CLINICAL MICROBIOLOGY REVIEWS,
Copyright © 2001, American Society for Microbiology. All Rights Reserved.
Jan. 2001, p. 114–128Vol. 14, No. 1
Treatment of Giardiasis
TIMOTHY B. GARDNER AND DAVID R. HILL*
Division of Infectious Diseases, University of Connecticut Health Center, Farmington, Connecticut
THERAPY OF GIARDIASIS.....................................................................................................................................116
Classes of Agents and Clinical Properties..........................................................................................................116
Emerging and experimental therapeutics........................................................................................................121
Special Situations ...................................................................................................................................................122
Pregnancy and lactation ....................................................................................................................................122
Resistance and relapse.......................................................................................................................................123
Giardia lamblia, also called Giardia duodenalis or Giardia
intestinalis, is a protozoan parasite of the small intestine that
causes extensive morbidity worldwide. It was first described in
the late 17th century by the Dutch microscopist Antonie van
Leeuwenhoek (62), and research into its epidemiology, patho-
genesis, and treatment has intensified since G. lamblia water-
borne outbreaks were reported in Europe and the United
States during the 1960s and 1970s (53, 81, 123, 128, 174).
Giardia infects approximately 2% of the adults and 6 to 8% of
the children in developed countries worldwide and is currently
responsible for the largest number of waterborne outbreaks of
diarrhea in the United States (54, 139).
Despite the recognition of G. lamblia clinical illness for the
last 40 years, the nearly 5,000 people hospitalized with giardi-
asis annually in the United States (149), and the millions in-
fected worldwide, there have been few reviews of therapy for
this infection and no definitive treatment protocols have been
published (58, 113, 150, 165, 261). In addition, only a handful
of agents have been used in therapy, and the agents which are
available may have adverse effects or be contraindicated in
certain clinical situations. Also, resistance may play a role in
some infections. This paper will review the agents currently
used for the treatment of giardiasis. The history, mechanism of
action, in vitro and clinical studies, and adverse effects are
detailed for each drug class. In addition, special clinical situa-
tions are discussed and recommendations for therapy are made.
The life cycle of G. lamblia has two forms: the trophozoite
(Fig. 1) and the cyst. The cyst is the infectious form and is
ingested in contaminated water or food or directly from fecal-
oral contact. As few as 10 cysts may establish infection (206).
After ingestion, excystation occurs. Excystation is thought to
be initiated by contact with acidic gastric contents, followed by
a highly coordinated sequence of events leading to the release
of one or two trophozoites (27, 109, 210). A parasite-derived
protease may be activated during the excystation process (252).
The trophozoite infects the duodenum and upper intestine,
which have a favorable alkaline pH, and gives rise to the
clinical sequelae. As trophozoites pass through the small in-
testine to the colon, encystation occurs. Encystation can be
initiated in vitro by culture of parasites in a reduced concen-
tration of bile salts and cholesterol followed by culture in an
increased concentration of bile at an alkaline pH (156). Cyst
wall proteins are then transcribed, secreted into encystment-
specific vesicles, and transported to the newly forming cell wall
over 14 to 16 h (75).
The wide variety of clinical presentations, from severe dis-
ease to an asymptomatic carrier state, makes the definitive
determination of pathogenesis difficult. However, several the-
ories have been put forward (83, 115). Some of the most likely
include the ability of the protozoan to cause direct damage to
the intestinal mucosa via adherence with the disk, disacchari-
dase enzyme reduction following brush border damage, the
release from Giardia of cytopathic substances such as thiol
proteinases and lectins, and the stimulation of a host immune
response with release of cytokines and mucosal inflammation
(41, 48, 61, 78, 83, 106, 110, 157, 259). Additionally, it is likely
that there are genetic differences between Giardia isolates
which may confer virulence (115, 173, 182, 190). The surface of
Giardia may also undergo antigenic variation in the human
* Corresponding author. Mailing address: Division of Infectious
Diseases, University of Connecticut Health Center, Farmington, CT
06030-3212. Phone: (860) 679-4700. Fax: (860) 679-4701. E-mail: dhill
host and thus evade immune detection (181). Given these
multiple potential mechanisms, a multifactoral process is
G. lamblia is found primarily in mammals including humans,
cats, dogs, beavers, and cattle (40, 74, 77, 257). Transmission of
the G. lamblia cyst to humans occurs most commonly following
ingestion of contaminated water (139). Transmission via sur-
face water is facilitated by the relative resistance of the cyst to
chlorination and its ability to survive in cold water for weeks
(59, 122). Transmission by food (22, 152, 187), by direct fecal-
oral contact among children in day care (28, 224, 237) or in
developing-world settings (96, 159), and by sexual practices
which include oral-anal contact (168) represent other common
modes of transmission (113). G. lamblia is also seen as a cause
of prolonged diarrhea in travelers (37, 66, 125, 136, 205; N.
Fiumara, Letter, N. Engl. J. Med. 288:1410–1411, 1973).
Worldwide, the majority of patients infected with G. lamblia
are asymptomatic. However, typical clinical symptoms of giar-
diasis usually begin 1 to 3 weeks after ingestion of cysts and are
marked by diarrhea, malaise, flatulence, greasy stools, and
abdominal cramps (113, 256). Other symptoms commonly in-
clude bloating, weight loss (174), and anorexia. Vomiting and
fever are less common, and blood- or mucus-tinged feces are
rare. Illness can last several months if untreated and can be
characterized by continued exacerbations of diarrheal symp-
toms. With chronic illness, malabsorption of fat, lactose, vita-
min A, and vitamin B12are reported, and failure of children to
thrive has been noted (86, 112, 149, 184, 227).
Giardiasis should be considered in the differential diagnosis
of many diarrheal syndromes. A careful history, which notes
any risk factors such as recent travel, wilderness exposure, or
situations involving poor fecal-oral hygiene, and a physical
examination are essential. Infection with G. lamblia can often
be distinguished from bacterial and viral infections because of
the longer duration of illness, 7 to 10 days by the time of
presentation, and the presence of weight loss (113). Parasitic
diarrhea with Cryptosporidium or Cyclospora can have similar
features in the immunologically normal host and would need to
be distinguished by specific diagnostic testing (50, 99).
