Hubbry Logo
Citrobacter koseriCitrobacter koseriMain
Open search
Citrobacter koseri
Community hub
Citrobacter koseri
logo
7 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Citrobacter koseri
Citrobacter koseri
Citrobacter koseri
View on Wikipedia
from Wikipedia

Citrobacter koseri
Scientific classification Edit this classification
Domain: Bacteria
Kingdom: Pseudomonadati
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Enterobacteriaceae
Genus: Citrobacter
Species:
C. koseri
Binomial name
Citrobacter koseri
Frederiksen 1970[1]
Synonyms
  • Citrobacter diversus
    (Burkey 1928)
    Werkman & Gillen 1932    [1]
Citrobacter koseri
SpecialtyInfectious disease

Citrobacter koseri, formerly known as Citrobacter diversus, is a Gram-negative non-spore forming, rod-shaped bacterium. It is a facultative anaerobe capable of aerobic respiration. It is motile via peritrichous flagella.[2] It is a member of the family of Enterobacteriaceae. The members of this family are part of the normal flora and commonly found in the digestive tracts of humans and animals.[1] C. koseri may act as an opportunistic pathogen in individuals who are immunocompromised.[3]

It rarely is community-acquired and mainly occurs as hospital-acquired infections. Infections caused by C. koseri can lead to various symptoms, including fever, chills, diarrhea, and abdominal pain. In severe cases, the bacterium can cause sepsis, meningitis, or brain abscesses. Brain abscesses have a high rate of mortality and complications, particularly in neonates. The transmission of C. koseri could be vertical from mother to fetus, and other sources can be horizontal by asymptomatic nursery staff.[4]

Signs and symptoms

[edit]

Neonates infected with C. koseri usually present with sepsis, meningitis, seizures, apnea, and a bulging fontanelle. No evidence of a stiff neck or high-grade fever is present.[5]

Complications

[edit]

Occasionally, it causes meningitis, but it can cause sepsis and ventriculitis.[5]

Arterial and venous infarctions are possible because of the bacterial infiltration along the main vessel; exudates within the ventricles and ventriculitis may obstruct the ventricular foramina and result in multicystic hydrocephalus with consequent long-lasting shunting difficulties and necrotizing meningoencephalitis with pneumocephalus has been reported.[5]

Pathogenicity

[edit]

The pathogenic mechanism is poorly understood. C. koseri may uniquely penetrate, survive, and replicate into vascular endothelial cells and macrophages. Furthermore, it survives in phagolysosomal fusion and replicates within macrophages, which may contribute to the establishment of chronic abscesses.[5][6]

Diagnosis

[edit]

Medical imaging

[edit]

Early and massive tissue necrosis is a specific feature of C. koseri brain infection. The early stage of the disease predominates in the white matter, causing cerebritis; the later stage is marked with necrotic cavities in multiple locations. The cavities are initially square and not tense, but when pus forms and collects in these cavities, they tend to become more rounded; a persisting cavity leads to septated ventriculitis that may result in multicystic hydrocephalus.[5]

Early cerebritis is seen, and multiple large cavities can be seen in the late stage of the disease; abscesses formation, contraction of the cavities, and hydrocephalus due to ventriculitis are observed in the late follow-up.[5][6]

Pathology

[edit]

Macroscopic findings include purulent exudates, opaque leptomeninges (thinning of meninges), pus, and ventriculitis/ ependymitis.

Microbiology

[edit]

In samples collected from cerebrospinal fluid, C. koseri grows well on any ordinary medium; they produce unpigmented, colorless mucoid colonies. If incubated for 24 hours in other media such as indole, citrate, and adonitol, C. koseri will be positive, hydrogen sulfide negative in Kligers’ iron agar, and negative results in lactose, salicin, and sucrose broth as well.[5][7]

Histology

[edit]

Citrobacter koseri may be identified in the walls of congested vessels; the presence of the cavities resulting from the infection does not develop a well-formed fibrotic wall.[5]

Differential diagnosis

[edit]

The differential diagnosis of C. koseri brain abscesses can be confused with other related diseases, so diagnostic imaging is essential to confirm this bacterium. The significant feature of C. koseri is the necrotic cavity which cannot be misidentified as an earlier ischemic or hemorrhagic insult or other mass lesions; congenital/neonatal tumors are uncommon (choroid plexus papillomas, craniopharyngiomas, teratomas); even when they present, they are different from the inflammatory ring of cerebral infection. Early cerebritis should not be mistaken for normal, immature white matter, nor cicatricial leukomalacia.[5][6]

Treatment

[edit]

A broad spectrum cephalosporin and meropenem are often used because of the good penetration into the central nervous system. If the response to the antibiotic is poor, the surgical aspiration of the collected pus reduces the mass effect and enhances the efficacy of the antibiotics.[5][7][8]

Prognosis

[edit]

