Human Protozoal Infections

Although all infectious agents in humans are parasites, by convention, parasitic diseases are defined as those caused by protozoa or helminths. The old classification, in which a single phylum of protozoa encompassed all unicellular eukaryotic microorganisms, is no longer valid because of new ultrastructural and molecular taxonomic information. For instance, Giardia lamblia has been shown to lack mitochondria and shown to contain ribosomal RNA sequences that resemble bacteria. These protozoa have been proposed to represent an evolutionary transition between prokaryotic and eukaryotic microorganisms. Both Giardia and Microsporidia(which also shares similarities with bacteria) have been reclassified as Archezoa, a term that reflects their evolutionary transitional nature. Clinicians can best classify unicellular eukaryotic microorganisms based on mode of transmission. The classification of representative protozoa according to modes of transmission is as follows: Enteric transmission -Balantidium, Giardia, Entamoeba, Cryptosporidium, Toxoplasma, Cyclospora, Microsporidia Sexual transmission -Trichomonas Arthropod transmission -Babesia, Plasmodium, Leishmania, Trypanosoma Other modes of transmission -Naegleria, Acanthamoeba, Toxoplasma Toxoplasma is the only pathogenic fecal-oral transmitted protozoa that has not been associated with gastroenteritis. Among all intestinal protozoa, those listed in Table 1 have been confirmed to cause GI disease. Others, such as Trichomonas hominis (in infants) andEntamoeba polecki (associated with pigs), have rarely been associated with diarrheal disease and are not discussed in this article. Table 1. Protozoa Associated with Intestinal Illness in Humans Name Flagellates G lamblia Contaminated fecal-oral water, Nausea, bloating, gas, diarrhea, anorexia Mode of Transmission Symptoms

Dientamoeba fragilis

Fecal-oral, associated Previously thought commensal; may cause withEnterobius diarrhea, abdominal, pain, nausea

Amebas Entamoeba histolytica Contaminated water, Colitis, dysentery, diarrhea, liver abscess, fecal-oral, contaminated other extraintestinal disease

food Spore-forming (Coccidia) Cryptosporidium parvum Contaminated water, Immunocompetent patients: Self-limited swimming pools, fecal- diarrhea Immunosuppressed patients: oral Severe and interminable diarrhea Fecal-oral Same as in Cryptosporidium

Isospora belli Cyclospora cayetanensis

Fecal-oral, contaminated Same as in Cryptosporidium water and food

Microsporidia (Septata Fecal-oral, contaminated Same as in Cryptosporidium intestinalis, Enterocytozoon water bieneusi) Ciliates Balantidium coli Fecal-oral (frequently Colitis, diarrhea associated with pigs)

Other Blastocystis hominis Fecal-oral May cause mild diarrhea

Pathophysiology:
Understanding the life cycle is essential to explain the pathophysiology of the diseases caused by these organisms. The life cycles of intestinal protozoa are very similar, with the exception of D fragilis, which lacks a cyst stage. Mechanisms of diarrhea production by intestinal protozoa are related to direct cytotoxic effects, the ability to invade, and/or effects of the immune response on the intestinal epithelium. No evidence suggests that intestinal protozoa produce enterotoxins.

Entamoeba histolytica
Mature cysts are ingested via contaminated water or food. After excystation in the small intestine, trophozoites inhabit the large intestine and can either invade the tissue (pathogenic amebas) or are eliminated in the stools. Trophozoites do not survive outside the body. This parasite was named for its remarkable ability to lyse human tissues. A prerequisite to amebic invasion is the parasite's ability to colonize and penetrate colonic mucins overlying the intestinal epithelium. At least 22 amebic strains or zymodemes have been identified based on pulsed-field gel electrophoresis patterns of the 4 isoenzymes isolated from ameba. Nine zymodemes have been associated inconsistently with invasiveness.

