1. Nematoda - the Unsegmented Roundworms Very abundant - Most are free-living Most are small and inconspicuous Most are not not important factors to man with the exception of the role they play in ecology. Pseudocoelomates We will only study some of parasitic ones

2. Nematode Form and Function Typically elongate and tapered at both ends. Pseudocoelomates Complete digestive tract - mouth and anus. Body is covered with a noncellular cuticle secreted by underlying hypodermis and shed four (4) times during ontogeny (development). d)have only longitudinal muscles.

3. Roundworm cuticle Most are dioecious and display sexual dimorphorism. Non-living cuticle forms the integument –Cuticle contains proteins similar to Keratin and collagen which are very important. –Fiber layers - contain bundles of collagen, give elasticity to cuticle, very important in hydrostatic skeleton.

4. Roundworm cuticle Cuticular markings and ornamentations of many types occur in different nematodes important taxonomically. Hypodermis lies just below or beneath the basal lamella and contains living cells.

5. Hydrostatic Skeleton. Based on incompressibility of fluids In nematodes, as longitudinal muscles on one side contract, bends worm. When muscle relaxes, fluid pressure and elastic component of cuticle causes the worm to bend the other way.

6. Sense organs and Taxonomy Papillae - sensory structures usually located on cephalic region but may be located in the caudal area. Amphids - sensory structures also present on head more conspicuous on marine, free living forms. Plasmids - one glandular type, one sensory.

7. Nematode Reproduction: Males have various structures spicules, bursae, gubernaculum etc that help hold vulva open during copulation Nematode sperm is unusual in that it lacks flagella. Movement of sperm is often descrived as “amoeboid like”

8. Nematode Reproduction: Number of reproductive tracts is important taxonomic feature. –Monodelphic - a single tract –Didelphic - Two tracts Ascaris –Polydelphic - many tracts Where do the tracts originate? –prodelphic - from anterior direction (Ascaris –opisthodelphic - from posterior direction

9. ORDER TRICHURA Morphology has thick relatively short, posterior end with long thread - like anterior end, whip like in appearance. Three Genera of medical importance-- Trichuris, Capillaria, and Trichinella.

10. Family Trichuridae - Whipworms Morphology thick relatively short, posterior end with long thread - like anterior end, whip like in appearance (Trichocephalus) thread-head used in some texts.

11. Trichuris trichiura 30-50mm long Produces 1000-7000 eggs per day - eggs embryonate in soil. When swallowed infective juvenile hatches in small intestine enters intestinal crypts. After development reenters lumen of intestine matures. Can live a long time (many years).

15. Epidemiology Poor sanitation-human feces deposited in soil Physical conditions allowing worm development in soil – warm climate – high rainfall high humidity – moisture retaining soil (clay soil) – shade

16. Epidemiology Some parts of world (Southeastern U. S. are fit these requirements and up to 20-25% of population especially small children are infected.

17. Pathology Usually asymptomatic if few worms. (<100) Heavy infection variety of symptoms. –anemia - hemorrhage of digestive tract –secondary bacterial infection –Prolapse rectum - see fig. 23-4 pg.387 –possible cause of appendicitis

18. Diagnosis and Prevention Diagnosis - presence of egg or worm in stool These are easy to distinguish Prevention –Proper sanitation in feces disposed and hand washing –Trichuris vulpis common whipworm of dogs of this area. It can infect humans.

19. Family Capillariiade Gradual change from stout posterior to anterior that is thin thread like –Capillaria hepatica Found in liver of rodents, other mammals (man) –Eggs locked in liver until host eaten or host dies –Eggs embryonate in soil- then ingested by new host –Pathology mainly results from damage of liver tissue –Hand washing of major importance Capillaria philippinensis - intestinal roundworm –Fish probably source of human infection, humans can become infected by ingesting fecal contaminated soil results diarrhea, emaciation and ion imbalance

21. Family Trichinellidae One of smallest nematodes of man, with very unusual life cycle of major importance to man. Trichinella spiralis - only species

22. Trichinella spiralis Causes disease trichinosis, trichiniasis, or trichinelliasis –Vague symptoms leads to misidentification –Morphology Males 1. 4-1.6mm long females 2.8-3.2mm long Slender at anterior end Biology –same animal can serve as definitive and intermediate host with juvenile and adults located in different organs.

