Parasitology
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Alan Gunn. Parasitology
Table of Contents
List of Tables
List of Illustrations
Guide
Pages
Parasitology. An Integrated Approach
Preface
About the Companion Website
1 Animal Associations and the Importance of Parasites. CONTENTS
1.1 Introduction
1.2 Animal Associations
1.2.1 Symbiosis
1.2.1.1 Symbionts
1.2.1.2 The Importance of Symbionts to Blood‐feeding Organisms
1.2.2 Commensalism
1.2.3 Phoresis
1.2.4 Mutualism
1.2.5 Parasitism
From Welcome Guest to Villain: The Derivation of the Term ‘Parasite’
1.2.5.1 Intra‐specific Parasites
1.2.6 Parasitoids
Parasitoid: Virus Interactions
1.2.7 The Concept of Harm
1.3 Parasite Hosts
Parasites of Parasites
1.4 Zoonotic Infections
1.5 The Co‐evolution of Parasites and Their Hosts
1.5.1 The Red Queen’s Race Hypothesis
1.5.2 Parasites in the Fossil Record
1.5.3 Parasites and the Evolution of Sexual Reproduction
1.6 Parasitism as a ‘Lifestyle’: Advantages and Limitations
1.7 The Economic Cost of Parasitic Diseases
1.7.1 DALYs: Disability‐Adjusted Life Years
1.8 Why Parasitic Diseases Remain a Problem
2 Taxonomy. CONTENTS
2.1 Introduction
2.2 Viruses: A Special (Unresolved) Case
2.3 Taxonomic Hierarchy
2.3.1 The Binomen System
2.4 Kingdom Protista
2.5 Kingdom Animalia
2.5.1 Parazoa
2.5.2 Eumetazoa
3 Parasitic Protozoa Part A: Phyla Rhizopoda, Metamonada, Apicomplexa. CONTENTS
3.1 Introduction
3.2 Phylum Rhizopoda
3.2.1 Entamoeba histolytica
Entamoebae and Amoebic Dysentery
3.2.2 Entamoeba dispar
3.2.3 Entamoeba moshkovskii
3.2.4 Entamoeba gingivalis
3.2.5 Naegleria fowleri
3.2.6 Balamuthia mandrillaris
3.2.7 Genus Acanthamoeba
3.3 Phylum Metamonada
3.3.1 Order Diplomonadida
3.3.1.1 Genus Giardia
3.3.1.1.1 Giardia duodenalis
3.3.2 Order Trichomonadida
3.3.2.1 Histomonas meleagradis
3.3.2.2 Trichomonas vaginalis
3.3.2.3 Trichomonas tenax
3.3.2.4 Trichomonas gallinae
3.3.2.5 Tritrichomonas foetus
3.3.2.6 Pentatrichomonas hominis
3.4 Phylum Apicomplexa
Plastids in Parasites
3.4.1 Genus Plasmodium
How Malaria Has Influenced the Course of History
3.4.1.1 Plasmodium Life Cycle
3.4.1.2 Plasmodium falciparum
3.4.1.3 Plasmodium vivax
3.4.1.4 Plasmodium ovale
3.4.1.5 Plasmodium malariae
3.4.1.6 Plasmodium knowlesi
3.4.2 Genus Theileria
3.4.2.1 Theileria Life Cycle
3.4.2.2 Theileria parva
3.4.3 Genus Babesia
3.4.3.1 Babesia Life Cycle
3.4.3.2 Babesia bigemina
3.5 Subclass Coccidiasina
3.5.1 Genus Eimeria
3.5.1.1 Eimeria tenella
3.5.2 Genus Isospora
3.5.3 Genus Cystoisospora
3.5.3.1 Cystoisospora (Isospora) belli
3.5.4 Genus Cyclospora
3.5.4.1 Cyclospora cayetanensis
3.5.5 Genus Sarcocystis
Human Sarcocystis Infections
3.5.6 Genus Toxoplasma, Toxoplasma gondii
Population structure of Toxoplasma gondii
3.5.7 Genus Neospora
3.5.7.1 Neospora caninum
3.5.8 Genus Cryptosporidium
4 Parasitic Protozoa Part B: Phylum Kinetoplastida; Parasitic Algae and Fungi. CONTENTS
4.1 Introduction
4.2 Phylum Kinetoplastida
4.2.1 Genus Leishmania
4.2.1.1 Leishmania Life Cycle
How Harming the Vector Facilitates Transmission
How Leishmania Establishes Within Mammalian Phagocytes
4.2.1.2 Visceral Leishmaniasis
4.2.1.3 Post Kala‐Azar Dermal Leishmaniasis
4.2.1.4 Cutaneous Leishmaniasis
4.2.2 Genus Trypanosoma
4.2.2.1 Trypanosoma brucei
Genomic Regulation in Trypanosomes
How Trypanosomes Alter Tsetse Fly Physiology to Facilitate Transmission
4.2.2.2 Trypanosoma congolense
4.2.2.3 Trypanosoma evansi
4.2.2.4 Trypanosoma equinum
4.2.2.5 Trypanosoma equiperdum
4.2.2.6 Trypanosoma cruzi
4.3 Phylum Chlorophyta
4.3.1 Genus Prototheca
