|
|
| (31 intermediate revisions by 6 users not shown) |
| Line 1: |
Line 1: |
| − | {{toplink
| + | #REDIRECT[[:Category:Immunodeficiencies]] |
| − | |backcolour = FFE4E1
| |
| − | |linkpage =WikiBlood
| |
| − | |linktext =WIKIBLOOD
| |
| − | |thispagemap= Immunodeficiencies(Concept Map) - WikiBlood
| |
| − | |sublink1 =Immunology - WikiBlood
| |
| − | |subtext1 =IMMUNOLOGY
| |
| − | |pagetype =Blood
| |
| − | }}
| |
| − | | |
| − | ==Introduction==
| |
| − | [[Image:Immunodeficiencies Map.jpg|thumb|right|150px|Immunodeficiency Diagram - Copyright nabrown RVC]]
| |
| − | Like any system in the body the immune system can go wrong. [[Autoimmune diseases - WikiClinical|Autoimmunity]] is when the immune system begins to attack itself. Immunodeficiency is when the immune system fails to protect itself from disease.
| |
| − | | |
| − | If the immunodeficient defect is present at birth and is therefore a result of a genetic or developmental abnormality, it is called a primary immunodeficiency.
| |
| − | | |
| − | Secondary immunodeficiency, sometimes called aquired immunodeficiency, is the loss of immune function during life, caused by exposure to harmful agents.
| |
| − | | |
| − | Immunodeficiencies can be treated by the replacement of the defective or missing protein, cells or gene. However, in veterinary medicine, [[Vaccines - WikiBlood|vaccinations]] and drugs are the most common treatments for immunodeficiency.
| |
| − | | |
| − | ==Primary Immunodeficiency==
| |
| − | | |
| − | *Primary immunodeficiencies may affect either the [[Innate Immune System - WikiBlood|innate immune system]] or the [[Adaptive Immune System - WikiBlood|adaptive immune system]]
| |
| − | *They are categorised by either the type or the developmental stage of the cells involved
| |
| − | *Lymphoid cell disorders affect [[Lymphocytes - WikiBlood#T cells|T cells]] or [[Lymphocytes - WikiBlood#B cells|B cells]] (or both)
| |
| − | *Myeloid cell disorders affect phagocytic function
| |
| − | *The severity of the immunodeficiency depends on at which stage in development the problem occurs
| |
| − | **E.g. Defects early on in development will affect the entire immune system
| |
| − | *[[Lymphocytes - WikiBlood#T cells|T cell]] deficiencies can affect both the cell-mediated and humoral response as [[Lymphocytes - WikiBlood#T cells|T cells]] play a central role in the immune system
| |
| − | | |
| − | ===Deficiencies of Innate Immunity===
| |
| − | [[Image:Grey Collie Syndrome.jpg|thumb|right|150px|Appearance of a puppy with Grey Collie syndrome - Copyright Michelle Tennis & Peggy Melton]] | |
| − | ====Canine Cyclic Haematopoiesis====
| |
| − | *Also called '''Grey Collie Syndrome'''
| |
| − | *Autosomal recessive
| |
| − | *Insertion mutation in AP3B1 gene
| |
| − | *Diluted grey coat colour, stunted growth, poor wound healing
| |
| − | *Neutropenia every 2 weeks which lasts 3-4 days due to cyclic production of cells from [[Bone Marrow - Anatomy & Physiology|bone marrow]]
| |
| − | *Animals are prone to recurrent infections, mainly from the respiratory and gastrointestinal tract
| |
| − | **E.g. pyrexia, [[Intestine Diarrhoea - Pathology|diarrhoea]], gingivitis and arthritis
| |
| − | *Puppies can be distinguised from other litter mates by the diluted grey collouring
| |
| − | *Affected puppies show symptoms such as fever, joint pain and eye, skin and respiratory infections from 8 weeks of age
| |
| − | *Affected animals rarely live beyond 2-3 years with most puppies dying withing a few weeks of birth
| |
| − | | |
| − | ====Canine Leukocyte Adhesion Deficiency (CLAD)====
| |
| − | *Occurs in Irish Setters
| |
| − | *Missence mutation of -Cys-36-Ser- in CD18 molecule
| |
| − | **CD18 is required for [[Neutrophils - WikiBlood|neutrophil]] migration and phagocytosis
| |
| − | *Recurrent bacterial infection
| |
| − | *Neutrophilia ([[Neutrophils - WikiBlood|neutrophils]] remain in the blood and are unable to fight infection in the tissue)
| |
| − | | |
| − | ====Bovine Leukocyte Adhesion Deficiency (BLAD)====
