Intro to parasitology + Hypo

Outline the 6 steps involved in the cycle of infection

1. parasite

2. susceptible host

3. portal of entry

4. mode of transmission

5. reservoir

6. portal of exit

Outline the general roundworm lifecycle (8)

1. adult worms sexually reproduce

2. eggs are excreted in faeces

3. L1 in faeces

4. L2 in faeces

5. L3, infectious stage (generally) on grass

6. infective L3 stage is ingested

7. develops into L4

8. develops into L5 → adult ready for reproduction

what are the 3 simple phases of a roundworm parasite infection?

1. contamination phase

2. free-living phase

3. parasitic phase

Define the pre paptent period (PPP)

• period b/w exposure to infection and when we can detect the parasite in blood/faeces

what do we call a parasite once it’s become detectable?

• patent

define the incubation period

• the period b/w exposure to infection by a parasite and appearance of clinical signs

state the stages of a common GI nematode life cycle

• it’s a direct life cycle

• egg → L1 → L2 → L3 (previous cuticle is retained and exsheathment occurs only when L3 enters host) → L4 → L5 → adult → egg

name a roundworm found in horses with a direct lifecycle

• parascaris equorum

what are 4 clinical signs of parascaris equorum

• reduced appetite

• diarrhoea

• death

• intestinal obstruction

what is the lifecycle and state whether it’s indirect/direct of the common trichostronglye

direct

1. eggs passes in faeces

2. L1 → L3 free living

3. L3 ingested

4. L3 exsheaths in the rumen

5. in the abomasum/SI → adult worm

3 clinical signs of the common trichostronglye

• reduced appetite

• diarrhoea

• death

state the life cycle of fasciola hepatica

1. eggs passed in faeces

2. miracidum larvae

3. intermediate host of a snail

4. cercariae

5. metacercariae cysts on grass

6. ingested

7. early immature fluke develops

8. into immature fluke

9. into adult fluke

what is fasciola hepatica

• fluke, trematodes

what is a cestode, tapeworm, that infects horses?

• Anoplocephala perfoliata

what are 3 symtpoms of anoplocephala perfoliata?

1. colic

2. diarrhoea

3. death

what is the life cycle of Anoplocephala perfoliata?

1. gravid segments pass into the faeces

2. they disintegrate, releasing eggs

3. mite ingests eggs (intermediate host)

4. mites are infected by cysticercoids

5. they move on vegetation

6. taken up by the horse

if a parasite ends up in a paratenic host, does this mean the end for its life cycle?

• no

• paratenic host could be ingested by the direct host e.g. snail by a dog, rat/bird by a cat

what is the life cycle in the paratenic host referred to as?

• quiescence

what are the 3 routes of toxocara canis transmission

1. transplacental migration to foetal liver → pups

2. transmammary

3. paratenic host

how does Toxocara canis transmit via mammary glands/placenta from the dam?

• somatic migration L3 in circulation and encyst in tisssue

• pregnant bitch → transferred either way.

how does transmission of Toxocara cati to kittens from a queen differ from that of T.canis from a dam to her pups?

• T.cati does not undergo transplacental transmission

State 7 areas agricultural economy is affected by GI nematodes

1. reproductive performance

2. wool production

3. milk production

4. carcass quality

5. weight gain

6. death

7. treatment + veterinary care

state 3 zoonotic transmissions of nematodes to humans

1. VLM - visceral larva migrans

2. OLM - occular - from Toxocara canis

3. CLM - cutaneous - larvae of hookworms migrating through skin

what is a highly dangerous zoonotic endoparasite?

• Echinococcus granulosus

what is the life cycle of E.granulosus?

• definitive host contains adult worms → in intestine → immature egg excreted in faeces → ingested by intermediate host → this host contains larval stage only, as cysts → infectious protoscoleces → scolex → adult worm in definitive host

what may affect the prevalence of an endoparasite

• seasonal trends

• time of disease

what may help diagnosis of GI parasites?

• clinical signs - there are general signs which can lead to diagnosis with sufficient accuracy

what are the diagnostic clinical signs of Oxyuris equi?

