Parasitology Flashcards
Identify this parasite ?
Rhipicephalus australis
- Australian economic impact $150 million a year
- legs pale whitish
- coxa with two small spurs
- wide distance between first gnathostome and first pair of legs
- mouth parts as long as basis capituli
- accessory and adenal shields present
- caudal process
- no festoons
- basis capituli is hexagonal
- anal groove posterior to anus shallow
Describe the life cycle of Rhipicephalus australis ?
Life cycle of Rhipicephalus australis
One host ticke
- engorged females drop off host (mainly in the morning) and seek shelter amongst plants and soil surfaces
- lay around 3000 eggs
- max egg production around 24 -27 degrees C
- egg production may cease at lower than 15 degress C
- larvae climb on grass and await host ( contact, CO2, odour) - questing position
- larvae - nymph - adult
- females usually drop after about three weeks after larvae attach to the host
- can survive upto nine months off the host
What is the questing position of tick larvae ?
Questing position = active waving of front legs in the air while standing on the tips of grass blades in preparation to attach to a host
Describe the epidemiology, tick movement and host susceptability of Rhipicephalus australis ?
Epidemiology Rhipicephalus
- Host predominantly cattle, can attach to horses, dogs, sheep
Distribution QLD, NT and WA
- dependant upon temperature and rainfall
- legislative tick line
Cattle susceptability depends on
- breed (bos indicus are less susceptable)
- stress, lactation, gestation
- grooming - restricted grooming = more ticks
- age calves prior to weaning are more susceptable
season - the resistance to tick wanes in Autumn due to reduced pasture quality and nutritional stress.
Movement of ticks
- cattle trucks
- herd movement
- wind dispersion (<1km)
- birds
Describe how the population of Rhipicephalus changes throughout the year ?
Population changes throughout the year
- can be seen almost anytime of the year
heaviest tick infestation occur November to July
- population size fluctuates throughout the year
- lowest winter early spring
- temperature, humidity affect the females reproductive activity + development and survival of larvae
- four generations each year with each generation becoming bigger than the last starting in November - December
What are the clinical signs of Rhipicephalus australis ?
Clinical signs
- damage to hides
- loss of production (anorexia, toxins produced by ticks, irritation etc)
- tick worry severe skin irritation, secondary infection of the attachment site, rapid loss of condition listlessness and possible death
Transmission of pathogens Babesia, and Anaplasm
How do we diagnose ticks ?
Diagnosis of ticks
- adult ticks easily observed on skin
- usually found around the base of the tail, escutcheon, belly, shoulder, dewlap and ears.
- Haemapphysalis preference for ears + inside ears
- nodules ulcers, wounds, and secondary infections
Identify this parasite and name its distinguishing features ?
Haemapphysalis longicornis
- legs dark brown
- anal groove behind anus
- festoons present
- second segment of palps extends laterally
- mouthparts as long as basis capituli
- basis capituli sub rectangular
Describe the life cycle of Haemapphysalis longicornis ?
Life cycle
three host tick
- fully engorged female drops off host lays more than 300 eggs
- larvae hatch, attach to host and drop off after about one week
- nymphs feed and drop off host after about one week
- the adult ticks attaches to a third host, drop off and lay eggs
Describe the epidemiology of Haemapphysalis longicornis ?
Haemapphysalis longicornis
cattle are preferreed host - may attach to horses, man, dogs, cats etc
- brahmen cattle develop quicker and stronger resistance
Distribution
- QLD (not north of Gympie), NSW, Victoria and WA
- larvae can survive upto one year on pasture
Describe the seasonal patterns of Haemapphysalis longicornis ?
The seasonal pattern
Adults increase in late spring and reach a peak over summer and decline in early autumn
- larvae feed mainly late summer and autumn
nymphs in autumn persist throughout winter - nymph appear on cattle late winter to early spring
Describe the pathogenesis and clinical signs of Haemapphysalis ?
Pathogenesis Haemapphysalis Longicornis
- found mainly around and inside of the ears
- also found escutcheon, flanks and anus
- cattle become resistant to tick infections - the most serious infections occur in naive cattle
Can transmit Theileria
Clinical signs
- lesions Wrythematous
- dark scab in the centre exudate
- young animals may suffer from loss of condition, anemia, weakness and some deaths may occur
What chemical controls can we use to reduce tick populations ?
Chemical control of ticks (4)
Synthetic pyrethroids
Amidines
Macrocyclic lactones (ML)
Acarine growth regulators - Fluazuron
What is the mechanism of action of synthetic Pyrethroids, and what species are they effective against ?
Synthetic Pyrethroids - Acaricides
Interfere with Na+ channels of the parasite nerve axons, delayed depolarisation and eventual paralysis
- derived from chrysantheum flower
- fast acting
- long residual activity
- low toxicity for host
Cypermethrin, (Flumethrin and Deltamethrin available Australia)
- 30-50% resistance in Rhipicephalus
- do not use in lactating dairy cows
Describe the mechanism of action for Amitraz and Amitic ? What species are these drugs effective against ?
What is the mechanism of action for macrocyclic lactones, and what species are they affective against ?
What is the mechanism of action for Acarine growth regulators provide examples and what species these drugs are effective against ?
Describe different methods of drug application and their associated positives and negatives ?
Describe the mechanism of action for tick guard plus ?
What techniques can we utilize to control tick populations without drug use ?
Tick population control principles
- use tick resistant breeds (Bos indicus)
- planned strategic treatments
- pasture spelling or rotation
- allow immunity to tick fever to develop / but not to numbers which affect animal productivity
- reduce larvae load on pasture
- rotate chemical agents to avoid strong selection for resistance
Describe the concept of eradication, reactive treatment and strategic programs when it comes to tick control ?
Eradication = continuously treat all possible hosts for the maximum period of time that larvae can survive in the environment - at intervals of time less than the minimum parasitic phase - mandatory for ticks outside of the tick zone
Reactive = Treatment of cattle when tick populations are high is not very effective - better to use strategic treatments
Strategic programs - start October
= aim to manage tick populations at levels which maintain immunity to tick babesia/ Anaplasma (tick fever), and severe clinical signs.
- treat at the beginning of tick breeding to prevent the subsequent surge in population
What is tick fever caused by ?
What is the economic importance of tick fever ?
In Australia 1800 caused the cattle population to decrease by 5.5 to 2.5 million
Describe the life cycle of Babesia inside the host cattle ?
Babesia life cycle
- female ticks become infected with babesia after feeding from an infected host (during the period of final engorgement)
- infection is transmitted by the next generation of ticks
- parasitemia is present 6-12 days B.bovis and 12-18 days B.bigemina
Development within the cow
- sporozoites with tick saliva
- sporozoites invade red blood cells and divide by binary fission - merozoites
merozoites enter red blood cells and divide by binary fission - more merozoites
- gametocytes develop and are ingested by adult ticks
Describe development of babesia species within the tick ?
Development within the vector babesia
- Transovarial transmission
- gametocytes to sporokinet
- sporokinets spread through the haemolymph to varous cells of the ticks (including ovaries and malpigian tubules)
sporonts - sporozoites transmit through tick saliva
Describe the epidemiology and susceptibility of Babesia.bovis ?
Epidemiology B.bovis
- Eastern and Northern parts of Australia - where the cattle tick Rhipicephalus australis is present
- environmental factors affect tick numbers
less ticks during the dry or winter season
Susceptibility
- Outbreaks are common in young cattle 1-3 years old or in naive cattle.
