Nematodes, Cestodes and Trematodes Flashcards
- Name 5 species of clinically significant Cestodes
- Taenia saginata - beef tapeworm
- Taenia solium - pork tapeworm
- Diphyllobothrium latum - broad/fish tapeworm
- Hymenolepsis nana - dwarf tapeworm
- Echinococcus spp. - hydatid
What are Helminths?
- ‘parasitic worms’
- 2 phyla
- Platyhelminthes - flatworms
- Cestodes - tapeworms
- Cyclophylidea ‘Land’
- Taenidae: T**aenia, Echinococcus
- Hymenolepidae: Hymenolepsis
- Pseudophyllidea ‘Water’
- Diphyllobothridae: Diphylobothrium
- Cyclophylidea ‘Land’
- Trematotodes - flukes
- Cestodes - tapeworms
- Nematodes - roundworms
- Platyhelminthes - flatworms
What is the Generalised Tapeworm Lifecycle?
- Adults ⇒ definitive hosts
- Eggs ⇒ external environment
- Juveniles ⇒ Intermediate host
- Hymenolepsis nana ⇒ humans
- Taenia saginata ⇒ cattle
- Taenia solium ⇒ pigs
- Diphylobothrum latum ⇒ copepods, fish
- Hymenolepsis nana ⇒ larvae of cereal meal worms or fleas (rodent reservoir)
- Hymenolepsis diminula ⇒ fleas or flour beatles
- Diphylobothrum caninum ⇒ dog or human flea (Ctenocephalides canis or C. felis)
Name 4 species of clinically significant Trematodes.
Etymology
- Fasciola hepatica - the liver fluke
- Paragonimus westermani - the lung fluke
- Opisthorchis sinensis - Chinese liver fluke (aka Clonorchis sinensis
- Schistosoma mansoni, S. japonicum, S. haematobium - schistosome or bilharzia flukes
- Etymology: old English word for Flounder
5 species of Clin. significant Nematodes.
What is the etymology?
- Strongyloides stercoralis - threadworm
- Necator americanus & Ancylostoma duodenale - the Hookworms
- Ascaris lumbricoides - the Large Roundworm of Man
- Tricuris trichuria - the Whipworm
- Enterobius vermicularis - the pinworm
- Toxocara canis & toxocara cati - Visceral and ocular larva migrans
- From Greek “nema” or thread
What is this?
Life cycle?
Symptoms?
- Ascaris
- largest of intestinal soil-transmitted helminths
- adults live in intestine, eggs passed in feces and contaminate environment, water and food
- Ascariasis caused by ingeting eggs on soiled hands or consuming fruit or veg that have not been washed or peeled
- eggs hatch into larva in small intesting, penetrate intestinal wall and migrate through blood and lungs where they may cause symptoms
- if coughed up and swallowed they return to gut to mature and reproduce
What are these?
- left to right
- Necator americanus or Cyclostoma duodenalis (hookworm) egg
- tricuriasis (whipworm) egg
- fertile ascaris egg
What is this?
Describe it.
- fertile Ascaris egg
- oval shape, about 60µm long
- brownish colour
- thick shell covered by a rough coat stained brown by bile in gut
What is this?
Describe it?
Describe it and what triggers it to dev
- infective Ascaris egg
- oval, thick wall, contains visible larvum
- as the fertile egg leaves host, reduction in temperature, oxygen and moisture levels trigger ovum to develop into this infective stage
- takes 20-40 days to do so
- if ingested in contaminated food, will hatch in intestine and person will become infected
What is this?
Describe.
- infertile Ascaris egg
- less common in feces than fertile eggs
- egg is longer an narrower than fertile ege, as large as 75-90µm long
- usually very dark in colour with flattened ends
What is this?
Where is it found?
Life cycle?
- adult pinworm (Enterobius)
- worldwide distribution, commonly affects children
- female deposits eggs on perianal skin during night, and within a few hours of being laid they contain infected larvae (embryonated eggs)
- child scratches and autoinoculates self, eggs travel to intestin and hatch
- sometimes larvae hatch on perinal skin and migrate back to the intestine and mature
What is this?
Describe.
Life Cycle
How diagnosed?
