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Several ligands have become available now, including radiolabelled analogues. In this book, the current state of affairs with regards to the medicinal chemistry and pharmacology of the H3 receptor and the several ligands available are presented by a number of experts in the field. The book presents an extended review of what has happened since the first H3 paper appeared.

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The editors hope that publication of this work will lead to an increase in interest of both academia and industry for the H3 receptor, especially as a target for drug development. This book will be of interest to medicinal chemists, pharmacologists, biochemists and neurologists and will also be a valuable source of reference for medical students and postgraduate students in related fields. Organic chemistry has a long-standing reputation as a difficult course. Organic Chemistry I For Dummies takes a simple approach to the topic, allowing you to grasp concepts at your own pace.

This fun, easy-to-understand guide explains the basic principles of organic chemistry in simple terms, providing insight into the language of organic chemists, the major classes of compounds, and top trouble spots. You'll also get the nuts and bolts of tackling organic chemistry problems, from knowing where to start to spotting sneaky tricks that professors like to incorporate. Baffled by benzines? Confused by carboxylic acids? Here's the help you need—in plain English! Readers are guided on planning and execution of multi-step synthetic reactions, with detailed descriptions of all the reactions.

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The last 10 chapters cover the nature and the scope of organic reactions and their mechanisms. The 7th edition proves again it is a must-have desktop reference and textbook for every student and professional working in organic chemistry or related fields. We are confident that this book will remain a dominant reference and that it will reside on many chemists' personal bookshelves. The authors are careful to present new information such that it links it to existing content, ever mindful that students assimilate new information only in the proper context. The enriched assessment content in WileyPLUS Learning Space offers students the opportunity to gauge their conceptual understanding and receive immediate feedback to address misconceptions.

This is a revised edition of a very successful book, which appeals to both academic and industrial markets. With its balanced presentation of polymer chemistry, physics, and engineering applications, the Third Edition of this classic text continues to instill readers with a solid understanding of the core concepts underlying polymeric materials. Both students and instructors have praised the text for its clear explanations and logical organization.

It begins with molecular-level considerations and then progressively builds the reader's knowledge with discussions of bulk properties, mechanical behavior, and processing methods. Following a brief introduction, Fundamental Principles of Polymeric Materials is divided into four parts:. Readers familiar with the previous edition of this text will find that the organization and style have been updated with new material to help them grasp key concepts and discover the latest science, techniques, and applications.

For example, there are new introductory sections on organic functional groups focusing on the structures found in condensation polymerizations.

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The text also features new techniques for polymer analysis, processing, and microencapsulation as well as emerging techniques such as atom transfer radical polymerization. At the end of each chapter are problems—including many that are new to this edition—to test the reader's grasp of core concepts as they advance through the text. There are also references leading to the primary literature for further investigation of individual topics. A classic in its field, this text enables students in chemistry, chemical engineering, materials science, and mechanical engineering to fully grasp and apply the fundamentals of polymeric materials, preparing them for more advanced coursework.

So, you survived the first semester of Organic Chemistry maybe even by the skin of your teeth and now it's time to get back to the classroom and lab! Organic Chemistry II For Dummies is an easy-to-understand reference to this often challenging subject. Thanks to this book, you'll get friendly and comprehensible guidance on everything you can expect to encounter in your Organic Chemistry II course.

Whether you're confused by composites, baffled by biomolecules, or anything in between, Organic Chemistry II For Dummies gives you the help you need — in plain English! Biomanufacturing facilities that are designed and built today are radically different than in the past. This is the first book for architects and designers that fills this void.

Process Architecture in Biomanufacturing Facility Design provides information on design principles of biopharmaceutical manufacturing facilities that support emerging innovative processes and technologies, use state-of-the-art equipment, are energy efficient and sustainable, and meet regulatory requirements. Relying on their many years of hands-on design and operations experience, the authors emphasize concepts and practical approaches toward design, construction, and operation of biomanufacturing facilities, including product-process-facility relationships, closed systems and single use equipment, aseptic manufacturing considerations, design of biocontainment facility and process based laboratory, and sustainability considerations, as well as an outlook on the facility of the future.

Process Architecture in Biomanufacturing Facility Design is an ideal text for professionals involved in the design of facilities for manufacturing of biopharmaceuticals and vaccines, biotechnology, and life-science industry, including architects and designers of industrial facilities, construction, equipment vendors, and mechanical engineers. It is also recommended for university instructors, advanced undergraduates, and graduate students in architecture, industrial engineering, mechanical engineering, industrial design, and industrial interior design.

Highly illustrated and clearly written, this award-winning reference work provides an excellent guide to this fast-growing field. The Immunoassay Handbook reviews a wide range of topics, now including lateral flow, microsphere multiplex assays, immunohistochemistry, practical ELISA development, assay interferences, pharmaceutical applications, qualitative immunoassays, antibody detection and lab-on-a-chip. This handbook is a must-read for all who use immunoassay as a tool, including clinicians, clinical and veterinary chemists, biochemists, food technologists, environmental scientists, and students and researchers in medicine, immunology and proteomics.

It is an essential reference for the immunoassay industry. Provides an excellent revised guide to this commercially highly successful technology in diagnostics and research, from consumer home pregnancy kits to AIDS testing. The content is designed to encourage purchases of single chapters or the entire book. David Wild is a healthcare industry veteran, with experience in biotechnology, pharmaceuticals, medical devices and immunodiagnostics, which remains his passion. He led research and development programs, design and construction of chemical and biotechnology plants, and integration of acquired companies.

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Main contents are comprehensive sample pyrograms, thermograms, identification tables, and representative mass spectra MS of pyrolyzates for synthetic polymers. This edition also highlights thermally-assisted hydrolysis and methylation technique effectively applied to 33 basic condensation polymers. Unlike humans, who gather information largely through sight and sound, most living creatures rely heavily on chemical compounds from other organisms for their basic knowledge of the world.

Among the various types of these compounds are the chemical signals exchanged between members of the same species that govern social interactions crucial to survival. These signals are called pheromones from the Greek "pherein"--to carry--and "hormon"--exciting and they are used to send warnings, establish territorial boundaries, provoke aggression, control sexual behavior, and locate food. In this volume, organic chemist William C. Agosta explores the chemistry of pheromones and the mechanisms by which they orchestrate animal behavior.

Professor Agosta details the intricate process of identifying pheromones and determining the active components within these sometimes highly complex mixtures. He also demonstrates the value of this growing body of knowledge to our understanding of evolution, ecology, human behavior, and agricultural production. The result is a fascinating look at a research area that brings together investigators, information, technologies, and procedures from the fields of biology, chemistry, and behavioral science. Chemical Communication spans the entire spectrum of life, from simple organisms, such as water molds and brown algae, to insects, birds, fish, reptiles, mammals, and in a provocative final chapter, human beings.

Along the way, Dr. Agosta provides dozens of captivating examples of pheromones in action: certain male red-sided garter snakes, which increase their chances of mating successfully by "impersonating" a female, thus distracting rivals; or the bolas spiders, which capture male moths by hitting them with an adhesive ball on a string after emitting a female moth pheromone that lures the males within range.

The book also includes important evidence that pheromones alter physiology as well as behavior. For example, young female mice reach maturity at an accelerated pace after constant exposure to adult male mice. With topics such as stereochemistry, carboxylic acids, and unsaturated hydrocarbons, it's no wonder so many students have a bad reaction to organic chemistry class.