In 1982, Sargeaunt postulated that instead of pathogenic and nonpathogenic zymodemes, 2 different amebas were present.[1] The concept of E histolyticaas a pathogenic ameba and E dispar as a nonpathogenic ameba is currently accepted. Furthermore, both immunologic assays and amplification tests have been developed to distinguish these two species among symptomatic and asymptomatic patients. Upon invasion of the host, amebas are capable of killing immune effector cells by contactdependent cytolysis, possibly by a calcium-dependent mechanism. They then disseminate to the liver or other tissues.

Giardia lamblia
After ingestion of mature cysts (infective dose varies from 10-100 cysts) via contaminated water or food, the trophozoite emerges in the small intestine, rapidly multiplies, and attaches to the small intestinal villi.[2] Mature infective cysts pass in feces and complete the cycle. The pathogenesis of diarrhea in giardiasis is thought to be related to the following factors: (1) the number of organisms ingested, (2) specific strain ingested, (3) nonantibody protective factors in the GI tract, and (4) the immune response of the host. Giardia trophozoites attach to the cell surface of villi by means of a disk on their posterior or ventral surface. Lectin, a protein on the trophozoite lining, recognizes specific receptors on the intestinal cell and may be partly responsible for the tight attachment between the parasite and the villi, which is followed by mucosal damage, mechanical obstruction (only caused in the presence of numerous organisms), and deconjugation of bile salts. Recent data has indicated that inflammatory mast cells may interfere with duodenal growth of G lamblia trophozoites.[3] Other inflammatory cells, as well as CD8+ T cells, contribute to villus-shortening and crypt hyperplasia. Strains that infect humans are biologically diverse, as shown by differences in antigens, restriction endonuclease patterns, DNA fingerprinting, isoenzyme patterns, and pulsed-field gel electrophoresis patterns. In giardiasis, secretory immunoglobulin A (IgA) is presumed to be important in host protection because invasion of the mucosa is not part of the pathogenic mechanism.

Spore-forming protozoa
Spore ingestion begins a life cycle that is similar in all 4 of the intestinal sporeforming protozoa (see Table 1). The ingested spores release sporozoites that invade enterocytes, primarily in the small intestine. The enterocyte infection progresses through 2 stages: merogenic and sporogonic. The merogenic (or schizogonic) stage involves the maturation and development of meronts to reproduce and multiply in the infected cell or to infect other enterocytes. This asexual stage allows the infection to spread to many enterocytes, even if the host is not exposed repeatedly to the organism. The sporogonic (ie, gametogonic, sexual) stage involves the maturation and development of sporozoites enclosed in cysts or spores. As the infected enterocytes die, cyst or spore shedding occurs. The spores are then excreted in the stool. The sporeforming protozoa are obligate intracellular pathogens. Infection by these protozoa has

been associated with substantial alterations in intestinal structure and function, but the pathogenesis of the predominant symptom, diarrhea, is not completely understood. Cryptosporidiosis is the best-studied spore-forming diarrhea, and its pathogenic mechanisms can also be related to other spore-forming protozoa. The hypothesized sequence of events is explained below. After invasion of the enterocytes, the epithelial cells release cytokines. These cytokinins activate phagocytes and recruit new leukocytes, which, in turn, release soluble factors (resulting in intestinal secretion of chloride and water) and inhibit absorption. Enterocyte damage may be a direct consequence of parasite invasion, multiplication, and extrusion. Regardless of the specific mechanism, marked distortion of the villus architecture is accompanied by nutrient malabsorption and osmotic diarrhea. With the exception of the microsporidia S intestinalis, none of the spore-forming protozoa have the ability to invade beneath the mucosal layer of the intestine.

Dientamoeba fragilis
The exact mode of transmission of D fragilis has not been confirmed. This parasite is speculated to be transmitted when pinworm eggs containing D fragilis trophozoites are ingested and, by this mechanism, resist the acid pH in the stomach. It is not invasive and mostly inhabits the large intestine. The exact mechanisms of diarrhea are not known.

