Anna-Kaisa Järvinen

Pneumocystis Carinii Pneumonia in Dogs -a Diagnostic Challenge

1. Beachey EH, Courtney HS: 1987, Bacterial adherence: the attachment of group A streptococci to mucosal surfaces. Rev Infect Dis 9(Suppl 5):S475-S481. 2. Collins JE, Bergeland ME, Lindeman CJ, Duimstra JR: 1988, Enterococcus (Streptococcus) durans adherence in the small intestine of a diarrheic pup. Vet Pathol 25:396-398. 3. Collins MD, Jones D, Far-row JAE, et al.: 1984, Enterococcus avium nom. rev., comb. nov.; E. casseliflavus nom. rev., comb. nov.; E. durans nom. rev., comb. nov.; E. gallinarium comb. nov.; and E. malodoratus sp. nov. Int J Syst Bacteriol 34:220223. 330-366. 5. Jergens AE, Moore FM, Prueter JC, Yankauskas PJ: 1991, Adherent gram-positive cocci on the intestinal villi of two dogs with gastrointestinal disease. J Am Vet Med Assoc 198( 11): 1950-1952. 6. Johnson DD, Dumimstra JR, Gates CE, McAdaragh JP: 1985, Enteric Streptococcus durans: an adhering streptococcus as a cause of diarrhea in suckling piglet? Proc George A Young Conf, Lincoln, NE, pp. 1-8. 7. Rogers DG, Zeman DH, Erickson ED: 1992, Diarrhea associated with Enterococcus durans in calves. J Vet Diagn Invest 4:471472. 8. Tzipori S, Hayes J, Sims L, Withers M: 1984, Streptococcus durans: an unexpected enteropathogen of foals. J Infect Dis 150: 589-593.

Size and shape of right heart chambers in mitral valve regurgitation in small-breed dogs.

BACKGROUND The contribution of right heart (RH) chamber enlargement to general heart enlargement seen on thoracic radiographs in mitral regurgitation (MR) is not known. OBJECTIVES To determine the size and shape of the RH chambers in normal dogs and dogs with varying degrees of MR. ANIMALS Fifty-four privately owned dogs: 13 normal, 41 with varying degrees of MR including 25 with congestive heart failure (CHF). METHODS Archived first pass radionuclide angiocardiograms were used to produce static images of the RH and left heart (LH) chambers. Indexes of size and shape of the RH and LH chambers were related to severity of MR determined by heart rate-normalized pulmonary transit time (nPTT), vertebral heart scale (VHS), and clinical status. RH shape was measured by a circularity index of RH short axis/long axis. RESULTS A 2nd degree polynomial fit best described the ratios; RH/LH dimension to nPTT (R(2)= 0.62) and to VHS (R(2)= 0.43), RH/LH area to nPTT (R(2)= 0.64) and to VHS (R(2)= 0.58), all P < .001. RH circularity was decreased in CHF, P < .001. In CHF, the RH chambers of 16 dogs were both flattened and enlarged, whereas 9 had convex septal borders. CONCLUSIONS RH chambers are not significantly dilated in dogs with mild to moderate MR without CHF. In CHF, RH chambers enlarge and also may be compressed by the LH chambers. Pulmonary hypertension probably is present in some dogs with CHF. Increased sternal contact is not a useful sign of right-sided heart dilatation in MR.

Comparison of results for weight-adjusted and fixed-amount bronchoalveolar lavage techniques in healthy Beagles

