Parasitology Flashcards
Identify this parasite, its epidemiology and describe its lifecycle ?
Hyostrongylus rubidus (red stomache worm)
Morphology
- slender reddish when fresh
- eggs thin shelled many cells
Epidemiology
- common in pigs reared on pasture
- signs observed usually in adult pigs, especially sows
Life cycle
- females lay strongyle eggs (low egg producing)
- infection of host through the ingestion of L3
L3 enter the pits of the gastric glands where they develop into adults within 3-4 weeks/ and then emerge from the glands
Describe the pathology and clinical signs of Hyostrongylus rubidus ?
Hyostrongylus rubidicans (red stomache worm)
Location = gastric glands of the stomache
Pathology
Caused by adults and larvae
- adult worms feed on blood - anemia
- penetration / development in the gastric glands of larvae / adults emerge resulting in nodules
- emergence of adults - inflammation, cytolysis, sloughing of mucosa
- congestion and haemorrhages
Clinical signs
- usually infections are benign - poor body condition, weightloss and ill thrift
- Heavy infections anaemia, loss of condition and reduced growth of progeny
Thin sow syndrome
How would you diagnose and treat Hyostrongylus rubidus ?
Hyostrongylus rubidus (red stomach worm)
Diagnose
faecal egg floatation + as clinical signs are not specific
Treatment
Benzimidazoles - Fenbendazole, Flubendazol
Tetrahydropyrimidines - pyrantel, morantel
Imidazothiazoles - Levamisole
Macrocyclic lactones - Abamectin, Ivermectin and Doramectin
Treatment is only temporary think to manage the parasite
Identify this parasite, describe its life cycle ?
Ascaris Suum
Morphology
- 45cm, stout body, pinkish yellow, three lips
- egg thick shell, yellow brown, mammilated outer layer
Life cycle
- prolific 200,000 eggs /day
- embryonate eggs not effective passed in faeces
- optimum temperature 30-33 forms quickly 13-18 days (below this temp slower development but eggs still survives).
- eggs sticky and can survive for years (6-9 years)
Infection occurs through ingestion of L3 food, water (potential for parental host earthworms, chicken, beetles)
Migration
Larvae hatch in the intestine and migrate to the liver - heart - lungs - pharynx and back to the small intestine to mature
PPT 6-8 weeks
Describe the epidemiology of Ascaris suum ?
Ascaris Suum (can infect and mature in humans)
Prevalence highest in 2-6 month old piglets
The most important / common gastrointestinal worm parasite in pigs with a prevalence of 50 - 75%
Location = adults small intestine
Larvae = migration small intestine - liver - heart - lungs - pharynx and back to the small intestine
- worldwide distribution
- common indoor and outdoor systems
- adults usually not infected or carry very few parasites - usually obtain immunity by four months
- young suckers may become infected early after birth - sows can be carriers with eggs adherent to their skin
Susceptability
- wooden floors > slats
- pig breed
- > free range organic
- seasonal variation peaking summer / autumn
Describe the pathology of Ascaris suum ?
Ascaris suum
Partial age immunity develops - 4 months, most worms expelled by six months
Adult - lesion digestive tract
Larvae lesions in liver (milk/ white spot)
Liver (larvae)
- milk white spots
- cloudy/ whitish spots upto 5mm on the surface of the liver
- economic loss from condemnation
Lungs (larvae)
- small haemorrhages into the alveoli, bronchioles and oedema
- lungs become compromised
Small intestine (adults)
- competition with host for nutrients
- heavy infections may block the gut
- perforate intestine
- block bile and pancreatic ducts (icterus)
What are the clinical signs of Ascaris suum ?
Ascaris suum
The effects of infection with A.suum are most obvious in pigs 2-6 months of age
Stunted growth - adult worms reduce food intake
Osmotic diarrhoea - impairment of lactase activity in the gut mucosa. (prevention of normal water and electrolyte absorption)
Note - in piglets less than 4 months with heavy infections you may see dyspnea (laboured breathing, cough and audible expiratory efforts (thumps) death.
How would you diagnose and treat Ascaris suum (5) ?
Ascaris suum
Diagnose
- history - environmental factors, age 2-6 months
- clinical signs - stunted growth, osmotic diarrhoea
- identification of eggs in faeces and identification of adult worms
Necropsy = ‘milk spots’
Treatment
Herterocyclic compounds - Piperazine
Benzimididazoles - Fenbendazole, Flubendazole
Imidazothiazoles - Levamisole
Tetrahydropirimidines - pyrantel, oxantal and morantel
ML = Abamectin, ivermectin and doramectin
Describe what management strategies should be implemented to control Ascaris suum ?
Ascaris suum
Management Boar
- treat 2-4 times per year
Sow
- treat pregnant sows two weeks prior to farrowing
- wash sow carefully 4-14 days before placing her in the farrowing pen.
- clean and disinfect farrowing pen
Piglets
- treat piglets 10-14 days before transfer to the fattening pen ( clean and disinfect)
- and 6 weeks later
Quarantine and treat any new pigs to the property
Destroy faeces for 3-4 days - improve hygiene to destroy eggs
Identify, describe the morphology, epidemiology and life cycle of this parasite ?
Strongyloides ransomi
Location = small intestine (F) embedded into the mucosa
Morphology
- thread like , oesophagus 2/3 of length
- eggs thin shelled, contain a larvae when laid
Epidemiology
- clinically significant in suckling pigs - sows are an important source of infection
- piglets quickly develop immunity
- present in outdoor and indoor systems
- infections are prevalent in warm climates
Life cycle
Parasitic and free living stages
- parasitic stage is only female
- homogenic or heterogenic development
Infection = L3 ingestion, transcutaneous or from milk
Within host L3 mature to female parasite in small intestine or enter hypobiosis.
PPT 4-9 days
What are the clinical signs of Strongyloides ransomi ?
Strongyloids ransomi
May appear in pigs as young as 5-10days (infection transcutaneous, milk and ingestion)
- diarrhoea
- dehydration
- emaciation
- anorexia
- anaemia
How would you diagnose and treat Strongyloides ransomi (thread worms) ?
Strongyloides ransomi (thread worms)
Diagnose
History - young age (could be 5-10 days)
Clinical signs
Faecal egg float (fresh samples L1 hatches quickly)
Fatal cases may occur before eggs appear in the faeces
Treatment
ML = Ivermectin, Doramectin (adult worms only)
Levamisole
Treatment of sows 3-16 days prior to parturition prevents transfer of larvae via milk
(hygiene cleaning of pens prior to farrowing).
Identify this parasite, describe its epidemiology, morphology and life cycle ?
Macracanthorchynchus hirudinace
Location = small intestine of pigs (humans)
Morphology
- upto 35cm
- proboscis provided with 6 transverse rows of hooks
- eggs thick shelled embrionated
Epidemiology
- common in feral pigs, relatively rare in free range systems
Life cycle
Intermediate host = May beetles, dung beetles and water beetles
Describe the clinical signs, diagnosis and treatment of Macracanthorhynchus hirudinace?
Macracanthorhyncus hirudinace
Clinical signs
- nodular lesions that may be invaded by bacteria
- perforation of the gut = peritonitis
- diarrhoea, weight loss
Diagnosis
Detection of eggs in faeces (sedimentation methods)
Treatment
- Ivermectin
- Doramectin
Identify this parasite ?
Describe its morphology and life cycle ?
Cystoispora / Isospora suis
Location = small intestine
Morphology
- sporolated oocyst contain 2 sporocyst each with four sporozites
Life cycle
- Infected animals shed in the environment unsporolated oocysts
- sporolation / sporogony the oocyst require humidity and temperature ( rapid 20-37*)
Ingestion = ingestion of sporolated oocyst
- oocyst excyst in the small intestine - sporozites are released and invade the epithelial cells
- develops (asexually) and sexually (gamogony) in the enterocytes of the small intestine
- oocyst released in faeces 4-5 days post infection in several peaks lasting upto two weeks
PPT 4-5 days
Describe the epidemiology of Coccidiosis Cystoispora / Isospora suis ?
Epidemiology Coccidiosis cystosporoa / Isospora
Epidemiology
Pigs younger than 2-3 weeks are most susceptable (immature immune systems).
- age resistance dose develop, recovered pigs are resistant to future infections
- worldwide distribution
(SOWS ARE NOT THE SOURCE)
Oocysts shed by previous piglets in the farrowing pen which survive on the floor and wall are the source of infection.
Sporolated oocyst survive for months in the environment and are resistant to most desinfectants
- not associated with a particular season
Note proven pathogen - > 20% of piglet diarrhoea, morbidity 100% of piglets and ,20% mortality
Describe the pathology and clinical signs of coccidiosis Cystoispora/ Isospora suis (4) ?
Coccidiosis Cystoispora / Isopora suis ?
Pathology
Depends upon the age of pigs and infective dose
- villous atrophy, necrosis and fusion
- crypt hyperplasia
- gaseous fluid filled intestinal content (without blood)
- synergistic effect with I. suis and salmonella
Clinical signs
Commonly occur in pigs 1-2 weeks of age
- apperas 3-5 days
- yellowish / greyish diarrhoea liquid to pasty, foul smelling and stains the perineum
- dehydration, piglets less active and depressed
- reduced weight gains, weight loss, not all piglets will be affected equally
How would you diagnose and treat Coccidiosis (Cystoispora / Isospor) suis ?
Coccidiosis suis
Diagnose
History and clinical signs
- piglets 1-2 weeks of age that do not respond to antibiotics
- identification of oocytes in faeces ( faecal floatation / direct smears), may be hard to detect
Necropsy - gut scrapings, histopathology differential diagnosis
Treatment
- Toltrazuril
- A single administration is highly effective if the disease is in its early stages
- treat all groups (metaphylactic) prevent deaths and loss of production
Identify four management strategies to prevent the spread of coccidiosis ?
Coccidiosis Cystoispora / Isospora suis ?
Management and hygiene
- all in and all out
- clean and disinfect the entire farrowing pen after all the litters are weaned (piglet to piglet disease)
- keep farrowing pens dry and clean
- disinfect with bleach (50%) or neopredisan
Identify this parasite, describe its morphology, and lifecycle ?
Trichuris suis
Location = caecum and colon
Morphology
Body made up of two segments - slender anterior and thick posterior
eggs = lemon shaped, smooth shell yellow brown and plugs at poles
Life cycle
Eggs are passed in faeces - infective larvae develops slowly 3-4 weeks
Infection = ingestion of embryonated eggs
PPT 6-8 weeks
Describe the epidemiology of Trichuris suis ?
Trichuris suis (may infect people)
Epidemiology
Most common in finisher / grower pigs 2-6 months of age
- prevalence higher in free range / organic farms
- common in pigs housed on dirt / inadequate drainage and pooling of water
- sows and boars lowest level of infection
Eggs highly resistant in the environment > 55*may
Describe the pathology and clinical signs of Trichuris suis ?
Trichuris suis
Location = caecum and colon
Pathology
Cause enterocyte destructive ulcers (local immune suppression
- predisposes to secondary infection (may mimic swine dysentery)
- erosion of the dilated blood vessels, mucosa, haemorrhage, anemia and hypoalbuminaemia
Clinical signs
Light infections no clinical signs
Massive infestation (1000s) = anorexia, anemia, mucoid to bloody diarrhea, dehydration, retarded development and death
How would you diagnose and treat an infection of Trichuris suis ?
Trichuris suis
Diagnosis
- Clinical signs and history are not specific
- detection of eggs in faeces ( easily missed as they are intermittent egg layers and the eggs do not float easily)
If suspected necropsy
Visualization of worms is relatively easy
Treatment
- Benzimidazoles - Fenbendazole, Flubendazole and Oxibendazole
- ML Doramectin
- Leviamisole
Identify this parasite and describe its morphology and life cycle ?
Oesophagostomum dentatum spp (nodular worms
Location = large intestine and feed upon tissue
Morphology
- anterior cephalic vesicle
- posterior ends in a bursa in the male
- Eggs, ovoid thin shelled morula stage
Life cycle
Infection = by ingestion of L3
- L3 can survive one year outdoors (eggs are susceptible to desiccation)
- L3 have low motility
- after ingestion of L3s enter the submucosa of the large intestine and moult to L4 (cause nodules)
- L4s return to the lumen to molt into adults
PPT 18-21 days
Describe the epidemiology of Oesophagostomum dentatum spp (nodular worms) ?
Oesophagostomum dentatum
Location = large intestine
Accumulates in adult pigs
- common in both outdoor and in door systems
- low immunogenicity - may accumulate in time, infections are common in adult animals
- pigs diet and age have a significant effect influence on establishment and fecundity ( higher protein and carb = reduced worm burden)
Describe the pathology and clinical signs of Oesophagostomum dentatum ?
Oesophagostomum dentatum
Location = large intestine
Pathology
L3s enters the submucosa of the caecums and colon - host responds by formaing a nodule
- Hypersensitivity reaction up to 5mm in diameter nodule
- inflammation and nodular reaction induced by invasion of the mucosa
- emergence of larvae from the mucosa
- thickening of intestinal wall, congestion
Clinical signs
- inappetence
- weight loss (thin sow syndrome)
- reduced litter size and weaning weight
How would we diagnose and treat an infection with Oesophagostomum dentatum ?
Oesophagostomum dentatum
Diagnose
Finding eggs in the faeces (patent infections)
- thin shell morula stage
Treatment
Pyrantel
Levamisole
Fenbendazole, Flubendazole
Abamectin, Ivermectin and Doramectin
Identify this parasite, describe its morphology and life cycle ?
Stephanurus dentatus
(kidney worm of pigs)
Location = adult; pelvis of kidney, perirenal fat (cyst), or the walls of ureters
young; liver and peritoneal cavity
Morphology
- stout worms
- buccal capsule cup shaped with with triangular teeth
Eggs = thin shelled morula stage
Life cycle
- eggs are passed in urine
- L! - L2 - L3 in the environment (earth worms may serve as transport host)
Infection
- ingestion of L3 from the environment
- ingestion infected earthworms
- transcutaneous
Larvae develop in the liver and migrate through the peritoneal cavity to the perirenal region.
PPT 6-11 months
Describe the epidemiology and clinical signs of Stephanurus dentatus (kidney worm) in pigs ?
Stephanurus dentatus pig kidney worm
Location = kidneys
Epidemiology
- common in feral pigs (N.QLD)
- limited to warm moist areas in Australia as the L3 stage is highly susceptable to desication
Clinical signs
- fibrosis in the liver
- abscesses in carcasses
- organs are often condemned at slaughter
- weight loss
How would you diagnose, treat and prevent infections with Stephanurus dentatus ?
Stephanurus dentatus
Detection = eggs in urine
Treatment
- Ivermectin, Doramectin
- Levamisole
- Fenbendazole
Prevention
- avoid exposure to L3 in wet/ muddy environments
- house on concrete or slabs
- seperate young pigs from those > 9 months of age (>9 months of age shed eggs long PP).
Identify this parasite and describe its life cycle ?
Metastrongylus spp
Location = bronchi, bronchioles
Morphology
- two tri lobed lips
- eggs = corrugated surface and embrrionated when layed
Life cycle
Intermediate host = earth worms
- out door systems
- pigs get infected after ingestion of infected earthworms
PPT 3-6 weeks
Describe the pathology and clinical signs of Metastrongylus spp ?
Metastrongylus spp
Pathology and clinical signs
- observed in pigs 4-6 months of age
- coughing, dyspnoea and unthriftiness
How would you diagnose and treat Metastrongylus spp ?
Metastrongylus spp
Diagnosis
clinical signs, out door systems and age 4-6 months
identification of eggs in faeces
Treatment
Fenbendazole, Flubendazole
Ivermectin, Doramectin
Levamisole
Describe the epidemiology of Sarcoptes scabiei var suis ?
