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- Herausgeber: Wiley-VCH Verlag GmbH & Co. KGaA
- Kategorie: Wissenschaft und neue Technologien
- Sprache: Englisch
This heavily illustrated text teaches parasitology from a biological perspective. It combines classical descriptive biology of parasites with modern cell and molecular biology approaches, and also addresses parasite evolution and ecology.
Parasites found in mammals, non-mammalian vertebrates, and invertebrates are systematically treated, incorporating the latest knowledge about their cell and molecular biology. In doing so, it greatly extends classical parasitology textbooks and prepares the reader for a career in basic and applied parasitology.
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Table of Contents
Cover
Title Page
Copyright
Preface
Chapter 1: General Aspects of Parasite Biology
1.1 Introduction to Parasitology and Its Terminology
Further Reading
1.2 What Is Unique About Parasites?
Further Reading
1.3 The Impact of Parasites on Host Individuals and Host Populations
Further Reading
1.4 Parasite–Host Coevolution
Further Reading
1.5 Influence of Parasites on Mate Choice
Further Reading
1.6 Immunobiology of Parasites
Further Reading
1.7 How Parasites Alter Their Hosts
Further Reading
Chapter 2: Biology of Parasitic Protozoa
2.1 Introduction
Further Reading
2.2 Metamonada
Further Reading
2.3 Parabasala
Further Reading
2.4 Amoebozoa
Further Reading
2.5 Euglenozoa
Further Reading
2.6 Alveolata
Further Reading
Chapter 3: Parasitic Worms
3.1 Platyhelminths
Further Reading
Further Reading
3.2 Acanthocephala
Further Reading
3.3 Nematoda
Further Reading
Chapter 4: Arthropods
4.1 Introduction
Further Reading
4.2 Acari – Mites and Ticks
Further Reading
4.3 Crustacea
Further Reading
4.4 Insecta
Further Reading
Answers to Test Questions
Chapter 1
Chapter 2
Chapter 3
Chapter 4
Index
End User License Agreement
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Guide
Cover
Table of Contents
Preface
Begin Reading
List of Illustrations
Chapter 1: General Aspects of Parasite Biology
Figure 1.1 Parasitos mask, a miniature of a theater mask of Greek comedy; terracotta, around 100 B.C. (From Myrine (Asia Minor); antiquities collection of the Berlin State Museums. Image: Courtesy of Thomas Schmid-Dankward.)
Figure 1.2 A clown fish in the tentacles of a sea anemone. The partners form a mutualistic symbiosis, but they can also survive independently. (Image: Richard Orr, courtesy of Random House Publishers, Munich.)
Figure 1.3 The pearlfish
Carapus
(syn.
Fierasfer
)
acus
lives in the water lungs of sea cucumbers. (Edited from Oche G. (1966) “The World of Parasites”, Springer-Verlag Heidelberg.)
Figure 1.4 Coexistence of a typical parasite with its host. Tapeworms draw nourishment from their host and exploit the host in the long term – they are, however, only moderately pathogenic. (De bouche à Oreille by Claude Serre © Editions Glénat 2016)
Figure 1.5 Brood parasitism: A young cuckoo is fed by a warbler. (Image: Courtesy of Oldrich Mikulica.)
Figure 1.6 Phoresy: Mites latch on to a sexton beetle, “hitching a ride” to the nearest carrion. (Drawing from a photo by Frank Köhler.)
Figure 1.7 Parasitoidism: A parasitic wasp of the genus
Ichneumon
lays its eggs in a caterpillar. (From a photo in “The Animal Kingdom,” courtesy of Marshall Cavendish Books Ltd.)
Figure 1.8 Predator–prey relationship: A lion attacks a wildebeest. (Image: Ingo Gerlach, www.tierphoto.de.)
Figure 1.9 Life cycles of parasites.
Left
: Monoxenous cycle with one host, for example,
Ascaris lumbricoides
.
Center
: Heteroxenous cycle with final and intermediate hosts, for example,
Trypanosoma brucei
. Right: Heteroxenous cycle with final host and two intermediate hosts, for example,
Dicrocoelium dendriticum
.
Figure 1.10 Distribution of various Mallophaga species on an Ibis (
Ibis falcinellus
), an example of high specificity for particular habitats on a host individual. (a)
Ibidoecus bisignatus
. (b)
Menopon plegradis
. (c)
Colpocephalum
and
Ferribia
species. (d)
Esthiopterum raphidium
. (From Dogiel, V.A. (1963)
Allgemeine Parasitologie (General Parasitology)
, VEB Gustav Fischer Verlag, Jena.)
Figure 1.11 Dimensions of various parasitic organisms.
Figure 1.12 Louse flies with varying degrees of wing reduction. (a)
Lynchia maura
(continuously flight-capable). (b)
Lipoptena cervi
, sheds its wings when it has alighted on a host. (c)
Melophagus ovinus
, wingless. (Compiled from various authors.)
Figure 1.13 Beach crab with the externa of
Sacculina carcini
. The brood sac – the only externally visible part of this extremely modified barnacle – juts out under the anal segments of the crab. (Image: Courtesy of M. Grabert)
Figure 1.14 Transition to endoparasitism in barnacles. (a): Barnacle on a firm surface. (b) Whale barnacle on whale skin. (c) The shark parasite
Anelasma squalicola
, forming root-like extensions that extend into the host's skin and absorb nutrients. (d) The root system of
Sacculina carcini
runs throughout the entire body of the host; the externa is under the anal segments. (Compiled from various sources.)
Figure 1.15 Adhesive and clasping organs in parasites. (a) Scolex of the pig tapeworm
Taenia solium
, front view. (b) Monogenean
Gyrodactylus elegans
. (c) Monogenean
Polystomum integerrimum
. (d) Acanthocephalan, or spiny-headed worm
Acanthorhynchus
. (e) Fish leech
Piscicola geometrica
. (f) Front end of the pentastomid, or tongue worm
Leiperia gracilis
as seen from the abdomen. (g) Larva of the pond mussel
Anodonta cygnea
. (h) Front end of the larva of a deer botfly (
Cephenomyia
). (i) Front end of a Gregarine (
Stylorhynchus
) from the intestine of a dragonfly larva. (j)
Argulus foliaceus
, a crustacean fish louse. (k) Crab louse (Insecta) of humans (
Pthirus pubis
). s: Sucker. (From Hesse-Doflein (1943) Tierbau und Tierleben, Verlag Gustav Fischer, Jena).)
Figure 1.16 Length of
Diphyllobothrium latum
compared to a medium-sized woman. (Image: Archive of the Department of Molecular Parasitology, Humboldt University, Berlin.)
Figure 1.17 Reproductive success of great tits from nests infected/not infected with
Ceratophyllus gallinae
. (According to data from Richner, H., Oppliger, A., and Christie, P. (1993)
J. Anim. Ecol
.,
62
, 703–710.)
Figure 1.18 Scottish grouse,
Lagopus lagopus scoticus
.
Figure 1.19 Fluctuation in the population of Scottish grouse due to infection with the intestinal nematode
Trichostrongylus tenuis
. Deworming (arrow) of a proportion of the birds prevents the decline of populations. (a) Course of events with two control populations; (b) Course of events in two populations after a single treatment; (c) Course of events in two populations after two treatments. (From Hudson, P.J., Dobson, A.P., and Newborn, D. (1999)
Science
,
282
, 2256–2258 with kind permission of the publisher.)
Figure 1.20 Development of green crabs from areas with and without their original parasites. (a) Width of shell. (b) Average weight of crabs in a trap (kg). (From Torchin, M.E., Lafferty, K.D., and Kuris, A.M. (2001)
Biol. Invasions
,
3
, 333–345, with kind permission of the publisher.)
Figure 1.21 Increase of infection with
Varroa destructor
in bees of different susceptibility. White bars: American bees; black bars: Primorsky bees. (Data from Rinderer, T.E., Guzman, L.I., Delatte, G.T., Stelzer, J.A., Lancaster, V.A., Kutznetsov, V., Beaman, L., Watts, R., and Harris, J.W. (2001)
Apidologie
,
32
, 381–394, by kind permission of the publisher.)
Figure 1.22
Anguillicola crassus
in the swim bladder of a European eel (
Anguilla anguilla
). (Image: Courtesy of Klaus Knopf.)
Figure 1.23 Various modes of coevolution of hosts and their parasites. For details see text. Black line: evolutionary line of parasite species; grey line: evolutionary line of host species. (From Paterson, A.M., Palma, R.L., and Gray, R.D. (1999) How frequently do avian lice miss the boat? Implications for coevolutionary studies.
Syst. Biol
.,
48
, 214–223 with kind permission of the publisher.)
Figure 1.24 Negative binomial frequency distribution of hookworms in a human population in Papua and New Guinea. A few individuals have many worms – but the majority of individuals have few or no worms. (From Pritchard
et al
. (1990), Parasitology 100, 259–267.)
Figure 1.25 Shift of allele frequencies of the β-tubulin gene of small strongyles parasitic in horses after several treatments with benzimidazole. The replacement of phenylalanine with tyrosine in position 200 of the protein leads to drug resistance. Heterozygous genotypes increase in frequency under the pressure of the drug treatment. (According to data from G. Samson-Himmelstjerna.)