Fortunately, this guide gives college students who are required to take organic chemistry an accessible, easy-to-follow companion to their textbooks. Account Options Prijavite se. Ljestvice popularnosti. Similar Ebooks. Knjiga The 8th Camerino-Noordwijkerhout Symposium has continued along its traditional path of interdisciplinary cooperation. Chemists, biochemists, pharmacologists, biophysicists and physiologists are all involved in the task of improving our knowledge of the mechanisms of drug-receptor interaction and of the heterogeneous nature of biological molecules.

In this volume, leading researchers have contributed state of the art information on receptor chemistry. Newest developments are covered with particular reference to receptors of the nervous system; SAR studies; receptor isolation; receptor cloning; receptor topography; biomedical consequences of occupancy; receptor regulation and receptor theory. This will be of great interest to pharmacologists, biochemists and medicinal chemists, as well as a valuable source of reference for medical students and postgraduate students in related fields.

Pharmacochemistry Library, Volume Small Peptides: Chemistry, Biology, and Clinical Studies focuses on the processes, reactions, properties, and characteristics of peptides, including analogues and proteases. The text then elaborates on bradykinin, cholecystokinin, and enkephalin analogues. The manuscript examines luteinizing hormone releasing hormone and somatostatin. Topics include enzymic degradation of somatostatin and analogues, clinical applications of somatostatin analogues, and pharmacological and clinical studies with LHRH agonists and antagonists. The formulation of peptides and inhibitors of aspartyl proteases are also mentioned.

The book is a valuable source of information for chemists, biologists, and readers interested in small peptides. Its current indications refractory ovarian and metastatic breast cancer may soon be expanded since the drug is showing activity against lung and head-and-neck cancers. Perspectives in Receptor Research.

Approaches to Design and Synthesis of Antiparasitic Drugs. This book presents a comprehensive and up to date account of the chemotherapy of parasitic diseases, both human and veterinary. The book starts with an overview of parasitic diseases. The body of the book is divided into two parts: antihelminthic drugs, and antiprotozoal drugs. Both parts start with chapters highlighting the 'biochemical targets' available for chemotherapeutic interference.

Individual chapters deal with one chemical class of compounds and describe their origin, structure-activity relationship, mode of action, and methods of synthesis and their status both in clinical and veterinary practice. The book will be useful to a wide spectrum of readers: students embarking on a research career in parasitic chemotherapy, clinicians and veterinarians and clinical pharmacologists desiring detailed information about the drugs currently in use, and pharmaceutical technologists wanting to update their knowledge of the methods of manufacture.

Serotonin Receptors and their Ligands. An international group of authors have produced an overview of the progress made in the medicinal chemistry of compounds selectively acting at serotonin receptors or serotonin transporters either as agonists, partial agonists or antagonists. The potential therapeutic applications of ligands of the different subtypes are described. Altogether an excellent addition to the Pharmacochemical Library series.

Vaso-occlusive disorders including unstable angina, myocardial infarction, transient ischemic attacks, stroke and peripheral artery disease remain the major sources of morbidity and mortality in western civilization. Platelet activation and resulting platelet aggregation play a major role in the pathogenesis of these thromboembolic diseases. Recognition of the contribution of platelets to the pathophysiology of cardiovascular disease has provided impetus for the continued search for new antiplatelet agents. Hence, over the past two decades many strategies have been evaluated in the search for efficacious mechanisms to reduce platelet function.

The medical need for more efficacious antithrombotic drugs and the growing understanding of the role of platelets in vascular injury have catalyzed the extensive evaluation of novel approaches to control platelet function. Along these lines, the volume therefore provides an in-depth assessment of ongoing clinical trials, new and clinically established agents, and other developments in this rapidly developing field. Trends in Drug Research II. This volume of Pharmacochemistry Library comprises the text of invited lectures presented at the 11th Noordwijkerhout-Camerino Symposium Trends in Drug Research, held in Noordwijkerhout, The Netherlands, from May In the early eighties when the H3 receptor was identified, many thought that an H3 ligand, an agonist or an antagonist, would become available as a therapeutic agent.

This has not occurred. The reason for this could be the fact that many investigators consider histamine mainly, if not only, as a mediator present in for example mast cells being released during allergic events. However, it has become apparent that histamine is an important neurotransmitter. Its role in the nervous system, especially in the central part of it, is rather extensive. Receptor Chemistry Towards the Third Millennium. Although much is known about the way ligands interact with receptors, which have now been isolated, characterized and cloned, many aspects still remain to be explored.

In particular, differentiation into distinct subpopulations and the multiplicity of transduction processes offer more specific targets in the search for new drugs. Arthur Winter. While this version features a new Dummies cover and design, the content is the same as the prior release and should not be considered a new or updated product. The easy way to take the confusion out of organic chemistry Organic chemistry has a long-standing reputation as a difficult course.

Refreshed example equations New explanations and practical examples that reflect today's teaching methods Fully worked-out organic chemistry problems Baffled by benzines? David R. Helps develop the skills needed to solve a variety of problem types. Presents the fundamental topics clearly with an informal, friendly tone. Describes the how-to of problem solving, including approaching problems strategically. Discusses the relationship between concepts and puts topics in context. Covers important areas such as resonance, nomenclature, conformations, substitution reactions, synthesis and more.

Charles Bamforth. Written by one of the world's leading authorities and hailed by American Brewer as "brilliant" and "by a wide margin the best reference now available," Beer offers an amusing and informative account of the art and science of brewing, examining the history of brewing and how the brewing process has evolved through the ages. The third edition features more information concerning the history of beer especially in the United States; British, Japanese, and Egyptian beer; beer in the context of health and nutrition; and the various styles of beer.

Author Charles Bamforth has also added detailed sidebars on prohibition, Sierra Nevada, life as a maltster, hopgrowing in the Northwestern U. Finally, the book includes new sections on beer in relation to food, contrasting attitudes towards beer in Europe and America, how beer is marketed, distributed, and retailed in the US, and modern ways of dealing with yeast. Readers continue to turn to Klein's Organic Chemistry As a Second Language: Second Semester Topics, 4th Edition because it enables them to better understand fundamental principles, solve problems, and focus on what they need to know to succeed.

The fourth edition explores the major principles in the field and explains why they are relevant. It is written in a way that clearly shows the patterns in organic chemistry so that readers can gain a deeper conceptual understanding of the material. Topics are presented clearly in an accessible writing style along with numerous hands-on problem solving exercises.

Introduction to Organic Chemistry, 6th Edition: Edition 6. William H. Introduction to Organic Chemistry, 6th Edition provides an introduction to organic chemistry for students who require the fundamentals of organic chemistry as a requirement for their major. It is most suited for a one semester organic chemistry course. In an attempt to highlight the relevance of the material to students, the authors place a strong emphasis on showing the interrelationship between organic chemistry and other areas of science, particularly the biological and health sciences.

The text illustrates the use of organic chemistry as a tool in these sciences; it also stresses the organic compounds, both natural and synthetic, that surround us in everyday life: in pharmaceuticals, plastics, fibers, agrochemicals, surface coatings, toiletry preparations and cosmetics, food additives, adhesives, and elastomers. James W. The book will help students understand and practice good lab safety. It will also help students become familiar with basic instrumentation, techniques and apparatus and help them master the latest techniques such as interpretation of infrared spectroscopy.

