Parasitology

Dr: Fadia Al-Khayat Lec: twelve -Protozoan

Mostly uninucleate organisms, that possess, at some time in the life cycle, one to many flagella for locomotion and sensation. (A is a hairlike structure capable of whiplike lashing movements that furnish locomotion.) Mastigophora - the flagellates. Inhabit the mouth, bloodstream, gastrointestinal, or urogenital tracts. Morphological Characteristics  Flagellum(ae) - organelles of locomotion; an extension of ectoplasm; moves with a whip-like motion.  Axostyle - a supporting mechanism, a rod-shaped structure; not all flagellates have these.  Undulating membrane - a protoplasmic membrane with a flagellar rim extending out like a fin along the outer edge of the body of some flagellates.  Costa - a thin, firm rod-like structure running along the base of the undulating membrane.  Cytosome - a rudimentary mouth; also referred to as a gullet. Identification of a is based upon:  Size.  Shape.  Motility.  Number and morphology of nuclei.  Number and location of flagella  Location in the body of the host. Flagellates are classified according to their occurrence in their vertebrate host body 1- intestinal and atrial flagellates which live in the alimentary canal and the urinogenital tract. 2-Blood and flagellates which live in the blood,lymph and tissue of the host.

Intestinal and atrial flagellates Giardia intestinalis (G.duodenalis, G.lamblia)

Is a flagellate protozoan, that colonizes and reproduces in the small intestine, causing . common to human and several other mammalian species such as dogs, cats, bovines .The life cycle includes trophozoite and cyst phases.

Morphology

 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).  The G. intestinalis cyst is egg-shaped, and measures 8-14µm by 7-10µm. 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. Upon excystation, each cyst produces two trophozoites.

Giardia intestinalis cyst

Life cycle

Trophozoites multiply by binary fission.Then the trophozoites encysted when the intestine contents leave the jejunum and begin to lose moisture.The encysted trophozoites undergoes another division and thus the mature cyst contain 4 nuclei.The cyst(infective stage) is passed to the environment with the feces, it is very resistant to environmental factors and can be survive more than 2 months in water at 8 C0 and about 1 month at 21 C0 and it is resistant to chlorinated ,dishnfectants.

The cyst is repeated when a new host ingests the cysts , the parasite frees it self from the cyst in the duodenum and emerges as a tetranucleate trophozoite that quickly divides into two binucleate trophozoite.

Pathogenecity

Infection with Giardia intestinalis can range from asymptomatic to severe diarrhea. Trophozoites attach themselves tightly to the free surface of the small intestinal epithelia through the adhesive discs.They cause marked increase of mucous production, diarrhea, dehydration, intestinal pain, flatulence and weight loss.Due to their attachment, the parasite prevent mechanically, the absorption of fats and fat- dissolved vitamins. Giardiasis demonstrated by the occurrence of greasy, mucous, watery but not bloody diarrhea. The parasite may enter the bile duct, and the gall bladder which can cause jaundice and colic.

Clinical signs

In symptomatic individual, the incubation period lasts 1-3 weeks. Symptoms consist of diarrhea frequently accompanied by abdominal pain, less often there is nausea and vomiting. The acute stage lasts about 3-4 days and in some patients may be prolonged illness with episodes of recurring diarrhea.

Trichomonas

Members of this genus are known as trophozoites only.Trophozoite is ovoid or pear- shaped,with 3-5 anterior flagella and another flagellum curving back along the margin of undulating membrane, which is supported at its base by a flexible structure known as costa. One nucleus is present in the anterior part of the body. One axostyle arise from the anterior end and extends from the posterior end as a hard spine.Three species of lives in human body.

Trichomonas tenax:

- oral trichomonas, is a species of trichomonas found in the oral cavity of humans, dogs and cats. Routine hygiene is generally not sufficient to eliminate the parasite. The parasite is frequently encountered in periodontal infections, affecting more than 50% of the population in some areas, but it is usually considered insignificant. However, it is not found on healthy gums. Its presence in necrotizing ulcerative gingivitis (GUNA) and necrotizing ulcerative periodontitis (PUNA) make it a possible pathogen worsening periodontal disease. This parasite is also present in some chronic lung diseases.

