L. adecarboxylata is an aero-anaerobic, pigmented, peritrichous-flagellated, mesophilic bacilli that belong to the Enterobacterals family. The term enteric group 41 or Escherichia adecarboxylata was initially described by Leclerc in 1962 as referring to the bacteria. However, various electrophoretic and nucleic acid methods separated it from the genus Escherichia and renamed it L. adecarboxylata [1-2]. L. adecarboxylata is commonly distributed in nature in ubiquity and has been isolated from various environmental sources such as water, soil, oil reservoirs, milk, industrial fat, and eggshells. It has been a normal flora of the gastrointestinal tract of normal humans and part of the gut flora in animals [16, 21]. Interestingly, it has been found in various clinical samples, such as urine, blood, wound, bone, bronchial wash, gall bladder, and cardiac valve [16, 22-25].
In the current report, L. adecarboxylata was isolated from a rectal swab to screen for the presence of multi-drug resistant organisms (MDROs). Less than 48 hours prior to the rectal swab collection, the patient suffered from an infected sacral bedsore where she was subjected to prompt surgical intervention and wound swab culture. The wound swab revealed significant growth of multidrug-resistant Acinetobacter baumannii (MDR-Ab) that exhibited a symmetrical antibiotic susceptibility testing to the detected MDR-Ab in rectal swab, Table 1.
Two studies have suggested a low pathogenic potential by L. adecarboxylata [7,14]. These findings are consistent with that of other studies, which asserted that the immunological status of infected patients by L. adecarboxylata tends to demand other germs as a co-infecting agent to establish an infection in immuno-competent patients. In contrast, it emerged as a monomicrobial infection in immunocompromised subjects . In the current case, both aerobic and anaerobic blood cultures were negative in all collection intervals, which supports previous reports suggesting that this bacterium is less invasive. Additionally, considering that the patient is non-immunocompromised and found as a polymicrobial infection, it seems likely that the strain is dependent on other co-infecting germs to establish an infection.
These results corroborate the findings of a previous study on the cytotoxic effect of L. adecarboxylata in human HeP-2 epithelial cells in an in-vitro study where the bacteria failed to invade or adhere to the cells . However, several cases presented as monomicrobial infections in subjects without pre-existing conditions (non-immunocompromised) [21,27, 29-32]. The contradicting scientific evidences highlight nothing but one notion that there are many gaps and unexplored spots in the analysis of the pathogenicity of L. adecarboxylata.
The source of infection by L. adecarboxylata is exceptionally blurry. Moreover, there is limited comprehensive knowledge about the route of transmission. However, there are several former hypotheses of infectious transmission that different authors have described: (I) bacterial translocation via the genitourinary tract, (II) host invasion through catheter or wounds access, and (III) bacterial translocation in the gastrointestinal tract across the mucosal barrier [15,24,26,27,34]. The second and third are possible routes of infection in our patient. Undeniably, catheter-induced infections are reported in the literature, with apparent evidence of the role of catheter and urinary tract infections [35-36]. A bacterial translocation through the genitourinary tract and catheter-induced implantation is less likely, as urine cultures were negative for L. adecarboxylata at all intervals. Keeping in mind that there are no reported cases of L. adecarboxylata in the same healthcare setting, positively favouring the argument to exclude transmission through healthcare workers' hands.
It is essential to note that our patient has a history of a long list of underlying conditions which lead to fluctuations in her immune system but with no diagnostic evidence of low numerical metrics in the white blood cell count in the general or absolute cell-cell count. In line with that, according to a study by Simpson , opportunistic infections were found in association with leukopenia in a context of bacterial infection caused by immunodeficiency in incidences other than AIDS. Other evidence has been reported demonstrating leukopenia, low CD4 count, and a significantly high vulnerability to opportunistic infections in a context other than AIDS as a causative agent for various opportunistic infections .
Another potential route of infection is the bacterial translocation in the gastrointestinal tract across the mucosal barrier. It is a multifaceted route of transmission, some have been investigated, and others are yet to be explained. It has been evidenced that bacteraemia could occur on such a transmission route. To date, only five cases reported in the literature will be used to evaluate the certainty of the previously stated route of transmission. A recent study reported bacteraemia by translocation of L. adecarboxylata into the gastrointestinal tract in a competent patient with Hirschsprung disease . Three other cases reported bacteraemia with no history or current record of undergoing invasive medical interventions [24, 40-41].
Furthermore, a 5th case reported bacteraemia due to an invasive intervention on the gastrointestinal tract, which led to severe alterations in the mucosal membranes.
