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Plesiomonas shigelloides
PART III Etiologic Agents of Infectious Diseases SECTION A Bacteria
143 Plesiomonas shigelloides Shai Ashkenazi
Plesiomonas shigelloides is a common inhabitant of surface water and fish. It causes acute gastroenteritis, mainly in travelers to tropical regions, and uncommonly severe extraintestinal infections in children.1–6
DESCRIPTION OF THE PATHOGEN P. shigelloides is the only species in the genus Plesiomonas. Based on phenotypic characteristics, P. shigelloides was classified in the Vibrionaceae family.4 However, sequence analysis indicates its phylogenetic ancestry is more closely aligned with the tribe Proteaceae in the Enterobacteriaceae family.7 P. shigelloides are facultative anaerobic, gram-negative rods, which are motile using a polar flagellum. Some isolates of P. shigelloides share the capsular O antigen with that of Shigella sonnei. P. shigelloides are oxidase, indole, and catalase positive. They also are ornithine, lysine, and arginine decarboxylase positive. P. shigelloides grow well on traditional enteric media, including MacConkey, Hektoen enteric deoxycholate citrate (Leifson), and SalmonellaShigella agars. Growth is enhanced when inoculated on selective media, such as trypticase soy broth with ampicillin.3 P. shigelloides produces gray, nonhemolytic colonies after 18 to 24 hours of incubation at 37°C; optimal growth occurs at temperatures of 40°C to 44°C.3
PATHOGENESIS P. shigelloides is epidemiologically associated with gastroenteritis, particularly in the first 2 years of life. However, when fed to adult human volunteers, the bacteria does not cause diarrhea.8,9 In vitro and in vivo studies suggest low pathogenicity.10 Clinical manifestations of gastroenteritis suggest enteroinvasion as a possible mechanism of disease. However, P. shigelloides yields negative or variable results by most standard assays of invasiveness.3,9–11 DNA probes for virulence genes of Shigella spp. and enteroinvasive Escherichia coli also are negative.9,11 Mutant studies have documented a crucial role of the lipopolysaccharide in pathogenicity through resistance to complement and adhesion to and invasion of some eukaryotic cells.12 Plesiomonas does not produce an enterotoxin; cytotoxin production has been demonstrated in some strains.9,11,13 A high-molecular-weight plasmid has been identified in most strains of P. shigelloides, but its role in the pathogenesis of diarrhea has not been determined.10 Investigations have demonstrated pronounced cell adhesion of P. shigelloides clinical isolates, a characteristic not observed in environmental isolates.14 It is unclear whether some strains are virulent but others are nonpathogenic or whether there is age- and immunity-related susceptibility. In a case-control study of childhood diarrhea in Bangladesh, P. shigelloides was isolated with similar frequency from stool specimens in cases and controls, but it was not isolated in nondiarrheal patients in China.1,15
EPIDEMIOLOGY P. shigelloides was isolated from 3% of outpatients with acute diarrhea in China and was the only pathogen isolated from 2%.1 Its natural reservoirs are water and fish in temperate and tropical regions. Humans are infected with P. shigelloides after ingestion of contaminated food or water or through contact with colonized animals.16 Plesiomonas colonizes the gut of various animals and has been isolated from cats, dogs, pigs, cows, snakes, newts, fish, shellfish, monkeys, and vultures; molecular studies suggest that P. shigelloides can be zoonotic.17 Although Plesiomonas has been identified in about 1% of tropical fish tanks, aquarium-associated illness is rare. Occupations associated with an increased risk of P. shigelloides infection include veterinarians, aqua culturists, fish handlers, and zoo keepers.3
832
P. shigelloides can be isolated from stools of patients with gastroenteritis who reside in tropical and subtropical regions of Africa, Asia, and Australia.3 Asymptomatic carriage of P. shigelloides in humans living in developed countries is uncommon. The organism has been isolated from coastal waters of the Gulf of Mexico and has been implicated as a cause of diarrhea in travelers to Mexico and the Caribbean. In the United States and Europe, most cases of gastroenteritis are associated with travel to tropical areas or with consumption of raw oysters or shellfish.3
CLINICAL MANIFESTATIONS After an incubation of 1 to 4 days, acute gastroenteritis is the most common clinical presentation.1–3 About 70% of gastroenteritis due to P. shigelloides is associated with an underlying illness or identifiable risk factor, such as travel or consumption of raw seafood.1,3,4 The clinical presentation varies; symptoms include abdominal cramps, dehydration, fever, headache, vomiting, and diarrhea, which usually last for a few days.1,2 A study from Bangladesh suggests that diarrhea primarily occurs in the first 2 years of life. Most illness (84%) manifests with acute watery diarrhea, although dysenteric disease (16%) and persistent diarrhea (13%) lasting more than 2 weeks also occur. A Canadian study documented persistent symptoms (>2 weeks in 76%, >4 weeks in 32%), mostly in people who recently had traveled, been exposed to seafood, or had contact with contaminated water. However, the high frequency of persistent symptoms may reflect selection biases. Extraintestinal manifestations are rare but include bacteremia, meningitis, osteomyelitis, septic arthritis, cellulitis, endophthalmitis, proctitis, peritonitis, pseudoappendicitis, pancreatitis, and cholecystitis.1,2,5,6,18–23 Underlying illnesses associated with extraintestinal infections include immunodeficiency, sickle cell disease, and cirrhosis and other hepatic diseases.1,2 P. shigelloides keratitis due to a laceration has been reported.24 There are cases of early-onset neonatal septicemia and meningitis.4,15,17 The mortality rate is high when extraintestinal infection occurs. For neonates with meningitis, the mortality rate can be greater than 80%.
