1-2. Enterobius vermicularis (pinworm). 1. Adult male (20) and 2. female (10).

These mature in the anterior

portion of the colon. The adult yellowish-white female worms are 8 to 13 mm and the male worms 2 to 5 mm
in size. Each has a bulbar esophagus as well as fin like projections, called cephalic alae, about the anterior
end. Male and female worms are further differentiated in that the male has a sharp curvature of the tail and
small posterior copulatory spicule, whereas the female has a long, straight, sharply pointed tail. When the
uterus is gravid with eggs, the female migrates from the colon (usually during sleeping hours of the host) to
the perianal area, where she deposits her eggs and dies. The adult may also migrate to the appendix, where
it can be found histologically. Pinworm disease is essentially an allergic reaction to the release of eggs and
other secreted materials from the gravid female, which causes severe rectal itching.

3. A higher-power view of the anterior end of the adult, clearly showing the alae.

4. Note the caudal curve and copulatory spicules of the male Enterobius vermicularis.

5. Enterobius vermicularis eggs (400). Eggs may be recovered from the perianal folds by applying the sticky
side of cellophane tape to the skin surfaces and then taping the cellophane, sticky side down, onto a
microscope side for examination. Eggs are rarely recovered in feces. The eggs are elongated (55 µm 25µm)
and tend to be flattened on one side. The thick shell is transparent and colorless and the folded larva may be
seen within. Pinworm eggs are infective for the host within a few hours of being released. Scratching of the
perianal region allows transfer of the eggs by hand to the mouth of the host. The eggs hatch soon after they
are swallowed and develop to mature worms within 2 weeks. Bedding, night clothing, and even house dust
may be sources of egg infection for others through ingestion or inhalation of airborne eggs. This is a very
common parasitic infection in this country and spreads easily, so that those living with an infected individual
are likely to become infected.

6. Enterobius vermicularis egg (900 ). This view shows an egg under oil immersion; the developed larva can
be clearly seen coiled inside the flattened shell.

7. Enterobius vermicularis egg (100). A low-power view of the egg as seen on a cellophane tape
preparation. Because of the transparency of the eggs, screening of the slides must be carefully performed
using low illumination.

8. Trichuris trichiura (whipworm) (4). Adult female, measuring 35 to 50 mm. The anterior ends of both male
and female worms are slender and threadlike, but the posterior one-third of the worm is wider. The posterior
end of the female appears club-shaped and straight; the male has a 360-degree coiled posterior with two
copulatory spicules. The adults in the intestine attach firmly by embedding a spear like projection at their
anterior end into the mucosa of the cecum and proximal colon. Distribution of this parasite is cosmopolitan,
especially in moist, warm areas. This is the most commonly reported parasitic infection in this country. Light
infections are usually asymptomatic, but heavy infections may cause enteritis and diarrhea with rectal
prolapse.
9. Trichuris trichiura egg (500). Diagnosis: recovery of eggs in feces. Concentration technique needed to detect a
light infection. The Trichuris egg is characteristically barrel-shaped and measures 20 µm 50 µm. Note the
undeveloped embryo; the clear, inner shell; the heavy, golden outer shell; and the transparent hyaline plugs at
the ends of the egg. Eggs passed in feces must remain in a favorable soil environment for at least 10 days until
larval development is complete; at this time the egg is infective. Ingestion of the egg from infected soil or
contaminated food is followed by hatching in the intestines. The larva molts and develops in the intestines to
become an adult. About 90 days are needed for a complete cycle from egg ingestion to egg output by the adults.

10. Trichuris trichiura egg. This view shows an egg at a magnification of 100. (Note: Dog whipworm is an
occasional zoonosis; the egg is much larger [35 µm 80 µm] and broader.)

11. Ascaris lumbricoides. Both male and female adults are shown. They are large, pinkish-white, and conically
tapered at the anterior end. A female measures 22 to 35 cm in length 3 to 6 mm in diameter and has a pinkish-
white and straight tail. A male measures 10 to 31 cm 2 to 4 mm and has a sharply curved tail with two copulatory
spicules. The adults live in the small intestine and can survive for over a year. Females lay up to 250,000 eggs
per day, which are passed in the feces and can be readily recovered by routine fecal examination. Passage of
adult worms from the rectum is often the first indication of infection. Light infections are asymptomatic. Heavy
infections may cause pneumonia early in the infection and, later, diarrhea, vomiting, or bowel obstruction.
Complications such as perforation of the intestinal wall or appendix, with resultant peritonitis or obstruction of
airways by vomited worms, may cause death. Known as the large intestinal roundworm.

12. An obstructed bowel from a heavily infected patient with Ascaris lumbricoites. Distribution of this parasite is
worldwide, although it is more frequently found in tropical areas.

13. Ascaris lumbricoides egg (400). Diagnosis: recognition of eggs (or adults) in feces. The fertilized egg
measures 40 µm 55 µm and contains an undeveloped embryo. This egg appears round, but Ascaris eggs are
slightly oval. The outer coat is albuminous and mamillated; occasionally, eggs without coats may be found
(decorticated). The thick, inner coat is of clear chitin. These characteristics are diagnostic. On reaching warm,
moist soil, larvae develop within the egg shells in 2 to 3 weeks and eggs are then infective for humans. Infection
occurs by ingestion of these infective eggs in contaminated food or drink. It is not uncommon for Ascaris and
Trichuris to coexist in the same person because of the same method of infection and the requirements for egg
development in the soil. Eggs hatch in the intestine and the Ascaris larvae rapidly penetrate the mucosal wall.
They reach the liver and then the lungs via the blood circulation. Larvae emerge from the circulation into the
lungs in about 9 days, migrate up the bronchi to the esophagus, and are swallowed. They mature in the intestine
in about 2 months. In an immune individual, most larvae are destroyed in the liver.

14. Ascaris lumbricoides egg. This view shows an egg at a magnification of 100. Ascarids of dogs and cats
(Toxocara spp.) can undergo partial development and produce pathology in humans. After ingestion of an egg
from soil, the Toxocara eggs hatch and the larvae penetrate the intestinal wall and enter the blood circulation but
are unable to complete the migratory route. They lodge in tissues and cause inflammatory reactions leading to
occlusions of capillaries of vital organs (e.g., eye, liver, brain, lungs). Symptoms vary depending on the location
of the parasite and the host’s reaction to it. The disease is called visceral larval migrans. It is seen most
commonly in children because they are more likely to ingest eggs from infected soil, such as at a playground
where dogs are walked. High eosinophilia is a very common sign. Diagnosis is made serologically or by
observing larvae in histopathological sections. Species identification is difficult but can be done.

15. Ascaris lumbricoides egg (400). An unfertilized egg. Note the elongated shape and the heavy, albuminous,
mamillated coat. This type of egg is occasionally seen.

16. Adult male hookworm (10). Adult hookworms are small, grayish-white nematodes. The anterior end is tapered
and curved and has an open buccal capsule. The posterior end of the male terminates in a fan-shaped
copulatory bursa and spicules. The ray-like pattern of the chitinous supportive structure in the bursa is different
for each species. Females (12 µm 0.5 µm) are larger than males (9 µm 0.4 µm). The female has a straight and
pointed tail and produces 5,000 to 10,000 eggs per day. She may live for up to 14 years.
17. Necator americanus (New World hookworm). The anterior end of an adult worm. Species identification is
helped by examining the buccal capsule. Note the pair of semilunar cutting plates in the upper side of the buccal
cavity. There is also a second, smaller set of plates on the lower side.

18. Ancylostoma duodenale (Old World hookworm). The anterior end of an adult worm. Note the two pairs of
teeth in the buccal cavity. The mouthparts of hookworms allow firm attachment to the mucosa of the small
intestine and ingestion of blood. N. americanus is found throughout Africa and the southeastern United States; A.
duodenale is found in southern Europe, northern Africa, the Far East, and the Mediterranean countries. Both are
found in parts of Asia, Central and South America, and the South Pacific. Symptoms of the disease depend on
the extent of the infection and the nutritional status of the patient and can appear clinically as a hypochromic
microcytic anemia because of the bloodsucking activity of worms. Only a heavy infection causes the disease
state.

19. Hookworm egg (500). Note the definite but thin shell and the clear area around the embryo. Diagnosis of the
presence of hookworms can be made on recognition of the eggs in feces, but adults must be examined for
species identification because the eggs and larvae of these worms look alike. Eggs usually contain an immature
embryo in the 4- to 8-cell stage of division if feces are promptly examined. Six cells are visible in this embryo.
Eggs measure about 30 µm 50 µm.

20. Hookworm eggs (500). This view shows more mature eggs containing developing rhabditiform larvae. Eggs
are shed in feces and the embryo rapidly develops to a larva in 1 to 2 days. Eggs hatch to liberate rhabditiform
larvae, which then further mature in the soil to become infective filariform larvae.
21. Hookworm rhabditiform larva, showing the anterior end of the first-stage larva (500). Although these larvae
are not usually seen in fresh fecal preparations, larvae may develop and hatch if feces are not promptly
examined. This view has been included so that differential characteristics between hookworm larvae and
Strongyloides stercoralis rhabditiform larvae may be studied. Note that the buccal cavity of a first-stage
hookworm larva is slightly longer than the width of the head, appearing as two parallel lines extending back from
the anterior edge of the larvae. It has a longer buccal cavity than that of S. stercoralis; this is the primary
characteristic differentiating the two (see Plate 25). In addition, the genital primordium is not obvious in hookworm
larvae but is visible in Strongyloides larvae. The hook worm larva measures 250 µm 17 µm.

22. Hookworm filariform larva (100). Infection occurs when infective stage (filariform) larvae penetrate skin,
especially between the toes. The larvae are carried throughout the body via lymphatic and blood circulation. Most
larvae emerge from the circulation in the lungs, migrate up the bronchi to the esophagus, and are swallowed.
They complete maturation in the intestine in about 2 weeks. Nonfeeding infective hookworm larvae in soil are
ensheathed and have pointed tails. A short esophagus extending about one-quarter of the way down from the
anterior end is another differentiating characteristic.

23. Infective filariform larvae of dog and cat hookworms, especially Ancylostoma braziliense, can invade human
skin, producing an allergic dermatitis called creeping eruption or cutaneous larval migrans. Inasmuch as the
human is an unnatural host for animal hookworms, further larval development does not occur. An itching, red
papule is produced at the site of larval entry with development of a serpentine tunnel between the epithelial
layers produced as the larva migrates. The larva moves several millimeters per day and may survive several
weeks or months. This disease is widely distributed and is common in sandy areas on the Atlantic coast from
New Jersey to the Florida Keys, along the Gulf of Mexico, and in many parts of Texas. It is also found in the
midwestern United States.

24. Strongyloides stercoralis (threadworm) (400). This view is of a rhabditiform larva (225 µm 15 µm) seen in
feces. Concentration techniques are helpful because numbers are low. The esophageal bulb is evident at the
junction of the esophagus and intestine, which is about one-fourth of the parasite’s length back from the anterior
end. This is one diagnostic feature that may be used to differentiate the hookworm from the Strongyloides
rhabditiform larvae because this structure is not as prominent in hookworm larvae. Adult parthenogenic female
worms (2.2 mm 50 µm) live in the submucosa of the upper small intestine. Eggs pass through the mucosa and
the rhabditiform larvae hatch in the lumen of the intestine to be shed in feces. The larvae may develop in soil to
become infective filariform larvae and penetrate the skin as do hookworm larvae. They may, however, also molt
and become infective before they pass in feces and penetrate the mucosa of the colon to cause autoinfection,
especially in debilitated or immunocompromised persons. In either case, they travel via the blood-lung route as
do hookworm larvae, returning to the intestine to develop into adults. The life cycle of this parasite may also
include a free-living cycle in the soil. In this case, rhabditiform larvae molt and develop in 2 to 3 days to become
free-living mature adults. The sexually mature free-living male and female mate and produce eggs that develop
into filariform larvae, which are infective to humans via skin penetration.
25. Strongyloides stercoralis (500). This view shows the short buccal cavity of the rhabditiform larva. The length
is one-third to one-half the width of the head of the larva (compare with Plate 21). Diagnosis is based on the
recovery of characteristic rhabditiform larvae from feces. The filariform (infective stage) larva of Strongyloides
recovered from soil or cultured in the laboratory has a notched tail, whereas the filariform larvae of hookworms
have pointed tails. This parasite is found worldwide, especially in warm climates. As with hookworm disease,
there is a dermatitis at the site of repeated larval entry, and respiratory symptoms may result from the larvae as
they migrate through the lungs. Abdominal symptoms vary with the extent of the infection, from mild epigastric
pain to vomiting, diarrhea, and weakness with weight loss. Moderate eosinophilia is common. Untreated, the
disease may last for many years because of autoinfection from larvae that develop in the colon and may cause
death in immunosuppressed patients.

26. Trichinella spiralis (trichina worm). Encysted larva in muscle tissue (400). Adult worms develop (in about 1
week) in the submucosal tissues of the small intestine. They are very small: the male measures 1.5 mm, and the
female measures 3.5 mm. Larvae (1 mm) produced by the female pass into the mesenteric venules or lymphatics
and are carried throughout the body. Within about 2 weeks they emerge from the blood to enter striated muscle
cells or other tissue, although they survive only if they enter striated muscle cells (for instance, in the tongue or
diaphragm). The 1-mm larvae become encysted in the muscle and calcify over time but remain alive for years.
Many hundreds of larvae may be produced over the female’s life span of 2 to 3 weeks. Infection occurs when
undercooked pork or bear meat containing encysted larvae is ingested; the larvae develop into adults in the
intestines in a few days. The disease state, trichinosis, is found worldwide among meat-eating populations (with
the highest prevalence in Europe and North America) and presents a variety of symptoms, including gastric
distress, fever, edema (especially of the face), and acute inflammation of muscle tissue. Daily study of blood
smears showing increasing eosinophilia is a useful diagnostic aid. A history of eating undercooked meat, skin
testing, and positive serologic tests are strongly suggestive of infection but are not conclusive. Definitive
diagnosis depends on demonstration of the encysted larvae in a muscle biopsy from the patient. Attempts at
recovery of adult parasites from feces are usually futile. Light infections have vague symptoms, which may be
missed.

27. Trichinella spiralis. A higher-power view of a stained section. Note the tissue inflammation around encysted
larvae in the muscle “nurse cells.”

28. Wuchereria bancrofti (Bancroft’s filaria) microfilaria (400). Diagnosis: recovery of characteristic microfilariae in
blood. A thick, peripheral blood smear, stained with Giemsa stain, showing the sheathed embryo, which
measures 250 mm in length. The ends of the sheath appear almost colorless and are noncellular, often staining
poorly with Giemsa. The presence of a sheath and the pattern of cell nuclei, which can be seen in the posterior
end of the microfilaria (upper center photograph), are diagnostic. In this species, a single column of cell nuclei
extends only to near the tip of the tail, which has no nuclei. Microfilariae are most prevalent in the peripheral
blood at night (nocturnal periodicity); therefore, they are best detected in blood specimens obtained between 9
P.M. and 3 A.M. Blood concentration is helpful. Adult nematodes live in the lymphatics. Prolonged infections
cause obstruction of lymph flow, resulting in elephantiasis of the lower extremities, genitalia, or breasts. Other
symptoms include fever and eosinophilia caused by allergic reactions to the parasite. Culex, Aedes, Mansonia,
and Anopheles mosquitoes serve as intermediate hosts of W.bancrofti and are found in tropical areas worldwide.

