Parasitology

• What is a parasite?

  Parasitism

  Intimate relationship between two organisms in which one (the parasite) lives at the expense of the other (the host).

  The relationship involves:

  nutritional dependence

  immunological defence

  integration of life-cycles
• Why are parasites important in veterinary medicine?

  Parasites may cause:

  • Death
  • Overt clinical disease
  • Sub-clinical disease
  • Less than optimum productivity (farm animal production)
  • LOP is when animals aren’t putting on as much weight as they normally would. Or cows not making as much milk, sheep not making as much wool, overall productivity from the parasite infected animal is reduced.
  • LOP = animals are not reaching their genetic potential in terms of their productivity

  
• Major parasite groups:

  • Helminths (worms)
  • Nematodes (roundworms)
  • Cestodes (tapeworms)
  • Trematodes (flukes)
  • Arthropods
  • Insects (fleas, lice, flies)
  • Acarina (mites, ticks)
  • Protozoa
  • Single celled organisms
• Parasite names

  sp = one unnamed species

  spp = more than one species

  
• Nematodes

  Morphology:

  • Long (mm to >50cm long)
  • Tough elastic cuticle
  • Muscular pharynx - draws food in
  • Nerve ring around pharynx and four longitudinal nerves - movement
  • Separate sexes
  • Female worms (blunt, pointed tail)
  • Male worms (spicules ± ‘bursa’ – cuticle covering male tail in bursate worms; absent in nonbursate)

  Feeding:

  • Swallow host food
  • Suck a plug of mucosa into their buccal cavity leaving a circular ulcer
  • Others bury heads deep into mucosa and suck blood

  Lifecycle:

  • Egg > L1 > L2 > L3 > L4 > Adult worm (L5)
  • L3 = infective stage
  • Once inside host, develops into L4 and L5

  
• Cestodes - Morphology

  • Chain (strobila) of progressively-maturing independent reproductive units (segments or proglottids)
  • Anchored to intestinal wall by hold-fast organ (scolex, head-end)
  • Pseudophyllidean tapeworms – scolex has 4 longitudinal ‘grooves’
  • Cyclophyllidean tapeworms – scolex often has hooks (armed)(global importance)
  • Each segment – male and female reproductive organs (Hermaphrodite)
  • Mature segments drop off adult tapeworm daily
  • Mature (gravid) segment > 100,000 eggs
  • Eggs immediately infective (contain tapeworm larva = oncosphere or hexacanth embryo with six hooks)

  
• Cestodes - Feeding

  No alimentary tract

  Absorb nutrients across body surface covered by a tegument (many minute projections, microthreces, increase the surface area)

  
• Cestodes - Lifecycle

  • Indirect life cycle e.g. echinococcus granulosus
  • two hosts involved - e.g. dog is final host
  • adult tapeworm is found in the small intestine, infected dog will pass either segments or eggs in its faeces and these will be ingested by a secondary or intermediate host. In Secondary host we don't get adult tapeworm, but a cyst like stage develops
  • metacestode = larval tapeworm

  
• Cestodes - epidemiological relationships

  • Examples of epidemiological relationships/how tapeworm lifecycles
  • Predator-prey (e.g. cat eating infected mouse)
  • Accidental (e.g. horse eating infected pasture mites)
  • Irritation (e.g. infected flea – swallowed during grooming)
  • Types of metacestode
  • Vary in the number of developing scolices they carry:
  • Cysticercus (one scolex)
  • Coenurus (many scolices)
  • Hydatid cyst (thousands of scolices)

  
• Trematodes - Morphology, Feeding & Lifecycle

  • Flat, leaf-like worms (mms to several cms long)
  • Oral and ventral suckers
  • Mouth leads from oral sucker to blind ending caecae
  • Most species hermaphrodite, but individuals cross-fertilize
  • Flukes covered by a metabolically, highly active tegument – important role in evasion of host immune response

  Feeding = Suck blood/ingest tissue debris

  Life cycle = Indirect life cycle, final host passes egg fluke in faeces. Has to find intermediate host in wet area (snail)-develops there. Is released, sits on grass waiting for a sheep to infect.

  
• Arthropods - Morphology & Feeding

  • Great diversity, e.g. insects & acarines
  • Separate sexes
  • Insects (3 body divisions, compound eyes, 3 pairs of legs, may have wings)
  • Acarines (2 body divisions, simple eyes, 4 pairs of legs, no wings, small size)

  Feeding

  • Mouthparts show a variety of adaptations:
  • Sucking up liquefied food
  • Sucking blood
  • Chewing skin debris
  • Not feeding at all

  
• Arthropods - Lifecycles

  Life cycle (insects)

  • Simple metamorphosis: egg – nymph – adult (e.g. lice)
  • Complex metamorphosis: egg – larva – pupa – adult (e.g. fleas, flies)

  Life cycle (acarines)

  Same for mites and ticks:

  Egg – larva – nymph – adult

  
• Protozoa:

  Morphology

  • Protozoa are motile, unicellular organisms with a nucleus, endoplasmic reticulum, mitochondria, Golgi body and lysosomes
  • Great diversity

