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519 Cards in this Set

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What is an Obligate Parasite?
Depend on their Hosts to maintain themselves within the environment
What is an Facultative Parasite?
Parasites can complete their life cycle w/o a period of parasitism
What is a temporary parasite?
Parasites that have one or more NONparasitic stages that live away from the host.
What is a permanent parasite?
Parasites complete their entire life cycle on a single host
What is highly host specific vs low specificity?
High host specificity = parasites are restricted to one host species
Low host specificity = can infect a wide range of host species
Charactoristics (6) of an "ideal" parasite
1. recognises host site
2. maintains its position
3. Utilizes host nutrients
4. Adapts to physio-chemical conditions at site
5. minimizes host immune response
6. Life cycle is synchronized with one of host
Definitive Host
host in which the parasite undergoes sexual reproduction
Intermediate (secondary) host
host other than final host that the parasite must infect to complete its life cycle (ANY REPRO IN THIS HOST IS ASEXUAL)
Transport host
host in which there is no parasite development but serves to distribute parasite into environment (NOT ESSENTIAL FOR COMPLETION OF LIFE CYCLE)
Paratenic Host
similar to transport hosts but limited parasite development (CYCLE CAN BE COMPLETED IN ABSENCE OF THIS HOST) (ALSO NOT AN OBLIGATE PART OF LIFE CYCLE)
Disease host
host in which disease is observed
Accidental host/incidental/dead-end host
some parasite development but no transmission
Reservoir host
host that maintains infxn in an environment, usually to the detriment of domestic livestock or man
Direct Life Cycle
parasite has a cycle of development in ONE DEFINITIVE HOST and the infective form is usually external, environmentally resistant, nonparasitic form.
Types of direct life cycles (3)
1. all stages parasitic
2. single non-parasitic stage
3. more than one non-parasitic stage
Indirect Life cycle
parasite needs to cycle btwn at least TWO different types of hosts to complete its life cycle. (THERE IS ALWAYS ONE DEF HOST AND ONE I. HOST)
-infective forms can be non-parasitic, parasitic or both
Types of Indirect life cycles (3)
1. predator-prey cycles (carnivore def host and herbivore as i. host)
2. Vertebrate - invertebrate cycle (def host always vertebrate and i.host is invertebrate)
3. Vector-borne parasites (flies adn ticks are the vector)
Cons to having an I. Host
-added complication for LC (life cycle)
-Reduces overall chance of success
-need for compensatory asexual repro in I.host
Pros to having an I. Host
-I.Host increases the range of the parsite in time and space
-Exploit transient environments
-Isolation from host extinction
How do ticks remain on host?
lipo-protein salivary secretion acts as glue to host epidermis and dermal collagen
Host reactions to ticks (immunological)?
In rxn to salivary secretion= inflammation followed by development of aquired immunity
-Delayed type 4 dermal hypersensitivity but type 1 immediate hypersensitivity involoved
-Effect of rxn = pruritis
What results due to pruritis associated to tick bites?
-excessive grooming
-vesiculation of epidermis to push tick off
-graqnuloma of dermis which cuts off bld to tick
-accum of eosinophils - poisons tick
Host Reaction to ticks (overall cost)
-Pruritis
-Stress
-Anorexia
-Anemia
(also hide damage, teat damage, paralysis)
Psoroptic Mites Location
ON SKIN SURFACE -penetrate outer layers of epidermis and feed on inflammatory exudate
Sarcoptic Mite Location
IN EPIDERMIS
Demodectic Mite Location
SUPERFICIAL TO EPIDERMIS BUT WITHIN THE HAIR FOLLICLE
Dermanyssid Mite Location
SUPERFICIAL AND TEMPORARY
Trombiculid Mite Location
FEED LIKE TICKS
PSOROPTES OVIS
-what is it?
-where is it found?
-what does it cause?
-Survival?
-most serious ectoparsatic infection in UK livestock
-doesn't burrow in epidermis but remains at base of hairs
-pierces skin with chelicerae
-exudate and scabbing takes place
-mites found around scabs and on wool (fomites)
-pruritis is intense, spreads quite quickly
-May survive off host for several days or weeks
What are chelicerae?
piercing mouthparts
What are chelae?
scissor like structures at the end of chelicerae
Effective control of PSOROPTES OVIS?
-tx of both infected livestock and either disinfection or 2-4 week vacating of contaminated enclosures and fomites.
Common name of PSOROPTES OVIS?
SHEEP SCAB
Common name of PSOROPTES CUNICULI?
RABBIT EAR CANKER
PSOROPTES CUNICULI
-Where does it infect?
-What does it infect?
-mange of auditory canal in rabbits can also infect horses
Larval stages of ticks and mites?
three pairs of legs
Nymphs and Adult stages of ticks and mites?
four pairs of legs
Body Design of Ticks and Mites?
-head, neck, thorax fused
-antennae and mandible absent
-Mouthparts: palps, chelicerae, hypostome
-together with basis capituli forms a capitulum or gnathosome
Common name for CHORIOPTES OVIS?
Cattle Scab
CHORIOPTES OVIS
-who does it infect?
-What is seen with infxn?
-cattle, sheep and (horses rarely causing severe effects)
-epidermal pustulation and thickening and wrinkling of skin
-horse lower legs where there is hair
Common name for OTODECTES CYNOTIS?
canine or feline otitis
OTODECTES CYNOTIS?
-who does it infect?>
-what is seen with infxn?
-common parasite of cats and dogs, increased amts is when dz is seen
-cerumen forming heavy waxy and crusted exudates blocking auditory canal
-pruritis is severe!
What do Sarcoptic Mites feed on?
keratinocytes within outer layers of epidermis
Sarcoptic Mites create skin reactions that lead to...
-acanthosis (thickening of stratum spinosum) and
-Hyperkeratosis (thickening of stratum corneum)
-self trauma due to excessive grooming
SARCOPTES SCABIEI
-who it infects?
-what is seen with infxn?
-common for pigs in UK and dogs (can infect cattle, sheep,fox and humans)
-papules form and skin thickens
-immediate and delayed dermal hypersensitivity to feces
-vigorous grooming and self trauma
-secondary rash may occur
NOTOEDRES CATI
-host?
-what is seen with infxn?
-cats around head and ears
-pruritis is intense and leads to self trauma
-rare in uk
KNEMIDOCOPTES MUTANS
-host?
-poultry
-skin under scales of legs become inflammed leads to distortion and lameness
KNEMIDOCOPTES GALLINAE
-poultry
-infests skin at base of feathers leads to depluming itch
KNEMIDOCOPTES PILAE
-ornamental cage birds
-infests the skin of the cere, head, neck, wings and feet
-leads to scaly face
On examination how can you distinguish between mange mites?
Look at Pretarsi

Sarcoptes and Notoedres: long unsegmented pedicel (stalk)

Psoroptes:
pretarsus has a long 3 segmented pedicel
Describe body structure of Demodex?
tiny, wormlike mites with short, stubby legs
What Demodex species are found on the human face?
D.folliculorum and D.brevis
Demodex disease?
-where?
-what happens?
-commensal on mammal species normally found without dz
-infestations transfer from mom to offspring
-live in hair follicles
-remain external to epidermis
-infestations localized due to nodules incasing thousands of mites
-occasionally infestation becomes severe and cause dz
What is a danger of demodex (secondary)?
Immune deficiency
WHat host is infected by demodex?
-dogs
-cattle and goats (ruins hides)
TROMBICULA AUTUMNALIS?
-who
-when
-how
-cats, dogs and humans
-edinburgh = summer
-parasitic ONLY AS LARVAE
-small with six legs
-adult free living
-attach to host in passing (as with ticks)
-use stylostome
-cause intense pruritis
What is a stylostome?
salivary feeding tube that can be secreted
CHEYLETIELLIDAE
-infests cats, dogs and rabbits
-alot of dandruff produced
-C.blakei (cat fur mite) easily transferred to humans.
what distinct feature allows for recognition of cheyletiellidae?
big palpal claws, M-shaped gnathosomal peritremes and comblike tarsal appendages
What species of Cheyletiellidae is a risk to humans?
C.blakei easily transferred from cats to humans
What species are bloodsucking mesostigmatid mites that parasitize birds?
Dermanyssus Gallinae
Ornithonyssus sylviarum
D. Gallinae
-host infects?
-how does it infect?
-what is seen with infxn?
-red mite of poultry, infests poultry houses
-Mites are free living and crawl onto poultry and feed rapidly on blood
-Feeding site becomes inflamed and pruritic
-leads to loss of productivity
-can infect workers of poultry houses too
ORNITHONYSSUS SYLVARIUM
-host?
-northern fowl mite similar to D.gallinae YET remains on its poultry host
ORNITHONYSSUS BACTI
-infests rodents and can cause problems in animal houses
-also can infect cats due to hunting (short lived infxn)
What are DERMATOPHAGOIDES MITES? (Acarus and Glycophagus)
-house dust mites
-cause asthma in humans via inhalation of feces in fomites
NONE of allergy causing mites are parasitic it is the protein from the dust and dead bodies
LAMINOSIOPTES CYSTICOLA
-endoparasite of poultry
-forms nodules in lungs, peritoneum and abd.
-no clinical dz seen but carcass is downgraded
PNEUMONYSSUS AND CYTODITES
-respiratory mites
TRIXACARUS CAVIAE
-infects g.pigs
-sarcoptic type mite
-causes acanthosis and hyperkeratosis..and death
Scab and mandatory tx??
-had probs in past with failed attempt to eradicate sheep scab using pesticides
-now mandatory tx abandoned
-Private good now (farmer pays)
as opposed to public good (management by govt)
-incidence of scab increasing throughout UK
Important things to remember about P. Ovis?
-resevoir can exist on cattle
-fomites can exist infected for up to 2 weeks
-Mites reproduce very rapidly (10 day cycle) at all seasons!!
-Have limited powers of dispersal
How do Arthropods evade Immune Reactions of their hosts?*****************
-blood sucking arthropods: saliva=anesthetic (so not felt right away) also antigenic material in glue along with proteo
What is Malpighian tubules and who has them?
Excretory organs branch off from gut
-Larval insects
What kind of metamorphosis does Mites and Ticks have?
All Have Incomplete Metamorphosis
Mite development?
-Larval stage develops into a nymph
-usually several nymph stages
-Mostly all stages are parasitic
-All stages are found on host
(moulting, mating and egg production)
Tick development?
-Larva develops into the nymph stage
-ONLY ONE nymph which then develops into adult
-Each stage feeds on a different host
-When feeding is complete engorged tick falls off to moult
-egg laying also occurs on the ground
3-HOST Cycle
Arthropods as Vectors of Pathogens:
1. Mechanical Transmission
-flies with spongy mouthparts
-move from host to host
-no involvement of pathogens with the LC of the vector or development within the vector
2. Biological Transmission
-movement from gut to mouthparts of pathogen and then transferred from one vert host to another
What is moulting?
-in order to grow from egg to adult, arthropod must shed its exoskeleton and grown a new larger one
What is Anaplasmosis?
-caused by Boophilus tick (and biting flies)
-dz Anaplasma Marginale rickettsia
What is Babesiosis?
-Babesia protozoa transmitted by:
Boophilus
Rhipicephalus
Ixodes ticks
What is Cowdriosis?
Ehrlichia ruminantium rickettsia
transmitted by:
Amblyomma ticks
What is Ehrlichiosis?
Ehrlichia species transmitted by:
several ticks
What is Theileriosis?
Theileria protozoa transmitted by:
Rhipicecphalus +
Hyalomma ticks
What is Tick Toxicosis?
-Hyalomma ticks feeding on cattle, sheep and camels
What is Dermatophilosis?
-Amblyomma ticks cause immune suppression in cattle
-this facilitates sever skin diseases due to Dermatophilus congolensis bacteria
-Not due to transmitted pathogen
Life Cycle:
3-stages of Tick development?
Associated with feedings:
1.larva to nymph
2.nymph to adult
3. reproduction of adults
What is transstadial transmission?
-pathogen has to get from vert host to vert host via tick so: must get into feeding larva or nymph and survive until larva or nymph in next stage feed on vert host
What is transovarial transmission?
if pathogen passes from infected mother to eggs and then to larvae
-also called vertical transmission
What pathogen is related to transovarial transmission?.
Babesia
All tick borne pathogens are transmitted biologically? what does that mean ?
They have an essential developmental cycle to complete within the tissues of the tick
**Few can be transmitted without any development*
Are ticks hardy? survival?
Yes in between feedings can live up to year or more if nymph or adult
-pathogens live for a long time in tick and thus ticks are imp reservoirs of infxn
What is the common name of Ehrlichiosis?
Tick Borne Fever
What species is affected by Tick Borne Fever?
-sheep mainly but also cattle and deer
What is TBF caused by?
MAINLY: -rickettsia Ehrlichia phagocytophila

