J. T. Lumeij

Avian Clinical Biochemistry

Publisher Summary This chapter presents basic concepts related to avian clinical biochemistry. Avian medicine and surgery is recognized as an official specialty in veterinary medicine in three continents: Europe, Australia, and North America. The increasing demand for veterinary care for individual birds with a high sentimental or economical value and efforts to conserve endangered species facilitated this awareness. The introduction of micromethods in clinical laboratories and the public demand for veterinary care for individual birds have removed many obstacles of this field. This chapter begins with discussing how blood samples of birds can be collected in the most efficient way. The chapter then discusses starvation, flight, and postprandial effects. The chapter also elaborates the biochemistry of plasma proteins, renal function, and hepatobiliary disease in birds. The chapter emphasizes that all efforts should be made to obtain a blood sample before any treatment is given. Treatments administered before samples are collected may severely affect plasma chemical values, which may jeopardize a correct diagnosis at a later stage. The time interval between restraint and blood sampling should be kept to a minimum to prevent stress-associated changes in clinical chemistry parameters. Blood samples should be obtained before an extensive clinical examination is performed to avoid iatrogenic changes in the samples.

The role of luteinizing hormone in the pathogenesis of hyperadrenocorticism in neutered ferrets

Four studies were performed to test the hypothesis that gonadotrophic hormones, and particularly luteinizing hormone (LH) play a role in the pathogenesis of ferrets: (I) adrenal glands of ferrets with hyperadrenocorticism were studied immunohistochemically to detect LH-receptors (LH-R); (II) gonadotrophin-releasing hormone (GnRH) stimulation tests were performed in 10 neutered ferrets, with measurement of androstenedione, 17alpha-hydroxyprogesterone and cortisol as endpoints; (III) GnRH stimulation tests were performed in 15 ferrets of which 8 had hyperadrenocorticism, via puncture of the vena cava under anesthesia; and (IV) urinary corticoid/creatinine (C/C) ratios were measured at 2-week intervals for 1 year in the same ferrets as used in study II. Clear cells in hyperplastic or neoplastic adrenal glands of hyperadrenocorticoid ferrets stained positive with the LH-R antibody. Plasma androstenedione and 17alpha-hydroxyprogesterone concentrations increased after stimulation with GnRH in 7 out of 8 hyperadrenocorticoid ferrets but in only 1 out of 7 healthy ferrets. Hyperadrenocorticoid ferrets had elevated urinary C/C ratios during the breeding season. The observations support the hypothesis that gonadotrophic hormones play a role in the pathogenesis of hyperadrenocorticism in ferrets. This condition may be defined as a disease resulting from the expression of LH-R on sex steroid-producing adrenocortical cells.

Plasma urea, creatinine and uric acid concentrations in relation to feeding in peregrine falcons (Falco peregrinus)

Significant post-prandial increases in plasma uric acid and plasma urea concentrations were observed in peregrine falcons. Post-prandial uric acid concentrations were similar to those in birds suffering from hyperuricaemia and gout and were well above the theoretical limit of solubility of sodium urate in plasma. It is not clear why under normal circumstances no urate deposits occur in peregrine falcons (and probably other raptorial birds), which show hyperuricaemia for at least 12 h after ingesting a natural meal. It is important to evaluate renal function in peregrine falcons (and perhaps other birds) after a 24-h fast to avoid misinterpretation due to physiological food-induced elevated concentrations of nonprotein nitrogen substances.

Electrocardiogram of the African grey (Psittacus erithacus) and Amazon (Amazona spp.) parrot.

Electrocardiographic reference values and configurations were established in apparently healthy African grey (Psittacus erithacus; n=45) and Amazon (Amazona spp.; n = 37) parrots, using standard limb leads. In 31 of the African grey parrots and 32 of the Amazon parrots electrocardiograms were made during isoflurane-anaesthesia. Significant differences between anaesthetized and unanaesthetized birds were found only for the median heart rate and QT-interval (P<0.05). Significant differences between the two genera were found for the duration of the P- and T-waves, the voltage of the T-wave and for the mean electrical axis. Sinus arrhythmias and ventricular premature beats were present in 5 to 10% of the tracings.

Severe leukopenia and liver necrosis in young African grey parrots (Psittacus erithacus erithacus) infected with psittacine circovirus.

This paper describes the signs, clinical pathology, and postmortem findings in 14 young African grey parrots (Psittacus erithacus erithacus) that were naturally infected with psittacine beak and feather disease (PBFD) virus (psittacine circovirus). All but two of the parrots had severe leukopenia at clinical presentation. Two other parrots also had severe anemia. All birds died within 3 wk after presentation. Postmortem examination documented liver necrosis in 11 of 14 birds and secondary bacterial or fungal infections in 9 of 14 birds. Tests for Chlamydia psittaci, polyomavirus, and Salmonella sp. were negative. PBFD viral infection could be demonstrated in all birds by polymerase chain reaction. Supporting evidence of PBFD viral infection was gathered by histologic examination of the bursa of Fabricius, electron microscopy, and DNA in situ hybridization. Electron microscopic examination of both the bursa of Fabricius and liver revealed virus particles resembling circovirus. DNA in situ hybridization of six liver tissue samples confirmed the presence of PBFD virus and excluded the presence of avian polyomavirus. Our findings suggest that a specific presentation of peracute PBFD viral infection, characterized by severe leukopenia, anemia, or pancytopenia and liver necrosis in the absence of feather and beak abnormalities, may occur in young African grey parrots.

