WikiVet English - User contributions [en]

Polyomavirus

2016-06-16T00:15:22Z

Kitnmre:

{{OpenPagesTop}}
Also known as: '''''Avian Polyomavirus — APV — Budgerigar Fledgling Disease Virus — BFD — BFDV — French Moult '''''

==Introduction==
APV was first isolated from '''Budgerigars''' from aviaries in the US and Canada in the early 1980s experiencing a high incidence of '''nestling mortality'''. It was subsequently shown to cause disease in love-birds, parrots, several species of passerines and various other wild birds.

A second avian polyomavirus called '''Goose Haemorrhagic Polyomavirus''' (GHP) was found in farm-raised geese in France in the year 2000. It is closely related to APV.

Infection in wild and captive-raised birds is widespread. All psittacine birds and many other species of birds are susceptible to infection. Disease is generally limited to Budgerigar and lovebird nestlings and hand-fed nestling parrots. It is seen less commonly in Amazon parrots and cockatoos.

APV is a non-envelopped, icosahedral virus that has a circular double-stranded DNA genome. There is little evidence to suggest any host specificity of the virus.

==Epidemiology==
Infections in susceptible non-Budgerigar species that are of the appropriate age result in a rapidly fatal disease, but slightly older nestlings survive and shed virus in faeces and possibly through feather dander for up to 16 weeks. The birds are important sources of infection for other birds.

In Budgerigars, shedding is believed to continue for '''up to 6 months'''. Concurrent APV and [[Psittacine Beak and Feather Disease]] virus infection may permit persistent shedding of APV.

Infection occurs through the '''respiratory tract''' and the mixing of birds at shows and sales and stocking pet shops with birds from multiple sources perpetuates infections.

The virus is also believed to be '''environmentally stable''' and can persist from one year to the next in nests.

==Clinical Signs==
The commonest presenting sign in Budgerigar aviaries is a '''sudden onset mortality''' in chicks 10-20 days old.

Live nestlings are stunted, have a distended abdomen and '''feather dystrophy'''.

Some nestlings survive with only feather dystrophy: grossly, primary wing [[Feather - Anatomy & Physiology|feathers]] and tail feathers are either absent entirely or have thick sheaths and there may be '''haemorrhage in their shafts'''.

These birds are sometimes also infected with '''Psittacine Beak and Feather Disease Virus'''.

In nestling parrots, most affected birds die suddenly. Clinical signs last less than 24 hours and include: weakness, pallor, '''subcutaneous haemorrhage''', anorexia, dehydration and crop stasis.

==Diagnosis==
Histologically, finding the characteristic lesions and '''inclusion bodies''' is diagnostic. Within the growing feather there is often massive infection of the cells in the zone of differentiation with inclusion bodies in nearly every cell. Inclusions in the epidermis of the skin can also be present.

'''Swabbing''' affected organs and submitting the swab for DNA probe testing is definitive, and, in cases with poorly developed lesions, may be the only way of making a positive diagnosis.

'''Cloacal and oral swabs''' may be assessed by PCR for the presence of polyomavirus.

Serology is of little use in predicting virus shedding as antibody titres persist for years and possibly for life.

==Treatment and Control==
There is '''no known treatment''' for APV infection.

Control in captive populations of birds is done through management and testing.

Breeding facilities can prevent the introduction of the disease by keeping a closed nursery and the use of '''quarantine and testing'''. Birds should not be expected to be shedding virus after 16 weeks of quarantine.

Birds should also be tested for Psittacine Beak and Feather Disease as this can cause persistend APV shedding.

Budgerigars and lovebirds should not be kept in the same premises as other parrots unless they are all tested.

{{Learning
|flashcards = [[Avian Medicine Q&A 03]]
}}

==References==

Schmidt, R. E. (2003) '''Pathology of pet and aviary birds''' ''Wiley-Blackwell''

Thomas, D. (2007) '''Infectious diseases of wild birds''' ''John Wiley and Sons''

{{review}}

{{OpenPages}}

[[Category:Viral Organisms]]
[[Category:Avian Viruses]]
[[Category:Expert Review - Bird]]

Category:Togaviridae

2016-06-16T00:14:09Z

Kitnmre:

{{frontpage
|pagetitle =Togaviridae
|pagebody = Togaviruses are so called because of their "cloak-like" appearance. They are often viruses that move through multiple hosts, as in the example of Equine Encephalitis Virus, which is transferred via vector to the horse and also has zoonotic potential
|contenttitle =Content
|contentbody =<big>
 
<categorytree mode=pages>Togaviridae</categorytree>
|logo =Alphavirus.gif
}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00121.asp Equine Viral Encephalitides]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Rhabdoviridae

2016-06-16T00:12:40Z

Kitnmre:

{{frontpage
|pagetitle =Rhabdoviridae
|pagebody =<div style="text-align: left; direction: ltr; margin-left: 1em;">
[[Rabies]] is a neurological killer that has evolved a fool-proof technique of transmission, and it cleverly evades the species barrier to present a potent threat to mammalian life. While the simplicity of the virus ensures its transmission, it also contributes to its weakness: its monoclonal antigenicity means that a single vaccination covers all strains of the disease. Though rabies is considered endemic in parts of the developed and undeveloped world, vaccination schemes have rendered the disease controllable to a satisfactory degree. Nonetheless, infection is still largely fatal and the disease should not be taken lightly.
</div>
|contenttitle =Content
|contentbody =<big>
 
<categorytree mode=pages>Rhabdoviridae</categorytree>
|logo =Vesicular stomatitis virus logo.png
}}

==Morphology==
*Large, enveloped, negative-sense RNA virus
*'''Bullet-shaped''' with short glycoprotein spikes

==Types and Subtypes==
Two Genera:
#Lyssaviruses: 7 genotypes
##'''Genotype 1''' is '''classical rabies'''
##Genotypes 2-7 more limited in distribution
##Genotype 4 infects '''insectivorous bats'''
#Vesiculoviruses are all '''exotic''' to the UK:
##[[Vesicular Stomatitis Virus]]
##Ephemeral Fever
##Fish Rhabdoviruses, such as viral hemorrhagic syndrome and infectious haematopoetic necrosis virus

{{Learning |Vetstream = [https://www.vetstream.com/felis/Content/Bug/bug00214.asp Rabies][https://www.vetstream.com/equis/Content/Disease/dis01018.asp Vesicular Stomatitis Virus]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Rhabdoviridae

2016-06-16T00:11:28Z

Kitnmre:

{{frontpage
|pagetitle =Rhabdoviridae
|pagebody =<div style="text-align: left; direction: ltr; margin-left: 1em;">
[[Rabies]] is a neurological killer that has evolved a fool-proof technique of transmission, and it cleverly evades the species barrier to present a potent threat to mammalian life. While the simplicity of the virus ensures its transmission, it also contributes to its weakness: its monoclonal antigenicity means that a single vaccination covers all strains of the disease. Though rabies is considered endemic in parts of the developed and undeveloped world, vaccination schemes have rendered the disease controllable to a satisfactory degree. Nonetheless, infection is still largely fatal and the disease should not be taken lightly.
</div>
|contenttitle =Content
|contentbody =<big>
 
<categorytree mode=pages>Rhabdoviridae</categorytree>
|logo =Vesicular stomatitis virus logo.png
}}

==Morphology==
*Large, enveloped, negative-sense RNA virus
*'''Bullet-shaped''' with short glycoprotein spikes

==Types and Subtypes==
Two Genera:
#Lyssaviruses: 7 genotypes
##'''Genotype 1''' is '''classical rabies'''
##Genotypes 2-7 more limited in distribution
##Genotype 4 infects '''insectivorous bats'''
#Vesiculoviruses are all '''exotic''' to the UK:
##[[Vesicular Stomatitis Virus]]
##Ephemeral Fever
##Fish Rhabdoviruses, such as viral hemorrhagic syndrome and infectious haematopoetic necrosis virus

{{Learning |Vetstream = [https://www.vetstream.com/felis/Content/Bug/bug00214.asp Rabies]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Retroviridae

2016-06-16T00:09:58Z

Kitnmre:

{{frontpage
|pagetitle =Retroviridae
|pagebody = Retroviruses are persistent, non-cytopathic, systemic viruses that give rise to secondary disease, such as tumors, immune-complex disease, or immunosuppression.
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Retroviridae</categorytree>

|logo =FeLV logo.jpg
}}

{{Learning |Vetstream = [https://www.vetstream.com/felis/Content/Bug/bug60015.asp Feline Immunodeficiency Virus][https://www.vetstream.com/felis/Content/Bug/bug60014.asp Feline Leukemia Virus]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Reoviridae

2016-06-16T00:08:18Z

Kitnmre:

{{frontpage
|pagetitle =Reoviridae
|pagebody =Reoviridae include rotaviruses and orbiviruses, such as African Horse Sickness and Bluetongue. Pathogenesis ranges from acute alimentary infections to infections of the vascular endothelium. "REO" stands for "Respiratory-Enteric-Orphan."
|contenttitle =Content
|contentbody =<big>
 
<categorytree mode=pages>Reoviridae</categorytree>
|logo =Rotavirus logo.jpg
}}

==Morphology==
*All are non-enveloped dsRNA viruses
*Spherical and medium-sized with characteristic appearances
*Segmented genome, with each segment encoding a separate viral protein

==Virulence and Pathogenesis==
*Reoviridae are '''resistant''' viruses that can persist in the environment for several weeks

==Epidemiology==
*Many reoviruses infect domestic animals without causing disease
*They have been implicated in stunting syndrome of chickens

{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00556.asp African Horse Sickness]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Poxviridae

2016-06-16T00:06:36Z

Kitnmre:

{{frontpage
|pagetitle =Poxviridae
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
Poxviruses are among the most easily recognized of all viruses, owing to the lesion by which they have gained their name. Once inside cell, they cause proliferation then lysis, giving way to a characteristic pock with a necrotic center. Poxviruses have risen to fame both for their ability to be eradicated (small pox) as well as their use in fighting other viruses (canarypox vaccines).
</div>
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Poxviridae</categorytree>
:''Small pox (variola)''
:''Pigeon pox''
:''Canary pox''
:''Camel pox''
:''Monkey pox''
:''Red squirrel parapox''
:''Red/Gray squirrel pox''
|logo =Orf logo.jpg
}}

==Morphology==
*Huge (up to 450nm), usually enveloped viruses, with a complex capsid symmetry
*Up to 30 different structural proteins
*Non-structural proteins:
**'''Viral epidermal growth factor''', which stimulates cell growth causing the raised edge of pustule
**'''Viral tumor necrosis factor''', which is non-functioning and acts as an anti-inflammatory by competing with TNF-alpha
**'''Viral IL-10''', which reduces the Th-1 cell mediated response

==Therapeutic Use==
Recombinant Vaccines
*Poxviruses can be used as heat-stable vectors for vaccines against other viruses
*Grown in host cell lines or on the surface of chick chorioallantoic membranes in ovo (primordial ectoderm)
*This was first accomplished by the recombination of cowpox and variola (smallpox) in the creation of the smallpox vaccine (vaccinia)
*More recently, the French used this technique in the creation of the oral rabies vaccine used among the wild fox population:
**Recombinant virus inserts a plasmid encoding rabies gene in place of thymidine kinase gene
*Canarypox vaccines now exist for [[Feline Leukemia Virus|FeLV]] and [[Rhabdoviridae|Rabies]]
**Undergoes a single cycle of replication without producing infectious virus in mammals

==Virulence and Pathogenesis==
*Primary replication in abraded squamous epithelium
*Viremia followed by multiple epidermal infections
*Ballooning then necrosis (hydropic degeneration) of epidermal cells
*Concurrent proliferation or adjacent epidermis (GF driven), creating more cells for the virus to infect
*All three result in classical sequence of lesions:
**Papule (proliferation)
**Vesicle (fluid filled)
**Pustule (lesion breaks)
**Scab formation (healing begins)
*Pock center can succumb to secondary infection
*Resolution in 3-4 weeks
*Some poxviruses can spread to the upper respiratory tract or viscera, causing more serious pathology

==Epidemiology==
*Spread quickly in unhygienic circumstances
*Can survive for years in dust

==Diagnosis==
*Clinical signs
*Histology
*Electron microscopy
*PCR, IIF

==Types and Subtypes==
* 6 Genera, all of which produce pox lesions
*Subdivided based on external structure by EM

{{Learning |Vetstream = [https://www.vetstream.com/felis/Content/Bug/bug60019.asp Feline Pox Virus][https://www.vetstream.com/lapis/Content/Freeform/fre00374.asp Rabbitpox]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Parvoviridae

2016-06-16T00:02:13Z

Kitnmre:

{{frontpage
|pagetitle =Parvoviridae
|pagebody = Parvoviruses are cleverly named for their extreme size (parve=small). They are species-specific and serious gastroenteric infections.
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Parvoviridae</categorytree>
|logo =Parvovirus logo.jpg
}}

=Morphology=
*Small, non-enveloped, icosahedral DNA virus with featureless virions

=Virulence and Pathogenesis=
*Resistant to pH (even gastric acidity), heat, and desiccation
*Infect rapidly dividing cells
*Target bone marrow, intestinal epithelium, and growing fetus (via viremia)
*Causes [[Parvovirus Enteritis|Parvovirus Enteritis]]

=Epidemiology=
*Can persist for years in the environment

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00213.asp Canine Parvovirus][https://www.vetstream.com/felis/Content/Bug/bug60013.asp Feline Panleukopenia]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Paramyxoviridae

2016-06-16T00:00:10Z

Kitnmre:

{{frontpage
|pagetitle =Paramyxoviridae
|pagebody =
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Paramyxoviridae</categorytree>
|logo =
}}

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00215.asp Canine Distemper][https://www.vetstream.com/canis/Content/Bug/bug00210.asp Canine Parainfluenza Virus 2]}}

[[Category:Viral Organisms]]

Category:Papillomaviridae

2016-06-15T23:57:30Z

Kitnmre:

{{frontpage
|pagetitle =Papillomaviridae
|pagebody = Papillomaviruses infect keratinized cells, giving rise to sarcoids, warts, and papillomas.
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Papillomaviridae</categorytree>
|logo =Papilloma virus logo.jpg
}}

