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Category: Clinical Microbiology
Parasitic Zoonoses, Page 1 of 2
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Parasitic zoonoses belong to the most important human diseases worldwide. They are caused by protozoa, helminths [trematodes (flukes), cestodes (tapeworms), and nematodes (round worms)], Acanthocephala (thorny-headed worms), pentastomids (tongue worms), and arthropods. The last of these plays an additional role as a transmitter of viruses, rickettsiae, bacteria, protozoa, and helminths.
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Entamoeba histolytica trophozoites with phagocytized erythrocytes (arrows) in feces of a patient with invasive amebiasis (picture: N. Fiege, Giessen, Germany).
Entamoeba histolytica trophozoites with phagocytized erythrocytes (arrows) in feces of a patient with invasive amebiasis (picture: N. Fiege, Giessen, Germany).
Developmental cycle of E. histolytica. (1) Cyst with four nuclei is ingested orally; (2) trophozoite with four nuclei leaves cyst within small intestine; (3) both cytoplasm and nuclei divide to form eight small amebae; (4) mature trophozoites (i.e., minuta forms) reproduce by constant binary fission in intestinal lumen; (5) uninucleate cyst (precyst) with marginal chromatoid bodies; (6) cyst with two nuclei and chromatoid bodies; (7) mature cyst with four nuclei (metacyst); (8) infectious cysts are set free with feces; (9) during acute amebic dysentery, minuta forms enlarge to large vegetative forms, i.e., magna or tissue forms; (10) magna forms enter submucosa of intestinal wall; (11) hematogenous spread to brain, lung, liver, skin, and other organs, with invasive, extraintestinal amebiasis with abscess formation.
Developmental cycle of E. histolytica. (1) Cyst with four nuclei is ingested orally; (2) trophozoite with four nuclei leaves cyst within small intestine; (3) both cytoplasm and nuclei divide to form eight small amebae; (4) mature trophozoites (i.e., minuta forms) reproduce by constant binary fission in intestinal lumen; (5) uninucleate cyst (precyst) with marginal chromatoid bodies; (6) cyst with two nuclei and chromatoid bodies; (7) mature cyst with four nuclei (metacyst); (8) infectious cysts are set free with feces; (9) during acute amebic dysentery, minuta forms enlarge to large vegetative forms, i.e., magna or tissue forms; (10) magna forms enter submucosa of intestinal wall; (11) hematogenous spread to brain, lung, liver, skin, and other organs, with invasive, extraintestinal amebiasis with abscess formation.
Developmental cycle of Babesia spp. (1) Sporozoites in saliva of feeding tick and invasion of erythrocytes of the vertebrate host; (2 and 3) asexual reproduction in erythrocytes by binary fission (formation of merozoites); (4) intraerythrocytic ovoid gamont develops (sexually differentiated stage); (5) after ingestion by ticks, gamonts form radiate protrusions in intestinal cells; (6) gamete (“ray body” as fertile stage); (7) fusion of two gametes; (8) formation of zygotes; (9) formation of sporokinetes (motile invasive forms); (10) sporokinetes leave intestinal cells and enter cells of various organs, e.g., epidermis, muscle, hemolymph, and ovaries and eggs; (11) invasion of salivary glands and formation of sporozoites; (12) transovarial transmission (transmission of sporozoites to next tick generation by infested eggs, heavy multiplication in gut epithelia of tick larvae and nymphs, and settlement in tick salivary glands).
Developmental cycle of Babesia spp. (1) Sporozoites in saliva of feeding tick and invasion of erythrocytes of the vertebrate host; (2 and 3) asexual reproduction in erythrocytes by binary fission (formation of merozoites); (4) intraerythrocytic ovoid gamont develops (sexually differentiated stage); (5) after ingestion by ticks, gamonts form radiate protrusions in intestinal cells; (6) gamete (“ray body” as fertile stage); (7) fusion of two gametes; (8) formation of zygotes; (9) formation of sporokinetes (motile invasive forms); (10) sporokinetes leave intestinal cells and enter cells of various organs, e.g., epidermis, muscle, hemolymph, and ovaries and eggs; (11) invasion of salivary glands and formation of sporozoites; (12) transovarial transmission (transmission of sporozoites to next tick generation by infested eggs, heavy multiplication in gut epithelia of tick larvae and nymphs, and settlement in tick salivary glands).
Babesia divergens. Thin blood smear from an experimentally infected bird; aberrant forms, partly Maltese cross forms as occurring in human blood (picture: Ute Mackenstedt, Hohenheim, Germany).
Babesia divergens. Thin blood smear from an experimentally infected bird; aberrant forms, partly Maltese cross forms as occurring in human blood (picture: Ute Mackenstedt, Hohenheim, Germany).
Developmental cycle of B. coli. (1) Cysts (40 to 60 µm) are excreted with feces; (2) cysts are ingested with food; (3) vegetative forms reproduce by repeated transverse binary fission and genetic information is exchanged by conjugation; (4) cyst formation is initiated by dehydration within feces in the rectum.
Developmental cycle of B. coli. (1) Cysts (40 to 60 µm) are excreted with feces; (2) cysts are ingested with food; (3) vegetative forms reproduce by repeated transverse binary fission and genetic information is exchanged by conjugation; (4) cyst formation is initiated by dehydration within feces in the rectum.