25. Trichinella spiralis Biology –Same animal can serve as definitive and intermediate host with juvenile and adult parasites located in different organs. –Infective juveniles -ingested, reach small intestine, molt 4 times, enter intestinal mucosa –Copulation occurs-male dies –Female migrates through epithelium giving live birth to juveniles-female dies

26. Trichinella spiralis Biology –Juveniles enter hepatoportal system carried to liver, heart, lungs-every part of body - prefer muscle tissue-but can be found elsewhere-most susceptible are muscles of eyes, tongue, mouth, arm and leg muscles –In tissue encysted by infiltrating leukocytes –After 2 months infective to new host

27. Trichinella spiralis Biology –Developmental arrest-up to 10 months-if not ingested usually become calcified but records of viability for 30 years –New host becomes infected by eating host in which these stages are found –In intestinal lumen-development occurs as above

28. Trichinella spiralis Biology –Sylvantic cycle-wild animals--such as bear, badgers, foxes, walruses-man –Urban cycle-humans, rats, pigs –Best considered a zoonotic disease humans rarely pass disease on. Why? –Man is not usually eaten-parasite dead end course in humans

29. Pathogenesis/clinical signs Nonpathogenic in swine  Edema of muscle fibers, periorbital swelling, extreme eosinophilia, persistent fever in other host species, incl. humans  May result in respiratory distress, swelling of tongue and other skeletal muscles, inability to move, death (usually at 28 dpi)  Recovery 6 mos. to 1 yr.

30. Epidemiology Sylvantic cycle- –Ingestion of poorly cooked bear, walruses, badgers, wild boar. –May be major cause in U.S. Today Urban cycle- –Man infected eating undercooked infected pork Pigs infected eating meat trimmings in garbage or by eating rats or nipping of each other tails or ears

31. Epidemiology Sylvantic cycle- –Ingestion of poorly cooked bear, walruses, badgers, wild boar. –May be major cause in U.S. Today Urban cycle- –Man infected eating undercooked infected pork Pigs infected eating meat trimmings in garbage or by eating rats or nipping of each other tails or ears

32. Epidemiology Pork must be cooked- all traces of pink removed –Sausage-raw delicacy some areas –100,000 individuals/ounce (5 juveniles per gram body weight usually fatal in humans –Back yard butcher - pg. 393

33. Pathology - 3 phases Adults penetrate mucosa - necrosis of host tissue-secondary infection, allergic reaction, vomiting, sweating diarrhea. 2.Migration of juveniles- damage to blood vessels, pneumonia, myocarditis, nephritis meningitis, encephalitis, eye damage Encystment in muscles - pain, difficult swallowing and/or breathing - heart failure- may lead to death

34. Pathology - 3 phases Penetration and encystment in muscle cells- muscle pain, difficulty swallowing, breathing - failure-may lead to death

35. Diagnosis Very difficult Xenodiagnosis-feed biopsy to lab animal, then dissect lab animal Immunodiagnostic techniques No satisfactory treatment-read pg.395

36. Public health significance Humans do serve as definitive and intermediate hosts  Usually occurs in a cluster-type epidemic  Humans typically become infected at pork roasts or barbecues, family picnics, where the source is local butchering of pigs; also, safaris into Alaska and Canada where poorly cooked bear or walrus is consumed

37. Prevention Cook meat well-all meat-especially pork, bear, etc. Cook garbage you would feed pigs Eliminate rats

38. Other control measures Do not allow pigs to eat pork scraps, other garbage, incl. rats, raccoon carcasses, etc.  Cook pork thoroughly; freeze carcasses - educate humans  Control rats (pigs are carnivores)  Not killed by curing, microwaving, or decomposition of meat

39. Order Dioctophymata Most members are parasites of aquatic birds and terrestrial mammals - only one organism will be discussed Dioctophyme renale - Giant kidney worm

40. Female reach length up to 1 meter long Blood red-blunt at ends Found in dogs, bears, humans, other large mammals

41. Biology Eggs hatch when eaten by aquatic oligochaete annelid Develops into 3rd stage juvenile When this host is ingested by fish or frog juvenile encysts in muscle or viscera with this animal serving as a paratenic host In the definite host the parasite migrates to liver, then to kidney where it matures.

