The hematopoietic System

The hematopoietic system includes bone marrow, thymus, lymph nodes and spleen. Hematopoietic  system produces the cellular components of the blood. Moreover of the reticuloendothelial cells are mainly contained in the blood forming organs (spleen, lymph nodes, nodules and Done marrow.

Bone Marrow (Hemic)

It is the primary, and usually the only, adult organ for hematopoiesis (erythropoiesis and leukopoiesis). In the young animals, the interior of all bones is occupied by red bone marrow, but as the animal becomes older, the red marrow, in the shaft of the long bones is replaced by yellow or fatty bone marrow. During fetal development hematopoiesis observed first in yolk sac and after that the liver, spleen, lymph node ad thymus. At birth, all marrow throughout the skeleton is active and occupies most of the marrow space.

In adult most of active marrow is in flat bones, ribs, vertebrae and proximal epiphyseal region of long bones. The remaining marrow becoming yellow, fatty and inactive.

• In adult mice and rat hematopoiesis continues in spleen and to lesser degree in other organ.

• Extramedullary hematopoiesis means the hematopoiesis occurs in liver, spleen and other organs in adult due to increase demand of erythrocytes as in case of anemia (Fig. 1).

Fig. 1: Spleen of mice suffering from anemia showing extramedullary hematopoieosis. H&E.

All circulating cellular elements of blood arise from a common hematopoietic stem cell. This cell give rise to:

a. Lymphoid stem cells which are the precursors of T and B lymphocytes.

b. Myeloid stem cells which gives rise to:

1. Erythrocytes and megakaryocytes (platelets).

2. Neutrophils and monocytes.

3. Eosinophils and basophils.

The recognition of cell types, developmental stages and differentiation of myeloid: erythroid ratio require bone marrow smears.

• Tissue secretion are necessary to evaluate aplasia, hyperplasia or focal lesions.

• The differentiation of stem cells into mature circulating cells is controlled by various factors such as interleukins, TNF-a, granulocyte-macrophage colony stimulating factor (CM-GSF) as well as nutritional factors (iron, vitamins, etc..).

Hyperplasia

When there is an increase in the demand of the red blood corpuscles or the leukocytes, the red bone marrow proliferates, and extends into the shaft of the long bones. These changes are known as hyperplasia

It is recognized grossly by increasing in the amount of active (red) bone marrow and a decrease of fatty marrow as compared with the normal for a given age. There are two varieties of myeloid hyperplasia.

Erythoblastic hyperplasia

• It is characterized by replacing the fat marrow by red marrow and represented microscopically by presence of precursors of erythrocytes (erythroblast).

• It is associated with anemia except toxic aplastic anemia.

Leukoblasitic hyperplasia

• It is characterized by replacing the yellow marrow by grayish marrow and represented microscopically by predominance of the precursors of leukocytes.

• It is associated with infections accompanied with leukocytosis and with pyogenic infection.

Hypoplasia

It is characterized by increase the proportion of fatty marrow. The remaining hematopoietic tissue scattered in little islands through the fatty marrow.

Agranulocytosis

It refers to complete absence of granulocytes from the circulating blood.

It is due to complete aplasia of leukoblastic cells of bone marrow. It is related to aplastic anemia and is attributed to similar causes.

Osteomyelitis

It is the inflammation of the bone marrow.

• The infection gain access to marrow through:

1. Local wound (fracture).

2. Hematogenous metastasis.

• It is usually localized process. The reaction usually purulent although specific infection as tuberculosis and brucellosis produce their typical lesions.

Macroscopic appearance

Accumulation of pus which cause softening and necrosis of overlying bone.

Microscopic appearance

Accumulation of polymorph nuclear leukocytes and fibrin are noticed (Fig. 2).

Fig. 2: Bone marrow showing osteomyelitis characterized by accumulation of polymorph nuclear cells and fibrin. H&E.