Several methods exist for detection of the parasite. Demon-
stration of trophozoites or cysts in the stool, called the ova and
parasite (O&P) examination, is the traditional means of diag-
nosis (167). One stool sample will allow the detection of 60 to
80% of infections, 2 stool samples will allow the detection of 80
to 90%, and three stool samples will allow the detection of over
90% (97, 111). However, in some instances, because of inter-
mittent or low levels of shedding, it is necessary to examine
more than three stool samples. The desire for more sensitive
and specific, as well as faster and reproducible, diagnostic
testing has led to the development of immunoassays. Fecal
FIG. 1. Ventral surface of a Giardia lamblia trophozoite imaged by scanning electron microscopy. It demonstrates the disk and flagella. A
second trophozoite is seen behind it. Magnification, ?8,100. Photo courtesy of David Dorward, Rocky Mountain Laboratory, National Institutes
of Health, Hamilton, Mont.
VOL. 14, 2001 TREATMENT OF GIARDIASIS115
antigen detection using enzyme-linked immunosorbent assays,
nonenzymatic immunoassays, or fluorescein-tagged monoclo-
nal antibodies can be superior diagnostic methods to the O&P
examination (7, 89, 90, 161, 262). It is particularly helpful in
assessing cure or in screening for Giardia infection. However,
when other parasites are in the differential diagnosis, a stool
sample for O&P examination should still be ordered. In the
unusual patient for whom a diagnosis cannot be made by O&P
examination of stool, endoscopy with duodenal fluid sampling
and biopsy may be performed (82, 113, 185, 256). An instance
in which this may be helpful is the human immunodeficiency
virus-infected patient with diarrhea, whose illness has multiple
potential etiologies. Culture and sensitivity testing is available
only in research settings (120, 138). DNA probes have been
generally limited to detection of parasites in water samples
(134, 158), and serologic testing is most useful in epidemiologic
surveys (118, 119, 170). Figure 2 outlines an approach to the
diagnosis and management of suspected cases of giardiasis and
is discussed further below (see “Recommendations”).
THERAPY OF GIARDIASIS
When evaluating the clinical efficacy of agents used against
Giardia, it is difficult to compare studies. They vary as to entry
methodology (whether randomization was done and if treat-
ment was blinded or open), population studied (children,
adults, symptomatic and/or asymptomatic patients), outcome
measures (clinical efficacy and/or stool negativity), and dura-
tion of follow-up. Nevertheless, conclusions may be drawn
from the studies when viewed as a whole, and statements can
be made about the relative efficacy of the agents.
Classes of Agents and Clinical Properties
Nitroimidazoles. The nitroimidazoles class of agents used to
treat G. lamblia infection includes metronidazole, tinidazole,
ornidazole, and secnidazole. This class was discovered in 1955
and was found to be highly effective against several protozoan
infections (240). Metronidazole [1-(?-hydroxyethyl)-2-methyl-
5-nitroimidazole; Flagyl] was determined to be therapeutic
against Trichomonas vaginalis and Entamoeba histolytica fol-
lowing its discovery in the late 1950s (67), and in 1962 Darbon
et al. reported that it could be used to treat giardiasis (57).
Since this discovery, metronidazole and other nitroimidazoles
have been used by clinicians as the mainstay of therapy of
Of the nitroimidazoles, the mechanism of killing of Giardia
by metronidazole has been the most thoroughly studied. Met-
ronidazole utilizes the anaerobic metabolic pathways present
in Giardia. The drug enters the trophozoite, and once it is
FIG. 2. Outline of the diagnosis and management of suspected cases of giardiasis.
116 GARDNER AND HILLCLIN. MICROBIOL. REV.
within the cell, electron transport protein ferredoxins from the
parasite donate electrons to the nitro group of the drug (223,
238, 244). The drug becomes “activated” by reduction of this
nitro group (223, 238, 240), and a gradient favoring the intra-
cellular transport of metronidazole is established by this re-
duction reaction. Reduced metronidazole serves as a terminal
electron acceptor which binds covalently to DNA macromole-
cules (72, 177). This results in DNA damage in the form of loss
of helical structure, impaired template function, and strand
breakage, with subsequent trophozoite death (95). In addition
to this effect, metronidazole inhibits trophozoite respiration
(81, 189). The reductive activation of metronidazole may also
lead to toxic radicals, which react with essential cellular com-
ponents (244). Trophozoites within cysts may be less affected
by nitroimidazoles, possibly because of poor penetration of
drug through the cyst wall (236). Resistance to metronidazole
has been induced in vitro (29). It correlates with decreased
activity of parasite pyruvate:ferredoxin oxidoreductase, which
is required for reductive activation of nitroimidazoles (239,
Metronidazole is quickly and completely absorbed after oral
administration and penetrates body tissues and secretions such
as saliva, breast milk, semen, and vaginal secretions (240). The
drug is metabolized mainly in the liver and is excreted in the
In vitro assays for nitroimidazole drug susceptibility have
been performed with G. lamblia since 1980 (112). Using mi-
croscopic evaluation of parasite morphology and mobility,
Jokipii and Jokipii first demonstrated that metronidazole and
tinidazole were effective (129). Subsequently, morphology (13,
166, 175), growth inhibition (56, 69, 94, 116, 160, 225), [3H]thy-
midine incorporation (32, 117, 164), serum killing (114), vital-
dye exclusion (114, 235), inhibition of adherence (21, 55, 79,
166, 192), metabolic (228), and colorimetric (133) assays have
been employed to measure the in vitro response of the drug to
many therapeutic agents. However, as indicated by the variety
of assays used, there is no standard for in vitro testing, making
it difficult to compare results and apply in vitro findings to the
Of the nitroimidazoles, tinidazole and metronidazole have
consistently demonstrated the greatest in vitro activity; tinida-
zole possesses a slight advantage (30, 32, 55, 101). More highly
substituted nitroimidazoles, such as miconazole, clotrimazole,
itraconazole, and ketoconazole, were developed for their an-
tifungal activity and are not effective agents against G. lamblia
(55). Sensitivity to nitroimidazoles can vary depending on the
stocks and clones of G. lamblia used in testing (29, 31, 79, 160).
In the United States, metronidazole is the only member of
the nitroimidazole class available to treat giardiasis; it is also
the most common drug used for treatment worldwide. In spite
of its widespread and accepted use against Giardia, the U.S.
Food and Drug Administration has never approved it for this
indication. Clinical trials have employed dosing two and three
times daily (usually 250 mg/dose) for 5 to 10 days and short-
course (1 to 3 days), daily single-dose therapy (2.0 or 2.4 g/
dose) (261). In the 5- to 10-day schedules the efficacy ranges
from 60 to 100% in adult and pediatric patients, with a median
efficacy in both groups of 92% (Table 1) (20, 49, 68, 91, 92, 100,
127, 132, 135, 150, 151, 191, 201, 202, 232, 256). In general, this
schedule is well tolerated, with most side effects involving gas-
trointestinal upset and metallic taste (Table 2).
