INTESTINAL PROTOZOA

The Prokaryotes:Domains Bacteria and Archaea 11

Eukaryotic Unicellular Chemoheterotrophs Vegetative form is a trophozoite. Asexual reproduction is by fission,budding, or schizogony. Sexual reproduction by conjugation. Some produce cysts. Protozoa Figure 12.16

No mitochondria Multiple flagella Giardia lamblia Trichomonas vaginalis (no cyst stage) Archaezoa Figure 12.17b–d

No mitochondria Nonmotile Intracellular parasites Nosema Microspora

Move by pseudopods Entamoeba Acanthamoeba Amoebozoa Figure 12.18a

Nonmotile Intracellular parasites Complex life cycles Plasmodium Babesia Cryptosporidium Cyclospora Apicomplexa

2 3 8 7 6 Plasmodium Figure 12.19

Move by cilia Complex cells Balantidium coli is the only human parasite. Figure 12.20 Ciliophora (Ciliates)

Move by flagella Photoautotrophs Euglenoids Chemoheterotrophs Naegleria: Flagellated and amoeboid forms; causes meningoencephalitis. Trypanosoma: Undulating membrane, transmitted by vectors. Leishmania: Flagellated form in sand fly vector, ovoid form in vertebrate host. Euglenozoa

Why are these studied with algae and protozoa? Dinoflagellates Figure 12.14

INTESTINAL PROTOZOA Ameba Flagellates Ciliates Intestinal Coccidia, Microsporidia, and Blastocystis hominis

Entamoebahistolytica ,[object Object]

Site in host:lumen & wall of LI

Source of infection:cysts in food & water, from fecesAMEBA

Causal Agent:Entamoebahistolytica pathogenic ameba associated with intestinal and extraintestinal infections. Amoebiasis

Cysts and trophozoites are passed in feces . ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine - trophozoitesare released, which migrate to the large intestine. The trophozoites multiply by binary fission - produce cysts , and both stages are passed in the feces . Pathogenecity

Cysts and trophozoites are passed in feces . ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . protection by their walls, the cysts can survive days to weeks in the external environment Pathogenecity

trophozoitesremain confined to the intestinal lumen ( noninvasive infection) individuals who are asymptomatic carriers, passing cysts in their stool. trophozoitesinvade the intestinal mucosa (intestinal disease) through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (extraintestinal disease), Pathogenecity

E. histolytica morphologically ingested red blood cells (erythrophagocystosis) Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). Pathogenecity

Worldwide, with higher incidence of amebiasis in developing countries. In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations. Geographic Distribution:

asymptomatic infection ("luminal amebiasis") invasive intestinal amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas) invasive extraintestinalamebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions). Clinical Features:

Fresh stool: wet mounts and permanently stained preparations (e.g., trichrome) Concentrates from fresh stool: wet mounts, with or without iodine stain, and permanently stained preparations E. histolyticatrophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery. Laboratory Diagnosis:

Microscopy Immunodiagnosis Molecular methods for discriminating between E. histolytica and E. dispar Morphologic comparison with other intestinal parasites Bench aid for E. histolytica Diagnostic findings:

Trophozoite:small, usually central karyosome; finely granular chromatin

Trophozoite with ingested RBCs

Cyst:4 nuclei in mature cyst; rod-like chromatoid bodies

Gross pathology of liver containing amebic abscess

Gross pathology of amebic abscess of liver. Tube of "chocolate" pus from abscess.

Entamoeba hartmanni Trophozoite: small, usually eccentric karyosome; finely granular chromatin

Cyst:4 nuclei in mature cyst; rod-like chromatoid bodies (6-8 um, smaller than E. histolytica cysts)

Entamoeba coli Trophozoite: 1 nucleus with large eccentric karyosome; coarse, irregular peripheral chromatin

Cyst:8 nuclei in mature cyst; splinter-like chromatoid bodies w/ pointed ends large, eccentric karyosome

Endolimax nana Trophozoites:1 nucleus w/ large, irregularly shaped, blot-like karyosome; has no peripheral chromatin; cytoplasm is granular and vacuolated

Cyst: mature cyst w/ 4 nuclei with large, blot-like karyosomes; no have chromatoid bodies

Iodamoeba butschlii Trophozoite: 1 nucleus w/ large, usually central karyosome surr by refractile, achromatic granules; cytoplasm coarsely granular, vacuolated & can contain bacteria, yeasts

Cyst: one nucleus with a large, usually eccentric karyosome; no chromatoid bodies but have a compact, well defined glycogen mass; shape varies from ovoidal to rounded.

For asymptomatic infections, iodoquinol, paromomycin, or diloxanidefuroate are the drugs of choice. For symptomatic intestinal disease, or extraintestinal, infections (e.g., hepatic abscess) the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanidefuroate. Treatment:

Balantidium coli ,[object Object]

Source of infection:stool (cysts)

Lab Dx: cysts/trophs in stoolCILIATES

Causal Agent Balantidium coli, a large ciliated protozoan parasite. Geographic Distribution: Worldwide. Because pigs are an animal reservoir. Other reservoirs include rodents and nonhuman primates. Balantidiasis

cysts – infective stage ingestion of contaminated food or water Life cycle

excystation occurs in the small intestine- trophozoitescolonize the large intestine Trophozoites undergo encystation to produce infective cysts . Some trophozoites invade the wall of the colon and multiply. Mature cysts are passed with feces . Life cycle

Most cases are asymptomatic. Clinical manifestations, when present, include persistent diarrhea occasionally dysentery abdominal pain weight loss. Symptoms can be severe in debilitated persons. Clinical Features:

trophozoites - stool specimens or in tissue Cysts are less frequently encountered. Laboratory Diagnosis:

Trophozoites: large size (50-70 µm); rows of cilia on the cell surface; a cytostome; a bean shaped macronucleus and a smaller, less conspicuous micronucleus

Cyst: spherical to oval; cilia present in the young cyst but are absent in older forms; large, kidney-shaped macronucleus & contractile vacuoles in cytoplasm

The drug of choice is tetracycline*, with metronidazole* and iodoquinol* as alternatives. Tetracycline is contraindicated in pregnancy and in children less than 8 years old. Treatment:

Currently classified as an amoebaBlastocystis hominis

Blastocystishominis Geographic Distribution:Worldwide. Causal Agent:

thick-walled cyst present in the stools (fecal-oral route) cysts infect epithelial cells of the digestive tract and multiply asexually Vacuolar forms - give origin to multi vacuolar and ameboidforms multi-vacuolar -- pre-cyst -- thin-walled cyst (autoinfection) ameboid-- pre-cyst --thick-walled cyst Life Cycle:

can cause both asymptomatic and symptomatic symptoms of illness including watery diarrhea, abdominal pain, perianalpruritus, and excessive flatulence. Clinical Features:

Cyst-like forms appear round with large, central vacuole-like body. The nuclei in the peripheral cytoplasmic rim are clearly visible, staining purple.

metronidazoleor iodoquinol Treatment:

Giardiaduodenalis (lamblia) ,[object Object]

Source of infection:cysts in food & water, from feces

Lab Dx: cysts/trophs in stool; IFA stain; Enterotest

Note: may be sexually transmittedFLAGELLATES

Causal Agent: Giardiaintestinalis Giardialamblia Geographic Distribution:Worldwide, more prevalent in warm climates, and in children. Giardisis