OBJECTIVE To compare recovery of epithelial lining fluid (ELF) in bronchoalveolar lavage fluid (BALF) by use of weight-adjusted or fixed-amount volumes of lavage fluid in dogs. ANIMALS 13 healthy Beagles. PROCEDURES Dogs were allocated to 2 groups. In 1 group, the right caudal lung lobe was lavaged on the basis of each dogs weight (2 mL/kg, divided into 2 aliquots) and the left caudal lung lobe was lavaged with a fixed amount of fluid (50 mL/dog, divided into 2 aliquots). In the second group, the right and left caudal lung lobes were lavaged by use of the fixed-amount and weight-adjusted techniques, respectively. The BALF was collected by use of bronchoscopy. A recovery percentage ≥ 40% was required. The proportion of ELF was calculated by use of the following equation: (concentration of urea in BALF/concentration of urea in serum) × 100. RESULTS Mean ± SD proportion of ELF in BALF was 2.28 ± 0.39% for the weight-adjusted technique and 2.89 ± 0.89% for the fixed-amount technique. The SDs between these 2 techniques differed significantly (calculated by comparing 2 covariance structures [unstructured and compound symmetry] in a repeated-measures mixed ANOVA). CONCLUSIONS AND CLINICAL RELEVANCE The findings strongly suggested that use of a weight-adjusted bronchoalveolar lavage technique provided a more uniform ELF recovery, compared with that for a fixed-amount bronchoalveolar lavage technique, when urea was used as a marker of dilution. A constant ELF fraction can facilitate more accurate comparisons of cellular and noncellular constituents in BALF among patients of various sizes.

Pulmonary Blood Volume in Mitral Regurgitation in Cavalier King Charles Spaniels

BACKGROUND Pulmonary edema and venous congestion are well-recognized signs of congestive heart failure (CHF) in advanced canine chronic mitral regurgitation (MR). However, little is known about pulmonary blood volume (PBV), blood pulmonary transit time (PTT), and the regulation of these. OBJECTIVES To measure and evaluate the relationships of PBV, forward stroke volume (FSV), and heart rate normalized blood pulmonary transit time (nPTT) in healthy dogs and dogs with MR. ANIMALS Thirty-three Cavalier King Charles Spaniels; 11 healthy, 4 in modified New York Heart Association (NYHA) class I, 11 in class II, and 7 in CHF. METHODS Heart rate normalized PTTs were measured by radionuclide angiocardiography. Left ventricular end diastolic and systolic diameter, left atrial/aortic root ratio, and FSV were measured by echocardiography. PBV and pulmonary blood volume index (PBVI) were calculated by established formulas. RESULTS PBVI was 308±56 (mean±SD) mL/m2 for healthy dogs, 287±51 mL/m2 in NYHA class I, 360±66 mL/m2 in Class II, and 623±232 mL/m2 in CHF (P=.0008). Heart rate normalized PTT, not FSV, was a predictor of PBV (r=0.92 and 0.02, respectively). CONCLUSIONS AND CLINICAL IMPORTANCE Increased PBV, not decreased FSV, is the main cause of increased nPTT in MR. Increased nPTT can be used as an indicator of abnormal cardiopulmonary function in dogs with MR.

Pulmonary histopathology in dalmatians with familial acute respiratory distress syndrome (ARDS).

The histopathological changes in the lungs of 12 related Dalmatians with idiopathic acute respiratory distress syndrome (ARDS) are described. Affected dogs had multiple foci of marked atypical hyperplasia and squamous metaplasia of the bronchiolar epithelium, patchy ongoing fibrosis with myofibroblastic metaplasia, smooth muscle hyperplasia and occasional honeycombing of alveolar walls, and hyperplasia of atypical type II pneumocytes. There was an abrupt transition between these proliferative lesions and areas of acute alveolar oedema with hyaline membranes in partially normal lung. Diseased areas were associated with moderate lymphohistiocytic interstitial inflammation. Immunohistochemical labelling for cytokeratin expression indicated that the metaplastic epithelium was of bronchiolar origin and that it extended into peribronchiolar alveolar spaces. Some of the bronchiolar lesions were pre-neoplastic and one adult dog suffered from bronchoalveolar carcinoma. These lesions are compared with the two forms of idiopathic interstitial pneumonia reported as causes of ARDS in man: acute interstitial pneumonia (AIP) and acute exacerbation of idiopathic pulmonary fibrosis (IPF). The observed lesions in the Dalmatians are distinct from the diffuse alveolar damage that characterizes AIP, but show some histological similarities to the usual interstitial pneumonia (UIP) that occurs in IPF with acute exacerbation in man. UIP has not previously been described in the dog.

Increased NT-proANP predicts risk of congestive heart failure in Cavalier King Charles spaniels with mitral regurgitation caused by myxomatous valve disease.

