Published on October 18, 2020
1. Soil- transmitted Helminths Arvin Ray M. delos Santos, RMT MPH – 1 | Lyceum Northwestern University
2. SOIL-TRANSMITTED HELMINTHS • This remain a major public health concern in developing countries like the Philippines, where poverty, poor environmental hygiene and impoverished health services exist. • Open defecation outside latrines by infected persons contributes significantly to the transmission of the diseases via contamination of soil and water supply.
3. SOIL-TRANSMITTED HELMINTHS (STH) • STH infections are caused by Ascaris lumbricoides, Trichuris trichiura, and the hookworms Necator americanus and Ancyclostoma duodenale. • High risk groups for STH infections include children, adolescent females, pregnant women and other occupational groups such as farmers, soldiers and indigenous groups.
4. SOIL-TRANSMITTED HELMINTHS (STH) • Helminth infections often result in subtle morbidities such as anemia, impaired physical and cognitive development, as well as poor school performance.
5. STH EPIDEMIOLOGY • Approximately 2 billion people worldwide are infected with soil-transmitted helminths. • It is estimated that 807 million individuals are infected with Ascaris, 604 million with Trichuris and 576 million with hookworms (Bethony et.al., 2006) • The burden caused by STH infection remains high in the Philippines according to results of studies supported by the Department of Health and UNICEF.
6. STH EPIDEMIOLOGY PARASITE LIGHT INTENSITY MODERATE INTENSITY HEAVY INTENSITY eggs per gram eggs per gram eggs per gram A. Lumbricoides 1 – 4,999 5,000 – 49,999 > 50,000 T. Trichiura 1 – 999 1,000 – 9,999 > 10,000 Hookworms 1 – 1,999 2,000 – 3,999 > 4,000 Threshold for the classification of intensity of STH infections in individuals
7. STH DIAGNOSIS • Parasitologic diagnosis of STH infections is made by analyzing stool samples for the presence of eggs. • Direct Fecal Smear (DFS) alone is the routine method for stool examination for the detection of motile protozoan trophozoites in diarrheic stool • DFS and Kato Thick method together are recommended for use in routine stool exam for STH infections and other helminths
8. Ascaris lumbricoides
9. Ascaris lumbricoides • Common name: Giant Roundworms • It is the most common intestinal roundworm of man. (Habitat: small intestine) • Causing the disease known as Ascariasis • It occurs frequently in tropical and subtropical regions of Asia, Central and South America and Africa where sanitation is lax.
10. Morphology 1. Ova 1.1. Fertilized egg: broadly oval, nearly spherical; golden brown in color; 45-75 x 35-45 microns 3 layers of egg shell a. albuminoid layer: outermost layer b. glycogen layer: a thick transparent middle layer c. lipoidal vitelline membrane: inner non-permeable membrane; absent in infertile eggs
11. Morphology 2. Ova 1.2. Unfertilized egg: never undergo further development; generally larger, narrower and elongated; 88-94 microns DECORTICATED EGG: an egg that has no albuminoid layer; it has smooth shell and appears pale yellow or colorless.
12. Morphology DECORTICATED EGG
13. Morphology 2. Adult: white, creamy or pinkish yellow when freshly expelled – Male: curve posterior end, mouth have 3 oval lips, usually shorter and slender, 15-30cm x 3 mm – Female: longer/stouter than male, 30-24cm x 5mm, straight posterior end – It lays 240,000 eggs per day – Approximately 65 to 85 million eggs during its life span of about 12 months
14. Adult A. lumbricoides
15. Adult A. lumbricoides
16. Pathology and Symptomatology • Due to larval migration LUNGS – petechial hemorrhage (larvae break out of the lung capillaries into the air sacs) Damage to the pulmonary tissues giving rise to Ascaris pneumonitis Symptoms manifested: asthmatic type of respitation; cough; bronchial rales (abnormall respiratory sound); urticarial rash(hives, vascular reaction of the upper dermis; eosinophilia in the circulatory blood
17. Pathology and Symptomatology • Due to adult worms Diarrhea, vague abdominal pain, nausea and loss of appetite Fever may stimulate the worms to migrate upward and be vomited and may pass through the nose Suffocation ( because vomited ascaris may pass into the larynx Pulmonary gangrene Otitis media (Eustachian tube)
18. Pathology and Symptomatology • Due to larval migration (con’t) Obstructive jaundice: due to obstruction of bile duct by the worms. Liver abscess (hepatic ascariasis) when worm force its body through gall bladder and enter the liver. The worms may enter the liver veins then carried to (brain, heart, lungs) causing serious complications. Pancreatitis when the worms migrate up enter and block the pancreatic duct. Appendicitis when the worm migrate down enter and block the appendix.