| |
| − | *Occurs in Holstein cattle
| |
| − | *Missence mutation of -Asp-128-Gly in CD18 molecule
| |
| − | *Recurrent infection, e.g. pneumonia
| |
| − | | |
| − | ===Deficiencies of Adaptive Immunity===
| |
| − | | |
| − | ====Equine Severe Combined Immune Deficiency (Equine SCID)====
| |
| − | *Autosomal recessive
| |
| − | *Occurs in 2-3% of Arabian foals
| |
| − | *Defect in DNA-dependent protein kinase gene
| |
| − | **Gene codes for a DNA repair enzyme involved in V(D)J recombination for antigen receptors of [[Lymphocytes - WikiBlood|lymphocytes]] (e.g. Ig and TCR)
| |
| − | *No functional [[Lymphocytes - WikiBlood#B cells|B cells]] or [[Lymphocytes - WikiBlood#T cells|T cells]]
| |
| − | *Foals develop infections (usually aorund 8 weeks of age as maternal [[Immunoglobulins - WikiBlood|antibody]] in [[Materno-fetal immunity - WikiBlood#Passive transfer via colostrum|colostrum]] wanes around this time)
| |
| − | *Foals usually die from bronchopneumonia
| |
| − | | |
| − | ====Canine X-Linked Severe Combined Immune Deficiency (Canine SCID)====
| |
| − | *Affects Basset Hounds and Corgis
| |
| − | *X-linked recessive defect in the gene conding for the IL-2 receptor
| |
| − | **IL-2 receptor is a receptor for the cytokine IL-2 which causes [[Lymphocytes - WikiBlood#T cells|T cells]] to proliferate
| |
| − | *Causes lymphoid hypoplasia, stunted growth and increases the animal's susceptibility to infection
| |
| − | *Animal usually dies from pneumonia or sepsis as the level of maternal [[Immunoglobulins - WikiBlood|antibody]] decreases
| |
| − | | |
| − | ====Selective IgA deficiency of German Shepherd Dogs====
| |
| − | *Poorly understood
| |
| − | *Linked to other disease syndromes such as deep pyoderma, inflammatory bowel disease, anal furunculosis and disseminated aspergillosis
| |
| − | *[[Immunoglobulin A - WikiBlood|IgA]] deficiency so more susceptible to mucosal disease
| |
| − | | |
| − | ====Immunodeficiency of Weimaraners, Irish Wolfhounds and Miniature Dachshunds====
| |
| − | *Unknown aetiology
| |
| − | *Inherited defects
| |
| − | *Low levels of circulating [[Immunoglobulin M - WikiBlood|IgM]] and [[Immunoglobulin G - WikiBlood|IgG]]
| |
| − | *Impaired [[Neutrophils - WikiBlood|neutrophil]] function
| |
| − | *Causes recurrent pyrexia and infections
| |
| − | **E.g. Rhinitis and bronchopneumonia in Irish Wolfhounds due to low [[Immunoglobulin A - WikiBlood|IgA]]
| |
| − | **E.g. Pneumocytosis in Miniature Dachshunds due to low [[Immunoglobulin G - WikiBlood|IgG]]
| |
| − | | |
| − | ===Labatory Examples of Severe Combined Deficiency===
| |
| − | | |
| − | *Severe Combined Immune Deficiency(SCID)
| |
| − | **No functional [[Lymphocytes - WikiBlood#B cells|B cells]] or [[Lymphocytes - WikiBlood#T cells|T cells]]
| |
| − | | |
| − | *Athymic nude mice (no [[Thymus - Anatomy & Physiology|thymus]])
| |
| − | **No functional [[Lymphocytes - WikiBlood#T cells|T cells]]
| |
| − | **Cell-mediated immunodeficiency
| |
| − | | |
| − | *Knock-out mice
| |
| − | **E.g. Gene coding for CD4, CD8, IL-10 removed
| |
| − | | |
| − | ==Secondary Immunodeficiency==
| |
| − | | |
| − | *There are many causes of secondary immunodeficiency
| |
| − | **Most deficiencies are not genetic
| |
| − | **Most are agent-induced, such as from X-ray radiation and immunosuppressive drugs
| |
| − | | |
| − | ===Viral Causes===
| |
| − | | |
| − | ====Feline Leukaemia Virus (FeLV)====
| |
| − | [[Image:FeLV Electron Micrograph.jpg|thumb|right|150px|FeLV Electron Micrograph [http://phil.cdc.gov/phil/home.asp Public Health Image Library] Image #5610]]
| |
| − | *Oncogenic retrovirus
| |
| − | *Causes neoplasia (lymphoma), myelosuppression (anaemia) and immunosuppression (of [[Lymphocytes - WikiBlood#T cells|T cells]])
| |
| − | *2 strains:
| |
| − | **FeLV-A
| |
| − | ***Natural strain
| |
| − | **FeLV-B
| |
| − | ***Formed through FeLV-A recombining with endogenous retroviral sequences in the feline genome
| |
| − | ***Increases the risks of lymphoma