- It is the smallest of the three Trichomonas, 6-8 µm long and 5-6 µm wide, and has a long axostyle and tail, 4 anterior flagella and a recurrent flagellum raising an undulating membrane to two third of the body.

- It feeds on and cellular debris. - Transmission is direct, usually by kissing or common use of eating and drinking utensils.

Trichomonas hominas

-T. hominis has no cystic stage. The trophozoite measures from 5-15μm in length by 7-10μm in width. The shape is pyriform and has an axostyle which runs from the nucleus down the centre of the body and extends from the end of the body and undulating membrane which extends the entire length of the body and projects from the body like a free flagellum. It has 4 free flagella and a single nucleus at the anterior end.

- It lives in the large intestine and caecum. -Transmission occurs by ingestion of the trophozoite with contaminated water and food.

Tricomonas vaginalis

-It is cause tricomonad vaginitis in women. -Both men and women are infected, the infection has spread from the vagina to other parts of the urogenital system and men remain asymptomatic. Morphology: T.vaginalis (pear-shaped) ranges in size from 4-32mm in length and 2- 7 µm in width. It has four anterior flagella and a recurrent flagellum attached to the body by undulating membrane, the recurrent flagellum does not extend beyond the posterior of the body. Life cycle: the organism reproduces by binary fission, it is transmitted fro one person to the next through sexual intercourse or may take place through the use of contaminated underwear, toilet seats and vaginal speculum. Clinical signs: cause an inflammation of the epithelium leads to tenderness, pain, itching and excessive production of mucus, also can infect parts of the urogenital system and has been found in the bladder, ureters and kidneys. Men usually remain asymptomatic ,but infrequently there is inflammation of the urethra and the prostate gland.

Blood and tissue flagellates

Members of this group live in the blood, lymph and tissues of vertebrate hosts and complete their life cycles in the gut of blood-sucking insects and other invertebrates.They are also known as haemoflagellates. They occur in four morphological forms.

Two genera within hemoflagellates infect human which are: Leishmania Trypanosoma

Morphological forms of hemoflagellates 1-Amastigote (Leishmania) form Round or oval in shape, 2-5 microns in diameter, have single nucleus with large central karyosome, the lies at right angle to the nucleus. This form (amastigote) has no flagellum. 2-Promastigote (leptomonad) form Elongated (spindle in shape) measuring 15-20 microns X 1-2 microns, have centrally located nucleus and the kinetoplast situated at the anterior end. Single free flagellum projects from the anterior end, equal or longer than the body length.This form has no undulating membrane. 3-Epimastigote form Elongated form, 15-20 microns long and slightly wider than promastigote, nucleus near middle, kinetoplast is anterior to the nucleus. Flagellum arise forming the undulating membrane extending half of the body length, and project from the anterior end as a free flagellum. 4-Trypomastigote (Trypanosome) form Elongated form with highly polymorphism from rather short and stumpy (15micron X 2-4micron) to a long slender from (35micron X 2-4micron). In stained blood film, appears as C or U shape. Nucleus near middle, kinetoplast is at the posterior end, the flagellum and undulating membrane pass anteriorly along entire body length and free flagellum extends from anterior end when present.

Genus Leishmania

General characters of genus Leishmania 1- Life cycle is indirect and completed in tow hosts, vertebrate (human, dog, rodent) as a final host and invertebrate; blood sucking insect (female of sand fly) as an intermediate host (vector). 2- Tow developmental forms are found, amastigote and promastigote ,amastigote in the final host (human) and promastigote in the vector (sand fly). 3- The vector is sand fly of genus Phlebotomus in Old World and genus Lutzomyia in New World. 4- Promastigote is the infective stage to final host (man) and amastigote is infective stage to sand fly (vector). 5- The parasite infects the reticuloendothelial cells of skin, mucus membrane or viscera (as liver, spleen and bone marrow) of the final host (man). 6- The parasite multiplies by binary fission (asexual). Life cycle Involves an alternative existence in a vertebrate (man,…ect) and an insect(sand fly).The flagellated promastigote enter the body (skin) of the final host through infected sand fly bite → the parasites engulfed by macrophage and endothelial cells of skin capillaries →promasitgote develops into amastigote (Leishman-Donovan (LD) bodies) →amastigote multiply inside macrophages by binary fission → cell burst → free amastigote either infect other cells (macrophages) in skin as in cutaneous or other cells in skin and the adjacent cells in mucous membrane as in mucocutaneousleishmaniasis or pass to different organ by blood stream (spleen, liver, bone marrow and lymph nodes) as in , then amastigotes engulfed by new reticuloendothelial cells →a blood sucking sand fly (female) draws amastigotes (L.D bodies) with its blood meal (by bites of proboscis) →amastigotes develop in promastigote forms in the mid gut of sand fly → multiply by longitudinal binary fission → solid mass of promastigotes fill up the anterior end of the mid gut and the esophagus , extending up to the pharynx → a heavy pharyngeal infection of the sand fly is known as anterior station development , which may block esophagus → at the time of sucking blood , regurgitation of promastigotes from their buccal cavity in the skin puncture by proboscis (biting organ) → infection of man. -Anterior station development is the anterior migration of the parasites from the mid gut to foregut, pharynx and buccal cavity of insect vector (as sand fly in Leishmania species). Posterior station development is the posterior migration of the parasite from the midgut to the hindgut and excreted with feces if insect vector (as Ruduviid bug in Trypanosoma cruzi).