Epidemiology Sarcoptes scabiei var suis
In several states of Australia it is a notifiable disease
S. Scabiei var suis is the most important ectoparasite of pigs
- 70-90% of herds are infected
- spread all over the world in both indoor and outdoor systems
Can temporarily infect humans (pig handlers)
(however unable to complete their life cycle 2-3 weeks)
Transmission = direct contact
- infection from the environment is less important but is possible
- highly contagious many pigs may become infested in a short period of time
- prevalence and severity of disease increases in the colder months
Sources of infestation
Animal with chronic/ hyperkeratotic lesions (ear, forehead and legs) especially adult breeding animals (sows boars where artificial insemination is not used).
Identify this parasite describe its morphology ?
Morphology Sarcoptes scabiei var suis
Body shape oval/ circular, ventral surface is flattened
- dorsal surface is convex
- Gnathosoma is almost square
Dorsal side of Idiosoma
- triangular scales
- transversal striations
- spines
The legs are short and conical
Describe the life cycle of Sarcoptes scabiei var suis ?
Sarcoptes scabiei life cycle
Egg, larva, two nymphal stages - adult (moult 2-3 weeks to complete)
- the parasites live in the superficial layers of the skin
- the fecundated female burrow/ tunnels in the skin and lays eggs (1-3 day over a period of two months)
- sex legged larvae hatch and most of them go to the surface of the skin
Describe the pathogenesis of sarcoptes scabiei var suis ?
Pathology
Burrowing mites cause irritation (secrete compounds which dissolve the epidermis)
- delayed and immediate hypersensitivity develop to parasite secretions, faeces and eggs
- hyperactive animals develop thick crusts that contain large numbers of parasites
Two groups
1) Larger group
- harbour few mites and develop a marked hypersensitivity reaction
- hypersensitivity up = mites down
2) Smaller group
This group of pigs harbour significant numbers of mites but do not develop a severe form of hypersensitivity
Hypersensitivity develops 3-4 weeks after infestation - congestion of the skin, papules and puritus
Describe how Sarcoptes Scabiei var suis is transmitted between pigs ?
Desribe the clinical signs you would observe with Sarcoptes scabiei var suis in pigs ?
Sarcoptes Scabiei
Clinical signs two main clinical forms
- ALLERGIC / HYPERSENSITIVITY FORM IN GROWING PIGS
- puritis
- scratching, rubbing against walls and fence
- head shaking
- hyperkeratosis (thickening of the skin)
-alopecia
-congestion of the skin papules
- nodules crust
- yellow brown crust within the ear, shaking - hYPERKERATOTIC CHRONIC FORM SEEN IN OLDER ANIMALS
- Lesions of the hyperkeratopic mange develops in only a few animals, those that fail to develop hypersensitivity reactions.
- thick crusts in the ears, very rich in parasites (18000 mites per gram ear material)
- clinical signs may regress after 2-3 months
- pruritis is reduced compared to the hypersensitivity form
- skin is thickened and wrinkled
Most sows boars might have lesions (crusts) only on the inner surface of the ears without other obvious clinical signs - source of infestation
What could we do to diagnose Sarcoptes scabiei var suis (4) ?
Diagnosis of Sarcoptes scabiei var suis (4)
Clinical signs - pruritus, papules, scratching etc
- estimate the level of pruritus by using a scratching / rubbing index
History - age (growing pigs), time of year, management and treatments
Serology
- Detection of antibodies by ELISA
Microscopic examination
- may be of value in the chronic form of disease
- examination of crust from ears (most likely to habour parasites )
Differential diagnosis
- Perakeratosis (incomplete maturation of skin cells nuclei still present)
- exudative dermatitis
- deficiencies in niacin and biotin
What control measures and treatment can we implement for Sarcoptes scabiei var suis ?
Sarcoptes scabiei var suis
Control
Target the breeding animals as they are the source of infection
- aim to prevent infestation of piglets from the sow
- all in all out
- treat boars regularly 2-3 months due to constant contact with sows
- treat sows gilts 7-14 days prior to farrowing
- treat piglets at weaning and during the growing period (clean shed)
- purchase pigs from an establishment free from parasites
Elimination is possible
Treatment
Formamidines Amitraz Taktic
Macrocyclic lactones Ivermectin and Doramectin
What management strategies should be implemented to stop reduce or eliminated Sarcoptes scabiei var suis ?
Sarcoptes scabiei var suis control
Target the breeding animals as they are the source of infestation
- aim to prevent infestation of the piglets from the sow
- all in all out
- boars treated regularly 2-3 months as they have regular contact with different sows
- treat sows/gilts 7-14 days prior to farrowing
- treat piglets during the growing period as required (prior to placement in a clean shed)
- purchase pigs from farms free of parasites and assess carefully during quarantine
Eradication is possible with careful management (most programmes ivermectin or doramectin)
Identify this parasite and describe its life cycle ?
Haematopinus suis life cycle
Spends their entire life on the host
- host specific
- females lay 3-4 eggs a a day which are cemented on the hair of the host
- three nymphal stages with the last one molting to an adult
- life cycle takes 23-30 days
- lifespan 35-40 days
Describe the morphology and epidemiology of Haematopinus suis ?
Haematopinus suis
Morphology
- head narrower than the thorax
- occular points behind antenae
- parategral plates
- three pairs of legs the same size
Epidemiology
Worldwide distribution but the prevalence is reduced in herds that are treated successfully for mange
- lice are host specific (introduced with infected livestock)
- boars and sows are usually the source of infection
- greater problem during the cold season
- larger populations develop on younger pigs and those with deficient diet/management
occasionally bite humans
- unable to complete lifecycle on human host
Describe the pathology and clinical signs of Haematopinus suis ?
Haematopinus suis
Pathology
H.suis may cause irritation (saliva and insertion of mouthparts which is painful)
- puritus - scratch - loss of hair - crusts
- excoriation and decreased weight gains
Clinical signs
- red spots from bites on the neck head and face
- scratching, rubbing, alopecia and anaemia in young pigs
What recomendations would you make to diagnose, control and treat Haematopinus suis ?
Haematopinus suis
Diagnose
- clinical signs
- visualization of lice and eggs on the body of the pig
Control
- treat all the breeding and feeding stock to break the cycle
- treat the sows before farrowing
- treat the newly brought stock before introducing to the herd
Treatment
- Formamidines - Amitraz Taktik
- Macrocyclic lactones Ivermectin, Doramectin
Identify this parasite and describe its life cycle ?
Capillaria spp hairworms
Different locations within the digestive tract - oesophagus, mouth, crop and small intestine etc
Life cycle
Indirect
IH represented by earth worms - birds become infected after ingesting earthworms containing infective larvae
Direct
Infective larvae develop inside eggs 1-4weeks - birds become infected after ingesting embryonated eggs
Describe the morphology and epidemiology of Capillaria spp (hairworms) in birds ?
Capillaria spp (hairworms)
Location = different regions of the digestive tract mouth, oesophagus, crop, small intestine, caecum
Morphology
Worms = small, slender body (difficult to see with the naked eye)
Eggs
- thick shell
- barrel shape and two plugs at each end (similar to trichuris)
Epidemiology
Distributed worldwide
-
- present in indoor and out door systems
- outdoor pens of poultry may remain contaminated (eggs survive years)
- young birds most susceptible to infection
- adult birds may act as carriers
Describe the pathology and clinical signs of Capillaria spp within the oesophagus and crop ?
Capillaria spp oesophagus and crop
Pathology
- marked thickening of the mucosa
- diptheric membranes
- sloughing of the mucosa
- food may accumulate in the crop etc
Clinical signs
- Inappetance, weakness and emaciation
- frequent swallowing attempts (stretch the neck)
- death
Describe the pathology and clinical signs of capillaria spp within the intestine ?
Capillaria species in birds
Clinical signs appear 12 days post infection
Pathology
- thickening of the mucosa
- congestion
- oedema
- haemorrhagic dots
- Catarrhal inflammation (build up of mucous) and sloughing of the mucosa
(this may eliminate worms few viewed upon necropsy)
Clinical signs
- pinkish mucoid material appears in faeces
- watery diarrhoea 4 days later
- depression, anemia
- wings and tail dropped, ruffled feathers etc
Describe how you would diagnose and treat an outbreak of Capillaria spp in chickens ?
Capilliaria
Diagnosis
Necropsy
- careful examination of the digestive tract
- microscopic examination of the mucosal scrappings - worm eggs
May detect eggs in faeces
- barrel shaped, two polar plugs transparent, and thick brown smooth shell
Treatment
Levamisole
Flubendazole and Fenbendazole
What management strategies should we implement to reduce Capillaria spp in chickens ?
Control Capillaria species
Species with intermediate host
- anthelmintics and move the birds inside
- or treat with anthelmintics and move to fresh ground
Species without IH
- hygiene and heat treatments of surfaces
- regular anthelmintic treatments
Identify this parasite and describe its morphology ?
Ascaridia galli
Location = small intestine of chicken, turkey and dove etc
Morphology
- white worms up-to 12 cm in length
- anterior three lips around mouth
- posterior end of male precloacal sucker and thick cuticle rim
Eggs
- ellipsoidal thick smooth shell
- one cell inside
- difficult to distinguish from Heterakis galinarum eggs
Describe the life cycle of Ascaridia galli ?
Life cycle Ascardia galli
Location small intestine
- infected birds shed eggs in their faeces
- development of L3 takes 10-20 days
Infection = ingestion of embryonated eggs
or paratenic host earthworms ( of less importance)
After infection the larvae develop within the wall of the small intestine (Histotrophic phase no migration)
- L3 undergo arrested development
- PPT 4-8 weeks, worms can live upto 14 months
Describe the epidemiology of Ascardia galli ?
Epidemiology of Ascardia galli
Spread all over the world
- indoor and outdoor systems (rare in caged birds)
Source of infection = birds with inapparent infections (adults) and the ground
- eggs may survive a long time in the environment
- common in chickens under 3 months
- larvae do not develop in adult birds
Describe the pathogenesis of Ascardia galli ?
Ascardia galli
Location small intestine
Pathology
1, Main effects
- penetration of the mucosa of the intestine by large numbers of larvae - enteritis
- haemorrhagic enteritis
- during histotrophic phase; haemorrhage and loss of blood, destruction of the glandular epithelium
- Large numbers of adults
- alter the intestinal function - reduced weight gain
- block the intestine (usually lower half) = DEATH
Describe the clinical signs of Ascaridia gallis ?
Ascaridia gallis
Location = small intestine
Clinical signs
- anaemia
- intermittent diarrhoea
- anorexia
- unthrifty
- weight loss etc
The parasite may migrate to the large intestine / cloaca and end up in the oviduct where they can be incorporated into eggs
How would you diagnose and control for Ascardia gallis ?
Ascardia gallis
Diagnosis
History - affected are under three months of age
Clinical signs - intermittent diarrhoea, unthrifty, anaemia etc
Visualisation of the eggs in faces (floatation methods)
Eggs = epsoidal, thick smooth shell with one egg inside
Treatment
- Piperazine food or water
- Imidazothiazoles = Levamisole water
- Benzimidazoles = Flubendazole water, and mebendazol (unregistered in Australia).
How would you go about controlling for Ascardia gallis ?
Control of Ascardia gallis
All in and all out
- rear the young birds separate from adults
- rear the young birds on pastures / grounds not previously used by adult birds
- use food and water systems which prevent faecal contamination
Identify this parasite in poultry and describe its epidemiology ?
Cestode tapeworm
Location = small intestine
Epidemiology
Birds younger than 3 months are most susceptible
There are many species of cestode in birds which differ in their pathogenicity
- an identification of species is required for control and assessment of pathological potential
- only common in out door system / IH host required
- in temperate areas infections are more common in warmer seasons (IH more abundant and active
Describe the life cycle of cestodes in poultry ?
Lifecycle of cestodes in poultry
various intermediate host = houseflies, beetles, ants, snails and slugs
- gravid proglottids/eggs are passed in the faeces of birds
- proglottids/egg are ingested by IH
- cystercercoid larvae
Infection of birds occurs through the ingestion of the intermediate host
Describe the pathology and clinical signs of cestodes in poultry ?
Cestodes in poultry
Pathology
- Raillietina echinobothria causes nodules (1-6mm) at the attachment site
Clinical signs
- emaciation
- dull plumage
- leg weakness
- slow movement
- paralysis and death
Identify these eggs ?
Identify these eggs
Pink = Ascaridia galli or Heterakis galinarum
Purple = cestode
How would you go about diagnosing cestodes in birds, and treating this parasite ?
Cestodes
Diagnosis
The clinical signs are unspecific, pay attention to individuals
affected under 3 months of age
History - free range birds, warm season, poor management etc
Visualization of proglottids or eggs in the faeces of birds - hexacanth
Necropsy = nodules
Histopathology = some species are very small difficult to sight
Treatment
Flubendazole in food
prevent contact with / or eliminate IH
Why is Coccidiosis Eimeriosis so important within the poultry industry ?
Coccidiosis / Eimeriosis
Severe cases usually seen in chickens 3-6 weeks old
Coccidiosis is the most important protozoan disease of chickens
- worldwide cost of 2.4 billion
- in chickens seven species have been described
develop at different sites along the intestine
have different degrees of pathogenicity
- significant losses of birds reared indoors and outdoors
Eimeriosis life cycle is short with a high reproductive potential = sever out breaks
- crowding and environment (humidity and temp) leads to outbreaks
Identify this parasite and describe how birds become infected ?
Coccidiosis / Eimeriosis
Sporolated oocyst = four sporocyst each with two sporozoites
Mode of infection
Birds shed unsporolated oocyst in their faeces
- the disease is self limiting unless the birds become reinfected
- oocyst is highly resistant in the environment months/ years
Host become infected after ingestion of the sporolated oocyst - the infective stage
Sporulation
The process by which the sporozoites are formed within the oocyst and become infective
- depends upon temperature 28
- depends on humidity 80%
- oxygen
This is asexual reproduction within the environment
Describe asexual reproduction / of Coccidiosis / Eimeriosis ?
Asexual reproduction in the host
Infection = ingestion of a sporolated oocyst
Sporozoite = banana shaped cells with a tapered anterior end
Invasive stage - invasion of host cell
- after invasion of the host cell the sporozoite grows and turns into a trophozoite (rounded shape)
- the nucleus of the trophozoite divides - immature schizont
- mature schizont the cytoplasm divides and merozoites are formed
Merozoites are similar in structure to sporozoites
- break out of the schizonts and host cell
- invade other host cells
- resume the schizogonic development multiple times
Merozoites are the invasive stage
Describe gamogony / gametogony with the host ?
Gamogony sexual reproduction
After n schizogonic cycles
- the merozoites invade other cells and begin sexual development
microgametocyte male and macrogametocyte female
which will give rise to a macrogamete
Fecundation zygote to oocyst
Oocyst are then shed in the environment
Describe the immune response of birds to Coccidiosis / Eimeria ?
Describe the pathogenesis of coccidiosis in Chickens ?
Pathogenesis Coccidiosis / Eimeria chickens
Rupture the cells
- they develop in causing villous atrophy, epithelial sloughing
Damage the stem cell of the crypts
- reduce turnover and renewal of epithelial cells
Produce toxins
- toxins that are released into the tissues, especially schizonts break out
Alter intestinal motility
- reduced in the ceca preventing parasite removal, nutrient absorption and changing the PH
Causes decrease in plasma carotenoids
- depigmentation of carcases and reduced value
What factors could affect the pathogenesis of coccidiosis/ Eimeria in birds ?
Factors affecting the pathogenesis of Coccidiosis in chickens
- Species and strain
- E. Tenella and E. necatrix are the most pathogenic - Dose and rate of infection
- infections with a high number of oocyst in a short time = disease - The host
- sever cases usually seen in chickens 3-6 weeks of age
- age, breed, immunological experience of birds
- feeding (maize fed birds have reduced pathogenicity of E.tenella).