- calves under nine months of age develop only mild or inapparent signs of infection
- Bos.indicus breeds more resistant
condition of host eg. stress of cows at calving make them susceptable
- Immunity - recovery from B.Bovis is accompanied by strong resistance to reinfection for life
Sources of infection
- Babesia may persist and be transmissable long after the animal is treated
- transmitted through ticks
- chances of being infected are greater the larger the population of ticks
At what time in the year are outbreaks of Babesia most likely to occur ?
South QLD
- most cases in Autumn
North QLD
- most cases in spring and winter
The greatest number of Babesia infections occur during the peaks of tick population
Describe the pathogenicity of Babesia. bovis ?
Pathogenicity of Babesia. bovis
Babesia. bovis is more pathogenic than B.bigemina
- hypotensive shock syndrome, parasitaemia 0.2%
- erythrocyte sludging
- cause adherence of rbc to the capillaries and to each other - blocking capillaries (brain, kidney)
- anorexia
- damage to organs - stasis, sequestration AND CHANGES TO THE RBC STRUCTURE
Haemolysis
- babesia multiply in rbc giving rise to 2-4 merozites that rupture the cells and invade other red blood cells
- b.bovis 1% parasitaemia may lead to massive lysis of rbc
What is the significance of sequestration, stasis and changes in the morphology of rbc in Babesia.bovis ?
Sequestration
- accumulation of reb infection with endothelium
- immune evasion (do not pass spleen + phag and opsonisation are prevented from accessing the infected cells
brain - cerebral babesiosis
- in the lung sequestion of rbc and neutrophils leads to increased permeability and oedema
What are the clinical signs of Babesia.bovis ?
Clinical signs Babesia.bovis - more pathogenic than B.bigemina
- mostly acute but paracute cases do occur
- clinical signs 6-12 days after the ticks begin to feed
- fever
-inappetence, depression, weakness, muscle tremor etc
- death may occur one week after the onset of fever
- anaemia
- haemoglobinuria (red water)
- jaundice
- diarrhoea sometimes followed by constipation
- cerebral babesiosis - hyperaesthesia, aggresion, coma, convulsion, paralysis etc, brain is characteristic pink coulour
What are the clinical signs of Babesia bigemina ?
Babesia. bigemina
Pathogenesis is almost entirely related to intravascular haemolysis
- parasitemia 20% or more
clinical signs are observed 8-16 days after the ticks begin to feed
- milder than babesia. bovis
- fever less of a feature and crebral signs not seen
- anemia, jaundice
- haemoglobinuria common consistent
What are the clinical signs of Babesia bigemina ?
Babesia. bigemina
Pathogenesis is almost entirely related to intravascular haemolysis
- parasitemia 20% or more
clinical signs are observed 8-16 days after the ticks begin to feed
- milder than babesia. bovis
- fever less of a feature and crebral signs not seen
- anemia, jaundice
- haemoglobinuria common consistent
What is the host immune response to babesia infection ?
Babesia
- immunity is host specific (however B. bigemina provides some protection against B. bovis)
- immunity develops 3-4 weeks after exposure / vaccination
- recovery is accompanied by strong resistance to reinfection
- Babesia may persist in the body of cattle that have recovered - they remain infective for ticks
- maternal antibodies protect calves for a couple of months, but calves remain protected upto nine months (protection from NO).
How would you go about diagnosing Babesia ?
Babesia
- clinical signs, fever, anorexia, jaundice
- history (naive, breed, Eastern and Northern Australia)
- thin and thick blood films stained by Giemsa (smears of B.Bovis of blood should be collected from capillaries of the ear or tail)
- serology
- ELISA
- PCR
How can we control and treat Babesia ?
Control
- remove cattle from tick infested pasture
- supportive therapy (fluids)
- vaccinate all at risk cattle (except those traeted with imidocarb
Vaccination
- Attentuation is not complete and reversion to virulence can occur after passage through the ticks or cattle
- immunity develops 3-4 weeks
- best to vaccinate between 3 and 9 months of age
- protection is usually life long
- DO NOT VACCINATE LATE PREGNANCY
Treatment Imidocarb diproprionate
- Imizol, Imidox
- do not administer to lactating dairy cows
- temporary solution only
Identify this parasite ?
Anaplasmosis
- Ricettsiae
- dense, rounded, dark blue spots irregular outline
- most occur close to the margin of the red blood cell
Describe the epidemiology of Anaplasmosis ?
Anaplasmosis
Distribution
- cattle tick area
Transmission
- Rhipicephalus australis is the vector in Australia
- transfer of infected larvae, nymphs, or adult tick from infected cattle to susceptible cattle: males are very important
- close contact with susceptible cattle
- Veterinary procedures (dirty tools)
- biting flies
- transplacental
- orally (licking blood from wounds)
Describe the clinical signs and pathology of Anaplasma ?
Anaplasma
- clinical signs appear one month after tick exposure
- more obvious in animals older than 1-2 years
- B.indicus + B.Taurus are equally susceptable
- sever infection upto 50% of rbc parasitised
Fever, depression, inapetance, jaundice, muscular weakness and tremor
- anaemia, watery blood, enlarged spleen and liver
- after recovery from illness long immunity develops but the animals remain infected
How do we treat for Anaplasma ?
Imidocarb
Oxytetracyclines
Where are the different nematode species located ?
Describe the economic significance of Gasterophilosis ?
Gasterophilosis
- the most common equine gastric parasite
- spread all over the world
- disease is caused by the larvae of Gasterophilosis
- has zoonotic potential - locating in the eye and skin of humans
Identify this species ?
Gasterophilosis intestinalis (common bot fly)
- mouth hook have a saddle like depression
- spines are slender and blunt tipped
- two rows of spines
Identify this species ?
Gasterophilosis nasalis (throat bot fly)
- one row of spines
Identify this species ?
Gasterophilosis haemorrhoidalis Nose bot fly
- mouth hooks are uniformly bent
- spines are smaller and pointed
- two spine rows
Describe the location and appearance of Gasterophilosis larvae ?
Gasterophilosis larvae
- larval stages 1-2 locate in the mouth
- larval stages 3 stomach/duodenum
- or rectum for L3 of horses
Appearance
- body is reddish brown, up to 20mm in length
- fusiform / cylindrical
- made up of 11 segments
- mouth appears robust laterally directed
- spines single or double rows encircle the body segments
Describe the life cycle of Gasterophilosis within the host ?
Life cycle of Gasterophilosis
- females lay operculated eggs (upto 160eggs) in specific locations, mostly the body of horses
- eggs are yellow layed on the intermandibular space, cheeks and front legs
Inside the eggs larvae form in five to ten days
they hatch by either
- spontaneously
- after stimulation by grooming ( warmth, moisture, and friction)
- larvae are then either ingested, or migrate to the mouth and pharynx where they can develop (beneath the mucosa of the oral cavity or beneath between the teeth) for about one month
- the larvae then moult to L2 or L3 where they migrate to the stomach or small intestine.
- larvae detach and are voided in the faeces
Describe the lifecycle of Gasterophilosis once voided into the environment ?
Life cycle Gasterophilosis
- in the environment larvae burrow into the soil and develop as pupae for about 4-6 weeks - adults emerge from pupae
- adult flys live for a few days ( rarely three weeks)
- mate and lay eggs
- in temperate areas larvae detach in spring and there is only one generation per year
- in warm tropical areas there may be more generations per year.
Describe the epidemiology of Gasterophilosis ?