  Feeding behaviour

  • Pinocytosis (small particles) or phagocytosis (larger particles)

  Life cycle

  • Asexual reproduction alone (e.g. simple binary fission)
  • Asexual and sexual reproduction (e.g. Eimeria, Toxoplasma)

  Number of hosts

  • HOMOXENOUS life cycle (=direct) single host
  • HETEROXENOUS life cycle (=indirect) 2 hosts
  • FACULTATIVELY HETEROXENOUS life cycle (may be >1 host, but not essential)

  
• Parasitic Gastro-Enteritis (PGE):

  Disease associated with a number of nematode species (singly or in combination)

  Characterised by:

  diarrhoea / weight loss (clinical disease)

  poor weight gain (sub-clinical disease)

  seasonal appearance

  hypoalbuminaemia – low blood protein

  
• Economic importance of PGE

  Considerable economic importance in grazing livestock

  Potential welfare problem (esp. organic farms)

  Losses associated with the cost of:

  replacement stock

  disruption of breeding programme

  impaired productivity

  treatment of clinically affected stock

  Prophylaxis
• Bovine PGE:

  Many worm species - few of significance:

  Abomasum

  • Ostertagia
  • Trichostrongylus
  • Haemonchus

  Small intestine

  • Cooperia
  • Nematodirus
  • Trichostrongylus
  • Bunostomum

  Large intestine

  • Oesophagostomum
  • Chabertia
  • Trichuris
• BOVINE OSTERTAGIOSIS

  Ostertagia ostertagi

  PRIMARY pathogen of cattle (temperate regions)

  Adult worms 1cm long, cotton-like, brown (when fresh)

  Abomasum (fundus)

  
• Lifecycle of Ostertagia

  • For nematodes, sexes are separate. After mating, female worms produce eggs which are passed onto pasture.
  • Eggs hatch, passing through L1, L2 phase and reaching the infective L3 stage. Move from poo, onto grass ready to be eaten.
  • The cycle is complete when calf ingests some infective L3 larvae with the grass and will enter the gastric glands in abomasum and emerge as adult parasite
  • Lifecycle = ~3 weeks
  • Pre-patent periods = time between infection of the calf (ingesting L3) and first case of eggs in poo/Time it takes for L3 to reach egg laying adult phase in host.

  
• RATE OF INFECTION depends on:

  • Host appetite
  • NUMBERS OF INFECTIVE LARVAE (L3) ON PASTURE
  • Risk of infection tells us how much at risk cattle are developing disease

  
• Disease commonest in calves

  • grazing permanent pasture - pasture that's been used for several years for rearing calves. infected at the start of the grazing season.
  • kept at high stocking density - if a farmer keeps a lot of calves on a relatively small area

  
• • Permanent pasture = was used to raise cattle the previous year. Therefore, there will be some left over L3 on pasture that will be present this year - Overwintering. L3 can survive cold temperatures. They rely on food reserves (L1,L2).
  • Farmer turns out young dairy cows in april/may and they pick up infective L3 larvae. 3 weeks later, worm eggs seen in calves poo. Eggs are not yet infective, need to develop to L3 stage to infect
  • The warmer it is, the faster the eggs will hatch and reach the L3 stage. All eggs will mature by the same time (summer) -> leading to rapid increase in infection

  
• • If calves are left to graze heavily contaminated pasture late in the autumn, the larvae ingested when it's getting cooler don't develop to adult worms in 3 weeks. Instead they go into gastric glands in the abomasum and go to sleep. They will become arrested for several months before resuming their development in February/March.
  • The calf may accumulate several hundred thousand to half a million arrested larvae - no clinical signs as arrested
  • Need ~40,000 worms to cause disease, calves have way more, theyre now ticking time bombs

  
• Why do L3 larvae become arrested after ingestion?

  • Late in the autumn calves are eating infective larvae, but they become arrested and sleep over winter.
  • By end of January, 20% of arrested worms will resume their development, reach adult stage 3 weeks later and cause clinical signs
  • A couple of weeks after that, another 20% would resume their development - Another bout of diarrhoea and so on.
  • What they're trying to do is wait for nice weather to increase their survival and spreading
  • short chilling will induce arrested development. But if prolonged chilling, it turns it off

  
• Type 2 disease: This is when successive waves of previously arrested worms resume their development and as they hit the adult stage, we get a bout of diarrhoea. So we see intermittent diarrhoea

  
• Immunity to Ostertagia ostertagi

  SLOW to develop (whole grazing season)

  May FALL over winter - RE-ESTABLISHED upon turnout (2nd grazing season)

  ADULT cattle solidly IMMUNE (no significant role in disease epidemiology)

   
• Type 1 disease or summer ostertagiosis occurs when overwintering has occured, calves have consumed last seasons L3 and excreted more eggs. Theres too much L3 larvae consumed, occurs mainly in summer as thats when they all develop (both new and overwintering L3 will mature all at once). Over a certain amount ingested leads to disease
• CONTROL (TYPE 1 DISEASE)

