Human parasites diagnosis treatment prevention

Heinz Mehlhorn

Human
Parasites
Diagnosis, Treatment,
Prevention


Human Parasites


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Heinz Mehlhorn

Human Parasites
Diagnosis, Treatment, Prevention


Heinz Mehlhorn
Department of Parasitology
Heinrich Heine University
D€
usseldorf, Germany
This is an updated translation of the 7th edition of the German book “Die Parasiten des
Menschen” (2012) published by Springer Spektrum.

ISBN 978-3-319-32801-0
ISBN 978-3-319-32802-7
DOI 10.1007/978-3-319-32802-7

(eBook)

Library of Congress Control Number: 2016941058
# Springer International Publishing Switzerland 2016
This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of
the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations,
recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission
or information storage and retrieval, electronic adaptation, computer software, or by similar or
dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this
publication does not imply, even in the absence of a specific statement, that such names are exempt
from the relevant protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this
book are believed to be true and accurate at the date of publication. Neither the publisher nor the
authors or the editors give a warranty, express or implied, with respect to the material contained
herein or for any errors or omissions that may have been made.
Cover illustration: Scanning electron micrograph of a couple of the species Schistosoma mansoni. See
also Fig. 4.1 a in this book. Photo Heinz Mehlhorn
Printed on acid-free paper
This Springer imprint is published by Springer Nature
The registered company is Springer International Publishing AG Switzerland


This edition is dedicated to my wife Birgit
on the occasion of our 42th wedding
anniversary.
February 2016

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Preface

Parasites threaten still today the health of humans and their animals, although
considerable progress had been achieved within the last century. However,
phenomena such as globalization with the daily transportations of millions of
containers and humans from one end of the world to the other make it easy
for agents of disease and their vectors to suddenly occur at places which were
thought to be safe. Thus, it is not astonishing that worldwide so-called
emerging diseases occur at a formerly unbelievable speed. The ongoing climate
change additionally offers better conditions for many agents of disease and
their vectors to enter and to settle in formerly untouched regions.
Therefore, it is needed to observe intensively the development and progress of
such aggressive organisms. Parasites belonging to the groups of protozoans,
worms or arthropods may harm humans and their animals directly by entering
them or indirectly as blood suckers, which may transmit other agents of diseases
such as “viruses, bacteria or even parasites.
Parasite-derived diseases cause still today a considerable number of deaths,
endangering millions of humans around the world, since still today the
measurements to control parasites are poor in many cases. The number of treatment
failures even increases constantly due to the fact that resistances of the parasites
against older medicaments are rising.
Parasitology is now an interdisciplinary science, since parasites are animals
which attack humans and animals. Thus, parasitic problems have to be considered
by physicians, veterinarians, biologists, pharmacists, chemists, epidemiologists,
etc., in order to develop successful control measurements.
The German Rudolf Leuckart (1822–1898) (Fig. 1) was the first to propose that
parasitology should handle all perspectives of parasites as an own interdisciplinary

field of science and not as an addendum to human or veterinary medicine.
This textbook considers the problems of humans with parasites. In order to make
it easy to find quickly the relevant information, each chapter on a parasite is
subdivided into 12 sections:
1. Name
2. Geographic distribution/epidemiology
3. Biology/morphology
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viii

Preface

Fig. 1 Medal showing Rudolf Leuckart (1822–1898), the “founder” of parasitology as a separate
branch connecting the knowledge of physicians, veterinarians and biologists. The German Society
of Parasitology honours internationally known scientists for their contributions in the fight against
parasites by awarding the Rudolf Leuckart medal

4.
5.
6.
7.
8.
9.
10.
11.
12.

Symptoms of disease

Diagnosis
Pathway of infection
Prophylaxis
Incubation period
Prepatency
Patency
Therapy
Further reading

More and detailed information is contained in the recently published 4th edition
of Mehlhorn H (ed.) (2016) Encyclopedia of Parasitology, Springer, Berlin,
New York. This book and an online version is a product of cooperation with
more than 50 colleagues worldwide.
D€usseldorf
April 2016

