List of antibiotic-resistant bacteria

The evolution of bacteria on a "Mega-Plate" petri dish[1]

A list of antibiotic resistant bacteria is provided below. These bacteria have shown antibiotic resistance (or antimicrobial resistance).

Enzyme NDM-1 (New Delhi Metallo-beta-lactamase-1)

NDM-1 is an enzyme that makes bacteria resistant to a broad range of beta-lactam antibiotics.

NDM-1 (New Delhi Metallo-beta-lactamase-1) originated in India. In Indian hospitals, hospital-acquired infections are common, and with the new super-bugs on rise in India, this can make them dangerous.[2] Mapping of sewage and water supply samples that were NDM-1-positive indicates widespread infection in New Delhi already back in 2011.[2]

NDM-1 was first detected in a Klebsiella pneumoniae isolate from a Swedish patient of Indian origin in 2008. It was later detected in bacteria in India, Pakistan, the United Kingdom, the United States,[3] Canada,[4] and Japan.[5]

Gram positive

Clostridium difficile

Clostridium difficile is a nosocomial pathogen that causes diarrheal disease worldwide.[6][7] Diarrhea caused by C. difficile can be life-threatening. Infections are most frequent in people who have had recent medical and/or antibiotic treatment. C. difficile infections commonly occur during hospitalization.[8]

According to a 2015 CDC report, C. difficile caused almost 500,000 infections in the United States over a year period. Associated with these infections were an estimated 15,000 deaths. The CDC estimates that C. difficile infection costs could amount to $3.8 billion over a 5-year span.[9]

C. difficile colitis is most strongly associated with fluoroquinolones, cephalosporins, carbapenems, and clindamycin.[10][11][12]

Some research suggests the overuse of antibiotics in the raising of livestock is contributing to outbreaks of bacterial infections such as C. difficile.[16]

Antibiotics, especially those with a broad activity spectrum (such as clindamycin) disrupt normal intestinal flora. This can lead to an overgrowth of C. difficile, which flourishes under these conditions. Pseudomembranous colitis can follow, creating generalized inflammation of the colon and the development of "pseudomembrane", a viscous collection of inflammatory cells, fibrin, and necrotic cells.[4] Clindamycin-resistant C. difficile was reported as the causative agent of large outbreaks of diarrheal disease in hospitals in New York, Arizona, Florida, and Massachusetts between 1989 and 1992.[13] Geographically dispersed outbreaks of C. difficile strains resistant to fluoroquinolone antibiotics, such as ciprofloxacin and levofloxacin, were also reported in North America in 2005.[14]

Enterococcus

Multidrug-resistant Enterococcus faecalis and Enterococcus faecium are associated with nosocomial infections.[15] These strains include: penicillin-resistant Enterococcus, vancomycin-resistant Enterococcus, and linezolid-resistant Enterococcus.[16]

Mycobacterium tuberculosis

Tuberculosis (TB) resistant to antibiotics is called MDR TB (multidrug-resistant TB). Globally, MDR TB causes 150,000 deaths annually.[17] The rise of the HIV/AIDS epidemic has contributed to this.[18]

Mycobacterium tuberculosis is an obligate pathogen that has evolved to ensure its persistence in human populations.[19] This is evident in that Mycobacterium tuberculosis must cause a pulmonary disease in order to be successfully transmitted from one person to another. Tuberculosis better known as TB has one of the highest mortality rates among pathogens in the world. Mortality rates have not seen a significant decrease due to its growing resistance to certain antibiotics.[17] Although years of research have been devoted to the creation of a vaccine, one still does not exist. TB is extremely transmissible, contributing significantly to its very high level of virulence. TB was considered one of the most prevalent diseases, and did not have a cure until the discovery of streptomycin by Selman Waksman in 1943.[20] However, the bacteria soon developed resistance. Since then, drugs such as isoniazid and rifampin have been used. M. tuberculosis develops resistance to drugs by spontaneous mutations in its genomes. These types of mutations can lead to genotype and phenotype changes that can contribute to reproductive success, leading to the evolution of resistant bacteria. Resistance to one drug is common, and this is why treatment is usually done with more than one drug. Extensively drug-resistant TB (XDR TB) is TB that is also resistant to the second line of drugs.[18][21]

