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Chapter 13 : Food-Borne Parasites

Authors: Dolores E. Hill1, J. P. Dubey2
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Affiliations: 1: U.S. Department of Agriculture, Agricultural Research Service, Animal and Natural Resources Institute, Animal Parasitic Diseases Laboratory, Building 1044, BARC-East, Beltsville, MD 20705-2350; 2: U.S. Department of Agriculture, Agricultural Research Service, Animal and Natural Resources Institute, Animal Parasitic Diseases Laboratory, Building 1001, BARC-East, Beltsville, MD 20705-2350
Content Type: Monograph
Publication Year: 2010

Category: Food Microbiology; Applied and Industrial Microbiology

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Abstract:

Food-borne infections are a significant cause of morbidity and mortality worldwide, and food-borne parasitic diseases, though not as widespread as bacterial and viral infections, are common on all continents and in most ecosystems, including arctic, temperate, and tropical regions. Major food-borne trematodiasis in humans has been discussed in this chapter. , the beef tapeworm, and and , the pork tapeworms, cause taeniasis in humans. and occur worldwide, endemically in underdeveloped regions where pork and beef are consumed and sporadically in developed nations, largely due to importation by immigrants and travelers. The neck of the tapeworm begins the process of strobilation, the production of proglottids. Humans and other piscivorous mammalian hosts harbor the adult tapeworm, which is attached to the small intestinal surface by the scoop-shaped scolex and bothria (or grooves), which are characteristic holdfast organs of pseudophyllidean tapeworms. Adult tapeworms are generally benign, but abdominal pain, nausea, and diarrhea may occur, and may absorb enough vitamin B to cause deficiency in malnourished individuals. Nematodes in the genus are some of the most commonly recognized agents of food-borne parasitic disease. Gnathostomes are species belonging to a geographically widespread genus but are most commonly found as adult worms in carnivorous mammals in Asia. The most widespread protozoan parasite affecting humans is . To prevent food-borne infection by , the hands of people handling meat should be washed thoroughly with soap and water before they go to other tasks.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Food-Borne Parasites
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Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
/content/10.1128/9781555815936.ch13.ch13fig01
Figure 1.
(A) Relative sizes of eggs produced by important digenetic trematode and cestode parasites of humans. (B) Life cycle of . i, infective stage; d, diagnostic stage. 1d, embryonated eggs, each with a fully developed miracidium, are passed in feces. 2, snail host ingests eggs; miracidia emerge from eggs and penetrate snail intestine; and sporocysts, rediae, and then cercariae develop in snail tissues. 3, cercariae released from snail. 4, cercariae penetrate skin of fresh/brackish water fish and encyst as metacercariae in fish tissues. 5i, humans become infected by ingesting undercooked fish containing metacercariae. 6, metacercariae excyst in small intestine and develop to adult stage. 7, fish-eating mammals and birds can also be infected.
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Image of Figure 1.
Figure 1.

(A) Relative sizes of eggs produced by important digenetic trematode and cestode parasites of humans. (B) Life cycle of . i, infective stage; d, diagnostic stage. 1d, embryonated eggs, each with a fully developed miracidium, are passed in feces. 2, snail host ingests eggs; miracidia emerge from eggs and penetrate snail intestine; and sporocysts, rediae, and then cercariae develop in snail tissues. 3, cercariae released from snail. 4, cercariae penetrate skin of fresh/brackish water fish and encyst as metacercariae in fish tissues. 5i, humans become infected by ingesting undercooked fish containing metacercariae. 6, metacercariae excyst in small intestine and develop to adult stage. 7, fish-eating mammals and birds can also be infected.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 2.
Life cycle of . i, infective stage; d, diagnostic stage. 1d, unembryonated eggs passed in feces. 2, embryonated eggs contaminate a body of water. 3, miracidia hatch from embryonated eggs and penetrate snail. 4, miracidia develop in snail tissue into sporocysts (4a), rediae (4b), and then cercariae (4c). 5, free-swimming cercariae encyst on water plants. 6i, metacercariae on water plant ingested by humans, sheep, or cattle. 7, metacercariae excyst in duodenum, penetrate the intestinal wall, and enter the liver to feed. 8, adults reside in hepatic biliary ducts.
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Figure 2.

