Aeromonas species
Authors: Po-Lin Chen, Chi-Jung Wu, Wen-Chien Ko
MICROBIOLOGY
Aeromonads, belonging to the genus Aeromonas, family Aeromonadaceae, are oxidase-producing gram-negative rods, grow on MacConkey agar and ferment carbohydrates. Separation from Vibrio species depends on resistance to the O/129 compound, no growth in 6% sodium chloride and absence of ornithine decarboxylase (except in A. veronii biovar veronii) (61). A. veronii contains two biovars (A. veronii bv. veronii and A. veronii bv. sobria). The species name A. sobria continues to be misused in publications and is A. veronii bv. sobria actually (106). In the past decade, several new species are discovered. Aeromonas species distribute widely in vertebrates, invertebrates, and the environment. Most clinical infections are associated with species A. hydrophila, A. veronii, A. caviae, and A. dhakensis. The other species are rarely or not associated with known human infections and therefore are not discussed in this chapter (Table 1). However, correct identification of aeromonads at the species level using phenotype-based methods is a challenge to most clinical microbiology laboratories (45). Recently, newer methods, including DNA sequencing of housekeeping genes, such as rpoB, rpoD, or gyrB (91, 140), and matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF), can achieve precise species identification (89).
EPIDEMIOLOGY
In nature, aeromonads are widely distributed in fresh and salt water, and also can be found in food (119), treated drinking or raw sewage water (93), fish, shellfish, meats, dairy products, fresh vegetables (67), domestic animals (such as horses, pigs, sheep, and cows) (67), and even in the hospital water supply system (127). Therefore, human infections caused by aeromonads most often occur in the community settings, but also can occur in healthcare facility settings (35, 108). Classically, susceptible individuals acquire aeromonads from oral consumption of or direct mucocutaneous contact with contaminated water, dirt, or seafood. Recently, Aeromonas species have been reported as an important bacterial wound pathogen in natural disaster situations, a phenomenon which may probably related to exposure to environmental mud or water or contaminated hospital water system (6, 68). Gastroenteritis and mild to moderate soft-tissue infections are the common presentations in immunocompetent individuals. The isolation rate from individuals with diarrheal illness ranges from 0.8% to 7.4%, but Aeromonas also can be isolated from the feces of up to 4% of asymptomatic persons (127). Not only causing community-acquired infections, Aeromonas species had been found to cause true indwelling-device related infections in healthcare facilities (65). In contrast, a pseudo-outbreak related to endoscopic equipment contaminated by A. hydrophila is an example of its ubiquity (42).
The population-based incidence of human Aeromonas infections in the literature was rarely reported. The first data came from California in 1988, with an annual incidence of 10.6 cases of Aeromonas infections per million population (79). In England and Wales in 2004, the estimated incidence of Aeromonas bacteremia was 1.5 cases per million population (68), and in French in 2006 the estimated figure was 0.66 cases per million population (90). In southern Taiwan between 2008 and 2010, the incidence of Aeromonas bacteremia, 76 cases per million inhabitants, was higher than the above figures (159). Therefore, these data suggest significant geographic variation of human Aeromonas diseases in different continents.
CLINICAL MANIFESTATIONS
Major clinical manifestations of invasive Aeromonas infections are primary bacteremia, hepatobiliary tract infections, and soft tissue-infections. Most human diseases were reported to be associated with three species, i.e., A. hydrophila, A. veronii, and A. caviae. With the changing taxonomy, the importance of some species in clinical infections increases. For example, A. dhakensis, previously named A. aquariorum or A. hydrophila sub. dhakensis, was often recognized as A. hydrophila by the current phenotype-based identification system (7, 27, 46). More and more evidences show A. dhakensis is widely distributed in the environment and causes a variety of infections in humans (7, 27, 46, 110). The virulence of this species has been recognized based on the evidences that it carries a number of putative virulence genes (46, 110) and has the most potent toxicity to human blood cell lines among the tested Aeromonas species (27, 110).
Aeromonas bacteremia usually occurs in patients with underlying illnesses, although it may occur in immunocompetent patients (56). Aeromonas species should be considered one of the causative pathogens of healthcare-associated bacteremia. In a study in southern Taiwan, about half of Aeromonas bacteremia develops in the setting of healthcare-associated infections, and most patients in this group had variable immunocompromised conditions, such as cancer, liver cirrhosis, receipt of immunosuppressant therapy, or diabetes mellitus (143). Neutropenic patients with hematological malignancy and patients with hepatic cirrhosis or hepatobiliary diseases are at particularly high risk (19, 41, 60, 81, 82, 164).
Primary bacteremia is not uncommon, although the presumed portal of entry in such cases is the gastrointestinal tract. Sepsis caused by Aeromonas is clinically indistinguishable from those caused by other gram-negative bacilli. Due to bacteremic spread, invasive soft-tissue infection, such as necrotizing fasciitis, may involve more than one site. The history of exposure to fresh or marine water or consumption of raw or semi-cooked seafood is helpful, when present. Some cases are hospital-acquired and water storage tanks in the hospitals are the potential sources (127). Most cases of bacteremia are caused by A. hydrophila, A. dhakensis, A. veronii, or A. caviae (31, 40, 46, 69, 82, 143, 164). Case fatality rate of Aeromonas bacteremia ranges from 24% to 63%. Underlying cancer, secondary bacteremia, and a higher severity for illness at the first presentation, were independently associated with a fatal outcome (82, 143).
Aeromonas species can cause biliary tract infections in both immunosuppressed and immunocompetent patients. Aeromonas biliary tract infections tend to occur in patients with biliary tract obstruction or stasis due to hepatobiliary cancer or stones (22). A. hydrophila is the most common causative species, followed by A. caviae and A. veronii (22). The majority of patients had polymicrobial infections and Escherichia coli, Enterococcus species, and Klebsiella species, are common concurrent isolates (22).