29. Brugia malayi (Malayan filaria) sheathed microfilaria (400). Diagnosis: recovery of characteristic microfilariae
in blood at night. The sheath stains pink with Giemsa. Note that the nuclei occur in groups to the end of the tail,
with two nuclei in the tip (middle right of photograph). These features are diagnostic. The disease produced is
essentially identical to W. bancrofti but is found primarily in Southeast Asia, India, and China. These microfilariae
also exhibit nocturnal periodicity in the blood and the mosquito vectors are species of Mansonia, Aedes, and
Anopheles.

30. Loa loa (African eyeworm) microfilaria (400). Diagnosis: recovery of characteristic microfilariae in blood. The
sheath does not stain with Giemsa. In this thick blood smear, the sheathed microfilaria can be seen, measuring
250 µm in length. Note that cell nuclei occur in groups through most of the body but are seen in a single line to
the tip of the posterior end of the tail (upper right of photograph). This feature is diagnostic. In humans, adults
migrate throughout the subcutaneous tissues, causing transient swellings called Calabar swellings. Adults may
be seen migrating through the conjunctiva of the eye. Microfilariae are most prevalent in the blood during the day
(diurnal periodicity), and the vector is the mango fly ( Chrysops). The disease is chronic and relatively benign,
although allergic reactions may occur, causing edema, itching, and eosinophilia. This parasite is found in West
and Central Africa.

31. Children with distinct fibrous nodules on their bodies, which contain adult worms and microfilariae of
Onchocerca volvulus. The female discharges microfilariae that migrate through the skin but do not enter the
blood. The disease is chronic and nonfatal. Allergic reactions to microfilariae cause local symptoms. If
microfilariae reach the eye, blindness may occur. This parasite is a major cause of blindness (river blindness) in
Africa. Diagnosis is made by excising a nodule with recovery of adult worms or by detecting microfilariae in a
tissue scraping of the nodule or a skin snip. When present in the eye, microfilariae may be observed with an
ophthalmic microscope. The vector is the black fly, Simulium, which breeds in running water, and the disease is
found in Central America, parts of northern South America, and west-central Africa.

32. Onchocerca volvulus diagnostic stage microfilaria (100) present in a tissue scraping of a skin nodule. The
microfilariae are unsheathed and the pointed, often flexed tail contains no cell nuclei. Differentiate from
Mansonella streptocerca microfilariae, which are also found in skin snips, by the tails, which, in M.streptocerca,
are bent into button-hook shapes and have nuclei extending into the tips
33. Dracunculus medinensis (Guinea worm). Diagnosis: detection of the adult in local lesions. This view shows
part of a female worm protruding from an ulcer and wrapped around a match stick. The female is 70 to 120 cm 2
mm in length. These worms release larvae into water. Infection occurs when a human drinks water containing
crustaceans of the genus Cyclops (the intermediate host) infected with a larva of D.medinensis. Larvae liberated
from the copepods in the human small intestine migrate through the viscera to the subcutaneous tissues and
become adults. In the subcutaneous tissues, the female induces an ulcer and releases larvae into water. Larvae
released into fresh water penetrate the Cyclops’s intermediate host. The major clinical manifestation of this
disease includes allergic symptoms, that is, fever, diarrhea, nausea, eosinophilia, and local symptoms caused by
ulcer formation. This parasite is found in the Middle East, Central Africa, the West Indies, and the Guianas.
Species that parasitize animals have been found in North America. The Cestoda are a subclass of endoparasitic
Platyhelminthes (flatworms); the cestodes are commonly known as the tapeworms. The adults live in the
intestinal tract of vertebrates, whereas larval forms inhabit tissues of vertebrates or invertebrates. The head
(scolex) is modified by suckers and sometimes hooks for attachment to the intestinal wall, and the segments
(proglottids), containing both male and female sex organs, bud from the posterior end of the scolex to form the
body of the tapeworm (the strobila). The length of tapeworms varies from 2 to 3 mm up to 10 meters. Infection in
humans produces primarily intestinal symptoms. Transmission to humans occurs (depending on the species)
when insufficiently cooked food containing larvae is eaten or when eggs are ingested.

34. Hymenolepis nana (dwarf tapeworm) egg (400). Diagnosis: recovery of characteristic clear, spherical, 30 to
47 µm eggs in feces. Note the threadlike filaments that radiate from two polar thickenings into the area between
the embryo and outer shell. Three pairs of hooklets may be seen on the embryo inside the inner shell. Infection is
by ingestion of the egg, which hatches in the duodenum. The embryo penetrates the mucosa, where it matures to
a cysticercoid larva in the intestinal wall. The larva emerges in a few days and develops to an adult worm. No
separate intermediate host is required.
35. Hymenolepis nana egg (100). A low-power view of another egg. The rat tapeworm ( H. diminuta) may also
infect humans; the egg is much larger (70 to 85 µm) and has no polar filaments.

36. Hymenolepis nana mature proglottids (100). The proglottid contains a bilobed ovary and three round testes.
The testes are visible but the ovary is not easily seen in this view. Segments are tiny and usually disintegrate in
the intestine before passage in the feces. The whole worm measures 2.5 to 4 cm and is the smallest tapeworm to
parasitize humans. Multiple infections are common because eggs can hatch in the intestinal tract and cause an
immediate autoinfection as the larvae enter the mucosa. The body of the worm (the strobila) contains about 200
proglottids. Each of these flattened segments contains complete male and female reproductive organs. All
nutrients are absorbed from the intestine of the host through the tegument of the tapeworm.

37. Hymenolepis nana scolex (100). The small scolex bears four suckers and a retractable rostellar crown with
one row of 20 to 30 hooklets. These structures provide for firm attachment to the intestinal mucosa. Light
infections may be asymptomatic but heavy infections produce diarrhea, vomiting, weight loss, and anal irritation.
This parasite is found in India and South America and is common in children in the southeastern United States.
Autoinfection may occur if eggs hatch inside the host but usually reinfection is caused by hand-to-mouth transfer
of eggs after scratching the irritated anal region.

38. Taenia species egg. Taenia solium (pork tapeworm) or T. saginata (beef tapeworm) egg (400 ). Taenia eggs
(30 to 45 µm) are diagnostic for the genus only. Notice the thick, yellow-brown outer shell with its radial striations.
The hexacanth embryo inside the eggshell bears six chitin hooklets. The six hooklets are not visible in this view.
Eggs of T. solium are infective for both pigs and humans. If eggs are accidentally ingested by humans, they
hatch, just as they do in pigs, in the small intestine. Larval forms ( Cysticercus cellulosae) develop in the
subcutaneous tissues, striated muscles, and other tissues of the body. Symptoms vary with the location of the
cyst. Eggs of T. saginata are not at all infective for humans. The source of human infection with the adult pork or
beef tapeworm is ingestion of insufficiently cooked pork or beef containing encysted Cysticercus larvae. After
being digested free, the scolex in the Cysticercus everts and attaches to the small intestine and the larva grows
to become an adult in 6 to 10 weeks.

39. Taenia spp. eggs (100). This view shows four eggs at low power. Pollen grains may resemble eggs under low
power.

40. Taenia solium (pork or “armed” tapeworm) scolex (100). Four suckers and a rostellum bearing 20 to 30 large
hooks are set in two rows at the anterior end of the scolex. T. saginata can be differentiated from T.solium
because the T. saginata scolex does not have hooks, only four suckers, and is therefore said to be “unarmed.”
41. Taenia saginata (beef tapeworm) scolex (100). This is the unarmed tapeworm; the scolex bears only four
large, cup-shaped suckers and no hooks.

42. Taenia solium gravid proglottid (5). The adult worm measures 2 to 8 meters in length, usually with fewer than
1,000 proglottids. The gravid proglottid has 7 to 13 (usually 9) lateral uterine branches (here stained dark brown)
filled with eggs, which is diagnostic for the species when recovered in the feces. Gravid proglottids of Taenia
species must burst open to release eggs because they have no uterine opening. ( Note: Handle with care
because eggs are infective.)

43. Taenia saginata (beef tapeworm) gravid proglottid (5). The adult measures 5 to 10 meters in length and has
1,000 to 2,000 proglottids. Each gravid proglottid has 15 to 30 lateral uterine branches containing about 80,000
eggs, which is diagnostic for the species when recovered in feces. The life cycle of both worms requires that the
eggs be ingested by the appropriate intermediate host (the pig or cow). The eggs hatch in the small intestine after
ingestion by the intermediate host and the six-hooked embryos penetrate the mucosal wall. They are carried by
the circulation (blood and lymphatic) to various tissues, where they encyst. Undercooked or raw beef or pork
containing cysticercus larvae, when ingested, allow larvae to develop into adults. Toxic metabolites and irritation
at the site of scolex attachment in the intestine by adult worms cause the human clinical symptoms. These are
variable and frequently vague and include abdominal distress, weight loss, and neuropathies.

44. Diphyllobothrium latum (broad fish tapeworm) egg (400). D. latum eggs (56 to 76 µm 40 to 50 µm) are
operculated (have a lid) and may be differentiated from operculated eggs of other helminths by the polar knob
seen opposite the operculum, the large size, and the undeveloped embryo seen within. Diagnosis is made when
these eggs are recovered in stool specimens. Undeveloped eggs discharged from segments of the adult
tapeworm must reach fresh water, where they mature and hatch, and the embryo infects the first intermediate
host (copepods). Fish ingest infected copepods (water fleas) and serve as the second intermediate host. Humans
and dogs acquire the infection by eating raw or undercooked parasitized fish containing the infective larval stage,
the plerocercoid.

45. Diphyllobothrium latum egg (400). The operculum (eggshell cap) of this egg is open. A polar knob is evident
at the opposite end of the shell.

46. Diphyllobothrium latum egg (100). A low-power view of the same egg.

47. Diphyllobothrium latem scolex (5). The scolex of this species does not have hooks or cup-shaped suckers but
is characterized by two grooved suckers (bothria), one on each side of the scolex. This worm attaches to the
mucosa of the small intestine by the bothria and can grow to 20 meters in length. Eggs develop in cold, clear
lakes in temperate regions, including the Great Lakes in North America.

48. Diphyllobothrium latum proglottid (10). The mature segment is much wider than it is tall and contains a
rosetteshaped uterus. There is a uterine pore through which eggs are discharged. This parasite is found
worldwide in areas around fresh water. In the United States, it is found in Florida, the Great Lakes region, and
Alaska. The disease is often asymptomatic or is accompanied by vague, digestive disturbances. Some patients
develop a macrocytic anemia of the pernicious anemia type because the worm successfully competes with the
host for dietary vitamin B12 and absorbs it before it can enter the host’s circulation. Chains of proglottids may be
found in feces.

49. Echinococcus granulosus (dog tapeworm or hydatid cyst tapeworm) adult (5). This view shows the entire
worm, which is 3 to 6 mm long and is found only in the small intestine of the canine host. The dog or wolf is the
definitive host and harbors the sexually mature adult parasites. Sheep and other ruminants are natural
intermediate hosts and harbor the asexual stage of the parasite in the tissues, but a human can be an accidental
intermediate host for E. granulosus. Infection of sheep or humans occurs when eggs are ingested in
contaminated food or water or by hand-to-mouth transfer from objects soiled with dog feces. Eggs hatch in the
small intestine and larvae migrate to various organs (usually the liver or lung) to produce cysts. Dogs and other
wild carnivores become infected by eating raw meat containing a hydatid cyst, thus completing the cycle. In
humans the produced disease varies with the location of the cyst. There may be no symptoms or death may
result if vital organs are involved. The parasite is found worldwide. Although rare in Europe and most of the
United States, except in sheep-raising areas, it is common in Alaska and Canada. Diagnosis in humans is by
history of possible exposure, by radiology, by immunodiagnostic skin testing or serologic testing, and by
observing hooklets, scolices, and larval cyst membranes in histopathological sections or other body fluids.

50. Echinococcus granulosus (100). A tissue section showing the wall of the hydatid cyst and three brood
capsules containing scolices growing into the cyst fluid from germinal tissue that underlies the outer cyst wall.

51. Echinococcus granulosus (500). A higher magnification of a single cyst. Each scolex clearly shows the
suckers and crown of hooks. Each scolex in a hydatid cyst will grow to an adult tapeworm after ingestion by a
dog.

52. Echinococcus granulosus cysts. This view shows several small cysts taken from the vertebral column of a
patient with spinal cord compression. Cysts in humans can be in any tissue, including bone, but are more
common in the liver, lung, or central nervous system (CNS).

The Digenea (flukes) are known as flatworms because they appear flat, elongated, and leaf-shaped. Both male
and female sex organs are found in each adult fluke that parasitizes the intestine, bile duct, or lungs. The blood
flukes (genus Schistosoma), however, are unisexual but live paired together in the blood vessels. Attachment is
by the oral and ventral cup-shaped suckers; moreover, the tegument of the flukes may bear small spines that aid
attachment. These parasites vary in size from less than 1 mm to several centimeters in length. All trematodes
require specific species of snail intermediate hosts and infection of humans occurs either by direct penetration of
the skin by a free-swimming cercaria (schistosome species) or by ingestion of an encysted metacercaria
(infective larva) of hermaphroditic flukes. Adult flukes live for many years.

53. Fasciola hepatica (sheep liver fluke) adult (2). This parasite is found in sheep- and cattle-raising areas
worldwide, including the United States. Encysted metacercariae on aquatic vegetation, eaten by humans, sheep,
or cattle, excyst, burrow through the intestinal wall, migrate to the liver, and work their way through the
parenchyma until they enter the proximal bile duct, where they become adults (3 cm 1.3 cm). Visible structures
include the anterior cone, the oral and ventral suckers located at the anterior end, the compact uterus (dark
brown) adjacent to the ventral sucker, Mehlis’ gland (a round structure centered beneath the uterus), and the
testes, occupying the central portion of the fluke. The vitellaria (finely branching, yolk-producing glands) extend
from top to bottom toward the outer edges of the parasite and partially cover the testes over the posterior one-
third. Disease symptoms reflect traumatic damage, with tissue necrosis and toxic irritation to the liver, bile duct,
and gallbladder. Diarrhea, vomiting, irregular fever, jaundice, and eosinophilia are characteristic symptoms.

54. Fasciola hepatica egg (400). Diagnosis: by recovery of this large, operculated egg in feces and by clinical
signs. This egg is very similar to that of Fasciolopsis buski (see Plate 57). Differentiation of eggs of these two
parasites is very difficult. Eggs of F. hepatica measure 140 µm 70 µm.

55. Fasciola hepatica egg (100). A low-power view of the large F. hepatica egg in the midst of naturally occurring
fecal debris.

