Medical Helminthology: Nematodes (Roundworms) Lecture Notes PDF

MEDICAL HELMINTHOLOGY 02/18/25 1  Introduction to Helminths Medical helminthology: Scientific study of parasitic worms and their medical consequences Laboratory diagnosis mainly depends on detection and identification of egg , larva and rarel...

MEDICAL HELMINTHOLOGY 02/18/25 1  Introduction to Helminths Medical helminthology: Scientific study of parasitic worms and their medical consequences Laboratory diagnosis mainly depends on detection and identification of egg , larva and rarely adults 2 Classification of helminths 3 Helminths can be classified as 1. Nematodes (Roundworms) 2. Trematodes (Flukes) 3. Cestodes (Tapeworms) 4  Nematodes (Roundworms)  Cylindrical worms  Have separate sex (bisexual)  Nematodes which infect humans include: A. Intestinal nematodes B. Blood and tissue nematodes 5  Intestinal Nematodes Intestinal nematodes infecting humans include: Ascaris lumbricoides Trichuris trichiura Enterobius vermicularis Strongyloides stercoralis Hookworms - Ancylostoma duodenale - Necator americanus 6  1. Ascaris lumbricoides Also known as the large intestinal roundworm Adult (male & female) live in the small intestine  Distribution: world wide 7  Ascaris… Habitat Adult: in the small intestine Egg : - Extremely resistant to adverse environmental condition 8 Ascaris… Transmission and Life Cycle Transmission: Ingestion of food or water contaminated with embryonated eggs Life Cycle Fully embryonated eggs are swallowed & larvae hatches & penetrate duodenal mucosa Larvae travel through the hepatic portal circulation to the liver, heart, pulmonary vessels and lungs They break out of the alveoli in to the air spaces ascend the bronchial tree to the throat swallowed and reach the small intestine again grow into mature worms 2-3 months after infection the adult worms start laying eggs (200,000/ day) 9 A. Lumbricoides life cycle 10  Ascaris… Clinical features and pathology Developing & mature worms in the intestine frequently cause abdominal pain. In heavy infections, especially in children, worm masses may cause obstruction or perforation of the intestine. Aberrant migration of “irritated” adult worms to bile duct, liver, Pharynx, peritoneal cavity, and damage tissue This migration can occur in response to fever, drugs other than those used to treat ascariasis, and some anesthetics. 11 Clinical… ith heavier worm loads a tangled mass of worms in the intestine can result in bowel obstruction or perforation as well as occlusion of appendix an individual worm can block a duct. 12 13 Laboratory Diagnosis Microscopy: - Detection and identification of eggs in the stool Eggs of Ascaris lumbricoides 14  Treatment Mebendazole: Drug of choice Prevention and control 1.Prevention of infection by washing hands before eating & after defecation Trimming finger nails Avoid consumption of uncooked food contaminated by soil 2. Preventing soil become faecally polluted by sanitary disposal of faeces in latrines avoiding the use of night soil as a fertilizer 3.Treatment and health education Mass de-worming programmes repeated at 3-6 month intervals, have been advocated in areas of high prevalence 15  2. Trichuris trichiura Common name : whipworm Distribution: world-wide Habitat: Adult: large intestine (caecum) & appendix Eggs: barrel shaped 16  Cont.. Adults: whip-like (shape) 17  Transmission and Life Cycle Transmission Ingestion of embryonated egg in contaminated food, water, or from contaminated hand life Cycle When embryonated eggs are swallowed larvae are released into the upper duodenum then attach themselves to the villi of small intestine or invade the intestinal walls  After 3-10 days they move down to the caecum & ascending colon where they mature into adult worms. 18 Life cycle 19  Clinical Features and pathology Are largely determined by the worm burden:  Heavy worm burden:  mechanical damage to the intestinal mucosa  Chronic profuse mucoid & bloody diarrhea, abdominal cramps and severe rectal tenesmus  Edematous prolapsed rectum ( in serious infection) 20 Cont… 21  Laboratory Diagnosis 1. Finding of characteristic eggs in faeces Treatment Mebendazole : Drug of choice Albendazole: Alternative Prevention and Control Sanitary disposal of faeces in latrine Avoidance of the use of night soil as a fertilizer Treatment of infected individuals and health education. 