Individuals with liver cirrhosis are susceptible to Aeromonas infections (82). Clinical cases of Aeromonas spontaneous bacterial peritonitis (SBP) have been occasionally encountered in the areas where the prevalence of viral hepatic disease is high. The Aeromonas species causing SBP are mainly A. hydrophila and A. veronii, while A. caviae was rarely reported (66, 162). Aeromonas SBP is a life-threatening infection and nearly half of the cases experience shock and conscious change initially. Aeromonas SBP associated in-hospital mortality rate is 50%-56% (66, 162), higher than those caused by other common pathogens, such as E. coli (141).
Musculoskeletal and soft-tissue infections, including cellulitis (133, 152), furunculosis (60), skin nodules (166), soft-tissue abscesses (55, 152), infected lacerations (152), necrotizing fasciitis (109), ecthyma gangrenosum (60, 75, 114, 158), osteomyelitis (152), and myonecrosis (112, 152, 153), are not uncommon clinical presentations of Aeromonas infections. Aeromonas soft-tissue infections vary geographically. For example, Aeromonas species is infrequently reported as a causative organism of necrotizing fasciitis in western countries, but appears to be more common in Taiwan (23, 27, 82, 164). Among the survivors of the tsunami in southern Thailand in 2004, the most common pathogens of skin and soft-tissue infections were Aeromonas species (62). Most infections were caused by A. hydrophila, followed by A. veronii. In a study in southern Taiwan, most A. hydrophila wound isolates were re-identified as A. dhakensis by the molecular typing (27). Identification of A. dhakensis is of clinical importance due to its virulence and more antimicrobial resistance toward third generation cephalosporins and imipenem than A. hydrophila (27). Clinical manifestations and outcomes of Aeromonas-associated soft-tissue infections vary by host immune status (21, 23). The affected patients often had antecedent water-related trauma. Such infections often were polymicrobial, suggestive of environmental contamination (55, 136, 152). In immunocompetent individuals, infections were localized, not associated with bacteremia, and had a favorable outcome. In immunocompromised hosts, Aeromonas-associated soft-tissue infections can be fulminant and fatal. Necrotizing fasciitis, myonecrosis, or both (myofascial necrosis) with or without soft-tissue gas formation (51, 153), had the following characteristic presentations. Typically they experienced minor injuries or had unrecognizable wounds in the extremities, and had a history of contact with soil, wood, or brackish water. Within 24 hours, rapid, centripetal progression of pain, erythema and swelling accompanied with hemorrhagic bullae, developed (146). Aeromonas necrotizing fasciitis is associated with systemic toxicity, a fulminant course and a high mortality rate (51, 145, 146). These invasive necrotizing infections frequently were monomicrobial and accompanied by bacteremia (22). Severe Aeromonas soft tissue infections are clinically similar to those caused by Vibrio vulnificus at the time of presentation, and always need emergent surgical intervention for limb or life-threatening infections (145). In burn patients, there is another soft-tissue infection entity similar to streptococcal, staphylococcal, pseudomonal, or clostridial infections (13, 77, 138). The cases of Aeromonas burn wound infections often had a history of immersion of the involved body surface in untreated water or rolling in soil to extinguish the flames (77). Furthermore, Aeromonas species is the most common cause of infections following medicinal leech therapy for local vascular congestion after reconstructive surgery. The incidence of soft-tissue infection after medicinal leech therapy ranges from 7% to 20%, but Aeromonas wound infection rarely develops after leech bites in the wild (32). Clinical features range from local wound infections, abscess formation, to myonecrosis, or even septic shock. However, in a review of 25 cases of leech-related infection, none died of Aeromonas infection (32).
There are several clinical presentations of gastrointestinal illness associated with Aeromonas infections: acute watery diarrhea, often with vomiting, dysenteric diarrhea, chronic diarrhea, choleraic and traveler's diarrhea (70). Moreover, complications related to gastroenteritis caused by cytotoxic Aeromonas, such as small bowel obstruction (14), acute renal failure (47) and hemolytic-uremic syndrome (15, 43), could be found in the English literature. Although Aeromonas-associated intestinal infections have been reported (2, 137, 148, 150), there are still some controversies about its role as an enteropathogen. The arguments arise from the following findings. First, there was no report identifying a clonally related outbreak of diarrhea caused by these pathogens, even though they are ubiquitous in environments. Secondly, direct clinical evidence proving experimental pathogenicity for human remains scare. Thirdly, so far the cases of Aeromonas-associated diarrhea frequently run a self-limited clinical course (151). In contrast, the data supporting aeromonads as enteropathogens comes from the facts that Aeromonas can be dominant in stool cultures in the persons with diarrhea (52, 64, 115, 116, 157), and ill patients in whom aeromonads are isolated from the gastrointestinal tract can produce intestinal secretory antibodies against the homologous strains (72). In a review article, A. caviae was referred to be the most common species in stool cultures, followed by A. hydrophila and A. veronii bv. sobria (151). Of the etiologies of travelers' diarrhea among Finnish tourists travelling to Morocco, A. veronii bv. sobria was the major species (59). These varied results may be related to heterogeneous hosts, geographic locations, seasons of collection, and different culture media (2).