DIAGNOSIS Isolation of the organism after growth in appropriate medium is essential for the diagnosis of P. shigelloides. Clinical laboratories sometimes underrecognize the organism because up to 30% of clinically significant isolates ferment lactose. If an oxidase test is not performed, these lactosefermenting isolates can be misidentified as normal enteric flora. When P. shigelloides is being considered on the basis of foreign travel or ingestion of raw seafood or untreated water, an oxidase test should be performed. Selective media also can be used. P. shigelloides is isolated readily from normally sterile body fluids in cases of extraintestinal infection.
TREATMENT Acute Gastroenteritis Because P. shigelloides–associated gastroenteritis is usually self-limited, replacement of fluid and electrolyte losses is the main treatment. The need for antimicrobial therapy is controversial because the disease is usually self-limited. In some studies, antimicrobial therapy appears to shorten the duration of illness, but a case-control study of Thai children found no difference in the duration of diarrhea in treated and untreated groups.25 Antimicrobial therapy is recommended for gastroenteritis in children with underlying conditions. P. shigelloides are usually resistant to penicillins (by β-lactamase production) and sometimes to trimethoprim-sulfamethoxazole, but they are usually susceptible to
Key Points: Epidemiology, Clinical Manifestations, and Management of Plesiomonas shigelloides Infection EPIDEMIOLOGY
MANAGEMENT
• Natural reservoirs are fresh water and fish in temperate and tropical regions. • Infections usually are associated with travel to tropical areas or consumption of raw seafood.
• Mainstay is replacement of fluid and electrolyte losses, preferably by oral rehydration. • Antimicrobial therapy is recommended for extraintestinal infections and for acute gastroenteritis in children with underlying conditions. • Most strains produce β-lactamase, but they are susceptible to cephalosporins, amoxicillin-clavulanate, carbapenems, and fluoroquinolones. • Recommended empiric antibiotic therapy usually is a thirdgeneration cephalosporin.
CLINICAL FEATURES • Incubation period: 1 to 4 days • Typical illness: acute onset of diarrhea (sometimes with blood or mucus), with nausea, vomiting, abdominal cramps, and sometimes fever • Extraintestinal manifestations: bloodstream and focal infections (rare, occurring mainly in neonates or children with chronic underlying conditions)
cephalosporins, amoxicillin-clavulanate, carbapenems, and fluoroquinolones.1,4,26,27 When antimicrobial therapy for Plesiomonas-gastroenteritis is indicated, the recommended empiric agent is ceftriaxone (50 mg/kg once daily for 5 days).
Extraintestinal Infections Intravenous antibiotic therapy is recommended for children with extraintestinal infections. It should be guided by local susceptibility data and then by the individual isolate because there is considerable variation in antimicrobial susceptibility. Empiric therapy with an extended-spectrum cephalosporin is reasonable because isolates typically are susceptible in vitro and because of good penetration into the cerebrospinal fluid.1,4,26,27 All references are available online at www.expertconsult.com.