==Morphology==
*Medium-sized, icosahedral, non-enveloped dsDNA viruses

==Virulence and Pathogenesis==
*Target actively-dividing cells
*Warts: genes expressed are associated with '''transformation''' (hyperplasia and delayed maturation)
*Virus is shed as cells exfoliate
*Oral papillomas in young animals often resolve spontaneously

==Epidemiology==
*'''Resistant''' viruses: can persist in environment for months
*Restricted to stratified squamous and mucosal epithelia with slow growth
*Usually species specific

==Types and Subtypes==

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00346.asp Canine Papillomavirus] [https://www.vetstream.com/equis/Content/Disease/dis01021.asp Equine Papillomatosis][https://www.vetstream.com/lapis/Content/Bug/bug00346.asp Rabbit Papillomatosis][https://www.vetstream.com/felis/Content/Bug/bug00346.asp Feline Sarcoids]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Papillomaviridae

2016-06-15T23:57:05Z

Kitnmre:

{{frontpage
|pagetitle =Papillomaviridae
|pagebody = Papillomaviruses infect keratinized cells, giving rise to sarcoids, warts, and papillomas.
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Papillomaviridae</categorytree>
|logo =Papilloma virus logo.jpg
}}

==Morphology==
*Medium-sized, icosahedral, non-enveloped dsDNA viruses

==Virulence and Pathogenesis==
*Target actively-dividing cells
*Warts: genes expressed are associated with '''transformation''' (hyperplasia and delayed maturation)
*Virus is shed as cells exfoliate
*Oral papillomas in young animals often resolve spontaneously

==Epidemiology==
*'''Resistant''' viruses: can persist in environment for months
*Restricted to stratified squamous and mucosal epithelia with slow growth
*Usually species specific

==Types and Subtypes==

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00346.asp Canine Papillomavirus] [https://www.vetstream.com/equis/Content/Disease/dis01021.asp Equine Papillomatosis][https://www.vetstream.com/lapis/Content/Bug/bug00346.asp Rabbit Papillomatosis][https://www.vetstream.com/felis/Content/Bug/bug00346.asp Feline Sarcoids]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Orthomyxoviridae

2016-06-15T23:54:13Z

Kitnmre:

{{frontpage
|pagetitle =Orthomyxoviridae
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
Influenza is a largely species-specific infection, but the threat of zoonotic potential is real. Virulence varies between strains, but all are spread by aerosol routes. They are typified by rhinitis, pyrexia, and anemia. Flu presents a particular challenge to vaccination as antigenic drift within the virus means that strains can vary from one year to the next. As such, vaccine produced from this year's virus may not give protection against next year's virus.
</div>
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Orthomyxoviridae</categorytree>
|logo =Equine influenza logo.jpg
}}

==Morphology==
*Enveloped, single-stranded RNA negative sense virus with a different gene on each of its 8 segments
*Each gene codes for one protein:
**Haemagglutinin ('''H''') spike
**Neuraminidase ('''N''') spike
**Matrix, which lines the envelope and acts as scaffolding
**Nucleic acid
**3 viral polymerases
**1 large non-structural protein
*Each strain of flu is named according to it's '''H''' and '''N''' number, eg. H5N1
**Haemagglutinin binds virus to respiratory epithelia via sialic acid
**Neuraminidase is a sialidase enzyme that prevents reattachment to the same host cell upon detachment

==Virulence==
Virulence depends on the tropism of the H molecule involved:
*H is formed by the cleavage of a precursor protein H0
*Cleavage typically happens in respiratory or enteric epithelia
*However, a virulent virus has more basic amino acids at it's H0 cleavage site, leaving it open for cleavage by other cells, such as neurons

==Types and Subtypes==
*Three genuses of Flu exist: A, B, and C, of which only A is of veterinary interest
*The subtype of a flu virus is described in terms of H (of H1-H15) and N (of N1 to N9)
*Subtype by species:
**Ducks: H1-H15
**Equine: H7 (previously Equine type 1) and H3 (previously Equine type 2)
**Harp seals: H4 and H7
**Pigs: H1, H3, H4, H5 (Asian), H9
**Human: H1-3, H7, H9
*Vaccines cannot cross protect against different subtypes within the same species

==Antigenic Shift and Drift==
*Flu continues to be a feared disease because of it's ability to evolve, both within a particular strain and into new and undefined strains
*'''Shift''' is the more serious of antigenic movements and is definied by:
**Gene reassortment
**Change of species specificity
*'''Drift''' is the evolution of a virus within its subtype, evidenced by the changing strains of human flu from year to year
**Each H spike carries 4 antigenic regions, and a change in any region results in drift
**Viral RNA is constantly evolving to evade immune detection and destruction
*Vaccination schemes are affected by both shift and drift:
**Complete change of H spike renders current vaccinations useless, and is the cause of an epidemic
**Current vaccines are always modeled on the most recent outbreaks of the flu in question, and cannot therefore protect against the evolution of the virus from year to year
**Partial protection can be provided against strains within the same ''subtype'', hence the continuation of vaccination shemes

==Literature Search==
[[File:CABI logo.jpg|left|90px]]

Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
 
[http://www.cabi.org/cabdirect/FullTextPDF/2006/20063206644.pdf '''Influenza in horses, birds, and humans.''' Naylor, J. M.; Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada, Large Animal Veterinary Rounds, 2004, 4, 6, pp 1-5, 18 ref. - '''Full Text Article''']

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Factsheets/FactSheet218.asp Canine Influenza] [https://www.vetstream.com/felis/Content/Bug/bug60085.asp Avian Influenza] [https://www.vetstream.com/equis/Content/Disease/dis00586.asp Equine Influenza]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Orthomyxoviridae

2016-06-15T23:53:32Z

Kitnmre:

{{frontpage
|pagetitle =Orthomyxoviridae
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
Influenza is a largely species-specific infection, but the threat of zoonotic potential is real. Virulence varies between strains, but all are spread by aerosol routes. They are typified by rhinitis, pyrexia, and anemia. Flu presents a particular challenge to vaccination as antigenic drift within the virus means that strains can vary from one year to the next. As such, vaccine produced from this year's virus may not give protection against next year's virus.
</div>
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Orthomyxoviridae</categorytree>
|logo =Equine influenza logo.jpg
}}

==Morphology==
*Enveloped, single-stranded RNA negative sense virus with a different gene on each of its 8 segments
*Each gene codes for one protein:
**Haemagglutinin ('''H''') spike
**Neuraminidase ('''N''') spike
**Matrix, which lines the envelope and acts as scaffolding
**Nucleic acid
**3 viral polymerases
**1 large non-structural protein
*Each strain of flu is named according to it's '''H''' and '''N''' number, eg. H5N1
**Haemagglutinin binds virus to respiratory epithelia via sialic acid
**Neuraminidase is a sialidase enzyme that prevents reattachment to the same host cell upon detachment

==Virulence==
Virulence depends on the tropism of the H molecule involved:
*H is formed by the cleavage of a precursor protein H0
*Cleavage typically happens in respiratory or enteric epithelia
*However, a virulent virus has more basic amino acids at it's H0 cleavage site, leaving it open for cleavage by other cells, such as neurons

==Types and Subtypes==
*Three genuses of Flu exist: A, B, and C, of which only A is of veterinary interest
*The subtype of a flu virus is described in terms of H (of H1-H15) and N (of N1 to N9)
*Subtype by species:
**Ducks: H1-H15
**Equine: H7 (previously Equine type 1) and H3 (previously Equine type 2)
**Harp seals: H4 and H7
**Pigs: H1, H3, H4, H5 (Asian), H9
**Human: H1-3, H7, H9
*Vaccines cannot cross protect against different subtypes within the same species

==Antigenic Shift and Drift==
*Flu continues to be a feared disease because of it's ability to evolve, both within a particular strain and into new and undefined strains
*'''Shift''' is the more serious of antigenic movements and is definied by:
**Gene reassortment
**Change of species specificity
*'''Drift''' is the evolution of a virus within its subtype, evidenced by the changing strains of human flu from year to year
**Each H spike carries 4 antigenic regions, and a change in any region results in drift
**Viral RNA is constantly evolving to evade immune detection and destruction
*Vaccination schemes are affected by both shift and drift:
**Complete change of H spike renders current vaccinations useless, and is the cause of an epidemic
**Current vaccines are always modeled on the most recent outbreaks of the flu in question, and cannot therefore protect against the evolution of the virus from year to year
**Partial protection can be provided against strains within the same ''subtype'', hence the continuation of vaccination shemes

==Literature Search==
[[File:CABI logo.jpg|left|90px]]

Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
 
[http://www.cabi.org/cabdirect/FullTextPDF/2006/20063206644.pdf '''Influenza in horses, birds, and humans.''' Naylor, J. M.; Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada, Large Animal Veterinary Rounds, 2004, 4, 6, pp 1-5, 18 ref. - '''Full Text Article''']

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Factsheets/FactSheet218.asp Canine Influenza] [https://www.vetstream.com/felis/Content/Bug/bug60085.asp Avian Influenza] [https://www.vetstream.com/equis/Content/Disease/dis00586.asp Equine Influenza]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Orthomyxoviridae

2016-06-15T23:52:54Z

Kitnmre:

{{frontpage
|pagetitle =Orthomyxoviridae
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
Influenza is a largely species-specific infection, but the threat of zoonotic potential is real. Virulence varies between strains, but all are spread by aerosol routes. They are typified by rhinitis, pyrexia, and anemia. Flu presents a particular challenge to vaccination as antigenic drift within the virus means that strains can vary from one year to the next. As such, vaccine produced from this year's virus may not give protection against next year's virus.
</div>
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Orthomyxoviridae</categorytree>
|logo =Equine influenza logo.jpg
}}

==Morphology==
*Enveloped, single-stranded RNA negative sense virus with a different gene on each of its 8 segments
*Each gene codes for one protein:
**Haemagglutinin ('''H''') spike
**Neuraminidase ('''N''') spike
**Matrix, which lines the envelope and acts as scaffolding
**Nucleic acid
**3 viral polymerases
**1 large non-structural protein
*Each strain of flu is named according to it's '''H''' and '''N''' number, eg. H5N1
**Haemagglutinin binds virus to respiratory epithelia via sialic acid
**Neuraminidase is a sialidase enzyme that prevents reattachment to the same host cell upon detachment

==Virulence==
Virulence depends on the tropism of the H molecule involved:
*H is formed by the cleavage of a precursor protein H0
*Cleavage typically happens in respiratory or enteric epithelia
*However, a virulent virus has more basic amino acids at it's H0 cleavage site, leaving it open for cleavage by other cells, such as neurons

==Types and Subtypes==
*Three genuses of Flu exist: A, B, and C, of which only A is of veterinary interest
*The subtype of a flu virus is described in terms of H (of H1-H15) and N (of N1 to N9)
*Subtype by species:
**Ducks: H1-H15
**Equine: H7 (previously Equine type 1) and H3 (previously Equine type 2)
**Harp seals: H4 and H7
**Pigs: H1, H3, H4, H5 (Asian), H9
**Human: H1-3, H7, H9
*Vaccines cannot cross protect against different subtypes within the same species

==Antigenic Shift and Drift==
*Flu continues to be a feared disease because of it's ability to evolve, both within a particular strain and into new and undefined strains
*'''Shift''' is the more serious of antigenic movements and is definied by:
**Gene reassortment
**Change of species specificity
*'''Drift''' is the evolution of a virus within its subtype, evidenced by the changing strains of human flu from year to year
**Each H spike carries 4 antigenic regions, and a change in any region results in drift
**Viral RNA is constantly evolving to evade immune detection and destruction
*Vaccination schemes are affected by both shift and drift:
**Complete change of H spike renders current vaccinations useless, and is the cause of an epidemic
**Current vaccines are always modeled on the most recent outbreaks of the flu in question, and cannot therefore protect against the evolution of the virus from year to year
**Partial protection can be provided against strains within the same ''subtype'', hence the continuation of vaccination shemes

==Literature Search==
[[File:CABI logo.jpg|left|90px]]

Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
 
[http://www.cabi.org/cabdirect/FullTextPDF/2006/20063206644.pdf '''Influenza in horses, birds, and humans.''' Naylor, J. M.; Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada, Large Animal Veterinary Rounds, 2004, 4, 6, pp 1-5, 18 ref. - '''Full Text Article''']

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Factsheets/FactSheet218.asp Canine Influenza] [https://www.vetstream.com/felis/Content/Bug/bug60085.asp Avian Influenza] [https://www.vetstream.com/equis/Content/Disease/dis00586.asp Equine Influenza]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Equine Influenza

2016-06-15T23:50:30Z

Kitnmre:

{{OpenPagesTop}}
Also known as: '''''Equine Flu'''''

== Introduction ==

There are two subtypes of Equine Influenza described in the world today. These are:

*H7N7 (Equine 1), which was prevalent in the UK between 1963-1977
*H3N8 (Equine 2), or the European strains, have been circulating since 1965.

Aerosol and fomite transmission infects the epithelium of the upper respiratory tract, resulting in cell necrosis, which then manifests as [[Bronchiolitis|bronchiolitis]] and serous exudation. There is a 1 - 3 day incubation period, with excretion of the virus in nasal secretions peaking at 3-4 days and finishing by 10 days.

The disease usually occurs as an outbreak with many horses on the yard becoming infected. The most common age to encounter the disease is around 2 years and stress is a predisposing factor, so this disease is most commonly seen in racing yards.

== Clinical Signs ==

There will be a harsh dry cough with pyrexia (39-410>C / 103-106F). The horse will appear generally depressed with a loss of appetite and decreased activity. Submandibular lymph nodes will be enlarged on physical examination. Secondary bacterial infection can follow defective muco-ciliary transport, eg ''[[Streptococcus zooepidemicus]]''.

== Diagnosis ==

Virus isolation by deep nasal swabs (12 inches) deposited into 10ml of transport medium and transported at 40C. An antigen detection [[ELISA testing|ELISA]] should then be performed. Blood samples for serology should also be taken on day one of the disease (acute phase) and then two weeks later (convalescent stage). A 4-fold increase of haemaglutination inhibition (HI) must be shown to confirm diagnosis.

== Treatment and Control ==

Isolate coughing horses at once to minimize spread and perform thorough disinfection of all shared tack, stables, vehicles, boot and feed buckets. Treat any secondary bacterial infections with suitable antibiotics.