The single-dose, short-course treatments (one high dose
given daily) were designed to improve compliance without
sacrificing efficacy. They have been used in both adults and
children. These regimens are generally less efficacious, partic-
ularly if only one dose of metronidazole is given. The efficacy
of single-dose therapy ranges from 36 to 60% if the drug is
given for 1 day (16, 93, 127, 130, 220, 229) and rises to 67 to
80% if the drug is given for 2 days (Table 1) (127, 130, 146; E.
Green, D. M. Lynch, J. A. McFadzean, and I. M. Pugh, Letter,
Br. Med. J. 2:411–412, 1974). Continuing single-dose treat-
ment for 3 days increases efficacy to the range seen with lower-
dose, longer-course therapies (229; Green et al., Letter). The
high-dose regimens may also carry more side effects (127).
Children have been included in many of the trials of both
long- and short-course therapy, with outcomes similar to those
in adults and 80 to 100% efficacy (median, 94%) in the 5- to
10-day regimens (91, 100, 132, 135, 186, 201, 232; A. Rastegar-
Lari and A. Salek-Moghaddam, Letter, J. Trop. Pediatr. 42:
184–185, 1996). Although metronidazole does not come in a
standard liquid form, a suspension can be prepared by thor-
oughly crushing metronidazole tablets, using a drop of glycerin
as a lubricant, and suspending the mixture in Cherry Syrup NF
The most common side effects of metronidazole treatment
include headache, vertigo, nausea, and a metallic taste in the
mouth (Table 2). Nausea occurs in 5 to 15% of patients given
standard multiday courses (135, 151). In addition, pancreatitis,
central nervous system toxicity at high doses (144, 212), and
transient, reversible neutropenia have been attributed to met-
ronidazole (147). Patients should be warned to avoid alcohol
while taking metronidazole. The inhibition of aldehyde dehy-
drogenase by metronidazole can cause severe vomiting, flush-
ing, headache, and gastrointestinal pain following alcohol in-
Metronidazole is mutagenic in bacteria and carcinogenic in
mice and rats at high doses over long periods (34, 153, 240,
251). However, mutagenicity has never been documented in
humans, suggesting that the use of metronidazole is safe in this
regard (23, 78, 98, 212). This may, however, mitigate against
the short-course high-dose regimens in children.
The finding of therapeutic efficacy with metronidazole
spurred investigators to develop and test other nitroimidazole
derivatives. The other agents, tinidazole, ornidazole, and sec-
nidazole, each have longer half-lives, making them suitable for
single daily-dose therapies (217). One dose of tinidazole
(Fasigyn) was successfully used in 1971 in a group of Swedish
students who acquired giardiasis during a visit to Russia (11).
This single, 2-g dose (or equivalent in children) has consis-
tently proven to have a clinical efficacy of 80 to 100% with a
median efficacy of 92% (Table 1) (16, 126, 130, 131, 146, 151,
193, 222, 229, 261; Z. Farid, N. A. El Masry, W. F. Miner, and
A. Hassan, Letter, Lancet ii:721, 1974; T. Pettersson, Letter,
Br. Med. J. 1:395, 1975) and is far superior to metronidazole
when single-dose regimens are directly compared (93, 130, 229,
261). There is also improved compliance with this dosing
schedule. The recommended dosing for pediatric populations
is usually 50 mg/kg for a single dose (Table 2) (82, 193, 232,
256), and the drug is available in a liquid suspension.
VOL. 14, 2001TREATMENT OF GIARDIASIS 117
Adverse effects reported with tinidazole are not as common
as with metronidazole but do include bitter taste, vertigo, and
gastrointestinal upset (Table 2) (130, 131; Pettersson, Letter).
Tinidazole is not available in the United States, but travel
health providers recommend that some travelers, particularly
long-term travelers or overland trekkers in Asia, purchase the
drug upon arrival at their country of destination and take it in
the event of acquiring giardiasis (113).
Another nitroimidazole derivative which is also not available
in the United States is ornidazole. There have been fewer
studies with ornidazole, but it has excellent efficacy when given
over several days and efficacy similar to tinidazole (92 to 100%)
when given as a single dose (19, 131, 145, 220, 232, 261).
Single-dose ornidazole (40 mg/kg) has also been given to chil-
dren, with obvious benefits regarding compliance and cost (39,
186). In one study the drug was given intravenously and was
associated with increased side effects, making the investigators
reluctant to recommend routine use of this drug in children
until large-scale studies of recurrence, carcinogenicity and side
effects are completed (39).
Secnidazole, a long-acting 5-nitroimidazole derivative, has
been used but is not available in the United States. Similar to
tinidazole and ornidazole, secnidazole is usually given as a
single dose. The most common regimen is 2 g in adults and 30
mg/kg in children (95). Clinical studies demonstrate efficacy
rates of over 85% with the single dose in adults (49; R. Baqai,
H. Qureshi, and S. J. Zuberi; Letter, J. Pak. Med. Assoc.
45:288, 1995), and in children, this dosing is as effective as a 7-
to 10-day course of metronidazole (100; Rastegar-Lari and
Salek-Moghaddam, Letter). The drug is rapidly and com-
pletely absorbed, has a half-life of 17 to 29 hours, and is
metabolized via oxidation in the liver (95). Adverse effects
have been reported, most notably gastrointestinal disturbance
(nausea, anorexia, and abdominal pain) and dizziness, but usu-
ally do not require discontinuation of the drug.
Quinacrine. Quinacrine (Atabrine) was first introduced as
an antimalarial agent in 1930, following the work of Kikuth,
and became the antimalarial of choice for allied troops in
World War II because of its greater availability and better
tolerance compared with quinine (240). After the war, it soon
became an important agent against G. lamblia, with a clinical
efficacy of 90% or more (20, 52, 105, 255). However, with a
U.S. market limited to the treatment of Giardia, the use of
quinacrine declined, and its production in the United States
was discontinued in 1992, although it may still be obtained
through alternative sources (Table 2).
