Parasitology Nematodes Nematodes “White worms” — Not segmented — Covered with a cuticle + Secreted by hypodermis + Grows as worm grows Sexes are separate — Find each other with pheromones — Male sperm lack flagellum + move by pseudopodia (Major sperm protein) Most are slender with few distinguishing characteristics. Cause of some of the most debilitating and disfiguring diseases in humansPhylum Nematoda _. * Most numerous animals = onearth — 90,000 in 1 rotting apple ~ 1074 in 6.7 ml of coastal mud — Estimated 9 billion per acre in good farmland — Parasitic infections can be enormous Phylum * More species than any other phylum — More insects have been described — Every insect studied has at least one nematode parasite ive in every habitat — Free-lving in marine, freshwater, terrestrial + Even between grains of sand ona beach — Parasitic on almost every animal — Parasitic on plants NematodaPhylum Nematoda + Pseudocoelom — Fluid-filled cavity that forms hydrostatic skeleton * Simple nervous system — May include sensory organs called phasmids/amphids * Complete digestive system * Four juvenile stages which all look similar — Separated by a molt of the cuticle — Called J1, J2, J3, J4 + Most juvenile stages are free-living — J3 is usually the stage that gets into the definitive host Phylum Nematoda Many species show eutely — After embryogenesis, the nuclei of the cells do not divide —The number of cells remains constant for the rest of worm’s life * The cells simply grow larger + Exception is the ovary/testes — Number of cells varies by species * Two classes —Enoplea —RhabditeaClass Enoplea « Amphids (sense organs) well developed * Most are non-parasitic * Order Trichurida = Trichuris, Capillaria, Trichinella * Order Dioctophymatida — Dioctophymata (Kidney worm) * Order Muspiceida * Order Mermithida — Parasite of insects Trichuris trichiura + Whipworm * Definitive Host; Humans — Dogs possibly + Intermediate Host: None — Pigs and chickens are transport hosts — Flies will transport eggs on legs * Geographic distribution: Cosmopolitan — Warm Climate — High rainfall — Unsanitary conditions asaTrichuris trichiura * Location: large intestine from caecum and appendix to rectum — Burrows head into mucosa * Transmission: Ingestion of embryonated eggs, usually in contaminated food — Requires high humid, warm climate and shade to develop properly. Trichuris trichiura satel Pathol: and S' loms: Low-level infections (<100 worms) are asymptomatic + Large infections can result in diarrhea, bloody stool, abdominal pain and rectal prolapse Chronic infections in children can lead to growth retardation and finger and toe clubbing. In Phils — 80-84% prevalence Often associated with Ascaris lumbricoides infections. — Mode of transmission sameTrichuris trichiura * Diagnosis: bipolar eggs in feces. Colonoscopy can also uncover worm infections Treatment: Mebendazole or albendazole. Rectal prolapse treated with surgery Troehuris * Females may lay 3,000 to iyi 20,000 eggs a day for trichiura many years. There are 60-70 species in this genus, all live in large intestine — T. felis— cats — T. discolor — cattle — T. muris — rodents — T. vulpis - canids + Occasionally infects humans — T. suis — pigsMOY eon o) Meee ree gen eee) Pte Naa) Eggs go Embryonate large out in —— in soil intestines bite) Eggs eaten Ba eal Tal Cem OL) | Juvenile Bre Ta) eo mature +——— penetrate Saas mucosa Definitive Host: migratory fish-eating birds — mammals including humans Intermediate Host: None. Geographic Distribution: Philippines (1967- 68:epidemic) and other parts of Asia Mode of Transmission: Ingestion of infected fish Location in D.H.: small intestine: Pathology: ulcerative and degenerative lesions in the intestinal muscosa; disruption to electrolyte balance leading to heart failure + Symptoms: abdominal pains, gurgling stomach and diarrhea + Diagnosis: Eggs may be found in feces * Treatment: Albendazole Life Cycle of C. philippinensis Eggs laid and BO Dire ios es Tea a CML) Sane cil a iteahinint i Man ingests ees we feces eal Bird ingest bell a ee eggs | ss Adult in the ~—— Ere BT aa relayTrichinella * Hosts: