Parasitology
Parasitology
is the branch of Science which mainly deals about all the Parasites and its
infectious diseases. Whole Parasitology covers mainly Parasites, Host and its
association between them.
Parasite
• A
living organism which receives nourishment and shelter from another organism
where it lives is called parasites.
• A
parasite does not necessarily cause disease.
• Simply
parasitism is living in association with the host.
• The
parasite derives all benefits from the association and the host may either not
be harmed or may suffer the consequences of this association, a parasite
disease.
• A
parasite is an organism that is entirely dependent on another organism,
referred to as its host, for all or part of its life cycle and metabolic
requirements.
Host:
An organism which harbors the parasite.
Terms
for association of Parasites:
Symbiosis
An
association in which both are so dependent upon each other that one can’t live
without the help of the other. None of the partners suffers any harm from
the association. The living together of two or more organism. One classic
example is the relationship between certain species of flagellated protozoa
living in the gut of termites. The protozoa, which depend entirely on a
carbohydrate diet, acquire their nutrients from termites. In return they are
capable of synthesizing and secreting cellulases; the cellulose digesting
enzymes, which are utilized by termites in their digestion.
Commensalisms
An
association in which the parasite only is deriving benefit without causing
injury to its host. A relationship between members of different species living
in proximity (the same cultural environment) in which one organism benefits
from the association but the other is not affected. An association in which the
commensal takes the benefit without causing injury to the host. E.g. Most of
the normal floras of the humans’ body can be considered as commensals.
Parasitism
An
association in which the parasite derives benefit and the host gets nothing in
return but always suffers some injury, however slight the injury may be. The
host, at the same time, offers some resistance to the injury done by the
parasite and there may be some adaptation (tolerance) between the parasite
and the host. A parasite has lost its power of independent life. An association
where one of the partners is harmed and the other lives at the expense of the
other. E.g. Worms like Ascaris
lumbricoides reside in the gastrointestinal tract of man, and feed on
important items of intestinal food causing various illnesses.
Classes
of parasites
Parasite
are mainly classified into following two catagories; along with some other
types of Parasites.
Ecto-parasite
(ectozoa): A parasitic organism that lives on the outer
surface of its host, e.g. lice, ticks, mites etc.
Endo-parasite (entozoa): A parasite
that live inside the body of their host, e.g. Entamoeba histolytica.
Temporary
parasite: The parasite visits its host for a short
period.
Permanent
parasite: A
parasitic life throughout the whole period of its life.
Obligatory
parasite: This parasite is completely dependent on the
host during a segment or all of its
life cycle, e.g. Plasmodium
spp.
Facultative
parasite: An organism that exhibits both parasitic and
non-parasitic modes of living and hence does not absolutely depend on the
parasitic way of life, but is capable of adapting to it if placed on a host.
E.g. Naegleria fowleri.
Occasional
or accidental parasite: When a parasite attacks an unnatural host and
survives. E.g. Hymenolepis diminuta (rat tapeworm).
Wandering
or aberrant parasite: One that wanders in to an organ in which it
is not usually found. E.g. Entamoeba
histolytica in the liver or lung of humans.
Opportunistic
parasites: The parasites which do not ordinarily produce
disease in healthy (immune-competent) individuals but do cause illness in
individuals with impaired defense mechanism (opportunistic parasites). It is
becoming of paramount importance because of the increasing prevalence of
HIV/AIDS in the world.
Classes
of host
Definitive
host:
Either
harbors the adult stage of the parasite or where the parasite utilizes the
sexual method of reproduction. The majority of human parasitic infections, man
is the definitive host; in malaria and hydatid disease, however, man acts as
the intermediate host.
Intermediate
host:
Harbours
the larval or asexual stages of the parasite. Some cases larval developments
are completed in two different intermediate hosts which are been referred to as
first and second intermediate hosts respectively. Some parasites require two
intermediate hosts in which to complete their life cycle. e.g., W.
brancrofti – intermediate host- mosquito (Culex, Aedes, Anopheles),
definitive host- man (lymphatic system).
Paratenic
host (a carrier or transport host):
A
host that serves as a temporary refuge and vehicle for reaching an obligatory
host, usually the definitive host, i.e. it is not necessary for the completion
of the parasites life cycle.
Reservoir host: A host
that makes the parasite available for the transmission to another host and is
usually not affected by the infection.
Natural
host: A host that is naturally infected with certain
species of parasite.
Accidental host: A
host that is under normal circumstances not infected with the parasite.