In our patient, blood culture bottles were negative during her lengthy hospital stay. These relationships can be hypothetically partly explained by another possible route of infection that has not yet been described: the possibility of gut flora borne by rectal bleeding (we describe it as rectal bleeding-borne gut flora). As it is known that L. adecarboxylata is part of the normal gastrointestinal flora [16,21], bearing in mind the chronic history of the patient having erosive gastropathy and heavy rectal bleeding before rectal swab collection, Hence, it could possibly be hypothesized that intestinal bleeding has been carried out by various sections of the intestinal microbiota in the rectal area. In reviewing the literature, no data was found on the association between rectal bleeding and L. adecarboxylata. However, dysbiosis in the gastrointestinal microbiota ecosystems could cause significant changes .
The frequency of L. adecarboxylata in human samples is unknown in Oman and it is the case in most other countries. However, a relatively recent 13-year retrospective single institutional study on Leclercia adecarboxylata infections in southern Hungary revealed 2-3 isolate frequency per year with a range of 1-4 . The same study  asserted a median age of 57 years old (age range:12-80) with more frequency in males (1.25 male-female ratio: 10 males: 8 females). Indeed, a variation in demographic characteristics could exist in other studies. The study also reported that 61.1% of the study population has underlying immunosuppression. In another study, the frequency of L. adecarboxylata in clinical specimens is estimated to be 0 to 5. However, the absolute frequency of infections caused by L. adecarboxylata is still to be determined, as it has been underreported for many decades since its first emergence .
The underestimation of L. adecarboxylata infections stemmed principally from the misidentification with other strains of the same family, Enterobacterals, such as Escherichia coli, as both strains share resemblance metabolic and morphological characteristics features [16, 45-56]. It should be noted that the two strains exhibited close and indistinguishable yields by automated systems, and it is misidentified if no further investigations have been carried out [15-16]. Thus, it indicates that the risk of misidentification is extremely eminent in the case where biochemical approaches are followed, which is the typical case in low setting laboratory. Despite that, the introduction of advanced automated systems, molecular sequencing, and MALDI-TOF MS revolutionized identification methods [47-48]. A similar situation was phased in our patient, L. adecarboxylata was misidentified as Citrobacter koseri using API and as Pantoea species using the Vitek2 system, which has not been reported in the literature, triggering an urgent comparative study in the same manner as conducted with E. coli [16,18]. The strain was correctly identified using MALDI-TOF, although a score of <2 triggered further identification through 16S rRNA.
It has been postulated that, in laboratories with low resources, the utility of chromogenic media such as CPS Elite agar and fosfomycin agar is promoted to differentiate between E. coli and L. adecarboxylata [16,18].
There are no guidelines for treating L. adecarboxylata infections, yet antibiotic regimens have shown efficient resolution of infections, including fluoroquinolones and beta-lactams [15,49]. Another study revealed more than 90% pan sensitivity in 31 of 34 L. adecarboxylata isolates . However, resistance has been reported commonly with fosfomycin . In the Spiegelhauer et al. study , 9 of 30 isolates showed resistance to ampicillin, and 8 of 10 isolates were resistant to fosfomycin. It can thus be suggested that these antibiotics are not recommended to treat L. adecarboxylata infections.
L. adecarboxylata resistant species producing ESBL were reported in the literature [39,45,50], which complicates therapeutic decisions leading to the use of broad-spectrum antibiotics such as carbapenems. More terrifying are the cases of Carbapnemase-Producing strains (CPE). In a study reported by Shin et al. , L. adecarboxylata was isolated from a blood culture of an immunocompromised patient with malignancy (breast cancer) in chemotherapy via a central catheter inserted peripherally. PCR confirmed the isolate for the presence of blaCTX-M-3 (resistant to aminoglycosides), blaTEM-1 (resistant to trimethoprim-sulfamethoxazole) and intl1 with aadA2 and dfrA12 genes. Sun et al.  reported isolation of L. adecarboxylata from a 43-year-old male sputum sample harboured the genes blaNDM-1, blaTEM, blaOXA-1, and blaCTX-M-1 that illustrated resistance to all antibiotics tested. Another study by Geffen et al.  revealed the blaKPC-2 gene in a rectal swab confirmed by 16S of rDNA sequencing. Only one reference in the literature has reported L. adecarboxylata with the resistant blaVIM-1 gene in a non-clinical sample . The study carried out by Papagiannitsis et al.  aimed to study the compliance to hand hygiene in Na Homolce Hospital staff, Prague, Czech Republic, that identified the strains with MALDI TOF MS confirmed it via 16s rRNA gene sequence. To our knowledge and through searching the literature, the current report is the first evidence to highlight L. adecarboxylata-resistant species producing blaVIM-1 in a rectal swab in the scientific literature.
Several limitations must be conveyed. The patient's death renders further examination to verify or falsify the previously described propositus concerning the possible route of infection. Not to mention the inability to pursue an accurate evaluation of the course of antibiotic therapy, although it was widely reported in the literature. There is ample room for further progress in determining the association of biofilms and bacterial resistance , because it has been neglected in discussing the possible path of infections of L. adecarboxylata.