56. Fasciolopsis buski (large intestinal fluke) (2). F. buski (2 to 7.5 cm 1 to 2 cm) is found primarily in Asia.
Encysted larvae (metacercariae) on vegetation eaten by humans or pigs mature to become adults and attach to
the mucosa of the small intestine. Identifiable and differential structures include the unbranched intestinal ceca
running laterally from top to bottom toward the outer edges; the two suckers of unequal size (round structures at
the top of the organism); the uterus (a dark canal centered under the ventral sucker, branching laterally); Mehlis’
gland with an attached ovary centered approximately one-third of the way posterior to the ventral sucker; and the
testes, branching laterally from the center, beneath the ovary. The anterior end tapers to form the oral sucker,
which is visible in this view. Disease symptoms caused by to1xic products absorbed into the host’s circulation
include general edema, diarrhea, vomiting, anorexia, and, possibly, malabsorption syndrome. Slight anemia and
eosinophilia occur in severe infections.
57. Fasciolopsis buski egg (400). Recovery of this large, thin-shelled, operculated egg (140 µm 70 µm) is
diagnostic. The operculum (lid) is visible here, open at the right end of the egg. This egg is empty; it was
previously incubated and the larva has hatched out of the shell.

58. Fasciolopsis buski egg (100). Immediately below this large egg appears a Trichuris trichiura egg; this is a
very good example of the difference in size between the eggs of the two organisms. The operculum is visible at
the left end of the fluke egg and the material inside of it is yolk. Most of the trematode eggs are undifferentiated
when found in fecal specimens. Eggs of all species must reach fresh water before further development occurs.
After full development, the first larval form (miracidium) hatches and penetrates the soft tissues of an appropriate
intermediate host, the snail. The miracidia develop through several stages to produce free-swimming cercariae,
which then (in this species) encyst on aquatic vegetation as metacercariae, which are infective when the
vegetation is eaten by a human. Fasciola hepatica eggs look identical.

59. Clonorchis sinensis (Oriental liver fluke) (4). This adult measures 1 to 2.5 cm 3 to 5 mm. Humans are infected
by eating raw fish, the second intermediate host, containing encysted metacercariae. Larvae excyst in the small
intestine and migrate to the bile ducts, where they develop into adult worms. Visible structures include the oral
sucker at the anterior end, the ventral sucker one-quarter posteriorly to the oral sucker, the uterus (a dark,
branching structure extending downward from the ventral sucker to the ovary), and the testes, immediately below
the large, oval Mehlis’ gland. The ceca extend from top to bottom toward the outer edge. The vitellaria are
parallel to the uterus. This parasite is found throughout Asia and causes obstructive liver damage with extensive
biliary fibrosis. Symptoms result from local irritation and systemic toxemia. Loss of appetite, diarrhea, abdominal
pain, and 5% to 40% eosinophilia are common symptoms.
60. Clonorchis sinensis egg (500). Eggs (15 µm 30 µm) are deposited in the bile duct and are evacuated in
feces. Diagnosis: recovery of this small, bile-stained egg in feces. Note the thick shell, the characteristic bell
shape, and the thickened opercular rim (the shoulders). There is usually a polar knob opposite the operculum.

61. Clonorchis sinensis egg (100). A low-power view of a developed C. sinensis egg. The eggs are difficult to
differentiate from those of other genera (e.g., Opisthorchis).

62. Paragonimus westermani (lung fluke) (4). This lung-dwelling adult measures 0.8 to 1.2 cm 4 to 6 mm.
Humans are infected by eating raw crab or crayfish, the second intermediate host, containing encysted
metacercariae. Larvae excyst in the small intestine; burrow through the mucosa; and migrate through the
peritoneal cavity, the diaphragm, and the pleural cavity to the lungs, where they develop into adult worms. Visible
structures include the oral sucker at the anterior end; the ovary, which is immediately below the ventral sucker
about midway down in the organism; the dark-staining uterus to the left of the ovary; and the testes, located in
the clear space beneath the ovary. The branching vitellaria are visible along the outer edges of the parasite. This
parasite is found throughout Asia and parts of Africa. It causes a chronic tuberculosis-type disease with fibrous
capsules forming around the adults. Eggs are coughed up in sputum and are visible as orange-brown flecks.
Clinical signs resemble those of tuberculosis, including cough with bloody sputum. Adults may invade other
organs. Symptoms vary with the location of the adult fluke.

63. Paragonimus westermani egg (300). Diagnosis: recovery of this operculated egg (80 to 120 µm 50 to 60 µm)
in sputum or feces. Eggs can be found in fecal specimens when sputum containing eggs is swallowed. Skin
testing may provide better evidence of infections than do fecal examinations. Notice the thin shell and the
thickened rim around the operculum. The shell also thickens at the end opposite the operculum.

64. Paragonimus westermani egg (100). A low-power view of the egg in the center of fecal debris.
65. Schistosoma species (blood flukes). Adults are in copula. The female (15 to 30 mm 0.2 mm) is seen lying
inside the gynecophoral canal of the male. These unisexual worms have a cylindroidal shape and live in pairs,
surviving for many years. Infection occurs when free-swimming, fork-tailed cercariae escape from the snail
intermediate host; burrow into the capillary bed of feet, legs, or arms of humans; and are carried to the blood
vessels of the liver, where they develop into adults. From there, S. mansoni and S. japonicum migrate to
mesenteric veins around the colon. S. haematobium migrates to pelvic veins around the urinary bladder.

66. Schistosoma mansoni egg (400). Diagnosis: recovery of eggs in feces. Unlike the other trematodes,
schistosome eggs do not have an operculum. Note the large size (115 to 175 µm 50 to 70 µm) and the
conspicuous lateral spine protruding from the side near one pole. A ciliated miracidium is indistinct but visible
inside this egg, but in fresh specimens it is generally distinct and motile, with active cilia and flame cells. Eggs are
deposited into venules, eventually rupture the wall to effect passage into the lumen of the intestine, and are
evacuated in the feces. Many eggs are caught in tissues of the liver and intestine, and a granuloma forms around
each egg in response to toxic enzymes released by the miracidium. Clinical manifestations include up to 50%
eosinophilia, gastrointestinal bleeding, rectal polyps, and hepatic cirrhosis. This parasite is found in Africa, the
Middle East, parts of South America, the West Indies, and Puerto Rico. Infected persons can frequently be found
in immigrant populations living in North American urban centers.

67. Schistosoma mansoni egg (100). A low-power view of several eggs. Note the lateral spines on the eggs.

68. Schistosoma japonicum egg (400). Diagnosis: recovery of eggs in feces. This egg measures 70 to 100 µm 50
to 60 µm. A small lateral spine on the eggshell is characteristic for this species. A ciliated miracidium is seen
inside the egg. The produced disease is similar to that of S. mansoni. Because S. japonicum produces 10 times
as many eggs as S. mansoni, the disease is more severe. Many eggs are swept back into the bloodstream to the
liver and are trapped, causing fibrosis and cirrhosis of the liver. Toxic symptoms are severe. This parasite is
found in Asia.

69. Schistosoma japonicum eggs (100). A low-power view of several eggs. The lateral spine is barely visible in
some eggs. S. mekongi eggs are similar but small (50 to 75 µm 40 to 65 µm). These eggs are often coated with
fecal debris and are more difficult to notice.

70. Schistosoma haematobium egg (400). Diagnosis: recovery of eggs in urine. This egg measures 115 to 175
µm 40 to 70 µm. A pointed terminal spine is characteristic for this species. A ciliated miracidium is visible inside.
Egg deposition by S. haematobium causes local traumatic damage to the rectum and the urinary bladder.
Bladder colic is a cardinal symptom. Blood, pus cells, and necrotic tissue debris are passed during urination.
Systemic symptoms are less severe than those produced by the other schistosomes. There is a high correlation
with bladder cancer in infected persons. This parasite is found in Africa, the Middle East, and Portugal.

71. Schistosoma haematobium egg (300). A high-power view of the egg, showing a differently shaped terminal
spine. Urine should be concentrated to aid detection. Eggs are most often in the last few drops expelled from the
bladder.

Amebae are unicellular protozoa, some of which may be parasitic in humans. These organisms are found
worldwide and some can live as parasitic or nonpathogenic trophozoites (the motile, feeding, reproductive
stage) in the lower gastrointestinal tract of humans. Most intestinal protozoa form a cyst stage (a dormant,
protective stage for the parasite in unfavorable environments after being evacuated in the host’s feces), and
in the cyst form may remain viable for long periods in warm, moist conditions. Transmission of intestinal
amebic diseases is from ingested cysts in fecally contaminated food, soil, or water. Cysts are most commonly
passed in feces by asymptomatic carriers.

72. Entamoeba histolytica/E. dispar trophozoite (10 to 60 µm) (1,000). This ameba is pathogenic for humans. It
can invade the intestinal mucosa, causing flask-shaped lesions and bloody diarrhea. The trophozoite releases
lytic enzymes and can also spread to other tissues, such as the liver, and cause amebic ulceration. E. dispar is
identical in appearance to E. histolytica, but is nonpathogenic. The differentiating characteristic of these two
forms is confirmed when engulfed red blood cells are visible inside E. histolytica trophozoites. Notice the nucleus,
which has a light chromatin ring at the edges, surrounding a centrally located karyosome (compare with
Entamoeba coli, Plate 78). The cytoplasm is finely granular as compared with that of E. coli. This is a trichrome-
stained organism.
73. Entamoeba histolytica (1,000). This trophozoite in feces contains five engulfed red blood cells, the presence
of which is a diagnostic feature, inasmuch as no other ameba contains these. This characteristic is used to
differentiate E. histolytica from E. dispar. In a saline solution, the trophozoite exhibits progressive, active motility,
with thin, fingerlike pseudopodia.

74. Entamoeba histolytica/E. dispar cyst (1,000). Cysts of E. histolytica/dispar are over 10 mm in size (10 to 20
µm). There are up to four typical nuclei in the mature cyst. One nucleus is clearly visible here. The nuclear
structure is identical in both trophozoites and cysts. The dark cigar-shaped bars are chromatoid bodies, which are
crystalline RNA. Iron hematoxylin stain.

75. Entamoeba histolytica/E. dispar cyst (1,000) showing four nuclei. Iodine stain.

76. Entamoeba hartmanni trophozoite (1,000). Note the morphologic similarity between the nucleus of this
commensal and that in Plate 72. This organism was previously identified as E. histolytica but is now known as E.
hartmanni. It is not pathogenic but morphologically resembles E. histolytica, differing only in size; it is less than 10
µm in size. This characteristic is important because correct diagnosis depends on the careful measurement of
the parasite. A trophozoite or cyst resembling E. histolytica that is less than 10 mm in diameter is classified as
E.hartmanni.

77. Entamoeba hartmanni cyst (1,000). The cyst (5 to 10 µm) resembles that of E. histolytica but is classified as
E. hartmanni because of its small size, the upper limits being 10 µm. This cyst is stained with iodine. It can have
up to four nuclei. It is important to differentiate E. histolytica from this and other nonpathogenic amebae to ensure
correct treatment of the patient.
78. Entamoeba coli trophozoite (1,000). This commonly-encountered nonpathogenic ameba must be
differentiated from E. histolytica. Notice the nucleus, which has a dark, irregularly thickened chromatin ring
around the membrane and a large, eccentrically located karyosome. This parasite is often larger than E.
histolytica (15 to 60 µm) and has coarser cytoplasm and sluggish motility, with blunt pseudopodia.

79. Entamoeba coli trophozoite (1,000). This trophozoite has a very large karyosome located next to the
chromatin ring.

80. Entamoeba coli cyst (1,000). Five nuclei are visible in the cyst (10 to 30 µm). E. coli is differentiated
from E. histolytica by the nuclear morphology and by the fact that the cyst may contain up to eight nuclei, rather
than four. Chromatoid bars in stained cysts are splinterlike, with pointed ends.

81. Entamoeba coli cysts (100). A low-power view of several cysts. One is seen at the center of the field and
several others are evident in the lower left area, all appearing as dark dots. This view demonstrates the
importance of scanning a part of all fecal slides under high power so that protozoa are not missed. These cysts
also should be examined at even higher magnifications to see the nuclei and other features for correct diagnosis
of the parasite species.

82. Endolimax nana trophozoite (1,000). Note the large karyosome in the nucleus. The fine chromatin ring is not
usually visible. This feature is diagnostic for this nonpathogen (6 to 12 µm). Note also the cytoplasmic vacuoles.

83. Endolimax nana cyst (2,000). The ovoid mature cyst has four nuclei. Note the large karyosome (dark dots).
The chromatin ring is not visible. These features are diagnostic. This parasite (8 to 10 µm) may be confused with
E. histolytica if care is not taken when examining the nuclear structure and the cyst shape.
84. Iodamoeba bütschlii trophozoite (1,000). Note the large karyosome and light chromatin ring in the nucleus of
the organism (12 to 15 µm). The cytoplasm is coarsely granular and a small, light vacuole that contains glycogen
is visible.

85. Iodamoeba bütschlii cyst (1,000). Note the large karyosome in the single nucleus of this trichrome-stained
cyst (5 to 20 µm). A large vacuole from which glycogen has been removed by the staining process is visible
(clear area inside the cyst), which is diagnostic for this nonpathogen. The glycogen vacuole stains dark brown
when an iodine wet mount is used. The nucleus of this species does not stain with iodine.

Flagellates are unicellular protozoa that move by means of flagella (motile fibrils extending from the body of
the organism). Many of the flagellates have a trophozoite stage, which is the active, feeding, motile form, and
also a cyst stage, which is a dormant, protective stage for the parasite in unfavorable environments outside
the host’s intestine. Transmission of the intestinal flagellates is by ingestion of fecally contaminated food or
drink, Trichomonas vaginalis trophozoites are directly transmitted during sexual intercourse, and the
hemoflagellates (found in the blood or tissues) are transmitted by arthropod intermediate hosts.

86. Dientamoeba fragilis trophozoite (1,000). This flagellate (5 to 12 µm) does not form cysts. Note that it has two
nuclei. This feature is diagnostic inasmuch as no other ameboid trophozoite has more than one nucleus. This
organism may be pathogenic and may cause diarrhea in humans.

87. D.fragilis.

88. Giardia lamblia trophozoites (1,000). These flagellates (10 to 20 µm15 µm) live in the duodenum and often
do not produce disease. When present in large numbers, they may cause epigastric pain and diarrhea. Note the
smiling face–like appearance of the trophozoite, which is bilaterally symmetric with two anterior nuclei, a central
axostyle, and four pairs of flagella. In fresh fecal wet-mount preparations, the motile trophozoite moves like a leaf
falling from a tree.
89. Giardia lamblia cyst (1,000). Diagnosis: recovery of trophozoites or cysts (8 µm 10 µm) in feces. The mature
cyst has four nuclei, although the immature cyst may have only two. Three are visible in the upper cyst in this
view.

90. Unusual sight of Entamoeba coli trophozoite containing several ingested Giardia lamblia cysts (1,000).

91. Giardia lamblia trophozoites (1,000). This stained section of duodenal mucosa shows two trophozoites
adhering. Note the two nuclei visible in the trophozoite centered in the field.