Example
of protozoa
v Amoeba: Entamoeba histolytica,
Entamoeba coli, Entamoeba gingivalis, Acanthamoeba species , Naegleria species
v Flagellates:
Giardia
lamblia, Trichomonas vaginalis,
Trypanosoma species,
Leishmania species
v Ciliates: Balantidium coli
v Coccidia:
Plasmodium
species,
Toxoplasma gondii, Isospora belli
Cryptosporidium parvum, Cyclospora cayetanensis
v Microsporidia: Encephalitozoon species, Enterocytozoon species
Helminthes
The
helminthic parasites are multicellular, bilaterally symmetrical animals having
three germ layer (triploblastic metazoa).
Entamoeba histolytica
Entamoeba
histolytica is one of six parasitic amebae of the genus
Entamoeba that are known to infect humans. Entamoeba coli, E.
gingivalis, E. moshkovskii, and E. hartmanni are no tassociated
with pathologic sequelae, but E. polecki and E. histolytica are
pathogenic. E. histolytica has recently been separated from E. dispar
on the basis of genetic differences. Both protozoa are morphologically
identical but have genetic, and functional differences; E. histolytica is
invasive and causes disease such as colitis and liver abscess, and E. dispar
causes a asympto-matic colonization which does not need to be medically
treated.
Epidemiology
In
1828, James Annesley wrote in Prevalent Diseases of India, `. hepatic disease
seems to be induced by the disorder of the bowels, more particularly when this
disorder is of a subacute or chronic
kind', recognizing for the first time a link between dysentery and liver
abscess. Approximately 30 years later, in 1855, Lambl described amebae in the
stool of a child who had diarrhea. Fedor Losch described amebae in the stool of a young
farmer with dysentery from his first evaluation in November 1873 until his
death in April 1874.
E.
histolytica infections occur worldwide but are more
prevalent in the tropics. It has been estimated that approximately 480 million
people, or 12% of the world's population are infected and that annual mortality
is 40,000 to 110,000 persons.
E.histolytica
is the most common intestinal protozoan
parasites in Nepal ranges less than 3% to high as 28.8%. Humans are the major
reservoir of infection with E. histolytica, although natural infections
in macaque monkeys and pigs have been reported.
Geographical distribution
Found
in all population throughout the world but more prevalent in the tropics than
in cooler climates. Found more in insanitary communities of temperate and subartic
areas. Occurs
worldwide, but is more common in areas or countries with poor sanitation,
particularly in the tropics.
Risk group
Worldwide,
with higher incidence of amoebiasis in developing countries due lack of
sanitary condition and poor water supplement system. High risk groups include
male homosexuals, travelers and recent immigrants.
Mode of transmission
Ingestion
of food and drink contaminated with E. histolytica cysts from human
feces and direct fecal-oral contact are the most common means of infection.
Morphology
Trophozoite
Outside
the cyst, the nuclei within the quadrinucleate ameba begin to separate from the
surrounding cytoplasm and undergo division to form eight uninucleate metacystic
trophozoites. The resulting trophozoites are always smaller (8μm) than the trophozoites seen
in the bowel of an infected human. The metacystic trophozoites continue to feed
and grow, finally achieving the size normally associated with the trophozoite.
Fig:
Trophozoite of E. histolytica
Precyst
In the precyst stage,
the trophozoite becomes approximately the same size as the cyst. The precystic
form is uninucleate, and the enlarged nucleus contains a karyosome that is more
or less escentric.
Cyst
A
cyst wall develops around the precystic form, and the single nucleus divides to
form the mature quadrinucleate stage. Again because of shrinkage caused by the
dehydration reagents, cysts may be 1 to 1.5 μm smaller than organisms seen
on wet preparations. They are usually spherical and contain four nuclei. The
nuclear membrane is uniformly lined with peripheral chromatin. The karyosome is
small and usually centrally located within the nucleus.
Fig: cyst of E.
histolytica
Metacyst
During the process of
excystation, the encysted ameba containing four nuclei becomes very active,
separating from the cyst wall. The quadrinucleate ameba escapes from the cyst
wall through a tiny pore, and the nuclei clump together.
Reproduction: various modes of reproduction seen in these
organism are
Encystatition:- This is
the process of tranformation of trophzoite into cysts which occurs in the lumen
of an infected individual.
Excystation:- This is the process of tranformation of
cysts into trophzoite and occurs only in the alimentary canal of the
susceptible host. During excystation a quadrinucleate cyst gives rise to eight
amoebulae each one of which is capable of developing into a trophozoite.