Resistance of Mycobacterium tuberculosis to isoniazid, rifampin, and other common treatments has become an increasingly relevant clinical challenge. Evidence is lacking for whether these bacteria have plasmids.[22] M. tuberculosis lack the opportunity to interact with other bacteria in order to share plasmids.[22][23]

Mycoplasma genitalium

Mycoplasma genitalium is a small pathogenic bacterium that lives on the ciliated epithelial cells of the urinary and genital tracts in humans. It is still controversial whether or not this bacterium is to be recognized as a sexually transmitted pathogen. Infection with Mycoplasma genitalium sometimes produces clinical symptoms, or a combination of symptoms, but sometimes can be asymptomatic. It causes inflammation in the urethra (urethritis) both in men and women, which is associated with mucopurulent discharge in the urinary tract, and burning while urinating.

Treatment of Mycoplasma genitalium infections is becoming increasingly difficult due to rapidly developing multi-drug resistance, and diagnosis and treatment is further hampered by the fact that M. genitalium infections are not routinely detected.[24] Azithromycin is the most common first-line treatment, but the commonly-used 1 gram single-dose azithromycin treatment can lead to the bacteria commonly developing resistance to azithromycin.[25] An alternative five-day treatment with azithromycin showed no development of antimicrobial resistance.[26] Efficacy of azithromycin against M. genitalium has decreased substantially, which is thought to occur through SNPs in the 23S rRNA gene. The same SNPs are thought to be responsible for resistance against josamycin, which is prescribed in some countries.[27] Moxifloxacin can be used as a second-line treatment in case azithromycin is not able to eradicate the infection. However, resistance against moxifloxacin has been observed since 2007, thought to be due to parC SNPs.[27][28] Tetracyclines, including doxycycline, have a low clinical eradication rate for M. genitalium infections.[29] A few cases have been described where doxycycline, azithromycin and moxifloxacin had all failed, but pristinamycin was still able to eradicate the infection.[27]

Staphylococcus aureus

Staphylococcus aureus is one of the major resistant pathogens. It caused more than 100,000 deaths attributed to AMR in 2019 and MRSA was present in 748,000 global deaths that year.[30] Found on the mucus membranes and the human skin of around a third of the population, it is extremely adaptable to antibiotic pressure. It was one of the earlier bacteria in which penicillin resistance was found, in 1947, just four years after mass-production began. Methicillin was then the antibiotic of choice, but has since been replaced by oxacillin because of significant kidney toxicity. Methicillin-resistant Staphylococcus aureus (MRSA) was first detected in Britain in 1961, and it is now "quite common" in hospitals. MRSA was responsible for 37% of fatal cases of sepsis in the UK in 1999, up from 4% in 1991. Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline, and erythromycin.

Streptococcus

Streptococcus pyogenes (Group A Streptococcus: GAS) infections can usually be treated with many different antibiotics. Strains of S. pyogenes resistant to macrolide antibiotics have emerged; however, all strains remain uniformly susceptible to penicillin.[31]

Resistance of Streptococcus pneumoniae to penicillin and other beta-lactams is increasing worldwide. It was identified as one of six leading pathogens for disease associated with resistance in 2019 and that year there were 596,000 deaths globally of people with drug-resistant infection from the pathogen.[30] The major mechanism of resistance involves the introduction of mutations in genes encoding penicillin-binding proteins. Selective pressure is thought to play an important role, and use of beta-lactam antibiotics has been implicated as a risk factor for infection and colonization. S. pneumoniae is responsible for pneumonia, bacteremia, otitis media, meningitis, sinusitis, peritonitis and arthritis.[31]

Gram negative

Campylobacter

Campylobacter causes diarrhea (often bloody), fever, and abdominal cramps. Serious complications such as temporary paralysis can also occur. Physicians rely on ciprofloxacin and azithromycin for treating patients with severe disease although Campylobacter is showing resistance to these antibiotics.[8]

Neisseria gonorrhoeae

Neisseria gonorrhoeae is a sexually transmitted pathogen that causes gonorrhea, a sexually transmitted disease that can result in discharge and inflammation at the urethra, cervix, pharynx, or rectum.[8] It can cause pelvic pain, pain on urination, penile and vaginal discharge, as well as systemic symptoms. It can also cause severe reproductive complications.[8]

