The role of the sequential organ failure assessment score in evaluating the outcome in dogs with parvoviral enteritis.

SCIENTIFIC BACKGROUND: The aim of this prospective study was to assess whether the Sequential Organ Failure Assessment (SOFA) score could be indicative of outcome (survival to discharge) in dogs with parvoviral enteritis. METHODS: In 35 naturally infected dogs, the SOFA score and clinical score were calculated and the presence of systemic inflammatory response syndrome was verified on admission and during the first four days of hospitalization. RESULTS: 26 dogs survived, and out of the 9 non-survivors, 6 dogs had positive blood cultures. Mean SOFA scores and clinical scores between survivors and non-survivors and between septic and non-septic dogs on admission and on each hospitalization day were significantly different. Trends in SOFA score indicated that in non-survivors and septic dogs there was an increase in SOFA score during the first four days of hospitalization and a decrease occurred in survivors and non-septic dogs. The area under the curve (ROC curve analysis) for SOFA score predicting the outcome was 0.797 and predicting sepsis was 0.834. The best cut-off point of SOFA score for predicting the final outcome was 3.5 and the best cut-off of SOFA score for predicting sepsis was also 3.5. CONCLUSIONS: Either single values or trends in SOFA score can assist in suspecting sepsis and reaching prognosis in parvoviral enteritis.

Canine and feline dirofilariosis in a highly enzootic area: first report of feline dirofilariosis in Greece.

Dirofilaria immitis (heartworm) is enzootic in many areas of the world and quite prevalent in southern European countries. Although dogs are the main host of the parasite, cats may also be infected, and the prevalence of feline dirofilariosis is associated with the respective prevalence of canine infection in any given area. The aim of the present study was to investigate the proportion of D. immitis infection among dogs and cats that were not under any kind of prophylactic treatment and were living in a heartworm enzootic area. In total, 180 stray animals (148 dogs and 32 cats) living in a shelter in Northern Greece were examined for heartworm infection by the Knott's test and serology (antigen and in cats also antibody detection), and additionally echocardiography in the infected cats. Thirty-seven (25%, CI 18.7-32.5%) of the dogs and 3 (9.4%, CI 3.2-24.2%) of cats were found to be positive, by at least one of the tests applied. In 2 of the infected cats, the parasites were also detected by echocardiography. One of the positive cats died suddenly 1 year after diagnosis and at necropsy two decomposing D. immitis were found in the right ventricle and pulmonary artery. This is the first report of confirmed feline dirofilariosis in Greece. The detected proportion of infection in cats was 38% of the respective canine infection in the examined shelter. The results of the present study underline the high risk of infection of cats living in enzootic areas and the imperative character of preventive measures in such conditions.

Multidetector computed tomographic pulmonary angiography in a cat with fatal heartworm disease.

A 17-month-old neutered male domestic shorthair cat was referred for a computed tomographic (CT) study of the thorax due to respiratory distress. Multidetector CT angiography showed a multifocal interstitial ground glass opacity, tortuous and blunted pulmonary arteries consistent with thromboembolism with perivascular lung infiltration and hypoventilation in multiple lung lobes. A blood antigen test was positive for Dirofilaria immitis. The cat's clinical condition rapidly declined and the owners elected euthanasia. The histopathologic examination confirmed heartworm disease with parasitic pulmonary thromboembolism.

Urinary Aldosterone/Creatinine Ratio After Fludrocortisone Suppression Consistent with PHA in a Cat.

A 9 yr old cat was presented with clinical signs and laboratory abnormalities attributed to arterial hypertension (mean systolic arterial pressure, 290 mm Hg). Plasma aldosterone concentration was increased at the time of admission (651 pmol/L), but serum creatinine and potassium concentrations were within the reference range. A second increased aldosterone (879 pmol/L) and normal plasma renin activity (1.85 ng/mL/hr) resulted in an increased aldosterone/renin ratio, which was suggestive of primary hyperaldosteronism (PHA). To further support the diagnosis of PHA, the urinary aldosterone/creatinine ratio was calculated both before and after oral administration of fludrocortisone acetate (0.05 mg/kg q 12 hr for 4 consecutive days). The urinary aldosterone/creatinine ratio was 92.6 × 10(-9) before fludrocortisone administration and 155.8 × 10(-9) 4 days later. Absence of suppression was typical of PHA. The cat had a limited response to antihypertensive medication and died before treatment for PHA could be instituted. A necropsy was not permitted by the owner.

Evaluation of a proposed therapeutic protocol in 12 dogs with tentative degenerative myelopathy.

The objective of this work was to evaluate the long-term efficacy of a proposed therapeutic protocol in 12 dogs with a tentative diagnosis of degenerative myelopathy, followed-up for a 6-month period. Twelve dogs fulfilling the antemortem inclusion criteria (breed, age, adequate vaccination, history of progressive posterior ataxia and/or paraparesis, no radiographic and myelographic abnormalities in the spinal cord and vertebral column) were allocated. All these dogs presented signs of thoracolumbar syndrome (T3-L3), scored as grade I (mild to moderate ataxia and paraparesis) in 10 and grade II (severe ataxia and ambulatory paraparesis) in 2 cases. Treatment included the use of epsilon-aminocaproic acid and N-acetylcysteine, supplemented with vitamins B, C and E. Prednisolone was given for the first two weeks and upon worsening of neurological signs. Daily exercise, performed as walking or swimming, was strongly recommended. Clinicopathological evaluation was normal in all 12 dogs, and survey radiographs and myelograms did not show spinal cord compression. Magnetic resonance imaging (MRI), performed only in 4 dogs, did not disclose compressive disorders or intramedullary lesions. Neurological signs were progressively worsening in all 12 animals, eventually resulting in severe paraparesis (grade III) or paraplegia (grade IV). The applied medications do not appear to be an attractive alternative to conservative management (physiotherapy) or euthanasia in canine degenerative myelopathy, irrespective of its chronicity.

Serum and liver iron concentration in dogs with experimentally induced hepatopathy.

BACKGROUND AND AIM: Iron (Fe) status is altered in human and experimental animal hepatopathies. In dogs limited data are available. The aim of this study was to investigate serum iron (SI), total iron binding capacity (TIBC), percentage transferrin saturation (SAT) and Fe status in the liver of dogs with experimentally induced hepatopathy. METHODS: Fourteen 1-year-old dogs were divided into two equal groups. In order for hepatopathy to be induced, 0.25 mL/kg body weight of carbon tetrachloride (CCl4) solution was administered once daily, orally, for a 10-week period in group B dogs, while group A dogs were used as controls. SI, TIBC and SAT values were measured 3 times before the beginning (baseline value) and 10 times at weekly intervals during the experiment. Liver samples, obtained before the administration of CCl4 and at the end of the experimental period (10 weeks), were subjected to Fe determination, as well as to histopathological and histochemical analysis. RESULTS: At the end of the experiment SI, TIBC and liver iron concentration, as well as liver total iron score were significantly increased in group B dogs. Distribution of granular hemosiderin iron in hepatocytes, Kupffer cells, and portal triads was noticed. Positive correlations were found between SI and liver Fe concentration, as well as histochemically determined Fe. Moreover, positive correlations were evident between liver fibrosis and serum, as well as liver Fe values. CONCLUSIONS: Experimentally induced chronic hepatopathy in dogs causes Fe status disturbances. Increased serum and liver iron concentration produces liver histopathological deterioration and it may be worth attention during laboratory evaluation in canine hepatopathy.