The Prokaryotes:Domains Bacteria and

Archaea

11

The Protozoa

Table 12.1

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 mitochondriaMultiple flagellaGiardia lambliaTrichomonas vaginalis

(no cyst stage)

Archaezoa

Figure 12.17b–d

No mitochondriaNonmotileIntracellular parasites

Nosema

Microspora

Move by pseudopodsEntamoebaAcanthamoeba

Amoebozoa

Figure 12.18a

NonmotileIntracellular parasitesComplex life cycles

PlasmodiumBabesiaCryptosporidiumCyclospora

Apicomplexa

2

3

67

8

Plasmodium

Figure 12.19

Cryptosporidium

Figure 25.19

Figure 12.20

Move by ciliaComplex cells

Balantidium coli is the only human parasite.

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

Euglenozoa

Figure 12.21

Why are these studied with algae and protozoa?

Dinoflagellates

Figure 12.14

AmebaFlagellatesCiliatesIntestinal Coccidia, Microsporidia, and Blastocystis hominis

INTESTINAL PROTOZOA

Entamoeba histolytica- Disease: Intestinal

amebiasis/amebic dysentery, extraintestinal amebiasis

- Site in host: lumen & wall of LI- Portal of entry: Mouth- Source of infection: cysts in food &

water, from feces

AMEBA

Causal Agent: Entamoeba histolytica

pathogenic amebaassociated 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 -

trophozoites are 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

1) trophozoites remain confined to the intestinal lumen ( noninvasive infection)

individuals who are asymptomatic carriers, passing cysts in their stool. 

2) trophozoites invade the intestinal mucosa (intestinal disease)

3) 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 extraintestinal amebiasis (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. histolytica trophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.

Laboratory Diagnosis:

MicroscopyImmunodiagnosisMolecular methods for discriminating betwee

n 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-likechromatoid 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-likechromatoid 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 diloxanide furoate

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 diloxanide furoate. 

Treatment:

Balantidium coli- Disease: Balantidiasis; balantidiosis;

balantidial dysentery - Site in host: LI- Portal of entry: Mouth- Source of infection: stool (cysts)- Lab Dx: cysts/trophs in stool

CILIATES

Causal AgentBalantidium 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 stageingestion of contaminated food or water

Life cycle

excystation occurs in the small intestine- trophozoites colonize 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 diarrheaoccasionally dysenteryabdominal painweight 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:

- May be pathogenic- Currently classified as an amoeba

Blastocystis hominis

Blastocystis hominis

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 ameboid forms

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, perianal pruritus, 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.

metronidazole or iodoquinol

Treatment:

Giardia duodenalis (lamblia)- Disease: Giardiasis; lambliasis - Site in host: upper SI- Portal of entry: Mouth- Source of infection: cysts in food &

water, from feces- Lab Dx: cysts/trophs in stool; IFA

stain; Enterotest- Note: may be sexually transmitted

FLAGELLATES

Causal Agent:Giardia intestinalisGiardia lamblia

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 (nondiarrheal feces )

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

metronidazole and tinidazole.  Nitazoxanide (giardiasis in children)

Treatment:

INTESTINAL COCCIDIA, MICROSPORIDIA, and BLASTOCYSTIS HOMINIS

Cryptosporidium parvum- Disease: Cryptosporidiosis- Transmission: contaminated food or

water by person to person contact- Lab Dx: Modified acid fast stain of a

fecal smear; PCR; IFA

Causal Agent:Cryptosporidium parvum and Cryptosporidium hominis are (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

Sporulated oocysts, 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 sourcesoutbreaks U S -- waterparks, community

swimming pools, and day care centers.  Zoonotic and anthroponotic transmission

Life cycle

Following ingestion (and possibly inhalation)

Excystation-- sporozoites are 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. 

Life cycle

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:

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.

Clinical Features:

Rapid loss of fluids -- fluid and electrolyte replacement.  

healthy, immunocompetent persons (self-limited)-- Nitazoxanide

 Immunocompromised and high risk pt.-- nitazoxanide is unclear.  For persons with AIDS, anti-retroviral therapy is

encourage

Treatment:

Acid-fast staining methods

immunofluorescence microscopy method of choice (followed closely by enzyme

immunoassays)

Laboratory Diagnosis:

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.

Cyclospora cayetanensis- Disease: Cyclosporiasis- Transmission: contaminated water - Lab Dx: Modified acid fast stain of a

fecal smear

Cyclospora oocysts from fresh stool fixed in 10% formalin and stained with modified acid-fast stain.  Compared to wet mount preparations, the oocysts are less perfectly round and have a wrinkled appearance.  Most importantly, the staining is variable among the four oocysts.

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- Cyclospora cayetanensis

Geographic Distribution:

most common in tropical and subtropical areas1990, foodborne outbreaks of cyclosporiasis,

3600 persons, in the United States and Canada.

sporulation -- sporont -- two sporocysts (contains 2 sporozoites ) 

sporulated oocysts are ingested (in contaminated food or water)

oocysts excyst in the gastrointestinal tract-- sporozoites invade the small intestine

asexual multiplication and sexual development -- oocysts

Life Cycle:

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.

Clinical Features:

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:

- Disease: Isosporiasis; intestinal coccidiosis- 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

Isospora belli

Oocysts: large (25 to 30 µm); typical ellipsoidal shape; when excreted, they are immature and contain one sporoblast; oocyst matures after excretion: the single sporoblast divides in two sporoblasts which develop cyst walls, becoming sporocysts, which eventually contain four sporozoites each

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 immunodepressed pt. and outbreaks in institutionalized groups in US

infection occurs by ingestion of sporocysts-containing oocysts

sporocysts excyst in the small intestine -- release their sporozoites, which invade the epithelial cells -- initiate schizogony . 

Life Cycle:

acute, nonbloody diarrhea with crampy abd pain (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:

Dientamoeba fragilis

- NO cyst stage

- not an ameba, but a flagellate!

- may possess some pathogenicity

- Site in host: LI

- Portal of entry: mout

- Source of infection: stool (trophs)

Causal Agent:Dientamoeba fragilis 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- Disease: Microsporidiosis- 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

- Infective form: spore- Lab Dx: Modified trichrome stain ; PCR

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.

