Elizabethkingia anophelis

Elizabethkingia anophelis
Scientific classification edit
Domain: Bacteria
Phylum: Bacteroidota
Class: Flavobacteriia
Order: Flavobacteriales
Family: Weeksellaceae
Genus: Elizabethkingia
Species:
E. anophelis
Binomial name
Elizabethkingia anophelis
Kämpfer et al. 2011

Elizabethkingia anophelis is a yellow-pigmented, rod-shaped, gram-negative bacterium in the Flavobacteriaceae family.[1] Elizabethkingia is isolated from the midgut of Anopheles gambiae G3 mosquitoes reared in captivity.[2][1] The genus Elizabethkingia, named for former US Centers for Disease Control and Prevention (CDC) microbiologist Elizabeth O. King,[3] also includes E. meningoseptica which causes neonatal sepsis and infections in immunocompromised persons, E. endophytica, and E. miricola.

The possibility of the role of mosquitoes in the maintenance and transmission of E. anophelis remains unclear.[4]

Biology and biochemistry

Genomic comparisons-The genome of E. anophelis 296-96 center compared to E. anophelis 344-1 innermost circle- ring 1

Morphology

E. anophelis is a Gram-negative bacterium that appears slightly yellow and is characterized by its non-motile and non-spore-forming nature.[1] Its cells typically have a rod-like shape and a size of around 4.03 Mbp, with an average GC content of 35.4%.[2] E. anophelis is known to be a prevalent inhabitant in the gut of Anopheles gambiae mosquitoes, the primary vector of malaria, and it is also capable of causing disease in humans.[3] In 2013, E. anophelis was identified as a human pathogen in Central Africa during an outbreak that occurred in an intensive care unit in Singapore. Both clinical cases reported multidrug resistance.[3]

Metabolism

Elizabethkingia anophelis uses complex carbohydrates, also known as glycans, in its metabolism. It has a starch-utilization system (Sus) that includes several proteins.[2] The bacterium's major fatty acids exhibit a complex polar lipid profile consisting of di-phosphatidylglycerol, phosphatidylinositol, the complex polar lipid profile also consists of an unknown phospholipid, and unknown polar lipids and glycolipids. E. anophelis produces several hemolysins that are thought to assist in the digestion of erythrocytes in the mosquito's gut.[2]

The bacterium utilizes polymers by using numerous TonB-dependent transporters (TBDTs) with various substrate specificities. These transporters actively take up essential nutrients and other substrates, including but not limited to iron complexes, vitamin B12, nickel, carbohydrates, and colicin.[2] To energize the transport process, TBDTs interact with the TonB complex, a cytoplasmic transmembrane assembly of proteins coupled with the TonB in the periplasm.[2]

E. anophelis is known for its intrinsic resistance to a wide range of antibiotics due to mechanisms such as enzymatic degradation of the drug, alteration of the target drug site, and direct extrusion of the drug from the cells using efflux pumps as well as β-lactamases.[2] The bacterium has also evolved to initiate a stress response when the cell begins to undergo oxidative stress. E. anophelis also produces OxyR regulon and antioxidants as a stress response to defend against the oxidative stress that can be associated with mosquitoes during the process of blood digestion. One study suggests that features of E. anophelis including growth, hydrogen peroxide tolerance, cell attachment, and biofilm formation are due to the presence of hemoglobin in the gut of the mosquito.[2]

Ecology

Anopheles mosquito

Elizabethkingia anophelis has a unique ecological niche, as it is primarily found in the midgut of the Anopheles mosquito, which is a known malaria vector.[5] It is also a pathogen that can cause infections in humans, particularly those with compromised immune systems. The bacterium has a mutualistic relationship with the mosquito, where it helps digest blood meals and promote the growth of other gut microbiota.[2] E. anophelis has also been found in diverse environments such as soil, water, and hospital settings. In hospital settings, it has been isolated from a range of sources including blood, respiratory secretions, and wounds.[6]

Role in disease

E. anophelis has been reported to cause neonatal meningitis in the Central African Republic, and a nosocomial outbreak has been reported in an intensive care unit in Singapore.[7]

Transmission

The transmission route remains unknown.[8]

Diagnosis

Cases are typically diagnosed through the culture of body fluids, most commonly blood testing. [9]

Treatment

The treatment of Elizabethkingia anophelis infections can vary depending on the severity of the infection and the susceptibility of the bacteria to antimicrobial agents. In general, treatment may involve the use of antibiotics E. anophelis has properties of antibiotic resistance making antibiotic susceptibility testing a must to guide the choice of antimicrobial therapy.[10]

E. anophelis has shown resistance to many antibiotics, which can complicate the treatment plan. Some of the antibiotic resistance occurs when the bacterium is introduced to carbapenems, cephalosporins, and aminoglycosides.[9] If deemed effective by the patient’s healthcare provider an antibiotic combination may be prescribed.