Balantidium coli
The cyst is the infectious stage and is acquired by ingestion of contaminated food or water. After excystation in the small intestine, the trophozoites colonize the terminal ileum and the large intestine. They can then invade tissues by mechanical action of ciliary movement and the secretion of hyaluronidase and probably other enzymes. Encystation occurs in the lumen of the colon or in freshly evacuated stools. As with E histolytica, invasiveness is the hallmark of the pathophysiology of balantidiasis.

Blastocystis hominis
Many experts believe that B hominis is pathogenic only when present in large numbers in the intestine (>5 organisms per 400X field) and when other infectious organisms are absent. Three distinct morphologic stages are recognized: vacuolar, granular, and ameboid. B hominis inhabits the large intestine and has no evident life cycle in humans. Cysticlike stages are rare and have been found in patients with acquired immunodeficiency syndrome (AIDS) and in vitro. The mechanisms of how this parasite causes illness have not been elucidated yet.

HISTORY
The spectrum of intestinal protozoal infections can range from asymptomatic to invasive disease (in the cases of E histolytica or B coli) to severe and/or chronic and protracted diarrhea (in the cases of giardiasis or in individuals who are severely immunosuppressed with spore-forming protozoal infections).
Amebiasis Noninvasive intestinal infection: Noninvasive amebiasis most frequently produces

no symptoms. Nevertheless, some patients may have some ill-defined GI tract

symptoms. These symptoms include alternating periods of mild diarrhea and constipation with or without mild abdominal pain; however, for the most part, patients tolerate the infection. Intestinal amebiasis or amebic colitis: Patients typically have 1-3 weeks of diarrhea to grossly bloody dysenteric stools with abdominal pain. Constitutional symptoms are often mild, and fever is present only in about 10-20% of cases; however, weight loss is common. Some patients manifest chronic nondysenteric diarrhea, combined with months or even years of abdominal pain associated with varying amounts of flatulence, mucus in stools, and weight loss. Acute fulminant or necrotizing colitis: This presentation occurs in only 0.5% of intestinal amebiasis cases and has been associated with patients inappropriately treated with corticosteroids. The patient develops sudden constipation following an acute and severe episode of dysenteric diarrhea that is followed by signs of shock. Ameboma: This is a mass of granulation tissue in the cecum or ascending colon, and it usually occurs in fewer than 1% of patients with intestinal amebiasis. Concurrent amebic dysentery is present in two thirds of patients. Patients usually report a tender, palpable, lower-left quadrant abdominal mass. Liver abscess: This occurs in 10% or fewer patients with invasiveE histolytica infections. Patients usually have a history of more than 1-2 weeks of fever, abdominal pain, poor appetite, and, less commonly, cough and pleuritic chest pain. Liver abscess is associated with diarrhea only in 20% of cases. Jaundice occurs only in severe cases. Giardiasis Following excystation and colonization, a spectrum of clinical manifestations can occur. Symptomatic infections are noted more frequently in children than in adults. Asymptomatic excretion: The asymptomatic carrier rate of G lamblia in the United States is estimated to be 3-7% but is as high as 20% in southern regions and possibly even higher in children attending childcare centers. In endemic giardiasis, most infections produce no symptoms. Acute infectious diarrhea: Infections resulting from waterborne outbreaks and infections in travelers and among children in childcare centers are associated more often with significant illness. Most patients have symptoms within 10 days of exposure, and more than 90% of patients have symptoms within 3 weeks. The usual symptoms are short-lasting acute diarrhea (with or without low-grade fever), nausea, abdominal distension, greasy stools, and anorexia. Acute giardiasis may spontaneously resolve. Parasites disappear from the stools within 4-6 weeks in both experimental and naturally acquired infections; however, giardiasis can sometimes occur as intermittent diarrheal episodes and/or evolve to chronic diarrhea, anorexia, bloating, and weight loss. Chronic diarrhea: Chronic giardiasis is usually associated with intermittent, loose, foul-smelling stools that resemble those of malabsorption states. Abdominal distension, sulfurous belching, flatulence, epigastric pain, substernal burning, nausea, anorexia, and failure to thrive may occur. Although severe forms of chronic giardiasis may occur in otherwise healthy individuals, they are common in patients with hypoglobulinemia, particularly IgA deficiency in association with lymphoid hyperplasia of the bowel. Chronic giardiasis may contribute to protein-energy malnutrition in children. Protein-losing enteropathy has also been described. Intestinal disaccharidase deficiency associated with giardiasis can be manifested by carbohydrate intolerance, especially lactose. Evidence suggests that giardiasis may be associated with chronic urticaria, gallbladder disease, and treatment failures because of malabsorption of antibiotics during episodes of otitis media.