Cysts for transmission Both cysts and trophozoites can be found in the feces (diagnostic stages) . Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . Life Cycle:

(small intestine) excystation Trophozoites multiply (lumen of the proximal small bowel )-- free or attached to the mucosa by a ventral sucking disk . Encystation(colon). cyst (nondiarrhealfeces ) Life Cycle:

The spectrum varies from asymptomatic carriage to severe diarrhea and malabsorption Acute giardiasis develops after an incubation period of 1 to 14 days (average of 7 days) and usually lasts 1 to 3 weeks Symptoms include diarrhea, abdominal pain, bloating, nausea, and vomiting. In chronic giardiasis the symptoms are recurrent and malabsorption and debilitation may occur. Clinical Features:

Trophozoite: pyriform shape w/ 2 nuclei & a large, central karyosome; large ventral sucking disc, 4 pairs of flagella, 2 curved median bodies

Cysts: ellipsoid shape w/ 2 nuclei each (more mature ones will have four); lengthwise running central fibrils; short fibers laterally or obliquely across fibrils in lower half of cyst

metronidazoleand tinidazole. Nitazoxanide(giardiasisin children) Treatment:

INTESTINAL COCCIDIA, MICROSPORIDIA, and BLASTOCYSTIS HOMINIS

Cryptosporidium parvum ,[object Object]

Transmission: contaminated food or water by person to person contact

Lab Dx: Modified acid fast stain of a fecal smear; PCR; IFA,[object Object]

Causal Agent:Cryptosporidium parvum and Cryptosporidium hominisare (most prevalent species) Geographic Distribution:first reports of human cases in 1976, worldwide. Waterborne outbreak in Milwaukee (Wisconsin) in 1993, that affected more than 400,000 people. Crytosporidiosis

Sporulatedoocysts, containing 4 sporozoites-- excreted by the infected host through feces and possibly other routes such as respiratory secretions . Transmission occurs mainly through contact with contaminated water (e.g., drinking or recreational water). food sources outbreaks U S -- waterparks, community swimming pools, and day care centers. Zoonotic and anthroponotictransmission Life cycle

Life cycle Following ingestion (and possibly inhalation) Excystation-- sporozoitesare released --parasitize gastrointestinal AND respiratory tract. asexual multiplication (schizogony or merogony) -- sexual multiplication (gametogony) -- producing microgamonts (male) and macrogamonts (female)

Life cycle Upon fertilization -- oocysts that sporulate in the infected host Two different types of oocysts are produced thick-walled, which is commonly excreted from the host thin-walled oocyst , which is primarily involved in autoinfection.

asymptomatic infections severe, life-threatening illness incubation period is an average of 7 days (2 to 10 days). Watery diarrhea is the most frequent symptom accompanied by dehydration, wt loss, abd. pain, fever, n/v immunocompetent persons, symptoms are usually short lived (1 to 2 weeks-- can be chronic and more severe in immunocompromised patients, especially those with CD4 counts <200/µl. Clinical Features:

asymptomatic infections severe, life-threatening illness incubation period is an average of 7 days (but can range from 2 to 10 days). Watery diarrhea is the most frequent symptom, and can be accompanied by dehydration, weight loss, abdominal pain, fever, nausea and vomiting. Clinical Features:

Clinical Features: In immunocompetent persons, symptoms are usually short lived (1 to 2 weeks); they can be chronic more severe in immunocompromised patients, especially those with CD4 counts <200/µl. also found in other digestive tract, lungs, and conjunctiva.

Treatment: Rapid loss of fluids -- fluid and electrolyte replacement. healthy, immunocompetent persons (self-limited)-- Nitazoxanide Immunocompromisedand high risk pt.-- nitazoxanide is unclear. For persons with AIDS, anti-retroviral therapyis encourage

Laboratory Diagnosis: Acid-fast staining methods immunofluorescencemicroscopy method of choice (followed closely by enzyme immunoassays)

Oocysts are rounded, 4.2 µm - 5.4 µm in diameter. Sporozoites are visible inside the oocysts, indicating that sporulation has occurred.

Oocysts stained by the modified acid-fast method: against a blue-green background, the oocysts stand out in a bright red stain. Sporozoites are visible inside the two oocysts to the right.

Oocysts of C. parvum (upper left) and cysts of Giardia intestinalis (lower right) labeled with immunofluorescent antibodies.

Cyclosporacayetanensis ,[object Object]

Transmission: contaminated water

Lab Dx: Modified acid fast stain of a fecal smear,[object Object]

Sporulation of Cyclospora oocysts. The sequence shows, as observed by DIC microscopy of wet mounts: an oocyst passed in fresh stool (Day 0); sporulated oocysts at days 5 (Day 5) and 10 (Day 10), which both contain 2 sporocysts; and a ruptured oocyst (Rupture), with a sporocyst still inside the oocyst and the other sporocyst just outside the coiled sporozoites are barely visible inside the sporocysts.

Causal Agent:unicellular coccidian parasite- Cyclosporacayetanensis Geographic Distribution: most common in tropical and subtropical areas 1990, foodborneoutbreaks of cyclosporiasis, 3600 persons, in the United States and Canada.

sporulation -- sporont -- two sporocysts (contains 2 sporozoites) sporulatedoocysts are ingested (in contaminated food or water) oocystsexcyst in the gastrointestinal tract-- sporozoites invade the small intestine asexual multiplication and sexual development -- oocysts Life Cycle:

Clinical Features: incubation period of 1 week—severe watery diarrhea s/sx- anorexia, wt loss, abd. pain, N/V, myalgias, low-grade fever, and fatigue. Untreated infections typically last for 10-12 weeks -- follow a relapsing course. In disease-endemic settings -- asymptomatic.

identification of oocysts in stool specimens Laboratory Diagnosis:

combination of two antibiotics, trimethoprim-sulfamethoxazole*, also known as Bactrim, Septra, or Cotrim. Supportive measures include management of fluid and electrolyte balance, and rest. Treatment:

Isospora belli ,[object Object]

Transmission: hand to mouth or through contaminated food or water

Lab Dx: wet mount of formalin-ethyl acetate conc. of fecal sample; modified acid fast stain,[object Object]

Causal Agent:coccidian parasite, Cystoisospora belli, is the least common of the three intestinal coccidia Geographic Distribution:Worldwide, especially in tropical and subtropical areas. Infection occurs in immunodepressedpt. and outbreaks in institutionalized groups in US

infection occurs by ingestion of sporocysts-containing oocysts sporocystsexcyst in the small intestine -- release their sporozoites, which invade the epithelial cells -- initiate schizogony . Life Cycle:

acute, nonbloody diarrhea with crampyabdpain (weeks)--malabsorption& wt loss. immuno-depressed patients , infants & children—severe diarrhea. Eosinophilia Clinical Features:

Microscopic wet mounts by bright-field, differential interference contrast (DIC), and epifluorescence modified acid-fast stain. Laboratory Diagnosis:

Trimethoprim-sulfamethoxazole is the drug of choice. Treatment:

Dientamoebafragilis - NO cyst stage ,[object Object]

may possess some pathogenicity

Source of infection: stool (trophs),[object Object]

Causal Agent:Dientamoebafragilis is not an ameba but a flagellate. parasite produces trophozoites; cysts have not been identified. Geographic Distribution:Worldwide.

the trophozoite is the only stage in stools Trophozoites have characteristically one or two nuclei Life Cycle:

children –intermittent diarrhea, abd pain, n/v, anorexia, fatigue, malaise, poor wt gain Clinical Features:

detection of trophozoites in permanently stained fecal smears (e.g., trichrome). Laboratory Diagnosis:

Nucleus: cluster of granules, with no peripheral chromatin; size range 5-15 µm.

