Haematology and oncology

Question 1

Response of spleen to injury

Answer 1

Acute inflammation – hyperaemia, microabscesses, abscesses
Hyperplasia of monocyte, macrophage system – granulomatous dx – fungal usually
Hyperplasia of lymphoid system – production of plasma cells and antibody, cell mediated immunity
Lymphoid atrophy/depletion – parvo or disease where lymphocytes being destroyed. Follicles shrink.
Storage of blood or contraction to expel reserve blood – can contract with death – red pulp lost
Neoplasia

Question 2

Causes of splenomegaly

Answer 2

Diffuse – uniform
- Infection/reactive hyperplasia
- Congestion (barbiturate euthanasia, anthrax, torsion/GDV, circulatory failure
- Neoplasia – uncommon to be diffuse
- Leukaemia, systemic tumours (mast cells, HS, myeloma, lymphoma)
- Haemolytic anaemia – most common

Question 3

What is autoimmune haemolytic anaemia/ IMHA

Answer 3

Diffuse marked anaemia and severe splenomegaly
Body decides to destroy RBC. So when enter spleen – being destroyed. Causes back up of dying RBC so debris can cause vessels to block – infarction.

Question 4

Splenic nodules

Answer 4

Haematoma - common
Hyperplasia (gross enlargement – cell proliferation)
Abscess – not as common
Can be seen in incomplete splenic contraction – so nodules of RBC.

Question 5

What is seen with splenic lymphoid follicular hyperplasia

Answer 5

Reactive hyperplasia of the white pulp lymphoid tissue
Can be in response to infection.

Question 6

What is spleen - senile nodular hyperplasia

Answer 6

A common, usually incidental change in older animals, particularly dogs.
Histologically a mixture of red and white pulp tissue. Possibly coincidental haemorrhage

Question 7

What can be seen with spleen inflammation

Answer 7

Spleen – inflammation
Capsule/peritonitis
Parenchyma – splenitis, splenic abscess.

Question 8

Splenic haemorrhage

Answer 8

Spleen – haemorrhage

Massive splenic congestion and capsular rupture, leading to marked acute haemoabdomen and death

Question 9

Splenic neoplasia

Answer 9

Hemangiosarcoma – Mesenchymal tumour – spindle cells. Pluripotent stem cells. Most often in spleen and left oracle of heart. Met to liver, kidney, brain, anywhere.

Look like blood filled channels.
Usually huge and look neoplastic.

Question 10

What is the Thymus

Answer 10

Where T cells develop
Regresses at puberty

Question 11

Response of thymus to injury and neoplasia

Answer 11

Responses of thymus to injury
- Lymphoid atrophy/depletion - parvo
- Inflammation – very rare
- Haemorrhage and haematomas
- Neoplasia – doesn’t completely go away at regression
- Cysts
- Hypoplasia (immunodeficiency)
- Atrophy – stress, age (involution)
- Depletion - viral infections
(EHV1; FPV; CPV; CDV; FIV)

Neoplasia:
- Thymic lymphoma (cats and calves) esp. Felv cats
- Thymoma (epithelial plus lymphoid cells)
(adult; dogs, sheep and goats) ?myasthenia gravis)

Question 12

What is SCID - severe combined immunodeficiency

Answer 12

Don’t have functional lymphocytes – no cell mediated immune response
SCID is not a specific condition, but a constellation of entities, which vary in severity and molecular basis, but which all result in failed production of functional lymphocytes (splenic and thymic hypoplasia).