also:
-Anaplasma phagocytophilum
How is TBF transmitted?
Ixodes ricinus ticks
Signs of dz of TBF
-lambs: pyrexic 5 days and immunity suppressed
-Ewes that are naive may abort
-Rams that are naive may become infertile
What does E.phagocytophila do? (TBF)
-infects neuts and other white cells
-can remain in carrier state (low) for several yrs
-ticks are reservoirs for infxn (deer too)
When E.phagocytophila is inside the tick what happens? (TBF)
-infects immune cells and develops and replicates in salivary glands
-at time of tick feeding, it becomes an infective form in salivary gland
How long does the infective stage last for TBF inside the tick?
-lasts from one stage to another over one year
What species support tick production which thus allows TBF to spread?
sheep and deer on rough hill pastures or woodlands
-ticks require high humidity in leaf litter layer above soil
Control of TBF
making sure young NOT WEANED lambs are exposed to infection via ticks--> develop good immunity with few clinical signs
--thus lambs will be fully susceptible to infection but have good resistance to clinical ehrlichiosis
What is Enzootic Stability? (endemic stability)
stable high level of infxn with ensuing immunity but low levels of dz.
Ticks can feed all year but are more active in Springtime. What problems does this cause?
Lambing, naive lambs that become infected after weaning or
-Naive older stock very important due to infertility or abortion
How to prevent problems (TBF)?
-fencing to prevent sheep from getting into ticky areas
-also do not put naive adults onto ticky pasture
-NO VAX avail but tx with abx
What is another name for Canine Ehrlichiosis?
Tropical Canine Pancytopenia
k-9 Ehrl is caused by?
Ehrlichia canis
k-9 Ehrl is transmitted by?
Rhipicephalus sanguineus (dog tick)
What does K9 Ehrl dz cause?
-severe haemorrhage and can be fatal
-residual infections occur in dogs for years
Problematic areas for K9 Ehrl?
Quarantine kennels in UK
-lg number of dogs moving in and out without quarantine rules
What is another name for CANINE BABESIOSIS?
CANINE MALIGNANT JAUNDICE
What is k9 babes caused by?
-Babesia canis
-Babesia gibsoni
What is the vector / transmission route? (k9 bab)
-same as k9 ehrlic
Rhipicephalus sanguineus
also:
-Dermacentor marginatus
What does the infection of k9 bab cause?
haemolytic anemia
-infected erythrocytes clump in capillaries and cause brain strokes
-dual infection with E.canis and B.canis can occur
What results if a dual infxn of E.canis and B.canis?
E.canis: inhibits erythropoesis while
B.canis: clumps erythrocytes
Together the infxn is compounded
Therapeutic agent for k9 bab?
Imidocarb and a vaccine in france called "pirodog"
Risk of spread for k9 bab?
same as with k9 ehrl:
traveling dogs and quarantine kennels
Looping Ill infects what species?
Sheep mainly
but also cattle, pig, horse, dog, deer and grouse
Pathogen is looping ill virus. How is it transmitted?
Ixodes ricinus ticks
Transstadially
-no complex development in tick BUT the virus replicates in salivary glands
What is seen with looping ill dz?
Sheep: pyrexia for several days then virus invades CNS if immunity fails neuro probs and paralysis, sometimes death
Hoggs most susceptible
How long is tick infected with looping ill as a vector?
FOr life therefore is a reservoir of infection
Control of looping ill?
Immune suppression from TBF predisposes looping ill severity therefore control methods involve:
-endemic stability as with TBF
-along with colostrum from immune dams protects lambs (immunity is sterile therefore sheep aren't a reservoir)
-there is also a vaccine available
What is another name for Tick Pyaemia?
Cripples
What kind of dz is Tick Pyaemia?
tick associated dz.
-Ticks are not vectors of causative agent
What causes Tick Pyaemia?
-Bacterium Staphyloccus Aureus
How does Tick Pyaemia infect?
Staphy proliferates systemically when lambs are immunosuppressed by E. phagocytophila
-Heavy infestations of ticks --> suppresses immunity
What is seen with Tick pyaemia?
-infection becomes systemic
-abscesses occur in many internal organs
-main clinical signs are abscesses in joints and brain leading to "crippling"
How to control Tick Pyaemia?
Much connected to that of TBF. !!!!!
-PROBLEM: Sufficient tick to ensure endemic stability of TBF are likely to cause a higher incidence of pyaemia
THEREFORE: difficult to control both
Pyaemia is more serious economic loss to farmer
Thus concentrate on pyaemia by good management to reduce lambs to stress so not hurt by Ehrlichia induced immune suppression.
What is Endemic instability?
challenge of infection is low, thus there are many susceptible hosts in the population --> gives risk of an epidemic with many patent infections if there is sudden contact with a new source of infection
-opposite of endemic stability
What is premunity?
resistance to infection established after an acute infection has become chronic and which lasts as long as the pathogen remains in the host (babesiosis)
What is Carrier state?
infection with pathogen in a state where it is not patent or easily found but can still be transmitted back to vectors feeding on the host
What is a Reservoir host?
host with carrier infection may also be known as carrier host
What causes Borreliosis?
Spirochete bacterium Borrelia Burgdorferi
How is the bacterium for Borreliosis transmitted?
Ixodes ricinus larvae and nymphs that feed on mice, voles, squirrels and birds
What are the natural hosts of borreliosis?
What hosts aren't the natural hosts yet it can survive in?
natural hosts: mice, voles, squirrels, and birds

Can survive in and cause dz in: human, dogs, sheep
What is the common name for Borreliosis?
Lyme Disease
Control Options for Tick Borne Disease (8):
1. None - rely on endemic stability and host resistance
2. Acaricide tx intensly
3. Acaricide tx strategically
4. Stock and pasture management (hostile environment for ticks)
5. Breed for resistance (cattle)
6. Drugs to tx transmitted pathogens
7. Live parasite vaccines
8. Synthetic antigen vaccine against the pathogen or the tick.
Body Design of Lice
-no wings
-flattening dorso-ventrally
-strong claws and spines to hold onto host
Lice are in the order of...
Phthiraptera
Suborders of Lice
Anoplura (sucking lice)

Ischnocera and Amblycera (chewing lice)
Where do lice live? Host finding?
-ectoparasites
-spend whole life on host w/transfer to others via close contact
-Lice prefer rough, dark surfaces
Use of antennae? (lice)
-well developed antennae to locate feeding sites by warmth and smell.
Life cycle of lice
-develop from egg to larva through several nymphal stages to sexually mature adults
-All active stages look similar
-Only lasts around 2 weeks duration
What kind of metamorphosis do lice have?
incomplete metamorphosis
Lice feeding and reproduction?
-Feed in small meals
-Females continuously lay eggs 10/day
Which species of lice produce asexually?
Bovicola - by parthenogenesis

!!Great advantage -don't have to find mates in low density populations!
How do lice survive against host defences?
-strong legs with curved claws to move thru and grip tightly to the pelage (hard to groom out)
-eggs glued onto pelage of host and eggs are resistant to dessication or grooming
Are lice host specific?
Yes highly host specific.
-sessile ectoparasites --> specialized digestion and feeding on specific tissues.

!!ANother great advantage because it allows evolving saliva and feeding mechanisms so specific to evade host immune system!
LINOGNATHUS VITULI
-what type of feeder?
-host?
-Where on host?
-any identifiable features?
-Anoplura (sucking)
-cattle
-head, neck, dewlap
-long nose
BOVICOLA BOVIS
-type of feeder?
-host?
-where located?
-Ischnocera (chewing)
-cattle
-top of head, neck, shoulders, back and rump
HAEMATOPINUS EURYSTERNUS
-type of feeder?
-host?
-where located?
-identifiable features?
-Anoplura (sucking)
-cattle
-base of horns, ears, eyelids
-short nose
SOLENOPOTES CAPILLATUS
-type of feeder?
-host?
-where located?
-Anoplura (sucking)
-cattle
-head, neck and dewlap
-little blue louse
LINOGNATHUS OVILLUS
-Anoplura (sucking)
-sheep
-head, ears, and neck
Linognathus pedalis
-anoplura (sucking)
-sheep
-hind legs to crutch
-!!!Adapted to low temps and can survive on pasture for up to one week!!
Bovicola ovis
-Ischnocera
-sheep
-whole body
Haematopinus Asini
-Anoplura
-horse
-mane, base of tail, fetlock - will spread over whole body
Damalinia Equi
Same as Haematopinus asini except Ischnocera
Haematopinus suis
-Anoplura
ONly pig louse
What is pediculosis?
Lice infestation of cattle
Predisposition to dz of lice?
Winter housing, or Dense housing of sheep, cattle and pigs predisposes for dz and easy spread
Clinical signs of heavy infestations of lice?
-pruritis
-anaemia
-loss of BCS
-wool loss due to excessive grooming
-"white powder" look on hair (eggs)
-or if hair parted can be seen crawling if large enough
Hide damage due to lice infestations?
fleck and spot on cattle hides

-due to granuloma formation at site of delayed dermal hypersensitivity rxn to the antigenic saliva
Felicola subrostratus
-Ischnocera
-cat
-only cat louse
Linognathus setosus
-Anoplura
-dog
Trichodectes canis
-Ischnocera lice
-dog
-Intermediate host of the tapeworm of dogs (Dipylidium caninum)
Clinical signs of lice on dogs and cats:
pruritis that leads to restlessness and excessive grooming
-can be seen in hair
Lipeurus caponis
-Ischnocera
-birds
-base of wing and tail feathers
-"wing louse"
Cuclotogaster heterographus
-Ischnocera
-birds
-"head louse"
Menacanthus stramineus
Amblycera (chewing)
-chicken
-skin of breast, thigh and around anus
-"chicken body louse" or "yellow body louse"
Menopon gallinae
-Amblycera
-bird
-"shaft louse"
Clinical signs of lice in birds:
L.caponis and M.stramineus cause worst probs.
-blood drawn
-inflammation
-pruritis
-Loss of BCS
-restlessness
-depluming
What kind of metamorphosis do fleas have?
Complete
Host finding for fleas?
-live partly off host
-can remain in the host's nest or housing
-jump onto the host to feed
-once on host tend to remain there
Environments preferred by fleas:
-warmth, CO2, smell and movement of host -specific to adults
-most are not highly host specific
Reproduction and life cycle of fleas:
-Eggs layed continuously 10-15/day, drop into host housing
-larvae remain in nest and feed on organic debris and on dry droppings of adult fleas which contain bld
-fully developed larva becomes a pupa which metamorphoses into the adult
Survival against host defenses (fleas)
-very strong back legs for mobility
-rows of spines and strong leg claws to hold and move
-flattened shape permits rapid travel thru hair without being groomed out
Flea feeding:
feeding is rapid and small meals repeated to provide for small batches of eggs

