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Bacterial meningitis

Pathogen:Bacteria →Gram-positive diplococci →Streptococcus pneumoniae
Transmission:Typically airborne – meningitis secondary to nasopharyngeal infection
Geographical range:Worldwide
Incidence:1.2 million infections per year

Case history

A 53-year old man experienced a headache, mild neck stiffness and high fever. He visited his general physician and the physician suspected a life-threatening subarachnoid haemorrhage or acute brain infection. He immediately indicated him for a lumbar puncture to sample cerebrospinal fluid (CSF). The puncture was performed and his CSF sample was sent to the laboratory to investigate the possible cause of his persisting symptoms.

Meningitis pathophysiology and diagnostics

Meningitis is an acute inflammation of the protective membranes covering the brain and spinal cord. The inflammation may be caused by an infection with viruses (most common cause), bacteria, fungi, protozoa and less commonly by certain drugs. The types of bacteria that cause bacterial meningitis vary according to the infected individual's age group. In adults, Neisseria meningitides (also called meningococcus) and Streptococcus pneumoniae (pneumococcus) together cause 80% of bacterial meningitis cases. Meningitis can be life-threatening because of the inflammation's proximity to the brain and spinal cord. In 2013, around 16 million people worldwide contracted meningitis, resulting in around 300,000 deaths (1).

Meningitis is caused by an infectious agent that has established a localized infection elsewhere in the body. Potential sites of infection include the skin, nasopharynx, respiratory tract, gastrointestinal tract and genitourinary tract. The bacteria invade the submucosa at these sites by circumventing the host immune response and gain access to the central nervous system by one of two main routes. Either through the bloodstream or through direct contact between the meninges and either the nasal cavity or the skin. In most cases, meningitis follows an invasion of the bloodstream by bacteria that live on mucous surfaces such as the nasal cavity. This is often preceded by viral infections, which weaken the normal barrier provided by the mucous surfaces. Once bacteria have entered the bloodstream, they enter the subarachnoid space in places where the blood-brain barrier is vulnerable, such as the choroid plexus.

When the body tries to fight the infection, blood vessels become leaky and allow fluid and WBC to pass through the meninges and enter the subarachnoid space. This process causes brain swelling and can eventually result in decreasing blood flow to parts of the brain, worsening the symptoms of infection (2). Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport and increased vascular and membrane permeability perpetuate the infectious process in bacterial meningitis. These processes account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose concentrations in patients with the disease.

A lumbar puncture and subsequent CSF analysis can typically confirm or exclude meningitis. The CSF sample is examined for the presence and types of white blood cells, red blood cells, protein content and glucose level. The predominant type of white blood cell indicates whether meningitis is bacterial (where neutrophils are usually predominant) or viral (where lymphocytes are usually predominant) (3), although this is not always a reliable indicator at the beginning of the disease. Less commonly, eosinophils may predominate, suggesting parasitic or fungal aetiology (4).

Various other specialized tests may be used to distinguish between different types of meningitis. Polymerase chain reaction (PCR) is a broadly used technique to amplify DNA in order to detect the presence of bacterial or viral DNA in cerebrospinal fluid.

Laboratory results

 

Case interpretation

The XN high sensitivity research mode for CSF revealed severe leukocytosis (2,770 WBC/µL) in the WDF scattergram with a dominant population of neutrophils (NEUT%=96.8%) and an increased monocyte fraction (MONO%=2.4%). The WDF scattergram also revealed cell counts in the abnormal cell areas of activated monocytes (research parameter Act Mono 1 = 17 cells/ µL), where various macrophage types such as erythrophages are detected when present.

Apart from the very high WBC count in this CSF sample, the RET scattergram showed a pathological RBC count (= 1,000 /µL). An increased RBC count detected in CSF can be caused by either a haemorrhage or an RBC contamination from small blood vessels that have been damaged during the lumbar puncture procedure (traumatic tap). It is often difficult to differentiate between these two possible causes without a further examination of CSF, e.g. through the detection of xantochromia or the ferritin level. In this case, a relatively low RBC count together with low level of ferritin (10 ng/ml) and negative spectrophotometry could differentiate between an artificial contamination of CSF during the lumbar puncture and a subarachnoid haemorrhage. The high number of activated monocytes (macrophages) in the WDF channel together with the very high pleocytosis and dominance of neutrophils indicated an acute bacterial meningitis and was likely to rule out a viral cause or subarachnoid haemorrhage. The diagnosis of bacterial meningitis was confirmed by a morphological observation of bacterial cocci in neutrophils (Figure 1.) and a positive PCR for Streptococcus pneumoniae.

Literature

  1. Vos T et al (2015): Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015 Aug 22; 386(9995):743-800.
  2. Koedel U, Klein M, Pfister HW (2010): New understandings on the pathophysiology of bacterial meningitis. Curr Opin Infect Dis. Jun; 23(3):217-23.
  3. Tunkel AR, Hartman BJ, Kaplan SL (2004): Practice guidelines for the management of bacterial meningitis. Clinical Infectious Diseases. 39 (9): 1267–84.
  4. Graeff-Teixeira C, da Silva AC, Yoshimura K (2009): Update on eosinophilic meningoencephalitis and its clinical relevance. Clin Microbiol Rev. Apr; 22(2):322-48.

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