Hypereosinophilia syndrome in dogs (domestic carnivore hemopathy)

Eosinophils are important components of the immune system, and they are often involved in hypersensitivity disorders and parasitic infestations. Eosinophilia is defined as an increase in the total number of eosinophils in the blood or tissues. In this article you will learn what to do if your dog has elevated eosinophils.

Although the upper range for blood eosinophil concentrations in dogs is 0.75 x 109/L , significant circulating eosinophilia is considered when the count exceeds 2.2-2.5 x 109/L . Most often this occurs as a leukemoid response or when eosinophil counts rise to high levels in response to an underlying cause.

Causes

Eosinophils are special leukocyte blood cells that are able to leave the circulatory system and accumulate in affected organs, for example, in the digestive organs, respiratory system and skin and soft tissues.

These cells are produced in the body's hematopoietic system, primarily concentrated in the peripheral circulatory system, and perform a protective function in the fight against parasitic infections and other problems. But too high a concentration of eosinophils in dogs often provokes the development of gastritis and myositis.

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The causes of elevated eosinophils include the following diseases and conditions::

1. Lots of stress.
2. Physical impact: injuries, burns, frostbite, etc.
3. Poisoning.
4. Helminthic infections.
5. Allergic reaction.
6. Asthma and other respiratory diseases.
7. Severe inflammation with the formation of pus.
8. Addison's disease.
9. Neoplastic processes, especially malignant neoplasms.
10. Repeated illness.

Since there are many reasons for changes in the level of eosinophils, it is possible to establish the real disease only with a thorough examination.

Hypereosinophilia syndrome in dogs (domestic carnivore hemopathy)

F. Gebert

The article describes a disease with blurred clinical symptoms, and only a very thorough examination allows diagnosis, treatment and prognosis to be established.

Hypereosinophilia syndrome is manifested by an increased concentration of eosinophils in the blood and their multiple infiltration in organs. In general, this pathology is rare; the largest number of publications is devoted to cats compared to dogs. To make a diagnosis and prognosis, it is necessary to know the pathophysiology of this disease.

Pathophysiology

Eosinophilia is a pathological condition in which the total number of eosinophils in the blood exceeds 1.9 × 109/L in a dog and 0.75 × 109/L in a cat. The number of eosinophils in the blood of a healthy body is limited. They belong to the myelomonocytic series and are formed from bone marrow cells. The process is regulated by granulocyte-macrophage colony-stimulating factor (GM CSF), interleukin 3 (IL3), but mainly interleukin 5 (IL5). These substances are synthesized by other cells, usually lymphocytes. Eosinophils then enter the blood, where they circulate for 24-36 hours. Next, they migrate to organs exposed to the most intense environmental aggression (skin, lungs and digestive tract), where they remain for several days until they undergo phagocytosis by macrophages.

The function of eosinophils is as follows:

• participation in the mechanisms of immunoresistance of the body during infestation of the latter with parasites or during hypersensitization;
• phagocytic activity towards bacteria or fungi;
• regulation of the inflammatory process due to peroxidases and other toxic proteins localized in the granules of their cytoplasm (prostaglandins, leukotrienes and some cytokines: interleukins 3 and 5, GM CSF) (Prelaud P., 1999). They may be regulators that primarily influence the inflammatory response of mast cells.

Eosinophils inactivate some molecules produced by mast cells, as they secrete histaminase, kinases and phospholipases in a type I hypersensitization reaction (Prelaud P., 1999). The mechanism of activation of eosinophil degranulation during the type I hypersensitization reaction is presented in Figure 1.

Picture 1

When an exogenous antigen (aeroallergen, antigen of a parasitic, bacterial, viral or nutritional nature) enters the body, it encounters T and B lymphocytes. In this case, B lymphocytes are stimulated and transformed into plasma cells, which synthesize immunoglobulins specific to this antigen. These immunoglobulins can belong to classes - G (IgG), M (IgM), A (IgA) or E (IgE). Immunoglobulins E adhere to the mast cell membrane. When the antigen re-enters the body, it is fixed on membrane IgE and provokes degranulation of mast cells, and chemical substances accumulated in eosinophils are also released: eosinophil chemotactic factor of anaphylaxis (ECF-A), interleukins 4 and 5. In paraneoplastic eosinophilia, the movement of eosinophils is carried out through chemotaxis due to the secretion of interleukin 2 and 5 by the neoplasm.

Etiology

Various disorders that may cause eosinophilia in domestic carnivores are presented in Appendix 1. The most common of these are: dermatitis caused by hypersensitization from flea bites; asthma and complex eosinophilic granuloma of cats (Appendix 2); eosinophilic enteritis and mastocytomas (Center SA, Randolf JB, Erb HN et col., 1990).

Appendix 1. Cause of eosinophilia

Appendix 2. Complex eosinophilic granuloma of the skin in a cat

The example of an eosinophilic disorder best described in domestic carnivores is complex eosinophilic cutaneous granuloma in the cat.

In this case we are talking about skin syndrome, which manifests itself in three forms: – ulcerative eosinophilia; – eosinophilic plaque; – linear eosinophilic granuloma. Differentiation between the ulcerative form and neoplastic processes (for example, epithelioma) requires a very careful approach in diagnosis.

The etiology is multivariate, often impossible to establish: – hypersensitivity (allergy due to flea bites, as well as nutritional nature, atopy); – injuries; – bacterial infection; – viral infection (FeLV); – autoimmune disease.

Only histomorphological examination allows a final diagnosis to be made. Diagnostic criteria are presented in Table 1 according to the function and clinical form of the disease.

Treatment requires elimination of the allergen responsible for hypersensitivity, if established. Otherwise, immunosuppressants prescribed orally are used, which include corticosteroids or megestrol acetate (pay attention to secondary effects: diabetes, diabetes mellitus, breast neoplasms, hypocortisolism, etc.). Methylprednisolone acetate is prescribed intramuscularly.

Histomorphological examination has revealed that many disorders in dogs and cats occur during infiltration of tissues or organs by eosinophils, which is accompanied or not by eosinophilia. Reactions can manifest themselves at the level of the skin, digestive tract (Calver CA, 1992; Rodriguez A., Rodriguez F., Pena L. et col., 1995), lungs (Calver CA, 1992; Smith-Maxie LL, et col., 1989) or the central nervous system (Bennet PF et col. 1997). Some breeds appear to have a predisposition to the manifestation of this pathology:

• granulomas in the vestibule of the oral cavity in the cheeks and lips of a Siberian husky;
• granulomas of the stomach and intestines in a Rottweiler (Gvilford WG, 1995; Strombeck DR, Gvilford WG, 1991);
• eosinophilic ulcerative stomatitis in Cavalier King Charles Spaniel (3 cases described) (Joffe DL, Allen AL, 1995).

Pleural and abdominal eosinophilic effusions in dogs and cats are described by Fossum TW et col. (1993). In 50% of cases they are associated with neoplasms. Cases of eosinophilic effusion are noted with: pneumothorax, interstitial infiltration of the lungs and peribronchial region; respiratory system and skin allergy syndrome; intestinal lymphangiectasia; volvulus of the lung lobe; chylothorax; intestinal perforation due to a bite and infection with feline leukemia virus (FeLV). Cases of eosinophilic gastroenteritis in mink have been described (Palley LS, Fox JG, 1992).

The cause of eosinophilic disorders is often impossible to determine. The first assumption about this pathology in domestic carnivores is based on infiltration of the digestive tract and type I hypersensitivity to allergens of alimentary nature. The second assumption is based on hypersensitization by bacteria or parasites of the intestine (Strombeck DR, Gvilford WG, 1991), or the respiratory apparatus (Calver CA, 1992). In eosinophilic pulmonary granulomatosis, the process is usually provoked by Dirofilaria immitis.

The cause of hypereosinophilia syndrome often remains unidentified. If the parasitic or allergic nature of the disease is established, then this pathology is not considered hypereosinophilia syndrome. The syndrome itself is characterized by circulatory hypereosinophilia (exceeding 1.9 × 109 cells/l in a dog and 0.75 × 109 cells/l in a cat), as well as eosinophilic infiltration of many organs from the bone marrow (Huibregste BA, Turner JL, 1994).

Clinical diagnosis

Diagnosis is usually based on the identification of damage to multiple organs and detection of eosinophilic infiltration. Symptoms are mostly poorly specific. The involvement of histomorphological and cytological studies is necessary to confirm the preliminary diagnosis of hypereosinophilia syndrome.