Heinz Mehlhorn


Acknowledgement

This English version is based on the 7th edition of a textbook in German
language. This volume condenses the contents of the common books and
publications with my colleagues D. D€uwel, D. Eichenlaub, A.O. Heydorn,
S. Klimpel, T. L€oscher, W. Peters, G. Piekarski, W. Raether, E. Schein,
E. Scholtyseck and many other parasitologists of my and foreign groups. I am
very grateful for their intense cooperation during the last 40 years.
My thanks go also to Dr. Volker Walldorf, who contributed a broad spectrum
of drawings. My wife Birgit Mehlhorn helped to collect literature and to translate
this volume into English. Mrs. Inge Schaefers and Mrs. Susanne Walter brought

the text in the present form. In addition, Mrs. Walter and Dipl. Ing. Isabelle
Mehlhorn organized the final presentation of the figures of this book.
Mrs. Andrea Schlitzberger and Mr. Lars K€orner at Springer Publishers
(Heidelberg) cared for the final version of this book, which hopefully makes it
easy for the reader to find quickly the wished information.
D€
usseldorf
March 2016

Heinz Mehlhorn

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Contents

1

The Phenomenon Parasitism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.1
Host Specificity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2
Ontogenetic Development of Parasites . . . . . . . . . . . . . . . . . . . .
1.3
Follow-Up of Different Generations . . . . . . . . . . . . . . . . . . . . .
1.4
Speed of Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1.5
Adaptations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.6
Pathogenicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.7
Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.8
Parasite Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Further Reading . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1
3
3
4
4
5
7
8
8
11

2

Which Parasites Are Important for Humans? . . . . . . . . . . . . . . . . .
2.1
Groups of Parasites . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2
Organs of Humans and Their Typical (Common) Parasites . . . . .

13

13
15

3

Protozoans Attacking Humans . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1
History and Relations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2
Trichomonas vaginalis (Trichomoniasis) . . . . . . . . . . . . . . . . . .
3.3
Flagellata of the Intestine . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.3.1
Trichomonas tenax . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.3.2
Entamoeba gingivalis . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4
Giardia lamblia (syn. G. duodenalis, G. intestinalis) . . . . . . . . .
3.5
Trypanosoma brucei Group (African Trypanosomiasis) . . . . . . .
3.6
South American Trypanosomes . . . . . . . . . . . . . . . . . . . . . . . . .
3.6.1
Trypanosoma cruzi (Chagas’ Disease) . . . . . . . . . . . . . .
3.6.2
Trypanosoma rangeli . . . . . . . . . . . . . . . . . . . . . . . . . .
3.7
Leishmania species (Agents of the Skin, Mucosa
and American Leishmaniasis) . . . . . . . . . . . . . . . . . . . . . . . . . .
3.8

Leishmania donovani complex (Visceral Leishmaniasis) . . . . . . .
3.9
Entamoeba histolytica (Entamobiasis, Amoebiasis and
Bloody Flu) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

19
19
20
24
26
26
27
30
37
37
42
43
52
55

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Contents

3.10

Facultatively Pathogenic Amoebae . . . . . . . . . . . . . . . . . . . . . .

3.10.1 Species of the Genera Acanthamoeba, Naegleria
and Balamuthia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.10.2 Dientamoeba fragilis . . . . . . . . . . . . . . . . . . . . . . . . . .
3.10.3 Apathogenic Amoebae or with a Low-Grade
Pathogenicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.11 Isospora belli . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.12 Cyclospora cayetanensis (Cyclosporiasis) . . . . . . . . . . . . . . . . .
3.13 Cryptosporidium Species (Cryptosporidiosis) . . . . . . . . . . . . . . .
3.14 Sarcosporidia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.14.1 Sarcocystis Species Inside the Human Intestine
(S. suihominis, S. bovihominis) . . . . . . . . . . . . . . . . . . .
3.14.2 Sarcocystis Species in Human Muscles . . . . . . . . . . . . .
3.15 Toxoplasma gondii (Toxoplasmosis) . . . . . . . . . . . . . . . . . . . . .
3.16 Plasmodium Species (Malaria) . . . . . . . . . . . . . . . . . . . . . . . . .
3.17 Babesia Species (Babesiasis, Babesiosis) . . . . . . . . . . . . . . . . . .
3.18 Balantidium coli (Balantidiasis) . . . . . . . . . . . . . . . . . . . . . . . . .
3.19 Pneumocystis jiroveci (Pneumocystosis) . . . . . . . . . . . . . . . . . .
3.20 Blastocystis Species (Blastocystosis) . . . . . . . . . . . . . . . . . . . . .
3.21 Microsporidia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.21.1 Enterocytozoon bieneusi (Enterocytozoonosis) . . . . . . .
3.21.2 Septata intestinalis . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.22 Encephalitozoon cuniculi (Encephalitozoonosis) . . . . . . . . . . . .
3.23 Encephalitozoon intestinalis (Encephalitozoonosis) . . . . . . . . . .
3.24 Nosema connori (syn. conneri) (Nosematosis) . . . . . . . . . . . . . .
Further Reading (Joint List for This Chapter) . . . . . . . . . . . . . . . . . . . .
4