swine, rats, humans, bear, walrus, and other carnivores. — Individual is the D.H. for the adults and |.H. for Juvenile Geographic Distribution: Cosmopolitan. More common in temperate areas than tropics. — There are at least seven sibling species and at least 3 strains + Different hosts, ribosomal DNA, gene sequences, and allozymes — Look identical Trichinella spiralis Location: Adults in wall of small intestine. Juvenile in striated muscles and organs. — Favorite are eye, tongue and masticatory muscles — Then diaphragm and intercostal — heavy muscles of arms and legs — Why they prefer certain muscles is are unclear Transmission: Ingestion of Juvenile in under cooked meat.Trichinella spiralis ee * Disease is trichinosis. — Pathology and — AKA. Trichiniasis or trichinelliasis Symptoms * The Great Mimic — Mimics many other conditions — Rarely exhibits a set of symptoms + Symptoms depend on location, number and age of larval worms + Most cases are asymptomatic + Initial phase: flu-like symptom — Caused by females penetrating mucosa + As worms mature, symptoms may include nausea, vomiting, sweating and diarrhea for five to seven days. — Body's reaction ta worm waste Trichinella spiralis = many symptoms symptoms and — Including pneumoni: pathology pleurisy, encephalitis, . meningitis, nephrit deafness, peritonitis, brain and eye damage, muscle stiffness, weak pulse, difficulty breathing, hallucinations Death is rare — Usually due to inflammation of heart muscle, respiratory complications or kidney malfunction+ Diagnosis: Antigenic and Trichinella serological tests, muscle aie biopsy plus case history. Spir alis + Treatment: No effective treatment. — Thiabendazole has worked in experimental animals but results in human mixed — Steroids reduce inflammation — Bed rest and analgesics help relieve pain and discomfort Trichinella spiralis Prevention: Cook meat well. —- Most cases are from undercooked pork - Includes processed meats, chops, sausages, ham, etc. —Can also occur in bears, walrus, fox, etc. + Rarely occurs in cattle and horses — How they get it is unknown + Can survive freezing down to —15°CTrit chinella Largest intracellular parasite : Ff — Juvenile invade a muscle cell and converts it into spiralis - ~ snusecat Notes = Alters the metabolism of the cell to do what it wants — Alters gene expression so it doesn't make contractile proteins « Releases Vascular endothelial growth factor (VEGF) — Stimulates formation of capillaries around cell + Nurse cell secretes collagen coating + Don't understand how worm does it - Eventually the body walls off the nurse cell by calcifying the walls | Immune system will eventually kill the Juvenile * But they can live over 39 years Trichinella spiralis - Notes Juvenile molt four times and become an adult in 30-32 hours from ingestion. + Female gives birth to live Juvenile - Noegg stage * Immunity has been demonstrated in mice — Can be passed to young from immune mothers. There are at least four variations of the life cycle which may be different species — Domestic + Use pigs and rats — Syivatic - Temperate zone + Fox, bears — Syivatic - Torrid zone * Hyenas, lions — Syivatic Frigid zone + Polar bears, walrusAdults inside Female BUT alt) estar) release ———> migrates to —>, mucosa cell Juvenile Ur its 6] Latte (oy Life Cycle of a wey T. spiralis WR | ! aL el Reach a Tere intestinal <—— small swallowed ~ 4-8 weeks lets es alg [istics (2) cell te mute} * Most are free-living nematodes. + Includes several families that were probably “pioneer parasites”. — Families Sterinernematididae and Heterorhabditidae (insects) - Family Rhabdiasidae (lung worms of frogs, snakes, cattle, and other animals) - Families Strongyloididae and Ancylostomatidae (medical importance to humans)Family Strongyloididae - Strongyloides sp. : Many different species. — §. stercoralis and S. fuelleborni in humans and primates — S.raitiin rats — S. ransomi in swine — Many other species parasitize birds, reptiles and amphibians Free-living stages mixed with parasitic stages. — Random mix — Free-living worms are male or female. — Parasitic worms are all parthenogenic females + No