 Spore-forming protozoa Asymptomatic infections: Asymptomatic infection is part of the clinical spectrum

of disease produced by these parasites. Asymptomatic infections with cryptosporidia occur in normal and immunodeficient hosts. Some data suggest that asymptomatic carriage of microsporidia in patients with AIDS may precede wasting and diarrheal illness. In one study, only 11-18% of immunocompetent Peruvian children with acute cyclosporal infections had diarrhea. The reported frequency of asymptomatic infection is controversial, especially with microsporidia, Isospora, and Cyclospora. The link between infection and clinically apparent disease is strong; however, the frequency that asymptomatic infection is identified depends on the sensitivity of the assay used to detect the parasite. Acute infectious diarrhea in immunocompetent hosts: Acute diarrhea in immunocompetent hosts has been shown to be a predominant clinical manifestation of infection with these parasites, except for microsporidia (only one case of microsporidial diarrhea has been reported in a normal host). In a study developed in Austria, the correlation between detection of microsporidia in stool and GI symptoms was transient, suggesting that microsporidia infection may cause clinical symptoms during the early stages of infection that resolve even though the microsporidia persist. Many studies report acute diarrhea in infants and children living in underdeveloped countries, medical personnel, travelers, and persons in institutions. In March 1993, the municipal water supply in Milwaukee became contaminated with cryptosporidia, and an estimated 403,000 residents developed diarrhea. In normal hosts, infections by cryptosporidia, Cyclospora, and Isospora are characterized by 3-25 days of diarrhea, malaise, abdominal pain with or without nausea, vomiting, and fever. However, studies performed in the United Kingdom have shown that cryptosporidiosis can cause recurrence of gastrointestinal symptoms in as many as 40% of immunocompetent patients (more with C hominis than with C parvum), and all episodes have been self limited. Giving specific treatment to immunocompetent patients with cryptosporidiosis is still not well supported. Disease in immunodeficient hosts All spore-forming protozoa have a predisposition for more frequent and prolonged infections in patients who are immunodeficient. Most reported cases are in patients with AIDS, but reports document severe cryptosporidia infections in patients with renal transplantation and persons with IgA deficiency. Isosporiasis has been reported in persons with cancer. The symptoms range from asymptomatic infection to severe life-threatening diarrhea, dehydration and chronic malabsorption leading to lethargy, failure to thrive, and malnutrition. The clinical features of 128 patients with AIDS-related cryptosporidiosis showed the following 4 patterns of disease: transient (29%), chronic (60%), fulminant (8%), and asymptomatic (4%). As mentioned above, more severe cases of cryptosporidiosis and microsporidiosis are observed in patients with AIDS who have very low CD4 counts (< 50-100/mL). A similar spectrum of disease severity is seen in AIDS-related intestinal infection with Cyclospora andIsospora. HIV-wasting syndrome is a well-established clinical syndrome in patients with AIDS characterized by chronic diarrhea, chronic weakness, and/or documented fever. The physiopathogenesis of this syndrome is multifactorial, from