22  3. Enetrobius vermicularis  Common name: “Pin Worm”  Geographical distribution Cosmopolitan, specially in temperate areas, children are more commonly infected than adults 23 Habitat Adult: Caecum, appendix and adjacent portion of the ascending colon Gravid female: Caecum and rectum Eggs: deposited on perianal skin and occasionally in faeces 24  Transmission and life cycle Transmission:  Person to person transmission (ingestion of eggs)  Exposure to viable eggs in the soil (Ingestion) Eggs remains viable for several weeks  Autoinfection: occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area Children who suck their fingers are more likely to be infected 25  Transmission…  Air borne: Some small number of eggs can also be inhaled and ingested  Retro infection : the migration of newly hatched larvae from the anal skin back into the rectum 26  Life Cycle The ingested embryonated eggs hatch in the small intestine, larvae migrate to caecal region where they mature into adults Gravid females migrate nocturnally outside the anus and oviposit on the perianal area With in 4-6 hours being laid the egg contain infective larvae Perianal itching from the eggs induces scratching, & hence the eggs are transferred to the mouth via fingers 27 Adult Pinworms on the perianal skin 28 28 Life cycle of E.vermicularis 29  Clinical features and pathoogy  Nocturnal anal pruritus ( Related to the migration of female worms from the anus onto the perianal skin before egg deposition )  Insomnia, nervousness, nightmares (particularly in children)  Abdominal pain or appendicitis resulting from the worms are considered to be very rare 30 Laboratory Diagnosis 1. Detecting eggs from perianal skin using adhesive tape or swab method 2. Detecting eggs in the faeces 3. Finding of female worms from perianal skin or faeces 31 Treatment Pyrantel Pamoate Mebendazole *The whole family should be treated, to avoid reinfection Prevention and control Treating all members of a family in which infection has occurred Wearing tight-fitting cotton pants to infected children Washing of the anal skin each morning Washing of clothing worn at night washing hands after using toilet and before eating 32 4. Strongyloides stercoralis Common name: Dwarf thread worm Geographical distribution: - world wide 33 Habitat Has both free living and parasitic generations Parasitic adult females : reside in the mucosal epithelium of the of small intestine of human Free living male and female: in the external environment Rhabditiform larvae ( diagnostic stage ) : Passed in the faeces & external environments Filariform larvae ( infective stage ) : in the soil & water 34 Eggs: As soon as they are laid in submucosa, the rhabditiform larvae will hatched. …. 35  Transmission and life cycle Transmission: Commonly - penetration of the skin by the filariform larvae from the soil Internal or external autoinfection Transmammary 36  Life cycle 1.Free-living (indirect) cycle Rhabditiform larvae (in stool): molt 4x and develop into free-living adult males and females, produce eggs → rhabditiform larvae → Filariform larvae Filariform larvae initiate parasitic life cycle 37  Trans… 2. Parasitic (direct) cycle Rhabditiform larvae(excreted in stool) → molt 2x → develop into filariform larvae → penetrate skin →heart → lung → Alveolar space → bronchial tree →pharynx → swallowed &develop into adult female in small intestine →produce egg which yield rhabditiform larvae( which excreted in stool) Autoinfection: the rhabditiform larvae become infective filariform larvae in the host tissue penetrate intestinal mucosa (internal autoinfection) or perianal area (external autoinfection) 38 Life cycle of S.stercoralis 39 39  Clinical features and pathology 1.Cutaneous phase: large number of larva produce itching & erythema at the site of infection within 24 hours of invasion 2.Pulmonary phase: larval migration through the lungs stimulate symptoms, depending on the burden of the larvae. Some patients may be asymptomatic , while others present with eosinophilia , bronchopneumonia and full blown pneumonitis 3. Intestinal phase : Invasion by adult worms may produce abdominal pain, mucoid diarrhea , nausea, vomiting, anemia and villous atrophy 40  Cont … Autoinfection: is probably the mechanism responsible for long- term infection Hyperinfection syndrome:  characterized by massive larval invasion of the lung or any other organ including CNS, which is fatal  occurs when the immune status of the host suppressed by either drugs, malnutrition or the concurrent diseases 41  Laboratory diagnosis Finding the rhabditiform larvae in faeces using direct or concentration method by microscopy In hyper-infection syndrome the larva may be found in sputum, urine and other specimens Examination of serial samples may be necessary because direct stool examination is relatively insensitive 42 Treatment - Ivermectin - Thiabendazole Prevention and Control Sanitary disposal of faeces in latrine Avoidance of use of night soil as a fertilizer Wearing protective footwear Treatment of infected individuals and Health education 43 Are hematophagous nematodes Two major species Ancylostoma duodenale Necator americanus Geographical distribution Found in all tropical and sub tropical countries N. americanus is the most widespread hookworm globally. 