KEY REFERENCES 1. Chen X, Chen Y, Yang Q, et al. Plesiomonas shigelloides infection in Southeast China. PLoS ONE 2013;8:e77877. 2. Escobar JC, Bhavnani D, Trueba G, et al. Plesiomonas shigelloides infection, Ecuador, 2004–2008. Emerg Infect Dis 2012;18:322–324. 5. Ozdemir O, Sari S, Terzioglu S, et al. Plesiomonas shigelloides sepsis and meningoencephalitis in a surviving neonate. J Microbiol Immunol Infect 2010;43: 344–346. 12. Aquillin E, Merino S, Tomas JM. The Plesiomonas shigelloides wb(O1) gene cluster and the role of O-antigen LPS in pathogenicity. Microb Pathog 2013;63:1–7. 18. Khan AM, Farugue ASG, Hossain MS, et al. Pleisiomonas shigelloides-associated diarrhea in Bangladeshi children: a hospital-based surveillance study. J Trop Pediatr 2004;50:354–356. 23. Xia FQ, Liu PN, Zhou YH. Meningoencephalitis caused by Plesiomonas shigelloides in a Chinese neonate: case report and literature review. Ital J Pediatr 2015; 41:1–3.
Plesiomonas shigelloides
REFERENCES 1. Chen X, Chen Y, Yang Q, et al. Plesiomonas shigelloides infection in Southeast China. PLoS ONE 2013;8:e77877. 2. Escobar JC, Bhavnani D, Trueba G, et al. Plesiomonas shigelloides infection, Ecuador, 2004–2008. Emerg Infect Dis 2012;18:322–324. 3. Brenden RA, Miller MA, Janda JM. Clinical disease spectrum and pathogenic factors associated with Plesiomonas shigelloides infections in humans. Rev Infect Dis 1988;10:303–316. 4. Kain KC, Kelly MT. Clinical features, epidemiology, and treatment of Plesiomonas shigelloides diarrhea. J Clin Microbiol 1989;27:998–1001. 5. Ozdemir O, Sari S, Terzioglu S, et al. Plesiomonas shigelloides sepsis and meningoencephalitis in a surviving neonate. J Microbiol Immunol Infect 2010;43: 344–346. 6. Auxilladora-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;39:335–339. 7. Martinez-Murci AJ, Benlloch S, Collins MD. Phylogenetic interrelationships of members of the genera Aeromonas and Plesiomonas as determined by 16S ribosomal DNA sequencing: lack of congruence with results of DNA-DNA hybridization. Int J Syst Bacteriol 1992;42:412–421. 8. Tseng HK, Liu CP, Li WC, et al. Characteristics of Pleisiomonas shigelloides infection in Taiwan. J Microbiol Immunol Infect 2002;35:47–52. 9. Herrington DA, Tzipori S, Robins-Browne RM, et al. In vivo and in vitro pathogenicity of Plesiomonas shigelloides. Infect Immun 1987;55:979–985. 10. Abbott SL, Kokka RP, Janda JM. Laboratory investigation on the low pathogenic potential of Plesiomonas shigelloides. J Clin Microbiol 1991;29:148–153. 11. Albert MJ, Ansuruzzaman M, Qadri F, et al. Characterization of Plesiomonas shigelloides strains that share type-specific antigen with Shigella flexneri 6 and common group 1 antigen with Shigella flexneri spp. and Shigella dysenteriae 1. J Med Microbiol 1993;39:211–217. 12. Aquillin E, Merino S, Tomas JM. The Plesiomonas shigelloides wb(O1) gene cluster and the role of O-antigen LPS in pathogenicity. Microb Pathog 2013;63:1–7. 13. Okawa Y, Ohtomo Y, Tsugawa H, et al. Isolation and characterization of a cytotoxin produced by Pleisiomonas shigelloides P-1 strain. FEMS Microbiol Lett 2004;239:125–130.