Worms of Humans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1
What Are Worms? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

4.2
Trematodes (Flukes) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.1
Schistosoma haematobium, Bladder Fluke
(Bladder bilharziasis) . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.2
Schistosoma mansoni and Other Species
(Intestinal Bilharziasis, i.e. Intestinal Schistosomiasis) . . .
4.2.3
Clonorchis and Opisthorchis Species, Chinese River
Fluke (Clonorchiasis, Opisthorchiasis) . . . . . . . . . . . . .
4.2.4
Paragonimus Species (Paragonimiasis) . . . . . . . . . . . . .
4.2.5
Fasciolopsis buski (Fasciolopsiasis) . . . . . . . . . . . . . . .
4.2.6
Fasciola hepatica (Fascioliasis) . . . . . . . . . . . . . . . . . .
4.2.7
Dicrocoelium dendriticum (syn. lanceolatum)
(Dicrocoeliasis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.8
Heterophyes Species (Heterophyiasis) . . . . . . . . . . . . . .
4.2.9
Metagonimus yokogawai and Related Species
(Metagonimiasis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.10 Echinostoma Species (Echinostomiasis) . . . . . . . . . . . .

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Contents

xiii

Gastrodiscoides hominis and Related Species
(Gastrodiscoidiasis) . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.12 Watsonius watsoni (Watsoniasis) . . . . . . . . . . . . . . . .
4.2.13 Nanophyetus Species (Nanophyetiasis) . . . . . . . . . . . .
4.2.14 Metorchis conjunctus (Meteorchiasis) . . . . . . . . . . . . .
4.2.15 Philophthalmus Species . . . . . . . . . . . . . . . . . . . . . . .
Tapeworms (Cestodes) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.1
Taenia solium, T. asiatica (Pork Tapeworm)
(Taeniasis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.2
Taenia saginata (Cattle Tapeworm) (Taeniasis) . . . . . .
4.3.3
Diphyllobothrium latum Species (Broad Tapeworm)
(Diphyllobothriasis) . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.4
Hymenolepis nana and Other Species
(Hymenolepiasis) . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.5
Echinococcus Species (Echinococciasis) . . . . . . . . . . .
4.3.6

Dipylidium caninum . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.7
Rare Tapeworms in the Intestine of Humans . . . . . . . .
4.3.8
Cysticercus Species (Cysticerciasis) . . . . . . . . . . . . . .
4.3.9
Coenurus Species . . . . . . . . . . . . . . . . . . . . . . . . . . .
Nematodes (Nematozoa, Roundworms) . . . . . . . . . . . . . . . . . .
4.4.1
Enterobius vermicularis (Enterobiasis) . . . . . . . . . . . .
4.4.2
Ascaris lumbricoides (Ascariasis) . . . . . . . . . . . . . . . .
4.4.3
Trichuris trichiura (Trichuriasis) . . . . . . . . . . . . . . . .
4.4.4
Ancylostoma and Necator Species
(Hookworm Disease, Ancylostomiasis, Necatoriasis) . .
4.4.5
Strongyloides stercoralis . . . . . . . . . . . . . . . . . . . . . .
4.4.6
Capillaria Species (Capillariasis) . . . . . . . . . . . . . . . .
4.4.7
Trichinella spiralis and Related Species
(Trichinellosis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.8
Angiostrongylus cantonensis (Angiostrongyliasis) . . . .
4.4.9
Angiostrongylus costaricensis (Angiostrongyliasis) . . .
4.4.10 Anisakis Species and Related Species (Anisakiasis) . . .
4.4.11 Gnathostoma Species (Gnathostomiasis) . . . . . . . . . . .

