Diagnosis may be made using observation under the microscope. ELISA and other immunoassay tests, including commercial direct fluorescence antibody kits, are also used. The most common treatments use metronidazole as the first-line choice, followed by tinidazole. If the infection becomes chronic, the parasites may become resistant to medications. Figure 1. Immunofluorescent staining allows for visualization of Cryptosporidium spp.
Another protozoan intestinal illness is cryptosporidiosis , which is usually caused by Cryptosporidium parvum or C. These pathogens are commonly found in animals and can be spread in feces from mice, birds, and farm animals. Contaminated water and food are most commonly responsible for transmission.
The protozoan can also be transmitted through human contact with infected animals or their feces. In the United States, outbreaks of cryptosporidiosis generally occur through contamination of the public water supply or contaminated water at water parks, swimming pools, and day-care centers.
The risk is greatest in areas with poor sanitation, making the disease more common in developing countries. Signs and symptoms include watery diarrhea, nausea, vomiting, cramps, fever, dehydration, and weight loss. The illness is generally self-limiting within a month. Diagnosis involves direct examination of stool samples, often over multiple days. Acid fast staining is often used. Enzyme immunoassays and molecular analysis PCR are available.
The first line of treatment is typically oral rehydration therapy. Medications are sometimes used to treat the diarrhea. The broad-range anti-parasitic drug nitazoxanide can be used to treat cryptosporidiosis.
Other anti-parasitic drugs that can be used include azithromycin and paromomycin. The protozoan parasite Entamoeba histolytica causes amoebiasis , which is known as amoebic dysentery in severe cases. The disease is most widespread in the developing world and is one of the leading causes of mortality from parasitic disease worldwide. Disease can be caused by as few as 10 cysts being transmitted.
The breakdown of the cyst wall is believed to be mediated by proteases. The trophozoite will undergo cytokinesis cell division without nuclear replication within 30 minutes after emerging from the cyst resulting in two binucleated trophozoites. The Giardia trophozoite exhibits a characteristic pear, or tear-drop, shape with bilateral symmetry when viewed from the top Figure. Characteristic features of the stained trophozoite include: two nuclei Nu with central karyosomes k , fibrils running the length of the parasite, and median bodies MB.
The large karyosome and lack of peripheral chromatin gives the nuclei a halo appearance. The fibrils are called axonemes Ax and are formed from the proximal regions of the flagella Fg within the body of the trophozoite. The median bodies are a pair of curved rod-shaped structures which lie posterior to the nuclei. At the ultrastructural level the median bodies contain an array of microtubules. The function of the median bodies is not known, but most believe they are somehow involved with the adhesive disk and its formation.
An adhesive disk AD , not always visible by light microscopy, occupies the ventral side of the anterior end. Giardia trophozoites possess four pairs of flagella and are motile. Three pairs of flagella emerge from the dorsal surface anterior, posterior-lateral, caudal and one pair emerges from the ventral surface. Trophozoites exhibit a distinctive erratic twisting motion, sometimes compared to that of a falling leaf.
However, the trophozoites are predominantly found attached to epithelial cells of the small intestine especially the duodenum and jejunum and are rarely found in stools, except in the cases of severe diarrhea.
This attachment to the intestinal epithelium is mediated by an organelle on the ventral side of the parasite referred to as the adhesive disk see below.
The trophozoite absorbs nutrients from the intestinal lumen via pinocytosis and no specialized feeding organelles have been described. The trophic stage is also characterized by an asexual replication. Both nuclei divide at about the same time and cytokinesis restores the binucleated state.
Each daughter cell receives one copy of each nuclei. Both nuclei appear equal in regards to gene expression and other properties. As an alternative to replication the trophozoite can encyst. During encystment the parasite rounds up, detaches from the intestinal epithelium, and secretes a cyst wall.
Encystation can also be carried out in vitro. Optimal induction of encystment is obtained by depriving the trophozoites of bile at pH 7 followed by an exposure to high concentrations of bile at pH 7. The lack of bile at neutral pH mimics the conditions under the mucus blanket adjacent to the intestinal epithelial cells, whereas exposure to high concentrations of bile at more alkaline pH is analogous to the intestinal lumen.
These studies highlight the extent to which Giardia has adapted to life within the gastrointestinal tract. Molecular and ultrastructural studies reveal the synthesis of cyst wall proteins and the appearance of large secretory vesicles in the parasite cytoplasm follow the induction of encystment.