It includes parasites cause three diseases in human: 1- infects the skin and cause or oriented sore.(CL) 2- Lieshmania donovani infects the spleen,liver ,bone marrow and cause Visceral Leishmaniasis or Kala-azar (VL) 3- Leishmania barasiliensis. Infects the mucous of the mouth,nose,pharynx an cause mucocutaneous Leishmaniasis(MCL).

Pathogenesis When the bite of infected sand fly liberate promastigotes into the skin → the parasite proliferates as amastigotes in the macrophages and other endothelial cells of the capillaries and small blood vessels of immediate area →lyses of the amastigotes occurs following activation of the macrophages by sensitized lymphocytes → a granulomatous reaction results in the formation of a localized nodule → which ulcerate when the blood supply to the area is compressed by the parasite-induced damage → a pyogenic infection develops in the open ulcer bed, and as host immunity increase → the ulcer heals.

Visceral leishmaniasis (VL) also known as kala-azar, black fever, and Dumdum fever is caused by obligate intracellular protozoan parasites, particularly by the species , L. infantum and L. chagasi. Transmission VL is predominantly transmitted through the bite of an infected female phlebotomine sand fly, although congenital and parenteral transmission (through blood transfusions and needle sharing) have been reported. Clinical signs: incubation period 2-6 months, but can vary from 10 days to several years. Some of macrophages enter the blood stream and reach the viscera, where the leishmanias multiply rapidly in the macrophages, which they destroy . fever is prolong and irregular ,coughing and diarrhea. The disease is characterized by splenomegaly and hepatomegaly, abdomen becomes distended, skin pigmentation.

Trypanosoma

They are microscopic unicellular flagellates , The genus Trypanosoma contains a large number of parasitic species which infect wild and domestic animals and humans and cause . include T.brucei gambian and T.brucei rhodesiense cause a disease commonly known as African sleeping sickness in which the host's central nervous system is infected at final stages. Transmitted to humans occurs through a vector tsetse fly

Trypanosoma cruzi, which causes American human trypanosomiasis, or Chagas' disease. This disease is found in humans in two forms: as an amastigote in the cells, and as a trypomastigote in the blood. The vectors for Trypanosoma cruzi is assassin flies, which ingest the amastigote or trypomastigote and carry them to animals or humans. The parasites enter the human host through mucus membranes in the nose, eye, or mouth upon release from the insect vectors

Parasitology

Dr: Fadia Al-Khayat Lec: thirteen

Sporozoa

The Sporozoa are parasitic protozoans that lack locomotor organs. They have no cilia, no flagella, no pseudopods, with most species presenting only gliding motility, except for male gametes in the sexual phase, which have a flagellated stage of motility. They are usually intracellular parasites. All species are parasitic and have elaborate life cycles, often requiring more than one host. The life cycle include asexual generation(reproduces by simple or multiple fission or internal budding) alternating with sexual generation(reproduces by isogametes or anisogametes). Four species of Plasmodium cause human malaria Plasmodium vivax, P.ovale, P.malaria, P.falciparum