4.4.12 Toxocara Species (Toxocariasis) . . . . . . . . . . . . . . . .
4.4.13 Dictyophyme renale (Dictyophymiasis) . . . . . . . . . . . .
4.4.14 Ternidens deminutus (syn. Triodontophorus deminutus,
Globocephalus macaci) (Ternidens Disease) . . . . . . . .
4.4.15 Trichostrongylus Species (Trichostrongyliasis) . . . . . .
4.4.16 Wuchereria bancrofti (Lymphatic Filariasis) . . . . . . . .
4.4.17 Brugia malayi (Lymphatic Filariasis) . . . . . . . . . . . . .
4.4.18 Loa loa (Loiasis) . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.19 Onchocerca volvulus (Onchocerciasis) . . . . . . . . . . . .
4.4.20 Mansonella Species (Mansonelliasis) . . . . . . . . . . . . .
4.4.21 Dirofilaria Species (Dirofilariasis) . . . . . . . . . . . . . . .
4.2.11

4.3

4.4

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Contents

Dracunculus medinensis (Dracontiasis) . . . . . . . . . . . .
Wandering Nematodes in Humans . . . . . . . . . . . . . . .
Microfilariae: Larvae of Filarial Nematodes . . . . . . . .
Skin Mole (Creeping Eruption, Larva Migrans
Cutanea) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.26 Thelazia Species (Thelaziasis) . . . . . . . . . . . . . . . . . .
4.5
Worms Belonging to Further Animal Phyla . . . . . . . . . . . . . . .
4.5.1
Pentastomida (Pentastomiasis) . . . . . . . . . . . . . . . . . .
4.5.2
Macracanthorhynchus hirudinaceus
(Acanthocephaliasis) . . . . . . . . . . . . . . . . . . . . . . . . .
4.5.3
Leeches (Annelida) . . . . . . . . . . . . . . . . . . . . . . . . . .
4.6
Available Compounds, Methods and Means to Control
Protozoan and Helminthic Parasites . . . . . . . . . . . . . . . . . . . . .
Further Reading (Joint List for This Chapter) . . . . . . . . . . . . . . . . . . .

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. 272

Arthropods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.1
Scorpions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.2
Spiders (Arachnida) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3
Ticks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3.1
Hard Ticks (Ixodidae) . . . . . . . . . . . . . . . . . . . . . . . .
5.3.2
Argasidae (So-Called Soft or Leather Ticks) . . . . . . . .
5.3.3
Skin Reactions After Tick Bites . . . . . . . . . . . . . . . . .
5.3.4
Tick Paralysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3.5
Treatment of Tick Bites . . . . . . . . . . . . . . . . . . . . . . .
5.3.6
Transmission of Agents of Disease . . . . . . . . . . . . . . .
5.3.7
Protection from Tick Bites . . . . . . . . . . . . . . . . . . . . .
5.3.8
Further Reading (Tick) . . . . . . . . . . . . . . . . . . . . . . . .
5.4
Mites . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.4.1
Chicken Mites (Dermanyssidae) . . . . . . . . . . . . . . . . .
5.4.2

Rat Mites (Liponyssidae) and Related Species . . . . . . .
5.4.3
Trombiculidae (Chigger Mites) . . . . . . . . . . . . . . . . . .
5.4.4
Fur Mites (Cheyletiellidae) . . . . . . . . . . . . . . . . . . . . .
5.4.5
Scabies Mites (Sarcoptidae) . . . . . . . . . . . . . . . . . . . .
5.4.6
Follicle Mites (Demodicidae) . . . . . . . . . . . . . . . . . . .
5.4.7
House Dust Mites (Tyroglyphidae) . . . . . . . . . . . . . . .
5.5
Insects (Insecta, Hexapoda) . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.5.1
Fleas (Siphonaptera) . . . . . . . . . . . . . . . . . . . . . . . . .
5.5.2
Lice (Phthiraptera) . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.5.3
Bugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.5.4
Mosquitoes (Nematocera) . . . . . . . . . . . . . . . . . . . . . .
5.5.5
Flies (Brachycera) . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.5.6
Horse Flies (Tabanidae) . . . . . . . . . . . . . . . . . . . . . . .
5.6
Protection from Insect Infestation . . . . . . . . . . . . . . . . . . . . . .
5.6.1
Protection from Mosquitoes . . . . . . . . . . . . . . . . . . . .
5.6.2

Protection from Flies . . . . . . . . . . . . . . . . . . . . . . . . .