The prognosis of the C. koseri infection is 20 to 30% of neonates die, and 75% of survivors have significant neurologic damage such as complex hydrocephalus, neurologic deficits, mental delay, and epilepsy.[5]

Control

[edit]

The most effective way to reduce transmission of organisms is regular handwashing.[5]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Citrobacter koseri

View on Grokipedia
from Grokipedia
Citrobacter koseri is a Gram-negative, rod-shaped, motile, non-spore-forming, facultative anaerobic bacterium belonging to the family . It utilizes citrate as a primary carbon source, ferments glucose and other carbohydrates to produce acid and gas, and is characterized as oxidase-negative and indole-positive. Formerly known as Citrobacter diversus, this species is ubiquitous in the environment, commonly inhabiting soil, sewage, water, food, and the intestinal tracts of humans and animals. As an opportunistic nosocomial pathogen, C. koseri primarily affects newborns, immunocompromised individuals, and patients with underlying conditions such as or cancer. It is particularly associated with severe infections, including and brain abscesses, which carry a of up to 30% and lead to neurological sequelae in approximately 80% of survivors. Other notable clinical manifestations include urinary tract infections, bacteremia, , , and sporadic musculoskeletal infections. C. koseri demonstrates significant , often mediated by chromosomal ampC β-lactamases and plasmid-encoded mechanisms, leading to multidrug resistance against β-lactams, , fluoroquinolones, aminoglycosides, and even . As of 2025, carbapenem-resistant clones have been reported spreading across hospitals globally, posing an increasing threat in healthcare settings. This resistance profile complicates treatment, especially in healthcare-associated outbreaks where the bacterium can contaminate equipment and colonize vulnerable populations.

Taxonomy and nomenclature

Etymology

The genus name Citrobacter derives from the Latin feminine citrus (referring to citrate) and the New Latin masculine bacter (a rod), collectively meaning a citrate-utilizing rod, reflecting the organisms' characteristic ability to use citrate as a sole carbon source. This was first proposed in by Werkman and Gillen to describe isolated from and other environments that exhibited this metabolic trait. The species epithet koseri is the New Latin genitive form of Koser, honoring Stewart A. Koser (1895–1973), an American bacteriologist renowned for his pioneering work on citrate utilization tests in the differentiation of enteric bacteria during the early . The species Citrobacter koseri was formally described as a novel taxon in 1970 by Frederiksen, based on phenotypic characteristics distinguishing it from other Citrobacter species within the family . An early name, diversus Werkman and Gillen 1932 (based on Aerobacter diversum Burkey 1928), was proposed but later rejected as a nomen dubium due to inadequate description. Strains now classified as C. koseri were subsequently designated under the later synonym Citrobacter diversus Ewing and Davis 1972 for similar citrate-positive, malonate-utilizing enterobacteria. In No. 67 (1993), the Judicial Commission of the International Committee on Systematic Bacteriology ruled C. koseri as the correct and priority name, rejecting both the 1932 and 1972 uses of C. diversus following evaluations of type strains, phenotypic data, and early DNA hybridization studies that confirmed the synonymy of C. koseri, Levinea malonatica Young et al. 1971, and the 1972 C. diversus.

Classification history

The genus Citrobacter was established in by Werkman and Gillen to accommodate Gram-negative, facultatively anaerobic rods capable of utilizing citrate as a sole carbon source, with C. freundii designated as the based on strains previously identified by Braak in 1928. Early classifications within the focused on biochemical traits such as citrate utilization and gas production from glucose, distinguishing from related like . An early species name, Citrobacter diversus Werkman and Gillen 1932 (from Aerobacter diversum Burkey 1928), was proposed for a citrate-utilizing bacterium but was later rejected as a nomen dubium in 1993 due to loss of the type strain and inadequate original description that did not match later taxa. In 1970, Frederiksen proposed Citrobacter koseri as a new species within the genus, based on biochemical profiling of clinical isolates that exhibited unique fermentation of dulcitol and sorbose, setting it apart from other Citrobacter taxa. Subsequently, in 1971, Young et al. erected the Levinea and named the L. malonatica for a group of strains sharing these traits, emphasizing malonate utilization and serological distinctions, though the genus was later deemed unnecessary. Ewing and Davis in 1972 applied the name C. diversus to the same , relying on expanded biochemical and serological data, but this was determined to be a misapplication of the rejected 1932 name. Nomenclatural confusion persisted due to overlapping descriptions, prompting Frederiksen in 1990 to request a formal opinion from the International Committee on Systematic , arguing that C. koseri, L. malonatica, and the 1972 C. diversus represented a single species distinguishable by at least eight biochemical characteristics from congeners and from the 1932 C. diversus. In No. 67 (1993), the Judicial Commission resolved the issue by designating Citrobacter koseri Frederiksen 1970 as the valid name, rejecting C. diversus (both 1932 and 1972 usages) as a for inadequate description and suppressing the Levinea. The current taxonomic placement of C. koseri in the class , order , and family has been robustly confirmed through 16S rRNA gene sequencing and multilocus sequence analysis, which demonstrate close phylogenetic relatedness to other species while affirming its distinct genomic identity. These molecular approaches, building on earlier biochemical foundations, have solidified its position without further revisions.