19. Pathology and Symptomatology
20. Laboratory Diagnosis • Direct Fecal Smear (DFS) • Kato-Thick Smear • Concentration Technique • ELISA • Indirect fluorescent antibody test (IFA) • Indirect hemagglutination test (IHA) • Eosinophilia is prominent during the early lung stage, but disappears later • Presence of Charcot Leyden crystals in sputum and stool Direct Fecal Smear
21. Transmission Soil eating Soil contaminated foodHuman manure as fertilizer Food handlers
22. Development of Ascaris Eggs
23. How man become infected? Man become infected by ingestion of infective Ascaris eggs; contain second stage larva L2 The larva hatch in the small intestine, and penetrate the wall of the intestine enter the portal circulation, carried to heart, then to lungs (Heart- Lung migration) Within 9-15 days in lungs, the larva develop to L3, which migrate through the bronchial tree, reach the throat the swallowed and enter the intestine. In the intestine the Ascaris larva grow into L4 then L5 which then mature into worm within 2-3 months The mature female will be fertilized by the male worms (mating). Each worm uteri may contain up to 27 million eggs at a time, but it produces about 200,000 eggs per day which deposit in feces
24. How life cycle continue? The life cycle continue when the eggs reach the soil When infected human defecate in soil, the eggs will reach the soil Under certain soil conditions: oxygen, shad, moisture, temperature (22-30 C), the fertilized egg develop into infective eggs. Ingesting those infective eggs by others (contamination of hands, foods, drinks with soil containing the eggs. While the infertile eggs don’t develop; they don’t have role in the life cycle
25. Life Cycle of A. lumbricoides
26. Ascaris worm coming through anus, nose and mouth
27. Obstruction of bowel by Ascaris Worm
28. Treatment • Albendazole • Levamisole • Mebendazole • Piperazine salts • Pyrantel pamoate Treatment is simple, effective and safe nowadays These drugs have neuromuscular blocking effect on the parasite causing paralysis Community based chemotheraphy done at interval of 4 months or 3x a year for 3 years appear to be promising in the control of Ascaris.
29. Prevention • Sanitary disposal of human excreta • Good personal hygiene • Avoid the use of fresh human feces as fertilizers in vegetable gardens and rice fields • Thorough cooking of food particularly vegetables • Washing fruits before eating
30. Trichuris trichiura
31. Trichuris trichiura • Common name: Whip Worm • Inhabits the human large intestine (ceacum) • Causing the disease known as trichiuriasis • It is soil transmitted infection (eggs are infective stage found in soil) • The adult worm looks like a whip, that is why it is called whip worm.
32. Trichuris trichiura
33. Trichuris trichiura • The worm has thin anterior and thick posterior part • They attached to intestinal mucosa by embedding the anterior part. • They feed on tissue fluid (not blood)
34. Morphology • Shape: Round; narrow long anterior part end and shorter and thicker posterior • Color: pinkish-white • Size: Female 35-50 mm long Male 30-45 mm, with a coiled posterior end
35. Eggs of Trichuris trichiura • Shape: oval (barrel-shaped) has polar hyaline mucoid blugs • Size: 60 x 40 µm • Color: honey brown • Shell: thick • Contents: mass of granules (unembryonated)
36. Development of Trichuris Eggs
37. How man become infected? Infection to man is by ingestion of the infective eggs (contain larva) that may be in contaminated food or drinks, hands with soil The larva hatch in the human small intestine then migrte to large intestine They attach to mucosa of the large intestine Then develop into mature worms within 3 months After mating, female produces 2,000-10,000 single-celled eggs per day which come out with feces Worms can live up to five years.
38. Life Cycle of Trichuris trichuira
39. Pathology and Symptomatology • People with light infections usually have no symptoms • People with heavy infection show symptoms like: Frequent defecation Painful passage of stool Stool appearance: contains a mixture of mucus and blood (dysentery) The clinical feature is identical to amebis dysentery.
40. Complications Colonic obstruction because of the tangled worms Ulceration of large intestine which result in blood loss Iron deficiency anemia Rectal prolapse
41. Complications: Rectal Prolapse
42. Laboratory Diagnosis Direct Fecal Smear Kato Thick Smear Concentration by sedimentation technique Floatation technique
43. Treatment Several antehelmintics drugs of choice: Albindazole Mebendazole Prognosis is good in light infection, but poor in heavy chronic infection.