Fibrosis

It is occurs as a sequelae of hypoplasia or aplasia.

It may accompany with myxyomatous degeneration.

Non neoplastic disorders of erythrocytes and myeloid leukocytes

Definition

It is a reduction below normal anemia of the number of erythrocytes and/or hemoglobin concentration per unit volume of blood.

In neonatal animals following ingestion of colostrums, erythrocytes numbers decrease and gradually return to adult level over succeeding weeks.

Animal residing at high altitudes have higher erythrocytes counts.

Classification of anemia

Anemia are classified in one of two ways:

1. Morphological classification

Based on MCV and MCHC anemia can classified to:

a. Macrocytic normochromic anemia occurs in vitamin B₁₂, folic acid deficiency and liver diseases.

b. Macrocytic hypochromic anemia occurs in case of acute blood loss or acute hemolysis.

c. Normocytic normochromic anemia (Aplastic anemia)due to depression of erythrogenesis. Neoplastic diseases, irradiation and certain toxicities may produce this form of anemia.

d. Microcytic hypochromic anemia is observed in case of iron deficiency, copper deficiency because copper is necessary for the utilization of iron in the production of hemoglobin.

2. Etiological classification

1. Hemorrhagic anemia

a. Acute blood loss: It is characterized initially by normal cell count, hemoglobin and hemocrit. Within hours, retention of water and electrolytes lead to dilution of blood with decrease in cell volume indices.

Regeneration of erythrocytes lost take about six weeks.

During this regeneration phase, the bone marrow shows erythroid hyperplasia and peripheral blood shows marked reticulocytosis.

b. Chronic blood loss: It results from continued loss of small amount of blood as in case of infestation with blood sucking parasites as Hemonchus contortus.

In early stage this type of anemia tend to be slight macrocytic or normocytic hypochromic. Poikilocytosis and hyperplasia of bone marrow are prominent. After some time iron stores exhaustion and the anemia becomes microcytic hypochromic.

2. Hemolytic anemia

It results from excessive destruction of the circulating erythrocytes, occurring within the blood stream.

It usually accompany by icterus, hemoglobinuria and hemoglobinuria in acute form, and with stimulation of bone marrow in chronic form.

Extravascular hemolytic anemia occur when erythrocytes phagocytized by macrophages due change in its shape or when recognized as foreign. In this form there is no hemoglobinemia or hemoglobinuria, but there is hemolytic icterus.

Causes

1. Infectious:

• Virus as Equine infectious anemia.

• Bacteria as Leptospirosis

• Protozoa as Babesiasis, Anaplasmosis, Trypanosomiasis and Hemobartonellosis.

2. Toxic

• Snake venoms, potassium and sodium chlorate, chronic lead poisoning and copper.

3- Autoimmune hemolytic anemia

It occur due to formation of antibodies against cell membrane of erythrocytes which become more susceptible to intravascular hemolysis. It may be

a) Isoimmune hemolytic anemia as erythroblastosis fetalis.

b) Idiopathic immune hemolytic anemia as canine immune mediated hemolytic anemia.

3. Deficiency anemia

a. Iron deficiency

Causes

1. Dietary deficiency of iron.

2. Malabsorption of iron.

3. Chronic blood loss.

It is hypochromic microcytic anemia with prominent poikilocytosis.

b) Copper deficiency

Minute traces of copper is needed for utilization of iron in the production of hemoglobin.

c) Vitamin B₁₂ deficiency

It is required for normal development and maturation of erythrocytes.

It leads to macrocytic normochromic anemia.

d) Cobalt and folic acid deficiencies

4. Toxic aplastic anemia

It occur due to failure of bone marrow to produce erythrocytes.

It is characterized by normal size, shape and color of erythrocytes beside absence of signs of active erythropoiesis “absence of megaloblasts, normoblaste and reticulocytes”. Moreover, the granulocytes formation is depressed.

