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Anatomy of body water and electrolytes

Rocky Mountain spotted fever (RMSF) is a life-threatening disease caused by Rickettsia rickettsii, an obligately intracellular bacterium that is spread to human beings by ticks. More than a century after its first clinical description, this disease is still among the most virulent human infections identified, being potentially fatal even in previously healthy young people. The diagnosis of RMSF is based on the patient's history and a physical examination, and often presents a dilemma for clinicians because of the non-specific presentation of the disease in its early course. Early empirical treatment is essential to prevent severe complications or a fatal outcome, and treatment should be initiated even in unconfirmed cases. Because there is no vaccine available against RMSF, avoidance of tick-infested areas is still the best way to prevent the infection.

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Rocky Mountain spotted fever.

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

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Pharmacology and toxicology.

It has become increasingly apparent that no single method for teaching anatomy is able to provide supremacy over another. In an effort to consolidate and enhance learning, a modernized anatomy curriculum was devised by attempting to take advantage of and maximize the benefits from different teaching methods. Both the more traditional approaches to anatomy teaching, as well as modern, innovative educational programs were embraced in a multimodal system implemented over a decade. In this effort, traditional teaching with lectures and dissection was supplemented with models, imaging, computer-assisted learning, problem-based learning through clinical cases, surface anatomy, clinical correlation lectures, peer teaching and team-based learning. Here, we review current thinking in medical education and present our transition from a passive, didactic, highly detailed anatomy course of the past, to a more interactive, as well as functionally and clinically relevant anatomy curriculum over the course of a decade.

Modernization of an anatomy class: From conceptualization to implementation. A case for integrated multimodal-multidisciplinary teaching.

PERIPHERAL circulatory failure is an important complication of Rocky Mountain spotted fever. Previous studies have shown that the collapse occurs usually in the second week of rash and that the disturbance can be alleviated by the administration of preformed protein. 1 The mechanism responsible for the circulatory changes is obscure, but the peripheral collapse is accompanied with a drop in serum proteins and with the development of visible generalized edema. 2 The resemblance of the clinical picture to "shock" suggests that a drop in the circulating blood volume occurs. The present studies were undertaken to determine whether the blood volume is altered, to observe the time at which the changes develop and to correlate the magnitude of the alterations with the clinical picture and other pertinent laboratory data. Determinations of the plasma volume and the thiocyanate space were done serially in a group of patients with rickettsial spotted fever,

PATHOGENESIS OF CIRCULATORY FAILURE IN ROCKY MOUNTAIN SPOTTED FEVER: Alterations in the Blood Volume and the Thiocyanate Space at Various Stages of the Disease

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The exchangeable potassium content of normal women.

Osler's practice.

Supportive therapy has not been as effectively used in Rocky Mountain spotted fever as it might be. Several misconceptions, including the idea that intravenous fluids are harmful, have been allowed to remain unchallenged in the literature. Specific therapy with hyperimmune antiserum is not widely used as yet and is usually given too late to be of greatest benefit. Before its efficacy can be evaluated, basic supportive therapy must be better standardized. The usual treatment of the disease consists in general supportive measures and the relief of symptoms. It is true that poorly directed or unwisely chosen parenteral supportive therapy may prove harmful. Because parenteral therapy has been given to poor advantage in some cases, statements such as the following have been made: "In recent years, many physicians of wide experience with spotted fever have advised against transfusions and intravenous fluids. They have observed that patients receiving this type of treatment

The treatment of rocky mountain spotted fever: with particular reference to intravenous fluids a new approach to basic supportive therapy

The underlying physiological disturbances responsible for death during the course of acute infections remain a mystery. Thousands of years ago men began to record descriptions of febrile illnesses. A particular type of rash might be accompanied by a slow or fast pulse and by a steady or remitting type of fever, which would run its course within a reasonably constant period of time and would be followed by a period of convalescence. On the basis of clinical observations, various specific diseases were separated from one another—the small from the great pox, the typhuslike, or typhoid, fever from typhus. In the course of some acute infections the appearance of edema was noted; in others edema was not visible, but diuresis occurred during recovery—an observation which suggested that fluid was retained in the tissues, whether it was obvious or not. With the introduction of immunologic techniques, it was recognized that the patient

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George T. Harrell

Papers

PATHOGENESIS OF CIRCULATORY FAILURE IN ROCKY MOUNTAIN SPOTTED FEVER: Alterations in the Blood Volume and the Thiocyanate Space at Various Stages of the Disease

The exchangeable potassium content of normal women.

Osler's practice.

The treatment of rocky mountain spotted fever: with particular reference to intravenous fluids a new approach to basic supportive therapy

Alterations in the permeability of membranes during infections.