| |
| − | **FeLV-C
| |
| − | ***Formed from the spontaneous mutation of FeLV-A
| |
| − | ***Is more myelosuppressive
| |
| − | *Virus replicates in the oropharyngeal lymphoid tissue causing a viraemia (virus circulating in the bloodstream) which then spreads to the systemic lymphoid tissue
| |
| − | *Shed in saliva
| |
| − | *Passed by oronasal route, e.g. mutual grooming
| |
| − | *Kittens between 6 weeks and 6 months are most susceptible
| |
| − | *60% of cats will become immune to the disease and recover
| |
| − | *Cats that are persistantly viraemic will progress to develop FeLV-associated diseases
| |
| − | *Some cats will become viraemic again if treated with corticosteroids or stressed if the infection lies dormant in the [[Bone Marrow - Anatomy & Physiology|bone marrow]]
| |
| − | *Diagnosis:
| |
| − | **ELISA
| |
| − | **Rapid-Immuno-Migration
| |
| − | **Western Blot
| |
| − | **Virus Isolation
| |
| − | **Immunofluorescence
| |
| − | **PCR
| |
| − | *Treatment:
| |
| − | **Antibiotics for secondary infection
| |
| − | **Anti-retroviral therapy
| |
| − | *For vaccinations see [[Vaccines - WikiBlood#Cat Vaccinations|here]]
| |
| − | | |
| − | ====Feline Immunodeficiency Virus (FIV)====
| |
| − | *Lentivirus
| |
| − | *Subtypes A, B and D
| |
| − | *Causes increased suscepitbilty to infections and neoplasia
| |
| − | *Specifically destroys [[Lymphocytes - WikiBlood#Helper CD4+|CD4+ T cells]]
| |
| − | *Virus is present in saliva, blood and other bodily fluids
| |
| − | *Feral and outdoor cats (mostly tom cats) are most at risk
| |
| − | *Virus replicates in lymphoid tissue
| |
| − | *Can remain asymptomatic
| |
| − | *Causes pyrexia and lymphadenopathy
| |
| − | *Transmitted by biting
| |
| − | *Diagnosis:
| |
| − | **ELISA
| |
| − | **Rapid-Immuno-Migration
| |
| − | **Western Blot
| |
| − | **Virus Isolation
| |
| − | **Immunofluorescence
| |
| − | **PCR
| |
| − | *Treatment:
| |
| − | **Antibiotics for secondary infection
| |
| − | **Anti-retroviral therapy
| |
| − | *For vaccinations see [[Vaccines - WikiBlood#Cat Vaccinations|here]]
| |
| − | | |
| − | ====Bovine Immunodeficiency Virus (BIV)====
| |
| − | *Lentivirus (non-oncogenic)
| |
| − | *Causes a persistent viral infection and lymphocytosis
| |
| − | *Immunocompromised cattle may develop secondary infections
| |
| − | *The tranmission is not well known, but the following possibilities are being researched:
| |
| − | **Through milk
| |
| − | **Through infected semen (e.g.artificial insemination)
| |
| − | **Placental transfer
| |
| − | *Diagnosis:
| |
| − | **Western Blot
| |
| − | **PCR
| |
| − | | |
| − | ===Toxic Causes===
| |
| − | | |
| − | *Poisons
| |
| − | | |
| − | ===Iatrogenic Causes===
| |
| − | | |
| − | *Drugs
| |
| − | **Corticosteroids
| |
| − | **Ciclosporin
| |
| − | **Cytoxic cancer therapy
| |
| − | | |
| − | ===Other Causes===
| |
| − | | |
| − | *Malnutrition
| |
| − | | |
| − | *Chronic disease
| |
| − | | |
| − | *Stress
| |
| − | | |
| − | *Senescence
| |
| − | | |
| − | ==Links==
| |
| − | | |
| − | *[http://www.bitoheavencollies.com/GrayCollie.html|Grey Collie Syndrome] ''Information on Grey Collie Syndrome including new research into treating the condition and a clinical example''
| |
| − | | |
| − | *[[Viruses|Viruses - WikiBugs]]
| |
| − | | |
| − | *[[Innate Immune System - WikiBlood]]
| |
| − | | |
| − | *[[Adaptive Immune System - WikiBlood]]
| |
| − | | |
| − | ==[[Immunodeficiencies Flashcards - WikiBlood|Immunodeficiencies Flashcards]]==
| |
| − | | |
| − | ==References==
| |
| − | '''Books'''
| |
| − | | |
| − | *Ivan Roitt: '''Essential Immunology,''' Ninth edition
| |
| − | | |
| − | *Goldsby, Kindt, & Osbourne '''KUBY Immunology,''' Fourth edition
| |
| − | | |
| − | '''Lecture Notes'''
| |
| − | | |
| − | *Dr Brian Catchpole BVetMed PhD MRCVS
| |
| − | | |
| − | '''Websites'''
| |
| − | | |
| − | *Michelle Tennis & Peggy Melton http://www.bitoheavencollies.com
| |
| − | | |
| − | ==Creators==
| |
| − | | |
| − | [[Natalie Brown]]
| |