Lymphoid Pathology

Question 1

1. What is the thymus and its main function?
2. Where is the thymus located?
3. Thymus in neonate?

Answer 1

1. For maturation and selection of T lymphocytes.
   Has a capsule, cortex and medulla and trabeculae.
2. Cervical region, thoracic inlet, proximity of heart.
3. Large.

Question 2

What are common responses of the thymus to injury? and which is the main response?

Answer 2

Hypoplasia, atrophy, haemorrhage/haematoma, inflammation, hyperplasia, neoplasia.
Atrophy is the main one.

Question 3

What is thymic hypoplasia secondary to?
Spp recognised in?
Effect on thymus?

Answer 3

Usually secondary to immunodeficiencies that affect T cells.
Recognised in foals and certain dog breeds.
Congenital disorder.
Smaller and less tissue.

Question 4

Premature atrophy vs physiological involution.

Answer 4

Thymus encounters a natural involution after sexual maturity.
Can be v difficult to differentiate between atrophy and involution.
Extremely small thymus in neonate should be considered abnormal.

Question 5

1. What is thymic atrophy?
2. What can commonly cause thymic atrophy?

Answer 5

1. Alteration of its cellular density and/or cellular composition and subsequent lobular shrinkage.
2. Infectious agents:
   - FIV, Parvo – cats.
   - Distemper, Parvo – dogs.
   - BVD virus – cattle.
   - Equine Herpes Virus 1 – horses.
   - Classical swine fever virus and PRRS – pigs.
   Stress – apoptosis of thymic T cells.
   Environmental contaminants – mycotoxins (e.g. fumonisins, aflatoxins), dioxins, PCB, heavy metal (lead, mercury).
   Malnutrition – (e.g. Vitamin B6 or zinc deficiencies) – immunosuppression.

Question 6

Possible causes of thymic haemorrhages/hematoma.

Answer 6

Thoracic trauma.
Overstretching of the neck.
Rupture of aortic aneurisms.
Neoplasms.
Intoxication with anticoagulant rodenticides.
Spontaneous idiopathic form (young dogs).

Question 7

Define hematoma.

Answer 7

A pocket of blood within the parenchyma/tissue.

Question 8

Thymic inflammation.

Answer 8

Rare – Usually, viral infections cause destruction of the lymphoid component (lymphocytolysis) and subsequent atrophy rather than an inflammatory response.

Question 9

1. What spp. is diffuse thymus hyperplasia observed in?
2. What is the usual cause for these spp.
3. What is follicular thymus hyperplasia indicative of?
4. What are the follicles?

Answer 9

1. Calves, rabbits and birds.
2. Repeat immunisation.
   Or a physiological variation.
   Findings are incidental and no clinical signs reported.
3. Chronic inflammation or immunologic response.
4. Germinal centres and expansion of the plasma cells.

Question 10

1. What is a thymoma?
2. What spp. most commonly affected by thymomas?
3. Thymoma location.
4. Malignant counterpart of thymoma?

Answer 10

1. Usually benign epithelial cell tumour, usually in older animals and is slow growing, can be encapsulated.
2. Goats, cats, dogs.
3. Cranial mediastinum.
4. Thymic carcinoma (v rare). – Highly invasive and most common subtype is squamous cell carcinoma which is common in dogs.

Question 11

1. What spp. thymic lymphoma common in?
2. Clinical signs?

Answer 11

1. Cats (1-10yrs), beef cattle (6-24mths).
2. Reflect compression of the adjacent anatomical structures e.g. dyspnoea, oedema, difficulty swallowing (dysphagia).

Question 12

1. What is the spleen?

Answer 12

1. Secondary lymphoid organ with capsule, trabeculae, red pulp, white pulp.
   Red pulp – erythrocyte storage, filters old/defective erythrocytes by macrophages, filter particles and pathogens by macrophages.
   White pulp – Macrophages, antigen presenting cells, B and T lymphocytes.
   Trabeculae – squeeze spleen when large amount of extra blood required.

Question 13

Causes of splenic atrophy?

Answer 13

Cachexia due to starvation, malignant neoplastic diseases, malabsorption syndromes.
Chronic radiation.
Senile (aging) atrophy common in elderly dogs and horses – small spleen w/ irregular pale surface.

