01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Giardia duodenalis is a flagellated protozoan that attaches to proximal small-bowel mucosa and impairs absorption without invading tissue. Infection ranges from asymptomatic carriage to prolonged greasy diarrhoea, bloating, fatigue and nutritional loss.
Entamoeba histolytica colonises the large bowel and may invade mucosa, creating flask-shaped ulcers and dysentery. Through portal spread it can cause a necrotic liver abscess, occasionally rupturing into pleura, lung, peritoneum or pericardium.
Routine microscopy has limitations. Giardia cyst shedding varies, and Entamoeba histolytica cannot be reliably distinguished morphologically from non-pathogenic E dispar. Targeted antigen or molecular testing improves specificity.
Treatment principles differ. Giardia needs luminal eradication with an effective course. Amoebiasis requires clearance of both invasive trophozoites and residual intestinal cysts; failure to prescribe the luminal phase permits ongoing transmission and relapse.
Key points
- Giardia usually causes foul-smelling watery or greasy diarrhoea, bloating, flatulence, nausea and weight loss after contaminated water, travel, childcare or close contact.
- Entamoeba histolytica causes variable disease from asymptomatic luminal infection to dysentery and liver abscess after exposure in endemic settings.
- Send stool antigen or PCR for Giardia; intermittent shedding can require additional specimens when probability remains high.
- Use species-specific PCR or antigen testing to distinguish pathogenic E histolytica from morphologically similar non-pathogenic Entamoeba species.
- Treat symptomatic giardiasis with a defined nitroimidazole regimen and investigate adherence, reinfection or immune deficiency if symptoms persist.
- Invasive amoebiasis needs a tissue-active nitroimidazole followed by a luminal amoebicide; metronidazole alone does not eradicate bowel cyst carriage.
- Amoebic liver abscess is often diagnosed through imaging plus serology and exposure because stool microscopy may be negative.
- Manage household, childcare, food-handling and sexual transmission through hygiene and health-protection advice rather than treating untested contacts automatically.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Giardia waterborne exposure
Cysts survive in untreated water and are ingested during travel, camping, swimming or sanitation failures. in susceptible exposed adults.
Close-contact Giardia spread
Childcare, household and faecal–oral sexual contact transmit cysts because only a modest inoculum is required. in susceptible exposed adults.
Endemic amoebic exposure
E histolytica cysts are acquired through food, water or hands contaminated by human faeces in endemic settings.
Sexual transmission
Direct faecal–oral contact can transmit intestinal protozoa within sexual networks even without international travel. in susceptible exposed adults.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Giardia attachment
Trophozoites adhere to duodenal and jejunal epithelium, disrupting brush border and fat and carbohydrate absorption. during active invasive disease.
- 2Giardia encystation
Organisms form environmentally resistant cysts during intestinal transit, enabling prolonged shedding and onward transmission. during active invasive disease.
- 3Amoebic mucosal invasion
E histolytica trophozoites lyse epithelium and extend into submucosa, producing flask-shaped ulcers and bloody diarrhoea. during active invasive disease.
- 4Portal dissemination
Invading amoebae enter portal blood and create a necrotic hepatic abscess, with possible extension across adjacent structures.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Greasy floating foul stool, bloating, sulphurous belching, flatulence, nausea, fatigue and weight loss without blood suggest proximal small-bowel infection.
Gradual abdominal pain, tenesmus and stool containing blood and mucus after endemic exposure indicates invasive colonic disease.
Fever, right-upper-quadrant pain, tender hepatomegaly and a solitary liver lesion may occur months after travel and without current diarrhoea.
Untreated stream or well water, swimming, nursery contact and household clusters increase Giardia probability.
Faecal–oral sexual contact can transmit either parasite and should be asked about neutrally to guide testing and prevention.
Continued diarrhoea may reflect non-adherence, reinfection, lactose intolerance, post-infectious symptoms, resistance or an incorrect initial diagnosis.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Stool Giardia antigen or PCRFirst step - Why
- Detect Giardia with greater sensitivity and specificity than a single routine microscopy specimen.
- Interpretation and limitations
- A positive result with compatible symptoms supports treatment; if negative despite strong probability, discuss repeat or additional stool specimens.
- 02
Stool ova, cysts and parasites - Why
- Identify Giardia and other parasites after prolonged, travel-associated or otherwise unexplained diarrhoea.
- Interpretation and limitations
- Send exposure details and often multiple specimens because shedding is intermittent; microscopy cannot reliably speciate Entamoeba histolytica.