4.4 Kingdom Fungi
4.4.1 Phylum Microspora
5 Platyhelminth and Acanthocephalan Parasites. CONTENTS
5.1 Introduction
5.2 Phylum Platyhelminthes
5.2.1 Trematoda
5.2.1.1 Family Fasciolidae
5.2.1.1.1 Fasciola hepatica/Fasciola gigantica
Environmental DNA (eDNA) and Parasite/Intermediate Host Monitoring
5.2.1.1.2 Fasciolopsis buski
5.2.1.2 Family Dicrocoeliidae
5.2.1.2.1 Dicrocoelium dendriticum
5.2.1.3 Family Paramphistomatidae
5.2.1.3.1 Genus Calicophoron: Calicophoron daubneyi
5.2.1.4 Family Opisthorchiformes
5.2.1.4.1 Clonorchis sinensis
5.2.1.4.2 Opisthorchis viverrini
5.2.1.4.3 Opisthorchis felineus
5.2.1.5 Family Paragonomidae
5.2.1.5.1 Paragonimus westermani
5.2.1.6 Family Cathaemasiidae: Genus Ribeiroia
5.2.1.7 Family Schistosomatidae: Schistosoma mansoni, Schistosoma japonicum, Schistosoma haematobium
5.3 Class Cestoda
5.3.1 Order Pseudophyllidea/Diphyllobothridea
5.3.1.1 Genus Diphyllobothrium
5.3.1.1.1 Diphyllobothrium latum
5.3.2 Order Cyclophyllidea
5.3.2.1 Family Taeniidae
5.3.2.1.1 Taenia solium
5.3.2.1.2 Taenia saginata
5.3.2.1.3 Taenia hydatigena
5.3.2.1.4 Taenia multiceps
5.3.2.2 Genus Echinococcus
5.3.2.2.1 Echinococcus granulosus
5.3.2.2.2 Echinococcus multilocularis
Has Successful Anti‐Rabies Control Resulted in an Increased Risk of Echinococcus multilocularis Infection in Europe?
5.3.2.3 Family Anoplocephalidae
5.3.2.3.1 Anoplocephala perfoliata
5.3.2.3.2 Moniezia expansa and Moniezia benedeni
5.4 Phylum Acanthocephala
Homosexual Interactions in the Acanthocephalan Moniliformis dubius
6 Nematode Parasites. CONTENTS
6.1 Introduction
6.2 Class Enoplea. 6.2.1 Genus Trichuris
6.2.2 Genus Trichinella
6.2.2.1 Trichinella spiralis
Invasion of Muscle Cells by Trichinella spiralis
6.3 Class Rhabdita. 6.3.1 Genus Strongyloides
6.3.1.1 Strongyloides stercoralis
6.3.2 Genus Ancylostoma
Arrested Development (Hypobiosis) in Hookworm Larvae
6.3.3 Genus Necator
6.3.4 Genus Ascaris
6.3.5 Genus Enterobius: Enterobius vermicularis
6.3.6 Genus Toxocara: Toxocara canis
6.3.7 Genus Anisakis
6.3.8 Family Onchocercidae
6.3.8.1 Genus Onchocerca
6.3.8.2 Genus Wuchereria, Wuchereria bancrofti
6.3.8.3 Genus Brugia
6.3.8.4 Genus Loa, Loa loa
6.3.9 Family Dracunculidae: Dracunculus medinensis
7 Arthropod Parasites. CONTENTS
7.1 Introduction
7.2 Phylum Chelicerata
7.2.1 Family Demodicidae
7.2.2 Family Sarcoptidae
7.2.2.1 Genus Sarcoptes
7.2.2.2 Genus Notoedres, Notoedres cati
7.2.2.3 Genus Knemidocoptes
7.2.3 Family Psoroptidae
7.2.3.1 Genus Psoroptes
7.2.4 Suborder Ixodida
7.2.4.1 Family Argasidae
7.2.4.1.1 Argas persicus
7.2.4.2 Family Ixodidae
7.3 Phylum Crustacea
7.3.1 Subclass Copepoda
7.3.2 Infraclass Cirripedia
7.3.3 Subclass Branchiura
7.3.4 Subclass Pentastomida
7.4 Subphylum Hexapoda
7.4.1 Order Phthiraptera (Lice)
7.4.2 Order Siphonaptera (Fleas)
Tungiasis
7.4.3 Order Diptera (True Flies)
7.4.3.1 Suborder Nematocera
7.4.3.2 Suborder Brachycera
Wound Myiasis
7.4.3.2.1 Family Calliphoridae
Blowfly Strike in Sheep
7.4.3.2.1.1 Genus Chrysomya
7.4.3.2.1.2 Genus Cochliomyia
7.4.3.2.1.3 Genus Auchmeromyia
7.4.3.2.1.4 Genus Cordylobia
7.4.3.2.2 Family Sarcophagidae
7.4.3.2.3 Family Oestridae
7.4.3.2.3.1 Subfamily Oestrinae
7.4.3.2.3.2 Subfamily Gasterophilinae
7.4.3.2.3.3 Subfamily Hypodermatinae
7.4.3.2.3.4 Subfamily Cuterebrinae
7.4.3.2.4 Family Streblidae
7.4.3.2.5 Family Nycteribiidae
8 Parasite Transmission. CONTENTS
8.1 Introduction
8.2 Contaminative Transmission
Geohelminths and Geophagy
Contaminative Transmission of Cyclospora spp
8.3 Transmission Associated with Reproduction. 8.3.1 Sexual (Venereal) Transmission