BLOOD and TISSUE PROTOZOA

BLOOD and TISSUE PROTOZOAPlasmodiumBabesiaTrypanosoma bruceiTrypanosoma cruziToxoplasma gondiiLeishmania

OTHER PROTOZOA

PROTOZOA FROM OTHER BODY SITESFree-living Amebae

NaegleriaAcanthamoeba

Trichomonas vaginalis

PLASMODIUM

Disease: MalariaP. vivax: Benign tertian malariaP. malariae: Quartan malariaP. falciparum: Malignant tertian

malariaP. ovale: Ovale tertian malaria

Lab Dx: Giemsa stained thick and thin blood smears; IFA; PCR

Infected RBC: P. vivax and P. ovale: reticulocytesP. malariae: senescent erythrocytesP. falciparum: erythrocytes of all ages

Cyclic paroxysm of fever:P. vivax and P. ovale: every 48 hoursP. malariae: every 72 hoursP. falciparum: every 36-48 hours

P. falciparum: Blood Stage ParasitesThin 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 SYMPTOMSFever, 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

• over 1 million deaths/year - mainly Africa

• Incubation period - 8-30 days

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

• sickle cell trait and P. falicparum

136

COMPLICATIONS P. ovale and vivax – relapse after 10 years of

first exposure

P. falciparum –

1. Cerebral malaria – severe headache, drowsiness, seizure, delirium, coma

2. Black water fever – jaundice, ARF, hemoglobinuria, black colored urine

137

MANAGEMENTP. Vivax and P. Ovale – Primaquine (relapse) P. falciparum - Chloroquine For chloroquine resistant plasmodium –

quinine* Prophylaxis – chloroquine or mefloquine,

pyrimethamine/ sulfadoxine (fansidar)

Disease: BabesiosisLab 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. 

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)

TRYPANOSOMA BRUCEI

Site in host: lymph glands, blood stream, brainPortal of entry: skinSource of infection: tsetse flyWinterbottom’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

Winterbottoms sign

Disease: American trypanosomiasis, Chaga’s disease

Lab Dx: Giemsa stained thick and thin blood smears for the trypomastigote; histopath exam for the amastigote

Site in host: Tissues – heart; bloodPortal of entry: skinSource of infection: Kissing bug Triatomidae

TRYPANOSOMA CRUZI

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 crithidia

Trypanosoma cruzi: Leishmanial form

Riduviid bug: the vector of American trypanosomiasis

Ramana's sign: unilateral conjunctivitis and orbital edema 

Chaga's Disease

• asymptomatic - mostly• acute - rash, edema on face (site of bite), flu-like symptoms• chronic – rare but serious• g.i. tract nerve damage leading to megacolon • heart - conductive problems and cardiomyopathy, sudden death

• "kissing bug" reduviid bug vector --(epimastigote replicative form)

Entry, Spread, Multiplication

• bug defecates on wound releasing trypomastigotes that get rubbed into wound and vasculature

• convert to amastigotes that invade and replicate in host cells

Diagnosis – clinical, serology, blood smear microscopy

Treatment - not very good, especially for late complications

Prevention – clear houses of bugs, use netting for sleeping

Disease: ToxoplasmosisSite in host: All organsPortal 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

TOXOPLASMA GONDII

- Definitive host: domestic cats - Intermediate host: infected rodents

Accidental intermediate host: humansLab Dx: IFAT and ELISA; Giemsa-stained smears

of exudates, aspirates or tissues

161

TOXOPLASMOSIS

Toxoplasma gondii, parasiteAffects birds, mammals i.e. catsInfected person may carry the organism for

life (reactivation is possible)

162

PATHOGENESISingestion 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. gondii tachyzoites: 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 SYMPTOMSMalaise, 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

DIAGNOSISSerology – high IgM or rising IgMCT scan

Mgmt:4-6 weeks of sulfadiazine + pyrimethamine

(take folic acid to counteract drug’s adverse effects)

- Disease: - L. tropica complex: Old Word Cutaneous

leishmaniasis (oriental sore, Aleppo boil, Delhi ulcer, Baghdad boil)

- L. mexicana complex: New Word Cutaneous leishmaniasis (chiclero ulcer, bay sore)

- L. braziliensis complex: Mucocutaneus leishmaniasis (espundia, uta)

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

LEISHMANIA

- Lab Dx: Giemsa stained tissue sections or impression smears

- Site in host: Monocytes/macrophages of skin & mucosa

- Portal of entry: Skin- Source of infection: Phlebotomus or Lutzomiya

fly

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

- Disease:

- Naegleria: Primary Amebic Meningoencephalitis (PAM)

- Acanthamoeba: Chronic Granulomatous Amebic Encephalitis and keratitis

- Lab Dx: Direct microscopic exam (Wheatley’s trichrome stain)

PROTOZOA FROM OTHER BODY SITES

FREE LIVING AMEBAE- Portal of Entry:

- Naegleria: nose- Acanthamoeba: respiratory tract or ulcers in

skin or mucosa / direct invasion of eye- Source of infection:

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

- Acanthamoeba: immunocompromised or debilitated host

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- Disease: Trichomonad vaginitis- Site in host: vagina & prostate- Portal of entry: genitalia- Sources of infection: trophs in vaginal &

prostatic secretions- NO cyst stage- Lab Dx: trophs in vaginal & prostatic fluids

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.

