Parasitology Flashcards

Question

Describe development of babesia species within the tick ?

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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

Answer 7

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

Answer 8

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

Answer 9

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).

Answer 10

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

Answer 11

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

Answer 12

Anaplasmosis - Ricettsiae - dense, rounded, dark blue spots irregular outline - most occur close to the margin of the red blood cell

Answer 13

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)

Answer 14

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

Answer 15

Imidocarb Oxytetracyclines

Answer 16

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

Answer 17

Gasterophilosis intestinalis (common bot fly) - mouth hook have a saddle like depression - spines are slender and blunt tipped - two rows of spines

Answer 18

Gasterophilosis nasalis (throat bot fly) - one row of spines

Answer 19

Gasterophilosis haemorrhoidalis Nose bot fly - mouth hooks are uniformly bent - spines are smaller and pointed - two spine rows

Answer 20

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

Answer 21

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

Answer 22

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.

Answer 23

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)

Answer 24

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

Answer 25

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.

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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.

Answer 32

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

Answer 33

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

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

note grows upto 15 - 50cm

Answer 40

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)

Answer 41

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

Answer 42

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) -

Answer 43

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

Answer 44

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.

Answer 45

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

Answer 46

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

Answer 47

Life cycle Strongyloide Westeri

Answer 48

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

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

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.

Answer 53

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

Answer 54

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

Answer 55

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

Answer 56

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

Answer 57

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

Answer 58

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

Answer 59

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

Answer 60

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.

Answer 61

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

Answer 62

Fenbendazole, ivermectin and moxidectin

Answer 63

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

Answer 64

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

Answer 65

Triodontophorous Tenuicollis identification of eggs in faeces faecal cultures for species identification

Answer 66

Treatment large Strongyles Anthelmintics from three different chemical families (MLs, BZs and tetra tetrahydropyrimidines) MLs = Ivermectin, Moxidectin BZs = Fenbendazole, Mebendazole tetraHydropyrimidines = Pyrantel

Answer 67

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

Answer 68

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

Answer 69

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

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

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 Strong resistance in Trichostrongyles - -

Answer 74

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

Answer 75

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

Answer 76

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

Answer 77

Benzimidazoles - Albendazole, Fenbendazole, Mebendazole Levamisole Tetrahydropyrimides - Pyrantel and Morantel Macrocyclic lactones - Ivermectin, abamectin and moxidectin Salicylanilides - Closantel Organophosphates - Naphthalophos

Answer 78

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

Answer 79

Paramphistomosis Adult - thick bodied more or less conical in shape - two suckers one anterior one posterior Eggs -

Answer 80

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

Answer 81

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

Answer 82

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

Answer 83

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

Answer 84

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

Answer 85

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

Answer 86

Pathology Moniezia expansa Clinical signs - lambs with heavy infections diarrhoea, constipation, nervous signs, anemia weight loss etc

Answer 87

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

Answer 88

Eimeria bovis Morphology - 4 sporocyst each with 2 sporozoites Life cycle

Answer 89

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

Answer 90

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

Answer 91

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

Answer 92

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

Answer 93

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

Answer 94

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

Answer 95

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

Answer 96

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

Answer 97

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

Answer 98

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

Answer 99

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

Answer 100

Treat adult and larval stages Benzimidazoles and tetrahydropyramides Incysted larvae can only be treated with two drugs Fenbendazole moxidectin

Answer 101

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

Answer 102

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.

Answer 103

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

Answer 104

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

Answer 105

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

Answer 106

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)

Answer 107

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

Answer 108

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

Answer 109

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

Answer 110

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

Answer 111

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

Answer 112

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

Answer 113

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)

Answer 114

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

Answer 115

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

Answer 116

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

Answer 117

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

Answer 118

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

Answer 119

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

Answer 120

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

Answer 121

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

Answer 122

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

Answer 123

Linognathus africanus * post antennal lateral margins are extended bulging * infects goats too

Answer 124

Long wool treatment will reduce lice numbers but not effectively eliminate them - always shear first

Answer 125

Effective drugs to utilise against lice Organophosphates synthetic pyrethroids Deltamethrin, Flumethrin Neonicotinoids Macrocyclic lactones - ivermectin magnesium fluorosilicate insect growth regulators Triflumuron

Answer 126

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

Answer 127

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

Answer 128

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

Answer 129

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

Answer 130

Haematobia exigua Synthetic pyrethroids deltamethrin, flumethrin Organophosphates diazinon, chlorpyrifos Macrocyclic lactones - abamectin, ivermectin

Parasitology Flashcards

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