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Neisseria meningitides is an aerobic, non-spore-forming Gram-negative coccobacilli that resides in its natural habitat within the nasopharyngeal tract of humans . 5-15% of the human population carries the bacteria in its nonpathogenic form .(a major step in infection is its colonization in the nasophrynx of the human carrier ) Neisseria meningitidis, also simply known as meningococcus is best known for its role in meningitis (meningitis is an inflammation of the membranes that cover the brain and spinal cord). It only infects humans, there is no animal reservoir. It is the only form of bacterial meningitis to cause epidemics.
Strains There are many strains of meningococcus, clinically the most important are A, B, C and W135:
• • • •
A - occurs most often in sub-sahara Africa and vaccination is recommended prior to travel B - is the most lethal form, comprising 40% of the cases. The changing nature of the B group has prevented formation of a general B vaccine in the UK.. C - caused approximately 60% of the cases before the introduction of successful vaccination programme for infants. W135 - is particularly a problem for those undergoing annual pilgrimage to Mecca. It is a requirement of Saudi Arabia that all those intending to go on Hajj have a certificate of Men W135 vaccination.
paralysis and mental retardation. become purpuric and eventually necrotic. Invasion of the mucosal cells occurs by a mechanism similar to that observed with gonococci. Meningococcemia alone o Meningococcemia is characterized by a low grade fever. Without treatment. skin lesions and arthritis developing over a period of days to weeks. Transmission and Invasion Transmission is via nasal droplets from asymptomatic carriers. o The key feature of meningitis due to N.uncommon o Virulence Factors • • • The major toxin of N. The lesions occur as the LOS is shipped out of the cell. meningitidis is its antiphagocytic polysaccharide capsule.LOS. including hearing loss. The other important determinant of virulence of N. They start as petechiae. Asymptomatic carriage is found in the nasopharynx in 5-10%. meningitidis is skin lesions (65%). the mortality is 85%. meningitidis is its lipooligosaccharide. The loss of leukotriene B4 deprives the leukocytes of a strong chemokinetic and chemotactic factor. Meningococcal LOS has been shown to suppress leukotriene B4 synthesis in human polymorphonuclear leukocytes. fulminating DIC and shock. Waterhouse-Friderichsen syndrome o Waterhouse-Friderichsen syndrome is a syndrome characterized by the bilateral hemorrhagic destruction of the adrenal glands. Attachment is mediated by fimbriae and possibly by other outer membrane components. Signs and symptoms of meningococcal disease: 2 . and systemic cytokine release leads to shock and DIC. Most of these strains are not pathogenic. and its mechanism is endotoxic. meningococcal LOS is highly toxic and is lethal for mice and causes a dermal Shwartzman phenomenon (a characteristic type of inflammatory reaction) in rabbits.• • • Local cytokine release causes brain damage. In as many as 10-15% of survivors. Pneumonia. there are persistent neurological defects. loss of limbs.
.e.) 3 . Agglutination reactions with immune serum subdivide the species into serogroups A. Currently. B. discomfort looking into bright lights. Y. low blood pressure. and W-135. (PCN cannot be used because it cannot get into the surface of the uninflammed nasopharyngeal mucosa. and in areas where elastic pressure is applied (like underwear and socks). N meningitidis ferments glucose and maltose. W135. vomiting. Oxidase and catalase are biochemical markers for preliminary identification of this organism. delirium. C. not sucrose or lactose. • Immunity and Vaccines • There is a quadrivalent polysaccharide vaccine that provides protection against serogroups A. sleepiness and. it is only required in high risk populations (i. depending on a group-specific capsular polysaccharide antigen. and ankles. groin. military recruits. Diagnosis • • • • Gram stain of CSF Culture of CSF.The symptoms of meningococcal meningitis are high fever. in the extreme. blood or skin lesions N meningitidis is a gram-negative diplococcus that grows well on solid media supplemented with blood and incubated in a moist atmosphere enriched with carbon dioxide. develops rapidly and usually appears on the armpits. Meningococcemic rash is non-blanching. X. Prophylaxis of carriers or those with close exposure with rifampin. seizures. C.) The vaccination of college students would be a good idea. weakness. Other signs and symptoms include nausea. and coma. These symptoms usually appear in a range of 2 to 10 days after exposure. Y. Sugar fermentations are required for final identification of the species. although not cost effective for society as a whole. fever and rash are symptoms of meningococcemia. confusion. and Z. travelers to Sub-Saharan Africa etc. headache and stiff neck. Treatment • • Treat with a high IV dose of penicillin (PCN) or a cephalosporin if meningococcemia or meningitis.
They are highly susceptible to heat. of 30-37oC. Neisseria are oxidase positive. They cannot tolerate free fatty acids in media. Media used to culture them include: o o Chocolate agar.Over view of Neisseria and a comparison between pathogenic N. gonorrhoeae and N. They are highly autolytic at stationary phase. trimethoprim (a broad spectrum antibiotic). vancomycin (to kill GM+). Other Neisseria species will grow at 22oC. They are fastidious organisms requiring: • • 4-8% CO2 to enhance growth. two of which are pathogenic. 4 . They have cytochrome c oxidase in the electron transport chain. cold and drying. Incubation temp. meningitidis Group Characteristics of Neisseria Neisseria are kidney bean shaped. Characteristics of the Pathogenic Members (Neisseria gonorrhoeae and Neisseria meningitidis) Pathogenic Neisseria are obligate human pathogens. and nystatin (to kill yeasts). which is chocolate agar plus the following antibiotics. Gram negative diplococci. There are 8 species of neisseria. Thayer Martin media. which is blood agar that has been heated. The freed hemoglobin binds up the free fatty acids. colistin (to kill other GM-). which will oxidize phenylethylene diamine dye to black.
3. lactose. maltose. They cause ciliostasis in ciliated cells with LOS and PDG. 7. The endocytosis is directed by porins. Neisseria spp. and sucrose. are used to identify Neisseria and related species. 5 . 2. Dissemination of the organisms into the bloodstream (if bacteremia occurs). such as glucose. Attachment to endothelial cells follows. Organisms resist killing by antibody and complement in inflammatory fluids and blood. 4. The Neisseria are transported through the cells. They are egested into the basement membrane leading to massive inflammation. Ciliated and non-ciliated host cells are destroyed 5.Comparison between both pathogenic members of Neisseria: 1)Sugar Utilization: • Patterns of acid production from sugars. produce acid by an oxidative pathway. In contrast to most bacteria that produce acid using fermentation. 2)Mechanism for Invasion of Epithelial Cells: (Deduced from Fallopian Tube Cell Culture with GC) 1. Neisseria stick to mucous secreting but not ciliated cells by their pili and opa proteins. 6.
gonorrhoeae (GC) Iron Binding • All organisms require an exogenous source of iron. meningitidis (MC) and N. • Porins are very wide channels that allow in a lot of hydrophilic solutes. (Remember Bacterial Structure?) 6 .) Capsule Major surface proteins: Pili Major surface proteins: Porins. (Review Bacterial Physiology for more information.3) Virulence Factors of N.
It cleaves IgA into Fab and Fc fragments. Remember that both S. influenzae had one. Major surface proteins: IgA protease • An IgA protease can be a handy virulence factor. It is a very potent endotoxin. and is called lipooligosaccharide or LOS. pneumoniae and H.Major surface proteins: Target of Blocking Antibody Major surface proteins: Adherence Major surface proteins: LOS • The lipopolysaccharide of Neisseria has a short side chain. 7 .
4) Diagnosis Epidemiology of Neisseria meningitidis A 8 .
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