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Listeriosis is a severe infectious disease occurring both in humans and in most other animal species caused by Listeria monocytogenes (L. monocytogenes) that can lead to severe meningoencephalitis. Elevated ADA activities have been demonstrated in the cerebrospinal fluid (CSF) in meningitis with different etiologies. However, data on ADA activities in CSF and serum associated with listerial meningoencephalitis is limited. Thus, the present study was designed to investigate the changes in the CSF and serum ADA activities and whether there is a correlation between CSF and serum ADA in the experimental model of listeriosis. Twenty adult white New Zealand rabbits of both sexes were used in this study. Fourteen rabbits were infected by intracerebral inoculation of L. monocytogenes 1/2a and 6 healthy rabbits were included in the study as the control group. CSF samples were obtained by puncture of the cisterna magna. Blood was sampled from the auricular vein of rabbits. ADA activity was determined using the colorimetric method. Mean±SD ADA activities in the CSF and serum were 14.98±3.26 U/L and 17.71±3.41 U/L in infected rabbits, respectively, while 4.72±1.86 U/L and 6.89±3.00 U/L in healthy rabbits. CSF and serum ADA activities showed significant alteration in rabbits with experimental listeriosis compared to control rabbits (p<0.001). A positive correlation was found between CSF and serum ADA activities in infected rabbits (r=0.65, p<0.05), but not in healthy rabbits. These findings imply that ADA plays a role in this disease process. In conclusion, CSF and serum ADA measurements may be used as a supplementary biochemical test in combination with clinical and laboratory findings of listerial meningoencephalitis
Listeriosis is a severe infectious disease occurring both in humans and in most other animal species caused by Listeria monocytogenes (L. monocytogenes) that can lead to severe meningoencephalitis. Elevated ADA activities have been demonstrated in the cerebrospinal fluid (CSF) in meningitis with different etiologies. However, data on ADA activities in CSF and serum associated with listerial meningoencephalitis is limited. Thus, the present study was designed to investigate the changes in the CSF and serum ADA activities and whether there is a correlation between CSF and serum ADA in the experimental model of listeriosis. Twenty adult white New Zealand rabbits of both sexes were used in this study. Fourteen rabbits were infected by intracerebral inoculation of L. monocytogenes 1/2a and 6 healthy rabbits were included in the study as the control group. CSF samples were obtained by puncture of the cisterna magna. Blood was sampled from the auricular vein of rabbits. ADA activity was determined using the colorimetric method. Mean±SD ADA activities in the CSF and serum were 14.98±3.26 U/L and 17.71±3.41 U/L in infected rabbits, respectively, while 4.72±1.86 U/L and 6.89±3.00 U/L in healthy rabbits. CSF and serum ADA activities showed significant alteration in rabbits with experimental listeriosis compared to control rabbits (p<0.001). A positive correlation was found between CSF and serum ADA activities in infected rabbits (r=0.65, p<0.05), but not in healthy rabbits. These findings imply that ADA plays a role in this disease process. In conclusion, CSF and serum ADA measurements may be used as a supplementary biochemical test in combination with clinical and laboratory findings of listerial meningoencephalitis
The level of adenosine deaminase (EC. 3.5.4.4), was estimated in plasma of 389 healthy males and 493 healthy females in order to establish a normal reference range for Saudis. Using the continuous spectrophotometric method, the reference ranges were calculated in two ways using the mean ± 2 SD and the 2.5th -97.5th percentile value methods. In both methods of calculation, a slightly higher range was observed for children as compared to adults. The method of 2.5th -97.5th percentile values brought almost all of our subjects within the recommended range of 11.5 -25 U/1. In the current study, the normal range for adenosine deaminase totalled 15.0 -23.2,14.8 -23.6,15.0 -23.0 and 16.7 -24.6 U/1 for the overall population, all males, females, and children, respectively. The ranges are discussed in the light of significantly different results obtained by the two calculation methods and recommendation of an appropriate method for healthy Saudis, namely the 2.5th -97.5th percentile values. The choice of the Ellis and Goldberg kinetic continuous monitoring method for the estimation of plasma ADA levels in the current investigation is also hereby justified.FJ. Al-Shammary, CC. Anokute, HK Ghneim, AM Na'seh, AD Al-Wazzan, SA Al-Majed,
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