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lecture handouts for zoo 173 1st sem AY 2010-2011

lecture handouts for zoo 173 1st sem AY 2010-2011



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    Nematodes Nematodes Document Transcript

    • Phylum Phylum Nematoda Nematoda • Pseudocoelom – Fluid-filled cavity that forms hydrostatic skeleton • Most numerous animals on earth • Simple nervous system – May include sensory organs called phasmids/amphids – 90,000 in 1 rotting apple Nematodes – 1074 in 6.7 ml of coastal • Complete digestive system mud • Four juvenile stages which all look similar – Estimated 9 billion per – Separated by a molt of the cuticle acre in good farmland – Called J1, J2, J3, J4 – Parasitic infections can be • Most juvenile stages are free-living enormous – J3 is usually the stage that gets into the definitive host Nematodes Phylum Nematoda • “White worms” Phylum • More species than any – Not segmented other phylum – Covered with a cuticle Nematoda • Many species show eutely – More insects have been • Secreted by hypodermis – After embryogenesis, the nuclei of the cells described • Grows as worm grows do not divide – Every insect studied has at • Sexes are separate – The number of cells remains constant for the – Find each other with pheromones least one nematode parasite rest of worm’s life – Male sperm lack flagellum • Live in every habitat • move by pseudopodia (Major sperm • The cells simply grow larger protein) – Free-living in marine, • Exception is the ovary/testes freshwater, terrestrial • Most are slender with few – Number of cells varies by species distinguishing characteristics. • Even between grains of sand on a beach • Two classes • Cause of some of the most debilitating and disfiguring diseases – Parasitic on almost every – Enoplea in humans animal – Rhabditea – Parasitic on plants 1
    • Class Enoplea Trichuris trichiura Trichuris trichiura • Location: large intestine from • Diagnosis: bipolar eggs • Amphids (sense organs) well developed caecum and appendix to rectum in feces. Colonoscopy • Most are non-parasitic – Burrows head into mucosa can also uncover worm • Order Trichurida • Transmission: Ingestion of infections – Trichuris, Capillaria, Trichinella embryonated eggs, usually in • Treatment: contaminated food Mebendazole or • Order Dioctophymatida – Requires high humid, warm albendazole. Rectal – Dioctophymata (Kidney worm) climate and shade to develop prolapse treated with • Order Muspiceida properly. surgery • Order Mermithida – Parasite of insects • Pathology and Symptoms: Trichuris trichiura Low-level infections (<100 Trichuris • Females may lay 3,000 to • Whipworm Trichuris worms) are asymptomatic 20,000 eggs a day for • Definitive Host: Humans trichiura • Large infections can result in trichiura many years. – Dogs possibly diarrhea, bloody stool, • There are 60-70 species in • Intermediate Host: None abdominal pain and rectal this genus, all live in large – Pigs and chickens are transport prolapse intestine hosts • Chronic infections in children – Flies will transport eggs on legs – T. felis – cats can lead to growth retardation • Geographic distribution: and finger and toe clubbing. – T. discolor – cattle Cosmopolitan • In Phils – 80-84% prevalence – T. muris – rodents – Warm Climate – T. vulpis – canids • Often associated with Ascaris – High rainfall • Occasionally infects lumbricoides infections. – Unsanitary conditions humans – Mode of transmission same – T. suis – pigs 2
    • Life Cycle of Trichuris trichiura Capillaria Capillaria sp. • Pathology: ulcerative and • Very large genus Adults in Eggs go philippinensis degenerative lesions in the – Infect every organ and tissue of all classes of Embryonate intestinal muscosa; disruption vertebrates. large out in in soil to electrolyte balance leading • C. hepatica zoonotic human parasite but intestines feces to heart failure normal host unknown Eggs eaten • Symptoms: abdominal – Rat intermediate host Emerge by humans pains, gurgling stomach and • C. aerophila live in lungs of carnivores into lumen diarrhea • C. annulata esophagus and crop of birds • Diagnosis: Eggs may be – Uses earthworm as intermediate host Juvenile Juvenile found in feces • C. plica kidneys and urinary bladder of canids Eggs mature penetrate • Treatment: Albendazole • C. linearis in cats hatch mucosa • C. procyonis lives in the tongue of raccoons Life Cycle of C. philippinensis Anatrichosoma • Definitive Host: migratory Capillaria fish-eating birds Eggs laid and Ingested by ocularis – mammals including humans embryonate in philippinensis FW fish • Lives in the corneal • Intermediate Host: None. freshwater epithelium of tree • Geographic Distribution: Man ingests shrews, Tupaia glis Philippines (1967- infected fish • Other Anatrichosoma 68:epidemic) and other Female sp. are parasitic in Bird ingest parts of Asia worms lay various tissues of many infected fish • Mode of Transmission: eggs mammals Ingestion of infected fish • Closely related to • Location in D.H.: small Juvenile in Trichuris and Capillaria Adult in the intestine small int small int. 3
    • • Hosts: swine, rats, Trichinella spiralis • Disease is trichinosis • Diagnosis: Antigenic and Trichinella humans, bear, walrus, and – Pathology and – A.K.A. Trichiniasis or trichinelliasis Trichinella serological tests, muscle other carnivores. Symptoms • The Great Mimic biopsy plus case history. spiralis – Individual is the D.H. for the – Mimics many other conditions spiralis adults and I.H. for Juvenile • Treatment: No effective – Rarely exhibits a set of symptoms • Geographic Distribution: • Symptoms depend on location, treatment. number and age of larval worms – Thiabendazole has worked in Cosmopolitan. More common in temperate • Most cases are asymptomatic experimental animals but areas than tropics. • Initial phase: flu-like symptom results in human mixed – There are at least seven – Caused by females penetrating – Steroids reduce inflammation mucosa – Bed rest and analgesics help sibling species and at least 3 strains • As worms mature, symptoms relieve pain and discomfort • Different hosts, ribosomal may include nausea, vomiting, DNA, gene sequences, and sweating and diarrhea for five allozymes to seven days. – Look identical – Body’s reaction to worm waste Trichinella spiralis Trichinella