The infection is initiated when sporozoites are injected with the saliva of a feeding mosquito. Sporozoites are carried by the circulatory system to the liver and invade hepatocytes (1). The intracellular parasite undergoes an asexual replication known as schizogony within the hepatocyte (2-4). schizogony culminates in the production of merozoites which are released into the bloodstream (5). A proportion of the liver- stage parasites from P. vivax and P. ovale go through a dormant period (not shown) instead of immediately undergoing asexual replication (i.e., stay temporarily at step 2). These hypnozoites will reactivate several weeks to months (or years) after the primary infection and are responsible for relapses Merozoites invade erythrocytes (6) and undergo a trophic period in which the parasite enlarges (7-8). The early trophozoite is often referred to as 'ring form' because of its morphology. Trophozoite enlargement is accompanied by an active metabolism including the ingestion of host cytoplasm and the proteolysis of hemoglobin into amino acids. The end of the trophic period is manifested by multiple rounds of nuclear division without cytokinesis resulting is a schizont (9). Merozoites bud from the mature schizont, also called a segmenter (10), and the merozoites are released following rupture of the infected erythrocyte (11). Invasion of erythrocytes reinitiates another round of the blood-stage replicative cycle (6-11). The blood stage is responsible for the pathology associated with malaria (see following pages). The intermittent fever paroxyms are due to the synchronous lysis of the infected erythrocytes. P. malariae exhibits a 72 hour periodicity, whereas the other three species exhibit 48 hour cycles. However, P. falciparum often exhibits a continuous fever rather than the periodic paroxyms. P.falciparum also is responsible for more morbidity and mortality than the other species. This increase virulence is due in part to the higher levels of parasitemia associated with P. falciparum infections. In addition, more complications are associated with P. falciparum because of thesequestration of the trophozoite- and schizont-infected erythrocytes in the deep tissues. As an alternative to the asexual replicative cycle, the parasite can differentiate into sexual forms known as macro- or microgametocytes (12). The gametocytes are large parasites which fill up the erythrocyte, but only contain one nucleus. Ingestion of gametocytes by the mosquito vector induces gametogenesis (i.e., the production of gametes) and escape from the host erythrocyte. Factors which participate in the induction of gametogenesis include: a drop in temperature, an increase in carbon dioxide, and mosquito metabolites. Microgametes, formed by a process known as exflagellation (13), are flagellated forms which will fertilize the macrogamete (14) leading to a zygote (15). The zygote develops into a motile ookinete (16) which penetrates the gut epithelial cells and develops into an oocyst (17). The oocyst undergoes multiple rounds of asexual replication (18)resulting in the production of sporozoites (19). Rupture of the mature oocyst releases the sporozoites into the hemocoel (i.e., body cavity) of the mosquito (20). The sporozoites migrate to and invade the salivary glands, thus completing the life cycle.In summary, malaria parasites undergo three distinct asexual replicative stages (exoerythrocytic schizogony, blood stage schizogony, and sporogony) resulting in the production of invasive forms (merozoites and sporozoites). A sexual occurs with the switch from vertebrate to invertebrate host and leads to the formation of the invasive ookinete. All invasive stages are characterized by the apical organelles typical of apicomplexan species.

Pathogenesis All of the pathology of malaria is due to parasites multiplying in erythrocytes(. The primary attack of malaria begins with headache, fever, anorexia, malaise, and myalgia. This is followed by paroxysms of chills, fever, and profuse sweating. There may be nausea, vomiting, and diarrhea. Then, depending on the species, the paroxysms tend to assume a characteristic periodicity. In P. vivax, P. ovale and P. falciparum the periodicity is 48hr and for P. malariae the periodicity is 72 hours.

Toxoplasma gondii Cellular stages During different periods of its lifecycle, individual parasites convert into various cellular stages, with each stage characterized by a distinct cellular morphology, biochemistry, and behavior. These stages include the tachyzoites, merozoites, bradyzoites (found in tissue cysts), and sporozoites (found in oocysts).

Tachyzoites Motile, and quickly multiplying, tachyzoites are responsible for expanding the population of the parasite in the host. When a host consumes a tissue cyst (containing bradyzoites) or an oocyst (containing sporozoites), the bradyzoites or sporozoites stage-convert into tachyzoites upon infecting the intestinal epithelium of the host. During the initial, acute period of infection, tachyzoites spread throughout the body via the blood stream. During the later, latent (chronic) stages of infection, tachyzoites stage-convert to bradyzoites to form tissue cysts.

