term 2 Flashcards
supra- omental recess in cattle
recess caudally abouve the two sections of omentum in whic the intestine is housed
name a general product of the rumen
volatile fatty acids
rumination
primary movment of rumen- Regurgitating food after a meal and then swallowing and digesting some of it. Cattle and other ruminant animals have a four-chambered stomach for the rumination of food and so can chew their cud
eruptation
secondary movemt of the rumen. burping, prevents bloat from gasses produced
how is the rumen inervated
Reticuloruminal movements are centrally regulated by the vagus.
Dorsal vagal nucleus of brainstem.
Afferents from the lumen of the ruminoreticulum monitor distension, ingesta consistency, pH, VFA concentration.
reticulum
sorts food particlales- regulates what moves to omasum
lies caudal to diaphram- when foreign object is injested strong contractions can cause it to pierce muscular wal and diaphram
omasum
same job a simple stomack
abomasum
glandular- protien digestion
proteoloitic enzymes- hca, pepsin
Gastric groove
In the unweaned animal the gastric groove forms a closed tube for milk to pass directly from the oesophagus to the abomasum.
Formation of the tube is a reflex action when the animal suckles.
The reflex is stimulated by ADH
The reflex may also be stimulated by chemicals such as copper sulphate
stomach of calf
rumen smaller
abomentum big
Motility of the omasum
Contractions are biphasic
Phase 1 squeezes ingesta into recesses between the laminae
Phase 2 is mass contraction of the omasum
Regulation of flow of ingesta from the reticulum to the omasum
The omasal orifice remains open.
Contraction of the reticulum causes substances to pass into the omasum. At this time the omasal orifice dilates further.
The omasal orifice then closes as it contracts to force the ingesta between the lamina
This requires innervation form the vagus nerve
Motility of the abomasum
General contraction of the abomasum with increased amount of peristalsis in the pyloric region.
Like simple stomach, regular flow of ingesta from abomasum to duodenum may be regulated by pylorus
Fibula of ruminentz
The shaft of the fibula regresses in ruminants. The proximal extremity persists as a tear-shaped process fused to the lateral condyle of the tibia. The distal extremity is isolated as a small compact malleolar bone that forms an interlocking joint with the tibia completing the articular surface of the talus.
describe the nerve origin, course, function and the consiquenses when damaged of the femoral nerve
L4-6
Short course within the thigh, finishing in the quadriceps (saphenous branch continues)
A saphenous branch arises from the femoral nerve close to its exit point from the iliopsoas and innervates the sartorius muscle. It then courses with the femoral artery distally
Femoral innervates:
the iliopsoas and quadriceps femoris muscles
The skin over the medial surface of the limb
Saphenous branch
providing general somatic afferents to the skin over the medial crus and, the dorsomedial metatarsus and fetlock joint
Newborn calves delivered by strong traction on hindlimbs may be unable to bear weight on the affected limb and have a loss of sensation on the medial aspect of the leg skin
describe the nerve origin, course, function and the consiquenses when damaged of the obturator nerve
L4-6
Crosses the ventral surface of the sacroiliac joint, runs medial to the shaft of the ilium, and penetrates the obturator foramen to reach the medial muscles of the thigh.
Innervates the adductor muscles
Loss of adduction:
Can be compressed during dystocia calvings-recumbency/dog sitting posture.
Fall-hind legs do the splits and may be unable to rise.
describe the nerve origin, course, function and the consiquenses when damaged of the sciatic nerve
L6-S2
On leaving the pelvis it passes around the dorsal and caudal aspects of the hip joint. Goes between the biceps and semi-membranosus. Divides into the tibial and common peroneal nerves before reaching the gastrocnemius.
Innervates the caudal thigh muscles.
Shared responsibility for innervating all structures distal to the stifle (except medial skin)
Goes between the biceps and semi-membranosus, a few centimeters caudal to the femur –at risk from damage by intramuscular injections.
Large/ill placed foetuses may damage the nerve during parturition. Affected limb hangs loose, stifle and hock extended, digits flexed, foot knuckled. No cutaneous sensation over the entire extremity except the area supplied by the saphenous.
describe the nerve origin, course, function and the consiquenses when tibial nerve
L6-S2
(branch of sciatic)
Passes between the heads of the gastrocnemius a short distance cranial to the popliteal lymph node. It branches to the caudal crural muscles. The main trunk (purely sensory) continues towards the hock. It divides opposite the point of the hock into the medial and lateral plantar nerves.
Innervates the caudal crural muscles.
Sensory: the lateral plantar nerve supplies the abaxial plantar portion of the lateral digit. The medial plantar nerve innervates the entire plantar medial digit and the axial surface of the lateral digit
Abnormal excessive innervation of the caudal crural muscles can cause spastic paresis.
Damage to the tibial nerve can cause over flexion of the hock, extension of the fetlock, producing a vertical pastern (innervation to the digital extensors remains intact so hoof placement is correct when the animal walks and weight is correctly carried)
No response to pain stimuli on plantar lower limb skin
describe the nerve origin, course, function and the consiquenses when damaged of the peroneal nerve
L6-S2
(branch of sciatic)
Crosses the lateral surface of the gastrocnemius under the cover of the biceps before becoming superficial and palpable as it passes caudal to the lateral collateral ligament of the stifle. Dives between the peroneus longus and lateral digital extensor muscles before dividing into superficial (3 divisions) and deep branches.
Generally:
Cranial crural muscles
Sensory nerves for the cranial aspect of the leg distal to the hock
Superficial:
medial branch that supplies digit III
middle branch that supplies the axial portions of digits III and IV
lateral branch that innervates the abaxial surface of digit IV
Deep:
sends branches that communicate with the middle branch of the superficial nerve to innervate the axial portions of the claws
Hyperextension of the hock, hyperflexion of the fetlock and digital joints. Unless passively placed in the correct position, the limb rests on the dorsal surface of the flexed digits.
The cow eventually learns to walk correctly by flicking the foot forwards and flat when taking a step.
No response to a pain stimuli on the cranial lower limb skin.
injection points on cattle
Pericardiocentesis - 5th intercostal space LHS abve costochondral junction
Blood sampling and IV injection– jugular groove, coccygeal vein
describe the dental formula of ruminents
Ruminants have a maxillary dental pad with no upper incisors or canines. This is followed by the diastema. They have 3 upper premolars and 3 upper molars.
On the mandible they have 3 incisors, 1 canine. Again, we have a matching diastema, then 3 lower premolars and 3 lower molars.
Ruminants have 20 deciduous teeth (no deciduous molars) and 32 permanent teeth
NB. It is customary to refer to the canine tooth as the fourth incisor in ruminants. The most rostral premolar is known as ‘PM2’ (there is no PM1). But molar 1 is still called M1.
Lack maxillary incisor - cornified dental pad
Mandibular brachydont incisors
Dental attrition is common
Hypsodont (long-crowned) premolar and molar teeth
describe the timeline of ruminent dentition
A: Deciduous incisors of a neonate.
The enamel still surrounds the crown
B: 2 years old, 1st incisor is permanent.
The distal border of I1 is slightly worn and dentine is exposed
C: 3.5yrs, I1+I2+I3 are permanent.
The occlusal surface of I2 is wider than I3.
D: 5yrs
E: 8yrs. The occlusal surface is at its greatest and the lingual surface of I1 and I2 is smooth, known as being ‘level’.
The facial muscles are supplied by the facial nerve (CNVII) which divides into its principle terminal branches underneath the parotid gland.
describe these branches
- The auriculopalpebral nerve supplies muscles of the external ear and eyelids. It reaches these by crossing the zygomatic arch directly in front of the temporomandibular joint where its superficial position makes it vulnerable. Damage to the nerve may be evident by drooping of the ear and sagging of the eyelids, and paralysis of the orbicularis muscle makes it impossible to close the eye-therefore blocking this nerve to eliminate the menace reflex (blink) is very handy for eye examinations. It is most easily palpated where it passes over the zygomatic arch.
- The dorsal buccal branch continues the parent trunk (facial), crossing the masseter muscle in an exposed and vulnerable position. Injury can cause loss of innervation to the muscles of the nose, upper lip and buccinator. The first loss leads to slight distortion of the face, which is pulled towards the unaffected side (as there are no counteracting muscles working), the second allow food to collect in a wad within the oral vestibule.
- The ventral buccal branch takes a more protected course caudomedial to the ramus of the mandible and reaches the face along with the facial artery and vein. It has limited distribution and so visible effects of injury are minimal.
Local anaesthetic points for disbudding, eye lid, nose/maxillary skin
The sensitive dermis of the horn is supplied mainly by the cornual nerve, which is a branch of the zygomaticotemporal division of the maxillary (lacrimal) nerve, plus a portion of the ophthalmic division of the trigeminal nerve.
The cornual nerve arises within the orbit and then passes backward through the temporal fossa where it is sheltered by the prominent ridge of the temporal line.
The nerve later divides into 2 or more branches that wind around this ridge and approach the horn separately under cover of the thin frontalis muscle.
The cornual nerve is blocked for disbudding and dehorning cattle. It can be found where it crosses the ridge-roughly midway between the postorbital bar and the horn (yellow dot).
Bovine specific Landmarks-Upper 3rd of the lateral temporal ridge of the frontal bone, 7-10mm deep, between the frontalis and temporal muscles. 2-3cm in front of the base of the horn
Infraorbital nerve which appears from the infraorbital foramen-anaesthesia of the nose and upper lip for placing a bull nose ring
Landmarks: Half way between the nasoincisive notch and the first upper premolar
Blue: Auriculopalpebral branch of the facial nerve-paralysis of the eyelids.
Landmarks: subcutaneously, where the supraorbital process of the frontal bone meets the zygomatic arch, point the needle posteriorly, inject for 3-5cm lateral to the zygomatic arch
describe the thymus in young ruminents
The thymus produces and secretes thymosin, a hormone necessary for T cell development and production. The thymus is special in that, unlike most organs, it is at its largest in children. Once you reach puberty, the thymus starts to slowly shrink and become replaced by fat
The thymus is large and lobulated. It extends from the larynx to the pericardium in young animals.