- 03
E histolytica-specific PCR or antigen - Why
- Distinguish pathogenic E histolytica from non-pathogenic look-alike species in stool or tissue.
- Interpretation and limitations
- Use before invasive treatment where feasible; visible trophozoites containing red cells support invasion but do not replace species-specific confirmation.
- 04
Full blood count, CRP, liver and renal profile - Why
- Assess inflammation, anaemia, dehydration, hepatic involvement and treatment safety.
- Interpretation and limitations
- Liver abscess commonly raises inflammatory markers and alkaline phosphatase, while eosinophilia is not a typical defining feature.
- 05
Liver ultrasound or contrast CT - Why
- Identify abscess number, size, lobe, rupture risk and alternative pyogenic or malignant lesions.
- Interpretation and limitations
- A usually solitary right-lobe lesion supports amoebiasis in context but imaging is not organism-specific; left-lobe, large or complicated lesions need urgent review.
- 06
E histolytica serology - Why
- Support extra-intestinal amoebiasis when stool tests are negative and exposure is plausible.
- Interpretation and limitations
- Antibodies are sensitive in liver abscess but may remain positive after remote infection, limiting specificity in endemic populations.
- 07
Abscess aspiration when indicated - Why
- Resolve diagnostic uncertainty or control a lesion at risk of rupture or failing medical treatment.
- Interpretation and limitations
- Routine aspiration is unnecessary for an uncomplicated responding abscess; aspirate with image guidance for left-lobe risk, impending rupture, bacterial differential or poor response.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Post-infectious lactose intolerance
Temporary lactase deficiency causes bloating and loose stool after infection despite parasite eradication and negative repeat testing.
Coeliac disease
Chronic malabsorption, weight loss and nutrient deficiency mimic Giardia but follow gluten-related immune enteropathy. on focused clinical assessment.
Bacterial dysentery
Shigella, Campylobacter, Salmonella and STEC cause blood and systemic inflammation and require organism-specific treatment decisions. on focused clinical assessment.
Inflammatory bowel disease
Ulcerative colitis and Crohn disease cause chronic or relapsing blood, urgency and inflammation but may worsen catastrophically with missed amoebiasis.
Pyogenic liver abscess
Bacterial hepatic infection often has bloodstream or biliary sources and may need drainage plus a different antimicrobial spectrum.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01GIARDIAConfirm and eradicate GiardiaFirst stepProlonged watery or greasy diarrhoea follows water, travel, childcare or close-contact exposure.+
- 1Assess hydration and send stool Giardia antigen or PCR with parasite testing appropriate to travel and duration.
- 2Give an exact locally approved metronidazole or tinidazole course after checking pregnancy, liver disease and interactions.
- 3Reinforce hand, toilet, laundry, food and sexual hygiene and seek health-protection advice for high-risk occupation or clusters.
- 4If symptoms continue, confirm adherence and repeat testing before changing treatment; assess reinfection, lactose intolerance and immune deficiency.
02DYSENTERYExclude invasive amoebiasisBlood and mucus, tenesmus or colitis occurs after exposure in an endemic area or faecal–oral contact.+
- 1Send stool for E histolytica-specific PCR or antigen and routine bacterial testing and assess full blood count, renal and inflammatory status.
- 2Avoid corticosteroids and antimotility drugs until amoebic and other invasive infection has been assessed.
- 3Begin specialist tissue-active treatment promptly in severe probable disease after diagnostic specimens, without waiting in a deteriorating patient.
- 4After the nitroimidazole course prescribe a complete luminal amoebicide and confirm symptom and transmission follow-up.
03LIVERTreat amoebic liver abscessFever and right-upper-quadrant pain accompany a compatible liver lesion and epidemiology.+
- 1Obtain liver imaging, E histolytica serology, blood cultures and stool testing while considering pyogenic abscess and malignancy.
- 2Start metronidazole 800 mg orally or intravenously three times daily for five to ten days under specialist direction, followed by a luminal agent.
- 3Seek urgent drainage review for left-lobe location, imminent rupture, severe compression, diagnostic uncertainty or inadequate response after several days.
- 4Monitor pleural, pericardial and peritoneal symptoms and arrange follow-up imaging according to lesion size and clinical recovery.
04PERSISTInvestigate apparent failureSymptoms or positive testing continue after a correctly prescribed protozoal regimen.+
- 1Verify exact doses, completion, vomiting, alcohol interaction and whether all amoebic phases were treated.