Causes

• Toxic substances as benzol and sulphonamides toxicosis.

• Ionizing radiation as X-ray, radium or others.

5. Myelophthistic anemia

It is type of anemia associated with physical destruction of bone marrow “erythropoietic tissue”.

Examples: anemia associated with leukemia or with leucosis of fowl.

Lesions of anemia

1. The mucous membranes are pale.

2. The blood may be pale and watery.

3. The skin is pale and become thin and inelastic due to atrophy of epidermis and dermis

4. Hemolytic jaundice “yellow skin, mucous membrane and others” are seen in case of extravascular and intravascular hemolytic anemia.

5. Gray dots in liver may be hematopoietic centers or may be minute foci of necrosis.

6. Hemoglobinemia and hemoglobinurea seen in hemolytic anemia characterized by intravascular hemolysis.

7. Erythroblastic hyperplasia characterized by replacement of fat in long bones by red marrow.

8. In toxic a plastic anemia the bone marrow shows markedly hypocellular with reduction of cell lines.

9. Blood film shows anisocytosis (variable sizes), poikilocytosis (variable shapes), nucleated erythrocytes. Also, basophilic stippling “minute dark spots in erythrocytes” is seen. In polychromatophilia, the erythrocytes don’t stain uniformly.

Heinz bodies are refractile bodies within erythrocytes which denaturated hemoglobin formed due to oxidative injury. It seen in toxic hemolytic anemia.

10. Section of spleen or liver may show extramedullary hematopoietic centers “hyperchromatic cells” (Figs 3 & 4).

Fig. 3: Spleen showing hemopoietic centers represented by dark basophilic bodies. Mason's Trichrom.

Fig. 4: Spleen of mice suffering from anemia showing extramedullary hematopoiesis. H&E.

1. Retrogressive changes and necrosis are noticed in cells of parenchymatous organs and muscles of heart.

12. Hemosiderosis is evident in case of hemolytic anemia.

Polycythemia

Polycythemia is defined as an increased number of red cells in peripheral blood.

It may result from:

1. An increase in the total red cell mass (absolute polycythemia).

2.  Decreased plasma volume without increase in total cell mass (relative polycythemia)

Neoplastic disorders of myeloid

leukocytes and erythrocytes

1. Lymphosarcoma

Four types of lymphosarcoma (lymphocytic, histiocytic, stem cell and poorly differentiated) are recognized lymphosarcoma may shows numerous malignant lymphoid cells circulating in the blood (leukemic) or a leukemic.

2. Myeloma

It is a malignant tumor of cells similar to plasma cell.

3. Thymoma

It is the benign tumor of thymus.

4.  Myeloid leukemia

It is a malignant tumor of precursors of granulocytes.

5.  Erythroid leukemia

It is a malignant tumor of the precursors of erythrocytes and leukocytes.

6.  Polycythemia vera

It is a neoplastic myeloproliferative disorder that affects chiefly the erythroid series. It is characterized by increased PCV without hypoxemia or reduced plasma volume.

Lymph nodes

They act as mechanical filters and settling chambers for the removal of bacteria, erythrocytes and particulate substances from the lymph.

The primary structure of lymph nodes is the lymphoid follicle, which is composed of a central area of B lymphocytes surrounded by a perifollicluar region of T lymphocytes. These are bathed by lymphatic entering at the cortex and blood vessels entering at hilus.

The structure of lymph node allow presentation of antigens by dendritic cells and macrophages.

Disturbances in growth

Aplasia means some lymph nodes fail to develop

Hypoplasia means some lymph nodes fail to attain their mature size and they are usually small.

Atrophy means there is diminution in size of some 1ymph nodes after they had reached their mature size. It occurs in old age and cachexia.

Reactive lymphoid hyperplasia

Antigenic stimulation leads to reactive hyperplasia and consists of three interrelated elements (Fig. 5).

Fig. 5: Lymph node showing reactive lymphoid hyperplasia. H&E.

