Cerebral cystic echinococcosis in Mongolian children caused by Echinococcus canadensis.

Recent molecular re-evaluation of Echinococcus granulosus, which causes cystic echinococcosis (CE), has revealed that it is not a single species, but instead consists of 5 cryptic species. Among them, E. granulosus (dog-sheep strain) is predominant (75%) followed by Echinococcus canadensis (22%). The major affected organs, in humans, are the liver (88%) and lungs (11%). Primary cerebral CE comprises less than 1% of all cases. As cerebral CE cases are rare, there are few reports with molecular confirmation of the causative species. This study reports mitochondrial gene analysis from 4 Mongolian pediatric cerebral CE cases. Molecular confirmation was obtained for 3 of the 4 cases, with all 3 cases determined to be due to E. canadensis (G6/G7) infection. None of the cases had other organ involvement. This is only the third report on the molecular identification of the Echinococcus species responsible for cerebral CE, and only the second report of E. canadensis (G6/G7) being the causative agent of cerebral CE.

Baylisascaris larva migrans.

Baylisascaris procyonis is a roundworm of the raccoon found primarily in North America but also known to occur in other parts of the world including South America, Europe, and Japan. Migration of the larvae of this parasite is recognized as a cause of clinical neural larva migrans (NLM) in humans, primarily children. It is manifested as meningoencephalitis associated with marked eosinophilia of the cerebrospinal fluid and peripheral blood. Diagnosis is made by recovering and identifying larvae in or from the tissues, epidemiological history, serology, and imaging of the central nervous system. Treatment is with albendazole and steroids, although the prognosis is generally poor. This parasite can also cause ocular larva migrans (OLM) which usually presents as diffuse unilateral subacute neuroretinitis (DUSN). The ocular diagnosis can be made by visualizing the larva in the eye and by serology. Intraocular larvae can be destroyed by photocoagulation although albendazole and steroids may also be used. However, once visual disturbance is established the prognosis for improved vision is poor. Related Baylisascaris species occur in skunks, badgers, and certain other carnivores, although most cases of NLM are caused by B. procyonis. Baylisascaris procyonis has also been found in kinkajous in the USA and South America and may also occur in related procyonids (coatis, olingos, etc.).

Direct and indirect affection of the central nervous system by Fasciola infection.

Fascioliasis is a worldwide, zoonotic disease caused by the liver trematodes Fasciola hepatica and Fasciola gigantica. Neurological fascioliasis has been widely reported in all continents, affecting both sexes and all ages. Two types of records related to two physiopathogenic mechanisms may be distinguished: cases in which the neurological symptoms are due to direct effects of a migrating juvenile present in the brain or neighboring organ and with cerebral lesions suggesting migration through the brain; and cases with neurological symptoms due to indirect immuno-allergic and toxic effects at distance from flukes in the liver. Neurological manifestations include minor symptoms, mainly cephalalgias, and major symptoms which are nonspecific, extremely diverse, varying from one patient to another and even within the same patient, and comprising meningeal manifestations and impressive neurological manifestations. The puzzling neurological polymorphism leads to confusion with cerebral tumors, multiple sclerosis, lesions of the brainstem, or cerebro-meningeal hemorrhages. Only blood eosinophilia and information on infection source guide toward correct diagnosis by appropriate coprological and/or serological techniques. Although neurological patients usually recover after fasciolicide treatment or surgical worm extraction, sequelae, which are sometimes important, remain in several patients. The need to include possible neurological complications within the general frame of fascioliasis becomes evident.

Imaging of rickettsial, spirochetal, and parasitic infections.

This article is an update and literature review of the clinical and neuroimaging findings of the commonly known rickettsial, spirochetal, and eukaryotic parasitic infections. Being familiar with clinical presentation and imaging findings of these infections is crucial for early diagnosis and treatment especially in patients who live in or have a travel history to endemic regions or are immunocompromised.

Spine infections.

Infections of the spine represent a rare but potentially debilitating and neurologically devastating condition for patients. Early diagnosis, imaging, and intervention may prevent some of the more critical complications that may ensue from this disease process, including alignment abnormalities, central canal compromise, nerve root impingement, vascular complications, and spinal cord injury. This article reviews the underlying pathophysiologic basis of infection, clinical manifestations, and imaging modalities used to diagnose infections of the spine and spinal cord.

Infectious myelitis.

Infections are an uncommon but very important etiology of myelitis as a correct diagnosis would allow for timely treatment and recovery. The term "myelitis" is generally used to describe an inflammatory pathologic process affecting the spinal cord and causing an interruption of the ascending and descending pathways, and, therefore, partial or complete loss of function. The onset may be acute or subacute, and the etiology may be cumbersome to determine. This article will review the most recently published literature regarding the infectious agents causing myelitis with an emphasis on diagnosis and treatment.

Trichobilharzia regenti: host immune response in the pathogenesis of neuroinfection in mice.

Besides their natural bird hosts, Trichobilharzia regenti cercariae are able to penetrate skin of mammals, including humans. Experimental infections of mice showed that schistosomula of this species are able to avoid the immune response in skin of their non-specific mammalian host and escape the skin to migrate to the CNS. Schistosomula do not mature in mammals, but can survive in nervous tissue for several days post infection. Neuroinfections of specific bird hosts as well as accidental mammalian hosts can lead to neuromotor effects, for example, leg paralysis and thus this parasite serves as a model of parasite invasion of the CNS. Here, we show by histological and immunohistochemical investigation of CNS invasion of immunocompetent (BALB/c) and immunodeficient (SCID) mice by T. regenti schistosomula that the presence of parasites in the nervous tissue initiated an influx of immune cells, activation of microglia, astrocytes and development of inflammatory lesions. Schistosomula elimination in the tissue depended on the host immune status. In the absence of CD3+ T-cells in immunodeficient SCID mice, parasite destruction was slower than that in immunocompetent BALB/c mice. Axon injury and subsequent secondary demyelination in the CNS were associated with mechanical damage due to migration of schistosomula through the nervous tissue, and not by host immune processes. Immunoreactivity of the parasite intestinal content for specific antigens of oligodendrocytes/myelin and neurofilaments showed for the first time that schistosomula ingest the nervous tissue components during their migration.

[Inflammatory and infectious manifestations of the nervous system]. / Manifestations inflammatoires et infectieuses du système nerveux.

The Central Nervous System is the site of a wide variety of inflammatory and infectious diseases. Some disease entities have been in the focus of interest in recent years and progress has been achieved in our understanding of some chosen domains. We will review recent progress in our knowledge about transmissible spongiformes encephalopathies and AIDS-associated lesions, and briefly discuss cerebral vasculitis, granulomatous diseases and the most frequent infections by parasites.