Figure 1.26 In the simplest case assumed here, with two types of hosts (A, B) and parasites (a, b), type a parasites can infect the hosts of type A and correspondingly, type b parasites can infect the hosts of type B. Infection leads to a decrease in the frequency of the corresponding type in the host population (fitness loss) and to an increase in the corresponding type in the parasite population (fitness gain). If, for example, there were currently many hosts of type B, but few parasites of type b, parasites of this type would have a high selective advantage. Selection of the type b now occurs causing — with a time delay — an increase in type b's frequency in the population. The various frequencies of host and parasite types alternate accordingly during the course of a cycle. In the longer term, however, none of the types disappear from the population, as each type is “protected” against elimination by negative frequency-dependent selection. From Schmid-Hempel, P. in Allgemeine Parasitologie (2006). Eds. Hiepe, Lucius, Gottstein, Parey in MVS Medizinverlage Stuttgart.
Figure 1.27 Chronological sequence of the worldwide spread of chloroquine resistance in
Plasmodium falciparum
. (Data from X. Su
et al
. (1997) Cell 91, 593–603.)
Figure 1.28 Sickle cell erythrocyte. (EM image: Courtesy of Eye of Science.)
Figure 1.29 Frequency of HbS alleles (in %). The distribution of sickle cell anemia correlates with the spread of
Plasmodium falciparum
. (Compiled from various sources.)
Figure 1.30 Ornaments such as the peacock's tail or deer antlers signal the genetic quality, including resistance against infections, of males to females.
Figure 1.31 Lower attractiveness of infected males: female mice sniff at the urine of healthy male mice significantly longer than at the urine of males infected with
Eimeria vermiformis
. (According to Kavaliers and Colwell (1995) Proc. Roy. Soc. B. 261, 31–35.)
Figure 1.32 Parasite-mediated sexual selection. A female is rejecting male 1, since its poorly developed tail does not allow a statement on its parasite burden. The female rejects male 2, since its ruffled tail signals a bad health status. Male 3 is accepted due to its healthy looking attractive tail. (According to Clayton, D.H. (1991)
Parasitol. Today
,
7
, 329–334, by courtesy of the publisher.)
Figure 1.33 Stickleback dance: The stickleback male tries to impress a female that is ready to lay eggs (noticeable by her bulging belly) through its red underbelly and lures the female into the nest. (According to J. Münzing in Grzimeks Tierleben (1970) Verlag Kindler Zürich.)
Figure 1.34 Time spent by female sticklebacks with male before and after infection with
I. multifiliis
. Before infection, males seen in white light (continuous line) are more attractive than in green light (broken line), because green light extinguishes the bright red color of males. Infection reduces the red color, such that males are less attractive, and attraction is similar in white and green lights. (Created from data of Milinski, M. and Bakker, T.C.M. (1990)
Nature
,
344
, 330–333.)
Figure 1.35 Schematic representation of premunition. The antigens of worms (gray ovals) induce immune responses that eliminate infective larvae; but established worms block these responses with immune evasion mechanisms (represented by a bar). (By R. Lucius (1996) in Allgemeine Parasitologie (2006). Eds. Hiepe, Lucius, Gottstein, Parey in MVS Medizinverlage Stuttgart.)
Figure 1.36 Example of the triggering of innate immunity. In dendritic cells (DC), parasite molecules (PAMPs) initiate an activation process, which leads to the formation of IL-12 and IL-18. In natural killer cells (NK), this leads to the production of IFN-γ, which affect other cells. For details, see text. (By R. Lucius In Allgemeine Parasitologie (2006) Eds. Hiepe, Lucius, Gottstein, Parey in MVS Medizinverlage Stuttgart.)
Figure 1.37 Differentiation of T cell subpopulations in the mouse. The differentiation is significantly influenced by the context of antigen presentation, in particular by the cytokine signals of antigen-presenting cells during the sensitization of T cells. In the presence of IL-4, there is a tendency to imprint Th2 cells (typical for helminth infections), producing a specific pattern of cytokines. Similarly, the presence of other cytokines results in Th1, Th17, or Treg responses. For details, see text. From Lucius, R. In Allgemeine Parasitologie (2006) Eds. Hiepe, Lucius, Gottstein, Parey in MVS Medizinverlage Stuttgart.
Figure 1.38 (a) Immune attack on extracellular protozoan parasites. Surface-bound antibodies make the parasite detectable for effector cells, resulting in phagocytosis. This process can be amplified by complement activation. (b) Killing of intracellular parasites. Th1 cells stimulate the host cell with IFN-γ to kill their intracellular parasites. IFN-γ can also result in the activation of macrophages that use their effector molecules to kill intracellular parasites in neighboring cells. From Lucius, R. in Allgemeine Parasitologie (2006). Eds. Hiepe, Lucius, Gottstein, Parey in MVS Medizinverlage Stuttgart.
Figure 1.39 Immune attack on worms. The allergens secreted by worms induce IgE antibodies, which make the worms detectable for attacking eosinophils. The IgE-dependent degranulation of mast cells facilitates the recruitment of eosinophils. For details, please see the text.
Figure 1.40 Eosinophils attack a third-stage larva of the filarial nematode
Acanthocheilonema viteae
in the tissue of a gerbil. (EM image: Department of Molecular Parasitology, Humboldt Universität.)
Figure 1.41 Immune attack on nematodes in the intestine. Worm antigens (
gray ovals
) passing into the sensitized tissues of the host that have already formed IgE antibodies, result in the degranulation of mast cells. The released mast cell products attract granulocytes and myeloid cells that release cytokines (black triangles), stimulate epithelial turnover and goblet cells to produce mucus. These factors loosen the association of epithelial cells, creating permeability for antibodies, eosinophils, and the effector molecules of mast cells. Some mast cell products also act directly on worms. The combination of these effects results in the rapid expulsion of nematodes. For details, see text. (From Lucius, R. in Allgemeine Parasitologie (2006). Eds. Hiepe, Lucius, Gottstein, Parey in MVS Medizinverlage Stuttgart.)
Figure 1.42 Myocarditis in Chagas disease. The muscle fibers have been infiltrated by inflammatory cells. Arrows: amastigote stages of
Trypanosoma cruzi
in muscle cells. (Image: Archive of the Department of Molecular Parasitology, Humboldt University, Berlin.)
Figure 1.43 Kidney damage due to immune complex-mediated inflammation in gerbils infected with the filarial nematode
Acanthocheilonema viteae
. Left, damaged kidney; right, healthy kidney. (Image: Richard Lucius.)
Figure 1.44 Cytoadherence.
Plasmodium falciparum
-infected erythrocytes (arrows) in a maternal blood vessel of the placenta. (Image: Courtesy of Mats Wahlgren.)
Figure 1.45 Sections of
Onchocerca volvulus
females in skin nodules. Note the absence of inflammatory cells in the connective tissue. (Image: Department of Molecular Parasitology, Humboldt University, Berlin.)
Figure 1.46 Occurrence of opportunistic infections depends on the density of CD4
+
T cell per µl of blood. (Composed from various sources by W. Presber.)
Figure 1.47 Reactivated toxoplasmosis in the brain of an AIDS patient. Note the necrotic area in the left hemisphere. (Image: Courtesy of Julio Martinez.)
Figure 1.48 Hatching larva of
Trichuris suis
. (Image: Courtesy of Ovamed.)
Figure 1.49 Muscle cyst of
Sarcocystis gigantea
on the pharynx of a sheep. (Image: Archive of the Department of Molecular Parasitology, Humboldt University, Berlin.)
Figure 1.50 Nurse cell first-stage larva of
Trichinella spiralis
in the muscle tissue of an infected rat. (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 1.51 Cross section of the liver of a
Biomphalaria glabrata
snail infected with
Schistosoma mansoni
(b) and the liver of a control animal (a). Note the degree of displacement of liver tissue (arrows) by parasitic stages (arrow heads). (Scale = 150 µm). (Image: Department of Molecular Parasitology, Humboldt University, Berlin.)
Figure 1.52 Growth of the snail
Galba truncatula
after infection with
Fasciola
, expressed by increase in dry weight. Uninfected snails (
circles
) begin to produce eggs after 20 days and grow only slightly. Infected snails (
squares
) are castrated, produce no eggs, and continue to grow. (From Wilson, R. A. and Denison, J. (1980) Z. Parasitenkd. 61, 109–119.)
Figure 1.53 Suggested mechanism of the feminization of male mice by metacestodes of
Taenia crassiceps
. The metacestodes stimulate the immune system toward a Th2-oriented response, leading to the expression of IL-6 in cells of the testes. IL-6 stimulates the expression of the enzyme aromatase p-450 (P-450 aro), which converts testosterone (Te) to estradiol (E2) rather than converting it into dihydroxytestosterone (DHT) by means of 5α-reductase (5α-red). Estradiol in turn acts as a growth factor for metacestodes and favors Th2 immune reactions. (From Morales-Montor, J. and Larralde, C. (2005)
Parasitology
,
131
, 287–294.)