After cyst wall formation the parasite undergoes one round of nuclear division without cytokinesis resulting in four nuclei. These four nuclei Nu are usually located at the anterior end of the cyst Figure.
The flagella and adhesive disk are lost as the cyst matures, but the axonemes Ax and median bodies MB persist. The distinctive fibrils ie, axonemes , which extend across the length of the cyst, result in Giardia being relatively easy to unambiguously identify. Other characteristics of Giardia cysts include a well-defined wall CW which is often set apart from the cytoplasm of the parasite. The cysts are passed in the feces and can survive for up to three months under appropriate temperature and moisture conditions.
Mature cysts are infective to the next host that happens to ingest them, thus completing the life cycle. A unique ultrastructural feature of Giardia is the adhesive disk also called ventral disk, sucking disk, sucker, or striated disk. The adhesive disk is a concave structure which occupies approximately two-thirds of the anterior end of the ventral surface Figure, left panel. As the names imply, this structure plays a role in the attachment of the trophozoite to the intestinal epithelium and ultrastructural studies reveal close associations between the adhesive disk and the intestinal brush border Figure, upper right panel.
Click here for larger image. The adhesive disk appears to be a relatively rigid structure and striations are evident by transmission electron microscopy. These striations are the result of microtubules mT and a unique cytoskeletal element called microribbons mR. Microribbons are long flattened structures and each microribbon is associated with a microtubule Figure, middle right panel. The combined microtubule-microribbon structure are arranged in concentric rows that form a flatten spiral with minimal overlap.
The outer rim of the adhesive disk, called the lateral crest, contains components of the actin-myosin cytoskeleton. This association of proteins involved in the generation of contractile force and other cytoskeletal elements in the adhesive disk suggests that attachment is mediated by mechanical forces generated by the parasite. The observation that imprints and circular dome-shaped lesions remain in the intestinal brush border ie, microvilli following detachment of trophozoites Figure, lower right panel is consistent with contractile forces playing a role in attachment.
Other proposed mechanisms for the attachment of Giardia to the intestinal epithelium include hydrodynamic forces generated by the ventral flagella and receptor-mediated binding via lectins on the trophozoite surface.
However, flagellar movement is poorly correlated with attachment and the surface lectins cover the entire trophozoite and are not specifically localized to the adhesive disk. The clinical features associated with Giardia infection range from total latency ie, asymptomatic , to acute self-resolving diarrhea, to chronic syndromes associated with nutritional disorders, weight loss and failure to thrive.
Children exhibit clinical symptoms more frequently that adults and subsequent infections tend to be less severe than initial infections. The incubation period is generally weeks, but ranges of days have been reported. The first signs of acute giardiasis include nausea, loss of appetite and an upper gastro-intestinal uneasiness. These signs are often followed or accompanied by a sudden onset of explosive, watery, foul-smelling diarrhea.
Other gastro-intestinal disturbances associated with giardiasis include: flatulence, bloating, anorexia, cramps, and foul sulfuric belching sometimes called 'purple burbs'. The acute stage usually resolves spontaneously in days and is often not recognized as being giardiasis. Occasionally, though, an acute infection will persist and lead to malabsorption, steatorrhea excessive loss of fat in the feces , debility loss of strength and weight loss.
Some of the individuals who resolve the acute symptoms do not clear the infection, but become asymptomatic cyst passers without clinical manifestations, whereas others may have a few sporadic recurrences of the acute symptoms. Acute infections can also develop into long-standing subacute or chronic infections which in rare cases last for years. The typical chronic stage patient presents with recurrent brief episodes of loose foul stools which may be yellowish, frothy and float, accompanied by intestinal gurgling, abdominal distention and flatulence.
Between episodes the stools are usually mushy, but normal stools or constipation can also occur. Cramps are uncommon during chronic infections, but sulfuric belching is frequent. Anorexia, nausea, and epigastric uneasiness are additional frequent complaints during chronic infections.
In the majority of chronic cases the parasites and symptoms spontaneously disappear. The specific mechanisms of Giardia pathogenesis leading to diarrhea and intestinal malabsorption are not completely understood and no specific virulence factors have been identified. Attachment of trophozoites to the brush border could produce a mechanical irritation or mucosal injury. In addition, normal villus structure is affected in some patients.
