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Two cases of central nervous system infections from which E. corrodens has been isolated are reported. The portals of entry, clinical course, and antimicrobial responses conform to other reports in the literature. The importance of obtaining careful anaerobic cultures is emphasized.
BACKGROUND: Central nervous system (CNS) infections caused by New Delhi metallo-β-lactamase-1 (NDM-1)-producing carbapenem-resistant Klebsiella pneumoniae (CRKP) are rare but associated with extremely high mortality because of extensive antimicrobial resistance and poor blood-brain barrier (BBB) penetration. To the best of our knowledge, there have been no published reports of pneumocephalus associated with infection caused by NDM-1-producing K. pneumoniae. CASE PRESENTATION: We report an 18-year-old woman who developed bloodstream infection and metastatic CNS infection following severe thoracoabdominal crush injury. Serial cerebrospinal fluid (CSF) cultures repeatedly yielded NDM-1-producing CRKP despite multiple adjustments of antimicrobial therapy. Retrospective whole-genome sequencing demonstrated that blood and CSF isolates belonged to the same clonal lineage carrying the blaNDM-1 gene on an IncX3 plasmid, confirming hematogenous dissemination. Serial cranial computed tomography revealed progressive diffuse cerebral edema and extensive pneumocephalus in the absence of skull fracture or neurosurgical intervention. Persistent microbiological failure was mainly attributed to the combination of NDM-1-mediated multidrug resistance and inadequate CNS antibiotic exposure, which ultimately led to the patient's death. CONCLUSION: This case illustrates the devastating clinical course of NDM-1-producing CRKP CNS infection and identifies extensive pneumocephalus as a rare but potentially fatal complication. It emphasizes the importance of early molecular diagnosis, repeated CSF microbiological assessment, optimization of antimicrobial regimens with adequate CNS penetration, and implementation of effective infection-control strategies. The case also highlights the urgent need for novel therapeutic approaches against metallo-β-lactamase-producing pathogens.
The present study demonstrated that the clinicopathological expression of the late demyelinating disease due to chronic central nervous system infection by Theiler's mouse encephalomyelitis virus was dependent, at least in part, on the strain of mouse used as host. A range of involvement was observed, with late disease being most severe in the SJL strain, intermediate in the CBA and C3H/He strains, and least in C57BL/6 mice. The lack of clinical signs in seven other inbred strains of mice indicates that their response to chronic infection was similar to C57BL/6 mice. SJL, CBA, C3H/He, and C57BL/6 mice all generated similar levels of neutralizing antibody. A correlation between the severity of late disease and central nervous system virus content was not demonstrated, which indirectly suggests an immunopathological rather than a cytolytic mechanism of myelin injury during the late disease period. Finally, in addition to being more extensive, SJL demyelinating lesions contained a disproportionately large number of macrophages compared with those of similar lesions in CBA and C3H/He mice.
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A morphologic study of demyelination produced by Theiler's encephalomyelitis virus (TMEV) infection in C3H/He mice was performed. Demyelination in this strain of mouse was less intense and had a milder gliomesodermal response than that observed in SJL mice. As early as 80 days after infection numerous remyelinated axons were present in C3H/He mice, and later, extensive remyelination was observed and was mainly by Schwann cells. About one-third of remyelinated plaques showed recurrent demyelinating activity at 200 days. The best evidence of recurrent demyelination was the loss of myelin by abons which had been previously remyelinated by Schwann cells. In addition, acute areas of demyelination were also seen in spinal cords which contained chronic or quiescent plaques. The demonstration of recurrent demyelination in TMEV infection is important for it increases the relevance of this model to multiple sclerosis (MS). In addition TMEV infection of C3H/He mice appears to be an excellent model for further studies of Schwann cell remyelination and recurrent demyelination in the central nervous system (CNS).
Cerebrospinal fluid (CSF) and sera from 129 patients of a study population of 139 were tested for antibody to herpes simplex, measles,and mumps viruses. Herpes simplex virus antibody was found in three of five patients with laboratory-confirmed herpes simplex infection and in eight patients without serological or virological evidence of current infection with this or other common neurotropic visuses. Eleven of the 139 patients were studied for antibody to lymphocytic choriomeningitis (LCM) virus. Eight of these had laboratory-confirmed LCM infection, and antibody was detected in the CSF of five of them. In one of these five, complement-fixing antibody appeared earlier in the CSF than in the blood. Assay of LCM virus antibody in the CSF may thus indicate infection with LCM virus more rapidly than serological and virological studies. The diagnostic and the possible prognostic significance of herpes simplex visus antibody in CSF remains to be ascertained.
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In a 50-year-old cook, partial motor seizures and signs of dominant hemisphere dysfunction developed after a brief nonspecific febrile illness. Pleocytosis was seen in the cerebrospinal fluid and findings on cerebral angiography and isotope brain scan suggested a subdural collection. Surgical exploration showed only thickening and inflammation of the dura. Cultures of this tissue and of the patient's blood were positive for Vibrio fetus, an organism common in sheep and cattle, but seen rarely in humans. Among the few reported cases of human infection, several have involved the brain and meninges.
