WikiVet English - User contributions [en]

User:Kthompson

2011-05-04T13:47:25Z

Kthompson: /* Hours worked table on user page */

{{UserPage
|Name=Katy Thompson
|Occupation= Veterinary Surgeon 
|School= UK - RVC (London)
|Year= 2010
|Email=
|Image=
}}

[[:Haemoabdomen|See:Haemoabdomen]]

 Pages I am working on: [[:Category:To Do - Kate]]

== Hours worked table on user page ==

Please ensure you have a table with your hours worked on your user pages - here's one as an example:

 

{| class="wikitable collapsible FCK__ShowTableBorders"
|-
| Day
| '''Week 1''' (28.2. - 6.3.)
| '''Week 2''' (7.3. - 13.3.)
| '''Week 3''' (14.3 - 20.3.)
| '''Week 4''' (21.3 - 27.3.)
| '''Week 5''' (28.3 - 3.4.)
| '''Week 6''' (4.4 - 10.4.)
| '''Week 7''' (11.4 - 17.4)
| '''Week 8''' (18.4 - 24.4)
| '''Week 9''' (25.4- 01.5)
| '''Week 10''' (02.5- 08.5)
| '''Week 11''' (09.5- 15.5)
|-
| Monday
| 3.5
| 2.5
| 5
| 6
| 5.5
| 5.5
| 1.5
|
|
|
|
|-
| Tuesday
| 9.5
| 3.5
| 6.5
| 6.5
| 1.5
| 4.5
|
| 2.5
|
|
|
|-
| Wednesday
| 6.5
| 6
| 5
| 8.5
| 7
| 6
|
|
|
|
|
|-
| Thursday
| 6
| 9
| 6.5
| 9
| 5.5
| 6
| 0.5
|
|
|
|
|-
| Friday
| 7
| 5.5
| 7.5
|
| 8
| 9
|
|
|
|
|
|-
| Saturday
|
| 5.5
|
|
| 5
|
|
|
|
|
|
|-
| Sunday
| 1
| 3
| 4.5
| 3.5
|
| 1
|
|
|
|
|
|-
| '''Total hours'''
| 33.5
| 35
| 35
| 33.5
| 32.5
| 32
| 2
| 2.5
| 0
|
|
|}

2011-04-08T14:28:05Z

Kthompson:

[[Image:Thyroid Gland Low Power.jpg|right|thumb|300px|©RVC 2008]]

== Embryological Origin ==
The thyroid gland is a downgrowth from the pharyngeal endoderm of the developing tongue.

 

==Anatomy==
The thyroid gland consists of two lobes (dog, horse), one on each lateral side of the cranial [[Trachea - Anatomy & Physiology|trachea]]. In the pig the lobes are connected by an ''isthmus'' with a small, central ''pyramidal lobe'' as part of that structure. Cattle have a particularly wide isthmus.
 

===Location===
The thyroid gland is located adjacent to the cranial trachea. Close to the ''Recurrent Laryngeal nerve'', carotid sheath and Sternohyoid and Sternothyroid muscles. The [[Parathyroid Glands - Anatomy & Physiology|'''Parathyroid Glands''']] are located dorsally to, or within the thyroid gland itself.
 

===Supply===
The thyroid gland is supplied by the '''Cranial Thyroid artery''' which is a branch of the common carotid artery. A subsidiary supply is provided by the '''Caudal Thyroid artery'''. The cranial and caudal thyroid arteries are united by substantial anastamoses along their caudal edge. Venous drainage is provided by the Internal Jugular vein and [[Lymph - Anatomy & Physiology|Lymph]] drains into the cranial Deep Cervical nodes.
 

===Ultrastructure and Histology===
[[Image:Thyroid Gland Labelled.jpg|right|thumb|300px|'''Normal Thyroid Gland. ©RVC 2008]]
 
The gland consists of varying sized follicles. These are a single layer of cuboidal epithelial cells: '''Follicular Cells''' surrounding a central lumen filled with a protein rich colloid (thyrogloblin). The apical surface of the cell membranes is covered with numerous micovilli to increase surface area. The follicular cells are connected by tight junctions, and have a dense capillary network.
 
Within the connective tissue close to the follicles are '''C-Cells''' alternatively known as '''Parafollicular Cells'''. These secrete ''Calcitonin'', a hormone which acts to lower plasma Ca2+ levels.
 

