26.2 Bacterial diseases of the nervous system  (Page 2/20)

Diagnosis of bacterial meningitis is best confirmed by analysis of CSF obtained by a lumbar puncture . Abnormal levels of polymorphonuclear neutrophils (PMNs) (>10 PMNs/mm ³ ), glucose (<45 mg/dL), and protein (>45 mg/dL) in the CSF are suggestive of bacterial meningitis. Popovic, T., et al. World Health Organization, “Laboratory Manual for the Diagnosis of Meningitis Caused by Neisseria meningitidis , Streptococcus pneumoniae , and Haemophilus influenza ,” 1999. Characteristics of specific forms of bacterial meningitis are detailed in the subsections that follow.

Meningococcal meningitis

Meningococcal meningitis is a serious infection caused by the gram-negative coccus N. meningitidis . In some cases, death can occur within a few hours of the onset of symptoms. Nonfatal cases can result in irreversible nerve damage, resulting in hearing loss and brain damage, or amputation of extremities because of tissue necrosis.

Meningococcal meningitis can infect people of any age, but its prevalence is highest among infants, adolescents, and young adults. US Centers for Disease Control and Prevention, “Meningococcal Disease,” August 5, 2015. Accessed June 28, 2015. http://www.cdc.gov/meningococcal/surveillance/index.html. Meningococcal meningitis was once the most common cause of meningitis epidemics in human populations. This is still the case in a swath of sub-Saharan Africa known as the meningitis belt , but meningococcal meningitis epidemics have become rare in most other regions, thanks to meningococcal vaccines. However, outbreaks can still occur in communities, schools, colleges, prisons, and other populations where people are in close direct contact.

N. meningitidis has a high affinity for mucosal membranes in the oropharynx and nasopharynx. Contact with respiratory secretions containing N. meningitidis is an effective mode of transmission. The pathogenicity of N. meningitidis is enhanced by virulence factors that contribute to the rapid progression of the disease. These include lipooligosaccharide (LOS) endotoxin , type IV pili for attachment to host tissues, and polysaccharide capsules that help the cells avoid phagocytosis and complement-mediated killing. Additional virulence factors include IgA protease (which breaks down IgA antibodies), the invasion factors Opa, Opc, and porin (which facilitate transcellular entry through the blood-brain barrier ), iron-uptake factors (which strip heme units from hemoglobin in host cells and use them for growth), and stress proteins that protect bacteria from reactive oxygen molecules.

A unique sign of meningococcal meningitis is the formation of a petechial rash on the skin or mucous membranes, characterized by tiny, red, flat, hemorrhagic lesions. This rash, which appears soon after disease onset, is a response to LOS endotoxin and adherence virulence factors that disrupt the endothelial cells of capillaries and small veins in the skin. The blood vessel disruption triggers the formation of tiny blood clots, causing blood to leak into the surrounding tissue. As the infection progresses, the levels of virulence factors increase, and the hemorrhagic lesions can increase in size as blood continues to leak into tissues. Lesions larger than 1.0 cm usually occur in patients developing shock, as virulence factors cause increased hemorrhage and clot formation. Sepsis, as a result of systemic damage from meningococcal virulence factors, can lead to rapid multiple organ failure, shock, disseminated intravascular coagulation, and death.