Gamma proteobacteria

Enterobacteriaceae

As of 2013 hard-to-treat or untreatable infections of carbapenem-resistant Enterobacteriaceae (CRE), also known as carbapenemase-producing Enterobacteriaceae (CPE), were increasing among patients in medical facilities. CRE are resistant to nearly all available antibiotics. Almost half of hospital patients who get bloodstream CRE infections die from the infection.[8]

Klebsiella pneumoniae

Klebsiella pneumoniae carbapenemase (KPC)-producing bacteria are a group of emerging highly drug-resistant Gram-negative bacilli causing infections associated with significant morbidity and mortality whose incidence is rapidly increasing in a variety of clinical settings around the world. Klebsiella pneumoniae was identified as one of six leading pathogens for disease associated with resistance in 2019 and that year there were 642,000 deaths globally of people with drug-resistant infection from the pathogen.[30] Klebsiella pneumoniae includes numerous mechanisms for antibiotic resistance, many of which are located on highly mobile genetic elements.[32] Carbapenem antibiotics (heretofore often the treatment of last resort for resistant infections) are generally not effective against KPC-producing organisms.[33]

Salmonella and E. coli

Infection with Escherichia coli and Salmonella can result from the consumption of contaminated food and polluted water. Both of these bacteria are well known for causing nosocomial (hospital-linked) infections, and often, these strains found in hospitals are antibiotic resistant because of adaptations to wide spread antibiotic use.[34] When both bacteria are spread, serious health conditions arise. Many people are hospitalized each year after becoming infected, with some dying as a result. Since 1993, some strains of E. coli have become resistant to multiple types of fluoroquinolone antibiotics. E. coli was identified as one of the six leading pathogens for deaths associated with resistance in 2019 and that year there were 829,000 deaths globally of people with drug-resistant infection from the pathogen.[30]

Although mutation alone plays a huge role in the development of antibiotic resistance, a 2008 study found that high survival rates after exposure to antibiotics could not be accounted for by mutation alone.[35] This study focused on the development of resistance in E. coli to three antibiotic drugs: ampicillin, tetracycline, and nalidixic acid. The researchers found that some antibiotic resistance in E. coli developed because of epigenetic inheritance rather than by direct inheritance of a mutated gene. This was further supported by data showing that reversion to antibiotic sensitivity was relatively common as well. This could only be explained by epigenetics.[35] Epigenetics is a type of inheritance in which gene expression is altered rather than the genetic code itself. There are many modes by which this alteration of gene expression can occur, including methylation of DNA and histone modification; however, the important point is that both inheritance of random mutations and epigenetic markers can result in the expression of antibiotic resistance genes.[35]

Resistance to polymyxins first appear in 2011.[36] An easier way for this resistance to spread, a plasmid known as MCR-1 was discovered in 2015.[36]

Pseudomonadales

Acinetobacter

Acinetobacter is a gram-negative bacteria that causes pneumonia or bloodstream infections in critically ill patients. Multidrug-resistant Acinetobacter have become very resistant to antibiotics.[8] Acinetobacter baumannii was identified as one of the six leading pathogens for deaths associated with resistance in 2019 and that year there were 423,000 deaths globally of people with drug-resistant infection from the pathogen.[30]

On November 5, 2004, the Centers for Disease Control and Prevention (CDC) reported an increasing number of Acinetobacter baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom and in Afghanistan during Operation Enduring Freedom were treated. Most of these showed multidrug resistance (MRAB), with a few isolates resistant to all drugs tested.[37][38]

Pseudomonas aeruginosa

Pseudomonas aeruginosa is a highly prevalent opportunistic pathogen. It was identified as one of the six leading pathogens for deaths associated with resistance in 2019 and that year there were 334,000 deaths globally of people with drug-resistant infection from the pathogen.[30] One of the most worrisome characteristics of P. aeruginosa is its low antibiotic susceptibility, which is attributable to a concerted action of multidrug efflux pumps with chromosomally encoded antibiotic resistance genes (e.g., mexAB-oprM, mexXY) and the low permeability of the bacterial cellular envelopes.[39] P. aeruginosa has the ability to produce 4-hydroxy-2-alkylquinolines (HAQs), and it has been found that HAQs have prooxidant effects and overexpressing modestly increased susceptibility to antibiotics. The study experimented with the P. aeruginosa biofilms and found that a disruption of relA and spoT genes produced an inactivation of the Stringent response (SR) in cells with nutrient limitation, which provides cells be more susceptible to antibiotics.[40]

