Citrobacter

Citrobacter
Citrobacter freundii Citrobacter freundii
Scientific classification
Kingdom: Bacteria Phylum: Proteobacteria Class: Gamma Proteobacteria Order: Enterobacteriales Family: Enterobacteriaceae Genus: Citrobacter Werkman and Gillen, 1932
Species
C. amalonaticus C. braakii C. farmeri C. freundii C. gillenii C. intermedius C. koseri aka C. diversus C. murliniae C. rodentium C. sedlakii C. werkmanii C. youngae

Citrobacter is a genus of gram-negative Coliform bacteria in the Enterobacteriaceae family.

The species C. amalonaticus, C. koseri, and C. freundii use solely citrate as a carbon source. These bacteria can be found almost everywhere in soil, water, wastewater, etc. It can also be found in the human intestine. They are rarely the source of illnesses, except for infections of the urinary tract and infant meningitis.

Citrobacter shows the ability to accumulate uranium by building phosphate complexes.

2. Bacteremias due to Citrobacter diversus and Citrobacter freundii. Incidence, risk factors, and clinical outcome AUTHORS: V. Drelichman and J. D. Band

From 1974 to 1982, 38 patients developed Citrobacter bacteremia at two adult community-teaching hospitals in the Detroit Medical Center (incidence, 1.2 cases per 10,000 discharges). Citrobacter accounted for 0.7% of all bacteremias during the study period. Of 31 cases reviewed, Citrobacter bacteremia frequently developed in elderly patients (65%) and was hospital acquired (77%). Initial sites of infection included the urinary tract (39%), gastrointestinal tract (27%), wound (10%), and unknown (13%). More bacteremias caused by Citrobacter diversus tended to arise from the urinary tract, while patients with Citrobacter freundii bacteremia had significantly more gallbladder disease. Patients with Citrobacter bacteremia were more likely than patients with Escherichia coli bacteremia to have had additional pathogens in the bloodstream, to develop bacteremia in the hospital, and to have undergone invasive procedures contributing to infection. Significant differences were not observed in demographic, host, or other epidemiologic or clinical factors examined. Of patients with Citrobacter bacteremia, 48% died.

3. Citrobacter freundii Invades and Replicates in Human Brain Microvascular Endothelial Cells AUTHORS Julie L. Badger,1 Monique F. Stins,1 and Kwang Sik Kim1,2,* Division of Infectious Diseases, Childrens Hospital Los Angeles,1 and University of Southern California School of Medicine,2 Los Angeles, California 90027 Received 12 February 1999/Accepted 4 May 1999 Neonatal bacterial meningitis remains a disease with unacceptable rates of morbidity and mortality despite the availability of effective antimicrobial therapy. Citrobacter spp. cause neonatal meningitis but are unique in their frequent association with brain abscess formation. The pathogenesis of Citrobacter spp. causing meningitis and brain abscess is not well characterized; however, as with other meningitis-causing bacteria (e.g., Escherichia coli K1 and group B streptococci), penetration of the blood-brain barrier must occur. In an effort to understand the pathogenesis of Citrobacter spp. causing meningitis, we have used the in vitro blood-brain barrier model of human brain microvascular endothelial cells (HBMEC) to study the interaction between C. freundii and HBMEC. In this study, we show that C. freundii is capable of invading and trancytosing HBMEC in vitro. Invasion of HBMEC by C. freundii was determined to be dependent on microfilaments, microtubules, endosome acidification, and de novo protein synthesis. Immunofluorescence microscopy studies revealed that microtubules aggregated after HBMEC came in contact with C. freundii; furthermore, the microtubule aggregation was time dependent and seen with C. freundii but not with noninvasive E. coli HB101 and meningitic E. coli K1. Also in contrast to other meningitis-causing bacteria, C. freundii is able to replicate within HBMEC. This is the first demonstration of a meningitis-causing bacterium capable of intracellular replication within BMEC. The important determinants of the pathogenesis of C. freundii causing meningitis and brain abscess may relate to invasion of and intracellular replication in HBME

Antimicrobial regimen

• Citrobacter freundii

• Preferred regimen (1): Meropenem 1-2 g IV q8h
• Preferred regimen (2): Imipenem 1 g IV q6h
• Preferred regimen (3): Doripenem 500 mg IV q8h
• Preferred regimen (4): Cefepime 1-2 g IV q8h
• Preferred regimen (5): Ciprofloxacin 400 mg IV q12h or 500 mg PO bid for UTI
• Preferred regimen (6): Gentamicin 5 mg/kg IV q24h
• Alternate regimen (1): Piperacillin-tazobactam 3.375 mg IV q6h
• Alternate regimen (2): Aztreonam 1-2 g IV q6h
• Alternate regimen (3): TMP-SMX 5 mg/kg q6h IV or DS PO bid for UTI
• Note: Usually carbenicillin sensitive, cephalothin resistant

• Citrobacter koseri

• Preferred regimen (1): Ceftriaxone 1-2 g IV q12-24h
• Preferred regimen (2): Cefotaxime 1-2 g IV q6h
• Preferred regimen (3): Cefepime 1-2 IV q8h
• Alternate regimen (1): Ciprofloxacin 400 mg IV q12h or 500 mg PO q12h for UTI
• Alternate regimen (2): Imipenem 1 g IV q6h
• Alternate regimen (3): Doripenem 500 mg IV q8h
• Alternate regimen (4): Meropenem 1-2 g IV q8h
• Alternate regimen (5): Aztreonam 1-2 g IV q6h
• Alternate regimen (6): TMP-SMX 5 mg/kg IV q6h or DS PO bid for UTI
• Note: Usually Ampicillin resistant, but may be sensitive to first generation cephalosporins

Gallery

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  Triple sugar iron agar (TSI) tested for Salmonella (H2S+) and (H2S-); Citrobacter sp. and S. arizonae. From Public Health Image Library (PHIL).

References

• Template:De

External links

• German National Resource Centre for Biological Material