Citrobacter koseri is a Gram-negative, nonspore-forming bacillus. It is a facultative anaerobe capable of aerobic respiration. It is motile via peritrichous flagella.[1] It is a member of the family of Enterobacteriaceae. The members of this family are the part of the normal flora of human and animal digestive tracts. [1] C. koseri may act as an opportunistic pathogen in a variety of human infections.[citation needed]
Contents
- 1 Citrobacter meningitis
- 1.1 Etiology
- 1.2 Pathogenicity
- 1.3 Differential diagnosis
- 1.4 Clinical findings
- 1.5 Pathology
- 1.6 Microbiology
- 1.7 Histology
- 1.8 Imaging
- 1.9 Treatment
- 1.10 Complications
- 1.11 Prognosis
- 2 Control
- 3 References
- 4 External Links
Citrobacter meningitis
Brain abscesses have a high rate of mortality and complications, therefore, neonates usually left with severe residual permanent damage. The transmission of C. koseri could be vertical from mother to fetus (local vaginal infection, rupture of the membranes, chorioamniotis may occur between the seventh and 11th day prior to delivery) and other sources can be horizontal nosocomial transmission by asymptomatic nursery staff.[2]
Etiology
Occasionally, it causes meningitis, but it can cause sepsis, ventriculitis, and cerebritis with 80% frequent multiple brain abscesses in low-birth-weight, immunocompromised neonates; rare cases have been reported in older children and adults, most of whom have underlying diseases.[3]
Pathogenicity
The pathogenic mechanism is poorly understood. C.koseri may have a unique ability to penetrate, survive, and replicate into vascular endothelial cells and macrophages. Furthermore, it survives in phagolysozomal fusion and replicates within macrophages, which may contribute to the establishment of chronic abscesses.[3][4]
Differential diagnosis
The differential diagnosis of C. koseri brain abscesses can be confused with other related diseases, so diagnostic imaging is important to confirm this bacterium. The significant feature of C. koseri is the necrotic cavity which cannot be misidentified as earlier ischemic or hemorrhagic insult or other mass lesions; congential/neonatal tumors are uncommon (choroid plexus papillomas, craniopharyngiomas, teratomas); even when they present, they are different from the inflammatory ring of a cerebral infection. Early cerebritis should not be mistaken for normal, immature white matter, nor for cicatricial leukomalacia.[3][4]
Clinical findings
The neonates become very sick and present sepsis, meningitis, and cerebritis, seizures, apnea, and a bulging fontanelle. No evidence of stiff neck or high-grade fever is present.[3]
Pathology
Macroscopic findings include purulent exudates, opaque leptomeninges (thinning of meninges), pus, and ventriculitis/ ependymitis.
Microbiology
In samples collected from cerebrospinal fluid, C. koseri grows well on an 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, negative results in lactose, salicin, and sucrose broth as well.[3][5]
Histology
C. koseri may be identified in the walls of congested vessels, presence of the cavities resulting from the infection do not develop well-formed fibrotic wall.[3]
Imaging
CT scan
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 in shape and not tense, but when pus forms and collects in these cavities, they tend to become more rounded in shape; a persisting cavity leads to septated ventriculitis that may result in multicyctic hydrocephalus.[3]
MRI
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.[3][4]
Treatment
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.[3][5][6]
Complications
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 a multicystis hydrocephalus with consequent long-lasting shunting difficulties, and necrotizing meningeoencephalitis with pneumocephalus has been reported.[3]
Prognosis
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.[3]
Control
The most effective way to reduce transmission of organisms is regular handwashing.[3]
References
- ^ Ong CL, Beatson SA, Totsika M, Forestier C, McEwan AG, Schembri MA (2010). "Molecular analysis of type 3 fimbrial genes from Escherichia coli, Klebsiella and Citrobacter species". BMC Microbiol. 10: 183. doi:10.1186/1471-2180-10-183. PMC 2900259. PMID 20576143.
- ^ Greenwood, David; Slack, Richard C. B.; Peutherer, John F.; Barer, Michael R. (2007). Medical Microbiology: A Guide to Microbial Infections: Pathogenesis, Immunity, Laboratory Diagnosis and Control (17th ed.). Elsevier. pp. 1264–6. ISBN 0-7020-4009-6.
- ^ a b c d e f g h i j k l Babyn, Paul S. (2011). "Section I: Neuroradiology: Case 3". Teaching Atlas of Pediatric Imaging. Thieme. pp. 44–7. ISBN 978-1-60406-494-0.
- ^ a b c Doran TI (1999). "The role of Citrobacter in clinical disease of children: review". Clin. Infect. Dis. 28 (2): 384–94. doi:10.1086/515106. PMID 10064257.
- ^ a b Feferbaum R, Diniz EM, Valente M, Giolo CR, Vieira RA, Galvani AL, Ceccon ME, Araujo MC, Krebs VL, Vaz FA (2000). "Brain abscess by Citrobacter diversus in infancy: case report". Arq Neuropsiquiatr 58 (3A): 736–40. doi:10.1590/s0004-282x2000000400023. PMID 10973119.
