Parasitology Lab 1 Flashcards
Angiostrongylus cantonensis Life cycle (rat)
Adult worms in pulmonary arteries of rats. Females lay eggs which mature to L1 larvae which migrate to pharynx, swallowed and passed in faeces. L1 larvae penetrate or ingested by intermediate hosts (snail or slug) -> mature to L3 infective larvae. Intermediate hosts may be eaten by paratenic (transport) hosts in which L3 survive but do not develop (shrimp, prawns, mussels, crabs, frogs, lizards) - if the intermediate or paratenic host is eaten by a rat, L3 migrate to the subarachnoid space in the brain and develop into young adults. Young adults return to the venous system and sit in the pulmonary arteries where they sexually mature
Angiostrongylus cantonensis Life cycle (human)
Humans acquire infection by eating raw or undercooked snails or slugs, undercooked paratenic hosts (raw shrimp, prawns, mussels, crabs, frogs, lizards), or salads and other leafy vegetables containing a small snail or slug (or L3 released in snail slime) - in humans the larvae (~2mm) migrate to the brain, lungs or the eye, where they ultimately die
Anisakis Life cycle (human)
Humans ingest infected raw fish or squid, L3 persist
Anisakis Life cycle (fish)
Adult worms in gut of marine mammals (seals, dolphins) -> eggs in faeces -> L1 -> L2 ingested by intermediate host (marine crustaceans) -> L3 infective larvae. Fish and squid eat crustaceans and L3s move to the body cavity and tissue (paratenic hosts), larger fish also become apratenic hosts
Ascaris lumbricoides Life cycle (human)
Human ingest eggs from environment, egg hatches in duodenum releasing L1 larvae mature to L3 larvae which penetrate intestinal wall into blood and lymphatic circulation. Larvae migrate to lung, break through alveoli, crawl up trachea, swallow into stomach, migrate to large intestine and mature into adult worms. Adult female worm creates eggs, larvae form within fertilised egg ready for ingestion. Adult worm may produce 200,000 eggs per day - thick outer layer of egg resistant to desiccation (not infective to human immediately)
Ascaris lumbricoides Life cycle (environment)
Unembryonated egg in soil embryonates to L2/L3 infective stage, eggs are very resistant to desiccation and can survive 8y in the environment. Human ingests embryonated egg
Ascaris lumbricoides Worm
15-40cm, male posterior tightly curled
Ascaris lumbricoides Egg
45-75x30-50um fertile corticated thick double wall with nobby structure, fertile decorticated egg have started to lose nobbliness. Infertile eggs occur because male cannot keep up with fertilising them, these are much darker, very nobbly and cannot see anything inside, tend to be more elongated - all of these eggs are diagnostic of an active infection
Balantioides coli Microscopy cysts
Round, 50-60um (large), dark iodophilic
Blastocystis Microscopy cysts
Round 5-13um shiny peripheral bodies
Capillaria philippinensis Life cycle (human)
Ingestion of raw or undercooked fish containing larvae. In the intestine some female worms may produce larvae that can reinvade the intestinal mucosa, resulting in internal autoinfection
Capillaria philippinensis Life cycle (birds)
Birds will have worms in their gut, eggs passed out of faeces of birds into water hatch into larvae, fish eat the larvae.