Microbiological characteristics

Morphology and physiology

Citrobacter koseri is a Gram-negative, non-spore-forming, rod-shaped bacillus belonging to the family Enterobacteriaceae. The cells are straight rods, typically measuring 0.5–1.0 μm in width and 1.0–2.0 μm in length. It is motile, propelled by peritrichous flagella distributed around the cell surface. As a facultative anaerobe, C. koseri can perform aerobic respiration in the presence of oxygen or switch to under anaerobic conditions. Optimal growth occurs at 37°C and within a range of 6.5–7.5, reflecting its adaptation to human physiological environments. On , it forms colorless colonies indicative of lactose negativity, though some strains exhibit late lactose fermentation. Certain strains of C. koseri produce a capsule, which may contribute to environmental resilience, while sporulation is absent across all isolates.

Biochemical properties

Citrobacter koseri exhibits a characteristic pattern of + + - +, indicating positive for production, , and citrate utilization, but negative for the Voges-Proskauer test. C. koseri is catalase-positive and oxidase-negative. The organism is urease-negative, further supporting its identification in clinical microbiology settings. In terms of fermentation, C. koseri ferments glucose and , producing acid and gas from glucose, which reflects its facultative anaerobic . It typically does not ferment or initially, although delayed positivity may occur in some strains after extended incubation, highlighting variability in sugar utilization that is key for differentiation. The species decarboxylates and positively but lacks activity for decarboxylase, a trait that contributes to its metabolic profile and separation from other species. Additionally, C. koseri reduces to , demonstrating its capability for under certain conditions. C. koseri is positive for activity, as detected by the o-nitrophenyl-β-D-galactopyranoside (ONPG) test, which correlates with its potential for late . A critical differentiator from C. freundii is its ability to utilize malonate as a sole carbon source (unlike most strains of C. freundii), underscoring the importance of this test in species-level identification.

Habitat and epidemiology

Natural reservoirs

Citrobacter koseri is ubiquitous in various environmental niches, primarily due to its enteric origins, and is frequently isolated from , where it contributes to natural microbial communities. It is also commonly detected in water bodies, including freshwater sediments, and in sewage systems, facilitating its persistence and potential dissemination. Additionally, the bacterium is found in various foods, such as ready-to-eat salads, underscoring its adaptability to organic-rich environments. As part of the normal , C. koseri inhabits the intestines of humans at low prevalence. It is similarly present in the gastrointestinal tracts of animals, including birds and mammals like chickens. In , such as the superworm Zophobas atratus, C. koseri has been isolated from the gut, highlighting its broad host range across vertebrates and . The organism is often recovered from food sources, including and contaminated , as well as dairy products like , where it can contaminate during production or handling. C. koseri persists in biofilms on environmental and industrial surfaces, enhancing its survival in moist, nutrient-limited settings. While direct human-to-human transmission is not typical, C. koseri can spread via the fecal-oral route in environments contaminated by or .

Prevalence and risk factors

_Citrobacter koseri is an opportunistic pathogen responsible for 3–6% of nosocomial infections attributed to species globally. This bacterium is particularly prevalent in hospital settings, where it contributes to urinary tract infections, bacteremia, and among vulnerable patients. In neonatal populations, C. koseri holds greater significance, accounting for approximately 4% of all bacterial cases, with rates reaching up to 5% in certain cohorts. The infection is rare yet has severe impact in this group. Infections with C. koseri are more predominant in developing countries, where inadequate and limited access to clean water exacerbate transmission through fecal-oral routes and contaminated environments. Key risk factors include prematurity and in neonates, which compromise immune defenses and increase susceptibility to invasive . Prolonged hospitalization, use of indwelling catheters, and —such as in patients with or undergoing —further elevate the risk of acquisition. Among adults, advanced age, particularly in those over 60 years, is associated with higher vulnerability due to comorbidities and reduced physiological reserves. Outbreaks of C. koseri are frequently traced to contaminated sources in healthcare environments, including and equipment in neonatal intensive care units. Since the , there has been a notable increase in among C. koseri isolates, with rising multidrug-resistant strains complicating treatment and contributing to higher morbidity in affected populations.