Control for this disease is by [[Vaccines|vaccination]]. All vaccines include H7 and varieties of the current circulating strains of H3. There are strict rules from the Jockey Club regarding timing of vaccinations: Horses must be certified as completing a vaccination course of 3 injections at least 8 days prior to racing. The course consists of a primary inoculation followed by a second within '''21-92 '''days and a third after a further '''150-215 '''days. Boosters are given annually on or before the anniversary of the third injection to maintain immunity, and in the event a year is missed, the initial course of three injections must be repeated.

== References ==

Brown, C.M, Bertone, J.J. (2002) The 5-Minute Veterinary Consult- Equine', Lippincott, Williams & Wilkins

Knottenbelt, D.C. A Handbook of Equine Medicine for Final Year Students University of Liverpool

Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders.

{{review}}

{{OpenPages}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00586.asp Equine Influenza]}}

[[Category:Orthomyxoviridae]] [[Category:Horse_Viruses]] [[Category:Expert_Review - Horse]] [[Category:Respiratory_Viral_Infections]] [[Category:Respiratory_Diseases_-_Horse]]

Category:Orthomyxoviridae

2016-06-15T23:48:32Z

Kitnmre:

{{frontpage
|pagetitle =Orthomyxoviridae
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
Influenza is a largely species-specific infection, but the threat of zoonotic potential is real. Virulence varies between strains, but all are spread by aerosol routes. They are typified by rhinitis, pyrexia, and anemia. Flu presents a particular challenge to vaccination as antigenic drift within the virus means that strains can vary from one year to the next. As such, vaccine produced from this year's virus may not give protection against next year's virus.
</div>
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Orthomyxoviridae</categorytree>
|logo =Equine influenza logo.jpg
}}

==Morphology==
*Enveloped, single-stranded RNA negative sense virus with a different gene on each of its 8 segments
*Each gene codes for one protein:
**Haemagglutinin ('''H''') spike
**Neuraminidase ('''N''') spike
**Matrix, which lines the envelope and acts as scaffolding
**Nucleic acid
**3 viral polymerases
**1 large non-structural protein
*Each strain of flu is named according to it's '''H''' and '''N''' number, eg. H5N1
**Haemagglutinin binds virus to respiratory epithelia via sialic acid
**Neuraminidase is a sialidase enzyme that prevents reattachment to the same host cell upon detachment

==Virulence==
Virulence depends on the tropism of the H molecule involved:
*H is formed by the cleavage of a precursor protein H0
*Cleavage typically happens in respiratory or enteric epithelia
*However, a virulent virus has more basic amino acids at it's H0 cleavage site, leaving it open for cleavage by other cells, such as neurons

==Types and Subtypes==
*Three genuses of Flu exist: A, B, and C, of which only A is of veterinary interest
*The subtype of a flu virus is described in terms of H (of H1-H15) and N (of N1 to N9)
*Subtype by species:
**Ducks: H1-H15
**Equine: H7 (previously Equine type 1) and H3 (previously Equine type 2)
**Harp seals: H4 and H7
**Pigs: H1, H3, H4, H5 (Asian), H9
**Human: H1-3, H7, H9
*Vaccines cannot cross protect against different subtypes within the same species

==Antigenic Shift and Drift==
*Flu continues to be a feared disease because of it's ability to evolve, both within a particular strain and into new and undefined strains
*'''Shift''' is the more serious of antigenic movements and is definied by:
**Gene reassortment
**Change of species specificity
*'''Drift''' is the evolution of a virus within its subtype, evidenced by the changing strains of human flu from year to year
**Each H spike carries 4 antigenic regions, and a change in any region results in drift
**Viral RNA is constantly evolving to evade immune detection and destruction
*Vaccination schemes are affected by both shift and drift:
**Complete change of H spike renders current vaccinations useless, and is the cause of an epidemic
**Current vaccines are always modeled on the most recent outbreaks of the flu in question, and cannot therefore protect against the evolution of the virus from year to year
**Partial protection can be provided against strains within the same ''subtype'', hence the continuation of vaccination shemes

==Literature Search==
[[File:CABI logo.jpg|left|90px]]

Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
 
[http://www.cabi.org/cabdirect/FullTextPDF/2006/20063206644.pdf '''Influenza in horses, birds, and humans.''' Naylor, J. M.; Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada, Large Animal Veterinary Rounds, 2004, 4, 6, pp 1-5, 18 ref. - '''Full Text Article''']

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Herpesviridae

2016-06-15T23:46:45Z

Kitnmre:

{{frontpage
|pagetitle =Herpesviridae
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
Herpes viruses are some of the more difficult viruses to combat as they quite contentedly go latent for long periods of time. They often produce an initial respiratory response but go subclinical until the animal becomes immunosuppressed. Protection against herpes is challenging, as immunity relies on stimulating a CD8+ T-cell response, which is difficult to provoke by conventional vaccination.
</div>
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Herpesviridae</categorytree>
|logo =Herpes logo.jpg
}}

==Morphology==
*Double stranded DNA that becomes a closed circle in the host nucleus
*Remains unintegrated while latent

==Virulence and Pathogenesis==
*Three types of genes involved in replication:
**'''Immediate early genes (IE genes)''': strong promoter of the expression of adjacent viral genes
**'''Early genes''': stimulate viral DN replication; potential cause of lymphoproliferation and tumors in the absence of cell lysis
**'''Late genes''': encode viral structural proteins
***Cause large intranuclear inclusion bodies typical of herpes viruses as capsid proteins are assembled
***Envelope buds through nuclear membrane, containing spike glycoproteins (gA to gE)
***Masses of virus then either lyse or fuse cells, causing ulceration, etc.
*Initial replication in '''respiratory tract'''
*Spread determines pathogenicity:
**Cell-associated spread means that virus is spread by cell fusion
**Can target crucial tissues: brain, placenta, etc
*All become '''latent''' and reactivate under stress
*Reactivation is associated with the presence of '''thymidine kinadse (tk) gene''' (which is deleted in GE vaccines)
**Accelerates DNA synthesis

==Research==
*Some herpes and pox viruses express non-structural proteins known as '''virokines'''
*Virokines appear to help the virus evade the Th-1 response by altering the inflammatory response

==Virus by Species==
{| style="width:60%; height:200px" border="1" align=center
!'''Virus'''
!'''Abbreviation'''
!'''Clinical signs'''
|-
|[[Equine Herpesvirus 1]]
|EHV1
|Respiratory disease, abortion, paresis
|-
|Equine Herpesvirus 2
|EHV2
|Avirulent
|-
|[[Equine Herpesvirus 3]]
|EHV3
|Pustular lesions on genitalia
|-
|Equine Herpesvirus 4
|EHV4
|Mild respiratory disease
|-
|[[Bovine Herpesvirus 1]]

[[Infectious Bovine Rhinotracheitis]] Virus

[[Infectious Pustular Vulvovaginitis]] Virus
|BHV 1

IBVR

IPVV
|IBRV: Upper respiratory disease, abortion

IPVV: Irritant pustular lesions on genitalia
|-
|[[Bovine Herpesvirus 2|Bovine Mammilitis Virus]]
|BHV2 (BHMV)
| Erosive lesions on teat and udder, '''Zoonotic'''
|-
|[[Malignant Catarrhal Fever Virus]]
|MCFV
|Infection of eye and upper respiratory
|-
|[[Suid Herpesvirus 1]] (Pseudorabies)
|PSV
|Respiratory disease, abortion (CNS in piglets, pruritis in cattle)
|-
|Suid Herpesvirus 2 (Porcine Cytomegalovirus)
|PCMV
|Subclinical, atrophic rhinitis
|-
|[[Canine Herpesvirus 1]]
|CHV1
|Fading puppies, repro failure
|-
|[[Feline Herpesvirus 1]]
|FHV1
|Rhinitis, bronchitis
|-
|Channel Catfish virus
|
|Death with hemorrhage
|-
|Koi herpes
|
|Death with gill necrosis
|-
|[[Herpesvirus cyprini]]
|
|Carp pox, also in goldfish
|-
|Elephant endotheiliotropic herpes virus
|
|African elephant: mild, skin papillomas

Indian elephant: FATAL with hemorrhage
|-
|[[Gallid Herpesvirus 1]]
|MDV
|Lymphoproliferative, invades CNS, visceral tumors
|-
|Gallid Herpesvirus 2
|HVT
|Avirulent, protective
|-
|Gallid Herpesvirus 3 (Infectious Laryngo-tracheitis)
|AHV1 (ILT)
|Tracheitis and bronchitis
|-
|[[Duck Plague Virus]]
|
|Endothelial and enteric lesions
|-
|Pigeon Herpesvirus
|
|Respiratory disease
|-
|[[Mareks Disease]]
|MDV
|Paralysis, encephalitis
|-
|Psittacid and Raptor Herpes
|
|Death with yellow diarrhoea and coma
|-
|Herpesvirus B (Monkeys)
|
|Potential zoonosis; oral ulcers in Asiatic monkeys, fatal encephalitis in man
|}

==Pathology==
Liver herpesvirus infections:
:Look for the intranuclear inclusions in surrounding surviving hepatocytes

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00212.asp Canine Herpesvirus][https://www.vetstream.com/felis/Content/Disease/dis60009.asp Feline Herpesvirus][https://www.vetstream.com/equis/Content/Bug/bug00053.asp Equine Herpesvirus]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Herpesviridae

2016-06-15T23:46:05Z

Kitnmre:

{{frontpage
|pagetitle =Herpesviridae
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
Herpes viruses are some of the more difficult viruses to combat as they quite contentedly go latent for long periods of time. They often produce an initial respiratory response but go subclinical until the animal becomes immunosuppressed. Protection against herpes is challenging, as immunity relies on stimulating a CD8+ T-cell response, which is difficult to provoke by conventional vaccination.
</div>
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Herpesviridae</categorytree>
|logo =Herpes logo.jpg
}}

==Morphology==
*Double stranded DNA that becomes a closed circle in the host nucleus
*Remains unintegrated while latent

==Virulence and Pathogenesis==
*Three types of genes involved in replication:
**'''Immediate early genes (IE genes)''': strong promoter of the expression of adjacent viral genes
**'''Early genes''': stimulate viral DN replication; potential cause of lymphoproliferation and tumors in the absence of cell lysis
**'''Late genes''': encode viral structural proteins
***Cause large intranuclear inclusion bodies typical of herpes viruses as capsid proteins are assembled
***Envelope buds through nuclear membrane, containing spike glycoproteins (gA to gE)
***Masses of virus then either lyse or fuse cells, causing ulceration, etc.
*Initial replication in '''respiratory tract'''
*Spread determines pathogenicity:
**Cell-associated spread means that virus is spread by cell fusion
**Can target crucial tissues: brain, placenta, etc
*All become '''latent''' and reactivate under stress
*Reactivation is associated with the presence of '''thymidine kinadse (tk) gene''' (which is deleted in GE vaccines)
**Accelerates DNA synthesis

==Research==
*Some herpes and pox viruses express non-structural proteins known as '''virokines'''
*Virokines appear to help the virus evade the Th-1 response by altering the inflammatory response

==Virus by Species==
{| style="width:60%; height:200px" border="1" align=center
!'''Virus'''
!'''Abbreviation'''
!'''Clinical signs'''
|-
|[[Equine Herpesvirus 1]]
|EHV1
|Respiratory disease, abortion, paresis
|-
|Equine Herpesvirus 2
|EHV2
|Avirulent
|-
|[[Equine Herpesvirus 3]]
|EHV3
|Pustular lesions on genitalia
|-
|Equine Herpesvirus 4
|EHV4
|Mild respiratory disease
|-
|[[Bovine Herpesvirus 1]]

[[Infectious Bovine Rhinotracheitis]] Virus

[[Infectious Pustular Vulvovaginitis]] Virus
|BHV 1

IBVR

IPVV
|IBRV: Upper respiratory disease, abortion

IPVV: Irritant pustular lesions on genitalia
|-
|[[Bovine Herpesvirus 2|Bovine Mammilitis Virus]]
|BHV2 (BHMV)
| Erosive lesions on teat and udder, '''Zoonotic'''
|-
|[[Malignant Catarrhal Fever Virus]]
|MCFV
|Infection of eye and upper respiratory
|-
|[[Suid Herpesvirus 1]] (Pseudorabies)
|PSV
|Respiratory disease, abortion (CNS in piglets, pruritis in cattle)
|-
|Suid Herpesvirus 2 (Porcine Cytomegalovirus)
|PCMV
|Subclinical, atrophic rhinitis
|-
|[[Canine Herpesvirus 1]]
|CHV1
|Fading puppies, repro failure
|-
|[[Feline Herpesvirus 1]]
|FHV1
|Rhinitis, bronchitis
|-
|Channel Catfish virus
|
|Death with hemorrhage
|-
|Koi herpes
|
|Death with gill necrosis
|-
|[[Herpesvirus cyprini]]
|
|Carp pox, also in goldfish
|-
|Elephant endotheiliotropic herpes virus
|
|African elephant: mild, skin papillomas

Indian elephant: FATAL with hemorrhage
|-
|[[Gallid Herpesvirus 1]]
|MDV
|Lymphoproliferative, invades CNS, visceral tumors
|-
|Gallid Herpesvirus 2
|HVT
|Avirulent, protective
|-
|Gallid Herpesvirus 3 (Infectious Laryngo-tracheitis)
|AHV1 (ILT)
|Tracheitis and bronchitis
|-
|[[Duck Plague Virus]]
|
|Endothelial and enteric lesions
|-
|Pigeon Herpesvirus
|
|Respiratory disease
|-
|[[Mareks Disease]]
|MDV
|Paralysis, encephalitis
|-
|Psittacid and Raptor Herpes
|
|Death with yellow diarrhoea and coma
|-
|Herpesvirus B (Monkeys)
|
|Potential zoonosis; oral ulcers in Asiatic monkeys, fatal encephalitis in man
|}

==Pathology==
Liver herpesvirus infections:
:Look for the intranuclear inclusions in surrounding surviving hepatocytes

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00212.asp Canine Herpesvirus][https://www.vetstream.com/felis/Content/Disease/dis60009.asp Feline Herpesvirus][https://www.vetstream.com/equis/Content/Bug/bug00053.asp Equine Herpesvirus]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Flaviviridae

2016-06-15T23:43:25Z

Kitnmre:

{{frontpage
|pagetitle =Flaviviridae
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
This group of viruses has three distinct genera, two of which are of veterinary concern. Flaviviruses, which are endemic vector-borne neurotropic viruses, include louping ill and West Nile Virus. Pestiviruses include Swine Fever and Bovine Virus Diarrhoea and present more hemorrhagic disease. Hepatitis C in man is also grouped in this classification.

