Lecture 4. Nematodes (Roundworm): Intestinal and Systemic J. D. MacLean
Trichuris (threadworm) oral hemorrhagic colitis
Enterobius (pinworm) oral perianal itch
Ascaris lumbricoides (round worm) oral small intestine obstruction(hookworm)
iron deficiency anemia
Strongyloides stercoralis duodenitis
cutaneous larva currens
hyperinfection in immunocompromised
Diagnosis: stool examination for larvae (strongyloides) or eggs (the rest)
Treatment: albendizole or ivermectin (strongyloides) or mebendazole (the rest)
Trichinella spiralis or nativa raw pork, bear,walrus
trichinosis diagnosis: eosinophilia, raised CPK, serology
Toxocara canis oral eosinophilia, hepatomegaly,
(visceral larva migrans) dx: serology
Wuchereria bancrofti mosquito vector adults block lymphatics;
(lymphatic filariasis) elephantiasis, chyluria or hydrocoele
dx: microfilaria in blood
Onchocera volvulus black fly vector itchiness, skin nodules,
(river blindness) blindness
dx: adults in skin nodules, microfilaria in skin biopsies (snips)
Loa loa horse fly vector Kalabar swellings (short
(eye worm) lived), eye worm
dx: microfilaria in blood
Diagnosis: blood or tissue examination for microfilaria; serology for Trichinella and Toxocara
Treatment: Wuchereria, Onchocerca, Loa- ivermectin, diethylcarbamazine
Trichinosis, Toxocara- thiabendizole, albendizole
The helminths (from the Greek meaning worm) are higher, multicellular forms of parasite with specialized organs. There are two basic groups
Nematodes - roundworms
Platyhelminths - flatworms - cestodes (tapeworm)
- trematodes (fluke)
Characteristics - round in cross section
- bilaterally symmetrical
- variable size - 1 mm to 1 meter
- organs - digestive, nervous, excretory, cuticle, muscle, sexual
- develops by molting (shedding cuticle)
- separate sexes
- reproduction and development: egg egg fertilization embryo in egg larva 4 molts adult
Bowel nematodes - with adults in bowel
Ancylostoma duodenale and Necator americanus
Tissue nematodes - adults or larval stage in tissue
Toxocara canis (visceral larva migrans)
Filaria - Wuchereria bancrofti
Trichuris trichiura (Whipworm)
Epidemiology:- about 350 million infected, in some areas 90-100% of population
- restricted to warm climate by necessity for egg to embryonate on moist warm soil for 10-14 days before becoming infective
- spread: fecal - oral (esp. via foods and hands)
Biology: - life cycle: people infected by swallowing embryonated egg egg hatches in small intestine attaches to colonic epithelium and matures to egg laying in 3 months.
- organism: adult female, approx. 45 mm
eggs approx. 52 mu long
Clinical - clinical: 99% assymptomatic
heavy load gives diarrhea dysentery anemia
Diagnosis: - examine stool (standard techniques) - pathognomonic egg
Treatment: - mebendizole, albendizole
Problems: - lack of cost effective control methods in LDC (least developed countries)
Enterobius vermicularis (Pinworm)
Epidemiology :-very common in all geographic areas - 20%+ in Toronto's children
- spread: fecal - oral; eggs can survive days to weeks in environment
Biology: - infected by swallowing egg which hatches after contact with stomach and matures to adult which then resides in lumen of caecum (from egg to adult maturation in 15-43 days) . Female migrates onto perianal skin to lay eggs at night.
- organism: adult female approx. 10 mm long; egg approx. 55 Ám long
Clinical: most asymptomatic
<10% anal pruritus; rarely vaginitis
Diagnosis: less then 10% found in stools, i.e. not a useful examination;
best is pinworm swab - cellophane tape swab, or sticky paddle
Problems: insensitivity of pinworm swabs (intermittent deposition of eggs) : eradication of infection from a family.
Ascaris lumbricoides (Roundworm)
Epidemiology: About 650 million infected worldwide mainly tropics. Transmission by faecal- oral; egg very resistant, can survive years
Biology: egg ingested, hatches in duodenum; larvae penetrate intestine wall, enter blood vessels and embolize through liver to lungs. They then migrate into airspaces, up trachea and are swallowed, taking up permanent adult residence in the small intestine - 2 months from egg to mature adult
Organism: adult female 20-35 cm long; egg approx. 68 mu long
Clinical: related to number of worms; small numbers asymptomatic
- large numbers of larva transiting lung -- Loefflers pneumonitis
- large numbers of adults in intestine -- obstruction, pains
- at times adults migrate into bile duct, up esophagus, through surgical anastomoses of intestine
- cause malnutrition if in large numbers
Diagnosis: stool examination
Epidemiology: The only important helminth that can complete its life cycle in the human host and hence increase its numbers. Special problem in immunocompromized because of this. Mainly a tropical parasite because requires warm moist soil for transmission.