• Classically affects horses, humans, mice, and dogs
• Autosomal recessive in Arabian horse and their crosses
• All foals die by 5 months of age as a result of infection by a variety of pathogens, with equine adenovirus, Pneumocystis carinii , Cryptosporidium parvum, and Rhodococcus equi being most important.
• More commonly, defects affect just T, or both B and T lymphocytes, resulting in impairment of both cell types (and thus both CMI and humoral immunity)

Two major molecular mechanisms of importance in animals:

– Autosomal recessive defect causing inhibition of DNA-dependent protein kinase (Arabian foals, Jack Russell terriers, CB-17 lab mice)

– X-linked defect in type I cytokine receptors (Basset hound, Cardigan Welsh Corgi)
Characteristic lesion in foals: Bilateral cranioventral bronchopneumonia with small spleen, lymph nodes and thymus (can be difficult to locate thymus)

Question 13

What is myeloid

Answer 13

Cells
- Granulocytes (neutrophils, eosinophils, mast cells)
- Monocytes
- Macrophages
- Erythrocytes
- Thrombocytes
- Other – dendritic cells

Tissue
- Bone marrow

Question 14

What is lymphoid

Answer 14

Lymphoid
Cells
- Lymphocytes

Tissues
- Lymph nodes
- Thymus
- Spleen
- Other – Peyer’s patches

Question 15

What do myeloid and lymphoid do?

Answer 15

Immunity – stimuli – infection, inflammation, fight/flight, antigens,

Question 16

When may you NOT see a stress leukogram?

Answer 16

May have hypoadrenocorticism - addisonian crisis - insufficient cortisol being produced to stimulate a stress leukogram

Question 17

Non-neoplastic lymphoid disease
Lymphadenopathy

Aitiology
Approach

Answer 17

Reactive hyperplasia – LN enlarges as part of immune response to lymphatic drainage from an affected site – usually localised

Lymphadenitis – infection/inflammation of LN
- Primary – LN itself
- Secondary – drainage, systemic
May be multiple or generalised – leishmania
Aitiology
- Often infection or inflammation
- Often a symptom, not disease itself.

Approach
History – concurrent infection/inflammation, medication
Physical exam – how many LN enlarged, which ones? – Source of infection/inflammation
Imaging
FNA
Submandibular LN
- Not uncommon to aspirate salivary tissue – if multiple LN enlarged, sample a variety
Good idea to warn client of inconclusive result.

Question 18

What is chyle

Answer 18

Chyle – Mixture of lymph and chylomicrons

Question 19

What are chylomicrons

Answer 19

Chylomicrons – lipids absorbed from intestine – transported via lymphatics

Question 20

What are chylous effusions

Answer 20

may result from rupture – trauma or obstruction (neoplasia) of thoracic duct or other major vessel
- Often idiopathic, site of leak not always determined
Both effusions (thoracic, abdominal) are rare
Immune response stimulated

Question 21

What is a chylothorax

Answer 21

Chylothorax is usually a bilateral pleural effusion
Can you stick a needle in it?
- Yes (thoracocentesis)
- Chylous effusion = modified transudate (progressing to exudate as inflammatory cells react to its presence)
Treatment may involve surgical closure of the thoracic duct

Question 22

Lymphangiectasia - lacteal dilation

Clinical findings
Diagnosis
Treatment

Answer 22

Lymphangiectasia – lacteal dilation
Pathophysiology: Intestinal lymphatics dilate and lose chyle into the lumen  protein-losing enteropathy
Aetiology (but most cases idiopathic):
- Congenital – may be inherited
- Acquired obstruction – e.g. neoplasia
Thought to be common in dogs; rare in cats
May be managed with low-fat diet +/- immunosuppressives (e.g. prednisolone)

History
- GI signs - weight loss, diarrhoea (chronic), vomiting

Physical exam - may present with - poor body condition, ascites

Biochemistry
- Parameters suggestive of PLE (protein losing enteropathy) - hypoalbuminaemia
- Hypocholesterolaemia - component of chyle

Haematology - lymphopenia - loss of chyle

Imaging - US - hyperechoic lacteals

Biopsy - consider endoscopic rather than surgical

Question 23

Non-neoplasia myeloid disease
Aplastic anaemia

Answer 23

Aplastic anaemia = failure of myeloid cell production
Multiple cell lines may be depleted (pancytopaenia)
Usually secondary
- Toxicity
- Adverse drug reaction
- Infection – Ehrlichia, parvovirus, feline leukaemia virus)
What could be the consequences of insufficient neutrophils?