Developmental cycle of T. cruzi. (1) Metacyclic (infectious) trypanosomes are transmitted by contaminated feces of triatomine bugs to humans. They enter the body through feeding lesions or via intact mucosa. (2) They spend a short time in the peripheral blood (no reproduction). (3) Parasites enter myocardial and endothelial cells of internal organs, e.g., spleen, RES, and liver. (4) Parasites reproduce in the amastigote (unflagellated) stage and form cysts. (5) Parasitized cells burst; organisms are transformed into trypomastigote (flagellated) forms, with a temporary appearance in the peripheral blood. Host cells are infected further. (6) Triatomine bugs ingest parasitized blood. (7) Parasites transform into epimastigote forms and rapidly reproduce in intestine of bugs. (8) Organisms are transformed into metacyclic trypanosomes and colonize the rectal ampoule.
Developmental cycle of T. cruzi. (1) Metacyclic (infectious) trypanosomes are transmitted by contaminated feces of triatomine bugs to humans. They enter the body through feeding lesions or via intact mucosa. (2) They spend a short time in the peripheral blood (no reproduction). (3) Parasites enter myocardial and endothelial cells of internal organs, e.g., spleen, RES, and liver. (4) Parasites reproduce in the amastigote (unflagellated) stage and form cysts. (5) Parasitized cells burst; organisms are transformed into trypomastigote (flagellated) forms, with a temporary appearance in the peripheral blood. Host cells are infected further. (6) Triatomine bugs ingest parasitized blood. (7) Parasites transform into epimastigote forms and rapidly reproduce in intestine of bugs. (8) Organisms are transformed into metacyclic trypanosomes and colonize the rectal ampoule.
Infection of humans with T. cruzi. An infected triatomine bug pierces the skin (a) and sucks blood and increases in size while feeding (b). After feeding, the bug sheds a fecal droplet containing infectious trypanosomes (c), which spreads on the skin (d). Through feeding lesions, abrasions, or mucous membranes (conjunctiva, etc.), trypanosomes reach blood vessels. (From product information for Lampit [nifurtimox; Bayer].)
Infection of humans with T. cruzi. An infected triatomine bug pierces the skin (a) and sucks blood and increases in size while feeding (b). After feeding, the bug sheds a fecal droplet containing infectious trypanosomes (c), which spreads on the skin (d). Through feeding lesions, abrasions, or mucous membranes (conjunctiva, etc.), trypanosomes reach blood vessels. (From product information for Lampit [nifurtimox; Bayer].)
Edema of the eyelids in a child with acute Chagas' disease as an early symptom of infection with T. cruzi (Romaña sign), a reaction to local multiplication of parasites.
Edema of the eyelids in a child with acute Chagas' disease as an early symptom of infection with T. cruzi (Romaña sign), a reaction to local multiplication of parasites.
Cryptosporidia (unstained oocysts) and yeasts in calf feces and “negative staining” with carbol-fuchsin (picture: Institute for Parasitology, Giessen, Germany).
Cryptosporidia (unstained oocysts) and yeasts in calf feces and “negative staining” with carbol-fuchsin (picture: Institute for Parasitology, Giessen, Germany).
Developmental cycle of Cryptosporidium spp. (modified from Eckert, 1984). (1) Sporozoite set free in stomach and duodenum approaching intestinal epithelium; (2) sporozoite with basal adhesive zone between microvilli of an intestinal cell; (3) young schizont within vacuole; (4) dividing schizont; (5) mature schizont with eight merozoites (type I meront); (6) free merozoite becomes attached to epithelial cell; (7) mature schizont with four merozoites (type II meront) (repeat of schizogonic process); (8) free merozoites; (9a) macrogamete; (9b) microgamont with nonflagellated microgametes; (10) thick-walled oocyst (permanent stage in environment); (11) thin-walled oocyst leading to endogenous autoinfection (ca. 20% of formed cysts); (12) sporulated oocyst containing four sporozoites, shed with feces (thick walled; oral infection).
Developmental cycle of Cryptosporidium spp. (modified from Eckert, 1984). (1) Sporozoite set free in stomach and duodenum approaching intestinal epithelium; (2) sporozoite with basal adhesive zone between microvilli of an intestinal cell; (3) young schizont within vacuole; (4) dividing schizont; (5) mature schizont with eight merozoites (type I meront); (6) free merozoite becomes attached to epithelial cell; (7) mature schizont with four merozoites (type II meront) (repeat of schizogonic process); (8) free merozoites; (9a) macrogamete; (9b) microgamont with nonflagellated microgametes; (10) thick-walled oocyst (permanent stage in environment); (11) thin-walled oocyst leading to endogenous autoinfection (ca. 20% of formed cysts); (12) sporulated oocyst containing four sporozoites, shed with feces (thick walled; oral infection).
Giardia duodenalis: trophozoit from feces. Interference contrast (picture: Institute of Parasitology, Zurich, Switzerland).
Giardia duodenalis: trophozoit from feces. Interference contrast (picture: Institute of Parasitology, Zurich, Switzerland).