The cervical part is connected to the thoracic by a narrow isthmus ventral to the trachea.
The cervical part divides into 2 horns that taper over the lateral aspects of the trachea. It may reach the larynx, with the cranial tip sometimes detached, fragmented and more closely associated with The medial retropharyngeal lymph node and the mandibular and parathyroid glands.
The thymus grows rapidly during the first 6-9monthds of life, although it reaches its greatest relative size much earlier. In some involution may begin as early as 8weeks old. But the tempo of regression varies and the thoracic part in particular may still be present in animals who are several years old. In general the isthmus and neck parts disappear completely.
The thymus in young calves is bright pink/red but lightens with age and the consistency firms as the active tissue is replaced by fatty fibrous tissue.
describe horns in cattle
The size and conformation of horns depends on their age, sex and breed. Function remains for attack, defence, maintaining social hierarchy and foraging.
The horns begin life as germinal epithelium which can be removed by disbudding, the surrounding epidermis which heals the wound, lacks the inductive capacity of the horn bud.
If not disbudded, the softer outermost layer (episceras) is produced by an irregular epithelial strip at the base which is transitional to the ordinary epidermis.
The cornual processes grow from the frontal bone at caudolateral angles to the head. It has a ridges and porous surface and is covered in papillated dermis that also serves as periosteum. The horn sheath/wall represents a modification of the cornified stratum of the epithelium and consists chiefly of tubules formed over the dermal papillae. The tubules run lengthways and are welded together by irregular, intertubular horn produced by the inter-papillary regions of the epithelium.
Since the whole epithelial surface is productive, the older horn is thrust apically by the newer horn, so the horn thickness increases towards the tip where it is all horn.
Horn growth is continuous but the rate may be slowed by periods of stress, similar to in the hooves, creating horn bands. Often produced at calving
An extension from the frontal sinus invades the cornual process at around 6months old.
describe the horn in sheep and goats
The size and conformation of horns depends on their age, sex and breed. Function remains for attack, defence, maintaining social hierarchy and foraging.
Small ruminants have a more domed head in comparison to cattle and the horns arrive closely behind the orbit in a parietal position unlike the temporal ones of cattle.
HORN BUDS: Each horn is based upon a separate ossification centre that makes a secondary fusion to a projection of the skull quite close to its contralateral fellow. Due to this specialised ossification to the skull, disbudding can only take place before this process occurs, which is very young at under a week old.
describe the vascuar supply of the horns
The cornual nerve is accompanied by a considerable artery and vein that branch from the superficial temporal vessels within the temporal fossa. The artery ramifies before it reaches the horn.
Its smaller branches run in the grooves and canals of the cornual process and retract when severed. Which is pretty impressive unless you are a very trying to tidily dehorn a cow and achieve good haemostasis without blood spurting everywhere. When they retract they cannot be easily grasped with haemostats to stop the bleeding, unless the cut is made close to the skull where the arteries are still embedded in soft tissue and easy to reach.
deascribe the interconnection between sinuses and horns
An extension from the frontal sinus invades the cornual process at around 6months old. Here we can see an opening into the caudal frontal sinus
However in both sheep and goats, the frontal sinus later excavates the horn core at the base but does not reach as far inside as in cattle.
describe sinuses in cattle
The paranasal sinus system is very poorly developed in the young calf and it must be several years old before it gets to full size. Even in a mature animal , the maxillary compartment continues to adjust to extrusion of the cheek teeth.
The complete set of sinuses is complicated:
Frontal compartments within the bones of the cranial roof and side walls
A palatomaxillary complex within the caudal part of the hard palate and the face, both before and below the orbit.
A lacrimal sinus within the medial orbital wall
Sphenoidal sinuses that extend past the orbit into the rostral part of the cranial floor
Conchal sinuses within the nasal conchae.
The maxillary sinus occupies much of the upper jaw above the alveoli of the cheek teeth. It communicates with the nasal cavity via a large nasomaxillary opening but natural drainage of pus or other fluid is hindered by the location of this opening high in the medial wall.
The maxillary sinus is continuous with the palatine sinus over the plate of bone that carries the infraorbital nerve in its free margin. It also extends caudally (as the lacrimal sinus in front of the orbit) and within the fragile lacrimal bulla that intrudes into the ventral part of the orbit.
The frontal sinus comprises of several compartments that communicate separately with ethmoidal meatuses. The 2 or occasionally 3, small rostral compartments are of little clinical interest. The caudal compartment is the largest and of most interest to us and spreads mainly within the frontal bone. It covers the dorsal part of the brain case and also extends into the lateral and nuchal walls and into the horn core as we saw earlier. It is separated from its fellow and from the smaller homolateral compartments by partitions which vary in position. The openings in these partitions are closed by mucosa. The major cavity, which continues to increase throughout life, is further subdivided by irregular and perforate septa. Inflammation of its mucosa is a common sequel to dehorning.
describe sinuses in small ruminents
The maxillary sinus is shallower and simpler. It does not communicate with the lacrimal sinus, which may open into the nasal cavity separately or via the lateral frontal sinus.
The frontal sinus comprises separate medial and lateral compartments. They lie medial to the orbit (and extend slightly beyond this both rostrally and caudally) and are of irregular form. The lateral compartment corresponds to the caudal sinus of cattle and provides the extension to the horn core.
The most common clinical involvement of the sinuses in sheep is that caused by the invasion of the frontal sinus by larvae of the nasal bot fly. Treatment involves surgical puncture to either the rostral to the horn or medial to the middle of the orbital rim where there is no risk to the frontal vein.
describe the reasons for ruminal acidosis
Often viewed as the most dramatic form of the forestomach fermentative disorders, clinical ruminal acidosis occurs when excessive levels of organic acids accumulate in the rumen, resulting in a rumen fluid pH of less than 5.2. Normal rumen pH=5.6-7
Subclinical rumen acidosis pH=5.2-5.6
Clinical acidosis pH= <5.2
Normally have a balance of fermentable carbohydrates and fibre, plus basic bicarbonate from saliva to help neutralise some of the acid.
Good rumination and chewing the cud stimulate saliva production
A common scenario for the development of clinical rumen acidosis is the excessive consumption of rapidly fermentable carbohydrates by ruminants that are unadapted to a high-concentrate diet. As a result, clinical rumen acidosis is often seen in the early feeding period when newly received growing beef cattle, accustomed to a primarily forage-based diet, are introduced to a primarily concentrate-based ration and the amount is increased too rapidly. Similar signs can also develop when concentrate-adapted ruminants are fed more concentrate than their ruminal microbial population can handle. This situation might occur following a feeding error, overprocessing of grain, changes in ration moisture, or when there is excessive competition for feed within an animal population. Excessive feeding of rapidly fermentable carbohydrates, commonly referred to as “grain overload,” is the classic scenario leading to clinical rumen acidosis. It is important to remember, however, that excess grain consumption is not essential to the development of the syndrome, because excess consumption of any rapidly fermentable carbohydrate (apples and other fruits, bakery waste products, incompletely fermented brewery products, and standing green corn) is capable of providing the necessary substrate for the development of clinical disease. Equally a sudden reduction I the amount of fibre fed, even when the carbohydrate amount stays the same can initiate a ruminal acidosis event due to the lack of buffering.
In non-production systems, ruminal acidosis can be seen in pet goats following consumption of excessive amounts of animal crackers or bread given by the owners as treats.
describe the pathogenisis of ruminal acidosis
Ruminal bacteria that digest starches and sugars proliferate and increase their rate of carbohydrate fermentation.
In the normal animal, or in animals with mild clinical disease, rumen buffering capacity and volatile fatty acid (VFA) absorption match the rate of carbohydrate fermentation. In this scenario, the pH within the rumen will stay in a normal range between 5.6 and 6.9, with the higher pH range being more common in New World camelids.
However, when production of VFAs and lactate exceeds the rate of absorption, rumen pH will begin to drop. VFAs and lactate increase in concentration within the rumen fluid and are subsequently absorbed into the systemic circulation.
Although numerous microorganisms have been implicated in the development of disease, the primary bacterium thought to be associated with the progression of clinical signs is Streptococcus bovis. S bovis, because of its rapid rate of division, ability to produce more ATP per unit time, and tolerance of a pH 4.5. As pH decreases, lactate production by S bovis decreases, and the growth of S bovis is slowed. At this point, the Lactobacilli become the dominant microbes present in the rumen and further serve to depress ruminal pH.
Describe the biochemical processes of acidosis
D- lactate is formed by fermentation and L-Lactate is formed during anaerobic glycolysis of hypoperfused tissues.
Both isomers are powerful corrosive agents that can cause severe damage to the rumen epithelium. In addition, lactate and VFAs are osmotically active.
Increased rumen osmolarity decreases absorption of lactate and VFAs, creating a cycle that perpetuates build up of these compounds and a continued drop in pH.
With the continued accumulation of these compounds and further increases in rumen fluid osmolarity, the rumen epithelium is further disrupted. Yeast and fungi that are resistant to highly acidic environments readily colonize the denuded sites and contribute to the development of mycotic rumenitis and omasitis.
In addition, organisms such as Fusobacterium necrophorum are able to invade the bloodstream and spread to the liver. In fact, rumen acidosis is thought to be one of the inciting causes for the development of liver abscesses in ruminants. In addition to their effects on the rumen, the osmotic pressure of these agents causes systemic dehydration and hypovolemia by pulling fluid from the circulation into the rumen, resulting in a reduction in tissue perfusion.
The loss of circulating blood volume leads to cardiovascular collapse, reduced renal perfusion, and anuria. Reduced peripheral circulation also leads to anaerobic cellular metabolism and systemic acidosis
Other compounds produced by rumen microbes
include endotoxins and histamine.
endotoxin concentrations will increase in the rumen of animals on a concentrate-based diet.
If these animals become acutely acidotic, cause microbial death and release of endotoxin in large quantities all at once.
histamine is also known to accumulate in the acidotic rumen.
Allisonellla histaminiformans thrives at low pH,
produces large quantities of histamine,
histamine can be absorbed through the damaged rumen wall and into the systemic circulation.