92. Chilomastix mesnili trophozoite (1,000). This nonpathogenic flagellate (7 µm20 µm) lives in the upper large
intestine and does not produce disease. Note the single prominent nucleus at the rounded anterior end. The
posterior is tapered with a noticeably angled projection. There are four anterior flagella and a distinct longitudinal
spiral groove. Viable trophozoites move in a spiral path.

93. Chilomastix mesnili cyst (1,000). Diagnosis: recovery of cysts (5 µm 8 µm) in feces. There is a single, large
nucleus in this lemon-shaped cyst. Correct diagnosis is important so that this is not confused with Giardia or
other pathogenic infection.

94. Trichomonas vaginalis trophozoite (1,000). This parasite (18 µm 25 µm) is recovered in urine or in urethral or
vaginal mucosal scrapings. Symptoms in women vary from mild irritation to painful itching, with a frothy, yellowish
vaginal discharge. Infected men are usually asymptomatic carriers. There are four anterior flagella, a large
nucleus, and an undulating membrane (not visible in this view) extending along one-half of the body. T. vaginalis
appears slightly larger than leukocytes, and the whipping motion of the flagella is clearly visible in fresh,
unstained urine. Trichomonas species do not form cysts. T. hominis is a nonpathogenic intestinal flagellate found
in feces; T. gingivalis trophozoite may be found in the mouth and is also nonpathogenic.
Two genera of flagellates are found as parasites of blood and tissue in humans. The Leishmania parasites have
two forms in their life cycle: the amastigote form, which multiplies in macrophages in humans, and the
promastigote form found in the midgut of the sandfly, Phlebotomus spp. (the intermediate host). The other
bloodborne genus parasitic in humans is Trypanosoma. These organisms are in trypomastigote form in the
bloodstream and other tissues in humans, and in the epimastigote form in the arthropod intermediate host
(except for T. cruzi, which is also seen as the amastigote form in human heart muscle).

95. Amastigote form (1,000). Many amastigotes (3 µm to 5 µm in diameter) are seen in this view. The nucleus
and the smaller, bar-shaped kinetoplast are visible in each organism as seen in the center of this field. The
leishmania invade reticuloendothelial cells and macrophages of humans. The disease produced by the
organisms of each species is as follows:
A. L. tropica (Old World leishmaniasis). Local lesions occur at the site of the sandfly bite, followed by focal
necrosis. Although it may be complicated by a secondary bacterial infection, the disease is usually self-limiting
and produces life-long immunity to reinfection. This parasite is found in Africa, India, and the Middle East.

B. L. braziliensis (New World leishmaniasis). The primary lesion is local, as with L. tropica, but the ulcer heals
slowly. Erosion of soft tissues, especially of the nose, mouth, ears, and cheeks, often occurs years later,
inasmuch as this organism tends to migrate to secondary sites, often complicated by a bacterial invasion followed
by local and systemic symptoms. This parasite is found in Central and South America.

C. L. donovani (kala-azar). The local primary lesion is usually not reported. The amastigotes gain access to the
bloodstream or lymphatics and eventually spread to fixed tissue macrophages in the viscera. Sites of this
invasion are the liver, spleen, and bone marrow, where multiplication usually proceeds unchecked. Anemia
usually follows because of increased production of macrophages and decreased erythropoietic activity. The acute
phase of the systemic disease is characterized by double spiking fever fluctuating daily (between 90ºF and
104ºF). There is moderate erythrocytopenia, absolute monocytosis, and neutropenia. Massive
hepatosplenomegaly occurs because of parasite multiplication and death frequently occurs if the patient is
untreated. This parasite is widely distributed, except in the United States.

96. Leishmania donovani (1,000) seen multiplying in a macrophage in a press preparation of spleen tissue.
97. Leishmaniasis. A typical skin lesion caused by L. braziliensis. Note the open ulcer on the man’s forehead.

98. Promastigote form (100). This stage is found in the midgut and proboscis of the sandfly, Phlebotomus. It is
the in fective form of leishmaniasis and is transferred to humans by the biting fly. The large nucleus, bar-shaped
kinetoplast, and flagellum are visible. Note the relative position of these structures.

99. Trypomastigote form (1,000). The trypanosome is found extracellularly, free in the blood. It is the infective
form transferred to humans by the biting arthropod vector (intermediate host). Trypanosome species are not
readily differentiated in peripheral blood. Visible structures include the flagellum, the large central nucleus, and
the undulating membrane that is attached to the kinetoplast at the posterior end of the organism. The diseases
produced by these organisms are as follows:
A. The sleeping sickness diseases produced by T. rhodesiense and T. gambiense are similar, differing
primarily in the severity of the second stage, which is so severe with T. rhodesiense infections that death
rapidly results. The disease begins with local inflammation at the site of the fly bite (tsetse fly). This
subsides as the trypanosomes enter the blood. They migrate to the lymph nodes, where severe
inflammation occurs because of rapid multiplication. Toxic metabolites and occlusion of vascular sinuses
by the proliferating organisms may cause death at this stage. Enlarged lymph nodes, myocarditis, fever
episodes, edema, and rapid weight loss are cardinal symptoms for T. rhodesiense. Trypanosomes invade
the central nervous system in the third stage to produce sleeping sickness and eventually death. T.
gambiense usually proceeds to this stage. The posterior cervical lymph nodes in the neck are invaded
and undergo massive swelling. This is called Winterbottom’s sign. Other nodes may be invaded,
producing weakness, pain, and cramps.

B. T. cruzi (Chagas’ disease). The primary lesion at the bite site of the reduviid bug intermediate host is
often near the eye, producing unilateral edema of the eyelid (Romaña’s sign). Next, primary parasitemia
 with S- or C-shaped trypanosomes with a large kinetoplast (as seen in this view) occurs in the blood,
causing fever and toxic conditions resembling typhoid fever (may be fatal in children). The chronic
disease is characterized by leishmanial forms multiplying in tissue macrophages, and symptoms of tissue
invasion, including enlargement of the spleen, occur. Cardiac and central nervous system pathology
occur as tissue destruction continues. There may be fever episodes and parasitemia when trypanosomes
are free in the blood. Diagnosis of these diseases is confirmed when parasites are recovered in blood or
seen in tissue specimens. Trypanosomes are 15 to 30 µm in length.

100. Trypanosoma cruzi (amastigote form) in cardiac tissue (1,000). The trypomastigote in reduviid bug feces is
pushed into the bite wound when the host scratches at the bite site, and these circulate in the blood until
phagocytized or they invade tissue macrophages, after which they change to the amastigote form. Note the nest
of multiplying amastigote forms in the heart muscle. Trypomastigote forms can be found in blood.

The Ciliata

101. Balantidium coli trophozoite (400). This organism (40 µm 60 µm) is a ciliate that is characterized by having
many short cilia on the surface of both the motile and encysted trophozoite. B. coli is the only ciliate pathogenic
for humans. The disease is characterized by invasion of the intestinal submucosa with inflammation and ulcer
formation. There may be fulminating diarrhea in heavy infections or an asymptomatic carrier state in light
infections. This organism has two nuclei: a large, kidney bean–shaped macronucleus and a small, round
micronucleus not visible in this view.

102. Balantidium coli cyst (400). This large, round cyst (50 µm) is characterized by the presence of macronuclei
and micronuclei; the latter are rarely seen, but when present, generally appear as small dots near the concavity
of the macronucleus. Cilia are evident around the inside edge of the cyst on the organism. This form, or the
trophozoite, is diagnostic when recovered in feces or seen in intestinal tissue.

103. Balantidium coli cyst (100). A low-power view of the cyst. This large parasite is easily recognized even at
this magnification. Sporozoa are protozoa that have both a sexual and an asexual phase in their life cycle. The
genus Plasmodium includes the malaria parasites. The asexual phase is found in the human intermediate host
and the sexual phase occurs in the definitive host, the Anopheles mosquito. Sporozoites are injected into the
blood by the biting mosquito and then invade liver cells. The asexual stages of malaria first multiply in the liver
and later in peripheral blood. Asexual schizogony results in the release of merozoites that may either invade new
red blood cells and develop into new schizonts or develop to become male and female gametocytes. If the
mosquito ingests gametocytes while feeding, these will develop throughout the sexual cycle to produce new
sporozoites, the infective form for humans. The clinical symptoms vary with the species of parasite but all cause
anemia (because of destruction of the red blood cells by the schizont form), headaches, general weakness, and a
characteristic repetitive fever and chills syndrome.

104. Plasmodium vivax (benign tertian malaria). This drawing shows the erythrocytic stages of P. vivax. The
prominent feature is the presence of Schüffner’s dots. These appear as red spots on infected red blood cells on a
stained blood smear and are seen in all developmental stages after the early trophozoite stage. The infected red
blood cell is larger than normal red blood cells because the parasites preferentially invade reticulocytes, the
larger, immature blood cell. The trophozoite divides to form a schizont containing 16 to 18 merozoites, which is a
differentiating characteristic for P. vivax. Plates 104 to 107 clearly illustrate the maturation of the trophozoite
stage of P. vivax. See enlarged version of image on p. 36.
105. Plasmodium vivax (100). A trophozoite is clearly visible in the center of the field. Note the red Schüffner’s
dots. Note also the ring (blue) and the chromatin dot (red) of the trophozoite. Each ring form (about one-third of
the cell diameter in size) represents one parasite; multiple parasites in a red cell are not commonly seen in this
species.

106. Plasmodium vivax (1,000). An older trophozoite than that in the previous plate is seen in the center of the
field. Note the larger size of the red cell, the bizarre ameboid shape of the motile trophozoite, and the
characteristic Schüffner’s dots.

107. Plasmodium vivax (1,000). An older trophozoite than that in the previous plate is shown. This cell is
enlarged and Schüffner’s dots are evident. The trophozoite is clearly ameboid in its movements.

108. Plasmodium vivax (1,000). Developing schizont. Many merozoites are seen inside the cell. A trophozoite
appears in the upper right of the field.

109. Plasmodium vivax (1,000). Mature schizont. Fourteen merozoites are visible inside the cell.
Characteristically, the schizont divides to form 16 to 18 merozoites. Development from the invasion of the red
blood cell by the trophozoite to the fully mature schizont occurs in 48 hours.

110. Plasmodium vivax (1,000). Mature schizont. Eighteen merozoites are visible inside the cell. The red blood
cell ruptures, releasing the merozoites, which may invade new red blood cells to repeat the asexual erythrocytic
cycle. Some merozoites invade red cells and become male or female gametocytes, which are part of the sexual
cycle in the mosquito after the gametocytes are ingested in a blood meal.
111. Plasmodium ovale. This drawing shows the erythrocytic stages of P. ovale. The red blood cells are enlarged
and oval in shape. This parasite is rare in humans and may be confused with P. malariae when Schüffner’s dots
are not present or with P. vivax when Schüffner’s dots are present. See enlarged version of image on p. 36.

112. Plasmodium ovale trophozoites (1,000). This parasite is similar to P. vivax because Schüffner’s dots are
visible. It also resembles P. malariae because the mature schizont usually contains 8 to 12 merozoites. The
diagnostic characteristic, when present, is the ragged, irregular appearance and oval shape of the host red blood
cell, as can be seen here.

113. Plasmodium ovale trophozoites (1,000). This is another view of this parasite's trophozoite. Seen in this view
are Schiiffner's dots and the characteristic ragged, irregular appearance and oval shape of the host red blood
cell.

114. Plasmodium malariae (quartan malaria). This drawing depicts erythrocytic stages of P. malariae. The
trophozoite measures about one-third of the diameter of the red blood cell. The prominent features include a
large ring form; the band form of the early schizont with coarse, dark granules; and the mature schizont,
containing 8 to 12 merozoites, assuming a characteristic rosette shape with malaria pigment deposited in the
center of the rosette. See enlarged version of image on p. 36.

115. Plasmodium malariae trophozoite (1,000). The band-form trophozoite across the red cell is characteristic
during the early development of the schizont.
116. Plasmodium malariae schizont (1,000). A schizont containing seven merozoites is seen in the upper left
corner. By 72 hours after the trophozoite enters the red blood cell, the mature form contains 8 to 10 merozoites
and assumes the characteristic rosette shape. Two young trophozoites are also seen in this view.

117. Plasmodium malariae schizont (1,000). Another view of a maturing schizont.

118. Plasmodium malariae gametocyte (1,000). This form is similar to that of P.vivax but is smaller and contains
less pigment.

119. Plasmodium falciparum (malignant subtertian malaria). This drawing demonstrates the erythrocytic stages of
P. falciparum. The prominent features are small ring forms with double chromatin dots, multiple rings in the same
cell, and crescentshaped gametocytes. Other stages in schizont formation are not seen in peripheral blood
because these (other) stages of maturation occur in the capillaries of internal organs. See enlarged version of
image on p. 36.

120. Plasmodium falciparum ring forms (1,000). Note the small ring size and multiple infections, not seen with P.
vivax or P. malariae.

121. Double malaria infection (1,000). A P. vivax trophozoite is shown in the center of the field. The small ring
form seen at the upper left has a double chromatin dot, a diagnostic feature of P. falciparum rings.

122. Plasmodium falciparum gametocyte (1,000). Note the characteristic crescent or banana shape of this form.
Malaria has been found worldwide but control measures have essentially eliminated the disease from many
countries, including the United States. It is still a major problem in Africa, Asia, Central and South America, and
the South Pacific. Diagnosis: clinical signs and observation of the parasite in thick and thin blood films obtained
ideally during the fever cycle. Other important sporozoan parasites are noted as follows.

123. Babesia microti ring forms (1,000). A pair of parasitic forms. Note the rings lie at right angles to each other.
When four rings are present they may form a tetrad known as a maltese cross. This parasite is transmitted by
ixodid ticks. Most cases are found in Europe and along the East Coast of the United States from Connecticut to
Nantucket.

124. Isospora belli oocyst (400). This oocyst containing one sporoblast is stained using the modified acid-fast
stain. Note that the oocyst wall does not stain but it is noted as an outline caused by precipitated stain.

125. Toxoplasma gondii trophozoites (1,000). T. gondii trophozoites viewed by fluorescence microscopy in the
indirect fluorescent antibody test (IFAT). This is a negative test result, indicating that patient’s serum, previously
incubated with these organisms, has no detectable antibody to T. gondii. No green fluorescence is observable.

126. Toxoplasma gondii trophozoites (1,000). This is a positive IFAT result for the detection of antibodies to T.
gondii in serum. Note the green fluorescence over the entire body of the organisms, indicating the presence of
antibodies bound to the surface.

127. Toxoplasma pseudocyst (400). A dormant pseudocyst filled with bradyzoites of T. gondii as seen in a brain
section. Immunosuppression of the host would allow these trophozoites to emerge and successfully invade new
host cells and to continue multiplication. Brain pseudocysts are also infective if ingested by the definitive host
(cats) from mouse brains.