The drug of choice is iodoquinol Paromomycin*, tetracycline*, (contraindicated in children under age 8, pregnant and lactating women) or metronidazole can also be used. Treatment:

Microsporidia ,[object Object]

Genera found in humans:Enterocytozoon, Encephalitozoon, Pleistophora, Nosema, & Microsporidium

Affects immunologically compromised hosts

E. bieneusi: found only in humans & most frequent cause of microsporidian enteritis in AIDS patients

Lab Dx: Modified trichrome stain ; PCR,[object Object]

Stool smear stained with Chromotrope 2R containing Enterocytozoon bieneusi spores. Black arrows indicate E. bieneusi spores with their belt-like stripe visible. Red arrow indicates an unidentified yeast. The yellow arrow indicates a vacuolated spore.

Stool smear stained with Quick-Hot Gram Chromotrope stain containing Enterocytozoon bieneusi spores. Black arrows indicate E. bieneusi spores with their belt-like stripe visible. The red arrow indicates an unidentified yeast. The yellow arrow indicates a vacuolated spore.

OTHER PROTOZOA BLOOD and TISSUE PROTOZOA Plasmodium Babesia Trypanosomabrucei Trypanosomacruzi Toxoplasmagondii Leishmania

PROTOZOA FROM OTHER BODY SITES Free-living Amebae Naegleria Acanthamoeba Trichomonasvaginalis

PLASMODIUM Disease: Malaria P. vivax: Benign tertian malaria P. malariae: Quartan malaria P. falciparum: Malignant tertian malaria P. ovale: Ovale tertian malaria Lab Dx: Giemsa stained thick and thin blood smears; IFA; PCR

Infected RBC: P. vivax and P. ovale: reticulocytes P. malariae: senescent erythrocytes P. falciparum: erythrocytes of all ages Cyclic paroxysm of fever: P. vivax and P. ovale: every 48 hours P. malariae: every 72 hours P. falciparum: every 36-48 hours

P. falciparum: Blood Stage Parasites Thin Blood Smears Fig. 1: Normal red cell; Figs. 2-18: Trophozoites (among these, Figs. 2-10 correspond to ring-stage trophozoites); Figs. 19-26:Schizonts (Fig. 26 is a ruptured schizont); Figs. 27, 28: Mature macrogametocytes (female); Figs. 29, 30: Mature microgametocytes (male).

Gametocytes of P. falciparum in thin blood smears. Note the presence of a “Laveran’s bib”, which is not always visible.

P. falciparum rings have delicate cytoplasm and 1 or 2 small chromatin dots. Red blood cells (RBCs) that are infected are not enlarged; multiple infection of RBCs more common in P. falciparum than in other species. Occasional appliqué forms (rings appearing on the periphery of the RBC) can be present.

P. falciparum schizonts: seldom seen in peripheral blood. Mature schizonts have 8 to 24 small merozoites; dark pigment, clumped in one mass.

P. malariae schizonts: have 6 to 12 merozoites with large nuclei, clustered around a mass of coarse, dark-brown pigment. Merozoites can occasionally be arranged as a rosette pattern.

P. malariae trophozoites: have compact cytoplasm and a large chromatin dot. Occasional band forms and/or "basket" forms with coarse, dark-brown pigment can be seen.

P. vivax gametocytes: round to oval with scattered brown pigment and may almost fill the red blood cell (RBC). RBCs are enlarged 1 1/2 to 2 × and may be distorted. Under optimal conditions, Schüffner's dots may appear more fine than those seen in P. ovale.

Rex Karl S. Teoxon, R.N, M.D 133 Vector: (night biting) anopheles mosquito minimus flavire

134 SIGNS AND SYMPTOMS Fever, chills, profuse sweating, convulsion, Anemia and fluid and electrolytes imbalance, hepatomegaly, splenomegaly Dx: blood extraction (extract blood at the height of fever) thin and thick smear. Fluorescently labeled Ab

influenza-like symptoms; paroxysms (fever, chills, rigors) every 36 to 48 hours, depending on species

sickle cell trait and P. falicparum,[object Object]

137 MANAGEMENT P. Vivax and P. Ovale – Primaquine (relapse) P. falciparum - Chloroquine For chloroquine resistant plasmodium – quinine * Prophylaxis – chloroquine or mefloquine, pyrimethamine/ sulfadoxine (fansidar)

Disease:Babesiosis Lab Dx:Giemsa stained thick and thin blood smears BABESIA

Babesia microti infection, Giemsa stained thin smear. The organisms resemble P. falciparum; however Babesia parasites present several distinguishing features: they vary more in shape and in size; and they do not produce pigment.

Infection with Babesia. Giemsa stained thin smears showing the tetrad, a dividing form pathognomonic for Babesia. Note also the variation in size and shape of the ring stage parasites and the absence of pigment.

TRYPANOSOMA BRUCEI Disease: African trypanosomiasis T. b. gambiense: Gambian trypanosomiasis, West & Mid-African sleeping sickness T. b. rhodesiense: Rhodesian trypanosomiasis, East African sleeping sickness Lab Dx:Giemsa stained thick and thin blood smears or lymph exudate (early stage); Giemsa stained smears of CSF (late stage)

Site in host: lymph glands, blood stream, brain Portal of entry: skin Source of infection: tsetse fly Winterbottom’s sign: enlargement of posterior cervical LNs

Trypomastigote: slender to fat and stumpy forms; in Giemsa stained films – C or U shaped forms NOT seen; small, oval kinetoplast located posterior to the nucleus; a centrally located nucleus, an undulating membrane, and an anterior flagellum. The trypanosomes length range is 14-33 µm

A dividing parasite is seen at the right. Dividing forms are seen in African trypanosomiasis, but not in American trypanosomiasis (Chagas' disease)

Tsetse fly. The vector of African trypanosomiasis

TRYPANOSOMA CRUZI Disease: American trypanosomiasis, Chaga’sdisease Lab Dx:Giemsa stained thick and thin blood smears for the trypomastigote; histopath exam for the amastigote Site in host: Tissues – heart; blood Portal of entry: skin Source of infection: Kissing bug Triatomidae

Trypomastigote: shape is short & stubby to long & slender; in Giemsa stained blood films – C or U shaped; kinetoplast is large, oval & located posterior to the nucleus; anterior long free flagellum

Trypanosoma cruzi: Leishmanial form

Riduviid bug: the vector of American trypanosomiasis

Ramana's sign: unilateral conjunctivitis and orbital edema

Chaga'sDisease ,[object Object]

acute- rash, edema on face (site of bite), flu-like symptoms ,[object Object]

g.i. tract nerve damage leading to megacolon

heart- conductive problems and cardiomyopathy, sudden death

[object Object],Entry, Spread, Multiplication ,[object Object]

convert to amastigotes that invade and replicate in host cells,[object Object]