43. Pathogenesis Kidney tissue destroyed, capsule distended, calcification occurs  Adhesions, peritonitis from worms in body cavity  Usually infects right kidney and left kidney often compensates. May be asymptomatic

44. Pathogenesis Possible pathogenic manifestations  Severe abdominal and lumbar pain  Sudden weight loss (up to 1/2), anorexia, vomiting  Hematuria - blood in urine  polydipsia - excessive thirst  uremia = azotemia - nitrogenous wastes

45. Epidemiology Any large mammal can serve as definitive host (bears, dogs, man). Most commonly fish or frog eating mammals –Fish and frogs serve as paratenic hosts. –Can become infected by ingesting infected annelid in contaminated water b.Cooking fish and drinking pure water prevents it in humans.

46. Order Rhabditata Go between free-living and parasitic cycles - have both parasitic and free living generations Most species inhabit decaying organic matter, soil, foul water, decaying, fruit, etc. Usually enter host through openings into body, wounds, etc.

47. Rhabdias bufonis-R. ranae Life cycle –Free living adult feeds on bacteria, etc. in soil –Offspring (Progeny) hatch within the uterus of female literally eating up the mother –3rd stage juveniles escape (filariform larvae) where they enter developmental arrest until they can enter skin of frog or toad –Those that reach lungs develop into hermaphroditic adults

48. Rhabdias bufonis-R. ranae Life cycle Protandrous hermaphrodite-male before it becomes a female-produces sperm stores it later produces eggs which are fertilized by stored sperm Fertilized egg passed up trachea of host swallowed hatch in intestine of frog-1st larval stage voided in feces-called rhaditiform larvae Juveniles undergo 4 molts to produce a generation of free living males and females (dioecious) This free living adult worm feeds on bacteria, etc. in soil

49. Strongyloides stercoralis a.Life cycle –Very complex –Parthenogenic females in layers of intestinal tissue (sometimes lungs, gall bladder, pancreas) and produce partially embryonated eggs –Juvenile hatches, escape into lumen-passed out in feces

50. Strongyloides stercoralis Juveniles can go one of two paths –Develop into free-living adults –Can produce successive generations of free- living adults –Can produce infective filariform juveniles strong evidence indicates that the environment has strong influence on the development of this organism

51. Strongyloides stercoralis Filariform juveniles develop when they enter host by skin penetration or by ingestion –Carried by blood to lungs, trachea swallowed- develop in intestine into parthenogenic adults –Embryonated eggs hatch, juvenile molts twice going down digestive tract larvae penetrate enter gut mucosa-blood-migration swallowed- develop into adults-(auto infection) –Man maintain infection up to 36 years

53. Epidemiology People become infected by larvae in contaminated soil or water Most common where poor sanitation conditions exist Prevention –Proper sanitation –Hand washing –Wear shoes/gloves when in contaminated soil

54. Pathology Invasion stage- intense itching at site of entry- creeping eruption Migratory stage (Pulmonary) - damage to lung tissue chest pain, cough, allergies. Can invade any organ. Intestinal phase - Frequently asymptomatic –Heavy infections - pain, vomiting, and diarrhea –Death is often result of imbalance of fluid and electrolyte levels

55. Order Strongylata Major medical importance Most species contain a broad, conspicuous copulatory bursa on males Most have a direct life cycle with no intermediate host

56. Family Ancylostomidae Commonly known as hookworms Live in intestines feed on blood and tissue fluids obtained from intestinal mucosa Morphology-especially important copulatory bursa of male.

59. Biology Mature worms mate in host small intestine –Embryonating eggs passed in feces If eggs land in warm, moist, shaded area, hatch feed molt twice form third stage filariform larvae. –When contact made with host skin, the filariform larvae burrow into it. –Enter blood vessels carried to heart, lungs, trachea-mouth swallowed-intestine where they develop into adult worms

60. Necator americanus "The American Killer" New World Hookworm –Probably introduced by slave trading –Major impact on development of southern U.S. –In 1947 estimated 1.5 million cases in North America –Current estimates in S.E.U.S. 4-5

62. Ancyclostoma duodenale - Old World Hookworm –Predominately found in southern Europe, –northern Africa, India, China, southeastern Asia –In mines of England and Belgium

64. Hookworm disease Sometimes asymptomatic-pathology depends on worm load and nutritional condition of the infected person Disease restricted to warmer regions of world also adequate amounts of moisture White people 10 (ten) times more susceptible to hookworm than black persons -"poor white trash"

65. Pathology Three phases of pathology –Cutaneous or invasion period –Pulmonary phase –Intestinal phase –Creeping eruption

