CRS 5 Flashcards
1
Q
Describe the cellular signalling mechanism of nitric oxide
A
- NO potent vasodilator
- Inhibits platelet aggregation and elevates cGMP
- Role in blood thinning
- Gas produced by endothelium from amino acids by nitric acid synthases
- NO passes from endothelium to VSMC via gap junctions
- ACh, bradykinin and serotonin act as 1st messengers in endothelial cells due to increased NO
- cGMP is 2nd messenger
- Ca2+ 3rd in VSMCs
- ACh released by nerve terminals in blood vessel wall activate NO synthase in endothelial cells lining blood vessels
- Endothelial cells produce NO
- NO diffuses out of endothelial cells and into underlying smoth muscle cells
- Binds to and activates guanylyl cyclase to produce cGMP
- cGMP tiggers response that causes smooth muscle cells to relax
- Enhances blood flow through vessels
- Occurs because cGP activates Ca2+ pump on membrane of intracellular stores
- Then pump Ca2+ out of intracellular environment
- Decreases concentration
- Reduction in Ca2+ causes contractile filaments in VSMC to slide apart and muscle cells relax
2
Q
Give examples of water vs lipid soluble signalling
A
- Steroids are lipid soluble while peptides are water soluble
3
Q
Describe the regulation of nitric oxide
A
- Different isoforms of NO synthase
- eNOS, nNOs, iNOS
- eNOS: found in cardiac cells, osteoclast and osteoblasts, platelets and endothelial cells
- iNOS: found in inflammatory cells, fibroblasts, endothelial cells and vascular smooth muscle
- Each of these have different metabolites
4
Q
Describe what happens during gram negative sepsis in relation to NO
A
- Massive activation of iNOS
- Excessive vasodilation
- Hypotension and vascular leakage
- Organ failure occurs
- Can be treated with the use of an NO blocker
5
Q
Explain why vasoconstriction is necessary
A
- Used to boost systemic pressure
- Not about reducing flow
- Blood vessels made narrower by VSMC contraction
- Increases vascular resistance
- Vasoconstriction is titrable (mild/moderate/severe) and can be increased by disease, drugs and short or long term physiological responses
- Smooth muscle cells are linked by gap junctions to underlying VSMCs forming functional syncytium
6
Q
Describe the receptors of blood pressure
A
- Detected by baroreceptors
- Sit on carotid sinus and aortic arch
- Sensory neurons with free sensory endings in walls of particular arteries
- Sensitive to stretch
- Detect changes in pressure within the artery
- Information collected by baroreceptors integrated in medulla oblongata
- ANS makes appropriate changes to cardiac function and degree of vasoconstriction
7
Q
Describe th autonomic pathways that regulat blood pressure
A
- SNS: vasoconstriction, increase heart rate and contractility, occurs when BP low
- PSNS: reduces heart rate and contracility, vasodilation, decrease high BP
8
Q
Differentiate between dehydration and hypovolaemia
A
- Dehydration is loss of fluid from ECF and ICF
- Hypovolaemia is loss of lfuid from vaculature
- In acute hypovolaemia, dehydration is unlikely to occur so skin tenting and altererd PCV will not be seen
9
Q
Describe the effect of hypovolaemia on cardiac function
A
- Preload decreases
- Stroke volume decreases
- MAP decreases
- Viscosity of blood unchanged
- Tissue oxygen decreased
- RAAS activated
- Heart rate increases to increase cardiac output and blood pressure
10
Q
Describe the paracrine, endocrine and autonomic responses to hypovolaemis
A
- Symapthetic tone increases, noradrenaline reelased
- Acts on beta1 receptors in heart
- Positive chronotropic and iontropic effect
- Sympathetic system stimulates adrenal galnd
- Release adrenaline
- Also acts on beta1 as agonist - increase HR and contractility further
- Increased sympathetic tone also stimulates vasoconstriction
- Indirect endocrine effects include: ADH released from pituitary in response to reduced blood volume, cause vasoconstrictioin and retention fo circulation volume through kidneys
- Angiotensin II in change of blood vessel tone
11
Q
Describe the difference between systolic and diastolic pressure
A
- Systolic pressure is highest pressure reached during ejection phase
- Diastolic pressure is lowest pressure reached during ventricular filling stage
12
Q
Explain what is meant by mean arterial pressure and its importance
A
- MAP is the average pressure over the whole cardiac cycle