Life cycle of . i, infective stage; d, diagnostic stage. 1d, unembryonated eggs passed in feces. 2, embryonated eggs contaminate a body of water. 3, miracidia hatch from embryonated eggs and penetrate snail. 4, miracidia develop in snail tissue into sporocysts (4a), rediae (4b), and then cercariae (4c). 5, free-swimming cercariae encyst on water plants. 6i, metacercariae on water plant ingested by humans, sheep, or cattle. 7, metacercariae excyst in duodenum, penetrate the intestinal wall, and enter the liver to feed. 8, adults reside in hepatic biliary ducts.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 3.
Life cycle of . i, infective stage; d, diagnostic stage. 1d, unembryonated eggs are released in sputum or in feces. 2, eggs embryonate in water. 3, miracidia hatch from eggs in water and penetrate snails. 4, miracidia develop in snail tissues into sporocysts (4a), rediae (4b), and cercariae (4c). 5i, cercariae leave snails, enter a crustacean host, and encyst as metacercariae. 6, humans ingest inadequately cooked or pickled crustaceans containing metacercariae. 7, metacercariae excyst in the duodenum, penetrate the intestinal wall, and enter the lungs. 8, adults in cystic cavities in lungs lay eggs which are excreted in sputum or are swallowed and passed in stool.
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Image of Figure 3.
Figure 3.

Life cycle of . i, infective stage; d, diagnostic stage. 1d, unembryonated eggs are released in sputum or in feces. 2, eggs embryonate in water. 3, miracidia hatch from eggs in water and penetrate snails. 4, miracidia develop in snail tissues into sporocysts (4a), rediae (4b), and cercariae (4c). 5i, cercariae leave snails, enter a crustacean host, and encyst as metacercariae. 6, humans ingest inadequately cooked or pickled crustaceans containing metacercariae. 7, metacercariae excyst in the duodenum, penetrate the intestinal wall, and enter the lungs. 8, adults in cystic cavities in lungs lay eggs which are excreted in sputum or are swallowed and passed in stool.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 4.
Life cycle of and . i, infective stage; d, diagnostic stage. 1d, eggs or gravid proglottids of (1A) or (1B) in feces are passed into the environment. 2, cattle and pigs become infected by ingesting vegetation contaminated by eggs or proglottids. 3, oncospheres hatch from eggs in gut, penetrate intestinal wall, and circulate to musculature. i, oncospheres develop into cysticerci in muscle. 4, humans are infected by ingesting raw or undercooked infected meat. 5, the (5A) or (5B) scolex evaginates and attaches to intestine using holdfast organs (hooks and suckers). 6, adult tapeworms reside in small intestine.
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Image of Figure 4.
Figure 4.

Life cycle of and . i, infective stage; d, diagnostic stage. 1d, eggs or gravid proglottids of (1A) or (1B) in feces are passed into the environment. 2, cattle and pigs become infected by ingesting vegetation contaminated by eggs or proglottids. 3, oncospheres hatch from eggs in gut, penetrate intestinal wall, and circulate to musculature. i, oncospheres develop into cysticerci in muscle. 4, humans are infected by ingesting raw or undercooked infected meat. 5, the (5A) or (5B) scolex evaginates and attaches to intestine using holdfast organs (hooks and suckers). 6, adult tapeworms reside in small intestine.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 5.
Scolex and egg of . (A) scolex, 1 mm in diameter, showing four suckers and rostellum with double row of hooks. Magnification, ×80. (B) egg (32 μm, with a range of 31 to 43 μm), indistinguishable from other taeniid eggs in feces; thick, striated shell enclosing hexacanth embryo (arrows). Magnification, ×400.
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Image of Figure 5.
Figure 5.

Scolex and egg of . (A) scolex, 1 mm in diameter, showing four suckers and rostellum with double row of hooks. Magnification, ×80. (B) egg (32 μm, with a range of 31 to 43 μm), indistinguishable from other taeniid eggs in feces; thick, striated shell enclosing hexacanth embryo (arrows). Magnification, ×400.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 6.
Life cycle of . i, infective stage; d, diagnostic stage. 1d, unembryonated eggs are passed in feces. 2, eggs embryonate in water. 3, coracidia hatch from eggs and are ingested by crustaceans. 4, procercoid larvae form in the body cavity of crustaceans. 5i, infected crustaceans are eaten by small freshwater fish. Procercoid larvae are released from crustaceans and develop into plerocercoid larvae. 6, predator fish eats the small infected fish. 7, humans ingest raw or undercooked infected fish. 8, adults live in small intestine. 9, proglottids release immature eggs.
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Figure 6.