Developmental cycle of L. donovani. (1) Transmission of flagellated leishmaniae by bite of bloodsucking Phlebotomus spp. (sand flies); (2) entrance of so-called promastigote forms into monocytes; (3) intracellular reproduction of now amastigote form leishmaniae (free of flagellae) by binary fission; (4) bursting of host cell and repeated infection of monocytes, predominantly in spleen and liver; (5) uptake of an infected host cell, containing amastigote leishmaniae, by sand flies; (6) transformation to ciliated promastigote stage and rapid multiplication by binary fission; (7) migration to proboscis of sand fly and formation of infectious metacyclic stage.
Developmental cycle of L. donovani. (1) Transmission of flagellated leishmaniae by bite of bloodsucking Phlebotomus spp. (sand flies); (2) entrance of so-called promastigote forms into monocytes; (3) intracellular reproduction of now amastigote form leishmaniae (free of flagellae) by binary fission; (4) bursting of host cell and repeated infection of monocytes, predominantly in spleen and liver; (5) uptake of an infected host cell, containing amastigote leishmaniae, by sand flies; (6) transformation to ciliated promastigote stage and rapid multiplication by binary fission; (7) migration to proboscis of sand fly and formation of infectious metacyclic stage.
Excessive growth of eyelashes in a child with kala-azar (Brazil).
Excessive growth of eyelashes in a child with kala-azar (Brazil).
Child with kala-azar (Brazil). Abdominal enlargement and considerable swelling of the inguinal lymph nodes are visible.
Child with kala-azar (Brazil). Abdominal enlargement and considerable swelling of the inguinal lymph nodes are visible.
Leishmania donovani: intracellular proliferation of the parasites in a macrophage (two nuclei). The amastigote stages (arrows) are characterized by a round nucleus and a rod-like kinetoplast (picture: T. Naucke, Bonn, Germany).
Leishmania donovani: intracellular proliferation of the parasites in a macrophage (two nuclei). The amastigote stages (arrows) are characterized by a round nucleus and a rod-like kinetoplast (picture: T. Naucke, Bonn, Germany).
Cutaneous leishmaniasis (Brazil).
Cutaneous leishmaniasis (Brazil).
Developmental cycle of microsporida. (1) Infectious spore; (2 and 3) extrusion of the tubular polar filament, penetration of the wall of an intestinal cell, and injection of the sporoplasm; (4 to 12) growth and asexual division via quadrinucleate stages (merogony) and finally encystment and formation of spores (sporogony); (13) rupture of host cell and liberation of infectious spores into the intestinal lumen.
Developmental cycle of microsporida. (1) Infectious spore; (2 and 3) extrusion of the tubular polar filament, penetration of the wall of an intestinal cell, and injection of the sporoplasm; (4 to 12) growth and asexual division via quadrinucleate stages (merogony) and finally encystment and formation of spores (sporogony); (13) rupture of host cell and liberation of infectious spores into the intestinal lumen.
Developmental cycle of Sarcocystis spp. with Homo sapiens as the definitive host. (1) Sporocyst with four infectious sporozoites, found in feces; (2) oral ingestion of sporocysts by intermediate hosts and liberation of sporozoites; (3) development of two generations of schizonts with 50 to 90 merozoites each by endopolygeny (multiple divisions) in endothelial cells of blood vessels (intestine, liver, kidney, lung, and other organs); (3a) free motile merozoite (second generation) entering a striated muscle cell; (3b) mature cyst (approximately 3 months p.i.) with cystozoites in skeletal muscle cells after a further schizogony (resting stages with thousands of cyst merozoites); (4) free cystozoite, after ingestion of a muscle cyst by the final host, entering cell of lamina propria; (5a) microgamont (male); (5b) macrogamont (female) in lamina propria (21 h p.i.); (5c) flagellated male microgamete; (6) macrogamete; (7) zygote (in intestinal epithelial cell); (8) sporogony within intestinal epithelial cell (formation of sporocysts); (9) sporulated oocyst (7 days p.i.) with two sporocysts, each containing four sporozoites, inside host cell.
Developmental cycle of Sarcocystis spp. with Homo sapiens as the definitive host. (1) Sporocyst with four infectious sporozoites, found in feces; (2) oral ingestion of sporocysts by intermediate hosts and liberation of sporozoites; (3) development of two generations of schizonts with 50 to 90 merozoites each by endopolygeny (multiple divisions) in endothelial cells of blood vessels (intestine, liver, kidney, lung, and other organs); (3a) free motile merozoite (second generation) entering a striated muscle cell; (3b) mature cyst (approximately 3 months p.i.) with cystozoites in skeletal muscle cells after a further schizogony (resting stages with thousands of cyst merozoites); (4) free cystozoite, after ingestion of a muscle cyst by the final host, entering cell of lamina propria; (5a) microgamont (male); (5b) macrogamont (female) in lamina propria (21 h p.i.); (5c) flagellated male microgamete; (6) macrogamete; (7) zygote (in intestinal epithelial cell); (8) sporogony within intestinal epithelial cell (formation of sporocysts); (9) sporulated oocyst (7 days p.i.) with two sporocysts, each containing four sporozoites, inside host cell.
T. brucei rhodesiense in blood smear (Giemsa stain).
T. brucei rhodesiense in blood smear (Giemsa stain).
Developmental cycle of salivary trypanosomes. (1) Trypanosomes (trypomastigote form) in peripheral blood after bite by tsetse fly (Glossina spp.). (2) Trypanosomes in stage of reproduction (peripheral blood); infection of CNS. (3) Development in the tsetse fly: (a) in stomach and crop; (b) epimastigote form in intestine in constant reproduction (binary fission); (c) metacyclic (trypomastigote) infectious form in salivary gland.