Gasterophilosis
- Gasterophilosis intestinalis is the most common species in Australia (prevalence 64% QLD)
- adult flies are usually active from September to January QLD
- in the more Southern states flies are more active later, and are not as active for as long
Adult flies cause considerable annoyance when ovipositing (dronning noise, sudden attacks)
Describe the pathogenesis of Gasterophilosis ?
Pathogenesis of Gasterophilosis
In the stomach and duodenum
- attach to the mucosa with mouth hooks
- feed on tissue exudate (not blood)
- may stay for at most 9-10 months
Adult flies also cause considerable annoyance with dronning and sudden attacks
- G.Nasalis is particularly problematic as the dart at the lips and throat
Describe the clinical signs of Gasterophilosis ?
All pathogenesis is caused by the larvae of Gasterophilosis
In the mouth
- penetrate gum tissue alongside or between the molar teeth causing pus sockets, excessive irritation
- pain on mastication leading to a loss in appetite and poor weight gain
In the stomach
- ulcers, erosions and perforation of the stomach
- peritonitis (swelling, inflammation) followed by death
- block the transit of food especially larvae which are located near the pylorus
- colic
- Gasterophilis intestinalis causes crater like attachment sites in the cardiac part of the stomach
Rectum
- parasites in this location could result in an anal prolapse
This disease usually results in a non specific syndrome of ill thrift, poor coat, mild colic and poor apetite.
How would you go about diagnosing and treating Gasterophilosis ?
Diagnosis
- Clinical signs, eggs on coat,
- damage to mouth and tongue, presence of larvae in faeces
- endoscopy
Treatment
macrocyclic lactones provided orally
- ivermectin, moxidectin
Organophosphates - also orally given
- Trichlofon, and Diclorvos
What strategies could we implement to prevent infestation with Gasterophilosis ?
Management of Gasterophilosis
- In temperate areas treat in winter when fly numbers are low (parasites are present in the stomach breaking the life cycle)
- washing sponging horses with insectocides
- grooming to remove eggs (bot knife)
- remove the faeces from pasture
What strategies could we implement to prevent infestation with Gasterophilosis ?
Management of Gasterophilosis
- In temperate areas treat in winter when fly numbers are low (parasites are present in the stomach breaking the life cycle)
- washing sponging horses with insectocides
- grooming to remove eggs (bot knife)
- remove the faeces from pasture
Identify this parasite ?
Draschia megastroma
- two lips separated from the rest of the body by a groove
- buccal vestibule : thickened funnel shaped with no teeth
- egg contains a larva
Identify this parasite ?
Habronema muscae
- two lateral lips
- mouth made up of two parts = with the anterior part being wider and then a cylindrical part
- egg contains a larva
Describe the life cycle of Habronemiasis ?
The life cycle of Habronemiasis
Intermediate host is muscid flys
- female worms lay embrionated eggs
- larvae hatch quickly - eggs or larvae are passed within the host faeces
worm larvae are ingested by fly larvae
- L1-L2-L3 develops inside the fly
- development of the fly and nematode are synchronised with L3 being reached as the fly emerges from the pupae
- L3 will reach the mouthparts of the adult fly
When the fly feeds on warm moist surfaces (body of host) the larva are stimulated to leave the fly.
Describe what happens to the larvae of Habronemiasis as it leaves the mouth parts of muscid flies into the equine host ?
Habronemiasis from leaving the intermediate host muscid flies
- when the fly feeds on the warm moist wet surfaces of the host, larvae are stimulated to exit through the flys mouth parts
- infective larvae L3 from the mouth parts of adult flies might be deposited in
Around mouth of horse
- L3 are digested and develop into adults
- within the stomach in about 2 months
On wounds, preocular area, penis, prepuce, nostrils (moist areas)
- larvae do not develop in these location but cause severe pathology
Describe what happens to the larvae of Habronemiasis as it leaves the mouth parts of muscid flies into the equine host ?
Habronemiasis from leaving the intermediate host muscid flies
- when the fly feeds on the warm moist wet surfaces of the host, larvae are stimulated to exit through the flys mouth parts
- infective larvae L3 from the mouth parts of adult flies might be deposited in
Around mouth of horse
- L3 are digested and develop into adults
- within the stomach in about 2 months
On wounds, preocular area, penis, prepuce, nostrils (moist areas)
- larvae do not develop in these location but cause severe pathology
Describe the pathology of adult stages of habronemiasis, and species differences ?
Habronemiasis
Draschia megastroma
- large nodules, tumors
- may block the pyloric region or may perforate the stomach leading to peritonitis
- nodules are divided into cavities where the worms live - these cavities open into the lumen
Habronema muscae
- free live in the stomach and are generally non pathogenic
- with very heavy infections may cause gastric ulcers and inflammation
Describe the pathology of cutaneous and pulmonary Habronemiasis ?
Habronemiasis
Cutaneous
- inflammation, hypersensitivity
- skin, ocular and praeputial lesions
Pulmonary
- larvae deposited around the nostrils migrate to the lungs
- multiple abscesses filled with necrotic debris containing parts of nematode larvae
What are the clinical signs of Habronemiasis ?
Clinical signs Habronemiasis
Cutaneous Habronemiasis
- caused by hypersensitivity to dead dying larvae
- failure of wounds to heal
- development of exuberant reddish brown granulation tissue
- usually start off irregular in shape but eventually become circular in shape
- protude above skin surface
- serosanguinous exudate
prepuce / urethral process = ulcerative lesions with yellowish granules
gastric and pulmonary habronemiasis = generally asymptomatic
How would you go about diagnosing Habronemiasis ?
Diagnosis
Clinical signs - hypersensitivity reddish brown granulation tissue
History - summer sores + lesions may recur over the years
Faecal floatation - eggs elongated contain larvae
- identification of yellowish granules
- microscopic scrapings and visulization of larvae
How would you go about treating Habronemiasis ?
Treatment
Antiparasitic therapy
MLs - Abamectin and Moxidectin are effective against adult stages of the worms
Benzmidazoles
- Fenbendazol
Organophosphates
Anti-inflammatory therapy
- Corticosteroids
Massive or medically refractory lesions may be eliminated surgically or by cryotherapy
How would you go about preventing Habronemiasis ?
Identify this parasite ?
note grows upto 15 - 50cm
Describe the significance of Parascaris equorum ?
The significance of Parascaris equorum
- very common in young horses
- most pathogenic parasite of horses
- economic loss due to reduced weight gain and death caused by rapture or blocking of the intestine
- widespread resistance to MLs
- foals with high parasitic burdens are at risk for developing small intestinal impaction after treatment (low survival rate)
Describe the life cycle of parascaris equorum ?
Life cycle Parascaris equorum
- eggs have a thick shell and are sticky = they survive for a long time in the environmnet and are resistant to disinfectants
Life cycle
- female worms are highly prolific egg layers (200,000 eggs a day)
- eggs reach the environment with faeces
- at 25-30 C eggs become infective in 9-14 days
- host becomes infected by ingesting embryonated eggs from the environment
- larvae hatch in the small intestine
- L3 reaches the liver - lungs - up the bronchial tree - pharynx - swallowed
- back to the small intestine
- grow and turn into adults
PPT 72-110 days
longevity - up to nine months but shorter in older horses
Describe the epidemiology of Parascaris equorum ?
Epidemiology Parascaris equorum
Infections are prevalent in young animals < 18 months of age
- most common in 5-8 month old foals
- exception horses and donkeys in tropical areas
- foals become infected soon after birth, from ingestion off pasture
Horses older than six months begin to become resistant to infection
- foal to foal disease (infected foals born this year shed eggs - eggs persist and infect next years foals)
- survival of worms in the small intestine is the major determinant of worm infection levels and infection levels
- female worms are very prolific and eggs may survive in the environment for many years (eg ten years)
-
Describe the pathology of Parascaris equorum ?