spiralis • Migration of larva causes • Location: Adults in wall many symptoms Trichinella spiralis – symptoms and – Including pneumonia, of small intestine. • Prevention: Cook meat well. Juvenile in striated pathology pleurisy, encephalitis, meningitis, nephritis, – Most cases are from undercooked pork muscles and organs. deafness, peritonitis, brain – Includes processed meats, chops, sausages, – Favorite are eye, tongue and eye damage, muscle and masticatory muscles ham, etc. stiffness, weak pulse, – Then diaphragm and difficulty breathing, intercostal – Can also occur in bears, walrus, fox, etc. hallucinations – heavy muscles of arms and • Rarely occurs in cattle and horses legs • Death is rare – How they get it is unknown – Why they prefer certain – Usually due to muscles is are unclear inflammation of heart • Can survive freezing down to –15oC • Transmission: Ingestion muscle, respiratory of Juvenile in under complications or kidney malfunction cooked meat. 4
    • Trichinella • Largest intracellular parasite Adults inside Female Juvenile Enter – Juvenile invade a muscle cell and converts it into intestinal release migrates to spiralis - a nurse cell muscle mucosa cell Juvenile striated • Alters the metabolism of the cell to do what it cell muscles Notes wants – Alters gene expression so it doesn’t make contractile proteins Life Cycle of Turns into • Releases Vascular endothelial growth factor Four molts (VEGF) nurse cell T. spiralis – Stimulates formation of capillaries around cell • Nurse cell secretes collagen coating Penetrate Reach Infective in • Don’t understand how worm does it Juveniles intestinal small 4-8 weeks – Eventually the body walls off the nurse cell by swallowed calcifying the walls mucosa intestine – Immune system will eventually kill the Juvenile • But they can live over 39 years Trichinella spiralis - Notes Dioctophyma renale Order Mermithida • Juvenile molt four times and become an adult in 30-32 • Order Dioctophymatida hours from ingestion. • Kidney worm • All are parasites of insects • Female gives birth to live Juvenile – Larval stages develop and grow in hemocoel of – No egg stage • Definite host are aquatic birds and mammals insect • Immunity has been demonstrated in mice – Can occur in dogs, cats, and humans – When nematode is nearly mature, it ruptures out – Can be passed to young from immune mothers • Adults take over one kidney of the definitive host of the body wall of the insect • There are at least four variations of the life cycle which and leaves other kidney alone • Usually when the insect is near water may be different species • Kills the insect – Domestic • Grows to several feet in length. • Use pigs and rats • Adults live in the soil, mate and lay eggs – Sylvatic – Temperate zone • Diagnosis by eggs in urine; worms (and kidney) should be removed. – Eggs may be eaten by host or juvenile may seek • Fox, bears out host – Sylvatic – Torrid zone • Uses two intermediate hosts • Hyenas, lions • May be used in future for biological control of – Sylvatic Frigid zone – First: freshwater oligochaete worm pests. • Polar bears, walrus – Second: a fish. 5
    • Mermithid- infected ant Familes Sterinernematidae and on left, Order Rhabditida Heterorhabditidae (con’t) normal ant • Most are free-living nematodes. • Worms reproduce for several generations on right while feeding on the bacteria and the insect’s • Includes several families that were probably “pioneer parasites”. organs until they run out of nutrients – then produce J3 which return to the soil – Families Sterinernematididae and • wait for the next host Heterorhabditidae (insects) – Family Rhabdiasidae (lung worms of frogs, • True mutualism between the worm and Mermithid bacteria snakes, cattle, and other animals) from – Neither can survive alone – Families Strongyloididae and abdomen Ancylostomatidae (medical importance to • May be a way of controlling insect pests. of ant humans) Familes • Includes two genera – Steinernema Family Rhabdiasidae Class Rhabditea Sterinernematidae • Rhabdias bufonis and R. ranae are lung – Heterorhabditis • Amphids (sense organs) are usually and worms of toads and frogs. • Important parasite of Heterorhabditidae – Parasitic Adults are protandrous hermaphrodites poorly developed. insects. • J3 juvenile invade host • Includes many free-living as well as • J3 juvenile invades • Male organs develop first and make sperm insect and releases • Then female organs develop and make eggs most parasitic round worms. – Use stored sperm to fertilize eggs bacteria • Some eggs leave in feces and hatch into free-living adult • Bacteria kill insect but males and females also retards growth of – Feed on soil bacteria other bacteria • Some eggs hatch in utero and feed on female internal organs until she is dead. – Insect doesn’t rot • J3 juvenile leave body to invade an insect. 6
    • Family Adults in Eggs go Hatch and • Well developed buccal Small Molt out in J1 develops Ancylostomatidae cavity with teeth. Intestine feces in soil - Hookworms • Four Larval stages. J2 – J1and J2 are free-living Molt – J3 burrows into definitive Molt J4 host skin and migrates to Hookworm intestine Molt Life Cycle J3 juvenile • Require warm, wet burrows into climate and shady areas Reach skin of host – J1 and J2 can’t tolerate intestine Family Rhabdiasidae drying, freezing, or Enters blood • Many other species of Rhabdias spp. are exposure to sun. Up or lymph Coughed Lungs Heart lung worms of frogs, snakes, cattle, and • Adults actively graze on up then trachea vessel other animals. intestinal mucosa swallowed • Many different species. Family • Definitive Host: Humans – S. stercoralis and S. fuelleborni • Symptoms of hookworm Necator Family in humans and primates – Most common human – S. ratti in rats Ancylostomatidae infection vary by species americanus hookworm Strongyloididae – S. ransomi in swine and number of worms. – Many other species parasitize - Hookworms – Most infections are • Intermediate Host: None - Strongyloides birds, reptiles and amphibians • Geographic Distribution: asymptomatic. sp. • Free-living stages mixed with Indigenous to Africa, India, parasitic stages. – A. duodenale causes more – Random mix damage than N. americana southeast Asia, China, islands – Free-living worms are male or – Nutrition of host also of sw Pacific. female. important in determining the – First found in Brazil and Texas – Parasitic worms are all degree of symptoms parthenogenic females – Brought to New World with slave • No sperm has been found in – Race also affects symptoms trade parasitic forms • Blacks are more resistant to – Autoinfection may also occur infection than whites • Transmission: J3 burrows into skin. 7