Developmental cycle of salivary trypanosomes. (1) Trypanosomes (trypomastigote form) in peripheral blood after bite by tsetse fly (Glossina spp.). (2) Trypanosomes in stage of reproduction (peripheral blood); infection of CNS. (3) Development in the tsetse fly: (a) in stomach and crop; (b) epimastigote form in intestine in constant reproduction (binary fission); (c) metacyclic (trypomastigote) infectious form in salivary gland.
Developmental cycle and transmission of T. gondii. (1) Sporulated oocyst or tissue cyst (5) is ingested orally by final host (cat) or unspecific (intermediate) host (mammals, birds, or humans). (2) Sporozoites and/or merozoites are set free in the gut and invade all types of nucleated cells. (3) Parasites multiply inside the cells by quick fissions (asexual reproduction: schizogony by endodyogeny); “pseudocysts” which contain numerous merozoites (tachyzoites) are formed. (4) Schizogony is repeated several times until the immune response of the host increases. (A) Diaplacental transmission is possible during this phase, leading to congenital toxoplasmosis. (5) Tissue cysts are formed under immune pressure with slowly multiplying merozoites (bradyzoites). (6) In cats, part of the merozoites reinvades epithelial cells of the gut and undergoes sexual differentiation. After fertilization (7), oocysts are formed (8). (9) Oocysts sporulate in the environment.
Developmental cycle and transmission of T. gondii. (1) Sporulated oocyst or tissue cyst (5) is ingested orally by final host (cat) or unspecific (intermediate) host (mammals, birds, or humans). (2) Sporozoites and/or merozoites are set free in the gut and invade all types of nucleated cells. (3) Parasites multiply inside the cells by quick fissions (asexual reproduction: schizogony by endodyogeny); “pseudocysts” which contain numerous merozoites (tachyzoites) are formed. (4) Schizogony is repeated several times until the immune response of the host increases. (A) Diaplacental transmission is possible during this phase, leading to congenital toxoplasmosis. (5) Tissue cysts are formed under immune pressure with slowly multiplying merozoites (bradyzoites). (6) In cats, part of the merozoites reinvades epithelial cells of the gut and undergoes sexual differentiation. After fertilization (7), oocysts are formed (8). (9) Oocysts sporulate in the environment.
Toxoplasma gondii: oocyst (diameter 12 µm) in feces of a cat (picture: Institute for Parasitology, Giessen, Germany).
Toxoplasma gondii: oocyst (diameter 12 µm) in feces of a cat (picture: Institute for Parasitology, Giessen, Germany).
Toxoplasma gondii: tissue cyst in the brain (mouse). Hematoxilin-eosin-staining (picture: Institute for Parasitology, Giessen, Germany).
Toxoplasma gondii: tissue cyst in the brain (mouse). Hematoxilin-eosin-staining (picture: Institute for Parasitology, Giessen, Germany).
Cercarial dermatitis: Cercaria of Trichobilharzia sp. after invasion of the skin. Hematoxilin-eosin-staining (picture: P. Kimmig, Hohemheim, Germany).
Cercarial dermatitis: Cercaria of Trichobilharzia sp. after invasion of the skin. Hematoxilin-eosin-staining (picture: P. Kimmig, Hohemheim, Germany).
Cercarial dermatitis: maculopapulous exanthema 24 h after infection (picture: P. Kimmig, Hohenheim, Stuttgart, Germany).
Cercarial dermatitis: maculopapulous exanthema 24 h after infection (picture: P. Kimmig, Hohenheim, Stuttgart, Germany).
Developmental cycle of C. sinensis. (1) Adult fluke (8 to 15 mm) in bile duct; (2) C. sinensis egg with miracidium (0.017 to 0.030 mm) excreted with feces (D, diagnostic phase); (3) miracidium (0.03 mm) hatched from egg within intestine of first intermediate host (freshwater snail, e.g., Parafossarulus manchuricus); (4) sporocyst (1.2 to 1.8 mm); (5) redia (>0.75 mm) in first intermediate host; (6) cercaria (about 0.5 mm) swimming actively in water; (7) metacercaria (≤0.285 mm; I, infectious stage) in second intermediate host (freshwater fish, e.g., a species of the Cyprinidae).
Developmental cycle of C. sinensis. (1) Adult fluke (8 to 15 mm) in bile duct; (2) C. sinensis egg with miracidium (0.017 to 0.030 mm) excreted with feces (D, diagnostic phase); (3) miracidium (0.03 mm) hatched from egg within intestine of first intermediate host (freshwater snail, e.g., Parafossarulus manchuricus); (4) sporocyst (1.2 to 1.8 mm); (5) redia (>0.75 mm) in first intermediate host; (6) cercaria (about 0.5 mm) swimming actively in water; (7) metacercaria (≤0.285 mm; I, infectious stage) in second intermediate host (freshwater fish, e.g., a species of the Cyprinidae).
Large liver fluke (Fasciola hepatica); original size: 2 cm). Carmin staining (picture: Institute for Parasitology, Giessen, Germany).
Large liver fluke (Fasciola hepatica); original size: 2 cm). Carmin staining (picture: Institute for Parasitology, Giessen, Germany).