The antiprotozoal mechanism of quinacrine is not fully elu-
cidated. The drug intercalates readily with G. lamblia DNA,
and it is this interaction which is thought to cause an inhibition
of nucleic acid synthesis (240). The differing relative quina-
crine uptake rate between human and G. lamblia cells may be
responsible for the selective toxicity of the drug (236). In vitro,
quinacrine reduces cyst viability and excystation rates (179,
189). Resistance has been induced in vitro, and in one study it
TABLE 1. Efficacy of anti-Giardia drugs in adult and pediatric infectiona
Median efficacy (%)c
Efficacy range (%)
Metronidazole500–750 mg/day ? 5–10 days
2.0–2.4 g, single dose
2.0–2.4 g, q.d. ? 2 days
2.0–2.4 g, q.d. ? 3 days
15–22.5 mg/kg/day ? 5–10 daysd
Tinidazole300 mg/day ? 7 days
1.0–2.0 g, single dose
50 mg/kg, single dosed
Ornidazole 1.0–2.0 g, single dose
40–50 mg/kg, single dosed
Secnidazole 2.0 g, single dose
30 mg/kg, 1 or 2 dosesd
Quinacrine300 mg/day ? 5–7 days
6–8 mg/kg/day ? 5–10 daysd
Furazolidone400 mg/day ? 7–10 days
8 mg/kg/day ? 7–10 daysd
Albendazole 200–800 mg/day ? 1–3 days
200–400 mg/day ? 5–7 days
Paromomycin 10–50 mg/kg/day or 1,500 mg/day ? 5–10 days55–88
Bacitracin zinc240,000 U/day ? 10 days95
aEfficacy is based on studies that may vary in design, entry methodology, or outcome measure. When separate pediatric populations were studied, they are designated.
See the text for references.
bDoses are total daily amounts, which may or may not have been given in divided doses. Actual treatment recommendations are presented in Table 2. q.d., once
cMedian efficacy is given when the results of four or more studies are included.
dPediatric population only.
118GARDNER AND HILLCLIN. MICROBIOL. REV.
was correlated with decreased uptake of the drug (246). Quin-
acrine is rapidly absorbed from the intestinal tract and is widely
distributed in body tissues.
Although results differ, depending on the in vitro sensitivity
testing assay used, metronidazole and furazolidone have been
shown to be slightly more potent than quinacrine (30, 32, 55,
94). However, in other studies the in vitro efficacies of quina-
crine and metronidazole are the same (21, 117, 164). Some of
this difference may be related to the greater variation in sen-
sitivity to quinacrine than to metronidazole or furazolidone
between clones of Giardia (31).
Clinically, quinacrine is very effective, with studies establish-
ing its efficacy over 5 to 10 days at about 95% (Table 1) (20,
135, 220, 255). Some researchers consider the drug to be the
most efficacious of any of the anti-Giardia therapeutics (256).
Dosing is usually 100 mg three times a day over 5 to 7 days for
adults and 6 mg/kg/day in three divided doses over 5 to 7 days
for children (Table 2) (150).
Side effects have precluded many clinicians from using quin-
acrine, particularly in children (Table 2). A bitter taste, along
with vomiting, has been reported in up to 28% of study par-
ticipants (20, 52), and led to a lower efficacy in children
younger than 5 years (52), probably due to low compliance.
Yellow/orange discoloration of the skin, sclerae, and urine
affects 4 to 5% of those taking quinacrine, beginning about 1
week after starting treatment, and can last up to 4 months after
discontinuation of therapy. Other common side effects include
nausea, vomiting, headache, and dizziness (254). Drug-induced
psychosis is uncommon, and exfoliative dermatitis and quina-
crine-induced retinopathy are rare (82). Quinacrine can exac-
erbate psoriasis, and in glucose-6-phosphate dehydrogenase
(G6PDH)-deficient individuals, it can precipitate hemolysis. It
is contraindicated in pregnancy due to a possible link with
spina bifida and renal agenesis. It has never been demon-
strated to be carcinogenic, even though it has a mechanism of
action of binding to DNA.
Furazolidone. Furazolidone (Furoxone) is one of the thou-
sands of nitrofuran compounds created since the class was
discovered in the 1940s (143). It is effective against many bac-
teria including Klebsiella spp., Clostridium spp., Escherichia
TABLE. 2. Recommended dosing and adverse effects of anti-Giardia drugs
Drug Adult dosef
Pediatric dose Adverse effects
250 mg t.i.d. ? 5–7 days 5 mg/kg t.i.d. ? 5–7 days Headache, vertigo, nausea, metallic taste,
Disulfiram-like reaction with alcohol
Rare: pancreatitis, central nervous system
toxicity, reversible neutropenia, peripheral
neutropathy, T-wave flattening with
2 g, single dose50 mg/kg, single dose (max, 2 g) As for metronidazole
2 g, single dose 40–50 mg/kg, single dose (max, 2 g)As for metronidazole
100 mg t.i.d. ? 5–7 days 2 mg/kg t.i.d. ? 7 days Nausea and vomiting, dizziness, headache
Yellow/orange discoloration of skin and
Rare: toxic psychosis
100 mg q.i.d. ? 7–10 days2 mg/kg q.i.d. ? 10 days Nausea, vomiting, diarrhea
Brown discoloration of urine; disulfiram-like
reaction with alcohol ingestion
Reacts unfavorably with MAO inhibitors
Mild hemolysis in G6PDH deficiency
500 mg t.i.d. ? 5–10 days 30 mg/kg/day in 3 doses ? 5–10 daysOtotoxicity and nephrotoxicity with systemic
400 mg q.d. ? 5 days 15 mg/kg/day ? 5–7 days (max, 400 mg)Anorexia, constipation
Rare: reversible neutropenia and elevated
liver function tests
120,000 U b.i.d. ? 10 days Not tested in children under 10 yr Nausea, vomiting, abdominal discomfort
Nephrotoxicity with systemic absorption
aNot a U.S. Food and Drug Administration-approved indication.
bNot available in the United States.
cNo longer produced in the United States. May be obtained from Panorama Pharmacy, Panorama City, Calif.
dAvailable in a liquid formulation.
eNot a U.S. Food and Drug Administration-approved indication. Information is based on only one study (14).
fq.d., once a day; b.i.d., twice a day; t.i.d., three times a day; q.i.d., four times a day.
VOL. 14, 2001 TREATMENT OF GIARDIASIS 119
coli, Campylobacter spp., and Staphylococcus aureus. As early
as the 1950s, furazolidone was being used in the treatment of
giardiasis (253). It is approved for use in the United States and
remains an important therapeutic agent worldwide. Of the
common anti-Giardia therapeutics, it is the only one available
in a liquid suspension in the United States; therefore, its use
has been advocated in pediatric populations (150).