Histamine may further intensify the symptoms of acute acidosis, including vasodilation and arterioconstriction, and increase vascular permeability
describe the Sequelae of acidosis
blood pressure to increase in capillaries and edema, resulting in swelling, hemorrhage, and even rupture of the vessels.
result in local ischemia and damage to the corium.
Laminitis is commonly seen with acidosis in cattle and sheep, but less so in goats.
Mild cases, animals can experience a transient lameness that seems to resolve following correction of the acidotic event. However, animals experiencing a severe acute case can have more serious lesions, and animals experiencing subacute acidosis can develop subclinical or chronic lesions because of long-term damage to the tissues of the hoof
describe ketosis in ruminents
Energy deficiency syndromes which focus around body fat metabolism, increased NEFAs and ketone bodies, and hepatic lipidosis.
Main syndromes are: Starvation ketosis (protein-energy malnutrition) Pregnancy toxaemia of beef cattle/sheep Fatty liver Fat cow syndrome Clinical ketosis (Type I or II) Chronic ketosis
It is exhibited in a range of ways depending on the species situation
Post partum in cattle forms
pre partum in sheep form
Starvation form (either species)
describe the normal metabolic pathway in the cow
Ruminants are in a vulnerable position with respect to their carbohydrate metabolism when compared to species with simple stomachs. Their GIT provides little glucose for intestinal absorption (up to 10% of total glucose). Instead dietary carbohydrates are converted by the rumen microflora to the VFAs. Consequently the glucose requirements in cattle must be largely met by gluconeogenesis using primarily proprionate and amino acids. Acetate and butyrate are converted to acetyl-co-enzyme (Acetyl CoA) and can thereafter be used for the synthesis of factor be converted into energy via the tricarboxylic acid (TCA, Krebs) cycle. Entry to the TCA cycle requires that acetyl CoA combines with oxaloacetate to form citrate. Citrate passes through a series of intermediate steps to become oxaloacetate again, during which energy is released and 2 molecules of CO2 are produced. Propionate can be converted into glucose, whereas acetate is mainly used for fat synthesis and is stored as lipids or secreted as milk fat. Butyrate can be partially oxidized to ketone bodies. Thus acetate and butyrate are ketogenic, whereas propionate is glycogenic.
Under normal conditions, these 2 groups of VFAs are produced in a ratio of 4:1.
describe clinical ketosis (type I, acetonaemia).
lactating dairy cows, first3-6weeks of lactation.
Characterized by
loss of bodyweight,
reduced milk yield,
Hypoglycaemia
presence of ketone bodies in all body tissues and fluids.
Occurrence: demands on their resources of glucose and glycogen cannot be met by their digestive and metabolic activity.
Begin lactating-increase in energy demand but decrease in feed intake
Negative Energy Balance (NEB).
several metabolic adaptations to manage NEB,
However, some animals will experience excessive NEB,
who are associated with increased risk of disease development and a decrease in both milk production and reproductive performance
Physiology of energy metabolism-Ketosis
In early lactation, homeorhesis is the driving physiologic force
breakdown of body stores of fat and protein
insulin resistance,
Milk production requires large amounts of glucose created by gluconeogenesis
This process is generally diminished in animals affected by ketosis, leading to hypoglycemia.
Providing glucose, stimulating gluconeogenesis, and decreasing fat breakdown form the foundation for rational ketosis treatment
Adipose Tissue
Glycerol and NEFA are released from adipose tissue in response to hormonal cues such as glucagon, corticosteroids, corticotropin, and catecholamines. Insulin is the only hormone that will act to inhibit lipolysis and therefore decrease the amount of NEFA released from adipose tissue. Early in the postpartum period, there is both a decrease in insulin production and a transient state of insulin resistance. These 2 mechanisms allow glucose sparing for lactogenesis by decreasing glucose use by insulin-sensitive tissues, and allowing continued lipolysis even when insulin concentrations increase.
Fatty acid oxidation: fatty acids are derived from the diet or adipose mobilisation. Ruminants have little preformed fat int heir diet and microflora cause little fat to be absorbed intact from the gut.
Fatty acids are taken up directly by the major energy requiring tissues of the body, where they can be oxidised completely to CO2 and energy. However in the absence of adequate gluose or precursors, fatty acids are more likely to be metabolised into ketone bodies
The continual release of NEFA into circulation is not always detrimental: NEFA is a good source of energy for several tissues in the body, and can be used to synthesize milk fat. However, elevated levels of NEFA can result in ab=n inability to oxidise them so they are converted into ketones or re-esterified into triglycerides in the liver and kidney, resulting in hepatic lipidosis.
Homeorhesis
the orchestrated or coordinated changes in metabolism of body tissues necessary to support a physiologic state
Biochemistry of ketosis
Several factors determine the amount and proportion of the 3 major volatile fatty acids (VFA; acetic acid, propionic acid, and butyric acid) produced by microbes in the rumen.
Acetic acid is used mainly in the liver as a major source of acetyl coenzyme A to generate adenosine triphosphate (ATP).
Butyric acid is absorbed from the rumen as a ketone body, βHB.
Propionic acid is taken up by the liver via portal circulation and serves as the major substrate for gluconeogenesis.
Liver
The liver receives approximately one-third of cardiac output and removes approximately 15% to 20% of the NEFA in circulation.
Once inside the liver, fatty acids can follow 4 pathways:
complete oxidation in the tricarboxylic acid cycle (TCA) pathway to produce ATP;
transport out of the liver in very low-density lipoproteins;
transformation to ketone bodies via the b-oxidation pathway or conversion to ketone bodies through peroxisomal oxidation;
or storage in the liver as triglycerides.
When levels of oxaloacetate are low and the cow is unable to oxidise all of the acetyl-CoA that she produces, excess acetyl-CoA is converted in the liver into the 3 major ketone bodies. The 3 major ketone bodies produced by the liver are
1. acetone,
2. acetoacetate (AcAc),
AcAc can convert to acetone and CO2, or alternatively into βHB.
3. βHB.
Acetone
is excreted in urine or exhaled;
it is responsible for the “pear drops/fruity” breath of ketotic cows.
While βHB accounts for most of the total ketone body pool in bovines, in lactating animals with NEB the equilibrium between AcAc and βHB may be shifted even farther toward βHB
Mammary Gland
The mammary gland is not dependent on insulin for glucose use. During excessive NEB, circulating NEFA are regularly incorporated into milk fat. During NEB in the postpartum period, milk fat concentrations tend to increase and milk protein concentrations tend to decrease; thus, the ratio between fat and protein can be used as an indicator of excessive NEB and as a predictor of the risk of developing metabolic diseases. To use milk fat and protein information as a predictor of metabolic diseases that commonly occurs within 30 days in milk (DIM), samples should be evaluated within 9 days postpartum
Sequalae of ketosis
Following ketosis we may see: Hepatic lipidosis Poor immune function, An excessive amount of circulating fatty acids may promote inflammation, which is an important factor in common diseases such as metritis and mastitis. Left Displaced Abomasum Chronic Ketosis Poor reproduction May not hit expected peak milk yield
list parts of the male reproductive anatomy in ruminents
Paired testes – in scrotum Paired spermatic cord Two epididymis Two ductus deferens Two ampullae Two vesicular glands One prostate Paired bulbourethral gland (Cowper’s) Fibroelastic penis – with sigmoid flexure Spermatic cord (containing ductus deferens, vessels including pamp plexus, nerves, connect tissue and cremaster)
what is the sigmoid flexure
At birth, the bull penis is short and slender and lacks a sigmoid flexure, and its apex is fused to the inner lining of the prepuce. With time (and under the influence of androgens), penile and preputial tissues separate, the penis elongates, and a sigmoid flexure develops
Image result for luteolysis
Luteolysis
structural demise of the corpus luteum, which is preceded by loss of the capacity to synthesize and secrete progesterone.
Changes that occur in the uterus with pregnancy
The progestational changes in the endometrium that are part of the normal reproductive cycle persist and intensify in the presence of an embryo. This response is evident from about 30days after fertilization. The blastocyst is first confined to one horn, and since ovulation is commoner from the right ovary (60%) the same preference for the side is present. The membranes soon spread into the other horn, but the embryo, and later the foetus, is almost always confined unilaterally; a pronounced asymmetry of the gravid uterus Is therefore the rule. Indeed the developing inequality in the size of the horns is one of the first clinically detectable signs of pregnancy in the cow. The distended amnion is palpable from 30days, and the foetus itself may be palpated around day 70.
The 80-90 caruncles in the gravid horn increase in size and become converted from low, 15mm long, smooth-surfaced ‘bumps’ on the mucosa to large sessile swellings with a surface pitted for the reception of the chorionic villi making a Velcro-like reationship. Later, those in the non gravid horn enlarge but to a lesser degree. At term the largest caruncles are the size of a clenched fist.
Broad ligament
Hypertrophy
After the 3rd month of gestation the ligament is fully stretched
Uterus slips down over the abdominal floor
placentome
Cotyledon + Caruncle
Cotyledon: the fetal side of the placenta. Caruncle: the maternal side of the placenta.
describe the changes in blood flow during pregnancy
Blood flow:
Increase
Greatest growth of the uterine artery on the pregnant side
Can be palpated per rectum as a mobile firm vessel passing forward across the shaft of the ilium
‘Fremitus’ of the uterine artery can be palpated
Similar but smaller changes occur in the non gravid horn, vaginal and ovarian arteries
Fremitus
Fremitus can be felt because of the hypertrophy of Middle Uterine Artery. There is a fluid turbulence that gives a ‘buzz’ feeling, or a kind of vibration to the artery. Middle Uterine Artery is located in the broad ligament
Uterine topography as gestation progresses:
enters the supraomental recess between the right face of the rumen and the double layer of the greater omentum
2-3months gestation: Sinks towards the abdominal floor
end of the fourth month: lies almost entirely within the abdomen, cervix carried across or beyond the pelvic brim
passes cranially below the right costal arch, pressing on the rumen to the left and the intestines dorsally. The vagina becomes stretched, and as the cervix slides down the caudal part of the abdominal floor, the uterus passes out of reach of the hand within the colon
5th month of gestation: Difficult to palpate the uterus
Further increase in size restores the uterus to reach, it extends forward to come into contact with the diaphragm and liver, pushing the diaphragm towards the thorax and reducing space available to the lungs.