    • • Pathology: Due to • Pathology: Due to damage Necator damage of tissue during Hookworm • Hookworm infection does not Ancyclostoma of tissue during migration of always lead to hookworm americanus migration of J3 juvenile and J3 juvenile and ingestion of Disease ingestion of intestinal duodenale disease. intestinal mucosa by J4 – Most infections are mucosa by J4 juvenile and juvenile and adults asymptomatic adults • Symptoms: Usually • Development and severity of • Symptoms: Usually asymptomatic. May cause asymptomatic. May cause Hookworm disease depends hookworm disease. on three factors. hookworm disease. – We will discuss Hookworm – Number of worms present – We will discuss Hookworm disease later. disease later. – Species of hookworm • Diagnosis: Eggs in feces – Nutritional status of the host. • Diagnosis: Eggs in feces • Treatment: Mebendazole • Treatment: Mebendazole • Definitive Host: Humans • Number of worms Ancyclostoma• Notes: First hookworm the – Less than 25 N. americanus are Ancyclostoma • Intermediate Host: None life cycle was determined Hookworm asymptomatic • Geographic Distribution: duodenale – 25-100 light symptoms – In 1896 Arthur Looss was Disease duodenale southern Europe, northern Africa, dropping cultures of worm into – 100-500 moderate symptoms India, southeast Asia, China. mouth of guinea pigs – 500-1000 severe symptoms – Scattered locations in United States, Caribbean Islands, and South – He accidentally dropped a drop – >1000 are frequently fatal. America. • Species of worm on his hand. – Found in 1000 year old mummy in • The area began to itch and turned – A. duodenale sucks more blood so fewer Peru red. worms required to cause symptoms • May not have been brought over with slave trade. • He wondered if the worm could • Nutritional status of Host – Frequently found in mines well north have penetrated skin – Poor nutrition leads to worse symptoms. of freeze line – He then started sampling his – Suppresses immune system • Provides stable climate, no own feces – Fewer nutrients to repair damage freezing, no sun. • Found hookworm eggs in feces a • Transmission: J3 burrows into few weeks skin. 8
    • Incidence of Hookworm Disease Incidence of Hookworm Disease Phases of Hookworm Disease • Unsanitary conditions: feces released into soil • Race • Intestinal Phase • Repeated contamination of soil – In general, whites are 10 times more susceptible – juvenile and adults suck blood from intestinal – Repeated visit to same area to defecate increases to hookworm disease than blacks. lining transmission • Exact mechanism isn’t clear • 0.03 ml/day for N. americanus • Environmental conditions: Warm, humid, – Gave rise to image of “poor white trash” in • 0.26 ml/day for A. duodenale climate without freezing, proper soil southern U.S. – Bleeding into intestines can occur – Must have loose, aerated soil, with lots of humus. • Whites were frequently victims of high hookworm • Most iron is reabsorbed in intestines – Warm, humid climate necessary for the worm to develop in soil in shady areas loads – Worms do not use the iron – Made them weak, apathetic, and lethargic • Exposure of skin to soil – Anemia can result if dietary intake isn’t • Blacks of the same socioeconomic situation were sufficient to replace the iron lost – Must have access to skin so it can burrow into the resistant to hookworm disease skin. • Severity depends on worm load and dietary intake. – They were industrious and hard-working Incidence of Hookworm Disease Phases of Hookworm Disease • Longevity of worm Phases of Hookworm Disease • Cutaneous Phase – Juveniles can live is soil for several weeks • Intestinal Phase • Up to a year in a mine. – Occurs when juvenile burrow into skin and enter vessels – Localized allergic reaction – Most common symptoms – Adults can live 5-15 years • Slight, intermittent abdominal pains • N. americanus lives up to 15 years, making 9,000 eggs/day. • Pulmonary Phase • Loss of normal appetite • A. duodenale lives up to 5 years but releases 25-30,000 – Caused by larval migration through lungs and up trachea eggs/day • Geophagy – desire to eat soil – Usually asymptomatic but can cause dry coughing and – Adults travel with host when host moves – Reason is unknown sore throat – Many areas of the southern U.S. have clay soil that • Paratenic Host – May allow for secondary bacteria infections seems to relieve symptoms – Recently discovered A. duodenale juvenile can – Pneumonitis can occur in very large infections » In 1920’s, a business person began to ship the burrow into “wrong” species and survive in muscle clay to people around the country. – Human infected when food is eaten 9
    • Phases of Hookworm Disease Ancyclostoma • • A.K.A. Creeping eruption Definitive Host: Dogs and • Chronic Heavy Infections Cutaneous • Hookworm juvenile caninum cats penetrates skin of the – Patient suffers from severe protein deficiency • Intermediate Host: None larval migrans wrong host • Can cause dry skin and hair, spoon nail, edema, • Distribution: Cosmopolitan • Juvenile dies during potbelly, delayed puberty, mental dullness, heart migration failure and death. – but particularly common in northern hemisphere – Body reacts to worm and – Hookworms don’t block absorption of nutrients creates nasty skin irritation • Transmission: J3 juvenile where every the worm went. • Disease complicated by malnutrition burrow into skin • Treat with thiabendazole • Loss of protein and iron to worm is catastrophic to • Location in definitive Host: • A. braziliensis most those subsisting on minimal diet common cause – Prolonged exposure during childhood can lead small intestine – A. caninum as well. to lower intelligence and “laziness” – Many other hookworms can cause it. Hookworm Disease Family • May explain the lower economic status in many Ancyclostoma • Pathology: damage to Strongylidae developing countries. – Lethargic population can’t produce as many goods as caninum intestinal mucosa by • Very important parasites of healthy population grazing and sucking horses. • Proper sanitation has eliminated it from most of blood. U.S., Caribbean, and many other areas. • Many species • Symptoms: – Large species – Strongylus – Latrines and treatment was provided by J.D. Rockefeller and lead to formation of Rockefeller Asymptomatic in most • Particularly S. vulgaris Foundation dogs and cats – Smaller species Cyathostomum • Incidence worldwide has increased in last 50 • Diagnosis: Eggs in years • J3 juvenile is ingested – 25% of world population still infected. feces. • Oesophagostomum sp. • Hookworms have evolved many ways to evade or • Treatment: – Important parasite of ruminates, suppress the immune system. Thiabendazole primates, and swine 10