The guide is mostly macroscale in its orientation. Michael B. Reviews of the previous edition: " Donald Voet. While continuing in its tradition of presenting complete and balanced coverage that is clearly written and relevant to human health and disease, Fundamentals of Biochemistry, 5e includes new pedagogy and enhanced visuals that provide a pathway for student learning. Richard B. The Organic Chemistry of Enzyme-Catalyzed Reactions is not a book on enzymes, but rather a book on the general mechanisms involved in chemical reactions involving enzymes. An enzyme is a protein molecule in a plant or animal that causes specific reactions without itself being permanently altered or destroyed.

Illustrates the organic mechanism associated with each enzyme-catalyzed reactionMakes the connection between organic reaction mechanisms and enzyme mechanismsCompiles the latest information about molecular mechanisms of enzyme reactionsAccompanied by clearly drawn structures, schemes, and figuresIncludes an extensive bibliography on enzyme mechanisms covering the last 30 yearsExplains how enzymes can accelerate the rates of chemical reactions with high specificityProvides approaches to the design of inhibitors of enzyme-catalyzed reactionsCategorizes the cofactors that are appropriate for catalyzing different classes of reactionsShows how chemical enzyme models are used for mechanistic studiesDescribes catalytic antibody design and mechanismIncludes problem sets and solutions for each chapter Written in an informal and didactic style.

The usual mode of infection is the consumption of water and vegetablescontaminated with the ova of T. The disease is usually asymptomatic in thecase of light infection; however, heavy infections may lead to anaemia, eosinophilia,abdominal pain, diarrhea, mucoid stool and occassional prolapse of the rectum.

The parasites possess slender andthread-like structures, hence called threadworms. They live burried in the intestinalmucosa of human. The movement of larval and adult parasites produces several pathologicalchanges like inflammation of the cells, allergic reactions and eosinophilia. The clinicalmanifestations of the disease include attacks of diarrhea, diffused abdominal pain,epigastric discomfort and hunger pains, which may lead to false diagnosis of pepticulcer. Heavy infections may cause malabsorption, flatulence and abdominal disten-sion.

The adult worms liveattached to the mucosa of the lower ileum, caecum and terminal parts of the colon. Man acquires the infection by ingestion of eggs of E. Since the eggs are resistant to desiccation, the infection also occurs bvconsuming raw vegetables, food and drinks contaminated with pinworm eggs. Scratching of the perianal skin may lead to dermatitis,eczema and secondary bacterial infections. The patient may also suffer from ano-rexia, restlessness, insomnia and mild to acute abdominal pain.

Occasionally,vulvovaginitis may also occur in young girls. Trichostrongylus orientalis is the main etiological agent in humans. The adultworms live embedded through their heads in the mucosa of the duodenum and jeju-num. Human acquires the infection when the semi-filariform larvae of Trichos-trongylus species enter the body through skin or mouth while consuming contami-nated drinks. The use of night-soil as fertilizer in some countries and resistant na-ture of the eggs provide a strong basis for propagation of this infection in farmingcommunities.

Trichostrongyloidiasis is generally symptomless and little is known about its. However, severe infections may give rise to mild anaemia as the wormsmay suck blood with their capillary heads embedded in the mucosa. Later the infection was reported from other adjacent provincesand from southern Thailand [27]. The adult worms of C. Some worms may also be seen moving free in other parts of the ali-mentary canal such as larynx, oesophagus, stomach and colon. The infection occurswhen infected fresh water fish and crustaceans are eaten raw by man.

The infectioncauses a syndrome which resembles with that of autoinfected and disseminatedstrongyloidiasis giving rise to abdominal pain, vomiting, malaise, nausea and ano-rexia. In chronic cases, there is cachexia with muscle weakness, muscle wasting anddepletion of minerals. In addition, there is protein losing enteropathy with extrememalabsorption of sugars and fat. There is continuous weight loss and often leads todeath of the patient within months [28].

The causative agents of the disease, Angiostrongylus costaricensis and A. Chemotherapy is usually not verysatisfactory. Sometimes surgical intervention may be required. The adult worms live in the small intestine of man. The infection alsooccurs in cats, dogs, pigs, polar bears, seals and whales. It is a widespread infectionoccuring throughout the temperate regions of the world and is found especially inpeople eating undercooked pork and pork products.

Trichinosis is transmitted to humans, when they eat infected pork. The hogsand rats serve as the reserviors of T.

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However two hosts are required to. This may be a hog-to-man, rat-to-hog or hog-to-hog cycle for the T. Humans, hogs and rats are infected by eat-ing infected pork containing the cysts of T. On reaching the digestive tract,the larvae emerge from the cysts and mature into adult males and females within afew davs. The fertilized females liberate larvae in the intestinal mucosa.

These cysts survive for several years and develop into adults on gettingfavourable conditions. The hogs become infected when they feed on the garbage containing infectedpork scraps hog-to-hog cycle. The hogs may also acquire the infection by eatingrats infected with T. The hog-to-man cycle arises when man eats the infected pork andpork products. The presence of larvae and cysts of T.

Sometimesdeath may occur due to toxemia, trichinous encephalitis or myocardial damagecaused by invasion of musculature by the larvae. The clinical symptoms of the disease are variable and depend upon the inten-siW of the infection. The presence of adult and larval parasites may give rise to ab-dominal pain, nausea, vomiting, diarrhea and blood in stool. The migration of larvaeleads to high fever, edema of face, eyelids, muscular pain in chest wall, cough, dysp-noea and stiffness of limbs.

In severe cases, neurotoxic symptoms, myocardiasis,meningitis and encephalitis may also be observed in some patients. Some other nematodes like Uncinaria stenocephala European dog hookworm andGnathostoma spinigerum also produce somewhat similar cutaneous lesions. The creep-ing eruption is prevalent in different regions of the warm climates, especially in theAmericas, Africa and Asia. It is estimated that nearly 10 million people around theworld suffer from this disease [24]. Both wild and domestic cats and dogs are the natural reservoir hosts of A. The female worms produce eggs which pass out with the stool and de-.

Man gets infected when these larvaepenetrate the skin. The larvae produce serpiginous tunnels under the skin and donot undergo further development. The epidemiology and life cycle of G. The adult wormslive in the alimentary canal of cats, dogs and tigers. The eggs produced by the adultfemales come out with the faeces and become embryonated in the soil.

They hatchupon coming in contact with water and give rise to cylindrical, ensheathed andrhabditiform larvae. These larvae are ingested by copepods where further develop-ment of the parasite takes place. When fish, frogs, birds and snakes eat these in-fected copepods, they become infected and third stage larvae are generated. Humanacquires the infection by eating the above infected intermediate hosts. After infecting the humans, the larvae move under the skin at the rate of cm per day producing linear, erythematous and serpiginous tunnels.

This causes in-flammation and pruritus and may also damage lungs, kidneys, eyes and other partsof the body. In the case of gnathostomiasis, the patient may show edema, eosino-philia and leukocytosis. Some fatal cases of eosinophilic myeloencephalitis caused bythe migration of immature worms of G. The larvae of G. The disease is more common in children than the adults who often come incontact with the eggs of T. The infection by Toxocara in dogs is cosmopolitan; however, sur-veys indicate that it is prevalent in the U. In humans the rate or incidence of visceral larva migran is low; neverthelessnearly 10, people are estimated to carry this disease around the world [24].