128. Sarcocystis spp. (1,000). A stained section of muscle tissue in which one can see a sarcocyst filled with
potentially infective organisms. These are infective if ingested by the definitive host.
129. Cryptosporidium parvum oocysts (1,000). The oocysts measuring 4 to 6 µm stain red (acid-fast stain)
against the blue-green background. Sporocysts are visible in the two oocysts on the right side of figure.

130. Cyclospora spp. oocysts (1,000). Note the variable staining and wrinkled appearance of these oocysts (8 to
10 mm) preserved in 10% formalin and stained using an acid-fast technique.

131. Enterocytozoon spp. Spores (0.7 to 1.01.1 to 1.6 µm). Several acid-fast spores are visible in this view (400).

132. Enterocytozoon spp. Spores. This view illustrates spores as seen at 1,000 magnification.

133. Encephalitozoon hellem. Spores. These spores were recovered in a bronchoalveolar lavage sample from a
30-year old patient with AIDS. This view (1,000) illustrates a monoclonal antibody-based immunofluorescent
identification technique. Polar tubules are visible as fluorescent strands extending from the spores.

134. Artifacts (400). Many fecal artifacts may be confused with parasitic forms to the untrained. A vegetable spiral
in the center of the field is superimposed over a form that may resemble a nematode egg.

135. Artifacts (500). The most notable artifact in this view is a plant hair that resembles a nematode. Hairs usually
have one blunt end and one tapered end, and nematodes have one tapered end and one round end, usually with
visible formed mouth structures.
INTRODUCTION CHAPTER 1
GLOSSARY
 accidental (or incidental) host. Infection of a host other than the normal host species. A parasite may or may
not continue full development in an accidental host.
 apical complex. Polar complex of secretory organelles in sporozoan protozoa.
 carrier. A host harboring a parasite but exhibiting no clinical signs or symptoms.
 commensalism. The association of two different species of organisms in which one partner is benefited and
the other is neither benefited nor injured.
 definitive host. The animal in which a parasite passes its adult existence, sexual reproductive phase, or
both.
 differential diagnosis. The clinical comparison of different diseases that exhibit similar symptoms; designed
to determine which disease the patient has.
 disease. A definite morbid process having a characteristic train of symptoms.
 ectoparasite. A parasite established on or in the body of its host.
 endoparasite. A parasite established within the body of its host.
 epidemiology. A field of science dealing with the relationships of the various factors that determine the
frequency and distribution of an infectious process or disease in a community.
 facultative parasite. An organism capable of living an independent or a parasitic existence; not an obligatory
parasite, but potentially parasitic.
 generic name (or scientific name). The name given to an organism consisting of its appropriate genus and
species title.
 genus (pl. genera). A taxonomic category subordinate to family (and tribe) and superior to species, grouping
those organisms that are alike in broad features but different in detail.
 host. The species of animal or plant that harbors a parasite and provides some metabolic resources to the
parasitic species.
 in vitro. Observable in a test tube or other nonliving system.
 in vivo. Within the living body.
 infections. Invasions of the body by a pathogenic organism (except arthropods), with accompanying
reaction of the host tissues to the presence of the parasite.
 infestation. The establishment of arthropods on or within a host (including insects, ticks, and mites).
 intermediate host. The animal in which a parasite passes its larval stage or asexual reproduction phase.
 metazoan. Belonging to a subkingdom of animals consisting of all multicellular animal organisms in which
cells are differentiated to form tissue. Includes all animals except protozoa.
 obligatory parasite. A parasite that cannot live apart from its host.
 parasitemia. The presence of parasites in the blood (e.g., malaria schizonts in red blood cells).
 parasitism. The association of two different species of organisms in which the smaller species lives on or
within the other and has a metabolic dependence on the larger host species.
 pathogenic. Production of tissue changes or disease.
 pathogenicity. The ability to produce pathogenic changes.
 reservoir host. An animal that harbors a species of parasite that is also parasitic for humans and from which
a human may become infected.
 serology. The study of antibody-antigen reactions in vitro, using host serum for study.
 species (abbr. spp.). A taxonomic category subordinate to a genus. A species maintains its classification by
not interbreeding with other species.
 symbiosis. The association of two different species of organisms exhibiting metabolic dependence by their
relationship.
 transport host. An animal that harbors a parasite that does not reproduce; it carries the parasite from one
location to another to infect a new host.
 vectors. Any arthropods or other living carriers that transport a pathogenic microorganism from an infected
to a noninfected host. A vector may transmit a disease passively (mechanical vector) or may be an
essential host in the life cycle of the pathogenicorganism (biological vector).
 zoonosis (pl. zoonoses). A disease involving a parasite that has accidentally infected a human; the normal
host for the parasite is an animal.

WHAT IS PARASITOLOGY?
Parasitology is the study of a particular relationship among certain species. Symbiosis means “living together”
and generally refers to a positive relationship between members of different species. Mutualism is
usually an obligatory relationship in which both organisms benefit. An example of mutualism is the termite
and its intestinal flagellate fauna. The termite benefits because it could not digest its cellulose-containing food
without the flagellate and the intestinal organism benefits by having a secure habitat in which to live and a good
source of food. Commensalism is usually not obligatory, but it reflects a relationship in which one
species of organism benefits and the other neither benefits nor is harmed. Humans can harbor several
species of ameba with no ill effects to the host but with benefit to the amebae. These nonpathogenic protozoa,
however, are not considered to be true commensals because it is generally accepted that they should not be a
normal part of the human intestinal flora. Parasitism is a relationship in which one species of organism lives on or
with another organism, with the parasite living at the expense of and often causing harm to the host. Most
parasites inflict varying degrees of harm depending on the general health and nutritional status of the host, the
size of the parasite, the number of parasites present, and the parasites’ location or migration path within the host.
Hosts
Hosts can be characterized as definitive, intermediate, transport, or reservoir. A definitive host is one in which the
parasite reaches sexual or reproductive maturity. An intermediate host is one that harbors parasites that engage
in asexual reproduction. Sometimes both types of hosts are required in a parasite’s life cycle. A transport host is
one that harbors a parasite that does not reproduce but merely goes on to infect a
new host. The transport host serves only to carry the parasite from one location to another. For example, a
house fly might passively transfer an ameba on its feet from contaminated feces to a cooking utensil in a
kitchen. A new host could then ingest the parasite stage, producing a new infection. A reservoir host
may harbor a parasite that is also infective for humans. For example, the bush buck antelope often
harbors the protozoa that causes sleeping sickness in humans, but the antelope suffers no ill effects.

CLASSIFICATION OF PARASITES
I. Metazoan helminths—wormlike invertebrates. (Only those parasitic for humans are included in this text.) The
following are considered:
A. Phylum Nemathelminthes
1. Class Nematoda: roundworms (body round in cross-section)
B. Phylum Platyhelminthes: flatworms
2. Class Cestoda: tapeworms (body flattened and segmented) Class Digenea: trematodes, flukes (body flattened,
leaf-shaped, and nonsegmented)
II. Protozoa*—unicellular eukaryotic microorganisms. The following are considered:
A. Phylum Sarcomastigophora
1. Class Lobosea: organisms that move by means of pseudopodia
2. Class Zoomastigophorea: organisms that move by means of flagella
B. Phylum Ciliophora
1. Class Kinetofragminophorea: organisms that move by means of cilia
C. Phylum Apicomplexa
1. Class Sporozoea: organisms with both sexual and asexual reproductive cycles; apical complex can be seen
with an electron microscope
III. Arthropods—possess a hard exoskeleton and jointed appendages. Only those that are parasitic to humans
and those that transmit parasitic diseases are included.
A. Phylum Arthropoda
1. Class Insecta: flies, mosquitoes, bugs, lice, fleas
2. Class Arachnida: ticks, mites
12. Define or explain the following terms:
a. Vector
b. Host
c. Proglottid
d. Definitive host
e. Operculum

NEMATODA CHAPTER 2
GLOSSARY
 autoreinfection. Reinfecting oneself. In the pinworm life cycle, infected individuals may reinfect themselves
via hand-to-mouth transfer from scratching the perianal region after the female worm has deposited eggs. In
other life cycles, infective eggs may hatch inside the host and then develop into an adult (e.g.,
Strongyloides stercoralis, Hymenolepis nana).
 buccal capsule (cavity). Oral cavity of roundworms. (In the case of hookworms, the cavity contains species-
specific cutting plates or cutting teeth.)
 bursa (pl. bursae). Fan-shaped cartilage expansion at the posterior end of some male nematodes (e.g.,
hookworms) that holds onto the female during copulation.
 copulatory spicules. Needlelike bodies possessed by some male nematodes; spicules lie in pouches near
the ejaculatory duct and may be inserted in the vagina of the female worm during copulation.
 corticated. Possessing an outer, mamillated, albuminous coating, as on the eggs of Ascaris lumbricoides.
 cutaneous larval migrans. A disease caused by the migration of larvae of Ancylostoma spp. (dog or cat
hookworm) or other helminth larvae traveling under the skin of humans. Larval migration is marked by thin,
red papular lines of eruption. Also termed creeping eruption.
 cuticle. The surface of roundworms; a tough protective covering that is resistant to digestion.
 dermatitis. Inflammation of the skin.
 diagnostic stage. A developmental stage of a pathogenic organism that can be detected in human body
secretions, discharges, feces, blood, or tissue by chemical means or microscopic observations.
Identification serves as an aid in diagnosis.
 diurnal. Occurring during the daytime.
 Edema. Unusual excess fluid in tissue, causing swelling.
 elephantiasis. Overgrowth of the skin and subcutaneous tissue in limbs or genitalia resulting from
obstructed circulation in the lymphatic vessels; can occur in the presence of some long-term chronic filaria
infections (e.g., Wuchereria bancrofti).
 enteritis. Inflammation of the intestine.
 eosinophilia. High levels of circulating eosinophils in the blood.
 fecundity. Reproductive capacity.
 filaria (pl. filariae). A nematode worm of the order Filariata; requires an arthropod intermediate host for
transmission of infection to humans.
 filariform larva. Infective, nonfeeding, sheathed, third-stage larva; larva has a long, slender esophagus.
 gravid. Pregnant; female has developing eggs, embryos, or larvae in reproductive organs.
 immunocompromised (immunosuppressed state). Depressed immune response system state; can
accompany various diseases or can be induced by drugs.
 incubation period. The time from initial infection until the onset of clinical symptoms of a disease.
 infective stage. The stage of the life cycle at which the parasite is capable of entering and continuing
development within the host.
 intermediate host. A species of animal that serves as a host for only the larval or sexually immature stages
of parasite development. Required part of the life cycle of that parasite.
 larva (pl. larvae). An immature stage in the development of a worm before becoming a mature adult.
Nematodes molt several times during development, and each subsequent larval stage is increasingly
mature.
 life cycle. Entrance into a host, growth, development, reproduction, and subsequent transmission of
offspring to a new host.
 microfilaria (pl. microfilariae). The embryo stage of a filaria parasite; usually in the blood or tissue of
humans; can be ingested by the arthropod intermediate host in which the microfilaria will develop to the
infective stage.
 molt. A process of replacement of the old cuticle with an inner, new one and subsequent shedding of the
old, outer cuticle to allow for the growth and development of the larva; the actual shedding of the old cuticle
is termed ecdysis.
 Nematoda. A class of the animal phylum Nemathelminthes–the roundworms.
 occult. Hidden; not apparent.
 pathenogenic. Capable of unisexual reproduction; no fertilization is required (e.g., Strongyloides stercoralis
parasitic female).
 pathognomonic. Indicative of disease; characteristic parthenogenic symptoms suggest the disease.
 periodicity. Recurring at a regular time period.
 pica. Habit of eating dirt or other unusual substances, such as chalk or plaster. Seen most often in children
or rarely, in adults.
 prepatent period. The time elapsing between initial infection with the immature parasite and reproduction by
the adult parasite.
 pruritus. Intense itching. Pruritus ani refers to anal itching, as in enterobiasis.
 rectal prolapse. Weakening of the rectal musculature resulting in a “falling down” of the rectum; occasion
ally seen in heavy whipworm infections, particularly in children.
 rhabditiform larvae. Noninfective, feeding, firststage larvae; the larvae have an hourglass-shaped
esophagus.
 tropical eosinophilia. A disease syndrome associated with high levels of blood eosinophils and an asthma-
like syndrome. Caused by zoonotic filaria (or other nematode) infections in which no microfilariae are
detectable in peripheral blood in most cases.
 visceral larval migrans. A disease in humans caused by the migration of the larval stage of the roundworm
Toxocara canis or T. cati through the liver, lungs, or other organs. The normal host of these ascarids is the
dog or cat. The disease is characterized by hypereosinophilia and hepatomegaly and often by pneumonia.
Migrating larvae can invade ocular spaces and cause retinal damage. This migration is called ocular larval
migrans (OLM).

Figure 2-1 is a generalized example of a life cycle that illustrates the key points to study while learning about any
parasite. Understanding the life cycle is the key to understanding how to break the cycle in nature and thereby
control the transmission of parasitic diseases. Minimally, you must know the five parts of a life cycle noted on the
sample figure:
1. Location of the parasite stage in a human host (e.g., adults in intestinal tract or in tissue site).
2. The means by which parasite stages leave the human host (e.g., eggs in feces; feeding insect ingests larval
stage from tissue). Usually, the parasite stage that is seen and identified in the laboratory is found when
examining a fecal or tissue specimen from an infected human. A parasite stage that is routinely recognized in a
biological specimen and thus serves as a key to diagnosis is termed the diagnostic stage.
3. When the parasite is infective. The parasite stage that is infective to humans (e.g., the third-stage larva) is
termed the infective stage. To understand how the potential spread of the disease can be halted, you must know
if external development is required for the parasite to reach infectivity (e.g., eggs develop in the soil) or if it
spends a part of the life cycle in another host.
4. The means by which a new human host is infected (e.g., egg is ingested; larvae enter through skin).
5. Sites of development and maturation of the parasite in humans (e.g., it migrates through the intestinal wall,
liver, and lungs and then is coughed up and re-swallowed into the intestinal tract).

INTESTINAL NEMATODES
Table 2-1 lists the scientific genus and species names and the common names for the intestinal roundworms
of medical importance that are included in this section. On the following pages are the life-cycle diagrams,
disease names, some of the major pathology and symptoms caused by infection with these roundworms,
distribution, and other points of diagnostic importance. Also see Atlas Plates 1 to 27 and their accompanying
descriptions. When you complete the study of each organism, you should be able to write:
1. The scientific name
2. The common name
3. The location of the adults in humans

4. The diagnostic stage and body specimen of choice for examination

5. The method of infection of humans
6. Other specific information pertinent to the diagnosis of each parasitic infection Proper pronunciation of the
scientific name is given beneath each name in Table 2-1.

Practice pronouncing the scientific name aloud and spelling it on paper. The correct pronunciation of each
parasite’s name can be heard in the DavisPlus online flash card activity. In addition to the life-cycle charts, Table
2-2 will help you review the pertinent information for each parasite, including the epidemiology and the major
disease manifestations that these parasites cause.
Enterobius vermicularis (pinworm, seatworm)

Method of Diagnosis
Recover eggs or yellowish white female adult from perianal region with a cellophane tape preparation taken early
in the morning when the patient first
Wakes.

