ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Plesiomonas shigelloides infections

Plesiomonas shigelloides infections
Literature review current through: Jan 2024.
This topic last updated: Dec 13, 2023.

INTRODUCTION — Plesiomonas shigelloides (formerly known Aeromonas shigelloides) is an oxidase-positive, facultatively anaerobic gram-negative bacillus commonly found in aquatic environments. It is an important pathogen of fish and has been implicated as a cause of enteric disease in humans, especially following the consumption of raw seafood. It has also been isolated from a number of extraintestinal sites [1,2].

Issues related to P. shigelloides infections are discussed here. The approach to diarrhea in adults and children is discussed in detail elsewhere. (See "Approach to the adult with acute diarrhea in resource-abundant settings" and "Diagnostic approach to diarrhea in children in resource-abundant settings".)

MICROBIOLOGY AND PATHOGENESIS — Molecular phylogenetic studies have shown that the ancestry of Plesiomonas is most closely aligned with the family Enterobacteriaceae [3]. Therefore, Plesiomonas has been re-categorized from the family Vibrionaceae to the family Enterobacteriaceae, in which it is the only oxidase-positive member [4]. The species name "shigelloides" is derived from the fact that many strains cross-react antigenically with Shigella, particularly Shigella sonnei [5].

Outbreaks of diarrheal disease have been associated with contaminated water and oysters containing P. shigelloides, and reduction in the severity and duration of symptoms following appropriate antimicrobial therapy has been observed [6-8]. However, efforts to confirm virulence in experimental settings (including one human volunteer study) have been inconclusive [2,9,10]. In a case-control study in Ecuador, detection of P. shigelloides alone was similar between patients with diarrhea and controls; co-infection with P. shigelloides and another gastrointestinal pathogen was associated with diarrhea [11]. This finding is consistent with the concept that isolation of P. shigelloides sometimes reflects its status as a "fellow traveler" with known pathogens, rather than the causative agent for the observed illness. Nonetheless, it is likely that certain strains of P. shigelloides are capable of causing diarrhea. Host susceptibility also influences the risk of illness. Plesiomonas has a type VI secretion system and carries a variety of putative virulence factors; however, their role in causing disease remains uncertain [12-16].

EPIDEMIOLOGY

Distribution — P. shigelloides is primarily a freshwater aquatic organism, with increased rates of isolation in the warmer months of the year [17]. The organism requires a minimum temperature of 8ºC and the absence of salt for growth, which limits its aquatic habitats [1]. Thus, P. shigelloides is generally found in fresh or estuarine (brackish) waters rather than marine environments. It is most frequently observed in tropical or subtropical areas, although it has been isolated from surface waters in Europe as far north as Sweden [18-20].

P. shigelloides is widely distributed among warm and coldblooded animals, including cats, dogs, pigs, poultry, cattle, vultures, toads, snakes, lizards, freshwater and tropical fish, newts, and shellfish, including shrimp and oysters [2,21-24]. P. shigelloides has also been identified in gull feces in southwestern Lake Michigan bathing beaches [25].

There have been several well documented outbreaks of diarrheal disease associated with P. shigelloides in Japan, China, and Cameroon [6,7,26,27]. In a study including 2500 cases of neonatal diarrhea in Bangladesh, 1.6 percent of cases were associated with infection with P. shigelloides [28]. In another study of 3536 patients with acute diarrhea in southeast China, P. shigelloides was isolated in 2.9 percent of cases [29]. In a study of travelers' diarrhea in Bangkok, Plesiomonas was isolated from 14 percent of patients compared with 8 percent of healthy controls [30].

Risk factors and sources of infection — Risk factors for P. shigelloides gastroenteritis include travel to tropical regions, consumption of raw or undercooked seafood, and/or exposure to reptiles or contaminated water sources [4,8,31]. Cases have also been associated with near drowning or other freshwater exposures.

