This document provides an overview of interpreting canine leukocyte responses, including causes and mechanisms of various conditions such as neutrophilia, neutropenia, eosinophilia, lymphocytosis, and lymphopenia. Key points discussed include the most common causes of neutrophilia being inflammation and stress, mechanisms of eosinophilia including parasite infection and inflammation, and causes of lymphocytosis including excitement, infection, and neoplasia. Morphologic alterations in leukocytes are also reviewed for various infectious agents and diseases.
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Interpretation of Canine Leukocyte Responses
1. Interpretation of Canine
Leukocyte Responses
Gaonkar Pankaj Prakash.
MVSc II year
pankajgaonkar12993@gmail.com
Department of Veterinary Pathology,
Nagpur Veterinary College,
Maharashtra Animal & Fishery Sciences University, Nagpur, India.
Masters Seminar – VPP 691
2. • Introduction
• Neutrophilia and Neutropenia
• Eosinophilia and Eosinopenia
• Basophilia and Basopenia
• Lymphocytosis and Lymphopenia
• Monocytosis and Monocytopenia
•Leukogram Differentiation Pattern
• Approach towards Interpretation of leukogram results.
INDEX
3. INTRODUCTION
•Total white blood cell (WBC) count - 5,000 to 14,100 cells/μL of blood.
•Neutrophil-commonly encountered leukocyte.
•Lymphocytes - less numerous than neutrophils.
•Monocytes and eosinophils - less frequently.
•Basophils are seen rarely.
The interpretation of result , while taking into account the basic factors that influence
alteration in :
Total number of leukocytes.
Proportion of different types of leukocytes.
Morphological alteration
5. Frequent causes of neutrophilia:
physiologic leukocytosis
corticosteroid- induced leukocytosis
inflammation
Other causes of neutrophilia:
haemolysis
hemorrhage
genetic defects in leukocyte adhesion molecules
immune- mediated diseases
Several benign and malignant neoplastic conditions cause paraneoplastic syndromes
that can result in neutrophilia
Thrombosis, infarction, burns, and uremia
NEUTROPHILIA
It is defined as > 12,000 neutrophils/ μL of blood, is a frequent observation in canine blood
films
6. Mechanism:
Shift from marginating to circulating pool
Increased release from bone marrow
Increased production by bone marrow
Delayed apoptosis
Decreased migration into tissue
Ref- A.J.ROSENFELD , S.M.DIAL. Clinical pathology for the veterinary team. 1st edition. Wiley-Blackwell publishing,2010
Normal neutrophil pool
7. Stress neutrophiliaExcitement neutrophilia (physiologic)
Inflammatory Neutrophilia
Ref- A.J.ROSENFELD , S.M.DIAL. Clinical pathology for the veterinary team. 1st edition. Wiley-Blackwell publishing,2010
8. Inflammation is the most frequent cause of neutrophilia !!!
The intensity of the underlying disease process has a direct effect on the magnitude of
the total neutrophil response.
Localized purulent lesions, like abscesses, induce greater neutrophilia than do more
generalized diseases, such as septicemia.
Neutrophilia with a left shift is the hallmark of acute inflammatory reactions.
The degree of the left shift is considered a direct indication of severity of disease.
Left shifts of great magnitude may occur in dogs that have pleuritis, peritonitis, pyoderma,
or pyometra.
Release of myelocytes and metamyeolcytes from bone marrow is related to the increased
tissue demand in purulent inflammation.
In some diseases, inflammation is too mild to induce a left shift.
Left shifts may be mild or nonexistent in seborrheic dermatitits, catarrhal enteritis, or
hemorrhagic cystitis, conditions in which tissue demand for neutrophils is minimal.
9. NEUTROPENIA
Neutropenia is decreased numbers of circulating segmented neutrophils.
Mechanisms:
• Estrogen ,chemotherapeutic agents
• Parvoviral
• Cytokines deficiency
• primary bone marrow disease
• Congenital defects in neutrophil production (elastase)
Decreased production of
neutrophils in bone
marrow
• endotoxemia
Cellular shifting from the
circulating to the marginal
pool
• severe acute inflammation (degenerative left shift
and toxic change).