Life cycle of . i, infective stage; d, diagnostic stage. 1d, unembryonated eggs are passed in feces. 2, eggs embryonate in water. 3, coracidia hatch from eggs and are ingested by crustaceans. 4, procercoid larvae form in the body cavity of crustaceans. 5i, infected crustaceans are eaten by small freshwater fish. Procercoid larvae are released from crustaceans and develop into plerocercoid larvae. 6, predator fish eats the small infected fish. 7, humans ingest raw or undercooked infected fish. 8, adults live in small intestine. 9, proglottids release immature eggs.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 7.
egg and strobila morphology. (A) Operculated egg of in feces; egg size of 61 μm (range of 58 to 76 μm). Magnification, ×400. (B) Proglottids of showing the craspedote strobilar arrangement. (C) Proglottid and scolex structures of , and acetabular (rounded sucker) structure of holdfast organs in species compared to bothridial (grooved sucker) holdfast structure in .
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Figure 7.

egg and strobila morphology. (A) Operculated egg of in feces; egg size of 61 μm (range of 58 to 76 μm). Magnification, ×400. (B) Proglottids of showing the craspedote strobilar arrangement. (C) Proglottid and scolex structures of , and acetabular (rounded sucker) structure of holdfast organs in species compared to bothridial (grooved sucker) holdfast structure in .

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 8.
Life cycle of . L1, larval stage 1.
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Image of Figure 8.
Figure 8.

Life cycle of . L1, larval stage 1.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 9.
infective muscle larvae in rat diaphragm muscle cells. Magnification, ×30.
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Image of Figure 9.
Figure 9.

infective muscle larvae in rat diaphragm muscle cells. Magnification, ×30.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 10.
(A) larvae within a muscle cell in horse tongue tissue. Hematoxylin-eosin-stained paraffin-embedded sections containing cellular infiltrates and encapsulated larvae in a nurse cell. CI, cellular infiltrates; ML, muscle larvae; N, nurse cell capsule. Magnification, ×160. (B) larvae within a nurse cell. Magnification, ×200.
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Image of Figure 10.
Figure 10.

(A) larvae within a muscle cell in horse tongue tissue. Hematoxylin-eosin-stained paraffin-embedded sections containing cellular infiltrates and encapsulated larvae in a nurse cell. CI, cellular infiltrates; ML, muscle larvae; N, nurse cell capsule. Magnification, ×160. (B) larvae within a nurse cell. Magnification, ×200.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 11.
Life cycle of . i, infective stage; d, diagnostic stage. 1, marine mammals excrete unembryonated eggs. 2a, eggs are embryonated in water and second-stage larvae (L2) form. 2b, larvae hatch from eggs and become free swimming. 3, larvae are ingested by crustaceans and mature to L3. 4, infected crustaceans are eaten by fish and squid. 5i, larvae can be maintained as L3 in paratenic fish hosts by predation, or 6, fish or squid are consumed by marine mammals, and the larvae molt twice and develop into adult worms that produce eggs that are shed in feces. 7d, humans become infected by eating raw or undercooked seafood. Diagnosis can be made by gastroscopic examination, and the larvae can be removed with forceps.
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Image of Figure 11.
Figure 11.

Life cycle of . i, infective stage; d, diagnostic stage. 1, marine mammals excrete unembryonated eggs. 2a, eggs are embryonated in water and second-stage larvae (L2) form. 2b, larvae hatch from eggs and become free swimming. 3, larvae are ingested by crustaceans and mature to L3. 4, infected crustaceans are eaten by fish and squid. 5i, larvae can be maintained as L3 in paratenic fish hosts by predation, or 6, fish or squid are consumed by marine mammals, and the larvae molt twice and develop into adult worms that produce eggs that are shed in feces. 7d, humans become infected by eating raw or undercooked seafood. Diagnosis can be made by gastroscopic examination, and the larvae can be removed with forceps.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 12.
(A) Life cycle of . i, infective stage; d, diagnostic stage. 1d, unembryonated eggs are passed in feces of infected humans or birds. 2, eggs embryonate in water and are eaten by fish. 3i, larvae hatch from eggs and juveniles develop to the infective stage in the fish intestine. 4, humans and birds become infected by consuming undercooked or raw, whole fishes. 5i, adult worms in the human intestine can release eggs, or 6, juvenile worms can invade the intestinal mucosa, leading to massive autoinfections and severe pathology. (B) Egg of in feces; range of 36 to 45 μm in length. Characteristic thick, striated shell and polar plugs visible.
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Figure 12.