Encysted metacercariae of Fasciola hepatica, attached to a blade of grass (picture: Institute for Parasitology, Giessen, Germany).
Encysted metacercariae of Fasciola hepatica, attached to a blade of grass (picture: Institute for Parasitology, Giessen, Germany).
Developmental cycle of F. hepatica. (1) Adult liver fluke (15 to 20 mm) in bile duct; (2) egg of liver fluke (0.09 to 0.15 mm) with zygote and nutrition cells (D, diagnostic stage); (3) miracidium (about 0.15 mm), hatched from egg and swimming in water; (4) sporocyst (0.3 to 0.5 mm) within snail (intermediate host, e.g., Lymnaea truncatula); (5) redia (1.5 to 2.5 mm) in a snail; (6) cercaria (0.67 to 1.45 mm), swimming in water; (7) metacercaria (encysted cercaria) (about 0.25 mm), adhering to a plant (I, infectious stage); (8) liver fluke (5 to 6 mm) in liver tissue, about 20 days old.
Developmental cycle of F. hepatica. (1) Adult liver fluke (15 to 20 mm) in bile duct; (2) egg of liver fluke (0.09 to 0.15 mm) with zygote and nutrition cells (D, diagnostic stage); (3) miracidium (about 0.15 mm), hatched from egg and swimming in water; (4) sporocyst (0.3 to 0.5 mm) within snail (intermediate host, e.g., Lymnaea truncatula); (5) redia (1.5 to 2.5 mm) in a snail; (6) cercaria (0.67 to 1.45 mm), swimming in water; (7) metacercaria (encysted cercaria) (about 0.25 mm), adhering to a plant (I, infectious stage); (8) liver fluke (5 to 6 mm) in liver tissue, about 20 days old.
Cercariae of Schistosoma mansoni: demonstrated by immunofluorscent staining (picture: Institute for Parasitology, Giessen, Germany).
Cercariae of Schistosoma mansoni: demonstrated by immunofluorscent staining (picture: Institute for Parasitology, Giessen, Germany).
Adult Schistosoma flukes (female and male in copulation), isolated from a mesenterial vein.
Adult Schistosoma flukes (female and male in copulation), isolated from a mesenterial vein.
Developmental cycle of S. mansoni. (1) Adult S. mansoni fluke (male, 6 to 10 mm; female, 7 to 15 mm) in intestinal and mesenterial veins or in the portal vein system (female fluke within the canalis gynaecophorus of the male); (2) S. mansoni egg (0.05 to 0.15 mm) shed with feces, with miracidium ready to hatch (D, diagnostic stage); (3) miracidium (ca. 0.13 mm), swimming in water; (4 and 5) mother sporocyst (4) and daughter sporocyst (5) in snail (intermediate host, e.g., Biomphalaria glabrata); (6) furcocercous cercaria (“furcocercaria”) (about 0.375 to 0.590 mm), swimming in water (I, infectious stage).
Developmental cycle of S. mansoni. (1) Adult S. mansoni fluke (male, 6 to 10 mm; female, 7 to 15 mm) in intestinal and mesenterial veins or in the portal vein system (female fluke within the canalis gynaecophorus of the male); (2) S. mansoni egg (0.05 to 0.15 mm) shed with feces, with miracidium ready to hatch (D, diagnostic stage); (3) miracidium (ca. 0.13 mm), swimming in water; (4 and 5) mother sporocyst (4) and daughter sporocyst (5) in snail (intermediate host, e.g., Biomphalaria glabrata); (6) furcocercous cercaria (“furcocercaria”) (about 0.375 to 0.590 mm), swimming in water (I, infectious stage).
Developmental cycle of D. latum. (1) Mature tapeworm (5 to >10 m in length) in the small intestine of humans and fish-eating mammals; (2) D. latum egg (0.045 by 0.070 mm) excreted with feces, with zygote and yolk cells (D, diagnostic stage); (3) egg with coracidium in water; (4) hatched motile coracidium (0.04 to 0.05 mm) swimming in water; (5) procercoid (0.5 to 0.6 mm; second larval stage) developed in a cyclopid copepod after ingestion of the coracidium; (6) plerocercoid (up to 50 mm; third larval stage developed in freshwater fish [second intermediate host] after ingestion of an infected copepod [I, infective stage]).
Developmental cycle of D. latum. (1) Mature tapeworm (5 to >10 m in length) in the small intestine of humans and fish-eating mammals; (2) D. latum egg (0.045 by 0.070 mm) excreted with feces, with zygote and yolk cells (D, diagnostic stage); (3) egg with coracidium in water; (4) hatched motile coracidium (0.04 to 0.05 mm) swimming in water; (5) procercoid (0.5 to 0.6 mm; second larval stage) developed in a cyclopid copepod after ingestion of the coracidium; (6) plerocercoid (up to 50 mm; third larval stage developed in freshwater fish [second intermediate host] after ingestion of an infected copepod [I, infective stage]).
Proglottid of Dipylidium caninum. Each proglottid contains two sets of genital organs and two genital pori (arrows): Giemsa staining (picture: Institute for Parasitology, Giessen, Germany).
Proglottid of Dipylidium caninum. Each proglottid contains two sets of genital organs and two genital pori (arrows): Giemsa staining (picture: Institute for Parasitology, Giessen, Germany).