Pure red cell aplasia = failure of erythrocyte production
- May be secondary to FeLV
Bone marrow infiltrates
- Myelofibrosis
- Gelatinous transformation

Question 24

Myeloid neoplasia

Answer 24

Myeloid leukaemia - rare - Acute (immature cells), chronic (differentiated cells), Polycythaemia vera (erythrocytes)

Mast cell tumour

Histiocytoma

Transmissible venereal tumour

Question 25

Histiocytoma

Answer 25

Common neoplasm in small animal practice
- Young dogs (< 2 years)
- Classically benign
- Can regress independently over several weeks
But use caution when advising clients
- Mast cell tumour can look a lot like histiocytoma

Question 26

Mast cell tumour

Answer 26

Mast cells are a form of granulocyte
- May appear in reactive lymph nodes
Malignant transformation - MCT
- Usually older dogs but any age at risk

MCTs usually present as skin masses
- Common – up to 20% of all canine skin tumours
- Cytology very sensitive – FNA of suspect skin masses recommended
- Some breeds more susceptible: boxers, Labradors, golden retrievers, Staffordshire bull terriers, Boston terriers, pugs

Grades - on histopathology
Lower grades - excision and monitoring
Higher grades - may spread to lymph nodes, liver, spleen, bone marrow - staging imporant
Locally invasive - high grades - margins of 3cm and 1-2 fascial plan deep to tumour
- Referral recommended with high grade

Degranulation
Histamine release can produce anaphylaxis
Recommend H1 blockers - chlorphenamine if tumour likely to be damaged during biopsy or surgery

Grading based on
- mitotic index
- Multinucleated cells
- atypical nuclei - size and shape
- anisokaryosis

Non resectable MCTs
- Tyrosine kinase inhibitors
- Mastinib

Question 27

Feline MCTs

Answer 27

Cutaneous form
- If well-differentiated may act benign
Visceral form – poorer prognosis
- Spleen, LN, liver
- Intestine may be diffuse
No grading system currently available
Association between mitotic index and survival time

Question 28

Transmissible venereal tumour

Answer 28

Infectious tumour
- Usually transmitted during mating
- Believed to be histiocytic but this is not confirmed
Not endemic to the UK
- May see more with increased number of imported dogs
Can respond to chemotherapy (e.g. vincristine)

Question 29

Lymphoid neoplasia

Answer 29

Lymphoid leukaemia
- T-, B-, or natural killer cell
- Acute or chronic
Lymphoid cells
- Plasmacytoma (plasma cells) – benign
Lymphoma
- B-cell (B = Better response to therapy)
- T-cell
T-zone ‘indolent’ lymphoma – surgical removal of affected node may be attempted
- Epitheliotropic (cutaneous) – rare

Question 30

Neutropenia - causes

Answer 30

Most common to least

Increased demand - migration to tissue (inflammation)
- Shift from circulating to marginating pool - acute endotoxaemia

Increased destruction
- Immune mediated neutropenia
- Drugs or toxins
- Viruses - parvo, feline panleukopenia

Decreased production by bone marrow
- FeLV, FIV
- drugs or toxins - anti-epileptic
- Primary BM disease - idiopathic aplasia, acute leukaemia
- Inherited defect

Unknown - feline idiopathic neutropenia

Question 31

What could circulating lymphoblasts indicate?