!!Also rapid feeding avoids local hypersensitivity rxns in dermis!
Ctenocephalides
-common flea
-felis and canis but can also infest goat and sheep in tropics
-cat flea most common
Spilopsyllus cuniculi
-rabbit flea
-can be picked up by cats and dogs when hunting
-tranmits myxoma virus --> myxomatosis in rabbits
Ctenocephalies is an intermediate host for:
both felis and canis species harbor immature stages of:
Diplyidium caninum (tapeworm of cats and dogs)
-Flea larvae ingest the oncosphere stage of tapeworm and then fleas are ingested by cat or dog when grooming

RARE: B/C the pathogen manages to survive the insect during complete metamorphosis
Why are fleas not true vectors when it comes to D. caninum?
Transmission does not occur via the active feeding of the flea
Best way to control tapeworm?
is to control both the tapeworm but also the fleas and lice that transmit it
Clinical signs associated with fleas:
-mild pruritis
-restlessness to groom
-flea bite allergies can arise
Name two main types of chicken fleas
1. Ceratophyllus gallinae
2. Echidnophaga gallinae
Best control of lice and fleas:
-good hygiene on farm and domestically
-antipest cleaning
-pasture management
-good hygiene with indoor or intensive housing (most at risk)
Flies:
-Class?
-Order?
-Metamorphosis?
-Insecta
-Diptera
-Complete metamorphosis
Life Cycle and Reproduction of Flies?
-Eggs
-Larvae (legless maggots or in aquatic environment)
-3 or 4 larval stages
-pupal stage
-adult
Reproduction rate for flies?
-repro rate is high with repeated batches of eggs of several hundred per female
-Breeding is in a favourable season and may be several weeks only
-!!CAn exploit temporary resources if needed!! (r)
What is larviparous?
larvae develop one at a time within a female to produce fully mature larvae which are laid at sites where they immediately pupate
What flies are larviparous? What is the benefit to doing this?
TseTse Flies and Keds

-low repro rate but high survival rate (b/c larvae are protected inside adult)
-!!! these exploit stable resources!! (k)
Host Finding capabilities of flies?
-Complex antennae: highly adapted to searching for hosts by perceiving warmth, Co2 and smell

-Daytime feeders have eyesight capable of discriminating hosts after located via smell
What Flies are daytime feeders?
Horse flies
Tsetse flies
Survival Against host defenses (flies):
-adult blood feeding flies are rapid feeders
-active flying and accurate host flying allows for rapid feeds
What special charactoristic for defense does larvae of Myiasis flies have?
-provoke hypersensitive rxns in skin BUT have an impermeable cuticle to provide protection.
Musca autumnalis
-face fly
-doesn't attack skin
-feeds on secretions from eyes, nose and mouth
-CAUSES NUISANCE - can disrupt grazing and create fly syndrome in cattle
Hydrotaea
-head fly
-Feed at eye secretion and at wounds on heads of sheep
-capable of abrading skin to feed on serum and bld
Haematobia
-horn fly
-cattle
-spend all time as adults on and around cattle
-Mouthparts are piercing proboscis
-occur in large numbers on the backs of cattle
CAUSE NUISANCES
Tabanidae
(Tabanus, Haematopota, Chrysops)
-Large complex mouthparts
-Painful Bite during bld feeding
-Crude wound
-Not in high density in UK
-Persistant biting leads to lack of BCS/production
-Larvae occur in wet soil/mud
Melophagus Ovinus
-Sheep ked
-Fly adapted for ectoparasitic life
-No wings, so is mistaken for ticks
-Adult holds onto wool and feeds on bld
-Heavy infestations=loss of production
Culicoides
-biting midges
-Habitat = bogs (larvae breed)
-Painful feeding
-Sheep, cattle, horses
-common in NW scotland
Describe mouthparts of Culicoides
-complex like a miniature version of those of a tabanid
Culicoides reaction on horses:
Severe immediate hypersensitive reaction called: sweet itch
Stomoxys
-stable flies
-modified piercing skin and feeding on blood
Control of Nuisance and biting flies:
Partially achieved via:
pour-ons
sprays
ear tags
attractant/bait systems
What is myiasis?
infestation of live flesh of vertebrates with maggot larva of Diptera flies
-very severe form of parasitism
Types of myiasis:
Facultative - maggots can survive on carrion

Obligate - parasitically adapted that fly has to infest correct species of live host at the correct site on host
Lucilia
-blowflies
-facultative myiasis (blowfly strike)
-attracted to protein food sources for egg laying
(carcasses, bld on wounds, soiled wool)
-Maggots hatch at such sites and invade existing wounds via: 1. lacerating mouthparts on existing wounds or 2. proteolytic enzymes in saliva
Results in: toxemia from ammonia and bacterial septicemia in combination leads to death
Which Lucilia is the main problem in the UK?
Lucilia sericata
Lucilia cuprina
"greenbottle flies"

-warm summers allow higher populations to build up
-Hypoderma bovis
-Hypoderma lineatum
-Warbles
-Obligate Myiasis
-Eggs laid on legs of cattle
-Larvae hatch and invade the host via hair follicles
-Larvae burrow thru muscle and viscera and end up as mature larvae along the back
-Emerge as larva, drop off and pupate

-Cattle recognize and panic when see adult flies and injure themselves
-Gasterophilus
-Oestrus ovis
-stomach bot of horses
-nasal bot of sheep
Factors favouring eradication of warble fly in 1970's
-fly has repro strategy of low production with high survival (get rid of low production may rid of all that survives)
-only one life cycle per year
-summer distinct season of adult activity
-larvae only occur on cattle No wild reservoir hosts
-cattle unable to escape attention of farmer
-Adults have limited dispersal capacity
Tx of warbles
ivermectin main tx now
-attempt at 5 year eradication scheme but failed
Name the vector:
1. African Horse Sickness (virus)
2. Bluetongue (virus)
3. Equine Encephalitis viruses
1. Culicoides (fly)
2. Culicoides
3. Mosquitos
What flies are vectors?
-Adults and usually females (females take repeated bld meals to support production of eggs)
Transmission of pathogen using flies as vectors require:
INTRA-STADIAL TRANSMISSION
pathogen must get into the vector at one bld meal then back to its mammal host at one of the next few meals within a few weeks.
(flies)IF the transmission is mechanical then...
it is rapid without development in vector
(flies)Extrinsic incubation period of the pathogen
if pathogen has a biological development in the vector then this must be fitted into the short period of feeding activity.
(flies)Intrinsic incubation period of the pathogen
time in the mammalian host from initial infection to a patent state of disease
(flies)If transmission is biological then...
biological route has to fit the egg laying and feeding cycle of the vector
Explain gonotrophic cylce of mosiquitos and Culicoides midges:
-take one large bld meal then rest and develop eggs
-After eggs are laid, female takes another meal
-cycle repeats 5-10 times
-Each feed after the first is an opportunity for the pathogen to be transmitted
Flies as vectors vs. Ticks as Vectors...
-Pathogens getting into ticks have only 1-2 opportunities of onward transmission at the future feedings (via transtadial rte)
-Yet can remain in the vector from months to years between bld meals
-With transovarial transmission (babesia) ticks can remain infected for several generations starting from one initial infection
Flies as vectors vs ticks as vectors continued....
-tick vectors can act as long term reservoirs
-Fly vectors cannot (pathogen must survive a carrier state infection in mammal hosts)
Flies as vectors...
-Fly populations are seasonal except in tropics where they feed all the time (this is why more fly borne diseases in tropics)
-Although climate warming may allow spread to temperate regions
Feeding mechanisms of flies that aids in them acting as vectors:
1. Musca flies and blowflies (Calliphora) have spongy mouthparts on which bacteria are transmitted mechanically (Moraxella bovis)
2. Tabanid flies - have complex cutting to produce bld flow which is taken up by sponge mouthparts and thus transmission of pathogens such as Trypanosoma evansi is transmitted mechanically
3. Mosqitoes have fine piercing mouthparts that transmit Dirofilaria immitis nematodes via saliva.
How is Keratoconjunctivitis Transmitted?
bacterium Moraxella bovis is transmitted by: Musca species and Hydrotaea
How: feed on lachrymal secretions at the eyes of cattle
How is Mastitis Transmitted?
Bacterium Corynebacterium pyogenes transmitted by: Htydrotaea

or Streptococcus species transmitted by: Musca species
Bluetongue Virus
-cattle (reservoir host, show little dz) and sheep (show dz)
-Culicoides
-warmer weather may influence midges
-vaccine avail
Rift Valley Fever