1. Clinical examination

The disease itself is characterized by polysymptoms, its severity depends on the degree of organ damage. In general, the symptoms of the clinical picture of the disease are vague (hyperthermia, anorexia and weight loss are noted quite often). During clinical examination, in the case of eosinophil infiltration of the intestines or stomach, cachexia, hyperthermia, hepatomegaly, splenomegaly, hypertrophy of peripheral or mesenteric lymph nodes and digestive tract disorders (diarrhea, vomiting) can be observed. The following organs may be involved in the pathological process: liver, spleen, kidneys, mucous membranes of the stomach or intestines, skin, thyroid gland, lungs, lymph nodes, adrenal glands and myocardium.

2. Additional research methods

Due to the fact that the symptoms are blurred, making a diagnosis of this disease requires the use of additional research methods.

• A blood test should detect at least hypereosinophilia. Biochemical parameters change depending on the severity of eosinophil infiltration of organs such as the liver and kidneys. A definitive diagnosis cannot be made using ultrasound examination alone. The observed changes are not pathognomonic, especially with liver infiltration. In any case, hypereosinophilia syndrome should be included in the list of suspected diseases if the echographic picture indicates anomalies identified simultaneously in several organs (liver, spleen, intestines, etc.).
• X-ray examination does not provide any additional information. All test results for parasitic infestation (scatology, serology) must be negative.
• Carrying out histomorphological analysis, starting with a biopsy, is necessary to make a final diagnosis (Table 1). Infiltration of eosinophils into the intestine, mesenteric lymph nodes, liver, spleen, medullary zone of the adrenal cortex and endocardium is possible. Simultaneous infiltration by plasma cells also occurs.

Table 1. Histomorphological modifications that appear in different forms during the development of eosinophilic granuloma of the skin in a cat.

• At autopsy, the presence of granulomas in the liver parenchyma can be detected in sizes ranging from 1 to 3 mm (Mac Even SA et col. 1985; Wilson SC et col. 1996).

3. Differential diagnosis

The differential diagnosis of hypereosinophilia syndrome should include eosinophilic leukemia (EL) (Couto CG, 1998; Hendricks MA, 1981; Latimer KS, 1995).

• Eosinophilic leukemia is characterized by persistent eosinophilia due to hyperplasia of eosinophil progenitor cells in the bone marrow and eosinophilic infiltration of multiple organs.
• Hypereosinophilia syndrome (HS) is identified when severe persistent eosinophilia is associated with infiltration of these cells into many organs and infiltration of the bone marrow by eosinophil precursors (Huibregste BA, Turner JL, 1994). In humanitarian medicine, hypereosinophilia syndrome has the following symptoms:

— eosinophilia in the blood exceeds 1500 eosinophils/mm3 at least six months after the disease; - absence of allergic or parasitic causes, as well as other disorders that usually cause eosinophilia; - the presence of symptoms associated with damage to many organs (Leiferman KM, 1995).

In humans, the criterion for differential diagnosis is the determination of the total level of IgE, which is often high in FH and is likely to be a predictive (prognostic) factor in assessing the possible effectiveness of treatment (Huibregste BA, Turner JL, 1994).

According to the same authors, the only reliable criterion in the differential diagnosis of EL and FH is the determination of incomplete maturation of eosinophils in EL.

Bone marrow puncture and myelogram can provide accurate information about the degree of maturity of cell clones.

Some authors are inclined to believe that EL and FH are two variants of the same disease (Huibregste BA, Turner JL, 1994) or that EL is an evolving form of SE, as well as granulocytic or myeloid leukemia (Mac Ewen SA, Vailli VE, Hulland TJ, 1985). Several cases of the spontaneous form have been reported in veterinary medicine, mostly in cats. FH is rare in dogs (Strombeck DR et col. 1991), and apparently no spontaneously occurring variant has been described. Experimental induction of hypereosinophilia syndrome is possible in many animal species, including dogs (Appendix 3).

Appendix 3. Experimental induction of hypereosinophilia syndrome

Hypereosinophilia syndrome can be induced experimentally.

Experimental contamination of a cat with Toxocara canis indicates the possibility of developing hypereosinophilia syndrome, manifested by granulomas of the liver, spleen, kidneys, lungs, omentum and blood eosinophilia (Moriello KA et coll., 1993; Parsons JS et coll., 1989).

In several dogs, after oral administration of Toxocara canis eggs, the development of granulomas (0.5-3 mm) was noted, localized in the liver, spleen, kidneys, small intestine, abdominal lymph nodes, as well as in the pancreas, heart, diaphragm and lungs (Hayden DW et coll., 1975).

In a hamster after inoculation with Schistosoma mansoni, histomorphological changes of the same nature were noted (Abou Rashed A., et coll. 1997).

In cattle with natural contamination of Fasciola hepatica, eosinophilic infiltration in the liver may occur (Tanimoto T. et coll., 1998).

Treatment and prognosis

• Treatment requires the use of corticosteroid therapy at an immunosuppressive dose (prednisolone 2-4 mg/kg per day orally) if the cause is unknown (Mac Even SA et col. 1985; Wilson SC et col. 1996). The maximum therapeutic dose of the drug is prescribed for a period of 4-6 weeks, then, when a positive effect occurs, it is reduced four times every 2 weeks. Currently, due to the small number of relapses, there is no information about the effectiveness of any other treatment options. None of the publications provide comparative study data on the use of immunosuppressants or immunomodulators.
• In general, the prognosis for FH syndrome is questionable. Sometimes cases of relapses are described, which does not allow the average survival of the patient to be established (Huibregste BA, Turner JL, 1994).

Conclusion

Hypereosinophilia syndrome is a clinical entity for which there are few publications in the dog (as opposed to the cat). The stomach, intestines and lymph nodes are most often damaged. Liver infiltration is probably much less common. Differential diagnosis of neoplasia, hypereosinophilia syndrome and eosinophilic leukemia requires a very delicate approach. Currently, information regarding this syndrome is limited. Experimental studies performed on laboratory animals, starting from the inoculation of pathogens of a parasitic nature, allow us to approach the most detailed approach to deciphering the pathophysiology. However, additional studies conducted in domestic carnivores with spontaneous hypereosinophilia syndrome rarely indicate a parasitic nature of the disease.

SVM No. 2/2003

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Diagnostics

Main symptoms

Signs of elevated eosinophils directly related to the disease that they provoked. The main symptoms are the following:

1. hepatosplenomegaly;
2. anemia;
3. lymphadenopathy;
4. gastritis;
5. indigestion, diarrhea;
6. nausea, vomiting;
7. fever;
8. signs of intoxication - fatigue, lethargy, apathy;
9. loss of appetite;
10. weight loss;
11. inflammatory conditions of blood vessels;
12. dryness and flaking of the skin;
13. signs of skin allergic reactions;
14. cough;
15. cyanosis of mucous membranes;
16. signs of helminthic infestation, etc.

After identifying these symptoms, you need to contact a veterinarian for an accurate diagnosis and initiation of treatment.

HAPPY NEW YEAR AND MERRY CHRISTMAS!

F. GEBERT

The article describes a disease with blurred clinical symptoms, and only a very thorough examination allows diagnosis, treatment and prognosis to be established.

CAUSE OF EOSINOPHILIA

Hypereosinophilia syndrome is manifested by an increased concentration of eosinophils in the blood and their multiple infiltration in organs. In general, this pathology is rare; the largest number of publications is devoted to cats compared to dogs. To make a diagnosis and prognosis, it is necessary to know the pathophysiology of this disease.

PATHOPHYSIOLOGY

Eosinophilia is a pathological condition in which the total number of eosinophils in the blood exceeds 1.9 × 10 e/l in a dog and 0.75 × 10/l in a cat. The number of eosinophils in the blood of a healthy body is limited. They belong to the myelomonocytic series and are formed from bone marrow cells. The process is regulated by granule oocyte-macrophage colony-stimulating factor (GM CSF), interleukin 3 (IL3), but mainly interleukin 5 (IL5). These substances are synthesized by other cells, usually lymphocytes. Eosinophils then enter the blood, where they circulate for 24-36 hours. Next, they migrate to organs exposed to the most intense environmental aggression (skin, lungs and digestive tract), where they remain for several days until they undergo phagocytosis by macrophages.

The function of eosinophils is as follows:

Picture 1.

- participation in the mechanisms of immunoresistance of the body during infestation of the latter with parasites or during hypersensitization;

- phagocytic activity towards bacteria or fungi;

- regulation of the inflammatory process due to peroxidases and other toxic proteins localized in the granules of their cytoplasm (prostaglandins, leukotrienes and some cytokines: interleukins 3 and 5, GM CSF) (Prelaud P., 1999). They may be regulators that primarily influence the inflammatory response of mast cells.