Pathogenesis and virulence

Virulence factors

Citrobacter koseri employs a range of factors to enhance its ability to colonize and damage host tissues. Type 1 fimbriae, also known as pili, are critical adhesins that mediate attachment to host epithelial cells, particularly in the urinary tract and . These structures are present in most clinical isolates of C. koseri, enabling initial host cell binding and facilitating subsequent establishment. Hemolysins, including homologs of alpha-hemolysin, contribute to the bacterium's tissue-damaging potential by lysing host cells and erythrocytes, which disrupts cellular and promotes release. Most C. koseri isolates exhibit hemolytic activity on blood agar, underscoring the prevalence of these pore-forming toxins in virulent strains. Iron acquisition systems are essential for C. koseri survival within the iron-limited host environment, with the bacterium uniquely possessing both yersiniabactin and aerobactin siderophores among species. These siderophores scavenge iron from host sources, supporting bacterial growth and persistence during infection. The high pathogenicity island (HPI), a genomic region homologous to that in Yersinia species, encodes the yersiniabactin system along with genes for flagellar and production, significantly enhancing overall ; experimental deletion of the HPI cluster reduces pathogenicity in animal models. Capsular polysaccharides form a protective layer around C. koseri cells, aiding evasion of host immune responses. Additionally, genes involved in biofilm formation allow C. koseri to produce extracellular matrices that promote adherence to surfaces and protect against antibiotics and host defenses. Motility conferred by flagella, encoded partly within the HPI, supports bacterial dissemination. A 36-kDa outer membrane protein has been identified as a potential virulence factor contributing to central nervous system invasion among strains causing brain abscesses.

Mechanisms of infection

Citrobacter koseri, a Gram-negative opportunistic , typically enters the host through the gastrointestinal or urinary tract, where it colonizes mucosal surfaces before ascending to the bloodstream, particularly in immunocompromised individuals such as neonates or those with underlying conditions. This entry route facilitates initial adhesion via structures like type 3 fimbriae, allowing the bacterium to establish infection in vulnerable hosts. In neonates, C. koseri demonstrates a remarkable ability to cross the blood-brain barrier through to and invasion of brain microvascular endothelial cells, which enables dissemination to the and initiation of . This process is exacerbated by the immature blood-brain barrier and underdeveloped immune responses in newborns, permitting rapid bacterial spread from the bloodstream to meningeal spaces. Once inside the host, C. koseri evades innate immunity by surviving and replicating intracellularly within macrophages, resisting through mechanisms that prevent phagolysosomal fusion, thereby subverting the host's antibacterial defenses. Additionally, the release of lipopolysaccharides (LPS) from the bacterial outer membrane acts as an endotoxin, triggering systemic inflammatory responses that can lead to in disseminated infections. Biofilm formation plays a critical role in persistent infections, particularly on indwelling devices like urinary catheters, where C. koseri adheres to surfaces and secretes extracellular polymeric substances, shielding communities of from antibiotics and host immune clearance. This persistence contributes to chronic urinary tract infections and recurrent bacteremia in at-risk patients.

Clinical features

Signs and symptoms

_Citrobacter koseri infections most commonly present in neonates as , characterized by fever, , poor feeding, bulging , and seizures that often occur within 24-48 hours of symptom onset. In addition to these signs, neonates may exhibit , , apneic spells, , temperature instability, and grunting respirations. These presentations are particularly associated with infections in neonates and immunocompromised individuals. In adults, urinary tract infections caused by C. koseri typically manifest with , urinary frequency, flank pain, and . Sepsis and bacteremia due to C. koseri often involve fever, chills, , and , with gastrointestinal symptoms such as noted in cases of enteric involvement. Pneumonia from C. koseri, frequently observed in ventilated or immunocompromised patients, presents with , dyspnea, and .

Complications

Citrobacter koseri infections, particularly in neonates, frequently lead to severe (CNS) complications, with brain abscesses occurring in approximately 75-77% of cases. These abscesses often result in due to obstruction and , contributing to significant neurological deficits such as , , and developmental delays in survivors. In bacteremic patients, C. koseri can cause with organ failure, including renal dysfunction, hepatic impairment, and . complicates about 4% of bloodstream infections, exacerbating multiorgan involvement and increasing mortality risk. Chronic urinary tract infections (UTIs) due to C. koseri in catheterized individuals often progress to or urosepsis, with over half of reported UTIs involving upper tract extension and potential formation. Rare disseminated infections may manifest as or , particularly in immunocompromised hosts, while neonatal cases carry a of up to 30%. Survivors of CNS infections face long-term sequelae, including developmental delays, , seizures, hemiplegia, and , affecting more than 80% of cases.