Describe the pathogenicity of Eimeria Acervulina ?
Eimera Acervulina
Locates in the duodenum may extend in severe infections
- scattered white plaque like lesions containing developing oocyst
- in heavier infections the lesions coalesce
- intestinal wall is thickened
- heavy infestations mucosa is bright red
Describe the pathogenicity of Eimeria maxima ?
Eimeria Maxima
Location jejunum
- most immunogenic
- small red petechia on the serosa surface
- orange coloured mucus or blood clots
- intestine is ballooned and the wall is thickened
Describe the pathogenicity of Eimeria necatrix ?
Eimeria Necatrix
Locates in the ceaca and jejunum
- one of the most pathogenic species
- 2nd generation schizonts cause the pathogenic stage
- white plaques or petechiae may be visable from the serosal surface
- intestinal content is streaked with blood
- ballooning, haemorrhages
Diagnostic - gut scrappings of the jejunum, large schizonts which are diagnostic for this species
Describe the pathogenicity of Eimeria tenella ?
Eimeria tenella
Locates in the ceca
- one of the most pathogenic species
- 2nd generation schizonts are the pathogenic stage
- scattered petechiae on the cecal wall
Bleeding with clotting caeca are most distended
- most birds die - if not the clot hardens as the mucosa cells join the blood to make a core
- cecal wall is thick, greatly distended containing blood and / or large caseous cores
What are the clinical signs of coccidia Eimeria in chickens ?
Clinical signs
Clinical
Common in infections with E.tenella and E.necatrix
- birds cease to drink or feed but later display polydipsisa
- huddle may let out a high pitched call
- the comb and wattles are pale atrophied
- wings are dropped, feathers ruffled and eyes closed
Haemorrhagic diarrhoea
Subclinical
- Birds do not show obvious signs but their performance is affected - difficult to diagnose
How would you go about diagnoses of Coccidioses / Eimeria in birds ?
Diagnoses of coccidioses in birds
History - age 3-6 weeks signs of severe disease, floor, overcrowding and potential chemoreresistance
Clinical signs
Identification of oocyte in faeces (direct smear)
- birds may shed oocyst without having any clinical signs
- schizonts, merozites, gametocytes, oocyst in gut scrappings or histological section
What treatments could we implement when dealing with coccidiosis / eimeria in chickens ?
Describe the management / prevention strategies in Coccidiosis / Eimeria ?
Prevention is best
Hygiene and poultry management
- all in all out
-feed
- bird density
- cleaning
Vaccination
- live vaccines and attenuated vaccines
- transfer of protective antibiotics from immunized hen to embryo
Broilers
- usually anticoccidial drugs are provided in the feed from one day of age until 5-7 days to market
Two programs are common
- Shuttle programs two or more anticoccidial are used in successive stages - in each growing cycle
- Straight programs a single coccidial is used through out
Identify this parasite and describe its morphology ?
Heterakis gallinarum
Location = caecae
Host = chicken, turkeys, geese, ducks etc
- mouth with three lips
- 2 lateral narrow alae extending the length of the body
- oesophagus ends in a well developed bulb
- posterior end female pointed, male pre cloacal sucker
Eggs
- elliptical lateral sides are almost parallel
- brown thick smooth one cell inside
resistant may survive a long period in the environment
Describe the lifecycle and epidemiology of Heterakis gallinarum ?
Heterakis gallinarum
Epidemiology
Location = caeca
- world wide distribution
- present in both indoor and outdoor systems
- eggs can survive for a long time in the environment up to 3 years
- earth worms may also survive a long time in the environment
Life cycle
Infected birds shed eggs in the environment
- eggs become embryonated with 2-3 weeks under optimal temperatures 26 degrees
Infection
- ingestion of embryonated eggs
- ingestions of earthworms, grasshoppers or flies which are contaminated
Larvae hatch within the small intestine than migrate to the ceca where they reach adulthood (lumen only) within 4 weeks
Describe the pathogenicity and clinical signs of Heterakis gallinarum
Heterakis gallinarum
Pathogenesis
- non pathogenic / low pathogenicity
- may cause slight inflammation or thickening of the mucosa
This parasite is important as it is a vector for
Histomonas meleagridis
What strategies should we implore to diagnose and treat Heterakis gallinarum ?
Heterakis Gallinarum
Prevention
- control is particularly hard especially in out door systems where earthworms are present
Diagnosis
- finding eggs within the faeces
- post mortem examination of the ceca (small slender worms)
Treatment
Levamisole water
Flubendazole food
What species does Heterakis Isolonche infect ?
Identify this parasite and describe its morphology and epidemiology ?
Histomonas meleagridis (black head disease, entero hepatitis)
Location = caeca and liver
Host = galliformes chickens, turkeys
Morphology
Pleomorphic = its appearance depends upon its location
- caecal lumen form = one flagellum
- tissue form rounded essentially the same but no flagellum
- acyst like form has also been described
Epidemiology
- mortality can exceed 85%
- outbreaks in the EU and Americas have been increasing
Describe the complex life cycle of Histomonas meleagridis ?
Histomonas meleagridis
Location = liver and caeca
In the ceca of the bird host Histomonas meleagrids infects Heterakis gallinum
- ovaries of the female become incorporated in to the eggs
- within the eggs Histomonas may survive 2-3 years
Transmission
- contaminated embryonated eggs of Heterakis gallinarum
- digesting paratenic host (earthworms) with Heterakis gallinarum infected with Histomonas
(direct transmission is possible)
- cloacal drinking
- after ingestion of contaminated food or water
In the caeca of the host Histomonads multiple (binary fission) and in 2-3 days enter the blood stream and reach the liver
Describe the epidemiology of Histomonas meleagridis ?
Epidemiology of Histomonas meleagridis
Host = galliform birds
Location = liver and ceaca
Age chicken between the ages of 4-6 weeks are most susceptible to disease
- distribution is all over the world
- severe disease in turkeys, partridge ruffled grouse
- chickens are often carriers - source of infection for turkeys
(Never rear turkeys and chickens together)
The role of Heterakis gallinarum and earthworms as vectors explain the long period of disease that might persist on farms
- Turkey farms are not usually contaminated with Heterakis gallinum
Once the infection is established on a farm it spreads quickly without the need for vectors - cloacal drinking and ingestion og Histomonas
What factors could affect the pathogenicity of Histomonas meleagridis in chickens ?
Pathogenicity of Histomonas meleagridis depends upon
Host species
- turkey more susceptable
Intestinal flora
- lesions can not be produced in germ free turkeys
- in chickens already infected with E.tenella the lesions were more severe and prevalent
Describe the pathogeniciy of Histomonas meleagridis in the ceca and liver of birds ?
Pathogenicity Histomonas meleagridis
Multiplication of the Histomonads in the cecal wall and liver = necrosis
Ceca
After tissue invasion - caecal wall develops thickened and hyperemic
- necrosis develops
- ceca become distended with a caseous / cheesy core made up of concentric layers
- ulcers - perforation of ceca - generalised peritonitis
Liver
Areas of depressed necrosis (underlying tissue is destroyed
- grow upto 1cm in diameter and are surrounded by a raised ring
- in heavy infections lesions may be small, numerous and they involve a large portion of the liver
Describe the clinical signs of Histomonas melegridis in turkeys ?
Clinical signs in turkeys
Incubation period 7-12 days (shorter after cloacal exposure)
- yellow faeces
- drowsiness, drooping of wings, closed eyes, head down close to body and head tucked under wing
- anorexia
- the head may or may not by cyanotic (increase methanoglobin levels)
emaciation and death in a high percentage (80-90%)
Describe the clinical signs of Histomonas melegridis in chickens ?
Clinical signs chickens
- rarely yellow faeces
- may shed bloody faeces and caseous caecal cores
- mortality may exceed 30%
Describe how you would diagnose Histomonas melegridis ?
Diagnosis of Histomonas melegridis
Clinical signs
History - most prevalent in chickens 4-6 weeks old
- identification of Histomonas in the caecal fluids or mucosal scrappings
- cultivation DWYERS MEDIUM
-Histopathology fresh samples as parasites autolyse fast
- PCR
What management strategies could we use to prevent and treat Histomonas melegridis
Histomonas melegridis
Treatment
5-Nitroimidazoles
Dimetridazole
Note products have been prohibited for use in food animals
- only use in breeders
Prevention
- do not grow chickens and turkeys together
- do not use chicken sheds for turkey use
- house flocks on concrete or wire floored pens
- hygiene, cleaning and disinfection
- before restocking quarantine new birds
Identify this parasite and describe its morphology ?
Morphology syngamosis trachea
Location = trachea
Host = turkey, pheasants and fowl
Adults
- female and male worm are always coupled - couple has the shape of the letter Y
- red colour when fresh as they feed on blood
Eggs
- an operculum at each pole
- relatively thick shell
- morula stage
Describe the life cycle of syngamous trachea ?
Syngamous trachea life cycle
Eggs are coughed up and swallowed - expelled into the environment with faeces
- L1-L3 within the egg - some L3s may hatch
Infection of host
1. eggs with L3
2. free L3 in the environment
3. paratenic host containing L3 (earthworms, slugs and snails)
L3 travel to the liver, lungs and trachea
PPT 12-17 days
Describe the epidemiology of Syngamous trachea ?
Syngamous trachea Epidemiology
Host = turkey (natural host), chickens, pheasant
- birds of all ages are susceptible to disease - but generally younger birds suffer a greater severity of disease
- common in outdoor systems
- infection seasonal warmer increased IH
- larvae can persist for long periods (4 years) within earthworms, the ground can remain contaminated for long periods
- wild birds are a potential source
Describe the pathogenesis of Syngamous trachea ?
Pathology Syngamous trachea
Caused by larvae while migrating in the lungs and adults within the trachea
Lungs larvae
- heavy infestations = oedema, pneumonia and death
Adult worms trachea
- feed on blood female, feed on tissue male
- grow rapidly
- haemorrhage inflammation, excessive mucous
- males are buried deeply in the wall of the mucosa
Describe the clinical signs of Syngamous trachea ?
Clinical signs of syngamous trachea
Suffocation - birds gasp for air and stand ‘gaping’
- coughing
- dyspnoea
- shaking of the head and extending of the neck
- death with 2-3 days
How would you diagnose, treat and control for syngamous trachea ?
Syngamous trachea
Location = trachea
Diagnosis
- Clinical signs
- History (young birds, outside and warm season)
- detection of eggs in faeces
- visualisation of worms within the trachea upon necropsy
Treatment
Levamisole water
Flubendazole administered in food
Prevention
- indoor systems
- separate young birds from older birds
- prevent contact with wild birds
- treat prophylactically before outbreaks
Identify this parasite and describe and life cycle ?
Oxyspirura mansoni
Host = chickens, turkeys and ducks
Location = inner corner of the orbit under the nictating membrane, causes blindness
- tropical and subtropical areas
Intermediate host = cockroaches
-eggs are deposited in the eye - secretions - lachrymal duct
- mouth swallowed and then passed out in faeces
- eggs are ingested by cockroaches in about 50 days the larvae reach the infective stage
- COCKROACHES ARE INGESTED BY BIRDS - larvae leave the cockroaches in the crop - to the oesophagus - mouth - lachrymal duct - eye
PPT 50 days
Describe the
epidemiology
pathogenesis / clinical signs
diagnoses
treatment
and prevention for Oxyspira mansoni ?
Oxyspira mansoni
Epidemiology
- tropical and subtropical areas
Pathology / Clinical signs
- Inflammation of the eye oedema, watery eyes, blindness
- scratching of the eye
Diagnosis
- visualisation of the parasite
- clinical signs
- examination of the lacrimal secretions may reveal eggs
Treatment
Ivermectin and moxidectin oral treatment
Prevention reduce the number of cockroaches
Identify this parasite and describe its epidemiology ?
Trichomonas gallinae
Clinical signs are usually evident in birds younger than one month
Trichomonas gallinae is a flagellate protozoan that occurs primarily in the upper digestive tract of columbiforms (doves, pigeons).
Location - upper disgestive tract, mouth, pharynx, oesophagus and crop
World wide distribution
- may infect a wide range of birds species
- may infect mammals including humans a zoonosis
- prevalence around 100% in pigeon / dove populations asymptomatic carriers
- significant impact on wildlife populations
Identify this parasite describe its morphology and life cycle ?
Trichomonas gallinae
Host = pigeons doves
Location upper digestive tract oesophagus, pharynx, crop etc
Morphology
- four anterior flagella and no posterior flagellum
- undulating membrane does not reach the posterior end of the body
- many strains vary in virulence
Transmission
- Columbiforms pigeon milk
- Galliforms feeding and watering from infected containers (wild birds)
Describe the pathology of Trichomonas gallinae ?
Pathology Trichomonas gallinae
Depends on the strain and immune status of birds
- secretes factors that initiate damage, separation and renewal of squamous cells
- invade the areas beneath the squamous cells
Accelerated desquamation, invasion of the mucosa and development of the canker
- ulcers covered by yellow membranes
- caseous necrosis
- build up of caseous material that may invade the roof of the mouth and sinuses - block oesophagus / pharynx
- yellow caseous nodules ‘yellow buttons’
- in the liver absesses, necrosis
Describe the clinical signs of Trichomonas gallinae ?
Trichomonas gallinae clinical signs
Excess of watery saliva and foul cheese like smell
- yellow caseous lesions around the beak and eyes
- yellow masses located on the floor - block the passage of food, trachea
- death from starvation or respiratory failure
weight loss, ruffled feathers and listlessness
How would you go about diagnosing Trichomonas gallinae ?
Diagnosis Trichomonas gallinae
History, clinical signs
Identification of the Trichomonads
wet smears - mucous lesions
culture - higher sensitivity then wet smears
PCR
Differential diagnosis = vitamin A deficiency
How would you go about treating or preventing Trichomonas gallinae ?
Trichomonas gallinae
Upper digestive tract oesophagus, crop, pharynx
5-nitroimidazoles
5nitroimidazoles have been prohibited for use in food animals in Australia
- Metronidazole
- spartrix
Prevention
- prevent flocks of doves, pigeons coming to feed from feedlots of livestock
- keep feeders and drinkers clean
- food and water should be changed regularly
Identify this parasite of birds and describe its life cycle ?
Poultry tick Argus persicus (fowl tick)
Host = chicken, turkey, duck - wild birds etc
can attack humans, dogs etc
Life cycle
Females lay eggs in the cracks and crevices of the shelter (batches 25-100eggs)
- each oviposition is preceeded by a blood meal
- eggs - larvae (permenant parasites (5-10 days) - nymphs (feed on host at night) - adult (feed on the host at night)
Can survive for long periods of time without feeding (>4 years) adults
(nymphs >2yrs, larvae >9months)
Describe the morphology and epidemiology of this parasite ?
Argas persicus (fowl tick)
Epidemiology
Host = chicken, turkey, duck - wild birds etc
- can attack humans and dogs
- generally only cause problems in outdoor systems
Morphology
- Gnathostome located on the ventral surface
Describe the pathology of Argus persicus (fowl tick) ?
Argus persicus Pathology
All stages remain around the roosting area
- nymphs and adults attack the host and feed during the night (5mins - 2hrs)
- larvae can attach and feed continuously (5-10 days) - may cause paralysis
- most larvae can be found on the neck, head and under the wings = diagnosis
vector = Borrelia anserina, Aegyptionella pullorum
Describe the clinical signs of Argus persicus ?
Argus persicus clinical signs
Heavy infestations - loss of blood - fatal anemia
- ruffled feathers
- poor apetite
- emaciation, weakness
- slow growth
- lowered production
turkeys will suffer more than chickens
Describe the process of diagnosing and treating an infection of Argus persicus ?