Increased tissue
emigration in excess of
bone marrow release of
neutrophils
•Breed-associated:
•Tervuren Shepherds , Australian Shepherds ,Labrador RetrieversUnknown mechanisms
11. Fig. Hypersegmented neutrophil from a dog. Wright’s stain.
Nuclear Hypersegmentation
•Characteristic changes-
Neutrophils with > 5 nuclear lobes are seldom observed in the blood of dogs.
.....Continued Morphologic Alterations in Neutrophils
12. Nuclear Hyposegmentation
•Associated with-
left shift of inflammation or infection
Fig. Late-band and metamyelocyte neutrophils from a dog that had inflammation.
Wright’s stain
.....Continued Morphologic Alterations in Neutrophils
13. Pelger - Huët Anomaly:
•Etiology - Autosomal dominant trait (hereditary disorder of granulocyte development)
Fig. Neutrophil from dog with Pelger-Huët anomaly.
Notice coarse mature chromatin pattern and hyopsegmented nucleus. Wright’s stain.
.....Continued Morphologic Alterations in Neutrophils
14. .....Continued Morphologic Alterations in Neutrophils
Ethylenediaminetetraacetic acid (EDTA) induced Artifact:
•Cause-When whole blood is collected in EDTA and allowed to incubate at room temperature
Cytoplasmic basophilia and foamy vacuolation (i.e. signs of toxic change) are not observed
as EDTA induced artifactual change.
15. Happens in-vitro if EDTA anticoagulated blood is allowed to stand.
Fig. Neutrophil aggregation
16. •Cytoplasmic vacuolation-
.....Continued Morphologic Alterations in Neutrophils
Fig. Toxic vacuolization.
Toxic Changes:
•A set of disease - induced morphologic alterations in neutrophils, including cytoplasmic vacuolation,
cytoplasmic basophilia, Döhle bodies, or prominently stained primary granules (toxic granulation) is
referred to as a toxic change.
.
17. •Döhle bodies-
Angular, blue - to - gray, cytoplasmic inclusions
Remnants of rough endoplasmic reticulum.
•Toxic Granulation- (B & D)
Increased permeability of primary granule
membranes to Romanowsky stains.
18. Infectious Agents :
Neutrophil with negatively stained intracellular bacillus (arrow) in blood smear from a dog that has
mycobacteriosis, Wright’ s stain.
.....Continued Morphologic Alterations in Neutrophils
19. .....Continued Morphologic Alterations in Neutrophils (Infectious Agent)
Canine distemper virus inclusion bodies :
Intracytoplasmic inclusions are round to irregularly shaped, homogeneous, magenta to
gray blue structures.
Fig. Magenta-colored canine distemper virus inclusion in a neutrophil, Wright’ s stain.
20. Hepatozoon canis and Hepatozoon americanum gametocytes:
Fig. Two segmented neutrophils with intracytoplasmic, clear to ice-blue H. canis gametocytes.
Wright’s stain.
.....Continued Morphologic Alterations in Neutrophils (Infectious Agent)
21. Histoplasma capsulatum
•They have a small round, purple nucleus, and can occur singly or in clusters within the
cytoplasm.
Fig . Segmented neutrophil with intracytoplasmic Histoplasma capsulatum . Wright’s stain
.....Continued Morphologic Alterations in Neutrophils
22. Ehrlichia canis morulae:
•The Ehrlichia morulae vary from magenta to blue- gray in color and resemble a mulberry.
Fig. Three neutrophils containing morulae of Ehrlichia ewingii, Wright’s stain.
.....Continued Morphologic Alterations in Neutrophils
23. Hemosiderin granules:
•The brown granules, that stain positive for iron.
•Multiple granules can be observed in some cells.
•The mechanism of their occurrence in neutrophils is uncertain.
Fig.Segmented neutrophil with hemosiderin crystal from a dog that had immune- mediated hemolytic
anemia.
Wright’ s stain.