Near term the pregnant uterus occupies most of the ventral and right sections of the abdomen and has raised the rumen from the abdominal floor and crushed the intestines upwards
Topography of the foetus:
First months of gestation: calf moves freely within the surrounding fluid
After 1st month: back is directed dorsally and to one side, toward the greater curvature of the uterus, and towards the mothers flank
bovien placenta
Separate maternal (endometrium) and foetal components.
Foetal placenta-chorioallantois,
feotal membranes- amnion and chorioallantois
Bovine placenta- synepitheliochorial.
The three characteristics of a synepitheliochorial placenta are:
presence of TGC in fetal tro-phectoderm,
formation of fetomaternal syncytia,
development of a placentomal chorioallantoic placental organization
development of the placenta in large animals
uterine epithelium persists although initially modified
trophoblastic binucleate/giant cells (TGCs) create fetomaternal hybrid syncytial plaques
syncytial plaques replaced by Uterine Epithelial cells by Day 40, only transient trinucleate mini syncytia produced throughout the remainder of pregnancy.
“cotyledonary” -localized areas of trophectodermal proliferation forming “cotyledons” in the placenta;
each cotyledon is the fetal part of a placentome.
The placentome is formed by the tuft of chorionic villi from the cotyledon enmeshed with corresponding maternal crypts of the caruncles.
These crypts develop from the preformed flat endometrial caruncles. Placentome formation with a synepitheliochorial interhemal barrier provides the vast increase in surface area. The gross morphology and the pattern of fetomaternal interdigitation differ considerably among bovid species
Pig placentas
non-invasive placenta classified as being epitheliaochorial and diffuse.
Pig blastocysts elongate extensively beginning about day 11 and become evenly spaced throughout both uterine horns.
The embryos become apposed to the uterine surface and begin to attach.
After attachment the endometrial epithelial cells become rounded with bulbous protuberances around which chorionic epithelial cells become moulded.
Processes from chorionic epithelial cells push between endometrial epithelial cells but do not penetrate the basement membrane.
Attachment is strengthened by intertwining of microvilli from chorionic and endometrial epithelial cells and interlocking ridges that act like “tongue and groove” fasteners between the two epithelia.
These attachments soon cover essentially the entire endometrial surface and the chorionic ridges become substantially larger as pregnancy progresses.
Vaginal palpation
Wear PPE=gloves, apply lube to hand, no jewellery, short nails
Approach cow safely, maintain contact
Clean vulva of faeces
Make hand into a beak shape and be gentle
Palpate the structures with flat fingers and palms
Scoop out vaginal discharge for examination
Structures
Vulva, external urethral opening, vaginal mucosa, caudal cervical ring
Cranial cervical ring, uterus, (foetal membranes, calf)
Rectal palpation
Wear PPE=gloves, apply lube to hand, no jewellery, short nails
Approach cow safely, maintain contact
Make hand into a beak shape and be gentle
Advance arm up to just past the elbow
Palpate the structures with flat fingers and palms
Structures
Rectum, cervix, uterus, uterine horns, ovaries, (Male: seminal vesicles, ampulla, prostate)
Iliac artery, pelvis, rumen, caudal pole of the left kidney, abnormal intestines/caecum (RHS)
uterine artery, foetus, placentomes, fluid filled amniotic vesicle,
Definitive signs of pregnancy in large animals
Foetus
Membrane slip (<45d) (feeling the chorioallantois in the uterine lumen)
Placentomes (>8wk, felt appreciably >3m)
Uterine artery fremitus (larger with gestation, don’t confuse with iliac artery which doesn’t move from bone)
Sexing foetuses
60-80days gestation
Male: hyperechoic umbilicus, penis (2 hyperechoic lines of the male genital tubercle), scrotum, followed by hindlimbs
Female: hyperechoic umbilicus, hind limbs, vulva (2 hyperechoic lines of the female genital tubercle), tail
camelid dental formula
1123/3123
describe the basics of mammary glands
Modified cutaneous (sweat) glands
Consists of body and papillae or opening (nipple/teat) – number varies across species
Attached to, and suspended from the ventral body wall
Typically paired structures
Function: to nourish
Each mammary gland is made of tubualveolar glands made of secretory units, grouped in lobules, separated by connective tissue septa
Mammary gland development begins with the growth of the epithelial tissue from the embryonic mammary ridge. The gland continues its development until puberty, when the first hormonal stimulus occurs.
Galactopoiesis
the phase during which the mammary glands maintain lactation
describe the development of mammary gland
Epithelial buds grow from mammary ridges (ectodermal thickenings)
Each bud raises a teat (papilla). In some species the draining point, at the teat is made of multiple duct systems.
Cows are single whereas in the bitch there can many other ducts draining into it.
Histological anatomy of the mammary gland
Each mammary complex comprises one of more mammary units. Mammary units are made of alveoli and ducts.
The body of the mammary glands is made of epithelial tissue (alveoli) and connective tissue with nerves, blood and lymph vessels.
Mammary units end in a system of ducts at the tip of the teat (papilla)
The milk producing part of the gland is divided in lobules (for anatomy purposes!) which are made of alveoli-epithelial tissue. The milk drains into the intralobular duct and from there to a larger interlobular duct and from there to the lactiferous sinus which opens in the teat orifice. This sinus has a little constriction, which creates the part of the sinus close to the gland and the part of the sinus inside the teat itself.
Glands separated by connective tissue
Teat - smooth muscle and elastic fibres
describe the streak canal of the mammary glands
Functions to keep milk in udder and bacteria out of udder
describe the teat cistern of the mammary glands
Duct in teat with capacity of 30-45 millilitres. Separated from streak canal by folds of tissue called Furstenberg’s rosette
describe the gland cistern of the mammary glands
Separated from teat cistern by the cricoid fold. Holds up to 400 millilitres of milk, collecting area for the mammary ducts
isometric growth of mammary glands
Birth -> puberty
allometric growth of mammary glands
Puberty -> pregnancy
Oestrogen – duct development
Progesterone (luteal phase) – alveoli formation
Prolactin, Growth hormone contribute
describe mammary growth in pregnancy
= final mammary development
Terminal alveoli grow into lobules
Prolactin, adrenal cortical hormones and placental lactogen for synthesis of milk
describe the process of lactogenisis
During lactogenesis, the mammary epithelium becomes highly differentiated. This period is associated with an overall increase in the size and metabolic activity of each cell, closure of tight junctions between cells, an increase in mitochondrial size, and development of the endoplasmic reticulum
In ruminants, PRL and glucocorticoids provide the primary stimulus for lactogenesis
Rise in progesterone
Tertiary branching of the ductal system
Rise in prolactin in dogs
Required for full development
Initiates lactation
Some species (similar action) Placental lactogen (ruminants) Relaxin (sow, horse)
Lactogenesis initiated
Alveoli accumulate colostrum
Increased prolactin (PRL) just before parturition
In other species it contributes to increase milk yield, but this has not been a consistent finding in ruminant
Cortisol stimulates differentiation of the glandular epithelium
GH – insulin growth factor signalling axis. At the start of lactation is a trigger, but mid-lactation GH increases milk yield
Oxytocin – simply helps with the release of milk
Milk ejection/let down
Milk ejection is active transfer of milk from alveoli and alveolar ducts into larger mammary ducts, cisterns and into the teat/nipples where it can be removed by the suckling neonate.
Active neuroendocrine reflex
Results in rapid transfer of milk from alveolus teat of mammary gland
Important to feed neonate and prevent pressure atrophy.
More frequent removal = less pressure atrophy = greater quantity of milk can be secreted
Majority of milk remains in alveoli
Milk letdown is a neuroendocrine reflex
Induces emptying of the mammary gland
Sensory activation Neural activation Oxytocin release: binds to myoepithelium in alveoli and ducts Causes smooth muscle in teat to relax
Tactile stimulation, sounds of neonate, visual triggers
Involution
Return to non-secretory state
Recovery time
Less suckling by neonate build up of pressure
pressure atrophy
Increase feedback inhibitor of lactation (FIL) – inhibits milk synthesis
Secretory cells remain non functional until next pregnancy
Next pregnancy Alveolar cells restimulated
Prolactin, adrenal cortical hormones, placental lactogen
what muscles are involved in the pelvic diaphram
coccygeus
levator ani
describe the origin, termination, inervation and function of the coccugeus
Spine of the ischichium and medial surface of the sacrosciatic ligament
Transverse process of the first 3 caudal vertebrae
Pudendal and caudorectal nerve from ventral branch of sacral nerve
Unilateral contralateral draws tail laterally; bilateral contralateral draws tail ventrally
describe the origin, termination, inervation and function of the levator ani
Spine of the ischichium and medial surface of the sacrosciatic ligament
External anal sphincter, caudal fascia
Pudendal and caudorectal nerve from ventral branch of sacral nerve
Holds anus against the contraction of the rectum, aids coccygeus
Innervation of and mechanisms involved in the erection of the cavernous tissue in males and females
Nerves: parasympathetic, from the pelvic nerves
Erection of the penis is brought about by engorgement of the cavernous and spongy spaces
2 distinct phases of erection are recognised:
Firstly : sexual excitement, blood flow into the penis increases as the walls of the supplying arteries relax.
Secondly: at the same time the venous outflow is obstructed.
Females: clitoris
Erection in the fibroelastic penis
slight increase in diameter and length
sigmoid flexure
little additional engorgement is required and erection may be rapidly achieved.