182

TRICHOMONIASIS

Trichomonas vaginalisparasite

183

SIGNS AND SYMPTOMSFemales: itching, burning on urination, yellow

gray frothy malodorous vaginal discharge, foul smelling

Males: usually asymptomatic

Dx: microscopic exam of vaginal discharge

184

MANAGEMENTMetronidazole (Flagyl)include partners

CX: PROM

The Helminths

Table 12.1

EukaryoticMulticellular animalsChemoheterotrophicKingdom: Animalia

Phylum: Platyhelminthes (flatworms)Class: Trematodes (flukes)Class: Cestodes (tapeworms)

Phylum: Nematodes (roundworms)

Helminths (Parasitic Worms)

Trematodes

Figure 12.25

Humans as Definitive Host

Figure 12.26

Cestodes

Figure 12.27

Humans as Intermediate Host

Figure 12.28

Nematodes: Eggs Infective for Humans

Figure 12.29

Nematodes: Larvae Infective for Humans

Figure 25.26

Kingdom: AnimaliaPhylum: Arthropoda

(exoskeleton, jointed legs)Class: Insecta (6 legs)

Lice, fleas, mosquitoesClass: Arachnida (8 legs)

Mites and ticksMay transmit diseases

(vectors)

Arthropods as Vectors

Figures 12.31a, 12.32

HELMINTHS INTESTINAL NEMATODES

Enterobius vermicularis Ascaris lumbricoides Necator americanus Ancylostoma duodenale Trichuris trichiura Strongyloides stercoralis

INTESTINAL CESTODES Taenia saginata Taenia solium Hymenolepis diminuta Diphyllobothrium latum Dipylidium caninum

INTESTINAL TREMATODES Clonorchis sinensis Fasciola hepatica Paragonimus westermani Fasciolopsis buski Heterophyes heterophyes Metagonimus yokogawai Schistosoma mansoni Schistosoma haematobium Schistosoma japonicum

TISSUE NEMATODES & CESTODES Trichinella spiralis Echinococcus granulosus Echinococcus multilocularis Spirometra species

Causal Agents:The nematode (roundworm) Capillaria

philippinensis causes human intestinal capillariasis

C. hepatica-- humans hepatic capillariasis C. aerophila-- humans pulmonary

capillariasis.

Geographic Distribution:Capillaria philippinensis 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 unembryonated eggs (autoinfection)  -- hyperinfection (a massive number of adult worms) . 

Life Cycle:Capillaria hepatica adult worms reside in the

liver of various animals, especially rats. 

Capillaria aerophila 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 -- cachexia and death

Hepatic capillariasis (C. hepatica) -- acute or subacute hepatitis with eosinophilia-- dissemination -- fatal

Pulmonary capillariasis (C. aerophila) -- fever, cough, asthma, and pneumonia-- fatal.

Diagnostic findingsMicroscopy

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

ASCARIS LUMBRICOIDES- Disease: Ascariasis; roundworm infection- Site in host: SI- Portal of entry: Mouth- Infective stage: ova containing second stage

larva- Sources of infection: eggs from soil or

vegetables- Lab Dx: eggs in stool

Fertilized Ascaris egg (A) still at the unicellular stage. Unfertilized and fertilized eggs, (B and C, respectively).

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:

Ascaris lumbricoides is 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 bil tract or

oral expulsion.  lung phase of larval migration, pulmonary

symptoms can occur (cough, dyspnea, hemoptysis, eosinophilic pneumonitis - Loeffler’s syndrome).

Diagnostic findingsMicroscopy

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 lumbricoidesIn GI tract, few symptoms in light infections

NauseaVomitingObstruction 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 loadEffects

Mechanical: obstruction, volvulus, intussusception, appendicitis, obstructive jaundice, liver abscesses, pancreatitis, asphyxia

Toxic and MetabolicMalnutrition (complex)

Ascaris lumbricoidesDiagnosisCharacteristic eggs on direct smear

examinationIf treating mixed infections, treat

Ascaris firstMebendazolePyrantel

Control: Periodic mass treatment of

children, health education, environmental sanitation

Causal Agent:The nematode (roundworm) Trichuris trichiura, 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 findingsmicroscopyExamination 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 138-yr-old schoolgirl visiting the U.S. from

Malaysia1 week history of epigastric pain,

flatulence, anorexia, bloody diarrheaNo eosinophilia notedClinical diagnosis of amoebic dysentery

made However, microscopy of stool prep…

Diagnosis?

Trichuris trichiura (Whipworm)Common in Southeast U.S. Frequently coexists with ascarisEntirely intraluminal life cycle—eggs are

ingestedFrequently asymptomaticSevere infections: diarrhea, abdominal

pain and tenesmusRectal prolapse in childrenDS-eggs in stoolMebendazole 100 mg bid x 3 days

ENTEROBIUS VERMICULARIS- Disease: Enterobiasis; pinworm infection;

seatworm infection; oxyuriasis- Site in host: LI, appendix- Portal of entry: Mouth- 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

Enterobius eggs: oval, asymmetric w/ one side noticeably flattened; smooth, thin-shelled, maycontain embryo 

Anterior end of Enterobius vermicularis adult worm.

Causal Agent:The nematode (roundworm) Enterobius vermicularis

(previously Oxyuris vermicularis) 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 FeaturesEnterobiasis is frequently asymptomatic.  The most typical symptom is perianal

pruritus, 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 findingsMicroscopy

Treatment:The drug of choice is pyrantel pamoate. 

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 femaleDoing poorly in schoolNot sleeping wellAnorecticComplains of itching in rectal region throughout the day

A Scotch-tape test reveals…

Diagnosis?

Enterobius (Pinworm)18 million infections in U.S.Incidence higher in whitesPreschool and elementary school most

oftenMostly asymptomaticNocturnal anal pruritis cardinal feature

due to migration and eggsMay have insomnia, possible emotional

symptomsDS-eggs or adults on perineum {scotch

tape}Mebendazole 100 mg. Repeat in 2 weeks.

Pyrantel pamoate 11 mg/kg; repeat 2 weeks

NECATOR AMERICANUS- Disease: New World Hookworm Disease- Site in host: SI, attached- Portal of entry: Skin- Infective stage: filariform larva- Sources of infection: infective filariform larvae

in soil- Lab Dx: eggs in stool

Hookworm egg: oval or ellipsoid; thin shell; usually embryo at four cell stage

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- Disease: Old World Hookworm Disease- Site in host: SI, attached- Portal of entry: skin, usually feet- Infective stage: filariform larva- Sources of infection: infective filariform larvae

in soil- Lab Dx: eggs in stool

Oral opening of Ancylostoma duodenale: presence of four cutting "teeth," two on each side.

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.

A B

Causal Agents:The human hookworms include two nematode

(roundworm) species, Ancylostoma duodenale and Necator americanus. 

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, Uncinaria stenocephala). 

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. 

Necator americanus 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 FindingsMicroscopybetween 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 pyrantel pamoate* can also be used. 

Eosinophilic enteritis caused by A. caninum and for cutaneous larva migrans(creeping eruption) caused by canine and feline hookworms.