Answer 31

In peripheral circulation these could be suggestive of leukaemia or lymphoma (leukaemic phase)
Given presence of a cytopaenia (rather than cytosis) more likely to be acute leukaemia

Question 32

Acute leukaemia

Answer 32

Phenotypes: myeloid (AML), lymphoid (ALL), mixed/undifferentiated
Most acute leukaemias in dogs are myeloid
Differentiation between AML and ALL is difficult – many are misclassified
- Is it worth trying…? – ALL may be more responsive to chemotherapy
Rare
Presenting signs vague: inappetence, lethargy
Prognosis poor
- AML survival usually < 3 months with treatment, as little as 2 weeks without
- 50% die during chemotherapy induction as cytopaenia(s) or anaemia worsens – sepsis, haemorrhage
Contrast with chronic ML (4-15 months with treatment) or chronic LL (some > 2 years)

Question 33

Leukaemia vs lymphoma

Answer 33

Stage V lymphoma infiltrates bone marrow – can be difficult to distinguish from leukaemia
Lymphoma clues:
- Cytosis more likely than cytopaenia
- Lymphadenopathy
- Organomegaly
- Bone marrow <25% blasts

Question 34

Types of tumours

Answer 34

Epithelial
Mesenchymal
Round cell

Question 35

Epithelial tumours

Answer 35

• Papilloma
• Squamous cell carcinoma
• Transitional cell carcinoma
• Adenoma
• Adenocarcinoma

Question 36

Mesenchymal tumours

Answer 36

• Fibroma/Fibrosarcoma
• Osteoma/Osteosarcoma
• Haemangioma/Haemangiosarcoma
• Lipoma/Liposarcoma
• Chondroma/Chondrosarcoma

Question 37

Round cell tumours

Answer 37

• Lymphoma
• Mast Cell Tumour
• Plasma Cell Tumour
• Histiocytic Sarcoma

Question 38

Why does tumour type matter?

Answer 38

Why does it matter?
Clinical behaviour
Metastasis – blood or lymph
Therapy
Getting a diagnosis
FNA – easy, conscious, cytology
Incisional biopsy – More tissue, anaesthesia req. histology
Excisional biopsy
First surgery is most important
Biopsy
- Know what tumour it is – cell of origin (epithelial, mesenchymal, round cell), grade
- Decide margins
- Think about staging
Grade – Features of the tumour on cytology/histopathology which allow predictions to be made about the tumours behaviour
High grade
- Higher mitotic count
- Poorly differentiated
- Locally invasive
- Nuclear/cellular/atypia
- Necrosis
Staging
An assessment combining features of the primary tumour and a measurement of where it has spread
TNM – Tumour, lymph node, distant metastasis
Stage I = small superficial low/intermediate grade tumours without nodal/distant metastasis
Stage II = Superficially large or deep small tumours (any grade) without nodal/distant metastasis
Stage III = Large deep tumours without nodal/distant metastasis
Stage IV = Any tumour with nodal or distant metastasis

Question 39

Tumour staging

Answer 39

TNM – Tumour, lymph node, distant metastasis
Stage I = small superficial low/intermediate grade tumours without nodal/distant metastasis
Stage II = Superficially large or deep small tumours (any grade) without nodal/distant metastasis
Stage III = Large deep tumours without nodal/distant metastasis
Stage IV = Any tumour with nodal or distant metastasis

Question 40

Types of tumour removal

Answer 40

Radical - entire component or structure containing mass
Curative intent - 2-3cm lateral margins and one fascial plane
Marginal - removing all the mass within pseudocapsule
Cytoreductive - removing the bulk of disease within pseudocapsule

Question 41

Why do animals with cancer get sick?

Answer 41

Pathophysiology
Functional
Bleeding
Infection
Effusions
Paraneoplastic syndromes

Functional
Pain, compression, obstruction

Effusions/bleeding
Pleural, pericardial, abdominal

Infections
Necrosis

Paraneoplastic syndrome
Hypercalcaemia
Hyperviscosity
Hormones (oestrogen)
Mast cell tumours – histamine, heparin

Chemotherapy
Medicinal therapy
Cytotoxic drugs
Anti-neoplastic agents
Immunosuppressive drugs
Maximum tolerated dose chemotherapy – given at spaced out intervals
Metronomic chemotherapy – regular intervals

Question 42

Chemotherapy side effects

Answer 42

Chemotherapy side effects
- Rapidly dividing tissues - kills
- Bone marrow – suppressed or killed
- Fur/whiskers
- Gastrointestinal tract