Capillaria philippinensis Egg
40x20um egg similar to T trichura but less of a cap on the operculum
Chilomastix mesnili Microscopy cysts
Lemon shaped, 7-10um, single nucleus, axonene
Cryptosporidium Microscopy cysts
5um (exactly) not usually seen on iodine, best seen on ZN bright cherry red, auramine, iodine
Cryptosporidium Lifecycle (human)
Human ingest thick-walled oocyst, small bowel oocyst releases sporozoite infects lumen, matures to trophozoite, asexual to meront or sexual to merozoite to gametes to zygote to oocyst if thin-walled (20%)- autoinfection cycle and thick-walled (80%) exits host ready to infect another human (oocyst > sporozoite > troph > meront > merozoite > gamete > oocyst)
Cyclospora catetanensis Life cycle (human)
Human ingest sporulated oocyst, small bowel excyst and release of sporocyst, sporozoite invasion of epithelium, asexual reproduction merozoite, then sexual reproduction gametocytes to zygote to faeces release of unsporulated oocyst
Cyclospora catetanensis Life cycle (environment)
Unsporulated oocyst, sporulates in the environment, ready for human ingestion in contaminated food/water
Cyclospora catetanensis Microscopy cysts
Round 8-10um, ZN variable stain with classic ‘ghost’, iodine classic ‘refractile’ wall (does not take up iodine) may see 2 sporocysts within
Cystoisospora belli Microscopy cysts
Oval, large 25-33um, may contain two sporocysts (often not visible), ZN stain
Diphyllobothrium latum Life cycle
Humans ingest raw or undercooked fish containing cysts, produces adult worms in human. Human pass eggs in faeces - larvae escape and infect cyclops, cyclops eaten by fresh water fish, procercoid develops into plerocercoid in fish ready for human to ingest
Dracunculis medinensis (Guinea worm) Life cycle (human)
Human ingest infected copepod, male and female larvae, reproduce, male dies. Female burrows through stomach, migrates to skin, penetrates through skin to deposit eggs in stagnant water
Dracunculis medinensis (Guinea worm) Life cycle (environment)
Eggs in stagnant water are consumed by copepod - need 14d in water, then 14d in copepod to become infective
Dracunculis medinensis (Guinea worm) Worm
60cm nematode
E histolytica/dispar Life cycle (human)
Ingestion of cyst from contaminated food or water -> excyst in stomach -> trophozoites in intestine -> cyst in faeces
E histolytica/dispar Microscopy
Round, 10-15um 1-4 ring dot nuclei. Cyst in faeces. Trophozoites last <2h in faeces (need to examine hot stool). Histo - look along edges of lumen for breaks in mucosal surface (ulcer), look beyond the necrosis, WBC = blue dots, flask shaped ulcer (small at top, broad underlying base), amoeba are found on leading edge (they will not be within the necrotic tissue (they’re finished with it) but will be heading into healthy tissue) - look for blue bodies (trophozoite) which may be foamy/vacuolated (containing RBC) - Trophozoites only have one ring and dot nucleus
Echinococcus granulosus Life cycle (human)
Human ingest egg, dead end host so hydatid cysts produced in liver, lungs, brain not transmissible. Egg hatch to produce oncospheres that invade through duodenum to the portal vein of the liver, grows out to establish cyst - membrane produces protoscolices floating in the cyst fluid, cyst can produce daughter cyst, displaces rather than invades tissue. If cysts rupture, the liberated protoscolices may create secondary cysts in other sites within the body
Echinococcus granulosus Life cycle (dog)
Dog ingests organs of sheep, cow, pig etc infected with hydatid cysts, adult worm in small intestine of dog, eggs passed in faeces
Echinococcus granulosus Egg
30-35um radially striated
Echinococcus granulosus Worm
4 suckers, 30-36 hooks. 3-8mm long with head and 3 segments
Echinococcus multilocularis Life cycle
Human ingest egg
Echinococcus multilocularis Life cycle (animal)
Rodent ingests egg, develops into larvae, rodent eaten by definitive host dog/cat > adult worm in gut of carnivore -> proglottid excreted in faeces contains egg -> egg ingested by intermediate host
Endolimax nana Microscopy cysts
Round-oval, 7-10um, 4 limax nuclei - black to bright to blink ‘wink’ as focus up and down
Entamoeba coli Microscopy cysts
Round, 15-30um, ~8 ring-dot nuclei (nuclei get smaller as they divide)
Entamoeba hartmanii Microscopy cysts
Round, 7-10um 1 ring-dot nucleus, paler (iodophobic)
Enterobius vermicularis Life cycle
Human ingests embryonated egg, egg hatches in small intestine, larvae move to large intestine. Over time (month) larvae mature to adult worms, accumulate in first part of large intestine (appendix/caecum) and mate. Female will migrate to anus and deposit eggs on skin around anus at night. Pruritis scratching -> contamination of hands -> spreading and ingestion of eggs
Enterobius vermicularis Worm
1-2mm Lateral alae - ridges that run down the side of the nematode (only Enterobius adults will have these in cross-section).