    • Family Trichostrongylidae Haemonchus • Pathology: Use lancet S. on anterior end to • Very large family with many genera and vulgaris species contortus pierce stomach lining in horse • Found in all classes of vertebrates. • Ingests blood intestine – Females have intestines • J3 are ingested – direct life cycle intertwined with ovaries – Heavily grazed pastures can have large • Gives the female the accumulation of juvenile alternating pattern similar to a barber pole • Very important parasite of domestic live stock. • Symptoms: anemia, – $222 million in annual cost to Australian sheep emaciation, edema, and industry intestinal disturbances. S. vulgaris ingesting – Controlled by Ivermectin. However, resistance is – Heavy infections can be becoming a problem. fatal. intestinal lining. – Also some resistance to the benzimidazole drugs – Survivors frequently has been reported. develop immunity Family Sygamidae • Barberpole worm Haemonchus Haemonchus • Diagnosis: Eggs in • Gapeworm of poultry • Definitive Host: feces. • Lives in the trachea contortus ruminants, including contortus – Trachea becomes blocked by cattle, sheep, goats. • Treatment: worms and mucus Mebendazole or – Causes bird to gasp for air – Human cases have been reported Ivermectin • Many species in Syngamus found in wild and domestic • Intermediate Host: None • Male do not show fowl the stripes of the • Geographic distribution: • Male is permanently barber pole but have attached to female. Cosmopolitan an unusual • J3 are ingested • Location: Abomasum – Use earthworms and asymmetrical (fourth stomach) terrestrial mollusks as copulatory bursa paratenic hosts • Transmission: ingestion of J3 juvenile 11
    • Adults in Eggs go out Metastrongyloids Angiostrongylus cantonensis Hatch Abomassum in feces • Transmission: J3 juvenile ingested • Lung parasites of many mammals. • Location: Pulmonary Artery and heart • Most require an invertebrate J1 and J2 • Pathology: Generally asymptomatic in rats. Life Cycle of intermediate host In all hosts, it undergoes a migration from Mature in develop in 3 days Haemonchus soil • May use several transport hosts. intestines to blood vessels near the brain. In • Metastrongylus apri important swine humans, it leaves vessels to wander through contortus brain and spinal cord. parasite J4 in Molts as it passes J3 ingested • Symptoms: None in rats. Causes – Uses earthworm intermediate host abomassum through first three with forage Eosinophilic Meningoencephalitis in humans stomachs – Cause pneumonia in pigs – Headache, fever, stiff neck – Vector/reservoir of swine influenza virus – Paralysis of fifth cranial nerve – Coma and death Other Trichostrongylids • Definitive Host: Rodents Angiostrongylus cantonensis • Trichostrongylus sp. are very small intestinal Angiostrongylus – Recently discovered in humans • Diagnosis: High eosinophil count in parasites of many animals • Intermediate Host: Snails, – T. colubriformis in sheep cantonensis spinal fluid. Sometimes worms are slugs, – T. tenuis in poultry collected in spinal fluid. • Paratenic hosts: terrestrial – T. axei in a variety of mammals planarians, freshwater – Symptoms similar to hydatidosis, • Ostertagia sp., particularly O. ostertagi, cause shrimp, land and freshwater cysticercosis, flukes, and other parasites $600 million in losses to U.S. cattle industry crabs, frogs, maybe clams – Symptoms also similar to bacterial or viral and oysters meningoencephalitis. • Dictyocaulus filaria is a lung parasite of sheep and goats. • Geographic Distribution: • Treatment: Thiabendazole treats the Human infections from SE • Nippostrongylus brasiliensis uses rats as Asia, East Indies, larval stages but no treatment is known definitive host. Madagascar and Oceania for adults. Spinal tap may relieve some – Easy to keep in lab so used to study nematode symptoms. Dead worms also present infections. problems. 12
    • Adults in Eggs laid Eggs break • Ingestion of eggs in J1 migrate • Largest of the nematode Ascaris contaminated food or water. pulmonary and carried into alveoli up trachea Ascarids artery to capillaries and hatch parasites – Use of night soils on crops – Some are over a foot long lumbricoides - increases transmission Molt • Stout, big worms Transmission • Require shade and mild Life Cycle of A. Swallowed temperatures and out in • Mouth surrounded with J4 migrates to • Eggs are very resistant cantonensis feces large lips, usually 3 pulmonary – Eggs can embryonate in very artery • Most are intestinal strong chemicals J2 survives J1 eaten parasites • 2% formalin if I.H. eaten by I.H. • Potassium dichromate Molt by P.H. • Infections are usually very • 50% hydrochloric, nitric, acetic, heavy and sulfuric acid J2 – Very long life Migrate to J3 ingested develops • At lest 10 years brain by D.H. in I.H. • Eggs can splash up onto Ascaris • Definitive Host: Humans Ascaris vegetables Intermediate Host: None Eggs can be picked up and lumbricoides • lumbricoides - • transported by cockroaches. • Geographic Distribution: Cosmopolitan Transmission • Wind borne dust may carry the – 25% of world population is eggs Nematodes II infected – Trapped on mucus membranes then swallowed – Has been known as human • Eggs have been found on parasite for over 2000 years German bank notes! • Found in writing of ancient Greeks • Children in infected much more • Location: small intestines frequently than adults – Dig in soil and put fingers in mouth 13
