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Human Protozoal Infections

Although all infectious agents in humans are parasites, by convention, parasiticdiseases are defined as those caused by protozoa or helminths. The old classification, in

which a single phylum of protozoa encompassed all unicellular eukaryoticmicroorganisms, is no longer valid because of new ultrastructural and molecular taxonomic information.

For instance, Giardia lamblia has been shown to lack mitochondria and shown tocontain ribosomal RNA sequences that resemble bacteria. These protozoa have beenproposed to represent an evolutionary transition between prokaryotic and eukaryoticmicroorganisms. Both Giardia and Microsporidia(which also shares similarities with

bacteria) have been reclassified as Archezoa, a term that reflects their evolutionarytransitional nature. Clinicians can best classify unicellular eukaryotic microorganismsbased on mode of transmission.

The classification of representative protozoa according to modes of transmissionis 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 beenassociated with gastroenteritis.

Among all intestinal protozoa, those listed in Table 1 have been confirmed tocause 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 Mode of Transmission Symptoms

Flagellates

G lamblia Contaminated water,fecal-oral

Nausea, bloating, gas, diarrhea, anorexia

Dientamoeba fragilis Fecal-oral, associated

with Enterobius

Previously thought commensal; may cause

diarrhea, abdominal, pain, nausea

Amebas

Entamoeba histolytica Contaminated water,

fecal-oral, contaminated

Colitis, dysentery, diarrhea, liver abscess,

other extraintestinal disease

http://emedicine.medscape.com/article/998168-overview






food

Spore-forming (Coccidia)

Cryptosporidium parvum Contaminated water,

swimming pools, fecal-oral

Immunocompetent patients: Self-limited

diarrhea Immunosuppressed patients:Severe and interminable diarrhea

Isospora belli Fecal-oral Same as in Cryptosporidium

Cyclospora cayetanensis Fecal-oral, contaminated

water and food

Same as in Cryptosporidium

Microsporidia (Septata

intestinalis, Enterocytozoon

bieneusi)

Fecal-oral, contaminated

water

Same as in Cryptosporidium

Ciliates

Balantidium coli Fecal-oral (frequently

associated with pigs)

Colitis, diarrhea

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 verysimilar, with the exception of D fragilis, which lacks a cyst stage.

Mechanisms of diarrhea production by intestinal protozoa are related to directcytotoxic effects, the ability to invade, and/or effects of the immune response on theintestinal epithelium. No evidence suggests that intestinal protozoa produceenterotoxins.

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 thetissue (pathogenic amebas) or are eliminated in the stools. Trophozoites do not surviveoutside the body. This parasite was named for its remarkable ability to lyse humantissues. A prerequisite to amebic invasion is the parasite's ability to colonize andpenetrate 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 associatedinconsistently with invasiveness.



In 1982, Sargeaunt postulated that instead of pathogenic and nonpathogeniczymodemes, 2 different amebas were present.[1] The concept of

E histolyticaas apathogenic ameba and E dispar

as a nonpathogenic ameba is currently accepted.Furthermore, both immunologic assays and amplification tests have been developed todistinguish these two species among symptomatic and asymptomatic patients. Uponinvasion of the host, amebas are capable of killing immune effector cells by contact-

dependent cytolysis, possibly by a calcium-dependent mechanism. They thendisseminate 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, rapidlymultiplies, and attaches to the small intestinal villi.[2] Mature infective cysts pass in fecesand complete the cycle. The pathogenesis of diarrhea in giardiasis is thought to berelated to the following factors: (1) the number of organisms ingested, (2) specific strainingested, (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 specificreceptors on the intestinal cell and may be partly responsible for the tight attachmentbetween the parasite and the villi, which is followed by mucosal damage, mechanicalobstruction (only caused in the presence of numerous organisms), and deconjugation of

bile salts. Recent data has indicated that inflammatory mast cells may interfere withduodenal growth of

G lamblia trophozoites. [3] Other inflammatory cells, as well as CD8+ Tcells, contribute to villus-shortening and crypt hyperplasia.

