Abstract:A rare case of primary cerebral abscess due to Nocardia asteroides, and its surgical removal, are described. Postoperative meningitis caused by the same fungi was succesfully cured with sulphadiazine and cycloserine. The nocardial disease, its neurological complications, and therapy are reviewed.
“…Frequently, nocardial lesions are localized in the parietal, frontal, and occipital cerebral cortex (132,228,503,562,658,715), basal ganglia (437,683), midbrain (682), and brain stem (pons) (109,138,309,484,505). Furthermore, there may be meningitis with or without involvement of other portions of the brain (138,142,228,267,378,430,517,625). Occasionally, the spinal cord represents the only location for CNS invasion by Nocardia spp.…”
The nocardiae are bacteria belonging to the aerobic actinomycetes. They are an important part of the normal soil microflora worldwide. The type species, Nocardia asteroides, and N. brasiliensis, N. farcinica, N. otitidiscaviarum, N. nova, and N. transvalensis cause a variety of diseases in both normal and immunocompromised humans and animals. The mechanisms of pathogenesis are complex, not fully understood, and include the capacity to evade or neutralize the myriad microbicidal activities of the host. The relative virulence of N. asteroides correlates with the ability to inhibit phagosome-lysosome fusion in phagocytes; to neutralize phagosomal acidification; to detoxify the microbicidal products of oxidative metabolism; to modify phagocyte function; to grow within phagocytic cells; and to attach to, penetrate, and grow within host cells. Both activated macrophages and immunologically specific T lymphocytes constitute the major mechanisms for host resistance to nocardial infection, whereas B lymphocytes and humoral immunity do not appear to be as important in protecting the host. Thus, the nocardiae are facultative intracellular pathogens that can persist within the host, probably in a cryptic form (L-form), for life. Silent invasion of brain cells by some Nocardia strains can induce neurodegeneration in experimental animals; however, the role of nocardiae in neurodegenerative diseases in humans needs to be investigated.
“…Frequently, nocardial lesions are localized in the parietal, frontal, and occipital cerebral cortex (132,228,503,562,658,715), basal ganglia (437,683), midbrain (682), and brain stem (pons) (109,138,309,484,505). Furthermore, there may be meningitis with or without involvement of other portions of the brain (138,142,228,267,378,430,517,625). Occasionally, the spinal cord represents the only location for CNS invasion by Nocardia spp.…”
The nocardiae are bacteria belonging to the aerobic actinomycetes. They are an important part of the normal soil microflora worldwide. The type species, Nocardia asteroides, and N. brasiliensis, N. farcinica, N. otitidiscaviarum, N. nova, and N. transvalensis cause a variety of diseases in both normal and immunocompromised humans and animals. The mechanisms of pathogenesis are complex, not fully understood, and include the capacity to evade or neutralize the myriad microbicidal activities of the host. The relative virulence of N. asteroides correlates with the ability to inhibit phagosome-lysosome fusion in phagocytes; to neutralize phagosomal acidification; to detoxify the microbicidal products of oxidative metabolism; to modify phagocyte function; to grow within phagocytic cells; and to attach to, penetrate, and grow within host cells. Both activated macrophages and immunologically specific T lymphocytes constitute the major mechanisms for host resistance to nocardial infection, whereas B lymphocytes and humoral immunity do not appear to be as important in protecting the host. Thus, the nocardiae are facultative intracellular pathogens that can persist within the host, probably in a cryptic form (L-form), for life. Silent invasion of brain cells by some Nocardia strains can induce neurodegeneration in experimental animals; however, the role of nocardiae in neurodegenerative diseases in humans needs to be investigated.
“…Frequently, nocardial lesions are localized in the parietal, frontal, and occipital cerebral cortex (132,228,503,562,658,715), basal ganglia (437, 683), midbrain (682), and brain stem (pons) (109,138,309,484,505). Furthermore, there may be meningitis with or without involvement of other portions of the brain (138,142,228,267,378,430,517,625). Occasionally, the spinal cord represents the only location for CNS invasion by Nocardia spp.…”
From the very beginning, there has been uncertainty over the taxonomic position of nocardioforms, i.e., bacteria that resemble Nocardia organisms. The specific taxonomy of isolates of this heterogenous group of organisms is still in flux and controversial (275, 278, 403, 404, 420, 584, 676, 699). During the ensuing 100 years, it has been shown that N. asteroides is a heterogeneous taxon (275, 403, 404, 420). It is not within the scope of this review to address this complex subject, yet it is important to note that N. asteroides, as currently defined, probably consists of several subtypes and/or species. These include N. asteroides sensu stricto, N. farcinica, N. nova, and several distinct serotypes and biotypes (278, 403, 404, 698, 699, 727). Regardless of their designation, all of these varieties of the N. asteroides taxon have been isolated from humans and animals with serious (often fatal) infections (93, 584, 698, 699). The other pathogenic Nocardia species appear to be taxonomically more homogeneous and include N. brasiliensis, N. otitidiscaviarum (N. caviae), and N. transvalensis (275, 420). There is even one Nocardia species that infects plants: N. vaccinii, which causes galls on blueberry plants (420).
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