- ^ McPherson C, Gal P, Ransom JL (2008). "Treatment of Citrobacter koseri infection with ciprofloxacin and cefotaxime in a preterm infant". Ann Pharmacother 42 (7): 1134–8. doi:10.1345/aph.1L008. PMID 18577764.
External Links
- "Citrobacter koseri". NCBI Taxonomy Browser. 545.
- Infectious diseases
- Bacterial disease: Proteobacterial G−
- primarily A00–A79, 001–041, 080–109
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| α |
| Rickettsiales |
Rickettsiaceae/
(Rickettsioses) |
| Typhus |
- Rickettsia typhi
- Rickettsia prowazekii
- Epidemic typhus, Brill–Zinsser disease, Flying squirrel typhus
|
|
Spotted
fever |
| Tick-borne |
- Rickettsia rickettsii
- Rocky Mountain spotted fever
- Rickettsia conorii
- Rickettsia japonica
- Rickettsia sibirica
- Rickettsia australis
- Rickettsia honei
- Flinders Island spotted fever
- Rickettsia africae
- Rickettsia parkeri
- Rickettsia aeschlimannii
- Rickettsia aeschlimannii infection
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| Mite-borne |
- Rickettsia akari
- Orientia tsutsugamushi
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| Flea-borne |
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|
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| Anaplasmataceae |
- Ehrlichiosis: Anaplasma phagocytophilum
- Human granulocytic anaplasmosis, Anaplasmosis
- Ehrlichia chaffeensis
- Human monocytotropic ehrlichiosis
- Ehrlichia ewingii
- Ehrlichiosis ewingii infection
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|
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| Rhizobiales |
| Brucellaceae |
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| Bartonellaceae |
- Bartonellosis: Bartonella henselae
- Bartonella quintana
- either henselae or quintana
- Bartonella bacilliformis
- Carrion's disease, Verruga peruana
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|
|
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| β |
| Neisseriales |
| M+ |
- Neisseria meningitidis/meningococcus
- Meningococcal disease, Waterhouse–Friderichsen syndrome, Meningococcal septicaemia
|
|
| M- |
- Neisseria gonorrhoeae/gonococcus
|
|
| ungrouped: |
- Eikenella corrodens/Kingella kingae
- Chromobacterium violaceum
- Chromobacteriosis infection
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|
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| Burkholderiales |
- Burkholderia pseudomallei
- Burkholderia mallei
- Burkholderia cepacia complex
- Bordetella pertussis/Bordetella parapertussis
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| γ |
Enterobacteriales
(OX-) |
| Lac+ |
- Klebsiella pneumoniae
- Rhinoscleroma, Klebsiella pneumonia
- Klebsiella granulomatis
- Klebsiella oxytoca
- Escherichia coli: Enterotoxigenic
- Enteroinvasive
- Enterohemorrhagic
- O157:H7
- O104:H4
- Hemolytic-uremic syndrome
- Enterobacter aerogenes/Enterobacter cloacae
|
|
| Slow/weak |
- Serratia marcescens
- Citrobacter koseri/Citrobacter freundii
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| Lac- |
| H2S+ |
- Salmonella enterica
- Typhoid fever, Paratyphoid fever, Salmonellosis
|
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| H2S- |
- Shigella dysenteriae/sonnei/flexneri/boydii
- Shigellosis, Bacillary dysentery
- Proteus mirabilis/Proteus vulgaris
- Yersinia pestis
- Yersinia enterocolitica
- Yersinia pseudotuberculosis
- Far East scarlet-like fever
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|
|
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| Pasteurellales |
| Haemophilus: |
- H. influenzae
- Haemophilus meningitis
- Brazilian purpuric fever
- H. ducreyi
- H. parainfluenzae
|
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| Pasteurella multocida |
- Pasteurellosis
- Actinobacillus
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| Aggregatibacter actinomycetemcomitans |
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|
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| Legionellales |
- Legionella pneumophila/Legionella longbeachae
- Coxiella burnetii
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| Thiotrichales |
|
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| Vibrionaceae |
- Vibrio cholerae
- Vibrio vulnificus
- Vibrio parahaemolyticus
- Vibrio alginolyticus
- Plesiomonas shigelloides
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| Pseudomonadales |
- Pseudomonas aeruginosa
- Moraxella catarrhalis
- Acinetobacter baumannii
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| Xanthomonadaceae |
- Stenotrophomonas maltophilia
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| Cardiobacteriaceae |
|
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| Aeromonadales |
- Aeromonas hydrophila/Aeromonas veronii
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| ε |
| Campylobacterales |
- Campylobacter jejuni
- Campylobacteriosis, Guillain–Barré syndrome
- Helicobacter pylori
- Peptic ulcer, MALT lymphoma, Gastric cancer
- Helicobacter cinaedi
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Index of bacterial disease
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| Description |
|
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| Disease |
- Gram-positive firmicutes
- Gram-positive actinobacteria
- Gram-negative proteobacteria
- Gram-negative non-proteobacteria
- Cholera
- Tuberculosis
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| Treatment |
- Antibiotics
- cell wall
- nucleic acid
- mycobacteria
- protein synthesis
- other
- Antibodies
- Vaccines
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