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The kidney of the one-humped camel has a remarkable capacity to preserve water and solute during extremes of long-term dehydration. We investigated the effects of dehydration and subsequent rehydration on camel kidney morphology at the ultrastructural level and the expression of aquaporins and solute carrier proteins. In light microscopy, dehydration induced few degenerative and necrotic changes in cells of the cortical tubules with little effect on medullary cells. Ultrastructural changes were mainly observed in some of the glomerular and tubular cells with insignificant changes in the collecting ducts of medulla. These changes included condensation of nuclear chromatin, vacuolization of cytoplasm, swelling of mitochondria, degradation or loss of brush borders of proximal tubules, cracking of major processes of some podocytes and degeneration of lysosomes and endoplasmic reticulum. Cell death, apoptotic-like bodies and changes in the basolateral membranes were infrequent and nephrolithiasis was not detected. Chronic nephropathy, mainly interstitial fibrosis and glomerular sclerosis induced by recurrent dehydration in human and animal models were not observed. Modulation of SLC proteins, AQP 1, 2, 3, 4, 9 and regulation of gene mRNAs expression levels during dehydration/rehydration play important role in water conservation and cell protection favoring kidney cellular restoration to near normal.

Hypothyroidism and iodine deficient disorders (IDD) are global problems affecting wide range of species. The camel is sensitive to iodine. This work was conducted to monitor thyroid hormones in group of camels at different physiological and pathological status. One hundred camels randomly selected were allocated into five groups including racing, late pregnant, lactating, aborted, and young calved. Four calves with congenital goiter (CCG) along with their mothers (MCCG) were also included. The affected calves were treated with two I/V doses of sodium iodide 1 week apart. T4 was highest in healthy calves followed by racing camels, which were significantly different from the rest of groups that displayed comparable values except for MCCG. T3 was highest in normal camel calves. The rest of groups illustrated comparable T3 levels although values for racing camels were slightly higher. The CCG group appeared smaller, weaker, and less active than their normal counterparts. They displayed enlarged thyroids, sometimes accompanied with difficult breathing and snoring. These calves and dams depicted comparable but very low T4 concentration; however, T3 was low only in the affected calves. Mild normocytic normochromic anemia, leukocytosis, neutrophilia, and elevated CK and LDH were evident in the CCG group. Sodium iodide injections significantly raised the thyroid hormones, reduced the thyroid size, and alleviated the adverse clinical signs. Monitoring of thyroid gland and hormones is necessary to avoid hypothyroidism. Iodine as feed supplements or boluses are recommended in affected herd especially during pregnancy, whereas iodine injections are indorsed for critical clinical cases.

Background Dehydration has deleterious effects in many species, but camels tolerate long periods of water deprivation without serious health compromise. The kidney plays crucial role in water conservation, however, some reports point to elevated kidney function tests in dehydrated camels. In this work, we investigated the effects of dehydration and rehydration on kidney cortex and medulla with respect to pro-inflammatory markers, oxidative stress and apoptosis along with corresponding gene expression. Results The cytokines IL-1β and IL-18 levels were significantly elevated in the kidney cortex of dehydrated camel, possibly expressed by tubular epithelium, podocytes and/or mesangial cells. Elevation of IL-18 persisted after rehydration. Dehydration induced oxidative stress in kidney cortex evident by significant increases in MDA and GSH, but significant decreases in SOD and CAT. In the medulla, CAT decreased significantly, but MDA, GSH and SOD levels were not affected. Rehydration abolished the oxidative stress. In parallel with the increased levels of MDA, we observed increased levels of PTGS1 mRNA, in MDA synthesis pathway. GCLC mRNA expression level, involved in GSH synthesis, was upregulated in kidney cortex by rehydration. However, both SOD1 and SOD3 mRNA levels dropped, in parallel with SOD activity, in the cortex by dehydration. There were significant increases in caspases 3 and 9, p53 and PARP1, indicating apoptosis was triggered by intrinsic pathway. Expression of BCL2l1 mRNA levels, encoding for BCL-xL, was down regulated by dehydration in cortex. CASP3 expression level increased significantly in medulla by dehydration and continued after rehydration whereas TP53 expression increased in cortex by rehydration. Changes in caspase 8 and TNF-α were negligible to instigate extrinsic apoptotic trail. Generally, apoptotic markers were extremely variable after rehydration indicating that animals did not fully recover within three days. Conclusions Dehydration causes oxidative stress in kidney cortex and apoptosis in cortex and medulla. Kidney cortex and medulla were not homogeneous in all parameters investigated indicating different response to dehydration/rehydration. Some changes in tested parameters directly correlate with alteration in steady-state mRNA levels.