- Enterobius eggs
- oval in shape, colourless, with clear shell
- about 55 µm long
- eggs laid on perianal skin, eggs become infective within few hours, itching causes host to scratch and then reinfects self by swallowing fertile egss, which hatch in the intestine
- best collected from perianal skin at night “sellotape method” or “Graham swab”, eggs visible under microscope
What is this?
Life Cycle?
Clinical disease?
Complications?
- trichuris (whipworm)
- round worm of humans found in warm moist climate and poor sanitation
- may occur in cecum, ileum, appendix and colon of humans
- ingestion of infective eggs in contaminated food/fingers
- light infections may cause few symptoms
- young children severe infections may cause chronic diarrhea, ulceration with blood and mucous passed in stool
- fe deficiency, wt loss
- prolapse rectum
What is this?
What other symptoms may occur?
- prolapsed rectum in child
- caused by whipworm (Trichuris)
- fe def anemia, wt loss
What is this?
Describe it.
Life Cycle.
How long does egg take to become infective.
- trichuris egg (whipworm)
- egg barrel-shaped, 50 µm long with clear mucoid plug at either end
- when passed in feces egg contains undeveloped ovum
- after about 3 weeks in soil becomes embryonated (infective)
- infective egg ingested from contaminated food or fingers, larvae hatch and develop in small intestine
- adult worms bore into wall of the large intestine and embed in anterior part of mucosa
- secretes digestive fluid into tissues of intestinal wall, liquefying surface, which is then taken up by the worm
What is this?
Describe it?
Size, distinctive characteristics.
Trichuris (whipworm) egg.
egg barrel-shaped, 50 µm long with clear mucoid plug at either end
What is this?
- hookworm (Ancylostoma duodenale or Necator americanus)
- adult parasites live in small intestine, sucking and ingesting blood through intestinal wall
- male worms 8-9 mm, females 11-12 mm, heads of both males and females are bent dorsally giving “fishing hook appearance”
What is this?
Geographic distribution?
Life Cycle?
Disease?
- Ancylostoma duodenale
- hookworm
- worldwide in areas with moist warm climate
- this species predominant in Middle East, Africa, Southern Europe
- transdermal entry via hair follicles, also ingested orally ⇒ Wakana syndrome
- preferred site upper small intestine, but in very heavy infections may extend as far as lower ileum
- hookworm mouthparts of adult penetrate blood vessels, nourish by sucking blood
- cause chronic anemia, blood loss
- differentiate from N. americanus by teeth in buccal cavity. N. americanus has flat cutting plate
What is this?
Geographical distribution?
How distinguished from similar parasite?
- Necator americanus
- hookworm
- this species predominates in America and Australia
- distinguished by flat cutting plates in N. americanus vs teeth in A. duodenale
What is this?
FOBT?
- adult hookworm, either Necator americanus or Ancylostoma duodenale
- teeth embedded in small intestine wall
- FOBT usually positive
What is this?
Life Cycle
- Hookwoorm eggs
- Ancylostoma duodenale and Necator americanus are indistinguishable
- Size: 57-76 µm, oval or ellipsoidal shape
- thin shell
- eggs passed into stool, hatch into rhabditiform larvae, which take about a week to develop into infective stage
- larvae penetrate skin usually of foot, travel through venous circulation through lungs up to trachea then swallowed, travel to small intestine, attach and mature into adults after feeding on blood
- female hookworms produce up to 30,000 eggs per day
What is this?
Characteristic features?
- hookworm larvae
- long buccal cavity at anterior end, which differentiates them from Strongyloides larvae
- no notch at the tail end
What is this?
sex?
Morphology? Identification
Life Cycle?
- Adults of Strongyloides stercoralis may be found in human host or soil
- in human host no parasitic males
- parasitic females are long and slender, measuring 2-3 mm
- in human host, female lays eggs in intestinal mucosa, larvae hatch almost immediately to only larvae are found in feces
- larvae similar to first stage Hookworm larve but have shorter mouth cavity and are found in freshly passed feces (hookworm larvae are found in stale faeces)
What is this?
What do the arrows indicate.
- female Strongyloides sterocralis larva passed in fresh species
- Red arrow indicates short (compared to hookworm larva) cavity and rhabditiform esophagus
- also differentiated by notch at tail end (not shown here)
What are the specific clinical features/syndromes associated with ascariasis?