Argus persicus
Diagnosis
- clinical signs, history (out door systems)
- if birds are examined at night visualisation of adults, nymphs and larvae
- If birds examined during the day observation of larvae as they remain attached to the skin
- neck, head and under wings
Treatment
Maldison
- spray or dust poultry shed with approved acaricides (forcing spray into cracks and crevices
- requires continuous monitoring prevent population from building up
Identify this parasite and describe its epidemiology ?
Dermanyssus gallinae (poultry red mite)
Able to bite mammals including humans zoonotic
Host = broad range of birds pigeons, canaries, sparrows, dogs, horses cattle and humans
- cases involving mammals usually occur in association with poultry houses or infested birds nest
Epidemiology
- common, prevalence increasing in poultry
- vector for bacteria salmonella, pasteurella and viruuses fowl pox and new castle disease
- present in all growing systems but most frequent in non intensive free range, barns, outdoor backyards
Identify this parasite describe it morphology and life cycle ?
Dermanyssus gallinae
Morphology
- oval body
- dorsal plate shield tapers posteriorly and its posterior margin is straight
- anal plate is triangular and the anus is located in the posterior half
Life cycle
Spend most of their lifetime in the poultry house, usually hidden in the cracks and crevices
- after feeding on the host at night females retreat to the cracks and crevices to lay eggs
- adults within seven days
egg - larvae (does not feed) - 2 nymphal stages
Large populations develop very quickly
Describe the clinical signs of Dermanyssus gallinae ?
Pathology Dermanyssus gallinae
Dermanyssus are very mobile, they bite and irritate the host
Birds become restless, do not feed and refuse to enter the infested sheds or lay in nest boxes
- feeding lesions (erythemia, vesicles)
- are frequently observed on the chest and legs
- anemia
- nervousness
- damage to plumage and feather loss
- rhinitus, conjunctivitis caused by invading mites
Chicks may die rapidly
Describe the pathology of Dermanyssus gallinae ?
Dermanyssus gallinae Pathology
Nocturnal blood feeders - during the day they remain hidden in cracks and crevices
- usually engorge completely in one feeding
- feeding female can live upto 7weeks, if unfeed upto 9 months
- remain on body while feeding 0.5-1.5hr after which they hide in crevices
Describe how you would go about diagnosing Dermanyssus ?
Diagnosis of Dermanayssus
- Clinical signs
- check the birds during the night
- during the day inspect the house and or the traps
Necropsy - dead mites within the oral cavity mucous / rarely in the ear canal or plumage
Describe how you would treat and control a outbreak of Dermanyssus ?
Dermanyssus
Control
Management is critical
- treatment of mites habitat is important
- clean, spray, dust poultry houses with acaricides (pyrethroids, organophosphates) pay attention to cracks and crevices
- vacuum clean the house and wash with scalding water
Use traps inpregnated with acaricides
- not parasites have the potential to build up to large number extremely quickly
Spinosad - treatment for environmnet
Treatment
Pestene (sulfur and rotenone powder for mites and lice)
Maldison (organophosphate)
Exolt in drinking water
Identify this parasite and describe its morphology ?
Ornithonyssus spp (fowl mites)
Morphology
They are similar to dermanyssus
- usually more spiny
- anus located anterior end of anal plate
- chelae well developed
Dark red post feeding
Describe the lifecycle of Ornithonyssus sylviarum and Ornithonyssus bursa ?
Ornithonyssus species life cycle
O. Sylviarum
Most eggs are laid on the host - usually mites will spend their entire lives on the host
- may leave the host when populations are high
- short life cycle (5-12 days) big populations may develop quickly
Infestation
- direct contact
- placing birds in accommodation previously infested
- mites may be seen off the host
Populations peak 4-10 weeks after infestation
O. Bursa
Similar to Sylviarum except
eggs may be laid on the host or in the litter/nests - the mites are only on the host for a short time to feed
Describe the epidemiology of Ornithonyssus species ?
Epidemiology of Ornithonyssus spp
O. Sylviarum
The most important and common ectoparasite in some countries
- Infestations are more common during the cold season
- present in all production systems
- spread all over the world in temperate regions
- infects domestic birds (chickens, turkeys) and wild birds
- severe problem in caged laying hens or breeding stock
- breeder flock males are generally more infested than females
Zoonoses also infects mammals including humans
Most mites on hen are located around the vent
O. bursa
The preferred breeding sites are the head and vent
- large numbers of parasites gives the feathers a dirty appearance
Describe the pathology of Ornithonyssus species ?
Pathology Ornithonyssus spp
Ornithonyssus sylviarum and bursa are blood feeders
- both species feed in the dark half light
- number of mites on the birds might be very high sometimes exceeding 100000 mites
In severe infestations with O. sylviarum may cause upto 6% blood loss per day in caged laying hens
Describe the clinical signs you would observe with an infestation of Ornithonyssus spp ?
Clinical signs of Ornithonyssus spp
O.sylviarum locates around the vent, but as the population increases it spreads to the breast and leg
- feathers may become mattered
- severe scabbing develops particularly around the vent
- may show a gre black discolouration of the faethers due to the heavy population of mites - mite skins, dead mites and dry blood
- restless, weight loss, anemia and production loss
Thickened crusty cracked skin and soiled feathers around the anus
Describe how you would diagnose Ornithonyssus spp
Diagnosis of Ornithonyssus
- clincal signs vent
- mites may be found on the birds during the day and night
- mites might be sighted crawling on eggs / hands of personnel handling the poultry and eggs
Note Ornithonyssus can attack people
What management strategies could we implement to control and treat Ornithonyssus spp populations ?
Ornithonyssus spp.
Treatment
Maldison organophosphate
Pestene (sulfur rotenone, powder for mites and lice)
Pyrethroids - oil solutions or plastic strips
Treatments are most effective when applied to feathers in the vent region
Chemoresistance to organophosphates has developed
In addition
- dry heat stem coop
- prevent introduction of the mites to the farm
- monitor flocks weekly
Identify this parasite describe its morphology and life cycle ?
Cnemidocoptes mutans
Host = domestic chicken, turkey usually older birds
Scaly leg mite on the legs of chickens
Location - under the scales of the legs
Morphology
- circular
- female dorsal surface scaly aspect
- gnathostome wider than it is long
- no dorsal spines
- legs are short and stubby
Life cycle
The life cycle is completed on the host within 2-3 weeks
- females give birth to hexapod larvae
- octopod protonymphs - tritonymphs - adults
Infection
- direct contact with infected birds
- mite may be picked up from the ground
- feathered parents to non feathered offspring-
Describe the pathology and clinical signs of Cnemidocoptes mutans
Cnemidocoptes mutans
Lesions are produced on the unfeathered portions of the legs
- the parasites burrow under the epidermal scales
- irritation, inflammation exudate which hardens to form crusty proliferative masses
- uplifting and upturning of the scales
Within the proliferative lesions mites cretae numerous tunnels - giving the lesions a honeycomb appearance under the microscope
In severe lesions the birds may become crippled and their legs become deformed
As the disease progresses birds stop eating and waste away
Describe how you would diagnose and treat Cnemidocoptes mutans ?
Cnemidocoptes mutans
Diagnosis
Clinical signs and identificaion of the mites in scrapping of the skin and lesions
Treatment
Birds may be treated by dipping the legs in acaricidal solutions
(treatment 10-14 days apart)
- prior to treatment warm soapy wtaer
- apply acaracide in a oil based product
Exalt - Fluralaner
Describe the morphology and clinical signs of Cnemidocoptes gallinae ?
Cnemidocoptes gallinae (depluming mite)
Host = chickens, pigeons and pheasants
Morphology
Similar to C.mutans but the females lack the scaly component
- striations are not broken interupted
Pathology/clinical signs
Mites burrow into the feather shfts and upper layers of the epidermis
- feeding tunnels in which larvae are born alive
- intense itching causes birds to pull out feathers “depluming itch”
- loss of feathers over the body, mites in the feather shafts
- redness
Causes
Hyperkertosis of the skin - wrinkling and thickening
Describe the clinical signs and treatment of Cnemidocoptes pilae ?
Cnemidocoptes pilae
Host = budgies, parrots, rainbow lorikeets
most common in fledging and young adults
Transmission = direct contact
Clinical signs
- thick crusts around the beak
- deformity of the beak
- difficulty in respiration and feeding
Treatment
- Ivermectin and Moxidectin via oral administration
Identify this parasite and describe its life cycle and morphology ?
Menacanthus stramineus (chicken body louse)
Host = chicken, turkey
most common pathogenic louse of turkeys
common on breast thigh and fillets
Morphology
- head is triangular wider than thorax
- two short spinelike processes on the ventral side of the head
- at least two rows of setae on each segment
Life cycle
All stages (eggs, 3 nymphal stages and adult) all occur on the host
- eggs are glued to hair shaftin clusters or individually at the base of feathers
PPT 3 weeks
Transmission = direct contact
Identify this parasite and describe its epidemiology ?
Menacanthus stramineus (chicken body louse)
Common in out door systems
- birds of all ages are suceptable
- within intensive systems louse are generally present in caged layers and floor breeders (rare in broilers)
- poor health (infection, nutrition, poor sanitation) will increase louse populations
Generally populations of louse increase in the cold climates
Describe the pathology and clinical signs of Menacanthus stramineus (chicken body louse) ?
Menacanthus stramineus
Host = chicken, turkey
Pathology / Clinical signs
Irritation - pruritus - scratching - damage
to the feathers, and skin crusts
Reddening of the skin which eventually becomes scabby
Describe how you would diagnose and treat/control for Menacanthus stramineus ?
Menacanthus stramineus
Diagnose
- clinical signs and history (outdoor, caged or floor breeders, nutrition, poor sanitation, other infections)
- identification of the louse on skin and feathers, part spread the feathers
-sighting of egg clusters on the feathers
Treatment and control
- Spray the poultry with an approved insecticide (ensure the whole bird is treated)
- generally insecticides are ineffective against the eggs - repeat treatment after 7-10 days
- check treat newly acquired birds
- remove manure and feather (egg clusters)
Identify this parasite and describe its life cycle and morphology ?
Echidnophaga gallinacea (stickfast flea)
Host = birds but also dogs, cats and humans etc
(zoonotic)
Morphology
- no ctenidia (combs)
- angular head
- reduced thorax
- mouthparts are long
Identify this parasite and describe its life cycle ?
Echinophaga gallinacea
Transmission = from the environment
Female fleas burrow into the skin where they attach firmly with their mouth parts
- after copulation females lay 1-4 eggs/day that fall to the ground (eggs in ulcerations - larvae will hatch then fall to the ground)
on the ground larvaehatch in 1-2 weeks - feed on chicken manure and flea excrement
L1 - L2 - L3 in 2-4 weeks - L3 spins a caccoon - pupa (3 weeks) then emerges as adult
entire life cycle in 1-2 months
Describe the epidemiology of Echinophaga gallinacea ?
Echinophaga gallinacea
Host = birds
zoonotic = cats, dogs, rabbits and humans
- common in the tropics
- may also be present in subtropical or temperate areas
- common in areas with sandy soil (larvae develop well in drained litter - out door environmnets)
Transmission = from the environmnet
Describe the pathology and clinical signs of Echinophaga gallinacea ?
Echinophaga gallinacea
Adults usually attach to the skin of the head, often in cluster of 100 or more (combs, wattles)
- females burrow into the skin with their mouth parts deeply embedded into the skin difficult to dislodge
- the skin around the point of attachment becomes ulcerated - bacterial complications
- irritation, scratching, birds may injure eyes, blindness, starvation
- in large numbers might cause anaemia and emaciation
Death may occur in young birds
Describe how you would conrol and treat for echidnophaga gallinacea ?
Echidnophaga gallinacea
Confinement of poultry
- provision of an impervious floor
- regular removal of faeces (contaminated) and cleaning of sheds
- eliminate shaded areas
- check and treat newly acquired birds
- prevent contact with wild birds, dogs, rats and cats
Pyrethrins, Pyrethroids
Maldison
Describe the morphology of Ceratophyllus gallinacea ?
Identify this parasite describe its morphology ?
Cystoisospora Isosporosis
Morphology
Unsporolated oocyst
- found in the faeces of infective animals, not effective for other animals
- thin shell
- contain one cell called a sporont
Sporolated oocyst (infective for other animals
- thin shell
- contains two sporocyst each with four sporozoites (banana shaped cells)
Describe the epidemiology of Cystoisospora Isosporosis in dogs and cats ?
Epidemiology Cystoispora Isosporosis
The most common coccidian parasites to infect dogs and cats
Location = small intestine (location varies with species)
- no significance for human health
- worldwide distribution - prevalence 3-38% of dogs
- young animals are more likely to be infected <1 month
- cross immunity is unlikely
- adult animals are likely to be resistant but can be sources of contamination with oocyst
- out breaks are common in breeding units, catteries and kennels
- prevalence is higher in strays
Describe the life cycle of Cystoisospora Isosporosis ?
Cytstoisospora Isosporosis
Life cycle
The infected host shed unsporolated oocyst into the environment
- sporulation 6-12hr fast
- some sporozoites will penetrate the intestinal wall and get to the mesenteric lymph nodes, liver, spleen etc where they may forms cyst
Transmission
The definitive host
- ingestion of a sporulated oocyst with contaminated foor or water
- or ingestion of parenetic /IH host mice rats shorter PPT
- the sporozoites excyst in the small intestine and invade the epithelial cells and divide
Paratenic / intermediary host
- Mice and rats might serve as a paratenic or intermediary host
- sporozoites grow in size and become surrounded by a cyst wall
(no replication within paratenic host)
Describe the pathology / clinical signs of Cystoisospora Isosporosis ?
Clinical signs Cystoisospora Isosporosis
Clinical signs are common in young animals < 1 month
- debilitated, immuno compromised and stressed animals
- may occur 2-3 days before the excretion of oocst in the faeces
- diarrhoea that sometimes (severe cases) may contain blood
- vomiting, abdominal pain and anorexia
- dehydration, weight loss and anemia
Describe how you would go about diagnosing and treating for Cystoisospora Isosporosis ?
Cystoisospora Isosporosis
Diagnosis
History - young animal < 1month, recurrent problem, stress + clinical signs
Detection of oocyst (faecal floatation) in the animals with clinical signs
- healthy animals may excrete oocyst
- clinical signs proceed oocyst shedding - must repeat faecal floatation
Treatment
Generally self limiting infection
Treatment speeds up resolution and reduces environmental contamination
- treat all animals within the litter metaphylactic treatment
treatment of bitches and new born may be indicated
Toltrazuril (baycox) off label dogs and cats
Procox approved for use in dogs
- do not use in collie or animals under two weeks
Describe how you would go about preventing an outbreak of Cystoisospora Isosporosis ?
Describe the epidemiology of fleas in cats and dogs ?
Epidemiology of fleas in cats and dogs
The most important ectoparasites of cats and dogs
About 5% of the flea population exist as adults on the host, the rest are in the environment as eggs, pupae, larvae
- spread all over the world
- higher prevalence during spring and summer
- may account for more than 50% of dermatological cases
- control cost 1billion a year in the US
- can feed on many host species
- houses offer conditions where the life cycle can be completed all year round
Intermediate host for Dipylidium caninum and Acanthocheilonema
- virauses and bacteria
There is a significance for humans zoonosis
Ctenocephalides will bite especially if pets temporily removed or flea populations are large
Identify this parasite and describe its morphology ?
Morphology Ctenocephalides
Brown black flattened laterally
- two sets of ctenidia
C. felis
- female head twice as long as it is wide
- dorsal border of hind tibia 6 notches
C. canis
- head is high rounded anteriorly
- dorsal border of hind tibia has 8 notches
- head rounded anteriorly
Describe the pathology of Ctenocephalides ?