Diagnosis– clinical, serology, blood smear microscopy Treatment- not very good, especially for late complications Prevention– clear houses of bugs, use netting for sleeping

TOXOPLASMA GONDII Disease: Toxoplasmosis Site in host: All organs Portal of entry: Ingestion of oocyst contaminated water Aerosolization of oocyst contaminated dust or litter Consumption of raw or undercooked cyst infected meat Transplacental passage of the tachyzoite

- Definitive host: domestic cats - Intermediate host: infected rodents Accidental intermediate host: humans Lab Dx: IFAT and ELISA; Giemsa-stained smears of exudates, aspirates or tissues

Toxoplasma gondii, parasite Affects birds, mammals i.e. cats Infected person may carry the organism for life (reactivation is possible) 161 TOXOPLASMOSIS

162 PATHOGENESIS ingestion of cyst from uncooked meat / fecal oral route from infected cats (feces) Quickly multiply in the GIT Distributed to CNS, lymphatic tissue, skeletal muscle, myocardium, retina and placenta

T. gondiitachyzoites:crescentic to pyriform shaped with a prominent, centrally placed nucleus.

Toxoplasma gondii cyst in brain tissue stained with hematoxylin and eosin (100×).

166 SIGNS AND SYMPTOMS Malaise, fever, myalgia, headache, fatigue, sore throat, lymphadenopathy or asymptomatic FULMINANT = vomiting, cough and dyspnea, hyperpyrexia, delirium and seizures, encephalopathy, meningitis INFANTS = hydrocephalus or microcephalus, seizure, jaundice later strabismus, blindness, epilepsy, mental retardation

167 DIAGNOSIS Serology – high IgM or rising IgM CT scan Mgmt: 4-6 weeks of sulfadiazine + pyrimethamine (take folic acid to counteract drug’s adverse effects)

L. tropica complex: Old Word Cutaneousleishmaniasis (oriental sore, Aleppo boil, Delhi ulcer, Baghdad boil)

L. mexicana complex: New Word Cutaneousleishmaniasis (chiclero ulcer, bay sore)

L. braziliensis complex: Mucocutaneusleishmaniasis (espundia, uta)

L. donovani: Visceral leishmaniasis (kala-azar or black disease, Dumdum fever),[object Object]

Site in host: Monocytes/macrophages of skin & mucosa

Source of infection: Phlebotomus or Lutzomiya fly,[object Object]

L. tropica amastigotes: ovoid in shape; large & eccentric nucleus; small, rodlike kinetoplast positioned opposite the nucleus; rodlike axoneme perpendicular to the kinetoplast

FREE LIVING AMEBAE ,[object Object]

Naegleria:Primary Amebic Meningoencephalitis (PAM)

Acanthamoeba:Chronic Granulomatous Amebic Encephalitis and keratitis

Lab Dx: Direct microscopic exam (Wheatley’s trichromestain)PROTOZOA FROM OTHER BODY SITES

Acanthamoeba:respiratory tract or ulcers in skin or mucosa / direct invasion of eye

Naegleria: warm lakes, streams, ponds or inadequately chlorinated swimming pools

Acanthamoeba: immunocompromised or debilitated host ,[object Object]

N. fowleri trophozoites cultured from cerebrospinal fluid: cells have characteristically large nuclei, with a large, dark staining karyosome. The amebae are very active and extend and retract broad pseudopods. Trichrome stain.

Acanthamoeba spp.:the cysts are spherical, 15-20 µm in diameter, having a thick double wall. The outer wall may be spherical or wrinkled, the inner wall appear stellate or polyhedral

Acanthamoeba spp.: cysts stained with Heidenhain’s iron alum-haematoxylin method.

TRICHOMONAS VAGINALIS ,[object Object]

Site in host: vagina & prostate

Sources of infection:trophs in vaginal & prostatic secretions

Lab Dx:trophs in vaginal & prostatic fluids,[object Object]

Trophozoites of T. vaginalis: large, pyriform flagellate exhibiting rapid & jerky motility. The wavelike motion of the undulating membrane is often apparent

Trichomonas vaginalis:flagellates are 10-30 µm in lenght and 6-20 µm in breadth. Flagella, nucleus, axostyle and undullating membrane are visible. Filamentous form of Lactobacillus Döderleini is present. Giemsa-Romanowski stain.

Trichomonas vaginalis parasite 182 TRICHOMONIASIS

183 SIGNS AND SYMPTOMS Females: itching, burning on urination, yellow gray frothy malodorous vaginal discharge, foul smelling Males: usually asymptomatic Dx: microscopic exam of vaginal discharge

184 MANAGEMENT Metronidazole (Flagyl) include partners CX: PROM

Eukaryotic Multicellular animals Chemoheterotrophic Kingdom: Animalia Phylum: Platyhelminthes (flatworms) Class: Trematodes (flukes) Class: Cestodes (tapeworms) Phylum: Nematodes (roundworms) Helminths (Parasitic Worms)

Humans as Definitive Host Figure 12.26

Humans as Intermediate Host Figure 12.28

Nematodes: Eggs Infective for Humans Figure 12.29

Nematodes: Larvae Infective for Humans Figure 25.26

Kingdom: Animalia Phylum: Arthropoda (exoskeleton, jointed legs) Class: Insecta (6 legs) Lice, fleas, mosquitoes Class: Arachnida (8 legs) Mites and ticks May transmit diseases (vectors) Arthropods as Vectors Figures 12.31a, 12.32

HELMINTHS INTESTINAL NEMATODES ,[object Object]

Strongyloides stercoralis,[object Object]

Dipylidium caninum,[object Object]

Schistosoma japonicum,[object Object]

Spirometra species,[object Object]

Geographic Distribution:Capillariaphilippinensis is endemic in the Philippines and also occurs in Thailand.

Life Cycle: unembryonated eggs are passed in the human stool and become embryonated after ingestion by freshwater fish-- larvae hatch & penetrate the intestine-- migrate to the tissues -Ingestion of raw or undercooked fish Adults worm -small intestine females deposit unembryonatedeggs (autoinfection) -- hyperinfection(a massive number of adult worms) .

Life Cycle: Capillaria hepatica adult worms reside in the liver of various animals, especially rats. Capillariaaerophila adult worms reside in the epithelium of the tracheo-bronchial tract of various animals.

Clinical Features: Intestinal capillariasis-- pain and diarrhea autoinfection. protein-losing enteropathy-- cachexiaand death Hepatic capillariasis (C. hepatica) -- acute or subacute hepatitis with eosinophilia-- dissemination -- fatal Pulmonary capillariasis (C. aerophila) -- fever, cough, asthma, and pneumonia-- fatal.

Diagnostic findings Microscopy Treatment:The drug of choice is mebendazole*, and albendazole* is an alternative.

ASCARIS LUMBRICOIDES ,[object Object]

Infective stage: ova containing second stage larva

Sources of infection: eggs from soil or vegetables

Lab Dx: eggs in stool,[object Object]

Adult Ascaris worm: tapered ends; length 15 to 35 cm (the females tend to be the larger ones). This worm is a female, as evidenced by the size and genital girdle (the dark circular groove at bottom area of image).