sperm has been found in parasitic forms — Autoinfection may also occur Family Ancylostomatidae * Well developed buccal cavity with teeth. + Four Larval stages. — Jiand J2 are free-living — J3 burrows into definitive host skin and migrates to intestine + Require warm, wet climate and shady areas - J1 and J2 can't tolerate drying, freezing, or exposure to sun. + Adults actively graze on intestinal mucosaSymptoms of hookworm infection vary by species and number of worms. — Most infections are asymptomatic. — A. duodenale causes more damage than N. americana — Nutrition of host also important in determining the degree of symptoms — Race also affects symptoms + Blacks are more resistant to infection than whites Ee Eggs go Hatch and ph Pera ABRs erie} met Intestine feces a=) | t ae s i" Hookworm re Hel Life Cycle Repo i. burrows into [tet tet] skin of host etd 1 ; Veli allege lees ee eS ee eee ee red a trachea vessel swallowedNecator ° —— Host; Humans. = — Most common human amerncanus hookworm Intermediate Host: None Geographic Distribution: Indigenous to Africa, India, southeast Asia, China, islands of sw Pacific. — First found in Brazil and Texas — Brought to New World with slave trade Transmission: J3 burrows into skin. * Pathology: Due to Necator damage of tissue during americanus migration of J3 juvenile and 7 ingestion of intestinal i mucosa by J4 juvenile and adults Symptoms: Usually asymptomatic. May cause hookworm disease. — We will discuss Hookworm disease later. Diagnosis: Eggs in feces Treatment: MebendazoleDefinitive Host: Humans Ancyclostoma Intermediate Host: None duodenale + Geographic Distribution: southern Europe, northem Africa, India, southeast Asia, China. — Scattered locations in United States, Caribbean Islands, and South America. — Found in 1000 year old mummy in Peru + May not have been brought over with slave trade. — Frequently found in mines well north of freeze line + Provides stable climate, no freezing, no sun. Transmission: J3 burrows into skin. + Pathology: Due to damage Ancyclostoma of tissue during migration of duodenale J3 juvenile and ingestion of intestinal mucosa by J4 juvenile and adults Symptoms: Usually asymptomatic. May cause hookworm disease. — We will discuss Hookworm disease later. Diagnosis: Eggs in feces Treatment: MebendazoleAncyclostoma@ Notes: First hookworm the life cycle was determined duoden al ce — In 1896 Arthur Looss was dropping cultures of worm into mouth of guinea pigs — He accidentally dropped a drop on his hand. * The area began to itch and turned red. + He wondered if the worm could have penetrated skin — He then started sampling his own feces + Found hookworm eggs in feces a few weeks Hookworm — + Hookworm infection does not : always lead to hookworm Disease Hinsaes) — Most infections are asymptomatic Development and severity of Hookworm disease depends on three factors. — Number of worms present — Species of hookworm — Nutritional status of the host.HOOKWOFMN — - tess than 25 1. americanus are asymptomatic — 25-100 light symptoms — 100-500 moderate symptoms — 500-1000 severe symptoms — >1000 are frequently fatal. Species of worm — A. duodenale sucks more blood so fewer worms required to cause symptoms Nutritional status of Host — Poor nutrition leads to worse symptoms. — Suppresses immune system — Fewer nutrients to repair damage Incidence of Hookworm Disease * Repeated contamination of soil — Repeated visit to same area to defecate increases transmission * Environmental conditions: Warm, humid, climate without freezing, proper soil — Must have loose, aerated soil, with lots of humus. - Warm, humid climate necessary for the worm to develop in soil in shady areas + Exposure of skin to soil — Must have access to skin so it can burrow into the skin.Incidence of Hookworm Disease + Longevity of worm - Juveniles can live is soil for several weeks + Up toa year in a mine. — Adults can live 5-15 years +N. americanus lives up to 15 years, making 9,000 eggs/day « A. duodenale lives up to 5 years but releases 25-30,000 eggsiday — Adults travel with host when host moves + Paratenic Host — Recently discovered A. duodenale