Other severe complications include Waterhouse–Friderichsen syndrome, a massive, usually bilateral, hemorrhage into the adrenal glands caused by fulminant meningococcemia, adrenal insufficiency, and disseminated intravascular coagulation.Not all instances of a purpura-like rash are due to meningococcal septicaemia; other possible causes, such as idiopathic thrombocytopenic purpura (ITP; a platelet disorder) and Henoch–Schönlein purpura, also need prompt investigation. Microbiology
N. meningitidis is a Gram-negative diplococcus since it has an outer and inner membranes with a thin layer of peptidoglycan in between. It is 0.6–1.0 micrometers in size. It tests positive for the enzyme cytochrome c oxidase. Habitat
N. meningitidis is a part of the normal nonpathogenic flora in the nasopharynx of up to 8–25% of adults. It colonizes and infects only humans, and has never been isolated from other animals. This is thought to result from the bacteriums inability to get iron from sources other than human transferrin and lactoferrin. Subtypes
Disease-causing strains are classified according to the antigenic structure of their polysaccharide capsule. Serotype distribution varies markedly around the world. Among the 13 identified capsular types of N. meningitidis, six (A, B, C, W135, X, and Y) account for most disease cases worldwide. Type A has been the most prevalent in Africa and Asia, but is rare/practically absent in North America. In the United States, serogroup B is the predominant cause of disease and mortality, followed by serogroup C. The multiple subtypes have hindered development of a universal vaccine for meningococcal disease. Pathogenesis
Virulence
Lipooligosaccharide (LOS) is a component of the outer membrane of N. meningitidis.
Macular corneal dystrophy, also known as Fehr corneal dystrophy named for German ophthalmologist Oskar Fehr (1871-1959), is a rare pathological condition affecting the stroma of cornea. The first signs are usually noticed in the first decade of life, and progress afterwards, with opacities developing in the cornea and attacks of pain. The condition was first described by Arthur Groenouw in 1890. Signs and symptoms
Onset occurs in the first decade, usually between ages 5 and 9. The disorder is progressive, vision changes with ageing from 2nd decade to 3rd visual impairment may seen in 4th and 5th decade severe visual impairment can be seen Minute, gray, punctate opacities develop. Corneal sensitivity is usually reduced. Painful attacks with photophobia, foreign body sensations, and recurrent erosions occur in most patients. Macular corneal dystrophy is very common in Iceland and accounts for almost one-third of all corneal grafts performed there. Genetics
Macular corneal dystrophy is inherited in autosomal recessive fashion and is thought to be caused by the lack or abnormal configuration of keratan sulfate. Most cases of MCD are caused by mutations in CHST6 gene.The gene CHST6 is a carbohydrate sulfotransferase encoding an enzyme designated corneal N-acetylglucosamine-6-sulfotransferase. In MCD type I, various mutations lead to inactivation of the enzyme, in MCD type II, inactivation is caused by large deletions and/or replacements in the gene. Diagnosis
Treatment
Corneal transplantation is often required. See also
Corneal dystrophy

References


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