After reaching the intestine of human, the eggs liberate larvae which pene-trate the bowel wall and enter the portal blood system from where they are carriedto the liver, lungs and different parts of the body. The larva seldom develops intothe adult in the human intestine as man is not its natural host.

In cats and dogs, thelarvae develop into male and female adults. Attacks of fever, malaise, nausea, vomit-ing, cough, abdominal pain, anorexia, weight loss and muscle and joint pain may beobserved occasionally. In chronic cases, the patient may report of some eye problemlike weak sight and impared vision resulting due to migration of larvae in the eyes. Liver complications like hepatitis and lung problems like cough and asthmatic at-tacks may occur due to migration of larvae to liver and lungs, respectively.

Similarly,involvement of brain in toxocariasis can give rise to an epilepsy like syndrome. According to recent esti-mates by the WHO, the world-wide prevalence of filariasis is about million[1,2]. The haematophagous arthopods, mosquitoes and flies, serve asthe intermediate hosts in the life cycle of the parasite. The transmission of the infec-tion to humans occurs when the mosquitoes feed on the blood of man. After reach-ing the blood circulation of man, the infective larvae undergo several moultings anddevelop into adult male and female worms living in lymph nodes, lymphatic ves-sels, connective tissues and other organs of the body.

The female worms produce mi-crofilariae which migrate to blood stream and are sucked by mosquitoes and flieswhere the life cycle of the parasite gets completed. The early phase of the infestation by W. Later the blockade of thelymphatic circulation occurs which leads to hydrocele and chyluria in thepatients. In chronic cases, the obstruction of the lymphatic system may takeplace causing massive enlargement of legs elephantiasis , arms, scrotum andbreasts.

The clinical characteristics of L. Sometimesthe adult worm may migrate in the eye ball giving rise to blindness and nervousdisorders. The O. The early stage of ocular onchocerciasis, caused by the presence of micro-filariae in the eyes, is marked by pain in the eyes, photophobia and lacrimationwhich gradually leads to conjunctivitis with eventual loss of vision. The infectionalso give rise to dermal problems and genital elephantiasis.

The filariases caused by M. However, M. Humans become infected with guinea worms by drinking water contami-nated by infected Cyclops. On reaching the intestine, the Cyclops get digested by gas-tric juice liberating free larvae which pierce the intestinal mucosa and reach the con-nective tissues where they live and attain sexual maturity in about a year.

After fertilization the female worms migrate under the skin and produce adermal blister which causes irritation. When the patient scratches the skin or theblisters come in contact with water, they burst liberating numerous motile rhabditi-form larvae which are soon engulfed by the Cyclops; thus the life cycle of the parasiteis completed.

The early stage of the infection produces no pathological sign. The worms re-quire months of incubation period before they are sexually mature. Symptomsappear only after the female is fertilized and is ready to discharge larvae. This stage ismarked by appearance of reddish papular lesions on legs and arms which cause itch-ing, fever, giddiness, utricaria and allergic reactions.

Repeated scratching of skin orcontact with water ruptures the blisters which release milky fluid with larvae whichmay lead to secondary infections. The migration of adult guinea worms to other partsof the body may result in neurological damage, joint swelling and arthritis. The disease has been reportedfrom different parts of Asia and Africa. Since the disease is associated with the respiratory system, its histopathologyis confusing. However, various lesions in the lungs may be seen with chest X-ray.

The clinical symptoms of the disease may range from mild to severe attacks ofcough, asthma and bronchitis. X-ray picture of lungs mayshow chronic bronchitis and other signs which are sometimes mistaken for Loeffler'ssyndrome or tuberculosis. In such cases, the antigen of D. Schistosoma haemato-bium, S. The adult worms of h u m a n schis-tosomes have separate sexes but they are dioecious existing together as males andfemales. The male worm has a groove gynecophoral canal along its ventral side inwhich it carries the female worm during most of its life span.

The adult worms of S. The worms excretetheir eggs in the urine of man but rarely in the faeces. The other three schistosomes S. Un-like the S. Schistosomiasis has a wide geographical distribution. It has been reportedfrom various parts of Africa, Asia and South America affecting nearly millionpeople around the world [2] of which 20 million people are estimated to suffer fromschistosomiasis in Egypt alone [36]. It has also been reported that S. Drinking of water containing cercariae of schistosomesmay also infect humans.

After reaching the blood circulation, the cercariae undergosome changes and eventually mature into male and female adults feeding on portalblood. When the female worms get fertilized they deposit their eggs on the walls ofthe urinary bladder S. When the eggs come in contact with water, they liberate free swimming em-bryos called miracidium which seeks its intermediate host, usually a fresh water oramphibious snail, and gets itself attached to the host's body.

If the miracidium doesnot find a snail it dies soon. After attaching to the body of a snail, the miracidiumpenetrates the musculature and reaches different parts of the body and produces amother sporocyst. The mother sporocyst then produces several daughter sporocystswhich later produce a large number of fork-tailed infective larvae called cercariae. These cercariae then leave the snail and swim freely in the water searching for theirdefinitive host, the humans, to complete the life cycle.

The pathological changes and clinical characteristics of schistosomiasis de-pends upon the nature and site of infestation in humans. The early phase of the dis-ease is marked by schistosoma dermatitis and katayama fever fever, chills, malaise. The main clinical manifestations of the disease are: a Urinogenital schistosomiasis: It is the most common form of schistosomiasisalong the Nile Valley in Egypt which involves different parts of the male and fe-male urinogenital system.

The main clinical symptoms may include formation ofkidney stones, renal failure, haematuria, renal and ureteric colic, fistula of bladder,penis and vagina, generation of ulcer leading to the formation of pus tracks in scro-tum and penis, swelling of testes and cancer of the bladder [38]. The liver also shows periportal cellular infiltration and fibrosis followedby wasting and swelling of the cells. The main diagnostic clinical symptoms ofhepatosplenic schistosomiasis are weakness, weight loss, epigastric discomfort, diar-rhea, enlargement of liver and spleen, swelling of limbs and clubbing of fingers.

The main clinical symptoms produced are peptic like ulceration,fistula of rectum and colon, rectal prolapse, rectal and anal polyposis leading to in-testinal obstruction due to large group of polyps, bouts of diarrhea and other gas-trointestinal disturbances. The penetration of worms into lungscauses fibrosis and obstruction of pulmonary blood circulation. The main clinicalmanifestations of this form of schistosomiasis are fatigue, palpitation, cardiac pain,giddiness and pulmonary hypertension.

Althoughseveral intestinal flukes such as Fasciolopsis buski, Heterophyes heterophyes, Metagonimusyokogawi, Echinostoma ilocanum and Gastrodiscoides hominis are parasitic to man, thepresent section is intended to deal only with the disease caused by the giant intestinalfluke, F. Fasciolopsiasis in man is acquired by eating raw stems, bulbs or fruits of somewater plants water chestnut or water caltrop infected heavily with the matacer-cariae of F.

These plants grow in ponds and other water reservoirs pollutedwith human excreta. The adult worms which are hermaphroditic, lay large number of eggs in theintestine of humans that are passed out with the faeces. These eggs hatch in freshwater and develop into miracidium and later enter the snail's body forming mothersporocysts, rediae, daughter rediae and finally cercariae. The cercariae encyst on dif-ferent parts of the edible aquatic plants from where they reach the human body andthe life cycle of the intestinal fluke is completed.

