Ortega Foodborne Parasites

1. Auflage 2006
ISBN: 978-0-387-31197-5
Verlag: Springer
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 284 Seiten

Reihe: Food Microbiology and Food Safety

This book examines the two major parasite groups that are transmitted via water or foods: the single-celled protozoa, and the helminths: cestodes (tapeworms), nematodes (round worms), and trematodes (flukes). Each chapter covers the biology, mechanisms of pathogenesis, epidemiology, treatment, and inactivation of these parasites. This important new text offers a better understanding of the biology and control of parasitic infections necessary to reduce or eliminate future outbreaks in the U.S. and elsewhere.

Autoren/Hrsg.

Ortega, Ynes R.

Inhaltsverzeichnis

1;Preface;6
2;Contributors;10
3;Contents;12
4;1 Amoeba and Ciliates;17
4.1;1.1 PREFACE;17
4.2;1.2 AMOEBA;17
4.2.1;1.2.1 Entamoeba histolytica;18
4.3;1.3 DIENTAMOEBA FRAGILIS;22
4.3.1;1.3.1 Morphology and Transmission;22
4.3.2;1.3.2 Therapy;23
4.4;1.4 NONPATHOGENIC AMOEBA;23
4.4.1;1.4.1 Entamoeba hartmanni;23
4.4.2;1.4.2 Entamoeba coli;23
4.4.3;1.4.3 Endolimax nana;23
4.4.4;1.4.4 Iodamoeba butschlii;23
4.5;1.5 FREE-LIVING AMOEBAE;24
4.6;1.6 CILIATES;24
4.6.1;1.6.1 Life Cycle and Morphology;25
4.6.2;1.6.2 Clinical Significance;25
4.6.3;1.6.3 Diagnosis and Treatment;27
4.6.4;1.6.4 Epidemiology and Prevention;27
4.7;REFERENCES;27
5;2 The Biology of Giardia Parasites;31
5.1;2.1 PREFACE;31
5.2;2.2 BIOLOGY;32
5.3;2.3 DETECTION AND CLASSIFICATION OF GIARDIA;33
5.3.1;2.3.1 Detection Methods;33
5.3.2;2.3.2 Classification of G. intestinalis;35
5.3.3;2.3.3 Genotyping of G. intestinalis;36
5.4;2.4 TRANSMISSION AND EPIDEMIOLOGY;39
5.4.1;2.4.1 Human;39
5.4.2;2.4.2 Environmental;40
5.5;2.5 CONTROL AND TREATMENT;41
5.6;REFERENCES;44
6;3 Coccidian Parasites;49
6.1;3.1 PREFACE;49
6.2;3.2 BACKGROUND/HISTORY;49
6.3;3.3 BIOLOGY;52
6.4;3.4 CLINICAL SIGNIFICANCE;54
6.5;3.5 TRANSMISSION AND EPIDEMIOLOGY;55
6.5.1;3.5.1 Cyclospora;55
6.5.2;3.5.2 Isospora;58
6.5.3;3.5.3 Sarcocystis;58
6.6;3.6 DIAGNOSIS;61
6.7;3.7 TREATMENT AND CONTROL;62
6.8;REFERENCES;63
7;4 Cryptosporidium and Cryptosporidiosis;73
7.1;4.1 PREFACE;73
7.2;4.2 TAXONOMY;73
7.3;4.3 LIFE CYCLE AND DEVELOPMENTAL BIOLOGY;76
7.4;4.4 EPIDEMIOLOGY AND TRANSMISSION;77
7.4.1;4.4.1 Cryptosporidiosis in Immunocompetent Persons;77
7.4.2;4.4.2 Cryptosporidiosis in Immunocompromised Persons;78
7.4.3;4.4.3 Transmission Routes and Infection Sources: Anthroponotic Versus Zoonotic Transmission;79
7.4.4;4.4.4 Waterborne Transmission;80
7.4.5;4.4.5 Foodborne Transmission;82
7.5;4.5 DETECTION AND DIAGNOSIS;85
7.5.1;4.5.1 Serologic Methods;85
7.5.2;4.5.2 Methods for Detection of Cryptosporidium in Stool Specimens;85
7.5.3;4.5.3 Methods for Detection of Cryptosporidium Oocysts in Environmental Samples;93
7.6;4.6 TREATMENT;97
7.7;4.7 CONTROL OF CRYPTOSPORIDIUM CONTAMINATION IN WATER AND FOOD;98
7.8;REFERENCES;102
8;5 Toxoplasmosis;125
8.1;5.1 PREFACE;125
8.2;5.2 PARASITE DESCRIPTION;125
8.3;5.3 LIFE CYCLE;126
8.4;5.4 TRANSMISSION;128
8.5;5.5 IDENTIFICATION;128
8.5.1;5.5.1 Molecular Assays;129
8.5.2;5.5.2 Riboprinting;130
8.6;5.6 PATHOGENICITY;131
8.7;5.7 EPIDEMIOLOGY;131
8.7.1;5.7.1 Humans;131
8.7.2;5.7.2 Swine;134
8.7.3;5.7.3 Poultry;136
8.7.4;5.7.4 Sheep and Goats;137
8.7.5;5.7.5 Other Animal Species;138
8.8;5.8 TREATMENT;139
8.9;5.9 INACTIVATION;140
8.10;REFERENCES;141