====Histology====
<center><gallery>
Image:Thyroid Gland Low Power.jpg|''' Thyroid Gland Low Power 1'''©RVC 2008
Image:Thyroid Gland Low Power 2.jpg|'''Thyroid Gland Low Power 2'''©RVC 2008
Image:Thyroid Gland Medium Power.jpg|'''Thyroid Gland Medium Power'''©RVC 2008
Image:Thyroid Gland High Power.jpg|'''Thyroid Gland High Power''' ©RVC 2008
Image:Normal thyroid.jpg|'''Normal Thyroid''' Courtesy of A. Jefferies
Image:Thyroid Gland High Power showing C Cells.jpg|'''Thyroid Gland High Power with C-Cells labelled''' ©RVC 2008
</gallery></center>

 

==Thyroid Hormone Physiology==
Follicular cells synthesize '''Thyroglobulin''' in their golgi apparatus. This is a glycoprotein consisting of 70 linked tyrosine molecules, 10% of which are ''iodinated'', and is stored in the colloid.
 
The thyroglobulin is then split to form the two amino acid derivative [[Hormones - Anatomy & Physiology|hormones]] produced in the thyroid gland which are Triiodothyronine (T3) and Thyroxine (T4). Thyroxine contains 4 iodine atoms, triiodothyronine contains 3. Creation of these two [[Hormones - Anatomy & Physiology|hormones]] is the only role of iodine in the body.
 
The majority (90%) of hormone produced by the follicular cells is T4. T4 can only be made in the thyroid gland. It can then be converted by other tissues into T3.
 

===Iodine Uptake===
Iodine circulates within the blood as Iodide (I-). It is actively transported into the follicular cells by an Na+/I- symport in the basal membrane. This pump concentrates iodine in the colloid at a level up to 250x greater than the plasma level. This process is known as ''Iodide Trapping.'' The pump is activated by Thyroid Stimulating Hormone (TSH) a hormone from the [[Pituitary Gland - Anatomy & Physiology|pituitary gland]].
Any excess iodide is excreted via the [[Urinary System Overview - Anatomy & Physiology#Upper Urinary Tract|kidneys]].
 

===Secretion of Thyroid Hormones===
Colloid uptake into the follicular cells takes place by endocytosis. The intracellular vesicles containing the colloid then fuse with lysosomes, where enzymes split the thyroglobulin into T3 and T4. The hormones diffuse across the basal plasma membrane into the interstitium (they are lipid soluble hormones).
 

===Transport===
Thyroid hormones are lipid soluble, thus need a transporting protein in order to travel in the blood.Half-life in the blood is 1 day for T3, 6 days for T4.
99% of thyroid hormones in circulation are bound.
The primary transport protein for thyroid hormones is '''Thyroid Binding Globulin''' (TBG). Synthesized in the [[Liver - Anatomy & Physiology|liver]], this protein binds 70-80% of the circulating thyroid hormones.
 
The remainder are carried by '''Thyroxine-binding prealbumin''' or '''albumin'''.
 

===Degradation===
Only free T3 and free T4 can enter cells to exert their actions. T4 is deiodinated to T3 in many cells of the body, particularly the liver and kidneys.
 
The thyroid secretes 90% T4, with 50% of this being deiodinated to T3. The remainder is converted to Reverse T3 (rT3). This is an inactive form of T3, and so creation of it is a regulatory mechanism. More rT3 is created when the body needs to reduce the action of T3 and T4.
 
The hormones are further deiodinated to diiodothyronine and monoiodothyronine in the liver and kidneys. Iodine is recycled or excreted in the urine.
 

===Regulation===
The Hypothalamus releases '''Thyrotropin Releasing Hormone''' (TRH) which stimulates the adenohypophysis (anterior [[Pituitary Gland - Anatomy & Physiology|pituitary gland]]) to release '''Thyroid Stimulating Hormone''' (TSH). This water soluble hormone travels in the blood to activate the thyroid gland by 5 actions:
#Increased endocytosis and proteolysis of thyroglobulin from colloid
#Increased activity of the Na+/I- Symport
#Increased iodination of tyrosine
#Increased size and secretory activity of thyroid follicular cells
#Increased number of follicular cells

[[Image:HypothalamicPituitaryThyroidAxis.jpg|thumb|240px|center|'''Schematic Diagram of the Hypothalamic - Pituitary - Thyroid Axis]]
 