- Drives tissue perfusion with blood result of discharge of volume of blood from heart
- Is not half way between systolic and diastolic pressure, 2/3 of cardiac cycle is diastole
- MAP = ((2xdiastolic)+systolic)/3
- MAP of 60mmHg is needed to perfuse the brain, normal range is 70-110mmHg
- Dependent on cardiac output, total peripheral resistance and blood volume
- Pressure = cardiac output x TPR
- Systolic ejection of blood creastes pressure waveform as blood passes from LV to aorta
- Arterial pulse walve in aorta is asymmetrical, transmitted to rest of arterial tree
- Pressure - time wave form also asymmetrical
- Peak of waveform is systolic pressuer (120mmHg) and base is diastolic pressure
- MAO is average effetive pressure forcing blood through circulatory system
13
Q
Describe the vascular responses to hypoxia other than the pulmonary vessels
A
- Vasodilate in response to hypoxemia
- Improve oxygen supply to the tissues
- Mediated by release of adenosine from hypoxic muscles or tissues
- Local acidosis leading to increased lactage
- Hyperpolarises cell membrane due to increased K+ reducing Ca2+ channel opening potential
- Release of NO from endothelium
14
Q
Describe the pulmonary vascular responses to hypoxia
A
- Vasoconstriction
- Mediated by fall in SaO2
- Response very fast but also patchy
- Dependent on individual
- Pulmonary vasoconstriction occur to maintain ventilation:perfusion relationships
- Mediated by vessel’s endothelium
- Adenosine or angiotensin
- Increases the resistance within pulmonary vasculature
- Tunica media of arterioles hypertrophies
- Hypertrophy of right ventricular myocardium in response to increased pressure within
15
Q
List the clinical manifestations of high altitude disease
A
- Fluid in the lungs
- Increased PCV
- Cerebral dysfunction
- Pulmonary hypertension
- Pulmonary oedema, RV hypertrophy, right sided heart failure, cerebral oedema,erythrocytosis, prevention of maturation of the foetal to adult circualtion, neurological signs, soft wet cough, shallow fast breathing
16
Q
Explain why fluid in the lungs occurs with high altitude disease
A
- Increased pressure within pulmonary arterioles and vasoconstriction of pulmonary veins
- Leakage of fluid from vessels into alveoli due to pulmonary capillary over distension
- Hydrostatic pressure within capillaries greater than that in alveoli
- Fluid floods alveoli (wet cough)
- Fluid contains protein and red cells
- Harder for alveolar macrophages and lymphatics to clear
- Shallow fast breathing
17
Q
Explain why increased OCV occurs with high altitude disease
A
- Erythrocytosis
- Erythropoeitin produced by interstitial capillary bed of kidneys
- In response to hypoxemia
- Released into circulation, triggers development of red cell precursors in the bone marrow
- Release of mature and immature RBCs
- Increased PCV and erythrocytosis
18
Q
Explain why cerebral dysfunction occurs with high altitude disease
A
- Low PaO2
- Vasodilation in the brain leading to cerebral oedema
- INcreased pressure = leakage of fluid from vessels ino cerebral tissues
- Can appear similar to BSE/ Pb toxicity/hypomagnaemic cows in mid to late stages
- Irritability, headaches, disorientation, ataxia, dysphoria, aggression, coma and death
19
Q
Describe the agricultural importance of high altitude disease in animals
A
- High altitude for animals as will be poor for crops
- Mainly cows
- European breeds badly affected (pigs, turkeys, horses, human)
- Sheep, goats, rabbits, guinea pigs, dogs, cats and South American camelids resistance
- Much greater losses when farming at high altitude
- Young do not adapt and are worse affected
- Susceptibility is also hereditary
20
Q
Define hypoxia
A
A deficiency in the amount of oxygen reaching the tissues
21
Q
Define hypoxemia
A
An abnormally low concentration of oxygen in the blood
22
Q
Give an explanation of what high altitude disease is
A
- Cor pulmonale/Mountain sickness/Brisket disease
- Primarily vascular disease seen at high altitudes
- Hypoxia
- Made worse by cold and exposure
- Can also be seen with lung disease
- Defined as right sided heart failure due to increased cardiac work secondary to pulmonary hypretension
23
Q
Describe the main ultrastructural features of a vascular smooth msucle cell
A
- State of constant tone
- Form a functional syncitium
- Internal elastic lamina between VSMC layer and endothelial cell layer of blood vessel
