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Shigellosis

From Wikipedia, the free encyclopedia
Infection of the intestines by Shigella bacteria

Medical condition
Shigellosis
Other namesBacillary dysentery, Marlow syndrome
Shigella seen in a stool sample
SpecialtyInfectious disease
SymptomsDiarrhea, fever, abdominal pain[1]
ComplicationsReactive arthritis,sepsis,seizures,hemolytic uremic syndrome[1]
Usual onset1–2 days post exposure[1]
DurationUsually 5–7 days[1]
CausesShigella[1]
Diagnostic methodStool culture[1]
PreventionHandwashing[1]
TreatmentDrinking fluids and rest[1]
MedicationAntibiotics (severe cases)[1]
Frequency>80 million[2]
Deaths700,000[2]

Shigellosis, known historically asdysentery, is an infection of theintestines caused byShigella bacteria.[1][3] Symptoms generally start one to two days after exposure and includediarrhea,fever,abdominal pain, andfeeling the need to pass stools even when the bowels are empty.[1] The diarrhea may be bloody.[1] Symptoms typically last five to seven days and it may take several months before bowel habits return entirely to normal.[1] Complications can includereactive arthritis,sepsis,seizures, andhemolytic uremic syndrome.[1]

Shigellosis is caused by four specific types ofShigella.[2] These are typically spread by exposure to infectedfeces.[1] This can occur via contaminated food, water, or hands orsexual contact.[1][4] Contamination may be spread byflies or when changingdiapers (nappies).[1] Diagnosis is bystool culture.[1]

The risk of infection can be reduced by properly washing the hands.[1] There is novaccine.[1] Shigellosis usually resolves without specific treatment.[1] Rest, and sufficient fluids by mouth, are recommended.[1]Bismuth subsalicylate may help with the symptoms; however, medications that slow the bowels such asloperamide are not recommended.[1] In severe casesantibiotics may be used butresistance is common.[1][5] Commonly used antibiotics includeciprofloxacin andazithromycin.[1]

A 2005 report by theWorld Health Organization estimated that shigellosis occurs in at least 80 million people and results in about 700,000 deaths a year globally.[2] Most cases occur in thedeveloping world.[2] Young children are most commonly affected.[1]Outbreaks of disease may occur in childcare settings and schools.[1] It is also relatively common among travelers.[1] In the United States about half a million cases occur a year.[1]

Signs and symptoms

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Signs and symptoms may range from mildabdominal discomfort to severedysentery characterized bycramps,diarrhea, with slimy-consistent stools, fever, blood,pus, ormucus in stools ortenesmus.[6][7] Onset time is 12 to 96 hours, and recovery takes 5 to 7 days.[8]Infections are associated withmucosal ulceration,rectal bleeding, and drasticdehydration.Reactive arthritis andhemolytic uremic syndrome are possible sequelae that have been reported in the aftermath of shigellosis.[citation needed]

The most common neurological symptom includesseizures.[9]

Cause

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Bacteria

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Shigellosis is caused by a bacterial infection withShigella,[1] a bacterium that is genetically similar to and was once classified asE. coli.[10] There are threeserogroups and oneserotype ofShigella:

The probability of being infected by any given strain ofShigella varies around the world. For instance,S. sonnei is the most common in the United States, whileS. dysenteriae andS. boydii are rare there.[1]

Transmission

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Shigella is transmitted through thefecal-oral route of individuals infected with the disease, whether or not they are exhibiting symptoms.[1][11] Long-termcarriers of the bacteria are rare.[11] The bacteria can infect not just humans but otherprimates as well.[12]

Mechanism

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Upon ingestion, the bacteria pass through thegastrointestinal tract until they reach thesmall intestine. There they begin to multiply until they reach thelarge intestine.[13] In the large intestine, the bacteria cause cell injury and the beginning stages of Shigellosis via two main mechanisms: direct invasion of epithelial cells in the large intestine and production of enterotoxin 1 and enterotoxin 2.[13]

