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Spinal Column - Anatomy & Physiology

2016-12-09T19:13:43Z

Rstanley2: /* Joints of the Spinal Column */

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==Introduction==
[[Image:Anatomy_and_physiology_of_animals_Regions_of_a_vertebral_column.jpg|thumb|right|250px|Divisions of the spinal cord- Copyright Ruth Lawson Otago Polytechnic ]]
The trunk consists of three segments; the thorax, the abdomen, and the pelvis, each of which is bounded by body wall and contains a cavity. The thoracic cavity lies cranial to the diaphragm, whereas the abdominal cavity lies caudal. The pelvic cavity is defined by the borders of the bony pelvis and communicates with the abdominal cavity. Dorsally, the roof of all three cavities is formed by the spinal column and associated muscles. Vertebrae develop segmentally from '''somitic sclerotomes''', whereas muscles develop from '''somitic myotomes'''. Within each myotome is a single nerve leaving the central neural tube. Motor innervation in the adult is therefore segmental. The ventral and lateral body walls are initially formed by '''somatopleure''' (ectoderm and lateral plate mesoderm), but is later invaded by somitic cells migrating ventrally. These differentiate to form ribs and sternum and associated muscles.

==Divisions and Landmarks==

The common pattern of canine landmarks, according to Dyce, Sack, et al, can be identified as:
[[Image:Spinal landmarks.jpg|center|500px|Spinal Landmarks - Copyright Becky Pocock 2008]]

==Vertebrae and Joints==

[[Image:Cervical Vertebra.png|thumb|right|250px|Cervical Vertebra - Wikimedia Commons 2008]]
Vertebrae consist of a body, which encloses the vertebral foramen (through which the spinal cord and meninges run), a spinous process, and a transverse process, as well as articular processes by which they join together. The form of the spinous process varies with respect to species and region.

===Cervical Vertebrae===

The first two cervical vertebrae are known as the '''atlas''' and the '''axis''' respectively, and are modified to allow movement of the head. The atlas has no conventional body, instead it is composed of two lateral masses joined by dorsal and ventral arches. The atlas and axis are fused in embryonic life. The '''wing of the atlas''' is the transverse process of this vertebra and allows the spinal column to articulate with the skull, by providing a resting place for the occipital condyles. The axis is the longest vertebra. The '''nuchal ligament''' connects the spinous process of the axis to the spinous process of the first thoracic vertebra (T1). The last (C7) cervical vertebra has a taller spinous process than those preceding it, and articulates with the first pair of ribs.

===Thoracic Vertebrae===

Thoracic vertebrae articulate with the ribs. They are distinguished by short bodies with flattened extremities, costal facets, short transverse processes and prominent spinous processes. They reach a maximum height, a few vertebrae behind the cervicothoracic junction (constituting the '''withers''' of the horse) and then decline. The orientation of spinous processes shifts from caudo- to craniodorsal.

===Lumbar Vertebrae===

The lumbar vertebrae are longer and more uniform in shape than the thoracic vertebrae. They are also shorter in height, with long, flattened transverse processes that project laterally.

===Sacral Vertebrae===

The '''sacrum''' is a single bone formed by the fusion of several vertebrae that articulates with the pelvic girdle. It allows the thrust of the hindlimbs to be transmitted to the trunk. The sacrum narrows caudally and is curved to present a concave surface to the pelvic cavity.

===Caudal Vertebrae===

The number of caudal vertebrae varies greatly even within species. There is a progressive simplification of their form.

==Joints of the Spinal Column==

There are two types of joints:

1. '''Cartilaginous''':

Provides direct connections between vertebral bodies. The bodies of adjacent vertebrae are connected by thick, flexible intervertebral discs, consisting of two parts:
:'''Nucleus pulposus''': slightly eccentric, notochord derivative, contained under pressure and prone to escape.
:'''Annulus fibrosus''': encircling bundles of fibrous tissue that pass obliquely from one vertebra to another, with changing orientation.

2. '''Synovial''':

Found between facets on vertebral arches. They are modified in the regions of the head and pelvis.

'''Joints of the atlas'''
#Atlanto-occipital joint - Between the condyles of the skull and corresponding cavities of the atlas. It functions as a ginglymus, movement is restricted to flexion/extension in the sagittal plane (eg nodding).
#Atlantoaxial joint - The ventral arch of atlas and the body of the axis face into a single synovial cavity with limited areas of contact. Movement is rotational about a longitudinal axis (eg. head shaking).

==Spinal Cord==

The details of the spinal cord are found on [[Spinal Cord - Anatomy & Physiology|spinal cord]] page.

==Hypaxial and Epaxial Muscles==

[[Image: epaxial muscles.JPG|thumb|right|250px|Epaxial muscles- Copyright C. Clarkson and T.F. Fletcher, University of Minnesota]]
[[Image: hypaxial muscles.JPG|thumb|right|250px|Hypaxial muscles- Copyright C. Clarkson and T.F. Fletcher, University of Minnesota]]
===Epaxial muscles===

The epaxial muscles are extensors of the vertebral column. They are found dorsal to the line of the transverse processes of the vertebrae and are arranged in three parallel columns.

1. Lateral column
:''Iliocostalis'' arises from the ilium and transverse processes of the lumbar vertebrae to insert on cranial lumbar vertebrae and ribs, spanning about 4 vertebrae.

2. Middle column
:''Longissimus'' is the strongest, extending from the ilium and sacrum to the head and neck.

3. Medial column
:''Transversospinalis'' is the most complex, lying between the medial vertebral arches and the spinous processes.

Innervation comes from the dorsal branches of the spinal nerves. They are rarely of clinical importance.

===Hypaxial Muscles===

The hypaxial muscles are flexors of the neck and tail.

'''Longus colli'''
:From the cranial thoracic region to the atlas, covering the ventral vertebral bodies

'''Rectus capitis ventralis'''
:From the atlas to ventral skull

'''Longus capitis'''
:From the midcervical vertebrae to the skull

'''Scalenus''' muscles
:From the caudal cervical vertebrae to first few ribs, which they stabilize on inspiration
 
{{Template:Learning
|dragster = [[Canine Spinal Skeletal Anatomy Resources (I, II & III)]] [[Canine Spinal Skeletal Anatomy Resources (IV & V)]] [[Canine Whole Spine Skeletal Anatomy Resource]] [[Canine Spine Radiographical Anatomy Resources (I & II)]]
|OVAM = [http://www.onlineveterinaryanatomy.net/content/muscle-flashcards-vertebral-mm-quicktime Muscle flashcards - canine vertebral muscles]
}}

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[[Category:Musculoskeletal System - Anatomy & Physiology]]
[[Category:A&P Done]]

IGF-1 - Anatomy & Physiology

2016-12-08T17:08:07Z

Rstanley2: /* Overview */

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==Overview==

[[Image:IGF1.png|250px|thumb|right|Danielle Keller
2007 '''Schematic structure of Insulin-like growth factor-1.''']]

IGF-1 is one of a number of insulin-like growth factors. Insulin-like growth factors are produced by many different tissues and have local paracrine and autocrine effects. (see [[Hormones - Anatomy & Physiology|hormones]] for further details). They bind to carrier proteins to extend their half life in the blood. The [[Liver - Anatomy & Physiology|'''liver''']] is the main source of IGF-1. Hormones that directly stimulate Insulin-like growth factor-I (IGF-I) include growth hormone, insulin and oestradiol.Growth hormone is the main regulator of IGF-I production in the liver and insulin and oestradiol are stimulatory in other tissues.

==Actions of IGF-1==

Increased '''protein synthesis''' and increased '''chondrogenesis''', both promoting growth.

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[[Category:Endocrine System - Anatomy & Physiology]]
[[Category:A&P Done]]

Infectious Bovine Rhinotracheitis

2016-12-08T16:30:28Z

Rstanley2: /* Diagnosis */

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== Introduction ==
[[Image:IBR nasal cavity.jpg|thumb|right|200px|<center>IBR in nasal cavity (Image sourced from Bristol Biomed Image Archive with permission)</center>]]
[[Image:IBR trachea.jpg|thumb|right|200px|<center>IBR in trachea (Image sourced from Bristol Biomed Image Archive with permission)</center>]]
This disease is also known as '''IBR''' and is caused by [[Bovine Herpesvirus 1]] (BHV-1) through aerosol transmission and close contact of infected animals. It is a highly infectious disease of cattle, causing upper respiratory tract disease. The virus is a [[:Category:Herpesviridae|herpesvirus]], meaning it has the ability to lie latent for a long period of time until reactivated by stress.

BHV-1 infects the respiratory mucosal epithelial cells (intranuclear eosinophilic inclusion bodies) from nasal mucosa down to bronchioles, which leads to neutrophilic inflammation of varying severity.

== Classification ==

BHV's Baltimore Classification is I, dsDNA virus, and is part of the Herpesviridae family. It is an enveloped virus with icosahedral capsid symmetry.