The mainclinical symptoms of the disease are abdominal pain and diarrhea with nausea, vom-iting and anorexia. Children show edema of the face; sometimes death may also oc-cur following cachexia. The main liver flukes infecting man are Fasciola hepatica, F. The liver rot disease, caused by F. Humans are infected by ingesting these encysted metacer-cariae through drinking water. The life cycle of F. The eggs excreted with the faeces of cattle, goats, sheep and humans hatch inwater giving rise to miracidia which infect a fresh water snail.

After undergoingsome development in the snail the parasite emerges out as cercariae which encyston aquatic plants as metacercariae. After reaching the intestine of the definite host,the metacercariae come out of the cyst and migrate through the intestinal wall andreach the liver parenchyma and bile ducts. The Chinese liver fluke disease is caused by C. Man is usually in-fected by eating raw, inadequately cooked or salted fish containing the metacer-cariae of C. The adult worms live in the bile duct and liver of cats, dogs,pigs and humans. They produce operculated eggs contanining fully developed mi-racidia.

The eggs are carried down through the bile to the duodenum from wherethey come out with the faeces. These eggs when ingested by the snail, develop intomother sporocysts, rediae and finally cercariae. After leaving the snail, the cercariaeswim in the water where they are swallowed by fishes. The cercariae may also pene-trate the skin of the fish below the scales and reach the musculature.

Here the cer-cariae get encysted and wait for the definite host to complete their life cycle. The lancet fluke infection is caused by D. The adult worms live in the bile duct of the host giving rise to various livertroubles. The disease is acquired by ingestion of metacercariae while snails and antsserve as the intermediate hosts in the worm's life cycle.

Since the seat of predilection of the liver flukes is liver or biliary passage, theclinical manifestations produced by them chiefly relate to liver and gastric problems. The early stage of the infection is marked by epigastric pain, fever and eosinophilia. Later the patient experiences diarrhea, anorexia, prolonged fever and abdominalpain. In chronic cases, the disease may lead to jaundice, cirrhosis of the liver andbiliary duct, ascites and cachexia. Sometimes the patient may die of serious livercomplications. The most common lung fluke infecting man is Paragonimus westermani.

Human acquires lung fluke infection by eating raw crabs and cray fishes in-fected with metacercariae. The adult worms live in the lungs of humans and pro-duce eggs which are excreted with sputum or swallowed to be passed out with fae-ces. The eggs hatch in water and liberate miracidia which later infect the snails andundergo luther development to mother sporocysts, rediae and cercariae.

The cer-cariae then attack their second intermediate hosts, the fresh water crabs and crayfishes where they encyst in the musculature and eventually develop into metacer-cariae. When humans eat these crabs and fish raw, the cysts dissolve and liberate themetacercariae in the duodenum. The liberated metacercariae penetrate the intestinalwall and migrate through different parts of the body to lungs where they developinto adults. Migration of the young flukes through different parts of the body producestunnels and cystic cavities giving rise to inflammatory reactions.

The main clinicalmanifestations of the disease are cough with gelatinous blood, stained sputum anddiscomfort in the chest. Mild anaemia, fever, body pain, adbominal pain and diar-rhea with occasional bloody mucus may also be observed. The parasite may migrateto the brain resulting in frequent Jacksonian type epilepsy. The intestinalcestode infections have a world-wide distribution, though they are more prevalent inthe tropical and sub-tropical regions.

Humansacquire the infection by eating raw or poorly cooked beef, pork or fish infected withthe larval cysts of tapeworms measly meat. The infection may also be acquired byingesting tapeworm eggs through drinking water, eating raw fruits and poorlycooked vegetables. The cestodes have a simple life cycle consisting of one or two hosts. The adulttapeworms living in the intestine of the definite host generally man produce ma-ture eggs which are shed out from gravid proglottids and pass out with the stool.

These eggs are then taken up by the intermediate hosts cattle, pigs and fishes. Onreaching the alimentary canal of the intermediate host, the eggs liberate on-chospheres which bore through the intestinal wall and enter the blood circulationfrom where they are carried to the different parts of the body.

On reaching the mus-culature, the worms develop into their second larval stage called Cysticercus or blad-der worms. These bladder worms get encysted and live in the muscles. When hu-mans eat poorly cooked meat of cattle, pigs or fishes, the scolices emerge out of thebladder worm and attach to the intestinal wall and slowly develop into adult tape-worms. This completes the life cycle of the parasite. The tapeworm infections generally do not produce significant pathologicalchanges; however, some of them may cause occasional appendicitis or increased eos-inophil counts.

The clinical symptoms of the disease are nausea, vomiting, generalweakness, weight loss, abdominal pain and diarrhea. In the case of D. This is due to the strongaffinity of D. The bladder worms may migrate in different parts of the body andmay cause serious clinical complications cysticercosis characterised by nervous sys-tem disorders and different problems of eyes, liver and brain. The disease is prevalent wherever man is closely associ-ated with cats, dogs and sheep.

The adult worms live in the alimentary canal of thedefinite host cats, dogs, wolves, foxes and jackals and shed eggs from gravid pro-. Sheep and cattle get infected by grazingon grass and vegetation contaminated with Echinococcus eggs. Dogs and cats get in-fected when they feed on the discarded viscera of slaughtered sheep and cattle al-ready infected with Echinococcus. Humans acquire the infection by ingestion of Echi-nococcus eggs through fruits, vegtables, salad or water.

On reaching the duodenum of the intermediate host man, sheep, cattle andcamel , the shell of the egg is digested liberating onchospheres which penetrate theintestinal wall and reach the blood circulation. The onchospheres are then carried todifferent parts of the body and get encysted. The liver is the most favoured sitewhere the majority of the cysts settle down. However, other parts of the body suchas lungs, spleen, brain, heart, kidneys, bones, abdominal cavity and musculaturemay also contain the hydatid cysts.

The main pathological changes during hydatid disease is inflammation andnecrosis of tissues around the cysts. Usually the hydatid disease is symptomless inits early stage; however, various clinical symptoms may appear later which dependupon the number, size and site of the cysts. The presence of hydatid cysts in livercauses nausea, vomiting, vague abdominal pain and bulging of right hypochon-drium or epigastrium due to hepatic enlargement.

If the cysts are located in lungs,they give rise to recurrent pyrexia and coughing paroxysms. The patient may alsoexhibit biliary colic and jaundice. Sometimes the cysts rupture into the peritonealcavity, lungs, kidneys and other organs of the body releasing hydatid fluid whichmay give rise to anaphylactic shock with vasomotor collaps, edema, utricaria andrespiratory discomfort which may be fatal in few cases.

The high prevalence of gastrointestinal nema-todiasis is due to the simpler life cycle of the parasite with no intermediates host andeasy access of eggs and larvae to the grazing animals. Placei, Trichostrongylus axei, T. The main nematodes which inhabit the digestive tract of sheep, goats anddeer are Gongylonema pulchrum, Gaigeria pachyscelis, Haemonchus contortus, H. The adult worms and developing forms of the nematodes may inhabit theabomasurn eg.

Haemonchus, Trichostrongylus etc. Cooperia, Bunos-tomum etc. The presence of nematodes in the intestinemay cause different types of gastrointestinal disturbances such as diarrhea, depletionof intestinal minerals and depressed enzymatic activities. The infestations may alsobe associated with anaemia and rnucoid hyperplasia. The economic loss during in-testinal nematode infections in ruminants may be due to decreased levels of mineralcausing reduced skeletal growth, weight loss, poor quality of meat and wool andless production of milk in dairy cattle.