Figure 1.54 Metacercariae of
Curtuteria australis
and
Acanthoparyphium
sp. encysted in the foot tissue of the bivalve
Austrovenus stutchburyi
. (Image: Tommy Leung and Robert Poulin, University of Otago.)
Figure 1.55 Scanning electron micrograph of a recently excysted metacercaria of
Acanthoparyphium
sp. (EM image: Haseeb Randhawa, Matthew Downes, and Robert Poulin, University of Otago.)
Figure 1.56 Bradyzoites of
Toxoplasma gondii
in a tissue cyst from the brain of a mouse. (Image: Archive of the Department of Molecular Parasitology, Humboldt University, Berlin.)
Figure 1.57 Behavioral alteration of rats infected with
Toxoplasma gondii
. Uninfected and infected rats were exposed to bobcat urine and rabbit urine in a circular arena. (a) Control animals visited the quadrant laced with bobcat urine significantly less often as compared with infected rats. (b, c) Representative scatter blots showing the movements of a control rat (left) and infected rat (right) within the arena. (From Vyas, A., Kim, S.-K., Giacomini, M., Boothroydt, J.C., and Sapolsky, R.M. (2007)
Proc. Natl. Acad. Sci. U.S.A
.,
104
, 6442–6447, with kind permission of the publisher.)
Figure 1.58 Behavioral changes in amphipods after infection with three different species of spiny-headed worms. Uninfected amphipods are primarily bottom dwellers, burying themselves in the mud when danger threatens. (a) Amphipods infected with
Polymorphus paradoxus
prefer the surface of the water, anchoring themselves rigidly in the aquatic vegetation when threatened, where they are taken by dabbling ducks (e.g., mallards). (b) Amphipods infected with
P. marilis
prefer better-lit areas in zones of average depth, where they are taken by diving ducks. (c) Amphipods infected by
Corynosoma constrictum
float on the surface. When danger threatens, however, they swim down to deeper zones, where they are taken by both dabbling and diving ducks. (From Moore, J. (1984)
Sci. Am
.,
250
, 2–89, by kind permission of the publisher.)
Figure 1.59
Dicrocoelium dendriticum-
infected
Formica
with mandibles firmly clenched on a blade of grass. (EM image: Courtesy of Eye of Science.)
Figure 1.60 Specific localization of the brain worms of
Dicrocoelium dendriticum
and
Dicrocoelium hospes
. In
D. dendriticum
infection, a brain worm usually penetrates into the subesophageal ganglion (a). In
D. hospes
infection, two brain worms are usually localized in the antennal lobes of the supraesophageal ganglion (b). Arrows: Brain worm. (Images: Courtesy of Thomas Romig.)
Figure 1.61 Oak bush cricket
Meconema thalassinum
from which the Gordian worm
Spinochordodes tellini
emerges. (Image: from http://en.wikipedia.org/wiki/Spinochordodes_tellinii.)
Chapter 2: Biology of Parasitic Protozoa
Figure 2.1 Phylogenetic tree of the eukaryotes. (Baldauf, S.L. (2003)
Science
,
300
, 1703–1706, with kind permission of Science Publishers.)
Figure 2.2
Giardia lamblia
trophozoites on the intestinal epithelium of a mouse. Inset: Underside of the parasite. (image: Department of Molecular Parasitology, Humboldt Universität.)
Figure 2.3
Giardia lamblia
. (a) Trophozoite. (b
)
Quadrinucleated cyst. (c) Trophozoite with its adhesive disk attached to the microvilli margin of an intestinal epithelial cell. (d) Trophozoite, during fission. A, adhesive disk; B, basal body of flagella; F, flagella; M, median body; N, nucleus. The scale is 5 µm for (a) and (b), 10 for (c) and (d). (Based on several authors.)
Figure 2.4 (a) Tear drop-shaped
Trichomonas vaginalis
trophozoite grown in liquid culture. (SEM Image: Courtesy of Eye of Science.) (b) Flattened
T. vaginalis
closely attached to vaginal epithelial cells. (SEM image: Rendon-Maldonaldo, JG
et al
. (1998) in Experimental Parasitology 89, 241–250. with kind permission by Elsevier.)
Figure 2.5 Ultrastructure of
Trichomonas vaginalis
. Ax, axostyle; C, costa; ER, endoplasmic reticulum; Ef, free flagella; Go, Golgi apparatus; H, hydrogenosomes; N, nucleus; Nu, nucleolus; P, pelta; Pf, parabasal filament; Tf, trailing flagellum; UM, undulating membrane; V, vacuole. (Adapted from Benchimol (2004) in “
Microscopy and Microanalysis
” with kind permission by Cambridge University Press.)
Figure 2.6 Membranous chancre caused by
Trichomonas gallinae
(yellow chancre) in the crop of a pigeon. (Image: Courtesy of T. Hiepe und R. Jungmann).
Figure 2.7 Life cycle of
Entamoeba histolytica
. (a) Hatching of tetranuclear amoeba. (b) Octanuclear amoeba with an amoebula being pinched off. (c) Amoebula. (d) Trophozoite. (e) Tissue-invading trophozoite with ingested erythrocytes. (f) Mononuclear cyst. (g) Binuclear cyst. (h) Tetranuclear cyst. (Based on several authors.)
Figure 2.8 Microscopy images of
Entamoeba histolytica
. (a) Trophozoite. (b) Tissue-invading trophozoite with ingested erythrocytes. (c) Tetranuclear cyst. (Images: Courtesy of E. Tannich.)
Figure 2.9 Trophozoite of
Entamoeba histolytica
with various vacuoles. (TEM image: Courtesy of E. Tannich.)
Figure 2.10 Liver abscesses as a result of an
Entamoeba histolytica
infection. The CT scan shows the two abscesses as light areas with diffuse outlines. (Image: Courtesy of E. Tannich.)
Figure 2.11 Early stage of tissue invasion by
Entamoeba histolytica
. Trophozoites kill the intestinal epithelial cells and penetrate deep into the mucosa through the resulting gaps. Neutrophils that have been attracted are also killed and the lytic products they contain contribute to dissolve the tissue. (Wyler, D.J. (1990)
Modern Parasite Biology
, W. H. Freeman & Company, New York, with kind permission by Freeman and Company.)
Figure 2.12 Killing of host cells by
Entamoeba histolytica
trophozoites. A trophozoite touches the target cell with its pseudopodium and kills it by secreting amoebapore. The dying target cell forms blisters. (SEM images: Courtesy of G. Kaplan, from Young, J.D., Cohn, Z.A. (1988) Sci. Am. 258, 38–44.)
Figure 2.13 Human pathogenic amoebae. (Adapted from various sources).
Figure 2.14 Schematic representation of the position of flagellum and the kinetoplast in
Trypanosomatidae
. (a) Trypomastigote. (b) Epimastigote. (c) Promastigote. (d) Amastigote. (Adapted from various authors.)
Figure 2.15 Ultrastructure of the trypomastigote (a) and epimastigote forms (b) of
Trypanosoma brucei
. ER, endoplasmic reticulum; F, flagellum; Go, Golgi apparatus; Fp, flagellar pocket; K, kinetoplast; M, mitochondrion; Mt, microtubules; N, nucleus. In order to better visualize the microtubules running below the surface, the anterior end of the trypomastigote form has been cut perpendicularly to the longitudinal section. (From Dönges (1988). Parasitology. Georg Thieme-Verlag, Stuttgart.)
Figure 2.16 Phylogeny of Kinetoplastea and representatives of outgroups, composed based on the phylogenetic analysis of
Trypanosomatidae
(based on Hamilton P.B.
et al.
(2004) Int. J. Parasitol. 34, 1393–1404)
Kinetoplastida
(based on Simpson, A.G.B.,
et al.
(2004).
Protist
,
155
, 407–422). Please note that
Stercoraria
(including
Trypanosoma cruzi
),
Salivaria
(including
T. brucei
), and
Leishmania
occupy different branches of the phylogenetic tree.
Figure 2.17 Life cycle of
Trypanosoma brucei
including mitochondrial function. (a) Slender trypomastigote blood form. (b) Trypomastigote intermediary form. (c) Stumpy trypomastigote blood form. (d) Procyclic trypomastigote form in intestinal lumen. (e) Mesocyclic trypomastigote form in the ectoperitrophic space. (f) Epimastigote form, with flagellipodia attached to microvilli of salivary gland cells. (g) Trypomastigote metacyclic form in the saliva of
Glossina
. Striped structure: Mitochondrion
.
(Adapted from Vickerman, K. (1985).
Br. Med. Bull
.,
41
, 105–114.)
Figure 2.18 Long slender trypomastigote blood form of
Trypanosoma brucei
, its anterior end lying on top of an erythrocyte. (SEM image: Courtesy of Eye of Science.)
Figure 2.19 Slender trypomastigote (a) and stumpy blood form (b) of
Trypanosoma brucei
. (Images: Courtesy of E. Vassella and M. Boshard.)
Figure 2.20 Changes in the prevalence of sleeping disease in the Central African Republic between 1950 and 2000. (Adapted from Cattand, P., Jannin, J., and Lucas, P. (2001).