44  Cont… Habitat – Adult: Jejunum & less often in the duodenum of human – Eggs: In the faeces; not infective to human – Rhabditiform & filariform larvae: free in the soil & water – filariform larvae are the infective stage 45  Cont… Egg: Hookworm rhabditiform larva Hookworm filariform larva 46  Transmission and life cycle Transmission Penetration of the skin by filariform larvae from the soil Ingestion of the filariform larvae present in the soil Transmammary and transplacental-- rare Life Cycle  Eggs are passed in the stool,  Under favorable conditions (moisture, warmth, shade): - Rhabditiform larvae hatch in the feces and/or soil - They become filariform (third-stage) larvae that are infective. … 47  cont… On contact with the human host, the filariform larvae penetrate the skin & are carried through the veins to the heart, then to the lungs They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and swallowed The larvae reach the small intestine, where they reside & mature into adults  they attach to the intestinal wall with resultant blood loss by the host. 48 Life cycle of Hookworm species 49 Life cycle of hookworm 50  Clinical features and pathology 1. Dermal (Cutaneous)phase ground itch : Local erythema, macules, papules 2. Pulmonary phase Migration of larvae through lung: - Bronchitis, pneumonitis and eosinophilia 3. Intestinal phase Pathogenic changes in hookworms infection is caused mainly by the adult worms Attachment of adult worms and injury to upper intestinal mucosa 51  Clinical… In the Intestine adult worms attach to the mucosa and feed on blood. Worms continuously move to new places exacerbating bleeding Estimated daily blood loss, 0.03 ml (N.americanus) 0.26 ml (A.duodnale) per worm Blood loss up to 200 ml per day in heavy infections 52 Clinical... High loads of the parasite coupled with poor nutrition (inadequate intake of protein & iron) eventually lead to anemia Malnutrition, stunt growth & poor mental development in children In chronic infection the main symptoms are: - Iron deficiency anemia (microcytic, hypochromic) with pallor, - Edema of the face and feet - Hemoglobin level 5 gm/dl or less 53 A. Teeth B. Cutting plates Head is slightly bend (hook) and the mouth carries characteristic teeth (Ancylostoma duodenale) or cutting plates (Necator americanus) 54 Laboratory diagnosis Finding eggs in faeces Microscopic identification of eggs in the stool is the most common method Treatment Mebendazole or albendazole If anemic : high protein diet supplemented with ferrous sulphate, folic acid and vitamin B12 Prevention and control Similar to Strongyloides stercoralis 55 Generalized life cycle of intestinal 56  Blood and tissue nematodes Include:  Filarial nematodes  Dracunculus medinensis (Guinea worm )  Trichinella species 57  Classification Three groups 1. Filarial nematodes (Filarial worms ) - Common/pathogenic filariae Wuchereria bancrofti  Brugia malayi  Brugia timori  Loa loa Onchocerca volvulus 2.Dracunculus medinensis ( Guinea worm) 3.Trichinella species 58  Filarial Nematodes General features Adults are long, thread - like worms Requires two host to complete their life cycle Females are viviparous, larvae hatch in the uterus The female produce first stage larvae (L1) The immature L1 stage larva is called Microfilaria Microfilariae: Require blood sucking insects (IH) to develop to infective form (L3) 59  Filarial worms cause 3 main diseases 1. lymphatic filariasis (Elephantiasis) 2. Loiasis 3. Onchocerciasis (river blindness) Lymphatic Filariasis Causative agents Wuchereria bancrofti Brugia malayi and Brugia timori These worms lodge in the lymphatic system Wuchereria bancrofti is the most widespread in the world (90% of the cases) 60 Lymphatic…  Social consequences It is one of the most debilitating and disfiguring diseases of the world 1. Disfigurement of the limbs and genitals leads to: Stigma Anxiety Ostracization Psychological trauma Sexual disability 61 Social… 2. The disease impeds  Mobility  Travel  Educational opportunity  Employment opportunity  Marriage prospect 62  Wuchereria bancrofti Disease: Bancroftian filariasis, Wuchereriasis, elephantiasis Distribution: Tropical and subtropical countries In Ethiopia: In people living adjecent to the baro river, near the town of Gambella Morphology: Adult: creamy white in colour with smooth surface 63  Cont… Habitat Adults: Coiled in lymphatic glands, or lying in lymphatic vessels, or wondering in retroperitoneal tissues Found usually in lymphatic of the lower limbs Microfilariae (diagnostic stage): In lymphatic vessels, in the peripheral blood , in lung and other internal organs Infective larvae: In the gut and muscles including mouth parts of certain species of mosquitoes. 