This shift from predominantly neutrophilic to lymphocytic pleocytosis was most consistent with viral meningitis, and the child was discharged home. The CSF protein was 0.85 g/L and CSF glucose 3.5 mmol/L. The decision was made to repeat the lumbar puncture, which now showed a total CSF WBC of 380×10 6/L, with 70% lymphocytes. There were no positive blood and CSF bacterial cultures, and it was too early for viral culture results. Twenty-four hours later, the child had improved clinically. Throat swab and stool specimen were also sent for viral culture. Blood culture, and bacterial and viral cultures of CSF were sent for study. Parenteral antibiotic therapy was not initiated, and the oral antibiotic was discontinued. CSF latex agglutination tests for Streptococcus pneumoniae, Hib, Neisseria meningitidis serogroups A, C, Y and W-135, and N meningitidis serogroup B/ Escherichia coli K1 were negative. CSF protein 0.78 g/L (normal 0.15 to 0.4 g/L) and CSF glucose 2.6 mmol/L (simultaneous blood glucose level of 5.3 mmol/L). CSF white blood cell (WBC) count was 420×10 6/L, with 80% neutrophils, 15% lymphocytes and 5% monocytes. Initial lumbar puncture revealed cloudy cerebrospinal fluid (CSF), and Gram stain showed moderate neutrophils but no bacteria. No rash was evident, and there were no swollen or painful joints. There were no enlarged cervical nodes, nor signs of hepatosplenomegaly. Tympanic membranes and pharynx appeared normal. Rectal temperature was 39.5☌, heart rate was 126 beats/min and respiratory rate was 24 breaths/min. He was lethargic and had nuchal rigidity. He was immunized previously with four doses of diphtheria- tetanus-acellular pertussis-polio- Haemphilius influenzae b (DTaP-polio-Hib) and a single dose of measles, mumps and rubella (MMR) at 12 months. He was prescribed amoxicillin two days before, and had taken six doses in total. There were no prodromal symptoms, no infectious contacts, no pets at home and no recent travels. CASE SCENARIOĪ two-year-old boy presented to an emergency room in July with a two-day history of fever, nausea and vomiting. The following case underscores the difficulties. Clinicians who assess children with aseptic meningitis recognize that the majority of cases are caused by viruses, but are often faced with having to exclude partially treated bacterial meningitis in children who had been on oral antibiotic(s). All contacts should be educated about the signs and symptoms of the infection and when to return to the emergency department.The term ‘aseptic meningitis’ refers to a meningitis for which an etiological agent is not apparent after Gram stain and bacterial culture of cerebrospinal fluid (CSF) ( 1). Family members should be educated about the need for prophylaxis when there is a family member with Neisseria and H. Across the board, the incidence of meningitis has decreased with the implementation of generalized vaccination. All healthcare workers (nurses, physicians, and pharmacists) should educate patients and parents in regards to vaccine-preventable meningitis ( H. To prevent this infection, the education of the public is vital. The pharmacist, preferably specializing in infectious diseases, should assist the clinical team in choosing the appropriate antibiotics based on the age of the patient and local sensitivities and correct dosing to ensure penetration into the central nervous system. If bacterial meningitis is suspected, prompt antibiotics should be started even in the absence of laboratory results. Other specialists who are usually involved in the care of these patients are neurologists, pediatricians, intensivists, infectious disease specialists, and pharmacists. The triage nurse must be fully aware of the signs and symptoms of the illness and refer the patient immediately to the emergency department clinician. The majority of patients with meningitis first present to the emergency department and a streamlined interprofessional approach is vital if one wants to lower the high morbidity. Meningitis is a serious disorder with high morbidity and mortality.
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