See also

References

  1. ↑ Baym, Michael; Lieberman, Tami D.; Kelsic, Eric D.; Chait, Remy; Gross, Rotem; Yelin, Idan; Kishony, Roy (2016-09-09). "Spatiotemporal microbial evolution on antibiotic landscapes". Science. 353 (6304): 1147–1151. Bibcode:2016Sci...353.1147B. doi:10.1126/science.aag0822. ISSN 0036-8075. PMC 5534434. PMID 27609891.
  2. 1 2 Walsh, Timothy R; Weeks, Janis; Livermore, David M; Toleman, Mark A (2011). "Dissemination of NDM-1 positive bacteria in the New Delhi environment and its implications for human health: an environmental point prevalence study". The Lancet Infectious Diseases. 11 (5): 355–362. doi:10.1016/s1473-3099(11)70059-7. PMID 21478057.
  3. ↑ Marilynn Marchione (13 September 2010). "New drug-resistant superbugs found in 3 states". Boston Globe.
  4. ↑ Madeleine White (21 August 2010). "Superbug detected in GTA". Toronto Star.
  5. ↑ Yuasa, Shino (8 September 2010). "Japan confirms first case of superbug gene". The Boston Globe.
  6. ↑ Gerding DN, Johnson S, Peterson LR, Mulligan ME, Silva J (1995). "Clostridium difficile-associated diarrhea and colitis". Infect. Control Hosp. Epidemiol. 16 (8): 459–477. doi:10.1086/648363. PMID 7594392.
  7. ↑ McDonald LC (2005). "Clostridium difficile: responding to a new threat from an old enemy". Infect. Control Hosp. Epidemiol. 26 (8): 672–5. doi:10.1086/502600. PMID 16156321.
  8. 1 2 3 4 5 6 "Biggest Threats – Antibiotic/Antimicrobial Resistance – CDC". www.cdc.gov. Retrieved 2016-05-05.
  9. ↑ "CDC Press Releases". CDC. January 2016. Retrieved 2016-05-05.
  10. ↑ Baxter R, Ray GT, Fireman BH (January 2008). "Case-control study of antibiotic use and subsequent Clostridium difficile-associated diarrhea in hospitalized patients". Infection Control and Hospital Epidemiology. 29 (1): 44–50. doi:10.1086/524320. PMID 18171186. S2CID 39290661.
  11. ↑ Gifford AH, Kirkland KB (December 2006). "Risk factors for Clostridium difficile-associated diarrhea on an adult hematology-oncology ward". European Journal of Clinical Microbiology & Infectious Diseases. 25 (12): 751–5. doi:10.1007/s10096-006-0220-1. PMID 17072575. S2CID 23822514.
  12. ↑ Palmore TN, Sohn S, Malak SF, Eagan J, Sepkowitz KA (August 2005). "Risk factors for acquisition of Clostridium difficile-associated diarrhea among outpatients at a cancer hospital". Infection Control and Hospital Epidemiology. 26 (8): 680–4. doi:10.1086/502602. PMC 5612438. PMID 16156323.
  13. ↑ Johnson S, Samore MH, Farrow KA, Killgore GE, Tenover FC, Lyras D, Rood JI, DeGirolami P, Baltch AL, Rafferty ME, Pear SM, Gerding DN (1999). "Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals". New England Journal of Medicine. 341 (23): 1645–1651. doi:10.1056/NEJM199911253412203. PMID 10572152.
  14. ↑ Loo VG, Poirier L, Miller MA, Oughton M, Libman MD, Michaud S, Bourgault AM, Nguyen T, Frenette C, Kelly M, Vibien A, Brassard P, Fenn S, Dewar K, Hudson TJ, Horn R, René P, Monczak Y, Dascal A (2005). "A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality". N Engl J Med. 353 (23): 2442–9. doi:10.1056/NEJMoa051639. PMID 16322602.
