Meningitis

Bosphore Bacterial Meningitis Panel Kit

Bosphore Viral Meningitis Panel Kit

Bosphore Neonatal Meningitis Panel Kit v1

Bosphore Neonatal Meningitis Panel Kit v2

 

Meningitis is caused by inflammation of the protective membranes covering brain and spinal cord (meninges). High risk of mortality and morbidity ratios might occur depending on the cause of the infection such as bacterial, viral agents or use of certain drugs.  Viral meningitis is a mild form of disease with higher incidence compared to acute bacterial meningitis. Acute bacterial meningitis is rarely seen, but it may cause hearing loss, brain damage and even death if the symptoms emerging instantly cannot be detected in the early stage.

 

Bosphore® Neonatal Meningitis Panel Kits detect and characterize Escherichia coli, Streptococcus agalactiae (Group B), Listeria monocytogenes and Streptococcus pneumoniae in human biological samples. Listeria monocytogenes is a gram-positive, anaerobic, facultative, ubiquitous intracellular pathogen and the causative agent of Listeriosis on humans and animals. Listeriosis – with a mortality rate of 24% - can lead to several consequences, including central nervous system infections, neonatal death, meningitis, septisemia, encephalitis and miscarriage. [1,2] Pregnant women, newborn, elderly and immunosuppressed persons are amongst the risk group to get Listeria infections [3].

 

There are 270 confirmed Listeriosis cases resulted in death between 2009-2015 within the European Union. [4] A multinational foodborne outbreak occurred on 6 March 2018. This outbreak -confirmed by 5 countries – caused 32 infections, 6 resulting in death [5].

 

Listeria monocytogenes is typically transmitted through contaminated food, processed meat, seafood, and poultry animals. Controlling Listeria expansion is still challenging due to the organism’s ubiquitous nature, intrinsic resistance and ability to grow under extreme environmental conditions.[6]

 

Streptococcus agalactiae, commonly known as Group B Streptococcus (GBS), is a diplococcal, gram positive pathogen responsible for infections affecting mainly neonates and immunocompromised patients. Organism may be found within the gastrointestinal and genitourinary tracts of healthy human beings as well. There are ten serotypes of Streptococcus agalacticae  but most of the invasive GBS diseases are caused by serotypes Ia, Ib, II, III and V. [7,8]. Pneumonia, meningitis and septicemia are considered to be the most prominent ones among GBS related infections [9].

 

According to recent studies, one in every 5 pregnant women carry Group B Streptococcus. More than 300.000 cases of invasive GBS disease occur worldwide and 90.000 of them results in stillbirth or infant death. Africa accounts for %54 of these cases. Countries with the highest numbers of invasive GBS cases are India, China, Nigeria, Democratic Republic of Congo and Egypt. [10] Streptococcus agalactiae harmlessly colonizes the microbiota of healthy adults in many cases without symptoms. Intrapartum transmission is common but mode of transmission in non-pregnant adults is still unknown. [11]

 

Escherichia coli is a Gram-negative, facultative aerobic, rod-shaped, coliform bacterium of the genus Escherichia found commonly in the gut of humans & warm-blooded animals [12]. Any age of people can be infected, the elderly and very young children are more prone to develop severe illness and hemolytic uremic syndrome (HUS), older children and young adults can become seriously ill as well. Most E. coli strains are harmless consisting of diverse group of bacteria. Strains of pathogenic E. coli are characterized into six patho types and are related with diarrhea and together referred to as diarrheagenic E. coli. (13) Shiga toxin-producing E. coli (STEC) also referred to as enterohemorrhagic E. coli (EHEC) or Verocytotoxin-producing E. coli (VTEC) a one of the most commonly heard when it comes to foodborne outbreaks, Enterotoxigenic E. coli (ETEC), Enteropathogenic E. coli (EPEC), Enteroaggregative E. coli (EAEC), Enteroinvasive E. coli (EIEC) and Diffusely adherent E. coli (DAEC) [13].

 

In tropical countries, EPEC is a major cause of childhood diarrhea. ETEC sources cases of 11-15% of traveler's diarrhea to those visiting developing countries and around 30-45% cases of traveler's diarrhea visiting Mexico. EAEC causes 30% of cases of traveler's diarrhea. An E coli in  neonatal meningitis carries a mortality rate of 8%, and most of the survivors have developed neurological or developmental abnormalities. The mortality and morbidity associated with E coli bacteremia is the same as that for other aerobic gram-negative bacilli [14] [15]. It is estimated that up to 10% of patients with STEC infection may develop Hemolytic-uremic syndrome (HUS), with a case-fatality rate ranging from 3 to 5%. Overall, HUS is the most common cause of acute renal failure in young children giving neurological complications (such as seizure, stroke and coma) in 25% of HUS patients and around 50% of survivors with chronic renal sequelae, usually mild [16].