- 2Assess untreated household or sexual exposure, contaminated water and high-risk occupation as sources of reinfection.
- 3Repeat organism-specific testing rather than assuming resistance and evaluate lactose intolerance, coeliac disease, IBD and post-infectious symptoms.
- 4AlternativeDiscuss true microbiological persistence, alternative regimens and immune deficiency with infection or gastroenterology specialists.
Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
Metronidazole for giardiasis
Give 400 mg orally three times daily for five days, or use another exact local first-choice regimen if specified by the current formulary.Avoid alcohol during and for at least 48 hours after treatment, review warfarin and lithium interactions, and seek specialist advice in pregnancy, liver disease or repeated failure.
Tinidazole for giardiasis
Give 2 g orally as a single dose with food when the local formulary selects tinidazole for an adult.Avoid alcohol during and for 72 hours afterwards; review pregnancy, breastfeeding, liver disease, neurological adverse effects and interacting anticoagulants.
Metronidazole for invasive amoebiasis
Give 800 mg orally three times daily for five days for amoebic dysentery; use five to ten days and intravenous administration when required for liver abscess or severe disease under specialist advice.It does not eradicate luminal cysts, so always follow with a luminal amoebicide; monitor neurological and hepatic toxicity and major interactions.
Luminal amoebicide
Give diloxanide furoate 500 mg orally three times daily for 10 days when available and specialist-selected, or the exact alternative luminal regimen supplied locally.Availability varies; obtain infection or tropical-medicine advice, review pregnancy and breastfeeding, and never omit this phase after invasive disease.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Nutritional deficiency
Persistent Giardia causes weight loss, fat-soluble vitamin deficiency and reduced growth or reserve through malabsorption. without timely definitive management.
Post-infectious bowel dysfunction
Lactose intolerance and functional symptoms can persist after microbiological cure and impair recovery. without timely definitive management.
Fulminant amoebic colitis
Extensive mucosal necrosis produces haemorrhage, toxic megacolon, perforation, shock and high mortality. without timely definitive management.
Liver-abscess rupture
Necrotic material extends into pleura, lung, peritoneum or pericardium, causing empyema, peritonitis or tamponade. without timely definitive management.
Amoeboma
Chronic focal inflammatory mass narrows colon and can mimic malignancy or inflammatory bowel disease. without timely definitive management.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Record stool frequency and character, weight, hydration, oral intake and return of functional activity.
- Recheck electrolytes and renal function when losses are substantial or treatment occurs during acute kidney injury.
- Monitor metronidazole or tinidazole intolerance, neurological symptoms, liver injury and relevant medicine interactions.
- For liver abscess follow fever, right-upper-quadrant pain, inflammatory markers and signs of pleural, peritoneal or pericardial rupture.
- Repeat imaging when clinical response is inadequate, rupture risk was present or diagnostic uncertainty remains.
- Do not use a persistently positive antibody titre as a test of cure for amoebic abscess.
- Address household, food-handling, childcare and sexual transmission with health-protection advice and retest persistent symptoms.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Greasy is different from bloody
Giardia impairs absorption without tissue invasion, whereas blood and mucus should redirect attention to amoebic or bacterial colitis.
Microscopy cannot reliably speciate
E histolytica resembles non-pathogenic Entamoeba species, so molecular or antigen confirmation prevents unnecessary invasive-disease treatment.
Liver disease may lack diarrhoea
Portal spread can produce an abscess after colonic symptoms have resolved or were never noticed.
Two compartments need treatment
A nitroimidazole clears invasive trophozoites but a separate luminal drug is required to eliminate intestinal cysts.
Routine drainage is unnecessary
Most uncomplicated amoebic liver abscesses respond to medicines; aspiration is reserved for risk, uncertainty or poor response.
Post-infectious symptoms persist
Temporary lactose intolerance or functional bowel disturbance can continue after Giardia eradication and should not prompt endless empirical courses.
11Common pitfallsFrequent interpretation and management errors.
- 01
Do not diagnose Giardia from bloating alone without appropriate stool testing.
- 02
Do not rely on one negative microscopy specimen when exposure and symptoms remain convincing.
- 03
Do not equate Entamoeba microscopy with confirmed pathogenic E histolytica.
- 04
Do not treat invasive amoebiasis with metronidazole alone and omit the luminal phase.
- 05
Do not give corticosteroids for presumed IBD before excluding amoebic colitis after relevant travel.
- 06
Do not aspirate every uncomplicated responding amoebic liver abscess.