  15. ↑ Hidron AI, Edwards JR, Patel J, Horan TC, Sievert DM, Pollock DA, Fridkin SK (November 2008). National Healthcare Safety Network Team; Participating National Healthcare Safety Network Facilities. "NHSN annual update: antimicrobial-resistant pathogens associated with healthcare-associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006–2007". Infect Control Hosp Epidemiol. 29 (11): 996–1011. doi:10.1086/591861. PMID 18947320. S2CID 205988392.
  16. ↑ Kristich, Christopher J.; Rice, Louis B.; Arias, Cesar A. (2014-01-01). Gilmore, Michael S.; Clewell, Don B.; Ike, Yasuyoshi; Shankar, Nathan (eds.). Enterococcal Infection—Treatment and Antibiotic Resistance. Boston: Massachusetts Eye and Ear Infirmary. PMID 24649502.
  17. 1 2 "Antimicrobial Resistance Still Poses a Public Health Threat: A Conversation With Edward J. Septimus, MD, FIDSA, FACP, FSHEA, Clinical Professor of Internal Medicine at Texas A&M Health Science Center". Agency for Healthcare Research and Quality. 2013-04-17. Retrieved 2013-09-26.
  18. 1 2 LoBue P (2009). "Extensively drug-resistant tuberculosis". Current Opinion in Infectious Diseases. 22 (2): 167–73. doi:10.1097/QCO.0b013e3283229fab. PMID 19283912. S2CID 24995375.
  19. ↑ Brites, D; Gagneux, S (2013-04-17). "Co-evolution of Mycobacterium tuberculosis and Homo sapiens, Brites, D., & Gagneux, S. (2015)". Immunol Rev. 264 (1): 6–24. doi:10.1111/imr.12264. PMC 4339235. PMID 25703549.
  20. ↑ Herzog H (1998). "History of Tuberculosis". Respiration. 65 (1): 5–15. doi:10.1159/000029220. PMID 9523361.
  21. ↑ Gao, Qian; Li, Xia (2010). "Transmission of MDR tuberculosis". Drug Discovery Today: Disease Mechanisms. 7: e61–e65. doi:10.1016/j.ddmec.2010.09.006.
  22. 1 2 Zainuddin ZF, Dale JW (1990). "Does Mycobacterium tuberculosis have plasmids?". Tubercle. 71 (1): 43–9. doi:10.1016/0041-3879(90)90060-l. PMID 2115217.
  23. ↑ Louw GE, Warren RM, Gey van Pittius NC, McEvoy CR, Van Helden PD, Victor TC (2009). "A Balancing Act: Efflux/Influx in Mycobacterial Drug Resistance". Antimicrobial Agents and Chemotherapy. 53 (8): 3181–9. doi:10.1128/AAC.01577-08. PMC 2715638. PMID 19451293.
  24. ↑ Suneta, Soni; Parkhouse, Andy; Gillian, Dean (24 April 2017). "Macrolide and quinolone-resistant Mycoplasma genitalium in a man with persistent urethritis: the tip of the British iceberg?". Sexually Transmitted Infections. 93 (8): 556–557. doi:10.1136/sextrans-2016-053077. PMID 28438948. S2CID 9178150. Retrieved 6 October 2017.
  25. ↑ Yew, H. S.; Anderson, T.; Coughlan, E.; Werno, A. (2011). "Induced macrolide resistance in Mycoplasma genitalium isolates from patients with recurrent nongonococcal urethritis". Journal of Clinical Microbiology. 49 (4): 1695–1696. doi:10.1128/JCM.02475-10. PMC 3122813. PMID 21346049.
  26. ↑ Anagrius, Carin; Loré, Britta; Jensen, Jørgen Skov; Coenye, Tom (2013). "Treatment of Mycoplasma genitalium. Observations from a Swedish STD Clinic". PLOS ONE. 8 (4): e61481. Bibcode:2013PLoSO...861481A. doi:10.1371/journal.pone.0061481. PMC 3620223. PMID 23593483.
  27. 1 2 3 Unemo, Magnus; Jensen, Jorgen S. (10 January 2017). "Antimicrobial-resistant sexually transmitted infections: gonorrhoea and Mycoplasma genitalium". Nature Reviews Urology. 14 (3): 139–125. doi:10.1038/nrurol.2016.268. PMID 28072403. S2CID 205521926.
  28. ↑ "Mycoplasma Genitalium Treatment Choices". www.theonlineclinic.co.uk.