juvenile can burrow into “wrong” species and survive in muscle — Human infected when food is eaten Incidence of Hookworm Disease » Race —In general, whites are 10 times more susceptible to haokworm disease than blacks. + Exact mechanism isn't clear — Gave rise to image of “poor white trash” in southern U.S. + Whites were frequently victims of high hookworm loads — Made them weak, apathetic, and lethargic + Blacks of the same socioeconomic situation were resistant to hookworm disease — They were industrious and hard-workingPhases of Hookworm Disease Cutaneous Phase — Occurs when juvenile burrow into skin and enter vessels — Localized allergic reaction Pulmonary Phase — Caused by larval migration through lungs and up trachea — Usually asymptomatic but can cause dry coughing and sore throat — May allow for secondary bacteria infections — Pneumonitis can occur in very large infections Phases of Hookworm Disease + Intestinal Phase = juvenile and adults suck blood from intestinal lining + 0,03 mi/day for N. americanus * 0.26 mi/day for A. duodenale — Bleeding into intestines can occur * Most iron is reabsorbed in intestines — Worms do not use the iron — Anemia can result if dietary intake isn’t sufficient to replace the iron lost + Severity depends on worm load and dietary intake.Phases of Hookworm Disease * Intestinal Phase — Most common symptoms + Slight, intermittent abdominal pains + Loss of normal appetite + Geophagy — desire to eat soil — Reason is unknown, — Many areas of the southem U.S. have clay soil that seems to relieve symptoms » In 1920's, a business person bagan to ship the clay to people around the country. Phases of Hookworm Disease + Intestinal Phase - Most common symptoms + Slight, intermittent abdominal pains + Loss of normal appetite + Geophagy — desire to eat soil — Reason is unknown — Many areas of the southem U.S. have clay soil that seems to relieve symptoms > In 1920's, 4 business person began to ship the clay to people around the country.Phases of Hookworm Disease * Chronic Heavy Infections — Patient suffers from severe protein deficiency + Can cause dry skin and hair, spoon nail, edema, potbelly, delayed puberty, mental dullness, heart failure and death. —Hookworms don’t block absorption of nutrients + Disease complicated by malnutrition + Loss of protein and iron to worm is catastrophic to those subsisting on minimal diet — Prolonged exposure during childhood can lead to lower intelligence and “laziness” Hookworm Disease * May explain the lower economic status in many developing countries. — Lethargic population can't produce as many goods as healthy population + Proper sanitation has eliminated it from most of U.S., Caribbean, and many other areas. — Latrines and treatment was provided by J.D. Rockefeller and lead to formation of Rockefeller Foundation + Incidence worldwide has increased in last 50 years — 25% of world population still infected. + Hookworms have evolved many ways to evade or suppress the immune system.Ancyclostoma , caninum Definitive Host: Dogs and cats Intermediate Host: None Distribution: Cosmopolitan — but particularly common in northern hemisphere Transmission: J3 juvenile burrow into skin Location in definitive Host: small intestine Ancyclostoma caninum + Pathology: damage to intestinal mucosa by grazing and sucking blood. Symptoms: Asymptomatic in most dogs and cats Diagnosis: Eggs in feces. Treatment: Thiabendazole.Cutaneous Lmigran + A.K.A. Creeping eruption Hookworm juvenile penetrates skin of the wrong host Juvenile dies during migration — Body reacts to worm and creates nasty skin irritation where every the worm went. Treat with thiabendazole A. braziliensis most common cause — A. caninumas well. — Many other hoakworms can cause it. Angiostrongylus cantonensis + Definitive Host: Rodents — Recently discovered in humans Intermediate Host: Snails, slugs, Paratenic hosts: terrestrial planarians, freshwater shrimp, land and freshwater crabs, frogs, maybe clams and oysters Geographic Distribution: Human infections from SE Asia, East Indies, Madagascar and OceaniaAngiostrongylus cantonensis * Transmission: J3 juvenile ingested * Location: Pulmonary Artery and heart + Pathology: Generally asymptomatic in rats. In all hosts, it undergoes a migration from intestines to blood vessels near the brain. In humans, it leaves vessels to wander through brain and spinal cord. * Symptoms: None in rats. Causes Eosinophilic Meningoencephalitis in humans — Headache, fever, stiff neck — Paralysis of fifth cranial nerve — Coma and death Angiostrongylus cantonensis * Diagnosis: High eosinophil count in spinal fluid. Sometimes worms are collected in spinal fluid. — Symptoms similar to hydatidosis, cysticercosis, flukes, and other parasites — Symptoms also similar to bacterial or viral meningoencephalitis. * Treatment: Thiabendazole treats the larval stages but no treatment is known for adults. Spinal tap may relieve some symptoms. Dead worms also present problems.vote iea ia) [fe ferow Ee) Eggs break pulmonary —— and carried into alveoli — artery to capillaries PUM arle a) i ve Life Cycle of A. 4migratesto Cantonensis felt Titel lag ETc fe Bre) Pam ene) J1 migrate Pe R ir: teat-s Boyles ls) and out in feces J1 eaten an Teli § ra ae Lae Se hs Migrate to , 3 ingested +————————— develops Pel er nee Largest of the nematode parasites — Some are overa Stout, big worms foot long Mouth surrounded with large lips, usually 3 Most are intestinal parasites Infections are usually very heavyCosmopolitan — 25% of world population is infected — Has been known as human parasite for over 2000 years + Found in writing of ancient Greeks * Location: small intestines 5 * Ingestion of eggs in Ascaris contaminated food or water. icol — — Use of night soil lumbricoides - - vse.tnight seis on core ‘TPANSMISSION + Require shade and mild temperatures Eggs are very resistant — Eggs can embryonate in very strong chemicals + 2% formalin * Potassium dichromate + 50% hydrochloric, nitric, acetic, and sulfuric acid — Very long life * Atlest 10 yearsAstais: Bie 1 ‘oid _* Eggs can be picked up and lumb re es transported by cockroaches. ‘TPansSimM/SSiON + wind bore dust may carry the r eggs — Trapped on mucus membranes then swallowed * Eggs have been found on German bank notes! * Children in infected much more frequently than adults — Dig in soil and put fingers in mouth * Ascariasis Ascaris * Depends on the number of ‘worms lumbricoides — , Worme subsist on liquid Pathology and _ content of small intestines — Do not suck blood or graze on Symptoms Pee, i Small to medium infections are usually asymptomatic — May cause “sensitization phenomenon” * Allergic reaction to worm waste. + Rashes, eye pain, asthma, insomnia, restlessnessAscaris lumbricoides — Pathology and Symptoms * Heavy infections can block intestines. — Sometimes fatal * Juveniles migrate through the lungs — Causes Asearis pnuemonitis — Fatal in heavy infections Penetration of intestine or appendix may occur — Frequently fatal Ascaris lumbricoide. S Diagnosis: — Eggs in feces. — Juveniles in sputum. * Difficult to identify to species. — Dead adults may be found in feces Treatment: Mebendazole will kill the adults but not the migrating larvae — May need to repeat treatment Dead adults usually pass out through the anusrece B a) irerdisted aan Eggs out et 7 poduicn ane in soil ila thal) ; ’ Coughed up ina andewslowee Life Cycle of ' t z Shelled — Ascaris ae lumbricoides “**"?"** Ltela ier Hatch from cle] eeu eee cma ‘ anaes elas el) Lert 1) ito airspace — Lo ahaa reeme Ce eee of lung Ot Uses pigs as definitive host. Frequently considered the same species as A. lumbricoides ~ Differences in DNA — Different lip morphology — Probably a recent split + Less gene flow between the two species. Biology is exactly the same as A. lumbricoides.Definitive Host: Dogs and other canids Distribution: Cosmopolitan Location: Small Intestines Transmission: Ingestion of embryonated egg in contaminated food and water. There is also fetal transmission from mother to puppies. If rodent eat eggs, becomes paratenic host. Toxocara + Pathology in dogs: Depends on age and immune status of host. If host is naive, goes on lung migrations like Ascaris, returns to intestine and lives on fluids If host is immune, juveniles