Amoebiasis, also known amoebic dysentery, is an infection caused by any of

the amobae of the Entamoeba group.[3] Symptoms are most common during infection

by Entamoeba histolytica.[3] Amoebiasis can be present with no, mild, or severe symptoms.
[3]
 Symptoms may include abdominal pain, diarrhea, or bloody diarrhea.[3] Complications can
include inflammation and ulceration of the colon with tissue death or perforation, which may
result in peritonitis.[3] People affected may develop anemia due to loss of blood.[3]
Cysts of Entamoeba can survive for up to a month in soil or for up to 45 minutes under
fingernails.[3] Invasion of the intestinal lining results in bloody diarrhea. [3] If the parasite
reaches the bloodstream it can spread through the body, most frequently ending up in the
liver where it can cause amoebic liver abscesses.[3] Liver abscesses can occur without
previous diarrhea.[3] Diagnosis is typical by stool examination using a microscope, but may
not reliably exclude infection or separate between specific types. [3] An increased white blood
cell count may be present in severe cases.[3] The most accurate test is finding
specific antibodies in the blood, but it may remain positive following treatment. [3] Bacterial
colitis can result in similar symptoms.[3]
Prevention of amoebiasis is by improved sanitation, including separating food and water
from faeces.[3] There is no vaccine.[3] There are two treatment options depending on the
location of the infection.[3] Amoebiasis in tissues is treated with
either metronidazole, tinidazole, nitazoxanide, dehydroemetine or chloroquine, while luminal
infection is treated with diloxanide furoate or iodoquinoline.[3] Effective treatment against all
stages of the disease may require a combination of medications. [3] Infections without
symptoms do not require treatment but infected individuals can spread the parasite to
others and treatment can be considered.[3] Treatment of other Entamoeba infections apart
from E. histolytica is not needed.[3]
Amoebiasis is present all over the world,[4] though most cases occur in the developing world.
[5]
 About 480 million people are infected with amoebiasis and this results in the death of
between 40,000–110,000 people a year.[3] Most infections are now believed due to E.
dispar.[3] E. dispar is more common in certain areas and symptomatic cases may be less
common than previously reported.[3] The first case of amoebiasis was documented in 1875
and in 1891 the disease was described in detail, resulting in the
terms amoebic dysentery and amoebic liver abscess.[3] Further evidence from the
Philippines in 1913 found that upon swallowing cysts of E. histolytica volunteers developed
the disease.[3]

Contents

 1Signs and symptoms

 2Cause
o 2.1Transmission
 3Pathogenesis
 4Diagnosis
 5Prevention
 6Treatment
 7Prognosis
 8Epidemiology
 9History
 10References
 11External links

Signs and symptoms[edit]

Most infected people, about 90%,[6] are asymptomatic, but this disease has the potential to
become serious. It is estimated that about 40,000 to 100,000 people worldwide die annually
due to amoebiasis.[7]
Infections can sometimes last for years if there is no treatment. Symptoms take from a few
days to a few weeks to develop and manifest themselves, but usually it is about two to four
weeks. Symptoms can range from mild diarrhea to dysentery with blood, coupled with
intense abdominal pains. The blood comes from bleeding lesions created by the amoebae
invading the lining of the colon. In about 10% of invasive cases the amoebae enter the
bloodstream and may travel to other organs in the body. Most commonly this means
the liver,[8] as this is where blood from the intestine reaches first, but they can end up almost
anywhere in the body.
Onset time is highly variable and the average asymptomatic infection persists for over a
year. It is theorized that the absence of symptoms or their intensity may vary with such
factors as strain of amoeba, immune response of the host, and perhaps
associated bacteria and viruses.
In asymptomatic infections, the amoeba lives by eating and digesting bacteria and food
particles in the gut, a part of the gastrointestinal tract.[citation needed] It does not usually come in
contact with the intestine itself due to the protective layer of mucus that lines the gut.
Disease occurs when amoeba comes in contact with the cells lining the intestine. It then
secretes the same substances it uses to digest bacteria, which include enzymes that
destroy cell membranes and proteins. This process can lead to penetration and digestion of
human tissues, resulting first in flask-shaped ulcerations in the intestine. Entamoeba
histolytica ingests the destroyed cells by phagocytosis and is often seen with red blood
cells (a process known as erythrophagocytosis) inside when viewed in stool samples.
Especially in Latin America,[citation needed] a granulomatous mass (known as an amoeboma) may
form in the wall of the ascending colon or rectum due to long-lasting immunological cellular
response, and is sometimes confused with cancer.[9]
The ingestion of one viable cyst may cause an infection. [10]
Steroid therapy can lead to severe amoebic colitis in persons with asymptomatic or
symptomatic E. histolytica infection.[11] Severe amoebic colitis is associated with high
mortality, and on average more than 50% with severe colitis die. [12]