66. Pathology Cutaneous or invasion period –When juveniles penetrate the shin –Tissue reaction worms may be killed-results in ground itch Pulmonary phase –Juveniles leave lung capillaries into alveoli –Usually asymptomatic –Hemorrhaging and inflammations may occur

67. Pathology Intestinal phase –Blood loss-iron deficient-anemia-up to 200ml of blood/day in heavy infections –Loss of appetite, pain-geophagy-see pg. 411 –Protein deficiency-edema –"Poor White Trash" –Creeping eruption-cutaneous larva migrans- species not able to mature in humans

71. Prevention Proper sanitation Wearing shoes and gloves Exposing contaminated land to sunlight

72. Order Ascaridata: The Large, Intestinal Roundworms Among the largest of all nematode parasites with some reaching 20 inches in length. Characterized by three large rounded lips The life cycle is usually simple, and no intermediate host is involved although a few species have more complex lifecycles.

73. Family Ascaridae - Ascaris lumbricoides (from humans) and (Ascaris suum from pigs) Because of size, cosmopolitan distribution, and size, these are well known parasites. Two species one in humans and the other in pigs. Thought to be the same specie but they show remarkable host specificity.

74. Ascaris lumbdrioides Large intestinal roundworm of man In some areas in the Orient, 100% of the population is infected. Most infections light but heavy infections may occur. Reported record (5,000) Glycogen consumption of Ascarids in China equal to glycogen of 143,000 tons of rice.

76. Morphology Large worms (males 15-30 cm long, females 20-50 cm long) Three prominent lips. Ovaries are extensive contain up to 27 million eggs at a given time. Eggs are characteristically lumpy. Non- fertilized eggs oval, fertilized eggs rounded.

78. Biology Female lays eggs into host intestine (200,000 per day), passed out in host feces. Eggs are resistant to low temperatures, dessication, and strong chemicals. Have remained viable for up to to 10 years.

79. Biology Eggs can embryonate in solutions of formalin, and 50% solutions of Sulfuric and hydrochloric acid to name a few). Sunlight and high temperatures are lethal in a short time.

80. Biology Eggs embryonate but do not hatch until ingested by man. When ingested, larvae escapes by way of operculum and burrows through intestinal mucosa.

81. Migration of Worms Larval forms enter blood and lymph capillaries and travel to heart. Heart to lungs, coughed up, swallowed to the intestine Then the worm can mature to an adult. Why such a pattern?

83. Epidemiology Indiscriminate defecation particularly near areas of habitation seeds the soil with eggs. Even if sanitation practices are initiated, the contaminated soil can lead to reinfection for many years. Children become infected by ingesting soil or putting soiled items in the mouth.

84. Epidemiology Nightsoil, the eggs may contaminate unwashed vegetables and water supplies. Eggs can be carried by cockroaches, flies, wind, and even on money. Ascariasis is present in epidemic proportions in the southeastern United States" (20 - 60) % of children infected.

85. Pathology Little damage is caused by the penetration Some worms migrate to ectopic sites (spleen, liver, lymph nodes, brain) and dependent upon number and where cause various inflammatory responses. These can lead to very severe allergic reactions. Transplacental migration can also occur.

86. Pathology Worms destroy capillaries in the lungs, causing hemorrhage. Heavy infections can lead to pools of blood which block air sacs. Migration of white blood cells lead to more congestion; a condition known as Ascaris pneumonitis (Loeffler's pneumonia). Lung tissue destroyed and bacterial infections occur may be fatal...

87. How the Worms Cause Pathology Normal worm activities Rob the host of nutrients Abdominal pain, restlessness, allergic reactions Intestinal blockage in heavy infections. Worms may knot up causing blockage which may be fatal.

88. How the Worms Cause Pathology Penetration of the intestine or appendix can lead to peritonitis which is often fatal. According to one researcher over 1/3 of all deaths caused in children because of abdominal emergencies in Capetown were causes by Ascaris.

89. How the Worms Cause Pathology Females wander in search for males. Overcrowding leads to wandering If worms migrate to stomach, acid irritates them leading to nauseous stomach. Aspiration of a vomited worm can result in death. If worms migrate to lungs, they can cause extensive damage and possible death.

90. Diagnosis and treatment Detection of larval worms in sputum or eggs in stool or the emergence of adult worm from anus or mouth or nose. Mebendazole is drug of choice but precaution must be taken in treatment as medications often cause adult worms to wander.