Anaemia – as lowered RBC count

Extravasation – leaks out of vessel when administering – can cause blistering, sloughing, necrosis

Cyclophosphamide - Sterile Haemorrhagic Cystitis

Doxorubicin – Cardiotoxicity

Doxorubicin (Cats) – Renal toxicity

Question 43

Lymphoma

Answer 43

Lymphoma
Malignant tumour of the WBC
- One of the most common tumours in the dog or cat.
- It can be seen in almost any organ
- Where it’s found will influence how it presents

Classification
Prognosis and treatment options
- B cell lymphomas better prognosis
- B and T cell lymphomas are known to respond differently to chemotherapy.
- High grade lymphoma – associated with poorer prognosis.

How are cats different?
- Multicentric form associated with FeLV.
- Greatly reduced since the introduction of vaccination against FeLV.
- Extranodal types are more common (e.g. alimentary, mediastinal, nasal and renal)

How do we diagnose lymphoma?
- FNA
- Trucut biopsy
- Excisional biopsy (e.g. removal of a lymph node)
- Flow cytometry

Question 44

Staging lymphoma

Answer 44

I - single lymph node
II - multiple lymph nodes
III - Generalised lymphadenopathy
IV - Liver and/or splenic involvement with or without stages I-III
V - Bone marrow or blood involvement and/or any non lymphoid organ - eyes/CNS - with or without stages I-IV

Substage - A without clinical signs of disease, B with clinical signs of disease

Question 45

Treatment protocol for lymphoma

Answer 45

C = Cyclophosphamide (capsule)
H = Doxorubicin (injection, care on handling)
O = Vincristine (injection)
P = prednisolone (tablet or injection)

Question 46

Differentials for splenomegaly

Answer 46

Differentials for splenomegaly –

Diffusely Infiltrative – neoplastic – lymphoma, malignant histiocytosis, multiple myeloma)

Infectious- septicaemia, viral (canine adenovirus)

IMHA IMT

Congestive – splenic torsion, portal hypertension, drug induced

Focal splenectomy – primary/secondary neoplasia, - hemangiosarcoma, haemangioma,

Non-neoplastic causes - nodular lymphoid hyperplasia, haematoma, abscess, granuloma.

Question 47

Canine splenic disease

Answer 47

Haemagiosarcoma is the most common primary splenic neoplasm.
- The spleen is a common site of secondary metastasis in dogs.
Caution with assuming that all masses are neoplastic.
- 2/3’s are reported to be benign (e.g. Haematomas/haemangioma) whilst 1/3 are malignant (haemangiosarcoma most likely)

Question 48

Feline splenic disease

Answer 48

Haemagisarcoma is rare
Splenic MCT is more common.
- Approximately half of MCT in cats are splenic
- They can be diagnosed via FNA
Even if they have metastasised splenectomy may be worthwhile as they often have a good median survival time (12-18 months)

Question 49

Haemangiosarcoma

Answer 49

GSD>Labrador and retriever, less common in cats
Extremely malignant tumour
Other common site right atrium
High metastatic rate of >90% to lungs, liver, nodes, brain and potentially skin/SC tissues
Surgery as primary treatment
- Thoroughly check abdomen for metastatic spread
- Post operative chemotherapy indicated in pretty much all cases
Splenectomy alone – survival ~ 3 months
Splenectomy plus chemotherapy ~ 6 months
- Survival of > 1 year even with drugs <10%
- Die of diffuse metastatic disease
- Prognosis better if spleen not ruptured?
- Chemo of choice doxorubicin every 3 weeks
- Prognosis from atrial masses similar

Don’t try and perform a partial splenectomy – splenectomy is more straightforward.
Check pcv/coagulation values – may need a transfusion.
Monitor for arrythmias

Question 50

Splenic torsion

Answer 50

Commonly seen as part of GDV
Classically large and giant breed dogs
May present with abdominal pain, collapse, pallor, tachydysrhythmia
May be chronic problem
Treat with splenectomy – risks as with other splenic surgery

Question 51

Define Immunocompromised, suppressed and deficient

Answer 51

Immunocompromised: any aspect of host defences is deficient.
Immunosuppressed: immune defences are specifically impaired.
Immunodeficient: body’s immune response is compromised or absent.