Ctenocephalides feeding
The adult fleas feed on blood (piercing sucking mouthparts)
- once on a host fleas start feeding within minutes
- fleas ingest more blood than they need - development of larvae (indirect parasitism)
220 females could consume 10% of a 0.45kg kittens blood per day = anemia
Describe the life cycle of Ctenocephalides and its various life stages ?
Ctenocephalides
Permanent parasites less than 15% would leave the host - the usual way of becoming infected is from the environment
Adults are permanent ectoparasites
- eggs; laid on the host but fall into the environment
Females begin laying 24-36 hours after their first blood meal
Most eggs fall of the host within 8hrs accumulating where the pet sleeps and rest
Most eggs are laid at night
- larvae develop in the environment
Most larvae develop at the base of carpet inaccessible to insecticides - pupae develop in the environment
L3 spins a silk cocoon which develops in the environment into a pupae
Best protected and resistant life stage - pre emerged adults environment
Emergence may occur after 6 weeks or 6 months causing issues for control
Host stimulated heat, light CO2 and air currents
Favourable conditions for development 50% humidity and 25 degrees
Various stages
Describe the clinical signs of Ctenocephalides ?
Ctenocephalides Clinical signs
1. Irritation
- presence of fleas
- flea movement
- action of sucking blood (red spot with a halo)
- injection of saliva (contains histamines)
- Anaemia (from blood loss)
In non allergic dogs clinical signs and lesions are minimal
(sometimes even in cases with high flea infestations)
Pruritus, scratching, alopecia, chewing may have tapeworms
Define FAD and discuss its pathology/ clinical signs ?
FAD Flea allergy dermatitis
Most if not all dogs become allergic to salivary antigens of fleas
- eryemthotous wheel at flea bite site develops into pruritic papule
- pruritis and repeated self trauma
- alopecia and stubbed broken fur
- dogs will bite at the fleas
Type 1, ( immediate IgE mediated mast cell degeneration)
Type 2 (delayed cell mediated T -DTH)
Cutaneous basophil hypersensitivity
(degranulation of basophils occurs 4-6 hours after the flea bites)
Dogs may become sensitized after 6-10 weeks of intermittent flea exposure
- may occur in age of dog but most common in animals 2-5 years of age
- the dermatitis is typically confined to the dorsal lumbosacral area
- forms a triangular shape
Describe the FAD of ctenocephalides felis in cats ?
FAD flea allergy dermatitis caused by Ctenocephalides
Fad is seen in cats of any age, sex and breed
- the primary clinical lesion seen in the cat is the erythematous papule covered by a small reddish brown crust
- these pruritic lesions are usually most severe on the head neck and dorsal lumbosacral regions
- alopecia is highly variable
Pruritus = moderate to severe pruritus licking, scratching and biting at the skin without visible provocation
- scaling
- broken skin
- restless
- loss of weight
Describe how you would go about diagnosing Ctenocephalides ?
Ctenocephalides fleas of dogs and cats
Diagnosis
- History and Clinical signs - lack of preventative treatment
- Response to insecticidal treatment or corticosteroids
- Visualization of fleas or flea faeces on the host
- fleas may be difficult to find in flea allergic animals
In difficult cases
- visualization of dipylidium caninum proglottids
- allergy testing intradermal
- ELISA detect specific IgE
- the use of a fine toothed comb to remove fleas as part of a physical examination
Identify this parasite and describe its morphology ?
Cryptosporidiosis
Location = intracellular but extracytoplasmic tip of epithelial cells
- changes in the parasite and host cell result in the formation of an attachment or feeder organelle
Morphology
- highly refractile
- contain four sporozoites (no sporocyst)
Two types of oocyst
1. Thick shell - 80% passed in the faeces of the host
2. Thin shell - autoinfection
Describe the life cycle and epidemiology of Cryptosporidosis ?
Cryptosporidosis
Location = intracellular of epithelial cells
Life cycle
Similar to Eimeria
Infection = ingestion of sporulated oocyst (contain 4 sporozoites)
- schizogony multiple times
- gametogony
Sporogony (in situ)
animals shed sporolated (infective oocysts)
- thick oocyst
- thin oocyst, autoinfection
Epidemiology
World wide distribution
- most infections are asymptomatic
- dogs and cats with diarrhoea are more likely to shed oocyst in the faeces
- young immunocompromised animals infected with other pathogens (Giardia) are more likely to have clinical signs
oocyst are highly resistant in the environment
There are implications for human health, but they are limited
Describe the clinical signs for cryptosporidiosis in dogs and cats ?
Cryptosporidiosis
Immunocompetent animals
- Asymptomatic
- excrete the oocyst for two weeks then stop shedding
Immunocompromised animals
- may develop signs of enteritis
- clinical signs observed in animals under six months
- diarrhea, anorexia and weight loss etc
Describe how you would diagnose Cryptosporidium and treat the infection ?
Cryptosporidium
Diagnosis
- clinical signs < 6 months
- identification of oocyst in the faeces
sugar and zinc floatation - oocyst are small and hard to see
Ziehl Nielson staining of faecal smears
Detection of DNA with PCR
Treatment
In most animals immunocompetent self limiting
- find and treat any underlying issue
- no drugs are registered for the treatment of infection
Trials are being run
Tylosin
Azithromycin
Paromysin
Nitazoxanide
Identify this parasites and describe its morphology ?
Giardiosis
Morphology
There are two form
Trophozoite
- pear shaped cut longitudinally
- rounded anteriorly, pointed posteriorly
- ventral adhesive disk
- two nuclei
- four pairs of flagella
usually passed in the diarrhoeic stools, does not survive in the environment
Cyst
- oval
- 2-4 nuclei, axonemes of the flagella and fragments of the adhesive disk
Passed in the well formed stools, may survive for several months in the environment
Describe the epidemiology and distribution within the host of Giardiosis ?
Epidemiology of Giardia
Infections with Giardia are found all over the world
- common in young animals < 1 year
- frequently prevalence is similar in animals with or without diarrhoea
In the environment the cyst can survive for months in wet and cold conditions
Zoonotic - but infection of humans from cats and dogs is minor
Distribution within animal - varies with host and diet
Dogs = duodenum and jejunum
Cats = throughout the intestinal tract
Describe the hosts, and location of these three species of Taenia - T. hydatigena, T. pisiformis and T . ovis ?
Taenia
DH = Adult worms locate in the small intestine of the dog, wolf, fox
Taenia Taeniaeformis = cat/fox SI
T. hydatigena
IH = Larval stage (cysticercus tenvicollis), develops in the peritoneum of cattle, sheep, goats, pigs and rarely horses
T. pisiformis
IH = Larval stages (cysticercus pisiformis) develop in the liver and peritoneum of rabbits
T. ovis
IH = Larval stages (cysticercus pisiformis) develop in the muscle of sheep and goats
Describe the life cycle of Taenia species ?
Life cycle Taenia species
The definitive host = the dog
- Adult Taenia live in the small intestine of the definitive host, usually up-to one year
- commonly shed 2-3 gravid proglottids in the faeces per day (100000eggs)
Eggs which are shed in the environment are infective (contain a hexacanth embryo) for the intermediate host.
The intermediate host
- infected through the ingestion of eggs or gravid proglottids
- oncospheres (hexacanth embryos) released from eggs
- penetrate the wall of the intestine, make their way to the organ of predilections (liver, muscle, brain) where they develop into mature metacestodes.
Describe the epidemiology of Taenia species ?
Taenia cestode
Definitive host = small intestine
Intermediate host = brain, liver, muscle depends on species of Taenia
Infections of Taenia are spread all over the world
- prevalence depends on the opportunities of the dogs to feed on viscera from slaughtered livestock or hunted animals
- infections are common in farm dogs, dogs from abattoirs and rural areas
- eggs of Taenia may survive upto one year on pasture
- eggs may be disseminated by wind, rain, floods and flies etc
Taenia spp may live 1-5 years in the definitive host and have a high reproductive potential.
Describe the clinical signs of Taenia species ?
Clinical signs Taenia species
Usually infections with adult tapeworms are not very harmful to dogs and cats - most infections are asymptomatic
- heavy infections cause non specific abdominal symptoms/ non-specifics
- diarrhoea or constipation
- the animals may have unthrifty pot bellied appearance
How would go about diagnosing Taenia infection within the definitive host ?
Taenia infection canine
Identification of proglottids in faeces, resting places and the coat of animals
- the proglottids are square rectangular shape (longer than wide) and have only one genital pore
- detection of eggs floatation methods or on the coats of dogs (perianal area = use adhesive tape).
Eggs of Taenia species can not be differentiated from Echinochococcus
- circular brown, embriophore is striated
- contain an oncosphere (hexacanth embryo)
Necropsy - visualization of the worms within the small intestine
Immunodiagnosis
- antibodies in serum
- coproantigens in the faeces
- detection of DNA in the faeces
How should Veterinarians go about control and treatment of Taenia infections ?
Taenia infections
To control
- deny dog access to potentially infected sheep, goat, rabbit carcasses etc
- reduce the number of stray dogs
- treat imported dogs
Treat dogs at intervals of time (PPT 6 weeks) and destroy all faeces post treatment.
Treatment
Praziquantel most effective
Epsiprantel
Nitroscanate
Benzimidazoles
Describe in detail the morphology of Echinococcus granulosus ?
Morphology Echinococcus granulosus
DH = small intestine of dogs, wolf, dingo, coyote, fox (not domestic cat
IH = Cystic Echinococcus in the intermediate host (sheep, cattle, horses, pigs, kangaroes, monkeys and humans etc)
Adult worm
- rostellum two rows of hooks
strobila is made up of 6-7 proglottids
- genital pore alternates regularly
Eggs
- brown
- striated embryophore
- oncosphere / hexacanth embryo
Metacestode hydatid cyst
- second stage larvae
- Two layers laminated and germinal layer
- not all hydatid cyst produce brood capsules, and/or protoscolices: sterile cyst
- hydatid sand
Larvae (cyst) of E. granulosus can occur in any tissue but most are found in the liver lungs.
Identify this parasite and describe its epidemiology ?
Spirocerca lupi
Host = dog, fox, coyote and jackel
Location = adult parasite wall of oesophagus in nodular masses
Immature stages stomach and dorsal aorta
Epidemiology
- high prevalence in South Africa
- In recent years a number of cases have been recorded in Mount Isa
Identify this parasite and describe its lifecycle ?
Life cycle Spirocerca lupi
Host = dog, fox, coyote and jackel
Location = adult parasite wall of oesophagus in nodular masses
Immature stages stomach and dorsal aorta
Life cycle
Intermediate host = dung beetles
- eggs are passed in the faeces and are then ingested by IH dung beetles
- With the IH reach mature to L3 the infective stage about 2 months
The definitive host becomes infected by ingesting beetles or paratenic host (birds, rodents, reptiles)
- Within the definitive host larvae are released into the stomach - penetrate the stomach wall - after ten days reach the aorta (stay 2.5months), then migrate to the oesophagus
PPT 5-6 months
Describe the clinical signs of Spirocerca Lupi ?
Clinical signs Spirocerca Lupi
- vomiting or regurgitation, dysphagia due to the development of oesophageal mass
- weight loss
- the dog may breath shallowly and sit with their head extended (pressure due to oesophageal mass)
- rupture of the aortic aneurism - haemothorax and acute death
Describe how you would go about diagnosing and treating Spirocerca lupi ?
Spirocerca Lupi
Diagnosis
- clinical signs (dysphagia, regurgitation etc)
- faecal floatation
- endoscopy
- radiography
Treatment
Ivermectin
Doramectin
Both are for off label use
Identify this parasite (cats, dogs) and describe its life cycle ?
Strongyloides stercolis and felis (threadworms)
Life cycle
Location = small intestine
Only the females are parasitic, lay embryonated eggs that hatch in the digestive tract - L1 are shed in the faeces of infected animals.
- in the environment L1 undergoes homogonic and heterogonic development
Infection of the host
- transcutaneous
- ingestions of embryonated eggs
- via milk
Note
- hypobiosis is uncommon in the species
- lung tracheal migration of larvae has a limited role in dogs
Identify this parasite and describe its epidemiology ?
Strongyloides stercoralis
Infections are the most common in tropical and subtropical areas, however can also occur in temperate zones.
Predisposing factors
- younger dogs more likely to display clinical signs
- kennels
- poor hygiene and overcrowding
Zoonotic
- causes a severe condition and potential death
- dogs may be a reservoir for human infection
What are the clinical signs of Strongyloides stercoralis ?
Strongyloides stercoralis
Clinical signs
Most infections in dogs and cats are asymptomatic
- heavy infestations in pups, watery mucus diarrhoea intermittent
- vomiting
dehydration, weight loss and sudden death
- bronchopneumonia (larvae migrate through lungs)
- pododermatitis (papules, puritis)
Describe how you would go about diagnosing Strongyloides stercoralis and felis ?
Strongyloides stercoralis / felis
Diagnosis
- clinical signs are not specific
- history young or immunocompromised
- faecal smears or faecal floats
- Baermann method (funnel, water allows sorting of larvae)
- dead animals gut scrapping’s and histological sections
Treatment
This is more difficult than for other nematode infections
Fenbendazole
Albendazole
Requires treatment over a five day period
Describe how you could control for Strongyloides stercolis ?
Control for Strongyloides stercoralis
- avoid overcrowding
- daily disposal of bedding and faeces
- regular deworming and routine faecal examinations
- hygiene, disinfection and maintenance of a dry environmnet
Identify this parasite and describe its epidemiology ?
Epidemiology Toxocara cani
Location = small intestine feed intestinal contents
- stout white worm with three lips and cervical papillae
One of the most frequent parasites of dogs with >80% of pups infected
- worldwide
- female very prolific
- prevalence affected by pup age, pup sex higher males, and source eg stray, castrated ?
- eggs sticky and resistant
Pups are the major source of environmental contamination (<5months).
Zoonotic
VLM visceral larval migrans
OLM ocular larval migrans
Transmission
- ingestion eggs
- paratenic host (rodents, birds and earthworms)
- tissues of female bitch - infection occurs over consecutive pregnancies in the absence of reinfection (transplacental, milk)-
Identify this parasite and describe its life cycle ?
Toxocara canis
Female T.canis are very prolific - eggs become infective L3 within the egg
< 3 month old pups ingest embryonated eggs = tracheal migration
> 3 months old pups/adults ingest embryonated eggs = somatic migration
In female dogs the hypobiotic larvae might get reactivated during pregnancy and they may migrate to
- foetus
- mammary gland
- intestine of the bitch
Describe the pathogenesis of Toxocara canis ?
Toxocara canis pathogenesis
Depends on many factors
- age host, parasite number and location of parasites (SI, bile ducts obstructive jaundice, stomach vomiting)
- adult worms may perforate the intestine, peritonitis
Stage of host development
- migrating larvae in utero - hepatic and pulmonary damage = still birth
- large number of migrating parasites = pneumonia followed by the death of the pup 2-3 days after birth
- maturation of the worms in the intestine, block transit and rupture intestinal wall
Describe the clinical signs of Toxocara canis ?
Clinical signs Toxocara canis
May appear in pups 2-3 weeks after birth, potentially before eggs can be detected in faeces
- coughing
- frothy nasal discharge (larval migration)
- anorexia, emaciation, abdominal distension
- diarrhoea, vomiting
- anaemia, rough hair coat and ill thrift
- death
Neurological signs restlessness, convulsions
Describe how you would diagnose Toxocara canis ?
Toxocara canis diagnosis
- Clinical signs (vomiting, frothy nasal discharge, rough coat etc)
- history (pups in the absence of regular treatments)
- visualisation of worms (may be in vomit / diarrhoea)
- faecal floatation / smear
Eggs
- sub spherical
- dark brown
- thick shelled and finely pitted outer coat
- contain one cell
Arrested larvae may be detected through Elisa but rarely used
Describe how you would go about treating Toxocara canis ?
