Almost all biological macromoleculess proteins
(enzymes) and DNAs are inactive in the absence of
water. Hydration of a protein/enzyme is particularly
important for the stability of the structure and for
the function, especially the recognition at a specific
site. This role of hydration in enzyme catalysis is well
known and has recently been reviewed in a number
of publications. In one of these studies it was
shown that the dehydration of a protein, which
makes it more rigid and increases its denaturation
temperature, is correlated with the loss of its physiological function.

Dynamics of water in biological recognition.

Human toxocariasis is a helminthozoonosis due to the migration of Toxocara species larvae through human organism. Humans become infected by ingesting either embryonated eggs from soil (geophagia, pica), dirty hands or raw vegetables, or larvae from undercooked giblets. The diagnosis relies upon sensitive immunological methods (ELISA or western-blot) which use Toxocara excretory-secretory antigens. Seroprevalence is high in developed countries, especially in rural areas, and also in some tropical islands. The clinical spectrum of the disease comprises four syndromes, namely visceral larva migrans, ocular larva migrans, and the more recently recognized "common" (in adults) and "covert" (in children) pictures. Therapy of ocular toxocariasis is primarily based upon corticosteroids use, when visceral larva migrans and few cases of common or covert toxocariasis can be treated by anthelmintics whose the most efficient appeared to be diethylcarbamazine. When diagnosed, all of these syndromes require thorough prevention of recontamination (especially by deworming pets) and sanitary education.

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Highlights of human toxocariasis.