Medium sized enveloped viruses
</div>
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Flaviviridae</categorytree>
|logo =
}}

{{Learning |Vetstream = [https://www.vetstream.com/lapis/Content/Bug/bug00361.asp West Nile Virus]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Coronaviridae

2016-06-15T23:41:30Z

Kitnmre:

{{frontpage
|pagetitle =Coronaviridae
|pagebody = Coronaviruses are perhaps most easily identified because of their classic "crown" appearance. They are quite common in the young of most species and can infect a wide range of tissues.
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Coronaviridae</categorytree>
|logo =
}}

==Classification==
Coronaviruses are viruses belonging to the family coronaviridae in the Order Nidovirales. Viruses in this order have a RNA genome ranging in size from 13 kb to 32 kb. Coronavirus genomes range from 26 to 32 kb making them the largest in this order. Coronaviruses are further grouped into two subfamilies namely coronavirinae and torovirinae. Subfamily coronavirinae contains 4 genera namely; alphacoronavirus, betacoronavirus, deltacoronavirus and gammacoronavirus while the subfamily torovirinae contains the genera bafinivirus and torovirus.

==Morphology==
Corona viruses are large, spherical enveloped RNA viruses. They contain a positive sense, single stranded polyadenylated and capped RNA. Their genome encodes for various structural, accessory and viral replication proteins. The structural proteins are hemaglutinin-esterase (HE), spike (S), envelope (E), nucleocaspid (N) and membrane (M) proteins. They can be identified by their '''crowns''', long bulbous widely-spaced spikes formed by the spike proteins.

==Virulence and Pathogenesis==
Pathogenesis varies widely based on each virus, but most commonly cause '''respiratory''' and '''enteric''' disturbances. Those described here will be the enteric variety.

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00211.asp Canine Coronavirus][https://www.vetstream.com/felis/Content/Disease/dis60142.asp Feline Infectious Peritonitis] [https://www.vetstream.com/lapis/Content/Bug/bug00368.asp Rabbit Coronavirus]}}

[[Category:Viral Organisms]]

[[Category:To_Do_-_Clinical/Viruses]]

Category:Coronaviridae

2016-06-15T23:40:44Z

Kitnmre:

{{frontpage
|pagetitle =Coronaviridae
|pagebody = Coronaviruses are perhaps most easily identified because of their classic "crown" appearance. They are quite common in the young of most species and can infect a wide range of tissues.
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Coronaviridae</categorytree>
|logo =
}}

==Classification==
Coronaviruses are viruses belonging to the family coronaviridae in the Order Nidovirales. Viruses in this order have a RNA genome ranging in size from 13 kb to 32 kb. Coronavirus genomes range from 26 to 32 kb making them the largest in this order. Coronaviruses are further grouped into two subfamilies namely coronavirinae and torovirinae. Subfamily coronavirinae contains 4 genera namely; alphacoronavirus, betacoronavirus, deltacoronavirus and gammacoronavirus while the subfamily torovirinae contains the genera bafinivirus and torovirus.

==Morphology==
Corona viruses are large, spherical enveloped RNA viruses. They contain a positive sense, single stranded polyadenylated and capped RNA. Their genome encodes for various structural, accessory and viral replication proteins. The structural proteins are hemaglutinin-esterase (HE), spike (S), envelope (E), nucleocaspid (N) and membrane (M) proteins. They can be identified by their '''crowns''', long bulbous widely-spaced spikes formed by the spike proteins.

==Virulence and Pathogenesis==
Pathogenesis varies widely based on each virus, but most commonly cause '''respiratory''' and '''enteric''' disturbances. Those described here will be the enteric variety.

{{Learning |Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00211.asp Canine Coronavirus][https://www.vetstream.com/felis/Content/Disease/dis60142.asp Feline Infectious Peritonitis] [https://www.vetstream.com/lapis/Content/Bug/bug00368.asp Rabbit Coronavirus]}}

[[Category:Viral Organisms]]

[[Category:To_Do_-_Clinical/Viruses]]

Category:Caliciviridae

2016-06-15T23:37:48Z

Kitnmre:

{{frontpage
|pagetitle =Caliciviridae
|pagebody =
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Caliciviridae</categorytree>
|logo =Calicivirus.jpg
}}

==Morphology==
*Caliciviruses are small, unenveloped, spherical RNA viruses
*They are recognized by '''cup-shaped surface depressions'''

==Virulence and Pathogenesis==
*Caliciviruses are moderately resistant and can survive in the environment for weeks
*They cause respiratory, enteric, and systemic disease
* Calicivirus may contribute to [[Calf Diarrhoea, Undifferentiated Neonatal|undifferentiated neonatal calf diarrhoea]], a mixed viral enteritis in calves.

{{Learning |Vetstream = [https://www.vetstream.com/felis/Content/Bug/bug60018.asp Feline Calicivirus] [https://www.vetstream.com/lapis/Content/Bug/bug60018.asp Rabbit Hemorrhagic Disease Virus]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Birnaviridae

2016-06-15T23:35:13Z

Kitnmre:

Birnaviridae is a family of viruses comprising two genera:-
:'''aquabirnavirus''': the virus of [[Infectious Pancreatic Necrosis|infectious pancreatic necrosis (IPN)]] of salmonid fishes
:'''avibirnavirus''' the virus of [[Infectious Bursal Disease|infectious bursal disease]] of fowls

{{unfinished}}

[[Category:Viral Organisms]]

Category:Astroviridae

2016-06-15T23:34:53Z

Kitnmre:

{{frontpage
|pagetitle =Astroviridae
|pagebody = Astroviridae is a family of viruses comprising two genera:-
:'''avastrovirus''': avastroviruses of types 1-3, including turkey avastrovirus.
:'''mamastrovirus''': mammallian astroviruses of types 1 to 19
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Astroviridae</categorytree>
|logo =
}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Asfarviridae

2016-06-15T23:34:29Z

Kitnmre:

{{frontpage
|pagetitle =Asfarviridae
|pagebody = Asfarviridae contains asfivirus, which is the virus of African Swine Fever. This is a serious exotic virus that should not be confused with [[Classical Swine Fever]].
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Asfarviridae</categorytree>
|logo =ASF logo.jpg
}}

==Morphology==
*Large, enveloped, icosahedral, '''cytoplasmic''' DNA virus

==Virulence and Pathogenesis==
*Infects either '''upper respiratory tract''' or '''skin''' via '''ticks'''
*Enters bloodstream in [[Monocytes|monocytes]]
*Reaches viscera and bone marrow within days
*Induces a '''clotting defect''' and '''hemolysis''' in red blood cells
*Also affects lymphocytes:
**Infects Th cells and causes them not to produce B-stimulating cytokines
**Antigen-stimulated B-cells undergo apoptosis rather than producing antibody
*General cell signal transduction is blocked, decreasing non-specific immunity

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Astroviridae

2016-06-15T23:34:16Z

Kitnmre:

{{frontpage
|pagetitle =Astroviridae
|pagebody = Astroviridae is a family of viruses comprising two genera:-
:'''avastrovirus''': avastroviruses of types 1-3, including turkey avastrovirus.
:'''mamastrovirus''': mammallian astroviruses of types 1 to 19
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Astroviridae</categorytree>
|logo =
}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Freeform/fre00370.asp Bacteriology]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Adenoviridae

2016-06-15T23:32:05Z

Kitnmre:

{{frontpage
|pagetitle =Adenoviridae
|pagebody = Adenoviruses are so named for the tissue from which they were first recovered: human adenoid tissue. Since then they have been found in most species and are generally harmless.
|contenttitle =Content
|contentbody =<big>

<categorytree mode=pages>Adenoviridae</categorytree>
|logo =
}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Bug/bug00020.asp Equine Adenovirus] [https://www.vetstream.com/canis/Content/Bug/bug00207.asp Canine Adenovirus Type 1] [https://www.vetstream.com/canis/Content/Bug/bug00208.asp Canine Adenovirus Type 2]}}

[[Category:Viral Organisms]]
[[Category:To_Do_-_Clinical/Viruses]]

Category:Horse Parasites

2016-06-15T23:19:57Z

Kitnmre:

{{frontpage
|pagetitle = Horse Parasites
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 
[[:Category:Horse Nematodes|Horse Nematodes]]

[[:Category:Horse Protozoa|Protozoa]]

[[:Category:Lice - Horse|Lice]]


[[Anoplocephala]]

[[Fasciola hepatica]]

[[Gasterophilus spp.]]

[[Otobius spp.]]

[[Psoroptes ovis]]
 
 
</big>
|logo=Horse-logo.png}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Parasitology Equine Parasitology]}}

[[Category:Horse]]

Category:Respiratory Diseases - Horse

2016-06-15T23:17:21Z

Kitnmre:

{{frontpage
|pagetitle = Respiratory Diseases of Horses
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 
Infectious:
:[[African Horse Sickness]]
:[[Aspergillosis]]
:[[Equine Influenza]]
:[[Equine Rhinopneumonitis]]
:[[Coccidiosis - Horse|Coccidiosis]]
:[[Equine Rhinovirus]]
:[[Equine Herpesvirus 1]]
:[[Equine Viral Arteritis]]
:[[Glanders]]
:[[Hendra Virus]]
:''[[Rhodococcus equi]]
:[[Strangles]]

Developmental:
:[[Alar Fold Stenosis]]
:[[Wry Nose]]

[[Recurrent Airway Obstruction]]

[[Summer Pasture-Associated Recurrent Airway Obstruction]]

[[Atheroma]]

[[Epistaxis - Horse|Epistaxis]]

[[Exercise Induced Pulmonary Haemorrhage]]

[[Maxillary Cysts]]

[[Nasal Amyloidosis]]

[[Nasal Septum Thickening]]

[[Pulmonary Oedema]]

[[Guttural Pouch Empyema]]

 
 
</big>
|righttitle =Literature Search
|righttext =
{{Template:CABIsmall}}
[http://www.cabi.org/cabdirect/FullTextPDF/2005/20053163998.pdf '''Equine infectious respiratory disease: prevention of disease and control of outbreaks.''' Weese, J. S.; Ontario Veterinary Medical Association, Milton, Canada, Better medicine, better life. OVMA Conference Proceedings 2005, 2005, pp 258-265, 6 ref. - '''Full Text Article''']
}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Respiratory Respiratory]}}

[[Category:Horse - Respiratory System]]
[[Category:WikiClinical Equine]]

Category:Reproductive Diseases - Horse

2016-06-15T23:15:55Z

Kitnmre:

{{frontpage
|pagetitle = Reproductive Diseases of Horses
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 
<categorytree mode=pages>Reproductive Diseases - Horse</categorytree>

 
 
</big>
|logo=Horse-logo.png}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Reproduction Reproduction]}}

[[Category:Horse - Reproductive System]]
[[Category:WikiClinical Equine]]

Category:Neurological Diseases - Horse

2016-06-15T23:14:50Z

Kitnmre:

{{frontpage
|pagetitle =Neurological Diseases of Horses
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">

</div>
|contenttitle =Content
|contentbody =<big>
<categorytree mode=pages>Neurological Diseases - Horse</categorytree>
</big>
|righttitle =Literature Search
|righttext =
{{Template:CABIsmall2}}
[http://www.cabi.org/cabdirect/FullTextPDF/2005/20053192998.pdf ''' Neurologic disease: current topics in-depth.''' Reed, S. M.; Saville, W. J. A.; Schneider, R. K.; American Association of Equine Practitioners (AAEP), Lexington, USA, Proceedings of the 49th Annual Convention of the American Association of Equine Practitioners, New Orleans, Louisiana, USA, 21-25 November 2003, 2003, pp 243-258, 94 ref. - '''Full Text Article''']
}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Neurology Neurology]}}

[[Category:Horse - Nervous System and Special Senses]]
[[Category:WikiClinical Equine]]

Category:Horse - Nervous System and Special Senses

2016-06-15T23:14:25Z

Kitnmre:

{{frontpage
|pagetitle = Horse Nervous System and Special Senses
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 
[[:Category:Neurological Diseases - Horse|Neurological Diseases]]
 
 
</big>
|logo=Horse-logo.png}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Neurology Neurology]}}

[[Category:Horse]]

Category:Alimentary Diseases - Horse

2016-06-15T23:03:22Z

Kitnmre:

{{frontpage
|pagetitle =Alimentary Diseases of Horses
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">
</div>
|contenttitle =Content
|contentbody =<big>
 
<categorytree mode=pages hideroot=on>Alimentary Diseases - Horse</categorytree>

</big>
|logo =Horse 1 logo.jpg
}}

 
 
 
 
 
 
 
 
 
 
 

{{Learning |Vetstream = [https://www.vetstream.com/equis/search?s=gastrointestinal Gastrointestinal]}}

[[Category:Horse - Alimentary System]]
[[Category:WikiClinical Equine]]

Category:Musculoskeletal Diseases - Horse

2016-06-15T22:59:55Z

Kitnmre:

{{frontpage
|pagetitle = Musculoskeletal Diseases of Horses
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 
<categorytree mode=pages>Musculoskeletal Diseases - Horse</categorytree>
 
 
</big>
|logo=Horse-logo.png}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Musculoskeletal Musculoskeletal]}}

[[Category:Horse - Musculoskeletal System]]
[[Category:WikiClinical Equine]]

Category:Horse - Musculoskeletal System

2016-06-15T22:59:22Z

Kitnmre:

{{frontpage
|pagetitle = Horse Musculoskeletal System
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 

[[:Category:Musculoskeletal Diseases - Horse|Musculoskeletal Diseases]]
 
 
</big>
|logo=Horse-logo.png}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Musculoskeletal Musculoskeletal]}}

[[Category:Horse]]

Regenerative and Non-Regenerative Anaemias

2016-06-15T22:57:45Z

Kitnmre:

==Introduction==
Anaemia refers to a reduction in [[Packed Cell Volume|packed cell volume]] (PCV), haemoglobin concentration or the level of total red blood cells. In the clinical approach to the anaemic patient, the initial step is to determine whether the anaemia is regenerative or non-regenerative. Regeneration refers to the production of new erythrocytes from the bone marrow and their subsequent release into the circulation. In dogs, there is a lag period of 48-72 hours before immature red blood cells (reticulocytes and nucleated red blood cells ) begin to appear in the circulation and the extent of the regenerative response is usually in proportion to the severity of the anaemic insult.