In the first phase of erection, there is parasympathetically mediated relaxation of the supplying arteries occurs. This raises the pressure within the corpus spongiosum and corpus cavernosum from the resting level (5 to 16mm Hg) to the arterial pressure (75 to 80mm Hg); the pressures within these bodies then fluctuate with the heart-beat. The apex of the penis protrudes at this stage, although the muscles of the penis (the ischiocavernosi and bulbospongiosus) are not yet active. Contractions of the ischiocavernosi now raise the pressure further and at the same time occlude both the arteries and the veins by compressing them against the ischial arch. These contractions impel blood forward through thick-walled dorsal and ventrolateral veins of the corpus cavernosum to discharge within the sigmoid flexure. The increase in pressure effaces the bends and straightens the penis, causing it to protrude about 25 to 40cm from the prepuce. After intromission, contact with the vaginal wall stimulates the receptors in the integument of the free part, reflexly stimulating completion of erection. During a short period pressure in the corpus cavernosum can rise remarkably, even to 60 to 100 times the arterial pressure
MOET
Multiple Ovulation Embryo Transfer (embryo flush)
Cause multiple ovulations from an ovary using hormonal therapy, inseminate the animal, retrieve the embryos and implant them into recipients/freeze
Advantages:
quickly multiply the genetics of the top females in the herd.
produce calves with superior genetics.
Females in the herd with less desirable genetics can serve as recipients
Embryos can be produced and sold to other producers who transfer them into their own recipient females.
Frozen embryos can be exported
Heterotrophs
need to consume other organisms to live
Chemoheterotrophs
use organic chemicals and compounds as carbon source
saprotrophs
live off dead or decomposing organic matter
heterotrophic fungi
Enzymes synthesised inside fungal hyphae
Excreted via exocytosis
Act on surrounding medium to break it down
Digested organic compounds are then reabsorbed in solution through the cell wall
Large surface area aids absorption
Biotrophic
feed off living cells
Necrotrophic:
invade living cells, kill them then digest
Moulds grow by
hyphal tip extension
Cell wall softened at tip
Turgor pressure extends wall
Increase in length as opposed to width
Increases surface area for absorption
cell wall of fungi
Cell wall is composed of β-glucan and chitin to provide strength and rigidity and resist osmotic stress
Cell membrane is similar to other eukaryotes but has ergosterol instead of cholesterol
mold
multicellular fungi
yeast
unicellular fungi
Unicellular, non-filamentous
Facultative anaerobes: carry out aerobic respiration when O₂ is available and anaerobic (fermentation) when no O₂ available
Reproduce by mitosis
dimorphic fungi
display both yeastlike and moldlike growth
mycelium
Made up of hyphae
Extensive tissue invasion
septate Hyphae:
cross walls that form between cells but often have pores to allow movement of cytoplasm and organelles (oposite of coenocytic hyphae
Ascomycetes produce
conidia on conidiophores
Zygomycetes
produce sporangiospores on sporangiophores
resting spores
Produced as a result of sexual reproduction
Thicker cell walls protect from abiotic and biotic factors
Harder to eradicat
mycosis
Infection by a fungal agent is called mycosis
Mycoses are generally chronic conditions because fungi grow slowly
Classification is based on the type of tissue infected and the mode of entry into the body - Systemic (lungs, deep tissue/organs) - Subcutaneous (beneath the skin) - Cutaneous (skin, hair and nails) - Superficial (skin surface, hair shafts) - Opportunistic (immune suppression)
Dermatophytoses:
the generamicrosporumandtrichophyton
Microsporum canis; gallinae; gypseum; nanum
Large, rough, thick-walled multiseptate macroconidia
Fusiform to obovate
Attack hair and skin
Most commondermatophyte
Trichophyton mentagrophytes; equinum; verrucosum
Rarely produce macroconidia
Single-cell microconidia are numerous
Solitary or in clusters
Attack hair, skin, nails, horns, claws
Dermatophytes
Arthrospores/conidia are source of infection
Entry via injured skin, scars and burns
Colonisation of keratinised layers
Invade and multiply within keratinised tissues
Produce keratinase
Induces inflammatory reactions
Move away from infection site
Need to overcome biotic and abiotic factors (primary defences)
Adherence and penetration is slow (2-5 days)
Carbohydrate-specific adhesins on surface of conidia
Secreted proteases can facilitate adherence
Fibrillar projections connect conidia to keratinocytes (skin surface
Hyphae grow centrifugally from the initial lesion towards normal skin, producing typical ringworm lesions
Alopecia, tissue repair and nonviable hyphae are found at the centres of lesions as they develop
Growth of hyphae can result in epidermal hyperplasia (overgrowth of skin cells) and hyperkeratosis (thickening of outer layer of skin).
Strategies:
Adherence
Invasion
Colonisation and spread
Immunosuppression
Aspergillus
Primarily a respiratory infection
Spores are very small
Can pass through upper respiratory tract
Carried to terminal part of bronchial tree
Spore germination and invasion of tissue is controlled by many factors
No true virulence factors
Combination of factors leads to disease state
fungal gleotoxin
assosiated with the hyphae
induces cell apoptosis, eithelial cell damage
inhibition of phagocitosis and t-cell response
fungal restrictocin
assosiated with hyphae
inhibitd neutrophil mediated hyphal damage
fungal verruculogen
assosiated with hyphae and condia
affects transepithelial resistance
fungal fumagillin
assosiated with the hyphae
damages epithelial cells and slows ciliary beating. angiogenesis inhibitor
fungal helvolic acid
assosiated with the hyphae
damages epithelial cells and slows ciliary beating.
describe the invasion of aspergillus
Hyphal invasion of blood vessels
Vasculitis and thrombus formation
Formation of mycotic granulomas in the lungs
Vascular dissemination
Colonisation and invasion of other internal organs
Additional mycotic granulomas
Candida albicans
Commensal yeast that lives on mucosal membranes
Pleomorphic switch from yeast to filamentous growth
Phagocytic clearance eliminates most yeast cells
Those that survive convert to hyphal forms
Enables tissue penetration and resistance to phagocytosis Adherence Avoidance Flexibility Integrin-like molecules on cell surface
Allows adhesion to matrix proteins on mucosal cells
Secretion of toxins; proteinases; lipases and phospholipases to aid tissue invasion
Msb2p counteracts complement system (antimicrobials)
Pre-disposing factors e.g. defective cell-mediated immunity, concurrent disease, prolonged use of antimicrobials, damage from catheters
Vascular invasion by hyphae
Haematogenous spread
Production of systemic lesions
Principal features of mycotoxicoses
Outbreaks are often seasonal and sporadic
- May be associated with particular batches of stored feed or certain types of pasture
- No evidence of transmission to in-contact animals
- Susceptibility can vary with the species, age and sex of the animals exposed
- Clinical presentation may be ill-defined
- Antimicrobial treatment is ineffective
- Recovery depends on type and amount of mycotoxin ingested and the duration of exposure to contaminated food
- Characteristic lesions in target organs of affected animals provide supporting diagnostic evidence
- Confirmation requires demonstration of significant levels of a specific mycotoxin in suspect feed or in tissues of affected animals
Aflatoxicosis
Aflatoxins are a group of approximately 20 related toxic compounds produced by some strains of Aspergillus flavus (Fig. 44.2), Aspergillus parasiticus and a number of other Aspergillus species during growth on natural substrates including growing crops and stored food. These fungi are ubiquitous, saprophytic moulds which grow on a variety of cereal grains and foodstuffs such as maize, cottonseed and groundnuts. About half of the strains of A. flavus and A. parasiticus are toxigenic under optimal environmental conditions. High humidity and high temperatures during preharvesting, harvesting, transportation and storage, as well as damage to field crops by insects, drought and mechanical injury during harvesting favour the growth of A. flavus and toxin production.
effects all animals
Aflatoxins
Aflatoxins are a group of related difuranocoumarin compounds with toxic, carcinogenic, teratogenic and mutagenic activity. The four major aflatoxins are B1, B2, G1 and G2. Aflatoxin B1 (AFB1) is the most commonly occurring and also the most toxic and carcinogenic member of the group
Most of the other aflatoxins are metabolites formed endogenously in animals after ingestion or administration of aflatoxins. Aflatoxins are stable compounds in food and feed products and are relatively resistant to heat. They retain much of their activity after exposure to dry heat at 250°C and moist heat at 120°C but may be degraded by sunlight. They have a low molecular weight and are nonantigenic in their native state.
The toxic effects of aflatoxins are dose-, time- and species-dependent. Mature ruminants are less susceptible to the effects of mycotoxins than young animals and monogastric animals. The toxins are absorbed from the stomach and metabolized in the liver to a range of toxic and nontoxic metabolites which are then excreted in urine and milk. The major biological effects of aflatoxins include inhibition of RNA and protein synthesis, impairment of hepatic function, carcinogenesis and immunosuppression.
AFB1 is bioactivated in the liver to a highly reactive intermediate compound which reacts with various nucleophiles in the cell and binds covalently with DNA, RNA and protein. After deliberate administration of AFB1 there is marked interference with protein synthesis at the translational level which seems to correlate with disaggregation of polyribosomes in the endoplasmic reticulum. Many of the toxic responses observed in animals resulting from AFB1 activity can be attributed to alterations in carbohydrate and lipid metabolism and interference with mitochondrial respiration.
Short-term effects include acute toxicity with clinical evidence of hepatic injury and nervous signs such as ataxia and convulsions. In acutely affected animals death may occur suddenly. Long-term consumption of low levels of aflatoxins probably constitutes a much more serious veterinary problem than acute, fulminating outbreaks of aflatoxicosis. With chronic aflatoxicosis there is reduction in efficiency of food conversion, depressed daily weight gain, decreased milk production in dairy cattle and enhanced susceptibility to intercurrent infections in most species due to immunosuppression.
AFB1 is also an extremely potent hepatocarcinogen in many species of animals.