.....Continued Morphologic Alterations in Neutrophils
24. Mucopolysaccharidosisis type VI (arylsulfatase B deficiency) and type VII :
•Autosomal recessive pattern
•Neutrophils and lymphocytes - large, pink to purple staining inclusions (Alder- Reilly bodies)
in the cytoplasm in routine Romanowsky - stained blood films (Fig.).
•The granules represent intermediate products that accumulate in cells caused by the
arylsulfatase B (type VI) or β - glucuronidase deficiency (type VII).
Fig. Segmented neutrophil with Alder - Reilly bodies from a dog that had mucopolysaccharidosis type VII.
Wright’ s stain.
.....Continued Morphologic Alterations in Neutrophils
25. Causes / Mechanism of Eosinophilia :
Parasitism : Eosinophil bind to parasite opsonized with IgG , IgE , complement.
Release of MBP,EPO
Toxic to parasite
Inflammation or local hypersensitivity:
•MBP Degranulation of mast cell and basophil.
•Eosinophil release histaminase Neutralize histamine
Paraneoplastic response:
•Release of cytokines by the neoplastic cells that promote eosinophil production.
(e.g. Interleukin-5).
EOSINOPHILIA
Eosinophilia, defined as > 1,300 eosinophils/ μ L of blood.
26. •Eosinopenia is a decreased numbers of circulating eosinophils.
•It may be difficult to document because the eosinophil normal range may go down
to zero.
•True eosinopenia is difficult to document and is of limited clinical significance.
•Eosinopenia is most commonly attributed to increased corticosteroids (stress
leukogram).
Etiology- emotional or physical stress,
hyperadrenocorticism (Cushing ’s syndrome).
High dose of corticosteroid for long term
It is hypothesized that corticosteroids inhibit histamine release, neutralize
circulating histamine, and initiate release of cytokines that mediate alterations in
eosinophil distribution.
Eosinopenia
27. BASOPHILIA & BASOPENIA
Basophils:
•Poorly lobulated nucleus- a twisted ribbon.
•blue - gray cytoplasm
•metachromatic granules -scattered , round, varied size
• Count: <2 % of the differential leukocyte count or an
absolute count of 0– 140 basophils/ μ L.
Basophilia:
•Defined as a increase in circulating numbers of basophils ( > 140 basophils/ μL of blood), is a
rare event.
•Parasite - Dirofilaria immitis, oslerus larvae.
Basopenia:
•Since most healthy animals have basophil counts of 0/ μL , therefore basopenia is not a
relevant finding.
28. Causes of Monocytosis:
•Stress response:
•Inflammation
•Recovery from acute marrow injury:
E.g. secondary to chemotherapeutic agents.
•Paraneoplastic response:
e.g. lymphoma
cytokine secretion (GMSF).
•Monocytic/ monoblastic leukemia:
A variant of acute or chronic myeloid leukemia.
Monocytopenia may be difficult to document because monocyte reference intervals
often go down to zero, and has no clinical significance.
Monocytosis & Monocytopenia
Monocytosis is defined by numbers that exceed 1,400 monocytes/μL.
29. LYMPHOCYTOSIS
Lymphocytosis: > 2,900 lymphocytes/ μ L of blood.
Cause :
Physiologic:
•Excitement - (epinephrine response)
•Vaccination
Antigenic stimulation:
Chronic Infection/inflammation : (long standing exposure)
Ehrlichia canis result in proliferation of lymphocytes and expansion of the blood
lymphocyte pool.
Trypanosomiasis,leishmaniasis and brucellosis also may cause lymphocytosis by a
similar mechanism.
30. Hypoadrenocorticism (Addison ’ s disease) :
•Reported to cause lymphocytosis in 11– 20% of affected dogs.
•The lack of lymphopenia in severely stressed dog provides supportive evidence for
glucocorticoid deficiency.
Fig. Lymphocytosis and Eosinophilia in dog with hypoadrenocorticism.
31. Lymphoid neoplasia :
•Malignant lymphoma, acute or chronic lymphocytic leukemia, and thymoma have been
associated with lymphocytosis
•The highest lymphocyte counts usually are associated with chronic lymphocytic leukemia.
This can occur in an animal of any age, but should be considered the main differential diagnosis
in an older animal with an unexplained lymphocytosis.