Goiter and other iodine deficiency disorders (IDD) are a worldwide problem. IDD prevalence rate of 52.7% has been reported among school children aged 9–12 years in Dhofar region, (WHO 2006) which resides adjacent to the Arabian Sea in the Sultanate of Oman. In a preliminary survey, 39.5 and 44.7% of the dromedary camels in the region exhibited low total T3 and total T4, respectively. An abattoir survey was carried out and the dromedary camels examined during the anti-mortem were clinically normal. Post-mortem examination of both thyroid lobes of slaughtered camel, revealed normal weight but 69.5% of these showed nodules of various sizes, numbers, shapes, colors and consistency in the capsular region and or deeply embedded in thyroid tissue. A wide range of histopathological changes were seen and categorized according to the dominant histological pattern into Hurthle cell nodules, papillary hyperplastic nodules, adenomatoid hyperplastic nodules and nodular colloid goiter only. The Hurthle cell nodules were either solid encapsulated cords or follicular variants of well-encapsulated macrofollicles and microfollicles of different sizes and shapes, and the Hurthle cells were seen lining the colloid follicles or forming the solid cords. In the papillary hyperplastic nodules, majority of cases lack capsule, the fronds were multiple and variable, and usually do not compress the surrounding parenchyma. Adenomatoid hyperplastic nodules formed of encapsulated follicular nodules with various sizes and shapes and containing little or no colloid. The nodular colloid goiter along with the papillary hyperplastic nodules had psammoma-like bodies without lamellation. No evidence was found of capsular or vascular invasion apart from one case which showed limited vascular and capsular invasion. The histopathology and immunohistochemistry using specific thyroid tumor markers did not reveal malignancy in all suspected cases. Total and free serum T3 and T4 and serum selenium were comparatively low, and CK enzyme was high in affected camels. The causes of the subclinical nodular goiter, probably multifactorial, were discussed.

We investigated the effects of 20 days of dehydration and 20 days of dehydration followed by 72 h of rehydration on the gastric mucosa of the one-humped dromedary camel. The parameters addressed include biomarkers of oxidative stress, apoptosis, gastric epithelial histology, gastric neuropeptides, and their receptors. Nineteen clinically healthy, 4–5 year-old male dromedary camels were divided into three groups (five control camels, eight dehydrated for 20 days, six dehydrated for 20 days and then rehydrated for 72 h). Dehydration affected the oxidative stress biomarkers causing a significant increase in malondialdehyde, glutathione, nitric oxide, and catalase values compared with controls. Also the results revealed that dehydration caused different size cellular vacuoles and focal necrosis in the gastric mucosa. Rehydration for 72 h resulted in improvement in some parameters but was not enough to fully abolish the effect of dehydration. Dehydration caused significant increase in apoptotic markers; tumor necrosis factor α, caspases 8 and 3, BcL-x1 and TGFβ whereas caspase 9, p53, Beclin 1, and PARP1 showed no significant change between the three groups indicating that apoptosis was initiated by the extrinsic pathway. Also there were significant increases in prostaglandin E2 receptors and somatostatin in plasma and gastric epithelium homogenate, and a significant decrease in cholecystokinin–8 receptors. A significant decrease of hydrogen potassium ATPase enzyme activity was also observed. Pepsinogen C was not affected by dehydration. It is concluded that long-term dehydration induces oxidative stress and apoptosis in camel gastric mucosa and that camels adjust gastric functions during dehydration towards water economy. More than 72 h are needed before all the effects of dehydration are reversed by rehydration.

In humans, spindle cell lesions associated with thyroid adenoma or carcinoma are rare. A cross section of the thyroid of a dromedary camel showed follicular cysts, and microscopically, both thyroid lobes showed colloid goitre. The left lobe showed spindle cell proliferation associated with follicular adenoma without evidence of capsular or vascular invasion. The spindle cell lesion had cells featuring ground glass or pseudoinclusion nuclei and showed extensive haemorrhage, hyalinization and thrombosis. The right thyroid lobe showed papillary adenoma. Immunohistochemistry showed negative expression for malignancy. Serum Se, free tri-iodothyronine (fT3) and free thyroxine (fT4) values were low and CK activity was high. The histological features were unusual and merit reporting.

Quality and patient safety are terms that both providers and recipients of healthcare are very familiar with. Accreditation is another term that is closely linked to quality and patient safety. Audit is a systematic, independent, and documented process for obtaining evidence and evaluating it objectively to determine the extent to which audit criteria are fulfilled. Accreditation and audit are integral components of the same process. Three different types of audit are well recognized—internal, external, and co-operative. Reading of relevant documents, observation of laboratory practices, and asking open-ended probing questions are important auditing techniques. For auditing to be successful, experienced, qualified, and well trained auditors are essential. Furthermore, the auditor should be open-minded, not prejudiced, a team player and effective communicator, both in writing and verbally. In many instances, the emphasis for seeking laboratory accreditation has shifted from building quality systems—to produce reliable results and ensure patient safety—to just passing the inspection. Recently, the emphasis for laboratory quality improvement has been placed on pre and post-analytical processes in preference to analytical quality. The analytical quality of laboratory results is still far from ideal and it may be detrimental if less emphasis is placed on this aspect of laboratory medicine. Auditing or on-site inspection as a regulatory tool does not work or present a realistic picture of laboratory quality. A continuous quality improvement approach will help laboratories to build quality into their systems.