Multiplication:-
Multiplication occurs by simple binary fission first of the nucleus and then of
cytoplasm.
Fig:
Excystation of E. histolytica
Life-cycle of Entamoeba histolytica
The active (trophozoite) stage exists only in the host and in fresh
loose feces; cysts survive outside the host in water, in soils,
and on foods, especially under moist conditions on the latter. The cysts are
readily killed by heat and by freezing temperatures, and survive for only a few
months outside of the host. When quadrinucleate cysts are swallowed they cause excysting
by releasing the trophozoite stage due to lysing the cyst cell wall by the action
of trypsin in the digestive tract. A single trophozoite of E.
histolytica with four nuclei is
liberated. The trophozoite
divides by binary fission giving rise to eight daughter trophozoites. The
daughter trophozoites are actively motile and are unique among the intestinal amebae parasitizing humans
because it is able to invade tissue. The amoeba can actually 'bore' into the intestinal wall, causing lesions and intestinal symptoms, and it may reach
the blood stream. From there, it can reach different vital organs of the human
body, usually the liver, but sometimes the lungs, brain, spleen, etc. When
the infection disseminates to extraintestinal sites, it is found most
frequently in the right lobe of the liver. Some trophozoites transformed to
cyst by the process of encystation, some cysts along with trophozoites
excreated in the feaces which are susceptible to human host. These remain
viable for 2 months if taken up by another host, its life cycle continue in another host.
Fig: Life-cycle of Entamoeba histolytica
Pathogenesis
Two mechanisms of pathogenesis
has evolved :
• A.
Secretion of soluble toxins
• B.
Cellular contact
A number of E. histolytica adherence receptors have
been identified, but the galactose-specific lectin receptor has been the most
thoroughly studied and is thought to be responsible for mediating attachment to
colonic mucus and colonic epithelial cells. Human colonic epithelial cells and
mucus contain large numbers of galactose or N-acetylgalactosamine residues. E.
histolytica also enhances mucus secretion, which correlates with its
pathogenicity. More virulent strains stimulated mucus secretion and depleted
goblet cells of mucin, thereby making epithelial surfaces more vulnerable to
invasion. Penetration of the mucous blanket was thought to be due primarily to
mechanical ameboid movement. The pore-forming amebapore protein is transferred
from the trophozoite to the target cell, causing a disruption of the
transmembrane gradient and contributing to the cell's death by the
colloid-osmosis lysis mechanism. They are involved in amebic invasiveness at
intercellular junctions, thereby allowing amebae to invade host tissues.
Cysteine proteinase can degrade cellular attachment and matrix proteins such as
collagen, laminin, and fibronectin. There is a direct correlation between the
amount of proteinase activity and the pathogenicity of E. histolytica. Furthermore
the extracellular products of E. histolytica cleaves the ground
substances and also cleave the complement components making them paralyse to
neutralize this parasite.
Clinical manifestation
Asymptomatic infection
Upto 90% of E. histolytica infections,
the symptoms are absent or very mild. These patients have normal
rectosigmoidoscopic findings, without a history of blood in stool samples. Cysts and trophozoites lacking ingested RBCs
may be visible on microscopy. Interestingly, most individuals infected with E.
histolytica, but not E. dispar, develop serum antibody responses to
the parasite even in the absence of invasive disease.
Symptomatic infections
Symptoms
commonly attributed to E. histolytica colitis or dysentery are abdominal
pain or tenderness and diarrhea (watery, bloody, or mucous). Diarrhea can occur
with up to 10 (or even more) bowel movements per day, and fever occurs in
one-third of the patients. Patients are often reluctant to eat, and one-fifth
develop weight loss. Although people can be asymptomatically colonized with E.
histolytica, they should be treated. Colonic findings in amebiasis have
varied from thickening of the mucosa to flask-shaped ulceration (mostly in the
cecum or appendix or near the ascending colon, but rarely in the sigmoidorectal
area). The development of fulminant colitis, ameboma, cutaneous amebiasis, and
rectovaginal fistulas can occur as complications of intestinal amebiasis.
Extraintestinal Amebiasis
Liver
abscess is the most common manifestation of extraintestinal amebiasis. Amebic
liver abscess (ALA) is associated with fever and abdominal pain in most
patients. Right upper abdominal pain or tenderness occurs in the acute phase,
while weight loss, fever, and more diffuse abdominal pain occur in the subacute
phase. ALA occurs more commonly in adults than in children. E. histolytica has been identified
microscopically in the stool samples of only a minority of patients.