64 Transmission and life cycle Transmission By the bite of infected female mosquitoes (Genera- Culex, Aedes, Anopheles) 65  Life cycle Requires two host  Human-DH, Mosquitoes-IH In humans:  Mosquito inject Infective larvae (L3) into human host, L3 enter into the lymphatic system and become adult male & female worms  Adult female worms (viviparous) produce thousands of sheathed microfilariae per day  Microfilariae found in peripheral circulation at night. 66  Life…  In mosquito:  Mosquito ingests microfilariae during blood meal from infected person  Microfilariae enter the body cavity (hemocoel) of mosquito lose their sheaths and migrate to thoracic muscles (flight muscles )for growth.  After 2 molts, microfilariae become L3 and migrate through the head, reach the proboscis of the mosquito. 67 Life cycle of W.bancrofti 68 Clinical feature and pathology  Many infections are asymptomatic Circulating microfilariae probably do not cause pathology  The main pathological lesions are due to: a)Inflammatory manifestations: due to toxic products of living or dead adult worms b) Obstructive manifestations 69 Clinical… a)Inflammatory manifestations: due to toxic products of living or dead adult worms Acute lymphatic filariasis:  High fever  Lymphadenitis and lymphangitis  usually the legs and genital organs (Microfilariae do not appear to be responsible for the major sequelae of lymphatic filariasis) 70  Clinical… b) Obstructive manifestations Chronic lymphatic filariasis: Obstructed lymphatics: obstructed genital lymphatics lead to hydrocele or scrotal lymphedema. Obstruction of the retroperitoneal lymphatics may cause the renal lymphatics to rupture in to the urinary tract, leading to chyluria ( the presence of lymph and emulsified fat in the urine ). Elephantiasis (non-pitting edema because there is proliferation of connective tissues, markedly thickened skin which become wart-like. 71  Clinical… Obstructive manifestations …  Fibrosis following the inflammatory process  Coiled worms inside lymphatics This may result in: Rupture of distended lymphatics (lymph leakage) - In the urinary passage – chyluria - In the testis – chylocoele 72  Clinical… Elephantiasis: Hard and thick, rough and fissured skin Frequently legs & genitalia (scrotum, penis & vulva) Less often arms and breasts. 73 Clinical… 74  Laboratory Diagnosis 1.Finding and identifying the microfilariae in blood by wet or stained blood films, blood collected at night. 2.Finding and identifying the microfilariae from urine, hydrocele fluid , lymphnode aspirates 3.Immunodiagnosis 75  Treatment Diethylcarbamazine (DEC) Ivermectin  Combination therapy DEC plus albendazole Ivermectin plus albendazole General measures: Rest, antibiotics, antihistamines, and bandaging 76 Clinical… 77  Treatment Surgical measures for elephantiasis: - Hydroceles can be drained repeatedly or managed surgically - Surgical removal of elephantoid tissue has been satisfactory for scrotal elephantiasis but not for effects on the extremities Prevention and control Control of mosquitoes Avoid mosquito bite Treat patients Health education Global lymphatic filariasis elimination program strategy: Mass drug administration Care for chronic cases 78  Causative agent of onchocerciasis also known as river blindness Geographical Distribution - Most infections in sub Sahara Africa - Some in Latin America and Middle East 79  Cont… Habitat – Adults:- Subcutaneous nodules and in skin – Microfilariae: Skin, eye & other organs of the body – Infective larvae: In the gut, mouth parts & muscles of Simulium black fly 80  Transmission and life cycle Transmission: - By the bite of infected black fly(genus Simulium ) Life cycle: During a blood meal, infected black fly introduces L3 (infective stage) into the human host In subcutaneous tissues the larvae develop into adult The female worms produce unsheathed microfilariae 81 In Black fly Black fly ingests the microfilariae during a blood meal Microfilariae migrate from the black fly's midgut through the hemocoel to the thoracic muscles Mf