Eosinophils inactivate some molecules produced by mast cells, as they secrete histaminase, kinases and phospholipases in a type I hypersensitization reaction (Prelaud P., 1999). The mechanism of activation of eosinophil degranulation during a type I hypersensitization reaction is presented in Figure 1. When an exogenous antigen (aeroallergen, antigen of a parasitic, bacterial, viral or nutritional nature) enters the body, it encounters T and B lymphocytes. In this case, B lymphocytes are stimulated and transformed into plasma cells, which synthesize immunoglobulins specific to this antigen. These immunoglobulins can belong to classes - G (IgG), M (IgM), A (IgA) or E (IgE). Immunoglobulins E adhere to the mast cell membrane. When the antigen re-enters the body, it is fixed on membrane IgE and provokes degranulation of mast cells, and chemical substances accumulated in eosinophils are also released: eosinophil chemotactic factor of anaphylaxis (ECF-A), interleukins 4 and 5. With paraneoplastic eosinophilia, the movement of eosinophils is carried out by chemotaxis due to the secretion of interleukin 2 and 5 by the neoplasm.

ETIOLOGY

Various disorders that may cause eosinophilia in domestic carnivores are presented in Appendix 1. The most common of these are: dermatitis caused by hypersensitization from flea bites; asthma and complex eosinophilic granuloma of cats (Appendix 2); eosinophilic enteritis and mastocytomas (Center SA, Randolf JB, Erb HN et col., 1990). Histomorphological examination has revealed that many disorders in dogs and cats occur during infiltration of tissues or organs by eosinophils, which is accompanied or not by eosinophilia. Reactions can manifest themselves at the level of the skin, digestive tract (Calver S.A., 1992; Rodriguez A., Rodriguez E, Turnip L. et col., 1995), lungs (Calver CA, 1992; Smith-Maxie LL, et col ., 1989) or the central nervous system (Bennet PF et col. 1997). Some breeds appear to have a predisposition to the manifestation of this pathology:

— granulomas in the vestibule of the oral cavity in the cheeks and lips of a Siberian husky;

— granulomas of the stomach and intestines in a Rottweiler (Gvilford W.G., 1995; Strombeck D.R., Gvilford W.G., 1991);

— eosinophilic ulcerative stomatitis in Covalerking Charles Spaniel (3 cases described) (JoffeD.L, Allen AL, 1995).

Pleural and abdominal eosinophilic effusions in dogs and cats are described by Fossum TW et col. (1993). In 50% of cases they are associated with neoplasms. Cases of eosinophilic effusion are noted with: pneumothorax, interstitial infiltration of the lungs and peribronchial region; respiratory system and skin allergy syndrome; intestinal lymphangiectasia; volvulus of the lung lobe; chylothorax; intestinal perforation due to a bite and infection with feline leukemia virus (FeLV). Cases of eosinophilic gastroenteritis in mink have been described (PalleyLS., Fox JG, 1992).

The cause of eosinophilic disorders is often impossible to determine. The first assumption about this pathology in domestic carnivores is based on infiltration of the digestive tract and type I hypersensitivity to allergens of alimentary nature. The second assumption is based on hypersensitization by bacteria or parasites of the intestine (Strombeck DR, Gvilford WG, 1991), or the respiratory apparatus (Calver S.A., 1992). Pryeosinophilic granulomatosis of the lungs is provoked, as a rule, by Dirofilaria immitis.

Table 1. Histomorphological modifications that appear in different forms during the development of eosinophilic granuloma of the skin in a cat.

The cause of hypereosinophilia syndrome often remains unidentified. If the parasitic or allergic nature of the disease is established, then this pathology is not considered hypereosinophilia syndrome. The syndrome itself is characterized by circulatory hypereosinophilia (exceeding 1.9 x 10 cells/l in a dog and 0.75 x 10 cells/l in a cat), as well as eosinophilic infiltration of many organs from the bone marrow (HuibregsteBA, Turner JL, 1994).

CLINICAL DIAGNOSIS

Diagnosis is usually based on the identification of damage to multiple organs and detection of eosinophilic infiltration. Symptoms are mostly poorly specific. The involvement of histomorphological and cytological studies is necessary to confirm the preliminary diagnosis of hypereosinophilia syndrome.

1. Clinical examination

The disease itself is characterized by polysymptoms, its severity depends on the degree of organ damage. In general, the symptoms of the clinical picture of the disease are vague (hyperthermia, anorexia and weight loss are noted quite often). During clinical examination, in the case of eosinophil infiltration of the intestines or stomach, cachexia, hyperthermia, hepatomegaly, splenomegaly, hypertrophy of peripheral or mesenteric lymph nodes and digestive tract disorders (diarrhea, vomiting) can be observed. The following organs may be involved in the pathological process: liver, spleen, kidneys, mucous membranes of the stomach or intestines, skin, thyroid gland, lungs, lymph nodes, adrenal glands and myocardium.

2. Additional research methods

Due to the fact that the symptoms are blurred, making a diagnosis of this disease requires the use of additional research methods.

• Blood tests should detect at least hypereosinophilia. Biochemical parameters change depending on the severity of eosinophil infiltration of organs such as the liver and kidneys. A definitive diagnosis cannot be made using ultrasound examination alone. The observed changes are not pathognomonic, especially with liver infiltration. In any case, hypereosinophilia syndrome should be included in the list of suspected diseases if the echographic picture indicates anomalies identified simultaneously in several organs (liver, spleen, intestines, etc.).

• X-ray examination does not provide any additional information. All test results for parasitic infestation (scatology, serology) must be negative.

• Histomorphological analysis, starting with biopsy, is necessary to make a final diagnosis (Table 2). Infiltration of eosinophils into the intestine, mesenteric lymph nodes, liver, spleen, medullary zone of the adrenal cortex and endocardium is possible. Simultaneous infiltration by plasma cells also occurs.

• At autopsy, it is possible to detect the presence of granulomas in the liver parenchyma in sizes ranging from 1 to 3mm (Mac Even SA etcol. 1985; Wilson SC etcol. 1996).

3. Differential diagnosis

The differential diagnosis of hypereosinophilia syndrome should include eosinophilic leukemia (EL) (Couto CG, 1998; Hendricks MA, 1981; Latimer KS, 1995).

• Eosinophilic leukemia is characterized by persistent eosinophilia due to hyperplasia of eosinophil progenitor cells in the bone marrow and eosinophilic infiltration of multiple organs.

• Hypereosinophilia syndrome (HS) is identified when severe persistent eosinophilia is associated with infiltration of these cells into many organs and infiltration of the bone marrow by eosinophil precursors (Huibregste BA, Turner JL, 1994). In humanitarian medicine, hypereosinophilia syndrome has the following symptoms:

— eosinophilia in the blood exceeds 1500 eosinophils/mm3 at least six months after the disease;

- absence of allergic or parasitic causes, as well as other disorders that usually cause eosinophilia;

- the presence of symptoms associated with damage to many organs (Leiferman KM, 1995).

In humans, the criterion for differential diagnosis is the determination of the total level of IgE, which is often high in FH and is likely to be a predictive (prognostic) factor in assessing the possible effectiveness of treatment (Huibregste BA, Turner JL, 1994).

According to the same authors, the only reliable criterion in the differential diagnosis of EL and FH is the determination of incomplete maturation of eosinophils in EL.

Bone marrow puncture and myelogram can provide accurate information about the degree of maturity of cell clones.

Some authors are inclined to believe that EL and FH are two variants of the same disease (Huibregste BA, Turner JL, 1994) or that EL is an evolving form of SE, as well as granulocytic or myeloid leukemia (Mae Ewen SA, Vailli VE, Hulland TJ, 1985). Several cases of the spontaneous form have been reported in veterinary medicine, mostly in cats. FH is rare in dogs (Strombeck DR etcol. 1991), and apparently no spontaneously occurring variant has been described. Experimental induction of hypereosinophilia syndrome is possible in many animal species, including dogs (Appendix 3).