Biochemically,
many patients also have elevated peripheral white blood cell counts and
alkaline phosphate levels. Unusual sites or complications of extraintestinal
amebiasis include direct extension from the liver to the pleura and/or
pericardium, brain abscess, and genitourinary amebiasis. A common outcome of this invasion of
tissues is a liver abscess, which can be fatal if untreated.
Laboratory Diagnosis
Diagnosis
depends primarily on demonstration of haematophagus trophozoite of E.
histolytica in stool samples, aspirates from intestinal and other organs,
biopsy materials(pinch biopsy at protoscopy or sigmoidoscopy and surgical
biopsy from elsewhere) and in mucus from rectal ulcers. Serology is the method of choice for diagnosis of amoebic liver
disease.
Microscopy
Diagnosis
of E. histolytica has historically relied on microscopic examination of
protozoan morphology.
Two
techniques are currently employed that is wet mount for the demonstration of trophozoites in freshly collected stool
specimen and iodine preparation for the demonstration of cystic form. Current
microscopy- and histology-based identification frameworks, however, are unable
to differentiate among protozoa with similar morphological features.
Culture
Boeck
and Drbohlav first cultivated E.
histolytica in a diphasic egg slant medium. Today, the National Institutes
of Health modification of Locke-egg medium has been used in some research
laboratories. However, Robinson medium
and TYSGM-9 of Diamond are more
often used for axenic cultivation of E. histolytica. After being used
successful axenic cultivation by Diamond, TYI-S-33 is one of the most widely used axenic media.
Molecular
technique
Molecular
biology-based diagnosis (PCR) seems to be a modern research tool that may
become the technique of choice in the future studies, because establishment of
these protozoa in culture is not a routine process and is less sensitive than
microscopy in detection.
Antibody and Antigen Detection
Serological
tests are more helpful for the identification of E. histolytica infection
that have been used so far involve IHA,
counter immune electrophoresis (CIE) , amoebic gel diffusion test , complement
fixation (CF) , indirect fluorescence assay(IFA), latex agglutination, and
ELISA.
Antigen-based
ELISA have several significant advantages over other methods currently used for
diagnosis of amebiasis. It also help to differentiate the different species of
amebiasis.
Treatment
·
Metronidazole is the mainstay
of therapy for invasive amebiasis.
·
Tinidazole has been approved by
the US Food and Drug Administration (FDA) for intestinal or extraintestinal
amebiasis. Other nitroimidazoles with longer half-lives (ie, secnidazole and
ornidazole) are can be used.
·
Asymptomatic E. dispar infections
should not be treated, but because this organism is a marker of fecal-oral
contamination, educational efforts should be initiated.
Prevention and Control
·
Public education on public and
personal hygiene, sanitary disposal of human feces, and food handling.
·
Provision of potable water devoid
of fecal contamination.
·
Chemoprophylaxis focused mainly
on the treatment of chronic cyst passers.
·
Education of high-risk groups
on sexual and other habitual practices that promote fecal-oral transmission.
·
Thorough washing of fruits and
vegetables using effective disinfectants before consumption.
Giardia
lamblia
Giardia lamblia (syn. Giardia intestinalis,
Giardia duodenalis) is a flagellated unicellular
eukaryotic microorganism that commonly causes diarrheal disease throughout the
world. The genus Giardia has
been isolated from more than 40 species. The species G. lamblia is
known to infect human, mammals, reptiles, and birds, cows, sheeps and pigs,
depending on the strain. It is the most common cause of waterborne
outbreaks of diarrhea in the developed countries and is occasionally seen as a
cause of food-borne diarrhea.
Geographical
distribution
In
developing countries, there is a very high prevalence and incidence of
infection, and data suggest that long-term growth retardation can result from
chronic giardiasis. In certain areas of the world, water contaminated with G.
lamblia cysts commonly causes travel related giardiasis in tourists.
Specific
areas of recognized increased risk for travelers include the Soviet Union,
Southeast and South Asia, tropical Africa, Mexico, and western South America.
Giardiasis is the most commonly reported pathogenic protozoan disease in the
United States.
Epideomology
Giardiasis
occurs worldwide, with higher prevalence where sanitation is poor. Persons of
all ages are affected, though in endemic areas infection is more frequent in
infants. The World Health Organization
reported that 200 million people in Asia, Africa and Latin America havesymptoms
of giardiasis with some 500,000 new cases a year, especially among children.