hypermetabolism, decreased oral intake, and cytokine dysregulation, to the coparticipation of various pathogens in which spore-forming protozoa are included. The advent of highly active antiretroviral therapy (HAART) has decreased the frequency and severity of cryptosporidiosis in HIV infected individuals. Recovery of CD4 with HAART has resulted in resolution of chronic diarrhea in many patients. Extraintestinal disease: The primary location of all intestinal spore-forming protozoal infections is the small intestine, predominately the distal small bowel. Colonic infection is common with microsporidiosis. Infection in the biliary tract has been reported with cryptosporidium, Isospora, and microsporidia leading to right upper quadrant abdominal pain, occasionally with jaundice and fever. Invasion by S intestinalis beneath the epithelial surface and dissemination to the liver, respiratory tract, or the kidney has been reported. The other intestinal microsporidia E bieneusi has also been isolated from the lungs in individuals with AIDS. Dientamoebiasis Symptoms commonly associated with D fragilis infection include abdominal pain, diarrhea, anorexia, nausea, vomiting, and flatulence. Bloody stools are not observed. In a study in Belgium of 448 patients with diarrhea, D fragilis was found in 6.3%, and G lamblia was found in 7.1%. Both parasites caused diarrhea and abdominal pain, but D fragilis was less frequently associated with nausea, vomiting, and weight loss. Less common symptoms include fever, weight loss, and fatigue. Diarrhea usually lasts 1-2 weeks, whereas abdominal pain can persist for 1-2 months. Because of its very high association with pinworms, some patients can also manifest anal pruritus, lower urinary tract infection (particularly young girls), or both. Balantidiasis Most infections with B coli are asymptomatic; however, some patients experience an acute or chronic illness. When acutely affected, the patient has diarrhea with stools containing abundant mucus and blood. Patients may also have concurrent nausea, vomiting, tenesmus, and intestinal colic, resembling an amebic colitis. In most patients, recovery occurs without treatment; however, in some patients, especially those who are malnourished or immunodeficient, the course can be fulminant and fatal. Usually, the course is long term with episodes of intermittent diarrhea and constipation, with or without abdominal pain, anorexia, weight loss, and weakness. Patients may present with an appendicitislike illness, and, in some patients, amebomalike presentations occur. Extraintestinal infection is rare. Blastocystosis Many experts believe that B hominis is pathogenic only when present in large numbers, but some studies have shown that the quantity of the parasite is not predictive of the presence (or severity) of the disease. The association of these protozoa with traveler's diarrhea and disease in the normal host is controversial. A study developed in Egypt found high concentrations of B hominis in symptomatic patients compared with asymptomatic patients, suggesting that blastocystosis may be an uncommon cause of gastroenteritis and travelers diarrhea; however, convincing information suggests thatB hominis causes diarrhea in immunosuppressed patients, such as patients with renal transplants and AIDS. The most common symptoms associated with infection include abdominal discomfort, diarrhea, flatulence, and sometimes fever and bloating. A study done in

Turkey showed an association between lower anthropometric indexes and B hominis infection.

PHYSICAL
Amebic or balantidic colitis Most patients have nonlocalized abdominal tenderness, and one third of patients

have fever (usually low-grade fever). Signs of dehydration are rare with these pathogens, although they can be present in young infants. An ameboma can be palpated on the lower right abdominal quadrant, and it is usually tender and mobile. Patients with acute or fulminant colitis present with severe abdominal pain, distension, and rebound tenderness, with or without fever. The patient may also present with signs of shock. In patients with amebic liver abscess, tender hepatomegaly is present in almost 100% of cases, and fever is present in 80-90% of cases, with or without hypoventilation of the lower right lung. Peritoneal signs and jaundice are unusual but, when present, are signs of severe disease. Giardiasis In children younger than 5 years, acute giardiasis can be complicated by signs of dehydration that may lead to hospitalization. However, these events are not as prominent as with other enteropathogens, such as rotavirus or enterotoxigenic bacteria. Signs of chronic giardiasis are more subtle. The patient may show some degree of protein-energy malnutrition, with a distended abdomen but no other pathognomonic signs. Spore-forming protozoa In immunocompetent patients, clinical findings are no different than the findings associated with giardiasis. Signs of dehydration are unusual but can occur. In immunodeficient hosts, especially patients with AIDS, diarrhea has been associated with accompanying signs of protein-energy malnutrition and even signs of hypokalemia with or without hyponatremia. Some patients with acute exacerbations can also manifest acute dehydration with or without metabolic acidosis. Dientamoebiasis and blastocystosis Clinical findings of dientamoebiasis and blastocystosis are no different than those found with acute giardiasis, although signs of dehydration are less frequent. Some immunosuppressed patients with blastocystosis may present with signs of malnutrition, but these observations can be more attributable to their underlying disease than to the parasitosis itself.