8.3.2 Transmission within Gametes
8.3.3 Congenital Transmission
8.4 Autoinfection
8.5 Nosocomial Transmission
8.6 Active Parasite Transmission
8.7 Hosts and Vectors. 8.7.1 Paratenic Hosts
8.7.2 Intermediate Hosts
8.7.3 Vectors
The Role of Symbionts in the Life of Tsetse Flies and Their Transmission of Trypanosome Parasites
8.8 Host Factors. 8.8.1 Host Identification
8.8.2 The Influence of Host Behaviour on Parasite Transmission
Baby Care and Strongyloides fuelleborni kellyi Infection
8.8.3 Religion and Parasite Transmission
8.8.4 War and Parasite Transmission
8.8.5 Parasites Influencing Host Behaviour
The Effect of Toxoplasma gondii on Human Behaviour
8.9 Co‐Transmission and Interactions Between Pathogens
8.10 Environmental Factors. 8.10.1 Natural Environmental Variables
8.10.2 Pollution
Sewage Effluent, Toxoplasma gondii and Marine Sentinel Species
8.10.3 Climate Change
A Perfect Storm: Did Global Warming Contribute to Disease in African Lions?
9 Immune Reactions to Parasitic Infections. CONTENTS
9.1 Introduction
9.2 Invertebrate Immunity
9.3 Vertebrate Immunity
9.3.1 Innate Immunity
Innate Immunity to Trypanosome Infection
9.3.2 Adaptive Immunity
9.3.3 Cell‐Mediated Immunity
9.4 Innate Immunity to Parasites. 9.4.1 Physical Factors
9.4.2 Chemical and Microbial Factors
9.4.3 Acute Inflammatory Response
9.4.4 Cell‐Mediated Immune Reactions
9.5 Adaptive Immune Reactions to Parasites
9.6 Microbiomes and Host Immune Reactions to Parasites
9.7 Avoiding the Host Immune Response
Hide in a ‘safe house’
Stay quiet and do not draw attention to yourself
Camouflage
Keep changing your disguise
Put out false information
Neutralise any threats
Exhaust the enemy
9.8 Immunity to Malaria
9.8.1 Plasmodium: Anopheles Interactions
9.8.2 Plasmodium: Human Interactions
9.8.2.1 Innate Immune Mechanisms Against Malaria
9.8.2.2 Antibodies Against Malaria
9.8.2.3 Why Humans Do Not Develop Protective Immunity Against Malaria
9.9 Schistosoma spp. and Hepatitis C Virus Interactions
9.10 HIV‐AIDS and Parasitic Infections
9.10.1 Parasites and the Transmission of HIV
9.10.2 Parasite‐HIV Co‐Infections
9.10.2.1 Leishmania‐HIV Co‐Infections
9.10.2.1.1 The Increasing Problem of HIV‐ Leishmania Co‐Infections
9.10.2.2 Malaria‐HIV Co‐Infections
9.10.2.3 Toxoplasma‐HIV Co‐Infections
9.10.2.4 Microsporidia‐HIV Co‐Infections
10 Pathology Part A: Factors Influencing Pathogenesis, How Parasites Cause Pathology, Types of Pathology. CONTENTS
10.1 Introduction
10.2 Factors Influencing Pathogenesis
10.2.1 Host Factors
10.2.2 Parasite Factors
10.3 Mechanisms By Which Parasites Cause Pathology
10.3.1 Direct Damage
10.3.2 Indirect Damage
10.4 Types of Pathology. 10.4.1 Abortion and Obstetric Pathology
10.4.2 Abscesses and Ulcers
10.4.3 Anaemia
10.4.4 Anorexia
10.4.5 Apoptosis
10.4.6 Autoimmunity
10.4.7 Calcification
10.4.8 Cancer
10.4.9 Castration
10.4.10 Delusional Parasitosis
10.4.11 Diarrhoea
10.4.12 Elephantiasis
10.4.13 Fever
10.4.14 Fibrosis
10.4.15 Granulation
10.4.16 Hyperplasia
10.4.17 Hypertrophy
10.4.18 Hypoplasia and Hypotrophy
10.4.19 Inflammation
10.4.20 Jaundice
10.4.21 Metaplasia
10.4.22 Pressure Atrophy
10.4.23 Psychological Disturbance
11 Pathology Part B: Damage to Specific Organs; Co‐Infections and Pathogenesis. CONTENTS
11.1 Introduction
11.2 Damage to Specific Organs. 11.2.1 Bladder
11.2.2 Brain and Nervous System
11.2.3 Gastrointestinal Tract
11.2.4 Gall Bladder and Bile Ducts
11.2.5 Genitalia
11.2.6 Kidney
11.2.7 Liver
11.2.8 Lungs
11.2.9 Skin
It Started with a Leech Bite
11.2.10 Spleen
