There are many stories, and many names well known to public health workers, as well as many whose work should be better known than it is. For example, in 1943 this reviewer was privileged to work with Benjamin E. Holsendorf in the East Harlem district of New York City in a rat control campaign, and it was a pleasure to find his important work on ratproofing given extensive and sympathetic consideration by Dr. Williams. This book is a notable contribution to the still unwritten history of American public health and will very probably be the standard work on the subject for many years to come. GEORGE ROSEN

https://ajph.aphapublications.org/doi/pdfplus/10.2105/AJPH.42.7.873-a

The Zoology of Tapeworms

Publisher Summary A number of studies have been made on the variation in morphology of fluke-host snails, apart from the problem of taxonomy. In order to clarify the taxonomy of these snails, a study was made of 61 populations from 42 localities in New South Wales, South Australia, Queensland, Victoria and Tasmania, and some specimens forwarded by several collaborators in New Zealand. Two extreme morphological types, “A” and “B,” were recognized, and both serve as intermediate hosts for F.hepatica. Snails collected in the field showed great variations in shell and body and there were many intermediates between the extreme variants. In the assessment of various factors influencing the epidemiology and control of fascioliasis because of F. hepatica or F. gigantica, it should be assumed that all lymnaeid snails may aestivate for a considerable time during dry periods at both low and high temperatures. Empirical screening for new and more efficient anthelmintics against F. hepatica has been fairly successful, but has still failed to produce the ideal drug for safe, economic, and preventive medication of fascioliasis. More knowledge on the intermediary metabolism of F. hepatica, particularly of enzyme activity in the pathways, may lead to a new revolutionary approach for selecting a substance for the elimination of the parasites.

Experimental fascioliasis in Australia.

In this review, we describe the current knowledge on the systematics, ecology and epidemiology of Trichinella and trichinellosis, and the impact of recent research discoveries on the understanding of this zoonosis The epidemiology of this zoonosis has experienced important changes over the past two decades, especially with regard to the importance of the sylvatic cycle and the sylvatic species Outbreaks of trichinellosis due to Trichinella spiralis from domestic swine, while still frequent, increasingly are caused by other Trichinella spp infecting hosts such as horses, dogs, wild boars, bears and walruses The latter revelations have occurred as a result of a series of discoveries on the systematics of Trichinella spp, facilitated by new molecular tools As a consequence, the genus is now composed of two clades, an encapsulated group (five species and three genotypes) and a non-encapsulated one (three species) This has sparked renewed investigations on the host range of these parasites and their epidemiological features Most dramatic, perhaps, is the recognition that reptiles may also serve as hosts for certain species This new knowledge base, in addition to having an important relevance for food safety policies and protection measures, is raising important questions on the phylogeny of Trichinella spp, the ecological characteristics of the species and their geographic histories Answers to these questions may have great value for the understanding of the evolutionary biology for other parasitic helminths, and may increase the value of this genus as models for research on parasitism in general

Systematics and epidemiology of trichinella.

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

Allergic inflammation as a hypothesis for the expulsion of worms from tissues: a review.

A histopathologic study of the anterior small intestine of immunized and nonimmunized mice infected with Trichinella spiralis.

Cercariae and adult males and females of Schistosoma mansoni were studied by scanning electronmicroscopy, and the eggs of this species were studied by this technique as well as by transmission electronmicroscopy. The observations of the eggs by the transmission technique revealed shell pores, epicuticular microbarbs, and other structures noted in our previous study. The various observations with the scanning technique used to study the eggs, cercariae, and adult worms are noted and illustrated by selected micrographs.

Scanning and transmission electronmicroscopy of Schistosoma mansoni eggs, cercariae, and adults.

Publisher Summary This chapter discusses cell-mediated immunity (CMI) against certain parasitic worms. The field of CMI evolved after many years of intensive studies of delayed hypersensitivity (DH); the paradigm for DH is seen in tuberculosis, which induces a characteristic delayed dermal sensitivity reaction after a skin test. The parasitic worms discussed in the chapter are nematodes, cestodes, and trematodes. The first successful adoptive transfer of immunity against an animal parasite was reported in 1964; lymph node cells and peritoneal-exudate cells were transferred in mice. Evidence for cell-mediated immunity against Trichinella spiralis (T. spirafis) in mice was suggested by the results of studies with antithymocyte serum (ATS). The chapter discusses the immune response to Nippostrongylus brasiliensis (N. brasiliensis) in rats as well as the effects of this response on the parasite itself. In studies with the Schistosoma mansoni -mouse model, it was shown that lymph node cells from infected mice underwent vigorous transformation (blastogenesis) in response in vitro to a soluble egg antigen.

John E. Larsh

Papers

Allergic inflammation as a hypothesis for the expulsion of worms from tissues: a review.

A histopathologic study of the anterior small intestine of immunized and nonimmunized mice infected with Trichinella spiralis.

Scanning and transmission electronmicroscopy of Schistosoma mansoni eggs, cercariae, and adults.

Cell-mediated immunity against certain parasitic worms.

Studies on delayed (cellular) hypersensitivity in mice infected with trichinella spiralis. ii. transfer of peritoneal exudate cells.