== Clinical Signs ==

Depending on severity, one will see serous, catarrhal or purulent nasal discharge, sneezing, coughing, dyspnoea and anorexia. There will be a rhinotracheitis that can develop into [[bronchopneumonia]]. An increased respiratory rate will also be present. Pregnant cows will also be seen to abort at 5 months or later in gestation.

Clinical disease is most severe in young calves, which can develop mucosal ulcerative lesions in the oesophagus and forestomachs and viraemia with multiorgan infection.

There is generally a high morbidity with low mortality, but up to 75% mortality if concurrent with [[Bovine Virus Diarrhoea Virus|BVDV]] resulting in meningo-encephalitis.

Signs can be made more severe by secondary bacterial infection such as [[:Category:Pasteurella and Mannheimia species|Pasteurella]] or [[:Category:Mycoplasmas|Mycoplasma]].

== Diagnosis ==

Clinical signs are suggestive. Definitive diagnosis can be achieved by virus isolation and [[immunofluorescence]].

On microscopic examination of infected tissue, one will see intranuclear inclusion bodies, which are indicative of the virus.

Test for serum antibodies against IBR and re-test in 2-3 weeks time.

== Control ==

'''[[Vaccines|Vaccination]] '''is available and commonly used in the UK. Both vaccines available in the UK are given intranasally and neither protects against re-infection when given during clinical outbreak, but can lessen the severity of the disease. There are also '''inactivated''' vaccines: intranasal/intramuscular administration, which have a gE deletion making this a '''marker vaccine'''. There is an ELISA for gE deletion, which can enable culling of carrier animals.

<big>For more information see [[Bovine Herpesvirus 1]]. </big>

{{Learning
|flashcards = [[Cattle Medicine Q&A 05]]
}}

== References ==

Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) '''Bovine Medicine '''(Second edition), ''Blackwell Publishing''

Divers, T.J. and Peek, S.F. (2008)''' Rebhun's diseases of dairy cattle,''''' Elsevier Health Scieneces''

Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) '''Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses, '''''Elsevier Health Sciences''

{{review}}

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[[Category:Respiratory_Diseases_-_Cattle]] [[Category:Expert_Review - Farm Animal]] [[Category:Respiratory_Viral_Infections]]

Large Colon Impaction - Horse

2016-04-24T12:03:44Z

Rstanley2: /* Clinical signs */

==Prevalence==
==Signalment==
==Pathophysiology==
==Anatomy==
Impactions of the large colon occur where the luminal diameter narrows, especially the pelvic flexure and the right dorsal colon (RDC) (83 in Bliks). Food impactions occur most often at the pelvic flexure, the site of the myoelectrical pacemaker. Sand impactions occur at various sites in the large intestine.
==Risk factors==
Sudden restriction in exercise associated with musculoskeletal injury (84) Twice daily feeding of concentrate - large fluxes of fluid into and out of colon, associated with readily fermentable carbohydrate in the colon and increases in serum aldosterone. Fluid fluxes may cause dehydration of ingesta during aldosterone-stimulated net fluid flux out of the colon (32). Amitraz - acaricide associated with clinical cases of colon impaction (85,86) - may alter pelvic flexure pacemaker activity resulting in uncoordinated motility patterns between the left ventral and left dorsal colon and excessive retention of ingesta. Absorption of water from ingesta increases with time, dehydrating the contents of the colon and resulting in impaction Parasite migration in the region of the pacemaker (87) Limited exercise Poor dentition Coarse roughage Dehydration

==Clinical signs==
Slow onset mild colic Reduced defecation Faeces hard, dry and mucus-covered because of delayed transit Heart rate mildly elevated during painful episodes but often normal Colic signs typically well controlled with analgesics but become increasingly more severe and refractory if impaction not resolved

==Diagnosis==
See colic diagnosis in horses
Firm mass in large colon but may underestimate extent of impaction because much of colon out of reach (83). Adjacent colon may be distended if impaction has resulted in complete obstruction. Impaction at other sites such as the transverse colon may not be palpable per rectum.

==Treatment==
===Medical===
See medical treatment of colic in horsesInitially intermittent abdominal pain controlled with analgesics: Flunixin meglumine IV every 6-12 hours Butorphanol IV every 6-8 hours Xylazine IV as needed Oral laxatives to soften the impaction: Liquid paraffin or mineral oil 2-4lites by nasogastric tube every 12 to 24 hours Anionic surfactant dioctyl sodium succinate (DSS) 6-12g/500kg diluted in 2-4litres of water by nasogastric tube every 12-24 hours Saline cathartics such as magnesium sulphate 0.1 mg/kg in 2-4litres by nasgastric tube may also be useful Prevent access to feed Aggressive oral and IV fluid therapy (2-4 times maintenance) if impactions persist(83)

===Surgical===
If impaction remains unresolved, pain becomes uncontrollable, or extensive gas distension of the colon occurs, surgery is indicated. Abodominocentesis can be used to monitor the onset of intestinal compromise.(83) At surgery the contents of the colon are evacuated via a pelvic flexure enterotomy.

==Prognosis==
Good for impactions that resolve medically (95% long term survival in one study) and fair in horses that require surgical intervention (58% long-term survival in the same study) (84)
==Prevention==
Frequent small feedings(32)
==References==

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[[Category:Impaction - Horse]][[Category:To Do - Alimentary]][[Category:To Do - Major]]

Haematuria

2015-09-22T19:29:08Z

Rstanley2: /* Differential Diagnoses */

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==Introduction==
Haematuria is the '''presence of blood in the urine''', which gives it a red colour.

It occurs in all species due to a variety of diseases and conditions.

==Differential Diagnoses==
It is important to distinguish haematuria from:
:'''haemoglobinuria and myoglobinuria'''. With haemoglobinuria, when the urine sample is spun down, the supernatant remains red/brown in colour. With haematuria a spun urine sample forms a reddish sediment. With myoglobinuria the spun sample appears clearer.
:'''porphyrin pigments in urine''': common in rabbits due to porphyrin pigments in diet, dipstick will differentiate, or porphyrin pigments will fluoresce under a Wood's lamp.

==Causes==
Haematuria may be caused by local or systemic disease.

'''Systemic disease''' is rare, but includes bleeding disorders such as [[thrombocytopaenia]], [[Coagulation Factor Deficiency|platelet dysfunction]] (von Willebrand's disease), defects in the coagulation cascade or bleeding due to toxins ([[Lead Poisoning|lead toxicity]]). There will usually be evidence of bleeding from other areas.

'''Local disease''' is much more common and haemorrhage can occur at all levels of the urinary and reproductive tract, leading to haematuria.

Local causes include: bacterial '''cystitis''', idiopathic cystitis, [[Urolithiasis|'''urinary calculi''']], [[pyelonephritis]], '''prostatitis''', polyps, '''bladder neoplasia''', neoplasia of the renal pelvis, idiopathic renal haemorrhage, vascular anomalies, '''trauma'''.

Reproductive tract diseases include: '''pyometra''', '''uterine neoplasia''', endometrial venous aneurysms.

==Diagnosis==
Haematuria can be diagnosed by using a '''dipstick''' for haemoglobin, but this will not differentiate haematuria from haemoglobinuria or myoglobinuria.

'''Urine sediment''' can be analysed to reveal red blood cells.

'''Clinical signs and physical examination''' may help localise the problem. The clinical signs of '''pollakiuria and dysuria''' indicate lower urinary tract inflammation but are not specific for a particular disorder.

Blood at the beginning of urination suggests bleeding from the bladder neck, urethra or genital tract. Blood present throughout urination is more consistent with diffuse bladder disease or upper urinary tract haemorrhage (kidneys and ureters). Also haemorrhage due to a bleeding disorder may present this way.

With focal lesions of the bladder or large dependent cystoliths, blood may enter urine at the end of voiding. Bleeding from the genital tract may occur independently of urination and may show blood clots.

'''Voided urine samples''' can be compared to samples collected during cystocentesis to establish the location of the disorder.

'''Radiographs, especially contrast studies, and ultrasonography''' may also be very helpful in identifying the urinary or genital tract pathology.

'''Full haematology and biochemistry''' may be indicated if the animal is showing systemic signs of illness. Usually, animals with lower urinary tract disorders do not exhibit these.

'''Cytology, biopsy or histopathology''' may be necessary if a mass is found or neoplasia is suspected.

==Treatment==
This will depend on the '''underlying cause''' of the haematuria.