Individuals who are immunocompromised, have hepatobiliary disease (including alcoholic cirrhosis), or hemochromatosis are at increased risk of extraintestinal infections. Infections have also been reported in patients with HIV [32,33] and inflammatory bowel disease [34,35].

Nosocomial transmission has also been reported in a study from China [29].

CLINICAL MANIFESTATIONS

Incubation period — The incubation period for illness ranges from 24 to 48 hours.

Gastrointestinal infection — Patients with diarrhea due to P. shigelloides most frequently develop watery or secretory diarrhea, but some have an invasive, dysenteric illness (ie, bloody or mucoid diarrhea) [2,21,23]. Severe abdominal pain and cramping are common in adults. In a study of Bangladeshi children, presenting symptoms included watery diarrhea (84 percent), dysentery (16 percent), vomiting (71 percent), and fever (8 percent) [36]. Diarrhea lasted 14 days or longer in 13 percent of cases. Symptoms are typically self-limited; in some patients, a subacute to chronic presentation lasting between two weeks and three months occurs.

Extraintestinal infection — Case reports of extraintestinal infections with P. shigelloides include:

Bacteremia (which may be preceded by enteric symptoms) [18,37-40]

Cellulitis and skin abscesses following trauma in fresh water [41]

Peritonitis (including infection associated with continuous ambulatory peritoneal dialysis) [42,43]

Meningoencephalitis (usually in neonates, with an associated case fatality rate of 80 percent) [44,45]

Eye infections [46,47]

Pneumonia [48]

Prosthetic joint infection following consumption of raw oysters [49]

Septic abortion [50]

Extraintestinal infections have frequently involved immunocompromised hosts, including neonates and patients with underlying hepatobiliary disease or hemochromatosis [37,38,44,51-54].

DIAGNOSIS — P. shigelloides infection can be diagnosed when the organism is isolated by culture of the relevant specimen. Molecular testing for P. shigelloides is also included on some diagnostic multiplex platforms for enteric pathogens. However, if P. shigelloides is detected by molecular testing in a patient who is seriously ill, we favor additional efforts to isolate the organism by culture to enable susceptibility testing to inform therapy. (See 'Treatment' below.)

Using traditional microbiologic techniques, P. shigelloides grows readily on nonselective media, including blood agar and other media used for isolation of pathogens from wound and blood.

In stool cultures, the organism is a nonlactose fermenter and therefore should be identified readily with routine stool culture on MacConkey agar. Colonies are oxidase positive, which provides a rapid differentiation from Shigella (with which Plesiomonas may cross-react on serologic testing). Some strains can be isolated from cefsulodin-irgasan-novobiocin (CIN) medium, normally used to isolate Yersinia and Aeromonas species [1].

Molecular tests for Plesiomonas appear accurate; as an example, reproducibility of positive tests for Plesiomonas with the FilmArray GI Panel was high (17 of 18 tests) [55].

TREATMENT — In general, gastroenteritis caused by P. shigelloides tends to be mild and self-limited. For diarrheal disease, supportive care (eg, with oral or intravenous rehydration) is the primary therapeutic intervention. Data informing the optimal approach to antibiotic therapy are limited. Our approach depends on the severity of illness (or the potential for severe illness):

For patients with diarrhea that is mild to moderate and does not require intravenous volume repletion, we recommend only supportive therapy with oral rehydration, without the addition of an antimicrobial agent.

For more severe diarrheal cases requiring intravenous volume repletion, for extraintestinal infections, and in immunocompromised patients, older adults, or very young children, we suggest antimicrobial therapy. For those who are severely ill, we suggest empiric therapy with a carbapenem. For patients who are not severely ill but still warrant antibiotic therapy, a fluoroquinolone can be used as empiric therapy. Once susceptibility testing results are available, the empiric regimen can be switched to an active agent with a narrower spectrum of activity to complete the duration, if necessary. Given concerns about potential adverse effects of fluoroquinolones, we favor using other active agents for directed therapy, if possible.