Cause[edit]
Amoebiasis is an infection caused by the amoeba Entamoeba histolytica. Likewise
amoebiasis is sometimes incorrectly used to refer to infection with other amoebae, but
strictly speaking it should be reserved for Entamoeba histolytica infection.[citation needed] Other
amoebae infecting humans include:[13]
 Parasites
o Dientamoeba fragilis, which causes Dientamoebiasis
o Entamoeba dispar
o Entamoeba hartmanni
o Entamoeba coli
o Entamoeba polecki
o Entamoeba bangladeshi
o Entamoeba moshkovskii
o Endolimax nana and
o Iodamoeba butschlii.
Except for Dientamoeba, the parasites above are not thought to cause disease.

 Free living amoebas.[14][15] These species are often described as "opportunistic free-

living amoebas" as human infection is not an obligate part of their life cycle.
o Naegleria fowleri, which causes primary amoebic meningoencephalitis
o Acanthamoeba, which causes cutaneous
amoebiasis[16] and Acanthamoeba keratitis and sometimes migrates to the brain.
o Balamuthia mandrillaris,[17] which causes both skin and brain infections.
o Sappinia diploidea
Transmission[edit]

Life-cycle of the Entamoeba histolytica

Amoebiasis is usually transmitted by the fecal-oral route, but it can also be transmitted

indirectly through contact with dirty hands or objects as well as by anal-oral contact.
Infection is spread through ingestion of the cyst form of the parasite, a semi-dormant and
hardy structure found in feces. Any non-encysted amoebae, or trophozoites, die quickly
after leaving the body but may also be present in stool: these are rarely the source of new
infections. Since amoebiasis is transmitted through contaminated food and water, it is often
endemic in regions of the world with limited modern sanitation systems, including México,
Central America, western South America, South Asia, and western and southern Africa.[18]
Amoebic dysentery is often confused with "traveler's diarrhea" because of its prevalence in
developing nations. In fact, most traveler's diarrhea is bacterial or viral in origin.

Pathogenesis[edit]
Tissue damage caused by E. histolytica is a result of three main events, host cell death,
inflammation, and parasite invasion. Abbreviations: EhMIF, E. histolytica macrophage migration
inhibitory factor; MMP, matrix metalloproteinases.

Amoebiasis results from tissue destruction induced by the E. histolytica parasite. E.

histolytica causes tissue damage by three main events: direct host cell killing, inflammation,
and parasite invasion.[19]