{{Learning
|flashcards = [[Rabbit Medicine and Surgery Q&A 20]]
}}

==References==
Wingfield, W. (2001) '''Veterinary emergency medicine secrets''' ''Elsevier Health Sciences''

Richardson, V. (2000) '''Rabbits: health, husbandry and disease''' ''John Wiley and Sons''

{{review}}

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[[Category:Urinary System - Pathology]]
[[Category:Expert Review]]

Heart Structure - Anatomy & Physiology

2014-05-12T15:51:25Z

Rstanley2: /* Right Atrium */

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==Structure of the Heart==
[[Image:Aspinall Slide7.JPG|thumb|right|350px|Image from [http://www.elsevierhealth.co.uk/veterinary-nursing/spe-60136/ Aspinall, The Complete Textbook of Veterinary Nursing], Elsevier Health Sciences, ''All rights reserved'']]
[[Image:Aspinall Slide8.JPG|thumb|right|350px|Image from [http://www.elsevierhealth.co.uk/veterinary-nursing/spe-60136/ Aspinall, The Complete Textbook of Veterinary Nursing], Elsevier Health Sciences, ''All rights reserved'']]
===Position and Shape of the Heart===

The heart is located in the thoracic cavity in between the [[Lungs - Anatomy & Physiology|lungs]], 60% of it lying to the left of the median plane. The heart’s lateral projection extends from [[Ribs and Sternum - Anatomy & Physiology|rib]] 3 to 6. Most of the heart’s surface is covered by the [[Lungs - Anatomy & Physiology|lungs]] and in juveniles it is bordered cranially by the [[Thymus - Anatomy & Physiology|thymus]]. Caudally the heart extends as far as the [[Diaphragm - Anatomy & Physiology|diaphragm]]. Variations in position and size exist among individuals depending on species, breed, age, fitness and pathology. Roughly speaking, the heart is responsible for about 0.75% of the bodyweight.

The heart is cone-shaped, with a broad base at the top from which the large blood vessels enter and exit. The tip, known as the apex, points downwards and lies close to the [[Ribs and Sternum - Anatomy & Physiology|sternum]]. The longitudinal axis of the heart is tilted to varying degrees depending on the species resulting in the base facing craniodorsally and the apex caudoventrally.

The heart has a right and left lateral surface, which meet cranially at the right ventricular border and caudally at the left ventricular border. The auricles of the atria are visible on the left side, surrounding the root of the aorta and the pulmonary trunk, whilst the large veins and the main parts of the atria are situated on the right.

Grooves on the surface represent the divisions of the internal structure of the heart. The right surface of the heart is marked by the subsinusoidal groove which extends from the coronary groove to the apex of the heart. The paraconal groove runs over the left surface of the heart from the coronary groove to the distal end of the cranial margin. The fat-filled coronary groove contains the coronary blood vessels and marks the separation of the atria and ventricles.

===Pericardium===

The pericardium is the membrane that surrounds and protects the heart. It is composed of two layers separated by a narrow cavity. The inner layer is firmly attached to the heart wall and is known as the visceral layer or epicardium. The outer layer is composed of relatively inelastic connective tissue and is termed the parietal layer. This fibrous layer prevents distension of the heart, thus preventing excessive stretching of the heart muscle fibres. The cavity between the two layers contains a small volume of fluid which serves as a lubricant, facilitating the movement of the heart by minimising friction. The sternopericardiac ligament connects the parietal layer to the sternum and the phrenopericardiac ligament joins the parietal layer to the diaphragm. The latter is present only in canine and swine.

===Layers of the Heart Wall===

The wall of the heart consists of three layers: the epicardium (external layer), the myocardium (middle layer) and the endocardium (inner layer). The epicardium is the thin, transparent outer layer of the wall and is composed of delicate connective tissue. The myocardium, comprised of cardiac muscle tissue, makes up the majority of the cardiac wall and is responsible for its pumping action. The thickness of the myocardium mirrors the load to which each specific region of the heart is subjected. The endocardium is a thin layer of endothelium overlying a thin layer of connective tissue. It provides a smooth lining for the chambers of the heart and covers the valves. The endocardium is continuous with the endothelial lining of the large blood vessels attached to the heart.

====Structure of Cardiac Muscle====

Cardiac muscle fibres are shorter in length and larger in diameter than skeletal muscle fibres. They also exhibit branching, which gives an individual fibre a Y-shaped appearance. A typical cardiac muscle fibre is 50-100μm long and has a diameter of about 14μm. Normally, there is only one centrally located nucleus, although occasionally a cell may have two nuclei. The sarcoplasm of cardiac muscle is more abundant than that of skeletal muscle and the mitochondria are larger and more numerous. Cardiac muscle fibres have actin and myosin filaments arranged in the same way as skeletal muscle fibres and possess a well-developed T-tubule system. In contrast to [[Muscles - Anatomy & Physiology#Skeletal Muscle|skeletal muscle]], cardiac muscle does not fatigue, cannot be repaired when damaged and is regulated by the autonomic nervous system.

Although cardiac muscle fibres branch and interconnect with each other, they form two separate functional syncytia, one for the atria and another for the ventricles. The ends of each fibre in a network connect to its neighbours by irregular transverse thickenings of the sarcolemma called intercalated discs. The discs contain desmosomes, which hold the fibres together, and gap junctions, which allow ions to travel between cells and permit the rapid propagation of action potentials. Consequently, excitement of a single fibre of either network results in stimulation of all the other fibres in the network. As a result, each network contracts as a functional unit.

====Fibrous Skeleton====

In addition to cardiac muscle tissue, the heart wall also contains dense connective tissue that forms the fibrous skeleton of the heart. The fibrous skeleton is composed of dense connective tissue rings that surround the four heart orifices. The skeleton contains fibrocartilage in which nodules of bones (ossa cordis) may develop in some species. Although these bones occur most commonly in cattle, they are not restricted to this species. The skeleton performs several functions:

* It serves as a point of attachment for the heart valves
* The cardiac muscle bundles insert onto the fibrous skeleton.
* It prevents the valves from overstretching as blood passes through them.
* It acts as an electrical insulator thereby preventing the direct spread of action potentials from the atria to the ventricles.

===Chambers of the Heart===

The heart contains four chambers. The two upper chambers are the atria and the two lower chambers are the ventricles. On the cranial surface of each atrium is a pouch-like appendage called an auricle which is thought to increase the capacity of the atrium slightly.

The thickness of the myocardium of the four chambers varies according to function. The atria are thin-walled because they deliver blood into the adjacent ventricles and the ventricles are equipped with thick muscular walls because they pump blood over greater distances. Even though the right and left ventricles act as two separate pumps that simultaneously eject equal volumes of blood, the right side has a much smaller workload. This is because the right ventricle only pumps blood into the lungs, which are close by and present little resistance to blood flow. On the other hand, the left ventricle pumps blood to the rest of the body, where the resistance to blood flow is considerably higher. Consequently, the left ventricle works harder than the right ventricle to maintain the same blood flow rate. This difference in workload affects the anatomy of the ventricular walls; the muscular wall of the left ventricle being significantly thicker than that of the right.

====Right Atrium====

The right atrium forms the dorsocranial section of the base of the heart and receives blood from the cranial vena cava, caudal vena cava and coronary sinus. The interatrial septum is a thin partition dividing the right and left atria and possesses a characteristic oval depression called the fossa ovalis which is a remnant of the foetal foramen ovalis. The right atrium also houses the sinoatrial node. Blood flows from the right atrium to the right ventricle through the tricuspid valve (also know as the right atrioventricular valve).
In rabbits the right atrioventricular valve is bicuspid not tricuspid.

====Right Ventricle====

The right ventricle forms most of the anterior surface of the heart and is crescent-shaped in cross-section. The cusps of the tricuspid valve are connected to tendon-like cords, the chordae tendinae, which, in turn, are connected to cone-shaped papillary muscles within the ventricular wall. The right ventricle is separated from the left by a partition called the interventricular septum. The trabecula septomarginalis is a muscular band that traverses the lumen of the right ventricle. Deoxygenated blood passes from the right ventricle through the pulmonary semi-lunar valve to the pulmonary trunk, which conveys the blood to the lungs.

====Left Atrium====

The left atrium forms the dorsocaudal section of the base of the heart and is similar to the right atrium in structure and shape. It receives oxygenated blood from the lungs via the pulmonary veins. Blood passes from the left atrium to the left ventricle through the bicuspid or left atrioventricular valve. The left atrium lies under the tracheal bifurcation and enlargement of this area of the heart can cause breathing difficulties.

====Left Ventricle====

The left ventricle forms the apex of the heart and is conical in shape. Blood passes from the left ventricle to the ascending aorta through the aortic semi-lunar valve. From here some of the blood flows into the coronary arteries, which branch from the ascending aorta and carry blood to the heart wall. The remainder of the blood travels throughout the body.
 