==Causes of Anaemia==
The major causes of anaemia are:
#'''Immune-mediated disease''' including [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]], a disease caused by an autoimmune response directed against endogenous erythrocytes, and [[Neonatal Isoerythrolysis|neonatal isoerythrolysis]], the result of a maternal immune response directed against foetal antigens inherited from the sire.
#'''Haemorrhage'''
#'''Haemolysis'''
#'''Anaemia of Chronic Disease'''
#'''Infectious Diseases''', notably:

*[[Equine Infectious Anaemia - Donkey|Equine Infectious Anaemia]] caused by EIA virus.
*Canine and feline infectious anemia caused by ''[[Mycoplasma haemocanis]]'' and ''[[Feline Infectious Anaemia|Mycoplasma haemofelis]]'' respectively. Candidata ''M. haemominutum'' and ''M. turicensis'' may also cause anaemia in cats.
*''[[Leptospira|Leptospira spp.]]'' may cause anaemia, usually when an animal is exposed to a non-host-adapted serovar.
*''[[Babesia|Babesia spp.]]'' may cause anaemia in dogs and cattle.
*''[[Hepatozoon|Hepatozoon spp.]]'' in dogs and pigs.
*''[[Clostridium haemolyticum]]'' causing Redwater Fever in cattle.

==Regenerative or Non Regenerative?==
The following features may be used to determine whether anaemia is regenerative or non-regenerative:
{| cellpadding="10" cellspacing="0" border="1"
| Feature
| Regenerative
| Non-regenerative
| Image
|-
| Mean Corpuscular Volume (MCV)
| '''Increased''' as reticulocytes are larger than mature erythrocytes
| '''Normal'''
|[[File:Polychromatic erythrocyte.png|thumb|150px|Reticulocyte Copyright Arcadian 2006 Wikimedia Commons]]
|-
| Mean Corpuscular Haemoglobin Concentration (MCHC)
| '''Decreased''' as reticulocytes are larger cells and less packed with haemoglobin (as the marrow is trying to produce cells at a faster rate it means they are not as well formed) and they also contain the remnant of the ribosomal RNA that is lost with progressive development of the cell
| '''Normal'''
|[[File:Erythrocyte.png|thumb|150px|Erythrocyte Copyright Arcadian 2006 Wikimedia Commons]]

|-
| Blood Smear
| '''Howell-Jolly bodies''' may be present as small basophilic spots within red blood cells. These represent the remnant of the endoplasmic reticulum of the erythrocyte. 
'''Large polychromatic''' red blood cells may be evident when the smear is stained with a Romanowsky stain. These cells probably represent reticulocytes but this cannot be confirmed unless a smear is also stained with a supra-vital stain such as new methylene blue. This latter procedure can be used to estimate the degree of reticulocytosis and to determine if this is appropriate to the severity of the anaemia.
| The red blood cells are usually normochromic and normocytic but poikilocytosis may be apparent in cases of maturation defect anaemia.
|[[File:Cabotsringbody.jpg|thumb|150px|Image of a Howell Jolly body (B)within a red blood cell Copyright Jarkeld 2009 Wikimedia Commons]]
|}

==Regenerative Anaemia==
The major causes of regenerative anaemia are '''[[Haemorrhage|haemorrhage]]''' and '''haemolysis'''.

===Haemorrhage===
Haemorrhage may occur from any site and it may be external (often due to trauma) or internal. Any form of spontaneous haemorrhage with no apparent cause may suggest the presence of an underlying coagulopathy. The most common haemorrhagic presentations are:
*'''Epistaxis''' due to disruption or erosion of blood vessels of the nasal cavity by trauma, neoplasia, fungal infection or a foreign body.
*'''Haematuria''' which may arise due to haemorrhage from any part of the urinary tract, especially the kidney (due to trauma, neoplasia or idiopathic haematuria) and bladder (due to trauma, cystitis, urolithiasis and neoplasia).
*'''Melaena''', '''haematochezia''' or '''haematemesis''' due to gastro-intestinal haemorrhage. Meleana refers to the production of black tarry faeces with digested blood whereas haematochezia refers to the production of fresh blood with the faeces. Classically, haematemesis is described as resembling 'coffee grounds' as blood is denatured by a low gastric pH but, as the gastric pH of the dog may vary widely between 2 and 6, vomited blood may also appear as fresh red blood.
*'''Haemoptysis''' refers to the production of blood from the respiratory tract. It may occur with severe forms of pneumonia and with pulmonary haemorrhage.
*'''[[Haemoabdomen]]''', '''haemothorax''' and '''haemopericardium''' are all forms of [[Haemorrhagic Effusion|haemorrhagic effusion]] that occur in body cavities.

===Haemolysis===
Haemolysis may occur in the following processes:
*'''Immune-mediated disease''' including [[Immune Mediated Haemolytic Anaemia]] and [[Neonatal Isoerythrolysis]].
*'''Infectious agents''' including ''[[Babesia|Babesia spp.]]'' in dogs and cattle, ''[[Feline Infectious Anaemia|Mycoplasma haemofelis]]'' in cats, ''[[Leptospira|Leptospira spp.]]'' in various species and ''[[Clostridium haemolyticum]]'' causing redwater fever in cattle.
*'''Inherited defects of red blood cells enzymes''' including pyruvate kinase (which is occur most commonly in West Highland white terriers) and phosphofructokinase (PFK).
*'''Hypophosphataemia''' which occurs in post-parturient cattle (causing post-parturient haemoglobinuria), with refeeding syndrome and when animals with [[Diabetes Mellitus|diabetes mellitus]] are stabilised with insulin.
*Exposure to '''toxins''' including rape and kale (which contain SMCO radicals) in cattle, onions and garlic in dogs and paracetamol in cats.
*'''Microangiopathic anaemia''' which occurs when red blood cells are forced through small meshworks of fibrin as with [[Haemangiosarcoma|haemangiosarcomas]], [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation]] (DIC) or bacterial endocarditis.
Haemolysis usually results in a more strongly regenerative response than haemorrhage and can be differentiated by plasma protein concentrations; these will fall with haemorrhage, but not with haemolysis.

==Non-regenerative Anaemia==
The failure to regenerate indicates that there is a failure to produce red blood cells in the bone marrow. Erythrocytes are produced from stem cells in the bone marrow and they then undergo sequential stages of maturation before and after they are released into the circulation.

===Failure of the bone marrow stem cells to produce erythroid cells===
This occurs in the following conditions:
*'''[[Immune Mediated Haemolytic Anaemia|Pure red cell aplasia]]'''
*Aplastic anaemia
*Bone marrow suppression
*Myelophthisis
*Myelodysplasia

===Failure of erythrocyte maturation===
This can occur with:
*Iron deficiency
*Vitamin B12/folate deficiency

{{Learning
|flashcards = [[Feline Medicine Q&A 08]] |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis01203.asp Anemia]
}}

{{review}}

[[Category:Anaemia|A]]
[[Category:Lymphoreticular and Haematopoietic Diseases - Dog]][[Category:Lymphoreticular and Haematopoietic Diseases - Cat]][[Category:Lymphoreticular and Haematopoietic Diseases - Horse]][[Category:Lymphoreticular and Haematopoietic Diseases - Cattle]][[Category:Donkey]][[Category:Lymphoreticular and Haematopoietic Diseases - Sheep]][[Category:Lymphoreticular and Haematopoietic Diseases - Pig]]

Equine Infectious Anemia

2016-06-15T22:55:51Z

Kitnmre:

{{OpenPagesTop}}
Also known as: '''''EIA, Swamp Fever

==Introduction==
Equine Infectious Anaemia (EIA) is an exotic viral disease affecting horses, donkeys and mules characterised by viraemia, anaemia and thrombocytopaenia. The disease is caused by Equine Infectious Anaemia Virus (EIAV), an equid-specific [[:Category:Lentiviruses|lentivirus]] in the [[:Category:Retroviridae|retrovirus]] family that is closely to related to HIV in humans. Cases of EIA in the UK are extremely rare and have previously occurred in horses that have travelled abroad or been imported from areas of endemic disease. In the UK the disease is notifiable and confirmed cases must be humanely destroyed.

==Signalment==
All equids are susceptible to EIA but [[Equine Infectious Anaemia - Donkey|donkeys]] and mules appear to be less severely affected. No breed, age or sex predilection has been reported.

==Pathogenesis==
EIA occurs worldwide but most commonly in countries with warm climates. The virus is usually transmitted via mechanical inoculation of blood via large biting flies such as [[Tabanidae|horseflies (''Tabanid'' spp)]] or stable flies (''[[Stomoxys calcitrans]]''). Additionally, transmission of the virus may occur through saliva, milk, body secretions or via contaminated needles and blood products. The virus may also be passed from pregnant mares to their foals across the placenta.

Viral replication occurs primarily in mature tissue macrophages located in the spleen. These macrophages act as the main source of high-titre viraemia during the course of the disease and also as a reservoir for infection during subclinical infection.
Infection in subclinically affected horses may be reactivated during times of stress, disease or during treatment with immunosuppressive drugs.

==Clinical signs==
The incubation period of the disease ranges from 10 to over 45 days and the clinical presentation is highly variable. EIA occurs in acute and subacute forms in susceptible animals but more commonly assumes a chronic course. However, a large number of affected horses do not display any clinical signs and unapparent carriers may be clinically normal.

In the acute stages, clinical signs may include mucosal petechial and ecchymotic haemorrhages, depression, lymphadenopathy, fever, lethargy and inappetance. In rare cases the disease may result in sudden death. Horses that have been infected for thirty days may display the characteristic signs of EIA including ventral and limb oedema, anemia, bloody diarrhoea, icterus, pyrexia and cachexia.

==Diagnosis==
The 'gold standard' for diagnostic confirmation is an '''agar gel immunodiffusion test (the Coggins test)''' which detects serum antibodies against the EIA virus. The test is 95% accurate for the diagnosis of EIA but false positives may be obtained from foals that have absorbed colostrum from affected mares and false negatives may occur during the acute stages of EIA. The Coggins test may be performed in combination with an '''[[ELISA]]''' or '''PCR''' test in order to increase the test sensitivity.

Additionally, haematology may reveal a moderate to marked [[Regenerative and Non-Regenerative Anaemias|anaemia]], leukopaenia and [[Bilirubin|bilirubinaemia]]. Mild [[Platelet Abnormalities|thrombocytopaenia]] is common in the acute phase of infection.

==Treatment==
No specific treatment or vaccine for EIA is available and strict procedures for affected horses are enforced in the UK. Until the presence of disease has been confirmed by a positive Coggins test, supportive treatment may be provided such as NSAIDs to reduce pyrexia and inflammation. Any horse that is suspected to be infected with EIA must be reported to the appropriate divisional veterinary manager of DEFRA. DEFRA policy is that horses with confirmed EIA must be slaughtered under Section 32 of the Animal Health Act 1981. Horses that have been in close contact with diseased animals must be kept in isolation for 90 days and tested on a monthly basis with regular veterinary assessment. After this period of testing, restrictions may be lifted if no disease is found.

==Control==
Although attenuated live vaccines are available in the United States, these are not in current use in the UK. Acutely affected horses carry high levels of virus in the blood and are a high risk source of infection to other horses so should be isolated immediately if EIA is suspected. All movement of horses on and off the premises must be prevented.

==Prognosis==
Foals exposed to EIAV have a high fatality rate but generally horses recover from the disease, becoming lifelong inapparent carriers. Relapse of the disease may occur during times of stress or illness. The current UK control measures dictate that confirmed cases of EIA carry a grave prognosis.

{{Learning
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=((title:(%22swamp+fever%22))+OR+(title:(%22Equine+Infectious%22+)+AND+(title:(Anaemia)+OR+title:(Anemia)))+OR+(title:(EIA)))+AND+od:(horses)&occuring1=freetext&rowId=2&options2=AND&q2=&occuring2=freetext&rowId=3&options3=AND&q3=&occuring3=freetext&publishedstart=2000&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all&x=50&y=8 Equine Infectious Anaemia publications since 2000]
}}

==References==
*Dwight, C., Hirsh, Y., Zee, Y. C. (1999) '''Veterinary Microbiology''' ''Wiley-Blackwell''
*Higgins, A., Snyder, J. R. (2006) '''The Equine Manual''' ''Elsevier Health Sciences''
*Jain, N. C. (1993) '''Essentials of Veterinary Haematology''' ''Wiley-Blackwell''
*Lavoie, J. P., Hinchcliff, K. W. (2009) '''Blackwell's Five-Minute Veterinary Consult: Equine''' ''John Wiley and Sons''

{{review}}

{{OpenPages}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00071.asp Equine Infectious Anemia]}}

[[Category:Lentiviruses]][[Category:Horse Viruses]]
[[Category:Lymphoreticular and Haematopoietic Diseases - Horse]]
[[Category:Anaemia]]

[[Category:Expert Review]]

Coagulation Factor Deficiency

2016-06-15T22:53:40Z

Kitnmre:

[[Image:2000px-Coagulation full svg.png|right|thumb|325px|'''Coagulation Cascade''' Source: Wikimedia Commons. Author: Joe D (2007)]]
==Introduction==
Factor deficiencies are often the result of congenital deficiency in one or more of the coagulation factors. Deficiencies lead to ineffective blood clotting and development of a disease syndrome characterized by excessive bleeding - deficiencies are often detected following trauma or surgery. Occasionally bleeding may be spontaneous (e.g. into alimentary or urinary tracts). Deficiencies are often seen as familial inherited problems. Haemophilia (factor VIII deficiency) is probably the best understood condition.

==Von Willebrand's Disease==
This condition is seen in the dog, most frequently in Scottish Terriers and Chesapeake Bay Retrievers. It has become more prevalent recently in Dobermanns, Setters and German Shepherd dogs. A similar disease has been recorded in the pig.

Von Willebrand's Disease is an inherited autosomal recessive trait. It is incompletely dominant, so there is variable expression. It can present as purpura and/or prolonged bleeding times. Pathologically, there is reduced platelet adhesiveness and low Factor XIII levels.

The disease can be assessed by the measurement of Von Willebrand Factor protein levels; levels are low in affected animals. The Von Willebrand Factor protein bind to Factor VIII, and is synthesised in endothelial cells and megakaryocytes and stored in platelets.