African Horse Sickness and Bluetongue (horses)
-Mosquitos


-Culicoides
-common in tropics with warmer weather may move
-vaccine avail
Leishmaniasis
-Leishmania species of protozoa transmitted to dogs by: Phlebotomus species of sandflys
-ingested by sandfly
-develop in fly gut to proliferateve promastigote forms which invade esophagus and mouthparts directly
-these are the infective forms for dogs
Transmitted by:
1. West Nile Virus
2.Trypanosomiasis (protozoa)
3. Leismaniasis (protozoa)
1. Anopheles (mosqito)
2. Glossina (tsetse flies in Africa) or Tabanids and Stomoxys in Africa, s.america or S.E.asia
3.Phlebotomus sandflies
Internal Parasites have one or more non-parasitic stages in their Life Cycle. These can be either:
1. dormant stages
2. free living
Economic impact of internal parasitism:
-reduced productivity due to subclinical infections
-Reduced productivity due to clinical dz
-cost of tx or prevention
-death of animals and loss of capital investment
Host specificity of internal parasites:
Most are HIGHLY host specific - limiting themselves to a single host genus or species and often within a particular site
Internal parasites that can infect a wide range of hosts and are not highly host specific:
Toxoplasmosa and Cyrptosporidium
2 Types of Parasitic lifecycles for internal parasites:
1. Direct/Monoxenous
2. Indirect/Heteroxenous
What is Direct/Monoxenous Life cycle?
LC is completed in an individual of a single host species
-Infective stage is non parasitic and environmentally resistant form
What is Indirect/Heterxenous Life Cycle?
Needs to infect two or more different types of hosts to complete life cycle
-Hosts are usually taxonomically unrelated (ie carnivore/herbivore or vert/invertebrate)
-Often has distinct phases of development in each host type
Definitive/Final host
one host in a direct lifecycle
or
host in which sexual reproduction takes place in indirect life cycle
Intermediate host
host in an indirect life cycle where any reproduction is entirely asexual
Vector
Arthropod that transmits a parasite between vertebrate hosts
Transport host
-NOT essential part of life cycle
-organisms such as flies or earthworms which take up parasite without any parasitic developement in host
Paratenic host
-NOT essential for life cycle
-as in transport host but limited parasite development (ie migration in host tissues)
Disease Host
the host in which the disease is seen
How to internal parasites get into host?
1. Mouth- mainly ingested (food or drink)
2. Skin (either direct skin penetration or indirect via blood sucking arthropod vector)
3. Iatrogenic -contaminated needles
4. Repro tract - coitus
5. Transplacental
6. Transmammary
Strategies of Internal parasites for dealing with Hosts Immune response:
1. inhabitating lumen of hollow organs
2. camo by mimicking host antigens
3. Changing antigens at diff stages in development
4. inhibiting parts of host immune system
5. rapid repro b4 immune response becomes effective
Internal Parasites:
Methods of feeding (4)
1 Passive absorption thru outer surface
2. Browsing on gut contents
3.Tissue feeders
4. blood feeders
Two types of reproduction seen in internal parasites:
1. Asexual
2. Sexual
Asexual reproduction
used to increase # of individual parasites within the host
(binary fission, shizogony)
Sexual Reproduction
repro using mating types, separately sexed individuals (dioecious) or doubly sexed individuals (monoecious)
Environmental Control of Internal parasites (4)
-stocking densities (high =bad)
- Pasture management
-Transport stress leads to egg output
-Selective breeding/genetic manipulation
Protozoa
-unicellular organisms
4 Main groups of Protozoa
1. Rhizopods
2. Ciliates
3. Flagellates
4. Sporozoan Protozoa
Parasitic Rhizopods:
-where do they feed
-Life cycle
-Location within host
-Reproduction
-"amoeba like"
-move via pseudopodia
-Extracellular
-feed via phagocytosis
-Cycle between Trophozoite and cyst forms
-Predominantly asexually
-Direct Life cycles
Parasitic Ciliates
-How do they move
-Where do they feed
-Location within host
-Reproduction
-Life cycle
-Move using cilia
-Extracellular
-Feed on particulate matter using cytosome
-Cycle between trophozoite and cyst form
-Asexual via binary fission and sexual via conjugation
-Direct Life cycles
Parasitic Flagellates
-how do they move
-how do they feed
- Reproduction
-Life cycle
-Move using flagellae
-Feed by uptake of soluble nutrients thru cell membrane or flagellar pocket
-Cycle between trophozoite and cyst forms (some exist solely as trophozoites)
-Asexual reproduction
-Most are extracellular with a few intracellular species (living in Macrophages)
-Extracellular species have direct life cycles
-Intracellular species transmitted being vector borne
Sporozoan Protozoa
-where are they located
-Reproduction
-Life cycles
-Intracellular
-Distinct phases of asexual and sexual repro
-Gives rise to many morphologically distinct forms
-Asexual repro - schizogony
-Sexual repro -fusion of dissimilar gametes --> gives rise to environmentally resistant oocysts
-Either Direct or Indirect Life cycles
Coccidia
Sporozoan Protozoa subgroup
-Intracellular gut phase with both sexual and asexual repro --> oocyst
-Direct or Indirect Life Cycles
Coccidia with direct life cycles:
infect gut cells of single host
Coccidia with Indirect Life cycles:
-Cycle between two host types
-Often based on prey - predator relationships
-Sexual or asexual repro takes place in def host (carnivore)
-Gives rise to oocysts
-In the I. Host only asexual repro takes place
-Gives rise to tissue cysts which lie dormant within soft tissue (muscle) until eaten by def host
Haemosporozoan Protozoa
-Intracellular bld protozoa infecting either erythrocytes or lymphocytes
-Transmitted by arthropods (ticks or insects)
What is an oocyst?
-spore phase of certain protists, such as Cryptosporidium and Toxoplasma.
- can survive for lengthy periods outside a host and is very resistant.
What is a cyst?
-a closed sac having a distinct membrane and develosion on the nearby tissue.
What is schizogony?
Reproduction by multiple asexual fission
-multiple nuclear divisions inside an infected cell
-cell division which each part turns into an indiv parasite
-merozites emerge - break out of infected cell to go attack other cells
What Internal Parsites live in:
1. Brain
2. Lungs
3. Blood
1. Toxo, Tapeworm Larvae
2. Lungworm, Tapeworm Larvae
3. Babesia
What internal parasite lives in:
1. Muscle
2. Small Intestine
3. Large Intestine
1. Toxo, Protozoan cysts, Tapeworm larvae,
2. Nematodes, Adult Tapeworms
3. Nematodes, coccidia
What internal parasites live in:
1. Abomasum
2. Liver
3. Foetus
1. Nematodes
2. Liver Flukes (trematodes)
3. Toxoplasma
Why are Protozoa with Direct Life Cycles Important?
1. Infections often lead to death of host
2. Infections lead to decreased productivity and welfare
3. Controlling them costs money and can lead to consumer resistance
4. Some are zoonotic
Where do protozoa with direct life cycles complete their life cycle?
complete life cycle in a single host
What is their feeding and reproduction schedule?
-they usually alternate between feeding (trophozoite) and repro stages (cysts and oocysts - environmentally resistant).
What is a trophozoite?
the activated, feeding stage in the life cycle of protozoan parasites
What body systems are protozoa with direct life cycles associated with? (majority)
Body systems that have access to outside such as the gut and the repro tract
Where are protozoa with direct life cycles found within host?
Extracellular in lumen of hollow organs usually motile with cilia or flagella (gut, vagina, uterus)
-CAN be located inside host cells but the extracellular stages are used for infection
Describe Extracellular Monoxenous Protozoa
-large, motile protozoa
-DLC -direct life cycle !!
-cyucle btween parasitic trophozoite and non parasitic forms (cysts)
-Infect digestive or repro tract
Entamaoeba
-What is it?
-Host affected?
-cycle summary
-Extracellular gut protozoa (DLC)
-Rhizopod parasite
-Dogs
-Trophozoite forms in gut, cysts pass out in feces to infect other dogs
Balantidium
-What is it?
-Host affected?
-cycle summary
-Extracellular gut protozoa (DLC)
-Ciliate protozoa
-Pigs but also humans
-Trophozoite forms in gut and cysts pass out in feces.
!! ONly causes dz if present in very large numbers
Giardia
-What is it?
-Host affected?
-cycle summary
-Extracellular Gut protozoa (DLC)
-Flagellate protozoa
-Young dogs and cats
-Trophozoite forms in gut and cysts pass out in feces
!!Easily dispersed by water "beaver fever"
Trichomonas
-What is it?
-Host affected?
-cycle summary
-Extracellular Gut protozoa (DLC)
-Flagellate
-Birds (esp game birds and pigeons)
-Two forms: esophageal or intestinal
-No cyst forms
-Contamination due to water supplies normally
Histomonas
-What is it?
-Host affected?
-cycle summary
-Extracellular gut protozoa (DLC)
-Flagellate
-Turkeys and game birds
-"blackhead"
-Flagellate form found in gut, amoeboid form in liver, no cyst form
-Transmitted via the eggs of the common Nematode: Heterakis Gallinarium
-Causes ulceration and necrosis of cecal mucosa and liver
Trichomonas foetus
-What is it?
-Host affected?
-Where in host affected?
-control
-Extracellular protozoa that affects Repro system
-Flagellate
-Lives in vagina and prepuce, can migrate to uterus and cause abortion
-Cattle
-Control via restricted breeding/AI
Trypanosoma equiperdum
-What is it?
-Host affected?
-Result of infection?
-Control
-Extracellular protozoa affecting Repro system (DLC)
-Flagellate
-related to pathogen: Vector borne Trypanosomes
-Causes VTD dourine in horses and donkey
-Results in infertility
-ONLY UK protozoan parasite with statutory testing regime
-control via control breeding
What are the most important Intracellular Monoxenous protozoa (gut dwelling)?
Coccidia
Name some features of coccidia:
-Very sm! intracellular!
-Principally found in Digestive tract
-Pass thru sporozoites, merozoites, gametes, and oocyts
How do coccidia get into host?
-Infective form (oocysts) picked up from environment
-Enter host cell by invagination of host cell membrane so that parasite is separated from the host cell cytoplasm by a parasitophorous vacuole
Describe the reproduction stages of coccidia:
-Distinct, sequential phases of asexual followed by sexual reproduction -- this results in oocyst formation
-Multiply using mutiple nuclear division to increase their numbers very rapidly at several stages in the life cycle (shizogony)
What is a sporozoite?
-cells that infect new hosts
-sporozoites eventually burst, releasing merozoites into the bloodstream.
What is merozoite?
-->a daughter cell of a protozoan parasite.
-Merozoites are the result of asexual reproduction (schizogony, merogony).
- In coccidiosis, merozoites form the first phase of the internal life cycle of coccidian.
Life cycle of Coccidia
-Direct life cycle
1. Oocyst shed in feces
2. Unsporulated oocyst = non infectious
3. Over several days and requiring oxygen = Sporulation takes place
4. Result is sporulated oocyst that is infectious
5. oocyst is swallowed and enters gut
6. Excystation - oocyst releases sporocysts
7. Sporocysts release sporozoites
8. Sporozoites invade gut cells
9. Trophozoite
10. Schizont
11. Merozoites are released from Schizont
12. Male and Female Gametes now rise from Merozoite
13. Create Developing oocyst that will be shed in feces
Eimeria sp.
-What is it?
-host infected?
-Host specific?
-Principal cause of Coccidiosis
- Poultry and Farmed rabbits, but seasonally affects lamb and cattle
-Highly host/site specific
-Sporulated oocyst contains four sporocysts each containing 2 sporozoites: 8 sporozoites/sporulated oocyst
Eimeria sp. and Poultry
-# of species
-control
-17 species can infect poultry
-control via good hygiene to prevent build up of infective oocysts (medicated feeds, vaccines, etc)
Caecal Coccidiosis in poultry is caused by:
Eimeria tenella
Intestinal coccidiosis in poultry is caused by:
E. necatrix
E. brunetti
E. mitis
E. maxima
E. acervulina
These 3 species cause what dz?
-E. ovoinoidales
-E. bakuensis
-E.Crandallis
-Ovine coccidiosis
-unweaned lambs 4-8wks old
-Affect small intestine
-Lambs become infected by oocysts passed by chronically infected adults and go on to shed more oocysts rapidly
These 2 species cause what dz?
-E. zuernii
-E. bovis
-Bovine coccidiosis
-cattle less than one year old
-infect the cecum and colon
These 3 species cause what dz?
-E. stiedae (bile duct)
-E. flavescence (intestine)
-E. intestinalis (intestine)
-Rabbit coccidiosis
-wild rabbits can act as a reservoir for farmed rabbits
What is Isospora sp?
-Form of coccida with direct life cycle
-usually non pathogenic but high levels may give rise to diarrhea
-OOCYSTS might be confused with other protozoa such as TOXOPLASMA
What is the main difference between Eimeria and Isospora?
-Isospora
Oocyst - 2 Sporocyst - 4 sporozoites

-Eimeria
Oocyst - 4 sporocysts - 2 sporozoites

(opposite)
What are the hosts infected with Isospora?
Mainly dogs, cats and pigs:
Dogs
I. canis and I. ohioensis
Cats
I. felis and I. rivolta
Pigs
I.suis
What is cryptosporidium?
-Coccidia with direct life cycle
-Pathogen of young animals (calves) also zoonotic
- Fecal contamination of meat
-Dangerous for immunosuppressed patients
Infection route of cryptosporidium?
-Parasite develops at jxn between BB and cytoplasm gut epithelium cells
-Produces small sporulated oocysts (immediately infective) which then...
a). initiate another cycle of asexual reproduction in the same host or
b). are shed from the body via feces.
Why are protozoa with Heteroxenous Life Cycles important?
-cause abortion in sheep,cattle and humans
-cause fetal abn in humans
-cause neuro dz in dogs and horses
-cause of meat condemnation in abbatoirs
General features of protozoa with indirect life cycles:
-all belong to group of coccidia
-intracellular w/in parasitophorous vacuole
-Alternate cycles of sexual and asexual repro with oocyst formation
-Final and I. host
-Life cycle based on predator (final host): prey (I. host)
What development takes place in the Final host involving protozoa with indirect life cycles (coccidia):
-Limited to gut producing oocysts that infect the intermediate host
What development takes place in the intermediate host involveing protozoa with indirect life cycles (coccidia):
-Initially in gut followed by extensive tissue migration of tachyzoites
-Finally resulting in tissue cysts containing bradyzoites which are the infective form for final host.
What is tachyzoite?
an asexual stage of rapid growth
Sarcocystis
-What is it?
-Hosts?
-Protozoa with Indirect LC
-Highly host specific host pairings
-dog: sheep-->S.bovicanis and
S.cruzi

-cat:sheep--> S.ovifelis and S.tenella

-Cattle:human-->S.bovihominis
Life Cycle of Sarcocystis?
-Final host: passes oocysts in feces
-I.Host: ingests oocysts
-Sporozoites hatch out
-Invade endothelial cells of capillaries of gut
-Asexual repro in gut endothelium
-Parasite then enters lymphocytes in bldstream
-carried to soft muscle sites and penetrate muscle
-Tachyzoites take place
-Sarcocysts form and fill with many slow growing bradyzoites
-Final Host ingests I.Host
-Bradyzoites are then released into gut of final host
-invade sub-epithelial cells
-differentiate into gametes
-sexual repro and fertilization
-give rise to thin walled oocysts
-Passed out in feces
-Oocysts are passed sporulated therefore are immediately infective
-contain 2 sporocysts each with 4 sporozoites
What clinical signs are seen in Final host with Sarcosystis?
-Signs rarely seen
-Occasional mild diarhea
What clinical signs are seen in I. Host with Sarcosystis?
sheep and cattle:
-condemnation of meat
-Anorexia
-Fever
-Anemia
-Wt loss, hair loss, BCS loss