32. LYMPHOPENIA
Lymphopenia, defined as < 400 lymphocytes/ μ L blood.
Causes :
Stress leukogram:
•This is due to endogenous or exogenous corticosteroids.
•It is due to a shift of lymphocytes from the circulating to other pools (such as decreased
efflux from lymph nodes or retention in bone marrow).
Acute infection:
•By means of stress - induced corticosteroid release and redistribution of lymphocytes.
•canine distemper virus and canine parvovirus, cause lymphocyte destruction, atrophy of
lymphoid tissues, and depletion of lymphocyte subpopulations.
Loss of lymphocytes:
•Chylothorax
•Loss of lymphocyte - rich fluid into the intestinal lumen.
(ulcerative enteritis , granulomatous enteritis).
33. Occlusion of the flow of lymph: Disseminated granulomatous infl ammation ,
Neoplasia
Autosomal recessive severe combined immunodeficiency:
•Jack Russell terrier puppies - marked lymphopenia and
decreases serum immunoglobulins
hypoplasia of all lymphoid tissues.
•Basset hounds that have combined immunodeficiency have lymphopenia.
•Recurrent infection.
34. Morphologic Alterations in Lymphocytes
Reactive Lymphocytes:
•Antigentically stimulated lymphoid cells that are seen in the blood of dogs.
•Morphology :
Deeply basophilic cytoplasm.
Vary in size, nuclear chromatin clumping, and number of nucleoli visualized.
Fig . Reactive lymphocyte in a canine blood smear. Wright’s stain
35. Granular lymphocytes :
•They have a few distinct azurophilic granules that tend to cluster at the nuclear margin or
indentation.
Fig . Large granular lymphocytes in a canine blood smear. Wright’ s stain
36. Lymphoblasts
•lymphoma and lymphoblastic leukemia .
•Morphology-
large nucleus with vesicular chromatin and prominent nucleoli.
The cytoplasm is abundant and has a deep blue hue.
Fig. Lymphoblast in blood smear of a dog that has malignant lymphoma. Notice the prominent nucleoli.
Wright’s stain.
37. Acute myeloid
leukemia
•Large number of
blasts
•multiple
cytopenias
Acute lymphoid
leukemia
•Large number of
blasts
•small to
intermediate
cells(Lymohocyte)
•multiple
cytopenia
LEUKEMIA
Lymphoma
•Variable number
of lymphoma cells
• Typically no or
mild cytopenias
Clinical Examination , phenotypic testing (e.g. Flowcytometry) are required for confirmative diagnosis.
Chronic leukemia
•Rarely Blasts
•Involved cell type
increased
•Mild cytopenias
43. supported by a lymphopenia and/or eosinopenia.
A neutrophilia, without a left shift, with or without a lymphopenia or eosinopenia could
be due to inflammation or corticosteroids, so you would need to evaluate other findings
(clinical and laboratory) for evidence of inflammation.
Is there evidence of endogenous corticosteroid release (“stress”) or is the animal on
corticosteroid treatment?
Are there abnormal cells in the blood or an unexplained lymphocytosis?
If yes, then you may have a leukemia (acute, chronic or the leukemia phase of lymphoma).
44. Is there an inflammatory leukogram?
Supported by –
Left shift (immature neutrophils in the circulation) .
Toxic change in neutrophils (which are usually found together, but not always).
If there is an inflammatory leukogram, how severe is it?
severity of the left shift (degenerative generally supports a severe inflammatory response).
degree of toxicity in neutrophils (marked toxic change in neutrophils would support severe
inflammation).
If there is inflammation, is the bone marrow responding?
Neutrophilia and mature neutrophils out number immature neutrophils , this would support
a bone marrow response.
45. If there is inflammation, who is winning? The animal or the inflammation?
This can be difficult to determine from a single hemogram.
A degenerative left shift, in the face of a Neutropenia or normal neutrophil count.
Thus depletion of marrow stores and failure of the bone marrow to keep up with the demand
from the tissue
The inflammation is winning...!!!
Neutrophilia and more immature than mature neutrophils
Marrow has had time to respond
Inflammation is worsening
Here, we are not sure who is winning.