Giardia intestinalis Microscopy cysts
Oval, 8-12um, axonene line, comma-shaped median body, 4 nuclei
Gnathostoma Life cycle (human)
L3 larvae ingested by humans, migrate around body
Gnathostoma Life cycle
Adult worms 2-3cm in stomach of carnivores (wild and domestic). Female releases eggs, hatch in water, L1 infects copepod (1st intermediate host) L1 -> L2, copepod eaten by fish or frog (2nd intermediate host) L2-> L3, bigger fish, snakes birds can be paratenic hosts, if 2nd or paratenic hosts are eaten by cats or dogs L3 larvae mature to adults
Helminths Lifecycle (feature)
All helminths pass through a series of developmental stages to complete their life cycle. If a parasite requires only one host to complete its life cycle the life cycle is ‘direct’ if it requires two or more it is ‘indirect’. The host harbouring the sexually mature adult worm is called the ‘definitive’ host, the host harbouring the larval stages is called the ‘intermediate’ host
Helminths Intestinal Transmission
Egg in soil (ingest): Trichuris trichura, Ascaris lumbricoides. Larvae in soil (penetrate): Hook worm & Strongyloides. Egg without soil: Enterobius vermicularis
Helminths Zoonotic Development
Develop fully in humans: Trichinella spp, Capillaria philippinensis. Arrest at larval stage: Toxocara canis, Angiostrongylus cantonensis, Anisakis, Gnathostoma spinigerum
Histopathology Liver
Malaria, Leishmania, Echinococcus
Histopathology Skin
Leishmania
Histopathology Brain
Malaria, Toxoplasma, T brucei
Histopathology Muscle
Cardiac: T cruzi
Histopathology Lung
PCP
Histopathology Large intestine
E histolytica, Ascaris, Trichuris
Histopathology Small intestine
Strongyloides stercoralis, Capillaria philippensis, Hook worm
Hook worm Worm
1cm, head bent dorsally with dorsal-facing buccal capsule, lives 5-10 years
Hook worm Egg
60x40um thin outer layer (need to hatch quickly in environment) - cannot differentiate Necator and Ancylostoma eggs
Hook worm Life cycle (human)
Human infected by penetration of unbroken skin by L3 filariform larvae, migrate to blood, circulate to lungs, through alveoli, crawl up trachea, swallowed. Mature to adult worm in jejunum and bites into the mucosa of small intestine and feeds on blood, male and female worms reproduce, eggs produced in small intestine and released in stool
Hook worm Life cycle (environment)
Eggs hatch in the environment (thin egg outer layer to facilitate this), L1 rhabditiform larvae will feed on bacterial in the soil, develop to L2 and then L3 filariform are infective by penetrating human skin. Needs moisture, warmth, shade and decaying vegetation
Hook worm vs Strongy Rhabditiform L1 buccal cavity
Strongy is short, Hookworm is deep
Hook worm vs Strongy Filariform L3 tail
Strongy is stubby - notched, Hookworm is pointed
Hook worm vs Strongy Filariform L3 oesophagus
Strongy oesophagus is half of body, Hookworm oesophagus is 1/3 of body
Hymenolepsis nana Life cycle
Human ingest eggs in contaminated water or food, cysteroid develops in villi of intestine, adult worm in upper part of ileum, eggs passed in faeces
Iodamoeba butschlii Microscopy cysts
Oval, 9-12um, single large limax nucleus - black to grey as focus up and down, orange glycogen vacuole
Leishmania Life cycle (human)
Phlebotamine blood meal transmits promastigote to human, phagocytosed by macrophage, promastigotes differentiate into amastigotes, multiply within phagolysosome, infected macrophage ingested by phlebotamine on taking blood meal (pro > amas)
Leishmania Life cycle (phlebotamine)
Phlebotamine blood meal ingests parasitised macrophage, cell lysis in midgut releasing amastigotes, amastigotes divide and differentiate into promastigote in midgut, multiply in midgut and migrate to proboscis, injected during blood meal (amas > pro)
Leishmania Microscopy