==Factor I ==
Factor 1 is fibrinogen.
'''Hyperfibrinogenaemia''' occurs in:
* Pregnancy
* Acute infections
* Post-operative states
* Pyometra
'''Hypofibrinogenaemia''' is seen in:
* Liver disease.
* disseminated intravascular coagulation (DIC).

==Factor II ==
Factor II is part of the prothrombin complex.
Hypoprothrombinaemia occurs when there is a lack of the components of the prothrombin complex - factors II, VII, IX, X. This can be caused by dicoumarol and its derivatives, as found in sweet clover and warfarin, which competitively inhibit Vitamin K activity in the liver, where the factors are synthesised.

==Factor IV ==
Factor IV is calcium, which is necessary at several stages of coagulation. Hypocalcaemia at a level sufficient to impair haemostasis is incompatible with life.

==Factor VII==
Factor VII is Proconvertin; deficiencies of factor VII do not appear to impair the formation of the haemostatic plug and any resulting bleeding defect is normally mild. Newborn pups have a very low plasma level of Factor VII and spontaneous and inherited deficiencies have been reported in Beagle colonies. Deficiencies may also occur associated with liver disease and in dicoumarol poisoning.

==Factor VIII ==
Factor VIII is known as antihaemophilic factor (AHF); a deficiency of this factor causes '''haemophilia A'''. In haemophilic conditions:
*The primary thrombocyte plug is abnormal with more vascular channels than usual and less fibrin-collagen contact around the edges.
*Plugs are therefore easily dislodged which results in rebleeding.
*Secondary plugs only form with difficulty.
Haemophilia is reported in horses and in around 20 breeds of dogs - it is known to be a sex-linked recessive condition associated with the X chromosome which affects only males.

The severity of the disease correlates with the Factor VIII levels. Haematomas and haemarthrosis are commonly seen as a result of this condition.

==Factor IX ==
Factor IX is 'Christmas Factor' and deficiency causes '''haemophilia B'''. This occurs presominantly in Cairn Terriers and Black and Tan Hounds. It is similar to Factor VIII deficiency; a sex-linked (X chromosome) recessive that results in a deficient haemostatic plug.

==Factor XI==
Factor XI is an antecedent to plasma Thromboplastin. Deficiencies have been reported in the cow, and reduced levels have been reported in the horse.

==Factor XII==
Factor XII is known as 'Hageman Factor'; low plasma levels had been reported in cats and horses.

{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/Dis01342.asp Coagulation Defects]}}

[[Category:Coagulation Defects]][[Category:Lymphoreticular and Haematopoietic Diseases - Dog]][[Category:Lymphoreticular and Haematopoietic Diseases - Cat]][[Category:Lymphoreticular and Haematopoietic Diseases - Cattle]][[Category:Lymphoreticular and Haematopoietic Diseases - Horse]]
[[Category:Haemorrhagic Diseases]]
[[Category:Cardiology Section]]

Urticaria

2016-06-15T22:51:42Z

Kitnmre:

{{OpenPagesTop}}
==Introduction==
Urticaria is a condition of the skin characterised by the development of multiple flat-topped, oedematous swellings (wheals) in the dermis that dent or 'pit' with digital pressure. Episodes may be acute, chronic or recurrent. The condition occurs in all domestic animals but most commonly in the horse.

==Pathogenesis==
The aetiopathogenesis of urticaria is complex and many causes have been suggested. The basic pathogenesis is thought to be due to degranulation of mast cells and basophils leading to the release of inflammatory mediators and an increase in vascular permeability. This may be due to either an exogenous or endogenous [[Type I Hypersensitivity|type I hypersensitivity]] reaction. Exogenous urticaria may occur as a result of exposure to chemicals, medication and insect bites or stings, shampoos or insecticides. Endogenous urticaria occurs following inhalation of allergens such as pollens. For a large number of cases no underlying cause is identified and these cases are termed idiopathic urticaria.

==Signalment==
Horses between 1 and 10 years of age are most prone to developing the condition. There is no sex predilection but Thoroughbreds and Arabs appear to be more commonly affected than other breeds.

==History and Clinical Signs==
Multiple wheals are often observed and occur within a few minutes or hours of exposure to the causative agent. A history of recurrence or repeated episodes is often reported. Affected areas can vary from small, localised lesions up to 3 cm in diameter, to extensive generalised areas involving large areas of skin. Lesions can occur on any part of the body but usually develop on the back, legs, flanks, neck and eyelids. Dermatographism is a specific pressure-induced type of urticaria in which wheals form in response to exogenous pressure, commonly these are observed in the saddle area of the horse. In severe cases the mucous membranes of the nose, mouth, anus and vulva may be involved. Pruritus may or may not be present and the lesions usually disappear rapidly.

==Diagnosis and Treatment==
Because of the numerous underlying causes of urticaria, definitive diagnosis may be difficult. Historical and clinical findings may lead to suspicion of the condition. The localisation of lesions (e.g. site of contact with saddle or insect repellent) or history of medication or exposure to chemicals may help to determine an underlying cause.

Acute urticaria often resolves spontaneouly without requiring treatment. If urticaria is suspected all current medications should be stopped. Dexamethasone given once usually results in resolution of clinical signs within 24 hours. In rare cases, epinephrine may be required if the urticaria is associated with signs of anaphylaxis.

Recurrent cases may require further investigation in order to determine the underlying cause. This may include further questioning about the animal's history and response to withdrawal of drugs or topical products. If no underlying cause is found, an investigation for allergies is indicated and may include intradermal allergy testing, insect control trials and an elimination (novel protein) diet. Biopsy of lesions is generally unrewarding but helps to rule out vasculitis as an underlying cause of the clinical signs. Antihistamines such as Hydroxyzine may be useful in the management of chronic urticaria but are ineffective in treating the acute form of the condition. Acupuncture has been reported to be effective in one horse.

==Prognosis==
The prognosis with urticaria is dependent on the underlying cause. If this can be identified and removed the prognosis is excellent. Horses with recurrent (idiopathic) urticaria generally have a poor prognosis.

{{Learning
|literature search = [http://www.cabdirect.org/search.html?it=any&q1=urticaria&calendarInput=yyyy-mm-dd&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&options1=AND&options2=AND&options3=AND&occuring3=freetext&occuring2=freetext&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc%3A%22ve%22&y=14&x=46 Urticaria publications]

[http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=urticaria&occuring1=title&rowId=2&options2=AND&q2=horses&occuring2=od&rowId=3&options3=AND&q3=&occuring3=freetext&x=47&y=11&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Urticaria in horses publications]

[http://www.cabdirect.org/search.html?q=title%3A%28urticaria%29+NOT+od%3A%28horses%29&fq=sc%3A%22ve%22 Urticaria in other species publications]
}}

==References==
*Mair, T. S., Love, S., Schumacher, J., Watson, A. E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''
*Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''
*Rose, R. J., Hodgson, D. R. (2000) '''Manual of Equine Practice''' ''Elsevier Health Sciences''
*Scott, D. W., Miller, W. H. (2003) '''Equine Dermatology''' ''Elsevier Health Sciences''

{{review}}

{{OpenPages}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Freeform/fre01331.asp Urticaria]}}

[[Category:Allergic Skin Diseases]]
[[Category:Dermatological Diseases - Horse]][[Category:Immunological Diseases - Horse]]
[[Category:Expert Review]]

Neonatal Isoerythrolysis

2016-06-15T22:50:18Z

Kitnmre:

{{OpenPagesTop}}
Also known as: '''''Feline Neonatal Isoerythrolysis (FNI) — NI — Equine Neonatal Erythrolysis — ENI

==Introduction==
Neonatal isoerythrolysis is a disease of humans and domestic animals and has been most commonly observed in newborn cats and horses. Rarely it has also been described in other species following [[:Category:Transfusion Medicine|blood transfusions]], [[Vaccines|vaccination]] or previous pregnancy. The disease is characterised by [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]] due to ingestion of maternal colostral antibody directed against surface antigens on neonatal red blood cells. This leads to a [[Type II Hypersensitivity|type II hypersensitivity]] reaction causing extravascular and intravascular haemolysis during the first few days of life.

==Pathogenesis==
===Equine Neonatal Isoerythrolysis===
In foals, the condition results when a foal inherits red blood cell antigens (which the dam does not have) from its sire. The Aa and Qa antigens are most strongly antigenic and exposure of the mare to these antigens during a previous pregnancy or whole blood transfusion leads to the mare producing alloantibodies to the foal's red blood cells. At birth the foal ingests large numbers of red blood cell antibodies in the colostrum, leading to severe haemolytic disease. During pregnancy however, the foal is unaffected because blood and antibodies are unable to cross the placenta. First foals are rarely affected, as a sensitization reaction (usually during an earlier pregnancy) is usually required.

===Feline Neonatal Isoerythrolysis===
[[Blood Groups - Cat|Cats have three main blood types]], type A, type B and type AB. Worldwide, the most common blood type in cats is type A and type A is dominant over type B. Queens with type B blood have high levels of naturally occurring alloantibodies to type A blood. Feline neonatal isoerythrolysis (FNI) develops when type B blood mothers mate with type A tomcats producing kittens with type A/B blood. The newborn kittens ingest maternal colostrum containing anti-A antibodies leading to the clinical signs of FNI.

==Clinical Signs==
===Horses===
Affected foals appear clinically normal at birth, and clinical signs develop from several hours up to a week after ingestion of colostrum. Foals with NI usually become progressively weak, lethargic and depressed and develop [[icterus]], tachycardia and tachypnoea. Although the signs are not pathognomonic for NI, a foal displaying '''haemoglobinuria and icterus''' born to a multiparous mare should be strongly suspected to have the disease. If the foal becomes severely hypoxic, seizures may occur. '''Neurological abnormalities''', such as somnolence or seizures, may also occur due to the phenomenon of '''kernicterus'''. Excessive amounts of unconjugated bilirubin are able to cross the blood-brain barrier in foals and lead to a bilirubin encphalopathy which can be permenent. '''Death''' usually occurs if NI is not diagnosed and treated promptly.

===Cats===
Although FNI is rare, the mortality associated with the disease is high. Purebred cats are more commonly affected than domestic shorthair cats. Similarly to affected foals, kittens are born and nurse normally and clinical signs develop within a few hours or days. Signs may be variable and kittens are occasionally found dead within a few hours of the onset of clinical signs. Clinical signs may include failure to thrive, weakness, dark red/brown urine, icterus, and [[Regenerative and Non-Regenerative Anaemias|anaemia]]. Affected kittens may separate themselves from the rest of the litter, stop nursing and appear weak. Signs may vary in severity within a single litter; this is thought to be related to differences in colostral intake. Other features of the disease may include necrosis and sloughing of the tail tip and [[DIC|disseminated intravascular coagulation]]. Affected kittens rarely survive the first week of life.

==Diagnosis==
To definitively diagnose the condition in '''horses''', a minor cross-match is performed using the foal's red blood cells and the mare's serum. A positive agglutination indicates a diagnosis of NI.

In '''cats''', diagnosis is performed on the basis of clinical signs and blood typing of the queen and kitten. If FNI is suspected all kittens should be blood typed; this can be achieved using placental blood.

==Treatment==
Treatment in '''foals''' depends on rapid identification of sick foals and prevention of suckling the dam for 48-72 hours. If the foal is less than 24 hours old at the time of diagnosis, it should be muzzled and fed supplemental milk. As the foal's intestine becomes impermeable to absorption of colostral antibodies by 24 hours of age, prevention of nursing until the foal is 30 hours of age should be sufficient. The mare should be milked every two hours during this period to ensure continued milk production. Separation of the mare and foal is not recommended as this may lead to unnecessary stress of the compromised foal.

A blood transfusion should be considered if the anaemia is severe (PCV less than 15%) or the foal is weak and shocked. The best donor of blood for transfusion is the dam, but this means that the serum containing the alloantibodies must be removed ('washing' of the red blood cells). This is achieved by mixing the mare's blood with saline and performing repeated centrifugation. If washed red blood cells from the mare are not available, blood from an acceptable blood-typed donor horse may be used.

Affected '''kittens''' should be removed from the queen for a period of 24 hours and fed milk replacer or fostered onto a lactating queen with blood type A. After this period, intestinal permeability to antibodies is greatly reduced and the kittens may be returned to the original queen. Supportive management of hypoglycaemia and hypothermia may be necessary. Severely affected kittens may require a blood transfusion, preferably with Oxyglobin if available. If this is not possible, washed type A blood is preferred. Intraosseous administration of blood is recommended due to the small size of the patient.

==Prevention==
The disease in horses is prevented by ensuring that mares are blood-typed before being mated. Mares who are negative for the blood antigens known for causing disease can be matched to stallions who are also negative. Similarly in cats, the disease is easily prevented if blood typing of cats is peformed prior to breeding.

{{Learning
|flashcards = [[Equine Internal Medicine Q&A 09]]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=neonat*&occuring1=title&rowId=2&options2=AND&q2=%22isoerythrolysis%22&occuring2=title&rowId=3&options3=AND&q3=cats&occuring3=od&x=53&y=9&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Neonatal Isoerythrolysis in cats publications]

[http://www.cabdirect.org/search.html?q=title%3A%28neonat*%29+AND+title%3A%28%22isoerythrolysis%22%29+AND+od%3A%28horses%29 Neonatal Isoerythrolysis in horses publications]
}}

==References==
Mair, T. S. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''

Norsworthy, G. D., Crystal, M., Grace, S. F. (2006) '''The Feline Patient''' ''Wiley-Blackwell''

Silvestre-Ferreira, A. C., Pastor, J. (2010) '''Feline Neonatal Isoerythrolysis and the Importance of Feline Blood Types''' ''Veterinary Medicine International Volume 2010''

{{review}}

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{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00064.asp Neonatal Isoerythrolysis]}}

[[Category:Materno-Fetal Immunity|E]]
[[Category:Immunological Disorders]]
[[Category:Immunological Diseases - Horse]][[Category:Immunological Diseases - Cat]]
[[Category:Expert Review]]

Failure of Passive Transfer

2016-06-15T22:48:43Z

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Also known as: '''''FPT'''''

==Introduction==
Transfer of passive immunity in the bovine neonate occurs solely through maternal colostrum. This is in contrast to humans where placental transfer of immunity via specific Fc receptors is the predominant mechanism. However, inadequate transfer of immunity is a relatively commonly diagnosed problem affecting young stock. This is particularly the case in modern Holstein dairy herds, where large milk yields dilute the antibody concentration in the colostrum meaning relatively more must be consumed to have the same immunity transferred. Due to the lower yields and possibly other genetic reasons, this tends to be less of a problem in suckler herds.