Approximate geographic distribution of E. multilocularis as of 1999. Shaded areas indicate that the organism is highly endemic (black) or endemic (gray). (Source: J. Eckert, F. Grimm, and H. Bucklar [Institute of Parasitology, University of Zürich, Zürich, Switzerland]. Reprinted from Eckert et al., 2000.)
Approximate geographic distribution of E. multilocularis as of 1999. Shaded areas indicate that the organism is highly endemic (black) or endemic (gray). (Source: J. Eckert, F. Grimm, and H. Bucklar [Institute of Parasitology, University of Zürich, Zürich, Switzerland]. Reprinted from Eckert et al., 2000.)
Alveolar echinococcosis (Echinococcus multilocularis) in the liver: human case. The tissue of the larva grows infiltratively and metastasizes. The cross section shows a sponge-like structure (picture: Parasitology, Hohenheim Germany)
Alveolar echinococcosis (Echinococcus multilocularis) in the liver: human case. The tissue of the larva grows infiltratively and metastasizes. The cross section shows a sponge-like structure (picture: Parasitology, Hohenheim Germany)
Approximate geographic distribution of E. granulosus as of 1999. F, free; PF, provisionally free. (Source: J. Eckert, F. Grimm, and H. Bucklar [Institute of Parasitology, University of Zürich]. Reprinted from Eckert et al., 2000.)
Approximate geographic distribution of E. granulosus as of 1999. F, free; PF, provisionally free. (Source: J. Eckert, F. Grimm, and H. Bucklar [Institute of Parasitology, University of Zürich]. Reprinted from Eckert et al., 2000.)
Developmental cycle of E. granulosus. (1) Mature tapeworm (3 to 6 mm) in the small intestine of a dog; (2) E. granulosus egg (0.032 by 0.036 mm) containing the oncosphere, passed in the feces either free or still included in the proglottid (D, diagnostic stage in the dog; I, infective stage for intermediate hosts, including humans); (3) free oncosphere (0.022 to 0.028 mm) in intermediate host; (4) hydatid cyst (echinococcus cysticus) (walnut to orange sized, sometimes even bigger) in liver, lung, or other organs of the intermediate host (I, infectious stage for the dog); (5) protoscolex (0.12 to 0.20 mm) liberated from the cyst in the intestine of the dog; (6) evaginated, maturing young tapeworm in the intestine of the dog.
Developmental cycle of E. granulosus. (1) Mature tapeworm (3 to 6 mm) in the small intestine of a dog; (2) E. granulosus egg (0.032 by 0.036 mm) containing the oncosphere, passed in the feces either free or still included in the proglottid (D, diagnostic stage in the dog; I, infective stage for intermediate hosts, including humans); (3) free oncosphere (0.022 to 0.028 mm) in intermediate host; (4) hydatid cyst (echinococcus cysticus) (walnut to orange sized, sometimes even bigger) in liver, lung, or other organs of the intermediate host (I, infectious stage for the dog); (5) protoscolex (0.12 to 0.20 mm) liberated from the cyst in the intestine of the dog; (6) evaginated, maturing young tapeworm in the intestine of the dog.
Multiple hydatid cysts (Echinococcus granulosus) in the liver: human case (picture: Media, Royal Tropical Institute Amsterdam, The Netherlands).
Multiple hydatid cysts (Echinococcus granulosus) in the liver: human case (picture: Media, Royal Tropical Institute Amsterdam, The Netherlands).
Clinical picture of cystic echinococcosis (picture: I. Mann, Nairobi, Kenya).
Clinical picture of cystic echinococcosis (picture: I. Mann, Nairobi, Kenya).
Developmental cycle of H. nana (direct cycle). (1) Adult tapeworm (10 to 90 mm) in the small intestine of rodents and humans; (2) H. nana egg (0.040 to 0.050 mm) with oncosphere passed with feces (D, diagnostic stage; I, infective stage); (3) cysticercoid (0.050 to 0.135 mm) in an intestinal villus.
Developmental cycle of H. nana (direct cycle). (1) Adult tapeworm (10 to 90 mm) in the small intestine of rodents and humans; (2) H. nana egg (0.040 to 0.050 mm) with oncosphere passed with feces (D, diagnostic stage; I, infective stage); (3) cysticercoid (0.050 to 0.135 mm) in an intestinal villus.
Developmental cycle of T. saginata. (1) Adult tapeworm (4 to 12 m) in the small intestine of a human; (2) mature proglottid (ca. 16 to 20 mm) passed with feces or actively emigrated, and egg (0.03 to 0.04 mm) of T. saginata with an oncosphere, in the feces (D, diagnostic stage); (3) free oncosphere (ca. 0.02 mm) in intestine and blood vessels of the intermediate host (cattle); (4) formation of the cysticercus (Cysticercus bovis) in striated muscle of the intermediate host; (5) mature C. bovis (5 to 8 mm) in striated muscle of cattle (I, infectious stage); (6) evaginated C. bovis in the human small intestine.