In addition to antibiotics, a healthcare provider can choose to supplement care with fluids and oxygen therapy. These additives may be necessary for severely ill patients.[11]

Epidemiology

A 2014 study showed that some Elizabethkingia infections that had been attributed to Elizabethkingia meningoseptica were instead caused by Elizabethkingia anophelis.[12]

An outbreak centered in Wisconsin began in early November 2015, with 48 people confirmed infected in 12 counties and at least 18 deaths by March 9, 2016, and four new cases documented just in the week of 2–9 March 2016.[13] By April 13, 2016, the infection had spread first to western Michigan and then to Illinois, with 61 confirmed cases and 21 deaths.[10]

The CDC notes that the infections leading to death occurred in persons over the age of 65 who had other health conditions, leading to uncertainty as to whether E. anophelis was the cause of death, or if the cause was a combination of E. anophelis and preexisting health conditions.[14]

History

Elizabeth King: E. anophelis was named after she discovered Elizabethkingia bacteria

In 1959, Elizabethkingia was discovered by a microbiologist at the United States Center for Disease Control, and in 2011, Kampfer et al. isolated Elizabethkingia anophelis from the midgut of Anopheles gambiae.[1]

References

  1. 1 2 3 4 Kämpfer, P; Matthews, H; Glaeser, SP; Martin, K; Lodders, N; Faye, I (November 2011). "Elizabethkingia anophelis sp. nov., isolated from the midgut of the mosquito Anopheles gambiae". International Journal of Systematic and Evolutionary Microbiology. 61 (Pt 11): 2670–5. doi:10.1099/ijs.0.026393-0. PMID 21169462.
  2. 1 2 3 4 5 6 7 8 9 Lindh, J.M.; Borg-Karlson, A.-K.; Faye, I. (2008). "Transstadial and horizontal transfer of bacteria within a colony of Anopheles gambiae (Diptera: Culicidae) and oviposition response to bacteria-containing water". Acta Tropica. 107 (3): 242–250. doi:10.1016/j.actatropica.2008.06.008. PMID 18671931.
  3. 1 2 3 Kim, Kwang Kyu; Kim, Myung Kyum; Lim, Ju Hyoung; Park, Hye Yoon; Lee, Sung-Taik (1 May 2005). "Transfer of Chryseobacterium meningosepticum and Chryseobacterium miricola to Elizabethkingia gen. nov. as Elizabethkingia meningoseptica comb. nov. and Elizabethkingia miricola comb. nov". International Journal of Systematic and Evolutionary Microbiology. 55 (3): 1287–1293. doi:10.1099/ijs.0.63541-0. PMID 15879269.
  4. ↑ Lau, Susanna K.P.; Wu, Alan K.L.; Teng, Jade L.L.; Tse, Herman; Curreem, Shirly O.T.; Tsui, Stephen K.W.; et al. (February 2015). "Evidence for Elizabethkingia anophelis Transmission from Mother to Infant, Hong Kong". Emerging Infectious Diseases. 21 (2): 232–241. doi:10.3201/eid2102.140623. PMC 4313635. PMID 25625669.
  5. ↑ Kukutla, Phanidhar; Lindberg, Bo G.; Pei, Dong; Rayl, Melanie; Yu, Wanqin; Steritz, Matthew; Faye, Ingrid; Xu, Jiannong (2014-05-19). Tu, Zhijian (ed.). "Insights from the Genome Annotation of Elizabethkingia anophelis from the Malaria Vector Anopheles gambiae". PLoS ONE. 9 (5): e97715. doi:10.1371/journal.pone.0097715. ISSN 1932-6203. Archived from the original on 2023-07-01. Retrieved 2023-05-13.
  6. ↑ "Elizabethkingia". Wisconsin Department of Health Services. 2021-09-28. Archived from the original on 2023-04-27. Retrieved 2023-05-02.
  7. ↑ Lau, Susanna K.P.; Wu, Alan K.L.; Teng, Jade L.L.; Tse, Herman; Curreem, Shirly O.T.; Tsui, Stephen K.W.; et al. (February 2015). "Evidence for Elizabethkingia anophelis Transmission from Mother to Infant, Hong Kong". Emerging Infectious Diseases. 21 (2): 232–241. doi:10.3201/eid2102.140623. PMC 4313635. PMID 25625669.
  8. ↑ "About Elizabethkingia | Elizabethkingia | CDC". www.cdc.gov. 2018-10-12. Archived from the original on 2023-04-27. Retrieved 2023-04-27.
  9. 1 2 Vallie, Sarah. "What Is Elizabethkingia?". WebMD. Archived from the original on 2023-04-27. Retrieved 2023-04-27.
  10. 1 2 "Multistate Outbreak of Infections Caused by Elizabethkingia anophelis". Centers for Disease Control and Prevention (CDC). March 30, 2016. Archived from the original on April 15, 2016. Retrieved April 13, 2016.
  11. ↑ "Elizabethkingia Infections Treatment & Management: Approach Considerations, Prevention". 2023-03-03. Archived from the original on 2023-05-03. Retrieved 2023-05-13. {{cite journal}}: Cite journal requires |journal= (help)
  12. ↑ Teo, J.; Tan, S. Y.-Y.; Liu, Y.; Tay, M.; Ding, Y.; Li, Y.; Kjelleberg, S.; Givskov, M.; Lin, R. T. P.; Yang, L. (6 May 2014). "Comparative Genomic Analysis of Malaria Mosquito Vector-Associated Novel Pathogen Elizabethkingia anophelis". Genome Biology and Evolution. 6 (5): 1158–1165. doi:10.1093/gbe/evu094. PMC 4041001. PMID 24803570.
  13. ↑ Baillon, Rachelle (9 March 2016). "Elizabethkingia: It may be "weeks rather than days" before we know source of infection". FOX6Now.com. Milwaukee, Wisconsin. Archived from the original on 14 April 2016. Retrieved 15 April 2016.
  14. ↑ "Recent Outbreaks". Centers for Disease Control and Prevention (CDC). June 16, 2016. Archived from the original on September 19, 2016. Retrieved September 18, 2016.
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