Unlike other bacteria,Shigella is not destroyed by thegastric acid in the stomach. As a result, it takes only 10 to 200 cells to cause an infection.[13] Thisinfectious dose is several orders of magnitude smaller than that of other species of bacteria (e.g.,cholera, caused by the bacteriumVibrio cholerae, has an infectious dose between 108 and 1011 cells).[14]

Diagnosis

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The diagnosis of shigellosis is made by isolating the organism from diarrheal fecal sample cultures.Shigella species are negative for motility and are generally not lactose fermenters, butS. sonnei can ferment lactose.[15] They typically do not produce gas from carbohydrates (with the exception of certain strains ofS. flexneri) and tend to be overall biochemically inert.Shigella should also be urea hydrolysis negative. When inoculated to atriple sugar iron slant, they react as follows: K/A, gas -, and H2S -. Indole reactions are mixed, positive and negative, with the exception ofS. sonnei, which is always indole negative. Growth onHektoen enteric agar produces bluish-green colonies forShigella and bluish-green colonies with black centers forSalmonella.[citation needed]

Prevention

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Simple precautions can be taken to prevent getting shigellosis: wash hands before handling food and thoroughly cook all food before eating. The primary prevention methods are improved sanitation and personal and food hygiene, but a low-cost and efficacious vaccine would complement these methods.[16]

Since shigellosis is spread very quickly among children, keeping infected children out of daycare for 24 hours after their symptoms have disappeared, will decrease the occurrence of shigellosis in daycares.[17]

Vaccine

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Currently, no licensed vaccine targetingShigella exists. Several vaccine candidates forShigella are in various stages of development including live attenuated, conjugate, ribosomal, and proteosome vaccines.[16][18][19]Shigella has been a longstandingWorld Health Organization target for vaccine development, and sharp declines in age-specific diarrhea/dysentery attack rates for this pathogen indicate that natural immunity does develop following exposure; thus, vaccination to prevent the disease should be feasible.Shigella species are resistant to many antibiotics,[1] so vaccination is an important part of the strategy to reduce morbidity and mortality.[16]

Treatment

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Treatment consists mainly of replacing fluids and salts lost because of diarrhea. Replacement by mouth is satisfactory for most people, but some may need to receive fluids intravenously. Antidiarrheal drugs (such asdiphenoxylate orloperamide) may prolong the infection and should not be used.[20]

Antibiotics

[edit]

Antibiotics should only be used in severe cases or for certain populations with mild symptoms (elderly, immunocompromised, food service industry workers, child care workers). ForShigella-associated diarrhea,antibiotics shorten the length of infection,[21] but they are usually avoided in mild cases because manyShigella strains are becoming resistant to common antibiotics.[22] Furthermore, effective medications are often in short supply in developing countries, which carry the majority of the disease burden fromShigella. Antidiarrheal agents may worsen the sickness, and should be avoided.[23]

In most cases, the disease resolves within four to eight days without antibiotics. Severe infections may last three to six weeks. Antibiotics, such astrimethoprim-sulfamethoxazole,ciprofloxacin may be given when the person is very young or very old, when the disease is severe, or when the risk of the infection spreading to other people is high. Additionally,ampicillin (but notamoxicillin) was effective in treating this disease previously, but now the first choice of drug ispivmecillinam.[24]

Epidemiology

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Insufficient data exist,[25] but it is estimated to have caused the death of 34,000 children under the age of five in 2013, and 40,000 deaths in people over five years of age.[16]Shigella also causes about 580,000 cases annually among travelers and military personnel from industrialized countries.[26]

An estimated 500,000 cases of shigellosis occur annually in the United States.[27] Infants, the elderly, and the critically ill are susceptible to the most severe symptoms of disease, but all humans are susceptible to some degree. Individuals with acquired immune deficiency syndrome (AIDS) are more frequently infected withShigella.[28] Shigellosis is a more common and serious condition in the developing world; fatality rates of shigellosis epidemics in developing countries can be 5–15%.[29]

