Parasitology - Nematodes 1

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Common features of Nematodes:

Cyclindrical (roundworms)

Separate sexes

Females produce eggs or L1

Wide size range

many different hosts and predilection sites

Life cycle:

Adult parasites produce eggs or L1

eggs hatch (L1)

L2

L3

L4

Adult parasite

*All nematodes have to undergo moulting process in order to develop from egg to adult

Moulting = shed exoskeleton and grow a new one, in order to allow growth and further development

PPP - pre patent period = time it takes from host ingesting infectious stages/being infected, and the parasites maturing and getting to dispersal stages

Toxocara canis (gut nematode) - eggs embryonate over 4 weeks and persist in environment for years

highly pitted thick eggshell

large adult forms

small infective stage larvae

adult head

Eggs = stage found in environment, larvae hatch from egg and are infectious stage that migrate through the tissues

Routes of infection:

Oral (direct) - infective larvae in egg

Transplacental - larvae arrested in tissues of dogs becomes re activated via placenta of milk = leads to infection of puppies

Transmammary (as above)

Paratenic host - transport host not obligate intermediate host, rodent (mouse) remain for life of the host, dogs affected if ingest host

*most common route = oral digestion of eggs

Infection in animals < 3 months old: PPP = 4-5 weeks

Egg matures in environment

egg containing L3 ingested

L3 hatches in the SI

hepatotracheal migration - via liver to lungs

L3 to SI via trachea

L3-L4 adult in SI

Adult in SI release eggs

Infection in older bitches - transplacental infection. PPP in pup = 16d-3 weeks

L3 in egg ingested

L3 hatches SI

L3 migrates into tissue: ARRESTS

L3 activates (3 weeks pre-partum)

In pup, L3 migrates to foetal lung

At birthL3 to SI via trachea

L3-L4 adult in SI

Adult in SI

*Ensures 100% infection

T. canis transmammary transmission

- L3 in the milk for up to 5 weeks = no migratory phase

*arrested larval development is re-activated when immunity is lowered in pregnancy

*unembryonated egg is not infected, eggs are sticky and resistant

Treatment of T.canis:

prevent environmental contamination with eggs

start treatment before parasite lays eggs, continue to remove milk-acquired infection

treat bitch at the same time

Hookworms:

1-3 cm, stout, hooked head

SI predilection site

direct life cycle

L3 infective

important pathogens in tropics - cause of severe anaemia

* re-activating L3 can produce patent infection in bitch, can infect 3 consecutive litters

Blood suckers:

- the hookworm head is buried in the mucosa and actively ingests blood and other tissues

- produce lytic factor, anti-coagulants and various proteases that degrade haemoglobin

A.caninum - clinical signs

young animals, severe acute haemorrhagic anaemia (bloody diarrhoea)

older animals - chronic haemorrhagic anaemia

respiratory signs due to larval damage

multiple infections (Skin reaction - dermatitis)

Sources of infection:

transmammary

percutaneous/oral from environment

Control:

Chemotherapy (3 monthly) - benzimidazoles + ivermect/moxidectin

High dose fenbendazole in pregnant

clean, dry bedding - earth or grass support survivial of L3

Vaccination against hookworms:

use gut membrane antigens

generate antibody response, ingest antibody when blood feeding

ihibits enzymes - haemoglobinase

worms starve - less fecund, shorter, reduced anaemia in host

Trichuris sp. or whipworms: PPP 6-12 weeks

Adults in large intestine

eggs passed in faeces

L1 develops in egg (resistant)

ingested

plugs digested, L1 released

penetrates mucosal glands

L2

L3

L4

Symptoms:

- usually asymptomatic

- occasionally diptheritic enteritis and haemorrhagic colitis

- watery diarrhoea + blood

Diagnosis = eggs in faeces