Definition, Etiology, PathogenesisTop
Giardiasis is a protozoal infection of the duodenum and the small intestine that manifests as protracted diarrhea.
1. Etiologic agent: Giardia duodenalis (also known as G lamblia or G intestinalis), a flagellated protozoal parasite of the duodenum and the jejunum. Its life cycle includes 2 stages: invasive (cyst) and mature (trophozoite). Ingestion of 10 to 100 cysts is sufficient to develop the disease. The release of trophozoites from the cysts is facilitated by hydrochloric acid. The trophozoites adhere to the jejunal mucosa and destroy the brush border of enterocytes and the structure of the intestinal villi (atrophy), thus leading to a reduction in absorption surface. Bile acids enable transformation of trophozoites into cysts, which are subsequently excreted in stool.
2. Reservoir and transmission: The reservoir is humans (predominantly) as well as a number of species of domestic mammals (dogs, cats) and wild mammals (eg, beavers). Infection spreads easily via the oral route, typically through contaminated hands (direct contact with an infected person), water (used either for drinking or recreation, as in the case of swimming pools, lakes, rivers), or less commonly through consumption of food contaminated with cysts.
3. Risk factors: Traveling to tropical countries (symptomatic G duodenalis infection accounts for 5% of traveler’s diarrhea cases); drinking unboiled water from streams, rivers, or lakes; poor sanitary conditions; working in daycare centers, preschools, orphanages; giardiasis in a household contact; anal-oral sexual contacts; significant malnutrition and cachexia; immunodeficiency (also due to immunosuppressive treatment), particularly hypogammaglobulinemia and IgA deficiency (a risk factor for severe and recurrent giardiasis); achlorhydria, treatment with drugs reducing gastric acid secretion, gastrectomy.
4. Incubation and contagious period: The incubation period usually lasts from 3 to 20 days (7 days on average); the patient is the source of infection for contacts. In a humid, cool environment the cysts remain infective for up to a few months; they are resistant to chlorine.
G duodenalis infection is the most prevalent protozoal infection worldwide (20%-40% of populations in developing countries; 0.5%-7% in industrialized areas; many cases remain undiagnosed).
Clinical Features and Natural HistoryTop
1) Asymptomatic colonization is the most common type of the infection, which resolves spontaneously in the majority of cases;
2) Acute giardiasis (lasts 2-4 weeks; usually the disease is self-limiting; 30%-50% of untreated patients develop chronic disease): Typically diarrhea (foul-smelling, watery stools, with no blood or mucus) and upper abdominal cramping (dyspepsia); in some cases asthenia, abdominal distention, nausea, anorexia and weight loss, less commonly vomiting and fever; no leukocytosis or eosinophilia on complete blood count (CBC).
3) Chronic giardiasis (steatorrhea): Follows acute giardiasis or develops independently; features similar to the acute disease but milder, may be recurrent; loose stools or steatorrhea, features of malabsorption, weight loss, asthenia flatulence, colicky pain, depression; in children leads to malnutrition and inhibition of growth.
4) Atypical manifestations: Urticaria, reactive arthritis. Some patients develop secondary lactose intolerance, cachexia, cholangitis, cholecystitis.
Giardiasis does not confer lifelong immunity; multiple reinfections are possible.
Identification of the etiologic agent:
1. Identification of G duodenalis by light microscopy (this unequivocally confirms the infection):
1) The key diagnostic method is examination of stool specimens for the presence of cysts; examine ≥3 samples collected every other day (sensitivity of a single test is ~30%, while sensitivity of repeated sampling is 100%; specificity of a single test is 100%).
2) Direct analysis of duodenal contents (gold diagnostic standard; gastroduodenoscopy required; sensitivity ~80%) for the presence of trophozoites of G duodenalis performed immediately after sample collection; the test is rarely performed.
3) Histologic examination of biopsy specimens of the duodenal or small intestinal mucosa (obtained using endoscopy): This should be performed in exceptional cases, when indications exist for either endoscopy (eg, dyspepsia) or histologic examination of the intestinal mucosa (eg, suspected enteropathy); in patients with giardiasis it reveals atrophy of the intestinal villi (usually partial) and the presence of trophozoites on the mucosal surface.
2. Detection of G duodenalis antigens in stool (enzyme-linked immunosorbent assay [ELISA], immunofluorescence assay): The test has a higher sensitivity than a single coproscopy, specificity of 95%, and a high proportion of false-positive results.
3. Detection of the DNA of G duodenalis in stool through polymerase chain reaction (PCR) testing: The test has high sensitivity and specificity and may replace microscopic testing.
4. Serologic tests should not be performed, as detection of antibodies against G duodenalis is not relevant for diagnosis.
Diagnosis is confirmed on the basis of identification of cysts or trophozoites in stool or duodenal contents (microscopic testing), detection of cysts in stool (direct immunofluorescence assay), or identification of the DNA of G duodenalis through PCR testing.
Empirical treatment may be considered in patients with clinical features of giardiasis and a typical epidemiologic history (stay in endemic areas, a household contact with giardiasis, epidemic outbreak in an institution); resolution of signs and symptoms following treatment confirms the diagnosis. Perform parasitologic studies in all of the patient’s household contacts.
As in diarrhea.
For epidemiologic reasons all infected individuals should be treated regardless of the presence of symptoms; this includes all of the patient’s household contacts.
1. First-line treatment: Oral tinidazole (acts on trophozoites, does not eradicate cysts) 2 g in a single dose or oral nitazoxanide 500 mg bid for 3 days (acts on trophozoites and eradicates cysts).
2. Second-line treatment (options): Oral metronidazole 250 mg tid or 500 mg bid for 5 to 7 days; oral albendazole 400 mg for 5 days, or oral mebendazole 200 mg tid for 5 days, or oral paromomycin 10 mg/kg tid for 5 to 10 days (eradicates cysts).
3. Treatment in pregnant patients: In mild cases treatment is not necessary; in patients with more severe manifestations, use oral paromomycin (the drug is not absorbed from the GI tract) 10 mg/kg tid for 5 to 10 days.
4. Treatment of patients with recurrence: Use a drug from a different group than previously; if there is subsequent recurrence or the treatment is ineffective, use combination therapy, eg, tinidazole or metronidazole with albendazole, paromomycin, or nitazoxanide (the effectiveness for eradication treatment is 80%-100%, depending on the combination used); paromomycin and nitazoxanide eradicate cysts.
The criterion for the complete cure is the absence of G duodenalis in stool 2 to 4 weeks after the discontinuation of treatment (follow-up antigen detection assay or microscopic examination). Recurrences after treatment typically occur within 2 to 8 weeks and may be clinically asymptomatic.
1. Maintaining good hygiene and sanitary standards.
2. Thorough washing of fruit and vegetables in clean water. Avoiding consumption of foods from unknown sources. Avoiding drinking water from unknown sources, streams, rivers, or lakes (boiling destroys the cysts).
3. Employees of daycare centers and preschools who develop diarrhea should refrain from work until the symptoms resolve.
4. Patients with giardiasis should not use recreational water facilities until 2 weeks after the resolution of signs and symptoms.
5. Breastfeeding prevents giardiasis in newborns.