Fumonisins
these substances are produced by several species of the genus Fusarium
The presence of fumonisins in corn grains has been associated with cases of esophageal cancer in inhabitants of the region of Transkei in southern Africa, in China and in northeastern Italy (Peraica, Radic, Lucic, & Pavlovic, 1999). Fumonisins are also responsible for the leukoencephalomacia in equine species and rabbits (Bucci et al., 1996, Fandohan et al., 2003, Marasas et al., 1988); pulmonary edema and hydrothorax in pigs (Harrison, Colvin, Greene, Newman, & Cole, 1990); and hepatotoxic, carcinogenic and apoptosis (programmed cell death) effects in the liver of rats
Trichothecenes
produced by fungi of the genera Fusarium, Myrothecium, Phomopsis, Stachybotrys, Trichoderma, Trichotecium, Verticimonosporium and possibly others
strong capacity to inhibit eukaryotic protein synthesis, interfering in the initiation, the elongation and termination steps of protein synthesis.#
DON is the mycotoxin most commonly found in grains. When ingested in high doses by animals it causes nausea, vomiting and diarrhea. When ingested by pigs and other animals in small doses it can cause weight loss and the refusal to eat. Due to these symptoms induced by deoxynivalenol it is known as vomitoxin or food refusal factor. Although less toxic than other trichothecenes, DON is more common in the seeds of safflower, barley, rye, and wheat and in feed mixtures
Zearalenone
this is a secondary metabolite produced mainly by Fusarium graminearum
The association between the consumption of moldy grains and hyperestrogenism in pigs has been observed since 1920. High concentrations of zearalenone in pig feed may cause disturbances related to conception, abortion and other problems
In Brazil this toxin has been found on cereals and oak flakes
Citrinin
Citrinin was first isolated from secondary metabolites of Penicillium citrinum, well before the Second World War (Hetherington & Raistrick, 1931). Subsequently, other species of Penicillium (Penicillium expansum and Penicillium viridicatum) and even of Aspergillus (Aspergillus niveus and Aspergillus terreus) also showed the capacity to produce these substances.
It has also been considered responsible for nephropathy in pigs and other animals, although its acute toxicity varies depending on the animal species (Carlton & Tuite, 1977). Oat (moldy), rye, barley, corn and wheat grains are excellent substrates for the formation of citrinin
Ergot alkaloids
cereal grains infected by Claviceps purpurea
Also known as ergotism, this intoxication occurs after the ingestion of bread or other products prepared with rye bread grains infected by fungus. Ergotism has two classic forms: gangrenous and convulsive. The gangrenous form affects the supply of blood to the extremities of the body, while the convulsive form acts directly on the central nervous system
With the modern techniques of grain cleaning the problem of ergotism has been practically eliminated from the human food chain. However, it remains a threat from the veterinary perspective. The animals which are susceptible to intoxication include cattle, ovine species, pigs and birds. The clinical symptoms of ergotism in these animals manifest in the form of gangrene, abortion, convulsions, suppression of lactation, hypersensitivity and ataxia (loss of coordination of voluntary muscular movements)
Ochratoxin A
Ochratoxin A has been found in oats, barley, wheat, coffee grains and other products for human and animal consumption
metabolite of Aspergillus ochraceus
associated with nephropathy in all animals studied to date
also shows hepatoxic, immunosuppressive, teratogenic and carcinogenic behavior
name the four main categories of authorized veterinary medicines:
POM-V medicines that can only be prescribed by a veterinary surgeon (veterinarian)
– POM-VPS medicines that can be prescribed by a veterinary surgeon, pharmacist or suitably qualified person
(SQP)
– NFA-VPS medicines that can be supplied by a veterinary surgeon, pharmacist or SQP
– AVM-GSL medicines that can be sold by anyone
The Veterinary Medicines Directorate (VMD)
an executive agency of the Department for Environment, Food and Rural Affairs
(Defra), is the UK regulatory authority for veterinary medicines and has responsibility for the development of the Veterinary
Medicines Regulations (VMR). The VMR regulate the authorization, manufacture, distribution and use of veterinary medicines
in the UK.
The VMR transpose EU legislation relating to veterinary medicinal products (VMP) and are explained in the Veterinary
Medicines Guidance pages of the VMD website
They are assessed for safety, efficacy and quality
■ All must have a Marketing Authorization (MA)
■ Authorized VMP must display a VM or EU code
All POM-V medicines supplied by the practice must be legibly and indelibly labelled with:
Name and address of the animal owner
■ Name and address of the veterinary practice supplying the medicine
■ Date of supply
■ Name, strength and quantity of product
■ Dosage and directions for use
■ ‘For animal treatment only’
■ For topical preparations: ‘For external use only’.
Written prescriptions for Controlled Drugs
If a written prescription is issued for a Controlled Drug (CD) it can be typed, computer generated or handwritten, but it must
be personally signed by the person issuing it.
It is an offence to supply a Schedule 2 or 3 CD against a faxed or emailed prescription.
In addition to the general prescription requirements above, a written prescription for a Schedule 2 or 3 CD should state
an exact dose in words as well as in figures (e.g. not ‘as directed’), and it must include the RCVS number of the veterinary
surgeon prescribing the drug.
A written prescription for Schedule 2 or 3 CDs can only be dispensed once and only within 28 days. Single prescriptions
with multiple dispenses (repeatable prescriptions) are not allowed for Schedule 2 and 3 CDs. It is good practice to mark the
prescription ’no repeats’.
It is a best practice recommendation to dispense only 28 days of CDs at a time. If it is considered necessary to dispense a
CD for a longer period (e.g. in the case of an epileptic dog on long-term medication), the veterinary surgeon must make sure
that the owner is competent to use and store it safely
Cryptococcosis
C. neoformans and C. gatti are dimorphic basidiomycetous fungi
Oval haploid budding yeast (vegetative growth)
Transition to filamentous sexual stage (Filobasidiella neoformans) known as a teleomorph
Important fungal infection of humans and animals
Primarily infects immune-compromised patients
Most common in cats
Also seen in dogs, cattle, horses, sheep, goats, birds and wild animals
Virulence factors:
Polysaccharide capsule
Melanin
Mannitol
Enzymes
“Sugar coated killer”
Phenotypic switching
Development of pulmonary lesions
Dissemination via hematogenous spread in macrophages
Localisation in central nervous system
Cross blood brain barrier (BBMB) via transcytosis or inside infected macrophages
Formation of lesions in the brain
Results in neurological signs
Infection can spread to the eye along optic nerves or hematogenous dissemination
Results in cryptococcal optic neuritis and retinitis
Most common systemic mycosis
Chronic infection causing listlessness and weight loss
Cutaneous legions, some large and ulcerative
Upper respiratory signs such as sneezing, chronic nasal discharge, polyp-like masses, subcutaneous swelling over the bridge of the nose
Neurological symptoms include depression, changes in temperament, seizures, circling, paresis and blindness
Optic signs include dilated, unresponsive pupils, blindness, inflammation of ocular structures
Dogs present meningoencephalitis, optic neuritis and granulomatous chorioretinitis
Disseminated disease with CNS or ocular involvement more common than respiratory
Cytologic evaluation of:
Nasal exudate
Skin exudate
Cerebrospinal fluid
Paracentesis of aqueous or vitreous chambers of the eye
Impression smears of nasal or cutaneous masses
Phenotypic switching
Alterations in cell membrane and capsule structure
Allows cells to persist in the host by minimising the inflammatory response
Sporotrichosis
Seen in cats, dogs, horses, donkeys, pigs, fowl, goats and cattle
Most common in cats and dogs
Entry of spores (conidia) or mycelia through broken skin
Directly through cut or puncture wound
Indirectly through contamination of existing wound
Also transmission in cat scratches
Subcutaneous/lymphocutaneous: most common form
Pulmonary: rare but possible via breathing in fungal spores
Disseminated: spread of infection to other parts of the body (immunocompromised patient
Conversion from mycelial to yeast form upon entry
Production of extracellular enzymes and adhesins allow adhesion to and invasion of cutaneous and subcutaneous tissue
Adhesion to extracellular protein fibronectin
Proteinases I and II hydrolyse stratum corneum cells
Definitive diagnosis relies on culture of both forms
Prognosis is good
Long treatment duration requires owner compliance
Itraconazole is feline drug of choice
expalne the mechanisms of common anti fungals
target the cell membrane- AMPHOTERICIN
ECHINOCANDINS
AZOLES
MACROLIDES
target mitosis/ replication- GRISEOFULVIN
target by DNA synthesis- FLUCYTOSINE
Amphotericin: Mechanism of Action
creates artificial ion channel
Amphotericin binds fungal membrane ergosterol (fungal cholesterol) causing:
Increased membrane permeability and
Creation of transmembrane channels (pores)
Resulting in:
Leakage of monovalent ions (K+, Na+, H+, and Cl-),
Leakage of macromolecules from fungal cell
Other mechanisms: Stimulates fungus to produce oxygen radicles Modulation of macrophage activity Stimulates pro-inflammatory cytokines Reactive oxygen intermediates Nitric oxide Eventually cell death
can enhance other antifungals
good for disseminated aspergillus
“Conventional”
Amphotericin B deoxycholate (AmB-d)
Newer (lipid-based) formulations
Liposomal amphotericin B (L-AmB)
Amphotericin B lipid complex (ABLC)
Amphotericin B colloidal dispersion (ABCD)
Many others- Fewer side effects: lipid vehicle acts as reservoirs, reducing binding to cells
Improved tolerability
Altered tissue penetration – more in liver, spleen and brain, less in lung and kidneys
Reduced toxicity (esp. nephrotoxicity and anaemia)
However, compared to AmB-D these formulations are less potent by mg dose
Resistance:
Dermatophytes- no ergosterol
Pythium
Candida- resistence
Antifungal Spectra: Candidaspp Rhodotorulaspp Cryptococcus neoformans Histoplasma capsulatum Blastomyces dermatitidis Coccidioides immitis Trichophyton Microsporum Epidermophytonspp
Amphotericin: Pharmacokinetics
Absorption
Poorly absorbed from the GI tract:
Amphotericin B (IV, Topical, Local, Intrathecally, Intraocularly)
Nystatin/Piramycin (Topically)
Distribution
Well distributed in most body compartments
CNS penetration ~0%- unless there is inflamation, good for crytococcal meningitis
Elimination
Initial Phase (24 hours): 70% plasma reduction, 50% Urine reduction
Second Elimination Phase: 15 day half life.
