SUSPECTED HYPOVITAMINOSIS A-ASSOCIATED SALT GLAND ADENITIS IN NORTHERN ROCKHOPPER PENGUINS ( EUDYPTES MOSELEYI).

Supraorbital salt-excreting glands are present in at least 10 avian orders and are largest in marine species, including penguins. Diseases of the avian salt gland have been described infrequently. From September 2015, five captive northern rockhopper penguins ( Eudyptes moseleyi) were presented over a 6-wk period for unilateral or bilateral supraorbital swellings. In September 2016, two cases recurred and two additional cases were identified. Histopathology demonstrated salt gland adenitis with extensive squamous metaplasia. Blood plasma testing demonstrated marked vitamin A and E deficiencies within the colony. Prolonged frozen storage of feed-fish was implicated as a cause of vitamin depletion; reducing storage times and addition of dietary supplementation prevented recurrence.

Salt gland adenitis as only cause of stranding of loggerhead sea turtles Caretta caretta.

The present study describes pathological and microbiological findings in 9 stranded loggerhead sea turtles Caretta caretta, whose only observed lesion was bilateral purulent salt gland adenitis. Histological lesions ranged from the presence of abundant eosinophilic material associated with bacterial colonies in the lumen of the central ducts of the glandular lobules to the destruction of the glandular tissue and presence of abundant eosinophilic material composed of heterophils and cell debris, lined by multinucleated giant cells. Aeromonas hydrophila, Staphylococcus sp., and Vibrio alginolyticus were the bacteria most frequently isolated. Plasma concentrations of sodium and chloride and plasma osmolality from 2 turtles suffering from salt gland adenitis were, respectively 45.7, 69.2, and 45.7% higher than the mean value for healthy turtles. These cases suggest that failure to maintain homeostasis due to severe lesions in the salt glands can cause stranding and/or death of loggerhead sea turtles.

Salt gland adenitis associated with bacteria in Blue Penguins (Eudyptula minor) from Hauraki Gulf (auckland, New Zealand).

Three Blue Penguins (Eudyptula minor) were rescued between July 2006 and January 2007 off the east coast of Auckland, New Zealand. They were taken to a rehabilitation center, where they subsequently died in May 2007 and were submitted for necropsy. There was unilateral enlargement of the salt glands with disseminated small, pale, and firm foci in all birds. Histologic examination of the affected glands demonstrated the presence of multifocal granulomas and areas of severe squamous metaplasia of the collecting ducts. The remaining gland had areas of hyperplasia, dysplasia, and necrosis with a severe granulomatous inflammatory reaction. Intralesional gram-negative bacteria were detected, but, unfortunately, bacterial culture was unrewarding. No further cases were observed in penguins in the subsequent year, and the primary cause of the salt gland adenitis remains uncertain.

Granulomatous inflammation of salt glands in ducklings (Anas platyrhynchos) associated with intralesional Gram-negative bacteria.

The "nasal glands" occur in many bird species and are powerful sodium ion-excretory organs. In ducks, they are located in supraorbital bony recesses. Granulomatous inflammation of these glands occurs with an incidence of approximately 1% in ducklings (Anas platyrhynchos), and is not associated with specific clinical symptoms. We investigated nine glands of eight animals with granulomas by gross pathology and histopathology, and compared results of bacteriology with 20 non-lesioned nasal glands. Adenitis was characterized by multifocal to coalescent heterophilic granulomas with central necrotic heterophils, and multinucleate giant cells, lymphocytes and plasma cells. Within the centres of the granulomas, there were clusters of Gram-negative bacteria that were identified as halo-tolerant Pseudomonas aeruginosa, Proteus mirabilis and Aeromonas hydrophila. Normal glands contained exclusively various halo-tolerant Gram-positive bacteria, mostly Streptococcus sp. and Enterococcus sp. The distribution of lesions and lack of clinical symptoms were suggestive of a localized ascending infection via the secretory ductules.

The microanatomy of the rectal salt gland of the Port Jackson Shark, Heterodontus portusjacksoni (Meyer) (Heterodontidae): suggestions for a counter-current exchange system.

A comprehensive anatomical study was undertaken to examine the rectal salt gland in the Port Jackson shark, Heterodontus portusjacksoni, a shark known to invade estuarine environments. The microstructure and vascular organisation of the rectal salt gland was investigated using histological observation and scanning electron microscopy of vascular corrosion casts. Cellular specialisation was observed in the lining of the central lumen of this gland. This may indicate that there is some modification of the principal product of the gland prior to its secretion. The rectal salt gland has a complex structure related to its function. Contrary to previous reports, the flow in secretory tubules is in the opposite direction to that of the capillaries and thus constitutes a counter-current arrangement. The similarity in the organisation of the counter-current and lobulate arrangement of salt-secreting glands through phylogenetically diverse organisms, such as sharks and birds, suggests that this arrangement is important in achieving efficient salt secretion.

Morphological and pathological effects of cadmium ingestion on Pekin ducks exposed to saline.