Question 52

Virus cell interactions

Answer 52

Productive – lytic – destroys.
Persistent – retroviruses, herpes

Non-productive – Viral destruction – transform to tumour cell
Latent – lie dormant

Question 53

How does a virus enter a cell?

Answer 53

Utilisation of naturally occurring and useful receptors on the cell surface.
Endocytosis: both enveloped and non-enveloped viruses.
Direct injection (bacteriophages)
Fusion of the envelope (some enveloped viruses)

Question 54

Canine distemper virus

Answer 54

Morbillivirus related to Measles, RNA enveloped virus (poor survival in the environment).
Infects a number of cells but has particular ‘tropism’ for lymphocytes (causes their destruction).
Oro-nasal infection (inhalation of aerosol) – replication in local lymphoid tissue-macrophages-dissemination to local lymph nodes – spread to other haemopoietic organs (spleen, bone marrow etc.)
RNA needs to be transcribed into DNA to start producing things.

Question 55

Canine parvovirus and feline pan leukopenia virus

Answer 55

CPV & FPV
Non-enveloped DNA virus
Tropism for fast dividing cells (gastrointestinal tract-crypts, bone marrow, lymphoid tissue)
Destruction of white blood cells precursors within bone marrow, sequestration of neutrophils within GI tract, damage to the barrier leading to bacterial translocation.
Parvo can infect cats so NO isolation in cat ward

Question 56

FeLV - feline leukaemia virus

Answer 56

FeLV – feline leukaemia virus
Retrovirus, RNA virus, Oncovirus family, worldwide distribution.
- 4 subtypes: A, B, C and T – all closely related antigenically.
Exogenous (from other cat) as well endogenous FeLV (incorporated into DNA long time ago).

Transmission through mutual grooming (‘love virus’) and rarely through bites.
- Risk factors: young age, increased population density, poor hygiene.
- In many areas low prevalence due to testing and vaccination

Antigen test rather than antibody as we vaccinate routinely for FeLV so antibodies will be present
Follow test instructions to get the best out of your test
- Room temperature
- Plasma, serum, or whole blood
- Do not mix samples – e.g. mix samples from same litter
Understand your tests sensitivity and specificity, calculate positive and negative predictive values taking prevalence into consideration

Pathophysiology:
- Each cat can present differently.
-Much more severe and less selective than FIV (lymphopenia, neutropenia, impaired neutrophil function, loss of CD4+ and CD8+ cells).
-Anaemia: regenerative (usually through secondary causes e.g. Mycoplasma haemofelis or immune-mediated destruction) or non-regenerative (direct effect of the virus on bone marrow).
-Neoplasia (lymphoma and leukaemia) though these days uncommonly associated.

Loss of appetite
Progressive weight loss
Poor coat condition
Enlarged lymph nodes
Persistent fever
Pale gums and other mucus membranes
Inflammation of the gums (gingivitis) and mouth (stomatitis)
Infections of the skin, urinary bladder, and upper respiratory tract
Persistent diarrhoea
Seizures, behaviour changes, and other neurological disorders
A variety of eye conditions
Abortion of kittens or other reproductive failures

Question 57

FIV - feline immunodeficiency virus

Answer 57

Retrovirus, RNA virus, Lentivirus genus, closely related to HIV but humans are not susceptible to this virus.
- 5 genetically distinct subtypes (important for PCR testing!)
- Seroprevalence highly variable between regions (1-14% in cats with no clinical signs and up to 44% in sick cats.

Transmission via deep wounds inoculation with saliva.
Transmission in stable households – uncommon!
- Related to aggressive behavior.