Case 1257 year old farmer from Dixie CountyPresents with profound SOBPhysical examination: anemic otherwise

unremarkableLaboratory examination reveals a

profound anemia (hct 24) with aniso and poikilocytosis

Remainder of laboratory examination normal.

Diagnosis?

HookwormHookworm responsible for development of

USPHSCaused by two different species (North

American and Old World)Very similar to strongyloides in life cycleAttaches to duodenum, feeds on bloodElaborates anticoagulant, attaches and

reattaches many timesLoss 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 rashUnable to sleepWBC 18,00065% eosinophils.

Case 15

An 8 year old boyPresents 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.

Diagnosis ?

Cutaneous Larva MigransCaused by filariform larvae of dog or cat

hookworm (Ancylostoma braziliense or Ancylostoma duodenale

Common in Southeast U.S.Red papule at entry with serpiginous

tunnelIntense pruritisSelf limiting conditionDiagnosis clinicalTopical or oral thiabendazole 25 mg/kg bid

for 3-5 daysMay 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 treatmentSkin lesions are readily recognizedUsually diagnosed clinicallyGenerally 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 wormsToxocara canis; Toxocara catisUnderdiagnosed based on

seroprevalence surveysHeavy infections associated with fever,

cough, nausea, vomiting, hepatomegaly, and eosinophilia

Uncommon in adultsOcular type more common in adultsDiagnosis-ELISAThiabendazole: 25 mg/kg bid X 5 days

Case 17

A 34 yr-old woman from Saudi ArabiaRadiation 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- Disease: Strongyloidiasis, Cochin-China

diarrhea or Vietnam diarrhea- Site in host: wall of SI- Portal of entry: skin- Infective stage: filariform larva- Sources of infection: larvae in soil;

autoinfection- Lab Dx: larvae in stool

Strongyloides stercoralis first-stage larva: The rhabditoid esophagus is clearly visible in this larva; it consists of a club-shaped anterior portion, a postmedian constriction, and a posterior bulb.

Causal Agent:The nematode (roundworm) Strongyloides

stercoralis.  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 Strongyloides stercoralis and Capillaria philippinensis infections. 

Clinical FeaturesFrequently 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 findingsMicroscopy

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 hospitalInitial blood work:

Elevated WBCRaised eosinophil count 4 times

normalUnderwent UGI endoscopyDuodenal biopsy obtained

Strongyloides: Crucial Aspects of Life CycleInfection acquired through

penetration of intact skinInfection may persist for many

years via autoinfectionIn immunocompromised patients,

there is risk of dissemination or hyperinfectionHyperinfection syndrome

Disseminated Strongyloidiasis

High mortality75%Penetration of gut wall by infective larvaeGut 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 painBloatingDiarrheaConstipation

Wheezing, SOB, hemoptysis

Summary—Clinical FindingsSkin rash or pruritis in ~ one-third Larva currens (racing larva)Intensely pruriticLinear 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- Disease: Diphyllobothriasis; fish tapeworm

infection; broad tapeworm infection- Site in host: SI- Portal of entry: mouth- 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- Lab Dx: eggs in stool

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 cestode Diphyllobothrium latum (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 findingsMicroscopy

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

DIPYLIDIUM CANINUM- Disease: Dipylidiasis; dog tapeworm

infection- Site in host: SI- Portal of entry: mouth- Definitive host: dog & cat (or humans)- Intermediate host: larval flea- Infective stage: eggs - Sources of infection: flea & louse- Lab Dx: eggs in stool or egg sacks in stool

Egg of Dipylidium caninum: round to oval (average size 35 to 40 µm) and contain an oncosphere that has 6 hooklets. Ovum contains hexacanth wmbryo (8-15 ova are usually enclosed within sac-like membrane) 

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:

Dipylidium caninum (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 Dipylidium caninum.  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 Dipylidium caninum 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 findingsMicroscopy

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- Disease: Hymenolepiasis; dwarf tapeworm

infection- Site in host: adults & cysts in SI- Portal of entry: mouth- Definitive host: human, mice & rats- Intermediate host: DO NOT require an IH- Infective stage: eggs - Sources of infection: eggs fr feces in soil;

autoinfection- Lab Dx: eggs in stool

Egg of Hymenolepis nana: oval or subspherical and smaller than those of H. diminuta, their size being 40 - 60 µm x 30 - 50 µm.  On the inner membrane are two poles, from which 4-8 polar filaments spread out between the two membranes. The oncosphere has six hooks (seen as dark lines at 8 o'clock). 

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- Disease: Hymenolepiasis; rat tapeworm

infection- Site in host: SI- Portal of entry: mouth- Definitive host: human, mice & rats- Intermediate host: insects (rat & mouse

flea, the flour moth and flour beetle)- Infective stage: eggs - Sources of infection: cysts from insects- Lab Dx: eggs in stool

Egg of Hymenolepis diminuta: round or slightly oval, size 70 - 86 µm X 60 - 80 µm, with a striated outer membrane and a thin inner membrane.  The space between the membranes is smooth or faintly granular.  The oncosphere has six hooks.

Mature proglottids of Hymenolepis diminuta.

Causal Agents:Hymenolepiasis is caused by two cestodes (tapeworm) species, Hymenolepis nana (the dwarf tapeworm,) and Hymenolepis dimnuta (rat tapeworm).  Hymenolepis diminuta 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.  Hymenolepis diminuta, 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 Hymenolepis diminuta 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.

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- Disease: Taeniasis; beef tapeworm

infection- Site in host: SI- Portal of entry: mouth- Definitive host: human- Intermediate host: grazing cattle- Infective stage: eggs - Sources of infection: cysts in beef- Lab Dx: segments and eggs in stool;

Scotch tape swab

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- Disease: Taeniasis; pork tapeworm

infection- Site in host: SI- Portal of entry: mouth- Definitive host: human- Intermediate host: pig- Infective stage: eggs - Sources of infection: cysts in pork;

autoinfection- Lab Dx: segments and eggs in stool;

Scotch tape swab

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

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) Taenia saginata (beef tapeworm) and T. solium (pork tapeworm).  Taenia solium can also cause cysticercosis.