Aeromonas respiratory tract infection, a rare disease, accounts for 6% of 78 cases of Aeromonas infections in a prospective study during six months in France (90). However, Aeromonas species should be considered as one of the causative pathogens in severe pneumonia in endemic areas. In a large-scale study on 84 patients with Aeromonas pneumonia in southern Taiwan, 85% of the affected patients were older than 65 years old and most of them had underlying diseases. The most commonly encountered underlying disease is malignancy, which was noted in a significant proportion (44%) of the patients. A. hydrophila was the most common pathogen, followed by A. caviae and A. veronii. Drowning-associated pneumonia was a fatal disease, especially in immunocompromised patients. In 6 patients with drowning-associated pneumonia, all of them needed ICU admission and mechanical ventilation, and all three patients with liver cirrhosis died. Similar to other Aeromonas infections, cirrhosis and cancer were associated with a poor outcome (24).
Aeromonas genitourinary tract infection was rarely reported in literature. It has been found to develop in patients with immunocompromised conditions (20). A. caviae and A. hydrophila were the common species causing urinary tract infections (20, 103). Most affected patients responded to antibiotic treatment and recovered well (20).
Aeromonas can cause ophthalmic infections, not only related to traumatic exposure to contaminated water or contact lens but also endogenous spread. Endogenous (76, 139) or exogenous endophthalmitis (96), post-traumatic or contact lens-related keratitis (128), and orbital cellulitis (30) have been reported. Endogenous ocular infections often affect immunocompromised hosts and exogenous ophthalmic infections following trauma are noted in those without underlying illness. The onset of endophthalmitis, the most severe ocular infection, is rapid and often results in enucleation. Outcome for other ophthalmic infections are usually good. Therefore, early recognition of endophthalmitis in patients having eye injuries associated with environmental contamination is critical in preventing serious sequelae of Aeromonas eye infections. With the increasing use of contact lens, the possibility of Aeromonas keratitis in the cases wearing contact lens needs to keep in mind (128, 149).
LABORATORY DIAGNOSIS
Aeromonas species are nonfastidious organisms and can grow readily on most common, routinely used media, such as blood, chocolate, or MacConkey agar (5). The genus Aeromonas is identified based on the findings of positive oxidase test, fermentation of D-glucose, motile, the absence of growth in 6.5% sodium chloride, and resistant to the vibriostatic agent O/129 (150 μg) (18). Correct identification of the species of the genus Aeromonas, especially those species that have implicated in human diseases is a microbiological challenge, as the number of taxa ascribed to the genus has increased during the last decade. The correct classification of microorganisms at species level on the basis of traditional methods (morphological, physiological, and biochemical), as well as commercial identification systems (i.e., API20E, Vitek, BBL Crystal, or MicroScan W/A) (5) is not universally achieved. In routine practice of microbiology laboratory, MALDI-TOF is a promising tool for rapid and precise identification of Aeromonas species (107).
PATHOGENESIS
Clinical data, ex vivo experiments, and animal studies suggest there is virulence variation among clinically important Aeromonas species (28). For example, A. dhakensis exhibits more potent virulence characteristics, as demonstrated by ex vivo and in vivo studies, and such a finding was in accordance with the clinical findings (28). In contrast, A. caviae is less virulent clinically, in cell cytotoxicity assay and in animal studies of mice and Caenorhabditis elegans. The so-called "virulent species", i.e., A. dhakensis, A. hydrophila, or A. veronii, harbor an array of virulence factors, such as hemolysin (ahh1), aerolysin (aerA), cytotoxin (ast), type III secretion system (ascV and ascF-G) (3, 46, 110). An array of putative virulence factors of aeromonads, such as aerolysin, enterotoxins, hemolysin, protease, hemoagglutinins, endotoxin, siderophores, type III secretion system (TISS), flagella, pili and biofilm regulated by quorum sensing system, may play roles in pathogenesis (17, 68, 71). However, the clinical role of these factors or proteins in human Aeromonas infections is not conclusive.
SUSCEPTIBILITY IN VITRO AND IN VIVO
The latest Clinical and Laboratory Standards Institute (CLSI) guideline for the antimicrobial susceptibility testing of Aeromonas spp., M45-A2, was revised in 2010 (34). Compared to the previous version, M45-A in 2006 (33), the minimal inhibitory concentration (MIC) breakpoints for cefazolin, cefotaxime, ceftazidime, and ceftriaxone susceptibility were lower in M45-A2. Therefore, the factor of changing interpretative breakpoint overtime should be taken into consideration when the antimicrobial susceptibility profiles of aeromonads were reviewed retrospectively. Most Aeromonas isolates in reports dealing with in vitro susceptibility were identified as three major phenospecies, i.e., A. hydrophila, A. caviae, and A. veronii bv. sobria (8, 16, 85, 111). The susceptibility profiles of less frequently encountered genomospecies, A. jandaei, A. schubertii, A. trota (122), and a newly described species in 2009, A. dhakensis, have also been reported (27, 46, 163) (Table 2). Several reports indicated that the isolates phenotypically identified as A. hydrophila were actually A. dhakensis, if rpoD or gyrB was sequenced (7, 110). Hence in the literature before 2009, A. hydrophila isolates for which antimicrobial susceptibility was reported would include A. dhakensis. Overall, there are not only interspecies differences but also geographic variability of antimicrobial susceptibility among aeromonads (8, 16, 27, 71, 85, 86, 111, 113). In general, except for A. enteropelogenes (formerly A. trota or A. tructi), aeromonads are uniformly resistant to ampicillin (31, 37, 85). Piperacillin shows variable activity but was more active than other penicillins (111). The activity of the 1st- , 2nd-, or 3rd-generation cephalosporins is variable. A. hydrophila, A. caviae, and A. dhakensis isolates are usually resistant to cephalothin and frequently display resistance to cefuroxime, ceftriaxone, or cefotaxime than do A. veronii isolates which are usually susceptible to cephalothin (71, 85, 163). It is noteworthy that imipenem resistance is commonly found among A. jandaei (65%) and A. veronii biotype veronii (67%) and occasionally in A. hydrophila and A. dhakensis (12, 122, 160). Aeromonads are usually susceptible to 4th-generation cephalosporins, aminoglycosides, fluoroquinolones, tetracycline, and trimethoprim-sulfamethoxazole (8, 16, 31, 86). However, increasing rates of resistance to fluoroquinolones, tetracycline or trimethoprim-sulfamethoxazole have been reported (85, 100, 101).