Receiving sufficient colostrum and having adequate immunity is important to reduce the risk of pre and post weaning morbidity and mortality. Good calf health is fundamental to achieving adequate weight gains and reaching the optimal age at first calving.

Inadequate absorption of [[Immunoglobulins|immunoglobulin]] occurs because:
# The neonate did '''not receive any''' colostrum.
# The neonate did '''not receive enough''' colostrum.
# The neonate did '''not absorb enough''' colostrum.
# The quality of the '''colostrum was inadequate'''.

==Colostrum quality (amount of IgG) depends on:==
* '''Breed''' - [[Immunoglobulins|antibody]] and milk fat are correlated, thus Jersey cows have the highest amount of immunoglobulin. Conversely, Holsteins have the lowest amount of immunoglobulin.
* '''Nutrition''' - it is especially important for cows during the dry period (last 2 months of pregnancy) to have the correct nutrition in order to produce [[Immunoglobulins|immunoglobulin]]. There is also some evidence that trace element deficiencies during the dry period may affect colostrum quality.
* '''Season''' - the lowest quality of colostrum is produced in the late winter months as this is correlated to the quality of forage available. High ambient temperatures may also have an adverse effect which is likely to be related to depressed dry matter intakes. In countries where this is a problem, heat abatement systems may help.
* '''Stress''' - dams under increased stress produce colostrum of reduced quality.
* '''Immunostatus of the dam''' - dams exposed to specific diseases mount an immune response and produce antibodies for that particular disease. These antibodies are then transferred to the neonate via colostrum. Dams may also be vaccinated which, if done during the colostrum production period (last 2 months of gestation), will also provide the neonate with some protection via passive transfer.
* '''Milk yield''' - increased yield dilutes the amount of immunoglobulins in the colostrum. The volume of colostrum produced at the first milking may be used as a guide of colostrum quality.
* '''Dry Period Length''' - excessively short dry periods, no dry period or mistakenly milking a cow during the dry period will have detrimental effects on colostrum quality.
* '''Dripping from teats''' - poor teat confirmation may result in a poor teat seal and thus dripping before the calf has been born or sucked.
* '''Parity''' - older cows have better quality colostrum as they have been exposed to more pathogens and may have had multiple vaccinations causing their colostrum to have a higher amount of immunoglobulin.
* '''[[Mastitis]]''' - A cow with clinical mastitis, or indeed any other illness, should not be used as source of colostrum.
* '''Pooling''' - Cow’s colostrum may be pooled to ease the calf management period. However, the larger volumes of lower quality colostrum tend to be relatively over-represented meaning this can be to the detriment of colostrum quality. Therefore this practice is to be discouraged. It is also a risk for the spread of [[Johne's Disease|Johnes disease]].
* '''Time of collection''' - The highest quality colostrum will be collected from the dam when milked within 1-2 hours of calving.

==Colostrum quantity depends on:==
* '''Amount the neonate suckles''' - a strong neonate and good mothering from the dam increases the amount the neonate suckles. Udder conformation also influences the accessibility of the teats to the neonate. Dystocia may reduce mothering and produce a weak calf that potentially causes an increased time to the first suck and/or reducing the amount the neonate consumes.
* '''Premature births''' - if born early the dam has a shorter period of time for concentration of antibodies from the blood to the colostrum. It is more likely that the neonate will also be weaker and smaller, causing the amount of colostrum sucked to be reduced.

==Failure of absorption from the intestines:==

The amount of colostrum recommended is a minimum of 3 liters within 6 hours of birth. This equates to 8-10% of the neonates body weight. If the colostrum is of sufficient quality, this should provide approximately 100-200g of IgG in the first feed. Timing is important and is considered '''optimal within the first four hours''' before progressively declining towards what is referred to as “gut closure”. The timing of the first feed can influence when this occurs and a delay can prolong the time before gut closure to approximately 36 hours. Therefore the first feed is the most important in the uptake of colostrum derived passive immunity.

==Diagnosis==

Failure of passive transfer can be a problem in the individual calf but more importantly can be a herd level problem which requires investigation. Diagnosing the problem can be done in a variety of ways each with their advantages and disadvantages. In all cases, calves should be sampled no earlier than 24 hours of age and up to a maximum of 7 days when the calf’s own endogenously produced antibodies can distort the results.

For more detail see [[Colostrum Quality Testing]]

==Prevention==
After diagnosis, herd level prevention strategies should be based around the following areas:-

====1. Method and amount of colostrum administration====

On a modern Holstein herd, leaving the calf to suckle from its dam is often inadequate to transfer sufficient passive immunity. Therefore, this process may be assisted by using a bottle or using a stomach tube. Farmers may need to be trained with the latter approach which is often preferred as it is more time efficient.

====2. Identification of high risk cows and calves====

From the risk factors for FPT stated above, at risk calves can be identified and action taken to ensure adequate colostrum intake.

====3. Colostrum storage====
[[File:Fresh colostrum in bucket.JPG|right|thumb|130px|<center>Freshly collected colostrum from a Holstein Friesian dairy cow</center>]]
It is often useful for the farmer to store colostrum in the freezer for use when needed. Anecdotally, storage has been reported as satisfactory for up to 12 months. However, repeat freeze thawing should be minimized as this can have adverse effects on colostrum quality. Microwaving the colostrum as part of the thaw is not recommended due to protein denaturing. Thawing should therefore be done slowly by putting the bottles into warm water.

On harvesting, the colostrum should not be maintained at room temperature for prolonged periods due to bacterial growth occurring which may harbour infectious agents. Bacterial contamination can be minimized by good udder preparation prior to milking and using clean equipment. Freezing should be performed as soon as possible after collection. If the colostrum is not going to be frozen but kept for later use, it should be refrigerated and used within a few days.

It is important to select the dam carefully when deciding which colostrum to store. The cow should be healthy and in good condition. It is advisable to check the colostrum with a [[Colostrum Quality Testing#Colostrometer|colostrometer]] before storage to try to ensure adequate quality. In herds with a history of Johnes disease, it may be worth testing the cow for infection, although due to the poor sensitivity of the test in clinically normal animals this is not a guarantee of uninfected colostrum.

[[File:colostrum in bottle.JPG|right|thumb|130px|Frozen colostrum in a plastic bottle]] [[File:colostrum in storage.JPG|right|thumb|130px|Frozen colostrum in storage]]

====4. Colostrum quality====

This can be done using a colostrometer.

====5. Colostrum supplements====

A colostrum supplement is added to normal colostrum to try to increase the IgG content. It is important that products of this type are not used as the sole source of colostrum which would confer inadequate immunity to the neonate.

====6. Colostrum replacers====

Colostrum replacers are designed to completely replace the need for normal colostrum from the dam. The advantages of these products are convenience and allowing some immunity to be conveyed to the calf when natural colostrum is not available. Their disadvantages are the cost and the lack of specific immunity to the pathogens present on the farm. They may be useful on particular farms affected with Johnes disease.

In situations where despite colostrum management practices being optimized, there is still evidence of FPT or high calf morbidity and mortality, other measures that may be more targeted to individual diseases may be more appropriate.

{{Learning
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103126499.pdf '''Colostral immunity in newborn calf: methods for improvement of immunoglobulins absorption.''' Zarcula, S.; Cernescu, H.; Knop, R.; Facultatea de Medicină Veterinară, Timişoara, Romania, Lucrari Stiintifice - Universitatea de Stiinte Agricole a Banatului Timisoara, Medicina Veterinara, 2008, 41, pp 195-202, 31 ref.]

[http://www.cabi.org/cabdirect/FullTextPDF/2006/20063206641.pdf ''' Failure of passive transfer in calves: a review.''' Richter, C.; Lohmann, K.; Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada, Large Animal Veterinary Rounds, 2005, 5, 10, pp 1-6, 56 ref.]
}}

==References==

McGuirk, S.M., Collins, M. (2004). '''Managing the production, storage, and delivery of colostrum. Veterinary Clinics of North America: '''''Food Animal Practice.'' 20(3):593-603.

Weaver, D.M., Tyler J.W., VanMetre, D.C., Hostetler, D.E., Barrington, G.M., (2000). '''Passive transfer of colostral immunoglobulins in calves.''''' Journal of Veterinary Internal Medicine.'' 14(6):569-77.

A.H. Andrews (2004) '''Bovine Medicine - Diseases and Husbandry of Cattle''' (2nd Edition) ''Blackwell Publishing ''

Koterba, Drummound and Kosch (1990) '''Equine Clinical Neonatology''''' Williams and Wilkins ''

P. Lydyard, A. Whelan and M.W. Fanger (2004) '''Immunology''''' Garland Science 2nd Edition ''

www.sheepandgoat.com

{{review}}

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{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00003.asp Failure of Passive Transfer]}}

[[Category:Materno-Fetal Immunity|C]]
[[Category:Immunological Disorders]]
[[Category:Immunological Diseases - Horse]][[Category:Immunological Diseases - Cattle]]
[[Category:Blood Samples and Coagulation Tests]]
[[Category:Expert Review - Farm Animal]]

Equine Severe Combined Immune Deficiency

2016-06-15T22:45:43Z

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Also known as: '''''Equine SCID — ESCID

==Introduction==
Severe combined immunodeficiency disease (SCID) of horses is an autosomal, recessive hereditary disease occurring in 2-3% of Arab or part-bred Arab foals. About 16-25% of Arabian horses are carriers of the disease and are phenotypically normal but pass on the defective gene to 50% of their offspring. Affected foals result from 25% of matings of two carrier horses.

SCID is characterised by a complete absence of functional B and T lymphocytes and affected (homozygous) foals fail to produce antigen-specific immune responses. The disease results in the absence of a functional immune system and affected foals are unable to resist or recover from infections. The most common opportunistic infections in affected foals are pneumonia caused by viral ([[Equine Adenovirus|Adenovirus]]), bacterial ([[Rhodococcus equi|''Rhodococcus equi'']]), fungal ([[Pneumocystis carinii|''Pneumocystis carinii'']] or protozoal (''[[Cryptosporidium]]'') organisms.

==Signalment==
Only Arab or cross-bred Arabs foals are affected. No sex predilection has been reported.

==Pathogenesis==
SCID occurs due to a mutation in the allele encoding for DNA-dependent protein kinase (DNA-PK) that is involved in V(D)J lymphocyte recombination. V(D)J recombination is required for antigenic receptor expression on B and T lymphocytes. Without these receptors, differentiation of B and T lymphocytes does not occur and lymphoid tissue fails to develop. The result of this mutation is a severe immunodeficiency.

==Clinical Signs==
Affected foals are clinically normal at birth and usually develop infections at around two to three months of age due to declining maternal antibodies in the colostrum. The most common clinical signs relate to infections of the respiratory tract such as nasal discharge, cough, dyspnoea or increased respiratory sounds. Other clinical signs may reflect further sites of infection including intermittent fever, pneumonia, colic, weight loss and diarrhoea. Infection of the pancreas may result in loss of functional endocrine tissue leading to stunted growth and weight loss.

==Diagnosis==
Diagnosis may not be straightforward as the clinical signs may resemble those of many other infections occurring in foals. The antemortem diagnosis of SCID is usually based on three criteria; a) a persistent lymphopaenia (occurring over 1-2 weeks) with less than 1000 lymphocytes per ml, b) a lack of serum IgM in foals over four weeks of age and c) lymphoid hypoplasia. Affected foals may also develop [[Regenerative and Non-Regenerative Anaemias|anaemia]] late in the course of the disease.

The '''intradermal phytohemagglutinin (PHA) test''' may be used as a test for immunocompetence and assesses T lymphocyte function. It can be performed in foals of all ages as the test is not affected by maternal antibodies. Intradermal PHA causes a [[Type IV Hypersensitivity|delayed hypersensitivity]] reaction, resulting in a skin swelling. A foal suffering from SCID fails to respond to intradermal PHA.

In order to obtain a definitive diagnosis, blood or cheek swabs may be submitted for '''PCR to identify the mutant allele of the DNA-PK gene'''. The test also identifies carriers of the disease which is important for screening prior to breeding. Additionally, post mortem findings of a small thymus and/or absent lymph nodes combined with the presence of opportunistic infections support a diagnosis of SCID. Histologically, lymph node follicles and germinal centres are absent with severe cellular hypoplasia of the thymus and lymph nodes.

==Treatment==
Medical treatment of foals with SCID is generally unrewarding. Treatment is supportive, consisting of antibiotics to treat secondary opportunistic infections.

==Prognosis==
The prognosis for affected foals is grave even with intensive treatment and most foals die within five months of birth.

==Prevention==
SCID may be prevented in foals by DNA testing of the mare and stallion and only breeding non-carrier animals.

{{Learning
|flashcards = [[Equine Internal Medicine Q&A 16]]
|literature search =[http://www.cabdirect.org/search.html?start=0&q=title:(%22Equine+Severe+Combined+Immune+Deficiency%22)+OR+((title:(%22Severe+Combined+Immune+Deficiency%22)++OR+title:(SCID))+AND+od:(horses))+OR+title:(ESCID) Equine Severe Combined Immune Deficiency publications]
}}

==References==
*Lavoie, J. P., Hinchcliff, K. W. (2009) '''Blackwell's Five-Minute Veterinary Consult: Equine''' ''John Wiley and Sons''
*McClure, J. T. (1997) '''New Developments in Severe Combined Immunodeficiency Disease''' ''Proceedings of the Annual Convention of the AAEP (43) pp61-64''
*Swinburne, J., Lockhart, L., Scott, M., Binns, M. M. (1999) '''Estimation of the prevalence of Severe Combined Immunodeficiency Disease in UK Arab horses as determined by a DNA-based test''' ''The Veterinary Record 145 22-23''

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{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00051.asp SCID]}}

[[Category:Primary Adaptive Immunity Deficiencies]]
[[Category:Expert Review - Horse]]
[[Category:Immunological Diseases - Horse]]

Category:Dermatological Diseases - Horse

2016-06-15T22:42:45Z

Kitnmre:

{{frontpage
|pagetitle =Dermatological Diseases of Horses
|pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;">

</div>
|contenttitle =Content
|contentbody =<big>
 
<categorytree mode=pages>Dermatological Diseases - Horse</categorytree>

</big>
|logo =Horse-logo.png
}}

==Equine Dermatology Virtual Patient:==
[[File:horse-logo.png|thumb|left|50px]]
<big>'''[http://www.nottingham.ac.uk/toolkits/play_2793 A horse with skin lesions]'''<big>
 

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Dermatology Dermatology]}}

[[Category:Horse - Integumentary System]]
[[Category:WikiClinical Equine]]

Thrombosis

2016-06-15T22:40:46Z

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== Introduction ==
[[Image:Pulmonary artery thrombus.jpg|thumb|right|200px|<center>Pulmonary artery thrombus. Courtesy of A. Jefferies</center>]]
[[Image:Thrombosis dog nose 2.jpg|thumb|right|200px|<center>Nasal thrombosis (dog). Courtesy of T. Scase</center>]]
A thrombus is a localized or generalized intravascular or intracardiac blood clot. Thrombosis is the method of formation of a thrombus. Thrombi may occur in any vasculature in the body and form as the result of trauma or pathological processes affecting the blood vessel endothelium or disturbances to blood flow and/or blood composition. Some diseases such as infective [[endocarditis]] and [[Dirofilaria immitis|heart worm]] increase the risk of thrombi formation.