    • • Ascariasis Ascaris • Depends on the number of A. lumbricoides – Pathology Ascaris worms and Symptoms lumbricoides – • Worms subsist on liquid lumbricoides • Wandering adults are dangerous. • Sperm does not Pathology and content of small intestines – Overcrowding can lead to wandering have a flagellum! – Do not suck blood or graze on Symptoms • Upstream to pancreatic or bile ducts • Crawls around like mucosa. – May cause liver damage • Small to medium infections an amoeba – If reaches stomach, causes vomiting of worm are usually asymptomatic – Unusual contractile • Downstream to appendix or out anus protein allows them – May cause “sensitization – Females like to crawl through small spaces to move. phenomenon” • Looking for curly tail of male • Allergic reaction to worm waste. • Females can lay • She may crawl through nose, ear, or any other opening • Rashes, eye pain, asthma, – Image the surprise as a 1.5 foot worm crawls out the nose 200,000 eggs a day insomnia, restlessness or ear! and have 27 million • Aspiration of worm can cause death eggs in uteri Ascaris • Diagnosis: Ascaris • Heavy infections can block – Eggs in feces. intestines. lumbricoides lumbricoides – – Juveniles in sputum. – Sometimes fatal • Difficult to identify to Pathology and species. • Juveniles migrate through – Dead adults may be found Symptoms the lungs in feces – Causes Ascaris pnuemonitis • Treatment: – Fatal in heavy infections Mebendazole will kill the • Penetration of intestine or adults but not the appendix may occur migrating larvae – Frequently fatal – May need to repeat treatment • Dead adults usually pass out through the anus 14
    • Adults in Molt into • Pathology in humans: Eggs out Embryonate Toxocara • Definitive Host: Dogs and small in feces in soil J1 Toxocara Causes visceral larval intestine canis other canids migrans (VLM) Molt into • Distribution: Cosmopolitan canis – Juveniles are in wrong host Coughed up J2 • They wander and some times and swallowed • Location: Small Intestines go dormant Life Cycle of • Transmission: Ingestion of • Body walls them off in a Shelled granuloma Move up larvae is Ascaris embryonated egg in – Pathology depends on trachea swallowed contaminated food and water. where they wander lumbricoides There is also fetal – Other species of nematodes Molt twice Hatch from transmission from mother to can cause VLM egg puppies. If rodent eat eggs, – Good reason to de-worm Break out Enter lymph dogs regularly into airspace Right side Penetrate becomes paratenic host. or blood of lung of heart mucosa vessel • Uses pigs as definitive host. • Pathology in dogs: Depends • Symptoms: Canine infections • Frequently considered the Toxocara on age and immune status of Toxocara are usually asymptomatic. Ascaris suum host. VLM can cause fever, same species as A. canis canis pulmonary symptoms, • If host is naïve, goes on lung lumbricoides migrations like Ascaris, returns hepatomegaly, and – Differences in DNA to intestine and lives on fluids eosinophila – Different lip morphology • If host is immune, juveniles – Depend on number of worms – Probably a recent split migrate but eventually go into – Can cause death when brain is developmental arrest infected. • Less gene flow between the two species. • When female dog becomes • Diagnosis: For dogs, eggs in pregnant, worm “wakes up” and feces. ELISA test for humans • Biology is exactly the same cross placenta • Treatment: None listed for as A. lumbricoides. – Almost all puppies born in the U.S. are infected dogs (deworming medicine). • Can also be transmitted in For humans, Mebendazole but mother’s milk. only in most severe cases. 15
    • T. canis • Prevention: Frequently de- Other • Toxocara cati - cats • Pathology and Symptoms: worm pets. • Toxocara vitulorum – cattle Anisakis sp. Usually asymptomatic. If juveniles – Cover sandboxes when not in Ascarids • Toxocara pteropodis – Australian fruit penetrate stomach, can cause use bats abdominal pain, nausea, – Keep animals from defecating • All three can infect young through sometimes vomiting. If juveniles where children play. mother’s milk but not through placenta wander, mimics other diseases. • Notes: Children are more • Toxoascaris leonina – dogs and cats • Diagnosis: Frequently seen with frequently infected than – Doesn’t cause visceral larval migrans endoscope. Immunodiagnosis. adults • Parascaris equorum is the only large • Treatment: Removal with biopsy – 4.6 to 7.3% of children in U.S. ascarid in horses forceps. No drug treatment. test positive • Baylisascaris procyonis in raccoons – May cause pathology in humans • Prevention: Don’t eat – Rates as high as 30% in undercooked, raw, salted, or pickled African American children • Lagochilascaris minor found in pharynx of wild cats in South America, fish. Can be prevented by blast – In developing countries, 50 to freezing or cooking. 80% of children test positive. North America and Africa – Has caused death in humans Adults in Eggs out Develop in Egg eaten by: Anisakis sp. • Definitive Host: wide variety of • Definitive host is birds, small in the egg to J2 marine fish, birds, and mammals Heterakis particularly poultry. naïve immune intestine feces larvae – Rarely humans dog dog gallinarum • Intermediate host is an • Intermediate Hosts: earthworm Mature crustaceans • Paratenic hosts: any marine • Eggs of the worm carry J2 hatches fish Histomonas meleagridis, a Migrates through • Geographic Range: flagellate protozoan lungs to small Life Cycle of Cosmopolitan – Causes blackhead disease in intestine Wanders – Human cases are from Japan, turkeys Europe, and Scandinavia. U.S. • Destroys the liver T. canis infections are increasing • Losses on turkey farms • Transmission: Eating infected – Has no effect on any other bird. Enters Female Goes Crosses crustaceans or fish puppies becomes dormant – Nematode is the intermediate placenta • Location: Stomach host for H. meleagridis pregnant • Eats the protozoan which multiples in its intestines 16
