Meningitis is a severe acute infectious disease caused by several microorganisms, including viruses, bacteria, parasites, and fungi. Fatality rates associated with this disease can be as low as 2% in infants and children, and as high as 20–30% in neonates and adults [1]. Transient or permanent deafness, or other neurological sequelae, arise in up to a third of survivors [2].

The frequency of neonatal meningitis varies greatly between different institutions and geographical areas, with rates of about two to ten cases per 10 000 live births [3]. More than two-thirds of all cases of neonatal meningitis in developed countries are caused by group B streptococci and gram-negative enteric bacilli. In developing countries, gram-negative enteric bacilli are the predominant organisms causing bacterial meningitis in newborns; however, group B streptococci and L. monocytogenes have been isolated increasingly [4]. Infections are mostly acquired by vertical transmission, but the nosocomial transmission is also important, especially in preterm infants with low birth weight who require long-term intensive care. Although nearly all newborn infants are colonized by many of the organisms with which they have contact, sepsis arises in less than 1% of these infants. About 25% of infants with septicemia develop meningitis [5].

In the neonatal period, pathogens are acquired mainly, although not exclusively, during birth by contact and aspiration of intestinal and genital tract secretions from the mother. In infants and children, meningitis usually develops after encapsulated bacteria that have colonized the nasopharynx are disseminated in the blood. Viral infections of the upper respiratory tract commonly precede invasion of the bloodstream. Subsequently, organisms penetrate vulnerable sites of the blood-brain barrier (e.g., choroid plexus and cerebral capillaries) and reach the subarachnoid space [6]. Meningitis can also develop by direct extension of infection from a paranasal sinus, middle ear, congenital dural defects, neurosurgical procedures, or head trauma with a skull fracture.

The intense inflammation within the subarachnoid space noted in lumbar CSF, and the resulting neurological damage, are not the direct result of the pathogenic bacteria but rather of activation [7] of the host’s inflammatory pathways by the microorganisms or their products.

Exclusion criteria: Children below 5 months of age and cases who had received antibiotics in the past seven days were excluded from the study.

Data collection procedure: All relevant demographic information as well as clinical symptoms and signs were recorded on admission on a self-structured proforma. Serum was separated from blood samples collected on admission from all patients and stored at −20⁰ C and used subsequently for assaying PCT. After 72 h of treatment, serum PCT levels were re-estimated. The prognosis of cases was followed over 7 days. Serum PCT was measured by a fluorescence immunoassay using QD_X Instacheck. It is a quantitative test requiring 150 μl of serum. The signal intensity of fluorescence on the detector antibody reflects the amount of antigen captured and is processed by the QD_X Instacheck Reader. The detection limit is 0.25-100 ng/ml. The normal serum procalcitonin with this is <0.5 ng/ml.

Ethical consideration and permission: Informed consent was taken from the parents for the participation of their children in the study. Permission for the study was sought from the institutional ethical committee (IEC SKIMS).

Data Analysis: Data was entered and analyzed by using standard statistical tests using SPSS 20. Variables were compared employing tests chi-square and student’s t-tests whichever feasible. Values were expressed as mean ± SD and p-value < 0.05 was considered significant.

Fig-1: Demographic profile of the study population.

Figure 1 shows the demographic features of the study population. Of the total 45 participants, 30 (66.7%) were males and 15(33.3%) were females. 11 (24.4%) had age <1 year, 15 (33.3%) were in the age group 1-5 years, 10(22.2%) in the age group of 6-10 years, and 9(20%) >10 years.

A total of 30(66.7%) males and 15 (33.3%) females participated in the study. Serum PCT was estimated on admission and also after 72 hours of starting treatment to study whether there is any significant drop in serum PCT, the mean serum PCT level at admission, and 72 hours of treatment of this group (n=45) were 14.9293; SD=4.4912 and 12.4386; SD=4.4096 respectively.

The drop in serum PCT was highly significant (p<0.001) and was consistent with the study conducted by Alavi SM, et al (2012) [12] with mean serum PCT at admission and 72 hours as 2.58±4.62 and 1.52±3.03 ng/ml, respectively and was also consistent with the study conducted by Ibrahim KA et al [13] in which follow up of the studied cases, showed a significant decrease in procalcitonin levels on day 3 and day 6 after antibiotic treatment.

Viallon A et al (2005) observed that median serum PCT levels on admission and at day 2 were 4.5 (2.8–10.8) mg/ml and 2 (0.9–5.0) mg/ml, respectively (P < 0.0001) [14].

This result is again consistent with that obtained by many authors, [15-17] who found that serum procalcitonin decreased to a very low, and may to an unidentifiable level with treatment, making it a valuable parameter for evaluating the efficacy of antibiotic treatment and hence diminishing the need for lumbar puncture performed 48-72 hours after admission to assess treatment efficacy.

Gendrel D et al (1997) observed that all the patients followed for PCT levels had < 1 mg/L of PCT at recovery [18].

Further, it was observed by Schwarz S et al (2000) that persistently elevated or increasing PCT levels after 2 days of admission were associated with unfavorable clinical outcomes [19].

These findings are in agreement with Monneret G et al (1997) study where they found that high levels of PCT correlated with bacterial invasion and PCT returned to normal range (< 0.1 micrograms) more quickly than C-reactive protein, suggesting that PCT may be an early marker of favorable outcome [20].

The study was dependent on the number of pediatric meningitis cases admitted to the hospital. Only 45 participants during the one year full filled the inclusion criteria.