This study examined the effects of simultaneous exposure to saline and cadmium (Cd) on organ mass and histology of a bird with salt glands, the Pekin duck, Anas platyrhynchos. Three mixed-sex groups, each containing 6 birds, ate duck pellets containing 0, 50, or 300 microg Cd/g, respectively, for 4 1/2 mo and drank 300 mM NaCl. Only females on the high-Cd diet lost body mass. Ingestion of Cd reduced heart mass in females. There was increased mass of Harderian and salt glands in both sexes. Mass of kidneys and liver increased only in males, and the gut mass (also length) increased more in males. Cadmium ingestion also induced (1) inflammation of renal interstitium and degenerative tubular changes, (2) marked degenerative changes in testes, (3) increased heart water content, (4) decreased cytoplasmic volume of liver cells, (5) reduced proportion of basophilic granular cells in chromaffin tissue of the adrenal glands, and (6) in the ileum, increased heterophilia in the lamina propria and, only in females, the apoptosis to mitosis ratio in crypt cells of the epithelium. The ducks' outward appearance gave no indication that ingesting large amounts of cadmium for 4 1/2 mo produced deleterious effects, but the physiological consequences were profound. Both sexes had greatly reduced gonadal mass and the males produced no sperm. The higher dietary level greatly hypertrophied the liver, kidneys, and gut only in males. The cadmium-induced changes in organs, particularly in the gonads, kidneys, and adrenal glands, should greatly impair the health and reproductive capacity of these ducks.

Inflammation of the nasal gland in domestic turkeys.

A prominent swelling above the eye of range-reared tom turkeys was found to be due to severe inflammation and hyperplasia of the nasal or salt gland. The incidence of affected turkeys was sporadic, and no mortality or other lesions were associated with the condition.

pCMBS-induced swelling of dogfish (Squalus acanthias) rectal gland cells: role of the Na+,K(+)-ATPase and the cytoskeleton.

(1) 0.1-1.0 mM p-chloromercuribenzene sulfonate (pCMBS) and some other organic mercurials produce a swelling of slices of dogfish shark (Squalus acanthias) rectal glands, with an uptake of cell Na+ and a loss of K+. In contrast, 1 mM N-ethylmaleimide (NEM) does not swell rectal gland cells (RGC), while affecting cell cations. (2) The slow entry of [203Hg]pCMBS is linearly related to its external concentration (10 microM-1 mM) and a small accumulation of pCMBS (apparent gradient about 3) in the cells occurs in 2 h. Cell 203Hg rapidly washes out of the cells (fast rate constant 0.153.min-1; slow rate constant 0.0067.min-1), and this efflux is accelerated by 1mM dithiothreitol. Thus, a major portion of pCMBS inter-acts rather loosely with cell components. (3) pCMBS and NEM share: (a) a negligible effect on the efflux of 86Rb+ and of [14C]urea; (b) a gradual inhibition of the cell Na+,K(+)-ATPase activity. (4) NEM as well as agents lowering cell glutathione accelerate and increase the pCMBS-induced cell swelling. Conditions inhibiting the Na+,K(+)-ATPase (ouabain, absence of Na+) have the same effect. (5) pCMBS, but not NEM produce a disappearance of the F-actin-phalloidin fluorescence independent of cell volume changes, particularly at the basolateral RGC membrane. (6) The data are consistent with the following set of events: (a) pCMBS (but not NEM) affects the cell membrane by increasing the efflux of the cell osmolyte taurine (Ziyadeh et al. (1988) Biochim. Biophys. Acta 943, 43-52 and unpublished data); (b) on entry into the cells, pCMBS and NEM interact with cell -SH, including those of the Na+,K(+)-ATPase; this action produces the observed changes in cell cations. Also, pCMBS, but not NEM, decrease F-actin at the membrane; (c) the inhibition of the Na+,K(+)-ATPase activity together with the decreased resistance of the cell membrane to stretch (absence of F-actin) produces the observed pCMBS-induced cell swelling by osmotic forces (intracellular non-diffusible anions).

Characterization of muscarinic acetylcholine receptors in the avian salt gland.

Electrolyte and fluid secretion by the avian salt gland is regulated by activation of muscarinic acetylcholine receptors (R). In this study, these receptors were characterized and quantitated in homogenates of salt gland from domestic ducks adapted to conditions of low (freshwater, FW) and high (saltwater, SW) salt stress using the cholinergic antagonist [3H]-quinuclidinyl benzilate (QNB). Specific binding of the antagonist to receptors in both FW- and SW-adapted glands reveals a single population of high affinity binding sites (KdFW = 40.1 +/- 3.0 pM; KdSW = 35.1 +/- 2.1 pM). Binding is saturable; RLmaxFW = 1.73 +/- 0.10 fmol/micrograms DNA; RLmaxSW = 4.16 +/- 0.31 fmol/micrograms DNA (where L is [3H]QNB and RL the high affinity complex). Calculated average cellular receptor populations of 5,800 sites/cell in FW-adapted glands and 14,100 sites/cell in SW-adapted glands demonstrate that upward regulation of acetylcholine receptors in the secretory epithelium follows chronic salt stress. The receptor exhibits typical pharmacological specificities for muscarinic cholinergic antagonists (QNB, atropine, scopolamine) and agonists (oxotremorine, methacholine, carbachol). In addition, the loop diuretic furosemide, which interferes with ion transport processes in the salt gland, competitively inhibits [3H]QNB binding. Preliminary studies of furosemide effects on [3H]QNB binding to rat exorbital lacrimal gland membranes showed a similar inhibition, although the diuretic had no effect on antagonist binding to rat brain or atrial receptors.