Transmission: skin contact with invasive larvae in soil.
Biology: larvae passed into soil in human feces where mature in several days to skin invasive (filariform) larvae. Can exist for months in soil "free living" by completing life cycle without contact with human host man. Larvae penetrate skin, move via blood vessels to lung, invade airspace, move up bronchi, are swallowed, and then penetrate small intestinal mucosa where they mature to adults in submucosa. They deposit eggs in submucosa and these hatch and migrate into intestinal lumen. Small numbers of larvae get into blood vessels and circulate again to produce more adults (internal autoinfective cycle) or invade perianal skin and enter blood vessels to eventually produce new adults (external autoinfective cycle).
Organism: female adult - 2.7 mm long, rhabditiform larvae approx. 0.38 mm, filariform larvae approx. 0.6 mm long
Clinical: - most asymptomatic
- GI - peptic ulcer like symptoms, diarrhea rarely, cutaneous larvae currens (buttock dermatitis)
- hyperinfection (disseminated strongyloides) in immunocompromised; spread of larvae to peritoneum, lung, CNS with contamination of those organs with gram negative bacteria; transmural small intestine spread of larvae and bacteria with necrosis of intestine
Diagnosis: stool examination . NB: difficult to find strongyloides
duodenal aspirate or Enterotest duodenal string test
culture of stool (Harada-Mori or Baerman) allows "free living" strongyloides to multiply
Treatment: albendazole, ivermectin
Problems: diagnostic techniques not sensitive
Ancylostoma duodenale and Necator mericanus
Epidemiology: transmission by contact of skin with soil contaminated with larvae.
Biology: eggs in feces hatch and mature as larvae in warm moist soil; develops into to infective (filariform) larvae in 7 days. Filariform larvae penetrate skin of host (e.g. bare feet), circulate to lungs where they penetrate alveoli, move up bronchi and are swallowed. Then, as adults, they attach by mouth to small intestinal mucosa and suck blood. (Necator 0.03 ml/day, Ancylostoma 0.15 ml/day). Prepatent period (time from skin penetration to egg production) is 4-5 weeks. Adults can live 5-15 years.
Organism: Adult female 12 mm long (A.d) ova approx. 60 mu long
Adult female 10 mm long (N.a) ova approx. 65 mu long
Clinical: Usually assymptomatic 90%
Heavy infections (20 - 100 worms)
- iron deficiency anemia
- malnutrition from protein loss
- rarely itch at skin entry site
Diagnosis: Stool examination for ova
Problems: Lack of cost effective LDC (least developed country) control
Cutaneous Larva Migrans
Non-human (dog, cat etc) hookworms that penetrate human skin (as does human hookworm) but cannot go further. Migrate and produce serpiginous itchy traits in subcutaneous tissue.
Treatment: albendizole, ivermectin.
Laboratory procedures for diagnosing intestinal helminths
Stool ova and parasite (O & P) examination
1. Direct microscopic examination: not very sensitive
2. Kato technique: uses glycerin mixed with stool which "clears" (makes transparent) fecal debris making eggs visable. Can be used for counting eggs/gram feces.
3. Concentration techniques: zinc sulfate solution - eggs float to top of solution
formal ethyl acetate
4. Culture: Harada Mori or Baerman culture - only strongyloides
will multiply in an incubated stool specimen - increases numbers of larvae and sensitivity of microscopy.
Increased blood eosinophil counts are normal host response to helminth infection; not seen in protozoan infections
very high moderate low or absent
% of total WBC count (30 - 80%) (10 - 30%) (0 - 10%)
Trichinella hookworm Ascaris
Toxocara Strongyloides Trichuris
Trichinella spiralis, nativa (Trichinosis, Trichinellosis)
Common in geographic areas where undercooked pork is eaten, in the Arctic where raw walrus is eaten and among bear hunters in North America; 5-15% of North American population infected at some time.This is a zoonosis infecting most carnivorous mammals; especially pigs, bear, walrus, and rats. Man infected by eating Trichinella infected uncooked meat.
Encysted larvae in meat, when eaten, excyst (hatch) and penetrate into small intestine submucosa where they mature to adults in 1-2 weeks producing larvae which penetrate blood vessels and diseminate to all muscles. There, they cause inflammation and encyst in muscle cells, remaining viable for many years. Adult female is 5 mm.long
Clinical: Early (1-2 weeks) - abdominal pain, diarrhea
Midterm (2-6 weeks) - myalgia, muscle weakness, facial and periferal edema, rash; sometimes encephalitis and myocarditis
Long term (months) - usually assymptomatic despite presence of trichinella cysts
Diagnosis: - clinical picture with laboratory support (eosinophilia and raised CPK)
- muscle biopsy with trichinoscopy
Treatment: steroids and mebendizole
Problems: education of meat consumers
lack of good drugs
Toxocara Canis (Visceral Larva Migrans)
Epidemiology: This is a zoonotic roundworm with the dog as reservoir. Uncommon human infection but consequences serious. Transmission is dog fecal (dog)-oral (human) .