For example, villus blunting atrophy and crypt cell hypertrophy and an increase in crypt depth have been observed to varying degrees. The increase in crypt cells will lead to a repopulation of the intestinal epithelium by relatively immature enterocytes with reduced absorptive capacities. An increased inflammatory cell infiltration in the lamina propria has also been observed and this inflammation may be associated with the pathology.
Giardia infection can also lead to lactase deficiency see lactose intolerance below as well as other enzyme deficiencies in the microvilli. This reduced digestion and absorption of solutes may lead to an osmotic diarrhea and could also explain the malabsorption syndromes. Thus far, no single virulence factor or unifying mechanism explains the pathogenesis of giardiasis. Post- Giardia Lactose Intolerance. Some patients may present with a lactose intolerence during active Giardia infections which can persist after parasite clearance.
This clinical manifestation is due to the parasite-induced lactase deficiency and is most common in ethnic groups with a predisposition for lactase deficiency. Lactase is an enzyme that breaks down lactose, a sugar found in milk, to monosaccharides which can be absorbed. This lactose intolerence syndrome should be considered in persons who still present mushy stools and excessive gas following treatment, but have no detectable parasites.
Diagnosis is confirmed by finding cysts or trophozoites in feces or in duodenojejunal aspirates or biopsies. Detection of the parasites can be difficult since Giardia does not appear consistently in the stools of all patients. Some patients will express high levels of cysts in nearly all the stools, whereas others will only exhibit low parasite counts in some of the stools. A mixed pattern, in which periods of high cyst excretion alternate with periods of low excretion, has also been observed.
In addition, parasites are easier to find during acute infections than chronic infections. Aspiration and biopsy may also fail to confirm the infection due to patchy loci of infection, and some question the usefulness of these invasive procedures.
Stool examination is the preferred method for Giardia diagnosis. Three stools taken at intervals of at least two days should be examined. Watery or loose stools may contain motile trophozoites which are detectable by the immediate examination of wet smears. Otherwise the specimen should be preserved and stained due to trophozoite lability.
The hardier cysts are relatively easy to recognize in either direct or stained smears see cyst morphology. In addition, diagnostic kits based on immunofluorescence or the detection of copro-antigens are also available. Diagnosis can also be made by examining duodenal fluid for trophozoites. The free end of the string is taped to the patient's face and the capsule is swallowed. After four hours to overnight the string is retrieved and the bile-stained mucus on the distal portion of the string is scraped off and examined by both wet mount and permanent staining.
A small intestinal biopsy, preferably from multiple duodenal and jejunal sites, may also reveal trophozoites attached to the intestinal epithelium. Infected individuals should be treated since Giardia can persist and lead to severe malabsorption syndromes and weight loss. Treatment is effective at reducing morbidity and there are no sequelae. Tinidazole is effective as a single two gram dose; paramomycin is not absorbed and may be useful during pregnancy. The widespread distribution of Giardia and the infectivity of the cysts make it unlikely that human infection will be completely eliminated.
Control measures to prevent or reduce Giardia infection will depend on the specific circumstances of transmission, but in general involve measures which prevent the ingestion of substances contaminated with fecal material see fecal-oral transmission factors. Health promotion and education aimed at improving personal hygiene, and emphasizing hand washing, sanitation and food handling, are effective control activities for the reduction of person-to-person transmission.
Special attention to personal hygiene in high-risk situations such as day-care centers and other institutions is needed. Treatment of asymptomatic household members prevents reinfection in non-endemic areas. However, the value of treating asymptomatic carriers in hyperendemic communities is questionable since reinfection rates are high. The socio-economic situation in many developing countries makes it difficult to prevent infection.
Public health measures to protect water supplies from contamination are required to prevent epidemics and to reduce endemicity. Tourists should not drink tap water without additional treatment in places where purity is questionable. Boiling or iodine treatment kills Giardia cysts, but standard chlorination does not. There are no safe or effective chemoprophylatic drugs for giardiasis.
The trichomonads are a group of flagellated protozoa. Most of the members of this group are parasitic and only a few free-living species have been identified. Generally the trichomonads are non-pathogenic commensals and only a few species are of importance in animals and humans.
Four species of trichomonads infect humans Table. Among these only Trichomonas vaginalis is clearly pathogenic and it is usually of low virulence. The others exhibit a questionable pathogenicity. Trichomonads of Humans. The trichomonads of humans inhabit different anatomical locations. Such cases have reported mainly in patients with underlying cancers or other lung diseases or following surgery.