Diagnostic Stage
Disease Names
■ Enterobiasis
■ Pinworm or seatworm infection

Major Pathology and Symptoms

1. Many cases are asymptomatic. Occasionally, severe clinical problems develop.
2. Rarely, the disease causes serious lesions, which are usually limited to minute ulcers and mild inflammation of
the intestine. About half of all patients report abdominal pain.
3. Other symptoms are associated with the migration of the gravid female out from the anus to lay her eggs on
the perianal region at night.
a. Cardinal feature: Hypersensitivity reaction from autoreinfection causing severe perianal itching; eggs get on
hands from scratching and are ingested; pruritus ani is pathognomonic
b. Mild nausea or vomiting
c. Loss of sleep and irritability
d. Slight irritation to intestinal mucosa
e. Vulval irritation in girls from migrating worms entering vagina

Treatment
Mebendazole or pyrantel pamoate; warm tap-water enemas; may need to treat the whole household be cause
eggs are easily spread in the environment.
Distribution
Distribution is worldwide, but it is more prevalent in temperate climates. E.vermicularis is the most common
helminth infection in the United States. It is a group infection, especially common among children.
Of Note
1. Humans are the only known host. Infection is generally self-limiting.
2. Each female produces up to 15,000 eggs. Most eggs become infective within 4 hours of release and

Trichuris trichiura (whipworm)

Method of Diagnosis
Recover and identify characteristic eggs in feces.
Diagnostic Stage

Disease Names
■ Trichuriasis
■ Whipworm infection

Major Pathology and Symptoms

1. Persons with slight infection are asymptomatic, with no treatment required.
2. Heavy infection (500 to 5,000 worms) simulates ulcerative colitis in children and inflammatory bowel disease in
adults. Histology reveals eosinophil infiltration but no decrease in goblet cells. The surface of the colon may be
matted with worms. Patients will have:
a. Bloody or mucoid diarrhea
b. Weight loss and weakness
c. Abdominal pain and tenderness (colitis may be seriously debilitating)
d. Increased peristalsis and rectal prolapse, especially in children
3. Chronic infections in children can stunt growth.
4. Stool is loose with mucus (and obvious blood) in heavy infection.

Treatment
Mebendazole
Distribution
T. trichiura is prevalent in warm countries and areas of poor sanitation. In the United States, it is prevalent in the
warm, humid climate of the South. It is the third most common intestinal helminth in the United States. It is more
common among children and mentally disabled people.
Of Note
1. Double infections commonly occur with Ascaris because of the similar method of human infection (i.e.,
ingestion o eggs from fecally contaminated soil). Pica is not an unusual occurrence in children.
2. Drug treatment may cause production of distorted eggs that have bizarre shapes when seen in a fecal
specimen.
3. Zoonosis infection can occur with pig or dog species of whipworm.

Ascaris lumbricoides (large intestinal roundworm)

Method of Diagnosis
Recover and identify fertile (corticated or not) or infertile eggs in feces. Sedimentation concentration test is
recommended instead of flotation. Enzyme-linked immunosorbent assay (ELISA) serologic test is available.

Diagnostic Stage

Disease Names
■ Ascariasis
■ Roundworm infection
■ Large intestinal roundworm infection

Major Pathology and Symptoms

1. Tissue phase: With heavy or repeated infection, pneumonia, cough, low-grade fever, and 30% to 50%
eosinophilia (Löffler’s syndrome) result from migration of larvae through the lungs (1 to 2 weeks after ingestion of
eggs). Allergic asthmatic reaction may occur with reinfection.
2. Intestinal phase: Intestinal or appendix obstruction results from migrating adults in heavy infections.
a. Vomiting and abdominal pain result from adult migration.
b. Protein malnutrition can occur in children with heavy infections and poor diets.
c. Some patients are asymptomatic.
3. Complications from intestinal obstruction are caused by tangling of the large worms or migration of adults to
other sites, such as the appendix, bile duct, or liver (detectable by radiograph).
4. Migrating adults (22 to 35 cm long) may exit by the nose, mouth, or anus. They are large, creamy, and white
and have a cone-shaped tapered anterior; the male has a curved tail.

Treatment
1. Mebendazole or pyrantel pamoate
2. Piperazine citrate
3. Levamisole
4. Corticosteroid treatment (helps symptoms of severe pulmonary phase)
5. Nasogastric suction and drug treatment or surgery for intestinal obstruction by adults
Distribution
A. lumbricoides is prevalent in warm countries and areas of poor sanitation. It coexists with T. trichiura in the
United States, which is found predominantly in the Appalachian Mountains and adjacent regions to the east,
south, and west. The eggs of these two species require the same soil conditions for development to the infective
state and infection for both is by ingestion of infective eggs.
Of Note
1. Ascaris is the largest adult intestinal nematode.
2. Adults are active migrators when provoked by fever, certain drugs, and anesthesia, and they may tangle and
block the intestine or migrate through the intestine or appendix and come out of the mouth or anus. Mortality
mainly results from intestinal complications in heavy infections.
3. Ascaris is the second most common intestinal helminth infection in the United States and the most common
infection worldwide.
4. The adult female lays up to 250,000 eggs per day.
5. Eggs may remain infective in soil or water for years; they are resistant to chemicals.

Necator americanus (New World hookworm) and Ancylostoma

duodenale (Old World hookworm)

Method of Diagnosis
Recover and identify hookworm eggs in fresh or preserved feces. Species cannot be differentiated by egg
appearance.

Diagnostic Stage

Note: Eggs of these species are almost identical.

Disease Name
Hookworm disease

Major Pathology and Symptoms

1. After repeated infection, severe allergic itching develops at site of skin penetration by infective larvae; this
condition is known as “ground itch.” Penetration stings and an erythematous papule forms.
2. Larvae migrate through lungs: Intra-alveolar hemorrhage and mild pneumonia with cough, wheezing, sore
throat, bloody sputum, and headache occur in heavy infections. Reaction is more severe in reinfections.
3. Intestinal phase of infection:
a. Acute (heavy worm burden producing more than 5,000 eggs per gram [EPG] of feces): enteritis, epigastric
distress in 20% to 50%, anorexia, diarrhea, pain, microcytic hypo-chromic iron deficiency anemia with
accompanying weakness, signs of hypoproteinemia, edema, and loss of strength from blood loss caused by adult
worms
b. Chronic light worm burden showing fewer than 500 EPG is the usual form of this infection; slight anemia,
weakness, or weight loss; non specific mild gastrointestinal symptoms (may be subclinical)
c. Symptoms secondary to the iron deficiency anemia caused by blood loss; hyperplasia of bone marrow and
spleen
d. High eosinophilia

Treatment
Mebendazole or pyrantel pamoate, iron-replacement therapy, thiabendazole ointment for cutaneous larval
migrans.
Distribution
N. americanus is found in North and South America; Asia, including China and India; and Africa. A. duodenaleis
found in Europe; South America; Asia, including China; Africa; and the Caribbean. Other Ancylostoma species
are found in the Far East. Hookworms are common in agrarian areas with poor sanitation. Almost one fourth of
the world’s population is assumed to be infected with hookworms.
Of Note
1. Moist, warm regions and bare-skin contact with sandy soil are optimal conditions for contracting heavy
infections in areas of poor sanitation. These parasites are often found in the same soil conditions as Ascaris and
Trichuris.
2. Delayed fecal examination can result in larval development and egg hatching; therefore, Strongyloides larvae
must be differentiated from hookworm larvae (see Atlas Plates 21 and 25). Hookworm rhabditiform larvae have a
long buccal capsule; Strongyloides rhabditiform larvae have a short buccal capsule and a bulbous esophagus.
3. Adults are voracious bloodsuckers. Heavy infection can result in 100 mL of blood loss per day; therefore,
provide dietary and iron therapy support along with drug treatment, as necessary.
4. Animal species of hookworm larvae such as
A. braziliense can migrate subcutaneously through the human skin after penetration, causing allergic reaction in
the migration tracks (cutaneous larval migrans).
5. Differentiate adults by buccal capsule and bursa (see Atlas Plates 21 and 25).
6. Ancylostoma filariform larvae can infect orally and possibly by transmammary or transplacental passage.
7. Pica contributes to infection and is a common symptom.

Strongyloides stercoralis (threadworm)

Method of Diagnosis
Recover and identify rhabditiform larvae in feces, which are present in low numbers. Also, the presence of
hookworm like eggs or larvae in duodenal drainage fluid or from Entero-Test capsule is diagnostic. (Larvae must
be differentiated from hookworm larvae when found in feces; see Atlas Plates 21 and 25.) Serology is EIA.
Larvae may be in sputum in disseminated strongy loidiasis. In severe cases, intestinal radiograph shows loss of
mucosal pattern, rigidity, and tubular narrowing.

Diagnostic Stage

Disease Names
■ Strongyloidiasis
■ Threadworm infection

Major Pathology and Symptoms

1. Major clinical features are abdominal pain, diarrhea, and urticaria, with eosinophilia.
2. Skin shows recurring allergic, raised, itchy, red wheals from larval penetration.
3. Migration of larvae: Primary symptoms are in the lungs; bronchial verminous (from worms) pneumonia.
4. Intestinal symptoms include abdominal pain, diarrhea, constipation, vomiting, weight loss, variable anemia,
eosinophilia, and protein-losing enteropathy. Light infections are often asymptomatic; gross lesions are usually
absent. The bowel is edematous and congested with heavy infection.
5. S. stercoralis has caused sudden deterioration and death in immunocompromised persons because of heavy
autoinfection and larval migration throughout body (hyperinfection), with bacterial infection secondary to larval
spread and intestinal leakage.

Treatment
1. Thiabendazole (not always successful)
2. Albendazole
3. Ivermectin
Distribution
Distribution is in warm areas, tropics, and subtropics worldwide (similar to hookworm).
Of Note
1. The parasitic female is parthenogenic; therefore, multiplication and autoreinfection can develop in the same
host.
2. Internal infection can continue for years because of maintenance of autoreinfection.
3. Strongyloidiasis is difficult to treat.
4. Often, T-lymphocyte function is defective.
5. Strongyloides larvae are not recovered using the zinc sulfate flotation technique; the sedimentation
concentration method is preferred.
6. Heterogonic development with its free-living cycle producing infectious larvae is influenced by environmental
conditions. S. stercoralis has a heterogonic life cycle that consists of a parasitic generation and a free-living
generation. The parasitic stage has a homogenic life cycle, while the free-living stage has a heterogonic life
cycle. The heterogonic life cycle is advantageous to the parasite because it allows reproduction for one or more
generations in the absence of a host.

Trichinella spiralis (trichinoses; trichinellosis)

Method of Diagnosis
Identification of encysted larvae in biopsied muscle; serologic testing (ELISA) 3 to 4 weeks after infection. A
history of eating undercooked pork or bear, fever, muscle pain, bilateral periorbital edema, and rising eosinophilia
warrants presumptive diagnosis.

Diagnostic Stage
Larva encysted in a muscle cell (called the “nurse cell”)

Note: Granuloma forms around nurse cell and becomes calcified over time.

Disease Names
■ Trichinosis
■ Trichinellosis

Major Pathology and Symptoms

1. Intestinal phase shows small intestine edema and inflammation, nausea, vomiting, abdominal pain, diarrhea,
headache, and fever (1st week after infection).
2. Migration phase shows high fever (104ºF), blurred vision, edema of the face and eyes, cough, pleural pains,
and eosinophilia (15% to 40%) lasting 1 month in heavy infection; death can occur during this phase in 4th to 8th
week after infection.
3. Muscular phase shows acute local inflammation with edema and pain of the musculature. Other symptoms
vary depending on the location and number of larvae present. Larvae encyst in skeletal muscles of limbs,
diaphragm, and face, but they invade other muscles as well. Weakness and fatigue develop.
4. Focal lesions show periorbital edema, splinter hemorrhages of fingernails, retinal hemorrhages, and rash.

Treatment
1. Nonlife-threatening infection (self-limiting): rest, analgesics, and antipyretics
2. Life-threatening infection: prednisone; thiabendazole (caution—effectiveness not proven; may have side
effects)
Distribution
Distribution is worldwide among meat-eating populations and rare in the tropics. The prevalence in the United
States is low with only about 12 cases recognized and reported per year in the United States from 1997 to 2001.
Most cases were acquired by eating undercooked, infected wild game, especially bear meat.
Of Note
1. Zoonosis: Carnivorous mammals are the primary hosts. This condition is found in most species.
2. Multiple cases are often related to one source of undercooked infected meat.
3. Cooking meat to 137ºF or freezing for 20 days at 5ºF will kill larvae.

Dracunculus medinensis (Guinea worm)

Method of Diagnosis
Visually observe painful skin blisters or emerging worm; induce release of larvae from skin ulcer when cold water
is applied.

Disease Names
■ Dracunculus
■ Guinea worm

Major Pathology and Symptoms

1. Allergic reaction occurs during migration.
2. The papule develops into a blister, usually on the feet or legs that ruptures.
3. Secondary bacterial infections or reaction to aberrant migration of larvae or adults may cause disability or
death.

Treatment
1. Removal of adult from skin (slow withdrawal from blister by wrapping it around a revolving small stick over
several days; this process may be completed in a few days but usually requires weeks or even months)
2. Surgical removal of adult
3. Aspirin for pain; antihistamines may reduce swelling
4. Prevention of secondary infection
Distribution
D. medinensis is found in the Middle East, India, Pakistan, and Africa.
Of Note
1. D. medinensis is the largest adult nematode parasitic in humans.
2. There is no effective immunity to reinfection.
3. The World Health Organization (WHO) is sponsoring an attempt at global eradication through the promotion of
drinking water filtration (T-shirts or gauze can be used) to strain out infected copepods. The WHO also sponsors
an education campaign to keep people out of the water when adult worms are protruding from the body. Since
1986 the total worldwide caseload has dropped from about 3.5 million to less than 18,000 cases in 2010 because
of the eradication efforts by many organizations.

FILARIAE: TISSUE NEMATODES

General Life Cycle
Adult filariae live in various human tissue locations. In general, fertilized adult female filariae living in the tissues
produce living embryos (microfilariae) that migrate into lymphatics, blood, or skin. These parasites require an
arthropod intermediate host for transmission of infection. If the arthropod ingests microfilariae while taking a
blood meal, the larvae molt twice inside the arthropod intermediate host and molts into the infective stage
filariform larvae.

These larvae are released from the insect’s proboscis and enter a new human definitive host when the arthropod
next feeds on blood. The entering larvae migrate to the appropriate tissue site and develop to become adults.
Maturation can take up to 1 year. In some species, the microfilariae are more prevalent in peripheral blood at
specific times of the day or evening (i.e., they exhibit periodicity). These times appear to coincide with the usual
feeding pattern of the arthropod intermediate host species. Nocturnal or diurnal periodicity is noted in Table 2-4.
At least three other species of filariae are common parasites of humans. Mansonella perstans, found in Africa
and Central and South America, and Mansonella ozzardi, found in Central and South America, apparently do not
induce pathology but do produce microfilariae in the blood. Mansonella streptocerca, found in tropical Africa,
produces microfilariae that are found in the skin, as does Onchocerca volvulus. Therefore, any microfilariae found
in blood or tissue must be differentiated; the diagnostic stages of the species are illustrated to aid in the
differential diagnosis of filariasis. Atlas Plates 28–33 further illustrate these parasites. Information on the following
pages is keyed by number according to genus and species. These numbers also will be used in the diagrams: 1
= Wuchereria bancrofti; 2 = Brugia malayi; 3 = Loa loa; 4 = Onchocerca volvulus.