===Thyroid Hormone Actions===
T3 and T4 have effects on all body systems and at all stages of life. These include '''Development''' where thyroid hormones are vital during the fetal period and the first few months after birth. T3 and T4 are the hormones for metamorphosis in frogs. Thyroid hormones also promote '''Growth''' as they enhance amino acid uptake by tissues and enzymatic systems involved in protein syntheis, promotes bone growth. They also help with metabolic actions such as '''Carbohydrate metabolism''', as thyroid hormones stimulate glucose uptake, glycogenolysis, gluconeogenesis. In '''Fat metabolism''' they mobilise lipids from adipose stores and accelerate oxidation of lipids to produce energy (occurs within mitochondria), as well as increasing the size and number of mitochondria. Thyroid hormones also '''Increase Basal Metabolic Rate''' (BMR) in all tissues except brain, spleen and gonads. The results in increased heat production, increased oxygen consumption. This increased metabolic rate also results in increased utilisation of energy substrates causing weight loss. Some of thyroid hormones [[Cardiorespiratory System Overview - Anatomy & Physiology#Cardiovascular System|'''Cardiovascular actions''']] are to increase cardiac output, heart rate and contractility. They affect the [[Cardiorespiratory System Overview - Anatomy & Physiology#Upper Respiratory Tract|'''Respiratory system''']] indirectly through increased BMR causing increased demand for oxygen and increased excretion of carbon dioxide. In the [[Nervous and Special Senses - Anatomy & Physiology#Nervous System|'''Nervous system''']] thyroid hormones are required for myelination of [[PNS Structure - Anatomy & Physiology#Neurons|neurons]] during the development of this system. They also enhance the sympathetic nervous system (by increasing epinephrine receptors). [[Reproductive System Overview - Anatomy & Physiology|'''Reproductive System''']] is affected if thyroid hormone levels decrease reduced levels of thyroid hormone causes irregular cycling, decreased libido. Finally, in the [[Alimentary System Overview - Anatomy & Physiology|'''Alimentary System''']] - Thyroid hormone increases appetite and feed intake, increases secretion of [[Pancreas - Anatomy & Physiology|pancreatic]] enzymes and increases motility.

 

==Problems associated with the Thyroid Gland==
Problems with the thyroid gland include enlargement, or [[Goitre|Goitre]] and also the effects of increased level of hormones in [[Hyperthyroidism|Hyperthyroidism]] or decreased levels of hormones in [[Hypothyroidism|Hypothyroidism]].

 

==Functional Anatomy (summary)==
The thyroid gland lies in the neck, in front of the upper part of the trachea. Two types of hormones are produced, which are the iodine containing hormones; '''Tri-iodothyronine'''(T3) and '''Thyroxine''' (T4). Thyroid hormones regulate the basal metabolic rate and are important in the regulation of growth of tissues, particularly nervous tissue. Release stimulated by TSH from the pituitary. The second type of hormone produced from the thyroid gland is '''Calcitonin''', which regulates blood calcium levels along with parathyroid hormone and acts to reduce blood calcium by inhibiting its removal from bone.
 
The majority of the gland is derived from a downgrowth of the foetal tongue. The calcitonin producing cells are different and are derived from the fourth branchial pouch.
[[Image:Normal thyroid.jpg|right|thumb|125px|<center>'''Normal Thyroid'''. Courtesy of A. Jefferies</center>]]
The throid gland is divided into follicles which are bounded by a single layer of cuboidal epithelial cells and a basement membrane. Follicles contain a homogenous colloid material called '''thyroglobulin'''. This is a store of thyroid hormones prior to secretion. The thyroid gland is the only endocrine gland to store its hormone in large quantities.
 
In the active gland colloid is diminished and epithelial cells are tall and columnar.
 
'''Parafollicular''' cells are found in clusters in the interfollicular space and are also known as '''clear''' cells as their cytoplasm doesn't stain with H and E.
These cells synthesise and secrete calcitonin in response to raised plasma calcium.

 

==Test yourself with the Thyroid Gland Flashcards==

[[Thyroid_Gland_Flash_Cards_- Anatomy & Physiology|Thyroid Gland Flashcards]]

[[Category:Endocrine System - Anatomy & Physiology]]
[[Category:To Do - Review]]

2011-04-06T14:39:51Z

Kthompson:

== Synonyms ==
Goat plague, pest of sheep and goats, pneumoenteritis complex, pseudorinderpest of small ruminants, stomatitis-pneumoenteritis syndrome.

