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Tag words: Neisseria, gonococcus, meningococcus, meningococcal meningitis, gonorrhea, nonatal ophthalmia, urethritis

Neisseria gonorrhoeae

Kingdom: Bacteria
Phylum: Proteobacteria
Class: Beta Proteobacteria
Order: Neisseriales
Family: Neisseriaceae
Genus: Neisseria
Species: N. gonohorrhoeae

Neisseria meningitidis

Kingdom: Bacteria
Phylum: Proteobacteria
Class: Beta Proteobacteria
Order: Neisseriales
Family: Neisseriaceae
Genus: Neisseria
Species: N. meningitidis

Common References: Neisseria, Neisseria meningitidis, Neisseria gonorrhoeae, N gonorrhoeae, N meningitidis, diplococcus, gonococcus, meningococcus, meningococcal meningitis, meningococcemia, meningitis, gonorrhea, nonatal ophthalmia, urethritis

Kenneth Todar currently teaches Microbiology 100 at the University of Wisconsin-Madison.  His main teaching interest include general microbiology, bacterial diversity, microbial ecology and pathogenic bacteriology.

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Pathogenic Neisseriae: Gonorrhea, Neonatal Ophthalmia and Meningococcal Meningitis (page 6)

(This chapter has 7 pages)

© Kenneth Todar, PhD

Clinical manifestations of N. meningitidis infection

The onset of meningococcal meningitis may be abrupt or insidious. Infants with meningococcal meningitis rarely display signs of meningeal irritation. Irritability and refusal to take food are typical; vomiting occurs early in the disease and may lead to dehydration. Fever is typically absent in children younger than 2 months of age. Hypothermia is more common in neonates. As the disease progresses, apnea, seizures, disturbances in motor tone, and coma may develop.

In older children and adults, specific symptoms and signs are usually present, with fever and altered mental status the most consistent findings. Headache is an early, prominent complaint and is usually very severe. Nausea, vomiting, and photophobia are also common symptoms.

Neurologic signs are common; approximately one-third of patients have convulsions or coma when first seen by a physician. Signs of meningeal irritation such as spinal rigidity, hamstring spasms and exaggerated reflexes are common.

Petechiae (minute hemorrhagic spots in the skin) or purpura (hemorrhages into the skin) occurs from the first to the third day of illness in 30 to 60% of patients with meningococcal disease, with or without meningitis. The lesions may be more prominent in areas of the skin subjected to pressure, such as the axillary folds, the belt line, or the back.

Fulminant meningococcemia occurs in 5 to 15% of patients with meningococcal disease and has a high mortality rate. It begins abruptly with sudden high fever, chills, myalgias, weakness, nausea, vomiting, and headache. Apprehension, restlessness, and delirium occur within the next few hours. Widespread purpuric and ecchymotic skin lesions appear suddenly. Typically, no signs of meningitis are present. Pulmonary insufficiency develops within a few hours, and many patients die within 24 hours of being hospitalized despite appropriate antibiotic therapy and intensive care.

Figure 4. The characteristic skin rash (purpura) of meningococcal septicemia, caused by Neisseria meningitidis

Virulence Factors

For a time, the virulence of Neisseria meningitidis was attributed to the production of an "exotoxin" that could be recovered from culture filtrates of the organism. But when studies revealed that antitoxin reacted equally well with washed cells as culture filtrate, it was realized that the bacteria underwent autolysis during growth and released parts of their cell walls in a soluble form. Hence, the major toxin of N. meningitidis is its lipooligosaccharide,LOS, and its mechanism is endotoxic. The other important determinant of virulence of N. meningitidis is its antiphagocytic polysaccharide capsule.

The human nasopharynx is the only known reservoir of N. meningitidis. Meningococci are spread via respiratory droplets, and transmission requires aspiration of infective particles. Meningococci attach to the nonciliated columnar epithelial cells of the nasopharynx. Attachment is mediated by fimbriae and possibly by other outer membrane components. Invasion of the mucosal cells occurs by a mechanism similar to that observed with gonococci. Events involved after bloodstream invasion are unclear and how the meningococcus enters the central nervous system is not known.

Purified meningococcal LOS is highly toxic and is as lethal for mice as the LOS from E. coli or Salmonella typhimurium; however, meningococcal LOS is 5 to 10 times more effective than enteric LPS in eliciting a dermal Shwartzman phenomenon (a characteristic type of inflammatory reaction) in rabbits. Meningococcal LOS has been shown to suppress leukotriene B4 synthesis in human polymorphonuclear leukocytes. The loss of leukotriene B4 deprives the leukocytes of a strong chemokinetic and chemotactic factor.

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Kenneth Todar has taught microbiology to undergraduate students at The University of Texas, University of Alaska and University of Wisconsin since 1969.

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