Most studies discussing beta-lactamases of Aeromonas species focused on three chromosomally encoded beta-lactamases, i.e., Ambler molecular class B (metallo-beta-lactamases, MBLs), C (AmpC cephalosporinase), and D beta-lactamases (penicillinases) (48, 68, 155). CphA harbored in A. hydrophila, A. veronii, A. jandaei, A. dhakensis is the principal chromosomal MBL recognized in aeromonads (130, 160). Compared with other class B enzymes, CphA MBL has a specific substrate profile, being active against penems and carbapenems, but not penicillins or cephalosporins (135). However, CphA carbapenemase production is not easily detected by the conventional in vitro susceptibility test, unless large inocula or a modified Hodge test (MHT) are adopted (130, 160). Chromosomal AmpC cephalosporinase in aeromonads included AsbA1 (A. jandaei), CepH and CepS (A. hydrophila), CAV1 (A. caviae), TRU-1 (A. enteropelogenes), and AQU-1 (A. dhakensis) (4, 10, 37, 49, 163). Of note, A. veronii bv. sobria 163a, from which CepS cephalosporinase was originally identified, was reclassified as A. hydrophila (144, 154). Recognized chromosomal penicillinases included AmpH and AmpS (A. hydrophila) and AsbB1 (A. jandaei) (4, 10, 154). Fosse et al. characterized a series of 417 wild-type Aeromonas strains into 5 predominant phenotypes based on biochemical identification and susceptibility testing by the disk-diffusion method: A. hydrophila complex/class B, C and D beta-lactamases; A. caviae complex/class C and D beta-lactamases; A. veronii complex/class B and D beta-lactamases; A. schubertii /class D beta-lactamase; A. trota (A. enteropelogenes)/class C beta-lactamase (48). Recently, A. enteropelogenes was shown to be susceptible to ampicillin and the only Aeromonas species that produces only one beta-lactamase (37). Furthermore, genomic studies indicated that A. dhakensis intrinsically harbors class B, C and D beta-lactamases and A. taiwanensis class C and D beta-lactamases (156, 163). Collectively, these observations suggested that the distribution of beta-lactamases is species specific among aeromonads (Table 3). These susceptibility profiles may be a useful scheme for taxonomic differentiation and a guide of antimicrobial therapy.
As other AmpC-carrying bacteria, aeromonads carrying AmpC genes do not always express AmpC beta-lactamases and may display susceptibility to 3rd-generation cephalosporins. The expression of three chromosomally mediated class B, C, and D beta-lactamases was co-regulated by a two component regulatory system (9). The mechanisms involved in the expression of beta-lactamases include inducible beta-lactamase production in the presence of suitable inducers (beta-lactam agents) or development of depressed mutation which lead to constitutive high-level production of beta-lactamases (154, 155). The frequency of in vitro development of resistant mutants in Aeromonas isolates was 10-6~10-9 (154, 155). Induction potential or the selection of resistant mutants among AmpC-carrying bacteria does not correlate with clinical risks, because a rapid bactericidal action will kill the organisms before a sufficient quantity of enzymes has been induced (74). For example, we reported a low incidence (3.4%) of emergence of broad-spectrum cephalosporin-resistant Aeromonas isolates when treating Aeromonas bacteremia with a beta-lactam (82). Although being rare scenarios, the emergence of beta-lactam resistance due to derepressed mutation for beta-lactamase hyper-production has occurred, mainly in patients with secondary bacteremia, such as bacteremia associated with burn wound infection or deep-seated infections which involved pneumonia, biliary tract infections, osteomyelitis, or skin and soft-tissue infection (11, 58, 82, 84, 95, 132, 163). Therefore, the use of a beta-lactam (except 4th-generation cephalosporins) for infections with a high bacterial load or accompanied with ischemic foci due to Aeromonas species carrying intrinsic beta-lactamases should be cautious for clinical failure (84, 160, 163).
In addition to intrinsic chromosomal beta-lactamases, acquired plasmid-mediated MOX-4 AmpC beta-lactamases and IMP-19 MBL, and integron-mediated VIM MBL have been detected in clinical A. caviae isolates, and acquired integron-mediated VIM MBL has been detected in a clinical A. hydrophila strain (1, 98, 118, 165). Notably, the acquired VIM MBL has a much broader substrate profile than that of CphA (98).
Ambler class A extended-spectrum beta-lactamases (ESBLs) have also been increasingly reported in both clinical and environmental aeromonads (5, 50, 54, 102, 104, 126, 129, 161, 165). The reported ESBL genotypes included TEM-24, CTX-M-3, CTX-15, PER-1, PER-3, PER-6, SHV-12, VEB-1a, TLA-2, and GES-7 (54, 57, 104, 126, 161, 165). These ESBL genes were found to be located in plasmids or integrons (54, 104, 126, 161). In one study investigating 156 Aeromonas blood isolates in southern Taiwan, 4 (2.6%) exhibited the ESBL phenotype, and two A. caviae isolates possessed blaPER-3 which was located in both chromosomes and plasmids (161). The optimal therapy for ESBL-producing Aeromonas infections remains undefined due to the rarity of clinical reports. With initial non-carbapenem antimicrobial therapy, two patients with pneumonia and one with necrotizing fasciitis failed (50, 129, 165), whereas three patients with non-critically ill bacteremia survived (161).