Question 14

Types of splenic overload and infiltration.

Answer 14

Siderotic plaques – incidental finding in old dogs. Previous trauma (maybe). Sider-calcic (Fe2+/Ca2+) impregnation.

Haemosiderosis – reduced rate of erythropoiesis.
Rapid destruction of erythrocytes.

Amyloidosis – Primary or secondary.
Most commonly secondary to chronic inflammation or neoplasia.
Amyloid protein.
Abnormal accumulation – yellowish appearance.

Question 15

Splenic vascular changes…
Active hyperaemia.

Answer 15

Active hyperaemia (increased blood flow to spleen).
- Acute systemic infections and bacterial intoxications.
– Spleen markedly larger and darker.

Question 16

…
Passive congestion.

Answer 16

Passive congestion.
- Disorders in the systemic circulation.
- Administration of barbiturates (act on smooth muscles which composes trabeculae).
- Hemolytic diseases.
- PM change.

Question 17

…
Infarction.

Answer 17

Infarction (death of tissue related to ischaemia).
- Thrombi and thromboembolism (diseases that cause vascular damage e.g. septicaemia, hypercoagulative states, endocarditis, septic thrombosis of vena cava (cows)).
- Neoplasia e.g. hyperviscosity syndrome associated to myelomas.
- Acute infarct – dark red, raised, haemorrhagic, demarcated area.
- Chronic infarct – wedge shaped, sharply demarcated, grey-white areas.
- Fibrous scar – final resolution.

Question 18

Torsion/volvulus of the spleen.

Answer 18

Large breed dogs – w/ or w/o gastric torsion.
Pig also affected – sows in particular.
Complete twist of the gastroesplenic ligament w/ splenic vein and artery occlusion.
Severe congestion and haemorrhagic infarction.
Asymptomatic until v severe.

Question 19

Splenic rupture.

Answer 19

Primary – trauma (e.g. RTA).
Secondary – splenomegaly, splenic neoplasia, heamatomas.
Poss. outcomes.
- Haematoma.
- Dissemination of small spleen fragments into the omentum (peritoneal splenosis).

Question 20

Splenic haematoma.

Answer 20

Single and large usually.
Causes:
- trauma, lymphoid hyperplasia nodules.
- May also be from rupture of splenic vascular tumours (haemangioma, hemangiosarcoma).

Question 21

Types of splenitis.

Answer 21

Suppurative, necrotising, pyogranulomatous, granulomatous.

Question 22

Common diseases where splenitis occurs.

Answer 22

Anthrax, Septicaemia salmonellosis, African and classic swine fever, erysipelas, Arcanobacterium pyogenes, Rhodococcus equi, Trueperella pyogenes, Streptococcus, CLA (caseous lymphadenitis) (sheep), Systemic mycoses, Bovine TB, FIP, Protozoal infections (Leishmania), Francisella tularensis.

Question 23

Extramedullary Haematopoiesis.

Answer 23

Related to the function of the spleen.
Chronic processes, esp. chronic anaemia in dogs and cats, can lead to this.
Producing precursor cells to try and supply RBCs.

Question 24

Lymphoid hyperplasia.

Answer 24

Diffuse or follicular.
Can be result of the response to blood-borne antigens (chronic antigenic stimulation).

Question 25

Nodular hyperplasia.

Answer 25

Incidental finding in older dogs and sometime old bulls.
A singular nodule or multiple nodule.
Mixed cell populations possible, but predominantly lymphocytes.
May predispose to splenic haematoma.
Not neoplastic lesions but may evolve into neoplasia.

Question 26

Neoplasia of the spleen.

Answer 26

Hemangiosarcoma (most common in dogs).
Lymphoma.
Mast cell tumours.
Haemangiomas.
Sarcomas.
Metastatic tumours (carcinoma, sarcoma).

Question 27

What are lymph nodes?

Answer 27

Small organs that filter out harmful substances from the lymph fluid, which drains from tissues and cells.
Has cortex, medulla etc. Usually APCs come through and activate and stimulate proliferation of the T and B lymphocytes.