Duration of therapy is dictated by clinical response. For most patients with diarrhea severe enough to require antimicrobial therapy, three to five days of therapy should be adequate. Patients with extraintestinal infections warrant more prolonged antimicrobial therapy, in the range of one to two weeks or more, depending on underlying conditions and clinical response.

However, clinical efficacy data for antibiotics are extremely limited. One retrospective study suggested that treatment with an appropriate antimicrobial agent shortens the course of diarrhea compared with no treatment or treatment with antibiotics to which the organism is not susceptible [56]. However, another retrospective series found no difference in the duration of fever or diarrhea among treated or untreated children with P. shigelloides [57].

Despite these ambivalent data, we favor antibiotic therapy in patients at risk for poor outcomes with infection.

Given the paucity of direct clinical data, our preference for empiric regimens is based on in vitro susceptibility patterns. Almost all strains remain susceptible to carbapenems [2]. Most are susceptible to fluoroquinolones, although reports of resistance are emerging globally [2]. Most strains of P. shigelloides carry a variety of beta-lactamases and therefore are resistant in vitro to ampicillin, carbenicillin, piperacillin, and ticarcillin [1,57-59]. Varying degrees of in vitro resistance have been reported to tetracycline, trimethoprim-sulfamethoxazole, erythromycin, and aminoglycosides [2].

SUMMARY AND RECOMMENDATIONS

Plesiomonas shigelloides is a facultatively anaerobic gram-negative bacillus common in the aquatic environment. It has emerged as a cause of enteric disease in humans, especially following the consumption of raw seafood. Not all strains appear to be capable of causing diarrhea. Host susceptibility may also influence the risk of illness. (See 'Microbiology and pathogenesis' above.)

The risk of P. shigelloides infection can be reduced by avoiding contact with untreated water supplies and consumption of raw or undercooked shellfish (particularly during warmer summer months). Individuals who are immunocompromised or have hepatobiliary disease are at increased risk of infection associated with water-related injuries. (See 'Epidemiology' above.)

Patients with diarrhea due to P. shigelloides most frequently develop watery or secretory diarrhea, but some have an invasive, dysenteric illness. Other symptoms include abdominal pain, cramping and vomiting; fever occurs occasionally. Extraintestinal manifestations have also been reported. (See 'Clinical manifestations' above.)

P. shigelloides can be detected on routine cultures of stool, wound, and blood cultures. It is also included in some multiplex diagnostic panels for enteric pathogens. (See 'Diagnosis' above.)

The gastroenteritis caused by P. shigelloides tends to be mild and self-limited and, in almost all instances, can be treated symptomatically with rehydration alone. For severe diarrhea requiring intravenous rehydration, for patients at risk for severe diarrhea (eg, extremes of age, immunocompromising condition), and for extraintestinal disease, we suggest antimicrobial therapy (Grade 2C). For empiric therapy of patients who are severely ill, we suggest a carbapenem (Grade 2C). For empiric therapy of patients who are less severely ill but still warrant antibiotic therapy, we suggest a fluoroquinolone (Grade 2C). Once susceptibility testing is available, an active agent with a narrower spectrum of activity should be chosen to complete the course, if necessary. (See 'Treatment' above.)