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4.4.22
4.4.23
4.4.24
4.4.25

5

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xv

5.7
Vampire Fish . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 425
5.8
Vampire Bats . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 426
Further Reading (Joint List for This Chapter) . . . . . . . . . . . . . . . . . . . . 426
Questions to Test Obtained Knowledge . . . . . . . . . . . . . . . . . . . . . . . . . 435
Solutions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444
Origin of Figures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 445
Photographs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 445
Diagrammatic Representations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 445
Author Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447
Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 449


ThiS is a FM Blank Page


About the Author

Prof. Dr. Heinz Mehlhorn has investigated
parasites, their transmission pathways and significant control measures for over 40 years. He has
published more than 20 books and 250 original
publications and received 25 patents on antiparasitic drugs, some of which he uses at
his university spin-off company Alpha-Biocare
(founded in 2000). As a university instructor, he
had the pleasure to introduce many students to the
topics in parasitology. Many of them are now
professors or in leading industrial positions. In television and radio broadcasts, he regularly informs the
public about relevant parasitological problems.

xvii


1

The Phenomenon Parasitism

The term parasite has its origin in the Greek word parasitos, which describes a
person that tests food of mighty, noble persons in order to avoid poisoning. Since
they obtained their food without paying or working for, the term got soon a negative
meaning characterizing tricky, unsocial persons. From there the term was later also
transferred to animals, which live fully or at least in part time on costs of their
human or animal hosts.
All animals and also humans have the same problem to obtain their daily food.
Apart from fully plant eaters, all other species have to strengthen their ability to
catch and ingest other specimens. Thus the fittest will kill smaller and weaker
individuals in order to succeed in the by Darwin (1809–1882) described struggle
for life. However, also the individuals of weaker (smaller) species developed skills
to survive either by ingesting the remnants of the meals of powerful species
(i.e. commensalism ¼ Latin ¼ eating together) or by living at the surface (skin,
hair) of larger animals as so-called ectoparasites (Greek ¼ ectos ¼ outside). Other
parasites started invasion from the outside when entering the mouth or anus
respectively started entering (totally or just by mouthparts) the skin of animals,
which thus become hosts ¼ prey animals.
Ectoparasites may stay stationary always or temporary for a while on their
host. For example, head lice (Pediculus humanus capitis) are stationary parasites,
since only pregnant female lice change the host, whereas female mosquitoes suck
blood only at intervals on various warm-blooded hosts and leave them immediately
after the successful blood meal. However, there are also many intermediate sucking
activities. For example, ixodid ticks such as Ixodes ricinus stay up to 10–12 days on

their hosts, before dropping down in order to proceed moult on the ground hidden in
grass, while Argas ticks stay only a few minutes on their hosts during their
blood meal.
Endoparasitism has its origin in activities, which are still today seen in the
behaviour of scabies mites (Sarcoptes scabies), which enter and stay in the host’s
epidermis, in the case of flagellates which enter and live inside the mouth or anal
regions or in Schistosoma species, where their free-living cercariae enter the body
# Springer International Publishing Switzerland 2016
H. Mehlhorn, Human Parasites, DOI 10.1007/978-3-319-32802-7_1

1


2

1

The Phenomenon Parasitism

of vertebrates in order to live as adult worms finally in the blood vessels of their
hosts. The intracellular way of life of stages of protozoans (e.g. Eimeria species,
Toxoplasma gondii) is apparently a peculiar type of the general endoparasitism
being based on the relative small size of the invading organism. But even larger
organisms such as the larvae of Trichinella spiralis are able to live for long
intracellularly.
Parasites may (depending on the species) invade one host species or several
ones. Those with only one host type are described as monoxenous, while others
with several hosts are termed heteroxenous. The latter parasites may be classified
according to the amount of different hosts as di-, poly- or even heteroxenous. If a
host change is absolutely needed, it is called obligatory; if several hosts may be