Causal Agent: Ascarislumbricoidesis the largest nematode (Adult females: 20 to 35 cm; adult male: 15 to 30 cm.) Geographic Distribution:most common human helminthic infection. Worldwide distribution. Highest prevalence in tropical and subtropical regions, and areas with inadequate sanitation.

Life Cycle: Adult worms live in the lumen of the small intestine--produce 200,000 eggs/day Fertile eggs embryonate- infective eggs swallowed -- the larvae hatch &, invade the intestinal mucosa-- portal-- systemic -- lungs . lungs -- alveolar walls-- bronchial tree – throat swallowed-- small intestine-- adult worms .

Clinical Features: adult worms usually cause no acute symptoms. High worm burdens –abd pain & obstruction. Migrating worms – occlusion of biltract or oral expulsion. lung phase of larval migration, pulmonary symptoms can occur (cough, dyspnea, hemoptysis, eosinophilicpneumonitis - Loeffler’s syndrome).

Diagnostic findings Microscopy Treatment:The drugs of choice for treatment of ascariasis are albendazole* with mebendazole, ivermectin*, and nitazoxanide as alternatives. In the United States, ascariasis is generally treated for 1-3 days with medication prescribed by a health care provider. The drugs are effective and appear to have few side effects.

Ascaris lumbricoides In GI tract, few symptoms in light infections Nausea Vomiting Obstruction of small bowel or common bile duct. Pulmonary: symptoms due to migration Alveoli (verminous pneumonia)—cough, fever wheeze, dyspnea, X-ray changes, eosinophilia

Effects of Adult Ascaris Worms Depends on worm load Effects Mechanical: obstruction, volvulus, intussusception, appendicitis, obstructive jaundice, liver abscesses, pancreatitis, asphyxia Toxic and Metabolic Malnutrition (complex)

Ascaris lumbricoidesDiagnosis Characteristic eggs on direct smear examination If treating mixed infections, treat Ascaris first Mebendazole Pyrantel Control: Periodic mass treatment of children, health education, environmental sanitation

Causal Agent:The nematode (roundworm) Trichuristrichiura, also called the human whipworm. Geographic Distribution:The third most common round worm of humans. Worldwide, with infections more frequent in areas with tropical weather and poor sanitation practices, and among children. It is estimated that 800 million people are infected worldwide. Trichuriasis occurs in the southern United States.

Life Cycle: The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage embryonate eggs After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine-larvae - adults in the cecum and ascending colon. Female worms in the cecum shed between 3,000 and 20,000 eggs per day.

Clinical Features: Most frequently asymptomatic. Heavy infections, especially in small children, can cause gastrointestinal problems (abdominal pain, diarrhea, rectal prolapse) and possibly growth retardation.

Diagnostic findings microscopy Examination of the rectal mucosa by proctoscopy (or directly in case of prolapses) can occasionally demonstrate adult worms. Treatment:Mebendazole is the drug of choice, with albendazole as an alternative.

Case 13 8-yr-old schoolgirl visiting the U.S. from Malaysia 1 week history of epigastric pain, flatulence, anorexia, bloody diarrhea No eosinophilia noted Clinical diagnosis of amoebic dysentery made However, microscopy of stool prep…

Trichuris trichiura (Whipworm) Common in Southeast U.S. Frequently coexists with ascaris Entirely intraluminal life cycle—eggs are ingested Frequently asymptomatic Severe infections: diarrhea, abdominal pain and tenesmus Rectal prolapse in children DS-eggs in stool Mebendazole 100 mg bid x 3 days

ENTEROBIUS VERMICULARIS ,[object Object]

Infective stage: ova containing rhabditiform larva

Sources of infection: oral-fecal route; through contaminated fomites/food; inhalation ff by ingestion of airborne ova; retroinfection

Lab Dx: eggs in perianal region; Scotch tape swab,[object Object]

Anterior end of Enterobius vermicularis adult worm.

Causal Agent: The nematode (roundworm) Enterobiusvermicularis (previously Oxyurisvermicularis) also called human pinworm. (Adult females: 8 to 13 mm, adult male: 2 to 5 mm.) Humans are considered to be the only hosts of E. vermicularis. Geographic Distribution:Worldwide, with infections more frequent in school- or preschool-children and in crowded conditions. Enterobiasis appears to be more common in temperate than tropical countries. The most common helminthic infection in the United States (an estimated 40 million persons infected).

Life Cycle: Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (e.g., curtains, carpeting). Some small number of eggs may become airborne and inhaled. .

Life Cycle: These would be swallowed and follow the same development as ingested eggs. -larvae hatch in the small intestine -adults in the colon . Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum

Clinical Features Enterobiasis is frequently asymptomatic. The most typical symptom is perianalpruritus, especially at night, which may lead to excoriations and bacterial superinfection. Occasionally, invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas can occur. Other symptoms include anorexia, irritability, and abdominal pain.

Diagnostic findings Microscopy Treatment:The drug of choice is pyrantelpamoate. Measures to prevent reinfection, such as personal hygiene and laundering of bedding, should be discussed and implemented in cases where infection affects other household members.

Case 10 11-year-old female Doing poorly in school Not sleeping well Anorectic Complains of itching in rectal region throughout the day A Scotch-tape test reveals…

Enterobius (Pinworm) 18 million infections in U.S. Incidence higher in whites Preschool and elementary school most often Mostly asymptomatic Nocturnal anal pruritis cardinal feature due to migration and eggs May have insomnia, possible emotional symptoms DS-eggs or adults on perineum {scotch tape} Mebendazole 100 mg. Repeat in 2 weeks. Pyrantel pamoate 11 mg/kg; repeat 2 weeks

NECATOR AMERICANUS ,[object Object]

Infective stage: filariform larva

Sources of infection: infective filariform larvae in soil

The embryo has begun cellular division and is at an early (gastrula) developmental stage.

Hookworm rhabditiform larva (wet preparation).

Hookworm filariform larva (wet preparation).

Anterior end of Necator americanus:oral opening of this species contains cutting "plates" . The muscular esophagus is labeled in this image (*).

ANCYLOSTOMA DUODENALE ,[object Object]

Portal of entry: skin, usually feet

B A A: Adult worm of Ancylostoma duodenale. Anterior end is depicted showing cutting teeth.B: Adult worm of Necator americanus. Anterior end showing mouth parts with cutting plates.

Causal Agents: The human hookworms include two nematode (roundworm) species, Ancylostomaduodenale and Necatoramericanus. A smaller group of hookworms infecting animals can invade and parasitize humans (A. ceylanicum) or can penetrate the human skin (causing cutaneous larva migrans), but do not develop any further (A. braziliense, A. caninum, Uncinariastenocephala). Occasionally A. caninum larva may migrate to the human intestine causing eosinophilic enteritis; this may happen when larva is ingested rather than through skin invasion.

Geographic Distribution: The second most common human helminthic infection (after ascariasis). Worldwide distribution, mostly in areas with moist, warm climate. Both N. americanus and A. duodenale are found in Africa, Asia and the Americas. Necatoramericanus predominates in the Americas and Australia, while only A. duodenale is found in the Middle East, North Africa and southern Europe.