Diagnosis

Laboratory identification

Citrobacter koseri is initially isolated from clinical specimens using standard microbiological culture techniques on non-selective and selective media. The organism grows well on blood agar, producing smooth, gray, non-hemolytic colonies measuring 2-4 mm in diameter after 24 hours of incubation at 35-37°C. On MacConkey agar, it appears as pink colonies due to lactose fermentation, facilitating differentiation from non-fermenters. Growth on eosin methylene blue (EMB) agar may yield colonies with a greenish metallic sheen, though less pronounced than in Escherichia coli. Direct microscopic examination via Gram staining reveals Gram-negative, straight rods, typically 1.0 × 2.0-6.0 µm in size. is confirmed as positive using a wet mount or semisolid motility medium, characteristic of peritrichous flagella. For definitive identification, automated biochemical systems such as API 20E or VITEK 2 are employed, relying on profiles including positive citrate utilization, decarboxylation, and beta-glucuronidase activity, which distinguish C. koseri from other species. Molecular methods provide rapid and specific confirmation. (PCR) targeting the uidA gene, encoding beta-glucuronidase, or 16S rRNA gene sequencing is used for accurate species-level identification, particularly in ambiguous cases. time-of-flight (MALDI-TOF) mass spectrometry offers a high-throughput alternative, achieving over 95% accuracy for Enterobacteriaceae including C. koseri when using updated databases. In outbreak investigations, serotyping based on O-antigens is performed using slide with specific antisera to subtype strains and trace . Antimicrobial susceptibility testing is essential due to potential multidrug resistance. Disk diffusion or for (MIC) determination follows Clinical and Laboratory Standards Institute (CLSI) guidelines, testing agents such as beta-lactams, aminoglycosides, and fluoroquinolones.

Imaging and pathology

Imaging findings in Citrobacter koseri infections vary by site but commonly reveal suppurative processes such as abscesses and inflammatory consolidations. In central nervous system (CNS) infections, particularly meningitis and ventriculitis in neonates, computed tomography (CT) often shows hypodense lesions indicative of early cerebritis or abscess formation in the frontal lobes or periventricular regions. Magnetic resonance imaging (MRI) provides superior detail, demonstrating ring-enhancing abscesses with surrounding edema, ventriculitis characterized by ependymal enhancement, and in severe neonatal cases, multiple lobulated masses with hemorrhagic components. These features are critical for early detection, as C. koseri has a high propensity for progressing to brain abscesses in up to 75% of neonatal meningitis cases. For urinary tract infections (UTIs), is the initial imaging modality of choice, frequently revealing due to obstruction from infection-related inflammation or calculi, as seen in cases of ascending C. koseri . Complicated UTIs may progress to perinephric abscesses, appearing as complex, hypoechoic or mixed solid-cystic collections adjacent to the , often measuring several centimeters and requiring drainage. In pulmonary infections like , chest typically demonstrates hazy opacities or consolidations, predominantly in the upper or lower lobes, reflecting lobar involvement. Computed tomography (CT) of the chest further delineates dense consolidative infiltrates with air bronchograms, patchy multifocal opacities, or pleural effusions, aiding in distinguishing C. koseri pneumonia from other etiologies in immunocompromised patients. Histopathological examination of infected tissues reveals characteristic features of acute bacterial suppuration. In general, biopsies or surgical specimens show dense neutrophilic infiltrates surrounding areas of necrosis, with Gram staining confirming the presence of gram-negative rods consistent with Citrobacter species. In CNS abscesses, brain tissue exhibits central liquefactive necrosis encapsulated by fibrous tissue, accompanied by reactive gliosis and perivascular inflammation, as observed in both human cases and animal models of neonatal infection. Laboratory culture from aspirated material confirms the pathogen, correlating imaging and pathology findings.

Differential diagnosis

Infections caused by Citrobacter koseri often present with nonspecific symptoms such as fever, , and in neonates or immunocompromised individuals, necessitating differentiation from other common pathogens through microbiological and molecular testing. In , C. koseri must be distinguished from predominant causes like group B Streptococcus (), , and , which together account for over 70% of cases; clinical features overlap, but (CSF) analysis reveals elevated lactate levels (>3.5 mmol/L) in bacterial etiologies including C. koseri, aiding separation from viral mimics, while definitive identification relies on CSF , culture, and PCR assays targeting specific pathogens like . For urinary tract infections (UTIs) and associated bacteremia, C. koseri resembles E. coli, , and in presentation with , flank pain, and systemic signs, but biochemical profiling differentiates them: C. koseri is motile, citrate-positive, indole-positive, and malonate-positive, contrasting with non-motile , oxidase-positive , and malonate-negative E. coli in standard tests; additionally, antimicrobial susceptibility patterns often show C. koseri resistance to similar to other , but species-specific identification via automated systems or 20E strips confirms the etiology. In cases of sepsis, particularly in neonates, C. koseri sepsis mimics viral infections such as or fungal causes like Candida species, with shared features of and multiorgan involvement; blood cultures positive for Gram-negative rods point toward bacterial sources including C. koseri, while multiplex PCR panels detect viral nucleic acids in enterovirus cases, and fungal cultures or beta-D-glucan assays help exclude Candida, emphasizing the need for broad empirical testing in high-risk neonates. Brain abscesses due to C. koseri, often a complication of meningitis, require distinction from those caused by Staphylococcus aureus or anaerobes like Bacteroides species, which present similarly with headache, focal deficits, and ring-enhancing lesions on imaging; aspiration of abscess fluid for culture is crucial, as C. koseri yields Gram-negative bacilli, whereas staphylococcal infections show Gram-positive cocci and anaerobes require prolonged incubation, guiding targeted therapy. A key microbiological feature distinguishing C. koseri from other Citrobacter species, such as C. freundii, is its positive malonate utilization, which supports rapid laboratory speciation.