    • Order • “Pinworms” • Transmission: Eggs are infective Enterobius vermicularis – • Females have slender, sharp- Enterobius stage. They are light and can float. Oxyurida pointed tails. vermicularis 3 modes: Pathology and Symptoms • Includes parasitic and free- – Hand to mouth (fecal/oral • Heavy infections may cause nervousness, living species contamination) restlessness, irritability, loss of appetite, • Eggs are picked up on the fingers • Uses invertebrates and nightmares, insomnia, bed wetting, vomiting and transferred to mouth vertebrates as definitive hosts – Inhalation • Rarely fatal. – No pinworms are found in dogs and cats • Eggs float and are inhaled, trapped – Worms do attach to the mucosa, resulting in by mucus membrane, then ulcerations • Only endoparasite with swallowed • Lead to secondary bacterial infections which can be fatal. haplodiploidy – Reinfection – Worms occasionally penetrate submucosa leading – Females are diploid • Develop from fertilized egg • Eggs hatch and larvae crawl back to death. – Males are haploid through anus – Worms may also wander up through the vagina, to • Develop from unfertilized egg • Location in definitive host: uterus, up oviducts and lodge in peritoneum – Also seen in rotifers, Intestines from stomach to anus • Causes peritonitis and granulomas around the worm. hymenopteran insects, and Acari – Most common in ileum-cecum region mites Enterobius vermicularis – Enterobius vermicularis – Pathology and Symptoms Pathology and Symptoms • Graze on epithelium cells and bacteria – Cause very little damage • Pinworm Neurosis – More of a mental condition Enterobius vermicularis • Disease is called enterobiasis than a medical one. • Definitive Host: Humans • 1/3 of cases are completely asymptomatic. – Female lays 15,000 eggs • Distribution: Cosmopolitan but more common in • Most cases, the worst symptom is intense itching. – The eggs get into everything temperate zones in industrialized countries. • Bedding – Female migrates out of anus at night to lay eggs • Clothing – Infects approximately 400,000,000 (10%) worldwide • Second only to Ascaris lumbricoides (1,000,000,000 or 25%) – Causes small breaks in skin which are invaded by • Curtains and drapery bacteria • Stuffed animals – Most common endoparasite in Europe and U.S. • Incidence between 30-80% in Caucasian children – Host scratches area, results in more breaks in skin and – People spend time and • Non-Caucasians seem to be more resistant more bacterial infections and more itching. money trying to eliminate the – Big problem in institutional situations eggs from the house. – Larvae may also invade the urethra, vagina, vulva • Causing itching around those openings as well 17
    • E. vermicularis – Life Cycle Enterobius vermicularis Adults in the Copulate Female Lays Spirurina: Acuariidae • Diagnosis: Two preferred techniques: Intestines and goes to eggs – Scotch tape technique Males die anus outside • All parasites of birds • Early morning, pat the area around the anus with a piece of anus – None infect humans Scotch tape (or any other transparent tape) Mature • Place tape on microscope slide with a drop of acetone. Eggs Eggs • Live in stomach and gizzard • Examine slide for eggs hatch become • Very unusual structures around head J3 larvae – Flashlight technique near airborne craw back – Called cordons • Shine a flashlight on the anus during the middle of the night anus • You can see the adult females crawling out to lay eggs. into anus – Function unknown • Treatment: Mebendazole (Vermox). Must Eggs – Aids with identification treat entire family and repeat after 10 days. coughed • Only Echinuria spp. are of economic Molt twice as J3 larvae Bedding, towels, and clothing should be up move to Large hatch in importance washed in hot water. Eggs Intestine small – Infect geese, ducks, and swans swallowed intestine Enterobius vermicularis Spirurina: Gnathostomatidae • Short life span Order Spirurida • Includes several large genera – Females die after oviposition – Tangqua sp. in reptiles – Males die after copulation • Divided into two suborders – Echinocephalus sp. in elasmobranchs • Infections become large, however, due to – Spirurina – Gnathostoma sp. in carnivorous mammals autoinfection and reinfection • Includes the filarial worms of humans • Gnathostoma spinigerum can cause • More common industrialized countries due to – Camallanina infections in humans increase in bedding, drapery, etc. in the • Includes Dracunculus medinensis – Most common in Japan and Far East home. – Usually from eating undercooked fish, chicken, • Most are parasites of wild animals • Because of low pathology, very little effort to ducks, or any other amphibian, reptile, or bird. eradicate this species. – First discovered in stomach of a tiger • Caucasians are much more susceptible than – Can cause cutaneous larval migrans (like A. non-Caucasians. caninum) 18
    • • Large, stout worms Live on the surface of the eye Spirurina: • Found in stomach or intestine Spirurina: Gongylonematidae Spirurina: •• Found in birds and mammals in all classes of vertebrates Physalopteridae• • Single genus Gongylonema Thelaziidae • Two species have been found Physaloptera sp. is largest in humans genus – About 25 species – Thelazia callipaeda parasite of – 3 spp. in amphibians • Live in the upper digestive tract dogs in Southeast Asia, China, – 45 spp. in reptiles and Korea – 24 spp. in birds • Birds and Mammals are definitive hosts – Thelazia californiensis parasite – 90 spp. in mammals of deer and other mammals in – P. praeputialis common in dogs • Only one, G. pulchrum, have been western U.S. of U.S. found in humans – P. rara most common one in • Use face flies as I.H. North America (edemic) – Wrong host so it wanders extensively • T. skrajabini and T. gulosa • Variety of mammals through upper G.I. tract and mouth occur in U.S. cattle • Appears to use field crickets for I.H. and snakes P.H. – Little pathology but very irritating • T. lacrymalis is found in U.S. – P. caucasica only species found – Treat with albendozole or surgery horses in humans • Primates normal host • Found in mammals only Spirurina: Tetrameridae Spirurina: Spirurina: Filarial Worms • Best known is Spirocerca lupi • Extreme sexual dimorphism Spirocercidae – Dogs are definitive host • Superfamily Filariodea – Males typical nematode – Female greatly swollen and – Uses dung beetle as I.H. • Live within the tissues of the body red – Paratenic hosts include birds, • More like a flatworm • Release live larvae reptiles, and mammals • Very commonly found in • Dogs usually get it from chickens – No egg stage gizzard or proventriculus of – Infected dogs may develop – Larval stage called microfilaria birds spondylosis • Very important causes of disease and • Cause very little damage • Deformation of the vertebrae disfigurement in humans • Use arthropods as – In dogs, it is the most frequent intermediate hosts • Most are in the family Onchocercidae cause of esophageal sarcoma • Relatively small family – Includes many species that parasitize wildlife – Much of the biology is still – Geopetitia – 5 rare species unknown – Several are very important human parasites – Tetrameres – 50 species • Wucheria, Brugia, Onchocerca, and Loa – Microtetrameres – 40 species – Distribution patchy 19