After (IC) inoculation of the DA strain of TMEV, SJL/J mice develop chronic CNS infection with marked mononuclear cell infiltration of spinal cord leptomeninges and white matter and concomitant demyelination. In the present study the temporal course of cell-mediated and humoral immune responses to virus were measured in this infection. It was shown that chronic TMEV infection is associated with the development of immunologically specific spleen cell reactivity as judged by in vitro incorporation of 3H-TdR into DNA in response to inactivated TMEV antigen. Spleen cell reactivity is first detectable about 2 months after infection, persists for at least 1 year, and correlates with the temporal development of serum-neutralizing antibody. The late development of sensitized spleen cells is not the result of an immunosuppressive effect of this virus infection since infected mice exhibit normal spleen cell proliferative responses to T cell mitogens and produce normal antibody responses to a heterologous protein antigen, sheep red blood cells. In addition, anti-viral antibody inhibits virus-induced spleen cell reactivity. Finally, the antigen-reactive lymphocyte subpopulation within the spleen responsible for proliferation to TMEV antigen are T cells and not B cells.
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Fungal infections of the central nervous system present a considerable challenge to available chemotherapy and other forms of treatment. The particular difficulties are discussed here, after an account of the fungi involved and their sensitivity to antifungal agents. Cryptococcal, coccidioidal and candidal infections are considered in more detail.
Viral infections of the central nervous system (CNS) are a major cause of morbidity largely due to lack of prevention and inadequate treatments. While mortality from viral CNS infections is significant, nearly two thirds of the patients survive. Thus, it is important to understand how the human CNS can successfully control virus infection and recover. Since it is not possible to study the human CNS throughout the course of viral infection at the cellular level, here we analyzed a non-lethal viral infection in the CNS of nonhuman primates (NHPs). We inoculated NHPs intracerebrally with a high dose of La Crosse virus (LACV), a bunyavirus that can infect neurons and cause encephalitis primarily in children, but with a very low (≤ 1%) mortality rate. To profile the CNS response to LACV infection, we used an integrative approach that was based on comprehensive analyses of (i) spatiotemporal dynamics of virus replication, (ii) identification of types of infected neurons, (iii) spatiotemporal transcriptomics, and (iv) morphological and functional changes in CNS intrinsic and extrinsic cells. We identified the location, timing, and functional repertoire of optimal transcriptional and translational regulation of the primate CNS in response to virus infection of neurons. These CNS responses involved a well-coordinated spatiotemporal interplay between astrocytes, lymphocytes, microglia, and CNS-border macrophages. Our findings suggest a multifaceted program governing an optimal CNS response to virus infection with specific events coordinated in space and time. This allowed the CNS to successfully control the infection by rapidly clearing the virus from infected neurons, mitigate damage to neurophysiology, activate and terminate immune responses in a timely manner, resolve inflammation, restore homeostasis, and initiate tissue repair. An increased understanding of these processes may provide new therapeutic opportunities to improve outcomes of viral CNS diseases in humans.
We observed persistent ECHOvirus infection of the central nervous system, as defined by continued presence of isolatable virus in cerebrospinal fluid, in five patients with agammaglobulinemia. The immunologic deficit in each was characterized by absence of surface-immunoglobulin-bearing B lymphocytes and of lymph-node cortical follicles, but normal T-cell function. ECHOviruses 30, 19, 9 and 33 were recovered from cerebrospinal fluid for periods varying from two months to three years. The patients had few signs of acute central-nervous-system infection. Three of the five patients had a dermatomyositis-like syndrome, with peripheral lymphocytes that reacted with anti-human leukemia-specific primate and rabbit serums in a cytotoxicity assay. These data suggest that intact B-cell function is essential for eradication of ECHOvirus infection of the central nervous system.
Propionibacterium acnes is a pleomorphic gram-positive anaerobic rod usually isolated as a contaminant from skin. We report three cases of P. acnes infection of central nervous system shunts for hydrocephalus. The organism was seen repeatedly on gram stain in a specimen of shunt fluid in all three cases; initially, it was regarded as a contaminant. In addition, two of the patients had precipitins to extracts of their organism. Serum from normal control subjects had no such precipitins. One of the patients had an immune-complex glomerulonephritis--an entity not previously associated with anaerobic organisms. All three patients recovered after removal of the shunt and treatment with antibiotics. P. acnes is a significant pathogen in patients with central nervous system shunts.
Two patients with cryptococcal infection of the central nervous system are described. The first presented with signs of an intracranial mass and was subsequently shown to have two lesions within the brain which were later identified as cryptococcal granulomata. Antifungal therapy did not eradicate the lesions; following their excision and continued therapy, the CSF became sterile however. The other patient had signs of a fulminant meningoencephalitis which initially were thought to represent the pathophysiological expression of an expanding brain tumor. These reports are used as a basis to review the various aspects of central nervous system cryptococcosis, particularly as they may relate to the neurosurgeon and the therapy of the disease.
The investigation of the central nervous system in generalized adenoviral infection in two children showed the presence in large nuclei of the nerve cells of hyperchromic inclusions containing the antigen of adenovirus. This testifies to the possibility of developing encephalites caused by respiratory viruses.