9;6 Food-Borne Nematode Infections;151
9.1;6.1 PREFACE;151
9.2;6.2 TRICHINELLA SPP.;151
9.2.1;6.2.1 Background;151
9.2.2;6.2.2 Speciation;152
9.2.3;6.2.3 Life Cycle;152
9.2.4;6.2.4 Epidemiology;153
9.2.5;6.2.5 Human Trichinellosis–Epidemiology;156
9.2.6;6.2.6 Clinical Manifestations;158
9.2.7;6.2.7 Diagnosis and Treatment;159
9.2.8;6.2.8 Prevention and Control;159
9.3;6.3 ANISAKIS SIMPLEX AND RELATED SPECIES;161
9.3.1;6.3.1 Background;161
9.3.2;6.3.2 Life Cycle;162
9.3.3;6.3.3 Epidemiology;162
9.3.4;6.3.4 Clinical Manifestations;163
9.3.5;6.3.5 Diagnosis and Treatment;163
9.3.6;6.3.6 Prevention and Control;164
9.4;6.4 ANGIOSTRONGYLUS CANTONENSIS AND ANGIOSTRONGYLUS COSTARICENSIS;164
9.5;6.5 GNATHOSTOMA SPP.;166
9.6;6.6 GONGYLONEMA SPP.;167
9.7;6.7 OTHER NEMATODE INFECTIONS WITH FOOD-BORNE ASSOCIATIONS;168
9.8;REFERENCES;169
10;7 Foodborne Trematodes;177
10.1;7.1 PREFACE;177
10.2;7.2 PARAGONIMUS SPP.;177
10.2.1;7.2.1 Introduction;177
10.2.2;7.2.2 Life Cycle;179
10.2.3;7.2.3 Epidemiology;181
10.2.4;7.2.4 Clinical Signs, Diagnosis, and Treatment;182
10.3;7.3 CLONORCHIS SINENSIS;184
10.3.1;7.3.1 Introduction;184
10.3.2;7.3.2 Life Cycle;185
10.3.3;7.3.3 Epidemiology;186
10.3.4;7.3.4 Clinical Signs, Diagnosis, and Treatment;187
10.4;7.4 OPISTHORCHIS VIVERRINI AND OPISTHORCHIS FELINEUS;190
10.4.1;7.4.1 Introduction;190
10.4.2;7.4.2 Life Cycle;190
10.4.3;7.4.3 Epidemiology;191
10.4.4;7.4.4 Clinical Signs, Diagnosis, and Treatment;192
10.5;7.5 NANOPHYETUS SALMINCOLA;193
10.5.1;7.5.1 Introduction;193
10.5.2;7.5.2 Life Cycle;193
10.5.3;7.5.3 Salmon Poisoning Disease;195
10.5.4;7.5.4 Clinical Signs, Diagnosis, and Treatment;196
10.6;7.6 FASCIOLA SPP.;198
10.6.1;7.6.1 Introduction;198
10.6.2;7.6.2 Life Cycle;198
10.6.3;7.6.3 Epidemiology;200
10.6.4;7.6.4 Clinical Signs, Diagnosis, and Treatment;200
10.7;7.7 FASCIOLOPSIS BUSKI;202
10.7.1;7.7.1 Introduction;202
10.7.2;7.7.2 Life Cycle;203
10.7.3;7.7.3 Epidemiology;204
10.7.4;7.7.4 Clinical Signs, Diagnosis, and Treatment;204
10.8;7.8 PREVENTION AND CONTROL;205
10.9;REFERENCES;207
11;8 Cestodes;213
11.1;8.1 PREFACE;213
11.2;8.2 TAENIA;213
11.2.1;8.2.1 Taenia solium;214
11.2.2;8.2.2 Taenia saginata;223
11.2.3;8.2.3 Taenia asiatica;225
11.3;8.3 DIPHYLLOBOTHRIUM;227
11.3.1;8.3.1 Diphyllobothrium Latum;227
11.3.2;8.3.2 Diphyllobothrium pacificum;230
11.4;8.4 SPIROMETRA;231
11.4.1;8.4.1 Spirometra mansoides;231
11.5;8.5 ECHINOCOCCUS;232
11.5.1;8.5.1 Echinococcus granulosus;232
11.5.2;8.5.2 Echinococcus multilocularis;237
11.6;8.6 HYMENOLEPIS;239
11.6.1;8.6.1 Hymenolepis nana;239
11.7;REFERENCES;241
12;9 Waterborne Parasites and Diagnostic Tools;247
12.1;9.1 PREFACE;247
12.2;9.2 PARASITES;248
12.3;9.3 CONCENTRATION AND ISOLATION TECHNIQUES;251
12.4;9.4 DETECTION METHODOLOGIES;253
12.4.1;9.4.1 Microscopic Techniques;253
12.4.2;9.4.2 Nucleic Acid Techniques;255
12.4.3;9.4.3 Immunological-based Techniques;264
12.4.4;9.4.4 Viability Techniques;266
12.5;9.5 PROPER EVALUATION (QA/QC);269
12.6;REFERENCES;271
13;10 Risk Assessment of Parasites in Food;291
13.1;10.1 PREFACE;291
13.2;10.2 THE RISK ASSESSMENT FRAMEWORK;292
13.3;10.2.1 Defining the Hazard;292
13.4;10.2.2 Exposure Assessment;293
13.5;10.2.3 Hazard Characterization (Dose-response Assessment);294
13.6;10.2.4 Risk Characterization;296
13.7;10.2.5 Assumptions, Assumptions, Assumptions;297
13.8;10.2.6 Emerging Applications of Microbial Risk Assessment;298
13.9;REFERENCES;298
14;Index;301