Pathology of Parascaris equorum - the cause
Hepatic migration of the larvae
- petechial haemorrages,
- periportal necrosis
- infiltration of eosinophils and lymphocytes results in widely scattered white foci
Larval migration in the lung
- petechial haemorrages
- oedema, atelectasis (lung collapse)
- infiltration of eosinophils and lymphocytes around the small airways and blood vessels
Intestinal stages are the most pathogenic
- mechanical obstruction of the bowel
- can lead to colic, bowel rapture and peritonitis
intussusception
- competes with host for nutrients
- the effects of parasitism may be compensated through good management
What are the clinical signs of parascaris equorum ?
Clinical signs of Parascaris Equorum
Obvious in foals younger than 6-8 months
Larval stages
- migrating through the lungs and bronchial tree (during 3rd to 4th weeks after infection)
- coughing, grayish white, purulent nasal discharge (bacterial complications possible severe pneumonia)
Adult stages of parasite
- inapetance
- ill thrift
- impaction of the small intestine - colic ( heavy infection + rapid growth of worms)
- volvulus, intussception, and intestinal rapture
- gastric reflux
- death
In horses older than 8 months most larvae die within the lungs and liver causing a more significant respiratory disease, however, few larvae reach the small intestine so no severe clinical signs.
How would we go about diagnosing Parascaris equorum ?
Diagnosis of Parascaris equorum
1) Clinical signs
2) History age eg young horses
3) identification of eggs in faeces eg egg floatation
Note disease may result from larvae so there would be no eggs in the faeces.
Best practice ultrasonography
- pressence of parasites in the faeces or naso gastric reflux
- surgery
- necropsy
What could be done to control for Parascaris eqorum ?
Treatment is difficult for Parascaris equorum
- resistance to MLS,
- resistance to pyrantel and Fenbendazole has been reported
- young horses with a high worm burden may be at risk of impaction
What to do
Heterocyclic compounds Piperazine
- highly effective against intestinal stages of parascaris equorum
- wide therapeutic index
Benzimidazoles - Fenbendazole and Mebendazole
- slow onset of anthelmintic activity
- drug of choice in foals suspected of having a large parasitic burden
Tetrahydroprimidines - Pyrantel and Morantel
Best to avoid drugs with a paralytic fast mode of action due to the risk of impaction eg MLs, pyrantel
How would you control parascaris equorum ?
Identify this parasite ?
Describe the life cycle of Strongyloide Westeri ?
Life cycle Strongyloide Westeri
Describe the epidemiology of Strongyloide Westeri ?
Epidemiology of Strongyloide Westeri
The earliest nematode of horses
- affects foals 2-4 weeks upto four months of age
- foals will develop a protective immunity at 5-6 months of age
- infections are common in warm humid invironments
- in farms with regular anthelmintic treatment prevalence is reduced
Three routes of infection
- via milk
- transcutaneously (larvae migrate through heart-lungs - trachea)
- ingestion
PPT 8-14 days
Common in wet dirty bedding
Describe the pathology and clinical signs of Strongyloides Westeri ?
Strongyloides Westeri
Pathology
- infections with large numbers of parasites are associated with inflammation, oedema and erosion of the intestinal epithelium = diarrhea
-migration of larvae through lungs = inflammation and hemorrhage
Clinical signs
Clinical signs occur in foals (2-7 weeks) infected with large numbers of parasites
- diarrhea
- emaciation
- dehydration
- weakness
There could also be skin lesion caused by transcutaneous entry of L3
Older foals may have high faecal egg count with no clinical signs
How would you go about diagnosing a case of Strongyloides Westeri ?
Diagnosis Strongyloides Westeri
Clinical signs and history - diarrhea in very young foals
presence of large numbers of eggs in the faeces ( high faecal egg counts may be found in healthy adults as well).
- oval thin shelled contain a larva
Management
- keep stales dry and clean remove manure
- in reacurring infection routine treatment of 1-2 week old foals with avermectins was beneficial
- treat mare late gestation to prevent infection of the foals through milk
How would we treat Strongyloides Westeri ?
Identify this parasite ?
Morphology anoplocephala perfoliata
- four spherical suckers
- four lappets
- scolex rounded
- no rostellum or hooks
- proglottids are wide and thin
- one set of genitals in mature proglottids
Eggs
- D shaped
- outer envelope is thick
- hexacanth embryo, enclosed by a large pyriform apparatus
- eggs can survive on the pasture upto nine months
Describe the life cycle of anoplocephala perfoliata ?
Describe the epidemiology of Anocephala perfoliata ?
Epidemiology Anocephala perfoliata
- spread all over the world high prevalence 14-81%
- an increase in A.Perfoliata has occured over time
- numbers are highest in countries with temperate climate
Certain animals will have high infection, whereas their neighbors have no infection (80% of parasites reside in 20% of horses).
- horses of all ages are affected, and there does not seem to be an acquired or age resistance
- young horses (0.5-2 years) are likely to harbour the highest tape worm burdens.
Describe the pathology and clinical signs of Anocephala perfoliata ?
Pathology of Anocephala perfoliata
- mechanical damage and parasite an - tigens play a role in pathogenesis
- the parasites cause ulcers at the attachment site
- A. Perfoliata attach in clusters primarily at the iliocaecal junction - clustering may exacerbate the lesions associated with the tapeworm attachment
- perforation, peritonitis, and death may result
Clinical signs heavy infections
- poor body condition, ill thrift, poor growth, recurring diarrhoea, progressive weight loss
- impaction, cecal perforation, colic, intussusception
How would you diagnose and treat Anoplocephala Perfoliata in horses ?
Diagnosis
- clinical signs are unspecific
- faecal egg count - floatation
- sodium chloride, zinc and sulphate solutions to float eggs
- saturated sucrose gives better answers
- sensitivity is low as many eggs may be within gravid proglottids
- Elisa
Treatment
- praziquantel
- pyrantel
- collect and destroy the faeces shed within 48 hr after treatment
Provide the taxonomy and morphology of large and small strongyles ?
Identify this parasite ?
Strongylus vulgaris
Location adult - large intestine; larvae cranial mesenteric artery
- large buccal capsule oval
- contains two ear shaped teeth and a dorsal gutter
- two leaf crowns external and internal
Describe the life cycle of large strongyles Vulgaris in horses ?
The life cycle of large strongyles
- eggs (thin shelled morula stage) are shed in the faeces
- larval development takes place between 8-39C
- optimum temperature 25C
- L3s emerge from the faeces and migrate into the soil/ grass blades
- Infection by ingesting L3 with herbage
Small intestine
- L3 exsheath
- burrow into the small intestine, caecum and colon where they moult to L4
- penetrate the submucosal arterioles and migrate on the intima towards the root of the cranial mesenteric artery
Cranial mesenteric artery
- remain for about four months as they develop to L5
- immature adults return to the intestine in the
blood stream
PPT 6-7 months
Describe the epidemiology of Strongylus Vulgaris ?
Epidemiology of Strongylus Vulgaris
Prevalence
- found worldwide
- common in the past, but significant decrease over the last twenty years
Susceptability
- no age related susceptability
- host horse, donkey, and zebra
- in temperate regions egg counts decrease over winter, increasing over summer and spring
Infective larvae are resistant to drying and freezing -
Animals with clinical or subclinical infections might shed millions of eggs in their faeces
The main source of infection for young is their dams
Describe the pathogenesis of Strongyles Vulgaris larvae ?