  1. Forsythe SJ, Abbot SL, Pitout J. Klebsiella, Enterobacter, Citrobacter, Cronobacter, Serratia, Plesiomonas, and other Enterobacteriaceae. In: Manual of Clinical Microbiology, 11th ed, Jorgensen JH, Pfaller MA, Carroll KC, et al (Eds), ASM Press, Washington, DC 2015.
  2. Janda JM, Abbott SL, McIver CJ. Plesiomonas shigelloides Revisited. Clin Microbiol Rev 2016; 29:349.
  3. MacDonell MT, Colwell RR. Phylogeny of the family Vibrionaceae and recommendation for two new genera: Listonella and Shewanella. Syst Appl Microbiol 1985; 6:171.
  4. Janda JM. Plesiomonas. Bergey's Manual of Systematic Bacteriology. In: Aeromonadacea, Second Ed, Garrity GM (Ed), Springer-Verlag, New York 2005. p.740.
  5. Chida T, Okamura N, Ohtani K, et al. The complete DNA sequence of the O antigen gene region of Plesiomonas shigelloides serotype O17 which is identical to Shigella sonnei form I antigen. Microbiol Immunol 2000; 44:161.
  6. Tsukamoto T, Kinoshita Y, Shimada T, Sakazaki R. Two epidemics of diarrhoeal disease possibly caused by Plesiomonas shigelloides. J Hyg (Lond) 1978; 80:275.
  7. Rutala WA, Sarubi FA Jr, Finch CS, et al. Oyster-associated outbreak of diarrhoeal disease possibly caused by Plesiomonas shigelloides. Lancet 1982; 1:739.
  8. Kauppinen A, Pitkänen T, Al-Hello H, et al. Two Drinking Water Outbreaks Caused by Wastewater Intrusion Including Sapovirus in Finland. Int J Environ Res Public Health 2019; 16.
  9. Herrington DA, Tzipori S, Robins-Browne RM, et al. In vitro and in vivo pathogenicity of Plesiomonas shigelloides. Infect Immun 1987; 55:979.
  10. Farmer JJ III, Arduino MJ, Hickman-Brenner FW, et al. The Genera Aeromonas and Plesiomonas. In: The Prokaryotes, Second Ed, Balows A, Truper HG, Sworkin M, et al (Eds), Springer-Verlag, New York 1992. Vol III, p.3028.
  11. Escobar JC, Bhavnani D, Trueba G, et al. Plesiomonas shigelloides infection, Ecuador, 2004-2008. Emerg Infect Dis 2012; 18:322.
  12. Okawa Y, Ohtomo Y, Tsugawa H, et al. Isolation and characterization of a cytotoxin produced by Plesiomonas shigelloides P-1 strain. FEMS Microbiol Lett 2004; 239:125.
  13. Ciznár I, Hostacka A, Gonzalez-Rey C, Krovacek K. Potential virulence-associated properties of Plesiomonas shigelloides strains. Folia Microbiol (Praha) 2004; 49:543.
  14. Tsugawa H, Ito H, Ohshima M, Okawa Y. Cell adherence-promoted activity of Plesiomonas shigelloides groEL. J Med Microbiol 2007; 56:23.
  15. González-Rodríguez N, Santos JA, Otero A, García-López ML. Cell-associated hemolytic activity in environmental strains of Plesiomonas shigelloides expressing cell-free, iron-influenced extracellular hemolysin. J Food Prot 2007; 70:885.
  16. Edwards MS, McLaughlin RW, Li J, et al. Putative virulence factors of Plesiomonas shigelloides. Antonie Van Leeuwenhoek 2019; 112:1815.
  17. Miller ML, Koburger JA. Plesiomonas shigelloides: an opportunistic food and waterborne pathogen. J Food Protect 1985; 48:449.
  18. Jönsson I, Monsen T, Wiström J. A case of Plesiomonas shigelloides cellulitis and bacteraemia from northern Europe. Scand J Infect Dis 1997; 29:631.
  19. Medema G, Schets C. Occurrence of Plesiomonas shigelloides in surface water: relationship with faecal pollution and trophic state. Zentralbl Hyg Umweltmed 1993; 194:398.
  20. Islam MS, Alam MJ, Khan SI. Distribution of Plesiomonas shigelloides in various components of pond ecosystems in Dhaka, Bangladesh. Microbiol Immunol 1991; 35:927.