Geographic Distribution:Both species are worldwide in distribution.  Taenia solium 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 Taenia saginata or Taenia solium.  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:Taenia saginata taeniasis 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.  

Taenia solium taeniasis is less frequently symptomatic than Taenia saginata taeniasis. 

The main symptom is often the passage (passive) of proglottids.  The most important feature of Taenia solium taeniasis 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.

Beef Tapeworm

TreatmentPraziquantelAlbendazoleNiclosamide

Tapeworms (Cestodes)

Adult worms inhabit GI tract of definitive vertebrate host

Larvae inhabit tissues of intermediate hostHumans

Definitive for T. saginataIntermediate for Echinococcus granulosus

(hydatid)Both definitive and intermediate for T.

soliumAdult worms shed egg-containing segments in

stool ingested by intermediate host larval form in tissues

CystercercosisSymptoms 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.

CysticercosisClinical manifestations

Adult worms rarely cause sxsLarvae penetrate intestine, enter blood, and

eventually encyst in the brain.Cerebral ventircles hydrocephalusSpinal cord compression, paraplegiaSubarachnoid space chronic meningitisCerebral 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

CysticercosisDiagnosis

CT and MRI preferred studiesDiscrete cysts that may enhanceUsually multiple lesions

Single lesions especially common in cases from India

Older lesions may calcifyCSF

Lymphs or eos, low glucose, elevated proteinSerology

Especially in cases with multiple cysts

CysticercosisTreatment

Complex and controversialPraziquantel 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

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Causal Agents:Schistosomiasis is caused by digenetic blood

trematodes.  The three main species infecting humans are Schistosoma haematobium, S. japonicum, and S. mansoni.  In addition, other species of schistosomes, which parasitize birds and mammals, can cause cercarial dermatitis in humans.

Geographic Distribution: Schistosoma mansoni 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. japonicum

schistosomiasis 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. haematobium schistosomiasis 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 FeaturesMany 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 FeaturesContinuing infection may cause granulomatous

reactions and fibrosis in the affected organs, which may result in manifestations that include: colonic polyposis with bloody diarrhea (Schistosoma mansoni 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 findingsmicroscopyAntobody detrectioncan 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- AKA: Sheep Liver Fluke- Disease: Fascioliasis, “liver rot”- Site in host: Bile ducts- Portal of entry: mouth- 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

Fasciola hepatica eggs: eggs are ellipsoidal, with small, barely distinct operculum. The operculum can be opened. The eggs have a thin shell which is slightly thicker at the abopercular end.  They are passed unembryonated. 

Causal Agents:

The trematodes Fasciola hepatica (the sheep liver fluke) and Fasciola gigantica, 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.

Life Cycle: Immature eggs are discharged in the biliary ducts and in the stool . 

Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria and Pseudosuccinea.  In the snail the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ).  The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces.  Mammals acquire the infection by eating vegetation containing metacercariae.  Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress .  After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults .  In humans, maturation from metacercariae into adult flukes takes approximately 3 to 4 months.  The adult flukes (Fasciola hepatica: up to 30 mm by 13 mm; F. gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host.  Fasciola hepatica infect various animal species, mostly herbivores.

Clinical Features:During the acute phase (caused by the migration of the immature fluke through the hepatic parenchyma), manifestations include abdominal pain, hepatomegaly, fever, vomiting, diarrhea, urticaria and eosinophilia, and can last for months.  In the chronic phase (caused by the adult fluke within the bile ducts), the symptoms are more discrete and reflect intermittent biliary obstruction and inflammation.  Occasionally, ectopic locations of infection (such as intestinal wall, lungs, subcutaneous tissue, and pharyngeal mucosa) can occur.

Diagnostic findingsMicroscopy and antibody detection

Treatment:Unlike infections with other flukes, Fasciola hepatica infections may not respond to praziquantel.  The drug of choice is triclabendazole with bithionol as an alternative. 

Causal Agent:The trematode Fasciolopsis buski, the largest intestinal fluke of humans.

Geographic Distribution:Asia and the Indian subcontinent, especially in areas where humans raise pigs and consume freshwater plants.

Life Cycle:

Immature eggs are discharged into the intestine and stool .  Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host . 

In the snail the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ).  The cercariae are released from the snail and encyst as metacercariae on aquatic plants .

The mammalian hosts become infected by ingesting metacercariae on the aquatic plants.  After ingestion, the metacercariae excyst in the duodenum and attach to the intestinal wall. .  The  adults have a life span of about one year.

Clinical Features:Most infections are light and asymptomatic.  In heavier infections, symptoms include diarrhea, abdominal pain, fever, ascites, anasarca and intestinal obstruction.

Diagnostic findingsMicroscopy

Treatment:Praziquantel* is the drug of choice. 

CLONORCHIS SINENSIS- AKA: Chinese or Oriental Liver Fluke- Disease: Clonorchiasis- Site in host: Bile ducts- Portal of entry: mouth- Definitive host: humans, dog & cat or other

mammals- 1st Intermediate host: freshwater snail

(Bulinus, Parafossarulus)- 2nd Intermediate host: freshwater fish

(Cyprinidae)- Infective stage: metacercariae - Lab Dx: eggs in stool

C. sinensis, adult: stained whole mount; approximate size = 15 mm.

C. sinensis egg: small operculated eggs.  Size 27 to 35 µm by 11 to 20 µm.  The operculum, at the smaller end of the egg,  is convex and rests on a visible "shoulder".  At the opposite (larger, abopercular) end, a small knob or hooklike protrusion is often visible (as is the case here).  The miracidium is visible inside the egg.

Causal Agent:The trematode Clonorchis sinensis (Chinese or oriental liver fluke).

Geographic Distribution:Endemic areas are in Asia including Korea, China, Taiwan, and Vietnam.  Clonorchiasis has been reported in non endemic areas (including the United States).  In such cases, the infection is found in Asian immigrants, or following ingestion of imported, undercooked or pickled freshwater fish containing metacercariae.

Life Cycle:Embryonated eggs are discharged in the biliary ducts and in

the stool .  Eggs are ingested by a suitable snail intermediate host ;

there are more than 100 species of snails that can serve as intermediate hosts.  Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ).  The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae .

  Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish .  After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater .  Maturation takes approximately 1 month.  The adult flukes reside in small and medium sized biliary ducts.  In addition to humans, carnivorous animals can serve as reservoir hosts.

Clinical Features:

Most pathologic manifestations result from inflammation and intermittent obstruction of the biliary ducts.  In the acute phase, abdominal pain, nausea, diarrhea, and eosinophilia can occur.  In long-standing infections, cholangitis, cholelithiasis, pancreatitis, and cholangiocarcinoma can develop, which may be fatal.

Diagnostic findingsMicroscopy.Treatment:

Praziquantel or albendazole* are the drugs of choice. 

Causal Agent:

Trematodes (flukes) Opisthorchis viverrini (Southeast Asian liver fluke) and O. felineus (cat liver fluke).

Geographic Distribution:O. viverrini is found mainly in northeast Thailand, Laos, and Kampuchea.  O. felineus is found mainly in Europe and Asia, including the former Soviet Union.

Life Cycle:The adult flukes deposit fully developed eggs that are passed

in the feces .  After ingestion by a suitable snail (first intermediate host) ,

the eggs release miracidia , which undergo in the snail several developmental stages (sporocysts , rediae , cercariae ).  Cercariae are released from the snail and penetrate freshwater fish (second intermediate host), encysting as metacercariae in the muscles or under the scales . 

The mammalian definitive host (cats, dogs, and various fish-eating mammals including humans) become infected by ingesting undercooked fish containing metacercariae.  After ingestion, the metacercariae excyst in the duodenum and ascend through the ampulla of Vater into the biliary ducts, where they attach and develop into adults, which lay eggs after 3 to 4 weeks . 

The adult flukes reside in the biliary and pancreatic ducts of the mammalian host, where they attach to the mucosa.

Clinical Features:Most infections are asymptomatic.  In mild cases, manifestations include dyspepsia,

abdominal pain, diarrhea or constipation.  With infections of longer duration, the symptoms can

be more severe, and hepatomegaly and malnutrition may be present. 

In rare cases, cholangitis, cholecystitis, and chlolangiocarcinoma may develop. 

infections due to O. felineus may present an acute phase resembling Katayama fever (schistosomiasis), with fever, facial edema, lymphadenopathy, arthralgias, rash, and eosinophilia. 

Chronic forms of O. felineus infections present the same manifestations as O. viverrini, with in addition involvement of the pancreatic ducts.

Diagnostic findingsMicroscopy

Treatment:Praziquantel is the drug of choice to treat opisthorchiasis. 

PARAGONIMUS WESTERMANI- AKA: Lung Fluke- Disease: Paragonimiasis, pulmonary distomiasis,

lung fluke disease- Site in host: Lungs- Portal of entry: mouth- Definitive host: humans & a variety of carnivores- 1st Intermediate host: freshwater snail (Family

Thieridae)- 2nd Intermediate host: freshwater crab (Eriocheir,

Patamon, Sesarma, Parathelphusa) or crayfish (Cambarus, Astacus)

- Source of infection: consumption of raw or undercooked infected freshwater crustaceans

- Infective stage: metacercariae - Lab Dx: eggs in sputum & stool

Egg of P. westermani: The average egg size is 85 µm by 53 µm (range: 68 to 118 µm by 39 to 67 µm).  They are yellow-brown, ovoidal or elongate, with a thick shell, and often asymmetrical with one end slightly flattened.  At the large end, the operculum is clearly visible.  The opposite (abopercular) end is thickened.  The eggs of P. westermani are excreted unembryonated.

Paragonimus westermani: Cross section of lung containing adult Paragonimus westermani.

Causal Agent:

More than 30 species of trematodes (flukes) of the genus Paragonimus have been reported which infect animals and humans.  Among the more than 10 species reported to infect humans, the most common is P. westermani, the oriental lung fluke.

Geographic Distribution:Paragonimus spp. are distributed throughout the Americas, Africa and southeast Asia.  Paragonimus westermani is distributed in southeast Asia and Japan.  Paragonimus kellicotti is endemic to North America.

Life Cycle:

The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stool . 

In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues .  Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail.  The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae.  This is the infective stage for the mammalian host . 

Life Cycle:

Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite .  The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (. 

The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively.  However, when this takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites.  Time from infection to oviposition is 65 to 90 days. 

Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani.

Clinical Features:The acute phase (invasion and migration)

may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia. 

During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum, hemoptysis, and chest radiographic abnormalities. 

Extrapulmonary locations of the adult worms result in more severe manifestations, especially when the brain is involved.

Diagnostic findingsMicroscopyAntibody detection is useful in light infections

and in the diagnosis of extrapulmonary paragonimiasis.

Treatment:Praziquantel* is the drug of choice to treat paragonimiasis.  Bithionol is an alternative drug for treatment of this disease. 

METAGONIMUS YOKOGAWAI- Disease: Metagonimiasis- Site in host: Bile ducts- Portal of entry: mouth- Definitive host: humans, dogs, cats, hogs,

pelicans & other fish-eating birds- 1st Intermediate host: snail

(Semisulcospira, Thiara and Hua)- 2nd Intermediate host: freshwater fish

(Salmonoids & cyprinoids)- Infective stage: metacercariae - Lab Dx: eggs in stool

M. yokogawai, adult fluke: the position of the ventral sucker is to the side of the midline with its axis in a diagonal line

Causal Agent:

Metagonimus yokogawai, a minute intestinal fluke (and the smallest human fluke).

Geographic Distribution:Mostly the Far East, as well as Siberia, Manchuria, the Balkan states, Israel, and Spain.

Life Cycle:

Adults release fully embryonated eggs each with a fully-developed miracidium, and eggs are passed in the host’s feces . 

After ingestion by a suitable snail (first intermediate host), the eggs hatch and release miracidia which penetrate the snail’s intestine .  Snails of the genus Semisulcospira are the most frequent intermediate host for Metagonimus yokogawai.  The miracidia undergo several developmental stages in the snail, i.e. sporocysts , rediae , and cercariae .  Many cercariae are produced from each redia.  The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable fresh/brackish water fish (second intermediate host) . 