  • Use clean pasture
  • New leys, pasture not grazed by cattle last year
  • BUT not always available
  • Eliminates the possibility of ingesting the overwintering L3 which is the source of infection
  • Delay turnout until after spring mortality in L3
  • BUT uneconomical use of pasture, supplementary feeding may be needed
  • Ensures any eggs left from overwintering die off from lack of food reserves
  • Dose ’n’ move to aftermath (mid-July)
  • wont control early season disease
  • increased anthelmintic resistance risk

  
• How Dose N Move works

  • We leave the calves on field A until mid-July then we dose them with a dewormer and move them on to field B for the rest of the year.
  • We've avoided the calves being exposed to the big auto infection peak that happens in the late summer

  
• Controlling Type 1 Disease

  IF NO ALTERNATIVE GRAZING AVAILABLE

  • Strategic anthelmintic treatment
  • Strategic treatment BEFORE mid-July, e.g. doramectin by injection) at 0 + 8 weeks post turnout (5 week residual activity v Ostertagia)
  • carefully timed treatments during the first part of the grazing season to stop the calves contaminating the pasture with eggs at all
  • Intra-ruminal anthelmintic devices
  • Minimise pasture contamination → prevents autoinfection peak in L3
  • e.g. Autoworm (Schering-Plough), Panacur bolus (Intervet)
  • BUT expensive
• CONTROL (TYPE 2 DISEASE):

  Cattle exposed to LOW challenge at pasture in late autumn

  UNLIKELY to require treatment at housing

  Cattle exposed to MEDIUM / HIGH challenge at pasture in late autumn or cattle of UNKNOWN origin

  LIKELY to require treatment at housing
• General importance of ticks

  Major cause of disease and production loss (US$7 billion annually worldwide):

  Blood losses (large numbers → anaemia)

  Tick worry (prevent animals feeding)

  Disease transmission

  Tick paralysis (ascending motor paralysis)

  Secondary infection / blowfly strike (at bite site)

  Production losses (farm animals)
• Divided on the basis of their MORPHOLOGY into:

  HARD ticks

  Important globally in both temperate and warmer climates

  SOFT ticks

  More important in warmer climates
• Identification - HARD ticks:

  • ORNATE ticks have coloured patches
  • FESTOONS (or notches) may be present
  • Prominent mouth-parts
  • SCUTUM - hard dorsal covering
  • BODY WALL - convoluted to accommodate blood meal (esp. female ticks)
  • Scutum smaller in female hard ticks as they need to take in more blood to produce eggs
  • in females the rear half of the body expands

  
• Identification - SOFT ticks:

  • Scutum – ABSENT
  • Mouthparts – NOT visible from dorsal surface
  • Do NOT swell much (feed little and often)

  
• Tick Feeding

  • Tick stands upright
  • Chelicerae cut through skin → pool of blood
  • Hypostome inserted deep into skin
  • Mouthparts CEMENTED in place
  • Tick feeds continuously + injects saliva (contains substances that reduce host inflammatory response, increase permeability of blood vessels → free flow of blood)

  
• Hard Tick Lifecycle - lasts from 1 month - 3 years

  Classified according to number of different hosts they need to complete the lifecycle:

  • ONE-host ticks: each stage (larva + nymph + adult) feed on one host, e.g. Boophilus
  • TWO-host ticks: larvae + nymphs feed on one host; adult ticks on a second host, e.g. Hyalomma
  • THREE-host ticks: each stage feeds + develops on a different host, i.e. three hosts, e.g. Ixodes
  • Not limited species wise

  
• Soft tick lifecycle

  • NOT classified like hard ticks
  • Feed little and often on many hosts
  • Some are host specific e.g. just feed on birds or just feed on mammals but it still depends on species of soft tick
• DISEASE TRANSMISSION - TICKS

  Ticks act as vectors of disease through the following ways:

  Trans-STADIAL transmission

  • Infectious agent ingested during feeding by larva
  • Passed on from one host to the next (in 2- & 3-host ticks) as tick develops to nymph + adult
  • NOT passed onto next generation via the egg

  Trans-OVARIAL transmission

  • Infectious agent is passed from one generation to the next through the egg, e.g. Babesia spp
  • When those eggs hatch, the larvae will be infected, trans-stadial transmission will kick in.
  • This method generates more infectious ticks via reproduction

  
• Ticks mouthparts

  • PALPS: (red arrows) sensory organs
  • CHELICERAE: puncture skin
  • HYPOSTOME: (green arrows) tube for sucking host blood, backward pointing teeth

  
• HARD TICKS - UK

  Ixodes spp. (3-host ticks)

  • Worldwide
  • I. ricinus, most important tick in UK
  • Distribution: western UK (mainly) - rough woodland
  • Wide host range
  • Vector for HUMAN disease:
  • Lyme disease (humans, dogs)
  • Vector for ANIMAL disease:
  • Bovine babesiosis, louping ill, tickborne fever & tick pyaemia
  • Paralysis in humans, dogs (warmer climates only)