Filariae
Method of Diagnosis
A. 1-3. (Numbers refer to organisms in the Filariae life cycle diagram.) Locate microfilariae (200 to 300 m) in
stained blood smear (see p. 152). Also, you can centrifuge blood samples and lyse red blood cells to concentrate
microfilariae in the specimen before staining (see p. 154, Knott technique).
4. Locate microfilariae in skin snips of tissue nodule.
B. Use serology (lacks specificity).

Differentiation of Microfilariae as Seen in a Stained Blood Smear

Examine for the presence or absence of a sheath (a thin, translucent eggshell remnant covering the body of the
microfilaria and extending past the head and tail). Also, examine the tail area of microfilaria for the presence or
absence of cells that exhibit a characteristic array of stained nuclei.

The tail of microfilaria of Onchocerca volvulus as seen in a tissue scraping from the nodular mass containing the
adult filaria or from a skin snip shows no sheath, nuclei not terminal, and a straight tail. The tail of Mansonella
streptocerca microfilaria is bent like a fishhook. These microfilariae are also found in skin snips.

Disease Names
Filariasis (generic)
1. Elephantiasis, Bancroft’s filariasis
2. Malayan filariasis
3. Eyeworm
4. Blinding filaria; river blindness

Major Pathology and Symptoms

Diagnosis is difficult because symptoms are broad in spectrum. The diagnosis depends on identification of
microfilariae.
1-2. In the early acute phase, fever and lymphangitis are seen; after years of repeated exposure, chronic
elephantiasis develops because of obstruction of lymphatics, lymph stasis, and lymphedematous changes. Adults
in lymphatics sequentially induce dilation, inflammation, and, after death of the adult worm, a surrounding
granulomatous thickening of lymphatic walls. Finally, obstruction and resultant enlargement occur below the
blocked area. Malayan filariasis is more often asymptomatic. In endemic areas, “filaria fevers” are seen, with
recurrent acute lymphangitis and adenolymphangitis without microfilariae. Also seen is tropical eosinophilia or
Weingarten’s syndrome (which resembles asthma) with high eosinophilia and no microfilariae.
3. Localized subcutaneous edema (Calabar swellings), particularly around the eye, are caused by microfilariae
migration and death in capillaries (more serious in visitors to endemic areas). Living adults cause no
inflammation; dying adults induce a granulomatous reaction. Proteinuria and endomyocardial fibrosis also occur.
4. Fibrotic nodules on the skin encapsulate adults (onchocercomas). Progressively severe allergic
onchodermatitis (pigmented rash) develops; blindness occurs from the presence of microfilariae in all ocular
structures (very prevalent in Africa and on Central American coffee plantations).

Treatment
1. Diethylcarbamazine; ivermectin kills microfilariae
2. Diethylcarbamazine
3. Diethylcarbamazine (also prophylactically)
4. Ivermectin
Distribution
1. Distribution is spotty worldwide; it occurs in tropical and subtropical areas.
2. Filiariae are found in East and Southeast Asia.
3. They are found in the rainforest belt in Africa.
4. They are found in Central America and equatorial Africa.
Of Note
1. Mosquito resistance to insecticides and coastaldwelling human populations are increasing the incidence of
exposure to infection.
2. Eosinophilic lung (tropical eosinophilia), an asthmalike syndrome, may be caused by occult filariasis or
zoonoses.
3. Onchocerciasis is the major cause of blindness in Africa; insect control is difficult because the Simulium spp.
(intermediate host) breeds in running water.
4. Filarial infection can induce an immunosuppressed state in the host that prevents a reaction to the parasite,
but immune-mediated inflammatory responses or immunologic hyperreactive immunopathology (elephantiasis
response) can still occur.

ZOONOSES
A zoonosis is a biological life-cycle situation—not a class of parasites. Some parasites that usually live only in
animals and survive in “the wild” without any life-cycle need for humans can sometimes infect humans. When this
happens, the parasite is living in an unnatural host and will cause symptoms in this accidental host. Many types
of parasites cause zoonotic infections but the nematode group comprises most of the important zoonotic
infections seen in humans. Zoonoses are accidental infections in humans by parasites that usually have other
animals as their hosts. Although the animal host and its parasites have evolved together and may tolerate each
other well, in an abnormal host, such as a human, the parasite can often cause serious pathology. Table 2-5 lists
the scientific names of some nematode zoonotic parasites, their geographic locations, usual animal hosts,
disease, and symptoms produced in humans after accidental infection. Although these parasites do not normally
complete a full life cycle in humans, it is nevertheless important to study these infections because of the
significant pathology they cause in infected individuals. For example, in the United States, there are large dog
and cat pet populations and these animals commonly have intestinal ascarids ( Toxocara spp.) and hookworms
(Ancylostoma spp.). When humans encounter pet feces–contaminated soil, roundworm eggs may be ingested or
hookworm larvae may invade exposed skin. Most pet owners do not realize that these dog and cat worms may
also infect humans and therefore do not take proper precautions to prevent infections. Small children are
particularly at risk because of their play habits (particularly in sandboxes or at public playgrounds) and pica.
Various workers (e.g., plumbers, electricians, others who often crawl under raised buildings) and sunbathers
sitting on wet beach sand may also be exposed to animal hookworm larvae and are susceptible to larval
penetration. Prevention of these infections may be accomplished by monitoring and treating infected pets
(especially puppies and kittens) for worms, avoiding potentially contaminated soil, and practicing good hygiene
and sanitation. Ingested eggs hatch in the intestine releasing larval forms, which migrate extensively throughout
the body. Eventually they become encapsulated in various tissues or organs. Often they are found in the liver,
eye, or central nervous system, resulting in organ damage with varying severity depending on the number of
larvae and their locations in the host. Blindness and severe brain damage have been associated with larvae of
Baylisascaris procyonis, an ascarid found in racoons in North America, Europe, and Japan.
CASE STUDY
A nurse from a psychiatric facility called the local hospital laboratory to find out how to perform a cellophane tape
test ordered for a 40-year-old patient who was exhibiting rectal digging. The technologist on duty explained the
procedure, and when the laboratory received it, the technologist noted the parasitic form in the accompanying
figure.
1. Was the correct test performed? Why?
2. How is this parasitic infection acquired? How is it maintained within the infected patient?
3. What other parasites may be transmitted with this organism?

A mother brought the parasite form shown in the accompanying figure to her 5-year-old daughter’s pediatrician.
She stated that her daughter had been complaining of an upset stomach, had a slight fever, and was having
diarrhea “a couple of times” during the last 10 days. Last night, the child vomited this “earthworm” into the toilet.
1. What is the probable identity of this parasite (genus and species)?
2. What other organs are invaded during this parasite’s life cycle?
3. What other nematode parasite might commonly be found in patients harboring the worm recovered in this
case?
4. What procedure should be performed to rule out other infections?
5. Why did the child vomit out the helminth?

A new internal medicine resident from the Philippines went to the hospital’s outpatient drawing area one evening
to have his pre-employment blood work done. His laboratory results indicated 1 + proteinuria and rare red blood
cells in the urinalysis report. The complete blood count (CBC) indicated mild anemia and the differential report
described the form seen in the accompanying figure.
1. What parasite do you suspect (genus and species)?
2. Would this infection be revealed if the resident had his blood drawn first thing in the morning? Explain your
answer.
3. What vector(s) are included in this parasite’s life cycle?
4. List other clinical symptoms that may be seen in this disease.
A 50-year-old special ops veteran came to the emergency department with severe respiratory symptoms,
including fever, wheezing, and a productive cough. Vague gastrointestinal symptoms were also present. The
patient had been receiving immunosuppressive therapy since his kidney transplant. He denied exposure to colds
or possible intestinal pathogens. The physician ordered a CBC and a sputum culture and Gram
stain. Mild eosinophilia was reported in the CBC. The parasite form in the accompanying figure was observed in
a wet mount of the patient’s sputum following its initial observation in the Gram stain.
1. What nematode parasites have a lung phase in their life cycle?
2. What parasite (genus and species) do you suspect in this case?
3. Describe the life cycle of this parasite and explain how it can survive for an extended period in the host.
4. List possible complications that may occur if the patient is not successfully treated.

A 25-year-old man went to the doctor complaining of blurred vision and swelling around his eyes. He had been
experiencing a low-grade fever and headache for the past 3 days. A CBC was performed and the differential
report revealed eosinophilia of 25%. On further questioning, the patient stated that he was a hunter and had
butchered, processed, and eaten a recently killed bear.
1. Based on the patient’s symptoms and history, what is the possible parasitic infection (genus and species)?
2. What classic signs are associated with this disease?
3. What other tests should be performed to confirm the diagnosis?
4. What precautions are necessary to prevent infections from this organism?

POST TEST

1. Draw the life cycle of Ascaris lumbricoides in diagram form. Indicate the diagnostic and infective stages. (10
points)
2. The night technician identified the following parasite below: (15 points)

a. What is the scientific name of the parasite?

b. What is the intermediate host?
c. In what body specimen was this organism identified and what laboratory technique was helpful in finding the
organism?

3. Briefly define each of the following: (25 points)

a. Cutaneous larval migrans
b. Diurnal
c. Diagnostic stage
d. Infective stage
e. Prepatent period

4. In which of the following sets of nematodes can each organism cause a pneumonia-like syndrome in a person
exposed to heavy infection with any of the three parasites? (5 points)
a. Ascaris lumbricoides, Trichuris trichiura, or Onchocerca volvulus
b. Enterobius vermicularis, Dracunculus medinensis, or Trichuris trichiura
c. Strongyloides stercoralis, Wuchereria bancrofti, or Angiostrongylus costaricensis
d. Necator americanus, Ascaris lumbricoides, or Strongyloides stercoralis

5. A patient presents with vague abdominal pains and a microcytic hypochromic anemia. A possible causative
parasite is: (2 points)
a. Enterobius vermicularis
b. Ancylostoma duodenale
c. Brugia malayi
d. Trichinella spiralis

6. An immunosuppressed patient is susceptible to autoreinfection with which one of the following nematodes? (2
points)
a. Strongyloides stercoralis
b. Trichinella spiralis
c. Ascaris lumbricoides
d. Trichuris trichiura

7. Infection with Enterobius vermicularis is best diagnosed by which one of the following? (2 points)
a. Examination of feces for eggs and adults
b. Serology tests
c. Perianal itching noted by patient
d. Examination of a cellophane tape preparation for eggs and adults
8. Human infection with Loa loa is best diagnosed by which of the following? (2 points)
a. Examination of an infected Anopheles mosquito
b. Examination of blood smears
c. Examination of feces
d. Examination of a skin scraping

9. A child who plays in dirt contaminated with human and pet feces is susceptible to which of the following set of
parasites? (5 points)
a. Ascaris lumbricoides, Trichuris trichiura, Trichinella spiralis, Wuchereria bancrofti
b. Loa loa, Capillaria philippinensis, Enterobius vermicularis, Trichinella spiralis
c. Strongyloides stercoralis, Toxocara canis, Ascaris lumbricoides, Necator americanus
d. Ancylostoma braziliense, Trichuris trichiura, Trichinella spiralis, Necator americanus

10. All of the following adult parasites live in the intestinal tract EXCEPT: (2 points)
a. Ascaris lumbricoides
b. Enterobius vermicularis
c. Loa loa
d. Trichinella spiralis

11. The largest adult nematode that is found subcutaneously in infected hosts is: (2 points)
a. Ascaris lumbricoides
b. Dracunculus medinensis
c. Onchocerca volvulus
d. Trichinella spiralis

12. Each of the following microfilaria has a sheath EXCEPT: (2 points)

a. Brugia malayi
b. Loa loa
c. Mansonella ozzardi
d. Wuchereria bancrofti

13. For each of the following, match the diagnostic technique(s) associated with the given parasite.
14. Note: Choices may be used more than once or not at all. (10 points)
a. Blood film examination
b. Cellophane tape test
c. Fecal concentration method
d. Tissue biopsy
e. Serologic test
_____. Ascaris lumbricoides
_____. Strongyloides stercoralis
_____. Trichinella spiralis
_____. Wuchereria bancrofti

14. For each of the following, match the insect(s) vector found in each filaria’s life cycle.
Note: Choices may be used more than once or not at all. (10 points)
a. Anopheles spp. (mosquito)
b. Culex spp. (mosquito)
c. Mansonia spp. (mosquito)
d. Chrysops (fly)
e. Simulium (fly)
_____. Brugia malayi
_____. Loa loa
_____. Onchocerca volvulus
_____. Wuchereria bancrofti

15. Visceral larval migrans is caused by: (3 points)

a. Ascaris lumbricoides
b. Ancylostoma braziliense
c. Dirofilaria spp.
d. Toxocara canis

16. The zoonotic disease known as creeping eruption is caused by: (3 points)
a. Ascaris lumbricoides
b. Ancylostoma braziliense
c. Dirofilaria spp.
d. Toxocara canis

CESTODA CHAPTER 3
GLOSSARY
 anaphylaxis (anaphylactic shock). An exaggerated histamine-release reaction by the host’s body to foreign
proteins, allergens, or other substances; may be fatal.
 anorexia. Loss of appetite.
 brood capsules. Structures within the daughter cyst in Echinococcus granulosus in which many scolices
grow. Each scolex can develop into an adult tapeworm in the definitive host.
 Cestoda. A class within the phylum Platyhelminthes that includes the tapeworms. These helminths have
flattened, ribbonlike, segmented bodies.
 copepod. A freshwater crustacean; intermediate host Iin the life cycle of Diphyllobothrium latum.
 coracidium. A ciliated hexacanth embryo; D. latum eggs develop to this stage and then can hatch in fresh
water.
 cysticercoid. The larval stage of some tapeworms (e.g., Hymenolepis nana); a small, bladderlike structure
containing little or no fluid in which the scolex is enclosed.
 cysticercus. A thin-walled, fluid-filled, bladderlike cyst that encloses a scolex. Also termed a bladder worm.
Some larvae develop in this form (e.g., Taenia spp.)
 embryophore. The shell of Taenia spp. eggs and certain other tapeworm eggs as seen in feces.
 hermaphroditic. Having both male and female reproductive organs within the same individual. All
tapeworms have both sets of reproductive organs in each segment of the adult.
 hexacanth embryo. A tapeworm larva having six hooklets (see oncosphere).
 hydatid cyst. A vesicular structure formed by E. granulosus larva in the intermediate host; contains fluid,
brood capsules, and daughter cysts in which the scolices of potential tapeworms are formed. Grows slowly
and can get quite large.
 hydatid sand. Granular material consisting of free scolices, hooklets, daughter cysts, and amorphous
material. Found in the fluid of older cysts of E. granulosus.
 oncosphere. The motile, first-stage larva of certain cestodes; armed with six hooklets (also termed
hexacanth embryo).
 operculum. The lid-like or cap-like cover on certain platyhelminth eggs (e.g., D. latum).
 parenchyma. Tissue in which the internal organs of platyhelminths are embedded.
 plerocercoid. The larval stage in the development of D. latum that develops after a freshwater fish ingests
the procercoid stage. This form has an immature scolex and is infective if eaten by humans.
 procercoid. The larval stage that develops from the
 coracidium of D. latum. It develops in the body of a freshwater crustacean.
 proglottid (pl. proglottids). One of the segments of a tapeworm. Each proglottid contains male and female
reproductive organs when mature.
 racemose. Clusters with branching, nodular terminations resembling a bunch of grapes. Used in reference
to larval cysticercosis caused by the migration and development of T. solium larvae in the brain tissue of
humans; an aberrant form.
 rostellum. The fleshy, anterior protuberance of the
 scolex of some tapeworms (species specific); may bear a circular row (or rows) of hooks; may be
retractable.
 scolex (pl. scolices). Anterior end of a tapeworm; attaches to the wall of the intestine of a host by means of
suckers and sometimes hooks.
 sparganosis. Plerocercoid in human tissue from accidental infection with procercoid of several species of
Cestodes.
 strobila. Entire body of a tapeworm.
 tegument (integument). The body surface of platyhelminths; the Cestode tegument is the site of nutrient and
oxygen absorption as well as waste excretion.
 transport hosts. Vectors; often bloodsucking insects.
 viscera (sing. viscus). Any of the large organs in the interior of any of the three great body cavities of
vertebrates.
Hymenolepis nana (dwarf tapeworm)

Method of Diagnosis
Recover and identify eggs in the feces.