Horse:
-Equine protozoal myeloencephalitis (neuro prob)
-caused by S. neruona
-horses ingest oocysts but are dead end hosts
What is the major species of Toxoplasma of vet imp?
T. gondii
What is dangerous about T. gondii?
-Intracellular but has the ability to develop in most cell types
Who is the host for T. gondii?
Final host: Cat
I. Host: mouse

**However can infect wide range of dead end hosts (including humans)
What is different about the life cycle of T. gondii?
Can be completed in the final host with absence of I. host
-Bradyzoites can develop in either final or i.host
-Both final and I. host can become infected by ingestion of tissue cysts and oocysts.
Describe the "natural" cat and mouse cycle of T. gondii?
-Infected cat pass oocysts in feces
-mice ingest oocysts
-sporozoites invade gut macrophage cells
-multiply and give rise to tachyzoites
-they invade other macrophages or are carried to other sites via blood and lymph
-eventually form bradyzoite cysts which remain in tissues until ingested by cat
-once mouse ingested, multiplies in gut wall
-gives rise to oocysts in 3-10 days
-oocysts passed unsporulated
-in 24 hrs: 2 sporocysts contain 4 sporozoites

**cats can also become infected by eating other cats or ingesting oocysts**
What is the strange behavior associated with T.gondii?
Bradyzoite cysts remain in mouse until ingested, may move to brain where they affect natural "cat avoidance" behavior
--> this increases a parasites chance of transmission
How do un-natural hosts become infected with T.gondii?
-ingest oocysts or bradyzoite cysts accidentally
What are risks if food animals ingest oocysts of T. gondii?
-bradyzoite cyst formation in muscles - danger if uncooked and eaten (humans)

-ingestion of oocysts and bradyzoite cysts by non feline carnivores (humans, dogs) can also lead to tissue migration and cause:

-abortion, fetal damage, visual disturbances, neurological symptoms
What is seen when T.gondii is found in the definitive host? (cats)
-most infections pass unnoticed
-fatalaties rare, usually involves infection of CNS, liver, lungs etc
-wt loss, fever, uveitis, anorexia, seizures, ataxia
-Transplacentally infected kittens usually die
How can sheep become infected with T.gondii?
-ingesting oocysts from pasture or feed contaminated with cat feces
What clinical signs are seen in sheep infected with T.gondii?
-If infected during early stages of pregnancy - abort
-Outcome depends on stage of pregnancy when infection aquired
-Abortion only associated with tachyzoite stage
-VAccine avail but is live so poses risk to vaccinator
How do humans become infected with T.gondii?
-ingesting oocysts from cat feces (cleaning, gardening, litter pan etc)
WHo is at the highest risk for T.gondii (humans?)
-early stage pregnancy
-immuno suppressed individuals (aids, transplant)
Neospora Caninum
-Hosts?
-Morphologically similiar to...
-Definitive host: dog
-Intermediate host: herbivores
-Morphologically similar to T.gondii
-Causes abortion and neonatal death in cattle, sheep, goats, and horses
-paralysis in puppies
What are Vector borne protozoa?
transmitted by one vertebrate host to another by an ARTHROPOD (vector)
Vectors are....
Blood sucking arthropods : TICKS AND FLIES
What are Haemoprotozoa?
-vector borne protozoa that have forms that develop in the blood of the vertebrate host at some point
What Reproduction cycle takes place where in vector borne protozoa?
-Asexual repro in both vert host and vector
-Sexual repro only takes place in vector
What is Cyclical or Biological Transmission?
-parasite must undergo a period of developement within the vector before it can be passed on to another host

--> this means that most vector: parasite relationships are highly specific
-Allows a good control point!
What is NON cyclical or Mechanical Transmission?
-some vbp can also be transmitted directly between hosts without any development in vector
What does it mean by Iatrogenically transmitted?
-transmission through use of contaminated needles
(mass vaccination or blood transfusion)
Babesia sp
-what are they?
-transmission by?
-main hosts?
-vbp - Intra-erythrocytic
-transmitted by Ixodidae
-highly host specific
-Mainly cattle in UK, but also sheep, goats, deer and dogs
(cattle forms can infect immunosuppressed humans)
Trypanosomes sp
-what are they?
-transmission by?
-main hosts?
-vbp - extracellular haemoflagellates
-Transmitted by: Tabanids and Sheep keds (biting flies)
-cattle and sheep (maj dz prob in tropics)
-in UK trympanosomes = nonpathogenic
Malaria sp
-What are they?
-transmission by?
-Main hosts?
-vbp - intra-erythrocytic
- transmitted by biting flies
-Affect wild and captive birds
Leishmania sp
-What are they?
-Transmitted by?
-Main hosts?
-vbp intracellular
-transmitted by sandflies
-dogs (not endemic in UK)
Name two species of Babesia that affect cattle in UK:
-transmitted by?
1. B.divergens
- "small" species
-mainly found on edge of rbc
-most pathogenic in UK
-Transmitted by Ixodes ricinus

2. B. major
-"large" species
-seen inside rbc "paired"
-transmitted by: Haemaphysalis punctata (tick)
Transmission of B.divergens is mainly dependant upon...
Where the vector Ixodes ricinus is located
Principal problems facing B. divergens in the UK (3):
1. tick can take up to 3 years to complete life cycle
2. each stage in life cycle feeds only once
3. ticks often inactive for long periods (winter)
What strategies have B. divergens evolved to in order to maximize its potentinal for transmission? (3)
1. Parasite repro synchronized to feeding behavior of tick

2. ability to be transmitted to a vertebrate host by each stage in the tick life cycle

3. ability to be passed between sequential stages in the tick life cycle without encountering another infected host.
Principal features of Helminths?
-multicellular
-multi organ
-endoparasites
-all reproduce sexually via eggs
-have a range of morphologically distinct larval stages
Name the three main groups of Helminths:
1.Platyhelminths (flatworms)
2.Nemathelminths (roundworms)
3.Acanthocephala (thorny or spiny headed worms)
Name two classes of Platyhelminths:
1. Trematodes
2. Cestodes
Trematodes
-body shape?
-life cycle/hosts?
-unsegmented, leaf like
-one or two suckers for attachment to host
-simple blind gut with single opening

-Direct OR indirect life cycles
-I. Host = invertebrates (mollusc)
Cestodes
-body shape?
-life cycle/hosts?
-segmented
-tape like
-can be up to several meters long
-distinct head (scolex) with hooks and suckers for attachment to host
-Gut is absent
-Nutrients via diffusion

-Indirect life cycles
-Vert or Invert can be I.host
Name the class of interest in the Nemathelminthes?
Nematodes
Nematodes
-body shape?
-life cycle/ hosts?
-cylindrical, tapering from either end
-shape maintained by fluid filled cavity
-true gut with mouth and anus
-Individuals are either MALE OR FEMALE

DIRECT OR INDIRECT LIFE CYCLES
-Invert hosts = I. host

**paratenic hosts and transport hosts imp!!
What is the prominent feature of Acanthocephala?
-spiny proboscis aka thorny or spiny head worms
-very few of vet importance!
Where do helminths live?
-can be found in most body systems of vertebrates either as adults or larvae
-some move around the body (migration)
before they find the final position and start reproduction (predilection site)
Why are helminths important?
1. production losses due to
-competition for nutrients
-damage to body systems
-death

2. Animal welfare
-companion animals
-food animals

3. Public health (zoonosis)
Helminth rate of reproduction?
large amounts of eggs (several million per day)
-all sexual reproduction but some can also carry out asexual repro and at cost to host!
Forms of Helminths: (sexual maturity)
1. larvae
2. Adult
1. sexually immature
2. sexually mature
Monoecious
male and female sex organs develop in SAME individual
-usually at different times and not self fertilizing
Dioecious
-male and female sex organs are found in seperate individuals
Definitive Host
host where adult sexually active forms are found
-found in direct or indirect life cycles
Intermediate Host
host where only immature (larval) forms are found
-essential part of indirect life cycle
Transport host
- host takes up an immature form but does not retain it
- no parasite development takes place in host
-NOT essential part of parasites life cycle
Paratenic host
-host takes up an immature form and retains it in its tissue
-no parasite development other than larval emergence from an egg
-NOT an essential part of parasite life cycle
Another name for a trematode?
fluke
What are monogean trematodes?
-Direct life cycles
-Ectoparasites of fish
What are digenean trematodes?
-Indirect life cycles
-Endoparasites of vet importance
Where are adult flukes found?
-Final (vert)host
Where are larval stages of flukes found?
-can be free living or parasitic within an I. Host
How many intermediate hosts can flukes have and what are the requirements?
-can have more than one intermediate host in life cycle
-BUT one MUST BE A MOLLUSC
What is a miracidium?
-Produced by adult flukes
-Infectious form to intermediate (first) host
-Develops from egg
What is the simplified life cycle of flukes?
-Adult produces egg
-Egg develops into miracidium
-Miracidium infects first I.host
-Inside the snail, the miracidium develops into a sporocyst
-Sporocyst gives rise to a number of redia
-Redia give rise to a number of cercaria
-Cercaria eventually develop into metacercaria forms which are infective for final host
Define the following terms:
1. redia
2. cercaria
3. metacercaria
All developmental stages in Trematodes
1. produces either more rediae, or cercariae
2. This is somewhat like a small adult, but has a large swimming tail somewhat like a tadpole's (but without a notochord or backbone, as it is not a chordate). It finds and settles in a host, and becomes an adult, or a mesocercaria, or a metacercaria, according to species.
3. A cercaria encysted and resting.
What stages of Trematode development are found in all species?
Miracidium and Cercarial Stages
Fasicola Hepatica
-What is it?
-Host?
-Life cycle?
-liver fluke
-ruminants (sheep and goats but also cattle, horses and humans)
-Digenean: with miracidium, sporocyst, redia, cercaria and metacercaria
-Single I. Host : Water snail (Lymnaea truncatula)
Effect of F. Hapatica on definitive host:
a) Acute Fasciolosis
1. Acute Fasciolosis
-assoc with migration of lg #'s of immature flukes thru liver as a result of ingesting lg #'s of metacercaria.
-Mass migration causes severe damage to the liver paranchyma and can result in death within 1-2 weeks of infection
Effect of F. Hapatica on definitive host:
b) Sub Acute Fasciolosis
2. Sub Acute Fasciolosis
-assoc w/the ingestions of smaller #'s of metacercaria over a longer period
-appears about 6-10 weeks after ingestion
-Dz damages liver and bile duct
Effect of F. Hapatica on definitive host:
c) Chronic Fasciolosis
3. Chronic Fasciolosis
-most common
-assoc w/ accum of lg #'s of adult liver flukes in bile duct resulting from ingestion of moderate amounts of metacercaria over a period of time.
- Appears several months after initial exposure and leads to general loss of condition, anemia, submandibular oedema (bottle jaw)
What Factors determine epidemiology of F. hepatica?
Mainly based on availability of viable metacercaria on the pasture.