- Main elements of VSMC are actin filaments, gap junctions, elastic elements and a sarcoplasmic reticulum
24
Q
State the roles of NO ion cahnnels in governing VSMC tone
A
- NO is a vasodilator
- Released from vascular endothelium of small muscular arteries and larger arterioles
- Released in response to shear stress but also ACh, polypeptides and kinins
25
State the role of endothelin ion cahnnels governing VSMC tone
- Family of peptides
- Different actions depending on organ/tissue
- e.g. in brain elicits initial vasodilation followed by potent, sustained vasoconstriction
26
Describe how metabolic factors operate loally to regulate arteries and veins
- Rate of blood flow infleunces local metabolic acitivity
- Shear stess
- O2 primary controlled - decreased O2 supply => vasodilation, continued demand stimulates angiogenesis
- Adenosine, phosphate ions, pCO2, lactate, K+ and osmolarity also regulate arteries and veins
- Functional hyperemia (functional demands i.e. if only legs working then more blood to legs) and reactive hyperemia (reaction to clear accumulated metabolites after ischemia) also affect arteria and veins
27
Describe how neural factors operate to regulate arteires and veins
- Arteries, arterioles, veins, muscular venules and arteriovenous anastomoses innervated by sympathetic fibres
- Resting sympathetic tone dominant through constant stimulation of alpha-adrenoceptors
- Leads to vasoconstrction (norepinephrine)
- Beta2-adrenoceptors cause vasodilation
28
Describe how alpha blockers work
- Block norepinephrine generation
- Less circulating IP3
- Less contraction of vessels and vasodilation occure
- Arterioles and venules sympathetically innervateed
- Some dilation will occur in both with an alpha blockade
29
Describe how hormonal factors regulate arteries and veins
- Vasoconstrictors: epinephrine, norepinephrine, prostaglandins, angiotensin II, vasopressin (at low concentrations called ADH)
- Vasodilators: bradykinin, histamine, prostaglandins
- Prostaglandins can be constrictors or dilators depending on species, concentration and local sensitivity but mainly constrictors
- Dilators can be beta and alpha blockers, sodium channel blockers, chlorine channel agonists
- Constrictors can be: sodium channel agonists, chlorine channel blockers, alpha and beta agonists
30
Describe how mechanical facotrs regulate arteries and veins
- Sudden rise in arterial pressure leads to an increase in blood flow
- Quickly restored to a normal value
- Myogenic autoregulation from direct response of VSMC to stretching and relaxation
- Endothelium forms bioactive interface
- Constant exposure of ECs to shear stess maintains vascular tone
- Mediated in part through regulation of eNOS
- Shear stress can be either atheroprotective or atheroprone
- Steady pulsatile flow in straight parts of arterial tree is atheroprotective (increases eNOS derived NO availability and exerts anti-inflammatory and antioxidative effects)
- In bends and bifurcations, distured flow patterns induce expression of molecules involved in atherogenesis
- Elevate level of reactive oxygen species in ECs
31
Describe how arteriolar flow is regulated
- Controlled centrally and locally
- Centrally is controlled by brain's cardiovascular centre
- Acts indirectly through baro- and chemoreceptor reflex arches
- Peripherally controlled by vascular beds and local fine tuning
- Acted directly upon through metabolic, mechanical and pharmacological stimuli
32
List the mecahnisms that maintain vasomotor tone
- Metabolic
- Neural
- Hormonal
- Mechanical
- Endothelial factors
- RAAS
- Intracellular calcium
33
Briefly outline the RAAS
- Renin angiotensin aldosterone system
- High concentration leads to vasoconstriction
- High blood pressure supresses RAAS, low stimulates it
- Angiotensin II ver vasoactive
- Increases blood pressure
- Short half life and is very potent
34
Explain how calcium ion concentration is kept low for signalling
- Calcium complexes insoluble
- Ca kept low by Ca transporters
- Means there is a steep concentratin gradient
- Offers potential to rapidly increase intracellular Ca and control VSMC contractility
- Calcium complexes of phosphorylated and carboxylated compounds often insoluble
- Intracellular levels of Ca2+ kept low
- Prevent precipitation of these compounds