Developmental cycle of T. saginata. (1) Adult tapeworm (4 to 12 m) in the small intestine of a human; (2) mature proglottid (ca. 16 to 20 mm) passed with feces or actively emigrated, and egg (0.03 to 0.04 mm) of T. saginata with an oncosphere, in the feces (D, diagnostic stage); (3) free oncosphere (ca. 0.02 mm) in intestine and blood vessels of the intermediate host (cattle); (4) formation of the cysticercus (Cysticercus bovis) in striated muscle of the intermediate host; (5) mature C. bovis (5 to 8 mm) in striated muscle of cattle (I, infectious stage); (6) evaginated C. bovis in the human small intestine.
Developmental cycle of marine anisakids. (1) Adult anisakids in the gastrointestinal tract of marine mammals produce eggs; (2) eggs excreted with feces; (3 and 4) development of first- and second-stage larvae (L1 and L2) in floating eggs, which are ingested by copepods (intermediate hosts); (5) development of third-stage larva (L3) in copepods; (6) ingestion of infected copepods by saltwater fishes (numerous species) and encapsulation of third-stage larvae in various organs (fishes serve as paratenic hosts, i.e., larvae do not develop further); (7) ingestion of infected fishes by predatory fishes may lead to accumulation of infective larvae in these fishes; (8 and 9) final hosts (8) and humans (9) are infected by ingestion of infected fishes.
Developmental cycle of marine anisakids. (1) Adult anisakids in the gastrointestinal tract of marine mammals produce eggs; (2) eggs excreted with feces; (3 and 4) development of first- and second-stage larvae (L1 and L2) in floating eggs, which are ingested by copepods (intermediate hosts); (5) development of third-stage larva (L3) in copepods; (6) ingestion of infected copepods by saltwater fishes (numerous species) and encapsulation of third-stage larvae in various organs (fishes serve as paratenic hosts, i.e., larvae do not develop further); (7) ingestion of infected fishes by predatory fishes may lead to accumulation of infective larvae in these fishes; (8 and 9) final hosts (8) and humans (9) are infected by ingestion of infected fishes.
Lymphatic filariasis: elephantiasis (picture: H. Zahner, Giessen, Germany).
Lymphatic filariasis: elephantiasis (picture: H. Zahner, Giessen, Germany).
Larva migrans cutanea (creeping eruption). Inflamed tracks of the dog hookworm Ancylostoma braziliense under the skin (picture: P. Janssen-Rosseck, Düsseldorf, Germany).
Larva migrans cutanea (creeping eruption). Inflamed tracks of the dog hookworm Ancylostoma braziliense under the skin (picture: P. Janssen-Rosseck, Düsseldorf, Germany).
Developmental cycle of S. stercoralis. (1) Adult parthenogenetic female S. stercoralis (2.2 to 2.5 mm) in the mucosa of the small intestine; (2) rhabditiform first-stage larva (0.20 to 0.25 mm) passed with feces (D, diagnostic stage); (2a) free-living male (0.7 to 0.9 mm) and female (ca. 1 mm) S. stercoralis; (2b) egg (0.07 mm) deposited by the free-living female; (2c) first-stage larva hatched from the egg; (3) filariform, infective third-stage larva (0.55 to 0.60 mm; I, infective stage) developed either via a free-living sexual worm generation or from a first-stage larva shed with the feces (2) invades percutaneously. The figure does not take into consideration endogenous autoinfections and possible repeated development of free-living generations.
Developmental cycle of S. stercoralis. (1) Adult parthenogenetic female S. stercoralis (2.2 to 2.5 mm) in the mucosa of the small intestine; (2) rhabditiform first-stage larva (0.20 to 0.25 mm) passed with feces (D, diagnostic stage); (2a) free-living male (0.7 to 0.9 mm) and female (ca. 1 mm) S. stercoralis; (2b) egg (0.07 mm) deposited by the free-living female; (2c) first-stage larva hatched from the egg; (3) filariform, infective third-stage larva (0.55 to 0.60 mm; I, infective stage) developed either via a free-living sexual worm generation or from a first-stage larva shed with the feces (2) invades percutaneously. The figure does not take into consideration endogenous autoinfections and possible repeated development of free-living generations.
Trichinella spiralis larvae in the musculature (squeezing preparation) (picture: Institute for Parasitology, Giessen, Germany).
Trichinella spiralis larvae in the musculature (squeezing preparation) (picture: Institute for Parasitology, Giessen, Germany).
Developmental cycle of Trichinella spiralis. (1) Adult male (1.0 to 1.6 mm) and female T. spiralis (3.0 to 4.0 mm) in the mucosa of the small intestine (e.g., of pigs, horses, humans); (2) encapsulated T. spiralis larva (capsule, 0.4 to 0.5 mm) in striated muscle (D, diagnostic stage; I. infective stage); (3) free larva of T. spiralis (0.8 to 1 mm) in the small intestine.
Developmental cycle of Trichinella spiralis. (1) Adult male (1.0 to 1.6 mm) and female T. spiralis (3.0 to 4.0 mm) in the mucosa of the small intestine (e.g., of pigs, horses, humans); (2) encapsulated T. spiralis larva (capsule, 0.4 to 0.5 mm) in striated muscle (D, diagnostic stage; I. infective stage); (3) free larva of T. spiralis (0.8 to 1 mm) in the small intestine.
Macracanthorhynchus hirudinaceus (Acanthocephala): front end with retractable proboscis (P) with hooks (H) and neck (H) (picture: H. Taraschewski, Karlsruhe, Germany).