1 Historical Introduction.- 1. Prologue: Ghosts of Christmas Past and Christmas Present.- 2. A Worm Discovered (1835).- 3. A Nematode Life Cycle Discovered (1835-1860).- 4. From Zoological Curiosity to Lethal Pathogen (1860-1900).- 5. Consequences (Politics and Parasites).- 6. The Recent Past.- References.- 2 Species, and Infraspecific Variation.- 1. Historical Perspective.- 2. A Working Definition of Species.- 3. Terminology.- 4. Distribution of Isolates.- 5. Criteria for Species and Isolates.- 5.1. Genetic Criteria.- 5.2. Morphological Criteria.- 5.3. Biochemical and Immunological Criteria.- 5.4. Sensitivity to Drug Treatment.- 5.5. Effect of Host on Reproductive-Capacity Index.- 5.6. Other Biological Characteristics.- 6. Trichinella spiralis var. pseudospiralis-an Enigma.- 7. Speciation in Trichinella.- 8. Future Considerations.- References.- 3 Biology.- 1. Introduction.- 2. Ingestion of the Infective First-Stage Larva.- 3. Digestion of Host Tissues away from the Infective First-Stage Larva.- 4. Intramulticellular Enterai Niche.- 4.1. Entrance of the Infective First-Stage Larva.- 4.2. Molting and Development.- 4.3. Mating.- 4.4. Fecundity.- 5. Intracellular Parenteral Niche.- 5.1. Migration of the First-Stage Larva to the Niche.- 5.2. Entrance of the Migratory First-Stage Larva.- 5.3. Growth and Development.- 5.4. Mature Nurse Cell-Infective First-Stage Larva Complex.- References.- 4 Biochemistry.- 1. Introduction.- 2. Carbohydrates and Carbohydrate Metabolism.- 2.1. Adult Worms.- 2.2. Muscle Larvae.- 3. Respiration.- 3.1. Adult Worms.- 3.2. Muscle Larvae.- 4. Lipids and Lipid Metabolism.- 4.1. Adult Worms.- 4.2. Muscle Larvae.- 5. Nucleic Acids and Nucleic Acid Metabolism: Muscle Larvae.- 6. Proteins and Protein Metabolism: Muscle Larvae and Adult Worms.- 7. Nutrition.- 7.1. Adult Worms.- 7.2. Muscle Larvae.- References.- 5 Anatomical Pathology.- 1. Introduction.- 2. Gastrointestinal Tract.- 2.1. Gross Changes.- 2.2. Microscopic Changes.- 3. Striated Muscle.- 3.1. Gross Changes.- 3.2. Microscopic Changes.- 3.3. Encapsulation.- 3.4. Calcification.- 4. Other Organs Involved.- 4.1. Heart.- 4.2. Liver.- 4.3. Spleen.- 4.4. Kidneys.- 4.5. Eyes.- 4.6. Lungs.- 4.7. Central Nervous System.- 4.8. Bone Marrow.- 4.9. Other Locations.- References.- 6 Pathophysiology of the Gastrointestinal Phase.- 1. Format of This Review.- 2. Gastrointestinal Symptoms.- 3. Morphological Changes.- 3.1. Macroscopic.- 3.2. Histological.- 4. Physiological Changes.- 4.1. Epithelium-Related.- 4.2. Smooth-Muscle-Related.- 5. Bases for Functional Changes.- 5.1. Direct Action of Parasite.- 5.2. Influence of Lamina Propria.- 5.3. Endocrine Disturbances.- 6. Host-Parasite Interrelationships.- 7. Relationships between Pathophysiology and Symptoms.- 8. Summary.- References.- 7 Pathophysiology of the Muscle Phase.- 1. Introduction.- 2. Parasite-Induced Modifications in Host Striated Skeletal Muscle.- 2.1. Alterations Induced in the Host Myofiber during Contact and Entry by the Newborn First-Stage Larva.- 2.2. Alterations in Host Muscle during Growth and Development of the Muscle Larva.- 2.3. Mature Nurse Cell.- 2.4. Hypothesis: A Possible Mechanism by Which the Parasite Initiates Redifferentiation in the Host Myofiber.- 2.5. Benefits Derived by the Muscle Larva from Pathophysiological Alterations in Host Muscle.- 3. Cardiopathophysiology in Trichinosis.- References.- 8 The Immune Response.- 1. Introduction.- 2. Immunity and the Intestinal Phase.- 2.1. Immunity against Adult Worms in Primary Infections.- 2.2. Immunity against Adult Worms in Reinfections.- 2.3. Immunity against Preadult Stages-Rapid Expulsion.- 3. Immunity and Newborn Larvae.- 3.1. Active Immunity in Mice and Rats.- 3.2. Passive Immunity in Mice.- 3.3. Effects of Cells and Serum Components in Vitro.- 4. Genetic Influences on Immunity to Trichinella.- 5. Stage Specificity of the Immune Response.- 5.1. "Dual-Antibody" Hypothesis of Oliver-Gonzalez.- 5.2. Immunological Evidence.- 5.3. Parasitological Evidence.- 5.4. A Revision of the Dual-Antibody Hypothesis.- References.- 9 Antigens.- 1. Introduction.- 2. Source of Antigens.- 2.1. Cuticular Antigens.- 2.2. Excretory-Secretory Antigens.- 2.3. Somatic Antigens.- 3. Enumeration, Isolation, and Characterization of Antigens.- 4. Concluding Remarks.- References.- 10 Chemotherapy.- 1. Introduction.- 2. Experimental Chemotherapy.- 2.1. Methods.- 2.2. Drug Efficacy.- 3. Clinical Chemotherapy.- 3.1. Clinical Prophylaxis.- 3.2. Clinical Therapy (Treatment of Patent Infections).- References.- 11 Clinical Aspects in Man.- 1. Introduction.- 2. Infection and Disease.- 2.1. Proportion of Symptomatic and Asymptomatic Cases in Trichinosis.