• female roundworm migrates out of rectum → lays eggs on skin

• migration + egg laying → itching which → severe anal pruritus

• eggs are yellow-white gelatinous streaks of perineal skin = highly diagnostic

• can cause secondary iinfection due to pruritus

what are some key aspects of controlling endoparasite outbreaks?

• maintain good husbandry and hygiene to reduce pasture contamination

• recognise + anticipate/prepare for high-risk reason

• recognise symptoms of disease early

• know the best time for intervention

• recognise pattern of life cycle

what can we call hypobiosis in terms of how it affects nematodes?

• arrested larval development - ALD

what is ALD?

• arrested larval development

  • it’s when the larvae of some nematodes stop developing in the host

what are 3 example species of nematode in which ALD can occur?

1. Ostertagia ostertagi

2. teladorsagia circumcinta

3. haemonchus contortus

what triggers hypobiosis?

• climactic factures - temperature and moisture - aka seasonally

  • environmental changes can be detected and arrest development of larva stages

what is required for hypobiosis?

• a biologicals switch must stimulate ALD and trigger reactivation of growth at a later stage

link immunity and larval arrest in lams and sheep

• in the spring, lambs will be susceptible and infected by L3s → patency reached

• in the autumn, immune response may induce hypobiosis

what are the effects of immunity (thinking about lambs exposed in a spring, then again in autumn)

• increased larval arrest

• reduced worm burden

• low FECs

what are the 2 mechanisms of spring rise?

1. overwintering - seasonal influences on infective larvae/eggs on pasture → revival in spring when temp increases

2. hypobiosis initiated by an environmental signal/immune response → increased faecal egg output by ewes after winter

why do preparturient ewes contribute to the risk of endoparasite contamination on pasture?

• serum prolactin levels are high in preparturient period → immune competency is low → arrested L4 → adults → eggs

• increase egg output around 2 weeks b4 birth, and 4-6 weeks after.

• L3 acquired from pasture are also more likely to establish in ewe at this time.

what are 3 sources of nematode larvae on pasture?

1. overwintered eggs and larvae

2. peri-parturient rise of pregnant ewes

3. rain is important in dispersing larvae

why may lambs be a source of larvae from Mid-summer-autumn?

• because they were infected in spring → now have egg producing adult nematoes.

are animals only affected by 1 nematode species on pasture?

• no

• may be affected by different species which peak at different times

  • immunity occurs quickly in some cases and slowly for other species

what are some example immune responses against N.battus in sheep?

• villus shedding as a clearance mechanism

• mast cells + eosinophils increasing at infection site

• sIgM → IgG as infection progresses

  • some mucosal IgA also present

outline Th2 cell involvement in N.battus immune response in sheep

Th2 → Il-5 + IL=13 → attract and activate eosinophils → site of infection

also → IL-4 → B-cells → plasma cells → IgA/M/G

what is hypobiosis an example of?

• an immune evasion mechanism - the larva is encapsulated in the tissue

why does sterile immunity never occur in cattle infected with O.ostertagi?

• L4 Ostertagia and adult suppress T-cell division

• dendritic cells and macrophages presenting its antigen induce regulatory T-cells

• cytokine production is decreased in calves

• TGF-beta is active and suppresses other cytokines

what protein can nematodes produce to avoid recognition by the immune system?

• cuticular proteins

Pinworms appear to cause little pathology, what may this be an example of?

• a parasite developing towards commensalism

why are neonates poor at developing immunity?

• neonatal immunological unresponsiveness is when they sometimes don’t produce a protective immune response until exposed by reinfection for a prolonged period

what is concomitant immunity

immunity protecting against subsequent infections but unable to clear the current one

how can nematodes influence IgE?

• some stimulate polyconal IgE → covers mast cells → less responsive to parasite antigens

in a host, what casues hypobiosis and then the resumption of larval development?

1. hypobiosis is caused by host immunity

2. relaxation of host immunity → resumed larval development

what is important to note about using anthelmintics and arrested larvae?

• some kill them, some don’t

why does a host want hypobiosis to occur?

• it’s a host-regulated phenomenon that limits the size of the worm populations during season of increasing larval activity

why do parasites want hypobiosis to occur?

• it’s a developmental adaptation process that enhances their own survival in adverse environmental conditions

• essential in epidemiology of infection