Pathogenesis of Strongyles Vulgaris
Infections with more than 800 larvae are lethal within three weeks are lethal
Migrating larvae
- haemorrhagic foci on the ileum
- severe inflammation in the submucosa
- movement of worms up the arteries leaves a trail of endothelial damage
Cranial mesenteric artery
- thrombosis
- thickening of the cranial mesentery artery
- fibrosis of the wall of the infected artery
Emboli from the thrombosis are carried distally where they occlude arterial supply of the gut infarction.
Larvae return to the intestine
- form nodules
- eventually the worm breaks into the lumen leaving behind a small ulcer
Describe the pathogenesis of Strongyles vulgaris adult worms ?
Pathology Strongyles vulgaris
Adult
- feed on blood
- take a plug of the mucosa into the buccal cavity
- slash it with teeth while secreting anticoagulants
- the worms move to new feeding sites leaving behind haemorrhage and ulers
- lesions are easily visible on the mucosa as red spots
Describe the clinical signs of Strongyles Vulgaris ?
The clinical signs of Strongyles Vulgaris ?
Clinical signs seem to be more severe in horses younger than three years
Larval stages
- no distinct clinical signs
- significantly higher incidence of colic
- pyrexia, anorexia, rapid loss of weight
- spending a large amount of time in sternal recumbency
- depending on the amount of larvae innoculated death may occur within three weeks
Adult stages of parasite
- weight loss, poor growth, rough coat
- compromised performance
- anemia
- most horses have a mixed infection and it can be difficult to distinguish the symptoms from large strongyles to small strongyles.
How would you go about diagnosing a case of Strongyles Vulgaris ?
Diagnose Strongyles Vulgaris
- Clinical signs, anorexia, poor growth, rough coat
- History of inadequate worm control
- response to treatment specific for the larvae
Arteriography
- may be able to palpate the main arterial lesion through rectal examination
To detect adult parasites
- Clinical signs
- Detection of eggs in faeces (faecal egg count) egg floatation
- PCR
What morphological features could you use to distinguish between Strongyles Edentatus, and Strongylus Equinus where are these parasites located ?
Provide a short over view of the life cycle of Strongyles edentatus and Strongyles equinus ?
Diagnose and list the clinical signs of S. Endentatus and S. Equinus ?
Identify this parasite, its distinguishing features and life cycle ?
Triodontophorus tenuicollis
Morphology
- well developed dorsal gutter
- three radially arranged teeth
- buccal capsule subglobular, thick walled
- mouth collar and corona radiata (leaf crowns)
Life cycle
- L3 migrate into the wall of the colon and caecum
- moult to L4
- L4 emerges into lumen - moult to adults
PPT 9 weeks
Describe the pathology and clinical signs of Triodontophorous tenuicollis ?
Triodontophorous Tenuicollis
Pathology
- caused mainly by adult worms
- plug feeder and blood suckers
- feed in groups or nests
- cause ulcers and blood loss
Clinical signs
- soft faeces and later diarrhea
- lost condition
- the animals tire easily and have a rough coat
Describe how you would diagnose
Triodontophorous Tenuicollis
identification of eggs in faeces
faecal cultures for species identification
How would you go about treating for Large Strongyles and Triodontophorus Tenuicollis ?
Treatment large Strongyles
Anthelmintics from three different chemical families (MLs, BZs and tetra tetrahydropyrimidines)
MLs = Ivermectin, Moxidectin
BZs = Fenbendazole, Mebendazole
tetraHydropyrimidines = Pyrantel
Describe the problem of resistance in the class nematodes gastrointestinal strongyles eg Haemonchus ?
The problem of chemoresistance
MLs Ivermectin, Moxidectin etc
- resistance in 90% of properties
BZs, fenbendazole, Mebendazole
- resistance in 90% of properties
Mixed BZs and BZs have 60 % resistance found on properties
low resistance to organophosphates
How can we use an integrated parasite management to prevent drug resistance ?
Integrated parasite management (7)
- timely worm testing (prior to opportune times of treatment eg shearing, lamb marking, weaning
- drench at the recommended times, and test for resistance with drench check
- management of drench resistance
- use grazing management to create low worm risk pastures
- using rams with better than average WEC ABSV ( breeding value)
- vaccination
- alternative methods
Provide recommendations for drenching ?
Recommendations for drenching
High rainfall areas
- drench breeding ewes prelamb
- drench lambs at weaning usually November, prior to spike in worm burden
- October, November drench all sheep if grass is actively growing, only drench young sheep of grass quality is poor
- drench sheep showing obvious signs of worm burden
- drench based on wormtest or drench guide
- quarantine drench
What can be done to prevent drench resistance ?
How to stop drench resistance
- avoid unnecessary drenching
- faecal egg count reduction test every 2-3 years
- use effective drenches and rotate amongst all drench groups in each paddock and mob
- in general utilise short acting drenches ( leaving long acting products for specific problems and high risk periods of the year)
- calibrate gear and dose to the heaviest animal in the flock
- follow label instructions
Management
- breed for worm resistant host
- reduce the exposure of animals to worms through grazing management
- prepare low worm risk paddocks for weaning and lambing
- rest, interchange with cattle grazing
- sheep to sheep short grazing rotational grazing
Describe Benzimidazoles, identify two drugs, provide mechanism of action, administration and which parasites its effective against ?
Benzimidazoles
Drugs - white drenches
- Albendazole, Fenbendazole, Mebendazole
Mechanism of action
- inhibit polymerisation of tubulin starving parasites
Effective against
- active against adults and larvae ( not all are effective against larvae in hypobiosis)
- effective against cestodes and tematodes
Administration
- wide safety margin
- not soluble in water oral administration only
- effectivity depends on the contact time with worms
- forms a reservoir in rumen, gradual uptake into blood stream
Widespread resistance in Trichostrongyles of ruminants
Describe Levamisole ?
Imidazthiazoles - Levamisole
yellow/ clear drenches
Effective against
- adult nematodes less active against larvae
- (not active against hypobiotic larvae)
Administration
- soluble in water
- may administer orally, injectable or and topically (pour on)
- absorbed and excreted quickly
- level of concentration is more important than time of exposure
Mechanism of action
- cholinergic agonist at the synaptic nicotinic receptor
- spastic paralysis of susceptable worms
Wide spread resistance in Trichostrongyles of ruminants
Describe tetrahydropyrimidines ?
Tetrahydropyrimidines = pyrantel, morantel
Effective against
- effective against adult worms less effective against larvae
- not effective against hypobiotic larvae
- less effective against Osteragia
Administration
- poorly absorbed, safe and gentle (uneffective against lung worms)
- orally administered
Mechanism of action
- Cholinergic agonist
- nicotinic receptor acetylcholine receptors on nematode muscle cells
- spastic paralysis of susceptible worms
- side resistance to Levamisole
-
Describe Macrocyclic lactones ?
Macrocyclic lactones
Ivermectin, Moxidectin, abamectin
Moxidectin tend to be more effective than the avermectins
Effective against
- adults, larvae and hypobiotic larvae
- also effective against arthropods ticks, lice and mites
Administration
- highly lipophilic stored in fat tissue and slowly released - provide residual activity against parasites and buffalo flys miasis
- wide safety margin
- administered orally, injectable and pour on
Mechanism of action
- They bind with a high affinity to glutamate - gated chloride ion channels
- triggers the influx of chloride ions that result in hyperpolarisation of the neuron
- paralysis and death of the target parasite
Describe Salicylanilides ?