- 2.2. Course of Trichinosis.- 2.3. Severity of Trichinosis.- 2.4. Factors That Influence the Severity of Trichinosis.- 3. Symptoms, Signs, and Clinical Pathology.- 3.1. Abdominal Syndrome.- 3.2. General Trichinosis Syndrome.- 3.3. Signs of Allergic Vasculitis.- 3.4. Symptoms and Signs Associated with Muscle Tissue.- 3.5. Signs of Metabolic Disorders.- 3.6. Complications of Trichinosis.- 3.7. Pathology in Laboratory Tests.- 4. Diagnosis.- 4.1. Clinical History-Taking.- 4.2. Physical Examination.- 4.3. Paraclinical Tests.- 4.4. Finding the Parasite.- 4.5. Differential Diagnosis of Trichinosis.- 5. Management and Treatment.- 5.1. Treatment of the Intestinal Infection.- 5.2. Acute Severe Trichinosis.- 5.3. Moderate or Mild Trichinosis.- 5.4. Late and Convalescent Phases of Trichinosis.- 5.5. Trichinosis in Children, Pregnant and Lactating Women, and Immunosuppressed Patients.- References.- 12 Immunodiagnosis in Man.- 1. Introduction.- 2. Immunodiagnostic Methods.- 2.1. Parasite Antigens.- 2.2. Indirect Immunofluorescence.- 2.3. Passive Hemagglutination.- 2.4. Enzyme-Linked Immunosorbent Assay.- 2.5. Counterimmunoelectrophoresis.- 2.6. Other Serological Methods.- 2.7. Skin Tests.- 3. Evaluation and Recommendation.- 4. Conclusions.- 5. Protocols for Indirect Immunofluorescence and Enzyme-Linked Immunosorbent Assay.- 5.1. Indirect Immunofluorescence.- 5.2. Enzyme-Linked Immunosorbent Assay.- References.- 13 Epidemiology I: Modes of Transmission.- 1. Introduction.- 2. Sylvatic Cycle.- 3. Domestic Cycle.- 4. Special Epidemiological Circumstances.- 5. Susceptible Host Species.- References.- 14 Epidemiology II: Geographic Distribution and Prevalence.- 1. Introduction.- 2. North America.- 2.1. Canada and Alaska.- 2.2. Greenland.- 2.3. United States.- 2.4. Latin America.- 3. Europe.- 3.1. British Isles.- 3.2. Germany.- 3.3. Austria.- 3.4. Switzerland.- 3.5. The Netherlands.- 3.6. Belgium.- 3.7. France.- 3.8. Spain.- 3.9. Portugal.- 3.10. Italy.- 3.11. Greece.- 4. Scandinavia.- 4.1. Norway.- 4.2. Sweden.- 4.3. Denmark.- 4.4. Finland.- 5. Eastern Europe.- 5.1. Poland.- 5.2. Czechoslovakia.- 5.3. Hungary.- 5.4. Romania.- 5.5. Yugoslavia.- 5.6. Bulgaria.- 6. Union of Soviet Socialist Republics.- 7. Asia.- 7.1. Middle East.- 7.2. Southeast Asia.- 7.3. Far East.- 8. Africa.- 9. Australia, New Zealand, and Pacific Islands.- References.- 15 Control I: Public-Health Aspects (with Special Reference to the United States).- 1. Introduction.- 2. Mechanisms of Control.- 2.1. Prevention of Swine Infections.- 2.2. Detection of Infected Swine.- 2.3. Rendering Infected Pork Noninfective.- 2.4. Game Foods.- 3. Measures Adopted in the United States.- 3.1. Control of Garbage.- 3.2. Regulation of Commercial Pork Products.- 3.3. Game Foods.- 3.4. Education.- 3.5. The Future.- References.- 16 Control II: Surveillance in Swine and other Animals by Muscle Examination.- 1. Introduction.- 1.1. General Methods and Uses.- 1.2. Criteria for Use.- 2. Trichinoscopic Method.- 2.1. Use.- 2.2. Procedure for Swine Diagnosis.- 2.3. Drawbacks.- 2.4. Other Uses.- 3. Basic Digestion Method.- 3.1. Basic Procedure.- 3.2. Modifications.- 3.3. Advantages and Disadvantages.- 4. Pooled Digestion Methods.- 4.1. Pooled-Sample Method: Procedure.- 4.2. Stomacher Method: Procedure.- 4.3. Other Modifications.- 5. Other Direct Diagnostic Methods.- 5.1. Mechanical Disintegration Method.- 5.2. Microscopic Section (Biopsy Method).- 5.3. Xenodiagnosis.- 6. Summary.- References.- 17 Control III: Surveillance in Swine by Immunodiagnostic Methods.- 1. Introduction.- 2. Serological Methods.- 2.1. Complement-Fixation Test.- 2.2. Particle-Agglutination Methods.- 2.3. Indirect Immunofluorescence Test.- 2.4. Enzyme Immunoassays.- 2.5. Radioimmunoassay.- 3. Sensitivity and Specificity.- 4. Antigen Preparation and Purification.- 5. Evaluation of Serological Methods in Various Geographic Areas.- 5.1. Evaluation of the Enzyme-Linked Immunosorbent Assay in the United States.- 5.2. Evaluation of the Enzyme-Linked Immunosorbent Assay in European Countries.- 6. Mechanization.- 6.1. Mechanized System for the Macro-Enzyme-Linked Immunosorbent Assay.- 6.2. Mechanized System for the Micro-Enzyme-Linked Immunosorbent Assay.- 7. Surveillance by Serological Methods.- 7.1. Inspection at the Slaughterhouse.- 7.2. Inspection at the Farm.- 7.3. Individual vs. Population Control.- 7.4. Legislation.- 8. Concluding Remarks.- References.- Appendix 1 Synopsis of Morphology.- 1. Introduction.- 2. Morphology of the Adult Male.- 3. Morphology of the Adult Female.- 4. Morphology of the Infective First-Stage Larva.- References.- Appendix 2 Laboratory Techniques.- Methods.- References.