(A) Life cycle of . i, infective stage; d, diagnostic stage. 1d, unembryonated eggs are passed in feces of infected humans or birds. 2, eggs embryonate in water and are eaten by fish. 3i, larvae hatch from eggs and juveniles develop to the infective stage in the fish intestine. 4, humans and birds become infected by consuming undercooked or raw, whole fishes. 5i, adult worms in the human intestine can release eggs, or 6, juvenile worms can invade the intestinal mucosa, leading to massive autoinfections and severe pathology. (B) Egg of in feces; range of 36 to 45 μm in length. Characteristic thick, striated shell and polar plugs visible.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 13.
Life cycle of and . (A) causes eosinophilic meningoencephalitis characterized by eosinophils in the cerebrospinal fluid. The infection is common in parts of Southeast Asia and the Pacific islands, Africa, and the Caribbean. Adult worms are found in pulmonary arteries of rodents; eggs are laid and hatch in the lungs. First-stage larvae migrate up the trachea, are coughed up, swallowed, and then are released in feces. Several types of aquatic and terrestrial mollusks serve as intermediate hosts; land crabs, shrimp, and frogs can serve as paratenic hosts. Infective third-stage larvae develop in intermediate hosts. Humans (and rats) become infected by eating undercooked and raw infected snails, slugs, crabs, or raw vegetables contaminated by snails or slugs. Humans are accidental hosts; completion of the life cycle has not been documented in humans. (B) causes eosinophilic enteritis, an eosinophilic inflammation of the mesenteric arterioles of the ileocecal region of the gastrointestinal tract. Common in parts of Central and South America. Adult worms are found in mesenteric arteries of rodents; eggs are released in feces. Other aspects of the life cycle are similar to that of , except that infective larvae invade the gastrointestinal tract in humans.
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Figure 13.

Life cycle of and . (A) causes eosinophilic meningoencephalitis characterized by eosinophils in the cerebrospinal fluid. The infection is common in parts of Southeast Asia and the Pacific islands, Africa, and the Caribbean. Adult worms are found in pulmonary arteries of rodents; eggs are laid and hatch in the lungs. First-stage larvae migrate up the trachea, are coughed up, swallowed, and then are released in feces. Several types of aquatic and terrestrial mollusks serve as intermediate hosts; land crabs, shrimp, and frogs can serve as paratenic hosts. Infective third-stage larvae develop in intermediate hosts. Humans (and rats) become infected by eating undercooked and raw infected snails, slugs, crabs, or raw vegetables contaminated by snails or slugs. Humans are accidental hosts; completion of the life cycle has not been documented in humans. (B) causes eosinophilic enteritis, an eosinophilic inflammation of the mesenteric arterioles of the ileocecal region of the gastrointestinal tract. Common in parts of Central and South America. Adult worms are found in mesenteric arteries of rodents; eggs are released in feces. Other aspects of the life cycle are similar to that of , except that infective larvae invade the gastrointestinal tract in humans.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 14.
Life cycle of and . i, infective stage; d, diagnostic stage. 1, unembryonated eggs released in feces and embryonate in water. 2, first-stage larvae (L1) hatch from eggs. 3i, larvae enter a copepod and develop to the second stage. 4i, when the copepod is eaten by a vertebrate second intermediate host, the L2 penetrate the intestine, enter muscle, and develop to L3. 5, if the second intermediate host is eaten by an appropriate definitive host, adult worms develop in the stomach. 6, numerous paratenic hosts (including humans) have been identified in which the L3 may wander without development if the second intermediate host or a paratenic host is ingested. 7d, in humans, L3 may wander in the skin, eye, viscera, spinal cord, or brain, with devastating results. Diagnosis is usually made by recovery of the migrating larvae.
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Figure 14.