OBJECTIVES To evaluate the predictive value of plasma N-terminal pro-atrial natriuretic peptide (NT-proANP) and nitric oxide end-products (NOx) as markers for progression of mitral regurgitation caused by myxomatous mitral valve disease. ANIMALS Seventy-eight privately owned Cavalier King Charles spaniels with naturally occurring myxomatous mitral valve disease. METHODS Prospective longitudinal study comprising 312 measurements over a 4.5 year period. Clinical values were recorded, NT-proANP concentrations were measured by radioimmunoassay, and NOx were analyzed colorimetrically. To predict congestive heart failure (CHF), Cox proportional hazards models with time-varying covariates were constructed. RESULTS The hazard ratio for NT-proANP (per 1000 pmol/l increase) to predict future CHF was 6.7 (95% confidence interval, 3.6-12.5; p < 0.001). The median time to CHF for dogs with NT-proANP levels >1000 pmol/l was 11 months (95% confidence interval, 5.6-12.6 months), compared to 54 months (46 - infinity) for dogs with concentrations ≤ 1000 pmol/l (p < 0.001). Due to intra- and inter-individual variability, most corresponding analyses for NOx were insignificant but dogs reaching CHF had a lower mean NOx concentration than dogs not reaching CHF (23 vs. 28 μmol/l, p = 0.016). Risk of CHF increased with increase in heart rate (>130 beats per minute) and grade of murmur (≥ 3/6). CONCLUSIONS The risk of CHF due to mitral regurgitation is increased in dogs with blood NT-proANP concentrations above 1000 pmol/l. Measurement of NT-proANP can be a valuable tool to identify dogs that may develop CHF within months.

Congestive heart failure and atrial fibrillation in a cat with myocardial fibro-fatty infiltration

Congestive heart failure and atrial fibrillation were diagnosed in a 4-year-old castrated Birman cat with progressive signs of dyspnea, tachypnea, and lethargy. Echocardiography revealed massive right-sided heart dilatation with ascites and hydrothorax. Electrocardiogram recording showed atrial fibrillation. Medical therapy with diuretics, benazepril, and antithrombotic agents was unsuccessful. The owner requested euthanasia. In post-mortem examination, changes associated with myocardial fibro-fatty infiltration were confirmed. Changes were most marked in the right ventricular wall but with left ventricular involvement was detected.

ANLN truncation causes a familial fatal acute respiratory distress syndrome in Dalmatian dogs

Acute respiratory distress syndrome (ARDS) is the leading cause of death in critical care medicine. The syndrome is typified by an exaggerated inflammatory response within the lungs. ARDS has been reported in many species, including dogs. We have previously reported a fatal familial juvenile respiratory disease accompanied by occasional unilateral renal aplasia and hydrocephalus, in Dalmatian dogs. The condition with a suggested recessive mode of inheritance resembles acute exacerbation of usual interstitial pneumonia in man. We combined SNP-based homozygosity mapping of two ARDS-affected Dalmatian dogs and whole genome sequencing of one affected dog to identify a case-specific homozygous nonsense variant, c.31C>T; p.R11* in the ANLN gene. Subsequent analysis of the variant in a total cohort of 188 Dalmatians, including seven cases, indicated complete segregation of the variant with the disease and confirmed an autosomal recessive mode of inheritance. Low carrier frequency of 1.7% was observed in a population cohort. The early nonsense variant results in a nearly complete truncation of the ANLN protein and immunohistochemical analysis of the affected lung tissue demonstrated the lack of the membranous and cytoplasmic staining of ANLN protein in the metaplastic bronchial epithelium. The ANLN gene encodes an anillin actin binding protein with a suggested regulatory role in the integrity of intercellular junctions. Our study suggests that defective ANLN results in abnormal cellular organization of the bronchiolar epithelium, which in turn predisposes to acute respiratory distress. ANLN has been previously linked to a dominant focal segmental glomerulosclerosis in human without pulmonary defects. However, the lack of similar renal manifestations in the affected Dalmatians suggest a novel ANLN-related pulmonary function and disease association.