The mechanism of action of furazolidone against G. lamblia,
like many of the antiparasitics, is not completely explained.
The drug undergoes reductive activation in the G. lamblia
trophozoite, but, unlike metronidazole, reduction possibly oc-
curs via an NADH oxidase (38, 244). Its killing effect correlates
with the toxicity of reduced products, which can damage im-
portant cellular components including DNA. Resistance to
furazolidone may be correlated with decreased entry of drug
(246) or with increased levels of thiol-cycling enzymes, which
can defend against toxic radicals (249). The drug is readily
absorbed via the gastrointestinal tract and is metabolized rap-
idly in tissues, leading to low concentrations in serum and urine
In in vitro susceptibility testing, furazolidone performs com-
parably to metronidazole and has consistently demonstrated
the highest activity of the nonimidazoles (32, 55, 101); it is
more active than quinacrine (30).
Clinical studies using furazolidone are numerous and have
been completed with a wide range of subjects, doses, and
administration schedules. Although its efficacy has generally
been considered to be slightly lower than those of metronida-
zole and quinacrine, curative rates between 80 and 96% have
been reported for 7- to 10-day courses (Table 1) (20, 52, 91,
151, 178, 191, 201, 255). It is when the drug is given for only 5
days that efficacy falls off considerably (151, 178). It is given as
four doses per day in both adults (100 mg per dose) and
children (1.5 mg/kg) (Table 2). In the pediatric suspension, two
tablespoonfuls substitute for a 100-mg tablet.
About 10% of patients report gastrointestinal symptoms
such as nausea, vomiting, and diarrhea (Table 2) (150, 256).
Other adverse effects can include a brown discoloration of the
urine; hemolysis can occur in G6PDH-deficient patients. The
drug has a monoamine oxidase (MAO) inhibitory effect and
should never be given concurrently to individuals already tak-
ing MAO inhibitors. There have been rare reports of disul-
firam-like reactions when it is taken with alcohol (164b). A
furazolidone-induced manic episode in a patient infected with
human immunodeficiency virus has been reported (73). Fura-
zolidone is also contraindicated in infants younger than 1
month of age, who could develop hemolytic anemia because of
their normally unstable glutathione. Finally, the drug is muta-
genic in bacteria and has been demonstrated to cause mam-
mary tumors in rats and pulmonary tumors in mice when given
in chronic high doses. However, the implication of this finding
for humans is not known and has not been adequately ad-
dressed (143, 164b, 236). When treating pediatric populations,
the advantages of its minimal adverse effects and the availabil-
ity of a liquid suspension must be weighed against the need for
frequent dosing over a 10-day treatment period.
Benzimidazoles. Two members of the benzimidazole class of
therapeutics, albendazole (Albenza) and mebendazole (Ver-
mox), have been used to treat G. lamblia infection (155). Clin-
ical and in vitro efficacy studies have produced different results
as to their effectiveness. However, a comparatively benign side
effect profile, combined with proven efficacy against many hel-
minths, renders them promising for treatment (208, 250).
The benzimidazoles exert their toxic effect on Giardia in part
by binding to the G. lamblia β-tubulin cytoskeleton (71, 175,
209). This binding causes both inhibition of cytoskeleton po-
lymerization and impaired glucose uptake (250). Although the
exact binding site on the cytoskeleton has not been deter-
mined, it is postulated that a benzimidazole-colchicine site
interaction may play a role (51, 166, 236). The benzimidazoles
are poorly absorbed from the gastrointestinal tract, although
this can be improved with the coingestion of a fatty meal. The
systemic effect of albendazole is due to its primary metabolite,
albendazole sulfoxide, which is rapidly formed in the liver
following absorption (3). Excretion by the kidneys is negligible.
In vitro susceptibility testing of G. lamblia to the benzimi-
dazoles is limited in comparison to the susceptibility of the
parasite to the nitroimidazoles or quinacrine. Nevertheless,
studies demonstrate a considerable in vitro effect (79, 175, 208,
209). One report showed that both albendazole and mebenda-
zole were 30- to 50-fold more active than metronidazole and 4-
to 40-fold more active than quinacrine in vitro (71). Another
demonstrated that the ability of albendazole to affect tropho-
zoite morphology, adherence, and viability was far greater than
that of metronidazole or tinidazole (166). However, their vari-
able clinical efficacy demonstrates the discordance between in
vitro testing and in vivo activity. Resistance to albendazole can
be induced in vitro (154) and correlates with changes in the
parasite cytoskeleton (243). Other benzimidazoles such as no-
codazole, oxfendazole, thiabendazole, and fenbendazole have
also demonstrated some in vitro efficacy (236).
Clinical trials have been limited to albendazole and meb-
endazole, with mixed results. Hall and Nahar reported equal
curative efficacy of albendazole and metronidazole in children
when albendazole was given for 5 days but not when it was
given in single or 3-day dosing (Table 1) (104). A decreased
efficacy of albendazole when given for 3 days or less was also
documented by Kollaritsch et al. in travelers with giardiasis
(137), by Pungpak et al. in children and adults (198), and by
Pengsaa et al. in children (193). Improved efficacy was seen in
other patients when the drug was given for 5 days (171, 207,
214) or 7 days (198). The exception to the need for longer
treatment courses was seen in one study in which a single dose
was administered (68). An albendazole-metronidazole combi-
nation was 100% effective in 20 patients with metronidazole-
resistant giardiasis who had failed three to five courses of
standard oral metronidazole therapy (44).
Treatment with mebendazole has resulted in widely diver-
gent clinical results. Al-Waili reported over 90% efficacy in two
studies in children (8, 9). However, other studies in both pe-
diatric and adult populations have not shown equal success but
instead have shown effectiveness in 80% (211) and in 60% or
less (39, 92, 132; L. di Martino, A. Nocerino, and M. Pettoello
Mantovani, Letter, Trans. R. Soc. Trop. Med. Hyg. 85:557–
558, 1991), as well as a failure to decrease the prevalence rates
of Giardia when mebendazole was used in mass treatment of
helminths (219). Because of this discrepancy, most interest has
focused on albendazole.