Amastigotes - splenic/bone marrow aspirate, tissue touch smears, punch biopsies. Amastigotes are intracellular however cells rupture in process of making slides. Histo: Liver and Skin. Liver hepatocytes are pink, Kuppfer (liver macrophages) are light purple, tiny dots are intracellular amastigotes. Lots of blue nuclei = inflammation. Impression smears extracellular due to cell rupture. Skin: inflammation (blue nuclei) in dermal layer, macrophages in skin (histiocytes) with intracellular pale blue dots that are much smaller = amastigotes
Leishmania Amastigote
In human only
Leishmania Promastigote
In phlebotamine sandfly only, not human
Leishmania Feature
Intracellular amastigote, reticuloendothelial system, e.g. macrophages of the liver, spleen, bone marrow and skin
Malaria RBC enlarged
Pv Po
Malaria Multiple trophozoites
Pf
Malaria Maurer’s clefts Pf
few, unevenly distributed
Malaria Schuffner’s dots Pv
many, evenly distributed
Malaria Fimbriation
Po
Malaria Lifecycle (exoerythrocytic human)
Malaria-infected female Anopheles mosquito inoculates sporozoites into human host dermis during blood meal, sporozoites migrate to blood stream, infect liver cells, mature into schizonts which rupture and release merozoites, Pv & Po have hypnozoites that can persist and cause relapse (sporozoite > schizonts > merozoites)
Malaria Life cycle (erythrocytic human)
Merozoites infect RBC, ring stage troph mature into schizonts which rupture releasing merozoites, most infect RBC continuing the cycle, some differentiate into sexual stage (gametocytes) esp as the human host becomes unwell (merozoites > troph > schizonts > merozoites OR gametocytes)
Malaria Life cycle (mosquito)
Female Anopheles takes blood meal from human ingesting female and male gametes, change in temperature inside mosquito -> fertilisation, motile ookinete penetrates midgut epithelium and differentiates into oocyst, sporozoites develop in oocyst, mature oocyst ruptures (2w), releasing motile sporozoites migrate to salivary glands awaiting blood meal. (gametocytes > zygotes > ookinetes > oocyst > sporozoites) Female anopheles must take a blood meal every 2-4 days to reproduce
Malaria Counting parasitaemia
Percentage of RBC infected (not no. of parasites). Want to count 2000 RBC, on x100 look within field where RBC do not overlap and count eight consecutive fields - count downwards as the density of the field will remain similar. Eg. 9 in 8 fields is 9 in 2000 is 4.5 in 1000, is 0.45 in 100 fields, is 0.45%
Malaria Microscopy
Brain: haemorrhage (orange areas), vessels that look dark, classic feature is ‘ring haemorrhage’ with capillary in centre - black dots stuck to capillary wall are schizonts - usually peripheral RBC sticking and block the capillaries, Liver tissue looks less tidy than normal liver. Pigment in sinusoidal spaces (within Kuppfer cells) not within hepatocytes. Will not see parasites, just evidence of macrophage clearing up. Liver is engorged
Malaria Peripheral blood stages
All present for Pv, Po, Pm. Mature troph of Pf tend to be sequestered in deep vessels
Microfilariae Life cycle
No multiplication of parasite in mosquito, sex and reproduction occurs in vertebrate host
Microsporidia Life cycle (human)
Human ingest spore (very hardy) germinate on lumen of gut, proliferate within cytosol or parasitophorous vacuole, replicate until host cell ruptures, mature spores released and can infect new cells continuing the cycle
Nematodes Body
Cylindrical body tapered at each end. Have a complete digestive system with mouth, intestine and anus. Body is covered by tough cuticle that resists drying and crushing. Nematodes use longitudinal muscles to produce a sideways thrashing motion. Most species are dioecious (separate males and females). Males are generally smaller than females. Infections are caused by eggs or larvae.