  21. Janda JM, Abbott SL. The Genus Plesiomonas. In: The Enterobacteria, Second Ed, AMS Press, Washington, DC 2006.
  22. Arai T, Ikejima N, Itoh T, et al. A survey of Plesiomonas shigelloides from aquatic environments, domestic animals, pets and humans. J Hyg (Lond) 1980; 84:203.
  23. Horneman A, Josko D. Vibrio, Aeromonas, Plesiomonas, and Campylobacter species. In: Textbook of Diagnostic Microbiology, Third Ed, Mahon, Lehman, Manuselis (Eds), WB Saunders Co, Philadelphia 2007.
  24. Davis WA 2nd, Chretien JH, Garagusi VF, Goldstein MA. Snake-to-human transmission of Aeromonas (Pl) shigelloides resulting in gastroenteritis. South Med J 1978; 71:474.
  25. Kinzelman J, McLellan SL, Amick A, et al. Identification of human enteric pathogens in gull feces at Southwestern Lake Michigan bathing beaches. Can J Microbiol 2008; 54:1006.
  26. Bai Y, Dai YC, Li JD, et al. Acute diarrhea during army field exercise in southern China. World J Gastroenterol 2004; 10:127.
  27. Wouafo M, Pouillot R, Kwetche PF, et al. An acute foodborne outbreak due to Plesiomonas shigelloides in Yaounde, Cameroon. Foodborne Pathog Dis 2006; 3:209.
  28. Khan AM, Hossain MS, Khan AI, et al. Bacterial enteropathogens of neonates admitted to an urban diarrhoeal hospital in Bangladesh. J Trop Pediatr 2009; 55:122.
  29. Chen X, Chen Y, Yang Q, et al. Plesiomonas shigelloides infection in Southeast China. PLoS One 2013; 8:e77877.
  30. Bodhidatta L, Anuras S, Sornsakrin S, et al. Epidemiology and etiology of Traveler's diarrhea in Bangkok, Thailand, a case-control study. Trop Dis Travel Med Vaccines 2019; 5:9.
  31. Shah N, DuPont HL, Ramsey DJ. Global etiology of travelers' diarrhea: systematic review from 1973 to the present. Am J Trop Med Hyg 2009; 80:609.
  32. Ahmad M, Aggarwal M, Ahmed A. Bloody diarrhea caused by Plesiomonas shigelloides proctitis in a human immunodeficiency virus-infected patient. Clin Infect Dis 1998; 27:657.
  33. Suthienkul O, Aiumlaor P, Siripanichgon K, et al. Bacterial causes of AIDS-associated diarrhea in Thailand. Southeast Asian J Trop Med Public Health 2001; 32:158.
  34. Meyer AM, Ramzan NN, Loftus EV Jr, et al. The diagnostic yield of stool pathogen studies during relapses of inflammatory bowel disease. J Clin Gastroenterol 2004; 38:772.
  35. Mylonaki M, Langmead L, Pantes A, et al. Enteric infection in relapse of inflammatory bowel disease: importance of microbiological examination of stool. Eur J Gastroenterol Hepatol 2004; 16:775.
  36. Khan AM, Faruque AS, Hossain MS, et al. Plesiomonas shigelloides-associated diarrhoea in Bangladeshi children: a hospital-based surveillance study. J Trop Pediatr 2004; 50:354.
  37. Lee AC, Yuen KY, Ha SY, et al. Plesiomonas shigelloides septicemia: case report and literature review. Pediatr Hematol Oncol 1996; 13:265.
  38. Woo PC, Lau SK, Yuen KY. Biliary tract disease as a risk factor for Plesiomonas shigelloides bacteraemia: a nine-year experience in a Hong Kong hospital and review of the literature. New Microbiol 2005; 28:45.
  39. Bonatti H, Sifri C, Sawyer RG. Successful liver transplantation from donor with Plesiomonas shigelloides sepsis after freshwater drowning: case report and review of literature on gram-negative bacterial aspiration during drowning and utilization of organs from bacteremic donors. Surg Infect (Larchmt) 2012; 13:114.