TREATMENT AND PROGNOSIS

• Treatment requires corticosteroid therapy at an immunosuppressive dose (prednisolone 2-4 mg/kg per day orally) if the cause is unknown (Mac Even SA et col. 1985; Wilson SC et col. 1996). The maximum therapeutic dose of the drug is prescribed for a period of 4-6 weeks,

CONCLUSION

Hypereosinophilia syndrome is a nosological entity about which there is a small number of publications in the dog (as opposed to the cat). The stomach, intestines and lymph nodes are most often damaged. Liver infiltration is probably much less common. Differential diagnosis of neoplasia, hypereosinophilia syndrome and eosinophilic leukemia requires a very delicate approach. Currently, information regarding this syndrome is limited. Experimental studies performed on laboratory animals, starting from the inoculation of pathogens of a parasitic nature, allow us to approach the most detailed approach to deciphering the pathophysiology. However, additional studies conducted in domestic carnivores with spontaneous hypereosinophilia syndrome rarely indicate a parasitic nature of the disease.

magazine "Veterinarian" No. 2 2003

Treatment

Most often, when eosinophils are elevated, a dog develops a specific form of gastritis. More than any other disease that affects acute and German Shepherds. The tendency to develop such a disease increases an unhealthy diet with a large amount of synthetic products, the presence of helminthiases, tumor processes and the presence of other problems with the digestive organs.

Characteristic features of eosinophilic gastritis are severe nausea and constant vomiting, which, when becoming chronic, leads to severe exhaustion and weakening of the dog. As a result, the skin and coat of dogs suffer - they become dry, brittle, damaged.

The dog doesn't just look skinny - his hair is dull and falling out, obviously unhealthy.

In severe cases and when a dog is exhausted and transferred to artificial feeding in the hospital, special medications are used.

In the presence of a disease, dietary nutrition plays an important role. Food allergies must be eliminated. With timely and correct treatment of the reaction, the prognosis is positive.

If measures are taken too late or treatment is not carried out properly, without consultation with an experienced veterinarian, the risk of complications and the disease becoming chronic increases dramatically. The disease weakens the dog, making it a target for a number of other diseases, especially infectious ones.

How to properly prepare an animal for blood donation

• Before taking blood for analysis, the dog is not fed for 10-12 hours, and the dog must have free access to water.
• We limit the animal’s physical activity (refusal of games, etc.).
• Taking any medications is prohibited. If your dog regularly takes any medications as prescribed by a veterinarian, consult them about stopping them.
• Before taking blood, therapeutic procedures, ultrasound, x-rays, and massage are unacceptable.

The procedure for taking blood for analysis

Blood is taken from a vein of the fore or hind limb by shaving off a small area of ​​hair. The injection site is treated with a disinfectant solution, a needle from a disposable syringe is inserted into the vein, blood in the amount of 2 ml is drawn into a test tube with heparin or sodium citrate.

What blood tests are performed in veterinary clinics?

In modern veterinary clinics, two laboratory blood tests are performed:

• General or clinical.
• Biochemical.

General blood test for a dog

A general blood test based on the number and condition of formed blood elements shows the health status of the dog’s body. When conducting a general blood test, parasites such as dirofilaria (dirofilariasis), babesia (pyroplasmosis - babesiosis) can be detected in a dog’s blood.

What indicators does the clinic’s veterinary specialist receive when conducting a general blood test:

• Hematocrit
• Hemoglobin.
• Average content and concentration of hemoglobin in an erythrocyte.
• Color indicator.
• ESR (erythrocyte sedimentation rate).
• Red blood cells.
• Leukocytes.
• Neutrophils.
• Lymphocytes.
• Eosinophils.
• Monocytes.
• Platelets.
• Basophils.
• Myelocytes.

Biochemical blood test in a dog

Biochemical blood tests allow veterinary specialists to identify subclinical (hidden) diseases of the dog. A biochemical blood test allows you to determine the functioning of the body’s enzymatic system and provide information about damage to a particular organ in a dog.

A biochemical blood test for a dog includes enzymatic, electrolyte, fat and substrate indicators.

Basic biochemical parameters:

• pH.
• Glucose.
• Protein and albumin.
• Cholesterol.
• Bilirubin is direct and total.
• Alanine aminotransferase (ALT).
• Aspartate aminotransferase (AST).
• Lactate dehydrogenase.
• Gamma glutamyl transferase.
• Alkaline and acid phosphatase.
• a –Amylase.
• Urea.
• Creatinine.
• Free fatty acids.
• Lipase level.
• Calcium.
• Magnesium.
• Creatine phosphokinase.
• Triglycerides.
• Phosphorus, inorganic.
• Electrolytes (potassium, calcium, sodium, iron, chlorine, phosphorus).

What to do at home

When your pet gets better and is allowed to go home, like any convalescent pet, it is important to provide a peaceful environment, warmth and comfort. The dog will be weakened, possibly exhausted, so it needs to be protected from stress, drafts and hypothermia.

© shutterstock

Good nutrition and love from their owners play an important role in recovery. The dog needs to be provided with light but high-calorie food, organic food, rest, and a sufficient amount of safe drinking water.

Complete recovery and normalization of the blood picture may take a long time.

What to do at home

When the pet gets better and is allowed to be taken home, like any convalescent, it needs to be provided with calm conditions, warmth and comfort. The animal will be weakened, possibly exhausted, so it must be protected from stress, drafts and hypothermia.

Proper nutrition and love from their owners play an important role in recovery. The dog needs to be provided with a light but high-calorie diet, natural products, rest, and a sufficient amount of clean drinking water.

Complete recovery and normalization of the blood picture may take a long time.

Possible complications

The type of complication depends on the underlying disease. If there are problems with the respiratory tract, the dog faces severe pneumonia, asthma and other diseases. Allergic reactions can cause hair loss and skin inflammation.

Problems with the digestive system are especially troublesome, since the dog loses weight, is weakened, cannot eat properly, and against this background a lot of dangerous diseases can develop.

The greatest threat from elevated eosinophils is background malignancy. Cancer can metastasize, which can quickly lead to the death of a pet.

Acute eosinophilic dermatitis with edema in dogs (Wells-Like syndrome)

170 skin diseases of dogs and cats with 1200 photos – translation SMALL ANIMAL DERMATOLOGY / Acute eosinophilic dermatitis with edema of dogs (Wells-Like syndrome)

Vet Clin Small Anim 49 (2019)

Translation from English: veterinarian Vasiliev AV

Key points

• · Canine acute eosinophilic dermatitis with edema (CAEDE) is a rare syndromic disease in dogs with a unique clinical presentation.
• · Most dogs with CAEDE have a history of gastrointestinal distress preceding or accompanying the skin disease.
• · Dogs with CAEDE have macular or generalized erythema that is most obvious on the hairless skin of the abdomen.
• Diagnosis of CAEDE is based on clinical and histological features, but some cases are difficult to distinguish from canine sterile neutrophilic dermatosis (Canine Sweet syndrome)
• · The etiology of CAEDE is unknown, but adverse drug reactions or systemic type I hypersensitivity may play a role in the pathogenesis.

Introduction

Canine acute eosinophilic dermatitis with edema (CAEDE) is a rare syndromic disease in dogs with a unique clinical presentation. Most dogs, but not all, have a history of moderate to severe gastrointestinal distress. Skin lesions occur during or after treatment for a gastrointestinal disease. Affected dogs develop bright red macules or generalized erythema that is most obvious on the non-hairy skin of the abdomen (Photo 1). Diagnosis is based on both clinical manifestations and histological features.

Although the etiology of this disease is unknown, adverse drug reactions or unknown systemic hypersensitivity may play a role. Some cases may be difficult to distinguish from canine sterile neutrophilic dermatosis (also known as Sweet syndrome [CSS]), due to overlap of clinical criteria and eosinophilic degranulation in the tissues.

Clinical features

In 1999, Holm et al published a case series of 9 dogs that presented with acute onset erythematous arcuate and serpentine macules and plaques with edema. Skin biopsy revealed a marked eosinophilic inflammatory infiltrate with edema. This syndrome was similar to eosinophilic cellulitis (Wells syndrome) in humans. The first dog described in the case series was a Labrador Retriever that developed skin lesions during treatment for giardiasis. Holm et al suggested that the skin lesions were triggered by a hypersensitivity reaction (eg, to drugs or arthropod stings), but a definitive cause was not has been installed.

It is important to differentiate this syndrome from canine atopic dermatitis (CAD). Although dogs with CAD could present with acute deterioration that could manifest as generalized erythema, the sudden appearance of maculopapular lesions, together with the histologic features, made the cases reported by Holm et al unique. Affected dogs did not have the flexural fold or distal limb lesions (eg, erythema, hyperpigmentation, and lichenification) that are characteristic of CAD,3 and pruritus was generally not observed.1

And, although CAD is an IgE-mediated disease, histologically, eosinophils are only an additional component of the inflammatory infiltrate. 3,4 The acute dermatitis reported by Holm et al was markedly eosinophilic and in some cases had collagen flame patterns. Collagen "flame patterns" (i.e., foci of dense deposits of eosinophilic protein on skin collagen) have been found in intense eosinophilic dermatoses such as feline eosinophilic granuloma complex.