These nematodes are responsi-ble for much morbidity in equines. For example, S. Westeri may cause acute diarrheain foals and donkeys. The migratory larvae of P. The adult worms of P. The presence of nematodes in the digestive tract of pigs is associated with. The common intestinal nematodes infecting pigs are Ascaris suum, Strongy-loides westeri, S. The pathology and clinical manifestations may depend on the type of the para-site infecting the animal.

For example, migration of larave of A. Animals with heavy worm burden may die due to severe lung damage. There is alsopoor weight gain in pigs infected with Ascaris. Similarly, Oesophagostolntlm spp. The cysts of T. In addition somehookworms, Ancylostoma caninum, A. Other roundworms found in the gastroin-testinal tract of cats and dogs are Strongyloides stercoralis, S. The intestinal nematode infections in cats and dogs occur throughout theworld.

The presence of ascarids may be responsible for gastrointestinal distur-bances and poor growth in the animals. The hookworms and some whipworms such as T. The common nematodes of the digestic tract of poultryare Heterakis gallinarum, H. The micro-filariae live in the peritoneal blood and skin while the adult filariids reside in theblood vessels, lymphatic system, subcutaneous tissues and body cavities. In addi-tion, the heartworm of the dog, Dirofilaria immitis, is found in the right ventricle andadjacent pulmonary arteries of carnivorous animals.

The important filariids infecting animals are Setaria cervi, Parafilaria bovicola,Stephanofilaria spp. Onchocerca armillata and Elaeophora poeli cattle ; Setaria equina horses , Setaria digitata sheep, goats , Setaria congolensis pigs and Dipetalonemadracunculoides cats, dogs. Some important lung worms of domestic animals are: Dictyocaulus viviparus cattle , D. Of these, D. Occasionally, the worms may block lungs of animalswhich may be fatal. The most notable parasites of this class areStephanurus dentatus kidney worm of pigs, Thelazia capillaria, T. The major liver flukes which infect ruminants are Fasciola hepatica,F.

These parasites usually cause hepatic problems in the animals. The most common lung flukes are Parago-nimus westermani and P. Some important flukes invading the blood circulatory system of cattle,sheep and goats are Schistosoma boris, S. This is becauseof the fact that tapeworm eggs are easily taken up by animals while feeding on thevegetation contaminated with human excreta.

For some cestodes like Taenia spp. The presence of cystic forms of the cestodes in the muscles of cattle and pigs give rise to 'measly beef' and 'measly pork', respectively, which are unsuitable for human con- sumption. The adult tapeworms live in the gastrointestinal tract and are responsible for various digestive system problems. The important tapeworms inhabiting the digestive tract of animals areMoniezia expansa, M.

A few tapeworms such as Stilesia hepatica and Thysanosomaactinioides are found in the bile duct of cattle. The larval forms of various cestodes are found in the musculature of someanimals. Thus, the bladder worms of T. Similarly larval stages of Echinococcus granulosus and E.

In hu-mans, the gastrointestinal tract is the seat of predilection of several amoebae, flagel-lates, ciliates and sporozoates causing from mild gastrointestinal disturbances tofatal clinical conditions like liver abscess and amoebic meningoencephalitis. The im-portant intestinal protozoal diseases of man are amoebiasis, giardiasis, trichomoni-asis, naegleriasis and toxoplasmosis. Of these, amoebiasis is estimated to affectnearly million people around the world of which nearly 40,, patientsdie every year [1,2]. Giardiasis is another widespread disease infecting nearly million people around the globe [1].

The major extraintestinal protozoal infections of man aremalaria, trypanosomiasis Chaga's Disease and African sleeping sickness and leish-maniasis, all of which are notorious for their detrimental effects on human health. Themedical problems associated with these vector-borne diseases are many and varied[40].

The clinical manifestations may range from fever and dermatological problems tograve clinical complications involving CNS, liver and tubular organs, many of whichare often difficult to treat resulting in high rate of mortality, especially in patients suf-fering from malnutrition.

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The cost of treatment may also sometime become a limitingfactor in curing the advanced cases of protozoan diseases [41]. It has been estimated. Similarly the number of persons infected with trypanosomi-asis and leishmamiasis are 25 and 1. The presence of pathogenic protozoans in domestic animals also produces de-bilitating effects and, therefore, eradication of these parasites is essential for betterhealth of livestock and improved socio-economic status of the farmers.

Another fatal protozoal infection of animals is Theil-eria parva parva responsible for East Coast fever in cattle. It has been estimated that nearly 1. The highest economic loss due to Babesia spp. Trypanosomiasis is an-other important disease of cattle. The impact of this infection is spread over 10 mil-lion square kilometers area of Africa extending from the Sahara to Limpopo andthreatens the health of over 25 million cattle and 35 million people.

This may be re-sponsible for severe economic losses, which is evident from the fact that livestock inAfrica are treated with more than 25 million doses of various trypanosomicidaldrugs every year [46]. Trypanosomiasis in cattle may, therefore, be one of the rea-sons why Africa produces about 70 times less animal protein per unit area thanEurope [47]. Some of these are nonpathogenic while others may produce a variety of clinicalmanifestations. The protozoans which belong to the class Plasmodium, Trypanosoma.

The major protozoa parasitic to humans are briefly described below. The disease has a cosmopolitan distribution, and is endemic in someparts of the world. The parasite enters a new host by the oralroute as a cyst. The amoebic cysts, discharged in the patient's stool are spread bypests, water streams and man himself through nightsoil fertilization of agriculturallands. Transmission of the disease occurs by consuming water, food and vegetablescontaminated by cysts. Direct faecal contact, person-to-person contact, flies and cock-roaches may also help in transmitting the amoebic cysts.

Amoebiasis is marked by two phases of the infection: a intestinal amoebiasischaracterised by dysentery and diarrhea, nondysenteric colitis, amoeboma amoebicgranuloma and amoebic appendicitis; and b extraintestinal amoebiasis hepaticamoebiasis marked by liver abscess [48]. Bothtrophozoite and encysted stages are seen in their life cycle.

The infection is associated with recurring episodes of abdominal dis-comfort which usually cease after treating the patient with an amoebicide. Although T. Coitus is probably the main source of transmission of the infec-tion. That is why it is usually advisable to treat both sexual partners. The infection isalso transmitted to humans by douche equipments, clothings and towels.

The infection is established when the pH of vagina goes below 3. Vaginal trichomoniasis is characterised by vulval pruritus with profuse andirritating vaginal discharge leading to excoriation of the vulva and dermatitis onthigh skin. In men, chronic urethritis may be observed. The flagellate is present only in the trophozoite form. Theparasite may be seen in very large numbers in stool during diarrhea of nonparasiticetiology.

The parasite occurs both in thetrophozoite and encysted forms. The infection is acquired by consuming food ordrink contaminated with cysts and, therefore, it is more prevalent in children thanthe adults. The clinical manifestations of the disease may include epigastric pain,nausea, flatulence and diarrhea. Acute giardiasis may be associated with steatorrheaand weight loss [49]. The infec-tion is reported to occur throughout the world producing diarrhea and dysentery.

Since B. Pigs are the main reserviors of B. The pathogenic protozoans of this class are lsospora belli and I. The infection may give rise to abdominal pain, di-arrhea, nausea, anorexia and headache. These are free living soil amoebae which occasionally infect the respiratoryand nervous systems of man. Naegleria spp. The parasite enters the nasal cavity and in-vades the brain via the olfactory nerve. Acanthamoeba Hartmannella spp.