Continued…
46. So how do we tell who is winning ?
When in doubt, always do serial hemograms – every 24 hours (or less if really needed)!
• Mature neutrophil - Increased
• Toxic change - Decreased
• Immature neutrophil - Decreased
Favourable
Prognosis
• Mature neutrophil - Decreased
• Toxic change - Increased
• Immature neutrophil - Increased
Guarded
Prognosis
Continued from….If there is inflammation , who is winning? The animal or the inflammation?
Disease processes can decrease or increase the no. of circulating leukocytes.
Total WBC count provides info on total no. of CIRCULATING leukocytes.
Whereas DLC allows characterization of each leukocyte.
Each leukogram pattern can be used to develop a list of possible diseases(diff. diagnosis).
Identification of of morphological changes provides valuable insight into diagnosis.
Challenge
Approach
Common causes of neutrophilia include inflammation (either infectious or non-infectious [trauma, surgery, burns, etc.]).
A neutrophilia is a feature of several different leukogram patterns, including an inflammatory leukogram, stress leukogram, and physiologic leukocytosis(epinephrine).
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Common causes of neutrophilia include inflammation (either infectious or non-infectious [trauma, surgery, burns, etc.]), exogenous or endogenous corticosteroids, and epinephrine. Immune-mediated diseases such as immune-mediated hemolytic anemia are also commonly associated with neutrophilia due to actions of inflammatory cytokines.
Neutrophilia
non-compensated left shift- (Storage pool contains no mature neutrophil).
Corticosteroids and epinephrine cause movement of neutrophils from the MNP to the CNP.
Only marginated pool is affected.
Stress neutrophilia-
Increased release of mature neutrophils from the bone marrow storage pool
Decreased margination of neutrophils.
Corticosteroids and epinephrine cause movement of neutrophils from the MNP to the CNP.
Because neutrophil cannot attach to the wall of vessle they cannot migrate to tissue.
The neutrophil uses cell adhesion molecules called L-selectin to loosely attach itself to the endothelial lining of the blood vessel.
Glucocorticoids are known to decrease gene transcription of L-selection thereby decreasing the amount produced and transferred to the surface to replace recently shed L-selectin. Without this replacement, the neutrophil will detach (or undergo "demargination") to then enter into the circulatory compartment.
Estrogen ,chemotherapeutic agents – kill HSC
Parvoviral – cytotoxic to HSC
Cytokines def. – GSF (granulocyte colony stimulating factor)
Bone marrow disease - ineffective hematopoiesis (leukemia , e.canis)
Congenital defects in neutrophil production - Attributed to a defect in intracellular trafficking of neutrophil elastase. Elastase - degrade cytokines.
Occurs in-
prolonged transit times in the vasculature and occur secondary to severe stress (endogenous corticosteroid release), hyperadrenocorticism, and exogenous corticosteroid administration.
Giant hypersegmented neutrophils have been observed in myelodysplastic syndromes and in granulocytic leukemia.
Associated with-
left shift of inflammation or infection
Pelger-Huët anomaly
pseudo-Pelger-Huët anomaly.
Characteristics-
granulocytes and monocytes with hyposegmented nuclei and mature chromatin patterns.
The nucleus of neutrophils, eosinophils, and basophils typically has a band or peanut-
shaped nucleus with tightly condensed chromatin.
Neutrophils have normal function.
Most dogs that have Pelger- Huët anomaly are heterozygous for the condition, and the neutrophils have normal function. Therefore, affected dogs have no predisposition for infection.
Characteristic changes:
neutrophils develop a few, clear vacuoles in the cytoplasm and an irregular distribution of cytoplasmic granules.
Cell membranes appear irregular, and mild pyknosis may occur.
bone marrow production of these cells is disrupted
resulting in loss of granule and membrane integrity.
Persistent ribosomes impart the cytoplasm with its characteristic basophilia.
Döhle bodies-
Associated - myeloid left shifts
Seen in conjunction with toxic granulation.
Fig. A&C-
Normally matured segmented and late band neutrophils.
white cytoplasm with pink granules,
long and fairly narrow nuclei,
tightly condensed chromatin.