Salicylanilides
Closantel (green drench)
Effective against
- all blood sucking nematodes (Haemonchus, Bunostomum)
- Fasiciola Hepatica, mites, ticks, lice, larvae of Ostrus Ovus
Administration
- soluble and well absorbed with either parental or enteral administration
-bioavailability is reduced when orally administrated
Mechanism of action
- uncouple oxidative phosphorylation, at the mitochondrial level and attach to plasma proteins
Resistance in Haemonchus contortus
Describe Organophosphates ?
Organophosphates
naphthalophos: white powder
Effective against
- highly effective against Haemonchus Contortus
- used only in sheep
- higher levels required to treat other nematodes
- do not use in debilitated thirsty, stressed and exhausted animals
Mechanism of action
- inhibits acetyl cholinesterase
Provide a list of drugs effective against gastrointestinal nematodes in ruminants ?
Benzimidazoles - Albendazole, Fenbendazole, Mebendazole
Levamisole
Tetrahydropyrimides - Pyrantel and Morantel
Macrocyclic lactones - Ivermectin, abamectin and moxidectin
Salicylanilides - Closantel
Organophosphates - Naphthalophos
What is anthelmintic resistance ?
When a drench fails to kill kill atleast 95-98% of parasites when used at the manufacturers recommended dose.
Heritable ability of the parasite which is passed onto its offspring
Identify this parasite and where does it locate in the host ?
Paramphistomosis
Adult
- thick bodied more or less conical in shape
- two suckers one anterior one posterior
Describe the lifecycle and epidemiology of Paramphistomosis ?
Life cycle of Paramphistomosis
Intermediate host = snails
- eggs are shed in the faeces
- Miracidium forms inside the eggs 2-4 weeks
- Cercaria forms in the snails
- Metacercaria may persist 1-3 months
PPT 1.5-3 months
Epidemiology
- distribution depends upon snail host
- more common in cattle than sheep especially around the irrigated areas of Victoria
Flooding - can result in the dispersion of snails from permanent water masses.
Infection = ingestion of metacercaria off pasture
- during the rainy season snails/metacercaria widely spread
- during the dry season snails take refuge near water sources reducing spread of the parasite
Susceptible animals
- weaner cattle and lambs
- protective immunity develops after infection
Describe the pathology of Paramphistomosis ?
Pathology Paramphistomosis
Immature stages (pathogenic)
- locate in the wall of the duodenum and abomasum
- feed on mainly tissue but also blood
- mechanic action and trauma by mechanical movement and sucker
- erosion of intestinal villi
antigenic activity acute inflammatory reaction
- oedema, congestive enteritus
- erosions and petechia surrounded by a necrotic zone
- atrophy of the villi
Adult stages low pathogenicity
What are the clinical signs seen in an infection with Paramphistomosis ?
Clinical signs Paramphistomosis
Most infections are light moderate, no to mild clinical signs
Moderate infections may cause reduced weight gain or loss in milk production
Heavy infections with larvae in young animals =
- clinical signs develop in two to four weeks
- anorexia, polydipsia (thirst), weight loss
- fluid foul smelling diarrhea
- dehydration, weakness, anemia, submandibular oedema and possible death
How would you go about diagnosing and treating Paramphistomosis ?
Paramphistomosis
Diagnosis
- clinical signs
- history
- note infection with immature parasite no eggs
- Coproscopy (microscope examination of stool sample)
- eggs are oviod with unequal poles
Treatment
- very few drugs are effective against Paramphistomosis
- supportive therapy remove animals from contaminated pasture
- Oxyclozanide
Identify this parasite ?
Moniezia expansa
- 4 suckers no rostellum and no hooks
- up to 2-3 metres long
- proglottids are wider then they are long
Eggs
- triangular
- the hexacanth embryo is enclosed by the pyriform apparatus
Describe the life cycle and epidemiology of Moniezia expansa ?
Moniezia expansa
Intermediate host = mites
Life cycle
- ruminants shed eggs proglottids in the faeces
- highly prolific worms
- eggs are ingested by mites - cystercoid larvae develop inside of the mites 2-4 months (temperature dependant)
- Definitive host become infected by ingesting mites during grazing
PPT 4-6 weeks
Epidemiology
- world wide distribution
- infections are more common in young animals
- within mites the cystercoid larvae can survive as long as the mites remain alive
Describe th clinical signs of moniezia expansa
Pathology Moniezia expansa
Clinical signs
- lambs with heavy infections diarrhoea, constipation, nervous signs, anemia weight loss etc
How would you go about diagnosing and treating Moniezia expansa ?
Moniezia expansa
Diagnosis
- clinical signs and history
- finding chains of proglottids and eggs floatation in the faeces
Treatment
- praziquantil
- benzamidazoles fenbendazole, mebendazole
control - plough and reseed pasture
- avoid using the same pastures for young animals over consecutive years
Identify this parasite and detail its life cycle ?
Eimeria bovis
Morphology - 4 sporocyst each with 2 sporozoites
Life cycle
Describe the epidemiology of Eimeria bovis ?
Epidemiology Eimeria Bovis
World wide
- common pathogen of cattle, most cattle become infected without any clinical signs
- oocyst are resistance can survive upto a year
- infections with a small number of oocyst will stimulate immunity
- infections with a large number of sporulated oocyst (heavily contaminated environment) in a short time will result in clinical disease
Susceptibility
- usually affects young animals 3 weeks to six months of age
- predisposing factors = crowding, poor nutrition and husbandry
- 2-3 month old calves have the highest excretion rates
- without reinfection it is a self limiting disease
Describe the pathology of Eimeria bovis ?
Eimeria bovis
Pathology
- depends upon species of parasite most infections are mixed
- pathogenesis is associated with levels of parasites in the coecum, lower ileum and colon
Disease caused by
- congested intestinal mucosa, catarrhal enteritis
- petechial haemorrhage
- bloody semiliquid fluid
What are the clinical signs of Eimeria bovis ?
Clinical signs of Eimeria bovis
Diarrhoea sometimes with blood
- anemia, weight loss, anorexia
- dehydration, weakness
- tenesmus, rectal prolapse
- yellow diarrhoea streaked with blood
Nervous coccidiosis - individuals fall to the ground, muscular tremors, convulsions, blindness
How would you go about diagnosing and treating Eimeria bovis
Eimeria bovis
Diagnosis
- clinical signs, history and age of animal
- detection of a large number of oocyst in the faeces
- during early stage oocyst may not be present
Treatment
- treat symptoms rehydrate
- Baycox Tetrazuril
What are the clinical signs of cryptosporidium ?
Cryptosporidium
Location = microvilli of the brush border in the DT and RT
Clinical signs
- affects calves younger than three weeks
- severe dehydration, diarrhoea, weakness and death
- high biological potential
No effective treatment available
Prevention is your only option
Describe the life cycle and epidemiology of Cryptosporidium ?
Epidemiology
C. parvum is one of the most common pathogens that causes diahorea in neonatal calves
- worldwide distribution
- most common in calves 1-3 weeks of age
- virtually all calves become infected in their first three weeks of life
- infected animals develop a strong immunity to future infections
highly common disease of dairy calves
Infection = ingestion of oocyst
Describe the epidemiology of small strongyles Cyathostomes ?