Influenced by:
-Presence of suitable snail habitats - wet mud, temperate, poorly drained pastures, ditches
-Temperature - excess of 10 degrees for snail manipulation and parasite development (if below 5 then snail activity ceases and fluke eggs fail to hatch)
-Moisture - high levels required
When are favourable conditions for F. hepatica found in UK?
May to October
When are large amounts of metacercaria likely to be present on pasture in the UK?
1. Metacercaria from snails infected in Summer will appear on pasture from Aug to Oct
-->these will come from snails which became infected w/miracidia from eggs passed onto pasture during spring/summer or overwintered eggs

2. Metacercaria from snails infected during the winter - appear on pasture between may and June
-->come from snails infected with miracidia from eggs passed previous autumn and have been overwintered by snail.
What is a major factor when predicting F. hepatica outbreaks?
Climate control/Rainfall seasons
How can we control F. Hepatica infection?
1. drug tx - use to reduce pasture contamination by fluke eggs or reduce effect of fluke population on host
**Check effectiveness of anthelmintic against immature vs adult stages**

2. Reduce snail populations - drain wet pasture and/or apply molluscicides
Dicrocoelium dendriticum
-What is it?
-small lancet liver fluke
-internal organs can be seen thru semi-transparent body
-Indirect life cycle with ant and mollusc as I. host and Def host is ruminant
How does Dicrocoelium differ from F. hepatica?
MIGRATION:
1a. Dicro doesn't migrate thru the liver paranchyma - Both adults and immature forms found in bild ducts.
vs.
1b. F.hepatica immature flukes migrate thru liver, Adults get in bile duct

CLINICAL SIGNS
2a. Dicro - rarely any clinical signs seen due to lack of cuticular spines
vs.
2b. Fasciolosis (sub, acute, chronic)

INTERMEDIATE HOST
3a. Dicro has 2 - Ant and mollosc = thus limiting parasites distribution to where both can be found
vs.
3b. JUST MOLLUSC for hepatica

EGGS and ENVIRONMENT
4a. Dicro adapted for transmission in dry areas:
Miracidium stage stays in egg, and Cercaria is protected in slime ball
vs.
4b. Hepatica: miracidium ciliated and swims to snail foot ... needs moisture

STAGES
5a. Dicro has no redia stage. It has two sporocyst generations instead in the snail
vs.
5b. one sporocyst and one redia stage in hepatic

HOST BEHAVIOR
6a. Dicro metacercaria develop in brain of ant and affect behavior enhancing transmission to final host
vs.
6b. Hepatic - no alternated behavior of host
Schistosomes
-What is it?
-Where in host is affected?
-Main host
-I. Host?
-Where are they found (location)?
-How do cercaria enter final host?
-Liver fluke
-Found in bld vessels of gut or bladder
-Ruminants
-Separte males and females
-I.Host = water snails
-Cercaria enter final host via the skin
-Imp in tropics and subtropics
Paramphistomes
-What is it?
-Where found in host?
-Main host?
-I.host?
-Body shape?
-Life cycle?
-liver flukes
-forestomachs
-ruminants (some pigs and horses)
-Conical shape rather than flattened
-I.Host = water snail
-Life cycle similar to F. hepatica
What is another name for Cestodes?
Tapeworms
Where is the adult cestode found?
-entire life within gut of host (final host)
-Devoted purely to egg making
-Eggs are voided with feces to environment (thick protective wall)
What is the life cycle of Cestodes?
INDIRECT CYCLE
-eggs in feces in environment
-ingested by I.host (herbivores/invertebrates)
-Herbivores are eaten by carnivore final host or Inverts are eaten accidentally by final host
-larva develops in I.Host into stage developed for waiting = cyst
-Larva fully develops within final host gut
-eggs then voided in feces
What stage of Cestodes does the:
Final host have?
I.Host have?
Final: Adult cestode (tapeworm form)

I.Host: Larval cystode : called Hexacanth larvae or onchosphere larvae
Disease seen with Adult cestodes in final host:
-little dz unless shortage of food (competes with host for nutrients)
-ulcers at pt of attachment
Disease seen with Larval Cestodes in I.host:
Acute dz: invation of CNS, cyst in liver
Describe the Adult Structure of Cestodes:
-adapted to live in sm intestine
-scolex has ring of hooks or suckers to stay attached
-Moving down from neck of scolex - proglottids form (flat, white, rectangular)
-Tape all the proglottids form is called strobila
-Proglottids are self containing egg units
-Each proglottid is a hermaphrodite
-hundreds of segments
-ones at posterior are voided full of eggs (gravid) or independantly crawl from anus
How do adult cestodes obtain nutrients?
-no gut
-nutrient derived from digestion process of the host absorbed directly thru proglottid
-flat shape of worm aids in absorption
How do larvae absorb nutrients?
-no gut
-absorb nutrients from surrounding lymph and tissue fluid
What is an oncoshpere?
-larva with six hooks found inside an environmentally resistant egg
How does the oncosphere get out of the egg?
-when ingested by I.host digestive secretions break down wall and larva is released
**At this point it is the hexacanth larva
-It burrows into the gut mucosa and enters the blood or lymph of vertebrate hosts (or body cavity of inverts)
Once a cestode is in the hexacanth larval stage where does it go/become?
-migrates to favored spot such as muscle and develops into a metacestode.
What is the reproduction plan for proglottids?
-hermaphrodite with one sex active at a time
-can be cross fertilization btwn worms clost together in the host's gut
What is the reproduction stradegy for cestodes?
-Massive egg production with low survival rate of eggs
While waiting for ingestion of I.host into final host can larvae multiply?
-Can multiply to increase chances of infection of final host
-HYDATID cyst is an example of this multiplication
Egg containg a larvae is called....
onchosphere
First larval stage of cestodes is the .....
(it has 6 hooks)
hexacanth larva
Second and Final larval stage of cestodes is called....
metacestode
Name 5 types of metacestodes and give examples of each:
1. Cystericerus = T.saginata
2.Coenurus = T.multiceps
3. Hydatid = Echinococcus
4.Cysticercoid =D. caninum
5. Stroboliocerus = T. taeniaformis
Describe a cysticercus and give an example:
-Fluid filled sac with one invaginated protoscolex
-Taenia saginata
Describe a coenurus and give an example:
-Fluid filled sac (like the cysticercus) with many protoscoleces
-Taenia multiceps
Describe a Hydatid and give an example:
-Large fluid filled sac containing protoscoleces detached from the cyst wall or forming further small cysts within the main one.
-Echinococcus
Describe a Cysticercoid and give an example:
-The protoscolex is contained within a solid cyst, these typically form in tape worms with invertebrate hosts
-Dipylidium caninum
Describe a Strobilocercus and give an example:
-Like a miniture strobila
-Taenia Taeniaformis
Taenia
-Final Host
-Intermediate Host
Final: Human, Dog, Cat

I. Host: Catte, pig, sheep, rodents
Echinococcus
-Final host
-I. host
Final: Dogs, Wild canids

I.Host: Ruminants, horses, rodents
Monieza
-Final host
-I.host
Final: Ruminants

I.host: Mites
Dipylidium
-Final Host
-I. Host
Final: Dog, Cat

I.Host: Fleas, Lice
Anoplocephala
-Final host
-I.host
Final: horses

I.Host: Mites
What are the two species of Taenia that affect Humans and Cattle/pigs?
T. saginata
T. solium
What species of Taenia affect Dog and sheep?
T. ovis
T. multiceps
What is the final host of both T. saginata and T. solium? and what are the intermediate hosts?
Final of T. saginata and T. solium = Humans

Intermediate of T. saginata = cattle

Intermediate of T. solium = Pigs
Disease associated with both final and i. host for Taenia saginata or solium?
Humans (final) = diarrhea and aesthetic problems

Cattle and Pigs (intermediate - with larval) = no known clinical dz
How can Larval stages of T. solium affect humans?
Poor hygiene leads to humans consuming larval stages
-Cysticercus cysts develop in CNS and eyes
-ZOONOTIC - common prob in tropics
What is the general name for the disease caused by infection of humans with cysts of Taenia?
cysticercosis
What is the best way to control cysticercosis?
1. Meat inspection for cysts (cysticercus type) in muscle

2. Human hygiene

3. Prevention of human sewage on fields of vegetables or for cattle pasture

4. Thorough cooking of meat
If humans are natural final host where in lies the problem with T. solium?
Infection of gut of humans w/ adult tapes of T. solium is part of a natural dz cycle BUT when a human becomes infected with the larval stages (CAUSING CYSTICERCOSIS) = unnatural relationship = zoonotic
What is the final host for T. ovis and how are they infected?
Dogs harbor T. ovis adults in gut
-get it from eating infected raw sheep meat with larval stages
Is there dz seen dogs from T. ovis?
-not considered a problem
What is ovine cysticercosis and what are its complications?
-Infection of sheep meat with cysticercus cyst type of larvae
-Economic loss of sheep meat
Best way to control T. ovis?
-Tx in dogs in combonation of control of Echinococcus granulosus
-Prevention of access to sheep carcasses
How do the final hosts become infected with T. multiceps?
-Dogs final host: harbor T. multicep adults
-Get from ingesting infected sheep meat
What is the path if T. multiceps is ingested:
-What stage is it ingested at by sheep?
-Where is the predilection site in sheep?
-What develops next?
-Onchosphere is larval stage of T. multicep that is ingested
-Penetrates bld stream
-Predilection site = brain
-Coenurus form of cyst 5-10cm develops and effects vision, gait and coordination
What is gid?
T. multiceps, affects sheep, clinical name for when coenurus cyst develops in brain and effects vision, gait and coordination
Echinococcus multilocularis
-What is it?
-Size
-Where is it found? Final host?
-I. Host?
-Dog tapeworm and Hydatid dz
-small tapeworm 3-5 proglottids
-Found in gut of dogs and wild canids
-Rodents
How do the I. host of E. multilocularis become infected?
-infected by eating vegetation contaminated with feces
Once I. host is infected with E. multilocularis what is the life cycle?
-infection from feces
-larvae develop into HYDATID cysts in rodents
- no harm in either hosts even with extreme #'s
How can humans become infected with E. multilocularis?
-Hydatid cysts occur in humans from contamination of vegetables from dog or fox feces
or
-direct contamination with dog adult tapes
What is the predilection site in humans for E. multilocularis?
liver
What is the other name for hydatid disease from E. multilocularis?
Alveolar Echinococcosis
-cyst grow abn large in humans
-cysts develop alveolar froms and may extend by metastatic budding from original cyst.

Can be life threatening and severe cases only treatable by liver resection or transplant!!
Does E. multilocularis occur in the UK?
NO - patchy distribution (usa, Central europe, eastwards to japan)

-IMPORTANT PET PASSPORTS FOR DOGS BEING BROUGHT IN TO UK (TAPEWORM CONTROL)
Echinococcus granulosus:
-What is it?
-Final host?
-I. host?
-Where is it found?
-Cestode - tapeworm
-Final host: dogs
-I. host - ruminants and horses (suffer little clinical dz from cysts)
-found in isolated areas of UK
Can E. granulosus infect humans? zoonotic?
YES same method as E. multilocularis. EXCEPT
-predilection site is: lung and liver

-Prevention same as with other one
What are Anoplocephalan Tapeworms?
-Do not have predator/prey life cycles
-Final host: herbivore or carnivore
-I. host: arthropod accidentally ingested
Dipylidium Caninum
-What is it?
-Size?
-Clinical Effect?
-Control?
-Final and Intermediate Host?
Dipylidium Caninum
-Anoplocephalan tapeworms
-20-50cm long
-no clinical affect
-Control: aesthetic reasons, slight risk of human infection, deworming, good hygiene (litter)
-Final: dog or cat
-I. host: Ctenocephalides (flea) and Trichodectes (lice)
Life cycle for Dipylidium Caninum?
1. larva develop into cysticercoid type of metacestode
2. Insects become infectd by eating the eggs
3. Larva in fleas remain during metamorphosis to infect the adult flea
4. Final host grooms the flea out of coat and ingests the infected flea or louse.
Moniezia expansa and M. benedeni
-What is it?
-Hosts affected?
-Life cycle?
- Clinical dz?
-Anoplocephalan tapeworm

-M. expansa: adults affect sheep
-M. benedri: adults affect cattle

-I. host: free living mites such as Acarnia/ Oribatidae(occurs in vegetation)