Excreted unchanged in urine (21%) and faeces (43%)
Imidazoles
enilconazole fluconazole itraconazole ketoconazole thiabendazole change permiability of membrane by inhibiting synthesis of ergosterol Resistance: No major Antifungal Spectra Blastomyces dermatitidis Paracoccidioides brasiliensis Histoplasma capsulatum Candidaspp Coccidioides immitis Cryptococcus neoformans Aspergillus fumigatus used in mild to moderate disease or in combination in severe disease
Inhibition of CYP450 results in reduction of: Progesterone Pregnenolone Corticosterone Aldosterone Cortisol Estrone Estradiol Estriol
toxicity more common in cats than dogs
Imidazoles: Pharmacokinetics
Absorption
Rapidly absorbed from the GI tract
Distribution
Well distributed in most body compartments
CNS penetration poor (Fluconazole about 50-90% plasma conc)
Highly protein bound (95%)
Elimination Initial Phase (1-2 hours): Rapid Second Elimination Phase (6-9 hours): Slower Roughly 5% unchanged in urine Roughly 80% bilary excretion
Flucytosine
enhances other anti fungals Mechanism Converted to fluorouracil Inhibits RNA synthesis Inhibits protein synthesis Resistance Can develop over course of treatment Antifungal Spectra Cryptococcus neoformans Candida albicans, Candida spp Torulopsis glabrata Sporothrix schenckii Aspergillus spp
Adverse Effects and Toxicity:
Vomiting
Diarrhoea
Reversible hepatic and hematologic effects (increased liver enzymes, anaemia, neutropenia, thrombocytopenia).
Interactions:
Synergistic antifungal activity between amphotericin B and ketoconazole.
Renal effects of amphotericin B prolong elimination of flucytosine.
Flucytosine: Pharmacokinetics
Absorption
Rapidly absorbed from the GI tract
Distribution
Well distributed in most body compartments
CNS Excellent
Minimal protein bound
Elimination
Roughly 85% unchanged in urine
Griseofulvin
Mitotic Inhibitor
Inhibits formation of the mitotic spindle.
Fungistatic Prevents fungi growth rather than killing the fungi. Use Dermatophyte infections Resistance Can develop over course of treatment Antifungal Spectra Microsporum Epidermophyton Trichophytonspp. Actinomyces Nocardiaspp Adverse Effects and Toxicity: Rare Vomiting Diarrhoea Teratogenic (contraindicated in pregnant animals especially mares and queens)
Interactions
Lipids increase GI absorption of griseofulvin.
Griseofulvin: Pharmacokinetics
Absorption
Rapidly absorbed from the GI tract, enhanced by high-fat diet.
Distribution
Well distributed in most body compartments
Binds well to keratin
Higher effect in growing nails/horn.
Elimination
Roughly 85% unchanged in urine
Virion
is the infectious particle
composed of nucleic acid, protein capsid, +/- envelope
may be extracellular or intracellular
Has viral surface proteins that attach to host cell surface proteins which allow entry into a cell.
describe the four aspects of virus replication
Four aspects of virus replication
Entry – binding to host cells and entering the cell
Replication – Producing new copies of the genome
Assesmbly – producing new virus particles
Release – Exiting the cell to infect a new host or a new cell within the current host
describe virus entry
Virus has to bind to cells
Binding can occur via cellular proteins that act as receptors
IMPORTANT to realize that receptors are normal cell proteins that viruses hijack they are not there just for the viruses – they have normal cellular functions
Receptors tend to be virus-specific
Multiple viruses can bind the same receptors
Some receptors bind viruses but don’t facilitate infection – pseudo receptors
Can also be cell type specific – if virus has specific host cell tropism
Not all cell-surface molecules are able to bind virus, if the virus binds to a different molecule no entry is possible
RSFV binds to lrp1
Found on all cell types a ubiquitous receptor allows the virus to enter lots of different cell types
Rabies virus binds to Acetylcholine receptor
Found on muscle cells and the synapses between the nerve and muscle cells – allows the virus to infect muscle and neurons
Poxviruses thought to bind to glycosaminoglycans
These are universal throughout the cells, but it is likely that the virus has specific tropisms to different cells, which is a result of downstream signalling within the cell, not binding
describe Basics of virus replication
Viruses hijack the cells systems to replicate – they cannot do it without the cellular machinery
Can occur in the cytoplasm or the nucleus – on membranes on in complexes
Viral proteins also interact with the cellular systems to inhibit cellular transcription or activate other cellular pathways to facilitate infection
Replication occurs in the nucleus for all but one group of DNA viruses
One exception to the rule is Pox viruses (monkeypox) that replicate in Cytoplasm
mRNA’s are then moved out to the cytoplasm for translation and assembly
Viruses uncoat once they enter the cell – Genomic material released for replication
Genomic material is either immediately transcribed (DNA/RNA viruses) or requires an extra step ( negative sense viruses, and retroviruses)
Viruses hijack the host cell systems and produce proteins using the host cell resources, though RNA viruses use their own replication complex proteins
Poxvirus Replication
complexes in the cytoplasm
No use of the DNA so must carry their own polymerase
Activation of various genes in early, intermediate and late phase to facilitate replication and assembly
Positive strand RNA virus replication
Virus enters the cell
Uncoats and the genomic RNA starts producing protein
RNA then generates a replicative intermediate to generate a new genomic RNA
Packaged and then exits the cell
Negative strand RNA virus replication
Virus enters cell and uncoats
mRNA is produced to produce protein
Replication occurs by way of a dsRNA intermediate
Virus assembly from proteins and the genomic RNA
Cell exit
Retrovirus replication
Virus enters the cell
The RNA is reverse transcribed and then imported into the nucleus
Integrated and then transcribed to produce mRNA
Translated into proteins and then assembly of the virus and release from the cell
describe Virus Assembly
Surface proteins, either envelope proteins and/or capsids packaged to produce new viruses
describe Virus release
2 main ways:
Budding from cell using host lipids and generating new enveloped viruses
Lysis of the cell releasing virus into the environment
list the aetiological agents that can contribute to the development of Kennel Cough in dogs in the UK (both bacterial and viral).
parainfluenza virus, canine adenovirus and Bordetella bronchiseptica, as well as mycoplasmas, Streptococcus equi subsp. zooepidemicus, canine herpesvirus and reovirus-1,-2 and -3.
parainfluenza virus
Type of virus: 50- to 200-nm virion consisting of a
nucleocapsid surrounded by a lipid envelope that is obtained as the nucelocapsid buds from the plasma membrane of an infected cell. 17 All PIVs, including CPIV,
have a single-stranded, nonsegmented, negative-sense
RNA genome
Pathogenesis and relevant virulence factors:
Incubation period: 3 to 10 days after infection, and viral shedding typically occurs 6 to 8 days after infection
Clinical signs and potential outcome:
Persistent cough
Fever
Nasal discharge
Sneezing
Eye inflammation
Lethargy
Loss of appetite
CPIV suppresses the innate branch of the immune system and causes the loss of cilia and ciliated epithelium, it makes conditions more favorable for coinfections. In puppies or immunosuppressed adult dogs, the presence of CPIV in coinfections can lead to a more severe pneumonia and can be fatal.
Diagnosis: based on the dog’s medical history, clinical signs, vaccination history and physical exam. If a specific diagnosis of canine parainfluenza is needed, ocular and oral swabs can be submitted to the lab for PCR testing to confirm the presence of CPIV.
CAV-2
Type of virus:
Pathogenesis and relevant virulence factors:
Incubation period:
Clinical signs and potential outcome:
Dry, hacking cough
Conjunctivitis (causing redness and inflammation of the eye)
Coughing up foamy discharge
Retching
Nasal discharge
Diagnosis: Your vet will want to hear some background history of your dog’s health, details of any symptoms and about any possible exposure to the virus through contact with other dogs. In addition to a thorough physical examination, blood and urine samples will be taken for testing and analysis as they will want to rule out any other more serious conditions such as canine adenovirus type-1, canine distemper and parvovirus which initially exhibit similar symptoms
canine parainfluenza vaccine
non-core
Administer at 6–8 weeks
of age, then every 2–4
weeks until 16 weeks of
age or older [EB4
Rabbit haemorrhagic disease virus
Infection is easily transmitted between infected rabbits by the oral, nasal or conjunctival routes, with the digestive system and respiratory tract as the main portals.
Only a few virions are required to produce infection.
Food bowls and bedding can transmit infection. Carcases from wild rabbits that died from RHD can be a source of infection, by spreading the virus via the faeces of scavengers.
RHD has a short incubation period of one to four days.
The virus replicates in many tissues, including the lung, liver and spleen, with subsequent viraemia and haemorrhage.
Viral tropism is for hepatocytes. The disease it causes is essentially a necrotising hepatitis, often associated with necrosis of the spleen. Disseminated intravascular coagulation produces fibrinous thrombi in small blood vessels in most organs, notably the lungs, heart and kidneys, resulting in haemorrhages. Death is due to disseminated intravascular coagulopathy or liver failure.
Peracute, with animals found dead within hours of eating and behaving normally. This is a common presentation
Acute, with affected rabbits showing lethargy, pyrexia (above 40°C) and increased respiratory rate. These animals usually die within 12 hours.
Subacute, with rabbits showing mild or subclinical signs from which they recover and become immune to infection.
Feline Enteric Coronavirus
Two forms of the disease
Mild enteric disease in kittens – GI tract
Feline Infectious Peritonitis – can be fatal
Mutations in the virus lead to the difference in the virus resulting in FIPV – lethal version of the disease
Mortality is high once symptoms occur
FECVs show a pronounced tropism toward epithelial cells in the gut, but they are also able to infect monocytes, albeit inefficiently. It was suggested that in monocytes—rather than in intestinal epithelial cells
FECV to FIPV
FIP develops in approximately 5% of cats that are persistently infected with FECV
FECVs acquire mutations that can convert them into FIPVs (Pedersen et al., 2012). The resulting FIPVs display an altered cell tropism; they infect and replicate efficiently in monocytes and macrophages. This property is considered a key step in the development of FIP.
