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Outbreaks of meningococcal meningitis in non-African countries over the last 50 years: a systematic review.

ABSTRACT: Background:Meningococcal disease is caused by the bacteria Neisseria meningitidis, leading to substantial mortality and severe morbidity; with serogroups A, B, C, W135, X and Y most significant in causing disease. An outbreak is defined as multiple cases of the same serogroup occurring in a population over a short time-period. A systematic review was performed to gain insight into outbreaks of meningococcal disease and to describe the temporal pattern over the last 50 years in non-African countries. Methods:PubMed and EMBASE were searched for English-language publications on outbreaks of meningococcal disease in non-African countries between January 1966 and July 2017, with an additional grey literature search. Articles and reports were considered eligible if they reported confirmed meningococcal outbreak cases, included the region, number of cases, and the start and end dates of the outbreak. Data on outbreaks was stratified by geographical region in accordance with the World Health Organization (WHO) regional classification, and case-fatality rates (CFRs) were calculated. Results:Of the identified publications, 3067 were screened and 73 included, reporting data from 83 outbreaks. The majority of outbreaks were identified in the regions of the Americas (41/83 outbreaks), followed by the European region (30/83 outbreaks). In each of the Western Pacific, Eastern Mediterranean, and South-East Asian regions there were <10 outbreaks reported. The predominant serogroup in the majority of outbreaks was serogroup C (61%), followed by serogroup B (29%), serogroup A (5%) and serogroup W135 (4%). Outbreaks showed a peak in the colder months of both the Northern and Southern Hemispheres. Of the 54 outbreaks where CFR was calculable for all outbreak cases, it ranged from 0%-80%. Conclusions:These data present a retrospective view of the patterns for meningococcal disease outbreaks in non-African countries, and provide valuable data for monitoring future changes in disease epidemiology and informing preventive measures.

SUBMITTER: van Kessel F

PROVIDER: S-EPMC6441124 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

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Project description:Herein partially summarizes one scientist-clinician's wanderings through the jungles of primate aqueous humor outflow over the past ~45 years. Totally removing the iris has no effect on outflow facility or its response to pilocarpine, whereas disinserting the ciliary muscle (CM) from the scleral spur/trabecular meshwork (TM) completely abolishes pilocarpine's effect. Epinephrine increases facility in CM disinserted eyes. Cytochalasins and latrunculins increase outflow facility, subthreshold doses of cytochalasins and epinephrine given together increase facility, and phalloidin, which has no effect on facility, partially blocks the effect of both cytochalasins and epinephrine. H-7, ML7, Y27632 and nitric oxide - donating compounds all increase facility, consistent with a mechanosensitive TM/SC. Adenosine A1 agonists increase and angiotensin II decrease facility. OCT and optical imaging techniques now permit visualization and digital recording of the distal outflow pathways in real time. Prostaglandin (PG) F2α analogues increase the synthesis and release of matrix metalloproteinases by the CM cells, causing remodeling and thinning of the interbundle extracellular matrix (ECM), thereby increasing uveoscleral outflow and reducing IOP. Combination molecules (one molecule, two or more effects) and fixed combination products (two molecules in one bottle) simplify drug regimens for patients. Gene and stem cell therapies to enhance aqueous outflow have been successful in laboratory models and may fill an unmet need in terms of patient compliance, taking the patient out of the delivery system. Functional transfer of genes inhibiting the rho cascade or decoupling actin from myosin increase facility, while genes preferentially expressed in the glaucomatous TM decrease facility. In live NHP, reporter genes are expressed for 2+ years in the TM after a single intracameral injection, with no adverse reaction. However, except for one recent report, injection of facility-effective genes in monkey organ cultured anterior segments (MOCAS) have no effect in live NHP. While intracameral injection of an FIV. BOVPGFS-myc.GFP PGF synthase vector construct reproducibly induces an ~2 mmHg reduction in IOP, the effect is much less than that of topical PGF2⍺ analogue eyedrops, and dissipates after 5 months. The turnoff mechanism has yet to be defeated, although proteasome inhibition enhances reporter gene expression in MOCAS. Intracanalicular injection might minimize off-target effects that activate turn-off mechanisms. An AD-P21 vector injected sub-tenon is effective in 'right-timing' wound healing after trabeculectomy in live laser-induced glaucomatous monkeys. In human (H)OCAS, depletion of TM cells by saponification eliminates the aqueous flow response to pressure elevation, which can be restored by either cultured TM cells or by IPSC-derived TM cells. There were many other steps along the way, but much was accomplished, biologically and therapeutically over the past half century of research and development focused on one very small but complex ocular apparatus. I am deeply grateful for this award, named for a giant in our field that none of us can live up to.

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Outbreaks of meningococcal meningitis in non-African countries over the last 50 years: a systematic review.

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