helminthology 2

• trematoda

  • schistosomosis (schistosoma spp)

• cestoda

  • echinococcosis (Echinococcus spp)

• nematoda

  • lymphatic filariosis (wucheria bancrofti)

  • onchocercosis (onchocerca volvulus)

  • STH (ascaris, Toxocara spp)

• diecious adults

• femals: 7-28mm

• males -> female resides in the gynacophoric canal of the male

• prepatency 5-11w

• patency 2-5y

• the main species infecting humans:

  • S. haematobium, S. japonicum, S. mansoni

• less infections caused by S. mekongi and S.intercalatum

1. Eggs shed from infected human in feces ( S.mansoni, S. japonicum, S mekongi) or in urine (S.haemmatobium) => diagnostic stage

2. eggs hatch and release miracidia

3. miracidia penetrate snail tissue (aquatic)

4. sporocysts develop in snail (successive generations)

5. Free swimming cercariae released from snail into water => infectious stage

6. ! Cercatiae penetrate skin of human (causing symptoms in humans)

7. cercariae lose tails during penetration and become schistosomulae

8. circulation

9. migration to portal blood in liver and maturation in adults

10. ! paired adult worm migrates to: (F into M to copulate)

    1. mesenteric venuel of bowel/rectum (laying eggs that circulate to the liver and shed in stools) (s.m; s.j/mekongi)

    2. venous plexus of bladder eggs shed in urine (s.h)

• acute and chronic disease

• penetrating cercariae cause skin reaction

• females excrete eggs that cause an immune reaction, mainly when trapped in body tissues

  • urinary schistosomosis: damage to the bladder, ureters and kidneys

  • intestinal schistosomosis: enlargement of the liver and spleen, intestinal damage and hypertension of the abdominal blood vessels

• schistosoma spp. parasiting birds and mammals can cause cercarial dermatitis in humans -> “bade-oder zerariendermatitis” (entenbilharziose)

• hook is typical for schistosomas eggs

• people get infected during routine agricultural, domestic, occupational and recreational activities

  • exposition to contaminated water

• children are espacially vulerable to infection

  • lack of hygiene and certain play habits such as swimming or fishing in contaminated water

• safe and effective medication with praziquantel

• people in need for preventive chemotherapy in 2020

  • 240mio in need

  • 77mio recieved PC

• since 2011 also reports from corsica

S. mansoni

• large

• conspicuous lateral spine

• excreted eggs in feces contain mature miracidium

S. haematobium

• large

• conspicuous terminal spine

• excreted eggs in urine contain mature miracidium - located to bladder

S. japonicum

• large, rounded

• small, incospicuous spine

• excreted eggs in feces contain mature miracidium - very small inconspicuous spine

• hermaprodited

• adults: 1.2-7mm

• prepatency

  • 4w e. multicolularis

  • 5-8w e. granulosus

• patency

  • few weeks, rarely 6-12m e.m.

  • 6m occasinally 2y e.g.

morphology

1. scolex with sucker and “armed” rostellim (ring of rostellar hooks)

2. proliferation zine

3. strobila often consiting of 3 segments

4. genital pore irregularly alternating, marginal (often difficult to detect) -> eggs excreted here. sometimes on the right, sometimes on the left side

5. uterus with lateral protrusions

morphology

1. scoley with sucker and “armed” rostellum

2. proliferation zone

3. strobila often consisting of 4-5 segments

4. genital pore irregularly alternating, marginal (often difficult to detect)

5. bad-shaped uterus

1. adult in small intestine for DH; proglottids can be shed so eggs can get free

2. embryonated eggs in feces (infection for DH & IH) => inectious stage

3. IH: not realla IH by not eaten..

   pathogen in different areas in the body - oncosphere released

4. hydatid cysts in various organs

1. DH: oncosphere hates penetrates intestinal wall

2. hydatid cyst in various organs

3. protoscolex from cyst

4. scolex attaches to intestine

1. adult in small intestine

2. embyonated egg in feces => infectious stage

3. Human: oncospheres released in darm

4. alveolar hydatid cysts in liver; may disseminate to other organs

1. ocosphere hatches; penetrates intestinal wall => IH

2. ! Alveolar hydatid cyst in visceral organs (usually liver) - diagnostic stage

3. protoscolex from cyst

4. scoley attaches to intestine

DH - fox -> ingestion of eggs in feces -> IH Rat -> ingestion of cysts in organs

DH -> adult tapeworm -> each gravid proglottis carris approx. 200 (EM) or 600 (EG) eggs, shed every 14d

IH -> metacestode/larva/cyst = echinococcus (metacestode names like the pathogen)