Larval migration?
Adult gastrointestinal parasitism?
General features?
- larval migration⇒verminous pneumonia
- adult GI parasitism⇒
- lactose intolerance
- vitamin A malabsorption
- intestinal obstruction
- hepatopancreatic ascariasis
- General
- impaired growth
- impaired physical fitness
- impaired cognition
- reductions in school attendance and performance
What are the specific clinical features/syndromes associated with trichuriasis?
Common name?
Larval migration?
Adult gastrointestinal parasitism?
General features?
- whipworm
- lm: none
- adult GI parasitism:
- colitis
- trichuris dysentery syndrome
- rectal prolapse
What are the specific clinical features/syndromes associated with hookworm
parasite name?
Larval migration?
Adult gastrointestinal parasitism?
General features?
- Ancylostoma duodenalis
- Necator americanis
- lm:
- ground itch
- cough
- Wakana disease: when A. duodenale transmitted orally, characterized by nausea, vomiting, pharyngeal irritation, cough, hoarseness, dyspnea
- adult gi parasitism
- intestinal blood loss
- fe def anemia
- protein malnutrition
Describe the lifecycle of Ascariasi lumbricoides.
- infection via fecal-oral transmission
- embryonated eggs swallowed, first stage larvae (L1) hatch, moult into L2 then penetrate intestinal mucosa and migrate to pulmonary circulation
- L3 migrate across alveolar wall, ascend tracheobronchial tree to larynx, then to small intestine
- Adult female A. lumbricoides produce thousands of eggs daily that pass into stool
- Egg production occurs 2-3 months after infection and worms can live for several years
- Eggs remain viable in warm moist soil for years
Describe Trichuris trichuria lifecycle.
- embryonated eggs ingested via food or hands, hatch into larvae that moult in small intestine
- larvae develop into adult worms in cecum and ascending colon
- female worms lay thousands of eggs daily for several years
- eggs pass into stool, embryonate over 2-4 weeks in warm, moist soil
- survive for months
Describe hookworm lifecycle.
Which species?
- Ancyclostoma duodenal and Necator americanus larvae free living in soil
- infect people by penetrating skin, usually feet
- larvae migrate to pulmonary capillaries, penetrate alveolare wall, migrate to larynx and are swallowed
- larvae moult and develop into mature worms in small intestine over 1-2 months
- can survive for months (A. duodenalis) or years (N. americanus)
- female worm releases thousands of eggs daily into stool
- after 5-10 days hatch in warm, moist, sandy soil or feces
- Rhabditiform larvae (L1) become infective after moulting to L2 & L3 larvae that survive for several weeks
- A. duodenalis can also be ingested orally and can cause Wakana syndrome (nausea, vomiting, pharyngeal irritation, cough, hoarseness, dyspnea)
- Zoonotic ancylostoma species can also infect people, causing cutaneous larva migrans (as well as possibly causing pathology similar to a. duodenalis or necator americanus in some people)
What is Wakana syndrome and how does it occur.
- hookworm Ancyclostoma duodenalis can also be ingested orally instead of penetrating skin resulting in Wakana syndrome (nausea, vomiting, pharyngeal irritation, cough, hoarseness, dyspnea)
What causes cutaneous larva migrans?
- infection by zoonotic ancyclostoma species
- eg dog or cat hookworm
Strongyloides stercoralis lifecycle.
- complex lifecycle, may take multiple routes including complete lifecycle outside human host
- filariform larvae inject human host orally or percutaneously
- skin, esp feet ⇒ pulmonary capillaries to alveoli, then larynx to small intestine
- oral ingestion same route after penetrating intestinal mucosa to lungs etc.
- female adults penetrate gut wall, lodging in duodenal & jejunal lamina propria, laying up to 50 eggs daily
- eggs hatch within gut wall, rhabditiform larvae migrate to lumen and are passed with stol
- larvae might penetrate colonic wall or perianal skin to enter a newy cycle or disseminate to other organs
- autoinfection may last decades without repeated external exposure
Describe possible clinical presentations with S. stercoralis.