Fluoroquinolone resistance among clinical Aeromonas isolates remained uncommon, < 10% (8, 31, 90, 99, 142, 143). However, an increasing ciprofloxacin resistance rate was noted in Aeromonas isolates associated with intra-abdominal infections in the Asia-Pacific region, from 7.8% between 2003 and 2006 to 16.6% between 2007 and 2010 (101). Fluoroquinolone-resistant Aeromonas infections following leech therapy (53, 147) and environmental Aeromonas isolates carrying plasmid-mediated qnrS2 gene have been reported (39, 105). Therapeutic efficacy of fluoroquinolones has been demonstrated in vivo for murine Aeromonas infections and clinically in a clinical study (80, 82).
Tetracycline resistance rate among clinical Aeromonas isolates varied geographically, 5% in Australia, 9%-25% in Europe and Latin America, 39%-49% in two hospitals in Taiwan (8, 85, 90, 100, 123, 142). The determinant of tetracycline resistance would be related to the plasmid (123). Minocycline and cefotaxime in combination have been demonstrated to be synergistic against a clinical isolate of A. hydrophila in vitro and in mice with Aeromonas peritonitis and bacteremia (83).
Tigecycline was active against nearly all Aeromonas isolates tested, with a susceptible rate of 99.5%-100%, whereas 43% of clinical isolates were resistant to colistin (8, 100). Aminoglycoside resistance remains rare worldwide (8, 31, 78, 101, 143). Overall, in addition to well-known chromosomally encoded beta-lactamases, aeromonads would acquire plasmids or integron-mediated resistance genes, expressing resistance to one or multiple classes of antimicrobial agents. These findings suggested the role of aeromonads as reservoirs or vectors of antimicrobial resistance determinants through horizontal gene transfer between aeromonads and coexistent bacteria in aquatic or gut microenvironments (25, 104). Therefore, the early impression that antimicrobial resistance by plasmid-mediated beta-lactamases would not be a problem in Aeromonas species may not be valid (73).
Given the varied susceptibility in Aeromonas species, antibiotic selection must be guided by species identification and in vitro susceptibility testing. However, there are discrepancies among various in vitro susceptibility test methods (92). Of disc diffusion, there was a good correlation with agar dilution method for piperacillin, cefotaxime, cefepime, ofloxacin, ciprofloxacin, gentamicin, amikacin, tetracycline and trimethoprim-sulfamethoxazole, but not for carbapenems, ticarcillin, ticarcillin-clavulanic acid, amoxicillin-clavulanic acid, tobramycin, and tigecycline (86, 92). Additional tests, such as cefepime-clavulanic acid synergy tests or MHT for screening of ESBL or carbapenemase production, respectively, should be performed in selected Aeromonas isolates and clinical conditions (160, 161).
ANTIMICROBIAL THERAPY
Antibiotic therapy with 3rd- or 4th-generation cephalosporins or fluoroquinolones for Aeromonas infection is rationale, especially for those patients with immunocompromised conditions, such as liver cirrhosis or malignancy. Drug of choices should be tailored according to local prevalence of drug-resistance in aeromonads. Antibiotics recommended for Aeromonas infections of different sites are summarized in Table 4 and discussed below in detail.
Gastrointestinal Infections
Aeromonas-associated gastroenteritis in immunocompetent persons is usually acute and self-limited. Therefore antimicrobial therapy is not routinely recommended. For those with intractable diarrhea, serious illness, or high risk of systemic infection, especially in patients with hematological malignancy or hepatobiliary diseases, therapy with antibiotics seems reasonable (63). Treatment of chronic diarrhea with trimethoprim-sulfamethoxazole (131) and acute diarrhea in a putative outbreak with ciprofloxacin (117) has been reported. Nevertheless, due to lack of controlled clinical trials and the increasing antibiotic resistance in Aeromonas species, the optimal regimen for such infections is not defined. Considering other co-pathogens, commonly causing bacterial gastroenteritis, such as Salmonella, Shiegella, Campylobacter, E. coli or Vibrio species, a fluoroquinolone is the drug of choice for severe gastroenteritis, if Aeromonas infection is suspected.
Biliary tract infections
Successful drainage in addition to appropriate antibiotic therapy is essential for successful treatment. Fluoroquinolones, 3rd- or 4th-generation cephalosporins, and aminoglycosides are considered the drugs of choice for patients with Aeromonas biliary tract infections (22, 125).
Spontaneous Bacterial Peritonitis
Immediate use of appropriate antibiotic is of clinical importance because Aeromonas SBP is a fatal disease in the patients with severely decompensated liver. However, it is important to perform ascites culture before or immediately after initiation of antimicrobial therapy, as cultures of ascitic fluid obtained 3 hours after antimicrobial therapy were sterile (162). Cefotaxime, a 3rd-generation cephalosporin with excellent penetration into ascites and without nephrotoxicity, is the appropriate drug as empirical therapy for SBP due to common Enterobacteriaceae pathogens (44). Antimicrobial therapy with a fluoroquinolone and the combination of a 3rd-generation cephalosporin and a tetracycline analogue are the plausible alternatives, if emergence of antimicrobial resistance during cefotaxime therapy is considered (162).