  29. ↑ Jensen, J.S.; Cusini, M.; Gomberg, M.; Moi, M. (9 August 2016). "2016 European guideline on Mycoplasma genitalium infections". Journal of the European Academy of Dermatology and Venereology. 30 (10): 1650–1656. doi:10.1111/jdv.13849. PMID 27505296.
  30. 1 2 3 4 5 6 Murray, Christopher JL; Ikuta, Kevin Shunji; Sharara, Fablina; Swetschinski, Lucien; Aguilar, Gisela Robles; Gray, Authia; Han, Chieh; Bisignano, Catherine; Rao, Puja; Wool, Eve; Johnson, Sarah C. (2022-01-19). "Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis". The Lancet. 0 (0). doi:10.1016/S0140-6736(21)02724-0. ISSN 0140-6736. PMID 35065702.
  31. 1 2 Albrich WC, Monnet DL, Harbarth S (2004). "Antibiotic selection pressure and resistance in Streptococcus pneumoniae and Streptococcus pyogenes". Emerg. Infect. Dis. 10 (3): 514–7. doi:10.3201/eid1003.030252. PMC 3322805. PMID 15109426.
  32. ↑ Hudson, Corey; Bent, Zachary; Meagher, Robert; Williams, Kelly (June 7, 2014). "Resistance Determinants and Mobile Genetic Elements of an NDM-1-Encoding Klebsiella pneumoniae Strain". PLOS ONE. 9 (6): e99209. Bibcode:2014PLoSO...999209H. doi:10.1371/journal.pone.0099209. PMC 4048246. PMID 24905728.
  33. ↑ Arnold RS, Thom KA, Sharma S, Phillips M, Kristie Johnson J, Morgan DJ (2011). "Emergence of Klebsiella pneumoniae Carbapenemase-Producing Bacteria". Southern Medical Journal. 104 (1): 40–5. doi:10.1097/SMJ.0b013e3181fd7d5a. PMC 3075864. PMID 21119555.
  34. ↑ Davies J, Davies D (2010). "Origins and Evolution of Antibiotic Resistance". Microbiol Mol Biol Rev. 74 (3): 417–433. doi:10.1128/MMBR.00016-10. PMC 2937522. PMID 20805405.
  35. 1 2 3 Adam M, Murali B, Glenn NO, Potter SS (2008). "Epigenetic inheritance based evolution of antibiotic resistance in bacteria". BMC Evol. Biol. 8: 52. doi:10.1186/1471-2148-8-52. PMC 2262874. PMID 18282299.
  36. 1 2 Reardon, Sara (21 December 2015). "Spread of antibiotic-resistance gene does not spell bacterial apocalypse — yet". Nature. doi:10.1038/nature.2015.19037. S2CID 182042290.
  37. ↑ Centers for Disease Control Prevention (CDC). (2004). "Acinetobacter baumannii infections among patients at military medical facilities treating injured U.S. service members, 2002–2004". MMWR Morb. Mortal. Wkly. Rep. 53 (45): 1063–6. PMID 15549020.
  38. ↑ "Medscape abstract on Acinetobacter baumannii: Acinetobacter baumannii: An Emerging Multidrug-resistant Threat". membership only website
  39. ↑ Poole K (2004). "Efflux-mediated multiresistance in Gram-negative bacteria". Clinical Microbiology and Infection. 10 (1): 12–26. doi:10.1111/j.1469-0691.2004.00763.x. PMID 14706082.
  40. ↑ Nguyen D, Joshi-Datar A, Lepine F, Bauerle E, Olakanmi O, Beer K, McKay G, Siehnel R, Schafhauser J, Wang Y, Britigan BE, Singh PK (2011). "Active Starvation Responses Mediate Antibiotic Tolerance in Biofilms and Nutrient-Limited Bacteria". Science. 334 (6058): 982–6. Bibcode:2011Sci...334..982N. doi:10.1126/science.1211037. PMC 4046891. PMID 22096200.
The offline app allows you to download all of Wikipedia's medical articles in an app to access them when you have no Internet.
Wikipedia's health care articles can be viewed offline with the Medical Wikipedia app.
This article is issued from Offline. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.