143
14. Schubert RH, Holz-Bremer A. Cell adhesion of Plesiomonas shigelloides. Zentralbl Hyg Umweltmed 1999;202:383–388. 15. Albert MJ, Faruque AS, Faruque SM, et al. Case-control study of enteropathogens associated with childhood diarrhea in Dhaka, Bangladesh. J Clin Microbiol 1999;37:3458–3464. 16. Wouafo M, Pouillot R, Kwetche PF, et al. An acute foodborne outbreak due to Pleisiomonas shigelloides in Yaounde, Cameroon. Foodborne Pathog Dis 2006;3:209–211. 17. Gonzalez-Rey C, Siitonen A, Pavlova A, et al. Molecular evidence of Plesiomonas shigelloides as possible zoonotic agent. Folia Microbiol 2011;56:178–184. 18. Khan AM, Farugue ASG, Hossain MS, et al. Pleisiomonas shigelloides-associated diarrhea in Bangladeshi children: a hospital-based surveillance study. J Trop Pediatr 2004;50:354–356. 19. Billiet J, Kuypers S, Van Lierde S, et al. Plesiomonas shigelloides meningitis and septicemia in neonates: report of a case and review of the literature. J Infect 1989;19:267–271. 20. Terpulek C, Goldmann A, Bartmann P, et al. Plesiomonas shigelloides sepsis and meningitis in a neonate. Eur J Pediatr 1992;501:499–501. 21. Fisher K, Chakraborty T, Hof H, et al. Pseudoappendicitis caused by Plesiomonas shigelloides. J Clin Microbiol 1985;26:2675–2677. 22. van Loon FPL, Rahim A, Chowdhury KA, et al. Case report of Plesiomonas shigelloides-associated persistent dysentery and pseudomembranous colitis. J Clin Microbiol 1989;27:1913–1915. 23. Xia FQ, Liu PN, Zhou YH. Meningoencephalitis caused by Plesiomonas shigelloides in a Chinese neonate: case report and literature review. Ital J Pediatr 2015;41:1–3. 24. Klatte JM, Dastjerdi MH, Clark K, et al. Hyperacute infectious keratitis with Plesiomonas shigelloides following traumatic lamellar corneal laceration. Pediatr Infect Dis J 2012;31:1200–1201. 25. Visitsunthorn N, Komolpis P. Antimicrobial therapy in Plesiomonas shigelloidesassociated diarrhea in Thai children. Southeast Asian J Trop Med Public Health 1995;26:86–90. 26. Kain KC, Kelly MT. Antimicrobial susceptibility of Plesiomonas shigelloides from patients with diarrhea. Antimicrob Agents Chemother 1989;33:1609–1610. 27. Maluping RP, Lavilla-Pitogo CR, DePaola A, et al. Antimicrobial susceptibility of Aeromonas spp., Vibrio spp. and Plesiomonas shigellosis isolates in the Philippines and Thailand. Int J Antimicrob Agents 2005;25:348–350.
833.e1
143 Plesiomonas shigelloides Shai Ashkenazi
Plesiomonas shigelloides is a common inhabitant of surface water and fish. It causes acute gastroenteritis, mainly in travelers to tropical regions, and uncommonly severe extraintestinal infections in children.1–6
DESCRIPTION OF THE PATHOGEN P. shigelloides is the only species in the genus Plesiomonas. Based on phenotypic characteristics, P. shigelloides was classified in the Vibrionaceae family.4 However, sequence analysis indicates its phylogenetic ancestry is more closely aligned with the tribe Proteaceae in the Enterobacteriaceae family.7 P. shigelloides are facultative anaerobic, gram-negative rods, which are motile using a polar flagellum. Some isolates of P. shigelloides share the capsular O antigen with that of Shigella sonnei. P. shigelloides are oxidase, indole, and catalase positive. They also are ornithine, lysine, and arginine decarboxylase positive. P. shigelloides grow well on traditional enteric media, including MacConkey, Hektoen enteric deoxycholate citrate (Leifson), and SalmonellaShigella agars. Growth is enhanced when inoculated on selective media, such as trypticase soy broth with ampicillin.3 P. shigelloides produces gray, nonhemolytic colonies after 18 to 24 hours of incubation at 37°C; optimal growth occurs at temperatures of 40°C to 44°C.3
PATHOGENESIS P. shigelloides is epidemiologically associated with gastroenteritis, particularly in the first 2 years of life. However, when fed to adult human volunteers, the bacteria does not cause diarrhea.8,9 In vitro and in vivo studies suggest low pathogenicity.10 Clinical manifestations of gastroenteritis suggest enteroinvasion as a possible mechanism of disease. However, P. shigelloides yields negative or variable results by most standard assays of invasiveness.3,9–11 DNA probes for virulence genes of Shigella spp. and enteroinvasive Escherichia coli also are negative.9,11 Mutant studies have documented a crucial role of the lipopolysaccharide in pathogenicity through resistance to complement and adhesion to and invasion of some eukaryotic cells.12 Plesiomonas does