Dog feces especially in sandboxes and parks where children play. Eggs in soil viable and infective for several months.
Biology: Adult has cycle in dog the same as Ascaris in man. Man an accidental "dead end" host. Eggs ingested by man/child, hatch after stomach passage and larvae migrate through small intestinal wall into vasculature and then to liver and lungs and beyond. Do not mature to adults but cause local inflammation.
Organism: In man larvae are 0. 5 mm long; egg in dog feces, looks like a round Ascaris egg.
Clinical: - Hepatomegaly, pneumonitis, encephalitis, fever and eosinophilia in heavy infections
- Retinal mass (similar to retinoblastoma) or focal retinitis when single larva reaches retina.
Diagnosis: - Clinical syndrome with very high eosinophilia
- Nothing in stools
Treatment: Steroids and thiabendizole or albendizole
Problems: - Control of dog and cat feces in parks and sandboxes
- Diagnosis difficult because of nonspecificity of symptoms
1. Anisakis sp: Salt water fish (cod, herring etc) roundworm that when ingested produces a nematode inflammatory mass in stomach of raw fish consumer or eosinophilic gastritis (mainly Japan, Holland).
2. Angiostrongylus cantonensis: nematode of amphibians producing eosinophilic meningitis (mainly SE Asia).
3. Gnathostoma spinigerum: nematode of cat producing migratory local subcutaneous swelling, and at times encephalomyelitis (mainly SE Asia).
4. Capillaria philippinensis: small intestine nematode producing diarrhea and malabsorption (Philippines).
This is a group of thread-like roundworms that are acquired via an insect (intermediate host) vector. The adults live in various tissues (lymphatics, subcutaneous etc.) Ansd are usually difficult to remove for diagnosis. The microscopic larvae (called microfilaria) of the adult female are very motile, circulating in blood or subcutaneously and because they are produced in such large numbers, are much easy to find. Disease can be produced by either the adults or the microfilaria or both, depending on the species.
Wuchereria bancrofti and Brugia malayi (lymphatic filariasis)
Cause lymphatic filariasis occasionally terminating in elephantiasis. 250 million humans affected; widely distributed throughout tropical and subtropical countries. Transmitted to humans by mosquitoes.
Organism: Adults live in afferent lymphatic vessels
Microfilariae born to female adult worms circulate in the blood. W. bancrofti microfilariae circulate preferentially from 10:00 p.m. to 2 a.m. - this corresponds to peak activity of vector mosquitoes.
Microfilaria develops to a 3rd stage juvenile larva in mosquito, and it is transmitted to new host at the time of feeding. Larva then matures to adult in the lymphatics; maturation to adult requires several months.
Adult 50 mm x 150 m
Lymphangitis and lymphadenitis
Orchitis and epididymitis
Blood examinations (esp. Night blood) for microfilaria
Treatment: Anti-inflammatory agents
Diethylcarbamazine (DEC), Ivermectin, albendizole
Prevention: Control of mosquitoes
Onchocerca volvulus (onchocerciasis) (River blindness)
Epidemiology: 20 million affected. Predominantly Africa and South and Central America, most commonly along rivers, the breeding site of the black fly vector.
Biology: Infective larvae transmitted to man by black flies of the genus Simulium.
Larvae develop to adults in subcutaneous tissue
Adult female produces microfilaria which wander in subcutaneous tissue, cornea, and anterior chamber of eye. Black flies acquire microfilaria on biting infected humans
Adult 33-50 cm x .3 mm Microfilaria 330 m x 6 m
Clinical : Skin nodules, onchocercal dermatitis, hanging groin, blindness
Diagnosis: Skin snip (small biopsy and incubation for microfilaria)
Treatment: Anti-inflammatory agents
Loa loa (loiasis)(Eye worm)
Biology: Adult worm lives in subcutaneous tissue and wanders freely
Microfilaria in subcutaneous tissues and blood
Transmitted by the bite of deer flies of the genus Chrysops
Adult: 55 mm x 0.5 mm Microfilaria: 280 m x 7m
Clinical: Calabar swelling, migrating worm in conjunctiva
Diagnosis: Excision of adult worm
Blood for microfilariae
Treatment: Diethylcarbamazine, Ivermectin