Treatment

Antimicrobial therapy

Citrobacter koseri exhibits intrinsic resistance to and first-generation cephalosporins, primarily due to the production of chromosomal AmpC β-lactamases, which hydrolyze these agents. However, the species generally remains susceptible to cefepime and like . Empirical therapy for infections caused by C. koseri should therefore avoid and first-generation cephalosporins, favoring cefepime or pending susceptibility testing, especially for invasive infections. Increasing rates of extended-spectrum β-lactamase (ESBL) production, with pooled prevalence around 22% among Citrobacter isolates as of 2022, and carbapenemase production, including metallo-β-lactamase (NDM), at approximately 18% as of 2022, complicate treatment options. Fluoroquinolones such as and aminoglycosides like gentamicin often retain activity against these strains, making them suitable alternatives or adjuncts in empirical regimens. For multidrug-resistant or carbapenem-resistant strains, consider newer beta-lactam/ inhibitors like ceftazidime-avibactam or , guided by susceptibility testing. All antibiotic selections must be guided by local susceptibility patterns and individual isolate testing to optimize outcomes. In cases of neonatal meningitis caused by C. koseri, at 120 mg/kg/day IV divided every 8 hours is recommended for at least 21 days, or until clinical resolution. An such as gentamicin may be added for severe cases to provide synergistic coverage. For urinary tract infections, treatment duration typically ranges from 7 to 14 days with an appropriate agent based on susceptibilities, while infections require 4-6 weeks of therapy.

Management of complications

Management of complications arising from Citrobacter koseri infections requires a tailored, supportive approach, particularly in vulnerable populations such as neonates, where (CNS) involvement is common. For CNS abscesses, which occur in up to 75% of cases caused by this pathogen, early surgical intervention is often essential to reduce mortality and morbidity. Surgical options include stereotactic needle aspiration or drainage to evacuate purulent material, frequently combined with therapy for at least 6-8 weeks. In cases with associated or , may be employed for diversion and to monitor (ICP), preventing further neurological deterioration. Sepsis, a frequent complication especially in immunocompromised or neonatal patients, demands prompt hemodynamic stabilization alongside source control measures. Initial fluid resuscitation with balanced crystalloids, targeting at least 30 mL/kg within the first 3 hours, is recommended to address hypoperfusion, followed by vasopressors such as norepinephrine if remains inadequate. Source control involves removing infected devices like central lines or catheters to halt bacterial dissemination, which is critical in C. koseri-associated bacteremia. In , supportive care in the , including for , further supports recovery. Renal complications, such as progressing to perinephric abscess or , are managed through drainage of abscesses via or surgical methods, with follow-up imaging like computed tomography to assess resolution. In severe cases leading to acute renal failure, or continuous may be initiated to manage fluid overload and electrolyte imbalances, particularly in patients with underlying comorbidities. In neonates, who face the highest risk from C. koseri infections, comprehensive supportive care includes for respiratory compromise and anticonvulsants such as for seizures secondary to or abscesses. Long-term neurodevelopmental monitoring is imperative, involving serial assessments for cognitive, motor, and sensory deficits, given the propensity for permanent sequelae from CNS involvement. A multidisciplinary approach enhances outcomes, incorporating infectious disease specialists for guiding , neurosurgeons for management, and rehabilitation teams for addressing neurological impairments through physical and . Early consultation facilitates coordinated care, reducing complication rates in this high-risk .

Prevention and control

Infection prevention strategies

Citrobacter koseri infections are primarily transmitted through the fecal-oral route, including via contaminated and water, so basic practices form the foundation of prevention. Thorough handwashing with soap and water after , before food preparation, and after contact with potentially contaminated surfaces is essential to interrupt transmission. Safe handling of and water, such as boiling or treating water supplies in areas with poor and ensuring proper cooking and storage of to avoid cross-contamination, further reduces community acquisition risk. In neonates, who are particularly vulnerable—especially premature infants—promoting exclusive provides protective factors like immunoglobulins that help prevent bacterial infections, including those caused by C. koseri. Powdered should be avoided when possible or prepared with strict using boiled water cooled to at least 70°C to kill potential contaminants, as Enterobacteriaceae like C. koseri can survive in improperly handled formula. For individuals undergoing high-risk procedures, such as urologic surgeries, prophylactic antibiotics selected based on local resistance patterns are recommended to cover , including C. koseri, thereby preventing postoperative infections. In vulnerable populations prone to urinary tract infections, education on care is vital; this includes using aseptic insertion techniques, maintaining a closed drainage system, the perineal area daily, and promptly removing catheters when no longer needed. Ongoing community surveillance of antibiotic resistance in C. koseri isolates is crucial for informing prevention efforts and ensuring effective use, as resistance patterns can vary geographically and influence empirical strategies.