Pneumocystis jirovecii Life cycle (human)
Inhalation, asexual replication, sexual conjugation, diploid precyst, maturation, excystment
Pneumocystis jirovecii Microscopy cysts
Black on green Grocott silver stain with frothy exudate
Protozoan cysts Examination technique
Size, nuclei - number and morphology (ring and dot vs limax), then look at specific features such as chromidial bars, median bodies, axonemes. Remember cysts are 3D - need to fine focus up and down planes to see all features including nuclei. Microscope - iris condenser on ‘two for poo’. Find coverslip and methodically scan every field at x40
Protozoan cysts Ring and dot nuclei
<10um E hartmanni, 10-15um E histolytica/displar (max 4), >15um E coli (lots of nuclei)
Protozoan cysts Calculating size
1 division x100 = 1um, x40 = 2.5um, x10 = 100um - generally faeces reviewed at x40 = times size by 2.5
Strongyloides stercoralis Life cycle (human)
Filariform larvae penetrate unbroken skin, migrate via venous system to lungs, cough/crawl up trachea, and swallowed. develop into adult worm in intestine, female worm asexually reproduces in intestine releases eggs which are hatched immediately to rhabditiform larvae which are passed in faeces. (can also penetrate through intestine [internal autoinfection], and can penetrate at perianal skin when defaecating [external autoinfection])
Strongyloides stercoralis Life cycle (environment)
Rhabditiform larvae in soil either mature into L3, or develop into free living adult males and females, mate to create rhabditiform larvae which transform to L3 filariform larva ready to infect another human. Free living stage allows for reproduction to be sustained in the absence of human host
Strongyloides stercoralis Life cycle (auto-infection)
Some rhabditiform larvae will mature to filariform larvae in intestine, penetrate the mucosa, migrate to the lung, and go through the process of climbing up the trachea again etc (Internal autoinfection). External autoinfection may also occur when the filariform L3 in faeces penetrate the perianal skin and start the process again (External autoinfection). Autoinfection occurs at low level in a normal host (persisting infections lasting >50 years), but in patients with severe cellular immunodeficiency vast numbers of larvae autoinfect -> hyperinfection syndrome. Overwhelming numbers of L3 larvae can cross the capillary bed of the lungs to infect all organs (eg brain, heart, liver (disseminated strongyloidiasis)
Strongyloides stercoralis Adult worm
1-2mm. Only female worms are found in humans, embedded in mucosa of small intestine. Females reproduce parthenogenetically (male not needed), eggs hatch quickly within the host (eggs not seen in faeces)
Strongyloides stercoralis Microscopy
Excretion of larvae is intermittent, direct faecal smear or concentration methods may be used such as formol-ether, or Baermann (20-50g) - leave the larvae to drop down to the bottom of the tube.
Strongyloides stercoralis Culture
Charcoal stool culture 7d room temperature, promotes free-living cycle, Nutrient agar. In disseminated disease larvae common in sputum
T brucei Vector
Tsetse fly (Glossina) - saw into skin and eat blood that pools, anticoagulants in saliva lead to transmission, Tsetse is found in vegetation, like to be under tree (either by rivers/lakes or wooded savannah)
T brucei T brucei
Motile, extracellular (in humans and tsetse) evades adaptic immune system by antigenic variation, mitochondria along length of body, glycosome, flagellar pocket under kinetoplast where flagellar comes out along length of cell,
T brucei Life cycle (human)
Tsetse fly takes blood meal injects metacyclic trypomastigotes (non-dividing form), once in bloodstream and/or tissue divide by binary fission into trypomastigotes in body fluids, these are infectious to tsetse fly on subsequent blood meal (metacyclic tryp > tryp)
T brucei Life cycle (tsetse fly)
Tsetse fly takes blood meal ingests bloodstream trypomastigotes, once in midgut transform into procyclic trypomastigotes (stumpy form that survives in 27C lower pH low sugar environment - uses active mitochondrial metabolism) and divide by binary fission, then transform into epimastigotes (sexual form) which multiply in salivary gland where they transform into metacyclic trypomastigotes ready to infect human host when tsetse fly takes a blood meal (tryp > procyclic tryp > epimastigotes > metacyclic tryp)
T brucei Microscopy
Small kinetoplast compared with T cruzi. Brain: Perivascular cuffing (groups of WBC around blood vessels), and Morula cells ‘orangey’ do not look like clear vacuoles on histo, these are seen in HAT and Tertiary Syphilis
T brucei Morula cells
CSF and brain tissue, lymphocytes with vacuoles (vesicles full of IgM) - IgM occurs due to changes in surface antigens. Other CSF findings: increased lymphocytes and protein
T cruzi Lifecycle (triatomine)
Triatomine takes a blood meal ingesting trypomastigotes (once infected, infected for life), transform to epimastigotes, multiply by binary fission, transform into infective metacyclic trypanosomes inside triatomine, excrete infective metacyclics in triatomine faeces onto host, parasite cannot enter intact skin - either goes through scratch in skin or mucus membrane (oral or eye) (tryp > epi midgut > tryp)