The infection may produce severe acute diarrhea in children less than five
years of age with chronic infections resulting in weight loss and growth
retardation.
Infections
occur in outbreak and endemic forms within nursery schools and other
institutional settings and among family members of infected children.
Transmission also occurs among male homosexuals engaging in oral-anal sexual
practices. Humans are the main reservoir of the parasite, but a variety of
animals carry Giardia spp. similar to those infecting humans.
Morphology
form of G. Lamblia
G. lamblia has two morphological
stages: the trophozoite and the cyst. Giardia lamblia exists in two forms, an active form called a
trophozoite, and an inactive form called a cyst. The active trophozoite attaches to the lining of the
small intestine with a "sucker" and is responsible for causing the
signs and symptoms of giardiasis.
Trophozoite
The
trophozoite is pear shaped, with a broad anterior and much attenuated
posterior. It is 10-12µm long and 5-7µm wide, bilaterally symmetrical, and has
two nuclei. It is also relatively flattened, with a large sucking disk on the
anterior ventral side, which serves as the parasite’s method of attachment to
the mucosa of the host. The trophozoite also has two median bodies and
four pairs of flagella (anterior, caudal, posterior and ventral). Upon
excystation, each cyst produces two trophozoites.
Fig: Trophozoite of G. lamblia
Cyst
The G. lamblia cyst is 7 to 10
um in diameter, and contains four nuclei. The cyst is covered by a
0.3~0.5um-thick cyst wall. The cyst wall is composed of two layers: outer
filamentous layer and an inner membranous layer. Cysts of Giardia are present in the feces of infected
persons. After
encystation, each organelle duplicates, so each cyst contains four nuclei, four
median bodies, eight pairs of flagella--although these organelles are not
arraigned in any clear pattern.
Fig: Cyst of G. lamblia
Risk group
There is a significant risk for
travellers in contact with recreational waters used by wildlife, with
unfiltered water in swimming pools or with contaminated municipal water
supplies.
Transmission
Infection
is spread directly from person to person by fecal-oral contamination with cysts
or indirectly by transmission in water and occasionally food. Cysts of Giardia
are present in the feces of infected persons. Thus, the infection is spread
from person to person by contamination of food with feces, or by direct
fecal-oral contamination.
Cysts
also survive in water, for example in fresh water lakes and streams. As a
result, giardiasis is the most common cause of water-borne, parasitic illness. Domestic
mammals (for example, dogs, cats, calves) and wild mammals (for example,
beavers) can become infected with Giardia; however, it is not clear how often
domestic or wild mammals transmit giardiasis to humans. The infection was found
more frequently in people living in close quarters and in children that shares
contaminated fomites (toys etc.).
Giardiasis
also has occurred as outbreaks from recreational water sources such as swimming
pools, water parks, and hot tubs, most likely because of an infected user rather
than a source of water that was contaminated.
Life
cycle of Giardia lamblia
Ingestion
of 100 or more cysts is required to ensure infection in humans, but ingestion
of as few as 10 cysts has resulted in infection. Cysts are resistant forms and
are responsible for transmission of giardiasis. Both cysts and trophozoites can
be found in the feces (diagnostic stages). The cysts are hardy and can survive
several months in cold water. In the small intestine, excystation releases
trophozoites (each cyst produces two trophozoites). Trophozoites multiply by
longitudinal binary fission, remaining in the lumen of the proximal small bowel
where they can be free or attached to the mucosa by a ventral sucking disk. Encystation
occurs as the parasites transit toward the colon. The cyst is the stage found
most commonly in nondiarrheal feces while trophozoite is found commonly in
diarrheal feces. Because the cysts are infectious when passed in the stool or
shortly afterward, person-to-person transmission or through contamination in
food and water may possible for continue their life cycle.
Fig:
life cycle of Giardia lamblia
Pathogenesis
An adhesive
disk on the ventral surface of the trophozoite facilitates attachment to the
mucosal surface of the duodenum and jejunum, although the trophozoite does not
invade the mucosal epithelium. Trophozoites that do not adhere to the small
bowel move forward to the large intestine where they revert to the infectious
cyst form; conjugated bile salts appear to foster encystation. Cysts are passed
back into the environment in excreted feces; in the setting of diarrhea,
trophozoites can also be found in the stool.