{{Template:Learning
|dragster = [[Canine Heart Dissection Anatomy Resources (I & II)]] [[Canine Heart Dissection Anatomy Resources (III & IV)]] [[Cardiovascular System Histology Resource (I)]]
|videos = [[Video: Heart potcast|Heart potcast]] [[Video: Heart (internal structure) potcast|Heart (internal structure) potcast]] [[Video: Dorsal view of the ventricles and valves of the heart|Dorsal view of the ventricles and valves of the heart]]
}}

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761535_sample.pdf
|chaptername = Normal Cardiovascular System
|book = Cardiovascular Disease in Small Animal Medicine
|author = Wendy A. Ware
|isbn = 9781840761535
}}

{{OpenPages}}
[[Category:Heart - Anatomy & Physiology]]
[[Category:Cardiology Section]]

Toxocara canis

2013-04-28T21:39:25Z

Rstanley2: /* Cycle 4 */

{{unfinished}}
{{Taxobox
|kingdom =Animalia
|phylum =Nematoda
|class =Secernentea
|sub-class =
|order =Ascaridida
|super-family =
|family =Toxocaridae
|sub-family =
|genus =Toxocara
|species =''T. canis''
}}

[[Image:Toxocara canis.jpg|thumb|150px|right|''T. canis'' egg - Joaquim Castellà - Veterinary Parasitology Universitat Autònoma de Barcelona]]

[[Image:Toxocara canis adult.jpg|thumb|150px|right|''T. canis'' adult worm from a puppy - Joel Mills, 2006 - Wikimedia commons]]

==Overview==
''Toxacara canis'' is a typical ascarid nematode that infects dogs where its predilection site is the small intestines. These worms can be found throughout the world with varying prevalence. Control of this ascarid is typically difficult due to its extended persistence in the environment. ''T. canis'' is also important in human medicine as the species most responsible for '''visceral larval migrans''' (VLM). The human is a non-permissive host of ''T. canis'' meaning it cannot complete its life cycle and reproduce, however the larval stages do migrate through the human body causing pathology.

==Identification==
''Toxacara canis'' has the typical gross morphology of an ascarid, it is a large, fleshy white worm and can be up to 18cm long. The females are longer than the males who can normally reach 10cm in length. Microscopically ''T. canis'' has a fairly standard [[:Category: Ascaridoidea|ascaridoid]] appearance, though the adult head is given an elliptical shape by large alae or 'wings'. The eggs of ''T. canis'' are dark brown with a thick, pitted shell, the thick shell makes them very resistant in the environment.

==Life cycle==
Typically of an ascarid ''T. canis'' has larvae have a migratory life cycle that is significance in the pathogenesis of infection. This species also has the most complex life cycle in the Ascaridoidea superfamily. There are four different life cycles that can occur dependant on the circumstances that the larvae or adult encounter.
====Cycle 1====
This is mostly a typical ascarid life cycle and commonly occurs in dogs that are infected between 2 and 3 months old. The infective eggs contain L2 larvae which hatch in the small intestine of the host dog after being ingested. The larvae then enter the hepatic portal vein and travel through the liver and further to the lungs where they moult to L3. The larvae then migrate to the trachea where they are coughed up and swallowed again by the host. This is known as hepato-tracheal migration. On returning to the small intestine they undergo the final moults (L3-->L4-->L5) before becoming adults.

====Cycle 2====
In older dogs (above 3 months) the migration changes and the hepato-tracheal route occurs far less often, though can still occur. In these animals the L2 larvae hatch in the small intestine and travel to a wide variety of tissues throughout the body. Once the larvae have reached a tissue they will begin hypobiosis and encyst in the tissue until reactivated. In some animals the hypobiotic larvae will not reactivate and this will be the end of their life cycle. Hypobiotic larvae in the tissues of the dog are known as '''somatic larvae''', although these do not grow or develop they are highly metabolically active. The produce large quantities of excretory/secretory antigens which are spread over the cuticle of the worm. These antigens are important in immune evasion by way of having a rapid turnover and sloughing off host antibodies and immune cells.

====Cycle 3====
In the pregnant bitch larvae that have become hypobiotic as described in cycle 2 above are reactivated by hormonal changes. These larvae become mobile about three weeks before parturition and migrate across the placenta to the lungs of the fetus. Within the fetal lungs the larvae moult just prior to birth (to L3). From the lungs the larvae complete their life cycle in the same way as in the young animal, by being coughed and swallowed to enter the small intestine. The adults will then produce eggs which are released in the faeces as normal.

====Cycle 4====
The final life cycle involves transmission of L2 larvae to pups through the milk. Hypobiotic L2 larvae are reactivated and are either already present in the mammary glands or travel to them and are capable of passing in the milk during the first 3 weeks of lactation. There is no further migration in the pup when the larvae are ingested in this way and the remaining life cycle of the worm is completed in the small intestine of the pup.

As well as the above life cycles ''T. canis'' can infect paratenic hosts such as mice, rats and some birds. Events occur just as in the older dog, i.e. larvae migrate → liver → lungs → heart → somatic tissues → granulomatous reactions → 'waiting phase'; but in this case, the somatic larvae are waiting for the animal that they are in (which is acting as a '''paratenic host''') to be eaten by a dog, fox, wolf or other canid, where they will establish as adults or somatic larvae (depending on the age of the predator). This explains how humans (as warm-blooded non-canid animals) enter into the epidemiological picture. The prepatent period of ''T. canis'' is 4 - 5 weeks in the canid host.

==Epidemiology==
''T. canis'' is present worldwide with a wide range of prevalances in different areas from 5 - 80%. Adult animals carry the fewest worms since initial infection causes immunity which leads to the shedding of adult worms from the intestines. The low parasite burden in adult animals can often lead to asymptomatic infection though the parasites wil still shed eggs in the faeces. The largest numbers of worms are found in dogs less than 6 months old who have not yet gained immunity to the worms. The high levels of prevalence of this species worldwide is largely due to the difficulty in controlling its spread. The eggs are extremely resistant in the environment and so can persist for several years. The females lay very large numbers of eggs, up to 700 per gram of faeces, making the removal of such a large number difficult. This final reason for such a large spread is the long lasting reservoir of hypobiotic larvae that can be reactivated in pregnancy in the bitch, these are not susceptible to anthelmintics and so are only eliminated by preventing pregnancy or the death of the host. As a result of the large number of infected bitches almost all puppies are born with ''T. canis'' infections which increases the spread of the eggs as they pass faeces in new environments once the litter is split up.

==Pathogenesis==
In puppies heavy infections can cause weight loss and poor growth as well as diarrhoea and vomiting. Pot belly may also be seen in pupies in some cases. With extremely heavy infections a plug may form that can cause intestinal impaction and prevent gastric movements. In adults, once immunity has developed, there are few clinical signs as most infections are too small for pathology to develop. In humans there is a zoonotic risk, as ''T. canis'' is the major agent of visceral larval migrans in children primarily with occular migration.

==Control==
Control of ''T. canis'' relies on effective clearing of the eggs form the environment as these can be infective in the environment for several years. This will prevent new infections of animals that have no been exposed previously as pups or as young dogs. However there are a number of endemic regions of the world where most animals have been exposed as pups and therefore can harbour hypobiotic larvae. These are difficult to eliminate and there are likely to be constantly be a small number of worms present, therefore regular treatment of dogs with anthelmintics is recommended.

* Causes eosinophilic enteritis in the dog

'''In warm-blooded non-canid animals''':
*Events occur just as in the older dog, i.e. larvae migrate → liver → lungs → heart → somatic tissues → granulomatous reactions → 'waiting phase'; but in this case, the somatic larvae are waiting for the animal that they are in (which is acting as a '''paratenic host''') to be eaten by a dog, fox, wolf or other canid, where they will establish as adults or somatic larvae (depending on the age of the predator).
*This explains how humans (as warm-blooded non-canid animals) enter into the epidemiological picture.

==== Epidemiology ====
*Infection of dogs is by ingestion of the L2 larvae, which can occur in four ways:

1) ingestion of the embryonated egg

2) prenatal infection

3) transmammary infection

4) ingestion of a paratenic host.

*Infection of a paratenic host can occur by:

1) ingestion of the embryonated egg

2) ingestion of larvae in the tissues of another paratenic host.

*Each female ''T. canis'' can lay up to 250,000 eggs per day:
**the eggs are not infective until the L2 is fully developed
**this process takes a few weeks in summer, but many weeks in the winter
**the embryonated egg is tough and can survive for 4-5years
**eggs therefore accumulate in the environment, and can easily be demonstrated in soil scrapings from, for example, breeding kennels or city parks
**when eggs from the environment are swallowed by a bitch, larvae accumulate in her somatic tissues - to be activated during pregnancy
**at birth, prenatally derived larvae are already migrating through the pups' liver and lungs
**adult worms reach the intestine and start to lay eggs when the pups are 2-3weeks old
**pups are therefore a potent source of environmental contamination (particularly in breeding kennels) until spontaneous expulsion occurs after approximately 6weeks of age.
**in general, only approximately 15% of adult dogs have patent infection - an exception is nursing bitches, who often pass large numbers of eggs
**up to 45% of foxes have patent infection, and are therefore a potent source of eggs in urban areas.

==== Human Infection ====
*Humans are infected by swallowing embryonated eggs from the environmental reservoir.
*This is most likely to happen in young children.
*Most infections are asymptomatic.
*Approsimately 2.5% of the British population are seropositive.