selected just by occasion, the host-parasite relation is called facultative.
Hosts are furthermore categorized according to the fact, whether they harbour
the sexual stages of the parasite (¼final host, definitive host) or whether they
contain asexually reproducing stages (¼intermediate hosts). For example, the cat
is the final host for Toxoplasma gondii, whereas humans and mice are intermediate
hosts. However, in the case of the tapeworms Echinococcus granulosus, humans are
only intermediate hosts (bearing the cyst with asexually reproduced protoscolices),
and dogs/foxes are the final hosts bearing the adult tapeworms.
The terms main host and accidental host are less accurate since this determination is often only based on the present status of knowledge and must perhaps be
changed if epidemiologic studies add other insights. For example, the main hosts
for Trichinella spiralis are pigs and rats, while humans are mainly accidental hosts.
Parasites such as Entamoeba histolytica, which have no (or a not yet proven) sexual
reproduction, cannot become classified into the above-cited host system.
Several species of ectoparasites are described acting as vectors, which are able
to transmit agents of diseases, which in most cases even may reproduce themselves
inside these insects, ticks or leeches. Inside these vectors even the sexual development of agents of disease may occur (e.g. Plasmodium species – agents of malaria
which proceed to gamogony in Anopheles mosquitoes). However, filarial worms let
only transport their asexual larvae to new hosts (e.g. humans), in which they
develop and reproduce in the sexual stages (adult male and female worms).
The life cycle of parasites mostly includes only one type of final host
(e.g. carnivores), while mostly several types of intermediate hosts become
involved (e.g. small crustaceans, fish). However, in the case of the species of the
genus Caryospora, two very different final hosts may be involved, since the sexual
process (¼formation of oocysts) occurs as well in the intestinal cells of the primary
final host (snakes) as well as inside their preys (rodents), which thus become
secondary final hosts. If such hosts are ingested by dogs, oocysts may in addition
develop inside their epithelial cells. Thus it can be stated that this parasite is very
unspecific with respect to its hosts, but thereby it increases considerably its chances
for propagation and thus for survival.
In a broad spectrum of meat feeding hosts – especially in cannibals ingesting

meat of their own species – some parasites exist, which use these animals as well as
final as intermediate hosts. Thus in some Sarcocystis species, lizards may have at


1.2

Ontogenetic Development of Parasites

3

the same time tissue cysts as well sexual stages in intestinal cells. The same occurs
in cats infected by Toxoplasma gondii or in the case of Trichinella spiralis, where,
e.g. adults may occur in the intestine of pigs and later asexual larvae inside their
muscle cells.
The propagation of parasites in a given region among peculiar hosts is furthermore supported by the help of further host types, which, however, may also act as
final or intermediate hosts at the same time:
1. Reservoir hosts
These are vertebrate hosts such as dogs and rodents, which, in the case of
human leishmaniasis, harbour parasite stages which can be transmitted through
bites of sandflies back to humans. On the other side, in the case of the agents of
human malaria, no further hosts exist.
2. Transportation host or paratenic host
This term describes intermediate hosts wherein no reproduction occurs, but
which accumulate parasitic stages, so that these are ingested in high numbers by
a final host thus increasing the chance for a successful transmission. Examples
are fish containing large numbers of tapeworm stages.
3. Incompetent host
This term describes hosts, wherein an accidentally penetrated parasite cannot
develop further on. Examples are the cercariae of various water bird
schistosomes in the skin of humans.

1.1

Host Specificity

The above-described host types are based on the varying adaptations of a parasite
species at a given host species. This relation may be:
(a) Very strong, so that only a single host species is parasitized: e.g. Isospora
hominis or Taenia saginata in humans and Eimeria maxima in chicken
(b) Rather variable, so that many hosts were used: e.g. Cryptosporidium species,
many trematodes or most blood-sucking ectoparasites
(c) Different in the host types: e.g. in Toxoplasma gondii, only felids act as final
hosts, while practically all warm-blooded animals may serve as intermediate
hosts

1.2

Ontogenetic Development of Parasites

The development of parasitic species may occur in different manners:
(a) Directly (i.e. without reproduction) via different larvae looking rather similar
to the adult stage (e.g. by metamorphosis in the case of some insects or
nematodes).


4

1

The Phenomenon Parasitism

(b) Indirectly, i.e. by inclusion of different reproduction processes (e.g. in the
case of coccidians, digenetic trematodes), where different generations follow
each other. This follow-up of different generations may occur obligatory
(e.g. in Sarcocystis species, digenetic trematodes) or facultatively (e.g. in
the case of Strongyloides nematodes).

