Thursday, November 30, 2017

Parasitology for B.Sc. Microbiology Level


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

 Fig:-E . histolytica and G. lamblia

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 cystGiardia 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
Metallic taste; nausea; vomiting; dizziness; headache; disulfiram-like effect; neutropenia
Single dose
Metallic taste; nausea; vomiting; belching; dizziness; headache; disulfiram-like effect
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.


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