CAUSES
Water and/or food contamination contributes to most, if not all, individual cases and outbreaks. Immunologic factors, such as IgA and T-cell responses, are important for giardiasis and spore-forming protozoa. Malnutrition is an important risk factor for susceptibility to all protozoa. Swine are, by far, the most important reservoir for balantidiasis.

 Dientamoebiasis is frequently associated with pinworm co-infection. For all intestinal protozoa, fecal-oral transmission is the primary route of transmission.

Human Helminth Infections

Nematode infections Enterobius vermicularis - Pinworm, Threadworm. An extremely common nematode infection, particularly in temperate areas such as Western Europe and North America, (it being relatively rare in the tropics) and particularly in children. It has been estimated that the annual incidence of infection is over 200 million, this probably being a conservative figure. Samples of caucasian children in the U. S. A. and Canada have shown incidences of infection of fro 30% to 80%, with similar levels in Europe. Ascaris lumbricoides - The Large Human Roundworm. Again the incidence rates for this parasite are very high with > 1500 million cases of infection annualy, of which ~210 million of these cases are symptomatic (* but see below). Trichuris trichuria - The Large Human Roundworm. The incidence rates for this parasite are also very high, with estimates of ~1300 million cases of infection annualy, of which >133 million of these cases are symptomatic (* again but see below). The Hookworms. These are represented by two parasites, Necator americanus in the tropics and sub tropics worlwide and the S. E. states of the U. S. A., and Ancylostoma duodenale, again with a worldwide distribution in the tropics and sub tropics as well as the Mediterranean region. In the case of these parasites there are > 1200 million cases of hookworm infection annualy, of which ~100 million of these cases are symptomatic (* again, but see below). Lymphatic filariasis - Elephatiasis This disease is caused principaly by two parasites, Wuchereria bancrofti with an annual rate of infection of ~106 million cases, and Brugia malayi with an annual rate of infection of ~12.5 million. The total number of people infected with other types of lymphatic filarial worms is much smaller, at ~1.5 million cases. These lymphatic filarial worms, (along with the related filarial parasiteOnchocerca volvulus, are unusual among the nematodes in that they deveope with, and are transmitted by insect vector intermediate hosts. Onchocerca volvulus - River Blindness. The incidence rates for this parasite are not as high as some of the previously described parasites, with an annual rate of infection of ~18 million, but due to the extreme pathology associated with this parasite, often with all adult members of affected villages losing their sight, along with severe skin conditions. Dracanculus medinensis - Guinea Worm. The incidence rates for this parasite are much lower, with an estimated annual rate of infection of ~100 000. This is much lower than in the recent past, when up to 50 million people were infected, and this