Merozoites

Like tachyzoites, merozoites divide quickly, and are responsible for expanding the population of the parasite inside the cat intestine prior to sexual reproduction. When a feline definitive host consumes a tissue cyst (containing bradyzoites), bradyzoites convert into merozoites inside intestinal epithelial cells. Following a brief period of rapid population growth in the intestinal epithelium, merozoites convert into the noninfectious sexual stages of the parasite to undergo sexual reproduction, eventually resulting in the formation of zygote-containing oocysts. Bradyzoites Bradyzoites are the slowly dividing stage of the parasite that make up tissue cysts. When an uninfected host consumes a tissue cyst, bradyzoites released from the cyst infect intestinal epithelial cells before converting to the proliferative tachyzoite stage. Following the initial period of proliferation throughout the host body, tachyzoites then convert back to bradyzoites, which reproduce inside host cells to form tissue cysts in the new host. Sporozoites Sporozoites are the stage of the parasite residing within oocysts. When a human or other warm-blooded host consumes an oocyst, sporozoites are released from it, infecting epithelial cells before converting to the proliferative tachyzoite stage.

Lifecycle The lifecycle of T. gondii can be broadly summarized into two components: 1) a sexual component that occurs only within cats (felids, wild or domestic) 2) an asexual component that can occur within virtually all warm-blooded animals, including humans, cats, and birds. Because T. gondii can sexually reproduce only within cats, they are defined as the definitive host of T. gondii. All other hosts – hosts in which only asexual reproduction can occur – are defined as intermediate hosts. Sexual reproduction in the feline definitive host When a member of the cat family is infected with T. gondii (e.g. by consuming an infected mouse laden with the parasite's tissue cysts), the parasite survives passage through the stomach, eventually infecting epithelial cells of the cat's small intestine. Inside these intestinal cells, the parasites undergo sexual development and reproduction, producing millions of thick-walled, zygote-containing cysts known as oocysts. Feline shedding of oocysts Infected epithelial cells eventually rupture and release oocysts into the intestinal lumen, whereupon they are shed in the cat's feces. Oocysts can then spread to soil, water, food, or anything potentially contaminated with the feces. Highly resilient, oocysts can survive and remain infective for many months in cold and dry climates. Ingestion of oocysts by humans or other warm-blooded animals is one of the common routes of infection. Humans can be exposed to oocysts by, for example, consuming unwashed vegetables or contaminated water, or by handling the feces (litter) of an infected cat. Although cats can also be infected by ingesting oocysts, they are much less sensitive to oocyst infection than are intermediate hosts. Initial infection of the intermediate host When an oocyst or tissue cyst is ingested by a human or other warm-blooded animal, the resilient cyst wall is dissolved by proteolytic enzymes in the stomach and small intestine, freeing infectious T. gondii parasites to invade host cells. The parasites first invade cells in and surrounding the intestinal epithelium, and inside these cells, the parasites convert to tachyzoites, the motile and quickly multiplying cellular stage of T. gondii. Asexual reproduction in the intermediate host Inside host cells, the tachyzoites replicate inside specialized vacuoles (called the parasitophorous vacuoles) created during parasitic entry into the cell. Tachyzoites multiply inside this vacuole until the host cell dies and ruptures, releasing and spreading the tachyzoites via the blood stream to all organs and tissues of the body, including the brain.