Fig. B&D-
Segmented and band neutrophils with toxic change.
less condensed chromatin than their normal counterparts.
Bluer cytoplasm due to retention of ribosomal RNA.
Bacterial rods and cocci can be infrequently detected in the cytoplasm of neutrophils and other blood phagocytes during septicemic crises.
Although clinical signs and leukograms can provide supportive evidence for bacteremia, the diagnosis is best confirmed by blood culture.
The bacteria stain positively or negatively in Romanowsky - stained blood films and buffy coat preparations (Fig. ).
Inclusion body indicates site of viral replication.
Canine distemper virus inclusion bodies can be infrequently observed in neutrophils from dogs that have naturally occurring viral disease or post- vaccination .
The intracytoplasmic inclusions are round to irregularly shaped, homogeneous, magenta to gray blue structures that may occur in blood cells, including erythrocytes and several types of leukocytes.
Detected - cytoplasm of neutrophils or monocytes.
The oval gametocytes measure 5 × 10μm and are unstained to ice- blue within the cytoplasm of monocytes and neutrophils in Romanowsky- stained blood smears.
Infection frequently is associated with neutrophilic leukocytosis.44
It is a yeast- like fungus that can be observed in neutrophils, monocytes, and eosinophils in Romanowsky- stained blood films.
The organisms are round, 2– 4 μm in diameter, and have thin walls.
Hemosiderin or haemosiderin is an iron-storage complex.
Haemosiderin often forms after bleeding (haemorrhage).[3] When blood leaves a ruptured blood vessel, the red blood cell dies, and the haemoglobin of the cell is released into the extracellular space.
Mucopolysaccharidosisis -Lysosomal storage diseases that have been reported rarely in the dog.
MBP –highly charged cationic protein
EPO- In presence of H2O2 and halide, generates oxygen radicals toxic to helminths, bacteria, mycoplasmas, fungi, protozoa, viruses, tumor cells;
MBP ,EPO also cause tissue damage.(lysis & oxidative stress respectively)
Activated Eosinophil – leukotrriene rich (C4)- amplify & sustain inflammation w/o antigen.
Emigration of eosinophil is controlled by adhesion molecules similar to neutrophils but E are recruited by specific chemokine i.e eotaxin.(expressed only by eosinophil)
----------------------------------------
Mast cells tumors(common), lymphoma (mostly T cell variants, but also B cell lymphoma), squamous cell carcinoma, and some other tumor types
Long - term use of high - dose corticosteroids depresses eosinophil production by the bone marrow. 40
Determination of absolute eosinophil counts with a hemocytometer and eosin - based diluent is recommended to confirm suspected cases of eosinopenia.
Host defense by means of immunoglobulin E (IgE)- mediated infl ammatory reactions . (Armed with IgE) – type 1 HS
Binding of an antigen to a specific, surface-bound IgE antibody, basophils are activated and release histamine and other mediators that contribute to the inflammation present in immediate hypersensitivity reactions.
B-cells are stimulated (by CD4+TH2 cells) to produce IgE antibodies specific to an antigen. The IgE antibodies bind to FcεRI receptors on the surface of tissue mast cells and blood basophils.
When stimulated, these cells synthesize platelet - activating factor; thromboxane A2; and leukotrienes C4, D4, and E4.
-----------------------------
Basophil function – heparin: anticoagulant. Histamine-promotes blood flow to tissue.
Action basophil-Basophil granules contain preformed mediators, including histamine and heparin (see Chapter 4 4) . When stimulated, these cells synthesize platelet - activating factor; thromboxane A2; and leukotrienes C4, D4, and E4.
Basophilia also is associated with infection with several other parasites and infectious agents.
Emigration of monocyte – same factor – neutrophil.
2nd line of defence
Phagocytosis
Beside phago they have potential to get activated by – 1. cytokine(Interferon gamma) from immune activated T cells.
2. endotoxin
Central figure of chronic inflammation bcoz activated M required for fibrosis (Growth factors,angiogenic factors,remodellinge collagenase)
Eventhough various factors makes M powerful cells, it can also inflict tissue damage (protease)
B and T cells appear similar by light microscopic examination of Romanowsky- stained blood films.