Life Cycle: Eggs are passed in the stool-released rhabditiform larvae grow in the feces and/or the soil , and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective . On contact with the human host, the larvae penetrate the skin and are carried through the veins to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed The larvae reach the small intestine- adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . In addition, infection by A. duodenale may probably also occur by the oral and transmammary route. N. americanus, however, requires a transpulmonary migration phase

Clinical Features: Iron deficiency anemia is the most common symptom of hookworm infection, and can be accompanied by cardiac complications. Gastrointestinal and nutritional/metabolic symptoms can also occur. local skin manifestations ("ground itch") can occur during penetration by the filariform (L3) larvae, and respiratory symptoms can be observed during pulmonary migration of the larvae.

Diagnostic Findings Microscopy between N. americanus and A. duodenale. Larvae can be used to differentiate between N. americanus and A. duodenale, by rearing filariform larvae in a fecal smear on a moist filter paper strip for 5 to 7 days (Harada-Mori).

Treatment: In countries where hookworm is common and reinfection is likely, light infections are often not treated. In the United States, hookworm infections are generally treated with albendazole* Mebendazole* or pyrantelpamoate* can also be used. Eosinophilic enteritis caused by A. caninum and for cutaneous larva migrans(creeping eruption) caused by canine and feline hookworms.

Case 12 57 year old farmer from Dixie County Presents with profound SOB Physical examination: anemic otherwise unremarkable Laboratory examination reveals a profound anemia (hct 24) with aniso and poikilocytosis Remainder of laboratory examination normal.

Hookworm Hookworm responsible for development of USPHS Caused by two different species (North American and Old World) Very similar to strongyloides in life cycle Attaches to duodenum, feeds on blood Elaborates anticoagulant, attaches and reattaches many times Loss of around 0.1 ml/d of blood per worm

Case 14 18-year-old trailer park handyman seen in ER Worked under trailers wearing shorts and no shirt Developed intensely pruritic skin rash Unable to sleep WBC 18,000 65% eosinophils.

Case 15 An 8 year old boy Presents with skin lesions and itching after spending the summer at a beach condo in St. Augustine with his family (mother, father, younger sister, dog and cat). Legs show several raised, reddened, serpiginous lesions that are intensely pruritic.

Cutaneous Larva Migrans Caused by filariform larvae of dog or cat hookworm (Ancylostoma braziliense or Ancylostoma duodenale Common in Southeast U.S. Red papule at entry with serpiginous tunnel Intense pruritis Self limiting condition Diagnosis clinical Topical or oral thiabendazole 25 mg/kg bid for 3-5 days May use ethyl chloride topically

Cutaneous larva migrans (creeping eruption) More common in children Larvae penetrate skin and cause tingling followed by intense itching. Eggs shed from dog and cat bowels develop into infectious larvae outside the body in places protected from desiccation and extremes of temperature Shady, sandy areas under houses, at beach, etc.

Cutaneous larva migrans (creeping eruption) Usually not associated with systemic symptoms

Cutaneous larva migrans (creeping eruption) Diagnosis and treatment Skin lesions are readily recognized Usually diagnosed clinically Generally do not require biopsy Reveal eosinophilia inflammatory infiltrate Migrating parasite is generally not seen Stool smear will reveal eggs

Visceral Larva Migrans Infection with dog or cat round worms Toxocara canis; Toxocara catis Underdiagnosed based on seroprevalence surveys Heavy infections associated with fever, cough, nausea, vomiting, hepatomegaly, and eosinophilia Uncommon in adults Ocular type more common in adults Diagnosis-ELISA Thiabendazole: 25 mg/kg bid X 5 days

Case 17 A 34 yr-old woman from Saudi Arabia Radiation and cyclophosphamide, adriamycin, vincristine and prednisone for diffuse large B cell lymphoma of the neck. Mild eosinophilia (AEC=500) at the time of diagnosis 4 months after initiation of chemo, c/o intermittent diffuse abdominal pain, bloating, constipation and occasional rectal bleeding. Absolute eosinophil count: 1000

Case 17 No evidence of lymphoma found on re-staging Completed chemo, was deemed to be in complete remission, but had persistence of GI complaints. Upper endoscopy was unrevealing. Colonoscopy and biopsy revealed granulomatous inflammation, prominent eosinophilic infiltrate, surrounding a collection of eggs.

STRONGYLOIDES STERCORALIS ,[object Object]

Sources of infection: larvae in soil; autoinfection

Lab Dx: larvae in stool,[object Object]

Causal Agent: The nematode (roundworm) Strongyloidesstercoralis. Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans. . Geographic Distribution:Tropical and subtropical areas, but cases also occur in temperate areas (including the South of the United States). More frequently found in rural areas, institutional settings, and lower socioeconomic groups

Life Cycle: The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist:

Life Cycle: Free-living cycle: The rhabditiform larvae passed in the stool (see "Parasitic cycle" below) can either molt twice and become infective filariform larvae (direct development) or molt four times and become free living adult males and females that mate and produce eggs from which rhabditiform larvae hatch . The latter in turn can either develop into a new generation of free-living adults (as represented in ), or into infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) .

Life Cycle: Parasitic cycle:Filariform larvae in contaminated soil penetrate the human skin , and are transported to the lungs where they penetrate the alveolar spaces; they are carried through the bronchial tree to the pharynx, are swallowed and then reach the small intestine . In the small intestine become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see "Free-living cycle" above), or can cause autoinfection .

Life Cycle: Parasitic cycle: In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloidesstercoralis and Capillariaphilippinensis infections.

Clinical Features Frequently asymptomatic. Gastrointestinal symptoms include abdominal pain and diarrhea. Pulmonary symptoms (including Loeffler’s syndrome) can occur during pulmonary migration of the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. Disseminated strongyloidiasis occurs in immunosuppressed patients, can present with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal. Blood eosinophilia is generally present during the acute and chronic stages, but may be absent with dissemination.

Diagnostic findings Microscopy Treatment:The drug of choice for the treatment of uncomplicated strongyloidiasis is ivermectin with albendazole* as the alternative. All patients who are at risk of disseminated strongyloidiasis should be treated.

On the day of admission… Fever, confusion, and not able to get out of bed---transported to the hospital Initial blood work: Elevated WBC Raised eosinophil count 4 times normal Underwent UGI endoscopy Duodenal biopsy obtained

Strongyloides: Crucial Aspects of Life Cycle Infection acquired through penetration of intact skin Infection may persist for many years via autoinfection In immunocompromised patients, there is risk of dissemination or hyperinfection Hyperinfection syndrome

Disseminated Strongyloidiasis High mortality75% Penetration of gut wall by infective larvae Gut organisms carried on the surface of larvae results in polymicrobial sepsis, meningitis Larvae disseminate into all parts of body: CNS, lungs, bladder, peritoneum

Summary—Clinical Findings Defective cell-meditated immunity: steroids, burns, lymphomas, AIDS (?) Gl symptoms in about two-thirds: Abdominal pain Bloating Diarrhea Constipation Wheezing, SOB, hemoptysis

Summary—Clinical Findings Skin rash or pruritis in ~ one-third Larva currens (racing larva) Intensely pruritic Linear or serpiginous urticaria with flare that moves 5-15 cm/hr Usually buttocks, groin, and trunk In dissemination, diffuse petechiae and purpura

Summary-Clinical Findings Eosinophilia 60-95% Less if on steroids

DIPHYLLOBOTHRIUM LATUM ,[object Object]

Definitive host: human, dogs, cats

1st Intermediate host: crustaceans (Cyclops or Diaptomus)

2nd Intermediate host: freshwater fish

Infective stage: plerocercoid larvae

Sources of infection: plerocercoid in freshwater fish

Eggs of D. latum:oval or ellipsoidal, with at one end an operculum that can be inconspicuous. At the opposite (abopercular) end is a small knob that can be barely discernible.