Treatment of Toxocara canis
Intestinal stages many anthelmintics are highly effective
- Piperazine
- Pyrantel, Oxantel
- Febantel
- Fenbendazole, mebendazole, flubendazole and oxibendazole
- Moxidectin, milbemycin, oxime
- Nitroscanate
- Emodepside
Arrested larvae area resistant to most drug treatments
- Fenbendazole for atleast 3 days
Migrating larvae might not be affected by some treatments
- piperazine, pyrantel, nitroscanate
- repeat treatment after 2-3 weeks
Identify this parasite and discuss its life cycle?
Toxocara cati
Significant for human health - VLM, OLM
Location = small intestine of cats
cervical alae are broad and end abruptly
Symptoms are more pronounced in kittens than in adult cats
Transmission
eggs
paratenic host
L3 with milk - no larval migration
no transplacental infection
Treatment
Piperazine
Pyrantel
Fenbendazole
Identify these three separate parasites and describe their morphology ?
Ancylostomosis hookworms
Location = small intestine
Anterior end bent dorsally
Ancylostoma caninum
- large buccal capsule
- 3 pairs of teeth on the ventral margin
Ancylostoma braziliense / ceylanicum
- buccal capsule with 2 pairs of teeth on the ventral margin
Uncinaria stenocephala
- buccal capsule with a pair of chitinous plates at the ventral margin
Describe the epidemiology of Ancylostoma caninum ?
Ancylostoma caninum
Location small intestine feed blood, mucosa and tissue fluids
- common tropical and subtropical areas
- pups may die suddenly 2-3 weeks after birth
- clinically significant infections frequent in pups <6months of age (usually not weaned)
- in endemic areas dogs usually build a strong resistance , however they often harbour a small number of parasites and contaminate the environment
- third stage larvae are able to survive for many weeks in the environment
Significance for human health
- A.ceylancium and A.caninum can develop to adults in the intestine of humans
- cutaneous larval migrans
- folliculitis
- eosinophilic pneumonitis etc
- able to regulate the immune system of the host (research).
Describe the life cycle of Ancylostoma caninum ?
Ancylostoma caninum
Adult female worms lay eggs which are passed with host faces into the environment where they develop L1-L2-L3.
- requires optimum temp and humidity 25-30 degrees C
L3 from the environment infect the host through
- transcutaneous heart - lungs - pharynx - swallow - SI adults
- Orally ingestion of embryonated eggs or paratenic host - small intestine no larvae migration
- Trans-mammary transmission (not A.braziliense & A.ceylanicum.
Arrested larvae
Some of the larvae that enter the host will not develop into adults
- they migrate to somatic tissues (muscle, subcutaneous) and enter ‘arrested development’
- this process is affected by age resistance of host and temperature of larvae subjected to prior to infection.
- the arrested larvae will be reactivated during late stages of pregnancy - migrate to mammary gland and infect the pups via milk.
- most anthelmintics are ineffective against ‘arrested larvae’
Describe the pathogenesis of Ancylostoma caninum ?
Pathogenesis of Ancylostoma caninum
Species of A. canimum is 50-100x more pathogenic than A.braziliense or Uncinaria stenocephala.
- only 50 -100 A. canimum parasites in pups might be fatal
Pathogenesis depends on
- age resistance < 6 months
- iron reserves, nutritional status and stress etc
Hook worms cause damage to the host at/during ?
1. The site of larval penetration
- foot pads and ventral abdomen
- inflammatory response erythema, papules, alopecia possible bacterial complications
2. Larvae migration through the lungs
- haemorrhage, inflammation, pneumonia and coughing
3. Adult worms buccal capsule attachment to the small intestine
- alternate feeding sites up-to 6 times daily
- essentially an open blood vessel
Describe the clinical signs of Ancylostoma caninum ?
Clinical signs Ancylostoma caninum
Hookworm disease is due to haemorrhage from multiple lacerations and blood feeding activity of worms
- clinical signs may appear in pups in just 2weeks after birth (severe clinical signs present before eggs are detected in faeces)
- anaemia, bloody faeces, lassitude, poor hair coat
- sudden death pups 2-3 weeks of age
- respiratory signs
- in sensitized dogs eczema, ulcers etc
- Uncinaria stenocephala in some cases causes haemorrhagic diarrhoea
Describe how you would go about diagnosing Ancylostomosis species ?
Diagnosis of Ancylostomosis species (hookworms)
Live animals
- clinical signs bloody faeces, anaemia
-history pups <6 month lack of treatments
- epidemiology (overcrowding, poor hygiene, time of year)
- faecal floatation or faecal smear
Severe disease may present before eggs appear in the faeces (trans-mammary transmission)
Dead animals
- lesions haemorrhagic enteritis
- visualisation of worms
- histopathology
Describe how you would go about treating a case of Ancylostoma caninum ?
Treatment of ancylostoma caninum
In severely affected animals eliminate the parasites as quickly as possible
- combine anthelmintic treatment with blood transfusions, iron and fluid therapy
Treatments effective for adult parasites
- Pyrantel
- Nitroscante
- Fenbendazole, Flubendazole, and mebendazole (safe in pups)
- Febantel
- Milbemycin, oxime and moxidectin
- Emodepside
Migrating larvae may not be affected by all drugs - repeat 2-3 weeks
Arrested larvae are not susceptible to routine therapy
Describe good management practices which can be used to prevent Ancylostoma and Toxocara infections ?
Prevention of Ancylostoma Caninum
1. Prevent clinical disease in pups infected vertically
- treat 2 weeks of age and than every two weeks until 2-3 months of age.
- when treating the pups treat the bitches too
Note treating while pregnant is of little use, as anthelmintics are ineffective against inhibited somatic larvae.
Older dogs
- prophylactics are recommended
- treat every 3-6 months or depending on the results of a faecal examination
Management
- remove faeces periodically
- clean hygienic
- keep environment dry
- regular treatments and treat newly acquired pups
- avoid overcrowding
- exercise dogs on concrete
Identify this worm (dog) and describe its epidemiology ?
Trichuris vulpis
Location = large intestine of dog, fox, coyote
Potentially zoonotic
- eggs are highly resistant in the environment (up-to seven years)
- world wide distribution
- common in kennels & stray dogs
- prevalence and worm burden higher in dogs older than 6 months.
The source of infection = contaminated moist soil where the eggs may survive for a long period of time. (eggs are susceptible to desiccation)
Describe the lifecycle of Trichuris Vulpis ?
Trichuris Vulpis
- females are highly proliferative
- the embryo develops inside the egg
- host becomes infected after ingestion of the embryonated egg.
PPT: 70-100 days
Describe how you would go about diagnosing and treating Trichuris Vulpis ?
Trichuris Vulpis
Diagnosis
- Clinical signs and history (age >6months) and detection of eggs in faeces
- faecal egg counts must be collected over several days as Trichuris are sporadic egg producers
- females lay only a few eggs, and the eggs do not float easily
- clinical signs may be seen before egg production begins
Sheathers sugar solution
Zinc sulphate solution
Treatment
Relatively drug resistant nematode as the odema of the caecum prevents passage of the drugs to the site of parasitism.
Febendazole
Flubendazole
Mebendazole
Febantel
Oxantel
Moxidectin
Emodipside
Eggs are very resistant so relapses are likely, it is reccomended to repeat treatments at 4 week intervals.
Describe the pathology and clinical signs of Trichuris Vulpis ?
Trichuris Vulpis
Pathology
-mechanical damage to the intestinal mucosa partially explains the clinical signs
- there are a variety of host responses as mucosa damage allows the entry of pathogenic bacterial microflora
- Balantidium colli
- inflammation of the mucosa, large amounts of mucous and occasionally haemorrhage
- fatal infections if high worm burden 1000s
Clinical signs
Most infections of Trichuris Vulpis are asymptomatic
Under high worm burden
- alternation between normal stools and diarrhea
- diarrhoea with blood and mucous
- fowl smelling
- abdominal discomfort tenesmus
- constipation
- weakness, weight loss and anaemia
Identify this parasite and describe its epidemiology (dog/cat) ?
Cystoisospora / Isosporosis
2 sporocyst and 4 sporozoites
Location = intestine
No significance for human health
- worldwide distribution - prevalence 3-38% in dogs
- young animals more likely to be affected
- cross immunity unlikely
- adult animals are often resistant but may be the source of contamination
Identify this parasite and describe its life cycle (dog/cat) ?
Cystoisospora / Isosporosis
The infected host shed un-sporolated oocyst in the environmnet
- sporolation 6-12 hrs
- some sporozoites penetrate the intestinal wall and get to the mesenteric lymph nodes, liver, spleen etc where they form a cyst.
The definitive host
- Ingestion of sporolated oocyst with food and water or paratenic host
- the sporozoites excist in the small intestine and invade the epithelial cells and divide.
Paratenic intermediate host
- mice, rats
- sporozoites grow in size and become surrounded by a cyst wall
- no replication
Describe the clinical signs of Cryptoisospora / Isospora in cats/dogs ?
Clinical signs Crytoispora /Isospora
Clinical signs are common in young <1month animals
- debiliatated, immunocompromised, stressed animals
- may occur 2-3 days before the excretion of oocyst in the faeces
- diarrhoea that in severe cases may contain blood
- vomiting
- abdominal pain
- anorexia
- dehydration
- weight loss
- anaemia
Disscuss how you could diagnose and treat a case of Cryptoisospora / Isospora in a dog ?
Cryptoisospora / Isospora
Diagnoses
history - pups<1 month of age, recurrent problems, stress and clinical signs
Faecal floatation
Healthy animals may excrete oocyst shedding - repeat floatation
Treatment
Generally self limiting - may resolve without therapy
- treatment speeds up resolution
- treat all animals in a litter
- improve hygiene
- fluid therapy
Toltrazuril baycox (off label use)
Procox
Describe how you would go about prevention with Cystoisospora / Isosporosis (dogs/cats) ?
Prevention Cystoisospora / Isosporosis
- improve hygiene
- remove faeces daily and destroy them
- runs cages, food utensils should be disinfected with steam
- immersion in boiling wtaer or by 10% ammonium
- prevent access to intermediate host
In shelters with recurrent problems - treat the animals every 2-3 weeks of age
Identify this parasite and describe its epidemiology and life cycle ?
Cryptosporidiosis
C. felis (cat intestine), C. canis (dog stomach, intestine), C. paruum (intestine many species including humans)
Location = intracellular but extra-cytoplasmic tip of epithelial cells
Ingestion of oocyst (4 sporocyst) highly refractile
Two types of oocyst
1. thick shelled excreted in faeces (contain 4 sporozoites)
2. Thin shelled autoinfection
Sporogony (in situ) - animals shed sporulated infective oocyst into the environment.
Epidemiology Cryptosporidium two
worldwide distribution
most infections are asymptomatic
- dogs and cats with secondary infections (Giardia) immunosuppression are more likely to develop symptoms
Identify this parasite and describe the clinical symptoms ?
Clinical signs Cryptosporidiosis
Immunocompetent animals
- asymptomatic (excrete oocyst for two weeks and then stop shedding)
Immunocompromised animals
- may develop signs of enteritis
- clinical signs observed in animals < 6months
- diarrhea, vomiting and weight loss
Describe how you would diagnose and treat Cryptosporidium ?
Cryptosporidium
Diagnoses
- clinical signs
- identification of oocyst in the faeces
- detection of DNA PCR
Sugar and zinc sulphate floatation
Ziehl Nielson staining
Treatment
In immunocompetent animals infection is self limiting
- find + treat underlying disease
- no drugs are registered for the treatment of this disease
Trials
Tylosin
Paromysin
Identify this parasite describe its two morphological forms and epidemiology ?
Giardia
Two morphological forms
Trophozoite
- pear shaped longitudinally
- ventral adhesive disk
- two nuclei
- four pairs of flagella
Cyst
- oval
- 2-4 nuclei and fragments of adhesive disk
Passed in well formed stools, may survive for several months in the environment.
Epidemiology
worldwide
common in young animals <1 year
zoonotic (minor role)
frequently prevalence is similar in animals displaying and not displaying symptoms
Describe the life cycle of Giardia ?
Giardia life cycle
Infection = ingestion of cyst with contaminated water, less commonly with food.
Excystation
- release of trophozoites
- triggered by exposure of cyst to gastric acid
- passage through the stomach and pancreatic secretions
Trophozoites divide by binary fission
- colonise large areas of the intestine causing pathology and may persist for years in the small intestine of the host.
Encystation
- Trophozoites takes place in the mid to lower jejunum after exposure to the bile salts and PH
Describe the clinical signs you would observe with a giardia infection ?
Clinical signs of Giardia
Most animals infected with Giardia do not show any clinical signs.
- young and immunocompromised
- diarrhoea watery pasty and semiformed faeces
-foul smelling and pale (increases fat secretion) - mucous on the surface
- weight loss
- abdominal pain
Describe how you would diagnose an infection with Giardia ?
Giardia
history (young, over-crowded)
Clinical signs - water pale mucoid diarrhoea
detection of parasites in the faeces
animals with diarrhoea are more likely to shed the parasite (no time to encyst)
- organisms shed intermittently
- cyst number in faeces dose not parallel the severity of infection
- cyst are small easily missed
- clinical signs precede shedding by 1-2 days
Direct smears (faces surface high numbers)
Zinc sulphate centrifugal floatation
Faecal immunoassays
Duodenal aspirate PCR
Describe what anthelmintics could be used to treat Giardia ?
Treatment of Giardia
Fenbendazole
Drontal plus
Oxfendazole
5-Nitroimidazoles
Metronidazole
Identify this parasite and describe its epidemiology ?
Tritrichomonas foetus / blagburni
Location = large intestine cat
one nucleus four flagella
rounded anteriorly pointed posteriorly
world wide distribution
infections common in young cats < 1 year
and in crowded environments such as catteries
Describe the clinical signs of Tritrichomonas / blagburni ?
Clinical signs Trittrichomonas blagburni
Diarrhoea that is of semi formed to liquid consistency, foul smelling and may contain blood or mucous
- increased frequency of defaecation
- flatulence, tenesmus
- the anus may appear oedematous and painful
Clinical signs are intermittent and improve with antimicrobial therapy to return after therapy is discontinued.
Describe how you would diagnose and treat a case of Tritrichomonas blagburni ?
Tritrichomonas blagburni
Diagnoses
direct smears using saline
culture Inpouch TF (fresh sample <6hrs)
PCR
Treatment
Ronidazol
Tinidazol
Prevention avoid dense housing and stress in kittens
Describe how you would treat Ctenocephalides ?
Identify this parasite and describe its morphology ?
Trichodectes canis
- head wider than thorax
- antennae are visible
- feed on epidermal debris and blood (biting lice)
Identify this parasite and describe its morphology ?
Heterodoxus springer (kangaroo louse)
Head is triangular
- provided with a pair of strong ventral spine like processes
- legs provided with two claws
Feeding seems to prefer blood
Identify this parasite and describe its morphology ?
Linognathus steosus
Head is narrower than the thorax
- head is small
- legs first pair is smaller than the second and the third
Feeding; blood
Describe the epidemiology and life cycle of small animal lice
Lice
Trichodectes canis, Heterodoxus springer, and Linognathus setosus
Life cycle
Eggs are glued at the base of hairs - nymphs hatch in 1-2 weeks - molt three times and become adults in 30 days.
Epidemiology
- most common in the cold season and group housing
- highly host specific
- common in young immunosupressed animals - massive populations rapidly rise in these animals
- Trichodectes and linognathus setosus have a global distribution
Describe the pathogenesis and clinical signs of Trichodectes canis, Heterodoxus springer and Linognathus setosus ?