 

Disease transmission and illness is due to consumption of contaminated food, unpasteurized (raw) milk, water that has not been disinfected, cattle contact, or interaction with infected people feces. Some selected foods are considered to carry such a high risk of E. coli O157 infection which includes unpasteurized (raw) milk, unpasteurized apple cider, and soft cheeses made from raw milk. Person-to-person contact is also an important mode of transmission through the oral-fecal route [16]. 

 

REFERENCES

1. Matthijs C. Brouwer, Diederik van de Beek, Sebastiaan G. B. Heckenberg, Lodewijk Spanjaard, Jan de Gans. (2006), Community-Acquired Listeria monocytogenes Meningitis in Adults. Clinical Infectious Diseases, Volume 43, Issue 10: 1233–1238. Doi:10.1086/508462.
2. Douglas A. Drevets, Michael S. Bronze. Listeria monocytogenes : epidemiology, human disease, and mechanisms of brain invasion. (2008). FEMS Immunology & Medical Microbiology, Volume 53, Issue 2: 151–165. Doi: 10.1111/j.1574-695X.2008.00404.x
3. J.M. Farber, P.I. Peterkin. (1991). Listeria monocytogenes, a Food-Borne Pathogen. Microbiological Revıews, Volume 53, No 3: 476-511. 
4. Veronica Martinez-Rios, Paw Dalgaard. (2017). Prevalence of Listeria monocytogenes in European cheeses: A systematic review and meta-analysis. Food Control Volume 84: 205-214. Doi:10.1016/j.foodcont.2017.07.020.
5. European Food Safety Authority. (2018). Multi-country outbreak of Listeria monocytogenes serogroup IVb, multi-locus sequence type 6, infections linked to frozen corn and possibly to other frozen vegetables. EFSA Supporting Publications. Volume 15, Issiu 7.  Doi: 10.2903/sp.efsa.2018.EN-1448.
6. Lungu B, Ricke SC, Johnson MG. (2009). Growth, survival, proliferation and pathogenesis of Listeria monocytogenes under low oxygen or anaerobic conditions: a review. Anaerobe: 7-17. Doi: 10.1016/j.anaerobe.2008.08.001.
7. Glaser, P. , Rusniok, C. , Buchrieser, . C., Chevalier, F. , Frangeul, L. , Msadek, T. , Zouine, M. , Couvé, E. , Lalioui, L. , Poyart, C. , Trieu-Cuot, . P. and Kunst, F. (2002), Genome sequence of Streptococcus agalactiae, a pathogen causing invasive neonatal disease. Molecular Microbiology, 45: 1499-1513. doi:10.1046/j.1365-2958.2002.03126.x.
8. Slotved HC, Kong F, Lambertsen L, Sauer S, Gilbert GL (2007). "Serotype IX, a proposed new Streptococcus agalactiae serotype" (PDF). J Clin Microbiol. 45: 2929–2936. doi:10.1128/jcm.00117-07.
9. State Government of Victoria, Department of Human Services. (2003) "Streptococcal infection - group B". Group B streptococcal disease [online].
10. Anna C Seale, Fiorella Bianchi-Jassir, Neal J Russell, Maya Kohli-Lynch, Cally J Tann, Jenny Hall, Lola Madrid, Hannah Blencowe, Simon Cousens, Carol J Baker, Linda Bartlett, Clare Cutland, Michael G Gravett, Paul T Heath, Margaret Ip, Kirsty Le Doare, Shabir A Madhi, Craig E Rubens, Samir K Saha, Stephanie J Schrag, Ajoke Sobanjo-ter Meulen, Johan Vekemans, Joy E Lawn; Estimates of the Burden of Group B Streptococcal Disease Worldwide for Pregnant Women, Stillbirths, and Children, Clinical Infectious Diseases, Volume 65, Issue suppl_2, 6 November 2017, Pages S200–S219, https://doi.org/10.1093/cid/cix664
11. Edwards MS, Baker CJ. (2010). Streptococcus agalactiae (group B streptococcus). "In" Mandell GL, Bennett JE, Dolin R (eds). Principles and practice of infectious diseases (7th. ed.). Elsevier. pp. Cap. 202. ISBN 978-0-443-06839-3.
12. P.L. Conway Microbial ecology of the human large intestine G.R. Gibson, G.T. Macfarlane (Eds.), Human Colonic Bacteria: Role in Nutrition, Physiology and Pathology, CRC Press, Boca Raton, FL, USA (1995), pp. 1-24
13. J.B. Kaper, J.P. Nataro, H.L.T. Mobley Pathogenic Escherichia coli Nat Rev Microbiol, 2 (2) (2004), pp. 123-140
14. Frank C, Werber D, Cramer JP, Askar M, Faber M, an der Heiden M, et al. Epidemic profile of Shiga-toxin-producing Escherichia coli O104:H4 outbreak in Germany. N Engl J Med. 2011 Nov 10. 365(19):1771-80.
15. Lepelletier D, Caroff N, Reynaud A, Richet H. Escherichia coli: epidemiology and analysis of risk factors for infections caused by resistant strains. Clin Infect Dis. 1999 Sep. 29(3):548-52. 
16. http://www.who.int/news-room/fact-sheets/detail/e-coli (Online).