1. Follicular hyperplasia (B cell response): The reactive follicles are large and consisting of activity proliferating B cells with few numbers of histiocytes and dendritic cells.

2. Paracortical hyperplasia (T cell response): Similar reaction occurs among T cells in the paracortex .

3. Sinus histiocytosis: It occurs in lymph nodes draining a malignant neoplasm.

The most prominent component is marked hyperplasia of sinus endothelial cells and their filling with histiocytes.

Processes involving deposition of various substances in the nodes:

Fat: Fat deposition occurs in mesenteric lymph node of fat pigs, supramammary nodes in lactating cows and in nodes draining areas of fat necrosis in cattle.

Macroscopically:

It appears as gray or grayish-yellow streaks or wavy lithe lymph nodes shows grayish yellow streaks

Microscopic appearance:

 Fat appears as droplets or liquid in the lymph sinuses. There is accumulation of lipoid material in the macrophages.

Amyloid infiltration

Deposition of amyloid in the lymph node result in amyloidosis of the lymph nodes. It associated with chronic diseases.

Erythrocytes: The deposition of erythrocytes occurs normal to certain extent. Erythrocytes appears either free in lymph vessel or inside macrophages.

Exogenous pigments

Anthracosis is the deposition of coal particles can be seen in pulmonary lymph nodes in animals living in industrial cities or working in coal mines.

Macroscopic appearance

The medulla of the node appears black and the cortex is normal gray.

Coat dust is seen particular in the pulmonary lymph node.

Endogenous pigments

Bile pigment are seen in jaundice.

Melanin is seen in nodes draining dark damaged skin. Also it occurs in dogs and swine heavily infested with lice, as lice inject melanin into the skin, then it is carried to lymph nodes.

Emphysema

It is the accumulation of gas occur in mesenteric nodes of swine in connection with intestinal emphysema, supramammary nodes due to inflation of the udder and bronchial and mediastinal nodes of horses due to pulmonary emphysema and in all animals suffering from pneumonia where there is interstitial emphysema, and in Lymph nodes draining the affected quarters in blackleg.

Macroscopic appearance

The lymph nodes are enlarged puffy and sometimes sponge like

Microscopic appearance

The sinuses contain gas bubbles of irregular size and shape and may be surrounded with macrophages and giant cells. The lymphoid tissue may undergo pressure atrophy.

Parasites

Several parasites including the mange mite (Demodix follicularum), Linguatula serrata larvae are seldom found in lymph nodes.

Lymphadenitis

It is the inflammation of lymph nodes.

Acute non specific lymphadenitis

Macroscopically, the lymph node become swollen, gray red and congested (Fig. 6).

Fig. 6: Swollen and congested lymph node suffering from lymphadenitis.

Microscopic picture

1. Hyperemia and edema with distension of the lymph sinuses.

2. The lymph sinuses usually contain a variable number of neutrophils. When pyogenic organisms are the cause of the inflammation, the reaction become clearly purulent.

3. Prominent lymphoid follicles and large germinal centers containing numerous mitotic Fig.s.

4. Lysis of lymphocytes are seen with viral diseases (Fig. 7).

Fig. 7: Bursa of Fabricius showing necrosis of lymphocytes in IBD. H&E

Chronic non specific lymphadenitis

Macroscopic picture

The lymph nodes are firm, dry and enlarged.

Microscopic picture

• It is characterized by lymphatic hyperplasia which may be B-cell hyperplasia, T cell hyperplasia or sinus histiocytic hyperplasia.

• The capsule and septae are thickened with increase of collagenous connective tissue (Figs  8 & 9).

Fig. 8: Lymph node showing thickening of capsule and septa in chronic lymphadenitis. H&E.

Fig. 9: Lymph node showing chronic lymphadenitis with thickening  septa. H&E.

