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|Year : 2009 | Volume
| Issue : 1 | Page : 37-40
Cerebritis: An unusual complication of Klebsiella pneumoniae
Mainak Majumdar1, David C Simes2, Ramesh D Prabha2
1 Department of Critical Care, Latrobe Regional Hospital, Traralgon, Vic 3844, Australia
2 Intensive Care Unit, Fremantle Hospital, Alma Street, Fremantle, WA6160, Australia
|Date of Web Publication||1-Jul-2009|
Department of Critical Care, Latrobe Regional Hospital, Traralgon, Vic 3844
Cerebritis is part of a continuum of brain infection and is difficult to diagnose. Cerebritis caused by Klebsiella in immunocompetent adults without predisposing factors such as neurosurgery or penetrating brain injury has not been reported before. We report a case of Klebsiella cerebritis in an adult patient with a proven extracranial focus of infection. We suggest considering cerebritis as a differential diagnosis for altered level of consciousness in patients of severe sepsis, even if an extracranial source of infection is proven.
Keywords: Alcohol, cerebritis, Klebsiella
|How to cite this article:|
Majumdar M, Simes DC, Prabha RD. Cerebritis: An unusual complication of Klebsiella pneumoniae. Indian J Crit Care Med 2009;13:37-40
|How to cite this URL:|
Majumdar M, Simes DC, Prabha RD. Cerebritis: An unusual complication of Klebsiella pneumoniae. Indian J Crit Care Med [serial online] 2009 [cited 2015 Mar 5];13:37-40. Available from: http://www.ijccm.org/text.asp?2009/13/1/37/53116
| » Introduction|| |
Cerebritis without a history of penetrating head trauma or neurosurgery is a rarely suspected cause of coma. Bacteria gain entry to brain tissue and cause infection either by direct spread or through hematogenous seeding.  In Gram-negative CNS infections, a primary focus of infection may be found in neonates and in trauma and neurosurgical patients, but in adults without antecedent surgery, there will be no primary focus of infection detected in up to 60% of cases.  Further, sedation in the intensive care unit (ICU) may mask progressive brain insult. Thus, cerebritis may be well advanced before measures are taken to curb its progression.
| » Case Report|| |
A 48-year-old lady presented with increasing confusion following a three-day history of fever, shortness of breath, and productive cough. Her background included heavy smoking, heavy ethanol use, and two prior hospital admissions for pneumonia and exacerbation of chronic obstructive airways disease.
At presentation she was febrile, delirious, and tachypneic with low oxygen saturations, relative hypotension, and new onset atrial fibrillation with a rapid ventricular response. Her chest X-ray revealed dense right upper and middle lobe consolidation. Initial treatment consisted of oxygen therapy, intravenous fluid resuscitation, noninvasive ventilation, and antibiotics (ceftriaxone and azithromycin) for her community acquired pneumonia. She reverted to sinus tachycardia after treatment with digoxin. She was prescribed benzodiazepines for apparent alcohol withdrawal agitation.
She was transferred to our institution after two days in established multiorgan failure with shock, respiratory failure, coagulopathy. Invasive organ support was initiated with intubation, mechanical ventilation, vigorous fluid resuscitation, vasopressors, and inotropes. Blood and sputum cultures taken at the time of her initial presentation grew Klebsiella pneumoniae sensitive to all antibiotics except amoxicillin. Antibiotics were changed to ceftriaxone and ciprofloxacin. Human immunodeficiency virus (HIV) screen was negative. Echocardiography revealed normal valve function, with no sign of vegetations and normal chamber size and function.
By day 3 in the ICU, her gas exchange had improved. Though tachycardic and febrile, she maintained sinus rhythm and sustained a mean arterial pressure above 70 mm Hg without vasopressor support. Sedation was then discontinued for the first time since intubation. Her pupils were noted to react to light but she was unresponsive to painful stimuli. There was no further change to her neurological status 24 hours after stopping sedation.
On day 5, she had a focal seizure limited to her left arm, lasting less than a minute. Her pupils were equal but noted to be unreactive, her gaze was divergent and a flaccid quadriplegia and absence of deep tendon reflexes were noted for the first time. An urgent CT brain demonstrated advanced cerebral injury [Figure 1], initially reported as extensive cortical necrosis of the frontal, parietal, and temporal lobes. To further define the extent of the inflammatory process, magnetic resonance imaging (MRI) [Figure 2] and [Figure 3] was performed. There was widespread nonvascular territory cortical infarction, particularly over both convexities. Given the additional patchy involvement of cortex elsewhere, particularly within the posterior fossa, hippocampi, and occipital horns of the lateral ventricles, the overall pathology was deemed to be cerebritis with hyperaemia and associated meningitis. There were no features suggestive of focal cerebral abscess and the dural venous sinuses appeared patent.
Neurosurgical advice was sought. It was felt that bifrontal craniotomy to reduce intracranial pressure would confer little benefit. In view of ongoing coagulopathy and thrombocytopenia, the risks of placing an intraventricular drain were considered to outweigh any benefits in guiding therapy. Spinal fluid was not sought for the same reasons.