The dosage in adults is usually 400 mg per day for 5 days for
albendazole and 200 to 400 mg per day for 5 to 10 days for
120 GARDNER AND HILLCLIN. MICROBIOL. REV.
mebendazole (Table 2). The usual dosage in children is 15
mg/kg per day for 5 to 7 days. Both drugs are available in
suspension. One advantage of using albendazole in children is
its efficacy against many helminths, allowing effective treat-
ment of multiple intestinal parasites (207, 208). Another ad-
vantage is its relative lack of side effects. However, with short-
term use, it may cause gastrointestinal problems of anorexia
and constipation. Long-term, high-dose use of albendazole,
such as when it is used for larval cestode infections, has caused
reversible neutropenia and elevated hepatic enzyme levels (3,
155, 258). Albendazole is contraindicated in pregnancy, due to
possible teratogenicity (pregnancy category C), but animal
studies have shown no increase in carcinogenic incidence.
Paromomycin. Paromomycin (Humatin), a member of the
aminoglycoside family, was first isolated in 1956. It is indicated
for the treatment of Entamoeba histolytica and Trichomonas
and has been proposed as a treatment for G. lamblia in resis-
tant infections and during pregnancy (113, 140). Paromomycin
is poorly absorbed from the intestinal lumen; even large-dose
oral administrations achieve only minimal concentrations in
the blood and urine of patients with normal renal function
(140). Paromomycin inhibits G. lamblia protein synthesis by
interfering with the 50S and 30S ribosomal subunits (the par-
asite rRNA has an unusual size and sequence) and causing
misreading of mRNA codons (69).
In vitro susceptibility testing demonstrates that paromomy-
cin has activity against G. lamblia, but the activity is generally
lower than that of the nitroimidazoles, quinacrine, or furazo-
lidone (30, 101). However, because of poor intestinal absorp-
tion, it compensates for its low antiprotozoal activity by achiev-
ing high levels in the gut. In a rat model, the drug showed
Clinical studies are limited, and therapeutic efficacy ranges
from 55 to nearly 90% (Table 1) (47, 63, 140, 191, 218). The
usual dose is 500 mg three times per day for 10 days in adults
and 25 to 30 mg/kg/day (divided into three doses) in children
As with other aminoglycosides, if absorbed systemically
paromomycin can cause ototoxicity and nephrotoxicity. How-
ever, it may be less ototoxic than other aminoglycosides (142),
and with limited systemic absorption, toxicity should not be a
concern in persons with normal kidneys. However, it should be
used with caution in those with impaired renal function.
Bacitracin zinc. The search for alternative, effective anti-
Giardia therapeutics has led investigators to consider bacitra-
cin. Bacitracin was first isolated in 1945 from a strain of Ba-
cillus and was used systemically against severe staphylococcal
infections until 1960, when its toxicity and the availability of
other antibiotics restricted it to mainly topical use (141). Zinc
was added to the bacitracin complex to promote stability. Bac-
itracin exerts its effect in bacteria by interfering with a dephos-
phorylation step in cell membrane synthesis. Following dem-
onstrated in vitro effectiveness against E. histolytica and
Trichomonas, bacitracin zinc was tested against Giardia in vitro
and found to be active (12, 13).
A clinical trial by Andrews et al. used twice-daily dosing over
10 days and compared the effectiveness of 120,000 U of baci-
tracin zinc, 120,000 U of bacitracin, 120,000 U of neomycin,
and 60,000 U of bacitracin zinc in combination with 60,000 U
of neomycin (14). Cure rates of 95% for bacitracin zinc, 88%
for either bacitracin or the bacitracin zinc-neomycin combina-
tion, and 86% for neomycin were demonstrated. Adverse ef-
fects were limited to a small number of patients who experi-
enced diarrhea, abdominal discomfort, constipation, and
nausea. Children younger than 10 years were excluded from
The disadvantages of using bacitracin zinc include a poten-
tial for nephrotoxicity with prolonged oral dosing and gastro-
intestinal disturbance. Furthermore, compliance can be af-
fected by the 10-day dosing period, and the formulations used
by Andrews in their study are not readily available. Although
bacitracin zinc is promising, more investigation is needed be-
fore it can gain wide acceptance as an agent against G. lamblia.
Emerging and experimental therapeutics. A wide variety of
chemotherapeutic agents including rifampin, bithionol, dichlo-
rophene, hexachlorophene, pyrimethamine, sodium fusidate,
chloroquine, and mefloquine have demonstrated in vitro activ-
ity against Giardia (81, 84, 233). Lipophilic tetracyclines, such
as doxycycline, are highly active in vitro; however, their clinical
efficacy is limited, perhaps because of their rapid absorption
from the intestine (70). Certain pentamidine analogs, as well as
azithromycin, have in vitro activity comparable to that of met-
ronidazole (25, 33).
Nitazoxanide, a 5-nitrothiazole derivative with broad-spec-
trum activity against protozoa, helminths, and some bacteria
has shown limited efficacy in adults and children in Mexico
(71%  and 78%  effectiveness, respectively) and in a
few AIDS patients in Mali (64). It has been given in a dose of
100 to 500 mg twice daily for 3 to 7 days.
Studies using a rat model have demonstrated the efficacy of
ivermectin under specific conditions (260). Disulfiram, a zinc
finger-active compound used for the treatment of alcoholism in
humans, shows significant cure rates and decreased parasitic
burdens in a mouse model of giardiasis (180).
In an ethnobotanical survey of the anti-Giardia gastrointes-
tinal remedies employed by the Luo tribes of East Africa,
methanolic extracts of 21 of the 36 taxa studied were lethal to
or inhibited the growth of G. lamblia in vitro (124). Geranium
nivem extracts have also shown in vitro activity (45). The im-
munomodulatory herbal drug Pippali rasayana, often pre-
scribed for the treatment of worm infections and chronic dys-
entery in India, achieved a 98% cure of murine infection with
G. lamblia (6). Extracts of Piper longum fruit were effective in
a mouse model of infection (241).
Proposlina, a bee glue preparation, demonstrated a 60%
parasitologic cure rate 1 week after treatment was completed
among 48 adults in Cuba (172, 261). In a patient with metron-
idazole-resistant Giardia infection, the ?-adrenergic antagonist
DL-propranolol, given in a dose of 40 mg three times a day with
400 mg of metronidazole three times a day for 10 days, cleared
infection, demonstrating clinical efficacy in humans (197). In
vitro studies demonstrate that propranolol exerts its effect by
inhibiting the motility and growth of the protozoan, most prob-
ably due to the membrane-stabilizing activity of the drug (85).
However, further studies with DL-propranolol and the related
compound D-propranolol are needed before they can be rec-
ommended as anti-Giardia agents.