Nosocomial measures

Nosocomial s caused by Citrobacter koseri are a significant concern in healthcare settings, particularly among immunocompromised patients, neonates, and those in intensive care units, where the bacterium can lead to outbreaks via contaminated environmental sources such as sinks, toilets, injection materials, and medical equipment. To mitigate transmission, healthcare facilities implement standard prevention protocols tailored to this opportunistic Gram-negative , which is often multidrug-resistant. Core nosocomial measures emphasize hand hygiene as the primary barrier to spread, with reinforced compliance using alcohol-based hand rubs or soap and water before and after patient contact, especially in outbreak scenarios. Contact precautions are recommended for patients colonized or infected with C. koseri, particularly strains exhibiting extended-spectrum β-lactamase (ESBL) or AmpC resistance, involving single-patient rooms, gowns, and gloves during care to prevent cross-contamination. Environmental cleaning with hospital-grade disinfectants targeting high-touch surfaces and water systems is crucial, as C. koseri persists in moist environments and over 70% of Citrobacter infections are nosocomial. Aseptic techniques during invasive procedures, such as insertions and pharmaceutical preparations, are essential to reduce entry points for the bacterium, which thrives in water supplies and contaminated fluids. Antibiotic stewardship programs play a pivotal role by promoting judicious use of broad-spectrum agents like and cephalosporins, thereby curbing the emergence of resistant strains that complicate C. koseri outbreaks, with many reported clusters successfully controlled through these interventions. Active , including routine screening of at-risk units like wards, enables early detection and , aligning with broader multidrug-resistant organism (MDRO) guidelines.