Diagnosis[edit]
With colonoscopy it is possible to detect small ulcers of between 3–5mm, but diagnosis may
be difficult as the mucous membrane between these areas can look either healthy or
inflamed.[3] Trophozoites may be identified at the ulcer edge or within the tissue, using
immunohistochemical staining with specific anti-E. histolytica antibodies. [5]
Asymptomatic human infections are usually diagnosed by finding cysts shed in the stool.
Various flotation or sedimentation procedures have been developed to recover the cysts
from fecal matter and stains help to visualize the isolated cysts for microscopic examination.
Since cysts are not shed constantly, a minimum of three stools are examined. In
symptomatic infections, the motile form (the trophozoite) is often seen in fresh
feces. Serological tests exist, and most infected individuals (with symptoms or not) test
positive for the presence of antibodies. The levels of antibody are much higher in individuals
with liver abscesses. Serology only becomes positive about two weeks after infection. More
recent developments include a kit that detects the presence of amoeba proteins in the
feces, and another that detects ameba DNA in feces. These tests are not in widespread use
due to their expense.
Microscopy is still by far the most widespread method of diagnosis around the world.
However it is not as sensitive or accurate in diagnosis as the other tests available. It is
important to distinguish the E. histolytica cyst from the cysts of nonpathogenic intestinal
protozoa such as Entamoeba coli by its appearance. E. histolytica cysts have a maximum of
four nuclei, while the commensal Entamoeba coli cyst has up to 8 nuclei. Additionally, in E.
histolytica, the endosome is centrally located in the nucleus, while it is usually off-center
in Entamoeba coli. Finally, chromatoidal bodies in E. histolytica cysts are rounded, while
they are jagged in Entamoeba coli. However, other species, Entamoeba dispar and E.
moshkovskii, are also commensals and cannot be distinguished from E. histolytica under
the microscope. As E. dispar is much more common than E. histolytica in most parts of the
world this means that there is a lot of incorrect diagnosis of E. histolytica infection taking
place. The WHO recommends that infections diagnosed by microscopy alone should not be
treated if they are asymptomatic and there is no other reason to suspect that the infection is
actually E. histolytica. Detection of cysts or trophozoites stools under microscope may
 require examination of several samples over several days to determine if they are present,
because cysts are shed intermittently and may not show up in every sample.
Typically, the organism can no longer be found in the feces once the disease goes extra-
intestinal.[citation needed] Serological tests are useful in detecting infection by E. histolytica if the
organism goes extra-intestinal and in excluding the organism from the diagnosis of other
disorders. An Ova & Parasite (O&P) test or an E. histolytica fecal antigen assay is the
proper assay for intestinal infections. Since antibodies may persist for years after clinical
cure, a positive serological result may not necessarily indicate an active infection. A
negative serological result, however, can be equally important in excluding suspected tissue
invasion by E. histolytica.[citation needed]
Stool antigen detection tests have helped to overcome some of the limitations of stool
microscopy. Antigen detection tests are easy to use, but they have variable sensitivity and
specificity, especially in low-endemic areas. [5]
Polymerase chain reaction (PCR) is considered the gold standard for diagnosis but remains
underutilized.[5][20]

Immature E. histolytica/E. dispar cyst in a concentrated wet mount stained with iodine. This
early cyst has only one nucleus and a glycogen mass is visible (brown stain).
 

Amoebae in a colon biopsy from a case of amoebic dysentery.

 
 Immunohistochemical staining of trophozoites (brown) using specific anti–Entamoeba
histolytica macrophage migration inhibitory factor antibodies in a patient with amebic colitis.

Prevention[edit]
Specimen of the human intestine that was damaged by amebic ulcer.

To help prevent the spread of amoebiasis around the home :

 Wash hands thoroughly with soap and hot running water for at least 10 seconds after
using the toilet or changing a baby's diaper, and before handling food.
 Clean bathrooms and toilets often; pay particular attention to toilet seats and taps.
 Avoid sharing towels or face washers.
To help prevent infection:

 Avoid raw vegetables when in endemic areas, as they may have been fertilized
using human feces.
 Boil water or treat with iodine tablets.
 Avoid eating street foods especially in public places where others are sharing sauces
in one container
Good sanitary practice, as well as responsible sewage disposal or treatment, are necessary
for the prevention of E. histolytica infection on an endemic level. E.histolytica cysts are
usually resistant to chlorination, therefore sedimentation and filtration of water supplies are
necessary to reduce the incidence of infection. [21]
E. histolytica cysts may be recovered from contaminated food by methods similar to those
used for recovering Giardia lamblia cysts from feces. Filtration is probably the most practical
method for recovery from drinking water and liquid foods. E. histolytica cysts must be
distinguished from cysts of other parasitic (but nonpathogenic) protozoa and from cysts of
free-living protozoa as discussed above. Recovery procedures are not very accurate; cysts
are easily lost or damaged beyond recognition, which leads to many falsely negative results
in recovery tests.[22]

Treatment[edit]
Main article: Amoebicide
E. histolytica infections occur in both the intestine and (in people with symptoms) in tissue of
the intestine and/or liver.[18] Those with symptoms require treatment with two medications, an
amoebicidal tissue-active agent and a luminal cysticidal agent. Individuals that are
asymptomatic only need a luminal cysticidal agent. [5]

Prognosis[edit]