Trop. Med. Int. Health,
6
, 348–361.)
Figure 2.21 Historic photograph of an African woman suffering from an advanced stage of sleeping sickness. (Image: Courtesy of G. Stich.)
Figure 2.22 Electron micrograph of the surface coat of
Trypanosoma brucei
. Please note the electron-dense, blurred layer of variable glycoproteins on cell body and flagellum. Inset: Detail of the surface with clearly recognizable elementary membrane and underlying microtubules. (From Wyler, D.J. (1990)
Modern Parasite Biology
, W. H. Freeman & Company, New York, with kind permission by Freeman and Company.)
Figure 2.23 Schematic representation of the glycosylphosphatidylinositol membrane anchor of a variable surface antigen of
Trypanosoma brucei
. (Based on Ferguson, M.A., Homans, S.W., Dwek, R.A., Rademacher, T. (1988) Biochem. Soc. Trans. 16, 265–268.)
Figure 2.24 Schematic view of antigen variation in
Trypanosoma brucei
. Ever-new clones of
T. brucei
blood forms develop, each of which has its specific variable surface antigens. By the time the host's antibody response has eliminated the predominant clone, a new variant has developed and continues to multiply until antibody responses to the new surface antigen develop. Although a small number of clones dominate each peak, there is a surprising amount of diversity as well, such that peaks are never homogeneous. (Top right: original patient data.)
Figure B2.1 Polycystronic transcription in
Trypanosoma brucei.
(Graphic: J. Donelson.)
Figure 2.25 West African dwarf shorthorn cattle. This dwarf variety has efficient immune responses against trypanosomes, as long as the animals are healthy. (Image: P. Agbadje with kind permission by W. Bernt.)
Figure 2.26 Life cycle of
Trypanosoma cruzi
. (a) Invasion of a cell by a trypomastigote metacyclic infective form from excrement of a reduviid bug. (b) Intracellular amastigotes. (c) Transformation into intracellular trypomastigotes. (d) Trypomastigote form in the bloodstream. (e, f) Epimastigote insect form. (g) Trypomastigote, metacyclic form. (Adapted from various authors.)
Figure 2.27 Stages of
Trypanosoma cruzi
. (a) Trypomastigote blood form, with distinct kinetoplast and a curved cell body. (b) Amastigote forms in a murine muscle cell. (Images: Courtesy of P. Kimmig.)
Figure 2.28 Reduviid bug
Dipetalogaster maximus
, an arthropod host of
Trypanosoma cruzi
, during a blood meal. Only reduviid bug species that defecate immediately after a blood meal can transmit
T. cruzi.
(Image: Courtesy of G. Schaub.)
Figure 2.29 Brazilian bank note with the image of Carlos Chagas, the discoverer of
Trypanosoma cruzi
and its life cycle.
Figure 2.30 Chagas disease. (a) Swollen eye lid (Chagoma or Romana's sign) after transmission of
Trypanosoma cruzi
by reduviid bugs. (b) Enlargement of the heart with thinned heart wall at the apex. (c) Intestinal ectasia (Images (a) and (b) archive of the Department of Parasitology, University of Hohenheim, Image: Courtesy of (c) J. S. Olivera, received from MA Miles.)
Figure 2.31 Transfer of sialic acid groups from the host cell to glycoproteins of
Trypanosoma cruzi
by virtue of trans-sialidases. (Adapted from Buscaglia, C.A., Campo, V.A., Frasch, A.C.C., and Di Noia, J.M. (2006)
Nat. Rev. Microbiol
.,
4
, 229–236, with kind permission by the publisher.)
Figure 2.35 Invasion of protozoan parasites into a host cell.
Leishmania
is taken up by phagocytosis.
Trypanosoma cruzi
invades by induced phagocytosis.
Toxoplasma gondii
invades by gliding motility. All parasites lie in a parasitophorous vacuole of different origin, from which
T. cruzi
escapes shortly after invasion. (From Sacks and Sher (2002) Nature Immunology 3, 1041–1047, with kind permission by the publisher.)
Figure 2.32 Life cycle of
Leishmania
sp. (a) Invasion of a macrophage by a metacyclic promastigote infective form. (b) Change into amastigote form. (c) Multiplication during the amastigote stage. (d) Released amastigote form. (e) Promastigote form from the insect foregut. (f) Promastigotes firmly attached to foregut cells. (g) Metacyclic promastigote form. (Adapted from various authors.)
Figure 2.33 Stages of
Leishmania
. (a) Promastigotes of
L. major
(image: Department of Molecular Parasitology, Humboldt Universität). (b) Amastigote stage of
L. mexicana
. Section through the flagellar pocket with longitudinal section of the flagellar stump. Lys, lysosome; Fp, flagellar pocket; M, mitochondrion. (From Waller and McConville (2002) Int. J. Parasitol. 32, 1435–1445, with kind permission by Elsevier Publishers.)
Figure 2.34 Surface components of the promastigote and amastigote stages of
Leishmania
. (From Naderer, T., Vince, J.E., and McConville, M.J. (2004)
Curr. Mol. Med
.,
4
, 649–665, with kind permission by Bentham Science Publisher Ltd.)
Figure B2.2
Figure 2.36 Manifestations of leishmaniosis. (a) Oriental boil after
Leishmania tropica
infection. (b) Child with hepatosplenomegaly following
Leishmania donovani
infestation. The outlines of the organs have been marked. (Image: Courtesy of W. Solbach.) (c) Mucocutaneous leishmaniosis in the corner of the mouth after
Leishmania braziliensis
infection. (d) Deformation of ear cartilage in chicleros' disease caused by
Leishmania mexicana
. (a, c, and d: Archive of the Department of Parasitology; University of Hohenheim.)
Figure 2.37 Stages of
Leishmania donovani
. (a)
In vitro
invasion by promastigotes into macrophages of a golden hamster. (b) Blood smear of a golden hamster with a macrophage containing amastigotes and some free amastigotes. (Images: archive of the Department of Parasitology, University of Hohenheim.)
Figure 2.38 Phylogeny of Alveolata. (According to Leander, B.S. and Keeling, P.J. (2003)
Trends Ecol. Evol
.,
8
, 395–402.)
Figure 2.39 Schematic representation of the surface of Alveolata. The plasma membrane is underlain by alveoli (=vesicles), which are filled in the thecate dinoflagellates, but empty in the Apicomplexa and Ciliophora and this results in a triple membrane. (From Hausmann, Hülsmann, Radeck (2003) Protistology, with permission from Scheizerbart'sche Verlagshandlung, Stuttgart, www.schweizerbart.de.)
Figure 2.40 Schematic life cycle of Apicomplexa.
Figure 2.41 Schematic representation of the different forms of Apicomplexan daughter cell formation. (a) Endodyogeny. Two daughter cells are formed inside the mother cell. (b) Typical schizogony. Two daughter cells are formed during the last nuclear division of the multipart schizonts. (c) Endopolygeniy. Many daughter cells are created simultaneously at the periphery of a polyploid nucleus. DCA, daughter cell anlage ( = primordium); N, nucleus; PN, polyploid giant nucleus. (From Mehlhorn and Piekarski: Grundriß der Parasitenkunde, (2002) with kind permission of Spektrum Akademischer Verlag, Heidelberg.)
Figure 2.42 Ultrastructure of an Apicomplexa merozoite. (a) Longitudinal section. A, amylopectin; Ap, apicoplast; C, conoid; DG, dense granules; ER, endoplasmic reticulum; ERh, efferent duct of the rhoptries; Go, Golgi apparatus; IM, inner membrane complex (flat vesicles); Mi, mitochondrion; Mn, micronemes; Mp, micropore; Mt, pellicular microtubules; N, nucleus; P, pole ring; Ppr, posterior pole ring; Rh, rhoptries. (Adapted from Scholtyseck und Mehlhorn (1973), Naturwissenschaftl. Rundsch. 26, 421–427.) (b) Detailed representation of the microtubular apical structures of a tachyzoite of
Toxoplasma gondii
. Apr, anterior preconoidal ring; Csu, conoid subunit; IMC, inner membrane complex; IMt, internal microtubules; Mt, microtubules; P, pole ring complex; Pm, plasma membrane; Ppr, posterior preconoidal ring. Nichols, B.A., Chiappino, M.L. (1987) J. Protozool. 34, 217–226.
Figure 2.43 Probable development of the apicoplast by secondary endosymbiosis. In the first step, uptake of a cyanobacterium resulted in a red alga with a plastid organelle. This alga was taken up by a single-celled eukaryote and became an endosymbiont. The respective membranes were retained. The result is an apicoplast with a quadruple membrane. Detail: TEM image of the apicoplast of
Plasmodium falciparum
. Pl, Plastid organelle; Arrow, quadruple membrane. (Photo from Ralph, S.A.
et al
. (2004) Nat. Rev. Microbiol. 2, 203–216, with kind permission of Macmillan Publishers Ltd.)
Figure 2.44 Schematic representation of the “gliding motility” of Apicomplexa. Details are in the text. (From: Soldati, D., and Meissner, M. (2004).