Eggs of Diphyllobothrium latum:are oval or ellipsoidal, with at one end an operculum (arrows) that can be inconspicuous. The eggs are passed in the stool unembryonated.

D. latum scolex and gravid proglottids

Proglottids of Diphyllobothrium latum. These proglottids tend to be passed in strands of variable length in the stool. The proglottids tend to be broader than long.

Proglottids of D. latum:broader than it is long; size 2 to 4 mm long by 10 to 12 mm wide; uterus coiled in rosette appearance; genital pore at the center of the proglottid.

Causal Agents: The cestodeDiphyllobothriumlatum (the fish or broad tapeworm), the largest human tapeworm. Geographic Distribution:Diphyllobothriasis occurs in the Northern Hemisphere Freshwater fish infected with Diphyllobothrium sp. larva may be transported to and consumed in geographic areas where active transmission does not occur, resulting in human diphyllobothriasis.

Life Cycle: Immature eggs are passed in feces -oncospheres -develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection.

Life Cycle: After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms which will reside in the small intestine. The adults of D. latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 m in length, with more than 3,000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces .

Clinical Features: Diphyllobothriasis can be a long-lasting infection (decades). Most infections are asymptomatic. Manifestations may include abdominal discomfort, diarrhea, vomiting, and weight loss. Vitamin B12 deficiency with pernicious anemia may occur. Massive infections may result in intestinal obstruction. Migration of proglottids can cause cholecystitis or cholangitis.

Diagnostic findings Microscopy Treatment:Praziquantel* is the drug of choice. Alternatively, Niclosamide can also be used to treat diphyllobothriasis.

DIPYLIDIUM CANINUM ,[object Object]

Definitive host: dog & cat (or humans)

Intermediate host: larval flea

Sources of infection: flea & louse

Lab Dx: eggs in stool or egg sacks in stool,[object Object]

Egg packets of Dipylidium caninum:Proglottids of Dipylidium caninum contain characteristic egg packets that are round to ovoid and contain 5 to 15 (sometimes more) eggs each.

Proglottids of D. caninum: barrel-shaped proglottids (average mature size 12 mm × 3 mm) have two genital pores, one in the middle of each lateral margin. Proglottids may be passed singly or in chains, and occasionally may be seen dangling from the anus. Proglottids are much longer than broad.

Adult tapeworm of Dipylidium caninum. The scolex of the worm is very narrow and the proglottids, as they mature, get larger.

Causal Agent: Dipylidiumcaninum(the double-pored dog tapeworm) mainly infects dogs and cats, but is occasionally found in humans. Geographic Distribution:Worldwide. Human infections have been reported in Europe, the Philippines, China, Japan, Argentina, and the United States

Life Cycle: Gravid proglottids are passed intact in the feces or emerge from the perianal region of the host . Subsequently they release typical egg packets . ingestion of an egg by the intermediate host (larval stages of the dog or cat flea Ctenocephalides spp.), an oncosphere is released into the flea's intestine. The oncosphere penetrates the intestinal wall, invades the insect's hemocoel (body cavity), and develops into a cysticercoid larva . The larva develops into an adult, and the adult flea harbours the infective cysticercoid . The vertebrate host becomes infected by ingesting the adult flea containing the cysticercoid . The dog is the principal definitive host for Dipylidiumcaninum. Other potential hosts include cats, foxes, and humans (mostly children) , .

Life Cycle: Humans acquire infection by ingesting the cysticercoid contaminated flea. This can be promulgated by close contact between children and their infected pets. In the small intestine of the vertebrate host the cysticercoid develops into the adult tapeworm (measuring up to 60 cm in length and 3 mm in width) reside in the small intestine of the host, where they each attach by their scolex. They produce proglottids (or segments) which have two genital pores (hence the name "double-pored" tapeworm). The proglottids mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool .

Clinical Features:Most infections with Dipylidiumcaninum are asymptomatic. Pets may exhibit behavior to relieve anal pruritis (such as scraping anal region across grass or carpeting). Mild gastrointestinal disturbances may occur. The most striking feature in animals and children consists of the passage of proglottids. These can be found in the perianal region, in the feces, on diapers, and occasionally on floor covering and furniture. The proglottids are motile when freshly passed and may be mistaken for maggots or fly larvae.

Diagnostic findings Microscopy Treatment:Treatment for both animals and humans is simple and very effective. Praziquantel is given either orally or by injection (pets only). The medication causes the tapeworm to dissolve within the intestines. Since the worm is usually digested before it passes, it may not be visible in the dog's stool. These drugs are generally well tolerated.

HYMENOLEPIS NANA ,[object Object]

Site in host: adults & cysts in SI

Definitive host: human, mice & rats

Intermediate host: DO NOT require an IH

Sources of infection: eggs fr feces in soil; autoinfection

Three adult Hymenolepis nana tapeworms. Each tapeworm (length: 15-40 mm) has a small, rounded scolex at the anterior end, and proglottids can be distinguished at the posterior, wider end.

HYMENOLEPIS DIMINUTA ,[object Object]

Intermediate host: insects (rat & mouse flea, the flour moth and flour beetle)

Sources of infection: cysts from insects

Mature proglottids of Hymenolepis diminuta.

Causal Agents:Hymenolepiasis is caused by two cestodes (tapeworm) species, Hymenolepis nana (the dwarf tapeworm,) and Hymenolepisdimnuta (rat tapeworm). Hymenolepisdiminuta is a cestode of rodents infrequently seen in humans and frequently found in rodents. Geographic Distribution:Hymenolepis nana is the most common cause of all cestode infections, and is encountered worldwide. In temperate areas its incidence is higher in children and institutionalized groups. Hymenolepisdiminuta, while less frequent, has been reported from various areas of the world.

Life Cycle: Eggs of Hymenolepis nana eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. When eggs are ingested (in contaminated food or water or from hands contaminated with feces- oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment .

Life Cycle: . Eggs of Hymenolepisdiminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H. diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H. diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (e.g., oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces .

Clinical Features:Hymenolepis nana and H. diminuta infections are most often asymptomatic. Heavy infections with H. nana can cause weakness, headaches, anorexia, abdominal pain, and diarrhea.

Treatment:Diagnostic findings Microscopy Treatment:Praziquantel* is the drug of choice.

TAENIA SAGINATA ,[object Object]

Intermediate host: grazing cattle

Sources of infection: cysts in beef

Lab Dx: segments and eggs in stool; Scotch tape swab,[object Object]

Taeniid eggs: rounded or subspherical, diameter 31 to 43 µm, with a thick radially striated brown shell. Inside each shell is an embryonated oncosphere with 6 hooks (hexacanth embryo).