not produce an enterotoxin; cytotoxin production has been demonstrated in some strains.9,11,13 A high-molecular-weight plasmid has been identified in most strains of P. shigelloides, but its role in the pathogenesis of diarrhea has not been determined.10 Investigations have demonstrated pronounced cell adhesion of P. shigelloides clinical isolates, a characteristic not observed in environmental isolates.14 It is unclear whether some strains are virulent but others are nonpathogenic or whether there is age- and immunity-related susceptibility. In a case-control study of childhood diarrhea in Bangladesh, P. shigelloides was isolated with similar frequency from stool specimens in cases and controls, but it was not isolated in nondiarrheal patients in China.1,15
EPIDEMIOLOGY P. shigelloides was isolated from 3% of outpatients with acute diarrhea in China and was the only pathogen isolated from 2%.1 Its natural reservoirs are water and fish in temperate and tropical regions. Humans are infected with P. shigelloides after ingestion of contaminated food or water or through contact with colonized animals.16 Plesiomonas colonizes the gut of various animals and has been isolated from cats, dogs, pigs, cows, snakes, newts, fish, shellfish, monkeys, and vultures; molecular studies suggest that P. shigelloides can be zoonotic.17 Although Plesiomonas has been identified in about 1% of tropical fish tanks, aquarium-associated illness is rare. Occupations associated with an increased risk of P. shigelloides infection include veterinarians, aqua culturists, fish handlers, and zoo keepers.3
832
P. shigelloides can be isolated from stools of patients with gastroenteritis who reside in tropical and subtropical regions of Africa, Asia, and Australia.3 Asymptomatic carriage of P. shigelloides in humans living in developed countries is uncommon. The organism has been isolated from coastal waters of the Gulf of Mexico and has been implicated as a cause of diarrhea in travelers to Mexico and the Caribbean. In the United States and Europe, most cases of gastroenteritis are associated with travel to tropical areas or with consumption of raw oysters or shellfish.3
CLINICAL MANIFESTATIONS After an incubation of 1 to 4 days, acute gastroenteritis is the most common clinical presentation.1–3 About 70% of gastroenteritis due to P. shigelloides is associated with an underlying illness or identifiable risk factor, such as travel or consumption of raw seafood.1,3,4 The clinical presentation varies; symptoms include abdominal cramps, dehydration, fever, headache, vomiting, and diarrhea, which usually last for a few days.1,2 A study from Bangladesh suggests that diarrhea primarily occurs in the first 2 years of life. Most illness (84%) manifests with acute watery diarrhea, although dysenteric disease (16%) and persistent diarrhea (13%) lasting more than 2 weeks also occur. A Canadian study documented persistent symptoms (>2 weeks in 76%, >4 weeks in 32%), mostly in people who recently had traveled, been exposed to seafood, or had contact with contaminated water. However, the high frequency of persistent symptoms may reflect selection biases. Extraintestinal manifestations are rare but include bacteremia, meningitis, osteomyelitis, septic arthritis, cellulitis, endophthalmitis, proctitis, peritonitis, pseudoappendicitis, pancreatitis, and cholecystitis.1,2,5,6,18–23 Underlying illnesses associated with extraintestinal infections include immunodeficiency, sickle cell disease, and cirrhosis and other hepatic diseases.1,2 P. shigelloides keratitis due to a laceration has been reported.24 There are cases of early-onset neonatal septicemia and meningitis.4,15,17 The mortality rate is high when extraintestinal infection occurs. For neonates with meningitis, the mortality rate can be greater than 80%.
DIAGNOSIS Isolation of the organism after growth in appropriate medium is essential for the diagnosis of P. shigelloides. Clinical laboratories sometimes underrecognize the organism because up to 30% of clinically significant isolates ferment lactose. If an oxidase test is not performed, these lactosefermenting isolates can be misidentified as normal enteric flora. When P. shigelloides is being considered on the basis of foreign travel or ingestion of raw seafood or untreated water, an oxidase test should be performed. Selective media also can be used. P. shigelloides is isolated readily from normally sterile body fluids in cases of extraintestinal infection.