It is inter-esting to note that Naegleria spp. The infectionmay be acquired while swimming in lakes and pools. Cats serveas the definite host. The sexual part of the life cycle of the parasite takes place in theintestinal cells of the felines. These animals pass out immature oocysts in their faeceswhich are taken up by sheep, pigs and cattle. Man becomes infected by eating poorlycooked or raw meat of sheep, pigs and cows containing toxoplasrna cysts. Sometimesoocyts from cat's faeces may also be ingested directly. The infection may also be ac-quired through the transplacental route.

The intermediate hosts man, pigs, rumi-nants harbour extraintestinal sexual forms, namely tachyzoites proliferative forms and bradyzoites encysted forms. Toxoplasrnosis produces a wide-spectrum of pathological and clinical mani-festations. The disease appears in two forms: congenital and acquired. Congenitaltoxoplasrnosis is usually fatal. The infection in newborns is marked by the presenceof hydorcephalus, encephalitis, bilateral retinochoroiditis, hepatosplenornegaly andjaundice. In some cases the disease may be inactive at birth, but may develop as thechild grows older.

Such children may show esotropia, strabismus, rnnicrophthalrnia,and cataract. Acquired toxoplasrnosis is characterised by retinochoroiditis, lyrnphade-nopathy and fever. In adult patients, retinochoroiditis, mononucleosis like syn-drome, fever and malaise may be frequently observed. The disease is also known torecrudesce in imrnunosuppressed patients. However, clinically significant parasitic pneumonia is mainly seen. The initial stage of the disease is characterised by anorexia, weightloss and dyspnea with bluish colouration around mouth and nostrils.

Later respira-tory problems become pronounced with marked tachypnea, cyanosis and spells ofnonproductive with pleurisy cough. This leads to diffused interstitial and alveolarinfiltrates resembling pulmonary edema. The patient usually dies if not treatedpromptly. This is a mild type of pathogen.

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Although the infections due to Crypto-sporidium usually subside without therapy, it may produce chronic debilitating diar-rhea, especially in patients with AIDS and low immunological profile. A number of species of Plasmodium invade the blood and liver causing malariain man and animals. The important pathogens of malaria in man are Plasmodiunl fah:i-parum, P.

The disease is transmitted to man by femalemosquitoes belonging to the genus Anopheles and is endemic in several parts of Asia,Africa and South America. The life cycle of Plasmodia involve the liver and erythrocytes of humans andthe stomach wall of mosquitoes. The sporozoites released into the blood by the biteof a mosquito are taken up by the hepatocytes and develop into schizonts. The tissueschizonts produce merozoites which are released into the circulation and infecterythrocytes and generate more merozoites as a result of an asexual cycle.

Some ofthe merozoites, thus formed, differentiate into male and female gametocytes whichare taken up by the mosquitoes while sucking human blood. In the mosquito, thesegametocytes fuse to form a zygote, thereby completing the sexual cycle of the para-site. The zygote give rise to sporozoites, which are stored in the salivary gland andare infective. These are released into blood through a mosquito bite. The main clinical manifestations of malaria are periodic fever with chills,splenomegaly, anaemia and leukopenia. The liver is occasionally enlarged. This leads to blockade of the blood circulation causing progres-sive increase in headache with little or no fever.

The final stage of the disease is char-acterised by coma and death of the patient. Several haemoflagellates of the genus Trypanosoma Trypanozoon are known toinvade the central nervous system, blood and tissues causing acute and chronic pro-tozoal diseases, collectively termed as 'trypanosomiasis'. Gambian sleeping sickness is caused by Trypanosoma brucei gambiense. The dis-ease is transmitted to man by the tsetse flies, Glossina palpalis. The Rhodesian sleep-ing sickness is caused by T. Both these forms of African trypanosomiasis areendemic in different parts of Africa.

The parasites of T. The early phase of the infection is marked by fever, headache,malaise and anaemia. The later stage of the disease is related to involvement of CNSand is characterised by meningoencephalitis, meningomyelitis and cachexia. The pa-tient becomes emaciated, falls in coma and finally dies.

Chaga's disease or American trypanosomiasis is caused by the invasion of theblood and tissues by the trypanosome T. The trypanosomes inhabit the bloodcirculation, while their leishmanial forms reside in the tissues. The main victims ofthis disease are children and young adults.

Transmission of Chaga's disease takesplace through the kissing bugs, Triatoma spp. Chaga's disease is widespread in several parts of South America; it is endemicin Brazil Argentina, Chile and Venezuela. The acute phase of the disease is markedby high fever, anorexia, vomiting, diarrhea and enlargement of the liver and spleen. The patients also suffer from various eye problems.

There is a continous damage oftissues in various organs like heart, liver and spleen. If the heart is affected by T. Another serious clinical feature of Chaga'sdisease is dilation of tubular organs such as oesophagus mega-oesophagus and co-lon megacolon in some patients. Depending upon the nature of infection, human leishmaniasis can bedivided into three forms: a Visceral leishmaniasis Kala-azar and post kala-azardermal leishamaniasis PKDL caused by Leishmania donovani complex; b cutaneousleishmaniasis caused by L.

Kala-azar visceral leishmaniasis gives rise to several clinical manifestations,the most notable being diarrhea, vomiting, cough, dizziness, weight loss, anaemia,malaise, bleeding gums, skin darkening, wasting and enlargement of spleen, liverand lymph nodes. The clinical features of PKDL include the cutaneous type of leish-maniasis with hypopigmentation and erythematous patches on face, limbs and bodytrunk. The main clinical symptoms of cutaneous leishmaniasis are related to dermalproblems like skin lesions and ulcerations.

The mucocutaneous leishmaniasis is thesevere and destructive form of cutaneous leishmaniasis that may occasionally causedestruction or disfiguration of tissues of nasal septum, lips and larynx. The important protozoaldiseases of domestic animals are described below. Coccidiosis in domestic fowl is responsible for considerable economicloss [53]. The coccidia are microscopic sporozoa belonging to the genera Eimeria andIsospora. Birds acquire coccidiosis when they ingest sporulated oocysts along with feedand water.

The disease is exacerbated due to poor nutritional conditions of chicken. In addition, environmental and climatic factors also add to the spread of the infec-tion. Faecal discharge of birds help oocysts to sporulate and become infective underwarm and humid conditions. Crowding of birds due to intensive rearing creates fa-vourable conditions for sudden outbreaks of severe forms of coccidiosis. Coccidiosis is usually marked by haemorrhagic enteritis resulting in devastat-ing bloody caecal coccidiosis E.

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The disease is further complicated by secondary bacterial infections. Otherclinical manifestations of the disease include poor weight gain weight loss , weak-ness and emaciation. In severe infection the animals die even before distinct clinicalsymptoms appear. Crypto-sporidium has been shown to be the main cause of respiratory infections in turkeysand chicken [54,55]. The in-fection in pregnant animals such as cattle, sheep and pigs may often cause abortion. Theamoeboid stage of the parasite causes enterohepatiUs in turkeys and chicken and,therefore, is responsible for high economic losses in the turkey industry.