Life cycle of and . i, infective stage; d, diagnostic stage. 1, unembryonated eggs released in feces and embryonate in water. 2, first-stage larvae (L1) hatch from eggs. 3i, larvae enter a copepod and develop to the second stage. 4i, when the copepod is eaten by a vertebrate second intermediate host, the L2 penetrate the intestine, enter muscle, and develop to L3. 5, if the second intermediate host is eaten by an appropriate definitive host, adult worms develop in the stomach. 6, numerous paratenic hosts (including humans) have been identified in which the L3 may wander without development if the second intermediate host or a paratenic host is ingested. 7d, in humans, L3 may wander in the skin, eye, viscera, spinal cord, or brain, with devastating results. Diagnosis is usually made by recovery of the migrating larvae.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 15.
Life cycle of .
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Figure 15.

Life cycle of .

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Figure 16.
Stages of . Scale bar in panels A to D, 20 μm, and in panels E to G, 10 μm. A. Tachyzoites in impression smear of lung. Note sizes of crescent-shaped individual tachyzoites (arrows) and dividing tachyzoites (arrowhead) compared with sizes of host red blood cells and leukocytes. Giemsa stain. B. Tissue cysts in section of muscle. The tissue cyst wall is very thin (arrow) and encloses many tiny bradyzoites (arrowheads). Hematoxylin and eosin stain. C. Tissue cyst separated from host tissue by homogenization of infected brain. Note tissue cyst wall (arrow) and hundreds of bradyzoites (arrowheads). Unstained. D. Schizont (arrow) with several merozoites (arrowheads) separating from the main mass. Impression smear of infected cat intestine. Giemsa stain. E. A male gamete with two flagella (arrows). Impression smear of infected cat intestine. Giemsa stain. F. Unsporulated oocyst in fecal float of cat feces. Unstained. Note double-layered oocyst wall (arrow) enclosing a central undivided mass. G. Sporulated oocyst with a thin oocyst wall (large arrow) and two sporocysts (arrowheads). Each sporocyst has four sporozoites (small arrow) which are not in complete focus. Unstained.
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Image of Figure 16.
Figure 16.

Stages of . Scale bar in panels A to D, 20 μm, and in panels E to G, 10 μm. A. Tachyzoites in impression smear of lung. Note sizes of crescent-shaped individual tachyzoites (arrows) and dividing tachyzoites (arrowhead) compared with sizes of host red blood cells and leukocytes. Giemsa stain. B. Tissue cysts in section of muscle. The tissue cyst wall is very thin (arrow) and encloses many tiny bradyzoites (arrowheads). Hematoxylin and eosin stain. C. Tissue cyst separated from host tissue by homogenization of infected brain. Note tissue cyst wall (arrow) and hundreds of bradyzoites (arrowheads). Unstained. D. Schizont (arrow) with several merozoites (arrowheads) separating from the main mass. Impression smear of infected cat intestine. Giemsa stain. E. A male gamete with two flagella (arrows). Impression smear of infected cat intestine. Giemsa stain. F. Unsporulated oocyst in fecal float of cat feces. Unstained. Note double-layered oocyst wall (arrow) enclosing a central undivided mass. G. Sporulated oocyst with a thin oocyst wall (large arrow) and two sporocysts (arrowheads). Each sporocyst has four sporozoites (small arrow) which are not in complete focus. Unstained.

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
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Tables

Food-Borne Parasites
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Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
/content/10.1128/9781555815936.ch13.ch13tab01
Table 1.
Major food-borne trematodiasis in humans
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Table 1.

Major food-borne trematodiasis in humans

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13
/content/10.1128/9781555815936.ch13.ch13tab02
Table 2.
Frequency of symptoms in people with postnatally acquired toxoplasmosis
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Table 2.

Frequency of symptoms in people with postnatally acquired toxoplasmosis

Citation: Hill D, Dubey J. 2010. Food-Borne Parasites, p 195-217. In Juneja V, Sofos J (ed), Pathogens and Toxins in Foods. ASM Press, Washington, DC. doi: 10.1128/9781555815936.ch13

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