Citrobacter koseri
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| Citrobacter | |
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| Species: | C. koseri
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'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 the enterobacteriaceae 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]
Citrobacter meningitis
Citrobacter koseri rarely cause neonate brain abcesses having 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 7th- 11th day prior to delivery) and other sources can be horizontal nosocomial transmission by asymptomatic nursery staff.[2]
Etiology
C. koseri occasionally causes meningitides but it can cause sepsis, ventriculitis, and cerebritis with 80% frequent multiple brain abscesses in low birth weight, immuno-compromised neonates; rare cases have been reported in older children and adults, most of which have underlying disease.[3]
Pathogenicity
The pathogenic mechanism is poorly understood. It has been suggested that C.koseri have a unique ability to penetrate, survive, and replicate into vascular endothelial cells and macrophages. Furthermore, C.koseri survives in phagolysozomal fusion and replicate within macrophages may contribute to the establishment of chronic abcesses.[3][4]
Differential Diagnosis
The differential diagnosis of the C. koseri brain abcesses can be confusing with other related disease, therefore, diagnostic imaging is important to confirm this bacterium. The significant feature of the Citrobacter.koseri is the necrotic cavity which cannot be mixed up with the earlier ischemic or hemmorhagic insult. 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 becomes very sick and presents sepsis, meningitides, and cerebritis, seizures, apnea, and a bulging fontanelle. There is no evidence of stiff neck or high grade fever.[3]
Pathology/Laboratory Findings
Macroscopic findings include purulent exudates, opaque leptomeninges (thining of meninges), pus, and ventriculitis/ ependymitis.
Microbiological Findings
If sample collected from cerebrospinal fluid, Citrobacter koseri grow well on an any ordinary microbiology media, 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]
Histological Findings
Citrobacter 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]
Brain Imaging Findings
CT Scan
Early and massive tissue necrosis is a specific feature of Citrobacter koseri brain infection. The early stage of the disease predominates in the white matter causes cerebritis, later stage marked with necrotic cavities in multiple locations. The cavities are initially square in shape and non-tense, but when pus forms and collects in these cavities, they tend to become more rounded in shape, persisting cavity leads to septated ventriculitis that may result in multicyctic hydrocephalus.[3]
MRI
Early cerebritis, multiple large cavities can be seen in the late stage of the disease, abcesses formation, contraction of the cavities, hydrocephalus due to ventriculitis 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 CNS. 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 infarction is possible because of the bacterial infiltration spread 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, necrotizing meningeoencephalitis with pneumocephalus has been reported.[3]
Prognosis
The prognosis of the Citrobacter. koseri is 20- 30% neonates die, 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 hand washing.[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.
{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - ^ A guide to microbial infections; David Greenwood, Richard Slack
- ^ a b c d e f g h i j k l Teaching Atlas of Pediatric Imaging; Paul S. Babyn
- ^ a b c The role of Citrobacter disease of children; Doran, T. I .
- ^ a b Brain abcesses by Citrobacter. koseri in infancy; Feferbaum, R. (58:736-740)
- ^ The Annals of Pharmacotherapy; J Laurence Ransom, MD