Strains that infect humans are biologically diverse, as shown by differences inantigens, restriction endonuclease patterns, DNA fingerprinting, isoenzyme patterns, andpulsed-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 pathogenicmechanism.

Spore-forming protozoa

Spore ingestion begins a life cycle that is similar in all 4 of the intestinal spore-forming protozoa (see Table 1). The ingested spores release sporozoites that invade

enterocytes, primarily in the small intestine. The enterocyte infection progresses through2 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 isnot exposed repeatedly to the organism.

The sporogonic (ie, gametogonic, sexual) stage involves the maturation anddevelopment 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 spore-forming protozoa are obligate intracellular pathogens. Infection by these protozoa has



been associated with substantial alterations in intestinal structure and function, but thepathogenesis of the predominant symptom, diarrhea, is not completely understood.

Cryptosporidiosis is the best-studied spore-forming diarrhea, and its pathogenicmechanisms can also be related to other spore-forming protozoa. The hypothesizedsequence of events is explained below.

After invasion of the enterocytes, the epithelial cells release cytokines. Thesecytokinins activate phagocytes and recruit new leukocytes, which, in turn, releasesoluble 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-formingprotozoa 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 containingDfragilis trophozoites are ingested and, by this mechanism, resist the acid pH in thestomach. It is not invasive and mostly inhabits the large intestine. The exactmechanisms of diarrhea are not known.

Balantidium coli

The cyst is the infectious stage and is acquired by ingestion of contaminated foodor water. After excystation in the small intestine, the trophozoites colonize the terminalileum 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 largenumbers 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 lifecycle in humans. Cysticlike stages are rare and have been found in patients withacquired immunodeficiency syndrome (AIDS) and in vitro. The mechanisms of how thisparasite causes illness have not been elucidated yet.

HISTORYThe 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 severelyimmunosuppressed with spore-forming protozoal infections).

Amebiasis Noninvasive intestinal infection: Noninvasive amebiasis most frequently producesno symptoms. Nevertheless, some patients may have some ill-defined GI tract



symptoms. These symptoms include alternating periods of mild diarrhea andconstipation with or without mild abdominal pain; however, for the most part, patientstolerate the infection. Intestinal amebiasis or amebic colitis: Patients typically have 1-3 weeks of diarrhea to grossly bloody dysenteric stools with abdominal pain. Constitutionalsymptoms are often mild, and fever is present only in about 10-20% of cases;

however, weight loss is common. Some patients manifest chronic nondysentericdiarrhea, combined with months or even years of abdominal pain associated withvarying 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 inappropriatelytreated with corticosteroids. The patient develops sudden constipation following anacute 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 usuallyreport 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 onlyin severe cases.

Giardiasis Following excystation and colonization, a spectrum of clinical manifestations canoccur. Symptomatic infections are noted more frequently in children than in adults. Asymptomatic excretion: The asymptomatic carrier rate of

G lamblia in the UnitedStates is estimated to be 3-7% but is as high as 20% in southern regions andpossibly 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 moreoften with significant illness. Most patients have symptoms within 10 days of exposure, and more than 90% of patients have symptoms within 3 weeks. The usualsymptoms are short-lasting acute diarrhea (with or without low-grade fever), nausea,abdominal distension, greasy stools, and anorexia. Acute giardiasis mayspontaneously resolve. Parasites disappear from the stools within 4-6 weeks in bothexperimental and naturally acquired infections; however, giardiasis can sometimesoccur 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. Abdominaldistension, sulfurous belching, flatulence, epigastric pain, substernal burning,

nausea, anorexia, and failure to thrive may occur. Although severe forms of chronicgiardiasis may occur in otherwise healthy individuals, they are common in patientswith hypoglobulinemia, particularly IgA deficiency in association with lymphoidhyperplasia of the bowel. Chronic giardiasis may contribute to protein-energymalnutrition in children. Protein-losing enteropathy has also been described.Intestinal disaccharidase deficiency associated with giardiasis can be manifested bycarbohydrate intolerance, especially lactose. Evidence suggests that giardiasis maybe associated with chronic urticaria, gallbladder disease, and treatment failuresbecause of malabsorption of antibiotics during episodes of otitis media.