A 2006 retrospective study documented the association of the CAEDE syndrome described by Holm et al with gastrointestinal disease. In this study, 22 of 29 dogs were treated for vomiting and/or diarrhea. Of these, 17 dogs developed skin lesions before the onset of gastrointestinal disease and 5 dogs developed skin lesions simultaneously. Severe diarrhea and vomiting were often associated with hematemesis and/or hematochezia and required hospitalization.

Most dogs had hypoalbuminemia. Similar to the cases described by Holm et al, clinical lesions consisted of bright red, sometimes target-like (ie, centrally cleared) macules and papules or plaques with or without generalized erythema and edema. The skin of the ventral abdomen was consistently and most severely affected.

A method of assessing skin drug reactions was used to determine the likelihood of an adverse drug reaction as an etiological mechanism. Although most dogs received multiple medications (eg, antiemetics, antihistamines, H2 receptor antagonists, and antibiotics) for the treatment of gastrointestinal disease, only 6 dogs with gastrointestinal disease had a positive skin response to the drug. Metronidazole has been taken by most dogs, but the cause and effect have not been proven.

Of the 7 dogs without gastrointestinal disease, one dog (Basenji) had a positive skin reaction to the drug. Lesions typical of CAEDE occurred while taking paroxetine, a drug used to treat behavioral disorders.5 In a follow-up study in 2022, Cain and colleagues 6 examined CAEDE with gastrointestinal disease. As in the first study, most dogs developed skin lesions after or during treatment for gastrointestinal distress, but 2 dogs developed skin lesions 1-2 days before the onset of gastrointestinal distress.

Of the 18 dogs, the cause of gastrointestinal disease was identified as pancreatitis in 3 dogs and adverse food reactions in 3 dogs, and inflammatory bowel disease was diagnosed in 5 dogs. The cause of gastrointestinal disease was not found in the remaining 8 dogs. Eight dogs had a skin drug reaction score consistent with a possible adverse drug reaction.

Histologically, a study by Cain et al 6 showed that skin inflammation varied in severity from very mild to severe.

Histological lesions can be divided into 3 patterns:

1) Very mild eosinophilic inflammation with or without neutrophilic inflammation in the superficial dermis with vascular ectasia

2) More extensive eosinophilic inflammation, which extended into the deeper layers of the dermis with mild “flame figures” of collagen.

3) The most severe and diffuse inflammation 6

It is important for pathologists to recognize the wide range of inflammation that can occur in CAEDE. Histological lesions likely reflect progression of skin lesions, but they do not provide information about patient outcome or triggering factor.6

Etiology

Although the pathogenesis of CAEDE remains unclear, studies by Mauldin and Cain generally reject the similarity of CAEDE to Wells syndrome in humans, in which lesions are more focally located on the extremities.5,6 Factors most commonly encountered in canine cases include the following: severe vomiting and diarrhea, which may require hospitalization; hypoproteinemia; treatment with multiple drugs; and acute onset of erythroderma and edema in a ventrally oriented distribution. Triggers such as adverse drug reactions may play a role but are not the definitive cause in all cases. This syndrome is likely a manifestation of a type I systemic hypersensitivity reaction.

Clinical differential diagnoses

Clinically, patients with CAEDE develop discrete, target-shaped, bull's-eye lesions that are similar to those seen in erythema multiforme and vasculitis. Some dogs may develop swelling with ulceration or swelling of the face, which is similar to hives. Although vascular involvement is histologically evident in many cases (eg, red blood cell diapedesis and perivascular fibrin accumulation), overt vasculitis (eg, fibrinoid necrosis or leukocytoclasia) is not usually observed. In addition, the skin does not show symptoms of vascular compromise (skin necrosis or ischemia)1,5,6 Generally, a good quality biopsy can distinguish between these conditions.

Treatment of acute eosinophilic dermatitis with edema in dogs

In each of the three CAEDE studies, medications prescribed before the onset of skin lesions were discontinued. 1,4,6 Commonly prescribed medications included antiemetics, H1 and H2 receptor antagonists, gastroprotectants, anthelmintics, and various antibiotics, including metronidazole. Skin medications included corticosteroids (eg, prednisolone) and antihistamines (eg, diphenhydramine, cetirizine, and hydroxyzine).

Gastrointestinal disease usually resolved before the appearance of skin lesions. In a study by Cain et al, 6 gastrointestinal symptoms resolved within a week, whereas skin lesions took 3 weeks to resolve. Skin lesions typically did not recur. Cain et al 6 reported one case of recurrent skin lesions, but these occurred without gastrointestinal symptoms.6

Canine sterile neutrophilic dermatosis (SWEET syndrome)

Sterile neutrophilic dermatosis (CSS) is a rare disease with features similar to CAEDE. This condition is equivalent to acute febrile neutrophilic dermatosis (also known as SWEET syndrome) in humans. Dogs and people with SWEET syndrome may exhibit symptoms of systemic illness (eg, fever, neutrophilia, arthritis, or pneumonia). 7–11 In dogs, skin lesions are similar but are probably more pustular than in CAEDE and may also be evident on non-hairy skin. Histologically, the dermis contains a marked neutrophilic infiltrate with or without eosinophils. Some cases are thought to be associated with adverse drug reactions. 10.11

Cases of similar presentations of canine acute eosinophilic dermatitis with edema and canine SWEET syndrome

Clinical and histological manifestations may be similar in cases of CAEDE and CSS. There are three main reasons why diagnosis can be difficult:

1) Eosinophils in tissues may undergo degranulation, making it difficult to distinguish them from neutrophils

2) Eosinophils are reported to be a component of the inflammatory infiltrate in CSS

3) Some cases in the older literature diagnosed with CSS may now be classified as CAEDE. Indeed, miniature schnauzer sterile pustular erythroderma is a condition whose histological features may be identical to both CAEDE and CSS, depending on whether eosinophils or neutrophils predominate in the inflammatory infiltrate of the skin.12

Miniature Schnauzers have been reported to have CAEDE in studies conducted by Mauldin and Cain et al.5,6 It is possible that these diseases are unrelated and represent a broad spectrum of systemic hypersensitivity with cutaneous manifestations. For pathologists having difficulty differentiating granulocytes in histological specimens, Luna histochemical staining can be used to evaluate granules in eosinophils.13

Figure 1: Severe abdominal erythroderma in dogs with CAEDE.

Photo 2 (a). Lateral view of the trunk demonstrating multifocal and severe erythematous maculopapular exanthema in a dog with CAEDE.

Photo 2 ((b). The configuration of the lesions in the area of ​​the ventral part of the neck is round or ring-shaped.

Photo 3. Ventral abdomen of the dog in Photo 2 with scattered hemorrhagic macules on diffusely erythematous skin.

Photo 4. Lateral view of the dog’s body from photo 2 one week after starting treatment with prednisolone (partial disappearance of skin lesions)

References:

1. Holm KS, Morris DO, Gomez SM, et al. Eosinophilic dermatitis with edema in nine dogs, compared with eosinophilic cellulitis in humans. J Am Vet Med Assoc 1999; 215(5):649–53. 2. Wells G, Smith NP. Eosinophilic cellulitis. Br J Dermatol 1979;100:101–9. 3. Olivry T, Hill PB. The ACVD task force on canine atopic dermatitis(XVIII): histopathology of skin lesions. Vet Immunol Immunopathol 2001;81:305–9. 4. Bizikova P, Santaro D, Marsella R, et al. Review: clinical and histological manifestations of canine atopic dermatitis. Vet Dermatol 2015;26:79-e24. 5. Mauldin EA, Palmeiro BS, Goldschmidt MH, et al. Comparison of clinical history and dermatologic findings in 29 dogs with severe eosinophilic dermatitis: a retrospective analysis. Vet Dermatol 2006;17(5):338–47. 6. Cain CL, Bradley CW 2nd, Mauldin EA. Clinical and histologic features of acute onset erythroderma in dogs with gastrointestinal disease: 18 cases (2005-2015). J Am Vet Med Assoc 2017;251(12):1439–49. 7. Gains MJ, Morency A, Sauve F, et al. Canine sterile neutrophilic dermatitis (resembling Sweet's syndrome) in a Dachshund. Can Vet J 2010;51(12):1397–9. 8. Johnson CS, May ER, Myers RK, et al. Extracutaneous neutrophilic inflammation in a dog with lesions resembling Sweet's Syndrome. Vet Dermatol 2009;20(3):200–5. 9. Cohen PR, Kurzrock R. Sweet's syndrome revisited: a review of disease concepts. Int J Dermatol 2003;42(10):761–78. 10. Mellor PJ, Roulois AJ, Day MJ, et al. Neutrophilic dermatitis and immunemediated haematological disorders in a dog: suspected adverse reaction to carprofen. J Small Anim Pract 2005;46(5):237–42. 11. Vitale CB, Ihrke PJ, Gross TL. Putative diethylcarbamazine-induced urticaria with eosinophilic dermatitis in a dog. Vet Dermatol 1994;5(4):197–203. 12. Okada K, Saegusa S, Yamaoka A, et al. Febrile neutrophilic dermatosis in a miniature schnauzer resembling Sweet's syndrome in humans. Vet Dermatol 2004; 15(s1). 13. Gomes P, Torres SM, Plager DA, et al. Comparison of three staining methods to identify eosinophils in formalin-fixed canine skin. Vet Dermatol 2013;24(3):323–8, e71–2.