Recirculate – detect transformed cell.
Majority – T lymphocytes (months to years).
B cells are short - lived (days to weeks).
Function by – Ab , cytotoxicity , signalling other cells
Excitement - transient lymphocytosis - avoided if animals are not overly excited at time of venipuncture.
second sample of blood, collected from the calmed or tranquilized dog, can be used to distinguish transient lymphocytosis of pathologic origin.
Vaccination – result of strong antigenic stimulation of immune system. (seen 1 to 2 week after vaccination)
Stressed animal showing lymphocytosis is evidence glucocorticoid deficiency. Because stress reults into lympholysis. (stress leukogram)
For lymphoid neoplasia(see Chapters 69 and 77 ).
This indicates they are either of cytotoxic T cell or natural killer cell origin. Flow cytometric analysis confirmed that the cells expressed CD3, CD5 and CD8, indicating they were cytotoxic T cells. They also expressed the antigen, CD11d, which supports the splenic red pulp as the origin for this leukemia (CD11d-positive granular lymphocytes are normal constituents in the red pulp of the spleen).
Leifer CE , Matus RE . C hronic lymphocytic leukemia in the dog: 22 cases (1974 – 1984) . J Am Vet Med Assoc 1986 ; 189 : 214 – 217 .
Physical stresses such as extremes in temperature or pain, which result in excess corticosteroid release, cause lymphopenia.
Chylothorax- leakage of chyle (lymphatic fluid of intestinal origin) into the pleural space. Loss into lymphocyte-rich effusions
Chapter 57-combined immunodeficiency-schalms book
CID - disturbed development of functional T cells and B cells caused by numerous genetic mutations. Both "arms" (B cells and T cells) of the adaptive immune system are impaired. SCID is the result of an immune system so highly compromised that it is considered almost absent. Characteristics include a poorly developed thymus gland. A common cause of death is canine distemper, which develops following vaccination with a modified live distemper virus vaccine.
Some resemble small lymphocytes with a basophilic cytoplasm, others resemble lymphoblasts.
----------------------------------
The cytoplasm may have a perinuclear Golgi zone and may contain a few vacuoles and resemble plasma cells.36,3
Basophilic – blue colour
Reactive Lymphocytes (also termed immunocytes and transformed lymphocytes)
Granular lymphocytes or natural killer cells
This indicates they are either of cytotoxic T cell or natural killer cell origin
Blast cells- AML,LL
Involved cell type – CL
Numerous large lymphocytes with occasional visible nucleoli (arrows) present in a canine patient with acute lymphoblastic lymphoma.
The cells could be readily mistaken for lymphocytes, however, they have fine chromatin (i.e. euchromatin indicating an actively synthetic nucleus), indicating they are an immature cell.
These results indicated a leukemia, however the lineage of the neoplastic cells could not be determined on the basis of morphologic features alone.
The dog had a "blast" count of 50,000/uL with a concurrent non-regenerative anemia and thrombocytopenia.
Flow cytometric analysis and cytochemical staining confirmed that the leukemia was an acute myeloid leukemia.
Note, that clinical information, results of other testing (e.g. imaging) and other clinical pathologic results will also assist with leukogram pattern differentiation (and there are exceptions to every rule).
“regenerative left shift” under these conditions, since they suspect a bone marrow response is occurring (i.e. myeloid hyperplasia),
but it is possible for the bone marrow to release a few immature neutrophils along with mature neutrophils in the storage pool in response to inflammation before the bone marrow has had time to increase granulopoiesis (i.e. first few days after onset of inflammation).
degenerative left shift:- more immature than mature neutrophils .
If Neutrophilia and more immature than mature neutrophils, this tells us that the marrow has had time to respond (there is a myeloid or neutrophilic hyperplasia)
inflammation is acutely worsening or a new inflammatory focus (severe) has developed (with cytokines causing release of immature cells from the marrow).
inflammation is acutely worsening or a new inflammatory focus (severe) has developed (with cytokines causing release of immature cells from the marrow).