It may occur due to endothelial injury, altered blood flow e.g. abnormal stasis or hypercoagulability.

Thrombosis is often associated with other disease processes such as [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]]. In cats with [[Hypertrophic Cardiomyopathy|hypertrophic cardiomyopathy]], thrombosis often causes [[Atrial Thrombosis|posterior paralysis]] in these animals, as it lodges in the branching of the abdominal aorta.

Spontaneous venous thrombosis is rare, but can be seen in cattle with [[Traumatic Reticulitis|traumatic reticulo-peritonitis]] in the caudal vena cava.

==Types==
There are many different types of thrombosis.

'''Arterial thrombosis''' is common in man, but it is uncommon in domestic animals; in man it is associated with atherosclerotic vascular disease. When they do occur in animals, arterial thrombi are usually small lesions but these may be sited strategically, thereby causing problems.

'''[[Arteriosclerosis]]''' is seen in aged dogs and horses affecting the coronary artery and other major arteries.

'''[[Intestinal Arterial Thromboembolism|Verminous arteritis]] may occur with or without [[aneurysm]] and is seen in horses as a result of ''[[Strongylus vulgaris]]'' infestation. It affects the root of cranial mesenteric artery, renal artery and aorta as a consequence of larval migration in the vessel walls.

'''Cardiac thrombosis''' is usually valvular, but can occasionally be mural. In farm animals, and rarely in the horse, infective/inflammatory thrombosis occurs subsequent to [[endocarditis]]. In dogs and horses, cardiac thrombosis is generally of degenerative/non-infectious cause; endocarditis may occur, though uncommonly.

'''Venous thrombosis''' is a fairly common type of thrombus in the veterinary species because veins are relatively thin-walled and are therefore more susceptible to distortion, inflammatory damage and iatrogenic venepuncture damage. Also,veins have relatively slower blood flow rates allowing cell aggregates to persist more readily. Most venous thrombosis in domestic animals results from extension of inflammatory reactions, erosion/disruption caused by malignant tumours, pressure from adjacent space-occupying masses or venepuncture damage.

'''Capillary thromboses''' are microthrombi that are only appreciable histologically. Their formation may be localised and associated with acute local inflammation or generalised. Localised microthrombi are rarely significant unless they are strategically sited. Generalised microthrombi may be seen in terminal diseases as a reflection of vascular failure, and are often associated with [[Shock|shock syndromes]] as part of [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation]]. Clinically, generalised capillary thrombosis is highly significant.

== Signalment ==

Can occur in any specie of animal, but is most commonly described in dogs and cats.

== Clinical Signs ==

Signs depend on the area affected and the size of the vessel blocked. There will always be poor perfusion below the affected area, or malfunction and necrosis of the affected organs. The area affected will often appear pale, cold, have poor perfusion and be painful to touch.

== Diagnosis ==
[[Image:Thrombosis dog nose.jpg|thumb|right|200px|<center>Nasal thrombosis (dog). Courtesy of T. Scase</center>]]
History and clinical signs can be indicative of the condition. On blood tests, one may see abnormalities associated with lack of blood perfusion in pathological conditions that can cause the thrombosis.

Ultrasonography may show blood stasis and may also demonstrate the presence of a thrombus.

Angiography may show lack of opacity in the affected region.

On microscopic examination, the thrombus appears as a layered mass which is attached to the vessel wall. The composition consists of [[Red Blood Cell|red blood cells]], [[neutrophils]] and [[platelets]] bound together by fibrin. Thrombi take different appearance depending on whether they are arterial or venous. '''Arterial thrombi''' tend to be '''pale''' and have a tail in the direction of blood flow. The high rate of blood flow sweeps red cells away - the thrombus is composed of mainly white cells, platelets and fibrin which are left behind. '''Venous thrombi''' tend to be a '''darker red'''. The slow blood flow allows the clot to form quicker which is loosely arranged and contains many red blood cells.

== Treatment ==

The mainstay of treatment is to diagnose and treat the underlying problem.

It is important to give pain relief and [[:Category:Fluid Therapy|IV Fluids]] as palliative care. The use of an anticoagulant such as heparin for short-term treatment or aspirin for long-term treatment should be considered.

== Prognosis ==
[[Image:DIC thrombus.jpg|thumb|right|200px|<center>DIC thrombus. Courtesy of A. Jefferies</center>]]
Prognosis depends upon the underlying condition.

If the animal survives the immediate effects of a thrombus, the thrombus may evolve in one of the following ways:

# The thrombus may gradually enlarge and eventually cause total obstruction of a vessel.
# The thrombus may be completely removed by fibrinolytic activity; fibrinolysis is a very active process and clots are usually removed within a few days of formation provided that blood flow is sufficient. An occlusive thrombus may prevent the necessary enzymes from reaching the clot but contraction of fresh clots under the influence of thrombasthenin (released by platelets) may provide a slit-like channel beside the thrombus that permits the blood flow to restart and completely dissolve the clot.
# Organisation; a thrombus acts as a foreign body, causing an inflammatory response in the underlying blood vessel or heart wall. The external surface of the thrombus then quickly becomes covered by endothelium and is excluded from the clotting mechanism. Neutrophils invade the mass and may reduce the centre. Occasionally, subsequent invasion by bacteria may lead to purulent inflammation. Normally, fibroblasts and capillary buds follow the neutrophils into the thrombus and a fibrous vascularised connective tissue forms. Capillaries channels anastomose to produce vessels that traverse the thrombus and re-establish blood flow - this is known as '''canalisation''' of a thrombus. Fibrous tissue matures and contracts, eventually causing the thrombus to become incorporated into the vessel wall as a fibrous lump. A piece of the thrombus may break off and form an [[Embolism|embolus]].

Also see: [[Thromboembolism]].

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 '''(Fifth Edition)'' W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine '''(6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition) ''Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual '''(Eighth Edition)'' Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition)'' Mosby Elsevie''

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{{Learning |Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00893.asp Aortoiliac Thrombosis]}}

[[Category:Cardiovascular_System_-_Vascular_Pathology]]
[[Category:Expert_Review]]
[[Category:Venous_Pathology]]
[[Category:Vascular_Diseases_-_Dog]]
[[Category:Vascular_Diseases_-_Cat]]
[[Category:Vascular_Diseases_-_Horse]]
[[Category:Circulatory_Disorders_-_Pathology]]
[[Category:Cardiology Section]]

Category:Cardiovascular Diseases - Horse

2016-06-15T22:37:49Z

Kitnmre:

{{frontpage
|pagetitle = Cardiovascular Diseases of Horses
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 
[[:Category:Cardiac Diseases - Horse|Cardiac Diseases]]

[[:Category:Vascular Diseases - Horse|Vascular Diseases]]
 
 
</big>
|logo=Horse-logo.png}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Cardiology Equine Cardiology]}}

[[Category:Horse - Cardiovascular System]]
[[Category:WikiClinical Equine]]

Category:Horse - Cardiovascular System

2016-06-15T22:37:28Z

Kitnmre:

{{frontpage
|pagetitle = Horse Cardiovascular System
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 

[[:Category:Cardiovascular Diseases - Horse|Cardiovascular Diseases]]
 
 
</big>
|logo=Horse-logo.png}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Cardiology Equine Cardiology]}}

[[Category:Horse]]

Category:Cardiac Diseases - Horse

2016-06-15T22:35:14Z

Kitnmre:

{{frontpage
|pagetitle = Cardiac Diseases of Horses
|pagebody =
|contenttitle = Content
|contentbody =
<big>
 

[[:Category:Arrhythmia|Arrhythmias]]

[[:Category:Cardiomyopathy|Cardiomyopathy]]

[[:Category:Heart Failure|Heart Failure]]

[[Heart Murmurs]]

Developmental:
:[[Atrial Septal Defect]]
:[[Patent Ductus Arteriosus]]
:[[Pulmonic Stenosis]]
:[[Tetralogy of Fallot]]
:[[Tricuspid Valve Dysplasia]]
:[[Vascular Ring Anomalies]]
:[[Ventricular Septal Defect]]

[[Endocardial Haemorrhage]]

[[Endocarditis]]

[[Pericardial Effusion]]

[[Valvulitis, Chronic|Chronic Valvulatis]]

 
 
</big>
|logo=Horse-logo.png}}

{{Learning |Vetstream = [https://www.vetstream.com/equis/browse/Cardiology Equine Cardiology]}}

[[Category:Cardiovascular Diseases - Horse]]

Potentiated-Sulphonamides

2016-05-23T02:53:29Z

Kitnmre:

{{review}}
{{toplink
|linkpage =WikiDrugs
|linktext =WikiDrugs
|sublink1 = Antibiotics
|subtext1 = Antibiotics
|pagetype = Drugs
}}

Potentiated-sulponamides are a combination of a [[sulphonamides|sulphonamide]] and trimethoprim. By combining the two types of antibiotics the mixture becomes bactericidal and increases their spectrum of activity. In practice they are often referred to as '''T.M.S''' or Trimethoprim Sulphate.

==Mechanism of Action==

The combination of sulphonamide and trimethoprim means that the bacterial nucleotide sythesis pathway is attacked at two seperate points. This produces a bactericidal, time-dependent killing affect. To find out how sulphonamides work click [[sulphonamides|here]] and to discover the same about trimethoprim click [[Trimethoprim - Dihydrofolate Reductase Inhibitors|here]].

==Spectrum of Activity==

The combined nature of the drug mean that they are very broad spectrum and the main species of note that isn't affected is ''Pseudomonas''.

==Pharmacokinetic Considerations==

The half-life of all these drugs are relatively short but their pharmacokinetic properties will depend upon the precise mixture of sulphonamide and trimethoprim, so it is best to check in a formulary before use.

They all have good tissue penetration and will readily cross the blood brain barrier. As resistance is now a problem with these drugs their efficacy is starting to become limited.

==Side Effects and Contraindications==

These drugs are relatively safe and have wide safety margins in all species except in cats. Again look at the individual drug combinations for specific mixture side-effects. Concern has been noted about immune-mediated reactions in dogs.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Generic/gen00290.asp Trimethoprim]}}

Sulphonamides

2016-05-23T02:52:29Z

Kitnmre:

{{review}}
==Introduction==
Sulphonamides are derivatives of sulphanilamide, an active metabolite of the pro-drug and dye prontosil. Commonly used ones are: '''sulphadiazine, sulphaquinoxaline, sulphadimethoxine, sulphadoxine''' and '''sulphanilamide'''.

==Mechanism of Action==
Sulphonamides act by competing with an essential precursor in folic acid synthesis in bacteria. Bacteria need to synthesise folic acid in order to grow as they are unable to obtain it from their 'diet' like mammals can. Since the bacterium is unable to synthesize RNA or DNA, due to its lack of folic acid, its growth is inhibited. As such, sulphonamides are '''bacteriostatic'''.

==Spectrum of Activity==
These are generally broad spectrum antibiotics.
* They are active against aerobic gram-positive cocci and some rods.
* They are active against gram-negative rods, including enterobacteriaceae.
* They are active against the anaerobes, ''Actinomyces'' and ''Fusobacterium'', but inactive against clostridial species and anaerobic cocci.
* Resistance is now widespread.
* Drugs which contain a PABA nuclear core, such as procaine, antagonise their actions.

==Pharmacokinetic Considerations==
* Sulphonamides are lipophilic weak acids of varying pKas.
* Most are absorbed readily from the gut, except Succinylsulphathiazole and Phthalylsuphathiazole.
* They tend to distribute widely throughout the body as the non-ionised form is able to cross cell membranes.
* The extent of binding to plasma proteins is very dependent on the individual drug and species involved and can vary between 20 and 90%.
* They are eliminate both by hepatic metabolism and renal excretion, the rate of both in each species and for each drug varies. This results in very different half-lives of each drug in each species.
* They are unable to work in pus or tissue debris as they contain thymidine and purines. This means that the bacteria can utilise these rather than folic acid for continued growth. This means that the drug will become obselete in such a circumstance.

==Side Effects and Contraindications==
Major reactions to sulphonamides are uncommon but the following are the most common of the side effects recorded:
* Rapid intravenous injection can lead to muscle weakness, ataxia and collapse. This has only been recorded in cattle and horses.
* They can precipitate in tubular fluid resulting in renal tubular damage.
* Dobermans have had serious allergic reactions to them including immune-mediated polyarthritis, thrombocytopenia and haemolytic anaemia.
* Severe hepatotoxicity has been noted in some dogs.
* Long dosage regimens of Sulphonamides have resulted in keratoconjunctivitis sicca/'dry eye' in dogs.
* Sulphonamides inhibit thyroid gland function and so mild signs of hypothyroidism have been seen in dogs that have had intesive dosage regimens.

===Hepatotoxicity===
*some of these casue hepatic necrosis in susceptible animals
*has been associated with a reduced capability of detoxifying the metabolites
*Doberman Pinscher breed appears to be susceptible
[[Category:Hepatotoxicity,_Drug_induced]]
[[Category:To_Do_-_Clinical]]

Sulphonamides

2016-05-23T02:50:46Z

Kitnmre: