Journal of Postgraduate Medicine
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Year : 1987  |  Volume : 33  |  Issue : 2  |  Page : 58-60  

Use of CSF C-reactive protein in differentiating bacterial and non-bacterial meningitis.

AK Vaidya, NM Wagle, SM Merchant 
 

Correspondence Address:
A K Vaidya





How to cite this article:
Vaidya A K, Wagle N M, Merchant S M. Use of CSF C-reactive protein in differentiating bacterial and non-bacterial meningitis. J Postgrad Med 1987;33:58-60


How to cite this URL:
Vaidya A K, Wagle N M, Merchant S M. Use of CSF C-reactive protein in differentiating bacterial and non-bacterial meningitis. J Postgrad Med [serial online] 1987 [cited 2022 Aug 12 ];33:58-60
Available from: https://www.jpgmonline.com/text.asp?1987/33/2/58/5293


Full Text



 INTRODUCTION



C-reactive protein (CRP) and the acute phase inflammatory response were discovered in 1930 by Tillett et al.[8] Almost any inflammatory disease will cause detectable quantities of CRP to be present in serum or fluids closely associated with affected tissues.[2],[4],[7] Increased CRP production is an early and sensitive response to most forms of microbial infections and the value of its measurement in the diagnosis and management of various infective conditions has been established.[3],[5] In western countries, attention was recently drawn to the value of serum CRP measurement in differentiating bacterial and viral infections.[5],[6]

However, routine diagnostic use of CSF- CRP in differentiating bacterial and non- bacterial meningitis has been evaluated by very few workers.[1],[2] Since meningitis is potentially hazardous disease of childhood, diagnostic test which is readily available, easy to interpret and simple to perform is of paramount importance. This report demonstrates the usefulness of a latex agglutination test for the detection of CSF-CKP as a rapid and simple, method in diagnosing and differentiating cases of bacterial and non-bacterial meningitis in children.[1]

 MATERIAL AND METHODS



A total of 130 CSF samples from clinically suspected cases of meningitis and 20 control samples in which clinical diagnosis was other than meningitis such as mental retardation, epilepsy, febrile convulsions were studied. The distribution of cases is shown in [Table 1]. Routine CSF examination included cell count, and protein, sugar and chlorides estimation. All CSF samples were processed for bacteriological examination by doing Gram-stained smear and culture. Isolated organisms were identified by standard methods. Latex agglutination test was done on all CSF samples using commercially available kit (obtained from Ortho Diagnostic System). A drop of CSF and a drop of latex reagent were mixed on a clean glass tile and the mixture observed for agglutination microscopically. Clumping of latex particles within 2 minutes was considered as positive. Known positive and negative samples served as controls.

 RESULTS



[Table 1] shows the results of all 150 cases. Out of these, 20 were controls in which CRP was negative. Protein, sugar, chlorides and ell count were normal. Bacteriologically, these samples were sterile. Out of 130 clinically suspected cases of meningitis, 100 cases were proved by positive culture as pyogenic meningitis. Cell count in these cases showed predominant polymorphs, increased protein level and low sugar. Twenty six cases were proved either by direct or indirect evidence as tuberculous meningitis. In all these cases, CSF-CRP was positive. Remaining 4 cases were bacteriologically sterile. In these 4 cases, CSF cell count was 100-200 cells, polymorph-lymphocyte ratio was overlapping, protein was marginally increased and sugar was normal. All these cases were clinically diagnosed as viral meningitis. CSF-CRP was negative. Three cases were followed up, and repeat CSF showed decrease in cell number and CRP was again negative.

 DISCUSSION



The etiological diagnosis of meningitis in developing countries remains a problem in clinical practice as CSF biochemical analysis and cellular response often overlap. This becomes even more difficult in a population where tuberculous meningitis is prevalent, as M. tuberculosis is not always easily and reliably identifiable in CSF by established methods. Our results indicate that demonstration of CSF-CRP in initial lumbar puncture is an ideal method in such situations. The mechanism by which CRP gains access to CSF is not known. Passive diffusion across the highly inflamed meninges would be a reasonable explanation.

Serum CRP levels have been used to monitor the infections of central nervous system[6] and also to differentiate between bacterial and viral meningitis, since the CRP levels have been found to be significantly lower in cases of viral meningitis.[3] Corral et al[2] have studied 56 children, aged 1 month to 15 years, with CSF pleocytosis. CRP was determined in the CSF by latex agglutination. On the first lumbar puncture, 24 patients with culture-proved bacterial meningitis had a positive CSF-CRP result and only 2 of 32 children with nonbacterial meningitis had positive CSF-CRP test. CSF- CRP values appeared to be more sensitive in differentiating bacterial and non-bacterial meningitis than the usual parameters measured in CSF like cell count, protein, sugar and Gram stain. Their study demonstrated that CSF-CRP levels are also useful in diagnosing partially treated cases of meningitis. Our results also correlate with their findings. All our four cases recovered within a week and in one case we could demonstrate plasmacytoid cells in the CSF. Such types of cells have been reported in acute viral meningitis.[3],[4] Unfortunately, we could not detect viral etiological agents responsible for meningitis. Thus, CRP detected by latex agglutination is a helpful screening test to differentiate bacterial and non-bacterial meningitis at the bedside and CRP detected patients should be considered to have bacterial meningitis until proved otherwise.

 ACKNOWLEDGEMENT



We thank the Dean, B. J. Wadia Hospital for Children for permission to publish this paper and faculty members of the Hospital for allowing the use of clinical material.

References

1Clarke, D. and Cost, K.: Use of serum C-reactive protein in differentiating septic from aseptic meningitis in children. J. Pediatr., 102: 718-720, 1983.
2Corral, C. J., Pepple, J. M., Moxon, R. and Hughes, W. T.: C-reactive protein in cerebrospinal fluid in children with meningitis. J. Pediatr., 99: 365-369, 1981.
3Debeer, F. C., Kirsten, G. F., Gie, R, P., Beyers, N. and Stachan, A. F.: Value of C-reactive protein measurement in tuberculous, bacterial and viral meningitis. Arch. Dis. Child., 59: 653-656, 1984.
4Horsfall, F. L. Jr. and Tamm, I.: "Viral and Rickettsial Infections of Man." J. B. Lippincott Company, Philadelphia, 1965, pp 1167-1168.
5McCarthy, P. L., Frank, A. L., Ablow, R. C. Masters, S. J. and Dolan, T. F. Jr.: Value of the C-reactive protein test in the differentiation of bacterial and viral pneumonia. J. Pediatr., 92: 454-456, 1978.
6Peltola, H. O.: C-reactive protein for rapid monitoring of infections of the central nervous system. Lancet, 1: 980-982, 1982.
7Pepys, M. B.: C-reactive protein-fifty years on. Lancet, 1: 653-656, 1981.
8Tillett, W. S. and Francis, T. Jr.: Serological reactions in pneumonia with a non- protein somatic fraction of pneumococcus, J. Exper. Med., 52: 561-571, 1980.

 
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