11.3 Co‐Infections and Pathogenesis
12 The Useful Parasite. CONTENTS
12.1 Introduction: The Goodness of Parasites?
12.2 The Importance of Parasites for the Maintenance of a Healthy Immune System
12.2.1 Type 1 Diabetes Mellitus
12.2.2 Type 2 Diabetes
12.2.3 Irritable Bowel Syndrome
12.2.4 Inflammatory Bowel Disease
12.3 The Use of Parasites to Treat Medical Conditions
12.3.1 Helminth Therapy
12.3.1.1 Helminth Therapy in Practice
12.3.2 Maggot Therapy
12.3.2.1 Maggot Therapy in Practice
12.3.2.2 How Maggot Therapy Works
12.3.3 Leech Therapy
12.3.3.1 Leech Therapy in Practice
12.3.4 Malaria Therapy (Malariotherapy)
12.4 Parasites as Sources of Novel Pharmaceutically Active Substances
12.5 Parasites as Biological Control Agents
12.5.1 Life Cycle of the Entomopathogenic Nematodes Heterorhabditis and Steinernema
Rhabditid Nematode–Bacteria Relationships
12.6 Parasites as Forensic Indicators
The Use of Parasitoid Wasps to Determine the Minimum Time Since Death
13 The Identification of Protozoan and Helminth Parasites. CONTENTS
13.1 Laboratory Testing for Parasitic Infections: Introduction
13.2 Importance of Correct Identification
13.3 Properties of an Ideal Diagnostic Test
13.4 Isolation of Parasites
Giardia String Test (Entero‐Test)
13.5 Identification from Gross Morphology
13.5.1 Morphological Identification of Entamoeba spp
13.5.2 Morphological Identification of Plasmodium spp. and Babesia spp
13.5.3 Morphological Identification of Taenia spp. Tapeworms
13.5.4 Morphological Identification of Filarial Nematode Infections
13.6 Biochemical Techniques for Identification
13.7 Immunological Techniques for Identification
13.8 Molecular Techniques for Identification
How Diagnostic Techniques Can Influence Epidemiological Studies
13.9 Diagnostic Testing of Parasitic Infections Outside the Laboratory: Introduction
13.9.1 Immunochromatographic (Lateral Flow) Tests
13.9.1.1 Detection of Parasites in Blood with LFDs. 13.9.1.1.1 Detection of Plasmodium spp. with LFDs
13.9.1.1.2 Detection of Leishmania spp. with LFDs
13.9.1.2 Detection of Parasites in Faeces with LFDs. 13.9.1.2.1 Detection of Faecal Protozoa with LFDs
13.9.1.2.2 Detection of Helminths in Faeces with LFDs
13.9.2 Point‐of‐Care Nucleic Acid Amplification Tests (NAATs)
13.9.2.1 Detection of Trichomonas vaginalis Using POCT NAATs
13.9.2.2 Detection of Plasmodium spp. Using POCT NAATs
13.9.2.3 Invertebrate Vector and Intermediate Host Monitoring Using POCT NAATs
14 Parasite Treatment. CONTENTS
14.1 Introduction
14.2 The Ideal Antiparasitic Drug
14.3 Pharmaceutical Drugs
14.4 DNA/RNA Technology
Antisense DNA and RNA
14.5 Molecular Chaperones (Heat Shock Proteins)
14.6 Nanotechnology
Gold Nanoparticles for the Diagnosis and Treatment of Parasitic Infections
14.7 Quantum Dots
14.8 Natural Remedies
Artemisinin and the Treatment of Malaria
14.9 Homeopathy
15 Parasite Vaccines. CONTENTS
15.1 Introduction
15.2 The Design and Use of Vaccines
15.3 Herd Immunity
15.4 Factors Limiting the Production of Commercial Antiparasitic Vaccines
15.5 Properties of an Ideal Vaccine
15.6 Types of Vaccine
15.6.1 Live Attenuated Vaccines
15.6.2 Inactivated Vaccines
15.6.3 Subunit/Recombinant Vaccines
15.6.4 Peptide/Polypeptide Vaccines
15.6.5 Carbohydrate Vaccines
15.6.6 Toxoid (Anti‐toxin) Vaccines
15.6.7 Virus‐Like Particles Vaccines
15.6.8 DNA/RNA Vaccines
15.7 Identification of Antigens for Use in Anti‐parasite Vaccines
15.8 Vaccine Delivery
15.9 Vaccines Against Malaria
15.10 Nanobodies (Single Domain Antibodies)
15.11 Problems with Vaccination Strategies