 

== Introduction ==
The disease was first described by workers in the Côté d’Ivoire (Gargadennec and Lalanne, 1942), and thereafter in other parts of West Africa in the 1950s and 1960s. It is now recognized to be distributed from south Asia through the Middle East, and from the horn of Africa through to West Africa. The similarity in clinical signs to that of rinderpest in cattle probably accounts for the number of reports of rinderpest in small ruminants from some countries, and delayed the recognition of the disease as a distinct entity in India until the early 1990s.
 
The infective agent was first considered a variant of rinderpest virus adapted to small ruminants, but was later shown to be antigenically (Gibbs et al., 1979) and genetically distinct (Diallo et al., 1989). Since PPRV isolates of West African, Middle Eastern and south Asian origin comprise distinct genetic groups, it is likely that the infections have circulated largely independently for long periods in each area.
 

The disease is recognized by the Office International des Epizooties (OIE) as a 'List A' pathogen on account of the high mortality and morbidity, and rapidity of spread by contagion. Recognition of PPR as a problem has increased in the 1990s, partly as a result of surveillance activities of the global rinderpest eradication programme (GREP), but also by the capacity of the infection to invade disease-free countries. The presence of infection restricts international trade in livestock and livestock products from infected countries, and is usually associated with ongoing severe losses where conditions exist that support epidemic spread among susceptible breeds, such as the incursions of infection into 'marginal' zones for persistence of infection such as humid zones of West Africa.
 

The development of tests for the confirmation of the agent and the differentiation from rinderpest was only achieved in the late 1980s, and recent recognition of the infection in many African and Asian countries can be attributed to availability of methods for specific detection of virus and antibodies. However, given the rapidity of spread of epidemics and the lack of a carrier state, it is likely that infection is not maintained in some areas because of inadequate supply of susceptible animals and some incursions of disease appear self-limiting. Presence of infection in a country in one year does not imply endemic infection. However, the risk of trans-boundary spread of this disease is high because sheep and goats are easily transported and trade across borders is difficult to control.
 

Disease occurs in goats and sheep, and has been recognized in captive wild ungulates from families of Gazellinae (Dorcas gazelle), Caprinae (Nubian ibex and Laristan sheep) and Hippotraginae (gemsbok). Experimentally, severe disease also occurs in white-tailed deer. Cattle undergo mainly subclinical reactions, and pigs develop a viraemia.
Seasonality in breeding, in marketing and in crop production all appear related to disease occurrence. In arid and semi-arid zones, surplus animals are sold during the dry season, which may lead to spread of infection into other areas, especially if sale occurs via markets. In humid zones, sale of surplus animals may occur at the start of the rains, with tethering of animals to avoid crop damage. Both sale of animals and close housing/tethering can increase risk of transmission if virus is introduced. The wet season can also predispose to secondary bacterial infections, exacerbating the viral pneumonia.
 

PPRV has a direct life cycle, maintained by infected animal to susceptible animal transmission, without involvement of carrier animals or vectors. The underlying requirement is a regular supply of susceptible hosts plus sufficient animal movement to allow mixing of the population (Rossiter and Taylor, 1993). Risk factors include unconfined husbandry, whether in urban or rural settings. The population size required to maintain infection is not known, but small populations probably cannot maintain infection for long and, therefore, given the rapid population turnover of small ruminants, disease associated with re-introduction can be severe. Severe epidemics probably reflect introduction of virus into areas with mainly susceptible populations and breeds, rather than endemic presence of infection throughout the year (Rossiter and Taylor, 1993). There is one serotype of virus, and immunity is long-lasting, probably life-long. Because colostral antibody protects young animals, in endemic areas most disease occurs in animals after waning of colostral immunity, from 4 months to 2 years of age, with protection of animals which have had previous exposure. Mortality rate in areas considered endemic may be in the region of 4-5% whereas rates from 20% to 90% in outbreaks have frequently been reported under epidemic conditions (Rossiter and Taylor, 1993). Climate appears to play a role in increasing the severity of disease, via secondary infections exacerbating the infection of the lung, but also affects the migration of pastoralist flocks in response to rainfall and drought and the resultant exposure to infection.

 

== Clinical Signs ==
Signs include pyrexia, depression, lethargy, weight loss or reducded weight gain and a reduced appetite. There will be ulcers, vesicles and erosion on the tongue and oral mucosa and the animal may be smacking its' lips, salivating excessively and grinding its teeth in pain. The animal will have foul smelling diarrhoea which may have mucous or blood in.
 