-1. Larval metacestode takes form of = cysticercoid and develops in mites
2. Mites are accidentally ingested with eaten vegetation or hay

- little clinical harm seen
Anoplocephala Perfoliata and A. magna
-Adults infect what host?
-I. Host?
-Why are they imp?
-Disease?
-Size?
-Anoplocephalan tapeworm

-Final host: horse

-I. host: oribatid mites

-Only tapeworm of horses

-cause ulcers and perforation of gut mucosa

-small 20cm
What plan was put into action to prevent Hydatid diseases in humans?
-PETS - dogs must be dewormed and deticked prior to entering the UK (24 hrs before)
What is the main problem with the plan to prevent hydatid dz from coming in thru PETS?
-Deworming with Droncit only kills adult infestations but not the eggs.
-Thus the first defecation after tx could heavily contaminate areas where rodent I. hosts are avail
-Localized endemic could establish if rodents did ingest and then were subsequently ingested by fox.
-THUS FOX CONTROL IS VITAL TO THE PREVENTION AS WELL.
What group of internal parasites poses the most threat to the UK?
Nematodes
Name basic features of Nematodes:
-body design
-Gut design
-Sexes?
-multicellular, elongate, unsegmented endoparasites
-shape maintained by a fluid filled body cavity
-external waxy cuticle
-all longitudinal muscles no circular
-simple gut and anus (no differentiation as with Trematodes and Cestodes)
-Seperately sexed individuals (compare with Trematodes and Cestodes)
What are the life cycles for Nematodes?
-Both parasitic and non-parasitic stages in LC
-Direct and indirect LC
-Indirect cycles= vert and invert hosts (vert is final)

**often paratenic and transport hosts
Are nematodes highly host specific?
yes
How do nematodes feed?
Can be BROWSERS or TISSUE FEEDERS or BLOOD FEEDERS

-gut is divided into muscular esophagus and non muscular intestine
- esophagus pumps food thru the intestine against the hydrostatic pressure of the body cavity
Describe Browsers (nematodes)
-feed on gut contents
-have simple mouth
-sometimes with lips
Describe Tissue feeders (nematodes)
-feed on gut contents
-have enlarged, cuticular buccal capsule around mouth with cutting plate hooks
Describe Blood feeders (nematodes)
-feed on gut contents
-feed directly on caplillaries with specialized stylets or by tissue destruction
How do nematodes reproduce?
-no multiplication in host
# of adults is determined by # of infective forms ingested by host

-Repro is usually sexual with seperate sexes

-Repro is confined to parasitic forms

-Eggs develop in uterus and pass with feces **some are ovo-viviparous

-Egg output can be millions
Name the 7 stages of the nematode life cycle?
1. Adult - M and F
2. Eggs - pass via feces
3. Five larval stages: L1 -L5

L1 and L2 = free living on pasture

L3 - L5 = parasitic
What are the different stages associated with the larvae of nematodes? (4)
- free living larvae
- ensheathed larvae
-larvae within eggs
- larvae within host

**INFECTIVE FORM IS USUALLY LARVAE BUT CAN VARY PER SPECIES FOR WHICH EXACT LARVAL STAGE**
Where do larval stages continue their development once inside the final host? (nematodes)
Either close to site of entry or they migrate to final adult location
What are the two forms of migration inside final host for nematodes?
1. Hepato-tracheal
-larva migrate from gut thru liver and lungs before arriving back to gut
-Most popular method


2. Somatic - larva
-migrate from gut thru various organ systems arrive back into the gut
-Target organs usually specific to parasite
How are nematodes able to survive the UK temperate conditions?
-free living larvae are susceptible to freezing and drought
-Therefore have come up with Principal Adaptions:
a. hypobiosis
b. periparturient (spring) rise
c. critical hatching conditions
What is Hypobiosis (nematodes)?
-Seasonal inhibition of development at a particular larval stage

USUALLY L4 WITHIN HOST

-Assoc. with autumn (unfavorable)

-Larval develop resumed in spring

-This allows overwintering and focus egg production on times when survival of free living forms is more favorable

**not exculsively seasonaly adapted
What is Periparturient (spring) rise for nematodes?
-Increase in parasite egg production seen around parturition time (sheep)

-Can arise from maturation of autumn inhibited larvae or from increased egg output by adult worms (due to changes in immunity, hormones etc assoc with birthing)

-Strategy aims: to synchronize the availability of infective forms with the presence of susceptible hosts ie YOUNG NAIVE LAMBS
What is Critical Hatching conditions? (nematodes)
-Larvae hatch from the egg only after a particular combination of weather conditions (ie cold followed by warm)

-Designed to deliver large numbers of infective forms onto the pasture when conditions are most favourable for survival of free living stages
How can we control nematodes?
1. Anthelmintics
a. Therapeutically
b. Strategically
c. Prophylactically

2. Using vaccines
3. Changing environment (reduce number of larvae on pasture - change location/stock)
4. Using resistant breeds
5. Using nematophagous fungi (reduce larval levels on pasture)
What are general features of Browsing nematodes?
1. adults = gut parasites
2. adults = simpler mouth with lips to esophagus
3. DIRECT LIFE CYCLES
4. External, non - parasitic larval stages
5. parasitic larval stages are either non migratory or migratory
6. Highly site and host specific
What are the 3 basic groups of Browsing nematodes
1. TRICHOSTRONGYLES

2. ASCARIDS

3. TRICHINELLA
General Features of Trichostrongyle Nematodes:
-Eggs are laid where?
-What forms are free-living and what do they feed on?
-What is the infective form?
-Major animals affected?
-Eggs laid on pasture

-L1 and L2 are free living
Feed on bacteria

-L3 within the cuticle of L2 (ensheathed) is infective form - LIMITED LIFE SPAN DOES NOT FEED

-Ruminants (sheep) and horses
What is the lifecycle for Trichostrongyle nematodes?
1. Eggs give rise to:
2. L1 and L2 free living
3. L3 stage is ensheathed in cuticle from L2 and is infective form
4. L3 exsheaths at site in gut of host due to response of environment
5. L3 penetrates gut mucosa and assoc. glands
6. Grow there and moult to L4 then L5
7. L5 emerges onto gut surface as male or female worm
What is the repro strategy and I.D. for trichostrongyle nematodes?
Males have copulatory bursa with supporting rays and spicules

Females have charactoristically shaped vulval flaps.
Trichostrongylus sp. (PGE)
-infective form?
-description?
-any diff sex ID?
-Where are they found in host?
-What hosts?
-Where does larval development take place?
-L3 infective form inside L2
-small and slender
-small bursa in males
-Found in Abomasum or small intesting of poultry and ruminants
-ALL LARVAL DEVELOPMENT TAKES PLACE IN GUT EPITHELIUM
Osteragia sp. (Bovine Ostertagiasis)
-what is it?
-description?
-Where is it found?
in what host?
-Differences in life cycle compared to overall plan?
-what causes any clinical dz?
-what is seen with dz?
-Trichostrongyle Nematode
-small, reddish brown
-found in abomasum of cattle
-L3>L4 in gastric glands of abomasum
-L4> adult in lumen
-Dz caused by lg #'s of L4 in gastric glands (emergence)
-Leakage of gut proteins into blood and pH changes
What are the two types of dz caused by Ostertagia in cattle?
1. Type I Ostertagiasis

2. Type II Ostertagiasis

**Seasonal**
What causes Type I Ostertagiasis?
L3 ingested in Spring/summer and develop into adults that year
What causes Type II Ostertagiasis?
L3 ingested in previous autumn and underwent hypobiosis in the gastric glands as L4.

Dz comes from mass emergence of larvae in following spring.
Nematodirus sp. (N. battus)(Nematodiriasis)
-what is it?
-describe?
-Male ID?
-Where is larval development?
-Trichostrongyle Nematode
-long, slender, whitish worm, with twisted body "cotton wool"

-Males have long fused spicules with specific end expansions, with small cephalic vesicle=helps it stick to villi

-Larval development on mucosal surface -->leads to damage of villi and thus diarrhea and dehydration

-L1>L2>L3 all retained within egg **CAN PERSIST FOR UP TO TWO YEARS ON PASTURE
What is required for development of larval stages of Nematodirus sp?
-Critical hatching temperature for L3 from egg

(usually only one batch of worms per year)
How can you prevent nematodiriasis?
Forcasting to prevent early year temps to give dewormers to coincide with hatching.
Haemonchus sp. (Haemonchosis)
-What is it?
-Where is it found..in host?
- Can it cross infect?
-Males ID
-Females ID
-Dz caused?
-Trichonstrongyle Nematode
-Lg blood-feeding worm
-Found in abomasum of cattle, sheep, and goats
-Can cross infect btween sheep and cattle

-Males large bursa
-Females: white ovaries twisted around the blood filled gut "barber's pole"

-Infestations lead to severe bld loss with anemia, wt loss, weakness, fatal hemorrhage gastritis
Control Options for Trichostrongyles of Ruminants:
-Aimed principally at limiting pasture contamination of L3 stages by reducing egg output
1. Anthelmintic
-effective?
-activity?
-timing?
-frequency?
-resistence?

2. Pasture management
-dose and move to new pasture
-alternate stock grazing
-rotational grazing
Ascarids
-Adult description
-Found in what host?
-Infective stage?
-Larval behavior?
-Nematodes
-Large white non bursate worms
-Intestines of pigs, horses, poultry, cats and dogs
-L2 either in egg or tissue of paratenic host
-can be migratory (either rte) or non migratory
Toxascaris leonina
-what is it?
-migratory?
-Location within what host?
-Dz causing?
-Life cycle?
-control?
-Ascarids
-Non migratory
-Sm. intestine CATS AND DOGS
- Patho in lg numbers

-Infection caused by: ingestion of L2 in egg or L2 in tissue of mice (PARATENIC HOST)

-control by dewormer and good hygiene
Heterakis
-What is it?
-Location in what host?
-Transport or paratenic host?
-Life cycle?
-Dz causing?
"browser nematode"
-Non migratory Ascarid
-Small white worms
-Lg intestine of domestic and wild birds
-Earthworms ingest infective eggs and become transport/paratenic hosts in which L2 migrate into tissues until eaten by bird

-Non pathogenic normally but Aids in transmission of Protozoan Histomonas meleagridis
Ascaridia
-What is it?
-Describe it?
-Location in what host?
-Life cycle, transport hosts?
-Major problem caused when?
"browser nematode"
-non migratory ascarid
-stout white worms
-sm. intestine of poultry and wild birds
-Earthworms act as transport hosts once eaten eggs - L2 passes thru to gut

-Mainly prob of young birds= hemorrhagic enteritis
Ascaris suum
- What is it?
-Migratory or not?
-Describe simply life cycle
Migratory AScarid "browser nematode"
**MOdel for HEPATO-TRACHEAL MIGRATION**

1. egg hatches in sm intest.
2. L2 passes to liver
3. In liver moults to L3
4. travels to lungs via bld
5. Then travels back to intestine
6. TWo final moults take place in intestine
What is milk spots and describe their significance?
In prev infected pigs of Ascaris suum:
-larvae travel to liver and stimulate an immune response
--> results in white spots and leads to meat condemnation
What is Ascaris Pneumonia?
Lg numbers of larvae of
Ascaris suum traveling thru lungs can give rise to transient Ascaris pneumonia
What do Adult Ascaris suum feed on?
"Browse" on gut contents causing little/no damage

Lg numbers can lead to Loss of BCS and all related
Control of Ascaris suum?
-dewormers
-good hygiene

-eggs can remain infective for years
Name the two important species of Toxocara and thier hosts:
Toxocara are migratory Ascarids