16 Parasite Control. CONTENTS
16.1 Introduction
16.2 Eradication, Elimination, and Control
16.3 Education
16.4 Environmental Modification and Cultural Control
Organic Livestock Farming and Parasitic Diseases
16.5 Remote Sensing and GIS Technology
16.6 Whether to Treat the Individual or the Population
16.7 Piggy‐Backing Control Programmes
16.8 Disruptions to Control Programmes
16.9 Role of Governments, Foundations, and Aid Organisations
References
Index. a
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Second Edition
Alan Gunn
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Evolution can be defined as a change in gene frequency between generations, but for this to occur three criteria need to be met. First, there must be genetic variation within the population. If the population is genetically homogeneous, then variation can only occur sporadically through random mutation. The second criterion is that the variation must be heritable: if the variation cannot be passed on to offspring, then it will be lost regardless of the benefits it imparts. The third and final criterion is that the variation must influence the probability of leaving reproductively viable offspring. If the variation is beneficial, then the organism possessing it will leave more offspring; however, unless these are reproductively viable, the variation would be quickly lost from the gene pool. Parasites live in close association with their hosts and the two organisms will co‐evolve. The nature of the host: parasite relationship may therefore change with time. For example, provided the three criteria are met, the host will evolve resistance/susceptibility factors depending upon the pressure exerted by the parasite. Although ever greater resistance to infection may appear to be ‘ideal’, this is unlikely to arise if the energetic cost impacts on the ability to leave viable offspring. At the same time, the parasite will evolve virulence/avirulence factors that promote its own survival.
It is often stated that long‐standing parasite: host relationships are less pathogenic than those that have established more recently. This is based on the reasoning that if the parasite kills its host, then it will effectively ‘commit suicide’ because it will have destroyed its food supply. Consequently, over time, it is to be expected that the parasite will become less harmful to its host – that is, it becomes less virulent. However, this assumption is questionable because a pathogen’s virulence often reflects its reproductive success. For example, let us consider two hypothetical strains, A and B, of the same nematode species that lives in the gut of sheep. Strain A is highly virulent and causes the death of the sheep whilst strain B is relatively benign and seldom causes any mortality. At first glance, one might expect that strain B would leave more offspring because its host lives for longer. However, if virulence was linked to the nematode’s reproductive output and the eggs were released at a time when they were likely to infect new hosts, then strain A would bequeath more of its genes to subsequent generations. Consequently, the proportion of strain A in the nematode population would increase with time and there would be constant selection for increasing virulence. The sheep and the parasites may eventually be driven to extinction by these changes, but individual animals (and humans) are almost always driven by their own immediate self‐interest rather than hypothetical future prospects.
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