Cyathostomes
The most common and pathogenically significant parasite to affect horses
- worldwide
- Location - become encysted in the mucosa and submucosa of the caecum and colon
- majority of horses on pasture are infected
- horses of any age can become infected, but young horses appear more susceptable
- temperate areas two peaks in parasite population spring and late summer
Infection by consuming L3 off pasture
Widespread resistance to benzimidazole
Describe the lifecycle of Cyathostomes ?
Cyathostome life cycle
Adult female cyathostomes lay eggs in the caecum, colon of the horse
- eggs reach the environment with host faeces
- the development of eggs to L3 depends upon the temperature, humidity and oxygen
- highly resistant larvae to environmental conditions
- optimum temperature is 25-33C
Infection of host = ingestion of L3 off the pasture
- after ingestion L3 exsheath and enter the glands of Lieberkuhn in the caecum and colon
- a cyst of host origin will be organised around the larvae
- The L3 larvae then moult or may persist within the cyst for months to years
- L4 excit the cyst and enter the lumen of the large bowel
- in the lumen L4 turn into adults
The emergence of larvae is the major pathogenic event
PPT 5-18 weeks
What factors affect the arrested development of cyathostomes ?
Describe the pathology of Cyathostomes ?
Cyathostomes pathology
Pathology is caused by the emergence of L4 from the cyst into the colon and caecum lumen where they develop into adults
- mechanical damage to the gut linning
- intense inflammatory reaction
- edema
- conjestion
- haemorrhage
- leakage of tissue fluids into the lumen
- disruption of gut motility
- adults cause limited pathology by mucosal plug feeding ulceration and potential leakage
Describe the clinical signs of Cyathostomes ?
Clinical signs Cyathostomes
Note immunity develops slowly and is incomplete
Larvae
- occurs during synchronous reactivation of large numbers of larvae
- most often a small number of horses affected in a herd
- usually clinical signs apparent in animals under five years
- spring
- sudden onset of diarrhoea
- rapid weight loss
- subcutaneous oedema
- colic
- anaemia, dehydration
- mortality
Symptoms may occur in horses recently treated with anthelmentics
How would you go about diagnosing Cyathostomes ?
Diagnosis
- clinical signs not specific
- history
- faecal egg count usually low or negative ( larvae emergence)
- may be able to observe L4 or adults in faeces
Haematology - neutrophilia
Serology - hypoalbuminemia, hyperglobulinemia
What drugs should we utilise for the treatment of Cyathostomes ?
Treat adult and larval stages
Benzimidazoles and tetrahydropyramides
Incysted larvae can only be treated with two drugs
Fenbendazole
moxidectin
Discuss anthelmintic resistance in gastrointestinal strongylosis in cattle ?
What is refugia ?
Describe the morphology and epidemiology of Theileriosis Orientalis ?
Epidemiology of Theileriosis Orientalis
Vector = Haemaphysalis Longicornus, Haemaphysalis bancrofti (kangaroe tick) three host ticks
Host = cattle infections and buffalo, location leukocytes and red blood cells
Distribution = worldwide, NZ, Australia and Japan
Morphology = straight line within red blood cell
Describe Theileriosis buffeli ?
Theileriosis buffeli
Host = cattle and water buffalo
Vector = three host tick Haemapphysalis longicornis
Distribution worldwide, QLD, NSW, NZ
Clinical signs = usually benign
Diagnosis = blood smears but complicated by the presence of babesia and anaplasma
Treatment = no need to control, as most calves are infected soon after birth with no evidence the infection is ever cleared and few clinical signs.
Describe the life cycle of Theileriosis Orientalis ?
Life cycle Theileriosis Orientalis
1) Infected ticks (nymphs, adult), inject sporozites with saliva into host
2) sporozoites invade the leukocytes and develop into schizonts
3) merozites released from the schizonts invade the red blood cells
It is the merozites which result in pathology
Transstadial transmission
* remain with vector from one life stage to another
* ticks ingest blood with parasitised RBC - gametocytes into gametes in the lumen of the ticks gut
* fuse to form zygote
* after the tick moults kinetes will penetrate the cells of the salivary glands, multiple and form sporozoites - injected into host with saliva
* note three tick host
Describe the pathogenesis and clinical signs of Theileriosis Orientalis ?
Theileriosis Orientalis
Pathology
* Destruction of red blood cells
* elevated levels of methemoglobin
* animals which recover , may have persistent infection and relapse when under stress
Clinical signs
* anaemia, anorexia, weakness, depression, jaundice
* abortion, ataxia, fever
* weight loss
* loss of production eg milk
* mortality upto 30%
* no haemoglobinuria
How would you go about diagnosing and treating Theilerosis Orientalis ?
Theilerosis Orientalis
Diagnosis
* Clinical signs - anemia, fever, weight loss
* History - naïve cattle, home bred cattle < 8-12 weeks
* presence of parasite in red blood cell - comma, signet or rod shaped
* blood smears (Gimsa stain)
* PCR and ELISA
Treatment
There is no registered drug for treatment of Theileriosis Orientalis in Australia
* in less severe cases can use Imidocarb, Oxytetracycline
* supportive therapy and blood transfusions
* reduce stress
Identify this parasite and describe its epidemiology ?
Mite Psoregates ovis - sheep itch mite
Morphology
* shape almost circular
* legs are short stout and arranged evenly around the body
*femur of each hind leg has one long pair of setae
Epidemiology
Transmission = direct contact only adult mites are motile
Host = sheep
Common = throughout Australia, America, Chile, South Africa etc
Highest number located on the dorsal side of the body in the stratem corneum (outermost layers of the epidermis)
Describe the life cycle of Psoregates ?
Life cycle Psoregates ovis mites
All stages are permanent parasites
* highest numbers are located on the dorsal side of the body
* egg, larva, three nymphal stages, adult
* the life cycle takes around five weeks to complete a slow breeder
* number build up slowly - it might take years to spread through a flock
The number of parasites are low in summer as they are sensitive to light heat, and high in autumn, winter and spring
Shearing has a negative effect on populations
Describe the pathology and clinical signs of Psoregates ovis mites ?
Psoregates ovis mites
Pathology = hypersenstivity reaction
Clinical signs
* most fleece damage occurs below a line drawn from the elbow to hip ( area accessible to mouth)
* sheep bite at their fleece - pulled wool on the sides of body and flanks
* sheep rub and scratch
* wool rugged tuft appearance
How would you go about diagnosing and treating Psoregates ovis ?
Psoregates Ovis
Diagnosis
Clinical signs - hip to elbow pulled wool
Suspect Psoregates ovis if clinical signs are present in the absence of lice
* sheep rub, scratch
* wool tufted appearance
Confirmation through skin scrappings
Treatment
* MLs ivermectin, abamectin and moxidectin
* will not eradicate the mite infection but will reduce numbers to a low level
* it takes a long time for mite populations to grwo to a level of clinical presentation
Identify this parasite describe its morphology and life cycle ?
Chorioptes bovis
Morphology
* gnathostome short and rounded in outline
* legs are long and protude beyond the tip of the gnathostome/ posterior margin of body
* posterior lobes well developed with 2 long broad setae
* pair of copulatory suckers
Life cycle
* all stages are permanent parasites
* egg, larva (three legs), nymph, adult
life cycle complete 3-4 weels
* common in temperate areas particularly housed dairy cows
Describe the epidemiology of Chorioptes bovis
Epidemiology Chorioptes bovis
Common parasite in temperate regions of Australia, particularly in indoor housed dairy cows.