migrate but eventually go into developmental arrest When female dog becomes Pregnant, worm “wakes up” and cross placenta — Almost all puppies born in the U.S. are infected Can also be transmitted in mother's milk.Toxocara canis + Pathology in humans: Causes visceral larval migrans (VLM) — Juveniles are in wrong host + They wander and some times go dormant * Body walls them off ina granuloma — Pathology depends on where they wander — Other species of nematodes can cause VLM - Good reason to de-worm dogs regularly Toxocara * Symptoms: Canine infections are usually asymptomatic. LM can cause fever, pulmonary symptoms, hepatomegaly, and eosinophila — Depend on number of worms — Can cause death when brain is infected. Diagnosis: For dogs, eggs in feces. ELISA test for humans Treatment: None listed for dogs (deworming medicine). For humans, Mebendazole but only in most severe cases.+ Prevention: Frequently de- worm pets. — Cover sandboxes when not in use — Keep animals from defecating where children play. Notes: Children are more frequently infected than adults — 4.6 to 7.3% of children in U.S. test positive — Rates as high as 30% in African American children — In developing countries, 50 to 80% of children test positive. CL Eggs out Develop in —+ Egg eaten by: small ~~ in the —> egg to J2 ie intestine feces Hee spate t % YET) s \ t SPA Dereon ure Poo Life Cycle of ital lat) T. canisDefinitive Host: wide variety of marine fish, birds, and mammals — Rarely humans Intermediate Hosts: crustaceans Paratenic hosts: any marine fish Geographic Range: ‘Cosmopolitan — Human cases are from Japan, Europe, and Scandinavia. U.S. infections are increasing Transmission: Eating infected crustaceans or fish Location: Stomach Anisakis sp. ° Pathology and Symptoms: Usually asymptomatic. If juveniles penetrate stomach, can cause abdominal pain, nausea, sometimes vomiting. If juveniles wander, mimics other diseases. Diagnosis: Frequently seen with endoscope. Immunodiagnosis. Treatment: Removal with biopsy forceps. No drug treatment. Prevention: Don't eat undercooked, raw, salted, or pickled fish. Can be prevented by blast freezing or cookingOrder + *Pinworms" + Females have slender, sharp- pointed tails. + Includes parasitic and free- living species + Uses invertebrates and vertebrates as definitive hosts — No pinworms are found in dogs and cats + Only endoparasite with haplodiploidy — Females are diploid + Develop from fertilized egg — Males are haploid + Develop from unfertilized egg — Also seen in rotifers, hymenopteran insects, and Acari mites Enterobius vermicularis + Definitive Host: Humans istribu: Cosmopolitan but more common in temperate zones in industrialized countries. — Infects approximately 400,000,000 (10%) worldwide + Second only to Ascaris Jumbricoides (1,000,000,000 or 25%) — Most common endoparasite in Europe and U.S. + Incidence between 30-80% in Caucasian children + Non-Caucasians seem to be more resistant — Big problem in institutional situationsEnferobius + Transmission: Eggs are infective Y 3 stage. They are light and can float. vermicularis 3 modes: — Hand to mouth (fecal/oral contamination) + Eggs are picked up on the fingers and transferred to mouth — Inhalation + Eggs float and are inhaled, trapped by mucus membrane, then swallowed — Reinfection + Eggs hatch and larvae crawl back through anus * Location in definitive host: Intestines from stomach to anus — Most common in ileum-cecum region Enterobius vermicularis — Pathology and Symptoms Graze on epithelium cells and bacteria — Cause very little damage + Disease is called enterobiasis 1/3 of cases are completely asymptomatic. Most cases, the worst symptom is intense itching. — Female migrates out of anus at night to lay eggs — Causes small breaks in skin which are invaded by bacteria . — Host scratches area, results in more breaks in skin and more bacterial infections and more itching. — Larvae may also invade the urethra, vagina, vulva + Causing itching around those openings as wellEnterobius vermicularis — Pathology and Symptoms * Heavy infections may cause nervousness, restlessness, irritability, loss of