- In eukaryotic cells 2 transport system
- Ca2+ ATPase pump and Na+/Ca2+ antiporter
- Steep concentration gradient, able to rapidly increase cystolic Ca2+ by opening Ca2+ channels in plasma membrane of in intracellular membrane
35
Explain the term EC50
The concentration of a drug that will give the half-maximal response
36
Explain the term Emax
The efficacy of a drug and refers to the maximum response achievable from a drug
37
Describe techniques used to investage receptor expression in arterial and vascular systems
- Administration of different drugs and combinations of drugs
- Measuring effect on blood pressure, heart rate, contractility etc
- If know what action drug has on a receptor, the know if response occurs and if the drug is antagonistic or agonistic
38
Explain the different causes of heart failure
- Usually chronic
- Acute can be vascular and AMI
- Chronic usually degenerative
- Fall in cardiac pressure detected as fall in blood pressure by baroreceptors
- In all cases, cardiac output falls
- Sympathetic activation, RAAS stimulation and cardiac enlargement
39
Compare concentric and eccentric cardiac hypertrophy and their causes and effects
- Concentric caused by pressure loading (hypertension, aortic pulmonary stress)
- Leads to stiff non-compliant heart due to thickening of the heart wall
- Eccentric caused by volume loading (valvular disease allowing regurgitation of blood back in to tha atria or ventricles)
- Leads to thin heart wall, overall increase in internal and external diameters of the heart
40
List the pathophysiological responses which occur in cases of cardiac failure
- Increased heart rate and contractility
- Vasoconstrction
- Salt and water retention
- Cardiac enlargement
- Backwards failure (congestion) more likely to occur than forwards failure (poor perfusion) as whole system is designed to maintain perfusion pressure
41
Describe clinical presentations of heart failure
- Heart rate and contractility increases (oxygen needs to increases so heart works harder to facilitate this)
- Vasoconstriction (increases afterload, cardiac output falls, valves more leaky)
- Salt and water retention (maintains blood pressure, volume returned to heart increases, oedema)
- cardiac enlargement (AV valves leak, oxygen needs to increase, cells die replaced by scar tissue, contractility falls)
- All compensatory mechanisms
- Generate more problems in the long term
42
Compare congenital and acquired heart diseases and give examples of each
- Congenital: less common, present at birth, patent ductus arteriosus
- Acquired: most common, few effective treatments, does not always lead to heart failure, degenerative valvular disease, valve/endocardial infection, pericardial disease, rate/rhythm abnormalities
43
Describe what occurs in degenerative valvular disease
- Later in life
- Cause unknown
- May not lead to heart failure
- Regurgitation of blood into atria duing systole
- Pressure in atrium lower than that in aorta, so if mitral is leaky then easier for blood to flow into artium
- Decreases cardiac output
- Total stroke volume increases
- Forward stroke volume decreases
44
Describe the consequences of AV valve degeneration
- Atrium has to deal with increased volume (normal + regurgitant)
- Increased diastolic volume in ventricle
- Atrial and ventricular pressure increases
- Heart volume increases
- Heart hypertrophies, valve leaflets pulled apart more, damage to chorda tendinae
- Continuous cycle
45
Describe the consequences of aortic valve degeneration
- Ventricle has increased blood volume (normal + regurgitant)
- diastolic pressure increases
- Atrial pressure increases
- Blood volume in ventricles increases, total heart volume increased
- Heart gets bigger
- AV valves leakier
- Cardiac output falls
46
Describe the pathology of valvular disease
- Weight of heart increases
- Increased volume loading
- Eccentric hypertrophy and dilated wall of heart is thin
47
Describe what occurs in heart muscle disease and its pathology
- Cardiomypothay
- Cause unknown
- Leads to heart failure
- Muscle function will be poor
- Heart does not pump effectively
- Cardiac output falls as stroke volume falls
- Systolic function of the valves compromised
- Weight of heart increases
- Increased volume loading
- Eccentric hypertrophy
48
Describe the consequences of dilated cardiomyopathy (aortic valve degeneration)