One gene the 3c shows a full-length gene in FECV
Essential for replication in the gut – pathogenesis of FECV
In FIPV this 3c gene shows mutations and a truncated gene
Hypothesise that this might result in increased tropisms for macrophages – FIPV
Spike protein can also show 2 mutations in the protein consistent in FIPV sequences – results in increased disease outcome
Bluetongue virus
Bluetongue is characterised by changes to the mucous membranes of the mouth and nose, and the coronary band of the foot.
Clinical signs are generally more severe in sheep but cattle can show signs of disease.
A veterinary surgeon must be contacted by the farmer where large numbers of sheep or cattle present with lameness, high rectal temperatures, salivation, lacrimation and ocular and nasal discharges.
Bluetongue is a notifiable disease in the UK
Midges – culicoides spp. are the vector
Ruminants can be infected, primarily sheep
Once the sheep is infected – enters the lymph nodes and then needs to get into the blood to continue transmission
Symptoms are a result of the prolonged viremia
Midge bite in the skin results in recruitment of APC’s at the bite site and virus migration to the lymphoid cells
BTV replicates within mononuclear phagocytic and endothelial cells, lymphocytes and possibly other cell types in lymphoid tissues, the lungs, skin and other tissues.
Followed by migration to the blood – circulates around the body
Infected ruminants may exhibit a prolonged but not persistent viraemia and BTV is associated with erythrocytes during the late stages of this prolonged viraemia.
The prolonged viremia results in injury to small blood vessels in target tissues – show the characteristic blue tongue
Shows haemorrhage and ulcers in the oral cavity and upper gastrointestinal tract; necrosis of skeletal and cardiac muscle; coronitis; subintimal haemorrhage in the pulmonary artery; oedema of the lungs, ventral subcutis, and fascia of the muscles of the neck and abdominal wall; and pericardial, pleural and abdominal effusions.
Canine Herpesvirus
Clinical signs of canine herpesvirusifpresented are:
Lethargy
Decreased suckling
Diarrhea
Nasal discharge
Conjunctivitis
Corneal edema
Red rash, rarely oral or genital vesicles
Soft, yellow-green feces
Notable absence of fever
CHV is primarily lethal in neonates (1-4 weeks old)
If infected after 1-2 weeks they will generally survive
Timing is therefore key to survival
Infection is by oronasal secretions of other dogs/mother or otherwise
Incubation period is 6-10 days
Duration of illness is 1-3 days
Herpesviruses only infect neonates due to the immature immune system
Not just in dogs, but also in humans very similar
disseminated herpes infection— the most dangerous type of herpes infection. The herpes virus is spread throughout the neonates body and can affect multiple organs, including the liver, brain, lungs, and kidney.
Why do adults not get it?
Functional immune system
Can result in latency
Latency is a hallmark of herpesvirus infections
The viral genome exists as an episome (naked, circular DNA) in the host cell nucleus
No virus is produced until reactivation
Not the same as persistent infection (continuous viral production)
E.g. VZV, which causes chickenpox in children, causes shingles when reactivated in the adult
Rift Valley Fever virus
Most commonly seen in domesticated animals in sub-Saharan Africa,
cattle, buffalo, sheep, goats, and camels.
People can get RVF through contact with blood, body fluids, or tissues of infected animals, or through bites from infected mosquitoes.
Mosquitoes are the main driver of transmission
Take a blood meal from an infected animal
Infected mosquitoes incubate for 7-14 days
Then once it reaches the saliva it can transmit to the next animal perpetuating the cycle
Cattle movement across boundaries
Climate change expands range of mosquitoes – increases disease range
Increased rains that allow increased mosquito numbers and therefore transmission rates
Notifiable disease DEFRA
High Pathogenic Avian Influenza H5N1
The flu virus is an RNA virus
The genome codes for five viral proteins and is made of eight fragments.
The virus has a lipid envelope with two glycoproteins present
Haemagglutinin - this glycoprotein plays a part in infection and provides the “H” in the strain type.
Haemagglutinin attaches the virus to cells and allows the viral envelope to fuse with the cell membrane and enter cells.
Neuraminidase –its role is to allow the release of viruses to infect other cells
Different combinations of H and N glycoproteins give rise to different strains
Mutations which produce small changes in antigens are referred to as antigenic drift and these occur in the same strain
Mutations which result in a major change and produce new strains are referred to as antigenic shifts
The virus is spread by inhalation or by direct contact.
Reservoirs of infection are primarily humans, but birds and pigs can act as reservoirs.
The multiple host status makes for mixing of flu types
Avian Influenza only transmits to humans in close contact
Evidence of HPAI Avian Influenza – reportable disease
African Swine Fever virus
Double stranded DNA virus
Only DNA virus known to be transmitted by arthropods.
Causes haemorrhagic fever- high mortality rate in domestic pigs
Has an enzootic cycle in addition
Warthogs and bushpigs with soft ticks as the vectors
Eradicated outside of Africa in 1990’s with exception of epidemic in Portugal in 1999
Endemic in Africa
Re-emerging in Europe
Zoonotic disease
Ticks bite wild animals – get infected with ASFV
Once infected, they are infected for life – can transmit even as they moult from larvae – nymph – adult tick
Bite domesticated animals – pigs get infected and can then transmit pig-pig.
No horizontal transmission in wild animals
If pigs are free-range – increased likelihood of contact with ticks
Like other DNA viruses had early, intermediate and late gene expression
Replicates in both nucleus and cytoplasm
Changes in the host result in increased pathogenesis
types of vaccine
whole innactivate virus- could cause outbreak
recombinanat viral vector-
DNA vaccine
virus like particles- just envelope/ protiens
recombinant bacterial vector vaccine
recombinant sub unit protein
live attenuated virus- very safe and good, basically non pathogenic virus
vacciens are inactivate dor activated
describe the benefits and draw backs of an innactivated vaccine
higher cost adjuvent needed good stability no reversion provided no mucosal immunity, antibody memory response the immunity is short lived
describe the benefits and draw backs of an activated protien
lower cost adjuvent not needed poor stability reversion is possible provides mucosal immunity, antibody an dCTL imunity and long term immunity
Issues with antivirals
Viruses use our own cells to replicate so anything that targets them also targets our cells
Can have some issues with toxicity – even long-term HIV drug use can affect the body – have some long-term events
Nucleoside analogues are commonly used in veterinary medicine
Squamata
Lizards and snakes
Chelonia
Tortoises and turtles
How are reptiles different to mammals
Poikilothermic ectotherm- interanl temp vairies and outside temp influnces
Jaw bones and auditory ossicles
Quadrate bone, Articular bone & Columella- the singular ear bone
Most reptiles are oviparous (some mammals are oviparous!)- egg laying
Temperature dependent sex determination
No mammary glands
3 chambered heart (Crocodilians - divided atrium, sometimes refered to as 4 chambered)
Homodont dentition- uniform continually growing teeth except fanged snakes
Scales instead of hair
Shed
No sweat glands
No diaphragm- no division between abdomine and thorax so not refered to as such- refered to as coelom
Nitrogenous waste product is uric acid, not urea
Anatomy of the reptile integument
Epidermis Keratinised scales Largely overlapping in squamates Shell in chelonians Hard scales in the limbs and tail 2 forms of Keratin Alpha Keratin Flexible, between scales & in hinges Beta Keratin Harder, found in scutes and scales Dermis- Highly vascular Sensory tissue Osteoderms-mineralised bony structures in dermis Chromatophores- pigment cells
Periodic sloughing and renewal Crocodilians and chelonians – continuous Lizards – cyclical - piecemeal Snakes – cyclical – single piece Resting phase & renewal phase Under thyroid control with multiple factors Vitamin D Activation Water uptake Desert species Anoxia tolerance Shells (Freshwater turtles)
Nociceceptors in reptiles
More mu opioid receptors cf kappa
Integument Overview - Snakes
Heavily keratinised epidermis Prevents water loss/waterproofs Protection Keratin formed into overlapping epidermal scales (non overlapping on head) Reptile skin is very inelastic Folds of skin between the scales to allow to expansion Single ventral scales – ‘gastropeges’ Thicker, larger scales for support Important for locomotion Scales caudal to cloaca – ‘subcaudal scales’ Usually paired Very few glands Cloacal glands Pits
Shedding
Growth
Replacement of worn out skin
Parasite disposal
Most snakes shed 2-4 times/year
Growth
Season (eg post hibernation)
Reproduction (shed 8-10 days before oviposition/parturition)
Shed more frequently when juvenile/rapid growth
Shed ‘in toto’ in one single piece (incl. spectacles)
Controlled by thyroid gland
Environmental conditions key
Lymph fluid builds up between old and new epidermal layers
Bluish colouration to skin ‘blue’
Spectacle opacity ‘in milk’ (inhibits visibility)
Reduced markings
Spectacle clears before shed
Skin circulation engorges to stretch and split old epidermal layer
Colourless
Pigment cells in the dermal layer
Changes in feeding behaviour and activity
Prior to shedding
Irritable/Reduced activity/Seek shelter/humidity
Post Shedding
Defaecation/Thirst
Ecdysis
shedding
Dysecdysis- Snakes
Abnormal or impaired shedding Can affect entire integument Spectacles ofter retained- Inhibit vision and can cause inappetence retention around Cloaca Patchy shed Usually husbandry related -Humidity -Temperatures -Substrate & -Furniture Never remove retained shed Soak/lubricate Husbandry
Integument Overview - Lizards
Heavily keratinised epidermis Prevents water loss/waterproofs Protection Keratin formed into epidermal scales similar to snakes Epidermal growth is cyclic Osteoderms in some species ‘Dermal Armour’ Modified scales Crests Spines Shields Dewlap Lamellae- allows geckops to cling- not lepord gecko
Cloacal glands Scenting Temporal glands Chameleon Function unknown but likely defence/lure Pre cloacal pores Geckos Femoral pores Iguanas, Many agamids Gender determination Salt glands Marine iguanas
Ecdysis - Lizards
Epidermal growth cyclic Regular patchy/piecemeal shed Some species eat shed skin Frequency varies: Species Size Growth – Juveniles may shed q. 2 weeks, Adults q. 3-4 times p.a. Temperature Humidity Nutrition Skin damage Endocrine function Controlled by thyroid gland