44. Prevention and Control Prevent contamination of soil with human feces Construction of toilet or latrines Washing hands before eating (children, soil workers) Washing of vegetables and fruits Do not use night soil as fertilizer
46. Hookworm • Ancylostoma duodenale and Necator americanus are nematode worms • Habitat: found in human small intestine • They are bloodsucking nematodes • Causing the disease known as hookworm infection, ground itch or tunnel disease • It is a soil transmitted infection (infective stage is larva found in soil)
47. Geographical distribution Hookworms are the second most common human worm after A. lumbricoides, mostly found in tropical and subtropical climates A. duodenale found in the Middle East, Southern Europe and North Africa. N. americanus predominates in the America (North, Central and South America) and Australia
48. The Worm: Morphology • Shape: cylindrical • Color: pink – red – brown – Female pointed at posterior end – Male in both species has broad posterior end (copulatory bursa)
49. What is Copulatory Bursa? • Is the cuticle expansion at the posterior end of the male worm • Contains the male genital organs (spicules) • Helps in capturing female worm during mating.
50. The Worm: Morphology • Size of worms A. duodenale Female: 10-13 x 0.6 mm Male: 8-11 x 0.5 mm N. americanus Female: 9-11 x 0.4 mm Male 7-9 x 0.3 mm
51. The Worm: Morphology • Buccal capsule (mouth) help differentiation of both species A. duodenale N. americanus Provided with teeth provided with cutting plates
52. The Worm: Morphology • The hookworms feed on blood, they are well adapted to suck blood from the capillaries of intestinal mucosa. • They use the teeth and cutting plates to attach and make wounds on the intestinal mucosa. • Their mouth is also provided by amphidial glands which secrete a potent anticoagulant on the wounds to ensure continuous blood flowing.
53. Eggs of A. duodenale and N. americanus Hookworms produce identical eggs • Shape: oval • Size: 60 x 40 µm • Content: has brown colored 4-8 cells (plastomers) • Surrounded by hyaline space • Shell: thin
54. Development of hookworm egg
55. How man become infected Man become infected when the infective larval stage (L3) which found in soil penetrate through the skin The larva enter the blood vessels in the epidermis, reach the heart then lungs (heart-lung migration) After 1 week the larva migrate from the lungs through the bronchial tree, reach the throat then swallowed and enter the intestines In the small intestine, the larva attach to intestinal mucosa, make wound and feed on blood. The grow into adult (male and female) worm in about 5 weeks. The mature worms mate. After mating the female worm start laying eggs. N. americanus produce up to 10,000 eggs per day A. duodenale produce up to 30000 eggs per day
56. Life cycle of Hookworm
57. Pathology and Symptomatology 1. Cutaneous Phase 1.1. Ground Itch • First sign after exposure to soil • Allergic reaction of the skin to penetrating larva (L3) • Characterized by itching, redness and skin rash
58. Pathology and Symptomatology 1. Cutaneous Phase 1.2. Creeping Eruption • An allergic reaction to the motile larva under the skin • Characterized by red tunnels, itching, may persists for weeks or months. • Usually caused by Necator americanus
59. Pathology and Symptomatology 2. Lung Phase • Inflammation due to entrance of larva in lungs (pneumonitis) • Severity of lung phase depends on the number of larvae
60. Pathology and Symptomatology 3. Intestinal Phase Presence of worms in small intestine will cause the following: Loss of apptite Nausea Stomach or abdominal pain Vomiting Weight loss Constipation / diarrhea Fatigue (tiredness) Black stool color
61. Complication of Hookworm Infection • Usually hookworms in human host live for a few years but can live up to 15 years • The main complication of hookworm is iron deficiency anemia (microcytic, hypochromic), the hemoglobin level may decrease to 5 g/dL or less • This occur in chronic infection or heavy infection, due to continuous blood loss from the wounds made by the worms on the intestines.
62. Laboratory Diagnosis Direct Fecal Smear Kato Thick Smear Brine flotation Technique Formalin-ether concentration technique (FECT)
63. Treatment Several antehelmintics drugs of choice Pyrantel pamoate Mebendazole Tetrachloroethylene Thiabendazole In addition to iron containing supplements Prognosis is good!
64. Prevention and Control Prevent direct contact with soil Prevent contamination of soil with human feces Construction of comfort rooms and encouragement of their use Disinfect the soil using aqueous iodine solution to kill the larva Disinfect the night soil before use as fertilizer.
65. Thank you…