- Increased diastolic ventricular volume
- Normal return to ventricle + afterload
- Ventricle dilates and walls thinner
- Heart hypertrophies
- AV valves leak
- Cardiac output falls
- In cats rarely filated and usually restrictive (stiff heart due to hypertrophy thickening the walls)
- Cardiac muscle fails, stroke volume falls, cardiac output falls
49
Describe the consequences of hypertrophic/restrictive cardiomyopathy
- Usually in cats
- Ventricle doesn't fill
- Diastolic ventricular pressure rises
- Ventricle contains less blood at end of diastole
- Ventricle ejects less blood
- Fall in cardiac output
- Atria get bigger
- Weight of heart increases
50
Describe what occurs in myocardial hypertrophy
- Eccentric and concentric hypertrophy
- Eccentric caused by volume loading and usually accompanies valvular disease
- Concentric caused by pressure loading, usually follows hypertension
- In hypertrophic cariomyopathy concentric hypertrophy is a consequence
51
Describe the physiological mechanisms by which heart failure can be managed
- Weight control
- Controlled exercise
- Drugs
- Regular reassessment
- Treatment of dysrhythmias
- Removal of fluid
52
Descriibe groups of drugs that can be used to manage heart failure
- Positive inotropes: increase contractility e.g. digoxin, pinobendan, dobutamine
- POsitive lusotropes: relax heart, restrictive cariomyopathy e.g, calcium channel blockers (diltiazem, verpamil) and beta blockers (propanolol, atenolol)
- Venodilators: increase venous capacity, reduce preload, reduce fluid build up
- Artierla dilators: reduce aferload, increase output, reduce valve leakage
- ACE inhibitors: reduce levels of angiotensin II and act as venodilators and arterial dilators, reduce levels of aldoserone and so reduce fluid accumulation, decongestion e.g. enalapril, benazepril, ramipril, imidapril
53
Understand the need for drug monitoring and combined treatment regimens for animals in heart failure
- Rarely true standard dose
- Regular reassessment importnat
- Rarely cure - simply treat primary clinical signs
- Tachyphylaxis possible
- May need to replace drug
- Important to control weight and exercise to allow drugs to work to full effect
54
Why might drugs fail to be effective?
- Dose too low
- Administration failure
- If given orally then full amount may not be absorbed
- Tachyphylaxis (drug stops working for the patient)
55
Describe the classifications of heart failure severity
Class I: no clinical signs, occult heart disease preset but with or without signs of compensation
Class II: mild-moderate, heart disease present, limited exercise tolerance (mild), progressively worsens, signs evident with mild exercise (moderate)
Class III: advanced, obvious clinical signs with minimal exercise, progressively worsens, obvious clinical signs at rest, usually results in death
56
Define symbiosis
2 organisms living together where neither benefits nor does it harm either one
57
Define mutualism
Organisms of different species both benefitting from an interaction e.g. a honey bee and a flowering plant
58
Define parasitism
One organism benefits from the interaction to the detriment of the other
59
Define commensalism
When only one organism benefits form the interaction but not to the detriment of the other
60
Define a facultative parasite
One that may survive in the absence of a host i.e. it is opportunistic
61
Define an obligate parasite
One that at some stages of the life cycle cannot survive in the absence of a host
62
Define an endoparasite
One that lives internally in the host
63
Define an ectoparasite
One that lives on teh outer surface of the host e.g. fleas
64
Define a direct life cycle
One where the parsitic stages occur in or on one host
65
Define an indirect life cycle
One where an intermediate host is needed for the development of some stages of the parasite
66
Describe the morphological features of major groups of parasites
- Many polymorphic (different body forms in life cycle)
- May be associated with free living and parasitic stages
- Highly modified to meet demands of teh environment
- No need for sense organs, organs of locomotion or digestive tract
- Prominent organs of fixation
- Well developed reproductive systems which produce millions of effs to ensure transfer
- Arthropods are inset like
- Nematheminths are thread like worms
- Platyhelminths are flat worms