Soft-tissue Infections
For patients with posttraumatic wound and a history of freshwater or seafood contact or medicinal leech therapy, particularly those with immunocompromised underlying illness, empirical therapy with a third cephalosporin with or without doxycycline, aztreonam, a 4th-generation cephalosporin, or a fluoroquinolone, may be indicated. In southern Taiwan, because of similar dermatological presentations in necrotizing fasciitis caused by V. vulnificus or Aeromonas species, cefotaxime (2g every 6 h) and minocycline (100 mg every 12 h), is recommended as the first-line therapy for those cases. For patients with a history of cephalosporin allergy, a fluoroquinolone, such as ciprofloxacin (i.v. 200-400 mg or p.o. 500 mg every 12 h), is an alternative regimen. The optimal antimicrobial agent would vary by different geographic regions and require the consideration of local susceptibility profile of Aeromonas strains. For example, A. dhakensis, as the major Aeromonas species causing soft tissue infections in southern Taiwan, has decreased susceptibility to ceftriaxone and imipenem (27). Therefore, these drugs should be used with caution when treating severe A. dhakensis infections. Piperacillin-tazobactam, cefepime, gentamicin, minocycline, and levofloxacin were in vitro active against A. dhakensis (27). Therapy should be modified according to the in vitro susceptibility for individual causative isolates. Surgical debridement of necrotic tissues is usually necessary.
Bacteremia
Although combination therapy of an aminoglycoside and a cephalosporin has been suggested as an appropriate regimen for Aeromonas bacteremia (60), no therapeutic superiority of combination therapy, as compared with monotherapy, has been demonstrated (82). Furthermore, selection of resistant mutants after beta-lactam therapy for Aeromonas bacteremia, was only documented in 2 (3.4%) of 58 episodes (82). A large-scale observational study also found that combination treatment showed no additional therapeutic benefit over beta-lactam monotherapy in non-neutropenic patients with gram-negative bacillary bacteremia (97). Therefore, for definite treatment of Aeromonas bacteremia, we recommend a beta-lactam agent: cefotaxime (1-2g every 6 h), ceftriaxone (1-2g every 12 h), or ceftazidime (1-2g every 8 h), with or without minocycline (i.v. or p.o. 100mg every 12 h), if they are active against the causative isolates. The duration of therapy should be no less than 10-14 days. Other bactericidal agents, such as aztreonam (1-2g every 8 h), cefepime (1-2g every 12 h), or a fluoroquinolone (ciprofloxacin i.v. 400mg or p.o. 500mg every 12 h, or i.v. or p.o. levofloxacin 500mg every 24 h) are reasonable alternatives.
However, given the risk of selection of the resistant subpopulation in Aeromonas with chromosomally encoded beta-lactamases, the use of a beta-lactam agent (except a 4th-generation cephalosporin) for bacteremia with a high bacterial burden or ischemic foci should be cautious. Hence, for severe infection due to Aeromonas spp. carrying AmpC beta-lactamase, such as A. hydrophila, A. caviae, or A. dhakensis, 4th-generation cephalosporins would be preferred if the causative isolate is not an EBSL producer. Carbapenems can be considered in severe bacteremia due to Aeromonas species without CphA carbapenemase, such as A. caviae, unless acquired carbapenem resistance is demonstrated. To avoid the complexity of beta-lactamase production, an in vitro active fluoroquinolone could be an alternative.
Pneumonia
According to a study of 84 cases of Aeromonas pneumonia in southern Taiwan, more than 80% of the clinical isolates were susceptible to 3rd- or 4th-generation cephalosporins, aminoglycosides, fluoroquinolones, and imipenem (24). In contrast, most of the isolates were not susceptible to ampicillin or 1st-generation cephalosporins. Therefore, 3rd- or 4th-generation cephalosporins as well as fluoroquinolones could be considered as the drug of choice for patients with severe Aeromonas pneumonia.
Specific Infections
Meningitis
Meningitis caused by Aeromonas species is rare. Ten cases, including 5 adults and 5 pediatric patients were summarized in a review (121), and thereafter at least another 3 cases were reported (38, 88, 134). Such a rare infection was generally secondary to metastatic dissemination from primary bacteremia, and diarrhea may or may not be present and sometimes associated with skin and soft-tissue manifestations. It occurred in individuals with underlying hepatic illness or neonates, or following medicinal leech therapy. High doses of 3rd-generation cephalosporins (cefotaxime 2g every 4 h or ceftriaxone 2g every 12 h) or meropenem (2g every 8 h) for three weeks could be considered for Aeromonas meningitis.
Endocarditis
With the exclusion of one case of unknown diagnostic details (29), two cases of Aeromonas endocarditis, involving aortic valve have been reported (36, 120). Both patients were elderly who had chronic underlying illness. Although endocarditis was controlled by beta-lactam-aminoglycoside combination therapy (carbenicillin plus gentamicin and cefazolin plus gentamicin, respectively), both died of their underlying illness. Given the favorable bacteriologic outcome from the above reported cases, combination therapy of an aminoglycoside plus a beta-lactam seems reasonable. Nevertheless, penicillins and narrow-spectrum cephalosporins have variable antimicrobial activity against clinical Aeromonas isolates, so we suggest a broad-spectrum cephalosporin (cefotaxime 2g every 4 h or ceftriaxone 2g every 12 h) for 4-6 weeks, in conjunction with an aminoglycoside (gentamicin 1.5-1.7mg/kg every 8 h) for 2 weeks. Fluoroquinolones may be useful, if the patient is allergic to beta-lactam agents or there is a concern for inducible beta-lactam resistance.
Eye Infections
Lipophilic drugs, such as chloramphenicol, trimethoprim-sulfamethoxazole and tetracyclines, show reasonably good vitreous penetration (124), but a bactericidal agent, i.e., trimethoprim-sulfamethoxazole, might be more reliable for severe, invasive infections. Ciprofloxacin is promising in systemic treatment of gram-negative bacterial endophthalmitis (87). In addition to virtrectomy, intra-vitreous administration of amikacin or ceftazidime plus systemic administration of ciprofloxacin or trimethoprim-sulfamethoxazole, if active in vitro, would be the preferred regimen. However, since the case number of Aeromonas endophthalmitis was small and therefore the optimal regimen remains undefined.