Spore-forming protozoa Asymptomatic infections: Asymptomatic infection is part of the clinical spectrumof disease produced by these parasites. Asymptomatic infections with cryptosporidiaoccur in normal and immunodeficient hosts. Some data suggest that asymptomaticcarriage of microsporidia in patients with AIDS may precede wasting and diarrhealillness. In one study, only 11-18% of immunocompetent Peruvian children with acute

cyclosporal infections had diarrhea. The reported frequency of asymptomaticinfection is controversial, especially withmicrosporidia, Isospora, and Cyclospora. The link between infection and clinicallyapparent disease is strong; however, the frequency that asymptomatic infection isidentified depends on the sensitivity of the assay used to detect the parasite. Acute infectious diarrhea in immunocompetent hosts: Acute diarrhea inimmunocompetent hosts has been shown to be a predominant clinical manifestationof 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 thatmicrosporidia infection may cause clinical symptoms during the early stages of

infection that resolve even though the microsporidia persist. Many studies reportacute diarrhea in infants and children living in underdeveloped countries, medicalpersonnel, travelers, and persons in institutions. In March 1993, the municipal water supply in Milwaukee becamecontaminated with cryptosporidia, and an estimated 403,000 residents developeddiarrhea. In normal hosts, infections bycryptosporidia, 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 thatcryptosporidiosis can cause recurrence of gastrointestinal symptoms in as many as40% 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 andprolonged infections in patients who are immunodeficient. Most reported cases arein patients with AIDS, but reports document severe cryptosporidia infections inpatients with renal transplantation and persons with IgA deficiency. Isosporiasis hasbeen reported in persons with cancer. The symptoms range from asymptomatic infection to severe life-threateningdiarrhea, dehydration and chronic malabsorption leading to lethargy, failure tothrive, and malnutrition. The clinical features of 128 patients with AIDS-related cryptosporidiosisshowed the following 4 patterns of disease: transient (29%), chronic (60%),

fulminant (8%), and asymptomatic (4%).

As mentioned above, more severe cases of cryptosporidiosis andmicrosporidiosis 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 documentedfever. The physiopathogenesis of this syndrome is multifactorial, from



hypermetabolism, decreased oral intake, and cytokine dysregulation, to thecoparticipation of various pathogens in which spore-forming protozoa are included. The advent of highly active antiretroviral therapy (HAART) has decreased thefrequency 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 hasbeen reported with cryptosporidium, Isospora, and microsporidia leading to rightupper quadrant abdominal pain, occasionally with jaundice and fever. Invasion by Sintestinalis

beneath the epithelial surface and dissemination to the liver, respiratorytract, 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 weightloss. Less common symptoms include fever, weight loss, and fatigue. Diarrhea usually lasts 1-2 weeks, whereas abdominal pain can persist for 1-2months. Because of its very high association with pinworms, some patients can alsomanifest anal pruritus, lower urinary tract infection (particularly young girls), or both.

Balantidiasis Most infections with B coli

are asymptomatic; however, some patients experiencean acute or chronic illness. When acutely affected, the patient has diarrhea with stools containing abundantmucus 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 befulminant and fatal. Usually, the course is long term with episodes of intermittentdiarrhea and constipation, with or without abdominal pain, anorexia, weight loss, andweakness. 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 largenumbers, but some studies have shown that the quantity of the parasite is notpredictive of the presence (or severity) of the disease.

The association of these protozoa with traveler's diarrhea and disease in thenormal host is controversial. A study developed in Egypt found highconcentrations of B hominis in symptomatic patients compared withasymptomatic patients, suggesting that blastocystosis may be an uncommoncause of gastroenteritis and travelers diarrhea; however, convincing informationsuggests thatB hominis causes diarrhea in immunosuppressed patients, such aspatients with renal transplants and AIDS.

