A 2-year-old female child with no significant previous medical history carried to the emergency department by her mother with a complaint that the child had flu-like symptoms started yesterday morning such as low energy levels, irritability and slight fever. She also mentioned that she is a working-mom and the child usually stays at the day-care center. Due to child's illness, mother decides to stay home with the child that day. However, symptoms have severely gotten worse through the night with high fever, high-pitched excessive crying along with nausea and vomiting. This is when the mother realized the severity of the child's condition and brought the child early in the morning to the hospital. At around 11:00 a.m. on the day of admission, she started having short periods of tonic-clonic movements on the right side of the body.
Upon the inspection of the child, there was a red rash on the skin with a slight bulging of the soft spot on the top of the head. The patient's mother claimed her child not to have a cough, shortness of breath, abdominal pain or diarrhea. Patient did not take any medications and had no known drug allergies. The child had high fever, headache, mildly dehydrated and stiff neck. There were no abnormal findings in cardiovascular and respiratory systems. The ears and throat were normal.
Further laboratory examinations have been conducted: Full Blood Count and CSF analysis. WBC count was 22,800/mm3 with 25 % band cells and 70 % polymorphonuclear leukocytes. Electrolyte levels and platelet counts fell within the normal range. A lumbar puncture was done, which involves withdrawing a small sample of cerebrospinal fluid (CSF) from the spinal canal with a needle. CSF findings display turbid fluid with increased neutrophil polymorphs which contained 860 white blood cells and the low glucose level: 1 mg/dL. The total protein level was 450 mg/dL. The gram stain and the latex agglutination test was further performed for bacterial antigens and found positive for Neisseria meningitis. Urine analysis revealed no abnormality. Repeatedly after 12 hours, the patient's blood and the CSF was sent for microscopy and culture .
Etiology
In acute meningitis, infection of the leptomeninges by bacteria induces an acute inflammatory response. The predominant bacterial pathogens in young children are Streptococcus pneumonia, Haemophilus influenenza and Neisseria meningitides (MENINGOCOCCAL MENINGITIS). The acute inflammatory response causes thrombosis of local blood vessels and prevents perfusion to the cerebral cortex, leading to the severe brain damage rather than the pathogenicity of the bacteria themselves. Through combating procedures with the acute inflammatory response to the infection causes more damage than the infective organism1.
Pathogenesis
Bacterial pathogens exploits host cell signaling pathways to promote its uptake by host cells. The pathogens follow with meningeal invasion and survive within the bloodstream and proliferate within the CSF. Chemical mediators such as inflammatory cytokines (eg, interleukin-1 (IL-1) interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF∝) attract neutrophils to the CSF. The neutrophils release large numbers of lysosomal cytoplasmic granules that are rich in proteolytic cellular martrix materials that break down cell membranes including those of the vascular endothelium. The neutrophil is the key cell to mediate the effects of acute inflammation1. The adhesion of neutrophils to endothelium causes them to aggregate along the vessel walls in a process termed margination. Endothelium in local vessels is activated both by products of tissue damage and by cytokines. Later, the endothelium is modified to become sticky for neutrophils, to secrete factors mediating vasodilation and to promote platelet adhesion and aggregation. Neutrophils also have great phagocytic potential and can actively ingest pathogens, which are then destroyed both by lysosomal enzymes and by mechanisms that generate toxic free radicals. Acute inflammatory response such as presence of endotoxin and inflammatory mediators results in thrombosis of local blood vessels and reduction in cerebral perfusion1. The vasculitis and thrombophlebitis can ultimately lead to brain damage. As a result there is an increase in brain edema and intracranial pressure. The cumulation of purulent exudate created when neutrophils dominate the composition, and material is liquefied to form pus in the CSF blocks CSF reabsorption1. An acute abscess is a mass of necrotic tissue, with dead and viable neutrophils. This leads to hydrocephalus. Brain edema and hydrocephalus increase intracranial pressure.
Diagnosis
CSF Analysis
Brain CT or MRI
The laboratory findings and clinical pictures such as CT suggested a diagnosis of acute bacterial (Meningococcal) meningitis. Definitive diagnosis is determined by CSF analysis. CSF pressure has been elevated. CSF examination also reveals cloudy fluid with many neutrophil polymorphs and a low sugar1. Increased protein level also suggests bacterial meningitis. Culturing the organism on chocolate agar plate to further differentiate the species and found that the patient is infected by Gram-negative cocci, Neisseria.
Clinical Manifestations
Signs and symptoms for acute bacterial meningitis among young children are often nonspecific especially in early disease. Fever, poor feeding, lethargy, vomiting, irritability and crying are common presenting symptoms. Seizures and bulging fontanelles are possible.
Treatment
Patient is hospitalized for treatment with antibiotics (penincilin G and cefotaxime) and corticosteroids given intravenously as soon as blood cultures identified the pathogen.
Prognosis
Prognosis depends partly on the number of organisms present in CSF at diagnosis and immediate treatment and supportive care can improve outcome and reduced mortality to less than 10%.