1.3

Follow-Up of Different Generations

In the case of many protozoan species, a so-called primary follow-up of generations
has been developed, since due to cell divisions, an enlargement of the numbers of
individuals occurs, while in the case of metazoans, cell reproduction only increases
the body size of the individual organism. Only by partial division of the whole body
a new generation occurs. Thus this process is called secondary follow-up of
generations. A typical primary follow-up of generations occurs among
coccidians comprising a sexual generation and one or several asexual
generations. The secondary follow-up of generations occurs in two different
ways:
(a) Metagenesis
Here occurs the follow-up of one (or several) asexual generation and a
sexual one (e.g. Echinococcus species).
(b) Heterogony
This term describes the follow-up of a single-sexual (female, parthenogenic)
and a typical two-sex (i.e. male/female) generation (e.g. Strongyloides
stercoralis).
Since rather few informations are available concerning sexuality and chromosomal equipment of many parasites, the determination of many life cycles is
difficult (e.g. in trematodes). In addition it occurs that the larvae of several parasites
may immediately reach maturity – a phenomenon, which is called neotenia (e.g. in

Monogenea). Another similar phenomenon is polyembryony.
The parasitic worm may be mono- or dioecious. However, in most dioecious
species, their sperms mostly reach maturity before eggs. This helps to avoid selfinfertilization, which, however, is common in large tapeworms such as Taenia
solium or T. saginata inside the intestine of humans.

1.4

Speed of Development

The larval development of ectoparasites depends on the local temperature, while in
the case of endoparasites, host defence reactions may have considerable influences
limiting on growth and ability to reproduce. Thus even in the same species, such
processes may need a range from a few days until months or even years. The period,
which is needed by a parasite to reach maturity (and production of transmittable


1.5

Adaptations

5

stages), is called prepatent period. The following period until the end of the
production of transmittable stages is named patency. The patent period of a
parasitic species is always species specific and may last a few days
(e.g. Coccidia) or even years (e.g. Taenia species, large filariae such as Onchocerca
volvulus). The period between infection day and the first occurrence of clinical
symptoms is termed incubation period (Latin: incubate ¼ embedding). This period
may be short (e.g. hours in case of amoebiasis) or even years (e.g. echinococcosis,
schistosomiasis, filariasis). A very important point is reached, when the incubation

periods need longer than the prepatent ones. This implicates that a human host does
not know that he/she is already able to infect other persons, since he/she is not
aware of his/her individual infection. This is, for example, the case in the transmission of the West Nile Virus disease in cases of transmission by clinical blood
transfusion or by mosquito bites.

1.5

Adaptations

Ectoparasites have developed peculiar mouth parts and digestion systems in order
to obtain and digest the food taken from their hosts. Often they are also using the
help of a broad spectrum of endosymbionts.
Endoparasites, however, have to solve several more problems. They must
develop:
–
–
–
–

Sophisticated invasion mechanisms
Techniques of anchoring themselves inside a host
Mechanism to protect their progeny inside the host organs
Mechanism to place their eggs/larvae inside their hosts at places from where
they may reach outside places and thus have the chance to become transmitted to
other hosts
(a)

Invasion mechanisms
The infection of a host by an endoparasite may occur passively by oral
uptake of persistent stages such as oocysts, eggs, cysts or tissue cysts, by

means of an injection process using ectoparasites as vectors or actively by
the use of own enzymes that enable them to pass the body surface
(e.g. miracidia larvae of trematodes or larvae of nematodes).
(b) Attachment and food uptake
Parasites have developed a large amount of sophisticated structures,
which help their attachment and fixation at inner and outer host tissues
and thus make them able to take up food. Examples of organs for fixation
are hooks, thorns, claws, suckers or bulbous like magnifications of the
cuticle. Food uptake of metazoans is in general done via an intestinal
system, which might be subdivided into different activity regions or not.
However, several intestinal worms (e.g. cestodes, acanthocephalans) are