- Acanthocephalan have thorns on their heads
67
List and define the different types of host in relation to parasitism
- Definitive: host in which parasite's sexual reproduction takes place
- Intermediate: host in which parasite's asexual reproduction takes place
- Permissive: host that is not usually utilised but facilitates life cycle completion
- Non-permissive: host in which parasite cannot complete life cycle (can still cause disease)
- Reservoir: temporary host used in absence of natural host
- Paratenic: host used for transport
68
Define a biological vector
A vectore needed by a parasite to complete part of its life cycle (e.g. mosquito)
69
Define a mechanical vector
A vector that can mechanically spread a parasite and is not utilised in the parasite life cycle e.g. tabanic flies in horse/deer fly
70
Give examples of parasitic phyla
- Arthropoda: flies, live, fleas, mites, ticks
- Platyhelminthes: flat worms, cestoda (tapeworms) and trematodes (liver fluke) infect GI
- Nemathelminth: worms - trichostrongyle, infect GI and CR
- Acanthophala (thorn head)
71
Describe different portals of entry for parasites into the animal body
- Ingestion
- Skin penetration
- Skin inoculation by insect bite
- Direct contact (mite)
- Transplacental (Strongyloides)
- Sexual intercourse (Trichomonas)
- Inhalation
72
Describe the basis of parasite control
Need to make environment unsuitable for parasite. Can be done as a vaccination or post infeciton
73
Define the prepatent period of parasites
The time take from infection for a parasite to become an adult and effective
74
Describe the epidemiology of cattle lungworm
- Dictyocaulus viviparus
- Usually seen in later half of first grazing season
- Exposed and survive gives immunity but most be maintained by exposure each year
- Hypobiosis of late larval stage
- L3 larvae overwinter on pastures in enough numbers to cause disease the following spring
75
Describe the symptoms of mild, moderate and severe infections of D. viviparus
- Mild: intermittent cough, normal resp rate, normal lung auscultation, sometimes occasional squeaks
- Moderate: frequent cough at rest, tachypnoea (40-60/min), pronounced sqeuaks and crackles in diaphragmatic lobes
- Severe: deep harsh cough, severe tachypnoea (>80/min), pronouned squeaks and crackles in lobes, respiratory distress, gasping for air with head and neck outstretched, salivation, loss of appetite, fever
76
Describe the life cycle of Dictyocaulus arnfieldi
- Similar to D. viviparus
- L1 not produced in lungs
- Eggs passed out of body but hatch very quickly
- L1 often detected in faeces
- In donkeys prepatent period of approx 13 weeks
- Adult parasites in donkeys found in small bronchi
77
Describe the diagnosis of D. arnfieldi in horses
- Usually not patent in horses
- Very few/no eggs or L1s
- Clinical signs include persistent cough, not responding to certain drugs e.g. antibiotics
- History that includes co-grazing with donkeys
- Bronchoalveolar lavage or traacheal wash may reveal worms and large numbers of eosinophils
78
Describe the diagnosis of D. arnfieldi in donkeys
- Shows as patent infection with eggs/L1 in faeces
| - Some clinical signs may be present e.g. lung sounds on auscultation
79
List the drugs that can be used to treat D. arnfieldi
- Ivermectin
- Fenbendazole
- moxidectin
80
List the drugs that can be used to treat D. viviparus
- Albendazole
- Doramectin
- Ivermectin
- Moxidectin
- Levamisole
81
List the 4 main spcies of lungworm in small ruminants
- Dictyocaulus filaria (direct)
- Muellerius capillaris (indirect)
- Prostrongylus (indirect)
- Cystocaulus (indirect)
- Sheep or goat ingest snail/slug with larvae
82
List the lungworms found in dogs
- Angiostrongylus
- Oslerus osleri
- Filaroides
- Crenasoma
83
Give the name of the lungworm found in cats
Aelurostrongylus
84
Describe the epidemiology of Angiostrongylus vasorum
- Adults live in pulmonary arteries
- Sometimes called heartworm (incorrect)
- Indirect life cycle
- Slug/snail intermediate host
- Clinical signs vary
- Endemic in some parts of UK
85
Outline the clinical signs of Angiostrongylus vasorum
- Coughing
- Dyspnoea
- Haemorrhage
- Pulmonary hypertension
- Lethargy
- Exercise intolerance
- Collapse
- Neurological signs
- Lumbar pain
- Ocular signs
- Can be asymptomatic
86
Outline the diagnosis of an infection with Angiostrongylus vasorum