Significance of Amebiasis

In the majority of cases, amoebas remain in the gastrointestinal tract of the hosts. Severe
ulceration of the gastrointestinal mucosal surfaces occurs in less than 16% of cases. In
fewer cases, the parasite invades the soft tissues, most commonly the liver. [8] Only rarely
are masses formed (amoebomas) that lead to intestinal obstruction.(Mistaken for Ca
caecum and appendicular mass) Other local complications include bloody diarrhea,
pericolic and pericaecal abscess.
Complications of hepatic amoebiasis includes subdiaphragmatic abscess, perforation of
diaphragm to pericardium and pleural cavity, perforation to abdominal cavital (amoebic
peritonitis) and perforation of skin (amoebiasis cutis).
Pulmonary amoebiasis can occur from liver lesions by spread through the blood or by
perforation of pleural cavity and lung. It can cause lung abscess, pulmono pleural fistula,
empyema lung and broncho pleural fistula. It can also reach the brain through blood vessels
and cause amoebic brain abscess and amoebic meningoencephalitis. Cutaneous
amoebiasis can also occur in skin around sites of colostomy wound, perianal region, region
overlying visceral lesion and at the site of drainage of liver abscess.
Urogenital tract amoebiasis derived from intestinal lesion can cause amoebic
vulvovaginitis (May's disease), rectovesicle fistula and rectovaginal fistula.
Entamoeba histolytica infection is associated with malnutrition and stunting of growth. [23]

Epidemiology[edit]
Amoebiasis caused about 55,000 deaths worldwide in 2010, down from 68,000 in 1990. [24]
[25]
 In older textbooks it is often stated that 10% of the world's population is infected
with Entamoeba histolytica.[citation needed] It is now known that at least 90% of these infections are
due to E. dispar.[citation needed] Nevertheless, this means that there are up to 50 million true E.
histolytica infections and approximately seventy thousand die each year, mostly from liver
abscesses or other complications. Although usually considered a tropical parasite, the first
case reported (in 1875) was actually in St Petersburg in Russia, near the Arctic Circle.
[26]
 Infection is more common in warmer areas, but this is because of both poorer hygiene
and the parasitic cysts surviving longer in warm moist conditions. [18]

History[edit]
Amoebiasis was first described by Lösh in 1875, in northern Russia. [3] The most dramatic
incident in the US was the Chicago World's Fair outbreak in 1933, caused by contaminated
drinking water. There were more than a thousand cases, with 98 deaths. [27][28] It has been
known since 1897 that at least one non-disease-causing species of Entamoeba existed
(Entamoeba coli), but it was first formally recognized by the WHO in 1997 that E.
histolytica was two species, despite this having first been proposed in 1925. [3] In addition to
the now-recognized E. dispar, evidence shows there are at least two other species
of Entamoeba that look the same in humans: E. moshkovskii and Entamoeba bangladeshi.
[3]
 The reason these species haven't been differentiated until recently is because of the
reliance on appearance.[3]
Joel Connolly of the Chicago Bureau of Sanitary Engineering brought the outbreak to an
end when he found that defective plumbing permitted sewage to contaminate drinking
water. In 1998 there was an outbreak of amoebiasis in the Republic of Georgia.[29] Between
26 May and 3 September 1998, 177 cases were reported, including 71 cases of intestinal
amoebiasis and 106 probable cases of liver abscess.
The Nicobarese people have attested to the medicinal properties found in Glochidion
calocarpum, a plant common to India, saying that its bark and seed are most effective in
curing abdominal disorders associated with amoebiasis. [30]
Giardiasis, popularly known as beaver fever,[3] is a parasitic disease caused by Giardia
duodenalis (also known as G. lamblia and G. intestinalis).[4] About 10% of those infected
have no symptoms.[1] When symptoms occur they may include diarrhea, abdominal pain,
and weight loss.[1] Vomiting, blood in the stool, and fever are less common.[1] Symptoms
usually begin 1 to 3 weeks after exposure and without treatment may last up to six weeks. [2]
Giardia usually spreads when Giardia duodenalis cysts within feces contaminate food or
water which is then eaten or drunk.[1] It may also spread between people and from other
animals.[1] Risk factors include travel in the developing world, changing diapers, eating food
without cooking it, and owning a dog.[1] Cysts may survive for nearly three months in cold
water.[1] Diagnosis is via stool tests.[1]
Prevention is typically by improved hygiene.[1] Those without symptoms do not usually need
treatment.[1] When symptoms are present treatment is typically with
either tinidazole or metronidazole.[1] People who are not already lactose intolerant may
become so temporarily after an infection and therefore it is often recommended milk be
avoided for a few weeks.[1] Resistance to treatment may occur.[1]
 Giardia is one of the most common parasitic human diseases globally.[4] In 2013, there were
about 280 million people worldwide with symptomatic giardiasis. [4] Rates are as high as 7%
in the developed world and 30% in the developing world.[1] The World Health Organization
classified it as a neglected disease.[1]