reduction illustrates how successfull helminth control programs can be effective in reducing the disease caused by these organisms. Other important nematode infections include Trichinella spiralis, Strongyloides stercoralis, and a number of more rare infections. Nematodes that normally infect other animals may still cause disease in man. These include Toxocara canis and a number of nematodes causing Anisakiasis. Digenean Trematode Infections Schistosomiasis - Bilharzia. This disease is the focus of this parasitology web site, and in terms of morbidity and mortality is the most important human helminthiasis. The numbers infected are lower than those of many of the nematode infections, with an estimated annual incidence of infection of > 200 million cases. In terms of active disease however the parasite is much more important, with an estimated annual mortality rate of ~1 million deaths directly due to infection with these parasites. Opisthorchis sinensis - The Chinese Liver Fluke This is also a very important trematode infection, with an estimated annual incidence of infection of ~20 - 30 million cases, mostly in the Far East, in Japan, China, Taiwan and South East Asia. Paragonimus sp. - The Lung Fluke This fluke causes a pulmonary disease, the adult parasites living in the lungs of their definitive hosts (e.g. man). There are a number of different species of this parasite, the most well documented being P. westermani in the Far East. Here it may be locally very common, with up to 40 to 50% of the population infected. There are a number of other digenean trematode infections. These include various Echinostomeinfections as well as a number of other flukes, described in a seperate Human fluke page within this site. In addition there are a number of these parasites that usually infect domesticated animals, but are also cause well known human infections as well. These include Fasciola hepaticaand Dicrocoelium dendriticum. Cestode (Tapeworm) Infections Taenia saginata - The Beef Tapeworm This only causes very limited pathology in man, but the anual incidence of infection is high, at an estimated 50 million cases. Taenia solium - The Pork Tapeworm This has a similar estimated annual incidence of infection of ~50 million cases. However in this case the consequences may be more severe, due to the added risk of contracting infection with the larval metacestode, (cysticercosis). This may have extreme consequences in terms of the pathology associated with infection, with an estimated annual mortality rate of ~50 000 deaths. For the Cestodes these annual incidence rates are based on detection of infection with the adult parasite. This is achieved by examination of faeces, urine or sputum for parasite eggs . Diagnosis of infection with larval metacestode parasites, such as Echinococcus sp. is very difficult, due to the lack of non invasive diagnostic techniques. It is in consequence very difficult to estimate annual rates of infection, even though these metacestodes may be very important pathogens.

References
1. Sargeaunt PG, Jackson TFGH, Simjee AE. Biochemical homogeneity of
Entamoeba histolytica isolates, especially those from liver abscess. Lancet. 1982;1:1386-8.

2. Carranza PG, Lujan HD. New insights regarding the biology of Giardia
lamblia. Microbes Infect. Sep 20 2009

3. Muller N, von Allmen N. Recent insights into the mucosal reactions associated
with Giardia lamblia infections. Int J Parasitol. Nov 2005;35:1339-47.

4. Karanis P, Kourenti C, Smith H. Waterborne transmission of protozoan parasites:

a worldwide review of outbreaks and lessons learnt.J Water Health. Mar 2007;5:1-38.

5. Hunter PR, Thompson RC. The zoonotic transmission of Giardia and

Cryptosporidium. Int j Parasitol. Oct 2005;35:1181-90.

6. Fleming CA, Caron D, Gunn JE, Barry MA. A foodborne outbreak of Cyclospora
cayetanensis at a wedding: clinical features and risk factors for illness. Arch Intern Med. May 25 1998;158(10):1121-5.

7. Huang P, Weber JT, Sosin DM, et al. The first reported outbreak of diarrheal
illness associated with Cyclospora in the United States.Ann Intern Med. Sep 15 1995;123(6):409-14.

8. Vandenberg O, Peek R, Souayah H, et al. Clinical and microbiological features of

dientamoebiasis in patients suspected of suffering from a parasitic gastrointestinal illness: a comparison of Dientamoeba fragilis and Giardia lamblia infections. Int J Infect Dis. May 2006;10(3):255-61.

9. Graczyk TK, Shiff CK, Tamang L, et al. The association of Blastocystis hominis
and Endolimax nana with diarrheal stools in Zambian school-age children. Parasitol Res. Dec 2005;98(1):38-43.

10. Ertug S, Karakas S, Okyay P, Ergin F, Oncu S. The effect of Blastocystis hominis on the growth status of children. Med Sci Monit. Jan 2007;13:CR40-3.

Catanduanes State Colleges COLLEGE OF HEALTH SCIENCES DEPARTMENT OF NURSING Virac, Catanduanes

Project In
Microbiology Parasitology
Prepared by:

and

MARIA TERESA Q. DELA ROSA

BSN 2A, Group 4

Submitted to:

ROSEL T. IBARDALOZA
Professor