Lice in dogs and cats
Pathology
Locate - neck, head, ears, back and trunk
- variation in symptom’s between individuals with similar numbers of parasite burden
- huge papules develop quickly on neglected, poorly nourished puppies
Chewing lice tend to be more of an irritant than suckling lice - itching, scratching, alopecia, excoriations and bacterial complications
Suckling lice cause anaemia and debilitation
Clinical signs
- pruritis, alopecia, restlessness
- thickly matted coats
- small papules and crusts
- in severe infestations anaemia, weakness and debilitation
Describe how you would go about diagnosing and treating Trichodectes canis, Heterodoxus springer and Linognathus setosus ?
Trichodectes canis, Heterodoxus springer and Linognathus setosus
Diagnosis
- History young pups in group housing
- Clinical signs
- Visualisation identification of lice/eggs
- adhesive tape
Treatment
Pyrethrin, pyrethroids
Fipronil
Imidacloprid
Selamectin
Identify this parasite and describe its life cycle ?
Felicola subrostrata(us)
Morphology
- shape of head is triangular pointed anteriorly
- median longitudinal groove on the head
Life cycle
Eggs are glued by female lice to the hair shaft - 3 nymphal stages - adults
- life completed in 30-40 days
- feed on skin debris and probably skin exudates
Describe the epidemiology and clinical signs of Felicola subrostrata(us) ?
Felicola subrostrata
Epidemiology
Transmitted mainly by direct contact but also indirectly (grooming supply’s)
- common in animals kept in poor conditions
- long haired cats which are unable to groom properly
Clinical signs
Areas most commonly affected head, face, pinnae, neck back and tail
- irritate the host
-restlessness
- scratching, alopecia, skin lesions
- scaling, papule, dulling, crusts
- coat may be matted and have a ruffled appearance
due to the accumulation of skin exudates in the hair
- anorexia, debiliatation
Describe how you would diagnose and treat Feliocola Subrostrata
Feliocola subrostrata
Diagnoses
- clinical signs and history
- Finding lice or eggs on the body of cats
(acetate tape impressions)
Treatment
Fibronil
Imidocloprid
Selamectin
treat all the cats in the household
Clean and treat bedding and cleaning supplies
Identify this parasite and describe its life cycle (dog) ?
Sarcoptes scabiei var canis
Morphology
- Oval circular
- Gnathostome is almost square
- Triangular scales
- Spines
Life cycle
Egg larva - two nymphal stages then the adult
The parasite lives in the superficial layers of the skin
The fecundated female burrows tunnels into the skin to lay eggs (1-3 day, for 1-2 months of life)
- six legged larvae hatch and most of them go to the surface of the skin
Describe the epidemiology of Sarcoptes scabiei var canis ?
Epidemiology of Sarcoptes var canis
Significance for humans
- self limited
- human involvement has been reported in 50% of canine cases
- reinfection possible
- lesions, pruritis, papules, erythema, pustules on arms and trunk
Sarcoptes scabiei var cani
The disease is highly contagious
- distributed worldwide
- often a history of being in animal shelters, contact with strays or visiting a boarding facility.
Transmission = direct contact
To a lesser extent indirect fomites (depending on the temperature and humidity may survive up-to 21 days in the environment but are only infective for 1-2 days)
Describe the pathology of Sarcoptes scabiei var canis ?
Pathology var canis
The mites act mechanically by burrowing in the skin too lay their eggs. (chelicerae, first pair of legs)
- irritation, hyperkeratosis
- secretions eggs and faeces induce both an immediate and delayed type of hypersensitivity
- reactions usually occur 3-4 weeks after contamination
- intense pruritus
Clinical signs
The mites prefer skin areas with little hair
- the elbows, ears, abdomen and hocks
-as the disease progresses the disease may infest large areas of the hosts body
- some animals may not present ear lesions
- intense pruritus
- congestions
- papules
- alopecia, scaling and crust
- thickening, wrinkling of the skin and in sever cases even death
- itching seems to be more severe in the warmer months
- uncommon but asymptomatic carriers exist
It becomes extremely intense about 30 days after exposure due to hypersensitivity
How would you go about diagnosing a infection of Sarcoptes scabiei var canis ?
Clinical signs Sarcoptes scabiei var cani
Diagnosis
Clinical signs - intense pruritis, alopecia, crusts, location
History - crowded situations
Skin scrapping’s, detection of mites eggs or faeces
- can be difficult to find mites in dogs with intense pruritus
- primary scraping sites the elbows, ear margins and hocks
- deep scraping
Finding a mite or egg is diagnostic, however not finding one dose not eliminate the possibility of disease.
- ELISA detection of specific antibodies
- Pennal pedal reflex (when rubbing the pinna dog will attempt to scratch the ear region).
Response to treatment ?
How would you treat a case of Sarcoptes scabiei var canis ?
Treatment
Treat all in contact dogs and animals suspected of being in contact.
Clean the bedding / environment, grooming equipment use acaricides
- Corticosteroids for pruritus
- Selamectin
- Moxidectin
- Afoxolaner
- Sarolaner
- Fluralaner
- Antibiotics for secondary pyoderma
Identify this parasite and describe its morphology and life cycle ?
Notoedres cati
Morphology
- body is circular, translucent and white
- Gnatosoma short and rounded
- concentrical striations
- blunt scales
- spine (4 anterior 6 posterior)
- legs short and conical
- anus is located dorsally
Life cycle (similar to sarcoptes scabiei)
- mites live in burrows within the epidermis
- eggs - larvae - two nymphal stages - adults
- life cycle last 2-3 weeks
Describe the epidemiology of Notoedres cati ?
Epidemiology of Notoedres cati
- distributed worldwide
The disease is highly infectious with all the cats within a household or neighbourhood potentially becoming infected.
Transmission is usually by direct contact
to a lesser extent indirect but adult mites can only live 1-2 days in the environment.
- usually affects adult cats
- may cause fulminating dermatitis in kittens
Describe the clinical signs of Notoedres cati ?
Notoedres cati clinical signs
Clinical signs appear around the pinna and they spread around the nose, eyes and face - head, neck and anterior legs
- alopecia
- erythema
- papules
- thick grey crust
- thickening of the skin and formation of wrinkles
Intense pruritus - excoriations and intense pruritus leading to bacterial complications.
Young cats may die
Older cats become emaciated, apathec and die in 3-4 months if left untreated
Discuss how you would diagnose and treat a case of Notoedres cati ?
Notoedres cati
History
Clinical signs
- visualisation of the mites in deep skin scrapings
- cats with hypersensitivity reactions may have very few mites but intense clinical signs
Treatment
All cats in the household or cattery should be treated
clean / remove bedding
bath cat with antiseborrheic shampoo to loosen crust
Moxidectin
Selamectin
Isoxazalines (off label may be lethal in kittens)
Identify this parasite describe its morphology and epidemiology ?
Otodectic mange
Host = cat, dog and fox and accidentally humans
Location = external ear canal and adjacent skin of the head
Morphology
- Gnathostoma as long as it is wide
- 4th pair of legs reduced
- posterior lobes in the male
Epidemiology
- worldwide
- 50-80% of otitis externa in cats but much less prevalent in dogs
<10%
- young animals more commonly infected
- asymptomatic carriers exist
Transmission = by direct contact (especially during nursing, may also be indirect).
Identify this parasite and describe its lifecycle ?
Otodectic mange
Host = dog and cat
Location = ear canal
Life cycle
This mite lives on the outside of skin and feeds on tissue fluids and debris.
The life cycle takes about 3 weeks
- egg (attached by females to the skin of the ear canal)
- hexapod larvae, two nymphal stages - adult
Mites locate in the ear canal but in heavy infestations may be found on the tail, back and head.
Describe the pathology and clinical signs of Otodectic mange ?
Otodectic mange
Pathology
Highly pathogenic (as few as three mites may cause symptoms)
- cats differ in their ability to serve as hosts for Otodectic
Physical presence of the mite feeding on the epithelium - mechanical irritation which accounts for some of the pruritis.
Hypersensitivity reaction to the saliva, that develops after two weeks is responsible for the majority of the pruritis.
- secondary bacterial infections may occur
Clinical signs
- brown waxy exudate / cerumen in the ear canal which may dry
- crusts might develop
- Pruritis, scratching or rubbing of the ears and shaking of the head
- hematoma formation and self trauma.
-
Describe how you would diagnose and treat a case of Otodectic mange ?
Otodectic mange (cat, dog)
Location = ear canal
Diagnosis
- Clinical signs and history
- Microscopic examination of the material collected from the ear canal (ear swabs mites eggs).
- Otoscopy direct visualization of the mites
- Positive pinna pedal reflex (cats), cat will move quickly the hindlimb where ear canal is massaged/swabbed
Treatment
Treat all affected animals and any dogs and cats that have contact
Cleaning of the house/ area where animals live is recommended
Topical otic acaricidal treatments
Acarexx
Milbemite
Cleaning the ears of affected animals is recommended before topical application of treatments
Combine whole body treatments
Fibronil
Selamectin
Moxidectin
Afoxolaner (dogs)
Sarolaner
Fluralaner
Identify this parasite describe it morphology and epidemiology ?
Domodex canis
Morphology
- body is elongated
- four short stumpy pairs of legs
- opistosoma is straited
- eggs are spindle shaped asymetrical
Epidemiology
Most dogs have demodex in their coat as a commensal
- pups usually acquire demodex by direct contact from their mother
- more common in pure bred dogs
- some breeds appear more susceptible Great-dane, English bull dog
Demodicosis is not infectious
No significance for humans
Describe the pathogenesis of Demodex canis ?
Pathology Demodex canis ?
Demidocosis is the result of excessive multiplication of the mites and development of huge populations in the skin of dogs.
Usually present as a commensal, only some dogs have a reaction - due to their altered immune response
1. Hereditary demodex canis specific T cell defect (pure bred, breed deposition
2. Immunosuppression induced by other conditions
A single bitch may produce multiple litters affected with Demodicosis - its hereditary
Describe juvenile and adult onset of Demodex canis ?
Demodex canis clinical signs
Generalised demodicosis
More than 6 focal lesions, involvement of two or more body regions or involvement of two or more feet
- serious skin disease possibly life threatening
- treatment is lengthy expensive / recent improvements
A) juvenile onset between 3-24 months
- inherited disease
- should not breed affected siblings parents
- pyoderma
B) Adult onset >24 months of age
- immunocompromised due to an underlying condition
- hyperadrenocortism, hyperthyroidism,
- immunosuppressive drug therapy
- Diabetes mellitus
- Neoplasms
- Stress (pregnancy, oestrus)
Describe the clinical signs of animals with juvenile or adult onset of Demodex canis ?
Clinical signs of Demodex canis
Squamous form
- patchy, regional, multi focal or diffuse
- Erythema
- Silvery greyish scaling comedoms
- hyperpigmentation
Pustular form
- secondary bacterial infection - papules, pustules, furuncles, pruritus
- affected skin becomes eroded ulcerated
- crust hyperpigmentation
- pyoderma
- pain, fever, lethargy, depression, debilatation
- odour
Dogs may appear older skin becomes wrinkled
Pododemodicosis
- interdigital erythema, pruritus, pain, hyperpigmentation
Describe your recommendations for managing generalised Demodex canis ?
Demodex canis
- need to identify and treat any underlying causes (stress, inherited or immunosuppression)
- acaricidal therapy
- treat the concurrent bacterial infection
- monitor efficiency of therapy
- the success is lower in dogs with adult onset of Demodex canis
Treatments are expensive and long - owner compliance
- acaricidal treatment may not be necessary in a localised demodex case (self limiting).
- Amitraz
- Milbemycin
- Fluralaner
- Sarolaner
- Afoxolaner
- the treatment of generalised demodex used to be difficult
Monitor for progression / resolution of disease
Scrape the 4-5 most severely affected areas and new lesions every 2-4 weeks to evaluate progress of treatment.
- if no improvement within 2 months change treatment
- determine the appropriate time to cease thearpy (2 negative scrapings one month apart)
Describe how you would go about diagnosing a case of Demodex canis ?
Demodex clinical diagnosis
Clinical signs and history
Microscopic examinations of skin scrapings
Deep scrapings until capillary bleeding
(squeezing the skin assist with mite extrusion)
Conformation by finding large numbers of mites or an increased ratio of juvenile mites to adult stages
Records should be made to monitor efficacy of therapy
- number of mites
- ratio dead to alive
- ratio of immature to mature mites
Trichography (microscopic examination of plucked hairs)
Exudate sampling
Acetate tape preparations
Otic swabs
Skin biopsies
Identify this parasite and describe its morphology and epidemiology ?
Cheyletiellosis
C blakei cat, C. yasguri dog and C parasitivorax rabbits
- legs end with comb like structures
- Gnathostome palps end with claws
- feather like setae
Epidemiology
All breeds and ages may become affected
- infestations are the most severe in young animals
- some usually adult animals may be infested but have no clinical signs = asymptomatic carrier
- highly contagious
- common in animals living with dense housing
- highly motile
- females can survive in the environment for up-to ten days
Identify the specific species of Cheyletiella which affect cats and dogs ?
Describe the life cycle of Cheyletiellosis species ?
Cheyletiellosis (walking dandraft)
Cheyletiella blakei = cat
Cheyletiella yasguri = dog
Feed on tissue fluids and lymph
The parasites spend their entire life on the host
- eggs are attached to the hairs of the host
- the life cycle comprises egg larvae and two nymphal stages before finally reaching the adult stage.
- life cycle is complete in 2-3 weeks
Eggs do not have an operculum.
Describe the pathogenesis and clinical signs of Cheyletiellosis ?
Cheyletiellosis
Pathology
Cheyletiella mites live in pseudotunnels they create on the skin surface in the keratin layer.
- pruritis because of the mechanical activity
- hypersensitivity the severity might not be proportional to the clinical signs
- Scaling seems to be the results of a host defence mechanism - epidermal cell turn over increases in response to injury of the epidermis
Clinical signs
- lesions occur mainly over the dorsum
- dandruff like giving the coat a powdery appearance
- pruritus may be mild to severe
- alopecia, erythema, papules, crusts
- Cat; miliary dermatitis (millet seeds)
Describe how you go about diagnosing a case of Cheyletiellosis in a dog or cat ?
Cheyletiellosis
The detection of Cheyletiella eggs or mites can be difficult
Sometimes a diagnosis is made by dermatitis being caused to the owners.
- clinical signs and history
- direct examination of the skin using a magnifying glass
- superficial skin scrappings
- Acetate tape impressions
- Combing flea comb or brushing of the hair
Describe the steps you would take in the treatment of Cheyletiellosis ?
Cheyletiellosis
All infected and in contact animals should be treated
- continue treatments for 2-4 weeks after the resolution of clinical signs and until mites / eggs are no longer visible
- the environment should be clean and treated with an acaricide
- females may be able to survive in the environmnet up to ten days
Permethrin (not for cats)
Selamectin spot on 3 times at one month intervals
moxidectin and imidacloprid (advocate at two month intervals)
Off label use
Milbemycon
Ivermectin
Amatraz
Identify this parasite and describe its morphology and life cycle ?
Ixodes holocyclus (Australia paralysis tick)
Morphology
- mouthparts are longer than the basis capituli
- anal groove anterior + join posteriorly
- spiracular plate
- no festoons
Life cycle Three host tick
- After engorgement the female drops off the host
- 2-3 weeks later lay 2000 to 3000 eggs in the environmnet
- Under suitable conditions the larvae hatch 1-2 months later
- The larvae (seed ticks) attach to a host (1st host) feed for 4-6 days then drop to the ground and moult to nymphs (19-41 days later).
- nymphs attach to second host feed for 4-7 days and then drop to the ground
- After 3-11 weeks the nymphs moult to adults (male, female)
The females attach to another host (3rd host) feed for 6-21
days and then drop off to lay their eggs.