Contents

 1Signs and symptoms

 2Cause
o 2.1Risk factors
o 2.2Transmission
 3Pathophysiology
 4Diagnosis
 5Prevention
 6Treatment
 7Prognosis
 8Epidemiology
 9Research
 10Other animals
 11References
 12External links

Signs and symptoms[edit]

Symptoms vary from none to severe diarrhea with poor absorption of nutrients. [5] The cause
for this wide-range in severity of symptoms has not been fully elucidated but the intestinal
flora of the infected host may play a role. [6][7] Diarrhea is less likely to occur in people from
developing countries.[6]
Symptoms typically develop 9–15 days after exposure,[8] but may occur as early as one day.
[5]
 The most common and prominent symptom is chronic diarrhea which can occur for weeks
or months if untreated.[9][10] Diarrhea is often greasy and foul-smelling, with a tendency to
float.[9][11] This characteristic diarrhea is often accompanied by a number of other symptoms,
including gas, abdominal cramps, and nausea or vomiting. [9][11] Some people also experience
symptoms outside of the gastrointestinal tract such as itchy skin, hives, and swelling of the
eyes and joints, although these are less common. [11] Despite its nickname "beaver fever",
fever occurs in only about 15% of people. [12]
Prolonged disease is often characterized by diarrhea along with malabsorption of
nutrients in the intestine.[9] This malabsorption results in fatty stools, substantial weight loss,
and fatigue.[9] Additionally, those suffering from giardiasis often have difficulty
absorbing lactose, vitamin A, folate, and vitamin B12.[10][11] In children, prolonged giardiasis can
cause failure to thrive and may impair mental development.[9][10]
Symptomatic infections are well recognized as causing lactose intolerance,[13] which, while
usually temporary, may become permanent.[14][15]
Cause[edit]
Giardiasis is caused by the protozoan Giardia duodenalis.[16] The infection occurs in many
animals including beavers (hence its nickname), as well as cows, other rodents, and sheep.
[16]
 Animals are believed to play a role in keeping infections present in an environment. [16]
G. duodenalis has been sub-classified into eight genetic assemblages (designated A–H).
[17]
 Genotyping of G. duodenalis isolated from various hosts has shown that assemblages A
and B infect the largest range of host species, and appear to be the main and possibly
only G. duodenalis assemblages that infect humans.[17][18]
Risk factors[edit]
According to the CDC, "Those at greatest risk are travelers to countries where giardiasis is
common, people in child care settings, those who are in close contact with someone who
has the disease, people who swallow contaminated drinking water, backpackers or campers
who drink untreated water from lakes or rivers, people who have contact with animals who
have the disease, and men who have sex with men." [19]
In the United States, giardiasis occurs more often during the summer. [16] This is believed to
be due to a greater amount of time spent on outdoor activities and traveling in the
wilderness.[16]
Transmission[edit]
Giardiasis is transmitted via the fecal-oral route with the ingestion of cysts.[8] Primary routes
are personal contact and contaminated water and food. [8] The cysts can stay infectious for
up to three months in cold water.[16]
Many people with Giardia infections have no or few symptoms.[20] They may, however, still
spread the disease.[20]

