Liver abscesses in dromedary camels: Pathological characteristics and aerobic bacterial aetiology.

The study was carried out at Nyala abattoirs, South Darfur State, Sudan during a period from 2009 to 2011. Slaughtered camels (822) were examined for pathological changes of liver abscesses and identification of the involved aerobic bacteria. Grossly, a total of 111 (13.5%) liver abscesses were recorded in different camel ages; 90 (81.1%) were less than seven years old and 21 (18.9%) were more than seven years old. Histopathology of sectioned tissues revealed necrotic abscesses with infiltration of inflammatory cells, hydropic degeneration with swelling of hepatocytes comprising the sinusoid and different size of vacuoles in the hepatic cells. Proliferation of bile ducts with fibrous tissue and infiltration of inflammatory cells was also recorded. Investigation of bacteria revealed 90 aerobic isolates; they were identified to 52 (57.8%) gram positive cocci, 20 (22.2%) gram positive rods and 18 (20.0%) gram negative rods. Staphylococcus spp. (41.1%), Corynebacterium spp. (17.9%) and Streptococcus spp. (13.3%) were the most frequently identified bacteria involved in liver abscesses of camels in the region. Further studies are required to assess the pathogenicity of bacterial isolates from camel livers. This is particularly important from a public health perspective, since some people of Sudan are known to consume raw camel liver.

Development and evaluation of a live attenuated camelpox vaccine from a local field isolate of the virus.

A strain of camelpox virus (CMLV) isolated in the Sudan was attenuated by serial passage in Vero cell monolayers for use as a future vaccine strain. The safety and potency of passage 115 virus (designated Sudan CMLV/115) was tested. Camels inoculated with CMLV/115 showed no clinical disease or skin lesions, developed low-level antibodies and cell-mediated immune response and resisted challenge with virulent wild-type CMLV. Field testing of the candidate vaccine showed that the developed vaccine induces immune response and is safe for young and pregnant camels.

Angiotensin-induced desensitization of the phosphoinositide pathway in cardiac cells occurs at the level of the receptor.

Previous studies show that angiotensin II (Ang II) increases phosphoinositide turnover in cultured neonatal heart cells. Ang II has also been shown to transiently increase spontaneous beating behavior in these cells. In this study we seek to identify the molecular mechanism underlying this rapid (3-5-minute) desensitization. Time-course studies on the accumulation of [3H]inositol phosphates indicate that the loss in functional responsiveness correlates with reduced efficacy of Ang II to activate the phosphoinositide path. Binding studies with 125I-Ang II revealed that there was no change in surface receptor binding capacity during the time in which desensitization developed. Normal phosphoinositide and functional responses are observed when desensitized cells are treated with probes that activate the cardiac phosphoinositide pathway at discrete steps. These studies reveal that the functional status of the major components of the phosphoinositide signaling pathway, including G proteins, phospholipase C, and protein kinase C (PKC), are normal during maintained Ang II desensitization. To study the potential role of PKC in Ang II desensitization, the cells are treated with TPA for 24 hours, which downregulates PKC activity. PKC-depleted cells rapidly desensitize after Ang II application. We conclude that the selective Ang II-evoked biochemical/functional desensitization involves inhibition at the level of the receptor, rather than at a component downstream in the path, and that this process is independent of PKC and loss of surface binding capacity.

Competitive interaction of pirenzepine with rat brain muscarinic acetylcholine receptors.

In the present work, we studied the details of the interaction of the nonclassical muscarinic receptor antagonist pirenzepine with [3H]quinuclidinyl benzilate binding sites in rat brain homogenates. Pirenzepine showed biphasic competition curves with a Hill coefficient lower than unity, and these curves were better described according to a two-site receptor model. The affinities and the relative preponderance of these sites were constant at different ligand concentrations, in accordance with a competitive type of interaction. Similarly, pirenzepine did not influence the rate of dissociation of the [3H]quinuclidinyl benzilate-receptor complex, even at relatively high concentrations. However, although low concentrations of pirenzepine decreased the affinity of [3H]quinuclidinyl benzilate for the receptor without affecting the density of the binding sites, higher concentrations of the antagonist decreased the receptor number in a reversible fashion. Schild plots of these data indicated an apparent deviation from simple competition in this experimental design, an observation which can be attributed to the selectivity of pirenzepine for different receptor subtypes. Furthermore, pirenzepine, at concentrations high enough to saturate both its high- and low-affinity sites protected [3H]quinuclidinyl benzilate binding sites in the brain against irreversible alkylation by propylbenzilylcholine mustard. Therefore, our data support a competitive nature of interaction of pirenzepine with rat brain muscarinic receptors.

Effect of oxotremorine and epinephrine on lung surfactant secretion in neonatal rabbits.

The phosphatidylcholine (PC) content (mg/g dry lung weight; mean +/- S.E.) of lung washes of 1 to 3-day-old rabbits was significantly greater 30 min after the injection of the muscarinic agonist oxotremorine (0.2 mg/kg; 50.5 +/- 2.9 mg/g; 2 P < 0.01) or epinephrine (50 micrograms/kg; 78.0 +/- 14.8 mg/g; 2 P < 0.001) than saline (25.7 +/- 1.9 mg/g). Injection of atropine (2 mg/kg), dl-propranolol (1 mg/kg) but not d-propranolol (1 mg/kg) at 40 min or adrenalectomy at 45 min before killing abolished the increase produced by oxotremorine (2 P < 0.001). Also, dl-propranolol antagonized the increase produced by epinephrine. Palmitic and myristic acids were the major fatty acids in the lung wash PC of control and oxotremorine-treated rabbits. The residual lung tissue PC content following atropine (2 mg/kg; 104.4 +/- 18.5 mg/g) was significantly greater (2 P < 0.05) than following saline (72.6 +/- 6.0 mg/g) but not different (2 P > 0.05) in other treatment groups. The total lung content of PC was 55% greater (2 P < 0.001) than controls 30 min after epinephrine (50 micrograms/kg). The surface activity of lung washes (mg/g dry lung weight; mean +/- S.E.), assayed on a surface tension balance using dipalmitoyl-phosphatidylcholine as standard, was significantly greater (2 P < 0.05) 30 min following injection of oxotremorine (0.2 mg/kg; 73.8 +/- 9.9 mg/g) or epinephrine (50 micrograms/kg; 72.2 +/- 10.2 mg/g) than saline (42.8 +/- 2.0 mg/g). Ten-min infusions of oxotremorine (0.34 micrograms/ml) into isolated, ventilated, perfused neonatal rabbit lung preparations failed to alter the PC content of the subsequent wash, but this was significantly (2 P < 0.05) raised from 3.7 (+/- 0.8) to 4.8 (+/- 0.8) mg/g dry lung wt by a 10 min infusion of epinephrine (3.4 micrograms/ml).