There may also be a foul odour to the breath and nasal discharge, dyspnoea, tachypnoea and coughing may be present. The animal may also be lacrimating excessively.

 

== Diagnosis ==
A manual on the diagnosis of PPR has been produced (FAO, 1998). Suspicion of PPR would be raised by signs of stomatitis – or pneumonitis, with enteritis in several animals. A high mortality and morbidity rate would be expected in outbreaks occurring in non-endemic areas, or where outbreaks have not occurred for some time and animals are not vaccinated.
 
Other conditions which need to be eliminated as differentials are rinderpest in small ruminants, contagious caprine pleuropneumonia, bluetongue, pasteurellosis, contagious ecthyma, foot-and-mouth disease, heartwater, coccidiosis and mineral poisoning. Rinderpest virus can cause disease in small ruminants, but where RP exists as a risk to small ruminants, disease in cattle would be expected, since many countries have ceased vaccination. Bluetongue infection occurs in many countries that are endemic or at-risk from PPR incursion. It can give rise to a muco-purulent discharge and high morbidity and mortality rate in susceptible sheep, but usually less so in goats. It does not usually result in a severe enteritis, although loose stools may occur, or erosions/ulcerations of epithelial surfaces. Bluetongue usually gives rise to visible signs of haemorrhage on the coronary band of the foot, in contrast to PPR. Foot-and-mouth disease affects other stock as well as sheep and goats; cattle in the region would be expected to show more severe signs than sheep or goats. On occasion though, the disease is more severe in the latter, and cattle may be absent. However, the enteritis usually present in PPR is not seen in FMD. The lesions of orf (contagious ecthyma) and sheep and goat pox differ in distribution to that of PPR, but animals recovering from PPR may develop proliferative growths on the lips resembling orf, and the virus may be involved in the pathogenesis of the condition. Contagious caprine pleuropneumonia occurs in many similar countries to PPR but does not usually give a high mortality in sheep, or have an accompanying severe enteritis. Heartwater can give a high mortality rate in susecptible breeds, but without a stomatitis.
 

PPRV is present at a high concentration in secretions and tissue samples in the early stages of the disease, but rapidly becomes difficult to detect after development of antibody responses. Collection of specimens from animals which have a serous ocular-nasal discharge and fever is preferable compared to later-stage signs of necrotic stomatitis-enteritis. In live animals, swabs should be made of the conjunctival discharges from the nasal and buccal mucosae. Whole blood should be collected in anticoagulant for virus isolation, polymerase chain reaction (PCR) and haematology. From the necropsy examination of two to three animals, lymph nodes, especially the mesenteric and bronchial nodes, lungs, spleen and intestinal mucosae should also be collected aseptically, chilled on ice and transported under refrigeration. Fragments of organs collected for histopathology are placed in 10% formalin. At the end of the outbreak, blood can be collected for serological diagnosis. Post-mortem examination of carcasses can be valuable, particularly in wildlife and in situations where samples cannot be kept in suitable conditions during transport to the laboratory, with a view to collection of specimens for detection of multi-nucleated giant cells by histopathology. Infection can be confirmed by identification of the agent with specific tests. Detection of a rise in titre of antibody could also be used, with paired samples collected 14-21 days apart.
 
Antigen-capture ELISA is sensitive and specific, using monoclonal antibodies to give a result with PPR virus and enabling differentiation from rinderpest in small ruminants (Libeau et al., 1994). The availability of the ELISA as a kit has undoubtedly assisted countries in the detection of PPR epidemics. PCR may be of advantage in testing tissues where virus cannot be detected by other means, including specimens for histopathology. However, the time taken to extract RNA, and undertake the RT-PCR is usually longer than that needed for CIEP, and higher technical standards are required to avoid false-positive reactions.
 
Antibodies are strongly induced by infection, and become detectable from the diarrheic stage onwards. The prescribed test for international trade (that which is accepted as a basis for the veterinary certification of animals as having evidence of presence or absence of antibodies) is virus neutralisation (VNT; OIE, 2000). Since there is cross-neutralisation between antibodies to PPR and RPV, a positive VNT result to PPR virus needs to be compared to the titre obtained with RPV. The OIE considers that a serum is considered to be positive for PPR when the neutralisation titre is at least two-fold higher for PPR than for rinderpest. Virus neutralisation tests involve use of live virus and cell cultures, and therefore require well-equipped laboratories and biosecurity to prevent escape of virus. VNT is therefore mainly restricted to laboratories with sufficient expertise and through-put of samples to justify the investment involved. The tests are sensitive and specific, and enable differentiation of antibodies to rinderpest virus, should these occur as a result of use of RP vaccine in small ruminants or exposure to the type 1 lineage of RPV. Haemagglutination inhibition tests for antibody have also been described with good correlation with VNT (Raj et al., 2000). After countries have been declared free of rinderpest infection, it may be sufficient to use more simple antibody detection methods that do not require differentiation of RPV infection of small ruminants.