On day 6 the patient developed dilated and fixed pupils, absent corneal reflexes, and absent plantar reflexes bilaterally. She still had a cough reflex and took spontaneous breaths on pressure support. A second CT brain [Figure 4] showed increasing areas of low attenuation within the frontoparietal and superior occipital cerebral cortex with evidence of mass effect.
A meeting was held with her family to inform them of her extremely poor prognosis. In keeping with her family's understanding of her previously expressed wishes, mechanical ventilation was withdrawn and palliative measures instituted. The patient died two days later.
| » Discussion|| |
Our patient was a 48-year-old female with good premorbid level of function, few hospital admissions, and no obvious risks for compromised or suppressed immune function. We did not expect her to develop a fatal CNS infection, while the extracranial focus of infection was demonstrably resolving (radiologically and in terms of measured gas exchange) on two antibiotics to which the pathogen was susceptible in vitro .
However, a review of literature suggests Klebsiella may possess unique infective and proinflammatory properties  that render it particularly virulent in the alcoholic host.  There is emerging laboratory data on murine models demonstrating reduced cytokine release (IL-17) in animals pretreated with alcohol prior to exposure to Klebsiella . The alcohol-treated animals also demonstrated distinctly worse clinical appearances.  A similar two-week alcohol exposure model showed increased mortality and decreased IL-17 production when Klebsiella pneumoniae was introduced to a murine pneumonia model.  Other studies also implicate IL-23 in the murine model.  Work on human endothelium and macrophage lines confirms that acute alcohol intoxication significantly inhibits lymphocyte expression during pulmonary inflammation. 
Klebsiella has been reported as a CNS pathogen with increasing frequency, with no improvement in prognosis over a 15-year period despite the availability of newer antibiotics. Particularly high mortality with Klebsiella septicemia and CNS spread has been noted. 
Diagnosing cerebritis requires a combination of high index of suspicion, diligent neurological examination during regular sedation holidays, and appropriate imaging studies. MRI images reflect the duration and severity of the illness. 
Given our experience, cerebritis should be considered a differential diagnosis in patients with a history of heavy ethanol consumption in the setting of Klebsiella sepsis and altered level of consciousness. Unfortunately, early diagnosis may only serve to allow appropriate counselling to relatives, without conferring a mortality advantage.
| » References|| |
|1.||Chun CH, Johnson JD, Hofstetter M, Raff MJ. Brain abscess: A study of 45 consecutive cases. Medicine (Baltimore) 1986;65:415-31. [PUBMED] |
|2.||Berk SL, McCabe WR. Meningitis caused by gram-negative bacilli. Ann Intern Med 1980;93:253-60. [PUBMED] |
|3.||Wen LL, Chiu CT, Huang YN, Chang CF, Wang JY. Rapid glia expression and release of proinflammatory cytokines in experimental Klebsiella pneumoniae meningoencephalitis. Exp Neurol 2007;205:270-8. [PUBMED] [FULLTEXT]|
|4.||Chang WN, Lu CH, Chang CS, Huang CR. Community-acquired spontaneous bacterial meningitis in patients with alcoholic liver disease. J Formos Med Assoc 2003;102:653-5. [PUBMED] |
|5.||Spies CD, Lanzke N, Schlichting U, Muehlbauer S, Pipolo C, von Mettenheim M, et al . Effects of ethanol on cytokine production after surgery in a murine model of gram-negative pneumonia. Alcohol Clin Exp Res 2008;32:331-8. [PUBMED] [FULLTEXT]|
|6.||Shellito JE, Quan Zheng M, Ye P, Ruan S, Shean MK, Kolls J. Effect of alcohol consumption on host release of interleukin-17 during pulmonary infection with Klebsiella pneumoniae . Alcohol Clin Exp Res 2001;25:872-81. [PUBMED] [FULLTEXT]|
|7.||Happel KI, Odden AR, Zhang P, Shellito JE, Bagby GJ, Nelson S. Acute alcohol intoxication suppresses the interleukin 23 response to Klebsiella pneumoniae infection. Alcohol Clin Exp Res 2006;30:1200-7. |
|8.||Happel KI, Rudner X, Quinton LJ, Movassaghi JL, Clark C, Odden AR, et al . Acute alcohol intoxication suppresses the pulmonary negative CXC chemokine response to lipopolysaccharides. Alcohol 2007;41:325-33. [PUBMED] [FULLTEXT]|
|9.||Lu CH, Chang WN, Chuang YC, Chang HW. The prognostic factors of adult gram-negative bacillary meningitis. J Hosp Infect 1998;40:27-34. [PUBMED] [FULLTEXT]|
|10.||Britt RH, Enzmann DR. Clinical stages of human brain abscesses on serial CT scans after contrast infusion: Computerized tomographic, neuropathological and clinical correlations. J Neurosurg 1983;59:972-89. [PUBMED] |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]