==== Efficacy of Anthelmintics Against Life-Cycle Stages of ''T. canis'' ====
{| style="width:75%; height:200px" border="1"

!'''Compound'''
!'''Trade-Name'''
!'''Intestinal Worms'''
!'''Migrating Larvae'''
!'''Somatic Larvae'''

|-
|
'''Piperazine'''

'''Pyrantel'''

'''Pyrantel + Febantel'''

'''Fenbendazole'''

'''Mebendazole'''

'''Flubendazole'''

'''Nitroscanate'''

'''Selamectin'''

'''Milbemycin'''

'''Moxidectin'''
|
various

Strongid

Drontal

Panacur

Telmin

Flubenol

Lopatol

Stronghold

Milbemax

Advocate
|
+

++

+++

+++

+++

+++

+++

+++

+++

+++
|
-

-

-

+++

?

?

?

?

?

?
|
-

-

-

-

-

-

-

?

-

?
|}

==== Control of ''T. canis'' ====
*The only satisfactory way of breaking the life-cycle in breeding kennels and reducing zoonotic risk is to eliminate ''T. canis'' eggs from the environment.
*Hygiene is important (but note that the eggs stick to surfaces and that few disinfectants will kill them).
*To prevent dogs excreting eggs, pups must be dosed regularly from 2weeks of age.
*Most anthelmintics are only active against adult worms in the intestine.
*These adult worms are quickly replaced by developing larvae that survived treatment.
*Therefore, pups should be dosed at 2, 4, 6, 8 and 12weeks of age.
*Fenbendazole is active against both adults and larvae.
*So, an equivalent result can be obtained with just two treatments: one in the third week of life, and again 3weeks later.
*Nursing bitches should also be treated.
*Otherwise, adult dogs should be dosed 2-4times a year.
*Current anthelmintics at normal dose-rates will not kill somatic larvae.
*This can be done, however, with daily high doses of fenbendazole.
*Pregnant bitches are given daily doses (25mg/kg) from the 42nd day of pregnancy.

==== ''T. canis'' in Veterinary Public Health ====
''T. canis'' is associated with at least three disease syndromes in humans:

1) '''visceral larval migrans''' (VLM) (→ eosinophilia, hepatomegaly, fever, asthma)

2) '''ocular larval migrans''' (OLM) (→ unilateral partial impairment of vision)

3) '''covert toxocarosis''' (non-specific clinical signs associated with high antibody titre)

Around 55cases, mostly OLM, are diagnosed in the UK each year.

[[Category:Ascaridoidea]]
[[Category:Zoonoses]][[Category:Dog Nematodes]]
[[Category:To_Do_-_Parasites]]

Toxocara canis

2013-04-28T21:28:35Z

Rstanley2: /* Cycle 3 */

{{unfinished}}
{{Taxobox
|kingdom =Animalia
|phylum =Nematoda
|class =Secernentea
|sub-class =
|order =Ascaridida
|super-family =
|family =Toxocaridae
|sub-family =
|genus =Toxocara
|species =''T. canis''
}}

[[Image:Toxocara canis.jpg|thumb|150px|right|''T. canis'' egg - Joaquim Castellà - Veterinary Parasitology Universitat Autònoma de Barcelona]]

[[Image:Toxocara canis adult.jpg|thumb|150px|right|''T. canis'' adult worm from a puppy - Joel Mills, 2006 - Wikimedia commons]]

==Overview==
''Toxacara canis'' is a typical ascarid nematode that infects dogs where its predilection site is the small intestines. These worms can be found throughout the world with varying prevalence. Control of this ascarid is typically difficult due to its extended persistence in the environment. ''T. canis'' is also important in human medicine as the species most responsible for '''visceral larval migrans''' (VLM). The human is a non-permissive host of ''T. canis'' meaning it cannot complete its life cycle and reproduce, however the larval stages do migrate through the human body causing pathology.

==Identification==
''Toxacara canis'' has the typical gross morphology of an ascarid, it is a large, fleshy white worm and can be up to 18cm long. The females are longer than the males who can normally reach 10cm in length. Microscopically ''T. canis'' has a fairly standard [[:Category: Ascaridoidea|ascaridoid]] appearance, though the adult head is given an elliptical shape by large alae or 'wings'. The eggs of ''T. canis'' are dark brown with a thick, pitted shell, the thick shell makes them very resistant in the environment.

==Life cycle==
Typically of an ascarid ''T. canis'' has larvae have a migratory life cycle that is significance in the pathogenesis of infection. This species also has the most complex life cycle in the Ascaridoidea superfamily. There are four different life cycles that can occur dependant on the circumstances that the larvae or adult encounter.
====Cycle 1====
This is mostly a typical ascarid life cycle and commonly occurs in dogs that are infected between 2 and 3 months old. The infective eggs contain L2 larvae which hatch in the small intestine of the host dog after being ingested. The larvae then enter the hepatic portal vein and travel through the liver and further to the lungs where they moult to L3. The larvae then migrate to the trachea where they are coughed up and swallowed again by the host. This is known as hepato-tracheal migration. On returning to the small intestine they undergo the final moults (L3-->L4-->L5) before becoming adults.

====Cycle 2====
In older dogs (above 3 months) the migration changes and the hepato-tracheal route occurs far less often, though can still occur. In these animals the L2 larvae hatch in the small intestine and travel to a wide variety of tissues throughout the body. Once the larvae have reached a tissue they will begin hypobiosis and encyst in the tissue until reactivated. In some animals the hypobiotic larvae will not reactivate and this will be the end of their life cycle. Hypobiotic larvae in the tissues of the dog are known as '''somatic larvae''', although these do not grow or develop they are highly metabolically active. The produce large quantities of excretory/secretory antigens which are spread over the cuticle of the worm. These antigens are important in immune evasion by way of having a rapid turnover and sloughing off host antibodies and immune cells.

====Cycle 3====
In the pregnant bitch larvae that have become hypobiotic as described in cycle 2 above are reactivated by hormonal changes. These larvae become mobile about three weeks before parturition and migrate across the placenta to the lungs of the fetus. Within the fetal lungs the larvae moult just prior to birth (to L3). From the lungs the larvae complete their life cycle in the same way as in the young animal, by being coughed and swallowed to enter the small intestine. The adults will then produce eggs which are released in the faeces as normal.

====Cycle 4====
The final life cycle involves transmission of L3 larvae to pups through the milk. Hypobiotic L3 larvae are reactivated and are either already present in the mammary glands or travel to them and are capable of passing in the milk during the first 3 weeks of lactation. There is no further migration in the pup when the larvae are ingested in this way and the remaining life cycle of the worm is completed in the small intestine of the pup.

As well as the above life cycles ''T. canis'' can infect paratenic hosts such as mice, rats and some birds. Events occur just as in the older dog, i.e. larvae migrate → liver → lungs → heart → somatic tissues → granulomatous reactions → 'waiting phase'; but in this case, the somatic larvae are waiting for the animal that they are in (which is acting as a '''paratenic host''') to be eaten by a dog, fox, wolf or other canid, where they will establish as adults or somatic larvae (depending on the age of the predator). This explains how humans (as warm-blooded non-canid animals) enter into the epidemiological picture. The prepatent period of ''T. canis'' is 4 - 5 weeks in the canid host.

==Epidemiology==
''T. canis'' is present worldwide with a wide range of prevalances in different areas from 5 - 80%. Adult animals carry the fewest worms since initial infection causes immunity which leads to the shedding of adult worms from the intestines. The low parasite burden in adult animals can often lead to asymptomatic infection though the parasites wil still shed eggs in the faeces. The largest numbers of worms are found in dogs less than 6 months old who have not yet gained immunity to the worms. The high levels of prevalence of this species worldwide is largely due to the difficulty in controlling its spread. The eggs are extremely resistant in the environment and so can persist for several years. The females lay very large numbers of eggs, up to 700 per gram of faeces, making the removal of such a large number difficult. This final reason for such a large spread is the long lasting reservoir of hypobiotic larvae that can be reactivated in pregnancy in the bitch, these are not susceptible to anthelmintics and so are only eliminated by preventing pregnancy or the death of the host. As a result of the large number of infected bitches almost all puppies are born with ''T. canis'' infections which increases the spread of the eggs as they pass faeces in new environments once the litter is split up.

==Pathogenesis==
In puppies heavy infections can cause weight loss and poor growth as well as diarrhoea and vomiting. Pot belly may also be seen in pupies in some cases. With extremely heavy infections a plug may form that can cause intestinal impaction and prevent gastric movements. In adults, once immunity has developed, there are few clinical signs as most infections are too small for pathology to develop. In humans there is a zoonotic risk, as ''T. canis'' is the major agent of visceral larval migrans in children primarily with occular migration.

==Control==
Control of ''T. canis'' relies on effective clearing of the eggs form the environment as these can be infective in the environment for several years. This will prevent new infections of animals that have no been exposed previously as pups or as young dogs. However there are a number of endemic regions of the world where most animals have been exposed as pups and therefore can harbour hypobiotic larvae. These are difficult to eliminate and there are likely to be constantly be a small number of worms present, therefore regular treatment of dogs with anthelmintics is recommended.

