Immunodeficiency and autoimmunity

Question 1

Innate immunity affected

Answer 1

Neutrophils and macrophages

Question 2

Acquired immunity affected

Answer 2

cell mediated

Question 3

Feline Immunodeficiency Virus (FIV)

Answer 3

Deficiency of T cells. Just like HIV. Retrovirus (RNA).
T lymphocytes undergo apoptosis. Drop in the level of CD4. Chronic infection (secondary infections). Cats are typically presented because of secondary infection in the URT or systems where you have normal flora (= oppotunistic infection)- digestive in general, oral cavity.
* Transmitted with blood/saliva (bite wound) (most imp. distinction between HIV, saliva too)
* Lifelong infection
* Vaccination (protective 75%-80%, 20% will still get FIV)/ maternal Ab (usually protective in kittens)
*Diagnosis, test: 98% sensitive to antibodies test

Question 4

FIV stages of infection

Answer 4

1. Acute phase- transient lymphadenopathy (due to rising immune response)- may not be visible. Severity depends on age. Several weeks.
2. Asymptomatic carrier- latency phase- can last weeks to years. Healthy, normal looking
3. Persistent generalized lymphadenopathy- non specific signs of illness (weight loss, large lymph nodes, stomatitis, anaemia, leucopenia)– majority of cats are presented at this stage
4. Terminal AIDs-like phase- lasts less than a year. Opportunistic infections, misc. disorders including neoplasm

Question 5

Stage 3-4

Answer 5

Mostly lymphocytes and erythrocytes and WBCs. Cells in the bone marrow are infected. (Penia of all of the above)

Question 6

Concurrently with FIV commonly??

Answer 6

Infection with mycoplasma (common infection of RBCs in cats or other species). Common presentation of FIV is anaemia. You would find Mycoplasma haemofelis. But the underlying condition is FIV.
* Anaemia, non regenative (can be regenerative at the beginning but when bone marrow suppression, it can become non)

Question 7

Secondary opportunistic infections with FIV

Answer 7

• Stomatitis/ gingivitis
• Toxoplasma gondii
• Cryptococcus sp.
• Mycoplasma haemofelis
• Calcivirus (URT)
• Herpesvirus (URT)
• Neurological disease
• Lymphoma (B cell, extranodal)

Question 8

Feline Leukaemia Virus (FeLV)

Answer 8

Retrovirus (RNA virus), Lentivirus
* lifelong
Drop in CD4 T lymphocytes (very similar to FIV)
Transmitted in blood and saliva
Clear associated with viral infection and Neoplasia (myelo and lymphoproliferative diseases)– 30% of FeLV + cats will develop lymphoma or leukaemia. 50% of thymic lymphomas are associated with FeLV
* Anaemia
* Immunosuppression (secondary infections)
* Diagnosis, test: 98% sensitive to antibodies test

Question 9

Chediak-Higashi Syndrome (innate)

Answer 9

Cattle, cats, mink, mice, humans
Big lysosome granules because they are building up and not released in Neutrophils. Size of eosinophilic granules. Vary in numbers. Can be mistaken for eosinophils- but the eosinophil granules are much brighter.
**every cell type in the body that contains granules will be affected by this disease- morphological and functional abnormalities
i.e. melanin- big clumps of melanin- causes hair frigidity- alopecia. Also depigmentation

Question 10

Pelger Huet Anomaly (innate)

Answer 10

Failure of segmentation of neutrophil nucleus. They all look like bands. You think persistent left shift.

Question 11

Canine Leukocyte Adhesion Deficiency (innate)

Answer 11

Affects bovine and canine.
Irish Wolfhound.
Caused by persistent leukocytosis. Impaired pus formation.
Autosomal recessive inheritance.

Leukocytes adhere to blood vessel wall and migrate for inflammation. Four phases.
Defect in the molecule that binds the leukocyte to endothelial wall and forms the adhesion. Therefore the rest cannot happen- no migration or stable adhesion. So they circulate in peripheral blood. Why you have a persistent leukocytosis.

Question 12

Bovine Leukocyte Adhesion Deficiency (innate)

Answer 12

Neutrophilia without left shift, lymphocytosis, and monocytosis.
Secondary infections will be overwhelming. (GI and resp)
Usually fatal within days of birth.

Question 13

Canine Cyclical Haematopoiesis (innate)

Answer 13

Collies, grey pigmentation, loss of neutrophils every 11-12 days, persists for 3-4 days. Total bone marrow suppression for that 3-4 days. So drop in neutrophils because they have the shortest life span, so they will be the ones that drop first. Recurrent infections, widespread lymphoid atrophy. Therefore secondary infections immediately- so most puppies die within hours or days from birth

Question 14

Severe Combined Immunodeficiency (SCID)

Answer 14

Arabian and Arabian cross
Autosomal recessive inheritance
Lymphopenia
Sopontaneous mutation of gene DNA Protein Kinase
B and T cells defective
** complete knock out of lymphocytes because it affects the lymphoid precursors
* can survive for a few weeks after birth but after maternal antibodies drop they will die, no cure

Question 15

X Linked Severe Combined Immunodeficiency (SCID)

Answer 15

Basset Hound, Welsh Corgi
Lymphopenia
Decreased number of CD8+T cells, normal B cells
only males
**thymus depleted (very small)

Question 16

Agammaglobulinaemia

Answer 16

Lack of production of all immunoglobulins.

Failure of passive transfer

Question 17

Autoimmunity

Answer 17

Immune response to self-antigens, organ specific, localized or systemic
Localized or systemic

Question 18

Systemic lupus erythematous

Answer 18

Not one single antigen attacked by Abs, multiple ones. Normally related to DNA. Every cell in the body affected
Failure of mechanisms that maintain immunological self-tolerance
* Autoantigen- antibody complexes deposit throughout the body–> type III hypersensitivity reaction (lupus is typical example)–> inflammation of joints, skin, and kidney
* UV exacerbated cutaneous lesions (humans)

Question 19

Clinical signs of Systemic Lupus Erythematosus

Answer 19

Variable, may mimic numerous diseases. “Great imitator”
Chronic illness characterized by pds of progression and remission
*Dermatitis, nonerosive polyarthritis, glomerulonephritis, pericarditiz, myocarditis, generalized muscle wasting (polymyositis), pneumonitis, pleuritis, meningitis, myleitis, polyneuropathy, and lymphoedema
* lethargy, anorexia, fever
*Proteinuria, hemolytic anemia, thrombocytopaenia, bone marrow necrosis

Question 20

Why ulceration and depigmentation?

Answer 20

Accum. of inflamm cells at the junction between epidermis and dermis. Mechanism is not known. They cause depigmentation because they affect the epidermal dermal junction where melanocytes normally site (at the level of basal cells)- so they leak pigment into the dermis. Nose will be depigmented. Later stages erosion and ulceration- separation of the epidermis from dermis.

Question 21

Pemphigus Foliaceus

Answer 21

11 or 12 types. 3 are the focus because they occurs in animals. Abs targeting molecules in the epidermis. Destruction of cell membrane junction. The only diff b/t 3- protein targeted is different and the level of destruction is different.
i.e. epidermis, dermis, collagen 18 (keeps dermis and epidermis together)
OUTCOME always the same vesicles and erosions. Difficult to diagnose when you only have crusts.
Confined to the head- lips, nose, tips of the ears.
Presentation- crusting, oedematous lesions