The definitive host becomes infected by ingesting undercooked or salted fish containing metacercariae .  After ingestion, the metacercariae excyst, attach to the mucosa of the small intestine and mature into adults (measuring 1.0 mm to 2.5 mm by 0.4 mm to 0.75 mm) .  In addition to humans, fish-eating mammals (e.g., cats and dogs) and birds can also be infected by M. yokogawai .

Clinical Features:The main symptoms are diarrhea and colicky abdominal pain.  Migration of the eggs to extraintestinal sites (heart, brain) can occur, with resulting symptoms.

Diagnostic findingsMicroscopy

Treatment:Praziquantel* is the drug of choice. 

HETEROPHYES HETEROPHYES- Disease: Heterophyiasis- Site in host: Bile ducts- Portal of entry: mouth- Definitive host: humans, dog & cat or other

fish eating mammals- 1st Intermediate host: brackish water snail

(Pirenella, Cerithidea)- 2nd Intermediate host: brackish water fish

(Mugil, Tilapia and Acanthogobus)- Infective stage: metacercariae - Lab Dx: eggs in stool

Causal Agent:

The trematode Heterophyes heterophyes, a minute intestinal fluke.

Geographic Distribution:Egypt, the Middle East, and Far East.

Life Cycle:Adults release embryonated eggs each with a fully-developed

miracidium, and eggs are passed in the host's feces .  After ingestion by a suitable snail (first intermediate host), the

eggs hatch and release miracidia which penetrate the snail’s intestine .  Genera Cerithidia and Pironella are important snail hosts in Asia and the Middle East respectively.  The miracidia undergo several developmental stages in the snail, i.e. sporocysts , rediae , and cercariae .  Many cercariae are produced from each redia.  The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable fresh/brackish water fish (second intermediate host) . 

The definitive host becomes infected by ingesting undercooked or salted fish containing metacercariae .  After ingestion, the metacercariae excyst, attach to the mucosa of the small intestine and mature into adults

.  In addition to humans, various fish-eating mammals (e.g., cats and dogs) and birds can be infected by Heterophyes heterophyes .

Clinical Features:

The main symptoms are diarrhea and colicky abdominal pain. 

Migration of the eggs to the heart, resulting in potentially fatal myocardial and valvular damage, has been reported from the Philippines. 

Migration to other organs (e.g., brain) has also been reported.

Laboratory Diagnosis:Microscopy

Treatment:Praziquantel* is the drug of choice. 

FASCIOLOPSIS BUSKI- AKA: Large or giant intestinal fluke- Disease: Fasciolopsiasis- Site in host: SI- Portal of entry: mouth- Definitive host: pig & humans- 1st Intermediate host: snail (Segmentina /

Hippeutis)- 2nd Intermediate host: water chestnuts &

lotus- Infective stage: metacercariae - Lab Dx: eggs in stool

Adult fluke of Fasciolopsis buski.

Egg of F. buski: eggs are ellipsoidal, with a thin shell, and a usually small, indistinct operculum.  In this particular egg, the operculum is open. 

SCHISTOSOMA MANSONI- Disease: Schistosomiasis, intestinal

schistosomiasis, bilharziasis “snail fever”- Site in host: veins of LI- Portal of entry: skin- Definitive host: humans, baboons &

rodents- Intermediate host: snail (Biomphalaria sp &

Tropicorbis sp)- Infective stage: cercariae - Lab Dx: eggs in stool; rectal or liver biopsy

Biomphalaria spp.

Schistosoma mansoni eggs: large (length 114 to 180 µm) and have a characteristic shape, with a prominent lateral spine near the posterior end.  The anterior end is tapered and slightly curved.  When the eggs are excreted, they contain a mature miracidium

Male and female schistosomes.

SCHISTOSOMA HAEMATOBIUM- Disease: Urinary schistosomiasis,

schistosomal hematuria, urinary bilharziasis

- Site in host: veins of urinary bladder- Portal of entry: skin- Definitive host: humans, monkeys &

baboons- Intermediate host: snail (Bulinus,

Physopsis, and Biomphalaria sp)- Infective stage: cercariae - Lab Dx: eggs in stool; cystoscopy

Bulinus spp.

S. haematobium eggs: large and have a prominent terminal spine at the posterior end

S.haematobium: adult schistosomes live in pairs in the pelvic veins (especially in the venous plexus surrounding the bladder); males are 10-15 mm in lenght by 0,8-1 mm in diameter, and have a ventral infolding from the ventral sucker to the posterior end forming the gynecophoric canal. Adult male with female in the copulatory groove.

SCHISTOSOMA JAPONICUM- Disease: Schistosomiasis, Katayama

fever- Site in host: veins of SI- Portal of entry: skin- Definitive host: humans, dogs, cats,

horses, pigs, cattle, deer, caribou & rodents

- Intermediate host: snail (Oncomelania)- Infective stage: cercariae - Lab Dx: eggs in stool; liver biopsy

Onchomelania, hupensis spp.

S. japonicum egg: typically oval or subspherical, and has a vestigial spine (smaller than those of the other species)

Cercaria

TISSUE NEMATODES and CESTODES

TRICHINELLA SPIRALIS- Disease: Trichinosis, trichiniasis,

trichinelliasis- Site in host: Adult – SI wall; Encysted

larvae – striated muscle- Portal of entry: Mouth- Definitive Host: human, pig, bear & other

carnivorous/omnivorous animals- Sources of infection: encysted larvae in

pork- Lab Dx: skin test, serology (slide

flocculation/ ELISA), muscle biopsy

Encysted larvae of Trichinella in pressed muscle tissue. The coiled larvae can be seen inside the cysts.

Larvae of Trichinella, freed from their cysts, typically coiled; length: .8 to 1 mm.

ECHINOCOCCUS GRANULOSUS- Disease: Echinococcosis, hydatid disease,

hydatid cyst- Site in host: liver, lungs, brain, bones- Portal of entry: Mouth- Definitive Host: dogs, wolves & other

Canidae- Sources of infection: eggs from dog feces

in soil- Lab Dx: skin test, X-ray, CAT scan, serology

"Hydatid sand". Fluid aspirated from a hydatid cyst shows multiple protoscolices (size approximately 100 µm), each of which has typical hooklets. The protoscolices are normally invaginated (left), and evaginate (middle, then right) when put in saline.