  40. Shinohara T, Okamoto K, Koyano S, et al. Plesiomonas shigelloides Septic Shock Following Ingestion of Dojo Nabe (Loach Hotpot). Open Forum Infect Dis 2021; 8:ofab401.
  41. Herve V, Bigaillon C, Duhamel P, et al. [Cutaneous abscess due to Plesiomonas shigelloïdes consecutive to a trauma in fresh water]. Med Mal Infect 2007; 37:840.
  42. Alcañiz JP, de Cuenca Morón B, Gómez Rubio M, et al. Spontaneous bacterial peritonitis due to Plesiomonas shigelloides. Am J Gastroenterol 1995; 90:1529.
  43. Woo PC, Lau SK, Wong SS, Yuen KY. Two cases of continuous ambulatory peritoneal dialysis-associated peritonitis due to Plesiomonas shigelloides. J Clin Microbiol 2004; 42:933.
  44. Terpeluk C, Goldmann A, Bartmann P, Pohlandt F. Plesiomonas shigelloides sepsis and meningoencephalitis in a neonate. Eur J Pediatr 1992; 151:499.
  45. Cavaliere AF, Perelli F, Mattei A, et al. Case report: vertical transmission of Plesiomonas shigelloides. Is it time to strengthen information on safety concerns for raw seafood dietary exposure in pregnancy? J Matern Fetal Neonatal Med 2023; 36:2220061.
  46. Marshman WE, Lyons CJ. Congenital endophthalmitis following maternal shellfish ingestion. Aust N Z J Ophthalmol 1998; 26:161.
  47. Klatte JM, Dastjerdi MH, Clark K, et al. Hyperacute infectious keratitis with Plesiomonas shigelloides following traumatic lamellar corneal laceration. Pediatr Infect Dis J 2012; 31:1200.
  48. Schneider F, Lang N, Reibke R, et al. Plesiomonas shigelloides pneumonia. Med Mal Infect 2009; 39:397.
  49. Hustedt JW, Ahmed S. Plesiomonas shigelloides Periprosthetic Knee Infection After Consumption of Raw Oysters. Am J Orthop (Belle Mead NJ) 2017; 46:E32.
  50. Cornut G, Marchand-Senecal X, Gaudreau C, et al. Plesiomonas shigelloides: An Unusual Cause of Septic Abortion. Case Rep Infect Dis 2017; 2017:9363707.
  51. Delforge ML, Devriendt J, Glupczynski Y, et al. Plesiomonas shigelloides septicemia in a patient with primary hemochromatosis. Clin Infect Dis 1995; 21:692.
  52. Riley PA, Parasakthi N, Abdullah WA. Plesiomonas shigelloides bacteremia in a child with leukemia. Clin Infect Dis 1996; 23:206.
  53. Ozdemir O, Sari S, Terzioglu S, Zenciroglu A. Plesiomonas shigelloides sepsis and meningoencephalitis in a surviving neonate. J Microbiol Immunol Infect 2010; 43:344.
  54. Auxiliadora-Martins M, Bellissimo-Rodrigues F, Viana JM, et al. Septic shock caused by Plesiomonas shigelloides in a patient with sickle beta-zero thalassemia. Heart Lung 2010; 39:335.
  55. Hitchcock MM, Hogan CA, Budvytiene I, Banaei N. Reproducibility of positive results for rare pathogens on the FilmArray GI Panel. Diagn Microbiol Infect Dis 2019; 95:10.
  56. Kain KC, Kelly MT. Clinical features, epidemiology, and treatment of Plesiomonas shigelloides diarrhea. J Clin Microbiol 1989; 27:998.
  57. Visitsunthorn N, Komolpis P. Antimicrobial therapy in Plesiomonas shigelloides-associated diarrhea in Thai children. Southeast Asian J Trop Med Public Health 1995; 26:86.
  58. Avison MB, Bennett PM, Walsh TR. beta-lactamase expression in Plesiomonas shigelloides. J Antimicrob Chemother 2000; 45:877.
  59. Wong TY, Tsui HY, So MK, et al. Plesiomonas shigelloides infection in Hong Kong: retrospective study of 167 laboratory-confirmed cases. Hong Kong Med J 2000; 6:375.
Topic 3132 Version 21.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