- commonly assymptomatic in otherwise healthy
-
pulmonary migration of larvae ⇒ eosinophilic pneumonia with cough, dyspnea, wheezing, hemoptysis
- in hyperinfection pneumonia may be severe, fatal
- chronic strongyloidiasis: asthenia, anorexia, nause, abd pain, diarrhea, abdominal tenderness
-
larva currens common in chronic infection, serpiginous urticaria, typically over abdomen, torso, buttocks, groin
- lesions last a few days
- rarely reactive arthritis
- in immunosupressed strongyloides hyperinfection syndrome leading to pulmonary or intestinal failure
- disseminated strongyloidiasis to any organ in immune suppressed
How many eggs will a femal ascaris worm produce per day?
- 200,000 sticky resistant eggs/day
Ascaris: how many infections per year?
how many deaths?
1 billion infections
20,000 deaths
What kinds of disease can ascaris larvae produce?
- A: pneumonitis
- seasonal fever, cough, hemoptysis, bronchospasm
- Dx: Eosinophilia, larvae in sputum, lobular consolidation
- B: ectopic e.g. brain
- C: allergy
What are possible effects of ascaris adult worms?
- GI
- intestinal obstruction, also volvulus, intussusception, gangrene, perforation, rectal prolapse
- malnutrition, stunting, developmental
- lactose intolerance
- vit A deficiency
- bile duct migration: biliary coli, stones, liver abscess (20 bacterial), pancreatic duct, ascending cholangitis
- migration to mouth, nose or anus during fever
Eosinophilia means …?
Worms
- predominantly nematodes (roundworms) and trematodes (flukes).
- non-invasive tapeworms (cestodes) dont usually cause it
- except Hymenolepsis nana
- Invasive tapeworms do. i.e. hydatid disease, but often not until rupture
Ascaris treatment?
What about intestinal obstruction?
- mebendazole 100 mg bid x 3 days or
- albendazole 400 mg one dose
- deal with the obstruction first, hydratin, ng suction acutely, then deworm
- may require laparotomy
What aspects of worm population dynamics limit success of mass deworming programs?
- heavy infections concentrated in few individuals
- worm “crowding” reduces egg output
- treatment rarely removes all worms
- surviving worm population compensates by producing mor eggs/worm
- worm prevalence in human population may diminish acutely but rises rapidly to baseline within a year
Summary of worm treatments:
First and alternative for
Ascaris
trichuris
hookworm
strongyloides
- For Ascaris and hookworm, first line treatments are
- albendazole 400 mg single dose or
- mebendazole 500 mg single dose or
- mebendazole 100 mg bid for 3 days
- Trichuris needs longer courses:
- albendazole 400 mg od x 3 days or
- mebendazole 500 mg od x 3 days or
- mebendazole 100 mg bid for 3 days
- ivermectin 200 µgm/kg daily x 3 d
- Strongyloides needs Ivermectin 200µgm/kg daily x 2 d
- with long high doses of albendazole as alternatives
- Of the four, only hookworm cannot be treated with ivermectin
- This poses a problem for mass deworming campaigns that would then have to include both albendazole and ivermectin in order to target all 4 STH
What are the early clinical features of hookworm disease?
- ground itch: unusual
- itch, edema, erythema, papulo-vesicular eruptions lasting 1-2 wks
- pulmonary sx: unusual
- cough (“foxhole cough” 1st WW), mucoid sputum, wheezing
- Initial intestinal sx
- abd pain, diarrhea, steatorrhea
- Initial eosinophilia
What is this and what is it caused by?
- cutaneous larva migrans
- cat or dog hookworm larvae
What are the chronic clinical effects of hookworm?
- chronic gi nutritional defects
- protein loss
- anemia esp if child has borderline iron intake/stores
What distinguishes hookworm from trichuriasis and ascariasis in terms of worm burden distribution and age.
- hookworm burden increases with age, in contrast with ascaris lumbricoides and trichuris trichiuria, whic are most intense in childhood.
How does skin pallor associated with hookworm respond to deworming.