Plasma chemistry references values in psittaciformes

Reference values for 17 plasma chemical variables in African greys. Amazons, cockatoos and macaws were established for use in avian clinical practice. The inner limits are given for the percentiles P(2.5) and P(97.5) with a probability of 90%. The following variables were studied: urea, creatinine, uric acid, urea/uric acid ratio, osmolality, sodium, potassium, calcium, glucose, aspartate aminotransferase, alanine aminotransferase, gamma glutamyltransferase, lactate dehydrogenase, creatine kinase, bile acids, total protein, albumin/globulin ratio. Differences between methods used and values found in this study and those reported previously are discussed.

Blood chemistry reference values in racing pigeons (Columba livia domestica).

Reference values for 23 blood chemical parameters in racing pigeons (Columba livia domestica) were established for use in clinical pathology. The inner limits are given for the percentiles P(2).(5) and P(97.5) with a probability of 90%. A minimum of 50 blood samples collected between September and January from different animals aged between 6 months and 12 years (median 1.5 years) was used for each parameter. Reference values obtained in the present study are compared with values published previously.

Comparison of different methods of measuring protein and albumin in pigeon sera.

Columbine serum total protein (TP) and albumin concentrations were determined using the biuret method and the bromocresol green dye binding (BCG) method or serum protein electrophoresis on cellulose acetate membranes (SPE). Results obtained using human and pigeon standards were compared. When pigeon albumin was used as a standard. TP values were consistently higher compared with values obtained using human protein as a standard. However, there was a high correlation between the results obtained with the two standards. The correlation between the BCG method and SPE for serum albumin determination was poor, irrespective of the standard used. The method cannot be recommended for pigeon blood. For avian clinical practice it is advised to establish TP concentration using the biuret method and a human standard and to calculate albumin concentration from the results of TP and SPE.

Changes in plasma chemistry after drug‐induced liver disease or muscle necrosis in racing pigeons (Columba livia domestica)

Changes in plasma variables as a result of liver damage induced by ethylene glycol (group A) or D-galactosamine (group B) and of muscle damage induced by doxycycline were compared. Plasma bile acid concentration was both a specific and a sensitive indicator of liver disease. Another specific, but less sensitive indicator of liver disease was 7-GT. Plasma AS AT activity was the most sensitive indicator of disease of the liver, but was not specific, since increased ASAT activities were also seen during muscle disease. ALAT activity was slightly more sensitive to liver damage than 7-GT, but was also not specific, being increased also after muscle damage. Plasma GLDH activity was increased only as a result of extensive liver necrosis. AP activity was of no value for detecting liver disease in the pigeon. CK activity was specific for muscle injury, though the activities of ALAT, ASAT and LD were also increased. Because of its long elimination half-life, increased ALAT activity persisted for 9 days after muscle damage, whereas CK activity returned to reference values within 3 days. LDH was a poor indicator of damage to liver and muscle, despite its relatively high tissue concentrations in both tissues. The rapid disappearance rate of LDH from plasma probably explains this observation.

Enzyme activities in tissues and elimination half‐lives of homologous muscle and liver enzymes in the racing pigeon (Columba Livia domestica)

Tissue enzyme profiles of heart, liver, pectoral muscle, quadriceps muscle, duodenum, kidney and brain from racing pigeons were established. The enzymes were alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), glutamate dehydrogenase (GLDH), lactate dehydrogenase (LDH), gamma glutamyltransferase (y-GT), alkaline phosphatase (AP), and creatine kinase (CK). Elimination half-lives (tybeta) of certain enzymes were also determined. The mean values (+/- SD) were: ASAT, 7.66 +/- 1.55 (liver) and 6.51 +/- 0.83 (muscle); ALAT, 15.69 + 1.70 (liver) and 11.99 +/- 1.32 (muscle); LDH, 0.71 + 0.10 (liver) and 0.48 +/- 0.07 (muscle); GLDH, 0.68 +/- 0.17 (liver), CK 3.07 +/- 0.59 hours (muscle). GLDH is the most liver-specific enzyme in the pigeon, but increased activities in the plasma are likely only in the acute stage of severe liver cell damage, since this enzyme is localised within the mitochondria and has a short half life. LDH and ASAT seem to be the most sensitive indicators of liver cell damage, though contributions come from muscle damage. Muscle cell damage can be differentiated from liver cell damage by measuring plasma CK activity, since CK is both a specific and a sensitive indicator of muscle cell damage. In a clinical setting the combined use of LDH, ASAT and CK permits differentiation between liver and muscle cell damage in racing pigeons.