Photo 1 from Vet Clin Small Anim 49 (2019)

Photo 2-4 from ournal of the Hellenic Veterinary Medical Society 62(4):320 · November 2017 

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Prevention

You can avoid illness if you try to provide your pet with the healthiest possible living conditions. The first is proper nutrition with natural products. To avoid developing gastritis caused by food allergies, you need to use only high-quality feed.

If you do not have experience creating a dog menu, pet owners should seek help from an experienced veterinarian. He will create an optimal diet based on the breed and age of the dog.

The dog needs regular walks and exercise. This is an important time to deworm because worms are often the cause of increased eosinophil counts.

It is impossible to completely protect against changes in the blood pattern, but the dog owner can reduce the risk of feeding.

Eosinophils in the general blood test of cats and dogs. Leukocyte formula

A general blood test is one of the main diagnostic methods

state of the animal.
It determines such indicators as the total number of leukocytes, erythrocytes and platelets, as well as hematocrit, hemoglobin, average volume of erythrocytes, average content and concentration of hemoglobin in an erythrocyte. Leukocytes
are white blood cells. These are cells of the blood vascular system, diverse in morphology and functions. White blood cells are produced in the bone marrow.

Leukocytes protect the body from infections through phagocytic activity, that is, they engulf foreign cells. They are also involved in the formation of humoral immunity (the formation of antibodies by lymphocytes) and in the recovery process in case of tissue damage.

According to morphology, leukocytes are divided into 2 groups, the cells of which differ in appearance and functions:

Granulocytes

– cells whose cytoplasm contains specific granularity. These include neutrophils, eosinophils, and basophils.

Agranulocytes are cells characterized by the absence of specific granularity in the cytoplasm and non-segmented nuclei. This group includes lymphocytes and monocytes.

In a general blood test, the total concentration of blood leukocytes and the percentage of the main subpopulations of leukocytes are determined.

Leukocyte formula (leukogram) is the percentage (or absolute) ratio of different types of leukocytes. The leukocyte formula is calculated in a stained blood smear under a microscope.

In clinical practice, the leukogram is of great importance, since with changes in the body, the content of some types of leukocytes increases or decreases due to changes in the number of others.

Eosinophils

– blood cells measuring 8 – 20 microns. Their entire cytoplasm is filled with large pink granules, since when stained according to Romanovsky, eosinophils are intensely stained with the acidic dye eosin. The eosinophil nucleus consists of 2 lobes. Eosinophils are granulocytic leukocytes. The pellets vary in appearance among different animal species. For example, in dogs they are round in shape and vary in size and number in the cytoplasm. In cats, the grains are rod-shaped and fill the entire cytoplasm.

Eosinophils have some phagocytic and motor activity and are involved in allergic reactions

. They are microphages, which means they absorb small foreign particles and cells. Eosinophils are capable of active amoeboid movement. They penetrate beyond the walls of blood vessels. Also, a property of these cells is chemotaxis - movement towards the site of inflammation or damaged tissue. Most eosinophils do not remain in the blood for long. Then they migrate to tissues, where they remain for a long time.

The main function of eosinophils is to fight parasites and participate in allergic reactions. They neutralize excess histamine

, which is released in large quantities during allergies. They participate in the transfer of breakdown products of proteins that have antigenic properties and prevent the local accumulation of a large number of antigens. Consequently, during allergic reactions, eosinophils bind and transport antigens and histamine to neutralizing organs (liver). Eosinophils are also capable of releasing histamine when necessary to prevent an allergic reaction.

The blood contains a small number of eosinophils. An increase in their level is called eosinophilia, a decrease is called eosinopenia.

Causes of eosinophilia:

Parasitic diseases

(for example, ascariasis, opisthorchiasis, trichinosis).

Allergic diseases (bronchial asthma, allergic dermatitis, drug allergies, food allergies).

Malignant neoplasms ( lymphogranulomatosis

, chronic myeloid leukemia and others). This is especially true for tumors accompanied by metastases and necrosis.

Connective tissue diseases (rheumatoid arthritis).

Eosinopenia is a relative concept. May be observed in healthy animals. In some cases it occurs with sepsis

, injuries, burns. Also, a decrease in eosinophils is characteristic of the initial phase of the infectious-toxic process. A favorable symptom is the appearance of eosinophils in the blood during an acute infectious disease. This is a sign that recovery is beginning.

If you notice a change in your pet's condition, please consult your primary care physician.

Clinical significance of UAC indicators

Currently, most indicators are determined on automatic hematology analyzers, which allow simultaneous examination of from 5 to 36 parameters, which provides a lot of additional information.

LEUCOCYTES (WBC) are produced in the red bone marrow and lymph nodes. Leukocytes include cells of the granulocytic (neutrophils, eosinophils, basophils), monocytic (monocytes) and lymphoid (lymphocytes) series.

The main function of leukocytes is to protect the body from foreign agents. Immunological reactions are realized due to the phagocytic activity of leukocytes, their participation in cellular and humoral immunity, and histamine metabolism.

Reference intervals:

dogs – 6.0 – 16.9 x 109 /l;

cats – 5.5 – 19.5 x 109 /l;

Leukocytosis is an increase in the number of white blood cells above normal limits.

Physiological leukocytosis:

• fear;
• excitation;
• rough treatment;
• physical exercise;
• convulsions.

Stress leukocytosis:

• injuries;
• surgical operations;
• attacks of pain;
• malignant neoplasms;
• spontaneous or iatrogenic Cushing's disease;
• second half of pregnancy (physiological with a shift to the right).

Inflammatory leukocytosis:

• infections (bacterial, fungal, viral, etc.);
• injuries;
• necrosis;
• allergies;
• bleeding;
• hemolysis;
• inflammatory conditions;
• acute local purulent processes.

Inappropriate reactions of leukocytes:

• severe purulent infections;
• gram-negative sepsis.

Leukopenia is a decrease in the number of leukocytes below normal limits.

Decrease in the number of leukocytes as a result of decreased hematopoiesis:

• infection with feline leukemia virus (cats);
• infection with feline immunodeficiency virus (cats);
• feline viral enteritis (cats);
• parvovirus enteritis (dogs);
• feline panleukopenia;
• hypoplasia and aplasia of bone marrow;
• damage to the bone marrow by chemicals, drugs, etc.
• myeloproliferative diseases;
• myelophthisis;
• taking cytotoxic drugs;
• ionizing radiation;
• acute leukemia;
• metastases of neoplasms to the bone marrow;
• cyclic leukopenia in marbled blue collies (hereditary, associated with cyclic hematopoiesis).

Leukocyte sequestration:

• endotoxic shock;
• septic shock;
• anaphylactic shock.

Increased utilization of leukocytes:

• gram-negative sepsis;
• endotoxic or septic shock;
• viremia;
• severe purulent infections;
• toxoplasmosis (cats).

Increased destruction of leukocytes:

• gram-negative sepsis;
• endotoxic or septic shock;
• DIC syndrome;
• hypersplenism (primary, secondary);
• immune-related leukopenia.

Result of the drugs:

• sulfonamides;
• some antibiotics;
• non-steroidal anti-inflammatory drugs;
• thyreostatics;
• antiepileptic drugs;
• antispasmodic oral drugs.

A decrease or increase in leukocytes in the blood may be due to certain types of leukocytes. An increase or decrease in the number of certain types of leukocytes in the blood can be absolute (with a decrease or increase in the total leukocyte content) or relative (with a normal total leukocyte content).