Curr. Opin. Cell Biol
.,
16
, 32–40, by kind permission of Elsevier.)
Figure 2.45 Model of the host cell invasion of a
Toxoplasma gondii
tachyzoite. See text for details. (a) Binding. (b) Protrusion of the conoid and secretion of components of the micronemes and rhoptries. (c–e) Formation of a
moving junction
between parasite pellicula and host cell surface, plus formation of the parasitophorous vacuole. (f) The membrane closes and the formation of the parasitophorous vacuole is completed. (From Wyler, D.J. (1990)
Modern Parasite Biology
, W. H. Freeman & Company, New York. By kind permission of W.H. Freeman and Company. Top left: Penetration of a host cell by a Toxoplasma tachyzoite. EM image: Courtesy of B. A. Nichols.)
Figure 2.46 Sporulated oocyst of
Eimeria
. (Image: R. Lucius/J. Gelnar.)
Figure 2.47 Lifecycle of
Cryptosporidium parvum
. (a) Sporozoite. (b) Trophozoite at the surface of an intestinal epithelial cell. (c) Schizont. (d) Merozoites. (e) Macrogametocyte. (f) Macrogamete. (g) Microgametocyte. (h) Microgametes. (i) Zygote. (j) Sporont with thin cyst wall. (k) Thin-walled oocyst. (l) Sporont with thick cyst wall. (m) Thick-walled oocyst. (Adapted from Mehlhorn H. (1998) Parasitology in Focus, with permission by Springer-Verlag, Heidelberg.)
Figure 2.48
Cryptosporidium parvum
. (a) Stages on the surface of a villus, 6 days after experimental infection of a pig (SEM). Note that the parasitophorous vacuoles of the major stages are broken open and the individual pathogens are lying free. (Image: Courtesy of Pohlenz.) (b) TEM image with different stages embedded by the intestinal microvilli of a calf. (Image: Courtesy of E. Goebel.)
Figure 2.49 Life cycle of
Eimeria tenella
. (a) Sporozoite. (b) Trophozoite in an intestinal epithelial cell. (c) Schizont. (d) Merozoites. (e) Free merozoite. (f) Dormant stage in intraepithelial lymphocytes. (g) Macrogametocyte. (h) Macrogamete. (i) Microgametocyte. (j) Microgametes. (k) Zygote. (l) Intracellular sporont. (m) Excreted sporont within the oocyst. (n) Excreted sporoblasts within the oocyst. (o) Oocyst with four sporocysts, each containing two sporozoites. (Adapted from Mehlhorn, H. (ed.) (1988) Parasitology in Focus, Springer-Verlag, Heidelberg.)
Figure 2.50 Stages of
Eimeria
. (a–e) Light microscope images of
E. tenella
stages. (Images: Courtesy of R. Entzeroth.)
Figure 2.51 Sporozoites of
Eimeria
. (a) A sporozoite of
E
.
falciformis
invades a host cell. (EM image: Department of Molecular Parasitology, Humboldt Universität.) (b) Sporozoite of
E. tenella
. (EM image by Institute for Animal Health, Compton, UK, with kind permission.)
Figure 2.52 Preferred colonization locations of
Eimeria
species in the intestine of the chicken. (Adapted from Ball, Pitilo and Long (1989) Adv. Parasitol. 28, 1–54.)
Figure 2.53 Life cycle of
Toxoplasma gondii
. (a) Sporozoite. (b, c) Tachyzoites in macrophage. (d) Bradyzoites in tissue cysts. (e) Bradyzoite. (f) Infection of intermediate hosts with bradyzoites from tissue cysts. (g) Trophozoite in intestinal epithelial cell. (h) Schizont. (i, j) Merozoites. (k) Macrogametocyte. (l) Macrogamete. (m) Microgametocyte. (n) Microgamete. (o) Zygote. (p) Sporont inside oocyst. (q) Sporulated oocyst with two sporocysts, each containing four sporozoites (infectious for cat or intermediate host). (r) Sporozoite, infectious for cat.
Figure 2.54 Stages of
Toxoplasma gondii
. (a) sporulated oocysts from cat feces. (Image: T. Jäkel.) (b) Tachyzoites in cultured fibroblasts. (Image: R. Lucius.). (c) Tissues cysts in the brain of a laboratory mouse. (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 2.55 Congenital toxoplasmosis. (a) Child with hydrocephalus. (From Dyke (1960)
Recent Advances in Clinical Pathology
, Vol.3. By kind permission of Elsevier.) (b) Cross section of a hydrocephalus brain with distinctly enlarged ventricles. (From: Schrod
et al
. (1991) Pädiat. Prax 43, 117–125. With kind permission by Hans Marseille Publisher.)
Figure 2.56 Estimated incidence of congenital toxoplasmosis in Germany in 2011, according to information of the Robert Koch-Institute Berlin. (Wilking, H., Thamm, M., Stark, K., Aebischer, T., and Seeber, F. (2014) Sci. Rep. 6, 22551. Wallon, M.
et al.
(2013) Clin. Infect. Dis. 56, 1223–1231.)
Figure 2.57 Tachyzoites of
Toxoplasma gondii
in a parasitophorous vacuole. The vacuole is surrounded by host-cell mitochondria and endoplasmic reticulum, which the parasite recruits. Image: Coppens and Joiner (2001) Exp. Review in Mol. Med. 2001, 1–20.
Figure B2.3
Figure 2.58 Oocysts of
Neospora caninum
. (Image: Institute of Parasitology, University of Bern.)
Figure 2.59 Life cycle
of Sarcocystis suihominis
. (a) Sporozoite. (b) Endopolygeny in endothelial cell. (c) Merozoite. (d) Tissue cysts in muscle cell. (e) Cystozoite. (f) Macrogametocyte. (g) Macrogamete. (h) Microgametocyte. (i) Microgametes. (j) Zygote. (k) Sporoblasts. (l) Sporocysts with sporozoites within the oocyst wall. (m) Excreted sporocyst. (Adapted from Mehlhorn, H. (ed.) (1988)
Parasitology in Focus
, Springer-Verlag, Heidelberg.)
Figure 2.60 Stages of
Sarcocystis suihominis
. (a) Free, sporulated oocysts. (b) Sporocysts within the thin oocyst sheath. (Images (a) and (b): Courtesy of H. Rommel.) (c) Schizont in the endothelial cell of a pig (d) Tissue cyst, Giemsa stain. (Images (c) and (d): Courtesy of A. O. Heydorn.)
Figure 2.61 Life cycle of
Plasmodium falciparum
. (a) Sporozoite. (b) Trophozoite in the liver cell. (c) Liver schizont. (d) Merozoite from liver cell. (e) Invasion of an erythrocyte. (f) Ring stage. (g) Schizont. (h) Merozoites. (i, j) Macrogametocyte. (k) Macrogamete. (l, m) Microgametocyte. (n) Exflagellation, resulting in the formation of microgametes. (o) Zygote. (p) Ookinete. (q) Oocyst. (r) Sporozoites are released from the oocyst and invade the salivary gland. (s) Transmission of sporozoites with the saliva. (Adapted from Mehlhorn, H. (ed.) (1988) Parasitology in Focus, Springer-Verlag, Heidelberg.)
Figure 2.62 Blood stages of human pathogenic Plasmodium species. Top row:
Plasmodium vivax
. Note the relatively large deformation of the erythrocyte and the formation of Schüffner's dots. Middle row:
Plasmodium malariae
. The ribbon shape of the trophozoite (does not always occur) and the shape of the schizont (“daisy”) is typical. Bottom row:
Plasmodium falciparum
. The delicate, relatively small ring shapes and the banana-shaped gametocytes are characteristic here. Maurer's clefts are shown in the older signet ring stages and in the young trophozoites. Note that only rings and gametocytes are usually found in the blood smear.
P. ovale
is not shown because the stages have the same appearance as those of
P. vivax
. (Courtesy of Bayer AG Leverkusen, from
The Microscopic Diagnosis of Tropical Diseases
(1955).)
Figure 2.63 Steps in the invasion of an erythrocyte by a
Plasmodium knowlesi
merozoite. Gk, Glycocalyx; mj,
moving junction
; Mn, micronemes; N, nucleus; PV, parasitophorous vacuole; Rh, rhoptries. From Hausmann, Hülsmann, Radeck (2003) Protistology, with permission from Scheizerbart'sche Verlagshandlung, Stuttgart, www.scheizerbart.de.
Figure 2.65 Distribution of
Plasmodium vivax
and
Plasmodium falciparum
. (From Global Malaria Mapper 2016, with kind permission.)
Figure 2.66 Types of fever in Malaria tropica, tertiana und malariae. (From W. Lang (1993),
Tropenmedizin in Klinik und Praxis
; by kind permission of Georg Thieme, Publishers, Stuttgart.)
Figure 2.64 Stages of
Plasmodium falciparum
. (a) Liver schizont in a histological section. (b) Ring stages in the blood. (c) Gametocyte in a blood smear. (Images: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 2.67 Children with splenomegaly caused by Malaria tropica – the photo was taken in a West African village. The second child from the left has an umbilical hernia, which was not caused by malaria. (Image: R. Lucius.)