Diagnostic Stage

Disease Name
Dwarf tapeworm infection

Major Pathology and Symptoms

1. Light infection is asymptomatic.
2. Heavy infection symptoms include intestinal enteritis, abdominal pain, diarrhea, headache, dizziness, and
anorexia.
4. Multiple adults are commonly present.
Treatment
Niclosamide
Distribution
Worldwide, H. nana is found in the tropics and subtropics; it most commonly occurs in children and in
institutionalized people living in close quarters. It is the most prevalent human tapeworm found throughout the
United States. Estimated infection rate is 3%.
Of Note
1. The dwarf tapeworm requires no intermediate host. The house mouse is also a common definitive host. Fleas
and beetles can serve as transport hosts. Cysticercoid larvae can develop in the body cavity of these insects and
are infective to either humans or rodents if accidentally ingested.
2. Eggs in feces from infected mice and rats are a common source of human infection.

Taenia saginata (beef tapeworm) and Taenia solium (pork tapeworm)

Method of Diagnosis
Recover egg or gravid proglottid (or scolex after drug treatment) in feces. Proglottid and scolex identification:
T.saginata has 15 to 30 lateral uterine branches in each side of the gravid proglottid (can be seen clearly after
dye injection into the uterine pore) and a scolex with only four suckers; T. solium has a gravid proglottid with 7 to
12 lateral uterine branches on each side of the gravid proglottid and the scolex has four suckers plus a central
crown of hooks. T. solium is called the “armed” tapeworm because of the crown of hooks by which the scolex
attaches to the intestinal wall (see Atlas Plate 40). The eggs of these two species are identical. Immunologic
methods for cysticercosis are enzyme-linked immunosorbent assay (ELISA) and indirect hemagglutination.

Diagnostic Stage
1. Eggs in feces
2. Intact gravid proglottids (usually in pairs or short chains, T. solium; usually singly, T. saginata) may be found in
feces and must be differentiated (see Atlas Plates 42 and 43)
3. Radiographic, computed tomography (CT), or magnetic resonance imaging demonstration of T. solium
cysticercus in tissue with accompanying symptoms

Disease Names
■ T. saginata: taeniasis, beef tapeworm infection
■ T. solium: taeniasis, pork tapeworm infection; cysticercosis (larval infection in tissue)

Major Pathology and Symptoms

1. Most infected people are asymptomatic. Abdominal pain, diarrhea, and weight loss can occur. Eosinophilia is
moderate.
2. Humans can serve as accidental intermediate hosts for T. solium. If eggs of T. solium are accidentally ingested
or released from a proglottid in the intestinal tract, the eggs can hatch in the intestine and the larvae will migrate
to form cysticercus bladders in any organ or nervous tissue (cysticercosis; neurocysticercosis [NCC] if in the
central nervous system). This larval migration can lead to a fatal outcome if the racemose form develops in the
brain. Arachnoiditis occurs in 50% of active NCC cases; obstructive hydrocephalus occurs in 25% of active
NCC cases. Symptoms include epilepsy, headache, papilledema, and vomiting.

Treatment
■ For adult tapeworm: praziquantel or niclosamide
■ For cysticercosis: albendazole or praziquantel, anticonvulsants for seizures, corticosteroids for NCC
symptoms, surgery
Distribution
T. saginata: cosmopolitan in countries in which beef is eaten raw or insufficiently cooked. It is found in the
southwestern United States. T. solium: cosmopolitan when pork is eaten raw or undercooked. It is less common
in the United States.
Of Note
1. Humans are the only known definitive host for these two Taenia spp.
2. The adult worms live for many years and usually only one worm is present in the intestine.
3. Human cysticercosis is common in Mexico and Central America.
4. Some 60% of patients with cysticercosis have larvae in the brain.

Diphyllobothrium latum (broadfish tapeworm)

Method of Diagnosis
Recover eggs in feces; evacuated proglottids usually in chains ranging from a few inches to several feet; scolices
are also diagnostic in feces but are rarely naturally evacuated intact.

Disease Names
■ Diphyllobothriasis
■ Dibothriocephalus anemia
■ Fish tapeworm infection
■ Broadfish tapeworm infection

Major Pathology and Symptoms

1. Major pathology and symptoms are intestinal obstruction (adult can grow to 20 meters) and abdominal pain.
Most infected people exhibit vague digestive symptoms.
2. Weight loss and weakness occur.
3. In about 1% of infected people (usually restricted to people of Scandinavian descent), anemia (macrocytic
type) and eventual nervous system disturbances result from a deficiency caused by the tapeworm’s utilization of
up to 100% of dietary B12.

Treatment
Niclosamide or praziquantel
Distribution
Distribution is in temperate regions where freshwater fish are a common part of the diet or raw fish are eaten (the
Great Lakes region of the United States, Alaska, Chile, Argentina, Central Africa, and parts of Asia). In Europe,
estimates of infection include 20% of the Finnish people and up to 100% of residents of the Baltic region. World
trade has increased the distribution of raw fish dishes to nonendemic areas with a concomitant increase in
tapeworm infections.
Of Note
1. Usually only one adult is present.
2. In addition to humans, a variety of fish-eating mammals can serve as definitive hosts.
3. The procercoid may be passed up the food chain in a dormant condition through small to large game fish (e.g.,
Northern or walleyed pike).
4. A human can develop a tissue plerocercoid if a procercoid in a copepod is accidentally ingested.
(See sparganosis in Table 3-2.)
5. The Japanese salmon tapeworm, Diphyllobothrium nihonkaiense, is causing increasing numbers of infections
in Japan, with emerging cases appearing in the United States and Europe. Consumption of sashimi and ceviche
promotes the possibility of infection with this parasite.

Echinococcus granulosus (hydatid tapeworm)

Method of Diagnosis
1. Serologic tests: indirect hemagglutination, ELISA
2. Presence of scolices, brood capsules, hydatid sand, or daughter cysts in the hydatid cyst fluid as detected by
biopsy (not recommended because leakage of cyst fluid can cause anaphylaxis)
3. X-ray examination, ultrasound scan, or CT detection of cyst mass in organ, especially if calcified

Diagnostic Stage

Hydatid cyst (partial cross-section)

Disease Names
■ Echinococcosis
■ Hydatid cyst
■ Hydatid disease
■ Hydatidosis

Major Pathology and Symptoms

1. Symptoms vary according to location and size of cyst. Expanding cyst causes pressure necrosis of
surrounding tissues.
a. In the liver (most common site), no symptoms develop until the cyst gets large (nearly a year after ingestion of
egg); then jaundice or portal hypertension develops.
b. In the lung, no symptoms appear until the cyst becomes large; then coughing, shortness of breath, and chest
pain develop.
c. In other sites, symptoms are related to enlarging cyst pressure.
2. Cyst growth or rupture can result in death.
3. Anaphylactic shock may occur if the cyst ruptures (may occur during biopsy procedure).
4. Other findings include eosinophilia, urticaria, and bronchospasm.

Treatment
1. Surgery
2. Mebendazole or albendazole
Distribution
Human infections occur as zoonoses primarily in sheep-raising areas where domestic dogs are used in herding.
Of Note
1. Hydatid disease in the United States is reported mainly in sheep-raising areas of the Southwest (chiefly among
the Navaho), Utah, and Alaska; it also is reported in Canada.
2. Echinococcus cysts in sheep or human tissues produce daughter cysts and brood capsules, all lined with
germinal tissue that buds off many protoscolices, each of which can form the scolex of an adult if ingested by a
canine.
3. E. multilocularis, which forms alveolar cysts, is rarer in humans but it is intensely pathogenic and generally
fatal without treatment. The disease develops slowly and may not produce symptoms for several years.
Symptoms often mimic those of cirrhosis of the liver or liver cancer. This parasite is found worldwide, mostly in
northern latitudes, and is harbored in wild canines (e.g., foxes, coyotes) and in rodents.
4. Hydatid cyst in bone has abnormal, disseminated development in the marrow.
5. A slow-leaking cyst causes allergic sensitization. Cyst rupture (occurring naturally or during surgery) can cause
anaphylaxis or spread of germinal tissue to other sites where new cysts can develop.

CASE STUDY

An elderly woman of Mediterranean heritage living in the Great Lakes area went to her doctor. She had been
suffering from intermittent diarrhea and abdominal pain for several weeks. After questioning, the patient revealed
that she regularly prepared gefilte fish (balls of boneless fish mixed with cracker meal) using freshwater fish
purchased from a local grocery store. She said she tasted it often during preparation to make sure the
seasonings were correct. Stool cultures and parasitic examinations were ordered. The culture results were
negative for enteric pathogens but the parasitic examination recovered the parasite form shown in the
accompanying figure.
1. What parasite (genus and species) do you suspect?
2. How is this parasitic infection acquired? What other parasitic infections could she have gotten by the same
means?
3. List other complications that may occur in long-standing infections.

POST TEST
1. Define and cite an example of each of the following: (20 points)
a. Hexacanth embryo
b. Hermaphroditic
c. “Armed” scolex
d. Proglottid
e. Hydatid cyst

2. Matching: Select correct intermediate host(s) for each parasite: (5 points)

a. _____Taenia solium
b. _____Hymenolepis nana
c. _____Hymenolepis diminuta
d. _____Diphyllobothrium latum
e. _____Echinococcus granulosus

1. Fish
2. Copepod
3. Cow
4. Human
5. Pig
6. Snail
7. Flea or beetle
8. Dog
9. Sheep
10. None

3. Draw and label the diagnostic stage(s) for each of the following as you would observe them microscopically in
human feces: (40 points)
a. Dwarf tapeworm
b. Broadfish tapeworm
c. Beef tapeworm
d. Pork tapeworm

4. Matching: Select one correct match for each parasite: (7 points)

a. _____Taenia solium
b. _____Hymenolepis nana
c. _____Diphyllobothrium latum
d. _____Echinococcus granulosus
e. _____Dipylidium caninum
f. _____Sparganosis
g. _____Cysticercosis
1. Macrocytic anemia, b. vitamin B12 deficiency
2. Plerocercoid subcutaneously
3. Neurological symptoms if in brain
4. Autoreinfection is common
5. Proglottid has 7 to 10 lateral uterine branches
6. Human accidentally ingests infected flea
7. Cysts found in liver, lungs, or other organs

Questions 5 to 18 are worth 2 points each.

5. A patient from the Great Lakes area presents with vague abdominal symptoms and a macrocytic anemia.
Which Cestoda would be the probable cause?
a. Diphyllobothrium latum
b. Echinococcus granulosus
c. Taenia saginata
d. Hymenolepis nana

6. A scolex is recovered in human feces after the patient is treated with medication. The scolex bears four cup-
shaped suckers. This parasite is:
a. Diphyllobothrium latum
b. Echinococcus granulosus
c. Taenia saginata
d. Hymenolepis nana

7. The eggs of which two species are infective to humans if ingested, resulting in larval stages and pathology in
the host’s tissues?
a. Taenia solium and T. saginata
b. Hymenolepis diminuta and Dipylidium caninum
c. Echinococcus granulosus and Taenia solium
d. Hymenolepis nana and Taenia saginata

8. The larval stage of which two species are infective to humans if the parasitized insect intermediate host is
ingested?
a. Taenia solium and T. saginata
b. Hymenolepis diminuta and Dipylidium caninum
c. Echinococcus granulosus and Taenia solium
d. Hymenolepis nana and Taenia saginata

9. Packets of tapeworm eggs encapsulated in a single membrane were recovered in feces. This parasite is:
a. Diphyllobothrium latum
b. Dipylidium caninum
c. Hymenolepis nana
d. Taenia saginata

10. The causative agent of cysticercosis is:

a. Echinococcus granulosus
b. Taenia saginata
c. Taenia solium
d. Trichinella spiralis

11. The examination of human feces is no help in the detection of:

a. Ancylostoma duodenale
b. Echinococcus granulosus
c. Hymenolepis nana
d. Strongyloides stercoralis

12. Mature eggs of an adult tapeworm accumulate in the:

a. Gravid proglottid
b. Mature proglottid
c. Neck region of the strobila
d. Scolex

13. A type of tapeworm larva with a large bladder, producing daughter cysts, brood capsules, and numerous
scolices is:
a. Cysticercus
b. Cysticercoid
c. Hydatid cyst
d. Plerocercoid
e. Procercoid

14. Eggs from which tapeworm, when passed, are immediately infective to humans?
a. Diphyllobothrium latum
b. Hymenolepsis nana
c. Taenia saginata
d. Echinococcus granulosus

15. In the Diphyllobothrium latum life cycle, the infective stage for humans is:
a. Cysticercus
b. Cysticercoid
c. Hydatid cyst
d. Procercoid
e. Plerocercoid

16. The human condition resulting from ingestion of the immature larval form of Diphyllobothrium latum is called:
a. Cysticercosis
b. Hydatid disease
c. Racemose
d. Sparganosis

17. The number of uterine branches in the mature proglottid of Taenia saginata is:
a. Less than 14
b. More than 14

18. The tapeworm scolex without cup-shaped suckers is:

a. Diphyllobothrium latum
b. Hymenolepsis nana
c. Taenia saginata
d. Taenia solium
e. Echinococcus granulosus