    • • Definitive Host: Humans • Symptoms: Filariasis – No known reservoir host Wuchereria • Three phases • Intermediate Host: Night- Asymptomatic Phase Wuchereria bancrofti • – Large number of microfilaria in blood feeding mosquitoes (wide – Some have swelling of lymph nodes bancrofti variety of genera and – May lead to other two phases species) • But not always • Geographic Range: • Inflammatory (Acute) Phase Around the equator, from – Due to antigens of adult worms Elephantiasis – a • No disease caused by microfilaria central Africa, to Turkey, symptom of W. – Dilate lymph channels India, Southeast Asia, • Interferes with lymph flow Philippines, Australia, and bancrofti infections – Attacks are marked by sudden onset of South America fever, chills, rigors, sweating, swollen, warm skin over lymph nodes, painful – Originally an Old World lymph node species spread to New – May also show orchitis (swelling of World by slave trade testes) and epididymitis. Location: Lymph channels Wuchereria• near major lymph glands Obstructive Phase Social and Psychological Impact Wuchereria • – Lymph channels become blocked by Wuchereria • – Elephantiasis can result in chronic bancrofti • Pathology: Depends on immune and inflammatory bancrofti dead worms bancrofti disfigurement response of host. – Lymph backs up and causes – May lead to sexual dysfunction • People with first exposure in swelling of the area • 27 million men have elephantiasis of adulthood quickly kill the worm scrotum – Area is then filled in with scar tissue and do not develop disease • 13 million people, mostly women, have – Of 10,431 U.S. naval personnel – Results in elephantiasis elephantiasis of breast that contracted W. bancrofti • Extreme enlargement of body parts • Can result in marriages devoid of during WWII, none developed • Particularly common in arm, legs, and physical and sexual intimacy elephantiasis scrotum • Where the parasite is endemic, – Elephantiasis of the scrotum can – May be due to repeated re- also cause leaking of lymph through fetus is exposed to parasite’s infections of the worm. scrotal skin antigens – Body’s immune system “learns” – Not fatal • Makes it look like person wet his pants that microfilaria are “normal” and • Can cause thoughts of suicide doesn’t kill them. 20
    • • Diagnosis: Microfilaria in peripheral blood sample at night Adults in Females Microfiliaria Microfilaria • Definitive Host: Humans Wuchereria – Blood should be taken between 10 lymph release are swept in peripheral Onchocerca – Up to 90% of people are p.m. and 2 a.m. channels microfiliara into blood blood at bancrofti • Microfilaria spend day in deep volvulus infected in some areas tissues night • Move to peripheral blood during • Intermediate Host: Black night to be picked up by mosquitoes Flies • Treatment: Hetrazan or DEC (Diethylcarbamazine) used to kill Molt and Mosquitoes • Distribution: Africa, adults. migrate to Life Cycle of pick up Arabia, Guatemala, – Nasty side effects lymph vessels microfilaria in – Repeated treatment needed W. bancrofti Mexico, Venezuela, and blood meal • Ivermectin prevents infection. Columbia – Cheaper and fewer side effects – Reached the New World • Best is combination of the two. with slave trade • DEC impregnated table salt is Injected with Move to J3 J2 J1 available as well. – Most common along rivers blood meal proboscis • Surgery for elephantiasis • Preferred habitat of I.H. Wuchereria • Avoid mosquito bites at night Onchocerca • Transmission: Larvae • Annual or semiannual doses of move into tissues through bancrofti - DEC (Diethylcarbamazine) and Brugia malayi volvulus wound made by bite Prevention Ivermectin • Very similar biology to W. bancrofti • Location in D.H.: Just – One of the diseases the Gates • Limited to Far East and Philippines foundation is fighting under the skin in nodules – Not found in Africa or the New World – most below waist in Africa • Education • Pathology and symptoms similar to W. – Most above waist, – In endemic areas, <50% knew particularly head, in New what caused filariasis bancrofti World – Only 6% knew you could catch it – Elephantiasis generally restricted to distal – Due to biting preferences from mosquitoes of the flies portions of arms and legs • 25% had microfilaria in their blood, • 5% of the women had elephantiasis • 30% of men had enlargement of testes 21
    • O. volvulus – • Most pathology due to immune • Definitive Host: Humans and inflammatory response of Onchocerca volvulus body. • Diagnosis: Microfilaria in bloodless skin snip. • Intermediate Host: Deer fly Pathology and Microfilaria can also be seen in eye during Loa loa • Adults live in skin nodules • Distribution: Rain forests Symptoms – Called onchocercomas exam. of west Africa and equatorial • Little pathology from live larvae • Treatment: Ivermectin kills microfilaria and and adults Sudan. eventually kills adults – Existed for short time in West • Dead worms cause – Also a preventative Indies but disappeared inflammatory response – Causes severe dermatitis over the – Fewer side effects than DEC (former treatment) • Transmission: Enters area – Gates Foundation is actively fighting this parasite – May result in thickening, wound from fly bite – Merck & Co. donated large quantities of the drug depigmentation of skin • Reduced the incidence of River Blindness significantly • Location: Just under skin • Often mistaken for leprosy – Causes “hanging groin” in Africa – May be eliminated soon and in eye. and Venezuela • Prevention: reduction of Black Fly populations – Elephantiasis is rare • Causes River Blindness Black fly O. volvulus – Adults Females Microfiliaria • Pathology and Symptoms: – Onchocerciasis Loa loa under release under the picks up Pathology and • Microfilaria migrate through the Infection called Loiasis. skin microfiliara skin microfilaria eyes in tissue • Causes very little pathology. Symptoms – Some times they die there fluids • Wander just under skin, causing • Inflammatory response causes allergic reactions the cornea to harden and become – Called Calabar swelling or fugitive opaque swelling Molt Life Cycle of Goes to – Causes blindness thoracic • Frequently wanders through eye • In many areas of Africa and O. volvulus muslces – Can cause emotional distress! Central America, everyone over the age of 40 is blind • Most frequent symptoms are – Little children guide blind adults to Enters itching, joint pain and fatigue. work in the fields wound Move to • Rarely, wanders deeper and can – Blindness is more common in J3 J2 J1 Central America than Africa made by fly cause fatal encephalitis proboscis • Flies prefer to bite on the head 22