T. canis -- dogs

T. cati -- cats
Toxocara cani
Infection prior to 3 months of age:
-route of migration
-Important sites
Hepato-tracheal migration rte
-L2>L3 moult takes place in lungs
-L3 returns to gut for final two moults to adults
Toxocara cani - Infection after 3 months of age
-migration
- Location sites?
-L2 migrate to a wide range of tissues including heart, liver, lungs, skeletal muscle
-In these tissues development is arrested (hypobiosis)
Toxocara cani becomes arrested in development, what are the two times when it is reactivated?
Reactivation leading to:
1. Pre-natal infection
2. Transmammary infection
Describe Pre-natal infection when it comes to Toxocara cani:
-3 weeks b4 birth L2 becomes activated
-migrates to the lungs of fetus
-here L2 moults to L3 just before birth
-soon after birth larvae migrate to intestine via trachea where they moult to adult
Describe Transmammary infection when it comes to Toxocara cani:
-Larvae can also be passed to pup via the milk and moult to adults WITHOUT TISSUE MIGRATION PHASE --> VERY UNUSUAL
Toxocara canis
-Who can act as paratenic hosts?
-What do heavy infestations lead to?
-What is a principal result of T. canis (infection)
-Control?
-rodents and birds containing L2
-Heavy infestations lead to pneumonia and occulsion of gut
-Principal cause of VISCERAL LARVA MIGRANS IN HUMANS (CHILDREN - BLINDNESS)
T. cati
-How is life cycle different than T. cani?
-somatic migration in adults after ingestion of the L2 in the egg.
-Kittens become infected via TRANSMAMMARY MILK not PRENATAL
-Paratenic hosts important!!
-rare cause of visceral larva migrans
Why are paratenic hosts important to T. cati life cycle?
Paratenic host play a role in epidemiology.
-->Infections derived from these hosts usually develop directly to adults in the gut WITHOUT MIGRATION.
Trichonella spiralis
-What is it?
-who does it infect?
-zoonotic?
-Migratory Ascarids - Example of "post adult" migration
-infects wild carnivores or pigs when they eat waste containing infected meat or from tail biting
-yes humans become infected by eating undercooked pork
What is the life cycle for Trichonella spiralis?
EXAMPLE OF "POST ADULT" MIGRATION

-L1 produced by female
-Migrate from gut
-Become arrested inside cells of skeletal muscle of host
-Muscle is eaten, larval development is resumed in intestine which is completed w/in two days.
General features of STrongyle Worms = aka Tissue Feeders
-size
-location
-ID features
-Where do they feed?
-infective form?
-migratory behavior of larvae?
-med to lg
-bursate worms of cecum, colon and sm intestine
-WELL DEVELOPED BUCCAL CAPSULE with a range of cutting features such as plates, hooks and teeth
-Feed directly on tissues of gut or blood
-ensheathed L3
-can be migratory or non migratory
Chabertia
-What is it?
-Migratory?
-Size
-Host?
-ID features?
-Life cycle?
-Control?
-Nematode - strongyle
-non migratory
-ALL STAGES FOUND IN GUT LUMEN OR MUCOSA
-largest nematode
-found in colon of sheep, goat and cattle

-VERY distinctive large bell-shaped buccal capsule

-L3 and L4 deep in mucosa of colon
-L4 found in lumen
-Adults are plug feeders and seldom cause dz in large numbers

-Control same as PGE (deworming and pasture management)
Oesophagostomum
-what is it?
-Host?
-ID features?
-Life cycle?
-Control?
-Nematode - Strongyle - Tissue feeder
-Ruminants (host)
-Head slightly bent dorsally, variety of cuticular ornamentation

-L3 develops in a fibrous nodule in gut wall
-L4 to adult on gut surface leaving behind charactoristic nodules

-Control dewormers and pasture management
Equine Strongyles (equine strongylosis)
-The infection...what is it?
Result of infection with a number of diff nematode species but usually tx as single clinical entity.
Name the two Major groups of Equine Strongyles?
1. Small Strongyles
--> Equine Cyathostomes (Trichonemes)

2. Large Strongyles
-->Strongylus
Cyathostomes
-What is it?
-Describe
-Location
-Migratory?
-Clinical dz?
-Control?
-1. Small Strongyles
--> Equine Cyathostomes (Trichonemes) - Tissue Feeder

-small, stout warms, L4 is red due to blood (others are white to dark red vary)

-Lg intestine of horses
- Larvae non migratory
-Infection usually well tolerated but increased #'s can lead to enteritis and fibrosis of gut (YOUNG ANIMALS BEWARE)

-Control: dewormer and pasture management
Life cycle of Cyathostomes (Trichonemes)
-L3 emerges in lumen of sm intes.
-moves to colon--> mucosa
-FIbrous nodule forms around larva
-moults to L4 inside nodule and emerges out to gut surface
-L4 and adults are plug feeders
-L4 sucks blood hence bright red
Large strongyle of Horses- Strongylus
-ID feature
-Location and host
-prepatent period?
-infective form?
-migration
-patho
-control
-lg buccal capsule
-adults found in lg intestine of horses and donkeys
-long prepatent periods (6-12 months)
-infective form= L3 ensheathed on pasture
-SOMATIC MIGRATION
-patho depends on tissue feeding habits of adults
-difficult to kill with dewormer
Three principal species of Strongylus based on larval target organs:
1. S. vulgaris
2. S. edentatus
3. S. equinus
Describe S. vulgaris
-what it is?
-migration?
-life cycle?
-Large strongylus horses
-somatic migration

-L3 penetrates int. mucosa
-moult to L4 in submucosa
-enters sm arteries
-migrates to MAIN MESENTERIC ARTERY
-several months later, moults to L5
-returns to intestinal wall via arterial lumen
-nodules form around the larvae
-nodules rupture releasing adult
-PREPATENT PERIOD 6 MONTHS
Patho associated with S. vulgaris?
once in main mesentaric artery:
-lesions can develop in artery and its branches arising from thrombus formation with inflammation and thickening of arterial wall
Describe S. edentatus
-what is it?
-migration?
-life cycle?
-Large strongylus horses
-somatic migration

-L3 penetrates int. mucosa
-travels to LIVER via parenchyma via bld stream
-forms nodules
-moult to L4 in liver
-Leaves liver via hepatic ligaments where the final moult takes place
-L5 travels back to wall of lg intestine
-LG nodule forms and ruptures releasing adult into lumen

PREPATENT PERIOD 11-12 MONTHS
Describe S. equinus
-what is it?
-migration?
life cycle?
-Large strongylus horses
-somatic migration

-L3 penetrates wall of intestine
-nodules form in MUSCLE LAYERS OF THE GUT
- moult to L4 takes place in nodules
-L4 migrate w/in parenchyma
-reappear in lumen of lg intestine w/out nodule formation

PREPATENT PERIOD 9 MONTHS
Hookworms
-what are they?
-where do they infect?
-who do they infect?
-ID shape?
-what type/where feed?
-infective form?
-Nematodes - tissue feeders
-sm intestine or colon
-ruminants and dogs
-dorsal bending of head "hook" shape
-blood feeders directly on arterial capillaries of mucosa
-infective form L3 (orally or percutaneously)
Ruminant Hookworm - Bunostomum
-what is it?
-size
-where of who
-how infected?
-patho?
-Tx?
-Control?
-bld feeder - nematode
-largest nematode
-sm. intestine of ruminants
-orally or percutaneous infection-> followed by migration to gut
-effects masked by other nematode infections
-tx under Ostertagia and Haemonchus and thus get tx anyway
good hygiene (thrive on damp conditions)
Unicinaria
-what is it?
-Host?
-how infected?
-control?
Northern hookworm of dogs and cats in temperate areas
-oral or L3 penetrates skin causing hypersensitivity rxn in feet
-good hygiene and dewormer
Ancylostoma
-what is it?
-Host?
-How infected?
-life cycle imp notes?
-Tropical canine hookworm
-dog
-oral or L3 skin penetration
-Larvae migrate to tissues and undergo hypobiosis and then are reactivated during later stages of pregnancy
Lungworms
-where are they located?
-how infected?
-life cycle?
Nematodes
-Adults in respiratory system
-eggs and larvae passed out in feces
-infection via ingested larvae that migrate from the gut to lungs
-direct or indirect life cycles
Dictyocaulus sp (husk)
-What is it?
-description
-Host?
-how infected?
-Life cycle?
Lungworm with direct life cycles tissue/blood feeder
-slender, thread like worm
-found in bronchi of cattle, sheep, goats, horses and donkeys (parasitic bronchitis in calves)

-L3 infective form

-penetrates intestinal mucosa and passes to mesenteric LN
-moult to L4 which travels to lungs via bld and lymph
-breaks out of capillary into alveoli
-Final moult in bronchioles
-Adults mature in bronchi
What is the repro strategy of Dictyocaulus?
-Females produce eggs containing fully developed L1 (ovo-viviparous) which hatch immediately
-migrate up trachea are swallowed and pass out feces
What is the feeding strategy of Dictyocaulus?
L1 to L3 stages do not feed but are reliant on stored food.

L3 leave fecal pat either by themselves or can be carried distances on spores of fungus PILOBOLUS which grows on feces.
Control of Dictyocaulus?
Vaccine avail irradiated L3 - less effective realted to earlier challenge resulting from more over-wintered larvae?
Syngamus sp. (gapeworm)
-What is it?
-who does it infect?
-size/description?
-ID features?
-infective form?
-Egg survival?
Lungworm - tissue feeder - nematode -
-birds
-large reddish
- Male and Female are in copula always Y shaped
-Variety of infective forms:
egg with L3
L3 hatched from egg
L3 in transport host (earthworm, slug, snail or beetle)
-Eggs survive for up to 9 months on soils or years as the L3 is within transport host
-Wild bird populations act as reservoirs for poultry and earthworms
Oslerus sp.
-What is it?
-Where is it found? Host?
-Repro?
-Patho?
Canine lungworm - tissue feeder - nematode -
- found in upper air passages of domestic and wild dogs
-Adults in nodules at tracheal bifurcation
-Ovoviviparous with larvae in feces

-Heavy infestations result in UR distress esp after exercise
Metastrongyles
-What is it?
-Def host/ I. host?
-Life cycle?
-how infected?
Obligate, Heterxenous - Lungworms with Indirect life cycles
-Invertebrate as I. host
-Transmission depends on avail of I. host

-Def host: pig
-I. host: earthworm

-Egg containing L1 ingested by earthworm
-Develops thru to ensheathed L3 IN TISSUES OF WORM
-EARTHWORM IS I. HOST NOT PARATENIC HOST OR TRANSPORT HOST

-Pigs becomes infected by eating earthworms
-L3 travel to lungs via lymphatic system
Mullerius sp.
-What is it?
-Def host/ I. host?
-Life cycle?
-how infected?
Obligate, Heterxenous - Lungworms with Indirect life cycles
-Invertebrate as I. host
-Transmission depends on avail of I. host

-Def host: sheep
-I. host: mollusc

-Adult found in alveolar tissue of sheep
-Gives rise to fibrous nodules
-Ovo-viviparous with L1 passed out with feces
-Infects molluscan I. host thru its feet
-Sheep infected by ingesting snail while grazing.
Filarial Nematodes
requirements
All have Indirect lifecycles with insects as intermediate hosts

Adults are found in bld system or CT

Larval stages = microfilaria
Parafilaria sp.
-what is it?
-hosts?
-life cycle
-how infected?
Filarial Nematode - tissue feeders

-Def host: cattle, horses
-I. host: Flies (Musca sp)

-Adults in nodules (verminous) in skin
-no egg stage

-Microfilaria in "bloody" secretions taken up by fly during feeding (NOT BLOOD SUCKING)

-Infect host by L3 breaking out of fly mouthparts and entering skin
Dirofilaria sp.
-what is it?
-hosts?
-life cycle
-how infected?
-Canine Heartworm - Filarial Nematode - Tissue feeder

-Def host: dog
-I. host: mosquitoes

-Adults found in pulmonary artery and "right" heart.
-Microfilaria circulate in the blood until taken up by mosquito

-After developing in mosquito tissues --> move to salivary glands and are then injected back into the dog via the mosquito saliva injected during feeding