Immunoprophylactic strategies to prevent or treat giardiasis
have generally not been effective (87). Passive transfer of anti-
Giardia immune serum did not facilitate parasite clearance in
VOL. 14, 2001TREATMENT OF GIARDIASIS 121
murine giardiasis (76, 242). Although patients with common
variable immunodeficiency do have symptomatic and pro-
longed infection with Giardia antiparasitic therapy is required
to control their infection (106, 216). Breast milk can be cyto-
toxic to Giardia via free fatty acids which are generated from
milk triglycerides by the action of a bile salt-stimulated lipase
(204). Also, breast feeding may confer some protection to
suckling infants (176, 183); however the approach of providing
enteral anti-Giardia antibody has not been studied.
Pregnancy and lactation. The management of symptomatic
G. lamblia infection during pregnancy is a challenge for the
clinician because no therapeutic agent combines optimal effi-
cacy and safety. Women who are asymptomatic, have mild
disease, or are in their first trimester should usually avoid being
treated. However, women in whom adequate hydration and
nutritional status cannot be maintained should be treated, even
in the first trimester.
Metronidazole, which rapidly enters the fetal circulation af-
ter absorption by the mother, has demonstrated mutagenicity
in bacteria and carcinogenicity in mice and rats (34, 36, 153,
240, 251). While this information raises concern about the use
of the drug during pregnancy, carcinogenicity has not been
demonstration in humans (23, 24, 78, 98, 212), nor has there
been teratogenicity in rodents (164a). Metronidazole has been
used extensively during pregnancy (pregnancy category B), pri-
marily for therapy of trichomoniasis in 7- to 10-day courses
(42). The results regarding safety to the fetus are conflicting
(36, 42, 107, 212, 215, 218). One retrospective study of 1,469
women who took metronidazole in pregnancy, with 206 using
the drug in the first trimester, found no evidence of congenital
abnormality (26). However, the Collaborative Perinatal
Project, including over 50,000 mother-child pairs, demon-
strated that first-trimester exposure to metronidazole in 31
women showed a possible association with malformations
(107). A meta-analysis of seven studies, prospectively monitor-
ing 253 mother-infant pairs and retrospectively monitoring
1,083 pairs, found no increased risk of fetal malformation in
association with first-trimester use of metronidazole (42), with
one report estimating a relative risk of 0.92 for birth defects
(215). On balance, there may be a slightly increased risk when
using metronidazole during the first trimester, and thus its use
should be avoided during this period. High-dose (?2.0 g),
short-course regimens should not be given during pregnancy.
Metronidazole is actively excreted in breast milk in concen-
trations similar to those in plasma. The American Academy of
Pediatrics (AAP) recommends giving a single 2-g dose in nurs-
ing mothers, followed by discontinuation of nursing for 12 to
24 h (10, 36). The AAP also recommends that mothers taking
tinidazole discontinue nursing for the same time period as
those taking metronidazole (10). However, metronidazole is
approved for use in children for therapy of amebiasis and is
used in children for therapy of anaerobic infections, so it would
seem that the small amount secreted in breast milk would not
be deleterious. Also, since single, high-dose regimens of met-
ronidazole have poor efficacy and would be expected to lead to
higher levels in breast milk, these findings favor traditional
treatment with lower doses over 5 to 7 days.
Paromomycin is generally considered safe because it is
poorly absorbed from the intestine and excreted almost 100%
unchanged in the feces. Therefore, little if any of the drug will
reach the fetus. However, it is not as effective as metronidazole
or quinacrine. In addition, no clinical trials have addressed the
effects of high serum concentrations of paromomycin during
pregnancy. Nevertheless, paromomycin has been used success-
fully to eradicate G. lamblia infection in the gravid patient and
is an important agent to consider during the first trimester,
when metronidazole should not be used (140, 218). Paromo-
mycin should also be safe in nursing mothers. A study in ewes
showed only a 0.018% drug recovery rate in breast milk for the
12 h following parenteral administration (36, 263). The AAP
does designate streptomycin and kanamycin, aminoglycoside
relatives of paromomycin, to be compatible with breast feeding
One expert on giardiasis has espoused quinacrine treatment
in pregnant patients due to its high cure rate (256). While the
drug is very effective, its slow excretion from the body and
proven teratogenicity in rats make it a suboptimal choice for
treatment in pregnancy. Although quinidine and quinine are
compatible with breast-feeding, no information regarding the
safety of quinacrine for the breast-fed child was available (10).
Furazolidone is not recommended for the pregnant patient.
Although it is efficacious, its has caused mammary tumors in
mice and mutations in bacteria, which should deter the physi-
cian from using it in this setting (164b). Its safety for breast-fed
children is not known. Albendazole is considered a pregnancy
category C agent, and has been teratogenic in rats and rabbits,
although there is little experience of its effects in pregnant
Asymptomatic infection. On a global basis, most persons
infected with G. lamblia are asymptomatic or minimally symp-
tomatic. Treating asymptomatic patients, particularly children,
is controversial, and there are several factors to consider be-
fore initiating therapy. The setting of the infection plays a key
role in the decision. In areas where G. lamblia is endemic,
treatment may not be desirable because the children are likely
to become rapidly reinfected following treatment (96, 231). If
Giardia contributes to failure of growth and development (86,
163, 227), treatment, even though reinfection may occur, might
allow catch-up growth (103) and might be worth the cost and
effort. A drug such as albendazole, which would also treat
nematode infections, might be useful in these settings; how-
ever, the requirement for 5-day dosing would make it difficult
to complete therapy in many situations.
In conditions in which the child’s nutritional baseline is
excellent, such as in day care centers in the developed world,
asymptomatic carriers may not always need therapy (5, 121,
195, 203, 221, 237). However, it should be noted, that aymp-
tomatically infected children may excrete Giardia for months
(195), carry it home to family members and thus initiate infec-
tion in the household, and even help maintain high levels of
Giardia infection in a community (4, 196, 224; G. D. Overturf,
Editorial, Clin. Infect. Dis. 18:764–765, 1994). It is not uncom-
mon for a mother of a young child in day care to become
symptomatic with giardiasis, identifying the presence in the
household of Giardia which has been introduced by the asymp-
tomatic child. If there is recurrent diarrhea attributed to Gi-
ardia in day care which cannot be controlled by improved
122GARDNER AND HILLCLIN. MICROBIOL. REV.
hygiene and by treatment and exclusion of children who are
symptomatic, consideration can be given to screening and
treating all the children in the day care setting (5, 18, 230).