TREATMENT Acute Gastroenteritis Because P. shigelloides–associated gastroenteritis is usually self-limited, replacement of fluid and electrolyte losses is the main treatment. The need for antimicrobial therapy is controversial because the disease is usually self-limited. In some studies, antimicrobial therapy appears to shorten the duration of illness, but a case-control study of Thai children found no difference in the duration of diarrhea in treated and untreated groups.25 Antimicrobial therapy is recommended for gastroenteritis in children with underlying conditions. P. shigelloides are usually resistant to penicillins (by β-lactamase production) and sometimes to trimethoprim-sulfamethoxazole, but they are usually susceptible to
Key Points: Epidemiology, Clinical Manifestations, and Management of Plesiomonas shigelloides Infection EPIDEMIOLOGY
MANAGEMENT
• Natural reservoirs are fresh water and fish in temperate and tropical regions. • Infections usually are associated with travel to tropical areas or consumption of raw seafood.
• Mainstay is replacement of fluid and electrolyte losses, preferably by oral rehydration. • Antimicrobial therapy is recommended for extraintestinal infections and for acute gastroenteritis in children with underlying conditions. • Most strains produce β-lactamase, but they are susceptible to cephalosporins, amoxicillin-clavulanate, carbapenems, and fluoroquinolones. • Recommended empiric antibiotic therapy usually is a thirdgeneration cephalosporin.
CLINICAL FEATURES • Incubation period: 1 to 4 days • Typical illness: acute onset of diarrhea (sometimes with blood or mucus), with nausea, vomiting, abdominal cramps, and sometimes fever • Extraintestinal manifestations: bloodstream and focal infections (rare, occurring mainly in neonates or children with chronic underlying conditions)
cephalosporins, amoxicillin-clavulanate, carbapenems, and fluoroquinolones.1,4,26,27 When antimicrobial therapy for Plesiomonas-gastroenteritis is indicated, the recommended empiric agent is ceftriaxone (50 mg/kg once daily for 5 days).
Extraintestinal Infections Intravenous antibiotic therapy is recommended for children with extraintestinal infections. It should be guided by local susceptibility data and then by the individual isolate because there is considerable variation in antimicrobial susceptibility. Empiric therapy with an extended-spectrum cephalosporin is reasonable because isolates typically are susceptible in vitro and because of good penetration into the cerebrospinal fluid.1,4,26,27 All references are available online at www.expertconsult.com.
KEY REFERENCES 1. Chen X, Chen Y, Yang Q, et al. Plesiomonas shigelloides infection in Southeast China. PLoS ONE 2013;8:e77877. 2. Escobar JC, Bhavnani D, Trueba G, et al. Plesiomonas shigelloides infection, Ecuador, 2004–2008. Emerg Infect Dis 2012;18:322–324. 5. Ozdemir O, Sari S, Terzioglu S, et al. Plesiomonas shigelloides sepsis and meningoencephalitis in a surviving neonate. J Microbiol Immunol Infect 2010;43: 344–346. 12. Aquillin E, Merino S, Tomas JM. The Plesiomonas shigelloides wb(O1) gene cluster and the role of O-antigen LPS in pathogenicity. Microb Pathog 2013;63:1–7. 18. Khan AM, Farugue ASG, Hossain MS, et al. Pleisiomonas shigelloides-associated diarrhea in Bangladeshi children: a hospital-based surveillance study. J Trop Pediatr 2004;50:354–356. 23. Xia FQ, Liu PN, Zhou YH. Meningoencephalitis caused by Plesiomonas shigelloides in a Chinese neonate: case report and literature review. Ital J Pediatr 2015; 41:1–3.
