Neonatal alloimmune thrombocytopenia, purpura, and anemia in 6 neonatal piglets.

A hemorrhagic diathesis due to neonatal alloimmune thrombocytopenia occurred in a sow herd consisting of F I large white X Landrace females. Colostrum, containing maternal antibodies incompatible with platelet antigens inherited from the sire, was ingested and absorbed by the piglets. Six piglets were affected and displayed signs of lethargy and depression with petechiation, ecchymosis, and severe bruising of the skin. All 6 piglets died or were euthanized by 3 days of age.

Vascular lesions in nine Göttingen minipigs with thrombocytopenic purpura syndrome.

Tissues from 9 Göttingen minipigs, aged 7 weeks to 1 year, with clinically diagnosed thrombocytopenic purpura syndrome were examined microscopically. All pigs had a history of spontaneous cutaneous purpura that was generally accompanied by disseminated visceral hemorrhages. Hematologic abnormalities included anemia (8 out of 9 pigs) and thrombocytopenia (7 out of 9 pigs), with platelet counts consistently below 20,000/microl. Microscopically, degenerative vascular lesions with morphologic features of arteriosclerosis were present in all 9 pigs. Vascular lesions affected small- to medium-sized muscular arteries and arterioles in various organs and extraparenchymal tissues; vessels of the renal pelvis and coronary arteries were consistently involved. Microscopic lesions in small- to medium-sized muscular arteries consisted of neointimal proliferation, medial thickening, luminal stenosis, thrombosis, disruption and fragmentation of the internal elastic lamina, necrosis of the tunica media, and medial deposits of myxoid matrix material. Microscopic lesions in arterioles included concentric laminar thickening of vessel walls (onion-skin pattern), endothelial cell hypertrophy, smooth muscle cell vacuolation, necrosis of the tunica media, thrombosis, and partial to complete luminal stenosis. Arteritis and/or periarteritis were also noted in 4 out of 9 pigs. Additional microscopic lesions included membranoproliferative glomerulonephritis (3 out of 9), myocardial microinfarcts (4 out of 7), renal interstitial fibrosis (2 out of 9), extramedullary hematopoiesis (6 out of 9), and intracapillary hyaline thrombi (2 out of 9). Degenerative vascular lesions have not been previously described in Göttingen minipigs with thrombocytopenic purpura syndrome. The etiopathogenesis of both the vascular lesions and thrombocytopenic purpura syndrome is currently unknown.

Immune complex-associated thrombocytopenic purpura syndrome in sexually mature Göttingen minipigs.

Eleven cases of thrombocytopenic purpura (TP) in sexually mature male or female Göttingen minipigs occurred sporadically over 3 1/2 years in a closed breeding colony protected by strict barrier conditions. Typical clinical signs of TP, including extensive subcutaneous haemorrhages, were seen in all affected animals. Haematological abnormalities included marked thrombocytopenia and anaemia. A consistent histopathological finding was the presence of membranoproliferative lesions in the renal glomeruli. Immunohistochemically, glomerular deposits were positively labelled for complement factor C1q and often also for immunoglobulins. Bone marrow findings consisting of increased numbers of immature and apoptotic megakaryocytes were compatible with a state of increased platelet consumption. Based on the combined presence of thrombocytopenia and renal immune complexes, it is suggested that the syndrome was related to a type III hypersensitivity reaction. However, further studies are needed to verify this hypothesis.

Thrombocytopenic purpura in lambs given bovine colostrum.

Newborn lambs which had been given colostrum from a single cow developed thrombocytopenia and seven died. The clinical signs included purpura, haemoglobinuria, melaena, dullness and lethargy. The lambs died at one to two days old. Post mortem examination revealed widespread haemorrhages throughout the body. Lambs given small amounts of colostrum developed a transient thrombocytopenia but did not die.

Focal ulcerative ileocolitis with terminal thrombocytopenic purpura in juvenile cotton top tamarins (Saguinus oedipus).

A newly recognized syndrome characterized by an acute focal ulcerative ileocolitis, anemia and thrombocytopenic purpura in five juvenile cotton-top tamarins is described. The presentation and morphology of this syndrome is distinct from any other reported gastrointestinal disease reported in tamarins. Traditional etiologies such as viruses, ingested toxins, Campylobacter, Salmonella and Yersinia and Clostridium difficile are not considered likely etiologic agents. Nontraditional etiologies such as anaerobes or pathologic strains of Escherichia coli are now being considered. This syndrome is of potential significance to ongoing research into the etiology of idiopathic tamarin colitis.

[The diagnosis of morbus maculosus in horses]. / Ein Beitrag zum Krankheitsbild des Morbus maculosus equorum.