Macracanthorhynchus hirudinaceus (Acanthocephala): front end with retractable proboscis (P) with hooks (H) and neck (H) (picture: H. Taraschewski, Karlsruhe, Germany).
Developmental stages of ixodid ticks, for example, Ixodes ricinus. (a) Larva (six legs), nymph and adult stages. The chitinous shield covers the whole body in case of the male and part of the body in case of the other stages (picture: www.zecken.de). (b) Engorged female tick with massively enlarged body (picture: H. Mehlhorn, Düsseldorf, Germany).
Developmental stages of ixodid ticks, for example, Ixodes ricinus. (a) Larva (six legs), nymph and adult stages. The chitinous shield covers the whole body in case of the male and part of the body in case of the other stages (picture: www.zecken.de). (b) Engorged female tick with massively enlarged body (picture: H. Mehlhorn, Düsseldorf, Germany).
Adult soft ticks (Argas reflexus); dorsal (left) and ventral aspects. Mouthpieces are only visible from the ventral aspect (picture: H. Mehlhorn, Düsseldorf, Germany).
Adult soft ticks (Argas reflexus); dorsal (left) and ventral aspects. Mouthpieces are only visible from the ventral aspect (picture: H. Mehlhorn, Düsseldorf, Germany).
Mouthparts of an ixodid tick (Ixodes ricinus); dorsal aspect with chelicerae (C), hypostome (H), and pedipalps (P) (picture: H. Mehlhorn, Düsseldorf, Germany).
Mouthparts of an ixodid tick (Ixodes ricinus); dorsal aspect with chelicerae (C), hypostome (H), and pedipalps (P) (picture: H. Mehlhorn, Düsseldorf, Germany).
Developmental cycle of a three-host tick (e.g., I. ricinus).
Developmental cycle of a three-host tick (e.g., I. ricinus).
Ornithonyssus sylvarum (northern poultry mite); 0.7 × 0.45 mm in size).
Ornithonyssus sylvarum (northern poultry mite); 0.7 × 0.45 mm in size).
Sarcoptes sp. (A) Adult (0.4 × 0.3 mm) and (N) nympheal stage out of the skin (picture: Institute for Parasitology, Giessen, Germany).
Sarcoptes sp. (A) Adult (0.4 × 0.3 mm) and (N) nympheal stage out of the skin (picture: Institute for Parasitology, Giessen, Germany).
Female mosquito (Aedes albopictus: tiger mosquitoe) during blood feeding (picture: R. Pospichil, Bergheim, Germany).
Female mosquito (Aedes albopictus: tiger mosquitoe) during blood feeding (picture: R. Pospichil, Bergheim, Germany).
Blackfly (Simulium sp.) causing painful lesions (picture: H. Mehlhorn, Düsseldorf, Germany).
Blackfly (Simulium sp.) causing painful lesions (picture: H. Mehlhorn, Düsseldorf, Germany).
Female sand fly (Phlebotomus mascittii) during blood feeding (picture: T. Naucke, Bonn, Germany).
Female sand fly (Phlebotomus mascittii) during blood feeding (picture: T. Naucke, Bonn, Germany).
Midge (Culicoides sp.), transmitter of various pathogens and cause of painful and itching biting lesions (picture: R. Pospischil, Bergheim, Germany).
Midge (Culicoides sp.), transmitter of various pathogens and cause of painful and itching biting lesions (picture: R. Pospischil, Bergheim, Germany).
Common horse fly (Haematopota pluvialis), an abundant species in Europe, the Near East and the Palearctic zone (picture: R. Pospischil, Bergheim, Germany)
Common horse fly (Haematopota pluvialis), an abundant species in Europe, the Near East and the Palearctic zone (picture: R. Pospischil, Bergheim, Germany)
Lucilia sericata (common green bottle fly or sheep blow fly): its larvae cause wound myiasis worldwide.
Lucilia sericata (common green bottle fly or sheep blow fly): its larvae cause wound myiasis worldwide.
Myiasis. Shown is a maggot (second-instar larva) of Dermatobia hominis removed from the subcutis. Note the opening at the migration channel (picture: P. Janssen-Rosseck, Düsseldorf, Germany).
Myiasis. Shown is a maggot (second-instar larva) of Dermatobia hominis removed from the subcutis. Note the opening at the migration channel (picture: P. Janssen-Rosseck, Düsseldorf, Germany).
Ctenocephalides felis (cat flea) (picture: H. Mehlhorn, Düsseldorf, Germany).
Ctenocephalides felis (cat flea) (picture: H. Mehlhorn, Düsseldorf, Germany).
Tungiasis. Multiple lesions on the heel caused by Tunga penetrans (picture: H. Feldmeier, Hamburg, Germany).
Tungiasis. Multiple lesions on the heel caused by Tunga penetrans (picture: H. Feldmeier, Hamburg, Germany).
Bed bug (Cimex lectularius) during the blood meal (picture: R. Pospischil, Bergheim, Germany).
Bed bug (Cimex lectularius) during the blood meal (picture: R. Pospischil, Bergheim, Germany).
Adult pentastomids and visceral (encysted) larval stages (nymphs) in a dog (picture: N. Pantchev, IDEXX Laboratories, Ludwigsburg, Germany).
Adult pentastomids and visceral (encysted) larval stages (nymphs) in a dog (picture: N. Pantchev, IDEXX Laboratories, Ludwigsburg, Germany).