The life cycle is complete within one year in tropical / sub tropical areas but usually takes longer (2 years) in temperate zones.
T
Identify this parasite and describe its epidemiology ?
Ixodes holocyclus
Host = monotremes and marsupials (but now a wide range of mammalsdogs, cats, horses, sheep,)
A single female tick can kill a dog
Zoonotic - 20 deaths recorded in Australia
- found mainly along coastal Eastern Australia (usually within 20km of the coast)
- distribution depends on Humidity (eggs, larvae sensitive to dessication)
- pressence of natural host possum, koali and bandicoot (reservoir)
- vegetation
- entire pets are more likely to be affected
Cases of tick paralysis can occur all year round but peak in spring. (previous years rainfall)
Describe the pathology of Ixodes holocyclus ?
Ixodes holocyclus
In general it is the female tick which causes paralysis
- a single female could cause death of the host
- there is no correlation between tick size and severity of clinical signs
- tick virulence might vary with the geographic area and the time of year
Pathology
- Salivary neurotoxins are transferred to the host during feeding
- no detectable amounts of toxin are secreted until the third day of attachment - onset of paralysis symptoms appear 3-5 days after attachment
The natural host bandicoots survive heavy infestations as a result of acquired immunity.
(adult males produce the toxin but do not feed on the host)
Describe the clinical signs resulting from Ixodes holocyclus ?
Ixodes holocyclus
Clinical signs
Usually observed 3-5 days after tick attachment
This depends on the rate of engorgement of the tick rather than a fixed time period.
- loss of appetite and voice (laryngeal paresis)
- Ascending flaccid paralysis, animals become weak in their back legs and ataxic
- wobbliness of the hindquarters rapidly worsens so that in a few hours the dog is unable to stand
Paralysis extends to affect the whole animal which becomes limp and flaccid
- drooling, regurgitation, vomiting, coughing
- become hypothermic
- pupils widely dilated
- respiration becomes slow and laboured, with a prolonged expiratory rate.
Death occurs from respiratory and cardiovascular failure.
- neuromuscular paralysis
- pulmonary oedema
Untreated dogs usually die within 24-48 hours after initial clinical signs
How would you go about diagnosing a case of Ixodes holocyclus ?
Ixodes holocyclus
Common location of tick head and forward of the shoulders
Clinical signs rapidly ascending paralysis
History - location where Ixodes holocyclus is endemic
Season - where ticks are at their peak (Spring)
Lack of tick prevention , drug when was it last used
- presence finding a female tick or a tick crater
- search for ticks or tick craters more than one tick may be present
- finger walking method
- perform physical and neurological examination
- full body clip (avoid stressing the patient)
- response to therapy
Describe how you would go about treating a severe case of Ixodes holocyclus ?
Ixodes holocyclus
1. Remove all parts of the tick ensuring all parts of the tick especially the mouth parts are removed
- will not immediately halt the progression of disease (clinical may even worsen up to 24hrs after tick removal).
- a thorough search of the animals coat is highly recommended more than one tick is possible
- Administration of anti toxin serum
- neutralise circulating toxins, effective only in the early stages of disease. (before toxins bind to the site of action at the neuromuscular junction)
- efficiency varies between manufacturers and batches so difficult to recommend a dose
- should we use a higher dose in cases with greater severity ?
TAS is injected slowly over a 20 minute interval
(if not possible intra peritoneal injection could be used)
reduce stress by the use of acepromazine
Some animals develop adverse reactions more common and fatal in cats.
- Supportive care and therapy
- oxygen therapy or mechanical ventilation
- Furosemid to reduce pulmonary oedema + intravenously fluids used cautiously
What management practices could we use to prevent paralysis ticks Ixodes holocyclus ?
Prevention is crucial
- Avoid tick infested areas especially within the peak season of spring
- Apply acaricides regularly and follow the manufactures instructions
- Thoroughly search animals daily for ticks and remove them
Acaricides for dogs
- Fipronil (spot on 2 weeks protection kills 100% of female ticks, spray 3 weeks protection)
- Afoxolaner (oral administration 4 weeks protection)
- Sarolaner (oral administration 4 weeks protection)
- Fluralaner (oral administration more than 4 months protection, spot on 6 months protection)
- Lotilaner ( safe use in young pups oral administration)
- Permethrin rinse weekly (do not use in cats)
(Permethrin and Imidacloprid spot on every two weeks)
- Flumethrin and imidacloprid eight months protection
- Deltamethrin collar
Takes around two weeks to achieve efficacy - the collar should be applied 2-4 weeks before the animal is exposed to parasites
Effective 12 weeks
- Amitraz collar - claims protection for eight weeks
Cats
Pyrethrins
Fibronil frontline spray
Sarolaner and selamectin 5 weeks
Fluralaner
It is unlikely any drug combination is 100 % effective so check and remove ticks daily
Identify this parasite describe its morphology and life cycle ?
Rhipicephalus sanguineus (kennel tick)
Host = dogs ( also found on cats, rabbits, humans).
Morphology
- mouth parts as long as basis capituli
- basis capituli is hexagonal with lateral sharp angles
- two pairs of ventral plates in the male
- festoons
- anal groove is posterior
Life cycle
Three host tick
- female ticks lay eggs in cracks and crevices houses and dog runs
- the cycle can be completed in about 2-3 months
egg - larvae, nymph - adult
Identify this parasite and describe its epidemiology ?
Rhipicephalus sanguineus (kennel tick)
Specific to dogs but also found on cats, rabbits, rodents and humans.
This parasite has a weak affinity for humans
- wide distribution within Australia
- Able to transmit many pathogens; Babesia, canis, Ehrlichia canis etc.
- unusual among ticks in that it may complete its entire life cycle indoors. Because of this it can establish entire populations in colder climates (found in much of the world).
- common in urban and suburban areas - heavy burdens may develop in dogs
Predilection
- younger dogs appear to carry a heavier parasite burden
- breed Cocker spaniel,
Active early spring to late autumn
In warmer areas may be active all year round.
Describe the pathogenesis and clinical signs of Ripicephalus sanguineus ?
Ripicephalus sanguineus
Predilection sites
- considered a hunting tick which moves towards its host when detected in the area
- found anywhere on the hosts skin
- commonly between paws and in host ears
Pathology
Dog appear to develop little to no resistance
- anaemia in heavy infestations
- inflamed nodule at the site of tick attachment
- erythema
- pruritus hypersensitivity
- self trauma
- signs of tick born diseases
Describe how you would treat a case of Ripicephalus sanguineus ?
Ripicephalus sanguineus
Treatment
Fipronil
Afoxolaner
Deltamethrin
Permethrin
Amitraz
Identify this parasite and describe its epidemiology ?
Epidemiology Dirofilaria immitis
Definitive host = dogs
Heartworm disease diroflilariosis
Morphology
- adult elongated filiform worms
- mouth is circular without lips
- male posterior is curled the spicules are unequal
Microfilaria
- Direct smears of fresh blood non progressive motility
- Knott preparations, straight body with a tapering cephalic end
Epidemiology
- common problem in many areas of the world
- especially in tropical and subtropical areas
- the geographical range of the disease has changed over the last ten years (used to be the highest prevalence in Northern QLD) reduced through the use of ML
- cats are more resistant than dogs
- prevalence higher in larger dogs
- prevalence higher in dogs > 3 years
- also higher in animals who live outside
Dirofilaria can infect humans but dose not mature.
Location = peripheral branches of the pulmonary arteries (granulomas coin lesions)
Harbours intracellular bacteria; Wolbachia pipientis
- removal of this bacteria leave the female parasites sterile and is followed by death
- target in the control and treatment of heart worms
Describe the pathogenesis and clinical signs of Difilaria immitis ?
Dirofilaria immitis
The location depends on depends on the size of dog and worm burden
Pulmonary artery = right ventricles
In heavy infections right atrium and caudal vena cava
Depends upon
- number of worms present
- duration of infection
- level of activity of the dog
- size of the dog (higher prevalence in larger dogs)
Multisystemic disease - pathology in lungs, heart, liver and kidneys.
Pathogenesis is initiated by the presence of adult worms in the pulmonary arteries - with primary lesions occur in the pulmonary arteries and lung parenchyma.
Clinical signs get worse when the heart worm dies, worm decomposition is followed by
- thrombosis (damage to the cuticle)
- blockage of distal arteries
- inflammation and platelet aggregation
- arterial injury
Contact of worms with the intima is the essential step
- Cor pulmonale right sided heart failure
- disruption of endothelial cell junctions and denuding of intimal surface
- smooth muscle cells multiple and migrate from the tunica media into the lumen of the vessel and start villus proliferation
- leads to blockage of the lumen
- tricuspid insufficiency
Microfilaria only play a minor role in disease by causing pneumonitis and glomerulonephritis.
Describe the life cycle of Dilfilaria immitis ?
Life cycle Difilaria immitis
Host = dogs
Location = pulmonary artery and right ventricles
Intermediate host = mosquitoes (Culex, Aedes, and Anopheles)
- mosquitoes become infected with microfliaria when taking a blood meal from an infected host.
- microfliariae may survive in the circulation up to 2.5 years
- concentration of microfilaria in peripheral blood varies; over a 24 hour period peak in the evening + higher in summer
Intermediate host
Within the mosquito at 26-28 degrees develop L1-L2-L3
- at <15 degrees the development of microfilaria is arrested
- third stage larvae migrate to the head and mouth parts of the mosquito.
Definitive host
The definitive host becomes infected while the mosquito is taking a blood meal
- L3 are deposited on the skin of the host in a drop of haemolymph and enter the body of the host through the puncture wound of the mosquito.
- day 70-120 worms reach the heart
The eventual location depends on the size of the dog and worm burden
PPt 6-9 months
Describe the clinical signs Dirofilaria immitis ?
Clinical signs Dirofilaria immitis
Caval syndrome (liver failure syndrome)
- failure of sufficient blood flow through the caudal vena cava
- anaemia, haemoglubinuria, metabolica acidosis, acites, jaundice
- acute onset and rapidly fatal course
Col pulmonale
Right sided heart failure
- pulmonary arteries become dilated
Glomerulonephritis
- proteinuria
- dark red kidneys
Heart worm disease may have an acute onset but usually begins with barely detectable signs.
- a very active dog is more likely to develop severe clinical signs
- reduced exercise tolerance and cough
- fatigue, lethargy
- weight loss despite a good appetite
- dyspnoea
- syncope and hemoptysis
- abnormal pulmonary sounds crackle and splitting of the secondary heart sound can be heard
- congestive heart failure
- right heart enlargement systolic murmer
Death following respiratory distress or cachexia
Describe how you would go about diagnosing a case of Dirofilaria immitis ?
Diagnosis Dirofilaria immitis
Clinical signs
History and physical examination
Confirmed by detection of
- microfilariae
- detection of parasite antigens or specific antibodies
Radiography (presence and severity)
Echcardiography
The presence of microfilaria in the blood of dogs ir relatively common. Not all dogs infected with heartworms will have microfilariae in the blood = occult infections.
- adult worms present but no microfilariae
- may be common up to 70% of infections in dogs
- immunologically or MLs may result in the absence of microfilaria in the blood
- single sex or geriatric infections
Microcapillary haematocrit tube
Direct smears non progressive movement
Modified Knotts test; filter test one MF per Ml of blood
Detection of antibodies and antigens (commercial test kits)
- antigen test have higher specificity and sensitivity
- antibody test only used in cats, mainly to rule out infection
- confirmation of diagnosis
- routine screening
- assessment of adulticide treatment
Note false negative antigen tests do occur (light infections only male worms)
Describe how you would go about treating a case of Dirofilaria immitis ?
Treating Dirofilaria immitis
Treatment is neither simple, safe or cheap
Before treatment dogs should be assessed for severity of disease and to predict potential complications.
Most complications result from death and decomposition of the worms followed by
- thrombosis
- arterial artery blockage
- arterial injury and thromboembolic disease
- right sided heart failure
- grade through history, physical examination and radiography
Before treatment and adulticide therapy
- patients should be stabilised
- begin exercise restriction for 6-8 weeks is mandatory after adulticide treatment
Marlarsomine is effective for treatment against worms older than 4 months
MLs for worms < 1month
This leaves a susceptibility gap
Treat dogs with MlLs for two month prior to Melarsomine treatment. Ivermectin Moxidectin + doxycycline
This eliminates the migrating larvae under two months of age, and allows the older parasites to reach an age where they become susceptible to Melarsomine.
- use MLs with caution in dogs with high microfilaria counts
- antihistamines, corticosteroids
Daily Doxycycline for one month prior to adulticide treatment to eliminate the Wombacha pipientis bacteria, which reduces the inflammatory response against dead worms.
Melarsomine deep intramuscular injection into the lumbar muscles three dose protocol - one injection followed one month later by the same dose 24 hrs apart.
CATS ADULTICIDE THERAPY NOT RECOMMENDED (prednisilone for 3-4 weeks).
Identify this parasite describe its morphology and life cycle ?
Angiostrongylosis vasorum (French heart worm)
Host = dog + fox
Location = pulmonary artery right side of the heart
Morphology
- small reddish worms
- white ovaries of females are coiled around the red intestine.
Life cycle Indirect
Intermediate host snails and slugs
Female parasites lay eggs which reach the capillary of the lung.
- the larvae hatch and reach the alveoli
- pharynx - swallowed - and exits with faeces into the environment.
- Ingested by snails and slugs
Transmission ingestion
- intermediate host
- paratenic host frogs
- food contaminated with slime from gastropods
L3 penetrate the GI tract and reach lymph nodes - liver - right ventricle and pulmonary arteries
PPT 208 days
Identify this parasite and describe its pathology and clinical signs ?
Angiostrongylus vasorum
Pathology
- nodules on the surface of the lungs
- emphysema
- haemorrhages
- granuloma
Clinical signs
- Coughing
- Dyspnea
- Depression
- Bleeding disorders DIC
- Exercise intolerance
Describe how you would go about diagnosing and treating a case of Angiostrongylosis vasorum ?
Angiostrongylosis vasorum
Diagnosis
- Identification of first stage larvae in the faeces
(Baerman method)
- collect faecal samples over three days
- Cytological examination of the bronchoalveolar lavage
- ELISA
Larvae have a kinked tail
Treatment
- Fenbendazole oral
- Milbemycin oxime oral
- Moxidectin topical
Describe the clinical signs, diagnosis and treatment of Angiostrongylus cantonensis ?
Angiostrongylus cantonensis
Host = rat
Accidental = dog horse humans
Ascending paresis, lumbar hyperalgesia
Diagnosis
- History
- Clinical signs
- Identification of larvae at necropsy
- ELISA
Treatment = Prednisolone
Identify this parasite and describe its clinical signs and transmission ?
Pneumonyssoides caninum (nasal mite)
Host = dog and foxes
Location = nasal cavities and sinuses
Yellowish mites
Transmission = direct contact
sneezing
coughing
epistaxis
nasal discharge
facial pruritus
head shaking etc
Describe how you would diagnose and treat Pneumonyssus ?
Pneumonyssus (nasal mite)
Diagnosis
visualisation of the mites
rhinoscopy or nasal flushes
Treatment
- selamectin
- Milbemycin oxime
Three treatments at two week intervals
Identify this parasite in a cat and what clinical signs you would expect ?
Capillaria aerophila
Host; dogs, cats, foxes, humans
Location; trachea, bronchi, bronchioles
More than half of the worm body is inside the mucosa
Australia present in cats
Clinical signs
Chronic dry cough that might become productive
when bacterial complications intervene.
Nasal discharge
Sneezing
Dyspnoea
Describe how you would diagnose and treat a case of Capillaria aerophila ?
Capillaria aerophila
Diagnosis
Clinical signs and finding eggs in the faeces/ bronchi smaples
Treatment
Dogs
Fenbendazole
Cats
Moxidectin
Eprinomectin