Pentatrichomonas hominis , formerly known as Trichomonas hominis , is a non-pathogenic commensal of the large intestine see non-pathogenic intestinal flagellates.
Some authors divide the trichomonads into three genera based on the number of free flagella. Species with three flagella are called Tritrichomonas , those with four are called Trichomonas , and Pentatrichomonas refers to trichomonads with five free anterior flagella. Dientamoeba fragilis was originally believed to be an ameba see non-pathogenic intestinal ameba.
Now it is know to be a flagellate—however without flagella—related to the trichomonads. A distinctive feature of the trichomonads is an axostyle ax which runs the length of the organism and appears to protrude from the posterior end Figure. The axostyle is a cytoskeletal element composed of concentric rows of microtubules and is believed to function in the attachment of the parasite to epithelial cells.
Trichomonads are also characterized by flagella fg emerging from the anterior end. One of the flagella is attached to the body of the organism and forms a posteriorly-directed undulating membrane um , whereas the remaining flagella are free. The combined basal bodies bb and the base of the undulating membrane, called the costa cs , are often seen is stained preparations. Less frequently seen is the cytostomal groove cy. A single nucleus nu is found at the anterior end of the parasite.
The trichomonads, like many other intestinal protozoa, exhibit an anerobic metabolism and lack mitochondria. Part of energy metabolism of trichomonads involves a unique organelle called the hydrogenosome. The hydrogenosome has a double membrane and is distantly related to the mitochondrion.
However, it lacks DNA, cytochromes and many typical mitochnondrial functions such as enzymes of the tricarboxylic acid cycle and oxidative phosphorylation. The primary function of the hydrogenosome is the metabolism of pyruvate, produced during glycolysis within the cytosol, to acetate and carbon dioxide with the concomitant production of ATP.
The electrons release from the oxidation of pyruvate are transferred to hydrogen ions to produce molecular hydrogen, hence the name hydrogenosome. Trichomonas vaginalis was first described from purulent vaginal discharges in and by the early part of the twentieth century was recognized as an etiological agent of vaginitis.
Trichomoniasis is a common sexually transmitted disease with a worldwide distribution and an estimated million people becoming infected per year worldwide and 5 million new infections per year in the United States.
Trichomoniasis is believed to be the most common non-viral sexually transmitted disease. Despite the frequency of trichomoniasis it has in the past been considered more of a nuisance parasite rather than a major pathogen. However it is now recognized a factor in promoting HIV infection see Box , causing low-weight and premature births, and predisposing women to substantial discomfort and stress.
Trichomonas and HIV. In females the organism primarily inhabits the vagina, and in males it is usually found in the urethra, prostate or epididymis. The life cycle consists only of a trophozoite stage which is transmitted by direct contact during sexual intercourse. Non-venereal transmission is rare, but possible since the trophozoites can survive days in urine and hours on a wet sponge. In addition, neonatals have been infected during the birth process. The trophozoites live closely associated or attached to the epithelium of the urogenital tract, where they replicate by binary fission.
Q10 a Highlight the role of thymus as a lymphoid organ. Q11 Some organisms suspend their metabolic activities to survive in Q12 a State the role of DNA ligase in biotechnology. Q13 Why do clown fish and sea anemone pair up?
What is this relatio Q14 a Name the Protozoan parasite that causes amoebic dysenter Previous Question Next Question. Popular Questions of Class 12th biology Q:- Why is reproduction essential for organisms? Answer Q:- What is spermatogenesis? Briefly describe the process of spermatogenesis. Q:- With a neat diagram explain the 7-celled, 8-nucleate nature of the female gametophyte.
Q:- Write a short note on a Adaptations of desert plants and animals b Adaptations of plants to water scarcity c Behavioural adaptations in animals d Importance of light to plants e Effect of temperature or water scarcity and the adaptations of animals. Q:- With a neat, labelled diagram, describe the parts of a typical angiosperm ovule. Q:- What is oogenesis?
Give a brief account of oogenesis. People who live in institutions, travellers who travel to or immigrants from developing countries with poor sanitary conditions, and men who have sex with men are at a higher risk of getting the disease. The incubation period is variable, and may range from a few days to several months.
It is usually 2 - 4 weeks.
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