References

  1. https://pmc.ncbi.nlm.nih.gov/articles/PMC11731968/
  2. https://journals.asm.org/doi/10.1128/mra.01228-20
  3. https://academic.oup.com/cid/article/28/2/384/410683
  4. https://publishing.rcseng.ac.uk/doi/10.1308/rcsann.2016.0209
  5. https://globalbiodefense.com/2025/07/21/global-drug-resistant-bacterial-clone-health-threat/
  6. https://www.thelancet.com/pdfs/journals/lanmic/PIIS2666-5247%2825%2900077-1.pdf
  7. https://www.hopkinsguides.com/hopkins/view/Johns_Hopkins_ABX_Guide/540129/all/Citrobacter_species
  8. https://medcraveonline.com/JMEN/antimicrobial-susceptibility-of-citrobacter-koseriisolated-on-clinical-samples-of-hospitalized-patients.html
  9. https://lpsn.dsmz.de/genus/citrobacter
  10. https://lpsn.dsmz.de/species/citrobacter-koseri
  11. https://doi.org/10.1099/00207713-43-2-392
  12. https://doi.org/10.1099/00207713-40-1-107
  13. https://doi.org/10.1128/jb.23.2.167-182.1932
  14. https://www.semanticscholar.org/paper/Biochemical-Characterization-of-Citrobacter-Werkman-Ewing-Davis/843ae136c08d88c14d2bac88b0252a19bb109ca6
  15. https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=info&id=545
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC6908497/
  17. https://doi.org/10.3389/fmicb.2019.02774
  18. https://www.ncbi.nlm.nih.gov/books/NBK8035/
  19. https://www.sciencedirect.com/topics/medicine-and-dentistry/citrobacter
  20. https://www.sciencedirect.com/topics/medicine-and-dentistry/citrobacter-koseri
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC7912136/
  22. https://www.mdpi.com/2076-3417/13/12/6907
  23. https://publications.aap.org/redbook/book/347/chapter/5751655/Serious-Neonatal-Bacterial-Infections-Caused-by
  24. https://medtigo.com/pathogen/citrobacter-koseri/
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC85297/
  26. https://www.sciencedirect.com/topics/immunology-and-microbiology/citrobacter-koseri
  27. https://journals.asm.org/doi/pdf/10.1128/jcm.32.8.1850-1854.1994
  28. https://doi.org/10.1111/1462-2920.15387
  29. https://microbiologyjournal.org/molecular-characterization-of-microbial-quality-of-ready-to-eat-salads-using-multi-locus-sequence-typing/
  30. https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2023.1175249/full
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC10457828/
  32. https://www.mdpi.com/2076-2607/11/8/2114
  33. https://publications.aap.org/pediatrics/article/118/5/e1576/69898/Diffuse-Pneumocephalus-in-Neonatal-Citrobacter
  34. https://pubmed.ncbi.nlm.nih.gov/10064257/
  35. https://www.scirp.org/journal/paperinformation?paperid=132941
  36. https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-025-11972-6
  37. https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-024-09575-8
  38. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/citrobacter-freundii
  39. https://pubmed.ncbi.nlm.nih.gov/31866966/
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC2900259/
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC201054/
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC4727638/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC2819382/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC162016/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC12422065/
  46. https://www.sciencedirect.com/science/article/pii/S2214250914000432
  47. https://publications.aap.org/redbook/book/755/chapter/14076955/Serious-Neonatal-Bacterial-Infections-Caused-by
  48. https://pubmed.ncbi.nlm.nih.gov/10530585/
  49. https://www.nature.com/articles/s41598-024-77342-5
  50. https://www.frontiersin.org/journals/antibiotics/articles/10.3389/frabi.2023.1276982/full
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC5054941/
  52. https://ijclinmedcasereports.com/pdf/IJCMCR-CR-01024.pdf
  53. https://journals.asm.org/doi/10.1128/iai.71.10.5871-5880.2003
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC3971854/
  55. https://www.sciencedirect.com/science/article/pii/S2214442016302157
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC9630887/
  57. https://jofem.org/index.php/jofem/article/view/42/58
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC10996352/
  59. https://www.researchgate.net/publication/375569801_Citrobacter_Infections_in_Children_and_Hearing_Loss
  60. https://microbe-canvas.com/Bacteria/gram-negative-rods/facultative-anaerobic-3/catalase-positive-3/oxidase-negative/colistin-susceptible-1/citrobacter-koseri.html
  61. https://basicmedicalkey.com/enterobacteriaceae-2/
  62. https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2023.1056790/full
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC10601122/
  64. https://pmc.ncbi.nlm.nih.gov/articles/PMC2849558/
  65. https://journals.asm.org/doi/10.1128/jcm.00343-12
  66. https://pmc.ncbi.nlm.nih.gov/articles/PMC5518651/
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC10778185/
  68. https://www.sciencedirect.com/science/article/abs/pii/S1090379809001524
  69. https://pmc.ncbi.nlm.nih.gov/articles/PMC5894052/
  70. https://pubmed.ncbi.nlm.nih.gov/10754158/
  71. https://ijop.net/index.php/ijocm/article/download/2929/2546/5726
  72. https://www.researchgate.net/publication/308929990_Citrobacter_koseri_Pneumonia_As_Initial_Presentation_of_Underlying_Pulmonary_Adenocarcinoma
  73. https://www.semanticscholar.org/paper/Abscess-caused-by-Citrobacter-koseri-infection%253A-and-Lin-Ho/1295e853733b13b6259832928b48df3c93d46fe4
  74. https://academic.oup.com/jid/article-abstract/157/1/106/807800
  75. https://www.ncbi.nlm.nih.gov/books/NBK532264/
  76. https://publications.aap.org/neoreviews/article/16/9/e535/88433/Neonatal-Bacterial-Meningitis
  77. https://journals.asm.org/doi/10.1128/cmr.00031-13
  78. https://pmc.ncbi.nlm.nih.gov/articles/PMC11761862/
  79. https://www.ncbi.nlm.nih.gov/books/NBK441841/
  80. https://www.hopkinsguides.com/hopkins/view/Johns_Hopkins_ABX_Guide/540065/all/Brain_Abscess
  81. https://pmc.ncbi.nlm.nih.gov/articles/PMC6630883/
  82. https://pmc.ncbi.nlm.nih.gov/articles/PMC3835999/
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC8429604/
  84. https://pmc.ncbi.nlm.nih.gov/articles/PMC11221093/
  85. https://www.idsociety.org/practice-guideline/amr-guidance/
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC3279664/
  87. https://pmc.ncbi.nlm.nih.gov/articles/PMC4672606/
  88. https://www.infectiousdiseaseadvisor.com/home/decision-support-in-medicine/infectious-diseases/brain-abscess/
  89. https://www.sccm.org/clinical-resources/guidelines/guidelines/surviving-sepsis-guidelines-2021
  90. https://www.nursingcenter.com/ncblog/february-2022/source-control-in-sepsis
  91. https://www.jognn.org/article/S0884-2175%2825%2900222-9/abstract
  92. https://pmc.ncbi.nlm.nih.gov/articles/PMC3714384/
  93. https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.063586-0
  94. https://www.ejcrim.com/index.php/EJCRIM/article/download/5290/4678/53373
  95. https://pmc.ncbi.nlm.nih.gov/articles/PMC6874386/
  96. https://www.idsociety.org/globalassets/idsa/practice-guidelines/clinical-practice-guidelines-for-antimicrobial-prophylaxis-in-surgery.pdf
  97. https://www.cdc.gov/uti/hcp/clinical-safety/index.html
  98. https://www.cdc.gov/infection-control/hcp/mdro-management/index.html
Add your contribution
Related Hubs
User Avatar
No comments yet.