appetite, nightmares, insomnia, bed wetting, vomiting + Rarely fatal. — Worms do attach to the mucosa, resulting in ulcerations + Lead to secondary bacterial infections which can be fatal — Worms occasionally penetrate submucosa leading to death. — Worms may also wander up through the vagina, to uterus, up oviducts and lodge in peritoneum + Causes peritonitis and granulomas around the worm Enterobius vermicularis — Pathology and Symptoms yy) + Pinworm Neurosis — More of a mental condition than a medical one. ‘emale lays 15,000 eggs — The eggs get into everything + Bedding + Clothing + Curtains and drapery + Stuffed animals — People spend time and money trying to eliminate the eggs from the house.Enterobius vermicularis + Diagnosis: Two preferred techniques: — Scotch tape technique * Early morning, pat the area around the anus with a piece of Scotch tape (or any other transparent tape) * Place tape on microscope slide with a drop of acetone + Examine slide for eggs — Flashlight technique + Shine a flashlight on the anus during the middle of the night + You can see the adult females crawling out to lay eggs * Treatment: Mebendazole (Vermox). Must treat entire family and repeat after 10 days. Bedding, towels, and clothing should be washed in hot water. Enterobius vermicularis Short life span — Females die after oviposition — Males die after copulation + Infections become large, however, due to autoinfection and reinfection + More common industrialized countries due to increase in bedding, drapery, etc. in the home. + Because of low pathology, very little effort to eradicate this species. * Caucasians are much more susceptible than non-Caucasians.E. vermicularis — Life Cycle Adults in the Copulate Female ___, Lays Lai > UL ane goes to eggs A Males die Ent} ed anus Ie} Ss il al Lele) Reyer Uhod Lato ert aecs eet cee Teeuty ci =r coughed Molt twice as BRT a1) “ 4 move to Large *—— een] or re . a Tiecstuted small Ply cl Tact + Divided into two suborders — Spirurina + Includes the filarial worms of humans —Camallanina + Includes Dracunculus medinensis * Most are parasites of wild animalsSpirurina: Filarial Worms Superfamily Filariodea Live within the tissues of the body Release live larvae — No egg stage — Larval stage called microfilaria Very important causes of disease and disfigurement in humans Most are in the family Onchocercidae — Includes many species that parasitize wildlife — Several are very important human parasites + Wucheria, Brugia, Onchocerca, and Loa * Definitive Host: Humans — No known reservoir host V/ucherena © Intermediate Host: Night- : feeding mosquitoes (wide bancrofti variety of genera and species) Geographic Range: Around the equator, from central Africa, to Turkey, India, Southeast Asia, Philippines, Australia, and South America — Originally an Old World species spread to New World by slave trade;=* Location: Lymph channels Wuchereria near major lymph glands ' « Pathology: Depends on bancrofti immune and inflammatory response of host. People with first exposure in adulthood quickly kill the worm and do not develop disease — Of 10,431 U.S. naval personnel that contracted W. bancrofti during WWII, none developed elephantiasis + Where the parasite is endemic, fetus is exposed to parasite’s antigens — Body's immune system “leams” that microfilaria are “normal” and doesn't kill them. Wuchereria * Symptoms: Filariasis + Three phases banerof) + Asymptomatic Phase — Large number of microfilaria in blood — Same have swelling of lymph nodes. — May lead to other two phases 4 + But not atways + Inflammatory (Acute) Phase — Due to antigens of adult worms + No disease caused by microfilaria — Dilate lymph channels + Interferes with lymph flow — Attacks are marked by sudden onset of fever, chills, rigors, sweating, swollen, warm skin over lymph nodes, painful lymph node — May also show orchitis (swelling of tesies) and epididymitis.