ADJUNCTIVE THERAPY
In invasive soft-tissue infections, early and aggressive surgical debridement is mandatory. Amputation of the affected extremity may be necessary. However, the prognosis of necrotizing soft-tissue infection remains poor. Among 52 cases of Aeromonas necrotizing soft-tissue infections with or without concomitant bacteremia from four reports from Taiwan (26, 82, 94, 145), even with aggressive surgical interventions for most cases, 17 (32.7%) eventually died.
VACCINES
There are no vaccines available for these organisms.
PREVENTION
The most important preventive measure is to avoid physical contact with marine microorganisms or wild water or incidental ingestion of contaminated food or water. Susceptible hosts, especially individuals with hepatic cirrhosis, biliary tract diseases, or malignancy, should avoid recreational activities in wild water, drinking of unprocessed water, and eating uncooked seafood.
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Tables
Table 1. Significance of Aeromonas Species for Human Infections.
| Clinical significance | Species |
|---|---|
| High | A. hydrophila, A. veronii, A. caviae, A. dhakensis |
| Medium | A. jandaei, A. media, A. bestiarum, A. trota, A. schubertii |
| Low or not reported in human infections | A. taiwanensis, A. sanarellii, A. allosaccharophila, A. bivalvium, A. encheleia, A. eucrenophila,A. molluscorum, A. popoffii, A. simiae, A. tecta, A. salmonicida |
Table 2. Summary of MIC50/MIC90 (μg/mL) of Aeromonas Species in the English Literature.
| Antibiotics | Morita (Asia) (111) | Burgos (Spain) (16) | |||||
|---|---|---|---|---|---|---|---|
| A. hydrophila, n=101 | A. caviae, n=12 | A. sobria, n=69 | A. hydrophila, n=87 | A. caviae, n=412 | A. sobria, n=23 | ||
| Amikacin | |||||||
| Amoxicilln/clavulanate | 10/20 | 10/20 | 20/40 | ||||
| Ampicillin | >256/>256 | >256/>256 | 128/>256 | 64/128 | 64/>128 | 128/>128 | |
| Ampicillin/sulbactam | |||||||
| Aztreonam | 1/0.5 | ≤0.06/0.12 | ≤0.06/0.12 | ≤0.06/0.25 | ≤0.06/0.25 | ≤0.06/0.13 | |
| Cefazolin | 16/>128 | 32/>128 | 8/32 | ||||
| Cefoperazone | 2/16 | 1/8 | 1/4 | ||||
| Cefotaxime | 2/8 | 1/4 | 1/4 | 0.13/0.5 | 0.23/1 | ≤0.06/0.25 | |
| Cefoxitin | 8/64 | 4/16 | 1/8 | ||||
| Ceftazidime | |||||||
| Cefepime | |||||||
| Ceftriaxone | 1/8 | 1/4 | 0.5/2 | ||||
| Cefuroxime | 2/16 | 2/4 | 1/8 | ||||
| Cephalothin | |||||||
| Chloramphenicol | 1/4 | 2/4 | 1/4 | ||||
| Ciprofloxacin | |||||||
| Levofloxacin | |||||||
| Gentamicin | |||||||
| Imipenem | 0.5/4 | 0.25/0.5 | 0.5/2 | ||||
| Minocycline | |||||||
| Moxalactam | 1/8 | 1/4 | 1/4 | ||||
| Ofloxacin | ≤0.06/≤0.06 | ≤0.06/≤0.06 | ≤0.06/≤0.06 | ||||
| Piperacillin | 64/128 | 32/128 | 64/128 | 2/4 | 2/8 | 0.5/32 | |
| Piperacillin/tazobactam | |||||||
| Tetracycline | 0.25/8 | 0.5/2 | 0.5/16 | ||||
| Ticarillin | 128/128 | 128/128 | 64/128 | 16/64 | 16/128 | 128/>128 | |
| Tobramycin | |||||||
| Co-trimoxazole | 8/128 | 4/>128 | 0.5/2 | ||||
Table 2 Cont'd
| Antibiotics | Ko (Taiwan) (85) | Overman (US) (122) | ||||||
|---|---|---|---|---|---|---|---|---|
| A. hydrophila, n=142 | A. caviae, n=32 | A. sobria, n=59 | A. jandaei, n=17 | A. schubterii, n=12 | A. trota, n=15 | A. veronii, n=12 | ||
| Amikacin | 4/8 | 2/4 | 4/8 | 4/8 | 4/16 | 4/8 | 8/16 | |
| Amoxicilln/clavulanate | ||||||||
| Ampicillin | 256/>512 | 128/>512 | 256/>512 | 4/8 | ||||
| Ampicillin/sulbactam | 8/16 | 8/8 | ||||||
| Aztreonam | 0.06/4 | 0.06/0.5 | 0.03/0.12 | 8/8 | 8/8 | 8/8 | 8/8 | |
| Cefazolin | 16/- | 4/- | 4/16 | 4/- | ||||
| Cefoperazone | ||||||||
| Cefotaxime | 0.5/32 | 0.25/32 | 0.06/32 | 4/4 | 4/4 | 4/4 | 4/4 | |
| Cefoxitin | 2/8 | 2/- | 8/16 | 2/4 | ||||
| Ceftazidime | 2/2 | 2/2 | 2/2 | 2/2 | ||||
| Cefepime | ||||||||
| Ceftriaxone | 1/128 | 0.5/32 | 0.006/4 | 4/4 | 4/4 | 4/4 | 4/4 | |