Question 28

Causes of LN atrophy.

Answer 28

Viral infections (BVD, FIV, Distemper, Feline Parvo).
Malnutrition / Cachexia.
Old age.
Toxins / chemotherapy / irradiation.

Question 29

LN overload and infiltration…
1. What if the LN is yellow?
2. What if LN is dark red/brown.
3. What if LN is black?
4. In what spp. would you see an accumulation of fat in LNs and for what reason?
5. In what situation would you get LN gas accumulation?
6. Cause of lymph cysts.

Answer 29

1. Jaundice.
2. Haemosiderin – haemorrhage/prolonged stasis.
   Iron injection – Piglet.
   Melanin.
   3, Melanin.
3. Mesenteric lymph nodes in pigs.
   Retromammary LNs in cows.
4. Drainage of emphysematous lesions.
5. Accumulation of intra-node lymph due to poor downstream srainage.

Question 30

LN hyperplasia.

Answer 30

Transient, benign, non-neoplastic process that may affect one or more LNs in relation to the antigen stimulation.
Lymphadenomegaly – LN enlargement. Localised or generalised, peripheral or internal.
Reactive – response to antigenic stimuli, production of follicles
- Benign, transient, local or systemic.

Question 31

1. What type of lymphadenitis affects sheep? – What type of exudate is present in the lesions? – what are the agents?
2. What type of lymphadenitises affect horses? – exudate? – agent?

Answer 31

1. Caseous lymphadenitis. – caseous/suppurative. – Corynebacterium pseudotuberculosis.
   Rhodococcus – pyogranulomatous – Rhodococcus equi.
2. Strangles – Suppurative – Streptococcus equi.

Question 32

1. What lymphadenitises affect pigs? – exudates? – agents?
2. What lymphadenitis affects bovine spp? – exudate? – agent?

Answer 32

1. “Jowl abscess” – suppurative – Streptococcus porcinus.
   PCV-AD – granulomatous – Porcine circovirus-2.
2. TB – Granulomatous – Mycobacterium bovis.

Question 33

1. What lymphadenitis affects ruminants? – exudate? – agent?
2. What lymphadenitis affects cats? – exudate? – agent?

Answer 33

1. Johne’s Disease – Granulomatous – myobacterium avium subsp. paratuberculosis.
2. FIP – Granulomatous – FCoV.

Question 34

Equine strangles mechanism of infection.

Answer 34

Bacterium inhaled/ingested > attaches to tonsils and penetrates into deeper tissues > drains into lymphatic vessels and regional LNs > large abscesses cause laryngeal compression so respirator stridor, dysphagia > rupture of abscesses > discharge to skin surface, spread medially into guttural pouches – reservoir and carrier state, spread via blood or lymph to other organs (‘Bastard Strangles’).

Question 35

Caseous lymphadenitis mechanism of infection.

Answer 35

Wound infection with Cornybacterium pseudotuberculosis > Drains into local LNs > Suppurative inflammation > Abscesses form > Abscesses are encapsulated > Capsule compromised, bacteria escape > Alternating necrosis, pus formation and reformation of the capsule > Drain externally through the skin and/or spread through lymph or blood to other organs.

Question 36

Granulomatous lymphadenitis – bovine TB mechanism of infection.

Answer 36

Mycobacterium bovis-containing aerosol droplets inhaled
Typical granuloma formula:
- Central macrophages w/ mycobacteria (+/- caseous necrosis +/- mineralisation).
- Halo of epithelioid and foamy macrophages and multinucleated giant cells .
- Outer layer of lymphocytes.
- Fibrous capsule.

Question 37

1. Name primary neoplasia of the lymph nodes.
2. Name secondary lymph node neoplasia.

Answer 37

1. Lymphoma.
2. Carcinomas – afferent lymphatic spread.

Question 38

Pathology types of the lymphatic vessels.

Answer 38

• Inflammation of lymphatics = lymphangitis.
• Obstructed flow = Lymphangiectasia (enlargement of vessels)/lymphoedema (accumulation of lymphatic fluid in the interstitial tissue).
• Lymphatic rupture = Rupture thoracic duct/chylothorax.