The most common symptoms associated with infection include abdominaldiscomfort, diarrhea, flatulence, and sometimes fever and bloating. A study done in



Turkey showed an association between lower anthropometric indexes and Bhominis infection.

PHYSICAL Amebic or balantidic colitis

Most patients have nonlocalized abdominal tenderness, and one third of patientshave fever (usually low-grade fever). Signs of dehydration are rare with these pathogens, although they can bepresent in young infants. An ameboma can be palpated on the lower right abdominal quadrant, and it isusually 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 almost100% of cases, and fever is present in 80-90% of cases, with or withouthypoventilation 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 asprominent as with other enteropathogens, such as rotavirus or enterotoxigenicbacteria. Signs of chronic giardiasis are more subtle. The patient may show some degreeof protein-energy malnutrition, with a distended abdomen but no other pathognomonicsigns.

Spore-forming protozoa In immunocompetent patients, clinical findings are no different than the findingsassociated with giardiasis.

Signs of dehydration are unusual but can occur. In immunodeficient hosts, especially patients with AIDS, diarrhea has beenassociated 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 dehydrationwith or without metabolic acidosis.

Dientamoebiasis and blastocystosis Clinical findings of dientamoebiasis and blastocystosis are no different than thosefound 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 underlyingdisease 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 giardiasisand 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 Europeand North America, (it being relatively rare in the tropics) and particularly in children. It has beenestimated that the annual incidence of infection is over 200 million, this probably being a conservativefigure. 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 worlwideand the S. E. states of the U. S. A., and Ancylostoma duodenale, again with a worldwide distribution inthe tropics and sub tropics as well as the Mediterranean region. In the case of these parasites thereare > 1200 million cases of hookworm infection annualy, of which ~100 million of these cases aresymptomatic (* 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. Thetotal 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 parasiteOnchocercavolvulus, are unusual among the nematodes in that they deveope with, and are transmitted by insectvector 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 thisparasite, often with all adult members of affected villages losing their sight, along with severe skinconditions.

Dracanculus medinensis - Guinea Worm.

The incidence rates for this parasite are much lower, with an estimated annual rate of infection of ~100000. 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 thedisease caused by these organisms.

Other important nematode infections include Trichinella spiralis, Strongyloides stercoralis, and anumber of more rare infections. Nematodes that normally infect other animals may still cause diseasein 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 themost important human helminthiasis. The numbers infected are lower than those of many of thenematode 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 documentedbeing P. westermani

in the Far East. Here it may be locally very common, with up to 40 to 50% of thepopulation infected.

There are a number of other digenean trematode infections. These includevarious Echinostomeinfections as well as a number of other flukes, described in a seperate Humanfluke page within this site. In addition there are a number of these parasites that usually infectdomesticated 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 anestimated 50 million cases.

Taenia solium - The Pork Tapeworm

This has a similar estimated annual incidence of infection of ~50 million cases. However in this casethe consequences may be more severe, due to the added risk of contracting infection with the larvalmetacestode, (cysticercosis). This may have extreme consequences in terms of the pathologyassociated 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 adultparasite. 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 lackof 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.



References1. 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 Giardialamblia. Microbes Infect . Sep 20 2009

3. Muller N, von Allmen N. Recent insights into the mucosal reactions associatedwith 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 andCryptosporidium. Int j Parasitol . Oct 2005;35:1181-90.

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

7. Huang P, Weber JT, Sosin DM, et al. The first reported outbreak of diarrhealillness associated with Cyclospora in the United States. Ann Intern Med . Sep 151995;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 lambliainfections. Int J Infect Dis. May 2006;10(3):255-61.

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

10. Ertug S, Karakas S, Okyay P, Ergin F, Oncu S. The effect of Blastocystis hominison 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 and

Parasitology

Prepared by:

MARIA TERESA Q. DELA ROSABSN 2A, Group 4

Submitted to:

ROSEL T. IBARDALOZAProfessor

project micro

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