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Micro 23: Neisseria and Related Genera

This episode introduces the Gram-negative diplococci of the genus Neisseria, organisms defined by their kidney-bean–shaped pairs and strict human host adaptation. Drawing from Murray’s Chapter 23, the focus centres on Neisseria gonorrhoeae and Neisseria meningitidis, two pathogens that share morphology yet diverge dramatically in clinical expression. The narrative begins at the mucosal surface. N. gonorrhoeae adheres to urogenital epithelium using pili and outer membrane proteins, evades immune detection through antigenic variation, and triggers intense neutrophilic inflammation. The result: urethritis, cervicitis, pelvic inflammatory disease, and disseminated gonococcal infection. N. meningitidis, by contrast, colonises the nasopharynx, occasionally breaching the epithelial barrier to enter the bloodstream. Its capsule enables survival in circulation, and endotoxin release drives fulminant meningococcaemia. The transition from asymptomatic carriage to life-threatening sepsis is rapid and unpredictable. Key mechanistic themes include: Antigenic variation IgA protease production Complement resistance Capsule-mediated immune evasion Clinically, this chapter underscores two patterns: Intense mucosal inflammation without systemic invasion (gonococcus) Rapid systemic dissemination with vascular collapse (meningococcus) Conceptually, Neisseria illustrates how small structural differences - particularly capsule expression - radically alter disease behaviour. Key Takeaways Neisseria are Gram-negative diplococci Pili and outer membrane proteins mediate mucosal adherence Antigenic variation enables immune evasion N. gonorrhoeae primarily causes mucosal infection N. meningitidis can cause fulminant septicaemia and meningitis Capsule presence is a major virulence determinant This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit drmanaankarray.substack.com/subscribe (https://drmanaankarray.substack.com/s...)