Orthodox Jewish communities (OJCs) are a known risk group for shigellosis;Shigella sonnei is cyclically epidemic in these communities in Israel, with sporadic outbreaks occurring elsewhere among these communities. "Through phylogenetic and genomic analysis, we showed that strains from outbreaks in OJCs outside of Israel are distinct from strains in the general population and relate to a single multidrug-resistant sublineage ofS. sonnei that prevails in Israel. FurtherBayesian phylogenetic analysis showed that this strain emerged approximately 30 years ago, demonstrating the speed at which antimicrobial drug–resistant pathogens can spread widely through geographically dispersed, but internationally connected, communities."[30]

See also

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References

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  1. ^abcdefghijklmnopqrstuvwxyzaaabacadaeafagah"General Information|Shigella – Shigellosis | CDC".www.cdc.gov. 3 August 2016.Archived from the original on 16 April 2017. Retrieved20 April 2017.
  2. ^abcdeGuidelines for the control of shigellosis, including epidemics due toShigella dysenteriae type 1(PDF). WHO. 2005. p. 2.ISBN 978-92-4-159330-4.Archived(PDF) from the original on 21 August 2017. Retrieved20 April 2017.
  3. ^"Factsheet about shigellosis".European Centre for Disease Prevention and Control. 8 July 2010.
  4. ^Antibiotic Resistance Threats in the United States, 2019(PDF). CDC. 2019. p. 9.Archived(PDF) from the original on 10 October 2022.
  5. ^"Update – CDC Recommendations for Managing and ReportingShigella Infections with Possible Reduced Susceptibility to Ciprofloxacin".emergency.cdc.gov. 7 June 2018. Retrieved16 June 2018.
  6. ^"Shigellosis". The Merck Manual Home Health Handbook.Archived from the original on 4 January 2012. Retrieved10 February 2012.
  7. ^Niyogi, SK (April 2005). "Shigellosis".Journal of Microbiology (Seoul, Korea).43 (2):133–43.PMID 15880088.
  8. ^"Symptoms ofShigella Infection".About Shigella.Archived from the original on 8 January 2012. Retrieved10 February 2012.
  9. ^"Diarrhoeal Diseases: Shigellosis".Initiative for Vaccine Research. World Health Organization. Archived fromthe original on 15 December 2008. Retrieved11 May 2012.
  10. ^Devanga Ragupathi, NK; Muthuirulandi Sethuvel, DP; Inbanathan, FY; Veeraraghavan, B (21 January 2018)."Accurate differentiation ofEscherichia coli andShigella serogroups: challenges and strategies".New Microbes New Infect.21:58–62.doi:10.1016/j.nmni.2017.09.003.PMC 5711669.PMID 29204286.
  11. ^ab"Shigellosis (Bacillary Dysentery)".Merck Manual Professional Version. Retrieved16 March 2018.
  12. ^Bowen, Anna (31 May 2017)."Travelers' Health, Chapter 3, Shigellosis (CDC)". Retrieved17 March 2018.
  13. ^abcAslam, A; Gossman, WG (14 February 2018).Shigella (Shigellosis). Treasure Island, FL: StatPearls.PMID 29493962.
  14. ^Nelson, EJ; Harris, JB; Glenn Morris Jr., J; Calderwood, SB; Camilli, A (October 2009)."Cholera transmission: the host, pathogen and bacteriophage dynamic".Nat Rev Microbiol.7 (10):693–702.doi:10.1038/nrmicro2204.PMC 3842031.PMID 19756008.