Figure 2.68 Cytoadherence of
Plasmodium falciparum
-infected erythrocytes. (a) Two erythrocytes adhere to an endothelial cell (EM image). (b) Higher resolution of (a). Note the strands of PfEMP1 between the knobs of the erythrocyte and the membrane of the endothelial cell. (c) SEM image of knobs on the surface of an infected erythrocyte. (Images: Courtesy of D. Ferguson, contributed by P. Horrocks
et al
. (2005) J. Cell Sci. 118: 2507–2518.)
Figure 2.69 Schematic representation of cytoadherence of
Plasmodium falciparum
-infected erythrocytes.
Gray
-highlighted erythrocytes are infected. They express PfEMP1 proteins, which bind to different ligands on endothelial cells, erythrocytes, and/or IgM and IgG in the plasma. Specific antibodies against PfEMP1 can block this binding process, resulting in clinical immunity. PfEMP1, Plasmodium falciparum erythrocyte membrane protein 1; CD36, CSA, ICAM-1, ELAM-1, thrombospondin and CD31 are cell surface components. (Adapted from Schlichtherle
et al
. (1996) Parasitology Today 12, 329–332.)
Figure 2.70 Prevalence of malaria in different age-groups changed. (Adapted from Wyler, D.J. (1990)
Modern Parasite Biology
, W. H. Freeman & Company, New York.)
Figure B2.4
Figure 2.71 Life cycle of
Babesia divergens
. (a) Sporozoite. (b) Invasion of an erythrocyte. (c) Schizogony. (d) Merozoite. (e) Macrogametocyte. (f, g) Ray bodies. (h) Microgametocyte. (i, j) Ray bodies. (k) Fusion of the ray bodies. (l) Zygote. (m, n) Formation of kinete in intestinal epithelial cell of the tick. (o) Kinete. (p, q) Multiple divisions in somatic cells with formation of other kinetes. (r) Kinete. (s) Sporozoite formation in the salivary gland. (Adapted from Mehlhorn, H. (ed.) (1988) Parasitology in Focus, Springer-Verlag, Heidelberg.)
Figure 2.72 Infection of cells with
Babesia
and
Theileria
. (a) Blood smear of a cow with
Babesia divergens
in erythrocytes (by kind permission of H. Mehlhorn). (b) Blood smear with
Theileria parva
in erythrocytes. (Image by Archive of the Department of Parasitology, University of Hohenheim). (c) T lymphocytes infected with schizonts of
Theileria parva
. (Image: Courtesy of D. Dobbelaere.)
Figure 2.73 Life cycle of
Theileria parva
. (a) Sporozoite. (b) Schizont in a lymphocyte. (c, d) Division of the lymphocyte with simultaneous division of the schizont. (e) Merozoite. (f) Schizogony in the erythrocyte. (g) Merozoite. (h–j) Macrogametocyte. (k) Macrogamete. (l–n) Microgametocyte. (o) Microgamete. (p) Zygote in intestinal epithelial cells of the tick. (q, r) Formation of kinetes. (s) Kinete. (t) Formation of sporozoites in the salivary gland. (Adapted from Mehlhorn, H. (ed.) (1988) Parasitology in Focus, Springer-Verlag, Heidelberg.)
Figure 2.74 Stages of
Balantidium coli
. (a) Schematic diagram of a trophozoite. Zs, cytostome; Ma, macronucleus; Mi, micronucleus; Nv, food vacuoles; PV, pulsating vacuole; Zp: =Cytopyge = cell anus. (b) Cyst from the feces of a pig. (Image: Courtesy of B. Bannert.)
Figure 2.75 Life cycle of
Ichthyophthirius multifiliis
. (a) Theront. (b, c) Trophont. (d) Cyst. (e) Tomites, which will break free of the cyst shell.
Figure 2.76
Ichthyophthirius multifiliis
. (a) Trophont, SEM image: Courtesy of W. Foissner. (b) Young eel with white spot disease. (Image: H. Taraschewski.)
Figure 2.77 Trophozoite of
Trichodina
sp. (a) SEM image: W. Foissner. acs, adoral cilial spiral; oacc, outer adoral cilial crown; lc, lateral cilia. (b) Drawing of
T. myicola
, semi-schematic. Part of the foreground has been omitted to show the structure of the ventral cilial crowns. PV, pulsating vacuole; Ma, Macronucleus, Mi, Micronucleus, Cs, Cytostome, Fv, Food vacuole. (From Hausmann, Hülsmann, Radeck (2003) Protistology, with permission from Scheizerbart'sche Verlagshandlung, Stuttgart, www.schweizerbart.de.)
Chapter 3: Parasitic Worms
Figure 3.1 Phylogeny of the Metazoa (according to Blaxter, M.L. (2003)
Adv. Parasitol
.,
54
, 101–195, some taxa omitted). Taxa containing parasites dealt with in this book are in
bold.
Figure 3.41 Eggs and larva of parasitic worms to be detected in feces. (a)
Dicrocoelium dendtriticum
, (b)
Fasciola hepatica
, (c)
Hymenolepis nana
, (d)
Taenia
sp., (e)
Moniezia expansa,
(f)
Capillaria aerophila,
(g)
Trichuris suis
, (h)
Enterobius vermicularis
, (i)
Ascaris lumbricoides
, (j)
Ancylostoma duodenale
, (k)
Haemonchus contortus
, (l) L1 of
Dictyocaulus viviparus
. (By courtesy of Janssen Animal Health, b2340 Beerse, Belgium. Image (I): Courtesy of Thomas Schnieder.)
Figure 3.2 Neodermis. (a–c) Schematic presentation of the development. (d) Cross section of the neodermis of a digenean trematode.
Figure 3.3 Typical life cycle of a digenean trematode (water-bound, marine). First intermediate host: marine snail. Depending on the taxon, development occurs through either sporocysts (black arrows) or rediae (gray arrows). The second intermediate host (a fish in this case) is an animal being part of the food chain of the definitive host (a seal in this case). Multiple arrows: asexual propagation of larval stages. Wave symbols: free swimming larval stages.
Figure 3.4 Developmental stages of Digenea. (a) Structure of a miracidium. (b) Epithelial cells of a miracidium, family Fasciolidae with five tiers of 6, 6, 3, 4, and 2 cells. (c) Epithelial cells of a miracidium (family Schistosomatidae) with four tiers of 6, 8, 4, and 3 cells. The cilia are omitted for ease of viewing. (d) Sporocyst of a
Schistosoma
species. (e) Redia of
Fasciola hepatica
filled with germ balls. (f) Schematic pattern of the cercarial excretory system, flame cell formula for the left side: (2+2)+2, for the right side: (3+3+3)+3+3). (g–l) Types of cercariae. (g) gymnocephalic amphistomous (
Paramphistomum
), (h) gymnocephalic xiphidiocerc (
Dicrocoelium
), (i) gymnocephalic lophocerc (
Psilochasmus
), (
j
) microcerc xiphidiocerc (
Paragonimus
), (k) furco-trichocerc (
Alaria
), (l) furco-zystocerc (
Azygia
).
Figure 3.5 Adult Digenea. (a)
Dicrocoelium dendriticum
. (b)
Opisthorchis felineus
. (c)
Paragonimus westermani
. (d)
Diplostomum spathaceum
. (e) Size proportions of the species depicted, from left to right:
P. westermani, D. dendriticum, D. spathaceum.
Figure 3.6 Genital organs of Digenea. (a) Female. (b) Male.
Figure 3.7
Schistosoma mansoni
, male and female in copula. (Top) Anterior end of male. (Left) Slender anterior part of female. (Image: Archive of the Department of Molecular Parasitology, Humboldt-University, Berlin.)
Figure 3.8 Life cycle of
Schistosoma mansoni
. (a) Pair of adults in humans. (b) Embryonated egg. (c) Miracidium. (d) Furcocercous cercaria having developed within sporocysts in a planorbid freshwater snail
Biomphalaria glabrata
.
Figure 3.9 Some details of human-pathogenic schistosomes. (a) Anterior end of a female
S. mansoni
. (b) Genital organs of female. (c) A male of
S. mansoni
, body laterally extended (os, oral sucker; vs, ventral sucker; go, genital opening; u, uterus; o, ovary; vit, vitallarium; oo, ootype; Mg, Mehlis' gland; vd, vitelline duct; t, testes; g, gut). (d) Embryonated egg of
S. mansoni
. (e) Intermediate host of
S. mansoni
:
Biomphalaria glabrata
. (f) Embryonated egg of
S
.
haematobium
. (g) Intermediate host of
S. haematobium
:
Bulinus truncatus
. (h) Embryonated egg of
S. japonicum
. (i) Intermediate host of
S. japonicum
: snail
Oncomelania hupensis
.