 

== Pathology ==
The carcass is usually dehydrated, and soiled with faeces. The peri-orbital and perinasal areas are usually encrusted with muco-purulent discharges. The erosions and ulcerations in the mouth and throat are usually prominent, as is the presence of the secondary broncho-pneumonia. The underlying primary viral pneumonia may be less obvious but is manifested by areas of level red consolidation (Rowland et al., 1969). 'Zebra striping' in the colon may also be seen, and lympadenopathy.
 
The most important histopathological indicator of PPRV is the presence of multi-nucleated giant cells containing intra-nuclear and intra-cytoplasmic inclusions. Multi-nucleated giant cells (syncytia) are most readily detected in the lungs, but also occur in bronchial, alveolar and ileal epithelium.

 

== Treatment and Control ==
Chloramphenicol, penicillin, streptomycin can each be used and should be given intramuscularly for 5 days. Fluid therapy is also useful as a supportive treatment aswell as electrolyte replacement.
 

A live, attenuated strain (PSRV 75/1) of the PPR virus has been developed for use as a vaccine and provides protection for over 3 years. Previous trials (usually with RP vaccine) usually reported reduction in mortality, particularly in weaned young stock, and positive benefit-to-cost ratios.
 
Risk factors for occurrence of disease are the purchase of animals from markets, and free-range husbandry of animals, when PPRV is known to be present in the region.
Movement control, at the level of total standstill of livestock movements and banning of markets may be effective if enforceable and short-lasting in duration, since the incubation period is short. However, an effective quarantine of affected and in-contact animals for one month after the recovery of the last clinically affected case has been recommended (Rossiter and Taylor, 1993). These measures may be accompanied by a slaughter policy of animals on infected and in-contact premises, in addition to the ban on livestock movements, if the aim is rapid eradication. Measures that negatively affect livelihoods will be unpopular and difficult to enforce unless accompanied by incentives, and have rarely been implemented by authorities.
 

PPR is a list A disease of the OIE, and thus member states are required to inform the OIE of the occurrence of the disease in their territory. The OIE publishes recommendations for zoo-sanitary conditions and certification of trade in animals and livestock products from countries which are not recognized as having freedom from PPR disease (OIE, 2001b). The OIE recommends sanitary prophylaxis (movement control, quarantine of infected premises, with slaughter of infected animals and in-contacts) when the disease appears in previously PPR-free countries. The use of a stamping-out policy, involving slaughter of infecteds and in-contact animals on infected premises, can lead to a reduced period of time elapsing after the last case of disease has been reported before the country is internationally recognized as free of PPR.

 

== References ==
Diallo A, Barrett T, Barbron M, Subbarao SM, Taylor WP, 1989. Differentiation of rinderpest and peste des petits ruminants viruses using specific cDNA clones. Journal of Virological Methods, 23(2):127-136; 24 ref.
 
FAO, 1998. Recognising peste des petits ruminants. A field manual. Rome, Italy: Food and Agriculture Organisation (FAO).
 
Gargadennec L, Lalanne A, 1942. La peste-des-petits-ruminants. Bulletin du Service Zootechnique Epizootique du Afrique Occidentale Francaise, 5:16-21.
 
Gibbs EPJ, Taylor WP, Lawman MJP, Bryant J, 1979. Classification of peste des petits ruminants virus as the fourth member of the genus Morbillivirus. Intervirology, 11(5):268-274.
 
OIE, 2000. The Manual of Standards for Diagnostic Tests and Vaccines. Paris, France: Office International Des Epizooties.
 
Rossiter PB, Taylor WP, 1993. Peste des Petits Ruminants. In: Infectious Diseases of Livestock, with special reference to Southern Africa. Chapter 75.
 
Rowland AC, Scott GR, Hill HD, 1969. The pathology of an erosive stomatitis and enteritis in West African Dwarf goats. Journal of Pathology, 98:83-87.

 

[[Category:To Do - CABI review]]
[[Category:Morbilliviruses]]