T. gondii tissue cyst in a mouse brain, individual bradyzoites can be seen Formation of tissue cysts Following the initial period of infection characterized by tachyzoite proliferation throughout the body, pressure from the host's immune system causes T. gondii tachyzoites to convert into bradyzoites, the semidormant, slowly dividing cellular stage of the parasite. Inside host cells, clusters of these bradyzoites are known as tissue cysts. The cyst wall is formed by the membrane. Although bradyzoite-containing tissue cysts can form in virtually any organ, tissue cysts predominantly form and persist in the brain, the eyes, and striated muscle (including the heart). However, specific tissue tropisms can vary between species; in pigs, the majority of tissue cysts are found in muscle tissue, whereas in mice, the majority of cysts are found in the brain. Cysts usually range in size between five and 50 µm in diameter, (with 50 µm being about two-thirds the width of the average human hair). Consumption of tissue cysts in meat is one of the primary means of T. gondii infection, both for humans and for meat-eating, warm-blooded animals. Humans consume tissue cysts when eating raw or undercooked meat (particularly pork and lamb). Tissue cyst consumption is also the primary means by which cats are infected. Chronic infection Tissue cysts can be maintained in host tissue for the lifetime of the animal. However, the perpetual presence of cysts appears to be due to a periodic process of cyst rupturing and re-encysting, rather than a perpetual lifespan of individual cysts or bradyzoites. At any given time in a chronically infected host, a very small percentage of cysts are rupturing, although the exact cause of this tissue cysts rupture is, as of 2010, not yet known. T. gondii can, theoretically, be passed between intermediate hosts indefinitely via a cycle of consumption of tissue cysts in meat. However, the parasite's lifecycle begins and completes only when the parasite is passed to a feline host, the only host within which the parasite can again undergo sexual development and reproduction

Pathogenesis Symptoms/Pathology Infection with Toxoplasma gondii is usually asymptomatic in healthy individuals. About 10-20% of those with an acute infection will have enlarged lymph nodes in the cervical and inguinal region as well as flu-like symptoms (fever, headache, muscle pain). The infection is generally self-limited and the symptoms usually resolve in a few months. Immunocomprimised persons often show involvement of the central nervous system but may also have heart and lung complications. In persons with AIDS, toxoplasmic encephalitis and brain lesions may occur. Congenital infection occurs if the mother is infected during pregnancy. Toxoxplasma gondii tachyzoites are thought to cross the placenta to the fetus which may lead to stillbirths or severe birth defects. Early diagnosis and treatment of the mother may reduce the probability of congenital infection.

Chronic infections may also lead to blindness over time as sarcocysts in the eye develop and rupture the infected cells.

Ciliates

Ciliates are single-celled organisms that, at some stage in their life cycle, possess cilia, short hairlike organelles used for locomotion and food gathering. Ciliates have one or more macronuclei and from one to several micronuclei. The macronuclei control metabolic and developmental functions while, the micronuclei are necessary for reproduction . Reproduction is typically asexual, although sexual exchange occurs as well. Asexual replication is usually by transverse binary fission or by budding. Sexual phenomena include conjugation (genetic exchange between individuals). Although most ciliates are free-living and aquatic, such as the Paramicium, some, such as the dysentery-causing Balantidium are parasitic Balantidium coli

Balantidium coli is an intestinal protozoan parasite that can infect humans. It is responsible for the disease Balantidiasis. These parasites can be transmitted through the fecal-oral route by contaminated food and water. Balantidium coli infection is mostly asymptomatic, but people with other serious illnesses can show diarrhea, abdominal pain, and sometimes a perforated colon. Balantidium coli has two developmental stages called the trophozoite stage (reproductive stage) and the cyst stage (infectious stage). In the trophozoite stage, Balantidium coli can measure between 50-130 µm long by 20-70 µm wide, it has a short ciliary covering and has spiraling motility. The two nuclei of Balantidium coli are clearly visible, the is a long, kidney-shaped structure while the is spherical. The peristome, which is an opening at the anterior end of cell, is also visible. The peristome leads to the (cell mouth).

The cyst is the infective stage, Cysts are smaller than trophozoites, measuring 40-60 m across. Cysts are round and have a tough, heavy cyst wall made of one or two layers. Usually only the macronucleus and perhaps cilia and contractile vacuoles are visible in the cyst Life cycle When cyst(infective stage) is ingested via feces-contaminated food or water, it passes through the host digestive system. The tough cyst wall allows the cyst to resist degradation in the acidic environment of the stomach and the basic environment of the small intestine until it reaches the large intestine. There, excystation takes place. Excystation produces a trophozoite from the cyst stage. The motile trophozoite then resides in the lumen of the large intestine, feeding on intestinal bacterial flora and intestinal nutrients. Trophozoites multiply by asexual binary fission or sexual conjugation (with the exchange of nuclear material). The trophozoite may become invasive and penetrate the mucosa of the large intestine. Trophozoites are released with the feces, and encyst to form new cysts. Encystation takes place in the rectum of the host as feces are dehydrated or soon after the feces have