Kittens born to persistently infected queens-rarely infected but antibodies may be present!

When thinking about FIV remember HIV (transmission and progression).
- Infects CD4+ T lymphocytes ( T helper cells) which are crucial for humoral and cell-medicated immunity.
- Invades dendritic cells, macrophages and CD4+ T-cells – can be detected in circulation, slow increase in viral particles and proviral DNA up to 12 weeks (clinical signs related to initial infection).
- Seroconversion within 2-4 weeks
- Decrease in viral load – entering asymptomatic phase.
- Latency – protection from immune system.
- Functional immunodeficiency through decline of CD4+ cells leading to AIDS-like deterioration.

• Late in the disease, antibodies level may decline and animal may test negative.
  Very few people will eliminate disease so test for antigens as antibodies can decline in late stage disease
  Cats at risk
  Promiscuous – unneutered
  Old
  Stray

Vaccination available but not licensed in Europe.
Induces humoral response.
Currently not recommended by ISFM and AAFP guidelines.
Huge genetic variation is a huge obstacle to vaccine protection

Weight loss.
Recurrent fever.
Lethargy.
Enlarged lymph nodes.
Gingivitis and stomatitis (inflammation of the gums and mouth)
Chronic or recurrent respiratory, ocular and intestinal disease.
Chronic skin disease.    Neurological disease (in some cats the virus can affect the brain)

Question 58

FIP - feline infectious peritonitis

Answer 58

Enveloped RNA virus
FCov – enteric virus, ubiquitous in the feline population
Only small proportion of cats will develop FIP, biphasic peak (weaning then >10y old)
Mutation that allows the virus to infect monocytes – macrophages, is the key part of the FIP pathophysiology
Presence of antibodies is not diagnostic for FIP
Uveitis and jaundice

2 forms: effusive (‘wet FIP’) and non-effusive (‘dry FIP)
Consider it a continuum (a spectrum) from non-effusive to effusive form.
Effusion is not related to ‘peritonitis’, it is MULTISYSTEMIC INFLAMMATORY VASCULITIS (PYOGRANULOMATOUS VASCULITIS)

Effusive form: any body cavity including pleural and pericardial cavities, as well as abdominal cavity.

Non-effusive form: usually ocular and neurological presentations

IL-6 = stimulates hepatocytes to release AGP (acute phase glycoprotein)
TNF-α = part of inflammatory response (lymphopaenia)
IL-1 = pyrogenic, activates B and T cells
Matrix metalloproteinases = increase ‘leakiness’ of the vessels

Antibody-dependent enhancement (ADE) = potential for exacerbation of the disease by pre-existing antibodies; similar concerns during Covid-19 pandemic.
- How do we diagnose FIP? How do we treat?
In cats that develop FIP disease, the first signs of illness may be very vague. Listlessness, lethargy, decreased or absent appetite, weight loss, and a fluctuating fever are commonly reported clinical signs.
At this stage, most cats will develop the ‘wet’ or effusive form of FIP, which refers to the accumulation of fluid in body cavities; fluid may accumulate in the abdomen, leading to a swollen abdomen, or in the chest cavity, resulting in difficulty with breathing.
Some cats develop ‘dry’ or non-effusive FIP where little to no fluid accumulates. The dry form often involves severe inflammation in one or more organs including the eyes, brain, liver, intestine, or other organs of the body, leading to a variety of clinical signs. Many cats with non-effusive FIP will have ocular (eye) symptoms as their only clinical sign.
Most cats exposed to feline coronavirus, even to the potentially FIP-inducing strains, are able to develop an immune response that protects them, therefore only a small proportion of infected cats actually develop clinical disease. However, those that do develop the disease almost invariably die.

Question 59

FeLV vs FIV

Answer 59

FeLV
- May be transient infection
- Curtailed lifespan
- Recurrent infections
- Anaemia
- Neoplasia - lymphoma

FIV
- Infected for life
- Relatively normal lifespan
- Recurrent infections
- Gingivitis
- Neoplasia