* Causes eosinophilic enteritis in the dog

'''In warm-blooded non-canid animals''':
*Events occur just as in the older dog, i.e. larvae migrate → liver → lungs → heart → somatic tissues → granulomatous reactions → 'waiting phase'; but in this case, the somatic larvae are waiting for the animal that they are in (which is acting as a '''paratenic host''') to be eaten by a dog, fox, wolf or other canid, where they will establish as adults or somatic larvae (depending on the age of the predator).
*This explains how humans (as warm-blooded non-canid animals) enter into the epidemiological picture.

==== Epidemiology ====
*Infection of dogs is by ingestion of the L2 larvae, which can occur in four ways:

1) ingestion of the embryonated egg

2) prenatal infection

3) transmammary infection

4) ingestion of a paratenic host.

*Infection of a paratenic host can occur by:

1) ingestion of the embryonated egg

2) ingestion of larvae in the tissues of another paratenic host.

*Each female ''T. canis'' can lay up to 250,000 eggs per day:
**the eggs are not infective until the L2 is fully developed
**this process takes a few weeks in summer, but many weeks in the winter
**the embryonated egg is tough and can survive for 4-5years
**eggs therefore accumulate in the environment, and can easily be demonstrated in soil scrapings from, for example, breeding kennels or city parks
**when eggs from the environment are swallowed by a bitch, larvae accumulate in her somatic tissues - to be activated during pregnancy
**at birth, prenatally derived larvae are already migrating through the pups' liver and lungs
**adult worms reach the intestine and start to lay eggs when the pups are 2-3weeks old
**pups are therefore a potent source of environmental contamination (particularly in breeding kennels) until spontaneous expulsion occurs after approximately 6weeks of age.
**in general, only approximately 15% of adult dogs have patent infection - an exception is nursing bitches, who often pass large numbers of eggs
**up to 45% of foxes have patent infection, and are therefore a potent source of eggs in urban areas.

==== Human Infection ====
*Humans are infected by swallowing embryonated eggs from the environmental reservoir.
*This is most likely to happen in young children.
*Most infections are asymptomatic.
*Approsimately 2.5% of the British population are seropositive.

==== Efficacy of Anthelmintics Against Life-Cycle Stages of ''T. canis'' ====
{| style="width:75%; height:200px" border="1"

!'''Compound'''
!'''Trade-Name'''
!'''Intestinal Worms'''
!'''Migrating Larvae'''
!'''Somatic Larvae'''

|-
|
'''Piperazine'''

'''Pyrantel'''

'''Pyrantel + Febantel'''

'''Fenbendazole'''

'''Mebendazole'''

'''Flubendazole'''

'''Nitroscanate'''

'''Selamectin'''

'''Milbemycin'''

'''Moxidectin'''
|
various

Strongid

Drontal

Panacur

Telmin

Flubenol

Lopatol

Stronghold

Milbemax

Advocate
|
+

++

+++

+++

+++

+++

+++

+++

+++

+++
|
-

-

-

+++

?

?

?

?

?

?
|
-

-

-

-

-

-

-

?

-

?
|}

==== Control of ''T. canis'' ====
*The only satisfactory way of breaking the life-cycle in breeding kennels and reducing zoonotic risk is to eliminate ''T. canis'' eggs from the environment.
*Hygiene is important (but note that the eggs stick to surfaces and that few disinfectants will kill them).
*To prevent dogs excreting eggs, pups must be dosed regularly from 2weeks of age.
*Most anthelmintics are only active against adult worms in the intestine.
*These adult worms are quickly replaced by developing larvae that survived treatment.
*Therefore, pups should be dosed at 2, 4, 6, 8 and 12weeks of age.
*Fenbendazole is active against both adults and larvae.
*So, an equivalent result can be obtained with just two treatments: one in the third week of life, and again 3weeks later.
*Nursing bitches should also be treated.
*Otherwise, adult dogs should be dosed 2-4times a year.
*Current anthelmintics at normal dose-rates will not kill somatic larvae.
*This can be done, however, with daily high doses of fenbendazole.
*Pregnant bitches are given daily doses (25mg/kg) from the 42nd day of pregnancy.

==== ''T. canis'' in Veterinary Public Health ====
''T. canis'' is associated with at least three disease syndromes in humans:

1) '''visceral larval migrans''' (VLM) (→ eosinophilia, hepatomegaly, fever, asthma)

2) '''ocular larval migrans''' (OLM) (→ unilateral partial impairment of vision)

3) '''covert toxocarosis''' (non-specific clinical signs associated with high antibody titre)

Around 55cases, mostly OLM, are diagnosed in the UK each year.

[[Category:Ascaridoidea]]
[[Category:Zoonoses]][[Category:Dog Nematodes]]
[[Category:To_Do_-_Parasites]]

Toxocara canis

2013-04-28T21:26:40Z

Rstanley2: /* Cycle 1 */

{{unfinished}}
{{Taxobox
|kingdom =Animalia
|phylum =Nematoda
|class =Secernentea
|sub-class =
|order =Ascaridida
|super-family =
|family =Toxocaridae
|sub-family =
|genus =Toxocara
|species =''T. canis''
}}

[[Image:Toxocara canis.jpg|thumb|150px|right|''T. canis'' egg - Joaquim Castellà - Veterinary Parasitology Universitat Autònoma de Barcelona]]

[[Image:Toxocara canis adult.jpg|thumb|150px|right|''T. canis'' adult worm from a puppy - Joel Mills, 2006 - Wikimedia commons]]

==Overview==
''Toxacara canis'' is a typical ascarid nematode that infects dogs where its predilection site is the small intestines. These worms can be found throughout the world with varying prevalence. Control of this ascarid is typically difficult due to its extended persistence in the environment. ''T. canis'' is also important in human medicine as the species most responsible for '''visceral larval migrans''' (VLM). The human is a non-permissive host of ''T. canis'' meaning it cannot complete its life cycle and reproduce, however the larval stages do migrate through the human body causing pathology.

==Identification==
''Toxacara canis'' has the typical gross morphology of an ascarid, it is a large, fleshy white worm and can be up to 18cm long. The females are longer than the males who can normally reach 10cm in length. Microscopically ''T. canis'' has a fairly standard [[:Category: Ascaridoidea|ascaridoid]] appearance, though the adult head is given an elliptical shape by large alae or 'wings'. The eggs of ''T. canis'' are dark brown with a thick, pitted shell, the thick shell makes them very resistant in the environment.

==Life cycle==
Typically of an ascarid ''T. canis'' has larvae have a migratory life cycle that is significance in the pathogenesis of infection. This species also has the most complex life cycle in the Ascaridoidea superfamily. There are four different life cycles that can occur dependant on the circumstances that the larvae or adult encounter.
====Cycle 1====
This is mostly a typical ascarid life cycle and commonly occurs in dogs that are infected between 2 and 3 months old. The infective eggs contain L2 larvae which hatch in the small intestine of the host dog after being ingested. The larvae then enter the hepatic portal vein and travel through the liver and further to the lungs where they moult to L3. The larvae then migrate to the trachea where they are coughed up and swallowed again by the host. This is known as hepato-tracheal migration. On returning to the small intestine they undergo the final moults (L3-->L4-->L5) before becoming adults.

====Cycle 2====
In older dogs (above 3 months) the migration changes and the hepato-tracheal route occurs far less often, though can still occur. In these animals the L2 larvae hatch in the small intestine and travel to a wide variety of tissues throughout the body. Once the larvae have reached a tissue they will begin hypobiosis and encyst in the tissue until reactivated. In some animals the hypobiotic larvae will not reactivate and this will be the end of their life cycle. Hypobiotic larvae in the tissues of the dog are known as '''somatic larvae''', although these do not grow or develop they are highly metabolically active. The produce large quantities of excretory/secretory antigens which are spread over the cuticle of the worm. These antigens are important in immune evasion by way of having a rapid turnover and sloughing off host antibodies and immune cells.

====Cycle 3====
In the pregnant bitch larvae that have become hypobiotic as described in cycle 2 above are reactivated by hormonal changes. These larvae become mobile about three weeks before parturition and migrate across the placenta to the lungs of the fetus. Within the fetal lungs the larvae moult just prior to birth. From the lungs the larvae complete their life cycle in the same way as in the young animal, by being coughed and swallowed to enter the small intestine. The adults will then produce eggs which are released in the faeces as normal.
====Cycle 4====
The final life cycle involves transmission of L3 larvae to pups through the milk. Hypobiotic L3 larvae are reactivated and are either already present in the mammary glands or travel to them and are capable of passing in the milk during the first 3 weeks of lactation. There is no further migration in the pup when the larvae are ingested in this way and the remaining life cycle of the worm is completed in the small intestine of the pup.

As well as the above life cycles ''T. canis'' can infect paratenic hosts such as mice, rats and some birds. Events occur just as in the older dog, i.e. larvae migrate → liver → lungs → heart → somatic tissues → granulomatous reactions → 'waiting phase'; but in this case, the somatic larvae are waiting for the animal that they are in (which is acting as a '''paratenic host''') to be eaten by a dog, fox, wolf or other canid, where they will establish as adults or somatic larvae (depending on the age of the predator). This explains how humans (as warm-blooded non-canid animals) enter into the epidemiological picture. The prepatent period of ''T. canis'' is 4 - 5 weeks in the canid host.