This is a review on Morbus maculosus equorum (purpura haemorrhagica) on the base of literature data and of a case report on 13 own patients. It is shown, that the clinical picture of this disease has not changed within the last 150 years. Clinical main symptoms are haemorrhagic diathesis (petechiae, ecchymosis, suggillations) as well as peripheral edema and fever. The main haematological findings are neutrophilia, mostly going along with shift to the left and lymphopenia. In the last few years thrombocytopenia was also described in some cases. Basic therapeutics are glucocorticoids and penicillins. Problems of differential diagnosis and of nomenclature are discussed.

[Neonatal thrombocytopenic purpura in a black and white male calf. Case report]. / Neonatale thrombozytopenische Purpura bei einem schwarzbunten Bullenkalb. Fallbericht.

A report is given on a newborn calf showing mucosal hemorrhage and melena. All blood clotting tests, except for prothrombin time (which proved to be initially prolonged), had normal results. The striking recurrent thrombocytopenia was successfully treated with prednisolone. Autoimmune idiopathic thrombocytopenia is suspected as a possible cause.

Immune complexes in purpura hemorrhagica of the horse contain IgA and M antigen of Streptococcus equi.

Purpura hemorrhagica is an acute disease of the horse characterized by edema of the head and limbs, leucocytoclastic vasculitis, petechial hemorrhages in mucosae, musculature and viscera, and sometimes glomerulonephritis. It is usually associated with strangles, an upper respiratory tract disease of the horse caused by Streptococcus equi. We have detected and characterized immune complexes in the sera of horses with poststrangles purpura hemorrhagica by using PEG precipitation and Western blot analysis. The immune complexes contained IgA and S. equi-specific antigens similar to those found in acid extracts. We propose that purpura hemorrhagica is an immune complex-mediated disease.

Application of the enzyme-linked immunosorbent assay for the detection of platelet antibodies in dogs.

An enzyme-linked immunosorbent assay (ELISA) was developed to detect serum antibodies reactive to canine platelets. The method used an anti-canine immunoglobulin G horseradish peroxidase conjugate, O-dianisidine, as a water-soluble chromagen, and pooled platelets as a temporary antibody support. The ELISA was compared with a conventional immunoinjury method measuring the accelerating effect of platelet factor 3 on coagulation. The ELISA was more sensitive in the detection of antiplatelet antibodies in canine patients with idiopathic thrombocytopenic purpura, autoimmune hemolytic anemia, and systemic lupus erythematosus. Serial dilution of rabbit anti-canine platelet serum revealed a positive correlation between the strength of the antiserum and the degree of color measured spectophotometrically, indicating that the absorbance value may be useful in estimating the amount of antibody present in the serum in indirect tests and on the platelets in direct tests.

Canine idiopathic thrombocytopenia: clinical observations and long-term follow-up in 54 cases.

Idiopathic thrombocytopenia purpura (ITP) was diagnosed in 54 dogs. Bleeding was associated with platelet counts less than or equal to 30,000/mm3, and occurred most frequently at mucosal surfaces and in the skin. Other hematologic changes were variable, the most common being regenerative anemia with leukocytosis. Bone marrow examination revealed variable megakaryocyte numbers, but hyperplasia was most commonly observed. Results of the platelet factor 3 test were positive in only 7 of 25 dogs so tested. Treatment included various combinations of corticosteroid, vincristine, cyclophosphamide, and splenectomy. The dogs could be classified into 4 groups on the basis of the course of disease: (1) 14 dogs that died or were euthanatized during the first episode of thrombocytopenia, (2) 17 dogs that recovered after a single episode of thrombocytopenia (acute ITP), (3) 8 dogs in which thrombocytopenia recurred over a period of up to 8 months before recovering (acute, recurrent ITP), and (4) 15 dogs that experienced repeated episodes of ITP for periods of up to 8 years (chronic ITP).

Isoimmune thrombocytopenic purpura in piglets.

A haemorrhagic diathesis due to isoimmune thrombocytopenia occurred in the fourth litter of a Landrace sow. Maternal antibodies, absorbed by piglets from the colostrum, were incompatible with platelet antigens inherited from the sire. The severity of haemorrhage varied between piglets although all were thrombocytopenic. Two deaths occurred, one at 24 h and the other at 3 weeks of age. The surviving 11 piglets were clinically and haematologically normal at 16 weeks of age.

Renal dysfunction in a case of purpura haemorrhagica in a horse.

A four-year-old thoroughbred was presented with clinical manifestations of purpura haemorrhagica. Evidence of renal involvement consistent with glomerulopathy and nephrotic syndrome, characterised by heavy proteinuria and azotaemia, became apparent and may have been exacerbated by diuretic therapy. Autopsy revealed membrano- and mesangial proliferative glomerulonephritis and chronic pleuritis. Circulating immune complexes may have been responsible for the renal diseases and the purpura.