- L1 in faecces or in bronchoalveolar lavage fluid
| - Radiography may also show signs of alveolar infiltrates
87
List the drugs that may be used to treat an infection with Angiostrongylus vasorum
- Fenbendazole
- Levamisole
- Ivermectin
88
Outline the key points about Oslerus osleri
- Metastrongyle nematode with direct life cycle
- Infetion occurs by ingestion of L1 infected faeces or direct transfer of L1 in sputum
- Adults live in trachea and bronchus
- Cause nodules
89
Describe the clinical signs and diagnosis of Oslerus osleri
- Chronic cough
- Immune response to adults in trachea and bronchus causes worm to encapsulate forming nodules
- Particularly at tracheal bifurcation
- L1 in faeces or BAL fluid also seen
- Resolution of tracheal or bronchiolar nodes can take several weeks post-treatment
90
Outline the key points about Aelurostrongylus abstrussus
- Cat lung worm
- Indirect life cycle
- Definitive host = cat
- Intermediate host = snails/slugs
- Paratenic host = host rodents, birds, amphibians
91
Describe how to diagnose Aelurostrongylus abstrussus
- Larvae in faeces
- May be intermittent so absence of larvae does not rule out aelurostrongylosis
- Larvae in BAL fluid
- Bronchointerstitial lung pattern visible on radiography
92
List the drugs that can be used to treat Aelurostrongylus abstrussus
- Fenbendazole
- Levamisole
- Ivermectin
93
Define visceral larva migrans
Larval migration through host organs e.g. ascarids
94
Define visceral larval migrans
Larval migration through the skin e.g. hookworms
95
Define ocular larva migrans
Larval migration through the eye e.g. Toxocara in humans
96
Name nematodes that have a lung phase but are not lungworms
- Ascaridae (Ascaris suum, Parascaris equorum)
- Toxocaridae (Toxocara cati, Toxocara canis)
- Strongyloididae (Ancylostoma caninum, Strongyloides sterocoralis)
97
Describe the life cycle of Oestrus ovis and discuss its importance in UK agriculture
- Myatic parasit
- L1 larvae deposited directly into living issue by adult bot flies
- Is a nasal bot fly of sheep and goats
- Once L1 deposited, migrate up nasal passages into the sinuses
- Here L1 develop into L3
- Can take weeks or months
- Once reach L3 are sneezed out onto pasture
- Pupate and develop into adults
- Once adults have very rudimental mouth parts so must get as much nutrition while in the sheep
- Clinical signs vary
- Include: sneezing, rhinitis, mucopurulent nasal discharge, obstruction of air flow, decrease in time spent grazng, avoidance behaviour and cause secondary bacterial infection leading to ascessation of lungs or interstitial pneumonia
- Decreases production
- Pupae survive over winter and flies so treatment needed in late summer
98
Describe the life cycle of Syngamus trachea and discuss its importance in UK agriculture
- Tracheal worm of birds
- Gapeworm
- Ingested directly as egg, as L3 or ingestion of paratenic host with encapsulated L3
- L1-L3 occur in the egg
- Once hatched, L4 migrate from duodenum through blood stream to lungs and then trachea
- Adults in trachea produce effs
- Coughed up and swallowed
- Eggs defecated
- Infection can be subclinical and depends on size and age ofbird
- Gaping very indicative
- Weight loss may also occur
- Difficult to control
99
Give examples of different ways in which nasal and tracheal parasites may be diagnosed
- Post mortem
- Nasal swabs
- Endoscopy
- Flushing of nasal cavities
- Eggs or larvae in faeces
100
Descrieb the life cycle and clinical features of canine heart worm
- Dirofilaria immitis
- Not present in UK
- Infection is seasonal
- Females longer
- Complex indirect life cycle
- Mosquitos as vector
- Female worms release microfilaria (MFF) into blood
- Taken up by mosquito during feeding
- MFF develop into L3 in mosquito
- Migrate to salivary glands
- L1s move down mouth parts onto skin and enter bite wound , into dog and to right heart and pulmonary vessels
- MFF cannot develop in dog
- Must pass through mosquito
- Prepatent period ~ 6-7 months
- Transplancental transfer of MFF can occur but no adults will develop
- Clinical signs can be asymptomatic through to heart failure
- 3 phases depending on severity
- Diagnostic tests: complete blood count, serum biochemical profile and urinanalysis, heartworm antigen tests, MFF identification tests, thoracic radiological exam, ECG, echocardiogram, angiography