Since Giardia
is not an invasive organism, the pathogenesis of diarrhea and malabsorption
that can occur in giardiasis is not fully understood; diarrhea may be a result
of both intestinal malabsorption and hypersecretion. The small intestine is the
site of the major structural and functional abnormalities associated with
giardiasis. Light microscopy may demonstrate no abnormalities, mild or moderate
partial villous atrophy, or subtotal villous atrophy in severe cases. An
increase in crypt depth may be seen, and microvilli shortening or disruption
may occur. Deficiencies in epithelial brush border enzymes, such as lactase,
may develop.
Clinical
manifestations
• Symptomatology
differs from person to person, depending on such factors as inoculum size,
duration of infection, and individual host and perhaps parasite factors. The
incubation period generally varies from 9 to 15 days. The acute stage usually
begins with a feeling of intestinal uneasiness, followed by nausea and
anorexia. Low-grade fever and chills may also be early symptoms. Subsequent
symptoms may include explosive, watery, foul-smelling diarrhea; marked abdominal
gurgling and distention associated with the passage of foul gas; and perhaps
belching, with a foul taste.
• During
this chronic phase, lassitude, headache, and myalgia may occur with continued
weight loss, anorexia, and malabsorption. Chronic infection in children may
present as failure to thrive. Urticaria, cholecystitis, and pancreatitis have
been reported with Giardia infections. Uncommon associated symptoms including
arthritis and retinal arteritis and iridocyclitis have responded to specific
anti-Giardia treatment. As stated by an experienced worker in the field,
"the symptomatology of giardiasis is rich and unpredictable; individual
variability and the intermittent nature and changing of the symptoms are
characteristic”.
• In
patients with giardiasis, the hemogram is usually normal and eosinophilia is
rare.
• Malabsorption
of fat, glucose, lactose, xylose, vitamin A, and vitamin B12 has been shown in
some patients.
• Lactose
intolerance, frequently present during infection, may persist for variable
periods following apparent eradication of giardiasis with specific treatment.
Treatment
|
Drug
|
Treatment
duration
|
Possible
side effects
|
|
5–7 days
|
||
|
Single dose
|
||
|
3 days
|
Abdominal pain; diarrhea;
vomiting; headache; yellow-green discolouration of urine
|
|
|
5 days
|
Dizziness; headache;
fever; nausea; vomiting; temporary hair loss.
|
Laboratory diagnosis
Stool examination
Most,
but not all, cases of giardiasis can be confirmed by stool examination. A
series of three stools, one collected each day on alternate days or within no
more than 10 days, is recommended.
A.
Macroscopy
examination
Faecal specimen containing Giardia lamblia may have an offensive odour and
are pale colored, fatty and float in water.
B.
Microscopy examination
Microscopic
examination of freshly passed stools is used for the demonstration of Giardia
trophozoite and cysts. Wet
Mount In bright-field microscopy, cysts appear ovoid to ellipsoid in shape and
usually measure 11 to 14 µm (range: 8 to 19 µm). Immature and mature cysts have
2 and 4 nuclei, respectively. Intracytoplasmic fibrils are visible in cysts.
Trophozoites appear as pear-shaped organisms (falling leaf motility), measuring
12 to 15 µm (range: 10 to 20 µm). Trophozoites contain two anteriorly placed nuclei
and 8 flagella (rarely seen). The use of collection kits containing stool preservatives is recommended
for inpatients and is mandatory for outpatient stool collections. If left
unpreserved for too long, the organisms tend to disintegrate, thus preventing
recognition of the typical trophozoite morphology. Use
of concentration method increases sensitivity.
Fig:
Cyst and trophozoite of Giardia
lamblia
Molecular diagnosis
·
DNA
Probe and PCR
can be used to identify the subtypes of Giardia lamblia.
Prevention and control
- Individuals
likely to be exposed to contaminated water (eg, travelers to
developing countries and backpackers and campers) should avoid drinking
from surface water, such as rivers and streams.
- Boiling
water is sufficient to kill all protozoal cysts. Halogenation of drinking
and washing water is generally effective
- Chlorine-based
preparations (halazone, 5 tablets/L for 30 minutes; chlorine bleach,
5.25%, 1 tsp/5 gal or iodine-based preparations (Potable Aqua, 1 tablet/L
for 30 minutes; saturated crystalline iodine, 12.5 mL/L for 30 minutes)
are effective against giardiasis
- Small-volume
direct personal water filters may be used, but the pore size may be
insufficient to filter out bacterial pathogens
- Uncooked
foods that may have been prepared using contaminated water should be
avoided when traveling.
• Eating
hot, cooked foods helps to prevent ingestion of viable cysts from foods
contaminated by infected water or fingers.