  15. ^Ito, Hideo; Kido, Nobuo; Arakawa, Yoshichika; Ohta, Michio; Sugiyama, Tsuyoshi; Kato, Nobuo (1991)."Possible mechanisms underlying the slow lactose fermentation phenotype inShigella spp".Applied and Environmental Microbiology.57 (10):2912–7.Bibcode:1991ApEnM..57.2912I.doi:10.1128/AEM.57.10.2912-2917.1991.PMC 183896.PMID 1746953.
  16. ^abcdMani, Sachin; Wierzba, Thomas; Walker, Richard I. (2016)."Status of vaccine research and development forShigella".Vaccine.34 (26):2887–2894.doi:10.1016/j.vaccine.2016.02.075.PMID 26979135.
  17. ^mayo clinic"Shigella infection - Symptoms and causes".Mayo Clinic.Archived from the original on 6 September 2015. Retrieved14 September 2015.
  18. ^"WHO vaccine pipeline tracker".World Health Organization. Archived fromthe original on 25 July 2016. Retrieved29 July 2016.
  19. ^"Vaccine Research And Development: New strategies for acceleratingShigella vaccine development"(PDF).Weekly Epidemiological Record.72 (11):73–80. 14 March 1997.PMID 9115858.Archived(PDF) from the original on 19 May 2009. Retrieved10 February 2012.
  20. ^"How canShigella infections be treated?".Shigellosis: General Information. Centers for Disease Control and Prevention. 17 January 2019.Archived from the original on 8 February 2016.
  21. ^Christopher, Prince RH; David, Kirubah V; John, Sushil M; Sankarapandian, Venkatesan; Christopher, Prince RH (2010)."Antibiotic therapy forShigella dysentery".The Cochrane Database of Systematic Reviews.2010 (8) CD006784.doi:10.1002/14651858.CD006784.pub4.PMC 6532574.PMID 20687081.
  22. ^Kahsay, AG; Muthupandian, S (30 August 2016)."A review on Sero diversity and antimicrobial resistance patterns ofShigella species in Africa, Asia and South America, 2001-2014".BMC Research Notes.9 (1): 422.doi:10.1186/s13104-016-2236-7.PMC 5004314.PMID 27576729.
  23. ^"How canShigella infections be treated?".Shigellosis: General Information. Centers for Disease Control and Prevention.Archived from the original on 11 February 2012. Retrieved11 February 2012.
  24. ^Katzung, Bertram G. (2007).Basic and Clinical Pharmacology. New York, NY: McGraw Hill Medical. p. 733.ISBN 978-0-07-145153-6.
  25. ^Ram, PK; Crump JA; Gupta SK; Miller MA; Mintz ED (2008)."Analysis of Data Gaps Pertaining toShigella Infections in Low and Medium Human Development Index Countries, 1984–2005".Epidemiology and Infection.136 (5):577–603.doi:10.1017/S0950268807009351.PMC 2870860.PMID 17686195.
  26. ^World Health Organization (2006).State of the art of new vaccine research and development(PDF).Archived(PDF) from the original on 4 March 2016.
  27. ^US Centers for Disease Control and Prevention."Shigella – Shigellosis".Archived from the original on 24 July 2016. Retrieved29 July 2016.
  28. ^Angulo, Frederick J.; Swerdlow, David L. (1995). "Bacterial Enteric Infections in Persons Infected with Human Immunodeficiency Virus".Clinical Infectious Diseases.21 (Supplement 1):S84 –S93.doi:10.1093/clinids/21.supplement_1.s84.PMID 8547518.
  29. ^Todar, Kenneth."Shigella and Shigellosis".Todar's Online Textbook of Bacteriology.Archived from the original on 9 February 2012. Retrieved10 February 2012.
  30. ^Baker, K; et al. (September 2016)."Travel- and Community-Based Transmission of Multidrug-ResistantShigella sonnei Lineage among International Orthodox Jewish Communities".Emerg Infect Dis.22 (9):1545–1553.doi:10.3201/eid2209.151953.PMC 4994374.PMID 27532625.

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