Leseproben

CHAPTER 4 Cryptosporidium and Cryptosporidiosis (p. 57-58)

Lihua Xiao and Vitaliano Cama

4.1 PREFACE

Cryptosporidium spp. are apicomplexan parasites that inhabit the brush-borders of the gastrointestinal epithelium (Bird and Smith, 1980). Initially thought to be only a pathogen of young animals such as calves, lambs, piglets, and foals, cryptosporidiosis is now known to be an important cause of enterocolitis, diarrhea, and cholangiopathy in humans (Current et al., 1983). Several Cryptosporidium spp. are now recognized to infect humans and more to infect other vertebrates (Xiao et al., 2004a). Healthy children and adults and young animals with cryptosporidiosis usually have a short-term illness accompanied by watery diarrhea, vomiting, malabsorption, and weight loss. In humans and animals with immunodeficiencies, and snakes, however, the infection can be protracted and life-threatening (Hunter and Nichols, 2002).

Cryptosporidium oocysts are environmentally resistant, retain their infectious potential for considerable time in moist environments, such as water, soil, fresh seafood and produce (Rose, 1997), and survive most water disinfection treatments as well (Korich et al., 1990). Two important fecal-oral transmission routes include direct contact with infected persons (person-to-person or anthroponotic transmission) or animals (zoonotic transmission), and consumption of contaminated water (waterborne transmission) or food (foodborne transmission). Thus, Cryptosporidium spp. are well recognized water and food-borne pathogens, having caused many outbreaks of human diarrheal disease in the United States and other developed countries (Anonymous, 1984, Current et al., 1983, D’Antonio et al., 1985, Joce et al., 1991, MacKenzie et al., 1994b, Millard et al., 1994).Water and food probably also play an important role in the transmission of cryptosporidiosis in endemic areas, even though the disease burden attributable to them is not fully clear.