microfilariae develop in to L3 L3 migrate to the black fly's proboscis Infection occurs when the fly takes a blood meal 82 Life cycle of O.volvulus 83  Clinical feature and Pathology Light to moderate infections may produce an itchy rash, while heavy infection may lead to severe sequelae. A.Onchocercoma (subcutaneous nodule containing adult worms ) Form under the skin when the adult worms become encapsulated in subcutaneous tissue 84  Clinical.. B. Skin diseases  Chronically infected skin loses its elasticity & becomes Wrinkled-- elephant skin. - Lose pigment :leopard skin (depigmentation surrounded by slightly hyperpigmented zone) Elephant or lizard Leopard skin skin 85 Clinical.. C. Ocular manifestation When microfilariae in the skin of face migrate in to the eye  consists of trapping of microfilaria in the cornea, iris & anterior chambers, leading to photophobia, lacrimation & blindness 86  Clinical.. Ocular Tissue: Visual impairment is the most serious complication of onchocerciasis and usually affects only those persons with moderate or heavy infections. Lesions may develop in all parts of the eye. The most common early finding is conjunctivitis with photophobia. 87 Lymph Nodes: Mild to moderate lymphadenopathy is frequent, particularly in the inguinal and femoral areas, where the enlarged nodes may hang down in response to gravity (“hanging groin”). 88  Laboratory diagnosis Microfilariae in skin snips Skin biopsy Mf in urine, blood & most body fluids (in heavy infection).  Wet mount preparation Staining 89  Treatment  Ivermectin is the first-line agent for the treatment of onchocerciasis  It is given orally in a single dose  Greatly reduce the microfilariae load in the skin and eye, thus diminishing the likelihood of development of a disabling onchocerciasis. Surgical Care:  Nodulectomy -Removes adult worms and stop production of microfilariae 90  Prevention and control Destruction of vector blackfly (Simulium): -Selective use of insecticides Using insect repellents, wear protective clothing - DEET (Diethyl toluamide) Treatment of communities – Mass chemotherapy Treatment of infected individuals and health education 91  Dracunculus medinenis Dracunculosis Synonyms: Dracontiasis, Dracunculiasis Causative agent Scientific name: Dracunculus medinensis Common name: Guinea worm 92  Epidemiology Distribution of Dracunculus medinensis Global: India, Africa ( especially west Africa) Nile valley, Middle East. Ethiopia: cases of dracunculiasis were reported from low lands of Ethiopia 93 Habitat: - Adults: in subcutaneous tissues of human - Infective stage (L3): in the copepods (Cyclops) Transmission and life cycle Humans become infected by drinking unfiltered water containing copepods (Cyclops) which are infected with third stage larvae of D. medinensis 94  Life Cycle…  Following ingestion, the copepods die and release the larvae, which penetrate the host (human) stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space  After maturation into adults and fertilization, the male worms die and the females migrate in the subcutaneous tissues towards the skin surface.  Approximately one year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures 95  Life…  When this lesion comes into contact with water , a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae  The larvae are ingested by a copepod and after two molts (two weeks) they are develop into infective larvae. Infective larvae 96 Dracunculus medinensis Common Name: Guinea worm 97  Clinical feature and Pathology Early manifestatiosn when the female worm approaches the skin (usually ankles or feet). It liberates a toxic substance that results in formation of papule, local erythema, and pain. The papule changes to a blister with in 24 h to several days Rupture of the blister ultimately ulcerates Local or systemic symptoms such as urticaria, pruritus, pain, dyspnea, nausea and vomiting, which subside with rupture of the blister The ulcer may be secondarily infected producing cellulitis and induration 98  Life… blister 99 Adult worm of D. medinensis 100 Laboratory Diagnosis Finding of worm or larvae from the local blister Treatment  Niridazole, Metronidazole  extraction of the adult guinea worm by rolling it on stick a few centimeters per day or preferably by multiple surgical incisions under local anaesthesia 101 Prevention and Control 1. Prevent water contamination with the larvae 2. Water can be boiled, filtered through tightly woven nylon cloth 3. Treatment of water using chemicals to destroy the Cyclops 4. Covering the blister with a water proof dressing 5. Treatment and health education 102