Figure 3.10 Eggs of
Schistosoma japonicum
(a),
Schistosoma haematobium
(b),
Schistosoma mansoni
(c). (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.11
Schistosoma mansoni
, antibody-coated schistosomulum with adhering eosinophils. The antibody-dependent cellular cytotoxicity is fatal for the parasite within 24–48 h. (Image: Courtesy of A.E. Butterworth)
Figure 3.12 Cross-section of an egg of
Schistosoma mansoni
in mouse liver surrounded by a granuloma. (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.13 Tegumental outer surface of adult
Schistosoma mansoni
. In the lowest magnification (a), the tegument is visible as a dark band surrounding an adult female
S. mansoni
worm (Bar = 20 µm). Panel (b) shows an enlargement of the area indicated by the white rectangle in panel (a). The folds in the outer tegumental membranes (surface pits) increase the area of the epithelium. The arrow indicates a multilamellar body moving from the cell body toward the tegument in a cytoplasmic connection spanning the superficial muscle layers (bar = 1 µm). Panel (c) shows a higher magnification image of the double phospholipid bilayer of the tegumental membranes (Bar = 75 nm). (From Van Hellemont
et al
. (2006)
Int. J. Parasitol
.,
36
, 691–699, with kind permission of Elsevier.)
Figure 3.14 Infection of the terrestrial pulmonate snail
Succinea putris
with
Leucochlori-dium paradoxum
. The left tentacle is filled with a pulsating sporocyst. (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.15 Life cycle of
Diplostomum spathaceum
. (a) Adult fluke. (b) Definitive host, the black-headed gull. (c) Unembryonated egg. (d) Embryonated egg. (e) Miracidium. (f) First intermediate host, a freshwater pulmonate
Radix peregra
. (g) Mother sporocyst. (h) Daughter sporocyst. (i) Furcocercous cercaria. (j) Cercaria in swimming position. (k) Freshwater fish. (l) Metacercaria (diplostomulum) in the eye of a fish.
Figure 3.16 Life cycle of
Fasciola hepatica
. (a) adult trematode in the bile ducts of ruminants (only the first part of the intestinal ceca are drawn). (b) Unembryonated egg. (c) Embryonated egg. (d) Miracidium. (e) Gymnocephalic cercaria developing within rediae in the first intermediate host
Galba truncatula
(Pulmonata). (f) Metacercariae on water plant. (g) Cross section of a metacercaria.
Figure 3.57
Wuchereria bancrofti
, lymphoedma (elephantiasis) of leg. (Image: Courtesy of Achim Hörauf.)
Figure 3.17
Fasciola hepatica
, stained whole mount (see also Figure 3.16a). (Image: Archive of the Department of Parasitology, University of Hohenheim)
Figure 3.18 Section through a cattle liver with
Fasciola hepatica
. Note the thickened walls of the bile ducts. Right middle: a whole fluke can be seen leaving a bile duct. (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.19 Life cycle of
Opisthorchis felineus
. (a) Adult trematode in the bile ducts of humans (see also Figure 3.9d). (b) Embryonated egg. (c) Lophocercous cercaria in the first-intermediate host snail
Bithynia leachi
. (d) Cercaria in characteristic floating position. (e) Enlarged metacercaria in the musculature of second intermediate host, a carp.
Figure 3.20 Stained whole mounts of the cat liver fluke
Opisthorchis felineus
(a) and the Chinese liver fluke
O. sinensis
with egg (b). Note the very different shapes of the testes in the hind body and of the ovary situated anterior to them. The seminal receptacle is found adjacent and in front of the ovary (not clear in
O. sinensis
). (Images: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.21 Life cycle of
Paragonimus westermani.
(a) Adult trematode in the lung of humans (see also Figure 3.5e). (b) Unembryonated egg. (c) Embryonated egg. (d) Miracidium. (e) Mircrocercous cercaria developing within rediae in the first-intermediate snail host
Semisulcospira
sp. (f) Enlarged metacercaria in a fresh water crab (black: excretory bladder, white and curled: intestinal ceca).
Figure 3.22 Life cycle (of
Dicrocoelium dendriticum
. (a) Adult trematode in the bile ducts of ruminants (see also Figure 3.9a). (b) Embryonated egg with fully developed miracidium. (c) Xiphidiocercous cercaria developing in sporocysts in the first-intermediate host
Zebrina detrita
(Pulmonata). (d) Second intermediate host
Formica
sp. eating from a slime ball released by the snail. (e) Ant's crop with melanized dots left behind from cercariae having penetrated its wall. (f) Ant clinging to a leaf with its mandibles. (g) “Brain worm” in the ant's subesophageal ganglion. (h) Infective metacercaria from the hindbody of the ant.
Figure 3.23
Zebrina detrita
with slime ball of
Dicrocoelium denriticum.
(Image: Loos-Frank.)
Figure 3.25 Types of metacestode stages of the Eucestoda (schematic).
Figure 3.26 Formation of genital organs in a tapeworm, in this case of
Taenia crassiceps
. Organs become visible for the first time in the numbered proglottids as follows: 39, first testes; 42, vagina; 57, vagina and vas deferens; 60, two-lobed ovary, vitellarium posterior; 70, uterus; 89, branched uterus; 126, gravid uterus with eggs.
Figure 3.27 Life cycle of
Diphyllobothrium latum
. (a) Anterior end of an adult worm. (b) Unembryonated operculated egg. (c) Embryonated egg containing a ciliated oncosphere, the coracidium. (d) Free-swimming coracidium. (e) Procercoid in the first intermediate host
Cyclops
(copepod). (f) Plerocercoid in the second intermediate host, a small fish. (g) Same larval form in paratenic host: pike. (h) Gravid proglottid.
Figure 3.28
Mesocestoides leptothylacus
. (a) Mature proglottid (vagina omitted). (b) Gravid proglottid. (c) Cirrus pouch with long thin cirrus, common genital opening at posterior end. (d) Scolex. (e) Tetrathyridium.
Figure 3.24 (a) Scolex of a tapeworm with two crowns of hooks and two of the four suckers. Note beginning of the proliferation zone in the lower part. (
Hydatigera taeniaeformis,
REM image: Courtesy of Eye of Science.) (b, c) Stained whole mount of a mature proglottid of
Taenia polyacantha
, containing male and female reproductive organs. (Image: Loos-Frank.)
Figure 3.29
Hymenolepis diminuta
, the rat tapeworm. (a) Eggs. (b) Cysticercoid from the beetle
Tenebrio molitor
. (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.30 Life cycle of
Rodentolepis nana
. (a) Scolex of the adult tapeworm in the human small intestine (note the presence of scolex hooks). (b) Egg containing oncosphere and polar filaments. (c) Cysticercoid in intestinal villi. (d) Cysticercoid in hemocoele of a beetle. (e) Mature proglottid of
R. nana
. (f) Scolex hook of
R. nana
. (g) Cysticercoid of
Hymenolepis diminuta
from a beetle.
Figure 3.31
Rodentolepis nana
. (a) Cysticercoid from a beetle. (b) Cysticercoid in the duodenal villious of a mouse. (Images: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.32
Taenia crassiceps,
double crown of isolated scolex hooks. Large hooks are approximately 180 µm long. (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.33 Life cycles of
Taenia saginata
(inner circle)
and Taenia solium
(outer circle
)
. (a) Adult worm in the small intestine of humans. (b) Egg. (c) Cysticercus (invaginated). (d) Intermediate host. (e) Cysticercus (evaginated). Morphology of
T. saginata
. (f) Scolex (no hooks!). (g) Mature proglottid. (h) Genital opening (on left side). (i) Gravid proglottid. Morphology of
T. solium
: (j) Scolex. (k) Scolex hooks. (l) Mature proglottid (note: the additional ovary lobe). (m) Genital opening (on right side). (n) Gravid proglottid.
Figure 3.34
Echinococcus granulosus
, hydatid with secondary and tertiary brood capsules in a human liver. (Image: Piekarski (1954)
Lehrbuch der Parasitologie
. Springer Verlag, Heidelberg.)
Figure 3.35 Sonography of human livers with
metacestodes of Echinococcus
: (a) bladder-like hydatid (arrow) of
Echinococcus granulosus
. (b) compact larval mass (arrow) of
Echinococcus multilocularis
. (Images: Courtesy of P. Kern.)
Figure 3.37 Life cycle of
Echinococcus multilocularis
. (a) Adult worm in the intestine of a fox. (b) Egg with oncosphere. (c) Humans as accidental intermediate hosts. (d) Larval mass in the true intermediate host, the common vole. (e) Section of vole liver with chambers containg protoscolices. (f, g) Protoscolices from a vole liver.
Figure 3.36
Echinococcus multilocularis
, adult from fox intestine. (Image: Archive of the Department of Parasitology, University of Hohenheim.)
Figure 3.38 Life cycle of
Plagiorhynchus cylindraceus
with three possible routes of transmission. (a, outer circle) Short two-host life cycle with the final host starling and the intermediate host pill bug
Armadillidium vulgare
(Crustacea, Isopoda). (b, middle circle) “postcyclic” transmission with hedgehog killed by traffic and carrion-eating bird as final hosts. (c, inner circle) three-host life cycle with shrew as paratenic host and barn owl as final host. For further explanations see text. (After Skuballa
et al
. (2010).
Parasit. Res
.
106
, 431–438.)