Echinococcus granulosus: the protoscolices then become invaginated and measure 90-140 by 70-120 µm. They can transform into daughter cysts.These cysts can proliferate both internally and externally giving exogenous cysts. Spontaneous or surgical rupture of the cyst can originate a secondary hydatidosis.

Histopathology of hydatid cyst.

Echinococcus granulosus: the presence of isolated hooklets is diagnostic for hydatidosis. Hooklets can be observed in hydatid fluid and must be searched in sputum after a vomica .

Hydatid cysts

ECHINOCOCCUS MULTILOCULARIS- Disease: Alveolar Echinococcosis- Site in host: liver, lungs, brain, bones- Portal of entry: Mouth- Definitive Host: foxes, cats, dogs, & other

carnivores- Intermediate Host: mouse, vole, &

lemming (human is an accidental host)- Sources of infection: eggs from dog/cat

feces in soil- Lab Dx: serologic tests (ELISA, IHA)

MICROFILARIAEWUCHERERIA BANCROFTI- Disease: Bancroftian filariasis, wuchereriasis- Site in host: Lymphatics- Portal of entry: Skin- Definitive Host: human- Intermediate Host: mosquito (Culex, Aedes,

Anopheles species)- Sources of infection: Mosquitoes- Lab Dx: Blood smear

Periodic form: between 10 am and 2amSubperiodic form: between 2 and 5 pm

- Microfilariae: sheathed; nuclei do not extend to tip of tail

Brugia malayi /Wuchereria bancrofti: B.malayi is transmitted by mosquitoes of the genus Mansonia, Anopheles and Aedes. W.bancrofti is transmitted by mosquitoes of the genus Culex, Anopheles and Aedes.

Microfilaria of Wuchereria bancrofti: sheathed, its body is gently curved, and the tail is tapered to a point. The nuclear column (the cells that constitute the body of themicrofilaria) is loosely packed, the cells can be visualized individually and do not extend to the tip of the tail.

Wuchereria bancrofti adults in section of lymph node

BRUGIA MALAYI- Disease: Malayan filariasis- Site in host: Lymphatics- Portal of entry: Skin- Definitive Host: human, monkey & cat- Intermediate Host: mosquito (Mansonia, Aedes,

Anopheles species)- Sources of infection: Mosquitoes- Lab Dx: Blood smear

Periodic (nocturnal) form: between 10 amand 2am

Subperiodic form: between 9 and 11 pm - Microfilariae: sheathed; nuclei exted to tip of tail

w/ 2 separated & swollen terminal nuclei

Microfilaria of Brugia malayi: has a sheath, are more tightly coiled, and the nuclear column is more tightly packed, preventing the visualization of individual cells.

Microfilaria of Brugia malayi, collected by the Knott (centrifugation) concentration technique, in 2% formalin wet preparation.  Note the clearly visible sheath that extends beyond the anterior and posterior ends of the microfilaria.  (There are four sheathed species: Wuchereria bancrofti, Brugia malayi, Brugia timori, and Loa loa.)

Detail from the microfilaria of Brugia malayi showing the tapered tail, with a subterminal and a terminal nuclei, separated by a gap without nuclei. 

LOA LOA- Disease: Loiasis, eye worm, fugitive

swellings, Calabar swellings- Site in host: Subcutaneous- Portal of entry: Skin- Definitive Host: human and monkey- Intermediate Host: fly (Chrysops)- Sources of infection: fly- Lab Dx: Blood smear

Diurnal periodicity: between 11 am and 1 pm

- Microfilariae: sheathed; nuclei extend to tipof tail

Microfilariae of Loa loa  (right) and Mansonella perstans (left). L. loa is sheathed, with a relatively dense nuclear column; its tail tapers and is frequently coiled, and nuclei extend to the end of the tail.  M. perstans is smaller, has no sheath, and has a blunt tail with nuclei extending to the end of the tail.

MANZONELLA OZZARDI and MANSONELLA PERSTANS

- Disease: Ozzardi filariasis/Perstan filariasis- Site in host: body cavities- Portal of entry: Skin- Definitive Host: human - Intermediate Host: midge (Culicoides &

Simulium)- Sources of infection: midge- Lab Dx: Blood smear- Microfilariae found in blood: No periodicity;

unsheathed; nuclei do not extend to tip of tail (M. ozzardi)/extend to tip of tail (M. perstan)

MANZONELLA STREPTOCERCA- Disease: Ozzardi filariasis/Perstan filariasis- Site in host: body cavities- Portal of entry: Skin- Definitive Host: human - Intermediate Host: midge (Culicoides &

Simulium)- Sources of infection: midge- Lab Dx: Blood smear- Microfilariae found in skin: No periodicity;

unsheathed; nuclei extend to tip of tail

Microfilaria of Mansonella streptocerca from a skin snip: unsheathed, has a nearly straight body attitude, the tail is typically coiled into a “shepherd’s crook”, and terminal nuclei extend as a single row to the end of the tail.

ONCHOCERCA VOLVULUS- Disease: Onchocerciasis, onchocercosis,

river blindness, “Sowda”- Site in host: Subcutaneous- Portal of entry: Skin- Definitive Host: human - Intermediate Host: fly (Simulium)- Sources of infection: fly- Lab Dx: skin biopsy or snips, nodule

aspirate- Microfilariae found in skin: No periodicity;

unsheathed; nuclei do not extend to tip of tail

Microfilaria of Onchocerca volvulus: tail is sharply and is s sharply angled at the end

Onchocerca volvulus, posterior end

Histopathology of Onchocerca volvulus nodule.

DRACUNCULUS MEDINENSIS, THE GUINEA WORM

- Disease: Dracontiasis, dracunculosis, guinea worm disease

- Site in host: Subcutaneous- Portal of entry: Mouth- Definitive Host: human & domesticated

and wild fur bearing animals - Intermediate Host: water flea (Cyclops)- Sources of infection: fly- Lab Dx: skin biopsy or snips, nodule

aspirate- Microfilariae found in skin: No periodicity

The female guinea worm induces a painful blister (A); after rupture of the blister, the worm emerges as a whitish filament (B) in the center of a painful ulcer which is often secondarily infected. 

D. medinensis worm wound around matchstick.This helminth is gradually withdrawn from the body by winding the stick.