| Cefuroxime | 2/128 | 8/128 | 0.5/32 | 2/2 | 2/8 | 2/4 | 2/2 | |
| Cephalothin | >128/>128 | >128/>128 | 8/>128 | |||||
| Chloramphenicol | ||||||||
| Ciprofloxacin | 0.008/0.5 | 0.004/0.06 | 0.008/0.25 | 1/1 | 1/1 | 1/1 | 1/1 | |
| Levofloxacin | ||||||||
| Gentamicin | 1/8 | 1/4 | 2/8 | 2/4 | 2/4 | 2/2 | 2/4 | |
| Imipenem | 2/4 | 0.12/0.25 | 2/8 | 8/- | 4/4 | 4/4 | 8/- | |
| Minocycline | ||||||||
| Moxalactam | 0.06/4 | 0.06/1 | 0.03/0.5 | |||||
| Ofloxacin | 0.03/0.5 | 0.03/0.5 | 0.015/0.5 | 2/2 | 2/2 | 2/2 | 2/2 | |
| Piperacillin | 32/- | 8/16 | 8/8 | 8/16 | ||||
| Piperacillin/tazobactam | ||||||||
| Tetracycline | 4/32 | 2/64 | 8/64 | |||||
| Ticarillin | 32/512 | 16/256 | 64/512 | 64/- | 8/32 | 8/8 | 32/64 | |
| Tobramycin | 1/32 | 2/16 | 2/32 | 4/4 | 4/- | 2/2 | 4/6 | |
| Co-trimoxazole | 0.5/128 | 2/128 | 1/256 | 0.5/0.5 | 0.5/0.5 | 0.5/0.5 | 0.5/0.5 | |
Table 2 Cont'd
| Antibiotics | Streit (Europe/Asia) (142) | Chen (Taiwan) (27) | ||
|---|---|---|---|---|
| Aeromonas spp., n=144 | A. hydrophila, n=13 | A. dhakensis, n=37 | ||
| Amikacin | ||||
| Amoxicilln/clavulanate | 16/>16 | |||
| Ampicillin | >16/>16 | |||
| Ampicillin/sulbactam | ||||
| Aztreonam | ||||
| Cefazolin | ||||
| Cefoperazone | ||||
| Cefotaxime | ||||
| Cefoxitin | ||||
| Ceftazidime | ||||
| Cefepime | <0.5/<0.5 | <0.5/<0.5 | ||
| Ceftriaxone | ≤0.25/1 | <0.125/0.25 | 1/2 | |
| Cefuroxime | 2/8 | 1/2 | 2/4 | |
| Cephalothin | ||||
| Chloramphenicol | ||||
| Ciprofloxacin | ≤0.03/0.12 | |||
| Levofloxacin | ≤0.03/0.25 | <0.125/0.5 | <0.125/0.25 | |
| Gentamicin | 0.25/0.5 | 0.5/0.5 | ||
| Imipenem | 0.5/4 | 2/16 | ||
| Minocycline | 1/2 | 1/4 | ||
| Moxalactam | ||||
| Ofloxacin | ||||
| Piperacillin | ||||
| Piperacillin/tazobactam | 2/2 | 2/2 | ||
| Tetracycline | ≤2/>8 | |||
| Ticarillin | ||||
| Tobramycin | ||||
| Co-trimoxazole | ≤0.5/>2 | |||
Table 3. Species-Specific Distribution of Chromosome-Mediated Beta-Lactamases Among Aeromoands.
| Species | Chromosome-mediated β-lactamases, Amber classification | ||
|---|---|---|---|
| Class B, MBL | Class C, AmpC | Class D, penicillinase | |
| A. hydrophila | + | + | + |
| A. caviae | - | + | + |
| A. veronii | + | - | + |
| A. dhakensis | + | + | + |
| A. enteropelogene (formerly A. trota) | - | + | - |
| A. taiwanensis | - | + | + |
| A. schubertii | - | - | + |
MBL = metallo-beta-lactamase.
Table 4. Recommendations of Antimicrobial Therapy for Aeromonas Infections.
| Sites of infection | Drug of choice | Duration of therapy | References |
|---|---|---|---|
| Primary bacteremia | 3rd- or 4th-generation cephalosporin, aztreonam, fluoroquinolone or in combination with a tetracycline analogue | 10-14 days | 83 |
| Biliary tract infection | Fluoroquinolone; 3rd- or 4th-generation cephalosporin | 10-14 days; drainage for biliary tract obstruction always necessary | 22, 32 |
| Spontaneous bacterial peritonitis | 3rd-generation cephalosporin; fluoroquinolone | 10-14 days | 163 |
| Skin and soft tissue infections | 3rd- or 4th-generation cephalosporin in combination with a tetracycline or gentamicin; piperacillin-tazobactam; fluoroquinolone | 10-14 days; surgical debridement if necessary | 27 |
| Gastrointestinal infections | Fluoroquinolone; trimethoprim-sulfamethoxazole | 5-7 days, if no complications | 118, 132 |
| Pneumonia | Fluoroquinolone; 3rd- or 4th-generation cephalosporin | 10-14 days | 24 |
| Meningitis | 3rd- or 4th-generation cephalosporin; meropenem | 3 weeks | 39, 89, 126, 135 |
| Endocarditis | 3rd- or 4th-generation cephalosporin in combination with an aminoglycoside; fluoroquinolone | 4-6 weeks (in combination with aminoglycoside for 2 weeks) | 121 |
What's New
None.
Guided Medline Search For:
Reviews
Baron EJ. Flow chart for identification of enteric fecal pathogens
Golnaz J, Zuravleff J. Retinitis and Endophthalmitis. 2007.