Pathophysiology[edit]
Life cycle of Giardia

The life cycle of Giardia consists of a cyst form and a trophozoite form. [7] The cyst form is
infectious and once it has found a host, transforms into the trophoziote form. [7] This
trophozoite attaches to the intestinal wall and replicates within the gut. [7] As trophozoites
continue along the gastrointestinal tract, they convert back to their cyst form which are then
excreted with feces.[1] Ingestion of only a few of these cysts is needed to generate infection
in another host.[21]
Infection with Giardia results in decreased expression of brush border enzymes,
morphological changes to the microvillus, increased intestinal permeability,
and programmed cell death of small intestinal epithelial cells.[22] Both trophozoites and cysts
are contained within the gastrointestinal tract and do not invade beyond it. [23]
The attachment of trophozoites causes villus flattening and inhibition of enzymes that break
down disaccharide sugars in the intestines.[6][22] Ultimately, the community of
microorganisms that lives in the intestine may overgrow and may be the cause of further
symptoms, though this idea has not been fully investigated. The alteration of the villi leads
to an inability of nutrient and water absorption from the intestine, resulting in diarrhea, one
of the predominant symptoms.[22] In the case of asymptomatic giardiasis, there can be
malabsorption with or without histological changes to the small intestine. The degree to
which malabsorption occurs in symptomatic and asymptomatic cases is highly varied.
The species Giardia intestinalis uses enzymes that break down proteins to attack the villi of
the brush border and appears to increase crypt cell proliferation and crypt length of crypt
cells existing on the sides of the villi. On an immunological level, activated host T
lymphocytes attack endothelial cells that have been injured in order to remove the cell.
  This occurs after the disruption of proteins that connect brush border endothelial cells to
[6]

one another.[22] The result is increased intestinal permeability. [22]

There appears to be a further increase in programmed enterocyte cell death by Giardia
intestinalis, which further damages the intestinal barrier and increases permeability. [22] There
is significant upregulation of the programmed cell death cascade by the parasite, and,
furthermore, substantial downregulation of the anti-apoptotic protein Bcl-2 and upregulation
of the proapoptotic protein Bax.[6] These connections suggest a role of caspase-dependent
apoptosis in the pathogenesis of giardiasis.[6]
Giardia protects its own growth by reducing the formation of the gas nitric oxide by
consuming all local arginine, which is the amino acid necessary to make nitric oxide.
[6]
 Arginine starvation is known to be a cause of programmed cell death, and local removal is
a strong apoptotic agent.[24]

Diagnosis[edit]
 According to the CDC, detection of antigens on the surface of organisms in stool
specimens is the current test of choice for diagnosis of giardiasis and provides
increased sensitivity over more common microscopy techniques. [25]
 A trichrome stain of preserved stool is another method used to detect Giardia.[26]
 Microscopic examination of the stool can be performed for diagnosis. [1] This method
is not preferred, however, due to inconsistent shedding of trophozoites and cysts in
infected hosts.[1] Multiple samples over a period time, typically one week, must be
examined.[1]
 The Entero-Test uses a gelatin capsule with an attached thread. One end is attached
to the inner aspect of the host's cheek, and the capsule is swallowed. Later, the thread
is withdrawn and shaken in saline to release trophozoites which can be detected with a
microscope. The sensitivity of this test is low, however, and is not routinely used for
diagnosis.[27]
 Immunologic enzyme-linked immunosorbent assay (ELISA) testing may be used for
diagnosis.[28] These tests are capable of a 90% detection rate or more. [28]
Although hydrogen breath tests indicate poorer rates of carbohydrate absorption in those
asymptomatically infected, such tests are not diagnostic of infection. [29] Serological tests are
not helpful in diagnosis.[1]

Prevention[edit]
The CDC recommends hand-washing and avoiding potentially contaminated food and
untreated water.[30]
Boiling water contaminated with Giardia effectively kills infectious cysts.[31] Chemical
disinfectants or filters may be used.[32][33] Iodine-based disinfectants are preferred over
chlorination as the latter is ineffective at destroying cysts. [34][35]
Although the evidence linking the drinking of water in the North American wilderness and
giardiasis has been questioned, a number of studies raise concern. [36] Most if not all CDC
verified backcountry giardiasis outbreaks have been attributed to water. Surveillance data
(for 2013 and 2014) reports six outbreaks (96 cases) of waterborne giardiasis contracted
from rivers, streams or springs[37] and less than 1% of reported giardiasis cases are
associated with outbreaks.[38]
Person-to-person transmission accounts for the majority of Giardia infections and is usually
associated with poor hygiene and sanitation. Giardia is found on the surface of the ground,
in the soil, in undercooked foods, and in water, and on hands without proper cleaning after
handling infected feces.[39] Water-borne transmission is associated with the ingestion of
contaminated water. In the U.S., outbreaks typically occur in small water systems using
inadequately treated surface water. Venereal transmission happens through fecal-oral
contamination. Additionally, diaper changing and inadequate hand washing are risk factors
for transmission from infected children. Lastly, food-borne epidemics of Giardia have
developed through the contamination of food by infected food-handlers. [40]