Trichinella and Trichinosis

The protective mucosal response against gastrointestinal nematodes in ruminants and laboratory animals

Generalized linear modelling for parasitologists

The clinical and autopsy findings of a two and a half year-old infant with Toxocara sp. infection of the brain and granulomatous lesions in the liver are reported. The cause of death was non-accidental injury. The relationship between Toxocara infection and behavioural disorders is discussed.

Toxocara canis larvae in the brain of a British child

A glass chamber method of counting living microfilariae in 20–100 c.mm. samples of freshly haemolyzed blood proved to be substantially more sensitive than, and as reliable as, the use of standard wet or stained dry films. The method has the further advantages of simplicity and brevity. The results showed that with the “normal” thick smear technique between 30 and 40% of microfilariae are lost during processing of the slide. It is suggested that the chamber counting method has practical field and laboratory utility.

Comparison of a counting chamber and thick smear methods of counting microfilariae

Studies with Brugia pahangi. I. Parasitological observations on primary infections of cats (Felis catus).

Studies with Brugia pahangi. II. The effect of repeated infection on parasite levels in cats.

The anthelmintic effects of flubendazole (methyl [5-(4-fluorobenzoyl)-1-H-benzimidazol-2-yl] carbamate) (Janssen Pharmaceutica) were evaluated in jirds (Meriones unguiculatus) and cats (Felis cattus) infected with Brugia pahangi. Flubendazole was macrofilaricidal at 5 × 2·5 mg/kg and 1 × 25 mg/kg in jirds and 1 × 100 mg/kg in cats when administered by subcutaneous injection. It also killed developing larvae in jirds. It was not microfilaricidal.

D. A. Denham

Papers

Toxocara canis larvae in the brain of a British child

Comparison of a counting chamber and thick smear methods of counting microfilariae

Studies with Brugia pahangi. I. Parasitological observations on primary infections of cats (Felis catus).

Studies with Brugia pahangi. II. The effect of repeated infection on parasite levels in cats.

The anthelmintic effects of flubendazole on Brugia pahangi