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Read-Only Case Details Reviewed: Apr 2008

JPC SYSTEMIC PATHOLOGY

Nervous System

February 2020

N-P06

 

Signalment (JPC #CG-4):  A duckling

 

HISTORY:  This is one of a flock of ducklings that became suddenly ill with signs of listlessness, anorexia, rapid breathing, and in some, nervous derangement prior to death.

 

HISTOPATHOLOGIC DESCRIPTION:  Cerebrum:  Multifocally expanding host endothelial cells and often occluding vascular lumina are moderate numbers of protozoal megaloschizonts. Meglaoschizonts are round, 60-100 µm in diameter, and contain multiple membrane bound basophilic cytomeres, each containing numerous 1 x 2 µm merozoites, which are separated by a homogenous purple proteinaceous material. In some megaloschizonts, a markedly hypertrophied endothelial cell nucleus is present. Degenerating megaloschozonts are surrounded by low numbers of lymphocytes, fewer heterophils and macrophages, necrotic debris, and mild hemorrhage, fibrin, and edema. There is mild gliosis of the surrounding neuroparenchyma, and vessels in this area are cuffed by low numbers of lymphocytes. Multifocally within blood vessels, erythrocytes contain one or more 1-3 µm, oval, clear to lightly basophilic gametocytes that peripheralize the nucleus. 

 

MORPHOLOGIC DIAGNOSIS:  Cerebrum, vessels: Intraendothelial megaloschizonts, multifocal, with variable vascular occlusion, intraerythrocytic gametocytes, and mild lymphohistiocytic encephalitis, duck, avian.

 

ETIOLOGIC DIAGNOSIS:  Cerebral leucocytozoonosis

 

CAUSE:  Leucocytozoon simondi

 

GENERAL DISCUSSION:

·      Leucocytozoonosis is a parasitic protozoal disease that infects many species of domestic and wild birds in Europe, Asia, and North America

·      Leucocytozoon sp. (phylum Apicomplexa, family Plasmodiidae), is closely related to Haemoproteus sp. and Plasmodium sp.

·      Often affects young ducks and geese and can result in sudden death

·      Highest incidence in the spring with a carrier state

 

PATHOGENESIS:

·      Vectors:  Transmitted by simuliid (black) flies (Simulium spp.) and biting culidoid midges (Culicoides spp.)

·      Schizogony in the liver, lung and vascular system

·      Anemia due to destruction of parasitized erythrocytes and parasitic production of anti-erythrocytic (AE) factor

 

LIFE CYCLE:

·      Insect bites bird > sporozoites in salivary gland of insect enter bloodstream > schizonts develop in liver > release merozoites (1 µm) > second generation develops in liver and phagocytic cells throughout body > become megaloschizonts (100 - 200 µm) > release merozoites (1 µm) > schizogony in liver or entry into circulating erythrocytes or leukocytes > development into microgamonts or macrogametes > insect feeds on bird > sexual maturation, fertilization and sporogony take place in insect

·      No merogony occurs in leukocytes or erythrocytes; merogony occurs in the parenchyma of brain, liver, heart (H-P06), kidney, or other organs

 

TYPICAL CLINICAL FINDINGS:

·      Course of disease is short; animals die or recover within a few days

·      Infections may or may not be clinically apparent

·      Sudden onset of depression, anorexia, weakness, loss of equilibrium, labored breathing, or sudden death

·      Clinical pathology: Intravascular hemolysis and anemia

 

TYPICAL GROSS FINDINGS:

·      Tissue pallor, thin blood, hepatomegaly, splenomegaly, and hemorrhage in the liver, lung and kidney

·      Megaloschizonts are grossly visible as multiple gray nodules in the brain, epicardium, liver, lung, kidney, intestine, and lymphoid tissue

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

·      Usually minimal host response

·      Lymphoplasmacytic infiltrates and multifocal ischemic necrosis due to occlusion of blood vessels by megaloschizonts in endothelial cells

·      Schizonts within hepatocytes may rupture and induce dilation and congestion of sinusoids and granulomatous reaction in the surrounding tissues

·      Megaloschizonts can be found in monocyte-macrophage lineage cells of spleen and other tissues

 

ULTRASTRUCTURAL FINDINGS:

·      Schizonts are composed of electron-dense cytomeres within membrane-bound vacuoles (parasitophorous vacuole)

·      Merozoites contains a large nucleus, a mitochondrion and well-developed apical complex consisting of three apical rings, paired rhoptries and numerous micronemes

 

ADDITIONAL DIAGNOSTIC TESTS:

·      Cytology: Gamonts markedly distort erythrocyte or leukocyte

·      Binucleate illusion – host cell nucleus at one end and the parasite nucleus at the other

·      Affected blood cells may be markedly elongated or spindle-shaped

 

DIFFERENTIAL DIAGNOSIS:

Intraerythrocytic gametocytes:

·      Haemoproteus sp.:  Primarily in birds (also found in turtles and lizards); insect vectors (midges, hippoboscids, tabanids); schizonts in visceral endothelial cells; gametocytes develop in circulating erythrocytes; birefringent pigment granules in infected erythrocytes, the gametocyte occupies over 50% of the of the red cell cytoplasm that partially encircles the nucleus; few clinical signs reported

·      Plasmodium sp. (P-P04):  Avian malaria; mosquito vector; contain birefringent pigment granules (malaria pigment); schizogony in peripheral blood; gametocytes in mature erythrocytes, gametocytes occupy less than 50% of the host cell cytoplasm

 

COMPARATIVE PATHOLOGY:

·      L. simondi: Ducks and geese

·      Rapid, fatal anemia, leukocytosis, splenomegaly, liver degeneration and hypotrophy

·      L. caulleryi: Chickens

·      Subcutaneous hemorrhages in the wings and legs, pectoral and thigh muscles, thymus, epicardium, pancreas and kidneys

·      L. smithi: Turkeys

·      Rapid course of disease; high mortality in young turkeys

·      L. grusi: Gruiformes (cranes)

·      L. tossi: Falconiformes (raptors)

·      L. marchouxi: Columbiformes (pigeons)

·      L. naevel: Guinea fowl

·      L. centropi: Cuculiformes (cuckoos, roadrunners)

·      L. tawaki: Penguin

·      L. ugwidi: Cape cormorant

 

References:

1.    Abdul-Aziz T, et al. Avian Histopathology. 4th ed. Jacksonville, FL: American Association of Avian Pathologists; 2016: 479,524,537.

2.    Bowman DD. Georgis’ Parasitology for Veterinarians. 10th ed. St. louis, MO: Elsevier Saunders; 2014: 114.

3.    Campbell TW. Exotic Animal Hematology and Cytology. 4th ed. Ames, IA: Wiley-Blackwell; 2015: 118-120.

4.    Fitz-Coy SH. Parasitic diseases. In: Boulianne M, ed. Avian Disease Manual. 7th ed. Jacksonville, FL: American Association of Avian Pathologists; 2013:159,163.

5.    Gardiner CH, et al. Apicomplexa. In: Gardiner CH, et al. eds. An Atlas of Protozoan Parasites in Animal Tissues. 2nd ed. Washington, DC: Armed Forces Institute of Pathology; 1998:65-68, 73-76.

6.    McDougald LR, et al. Protozoal Infections. In: Swayne DE, et al. eds. Diseases of Poultry. 13th ed. Ames, IA: Wiley-Blackwell; 2013: 1185-1188.

7.    Terio KA, Mcaloose D, G. SLJ. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Academic Press; 2018: 677, 717, 741-742, 766-769, 818.

 


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