6

1

The Phenomenon Parasitism

able to take up all needed substances via their own surface layers, which
even morphologically look similar to the surface of the intestines of
vertebrates. Protozoans take up their food by the help of peculiar
cytostomes or just via vesiculation at the surface.
(c) Protection from host influences (immune-evasion)
Endoparasites which live in the intestines of their hosts have to protect
themselves from the host’s digestive fluids. This is done in many parasitic
species by the help of a layer of mucopolysaccharides, which form together
with other chemical compound a very resistant surface coat, the composition of which is very often changed by the parasite so that its chances in the
“fight for survival” become considerably enhanced. Thus this permanent
change of the antigenic components at the surface helps that the parasite

remains undetected by the host defence system (¼eclipse), which produces
constant antibodies/immuno-globulines (e.g. IgE, IgG, IgM) besides unspecific phagocytic and lytic cells.
Many parasites developed as peculiar protection of their surface the
so-called molecular mimicry, which is based on the inclusion of hostderived components into their surface (e.g. seen in schistosomes, filarial
worms, Fasciola hepatica, etc.). Other parasites interrupt or reduce the
formation of the host’s MHC-complex (major histocompatibility complex). Again other parasites settle in host tissues, which have a low
immune-activity such as brain, where tapeworms settle very often. This
phenomenon of targeting host organs with low immune-reactivity is
described as sequestration (Latin: sequestratio ¼ separation). Since the
above-cited systems are rather rough methods to escape host’s immune
defence, some parasites have developed further methods. Thus some block
or suppress completely the activity of the host’s defence system by production and excretion of large amounts of antigenic material which binds the
limited number of antibodies produced by the host, so that, e.g. in the case
of trypanosomes inside the host’s blood vessels, they are able to survive. In
another approach some trypanosomes set such a strong stimulus to produce
antibodies that this system becomes exhausted and thus at least several
trypanosomes may survive.
As soon as (by any many possible reasons) the immune system of a host
is exhausted, the so-called opportunistic agents of disease may overwhelm
the defence system of the host completely and endanger its life. This
phenomenon mainly occurs as soon as the host defence system is weakened
by another agent of disease (e.g. in cases of infections with Cryptosporidium species or Pneumocystis jiroveci).
Nematodes and larvae of insects protect themselves inside host tissues by
the help of their cuticle, which can be exchanged from time to time, so that
host defence systems have problems to detect them. Other parasites protect
themselves inside host tissues by formation of so-called tissue cysts
(e.g. Sarcocystis species, Trichinella spiralis, Onchocerca volvulus). In
many cases the parasites overwhelm the host cells intensely that the host

1.6

Pathogenicity

7

cells appear completely different from the uninfected ones. Furthermore
some parasites, which enter cells, which normally have finished their
division process, stimulate these cells to new repeated divisions and thus
increase the propagation chances of this parasite. This is, for example,
initiated by Theileria species inside their host cells (lymphocytes of cattle).
(d) Host specificity
This phenomenon is only poorly understood: why are some parasites able
to develop in different hosts and other species not. Some studies dealing
with the metabolism of parasites may perhaps contribute to the above-cited
phenomenon. One reason might be that many parasite worms have lost the
ability to produce lipid complexes de novo. Thus the host specificity may
depend on the lipids that they need and get from their hosts. Other worms
which use several hosts may not as specific with respect to their lipid
dependence. Such a close dependence is apparently not developed with
respect to the use of carbohydrates and proteins, which derive from rather
simple, nonspecific molecules.
(e) Brood protection
The successful parasite is able to protect its progeny not only from the
aggression of the host’s defence system, but also outside of the body. This
is, for example, done by the development of thick shells around eggs.
Furthermore it is needed to depone their progeny in a parasitized body at
places, from where the young generation has the chance to get out of the
host’s body. For example, schistosomes depone their eggs in blood vessels
either close to the urogenital or intestinal blood vessels or Paragonimus

trematodes place their eggs close to blood vessels of the host’s lungs and
thus enable the eggs to become excreted either with sputum (saliva) or feces
or their hosts.

1.6

Pathogenicity

Parasites may harm their hosts in many ways:
– Cells and organs may become destroyed mechanically (e.g. Plasmodium spp.,
Onchocerca volvulus, Ancylostoma duodenale).
– Host tissues are stimulated to grow to an unphysiological size or tumour
development is induced (e.g. in cases of liver flukes, schistosomes).
– Peculiar compounds are extracted from hosts (e.g. vitamin B12 extraction by
Diphyllobothrium latum).
– Intoxications are induced by discharge of own metabolic excretions
(e.g. Trypanosoma cruzi, Plasmodium stages, ticks).
– Introduction of secondary infections due to bacteria glueing on the surface of
parasitic stages (e.g. Entamoeba histolytica, surface of nematodes).
– Inoculation of agents of diseases during blood meals of insects and ticks.