Leukocyte formula is the percentage of different types of leukocytes in a blood smear. It has great diagnostic value.

Neutrophils in peripheral blood are represented by segmented and a relatively small number of band forms. The main function of these cells is to protect the body from infections; their main property is the ability to phagocytose.

Neutrophilia – increased number of neutophils:

Physiological:

• excitation;
• fright;
• physical exercise.

Stressful:

• pain;
• prolonged stress;
• Cushing's syndrome.

Inflammatory:

• bacterial infections (sepsis, pyometra, peritonitis, abscesses, pneumonia, etc.);
• inflammation or tissue necrosis (rheumatoid attack, heart attacks, gangrene, burns);
• progressive tumor with decay;
• acute and chronic leukemia;
• exogenous intoxication (the result of the action of poisons of insects, snakes, endotoxins, vaccines, medications);
• acute hemorrhages;
• parasitic diseases;
• endogenous intoxications (uremia, ketoacidosis, eclampsia, etc.);
• hereditary pathologies;
• increase in carbon dioxide concentration.

Neutropenia is a decrease in the number of neutrophils.

Causes:

• viral (canine distemper, feline panleukopenia, parvovirus gastroenteritis, etc.)
• some bacterial infections (salmonellosis, brucellosis, tuberculosis, bacterial endocarditis, other chronic infections);
• infections caused by protozoa, fungi, rickettsia;
• aplasia and hypoplasia of the bone marrow, metastases of neoplasms in the bone marrow;
• ionizing radiation;
• hypersplenism (splenomegaly);
• aleukemic forms of leukemia;
• anaphylactic shock;
• collagenoses;
• hereditary forms;
• the use of sulfonamides, analgesics, anticonvulsants, antithyroid and other drugs.

Agranulocytosis is a sharp decrease in the number of granulocytes in the peripheral blood until their complete disappearance, leading to a decrease in the body's resistance to infection and the development of bacterial complications.

Leukemoid reaction of the neutrophil type is a sharp increase in the number of neutrophil leukocytes in the blood with the appearance of a large number of hematopoietic elements, up to myeloblasts.

Causes:

• acute bacterial pneumonia;
• malignant tumors with multiple metastases to the bone marrow.

Eosinophils are blood cells that phagocytose antigen-antibody complexes. Participate in immediate and delayed hypersensitivity reactions.

Eosinophilia is an increase in eosinophils in the blood. Most often accompanies parasitic infestations and atopic diseases.

The most common reasons:

• allergies;
• parasitic diseases;
• drug intolerance;
• eosinophilic granulomas;
• eosinophilic leukemia;
• inflammatory reactions in organs that normally contain a large number of mast cells (skin, lungs, intestines, uterus).

Eosinopenia - a decrease in the content of eosinophils - is in most cases caused by an increase in adrenocorticoid activity. The concept is relative, since they may not be normally present in healthy animals.

Basophils are blood cells containing histamine granules in the cytoplasm. The main function of these cells is to participate in immediate-type hypersensitivity reactions, as well as in inflammatory, allergic and delayed-type hypersensitivity reactions.

Basophilia - increased basophils in the blood .

Causes:

• allergic reactions to the introduction of a foreign protein, including allergies to food;
• chronic inflammatory processes in the gastrointestinal tract;
• blood diseases (acute leukemia, lymphogranulomatosis);
• myxedema (hypothyroidism);
• lipid metabolism disorder;
• the result of the action of estrogens and antithyroid drugs.

Lymphocytes are a central link in specific immunological reactions. The main function is to recognize the antigen and participate in an adequate immune response of the body. T lymphocytes determine cellular immunity. B lymphocytes participate in humoral immunity and differentiate into plasma cells that secrete immunoglobulins in response to stimulation by foreign antigens. They actively participate in the pathogenesis of immunodeficiency conditions, infectious, allergic, lymphoproliferative, oncological diseases, and autoimmune processes.

Absolute lymphocytosis is an increase in the number of lymphocytes in the blood.

Causes:

• viral infections;
• chronic allergic reactions;
• reaction to vaccination in young dogs;
• blood diseases (lymphocytic leukemia, lymphosarcoma);
• toxoplasmosis;
• hyperthyroidism;
• the use of non-steroidal anti-inflammatory drugs (NSAIDs), griseofulvin, haloperidol, etc.;
• relative lymphocytosis with neutropenia.

Absolute lymphopenia is a decrease in the number of lymphocytes in the blood.

Causes:

• pancytopenia;
• use of corticosteroids, immunosuppressants;
• malignant neoplasms;
• immunodeficiency states;
• renal failure;
• chronic liver diseases;
• loss of lymphocyte-rich lymph;
• circulatory failure.

Monocytes are cells belonging to the mononuclear phagocyte system (MPS). Removes dying cells, denatured protein, bacteria and antigen-antibody complexes from the body.

Monocytosis is an increase in the number of blood monocytes.

Causes:

• infections (viral, fungal, rickettsial, protozoal);
• blood parasitic diseases (pyroplasmoidosis, including canine babesiosis);
• acute and chronic inflammatory processes;
• collagenoses;
• blood diseases;
• tissue inflammatory processes;
• granulomatosis (tuberculosis, brucellosis, ulcerative colitis, enteritis);
• surgical interventions.

Monocytopenia is a decrease in the number of monocytes. It is difficult to assess due to the low level of monocytes in the blood under normal conditions.

HEMOGLOBIN (HGB) is the main component of red blood cells. The main function of HGB is the transfer of oxygen from the lungs to the tissues, as well as the removal of carbon dioxide from the body and the regulation of acid-base status. HGB concentration is the main indicator in the diagnosis of anemia.

Reference intervals:

dogs – 120 – 180 g/l;

cats – 80 – 150 g/l;

Reasons for the increase:

• primary and secondary erythrocytosis;
• excessive exercise or agitation;
• relative erythrocytosis during dehydration;

Reasons for downgrade:

• anemia (iron deficiency, hemolytic, hypoplastic, B12-folate deficiency);
• acute blood loss (on the first day of blood loss due to blood thickening caused by large loss of fluid, the hemoglobin concentration does not correspond to the picture of true anemia);
• hidden bleeding;
• endogenous intoxication (malignant tumors and their metastases);
• damage to the bone marrow, kidneys and some other organs;
• hemodilution (intravenous fluids, false anemia).

Reasons for a false increase in hemoglobin:

• high leukocytosis;
• progressive liver diseases;
• multiple myeloma.

HEMATOCRIT (HCT) is the volume fraction of formed elements in whole blood. The second most important indicator of a general blood test after HGB, showing the severity of anemia. This is an approximate indicator of hemoconcentration shifts and hemodilution.

Reference intervals:

dogs – 37 – 55%;

cats – 25 – 45%.

Reasons for the increase:

• primary and secondary erythrocytosis (increased number of red blood cells);
• dehydration (gastrointestinal diseases accompanied by profuse diarrhea, vomiting; diabetes);
• decrease in the volume of circulating plasma (peritonitis, burn disease);

Reasons for downgrade:

• anemia;
• increased circulating plasma volume (heart and kidney failure, hyperproteinemia);
• chronic inflammatory process, trauma, fasting, chronic hyperazotemia, cancer;
• hemodilution (intravenous administration of fluids, especially with reduced renal function).

RED CELLS (RBC) are the most numerous representatives of the formed elements of blood. Red blood cells contain HGB. The main function of red blood cells is to supply tissues with oxygen and remove carbon dioxide from them. They are formed from reticulocytes as they exit the red bone marrow. The reticulocyte finally matures within a few hours.

Reference intervals:

dogs – 5.5 – 8.5 x 1012 /l;

cats – 5.0 – 11.0 x 1012 /l;

Erythrocytosis is an increase in the number of red blood cells, which can be absolute or relative.

Relative erythrocytosis - due to a decrease in circulating blood volume or the release of red blood cells from blood depots.

Causes:

• excitation;
• exercise stress;
• pain;
• fluid loss (diarrhea, vomiting, excessive diuresis, excessive sweating);
• drinking deprivation;
• increased vascular permeability with the release of fluid and proteins into the tissue.

Absolute erythrocytosis is an increase in the mass of circulating red blood cells due to increased hematopoiesis.

Erythremia is primary erythrocytosis, resulting from the autonomous (independent of the production of erythropoietin) proliferation of erythroid progenitor cells in the red bone marrow and the entry into the blood of a large number of mature red blood cells.