==Epidemiology==
''T. canis'' is present worldwide with a wide range of prevalances in different areas from 5 - 80%. Adult animals carry the fewest worms since initial infection causes immunity which leads to the shedding of adult worms from the intestines. The low parasite burden in adult animals can often lead to asymptomatic infection though the parasites wil still shed eggs in the faeces. The largest numbers of worms are found in dogs less than 6 months old who have not yet gained immunity to the worms. The high levels of prevalence of this species worldwide is largely due to the difficulty in controlling its spread. The eggs are extremely resistant in the environment and so can persist for several years. The females lay very large numbers of eggs, up to 700 per gram of faeces, making the removal of such a large number difficult. This final reason for such a large spread is the long lasting reservoir of hypobiotic larvae that can be reactivated in pregnancy in the bitch, these are not susceptible to anthelmintics and so are only eliminated by preventing pregnancy or the death of the host. As a result of the large number of infected bitches almost all puppies are born with ''T. canis'' infections which increases the spread of the eggs as they pass faeces in new environments once the litter is split up.

==Pathogenesis==
In puppies heavy infections can cause weight loss and poor growth as well as diarrhoea and vomiting. Pot belly may also be seen in pupies in some cases. With extremely heavy infections a plug may form that can cause intestinal impaction and prevent gastric movements. In adults, once immunity has developed, there are few clinical signs as most infections are too small for pathology to develop. In humans there is a zoonotic risk, as ''T. canis'' is the major agent of visceral larval migrans in children primarily with occular migration.

==Control==
Control of ''T. canis'' relies on effective clearing of the eggs form the environment as these can be infective in the environment for several years. This will prevent new infections of animals that have no been exposed previously as pups or as young dogs. However there are a number of endemic regions of the world where most animals have been exposed as pups and therefore can harbour hypobiotic larvae. These are difficult to eliminate and there are likely to be constantly be a small number of worms present, therefore regular treatment of dogs with anthelmintics is recommended.

* Causes eosinophilic enteritis in the dog

'''In warm-blooded non-canid animals''':
*Events occur just as in the older dog, i.e. larvae migrate → liver → lungs → heart → somatic tissues → granulomatous reactions → 'waiting phase'; but in this case, the somatic larvae are waiting for the animal that they are in (which is acting as a '''paratenic host''') to be eaten by a dog, fox, wolf or other canid, where they will establish as adults or somatic larvae (depending on the age of the predator).
*This explains how humans (as warm-blooded non-canid animals) enter into the epidemiological picture.

==== Epidemiology ====
*Infection of dogs is by ingestion of the L2 larvae, which can occur in four ways:

1) ingestion of the embryonated egg

2) prenatal infection

3) transmammary infection

4) ingestion of a paratenic host.

*Infection of a paratenic host can occur by:

1) ingestion of the embryonated egg

2) ingestion of larvae in the tissues of another paratenic host.

*Each female ''T. canis'' can lay up to 250,000 eggs per day:
**the eggs are not infective until the L2 is fully developed
**this process takes a few weeks in summer, but many weeks in the winter
**the embryonated egg is tough and can survive for 4-5years
**eggs therefore accumulate in the environment, and can easily be demonstrated in soil scrapings from, for example, breeding kennels or city parks
**when eggs from the environment are swallowed by a bitch, larvae accumulate in her somatic tissues - to be activated during pregnancy
**at birth, prenatally derived larvae are already migrating through the pups' liver and lungs
**adult worms reach the intestine and start to lay eggs when the pups are 2-3weeks old
**pups are therefore a potent source of environmental contamination (particularly in breeding kennels) until spontaneous expulsion occurs after approximately 6weeks of age.
**in general, only approximately 15% of adult dogs have patent infection - an exception is nursing bitches, who often pass large numbers of eggs
**up to 45% of foxes have patent infection, and are therefore a potent source of eggs in urban areas.

==== Human Infection ====
*Humans are infected by swallowing embryonated eggs from the environmental reservoir.
*This is most likely to happen in young children.
*Most infections are asymptomatic.
*Approsimately 2.5% of the British population are seropositive.

==== Efficacy of Anthelmintics Against Life-Cycle Stages of ''T. canis'' ====
{| style="width:75%; height:200px" border="1"

!'''Compound'''
!'''Trade-Name'''
!'''Intestinal Worms'''
!'''Migrating Larvae'''
!'''Somatic Larvae'''

|-
|
'''Piperazine'''

'''Pyrantel'''

'''Pyrantel + Febantel'''

'''Fenbendazole'''

'''Mebendazole'''

'''Flubendazole'''

'''Nitroscanate'''

'''Selamectin'''

'''Milbemycin'''

'''Moxidectin'''
|
various

Strongid

Drontal

Panacur

Telmin

Flubenol

Lopatol

Stronghold

Milbemax

Advocate
|
+

++

+++

+++

+++

+++

+++

+++

+++

+++
|
-

-

-

+++

?

?

?

?

?

?
|
-

-

-

-

-

-

-

?

-

?
|}

==== Control of ''T. canis'' ====
*The only satisfactory way of breaking the life-cycle in breeding kennels and reducing zoonotic risk is to eliminate ''T. canis'' eggs from the environment.
*Hygiene is important (but note that the eggs stick to surfaces and that few disinfectants will kill them).
*To prevent dogs excreting eggs, pups must be dosed regularly from 2weeks of age.
*Most anthelmintics are only active against adult worms in the intestine.
*These adult worms are quickly replaced by developing larvae that survived treatment.
*Therefore, pups should be dosed at 2, 4, 6, 8 and 12weeks of age.
*Fenbendazole is active against both adults and larvae.
*So, an equivalent result can be obtained with just two treatments: one in the third week of life, and again 3weeks later.
*Nursing bitches should also be treated.
*Otherwise, adult dogs should be dosed 2-4times a year.
*Current anthelmintics at normal dose-rates will not kill somatic larvae.
*This can be done, however, with daily high doses of fenbendazole.
*Pregnant bitches are given daily doses (25mg/kg) from the 42nd day of pregnancy.

==== ''T. canis'' in Veterinary Public Health ====
''T. canis'' is associated with at least three disease syndromes in humans:

1) '''visceral larval migrans''' (VLM) (→ eosinophilia, hepatomegaly, fever, asthma)

2) '''ocular larval migrans''' (OLM) (→ unilateral partial impairment of vision)

3) '''covert toxocarosis''' (non-specific clinical signs associated with high antibody titre)

Around 55cases, mostly OLM, are diagnosed in the UK each year.

[[Category:Ascaridoidea]]
[[Category:Zoonoses]][[Category:Dog Nematodes]]
[[Category:To_Do_-_Parasites]]

Toxocara canis

2013-04-28T21:19:46Z

Rstanley2: /* Cycle 2 */

{{unfinished}}
{{Taxobox
|kingdom =Animalia
|phylum =Nematoda
|class =Secernentea
|sub-class =
|order =Ascaridida
|super-family =
|family =Toxocaridae
|sub-family =
|genus =Toxocara
|species =''T. canis''
}}

[[Image:Toxocara canis.jpg|thumb|150px|right|''T. canis'' egg - Joaquim Castellà - Veterinary Parasitology Universitat Autònoma de Barcelona]]

[[Image:Toxocara canis adult.jpg|thumb|150px|right|''T. canis'' adult worm from a puppy - Joel Mills, 2006 - Wikimedia commons]]

==Overview==
''Toxacara canis'' is a typical ascarid nematode that infects dogs where its predilection site is the small intestines. These worms can be found throughout the world with varying prevalence. Control of this ascarid is typically difficult due to its extended persistence in the environment. ''T. canis'' is also important in human medicine as the species most responsible for '''visceral larval migrans''' (VLM). The human is a non-permissive host of ''T. canis'' meaning it cannot complete its life cycle and reproduce, however the larval stages do migrate through the human body causing pathology.

==Identification==
''Toxacara canis'' has the typical gross morphology of an ascarid, it is a large, fleshy white worm and can be up to 18cm long. The females are longer than the males who can normally reach 10cm in length. Microscopically ''T. canis'' has a fairly standard [[:Category: Ascaridoidea|ascaridoid]] appearance, though the adult head is given an elliptical shape by large alae or 'wings'. The eggs of ''T. canis'' are dark brown with a thick, pitted shell, the thick shell makes them very resistant in the environment.