Plesiomonas shigelloides
REFERENCES 1. Chen X, Chen Y, Yang Q, et al. Plesiomonas shigelloides infection in Southeast China. PLoS ONE 2013;8:e77877. 2. Escobar JC, Bhavnani D, Trueba G, et al. Plesiomonas shigelloides infection, Ecuador, 2004–2008. Emerg Infect Dis 2012;18:322–324. 3. Brenden RA, Miller MA, Janda JM. Clinical disease spectrum and pathogenic factors associated with Plesiomonas shigelloides infections in humans. Rev Infect Dis 1988;10:303–316. 4. Kain KC, Kelly MT. Clinical features, epidemiology, and treatment of Plesiomonas shigelloides diarrhea. J Clin Microbiol 1989;27:998–1001. 5. Ozdemir O, Sari S, Terzioglu S, et al. Plesiomonas shigelloides sepsis and meningoencephalitis in a surviving neonate. J Microbiol Immunol Infect 2010;43: 344–346. 6. Auxilladora-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;39:335–339. 7. Martinez-Murci AJ, Benlloch S, Collins MD. Phylogenetic interrelationships of members of the genera Aeromonas and Plesiomonas as determined by 16S ribosomal DNA sequencing: lack of congruence with results of DNA-DNA hybridization. Int J Syst Bacteriol 1992;42:412–421. 8. Tseng HK, Liu CP, Li WC, et al. Characteristics of Pleisiomonas shigelloides infection in Taiwan. J Microbiol Immunol Infect 2002;35:47–52. 9. Herrington DA, Tzipori S, Robins-Browne RM, et al. In vivo and in vitro pathogenicity of Plesiomonas shigelloides. Infect Immun 1987;55:979–985. 10. Abbott SL, Kokka RP, Janda JM. Laboratory investigation on the low pathogenic potential of Plesiomonas shigelloides. J Clin Microbiol 1991;29:148–153. 11. Albert MJ, Ansuruzzaman M, Qadri F, et al. Characterization of Plesiomonas shigelloides strains that share type-specific antigen with Shigella flexneri 6 and common group 1 antigen with Shigella flexneri spp. and Shigella dysenteriae 1. J Med Microbiol 1993;39:211–217. 12. Aquillin E, Merino S, Tomas JM. The Plesiomonas shigelloides wb(O1) gene cluster and the role of O-antigen LPS in pathogenicity. Microb Pathog 2013;63:1–7. 13. Okawa Y, Ohtomo Y, Tsugawa H, et al. Isolation and characterization of a cytotoxin produced by Pleisiomonas shigelloides P-1 strain. FEMS Microbiol Lett 2004;239:125–130.
143
14. Schubert RH, Holz-Bremer A. Cell adhesion of Plesiomonas shigelloides. Zentralbl Hyg Umweltmed 1999;202:383–388. 15. Albert MJ, Faruque AS, Faruque SM, et al. Case-control study of enteropathogens associated with childhood diarrhea in Dhaka, Bangladesh. J Clin Microbiol 1999;37:3458–3464. 16. Wouafo M, Pouillot R, Kwetche PF, et al. An acute foodborne outbreak due to Pleisiomonas shigelloides in Yaounde, Cameroon. Foodborne Pathog Dis 2006;3:209–211. 17. Gonzalez-Rey C, Siitonen A, Pavlova A, et al. Molecular evidence of Plesiomonas shigelloides as possible zoonotic agent. Folia Microbiol 2011;56:178–184. 18. Khan AM, Farugue ASG, Hossain MS, et al. Pleisiomonas shigelloides-associated diarrhea in Bangladeshi children: a hospital-based surveillance study. J Trop Pediatr 2004;50:354–356. 19. Billiet J, Kuypers S, Van Lierde S, et al. Plesiomonas shigelloides meningitis and septicemia in neonates: report of a case and review of the literature. J Infect 1989;19:267–271. 20. Terpulek C, Goldmann A, Bartmann P, et al. Plesiomonas shigelloides sepsis and meningitis in a neonate. Eur J Pediatr 1992;501:499–501. 21. Fisher K, Chakraborty T, Hof H, et al. Pseudoappendicitis caused by Plesiomonas shigelloides. J Clin Microbiol 1985;26:2675–2677. 22. van Loon FPL, Rahim A, Chowdhury KA, et al. Case report of Plesiomonas shigelloides-associated persistent dysentery and pseudomembranous colitis. J Clin Microbiol 1989;27:1913–1915. 23. Xia FQ, Liu PN, Zhou YH. Meningoencephalitis caused by Plesiomonas shigelloides in a Chinese neonate: case report and literature review. Ital J Pediatr 2015;41:1–3. 24. Klatte JM, Dastjerdi MH, Clark K, et al. Hyperacute infectious keratitis with Plesiomonas shigelloides following traumatic lamellar corneal laceration. Pediatr Infect Dis J 2012;31:1200–1201. 25. Visitsunthorn N, Komolpis P. Antimicrobial therapy in Plesiomonas shigelloidesassociated diarrhea in Thai children. Southeast Asian J Trop Med Public Health 1995;26:86–90. 26. Kain KC, Kelly MT. Antimicrobial susceptibility of Plesiomonas shigelloides from patients with diarrhea. Antimicrob Agents Chemother 1989;33:1609–1610. 27. Maluping RP, Lavilla-Pitogo CR, DePaola A, et al. Antimicrobial susceptibility of Aeromonas spp., Vibrio spp. and Plesiomonas shigellosis isolates in the Philippines and Thailand. Int J Antimicrob Agents 2005;25:348–350.
833.e1