Specific lymphadenitis

1. Serous lymphadenitis

Cause

It usually observes with many acute septicemic diseases. Also it seen in lymph nodes draining an area or organ undergoing inflammation.

Macroscopically,  The lymph nodes are enlarged and soft. Moreover, the cut surface is moist, reddened and slightly bulges.

Microscopically, the lymph node shows hyperemia and edema and some erythrocytes.  There is hyperplasia of lymphocytes and reticuloendothelial cells.

2. Suppurative lymphadenitis:

Causes

1. The cause is pyogenic    microorganisms or associated with some specific infectious suppurative diseases as strangles in equines and ovine caseous lymphadenitis in sheep.

Macroscopically, lymphadenitis may be diffuse or focal. In the diffuse form pus is present al lover the node but in the focal form pus is found in local areas of the node as abscesses.

Microscopically, the lymphoid tissue is heavily infiltrated with neutrophils (Fig. 10).

Fig. 10: Lymph node showing suppurative lymphadenitis characterized by infiltration of the lymphoid tissue with neutrophils. H&E.

Moreover, the vascular and cellular alterations In inflammation are present. Hyperplasia of reticuloendothelial cells may occur if infection persists for several days.

3. Fibrinous lymphadenitis:

Causes

It occur in lymph-nodes draining areas of  acute fibrinous inflammation as in lymph node draining area of blackleg and malignant edema or burned skin.

Macroscopically, The affected nodes show the cardinal signs of very acute inflammation. They are quite firm and are incised easily.

Microscopically, The fibrin is the main constituent of exudate besides vascular and cellular changes of acute inflammation.

4. Hemorrhagic lymphadenitis

Causes

It is associated with several acute septicemic diseases as anthrax, pasteurellosis, blackleg and malignant edema.

Macroscopically, The lymph nodes are enlarged and dark red. The cut surface is moist and dark red. Microscopically, erythrocytes are the main constituent of the exudate. The vascular and cellular alterations of acute inflammation are present.

5. Chronic  lymphadenitis:

It may be associated with several chronic or granulomatous diseases as Tuberculosis, glanders, caseous     lymphadenitis, actinobacillosis and paratuberculosis or follow acute lymphadenitis.

Macroscopically, The affected lymph nodes are enlarged and firm (Figs 11 &12 ).

Fig. 11:  Lymph node of sheep showing gross picture of  caseous lymphadenitis characterized by presence of caseated material with concentric lamination.

Fig. 12: Lymph node of sheep showing gross picture of  caseous lymphadenitis characterized by presence of caseated material with concentric lamination.

Microscopically, aggregation of rnacrophages lymphocytes, plasma cells and giant cells are seen besides caseous necrosis and calcification,  Hyperplasia of the reticuloendothelial tissue and fibrous tissue proliferation are noticed. Chronic suppurative lymphadenitis is seen in glanders, actinobacillosis and actinomycosis. Granulomatous lymphadenitis is a feature of tuberculosis, caseous lymphadenitis and mycotic diseases (Figs 13, 14 & 15 ).

Fig. 13: Lymph node of cattle infected with tuberculosis showing granulomatous lymphadenitis. H&E.

Fig. 14: Lymph node showing caseous necrosis represented by eosinophilic and basophilic debri. H&E

Fig. 15: Lymph node showing caseous necrosis and calcification which stained stained black with Von kossa stain.

N.B. The pathological picture in viral induced lymphadenitis is extensive necrosis of lymphocytes as in case of rinderpest.

Lymph vessels

1. Dilatation of lymph vessels

Lymph vessels may undergo focal or diffuse dilatations (Fig. 16).

Fig. 16: Intestinal villi showing dilatation of lymph vessel. H&E.

Causes:

1. The dilatation of lymph vessels may be due to obstructions in lymph vessels as in case of chronic lymphangitis.

2- Thrombosis of lymph vessels is seen in lymph vessels in inflamed area.

Lymphangitis is the inflammation of the lymph vessels.