* Obstructive Phase — Lymph channels become blocked by’ dead worms g] — Lymph backs up and causes swelling of the area — Area is then filled in with scar tissue | — Results in elephantiasis + Extreme enlargement of body parts + Particularly common in arm, legs, and scrotum — May be due to repeated re- infections of the worm. — Not fatal Elephantiasis — a symptom of W. bancrofti infectionsWuche reria * Social and Psychological Impact — Elephantiasis can result in chronic bancrofti disfigurement — May lead to sexual dysfunction + 27 million men have elephantiasis of scrotum * 13 million people, mostly women, have elephantiasis of breast * Can result in marriages devoid of physical and sexual intimacy — Elephantiasis of the scrotum can also cause leaking of lymph through ‘scrotal skin * Makes it look like person wet his pants * Can cause thoughts of suicide + Diagnosis: Microfilaria in j peripheral blood sample at night Wuchereria — Blood should be taken between 10 per p.m. and 2.a.m + Microfilaria spend day in deep tissues: + Move to peripheral blood during night to be picked up by mosquitoes Treatment: Hetrazan or DEC Icarbamazine) used to kill Nasty side effects — Repeated treatment needed Ivermectin prevents infection. — Cheaper and fewer side effects Best is combination of the two. DEC impregnated table salt is available as well. + Surgery for elephantiasis+ Avoid mosquito bites at night + Annual or semiannual doses of DEC (Diethylcarbamazine) and Ivermectin — One of the diseases the Gates foundation is fighting Education — In endemic areas, <50% knew what caused filariasis — Only 6% knew you could catch it from mosquitoes + 25% had microfilaria in their blood, + 5% of the women had elephantiasis * 30% of men had enlargement of testes EC Tcaiy aur: ty Microfiliaria Wolves ETT) lymph ——*+ release ——+ are swept —+ in peripheral Ce Taal) Puerco) flu Coll elise] 1s [elero 14 Gallia Molt and T iT ite eae LEM =o) asa Misa lcd W. bancrofti Ree GEN) 1s elolo Nuit) Tiere mT) fel Be) | —_ J3+—J2 +— Ji blood meal proboscisDracunculus * Definitive Host: Humans medinensis — Rhesus monkeys have been infected in the lab Intermediate host: Cyclopoid copepods Distribution: Africa, India, Middle East — Reports from North America are probably different species, D. insignis Transmission: Ingestion of copepods in drinking water. Dracunculus + Female becomes swollen medinensis a with larvae and body wall breaks Pathology — Releasing juveniles just under skin. Causes inflammation which results in a blister Blister breaks and part of worm sticks out Area of blister is very hot * Relief comes from putting area in cold water * Stimulate uterine contractions * Female releases up to half a million larvae in waterDracunculus medinensis - Symptoms * Dracunculiasis * Caused by three factors — Emerging worms cause severe allergic reaction to worm waste + Rash, nausea, diarrhea, dizziness, localized swelling + Symptoms stop after female emerges — Bacterial infections are common at site of emergence. — Nonemergent “dead” worms can cause inflammatory response. + Symptoms can include arthritis and paralysis Dracunculus* Pisttd a cee tare fi z white worm protruding fram medinen. Si $ wound also diagnostic. Treatment: Adult female is removed by slowly winding her on a stick. — Cold water is washed over the worm — She expels juveniles and can be pulled out about 5 cm — Takes about 3 weeks to remove entire worm Breaking the worm can result in massive allergic reaction Surgery can be used to remove calcified wormsDracunculus medinensis + Eradication: WHO predicted it would be eradicated by 1995. Missed the deadline but incidence continues to decline. * Involves — Supplying safe drinking water — Education about transmission in unclean water — Early case containment and keeping infected body parts out of drinking water — Vector control — using chemical that kills copepods but had very little effect on other animals * Incidence increases during droughts — Larvae and |.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 |.H. wasn't discovered until 1869 Males are rarely observed, reach 40 mm Females frequently grow up to 800 mmrl Mey letter) Beart) to just under ——blister which —> _J11 into water rea Met en ay when D.H. puts Et) be Cla R lle ECE) males die Life Cycle of D. A 5 BT) Ree plete =e} by copepod en rn Penetrate fi foferl te Pee Saal}