Figure 3.39 Acanthocephala: (a) Diagram of a female with floating ovaries (eggs not depicted). (b) Diagram of a male Palaeoacanthocephalan. (c) Proboscis of a thorny-headed worm. (d) Egg with acanthor larva. (e) Acanthella (on the outer right side: apex of the acanthor). (f) Ovary from the body cavity of a female worm.
Figure 3.40 Acanthocephala. Presoma with proboscis of various species. (1)
Neoechinorhynchus rutili
, (2)
Paratenuisentis ambiguus
, (3)
Acanthocephalus anguillae
, (4)
A. lucii
, (5)
Echinorhynchus truttae
, (6)
Pomphorhynchus laevis
. B, Bulbus; FW, fibrous wall between the tegument of presoma and metasoma; N, neck; P, proboscis. (SEM image: Courtesy of H. Taraschewski.)
Figure 3.49 Life cycle of
Haemonchus contortus
. Female (a) and male (b) in abomasum of sheep. Young (c) and fully developed (d) egg in feces. L1 (e) and L2 (f) in feces. Sheathed L3 (g) leaves feces and crawls onto plants (g). When eaten by sheep it sheds its sheath to become an L4 (i).
Figure 3.56 Life cycle and morphology of
Wuchereria bancrofti
. (a) adult male, (b) adult female, (c) elephantiasis, (d) microfilariae, (e) L2 larva, (f) female mosquito, (g) L3 larva.
Figure 3.42 Structures of nematodes. (a) Scheme of a didelphic female. (b) Scheme of a male. (c) Cross section of an
Ascaris
male. (d) Copulatory bursa of
Trichostrongylus
(two copulatory spicules). (e) Position of the copulatory bursa of Strongyloidea (the male copulatory bursa envelops the female body at her genital opening). (f) Cervical alae of
Toxocara cati
.
Figure 3.51 Life cycle of
Ascaris lumbricoides
. Circle: in eggs, released by humans, larval stages develop in the external environment to the infective L3, which then has to be ingested. Within humans: (1) L3 hatches in the small intestine. (2) Following penetration larvae are carried by venous blood via intestinal wall and portal vein to the liver, where they molt to L4. (3) Transportation via vena cava to the right ventricle and (4) to the lung. (5) L4 penetrate the alveolar walls, are coughed up into the trachea, swallowed and carried to the small intestine, where the last moult occurs. (a) Hand with adult male and female. (b) Head region with three lips and oral opening. (c) Distal end of male with the two spicules. Combined after several authors.
Figure 3.59 Life cycle and morphology of
Onchocerca volvulus
. (a) Adult males and females in connective tissue of humans. (b) Microfilaria in skin. (c) Blackfly (
Simulium
). (d) L2, sausage stage. (e) Infective L3. (f) Mouth region of adult with papillae and mouth opening. (g) Anterior end of female with vagina. (h) Posterior end of male with the two unequal spicules.
Figure 3.43 Life cycle of
Trichinella spiralis
. (A) (above) Pig, (A) (below) Rat. (a) male worm. (b) female worm, giving birth to (b) larvae, which settle (c) in skeletal muscle. Cycle repeats if pig eats rat, if rat eats pig slaughtering waste, or humans (B) eat infected pork. All stages develop also in man, who is, though, a dead-end host.
Figure 3.44
Trichinelloidea
. (a)
Trichuris trichiura
, female, (b)
T. trichiura
, posterior end of male, (c)
Trichinella spiralis,
posterior end of male, (d) muscle larva of
T. spiralis
, nurse cell complex surrounded by blood vessels, (e)
T. spiralis
, cross section of muscle larva.
Figure 3.45
Trichinella spiralis
, L1 digested from infected muscle tissue. (EM image: Courtesy of Eye of Science.)
Figure 3.46 Life cycle of
Strongyloides stercoralis
(L in cycle = larval stages). (a) Parasitic female. (b) Free-living female. (c) Free-living male. (d) Anterior end of filariform larva with typical esophagus. (e) Anterior end of rhabditiform larva with typical esophagus.
Figure 3.47 Life cycle of
Necator americanus
. (a) female, (b) male, (c) young egg, to develop in human feces, (d) L1, (e) L2, (f) in soil and feces. Sheathed L3 (g) invades the skin (h). Migration in human body not shown.
Figure 3.48 Hookworms (Ancylostomatidae). (a) Mouth capsule of
Ancylostoma duodenale
. (b) Mouth capsule of
Necator americanus
. (c) Copulatory bursa of
A. duodenale
with spicules.
Figure 3.50
Haemonchus contortus
. (a) Male and female at equal magnification (arrow: valvular flap). (b) Anterior end with cervical papillae. (c) Copulatory bursa with spicules. (d) Mouth capsule with hook and muscular pharynx. (e) Female genital opening with vulvar process (arrow). (f) Egg.
Figure 3.52 Life cycle of
Toxocara canis
(rectangular frames in cycle refer to worm stages shown in boxes). (a) Infective L3. (b) Head region of adult with cervical alae, shaded in grey.
Figure 3.54
Dracunculus medinensis
. (a) X-ray of female in human leg. (From Piekarski (1954)
Lehrbuch der Parasitologie
. Spinger-Verlag Heidelberg.) (b) Aesculapian staff.
Figure 3.53
Dracunculus medinensis
. (a) L1 released into water. (b) L3 in the body cavity of a copepode. (c) Extraction of a female worm.
Figure 3.55
Enterobius vermicularis
. (a) Female, didelphic. (b) Posterior part of a male worm. (c) Newly released egg. (d) Egg with infectious L3 stage. (e) Egg of
Oxyuris equi
.
Figure 3.58 Stages of Onchocercidae. (a) Sheathed microfilaria of
Wuchereria bancrofti
. (b) Sheathed microfilaria of
Loa loa
. (c) L2 stage larvae of
W. bancrofti
. (d) A mouse macrophages attack a microfilaria of the rodent filaria
Acanthocheilobema viteae
. EM image: Department of Molecular Parasitology, Humboldt Universität.
Figure 3.60
Onchocerca volvulus
. (a) Skin nodules, Onchocercoma. (b) Sowda, a clinical picture of onchodermatitis. (Images: Courtesy of: Dietrich Büttner.)
Chapter 4: Arthropods
Figure 4.1 Phylogeny of arthropods. (After Giribet, G. and Edgecombe, G.D. (2013) in
Arthropod Biology and Evolution: Molecules, Development, Morphology
(eds A. Minelli, G. Boxshall, and G. Fusco), Springer, pp. 17–40.)
Figure 4.2 Acari: Mesostigmata. (a) Female (ventral aspect). (b) Gnathosoma in cross section. (c) Pretarsus.
Figure 4.3 Life cycle of
Varroa destructor
. (a) Female mite in brood cell of worker bee. (b) From eggs laid on a bee larva one male and up to six female mites develop. (c) Copulation within brood cell. (d) Fertilized female mite enters the outside world when adult bee hatches. (e) Mites suck hemolymph from flying bee. (f) Female of
Varroa
. (g) Male of
Varroa.
Figure 4.4 Metastigmata, ticks. (a)
Ixodes ricinus
, female, dorsal view. (b)
I. ricinus
female, ventral view. (c) Capitulum with mouthparts of
I. persulcatus
, dorsal view. (d) Tarsus of a tick with Haller's organ. (e) Tick chelicera. (f) Hypostome of female
I. ricinus
. (g) Hypostome of male
I. ricinus
. (h) Male of
Rhipicephalus sanguineus
, ventral view. (i) Capitulum of
R. sanguineus
, ventral view. (j) Female
Ornithodoros moubata
, ventral view.
Figure 4.5
Ixodes ricinus. (
a) Young female, nymph, and two six-legged larvae. (b) Young female questing for place of penetration. (c) Replete female. (Images: Courtesy of Heiko Bellmann.)
Figure 4.6
Ixodes ricinus
. (a) Capitulum, frontal view, below: hypostome, above: chelicerae, right and left: pedipalps, on capitulum: the two areae porosae. (b) Hypostome, ventral view, tip of a chelicera underneath left-hand side. (EM Images: Courtesy of Eye of Science.)
Figure 4.7 Female of
Dermacentor
sp. (Image: Courtesy of Heiko Bellmann.)
Figure 4.8 Female
Rhipicephalus sanguineus
. (EM Image: Courtesy of Eye of Science.)
Figure 4.9 Acari, Prostigmata. (a) Female
Demodex folliculorum
, ventral view. (b) Egg of
D. folliculorum
. (c) Egg of
D. brevis
. (d)
D. canis
sticking head first within a hair follicle from the skin of a dog. (Image: Courtesy of Eye of Science.)
Figure 4.10 Life cycle of
Neotrombicula autumnalis
. (a) Replete larva (chigger) on humans. (b) Hypobiotic protonymph. (c) Free-living deutonymph. (d) Hypobiotic tritonymph. (e) Adult mite. (f) Egg. (According to Jones, B.M. (1951) Parasitology 41, 229–248.)
Figure 4.11 (a)
Sarcoptes scabiei
var.
suis
, frontal view from above. Some bristles on the back lost. (EM Image: Department of Molecular Parasitology, Humboldt Universität.) (b) Female
Sarcoptes scabiei