The birds ac-quire the infection by ingesting either the trophozoites or the embryonated eggs ofcaecal worms, Heterakis gallinarium containing H. The vectors of the disease are Simulium spp. The im-portant parasites are L. This results in sig-nificant economic losses in poultry industry in Japan and other parts of SoutheastAsia [6]. The importantparasites infecting cattle are Theileria parva parve East coast fever , T. The clinical symptoms of acute and subacute forms of theileriasis in cattle arefever at irregular intervals, enlarged lymph nodes, diarrhea, anaemia, dyspnea, leuk-openia and weakness.

The important Babesia spp. Babesiasis is ahighly pathogenic disease characterised by haemolytic anaemia, jaundice andhaemoglobinuria, causing occasional death of the animals. The erythrocytes parasit-ized with B. This can block bloodvessels in brain, liver, kidneys and lungs producing necrosis of adjacent tissues [60].

The infection is mainly transmitted by tsetse flies, thoughsalivarian or stercoranian methods of infection are also known. Some blood suckinginsects such as Tabanus and Stomoxys flies, and also vampire bats may transmit try-panosomiasis in animals. Infections with Trypanosoma equiperdum in horses and don-keys may also be transmitted during coitus. The major trypanosomes infecting domestic animals are: Trypanosoma vivaxand T. All these parasites invade the blood cells in the early stage.

Later the trypano-. Typical clinical symptoms of try-panosomiasis are characterised by wasting with progressive deterioration of generalhealth leading to extreme emaciation, collaps and death of the animals. In addition to the pathogenic trypanosomes, some nonpathogenic speciessuch as T. The disease is caused by Anaplasma ovis sheep and A. Since anaplasmosisis a tick-borne disease, it is usually grouped with babesiasis and theileriasis. How-ever, some workers consider Anaplasma to belong to order Rickettsiales and, therefore,should not be treated as protozoa at all [61].

However, during the period , often referred to as the golden-age of medicinal science [16], parasitic chemo-therapy did not receive the attention it deserved considering the extensive morbidityand mortality and the associated socio-economic loss caused by them vide infra. Thus, while the progress during this period in antibacterial chemotherapy was spec-tacular, rather few new classes of antiparasitic drugs were added [62]. The drugsused at present to treat the major parasitic infections in humans and domestic ani-mals are listed in Table 1 and 2, respectively []. A perusal of the table wouldshow that parasitic chemotherapy at present is rather inadequate.

There are big gapsin the therapeutic armementarium for these infections. There are very few drugsavailable for systematic protozoal and helminth infections; no suitable antileish-manicidal or macrofilarial drug is available. Primaquine, the only drug available forrelapse of vivox malaria, is not very safe to use.

There are very few drugs availableagainst multidrug resistent P. These gaps needed to be filled urgently. Recent advances in molecular and cellular biology and in instrumentationtechniques have provided new insights into the etiology, physiology and pathologyof these diseases and elucidated complex molecular structures and their function,uncovering new targets for drug-interference and design.

Developments in new in-strumentation techniques have also provided new non-invasive approaches to. Amphotericin Bamoebicmeningoence- T. Blood flukeinfections Hetol, bithionolTapeworm Cestodes Tartar emetic, stibophene, sodium an-infections timony dimercaptosuccinate, lucan- thone, hycanthone, niridazole,Protozoal diseases haloxon, trichlorphon, amoscanate, praziquantel.

Coccidiosis Eimeria,Isospora spp. Arecoline hydrobromide di-n- butyltin, dichlorophene, bunamid- ine, niclosamide, terenol, nitroscanate, praziquantel, fenbenda- zole, albendazole, oxfendazole, luxa- bendazole, paromomycine sulphate. Sulpha drugs sulphaquinoxaline, sul- phadimethoxine, sulphaguanidine, sulphamethazine etc. Theileria spp. Probably noneLeucocyto-zoonosis Amoprolium, Sulfadiazine plus pyrimethamine. Theileriasis Dimetridazole, ipronidazole, ronida-Babesiasis Babesia spp. Trypanosomiasis Trypanosoma spp.

Combination of pyrimethamine withAnaplasmosis Anaplasma spp. Tetracyclines oxytetracycline, chlor- tetracycline, rolitetracycline , menoc- tone, BWC clexon , BWC buparvaquone , halofuginone lactate. Trypan blue, acriflavine hydrochlo- ride, quinuronium sulphate, dimi- nazene, pentamidine, phenamidine, imicarbalide, imidocarb, primaquine, oxytetracycline, chlortetracycline, clin- damycin. Tartar emetic, suramin, quinapyra- mine, homidium chloride, dimi- nazene, isometamidium chloride.

Tetracycline, oxytetracycline, chlortet- racycline, imidocarb dipropionate, gloxazone. These developments provide great opportunities for new drug development. Similarly, the lead-optimization approach in drug research has further been mademore scientific and less time consuming by using well defined methods of QSARproposed by Hansch and Fujita [71], Free and Wilson [72] and Bocek and co-workers[73]. For example a number of biochemical targets such as glucose metabolism,neuromuscular transmission, tubulin polymerisation and interference with ion-fluxin helminths appear suitable for rationale design of new anthelrnintics [74].

Simi-larly, inhibition of DNA functions, antagonism of folate, coenzyme A and Q, hypox-anthine-guanine phosphoribosyl transferase HGPRT , catalase and glutathione per-oxidase in protozoans have been used to develop better agents. In addition, designof suicide enzyme inhibitors, prodrugs and agents that would interfere with lipidand polyamine metabolism has helped to throw light on newer template structuresfor generating potent antiparasitic agents.

More recently computer assisted molecu-lar modelling and drug design is being used to solve intricate problems of conforma-tional analysis and other structural requirements for a fruitful prediction and selec-tion of an active molecule of desired biological profile. Nevertheless, intuition andexperience of a medicinal chemist would continue to guide to arrive at new mole-cules that may turn into potential drugs if subjected to reliable in vitro and in vivoscreening systems.

It is hoped that with the help of the knowledge regarding diseaseprocess es of various protozoal and helminth infections, the biochemistry of para-sites and newer strategies of drug design would lead us to develop ideal drugs forfilariasis, trichinosis, guinea worm infections, hydatidosis, malaria, leishmaniasis,trypanosomiasis and a few protozoal diseases of the gastrointestinal tract [40,]which still pose a challenge to scientists engaged in drug development for parasiticdiseases.

Hopkins, D. Hunter, III, G. Saunders Company, Philadelphia Mehlhorn, H. Katiyar, J. Stephenson, L. Cabrera, B. Hayashi, S.

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Burger, A. Simpson, J. Campbell, W. Guerrero, J. Stoll, N. Walsh, J. Janssen, P. D'Arcy, P. Horton, R. Anond, P. Whalen, G. Chitanondh, H. Nitidandhaprabhas, P. Woodruff, A. Wiseman, R. Laemmler, G. Maddison, S. Pesigan, T. Katz, N. Ghoneim, M. Sharma, S. McGreevy, P. Campbell, and R. Rew, Plenum Press, New York, , pp. McDougald, L. Rew, Plenum Press. New York , pp. Raether, W. Mehlhorn, Springer-Verlag, Heidelberg, pp. McCosker, P. Ristic, and J. Kreier, Academic Press, New York , pp. Nantulya, V.

Ellis, C. Allsopp, R. Eldson-Dew, R. Wolfe, M. Culbertson, C. Duma, R. Long, P. Rommel, M. Hoerr, F. Dhillon, A. Uilenberg, G. Irvin, M. Cunningham, and A.