T cruzi Lifecycle (human)
Triatomine takes blood meal and defaecates on human. Human scratches into skin, eye or ingests infective trypomastigotes, can infect any host cell, usually cardiac muscle or lipid, or smooth muscle of intestinal tract (in theory found in many other cell types), circulating as trypomastigotes, develop pseudocyst inside host cell (containing 2-400 amastigotes then rupture), ingestion of trypomastigotes by insect vector (when taking blood meal from mammal) (tryp > amas in pseudocyst > tryp)
T cruzi Morphology
Blood trypomastigotes - large stained nucleus, bar shaped kinetoplast
T cruzi Vector
Triatoma, Rhodnius, Panstrongulus all referred to as ‘Triatomine” - take a blood meal but transmit via faeces
T cruzi Microscopy
Large kinetoplast compared with T brucei. Cardiac muscle: striated/interwoven muscle (fibres interlink, whereas skeletal interlink), nuclei are at centre (‘heart’ of cell), will see amastigotes in muscle - look for inflammation at low power, may see pseudocyst with amastigotes (kinetoplast may be seen as a little line in loosely packed pseudocyst, but not always)
Taenia Distinguish T saginata from T solium
Scolex T saginata 4 suckers, no hooks or rostellum. Gravid proglottid >16 uterine branches. Ovary 2 lobes, vaginal with sphincter muscle. T solium scolex 4 suckers, rostellum with hooks, Gravid proglottid <10 uterine branches, Ovary 3 lobes, no vaginal sphincter muscle
Taenia solium Life cycle (human)
Humans ingest raw or undercooked meat containing cysts - cysts develop into adult worms in small intestine. Humans excrete segments of worm and eggs. If human ingests eggs (or gravid proglottids containing eggs) - cause neurocysticercosis - development of cysts in brain
Taenia solium Worm
Scolex attaches to the intestinal wall, hangs in the intestine from the head, inflammatory around it trying to release the parasite, when it breaks it will continue making proglottids - the bigger proglottids are the older ones at the end of the worm. No intestinal tube, it ingests nutrients from the skin of the worm, but has a fully developed reproductive system - each proglottid has 30-50,000 infective eggs
Toxocara canis Life cycle (human)
Humans ingest eggs, somatic migration of L2 only (visceral larval migrans)
Toxocara canis Life cycle (dog)
Puppies ingest eggs, somatic migration in tissues -> infected female dog -> infection of puppies in utero -> puppies develop adult worm in intestine and shed eggs
Toxoplasma gondii Lifecycle (human)
Ingestion of free oocysts (cat faeces) or tissue bradycysts (undercooked meat) - release sporozoites (cyst) or bradyzoites (tissue) transform into tachyzoites shortly after ingestion, invade leukocytes (promote dissemination) tachyzoites replicate rapidly, cell ruptures, tachyzoites released, tissue cysts (esp brain, muscle) are bradycysts containing bradyzoites (slow multiplication), tachyzoites can cross the placenta (bradyzoites do not) (sporo or brady > tachy > brady)
Toxoplasma gondii Microscopy
Histo of brain: Perivascular cuffing, necrosis, haemorrhage, inflammation - tachycyst (loosely packed with tachyzoites) adjacent to necrotic tissue (inside normalish tissue), bradycyst are tightly packed.
Trichinella spp Life cycle (human)
Human ingest raw or undercooked pork containing L1 larvae, larvae emerge in duodenum, mature to tiny adult worms which migrate through intestinal wall into lymphatics and blood to skeletal muscles, penetrate striated muscle cell, develop ‘nursed cell’ (cyst) containing a coiled L1 larva (intracellular larvae). Muscle cysts calcify over time but larvae remain dormant and infective for years. Viable larvae can be readily digested from infected muscle. Humans are accidental dead-end hosts
Trichinella spp Life cycle (animal)
Pigs and rats are main hosts. Rat ingests raw or undercooked pork containing larvae, larvae migrate, adult worm in small intestine liberates larvae which migrate to muscles and encyst. Infected flesh of rat and offal eaten by pig. Liberated larvae from rat muscle become adult worms in pig intestine, female worms produce larvae which migrate to pig muscle and encyst
Trichuris trichura Life cycle (human)
Human ingests egg (from contaminated food/water), larvae hatch in small intestine, mature and migrate to Adult worm in caecum, pass unembryonated eggs in faeces, infective larvae develop within eggs in soil, embryonated eggs contaminate water, ready for ingestion by human
Trichuris trichura Life cycle (environment)
Eggs need shade and moisture to become infective in soil (L1 stage)
Trichuris trichura Adult worm
2-5cm whip-like appearance. Thin end is the front of the worm and burrows into the epithelial layer of the caecum and colon. Thick layer hangs into the lumen and facilitates mating between male and female
Trichuris trichura Egg
50-55um lemon shaped with translucent polar plugs. Smooth yellow brown colour (naturally stained by bile) TT - tea tray