• metacestode filled with fluis (EG) or gelatinous mass (EM)

  • single or multi-chambered for EG

  • conglomerate of many single vesicles for EM

• main localisation liver or lung -> but can also spread into brain and other organs

E ganulosus group -> disease cystic echinococosis, syncidiale hydatid disease (CE)

e multilocularis -> disease alveolar echinococcosis (AE) ONLY ONE

• there is also the so calles “neotropical echinococcosis” NE which is caused by E. oligarthra and e.vogeli in South amerika

• names from the different metacestode

• most frewuent ophthalmological echinococcosis manifestation: orbita, rarely vitreous body ir anterior chamber of the eye

• accounts for 1-2% of all hydatid cysts

• hydatod sand appears granular and consists of:

  • blood capsules

  • protoscoleces fro ruptured blood capsules

  • debris of former brood capsules

  • detached hook of the protoscoleces

  • calcareousbodies

• a “mature” hydatid contains approc. 500ml hydatid sand

  • 1 ml of hydatid sand can contain up to 400000 protoscoleces

• sponge like structure as it is composed of many single vesicles

• vesicles germ eogenously, likewise extensions of the germinal layer spread root-like into the surrounding tissue

  -> tumorous and infiltrative growth

• -> spreading all over the abdominal cavaty

• cancer of parasites

• infection of humans only via eggs, not via the metacestode (humans are not the DH)!

• infection by hand-moth contact after contamination of hands with eggs

• 5-15y incubation period for AE, untreated >94% lethality

• if possible, total surgical resection of the echinococcus, additionally therapy with benizimidazoles for years/life -> are not destroying in the cyst - cant get rid of it. - hard treatment

• due to the high untreated lethaoty and the high burden of therapy as well as the high costs for AE patients (on average 182,000.-) AE is one of the most important zoonoses despite its low incidence!!

• infection with parasite filarial worms

• localisation is species-dependent

  • filariae in lymphatics - lymphatic filariosis (Wuchereria bancrofti)

  • filariae in hypodermis - onchocercosis (onchocerca volvulus)

  • filariae in hypodermis - loasis (loa loa)

• f 8-10cm, m 40mm

  • lymphatics

• microfilariae 240-300µm -> larvae

  • lymphatics - peripheral blood

• prepatency 7-24m

• patency 6-8y

• approx. 90% of lymphatic filariosis cases are caused by W.bancrofti

  • other pathogenic agents are brugia malayi and brugia timori

1. Mosquito takes a blood meal (L3 larvae enter skin)

2. human stages: Adults in lympatics -> 3 stage larvae (microfilarae) develop in human - to adult in the lymphatic system

3. adults produce sheathed microfilariae that migrate into lymphatic and peripheral blood circulation -> depending on daytime where they are! when mosquito are active -> in the blood

4. mosquito takes a blood meal - ingests microfilariae

5. microfilariae shed sheats, penetrate mosquitos midgut and migrate to throacic muscles

6. L1 larvae

7. L3 larvae

8. migration to mosquito head and proboscis

• filaria L3,L4, adults inside the lymphatic system -> lead to multiple inflammatory reactions and accumulation of lymph

• often asymptmatic, but with subclinical damage of th lymphatic system

• when it gets worse: lymphedema (tissue swelling)

  • advanced stage: elephantiasis (skin/tissue thickening), often with secondary bacterial infections

  • hydrocele, chylocele, swelling of scrotum or vulva

• periodic appearance of of pain and fever

• 40% kidney damage - proteinuria, hematuria

• enlargement of parts of the body due to defective drain of the lymph -> blocked or damages due to inflammatory reactions

• leads to aggregation of water and proliferation of connective tissue

• most freqeuently affected: limbs, particularly legs

• distribution predominantly in developing countires

• innate and acquired form elephantiasis tropica - filarial infection

• transmission through bites of infected mosquitoes (anopheles, aedes, culex, a.o.)

• diethylcarbamazin citrate (DEC, effective against microfilariae in adults) but side effects possible

• ivermectine (effective against microfilariae) have to take it over all the time the adults are viable

• mosquito net

• insect repellant

makrofilariae-adults

• f: 33-50cm, m 19-42mm

  • nodules in subcutaneous tissues

• microfilaria: 220-360µm

  • skin, lymphatocs of connective tissues

• prepatency 12-18m

• patency 10-15y

1. IH Blackflie (genus simulium) takes a blood meal (L3 larvae enter bite wound)

2. human stages - subcutaneous tissues

3. adutls in subcutaneous nodules

4. adults produce unsheathed microfilariae that typically are found in skin and in lymphatics of connective tissues, but also occasionally in peripheral blood, urine and sputum!