4.2 TAXONOMY

Cryptosporidium spp. belong to the family Cryptosporidiidae, which is a member of the phylum Apicomplexa. The exact placement of Cryptosporidiidae in Apicomplexa is uncertain. It was long considered a member of the class Coccidea, in the order of Eimeriida or Eucoccidiorida (Corlis, 1994). Recent phylogenetic studies, however, indicate that Cryptosporidium spp. are more related to gregarines than to coccidia (Carreno et al., 1999). Extra-celluar gregarine-like reproductive stages have been described in Cryptosporidium andersoni and Cryptosporidium parvum (Hijjawi et al., 2002). Thus, Cryptosporidium spp. are no longer considered coccidian parasites.

Cryptosporidium spp. were first recognized by Tyzzer in 1907, who described Cryptosporidium muris in the stomach of laboratory mice (Tyzzer, 1907, 1910). Later in 1912, Tyzzer described a second species in laboratory mice, C. parvum (Tyzzer, 1912). This new species differed from C. muris not only by infecting the small intestine instead of the stomach, but also by having smaller oocysts, the environmentally robust stage of the parasite (Upton and Current, 1985). Over the next 50 years following the initial description of Cryptosporidium, these parasites were commonly confused with sporocysts of Sarcocystis. Several new Cryptosporidium species were described during the period, mostly based on sporocysts of Sarcocystis spp. Subsequently, it was thought that because Cryptosporidium was closely related to Eimeria, Cryptosporidium spp. also could not normally be transmitted from one species of animals to another (Levine, 1980). This erroneous concept of strict host specificity led to the description and report of multiple new species during the 1960–1980s, which are no longer considered valid, such as Cryptosporidium anserinum in geese (Proctor and Kemp, 1974), Cryptosporidium agni in sheep (Barker and Carbonell, 1974), Cryptosporidium bovis in neonatal calves (Barker and Carbonell, 1974), Cryptosporidium rhesi in monkeys (Levine, 1980), and Cryptosporidium cuniculus in rabbits (Inman and Takeuchi, 1979). Infection and cross-transmission studies conducted in the 1970s and 1980s demonstrated that Cryptosporidium isolates could indeed frequently be transmitted from one host species to another (Tzipori et al., 1981a, 1981b, 1982). These findings led to the synonymization of many species into C. parvum, and were the basis for proposing the monospecific structure of the genus Cryptosporidium. As a result, C. parvum was used extensively for the description of Cryptosporidium spp. from most mammals including humans (Tzipori et al., 1980, Upton and Current, 1985).

The recent use of molecular methods in the characterization of Cryptosporidium has helped to resolve existing confusions in the taxonomy of this genus (Fayer et al., 2000a, Morgan et al., 1999b, Xiao et al., 2000b, 2004a). These molecular tools have been very valuable when used in conjunction with morphological, biological, or host specificity studies. This has resulted in the validation of several Cryptosporidium described earlier, such as Cryptosporidium meleagridis in birds, Cryptosporidium wrairi in guinea pigs, and Cryptosporidium felis in cats. It is now well known that various Cryptosporidium isolates do have differences in host specificity, but one Cryptosporidium sp. usually infect a limited spectrum of animals, especially if the host animals are related. This new Cryptosporidium taxonomic paradigm has also led to the establishment of several new Cryptosporidium species, such as Cryptosporidium hominis (previously known as C. parvum genotype 1 or the human genotype) in humans, C. andersoni (previously known as C. muris-like or C. muris bovine genotype) and C. bovis (previously known as Cryptosporidium bovine genotype B) in weanling calves and adult cattle, Cryptosporidium canis (previously known as C. parvum dog genotype) in dogs, and Cryptosporidium suis (previously known as Cryptosporidium pig genotype I) in pigs.