Symptomatic erythrocytosis caused by hypoxia:

• lung diseases;
• heart defects;
• presence of abnormal hemoglobins;
• increased physical activity;
• staying at high altitudes above sea level;
• obesity;
• chronic methemoglobinemia (rare).

Symptomatic erythrocytosis associated with inappropriately increased production of erythropoietin:

• hydronephrosis and polycystic kidney disease (with local hypoxia of kidney tissue);
• kidney parenchyma cancer (produces erythropoietin);
• liver parenchyma cancer (produces erythropoietin-like proteins).

Symptomatic erythrocytosis associated with an excess of adrenocorticosteroids or androgens in the body:

• Cushing's syndrome;
• pheochromocytoma;
• hyperaldesteronism.

Erythrocytopenia is a decrease in the number of red blood cells in the blood.

Causes:

1. Anemia of various origins.
2. Increased circulating blood volume (relative anemia):

• overhydration;
• sequestration of red blood cells in the spleen;
• hyperproteinemia;
• hemodelution (blood dilution) in case of advanced expansion of the vascular space and distribution of the total red blood cell mass in the body (anemia of newborns, anemia of pregnant women);
• increased concentration of cytotoxic estrogens in functioning cystic ovaries (dogs).

1. Infectious agents:

• Ehrlichia canis (dogs);
• parvovirus (dogs);
• infection with feline leukemia virus (FLV infection);
• panleukopenia (cats – rare);
• infection with feline immunodeficiency virus (FIV infection).

1. Immune-mediated - idiopathic aplastic anemia.
2. Radiation therapy.
3. Myelophthisis (a disorder characterized by the replacement of hematopoietic cells with abnormal cells):

• myelogenous leukemia;
• lymphoid leukemia;
• multiple myeloma;
• myelodysplastic syndromes;
• myelofibrosis;
• osteosclerosis;
• metastatic lymphomas;
• metastatic mast cell tumors.

Classification of anemia according to erythrocyte parameters, taking into account the mean erythrocyte volume (MCV) and the mean hemoglobin concentration in the cell (MCHC)

Normocytic normochromic anemia:

• acute hemolysis in the first 1-4 days;
• acute bleeding in the first 1-4 days;
• moderate blood loss that does not stimulate a significant response from the bone marrow;
• early period of iron deficiency;
• chronic inflammation;
• chronic neoplasia;
• chronic kidney disease (with insufficient production of erythropoietin);
• endocrine insufficiency (hypofunction of the pituitary gland, adrenal glands, thyroid gland or sex hormones);
• selective erythroid aplasia;
• aplasia and hypoplasia of the bone marrow of various origins;
• lead poisoning;
• lack of cobalamin (vitamin B12).

Macrocytic normochromic anemia:

• regenerative anemia;
• for infections caused by feline leukemia virus;
• erythroleukemia and myelodysplastic syndromes;
• non-regenerative immune system-mediated anemia;
• macrocytosis in poodles (healthy mini-poodles without anemia);
• cats with hyperthyroidism (weak macrocytosis without anemia);
• folate deficiency.

Macrocytic hypochromic anemia:

• regenerative anemia with noticeable reticulocytosis;
• hereditary stomatocytosis in dogs;
• increased osmotic instability of erythrocytes of Abyssinian and Somali cats.

Microcytic or normocytic hypochromic anemia:

• chronic iron deficiency;
• portosystemic shunts;
• anemia in inflammatory diseases;
• hepatic lipidosis in cats;
• normal condition for Japanese Great Danes, Akitas and Shibas;
• long-term treatment with recombinant human erythropoietin;
• copper deficiency;
• drugs or agents that inhibit heme synthesis;
• myeloproliferative disorders with impaired iron metabolism;
• pyridoxine deficiency;
• familial disorder of erythropoiesis in English springer spaniels.

MEAN ERYTHROCYTE VOLUME (MCV) is an indicator used to characterize the type of anemia. The MCV value within the normal range characterizes the erythrocyte as a normocyte, less than normal as a microcyte, more than the normal range as a macrocyte

Reference intervals:

dogs – 60–72 fL

cats – 39 – 50 fL;

Increased (macrocytosis):

• macrocytic and megaloblastic anemia (B12-folate deficiency);
• anemia that may be accompanied by macrocytosis (hemolytic);
• healthy greyhounds;
• congenital macrocytosis in poodles;
• regenerative anemia;

Decreased (microcytosis):

• microcytic anemia (iron deficiency, sideroblastic, thalassemia);
• anemia that is accompanied by microcytosis (hemolytic, hemoglobinopathies);
• portosystemic anastomoses and lipidosis in cats;
• liver failure;
• healthy dogs of Asian breeds (Shiba Inu, Akita, Jindo);
• young animals;
• hypertensive characteristics of water-salt imbalance.

AVERAGE CONTENT OF HEMOGLOBIN IN AN INDIVIDUAL ERYTHROCYTE (MCH) - this indicator has no independent significance, since it directly depends on the average volume of the erythrocyte (MCV) and the average concentration of hemoglobin in the erythrocyte (MCHC).

Reference intervals:

dogs – 19.5 – 25.5 Pg

Cats –12.5 – 17.5 Pg

Increased:

• hyperchromic anemia (megaloblastic, liver cirrhosis);
• lipemia;
• Heinz bodies;
• pronounced leukocytosis.

Downgraded:

• hypochromic anemia (iron deficiency);
• reticulocytosis;
• anemia in malignant tumors.

INDICATOR OF ANISOCYTOSIS OF RED CYTES (RDW) – coefficient of variation in the distribution of erythrocytes by volume. A condition in which red blood cells of different sizes are simultaneously detected (anisocytosis).

Reference intervals:

Dogs – 11.0 – 16.0%;

Cats – 13.5 – 18.0%;

Increased:

• macrocytic anemia;
• myelodysplastic syndromes;
• metastases of neoplasms to the bone marrow;
• iron deficiency anemia.

AVERAGE CONCENTRATION OF HEMOGLOBIN IN erythrocytes (MCHC) – reflects the relative content of HGB in the erythrocyte.

Reference intervals:

dogs – 320-385 g/l

cats – 310 – 385 g/l

Increased MSHC (extremely rare) – reasons:

• hyperchromic anemia (spherocytosis, ovalocytosis);
• hyperosmolar disturbances of water and electrolyte metabolism.

False increase in MSHC (artifact) – reasons:

• hemolysis of erythrocytes in vivo and in vitro;.
• lipemia;
• the presence of Heinz bodies in erythrocytes;
• agglutination of erythrocytes in the presence of cold agglutinins.

Decrease in MCHC reasons:

• regenerative anemia (if there are a lot of stressed reticulocytes in the blood);
• chronic iron deficiency anemia;
• hereditary stomatocytosis (dogs);
• hypoosmolar disturbances of water and electrolyte metabolism.

False decrease in MSHC – in dogs and cats with hypernatremia.

PLATELETS (PLT) are a formed element of blood, part of the cytoplasm of bone marrow megakaryocytes. Platelets perform angiotrophic, adhesive-aggregation functions, participate in the processes of blood coagulation and fibrinolysis, and ensure retraction of a blood clot. A decrease in the number of platelets in the blood (thrombocytopenia) can be caused by a decrease in their formation (hematopoietic insufficiency), an increase in their destruction or sequestration, as well as increased consumption.

Reference intervals:

dogs – 200 – 500 x 109 /l;

cats – 300 – 700 x 109 /l;

Thrombocytosis - an increase in the number of platelets can be primary (the result of primary proliferation of megakaryocytes) and secondary (reactive), occurring against the background of any disease.

Causes:

• myeloproliferative processes (erythremia, myelofibrosis);
• chronic inflammatory diseases;
• malignant neoplasms;
• bleeding, hemolytic anemia;
• after surgical operations;
• after splenectomy;
• use of corticosteroids.

Thrombocytopenia - a decrease in the number of platelets in the blood can be caused by a decrease in their formation (hematopoietic insufficiency), an increase in their destruction or sequestration, as well as increased consumption.

Causes:

• hereditary thrombocytopenia;
• DIC syndrome;
• bone marrow damage;
• infections;
• thromboembolic disease;
• hypersplenism;
• vasculitis;
• immune-related diseases;
• radiation therapy;
• the use of antihistamines, antibiotics, diuretics, anticonvulsants, Vicasol, heparin, digitalis preparations, nitrites, estrogens, etc.

More detailed information on taking a general blood test and the results of the study can be obtained in our clinics in Vitebsk and St. Petersburg at the Veterinary Center of Dr. Bazylevsky A.A.

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