    • Other filarial worms of humans Dirofilaria • Location: Right side of Loa loa heart and pulmonary artery • Mansonella ozzardi • Diagnosis: Microfilaria in the peripheral blood – Live in the mesenteries and peritoneum immitis • Transmission: Injected during the day – Found in New World only during blood meal. – Microfilaria move to lungs at night – Uses mosquitoes and black flies as I.H. • Pathology: Large number • Treatment: DEC (Diethylcarbamazine) is usual • Mansonella perstans of worms block the valves of treatment but is worse than the worm. – Tropical Africa and South America heart Ivermectin does not kill adults but prevents – Uses primates as reservoir host – Results in inefficient pumping reinfection. Adults just under the skin or in eye – Live in coelom of blood can be removed surgically. – Use mosquitoes as I.H. • Respiratory complications • Prevention: Avoid deer fly bites and reduction • Mansonella streptocerca can occur of deer fly populations. – Lives just under skin of humans in rainforest of Africa Adults Females Microfiliaria Deer fly • Heartworm under release to picks up Dirofilaria • Definitive Host: Dogs, cats, Dirofilaria immitis skin microfiliara bloodstream microfilaria • Symptoms: Vomiting, Respiratory insufficiency, ferrets, sea lions, and other in tissue immitis chronic cough, exercise intolerance. Death fluids mammals including humans. usually comes from cardiopulmonary failure • Intermediate Host: – Human cases are rare but can result in chest pain, Mosquitoes cough, coughing up blood, fever, malaise Molt Life Cycle of Goes to • Distribution: Cosmopolitan • Diagnosis: ELISA test. Microfilaria not Loa loa fat body diagnostic – In U.S., most common along Mississippi River, Atlantic and • Treatment: Difficult. Early cases can be cured. Gulf Coast states Dead adult worms may cause more damage Enters • Incidence 45% in dogs than live ones. Can be prevented by giving wound Move to – Rare in the western U.S. Ivermectin (Heartguard) during mosquito season made by fly J3 J2 J1 proboscis • Incidence can be as high as 5% or year round. in California and Oregon dogs 23
    • Adults in Females Microfilaria • Definitive Host: Humans Dracunculus medinensis - heart or release in peripheral Dracunculus – Rhesus monkeys have been Symptoms pulmonary microfilaria blood infected in the lab artery medinensis • Intermediate host: Cyclopoid • Dracunculiasis copepods • Caused by three factors • Distribution: Africa, India, – Emerging worms cause severe allergic reaction to Mosquitoes Middle East worm waste Molt Life Cycle of pick up – Reports from North America are • Rash, nausea, diarrhea, dizziness, localized swelling D. immitis microfilaria in probably different species, D. • Symptoms stop after female emerges blood meal insignis – Bacterial infections are common at site of • Transmission: Ingestion of emergence. copepods in drinking water. – Nonemergent “dead” worms can cause Injected with Move to • Location: just under the skin inflammatory response. J3 J2 J1 blood meal proboscis • Symptoms can include arthritis and paralysis Dracunculus • Female becomes swollen Diagnosis: Larvae can be Suborder Camallanina with larvae and body wall Dracunculus • found in fluid of blister. Large medinensis - white worm protruding from • Three families breaks Pathology medinensis wound also diagnostic. – Family Camallanidae – Releasing juveniles just under • Treatment: Adult female is • Inhabit intestines of fish, amphibians, and reptiles skin. removed by slowly winding her • Use cyclopoid copepod as I.H. – Causes inflammation which on a stick. • No tissue migration results in a blister – Cold water is washed over the worm – Family Philometridae – Blister breaks and part of worm – She expels juveniles and can be • Tissue parasites of fishes sticks out pulled out about 5 cm – Family Dracunculidae – Area of blister is very hot – Takes about 3 weeks to remove entire worm • Tissue parasites of reptiles, birds, and mammals • Relief comes from putting area in cold water • Breaking the worm can result • Dracunculus medinensis and D. insignis have been found in • Stimulate uterine contractions in massive allergic reaction humans – D. insignis is zoonosis from muskrats, opossums, and raccoons. • Female releases up to half a • Surgery can be used to million larvae in water remove calcified worms 24
    • Dracunculus medinensis Female moves Creates Female releases to just under blister which J1 into water • Eradication: WHO predicted it would be the skin ruptures the when D.H. puts eradicated by 1995. Missed the deadline but skin blister in water incidence continues to decline. • Involves Mates and – Supplying safe drinking water males die Life Cycle of D. – Education about transmission in unclean water J1 eaten – Early case containment and keeping infected body Mature medinenesis by parts out of drinking water copepod – Vector control – using chemical that kills copepods but had very little effect on other animals Copepod Penetrate J3 J2 • Incidence increases during droughts ingested hemocoel by human – Larvae and I.H. host concentrated and more likely to be ingested. Dracunculus • Long history with humans – “Fiery serpent” of Bible medinensis – Found in the writings of ancient Greeks and Romans – Caduceus carried by God of Medicine probably depicts worm on stick – Treatment officially described in 1674 • But I.H. wasn’t discovered until 1869 • Males are rarely observed, reach 40 mm • Females frequently grow up to 800 mm 25