Investigation of Mycobacterium paratuberculosis in Arabian dromedary camels (Camelus dromedarius)

Aim: Mycobacterium avium subspecies paratuberculosis (MAP) causes Johne's disease in ruminants. This study aimed to investigate Mycobacterium paratuberculosis infection in clinically infected camels on the immunological, conventional bacteriological, and molecular biological basis. Materials and Methods: A total of 30 Arabian camels (Camelus dromedarius) were examined in this study. The camels were suffering from signs ranging from mild to severe infections (that did not respond to antibiotic treatment) to chronic or intermittent diarrhea. Camels were grouped into three groups based on their age, sex, and breed. Detection of anti-MAP antibodies in camels' serum, Ziehl-Neelsen (ZN) staining technique on rectal scraps, direct recognition of MAP in stool and tissue specimens by IS900 polymerase chain reaction (PCR) assay, and finally isolation and molecular description of MAP from fecal and tissue samples were carried out. Results: Five MAP isolates were recovered from these investigated camel samples giving an isolation rate of 16.6%, while eight camels were identified by PCR (26.6%). Five camels yielded MAP in their feces by ZN fecal staining (16.6%), whereas ELISA detected anti-MAP antibodies in nine camels only (30%). Conclusion: From the obtained results, we concluded that the gold standard for the diagnosis of MAP is the culture method despite its limitations. Molecular diagnosis (PCR) could be a useful tool in the identification of truly positive and negative camels; however, great care should be given regarding the primers specificity and sensitivity

Vitamin D Metabolites and Their Association with Calcium, Phosphorus, and PTH Concentrations, Severity of Illness, and Mortality in Hospitalized Equine Neonates

<div><p>Background</p><p>Hypocalcemia is a frequent abnormality that has been associated with disease severity and outcome in hospitalized foals. However, the pathogenesis of equine neonatal hypocalcemia is poorly understood. Hypovitaminosis D in critically ill people has been linked to hypocalcemia and mortality; however, information on vitamin D metabolites and their association with clinical findings and outcome in critically ill foals is lacking. The goal of this study was to determine the prevalence of vitamin D deficiency (hypovitaminosis D) and its association with serum calcium, phosphorus, and parathyroid hormone (PTH) concentrations, disease severity, and mortality in hospitalized newborn foals.</p><p>Methods and Results</p><p>One hundred newborn foals ≤72 hours old divided into hospitalized (n = 83; 59 septic, 24 sick non-septic [SNS]) and healthy (n = 17) groups were included. Blood samples were collected on admission to measure serum 25-hydroxyvitamin D₃ [25(OH)D₃], 1,25-dihydroxyvitamin D₃ [1,25(OH) ₂D₃], and PTH concentrations. Data were analyzed by nonparametric methods and univariate logistic regression. The prevalence of hypovitaminosis D [defined as 25(OH)D₃ <9.51 ng/mL] was 63% for hospitalized, 64% for septic, and 63% for SNS foals. Serum 25(OH)D₃ and 1,25(OH) ₂D₃ concentrations were significantly lower in septic and SNS compared to healthy foals (P<0.0001; P = 0.037). Septic foals had significantly lower calcium and higher phosphorus and PTH concentrations than healthy and SNS foals (P<0.05). In hospitalized and septic foals, low 1,25(OH)₂D₃ concentrations were associated with increased PTH but not with calcium or phosphorus concentrations. Septic foals with 25(OH)D₃ <9.51 ng/mL and 1,25(OH) ₂D₃ <7.09 pmol/L were more likely to die (OR=3.62; 95% CI = 1.1-12.40; OR = 5.41; 95% CI = 1.19-24.52, respectively).</p><p>Conclusions</p><p>Low 25(OH)D₃ and 1,25(OH)₂D₃ concentrations are associated with disease severity and mortality in hospitalized foals. Vitamin D deficiency may contribute to a pro-inflammatory state in equine perinatal diseases. Hypocalcemia and hyperphosphatemia together with decreased 1,25(OH)₂D₃ but increased PTH concentrations in septic foals indicates that PTH resistance may be associated with the development of these abnormalities.</p></div

Serum 25(OH)D₃ and 1,25(OH)₂D₃ concentrations in healthy, SNS, and septic foals.

<p>Values are expressed as median and 95% CI. (A) Septic and SNS foals had significantly lower serum 25(OH)D_<b>3</b> concentrations compared to healthy foals (P < 0.0001). (B) Septic and SNS foals had significantly lower serum 1,25(OH)_<b>2</b>D_<b>3</b> concentrations compared to healthy foals (P = 0.037). * indicates a statistically significant difference from healthy foals.</p

Serum total calcium and phosphorus concentrations in healthy, SNS, and septic foals.

<p>Values are expressed as median and 95% CI. (A) Septic foals had significantly lower serum total calcium concentrations compared to healthy and SNS foals (P = 0.01). (B) Septic foals had significantly higher serum phosphorus concentrations compared to healthy and SNS foals (P = 0.02). * indicates a statistically significant difference from healthy and SNS foals.</p

Percent distribution of serum 25(OH)D₃, total calcium, and phosphorus concentrations in hospitalized, septic, and SNS foals, based on 95% CI values from healthy foals.

<p>*P < 0.05</p><p>**P < 0.01; SNS—sick non-septic foals</p><p>For vitamin D, * = statistically different from hypervitaminosis D; ** = statistically different from normovitaminosis D and hypervitaminosis D in all foal groups.</p><p>For calcium, ** = statistically different from hypercalcemia in hospitalized and septic foals, and statistically different from hypocalcemia in SNS foals.</p><p>For phosphorus, ** = statistically different from normophosphatemia and hypophosphatemia.</p><p>Percent distribution of serum 25(OH)D₃, total calcium, and phosphorus concentrations in hospitalized, septic, and SNS foals, based on 95% CI values from healthy foals.</p

Interaction between Bovine leukemia virus (BLV) infection and age on telomerase misregulation

Bovine leukemia virus (BLV) is the causative agent of enzootic bovine leukosis (EBL). BLV can interact with telomerase and inhibits telomere shortening, contributing in leukemogenesis and tumour induction. The role of telomerase in BLV-induced lymphosarcoma and aging has been extensively studied. To date, the interaction of both BLV and aging on telomerase mis-regulation have, however, not been investigated. In the present study, telomerase activity in BLV positive and negative cows was compared over a wide range of ages (11-85 months). Lymphocyte counts were also measured in both BLV positive and negative groups. Telomerase activity was detected in all BLV infected animals with persistent lymphocytosis (PL), especially in older individuals. This study revealed that the cells undergo the natural telomerase shortening even in the presence of an existing viral infection. We also show that viral infection, especially during the PL phase of the disease, increases telomerase activity. A statistically significant interaction between age and viral infection was observed for telomere shortening during BLV infection. Older animals with BLV infection, especially those with persistent lymphocytosis or visible tumors, exhibited a sharp increase in telomerase activity. This study demonstrates that there is a significant interaction between BLV infection and telomerase up-regulation and lymphocytosis.Farhid Hemmatzadeh, Hadi Keyvanfar, Noor Haliza Hasan, Faustina Niap, Ebrahim Bani Hassan, Azar Hematzade, Esmaeil Ebrahimie, Andrea McWhorter, Jagoda Ignjatovi