Spleen

The spleen can be defined as hemopoietic organ which filter blood through a sinusoidal system. It is a great reticuloendothelial sponge, which hold a large amount of blood. The red pulp of spleen is consisted of thin wall vascular sinusoids which are lined by discontinuous endothelium and separated by the splenic cords (cords of Billroth). The splenic cords consist of macrophages. The while pulp consist of central artery surrounded eccentrically by a collar of T lymphocytes (periarteriolar lymph sheath). Bulging from and surrounded by this collar is a lymphoid follicle composed of B lymphocytes. The central artery and its collar of lymphocytes continue beyond the follicle until it terminates into penicillary arterioles.

Blood entering the spleen circulates through splenic sinusoids of red pulp and passes directly to splenic veins (closed circulation). Blood may also pass outside the sinusoids to enter the splenic cords (open circulation) and entering the sinusoids and continuing to splenic vein. The function of the spleen can be segregated into four categories.

1. Filtration of unwanted elements from the blood.

2. Its role as a major secondary organ in the immune system.

3. It is a source of lymph reticular cells and some hematopoietic cells.

4. It constitute a reserve pool and storage site.

1. Developmental diseases of spleen

The spleen may be congenitally absent (aplasia). It occur in inbred strain of mice.

1. Disturbances in development

A. Accessory spleen:

Accessory spleen are small spherical masses of splenic tissue small spherical structure that are histologically and functionally identical with normal spleen) attached to the visceral surface of the spleen or present in the gastro-splenic omentum.

B-Duplication of spleen is occasionally observed in normal swine.

2. Degenerative diseases of spleen

Senile atrophy

It is seen in old dogs and horses. Microscopically, the capsule appears thickened with lymphoid atrophy. The red pulp appears fibrotic due to condensation of sinusoids and lack of blood.

Hyaline degeneration

It occurs in small arterioles associated with septicemic diseases and intoxication.

Siderotic nodules (Gamna-Gandy bodies)

It occurs mainly in old dogs as yellowish encrustation along the splenic margins or even covering most of the capsule (Fig. 17) . Microscopically, there is thickening of the capsule and trabeculae and perivascular tissue with deposition of iron and calcium.

Amyloidosis

It is rare except in animals, which have been used for hyper immune serum production (Fig.s 17 &1 8).

Fig. 17: Spleen of dog showing Siderotic nodules characterized by yellowish encrustation along the splenic margin.

Fig. 18: Spleen showing pale Eosinophilic homogenous structure less materials (amyloidosis). H&E.  

3. Rupture of the spleen

it is frequent in dogs and cats run over by automobile. Rupture is usually followed by massive intraperitoneal hemorrhage and death. In rare instances clotting stop the flow of blood. A considerable number of dogs survive and the two or more healed fragments are found at necropsy years later. Pathologic picture may occurs in any species with minor trauma if the spleen is enlarged and capsule thinned.

4. Torsion of the spleen

it occurs when spleen is twisted on its mesentery. It affects spleen of dogs, pigs and rarely horses.

5. Displacement of the spleen

It is common on dogs and cats.

6. Cysts and parasites

Occasionally, Cysticercus tenuicollis and Hydateds are found.

Pseudocyst may result from cystic degeneration of hematoma. Moreover Toxicara larvae can be seen (Fig. 19).  

Fig. 19: Parasitic splenitis due to Toxicara larvae. The larva surrounded with numerous eosinophils. H&E.  

Neoplastic cysts are hemangiomas or hemangiosarcomas.

7. Splenic enlargements, splenomegaly

Enlargement of the spleen (Fig. 20)   can results from several different mechanisms, including circulatory disturbances, inflammatory diseases, metabolic diseases and neoplastic diseases.

N.B.

Hypersplenism: • It is overactive of spleen in cell destruction. It lead to reduction of one or more of cellular elements of blood leading to anemia, leucopenia or thrombocytopenia.