5. blackflie takes a blood meal and ingests microfilariae

6. microfilariae penetrate blackflys midgut and migrate to thoracic muscles

7. L1 larvae

8. L3 larvae

9. migrate to head and blacklfly’s proboscis

• eye and skin disease

• skin nodules are frequently forming around the adult worms

• f produce microfilariaw (220-360µm) that migrate through the body (skin, lymphatics of connective tissue)

  • dead or dying larvae provoke an immune reaction

• severe itching and various skin changes

• sometimes eye lesions leading to visual impairment and permanent blindness

  • clouding of the cornea by inflammatory reactions

• transmission through repeated bites of infected blackflies of the genus simulium

• ivermectin every 6m for the lifespan of the adults (effective againt microfilariae)

• doxycycline (effective against Wolbachia symbiont)-> antibiotika which kill the symbiont, cant get 100% rid of the adult

• insect repellant

most common are infectious wiith:

ascarids- ascaris lubricoides

whipworms - trichuris trichiura

hook worms - ancylostoma duodenale, necator americanus

threadworms - strongyloides stercoralis

ascarids:

• a. lubricoides

• Toxocara spp

whipworms

• t. trichiura

• thrichuris suis

hookworms

• a. duodenale

• n. americanus

• ancylostoma caninum u.a.

strongyloides spp

Ascaris of humans - a.lubricoides, of pigs - a.suum

• presumed to be the same species

adults - are located in the small intestine

f 20-35cm, m 15-30cm

• prepatency 2m

• patency 12-18m

1. adults in small intestine => diagnositc stage

2. unfertilized egg (will not undergo furhter developemnt) in feces

1. fertilized egg - also in feces but undergoes development

2. emryonated egg with L3 larvae

3. ingestion of embryonated eggs => infectious stage

4. hatched larvae enter circulation and migrate to lungs

5. from intetine to lungs

6. larvae are coughed up and swallowed, re-entering the gastrointestinal tract. maturation proceeds in the small intestine.

• allergic reactions (sensitisation)

• pneumonia with cough, fever, mucus, asthma-like attacks

• colics (due to blocking of the pancreatic and bile ducts)

• ileus (massive infection)

• malnutrition (massive infection)

  • take up the nutrition out of our body

canis:

• dog roundworm

• adults: 10-18cm

• long, narrow alae

• in small intestine

• prepatency3-6w

• patency 4m

cati:

• cat roundworm

• adults: 3-12cm

• short and broad alae

• in small intestine

• prepatency: 4-8w

• patency: up to 8m

1. eggs passed in feces - larvae also gets into the placenta -> just in canis, puppies then get born infected and can reinfet the parents

2. external envirnoment : unembryonated -> embryonated egg with L3

3. ingestion of eggs

4. adults in small intestine of DH!

5. vertival transmission to puppy

6. adults in small intestine of offspring

7. uptake in paratenic host

8. ingestion of PH

9. Ingestion of eggs of Human (infectiozs stage)

10. food borne transmission via bunny (PH)

11. L3 migrate in tissue

• larva migrans

  • visceral toxocarosis

  • ocular toxocarosis

  • neurotoxocarosis

  • “covert” toxocarosis

• visceral toxocarosis

  • abdominal pain

  • respiratory symptoms

• "covert” toxocarosis

  • unspecific symptoms

• ocular toxocarosis

  • blindness

humans: epilepsy, ataxia, pareses, neuropsychological disturbances

memory impairment

mouse: epileptical seisures?, ataxia, pareses, paralysis, balance disorders, memory impairment

challenge of C57BL/6J mice with 2000 infective eggs of T canis or T cati

around 79 dpi neurotoxocarosis kicks in

tested with neurobehaviour/memory funciton, neurotropism and histopathology

memory impairment: more pronounced and severe in T.canis infected mice.

higher affinity of T.canis towards the brain

microglia activation

ß-APP accumulation

degeneraive myelin changes: vacuolisation, gitter cells and demyelination

AD is induced by formation of ß-amyloid aggregates and intercellular neurofobrillary tangles

NT and AD share prodound similarities:

1. memory impairment

2. microglia activation

3. ß-APP accumulation

4. demyelination

silent progression of NT to AD is being discussed

• a. lumbricoides: albendazole and mebendazole -> good treatable

• toxocara spp. human: thiabendazole, mebendazole, albendazole, diethylcarbamacine (DEC)

  • only indicated if patient suffer from infection

  • symptomatic treatment of ocular and neurotoxocarosis patients with corticosteroids and anticonvulsants

• strategic use of anthelmintics accodring to the individual risk of infection of the dog or cat

  • treatment of animals lowers the risk of human infection!