Host = cows Location = surface of skin
Transmission = direct contact
Feed upon = skin debris
- mite populations increase in autumn reaching a peak over winter
- clinical signs are the most severe during cold weather
- in summer months the mites persist in areas not exposed to the sun
- often asymptomatic and condition may be overlooked
Describe the pathology and clinical signs of Chorioptes bovis ?
Chorioptes bovis
Pathology
Clinical signs are a result of hypersensitivity reaction to mite antigens, present in faeces and saliva (mechanical action less important)
* clinical signs are most severe during the winter months (huddling, sun)
Clinical signs
* can be asymptomatic to severe
* lesions common on tail, perineum, rump, udder and scrotum
* base of tail crust crevices and mild puritis
* nodules progress to alopecia, fine grayish scales, oozing thick crusts
*skin is thick and wrinkled, crevices predisposing animal to secondary bacterial infections
What are the clinical signs of Chorioptes ovis ?
How would you go about diagnosing and treating Chorioptes Ovis ?
Chorioptes
Diagnose
- clinical signs more severe in cold weather
- history housed dairy cows increasing direct contact
Microscopic examination of the superficial skin scrappings
Treatment
- Macrocyclic lactones Ivermectin, moxidectin
- Amitraz however, only registered for tick use in Australia
- Synthetic pyrethoids Flumethrin, Deltamethrin (only registered for tick use in Australia)
Identify and discuss this parasite ?
Demodex bovis
Host - cattle
Location - hair follicles and sebacious glands
Transmitted by prolonged contact
Clinical signs
- nodules and papules
- localised mainly on the shoulder and brisket
- nodules contain caseous material and many mites - damage to hide
- ulcers absesses, alopecia and crusts etc
Treatment
ML Ivermectin, Moxedectin
Organophosphates
Describe the life cycle of lice ?
Lice life cycle
* spend entire life on the host
* generally lice are highly host spceific
* dorso ventrally flattened with claws to cling tightly to fur and hair
* life cycle is incomplete hemimetabolous development egg, three nymphal stages, adults
* malnutrition and overcrowding favour heavy infestations and enhance transmission
* bovicola ovis has a low rate of increase and spreads slowly among sheep
Identify this parasite ?
Bovicola ovis
- head is broad > thorax
- the abdomen is pale with dark transverse stripes
- legs are short of a similar size
cost to the wool industry $122 million annually
* reduce wool quantity and quality
* discolouration, reduced staple strength
What is the effect of shearing, temperature and humidity on Bovicola ovis ?
Bovicola ovis
Shearing
*can cause a loss of 35-5% of lice that are present in spring
* render the microclimate of the remaining 6mm of wool unsuitable for lice
* many lice will be killed by exposure to the sun and higher temperature
(negatively phototactic)
* prefer to remain in parts of the fleece that are 37.5 degrees - a favourable temperature for oviposition, feeding and development
Temperature
* lice may be killed if temps exceed 45 degree
Humidity
* Nymphs and adults tolerate humidity for 24 hours, but emersion > 6 hrs is lethal
* a rain soaked fleece which may remain wet for many hours can cause considerable mortality of sheep biting lice
Describe the epidemiology of Bovicola ovis ?
Epidemiology of Bovicola ovis
Host = sheep, but can transfer and reproduce on goats
Transmission = direct contact or indirect (environment fomites, shearing shed, races)
Sheep which are more prone to infection
* merino breed
* young lambs
* old, sick or poor sheep
Lice spread slowly through the flock and may be present for years prior to a heavy infestation
Spring shorn flocks - lice populations generally increase over winter and fall over summer - effects of shearing
What is the spatial distribution of lice on sheep ?
Lice spatial distribution on sheep
At most points in the year the highest numbers are located dorsally on the back, and along the sides.
After shearing this may change as the lice locate under the neck, lower flanks and upper legs
What are the clinical signs of bovicola ovis ?
Clinical signs
* irritation - rubbing, scratching and biting at wool (pruritis)
* ragged appearance
* reduced quality and quantity of wool
* wool loses its brightness and becomes more yellow
*fleece derangement (wool rub is a good indicator)
* visual inspection - lice can be difficult to detect (light in colour, photophobic)
If one louse is sighted the entire mob is considered lousy
How would you go about diagnosing Bovicola ovis ?
Detection of Bovicola ovis
- detection of lice antigen on shearing tools
eg debris from the shearers comb and ELISA - there exist a scoring system light - medium - heavy
Identify this parasite ?
Lignathus pedalis (foot louse)
Indirect infestation is possible = environment + direct
- short head about as broad as it is long
- not prolonged in-front of the antennae
- heaviest infestations in young lambs and rams
- parasite populations peak in winter
- Clinical signs = biting and stamping of infected parts
Identify this parasite ?
Linognathus africanus
- post antennal lateral margins are extended bulging
- infects goats too
What management techniques could be employed to eradicate lice ?
Long wool treatment will reduce lice numbers but not effectively eliminate them - always shear first
What drugs are effective against lice
Effective drugs to utilise against lice
Organophosphates
synthetic pyrethroids Deltamethrin, Flumethrin
Neonicotinoids
Macrocyclic lactones - ivermectin
magnesium fluorosilicate
insect growth regulators Triflumuron
Identify this parasite, describe its economic importance ?
Haematobia exigua
Morphology
* the eyes are large and red
* maxillary pulps are longer than half of the length of the proboscis
* thorax two dark stripes
* the wings are held in a V shape at rest
Economic importance
The most important animal health issue affecting beef cattle profitability
* 78 million per year
* lesions cause by Haematobia exigua (buffalo fly) and stephanofilaria spp cause hide damage and severe welfare issues
Describe the life cycle and feeding habits of Haematobia exigua (buffalo fly) ?
Buffalo fly
Both sexes feed on blood - 20-40 times per day
* bites are painful
* the prestomal teeth are rotated to drill into tissues - very painful bleeding under the skin on which the fly feeds.
Adult flies live about 10-20 days on a cattle host
* permanently associated with host
* female only leaves host to lay eggs in freshly layed faeces of the host (within 15 sec of cow defaecation)
* female requires blood meals for egg production and lay batches of eggs (14-20)/ under the dung or in crevices of the dung pad
* life cycle can be as short as 9-11 days, but may take longer in cooler weather
Describe the epidemiology of Haematobia exigua ?
Epidemiology
Northern Australia and Asia
Movement throughout Australia mainly occurs through the movement of cattle
- numbers are the highest in summer and autumn (temp and humidity)
Location = found in high numbers on withers, shoulders and flanks - with heavy infestations found around the head, ribs, back and head (around eyes) and legs
Susceptability
* cattle and buffalo ( may attack other species)
* Bos indicus more resistance
* Bulls more heavily affected then cows
* More heavy infestation on old, dark, poor condition animals
* do not like dusty animals
Describe the pathology and clinical signs that result from Haematobia exigua ?
Pathology
The prestomal teeth rotate to drill into tissues, causing a very painful bite. The insects feed on the blood under the skin.
Clinical signs
Feed on blood - painful bite + irritation - distress - reduced grazing time
* restlessness
* rubbing against fences, trees
* skin lesions - inner corner of mouth, neck, face, shoulders and underline
* lowered weight gain and milk production
Describe how you could implement IPM with relation to Haematobia exigua ?
What chemicals can we use to treat Haematobia exigua ?
Haematobia exigua
Synthetic pyrethroids deltamethrin, flumethrin
Organophosphates diazinon, chlorpyrifos
Macrocyclic lactones - abamectin, ivermectin
Describe the life cycle of a nematode strongylida species ?