• It is encountered in patients with splenomegaly.

• Splenectomy is indicated in this case.

The cause of this syndrome is still uncertain but increased sequestration of the cells lead to damaged cell membrane and enhanced lysis by splenic macrophages

Fig. 20: Splenomegaly (below) in compare with normal one.

.a. Acute congestion

Causes

1. Acute myocardial failure.

2. It occurs following euthanasia with barbiturate.

3. Acute systemic infections and intoxication.

4. Splenic torsion.

Macroscopic picture

1. Spleen is enlarged and soft.

2. Cut surface is dark, plugged and oozed blood.

Microscopic picture

• There are a little changes except presence of large number of erythrocytes in sinuses and cord of billroth.

b. Chronic passive congestion

Causes

1. Liver cirrhosis.

2. Systemic venous congestion as in cardiac decompositions involving right side of heart.

3. Other disorders which cause increase pressure on splenic vein.

Macroscopic picture

• Marked enlargement of spleen which become little tough or firm.

Microscopic picture

1. Distension of sinusoids and cords with blood.

2. Hyperplasia of endothelial lining of sinusoids which become cuboidal.

3. Marked diffuse fibrosis with thickening trabeculae.

4. Hemosiderosis is noticed (Gandy Gamna bodies).

c.  Hematoma

It occurs frequent in dogs due to trauma. It may be pool of blood (recent) or lysed blood and fibrin surrounded by degenerating granulocytes and fibrous capsules.

d.  Splenitis

It may be acute to chronic splenitis.

Acute splenitis

It occurs with septicemic disease as anthrax.

Macroscopically, severe enlargement of spleen (black berry jam spleen) is noticed (Fig. 22 )   .

Microscopically, congestion of splenic sinusoids and vessels beside infiltration of spleen with neutrophils and macrophages.

Some septicemia associated with destruction of lymphocytes particularly in germinal center.

Fig. 21: Dark an enlarged spleen in case of anthrax.  

Chronic splenitis

It may be diffuse or focal.

It associated with some infectious diseases as brucellosis, tuberculosis and caseous lymphadenitis. Moreover chronic splenitis can be seen with schistosomal egg. (Fig. 22)  

The nature of inflammatory reaction is differ from disease to other but usually accompany with lymphoid hyperplasia.

Fig. 22: Chronic splenitis due to infection with Schistosomiasis characterized by egg granuloma. H&E.  

e. Anemia

It is usually associated with splenic enlargement through two mechanisms.

1-Hemolytic anemia especially those characterized by extravasated hemolysis, spleen is engorged with disintegrating erythrocytes and there is hyperplasia of macrophages.

2-In chronic anemia, extramedullary hematopoies may be extensive enough to cause enlargement.

f. Storage disease and deposition

• Amyloidosis (Fig.s 23 & 24).  

• Siderotic (Gandy Gamna bodies).

Fig. 23: Spleen showed diffuse amyloidosis. H&E  

Fig. 24: Spleen showing focal amyloidosis. Crystal violet.  

g. Nodular hyperplasia

It is frequent in old dogs (Fig. 25).  

One or more sharply demarcated nodules which elevate the splenic capsules.

Microscopically, the malpighian bodies are enlarged and surrounded by a prominent red pulp. The architecture of splenic bodies is distorted by a dense accumulation of lymphocytes.

Fig. 25: Spleen of dog showing nodular hyperplasia.  

h. Neoplasm of spleen

lymphosarcoma (Fig. 26)   , malignant lymphoma, hemangiosarcoma, hemangioendothelioma, leimyosarcoma are primary tumor encountered in spleen.

Fig. 26: Spleen showing lymphosarcoma.

8. Splenic infarction

Infarction occur occasionally in spleen, usually hemorrhagic. It tend to be conical with the base at capsule (Fig. 27).  

Fig. 27: Spleen showing infarction.