Taenia egg. Note the thick, "striated" shell and several of the larval hooks; approximate size = 40 µm.

T. Saginata gravid proglottid:has 15 to 30 main uterine branches on each side of central stem; proglottids are much longer than wide

TAENIA SOLIUM ,[object Object]

Sources of infection: cysts in pork; autoinfection

Scoleces of Taenia saginata and Taenia solium: Scolex of T. saginata has 4 suckers and no hooks. T. solium has 4 suckers in addition to a double row of hooks.

Scolex of Taenia solium:measures approximately 1 mm across. The four suckers are numbered. Note the presence of an armed (hooked) rostellum (*); the scolex of Taenia saginata, the beef tapeworm, does not have an armed rostellum.

A cysticercus of Taenia in muscle. Note the fibrous capsule (*) around the cysticercus.

Causal Agents: The cestodes (tapeworms) Taeniasaginata (beef tapeworm) and T. solium (pork tapeworm). Taeniasolium can also cause cysticercosis. Geographic Distribution:Both species are worldwide in distribution. Taeniasolium is more prevalent in poorer communities where humans live in close contact with pigs and eat undercooked pork and is very rare in Muslim countries

Life Cycle: Taeniasis is the infection of humans with the adult tapeworm of Taeniasaginata or Taeniasolium. Humans are the only definitive hosts for T. saginata and T. solium. Eggs or gravid proglottids are passed with feces ; Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops into an adult tapeworm The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine .

Life Cycle: Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25 m) and 2 to 7 m for T. solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T. saginata adults usually have 1,000 to 2,000 proglottids, while T. solium adults have an average of 1,000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T. saginata may produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid respectively.

Clinical Features: Taeniasaginatataeniasis produces only mild abdominal symptoms. The most striking feature consists of the passage (active and passive) of proglottids. Occasionally, appendicitis or cholangitis can result from migrating proglottids. Taeniasoliumtaeniasis is less frequently symptomatic than Taeniasaginatataeniasis. The main symptom is often the passage (passive) of proglottids. The most important feature of Taeniasoliumtaeniasis is the risk of development of cysticercosis.

Diagnostic findings TAKE EXTREME CARE IN PROCESSING THE SAMPLES! INGESTION OF EGGS CAN RESULT IN CYSTICERCOSIS! Microscopy Antibody detection may prove useful especially in the early invasive stages, when the eggs and proglottids are not yet apparent in the stools. Treatment:Treatment is simple and very effective. Praziquantel* is the drug of choice.

Taenia saginata Ingestion of raw or poorly cooked beef Cows infected via the ingestion of human waste containing the eggs of the parasite Cows contain viable cysticercus larvae in the muscle Humans act as the host only to the adult tapeworms Up to 25 meters in the lumen of intestine Found all over the world, including the U.S.

Treatment Praziquantel Albendazole Niclosamide

Tapeworms (Cestodes) Adult worms inhabit GI tract of definitive vertebrate host Larvae inhabit tissues of intermediate host Humans Definitive for T. saginata Intermediate for Echinococcus granulosus (hydatid) Both definitive and intermediate for T. solium Adult worms shed egg-containing segments in stool ingested by intermediate host larval form in tissues

Cystercercosis Symptoms depend on location of cysts, but frequently include motor spasms, seizures, confusion, irritability, and personality change In the eye, often subretinal or in vitreous. Movement may be seen by the patient. Pain, amaurosis, and loss of vision may occur.

Cysticercosis Clinical manifestations Adult worms rarely cause sxs Larvae penetrate intestine, enter blood, and eventually encyst in the brain. Cerebral ventircles  hydrocephalus Spinal cord  compression, paraplegia Subarachnoid space  chronic meningitis Cerebral cortex  seizures Cysts may remain asymptomatic for years, and become clinically apparent when larvae die Larvae may encyst in other organs, but are rarely symptomatic

Cysticercosis Diagnosis CT and MRI preferred studies Discrete cysts that may enhance Usually multiple lesions Single lesions especially common in cases from India Older lesions may calcify CSF Lymphs or eos, low glucose, elevated protein Serology Especially in cases with multiple cysts

Cysticercosis Treatment Complex and controversial Praziquantel and albendazole may kill cysts, but death of larvae can increase inflammation, edema and exacerbate sxs When possible, surgical resection of symptomatic cyst is preferred Corticosteroids vs. edema and inflammation; antiseizure meds

Causal Agents: Schistosomiasis is caused by digenetic blood trematodes. The three main species infecting humans are Schistosomahaematobium, S. japonicum, and S. mansoni. In addition, other species of schistosomes, which parasitize birds and mammals, can cause cercarial dermatitis in humans. Geographic Distribution: Schistosomamansoni is found in parts of South America and the Caribbean, Africa, and the Middle East; S. haematobium in Africa and the Middle East; and S. japonicum in the Far East.

Life Cycle: Eggs are eliminated with feces or urine .- eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include 2 generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins (, ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . S. japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and S. mansoni occurs more often in the superior mesenteric veins draining the large intestine . S. haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules.

Life Cycle: . Pathology of S. mansoni and S. japonicumschistosomiasis includes: Katayama fever, hepatic perisinusoidal egg granulomas, Symmers’ pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S. haematobiumschistosomiasis includes: hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, hourse and goats, serve as reservoirs for S. japonicum, and dogs for S. mekongi.

Clinical Features Many infections are asymptomatic. Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by S. mansoni and S. japonicum. Manifestations include fever, cough, abdominal pain, diarrhea, hepatospenomegaly, and eosinophilia. Occasionally central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord from S. mansoni and S. haematobium infections may result in a transverse myelitis with flaccid paraplegia. .

Clinical Features Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include: colonic polyposis with bloody diarrhea (Schistosomamansoni mostly); portal hypertension with hematemesis and splenomegaly (S. mansoni, S. japonicum, S. mansoni); cystitis and ureteritis (S. haematobium) with hematuria, which can progress to bladder cancer; pulmonary hypertension (S. mansoni, S. japonicum, more rarely S. haematobium); glomerulonephritis; and central nervous system lesions.

Diagnostic findings microscopy Antobodydetrectioncan be useful in both in clinical management (e.g., recent infections) and for epidemiologic surveys. Treatment:Safe and effective drugs are available for the treatment of schistosomiasis. The drug of choice is praziquantel for infections caused by all Schistosoma species. Oxamniquine has been effective in treating infections caused by S. mansoni in some areas in which praziquantel is less effective.

FASCIOLA HEPATICA ,[object Object]

Disease: Fascioliasis, “liver rot”

Definitive host: sheep, cattle & other mammals, including humans

Intermediate host: snail (Lymnaea)

Source of infection: eating watercress, lettuce or radishes or drinking water infested with metacercariae

Infective stage: metacercariae

Lab Dx: eggs in stool ,[object Object]

Causal Agents: The trematodesFasciola hepatica (the sheep liver fluke) and Fasciolagigantica, parasites of herbivores that can infect humans accidentally. Geographic Distribution:Fascioliasis occurs worldwide. Human infections with F. hepatica are found in areas where sheep and cattle are raised, and where humans consume raw watercress, including Europe, the Middle East, and Asia. Infections with F. gigantica have been reported, more rarely, in Asia, Africa, and Hawaii.

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