- skin pallor associated with hookworm disease due to fe deficiency, which recovers quickly after deworming
- Pallor due to hypoproteinemia is slower to recover
Treatment of hookworm anemia
- oral iron eg Ferrous sulfate 200 mg tid x 3 months after hgb normal
- folic acid 5 mg daily at least 1 month
- vit c if not present in diet
- deworm with albendazole or mebendazole
- nb NOT ivermectin
What is this?
Outline diagnosis and treatment
- barrel shaped eggs in faeces
- proctoscopy shows worms in heavy infections
- treat with mebendazole or albendazole (or thiabendazole) - only moderately effective so REPEAT
- oral iron, hydration
What are these and how are the species distinguished?
How many suckers?
- Taenia saginatum (left) - beef tapeworm
-
Taenia soleum (right) - pork tapeworm
- 13-30 primary lateral uterine branches on T. saginatum; 7-13 on T. soleum
- scolex on both have 4 suckers, but T. soleum has hooks, T. saginatum does not
- Eggs from both are identical
What are these and how are they distinguished from other species?
-
Taenia species ova
- T. saginatum and T. soleum eggs indistinguishable
- eggs round, 33 -43 µm with thick radially striated dark brown wall
- inside each shell an embryonated oncosphere with 3 pairs of hooks
- egg in figure C still has primary membrane (yolk sac) that surrounds eggs in uterine branches
- distinguish T. saginatum and T. soleum by presence of hooks on scolex of latter
What are these?
Distinguishing features?
- Diphyllobothrium latum ova
- egg pale yellow-brown and oval shape
- 65-70 µm
- operculum at one end can be hard to see
- egg contains mass of granulated yolk cells surrounding undeveloped ovum
- eggs mature and hatch in freshwater and after 1-2 wks hatch to release ciliated coracidium stage
What are these?
How is the diagnosis made?
How long are the eggs infective in the environment?
What are the intermediate hosts?
What are the definitive hosts?
- Eggs of H. nana in an unstained wet mount. Note the presence of hooks in the central oncosphere and polar filaments within the space between the oncosphere and outer shell.
Diagnosis is by identifying the distinctive eggs in faeces: eggs of Hymenolepis nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment.
When eggs are ingested by an arthropod intermediate host (beetles and fleas may serve as intermediate hosts) they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine
What is this?
Hydatid Sand
What is this?
Hydatid Cyst Cross Section
Name the four main clinically significant species of tissue flukes and their 2nd intermediate hosts.
Praziquantel dosing (fix this card)
tabs 600 mg, can be broken in 1/4 or have
child dose is 15 mg/kg
use height scale
Describe the lifecycle of Necator americanus.
What are the clinical features of acute infection and the consequences of that infection.
- eggs are passed in the soil and embryonate there, hatching into larvae
- larvae “quest” on grass or pass through skin from ground, migrate through heart and lungs, coming out through trachea then descending into GI tract
- In some areas, oral ingestion of cysts is very common⇒Wakana syndrome
- larvae mature into adults after passing down GI tract to duodenum, anchor there and small intestine consuming blood
- Syndromes:
- ground itch
- cough
- Wakana disease: when larvae are transmitted orrally, they produce nausea, vomiting, pharyngel irritation, cough, hoarseness, dyspnea
- Adult GI parasitism in small intestine leads to
- intestinal blood loss
- fe def anemia
- protein malnutrition
- What is the best initial treatment of a patient with high Loa loa microfilaraemia?
- Albendazole
- Treatment of individuals with high Loa loa microfilaraemia is associated with a risk of encephalopahty if ivermectin or DEC is used. Albendazole administration for 3 weeks initially reduces the microfilarial load and the risk of encephalopathy. Doxycycline is used in other filarial worms that carry Wolbachia, but this does not apply to Loa loa. Praziquantel is used in other parasitic infections, eg schistosomiasis, taeniasis.
- How can the differentiation of adult Taenia species in humans most accurately be achieved?
- By examining the scolex
- The eggs of Taenia solium and T. saginata are identical in morphology and can’t be distinguished. Both may appear in faeces. Microscopy of mature proglottids can indicate species, as T. saginata proglottids have more uterine branches than those of T. solium (12-30 vs. 7-13), but since this is variable it is not very accurate. The scolices (heads) of T. saginata and T. solium are different: T. solium has hooks and suckers, whereas T. saginata has only suckers.