==Life cycle==
Typically of an ascarid ''T. canis'' has larvae have a migratory life cycle that is significance in the pathogenesis of infection. This species also has the most complex life cycle in the Ascaridoidea superfamily. There are four different life cycles that can occur dependant on the circumstances that the larvae or adult encounter.
====Cycle 1====
This is mostly a typical ascarid life cycle and commonly occurs in dogs that are infected between 2 and 3 months old. The infective eggs contain L3 larvae which hatch in the small intestine of the host dog after being ingested. The larvae then enter the hepatic portal vein and travel through the liver and further to the lungs where they moult to L4. The larvae then migrate to the trachea where they are coughed up and swallows again by the host. This is known as hepato-tracheal migration. On returning to the small intestine they undergo two further moults before becoming adults.
====Cycle 2====
In older dogs (above 3 months) the migration changes and the hepato-tracheal route occurs far less often, though can still occur. In these animals the L2 larvae hatch in the small intestine and travel to a wide variety of tissues throughout the body. Once the larvae have reached a tissue they will begin hypobiosis and encyst in the tissue until reactivated. In some animals the hypobiotic larvae will not reactivate and this will be the end of their life cycle. Hypobiotic larvae in the tissues of the dog are known as '''somatic larvae''', although these do not grow or develop they are highly metabolically active. The produce large quantities of excretory/secretory antigens which are spread over the cuticle of the worm. These antigens are important in immune evasion by way of having a rapid turnover and sloughing off host antibodies and immune cells.

====Cycle 3====
In the pregnant bitch larvae that have become hypobiotic as described in cycle 2 above are reactivated by hormonal changes. These larvae become mobile about three weeks before parturition and migrate across the placenta to the lungs of the fetus. Within the fetal lungs the larvae moult just prior to birth. From the lungs the larvae complete their life cycle in the same way as in the young animal, by being coughed and swallowed to enter the small intestine. The adults will then produce eggs which are released in the faeces as normal.
====Cycle 4====
The final life cycle involves transmission of L3 larvae to pups through the milk. Hypobiotic L3 larvae are reactivated and are either already present in the mammary glands or travel to them and are capable of passing in the milk during the first 3 weeks of lactation. There is no further migration in the pup when the larvae are ingested in this way and the remaining life cycle of the worm is completed in the small intestine of the pup.

As well as the above life cycles ''T. canis'' can infect paratenic hosts such as mice, rats and some birds. Events occur just as in the older dog, i.e. larvae migrate → liver → lungs → heart → somatic tissues → granulomatous reactions → 'waiting phase'; but in this case, the somatic larvae are waiting for the animal that they are in (which is acting as a '''paratenic host''') to be eaten by a dog, fox, wolf or other canid, where they will establish as adults or somatic larvae (depending on the age of the predator). This explains how humans (as warm-blooded non-canid animals) enter into the epidemiological picture. The prepatent period of ''T. canis'' is 4 - 5 weeks in the canid host.

==Epidemiology==
''T. canis'' is present worldwide with a wide range of prevalances in different areas from 5 - 80%. Adult animals carry the fewest worms since initial infection causes immunity which leads to the shedding of adult worms from the intestines. The low parasite burden in adult animals can often lead to asymptomatic infection though the parasites wil still shed eggs in the faeces. The largest numbers of worms are found in dogs less than 6 months old who have not yet gained immunity to the worms. The high levels of prevalence of this species worldwide is largely due to the difficulty in controlling its spread. The eggs are extremely resistant in the environment and so can persist for several years. The females lay very large numbers of eggs, up to 700 per gram of faeces, making the removal of such a large number difficult. This final reason for such a large spread is the long lasting reservoir of hypobiotic larvae that can be reactivated in pregnancy in the bitch, these are not susceptible to anthelmintics and so are only eliminated by preventing pregnancy or the death of the host. As a result of the large number of infected bitches almost all puppies are born with ''T. canis'' infections which increases the spread of the eggs as they pass faeces in new environments once the litter is split up.

==Pathogenesis==
In puppies heavy infections can cause weight loss and poor growth as well as diarrhoea and vomiting. Pot belly may also be seen in pupies in some cases. With extremely heavy infections a plug may form that can cause intestinal impaction and prevent gastric movements. In adults, once immunity has developed, there are few clinical signs as most infections are too small for pathology to develop. In humans there is a zoonotic risk, as ''T. canis'' is the major agent of visceral larval migrans in children primarily with occular migration.

==Control==
Control of ''T. canis'' relies on effective clearing of the eggs form the environment as these can be infective in the environment for several years. This will prevent new infections of animals that have no been exposed previously as pups or as young dogs. However there are a number of endemic regions of the world where most animals have been exposed as pups and therefore can harbour hypobiotic larvae. These are difficult to eliminate and there are likely to be constantly be a small number of worms present, therefore regular treatment of dogs with anthelmintics is recommended.

* Causes eosinophilic enteritis in the dog

'''In warm-blooded non-canid animals''':
*Events occur just as in the older dog, i.e. larvae migrate → liver → lungs → heart → somatic tissues → granulomatous reactions → 'waiting phase'; but in this case, the somatic larvae are waiting for the animal that they are in (which is acting as a '''paratenic host''') to be eaten by a dog, fox, wolf or other canid, where they will establish as adults or somatic larvae (depending on the age of the predator).
*This explains how humans (as warm-blooded non-canid animals) enter into the epidemiological picture.

==== Epidemiology ====
*Infection of dogs is by ingestion of the L2 larvae, which can occur in four ways:

1) ingestion of the embryonated egg

2) prenatal infection

3) transmammary infection

4) ingestion of a paratenic host.

*Infection of a paratenic host can occur by:

1) ingestion of the embryonated egg

2) ingestion of larvae in the tissues of another paratenic host.

*Each female ''T. canis'' can lay up to 250,000 eggs per day:
**the eggs are not infective until the L2 is fully developed
**this process takes a few weeks in summer, but many weeks in the winter
**the embryonated egg is tough and can survive for 4-5years
**eggs therefore accumulate in the environment, and can easily be demonstrated in soil scrapings from, for example, breeding kennels or city parks
**when eggs from the environment are swallowed by a bitch, larvae accumulate in her somatic tissues - to be activated during pregnancy
**at birth, prenatally derived larvae are already migrating through the pups' liver and lungs
**adult worms reach the intestine and start to lay eggs when the pups are 2-3weeks old
**pups are therefore a potent source of environmental contamination (particularly in breeding kennels) until spontaneous expulsion occurs after approximately 6weeks of age.
**in general, only approximately 15% of adult dogs have patent infection - an exception is nursing bitches, who often pass large numbers of eggs
**up to 45% of foxes have patent infection, and are therefore a potent source of eggs in urban areas.

==== Human Infection ====
*Humans are infected by swallowing embryonated eggs from the environmental reservoir.
*This is most likely to happen in young children.
*Most infections are asymptomatic.
*Approsimately 2.5% of the British population are seropositive.

==== Efficacy of Anthelmintics Against Life-Cycle Stages of ''T. canis'' ====
{| style="width:75%; height:200px" border="1"

!'''Compound'''
!'''Trade-Name'''
!'''Intestinal Worms'''
!'''Migrating Larvae'''
!'''Somatic Larvae'''

|-
|
'''Piperazine'''

'''Pyrantel'''

'''Pyrantel + Febantel'''

'''Fenbendazole'''

'''Mebendazole'''

'''Flubendazole'''

'''Nitroscanate'''

'''Selamectin'''

'''Milbemycin'''

'''Moxidectin'''
|
various

Strongid

Drontal

Panacur

Telmin

Flubenol

Lopatol

Stronghold

Milbemax

Advocate
|
+

++

+++

+++

+++

+++

+++

+++

+++

+++
|
-

-

-

+++

?

?

?

?

?

?
|
-

-

-

-

-

-

-

?

-

?
|}

==== Control of ''T. canis'' ====
*The only satisfactory way of breaking the life-cycle in breeding kennels and reducing zoonotic risk is to eliminate ''T. canis'' eggs from the environment.
*Hygiene is important (but note that the eggs stick to surfaces and that few disinfectants will kill them).
*To prevent dogs excreting eggs, pups must be dosed regularly from 2weeks of age.
*Most anthelmintics are only active against adult worms in the intestine.
*These adult worms are quickly replaced by developing larvae that survived treatment.
*Therefore, pups should be dosed at 2, 4, 6, 8 and 12weeks of age.
*Fenbendazole is active against both adults and larvae.
*So, an equivalent result can be obtained with just two treatments: one in the third week of life, and again 3weeks later.
*Nursing bitches should also be treated.
*Otherwise, adult dogs should be dosed 2-4times a year.
*Current anthelmintics at normal dose-rates will not kill somatic larvae.
*This can be done, however, with daily high doses of fenbendazole.
*Pregnant bitches are given daily doses (25mg/kg) from the 42nd day of pregnancy.

==== ''T. canis'' in Veterinary Public Health ====
''T. canis'' is associated with at least three disease syndromes in humans:

1) '''visceral larval migrans''' (VLM) (→ eosinophilia, hepatomegaly, fever, asthma)

2) '''ocular larval migrans''' (OLM) (→ unilateral partial impairment of vision)

3) '''covert toxocarosis''' (non-specific clinical signs associated with high antibody titre)

Around 55cases, mostly OLM, are diagnosed in the UK each year.

[[Category:Ascaridoidea]]
[[Category:Zoonoses]][[Category:Dog Nematodes]]
[[Category:To_Do_-_Parasites]]