Treatment[edit]
Treatment is not always necessary as the infection usually resolves on its own. [6] However, if
the illness is acute or symptoms persist and medications are needed to treat it,
a nitroimidazole medication is used such
as metronidazole, tinidazole, secnidazole or ornidazole.[8]
The World Health Organization and Infectious Disease Society of America recommend
metronidazole as first line therapy.[41][42] The US CDC lists metronidazole, tinidazole,
and nitazoxanide as effective first-line therapies;[43] of these three, only nitazoxanide and
tinidazole are approved for the treatment of giardiasis by the US FDA.[44][45][46] A meta-analysis
done by the Cochrane Collaboration found that compared to the standard of metronidazole,
albendazole had equivalent efficacy while having fewer side effects, such as gastrointestinal
or neurologic issues.[47] Other meta-analyses have reached similar conclusions. [48] Both
medications need a five to 10 day long course; albendazole is taken once a day, while
metronidazole needs to be taken three times a day. The evidence for comparing
metronidazole to other alternatives such as mebendazole, tinidazole or nitazoxanide was
felt to be of very low quality.[47] While tinidazole has side effects and efficacy similar to those
of metronidazole, it is administered with a single dose. [20]
Resistance has been seen clinically to both nitroimidazoles and albendazole, but not
nitazoxanide, though nitazoxanide resistance has been induced in research laboratories. [21]
[49]
 The exact mechanism of resistance to all of these medications is not well understood.
[49]
 In the case of nitroimidazole-resistant strains of Giardia, other drugs are available which
have showed efficacy in treatment including quinacrine, nitazoxanide, bacitracin
zinc, furazolidone and paromomycin.[20] Mepacrine may also be used for refractory cases. [21]
Probiotics, when given in combination with the standard treatment, has been shown to
assist with clearance of Giardia.[50]
During pregnancy, paromomycin is the preferred treatment drug because of its poor
intestinal absorption, resulting in less exposure to the fetus. [51] Alternatively, metronidazole
can be used after the first trimester as there has been wide experience in its use
for trichomonas in pregnancy.[52][53]

Prognosis[edit]
In people with a properly functioning immune system, infection may resolve without
medication.[6] A small portion, however, develop a chronic infection. [6] People with an
impaired immune system are at higher risk of chronic infection. [6] Medication is an effective
cure for nearly all people although there is growing drug-resistance. [1][54][21]
Children with chronic giardiasis are at risk for failure to thrive as well as more long-lasting
sequelae such as growth stunting.[55] Up to half of infected people develop a
temporary lactose intolerance leading symptoms that may mimic a chronic infection. [1] Some
people experience post-infectious irritable bowel syndrome after the infection has cleared.
[6]
 Giardiasis has also been implicated in the development of food allergies.[6] This is thought
to be due to its effect on intestinal permeability. [6]

Epidemiology[edit]

Rates of giardiasis in 2005 in the United States

In some developing countries Giardia is present in 30% of the population.[16] In the United

States it is estimated that it is present in 3–7% of the population. [16]
The number of reported cases in the United States in 2018 was 15,584. [56] All states that
classify giardiasis as a notifiable disease had cases of giardiasis. [56] The states of Illinois,
Kentucky, Mississippi, North Carolina, Oklahoma, Tennessee, Texas, and Vermont did not
notify the Center for Disease Control regarding cases in 2018. [56] The states with the highest
number of cases in 2018 were California, New York, Florida, and Wisconsin. [56] There are
seasonal trends associated with giardiasis. [57] July, August, and September are the months
with the highest incidence of giardiasis in the United States. [58]
In the ECDC's (European Centre for Disease Prevention Control) annual epidemiological
report containing 2014 data, 17,278 confirmed giardiasis cases were reported by 23 of the
31 countries that are members of the EU/EEA. [59] Germany reported the highest number at
4,011 cases.[59] Following Germany, the UK reported 3,628 confirmed giardiasis cases.
Together, this accounts for 44% of total reported cases. [59]