwater exposure, childcare setting contact, or relevant sexual history) together with the characteristic symptom pattern.
• The absence of blood or significant fever distinguishes the pattern from many bacterial causes of travellers' diarrhoea.

• Stool antigen testing (enzyme immunoassay) offers good sensitivity and is widely used as a practical first line diagnostic test.
• Polymerase chain reaction testing, where available, further improves sensitivity. This is particularly valuable given the historically recognised limitations of stool microscopy with intermittent, variable cyst shedding.
• Stool microscopy for ova and parasites can identify characteristic cysts or, less commonly on a formed stool sample, trophozoites. Sensitivity with a single sample is imperfect because of intermittent shedding.
• Multiple samples (typically three, on separate days) improve diagnostic yield where initial testing is negative but clinical suspicion remains significant.
• Duodenal aspirate or biopsy, obtained at upper gastrointestinal endoscopy, is reserved for persistent diagnostic uncertainty despite negative stool testing. Trophozoites may then be directly visualised attached to the duodenal mucosa.

• Metronidazole 400 to 500 mg orally three times daily for five to seven days is a standard, widely used and effective first line treatment.
• Tinidazole 2 g orally as a single dose is a more convenient alternative, with comparable and in some studies superior cure rates and improved adherence given the single dose regimen.
• Nitazoxanide 500 mg orally twice daily for three days is a further effective option. It is particularly useful in young children given its oral suspension formulation and generally favourable tolerability.
• Treatment failure occurs in a meaningful minority. It may reflect genuine drug resistance, reinfection (particularly where ongoing environmental or contact exposure has not been addressed), or an alternative or coexisting diagnosis contributing to persistent symptoms.
• Failure warrants reassessment, repeat stool testing, and consideration of an alternative agent or extended treatment course where appropriate.
• Symptomatic and nutritional support is an important adjunct to antiparasitic treatment. This includes temporary dietary lactose restriction for secondary lactose intolerance where relevant, adequate hydration, and nutritional supplementation in more significant or prolonged infection.
• Prevention is the primary strategy, as no vaccine is available. It relies on safe water practices (boiling or appropriate filtration of water in endemic settings or during relevant recreational activity, given resistance to standard chlorination levels), good hand hygiene, particularly in childcare settings, and appropriate food handling and hygiene.