If Giardia is detected in the stool and there is little likelihood
of reinfection, such as in a returned traveler, treatment can be
given. In the household, if one member is symptomatic and
there is the possibility that fecal-oral spread has occurred
within the family or that there is a common source of infection,
all family members should be screened and treated so that
reinfection will not occur.
Another factor to consider in deciding whether to treat
asymptomatic carriers is the consequences of transmission of
infection if the carrier is not treated, e.g., infection in food
handlers (169, 199). This group should be treated to prevent
Resistance and relapse. Treatment failures have been re-
ported with all of the common anti-Giardia agents including
metronidazole, quinacrine, furazolidone, and albendazole.
However, it is important for the clinician faced with recurrence
of symptoms after therapy to differentiate between actual drug
resistance, cure followed by reinfection, and post-Giardia lac-
tose intolerance. Therefore, the first step is to document true,
persistent infection by sending a stool sample for O&P exam-
ination or Giardia antigen detection. If the sample is positive,
a careful exposure history should provide information about
the likelihood of reinfection, and reinfected individuals should
respond to the original therapeutic agent. Reinfection would
be common in regions of endemicity around the world and in
situations of poor fecal-oral hygiene. If a patient has become
reinfected, risk factors should be identified and the patient
should be counseled regarding proper hygiene and prevention
Post-Giardia lactose intolerance is the most common of the
disaccharidase deficiencies associated with giardiasis and may
occur in 20 to 40% of patients (65). Thus, if the stool is
negative for Giardia, a trial of avoiding lactose-containing
foods and liquids should be instituted. This syndrome may take
several weeks to resolve.
True treatment failure could mean infection with a drug-
resistant isolate of Giardia. Resistance to most anti-Giardia
agents has been documented or induced in vitro (29, 154,
245–247), and multiple, genotypically different clones of G.
lamblia with different drug class susceptibilities have been
found in the human duodenum (46, 81, 160, 248). However,
there has not been a consistent correlation between in vitro
resistance or sensitivity and clinical failure or success (43, 160,
164, 225, 249), still leaving open the question of true parasite
Clinically resistant strains have been treated with longer
repeat courses or higher doses of the original agent (91, 165,
178). However, the most efficacious means of eradicating these
infections seems to involve using a drug from a different class
to avoid potential cross-resistance (52, 92). An initial switch to
a drug of a different class may not always be effective as dem-
onstrated in two French patients who failed albendazole treat-
ment following two courses of metronidazole but did respond
to quinacrine (P. Brasseur and L. Favennec, Letter, Parasite
2:422, 1995). Combination regimens using metronidazole-al-
bendazole, metronidazole-quinacrine, or other active drugs or
giving a nitroimidazole plus quinacrine for courses of at least 2
weeks have proven successful against refractory infection (44,
182a, 197, 225, 234). On occasion, several different combina-
tions or approaches will be necessary to effect cure.
In cases of giardiasis in which alternative therapy is not
effective, other possibilities should be considered, such as the
presence of immunologic deficiency. Chronic giardiasis in pa-
tients with hypogammaglobulinemia is well recorded (106, 108,
216) and can be difficult to treat, often requiring prolonged
courses of therapy. Although Giardia is seen in homosexual
men who engage in oral-anal sexual practices (162, 200, 226),
illness may often be neither severe nor prolonged (148). Nev-
ertheless, in AIDS patients with severe giardiasis, prolonged or
combination therapy may be necessary (182a).
An approach to the diagnosis and management of suspected
giardiasis is illustrated in Fig. 2 and discussed in more detail
above (see “Background”). If stools are negative, an empiric
course of therapy can be given; however, an alternative diag-
nosis should be considered. If there is no response to therapy
in stool-negative cases, invasive testing by endoscopy can be
performed to help determine the diagnosis, particularly if the
patient is immunocompromised.
When treatment is carried out, the agents of choice are
listed in Table 3 and the dosages are given in Table 2. The most
effective agents for therapy of giardiasis are single doses of
tinidazole or ornidazole, 5 to 7 days of quinacrine, and 5 to 7
days of metronidazole. Tinidazole and ornidazole are not ap-
proved or available in the United States. Production of quin-
acrine has been discontinued, but it still may be obtained on a
limited basis; however, it has significant side effects, particu-
larly in children. Therefore, the treatment of choice in the
United States for both adults and children is metronidazole. A
standard course of 5 to 7 days should effectively treat 90% or
more of infected individuals. Although the efficacy of 3 days of
2 to 2.4 g in a single daily dose approaches that of longer
regimens, this regimen is not recommended. The drug has not
TABLE 3. Recommendations for therapy of giardiasis
Clinical scenario Drug and duration of treatmenta
Symptomatic infection, USA
Adult and pediatric
Metronidazole for 5–7 days
Furazolidone for 7–10 days
or quinacrine for 5–7 days
or albendazole for 5–7 days
Symptomatic infection, overseas
Adult and pediatric Tinidazole (single dose) or
ornidazole (single dose)
Second and third trimesters
Paromomycin for 5–10 days
Paromomycin for 5–10 days
or metronidazole for 5–7
Resistant infection or relapseDrug of different class or
plus quinacrine for 2 wk or
aFor drug dosing, see Table 2.
VOL. 14, 2001 TREATMENT OF GIARDIASIS123
received a Food and Drug Administration indication for giar-
diasis, and these high doses may have increased side effects.
Furazolidone is an effective alternative but requires 7 to 10
days of treatment four times a day, which will probably affect
compliance. Of the newer therapeutics, albendazole in a 5-day
regimen seems most promising, but additional studies are
needed. It has the advantage of having broad antiparasitic
effect, which may be beneficial in developing-world settings.
In pregnancy, if treatment is required, paromomycin should
be tried in the first trimester and paromomycin or metronida-
zole should be used in the second and third trimesters.
Treatment of all asymptomatic patients calls for careful in-
terpretation of the clinical situation, but they may not always
It can be expected that parasites will be cleared from the
stool in 3 to 5 days and that symptoms will resolve in 5 to 7 days
(91, 100, 131, 171). If the symptoms do not abate, the patient
should be evaluated for treatment failure or lactose intoler-
ance. If resistance or relapse has occurred, treatment with a
drug of a different class or with a combination of a nitroimid-
azole and quinacrine for at least 2 weeks should eradicate
We thank Theodore Nash for helpful comments and suggestions.
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