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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spiroplasmas are mollicutes characterized by motility and helical morphology. They were discovered through studies on corn stunt and citrus stubborn diseases. The stubborn agent was the first mollicute of plant origin to be obtained in culture and the first cultured mollicute to possess a helical morphology. The citrus pathogen has been known as Spiroplasma citri since 1973. The corn stunt agent was cultured in 1975 and fully characterized as Spiroplasma kunkelii by 1986. The third and only other phytopathogenic spiroplasma is Spiroplasma phoeniceum, cultured from naturally infected periwinkle plants in Syria and described in 1986. These three spiroplasmas are restricted to the phloem sievetubes of the infected plants and are transmitted from plant by various phloem feeding leafhopper vectors in which the spiroplasmas multiply. Following the pioneering work on S. citri and S. kunkelii, close to fifty other spiroplasma species or proposed species have been discovered. All spiroplasmas have been isolated from insects, ticks and plants. Insects are particularly rich sources of spiroplasmas. Some insect-derived spiroplasmas are entomopathogens. S. melliferum and S. apis are honey bee pathogens. They cross the insect-gut barrier and reach the hemolymph, where they multiply abundantly and kill the bee. Spiroplasma floricola is the agent of lethargy disease of Melolontha melolontha (cockchafer). Spiroplasma poulsonii infects the neotropical species of Drosophila, is transmitted transovarially and kills the male progeny of an infected female fly, hence the name sex ratio spiroplasma. Some insect-derived spiroplasmas are also found on plant (flower) surfaces. For instance, S. apis was cultured from the surfaces of flowers growing in the vicinity of affected beehives. This suggests that the plant surface spiroplasmas are deposited on these surfaces by contaminated insects. Many insect spiroplasmas are not pathogenic, are often restricted to the gut and may be regarded as mutualists or incidental commensals. Of the three known tick spiroplasmas, only Spiroplasma mirum obtained from rabbit ticks is pathogenic to the vertebrate animal (chick embryo, new-born rodents, adult rabbit), but only upon experimental inoculation of the spiroplasma. Strain SMCA induces high incidence of cataracts in new born rodents. With strain GT-48 no cataracts are observed, but fatal encephalitis occurs. Spiral membranous inclusions resembling spiroplasmas have been seen in brain biopsies taken from patients with Creutzfeldt-Jakob disease. However, failure to detect spiroplasmas by serology and culture points to the absence of spiroplasmal involvement in spongiform encephalopathies. Transposon Tn 4001 mutagenesis has been applied for the first time to Spiroplasma citri, and pathogenicity can now be studied at the genetic level. One Tn 4001 mutant does not multiply in the leafhoppers and is, therefore, not transmitted to the plant. Another mutant multiplies well in the plant and is transmitted to the plant, where it reaches high titers, but without inducing symptoms in the plant. In this non-phytopathogenic mutant, Tn 4001 is inserted in the spiroplasmal fructose operon, and the mutant is unable to use fructose. Finally, to study involvement of spiroplasmal motility in pathogenicity, a non-motile mutant has been obtained. Motility was restored by complementation with the wild type genes. This is the first time that successful complementation has been reported, not only in the spiroplasmas but in the mollicutes in general. Undoubtedly, studies on pathogenicity have entered a new era.
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PMID:Spiroplasmas: infectious agents of plants, arthropods and vertebrates. 928 68

We presented a case of Creutzfeldt-Jakob disease (CJD) associated with ocular dipping (OD). A 65-year-old woman was hospitalized with two months history of progressive ataxia and mental deterioration. On admission, she was bed-ridden and stuporous with rigidity of the four limbs. Her both eyes were noted to deviate downward slowly from midpossition, taking 1 to 3 seconds to reach the nadir and rapidly returned to midpossition. It was felt that these abnormal eye movements are compatible with OD. Findings of EOG were compatible with that of typical OD. Electroencephalogram obtained a few months later revealed periodic synchronous discharge. Magnetic resonance imaging of the brain which had demonstrated mild cerebral atrophy in the beginning subsequently revealed full-brown cerebral atrophy. Hence, she was diagnosed of having CJD. There has been no report of CJD associated with OD. The OD was observed to last as long as 110 days. When the above described abnormal eye movements were noted, there was no signs indicative of brain stem dysfunction present. Therefore, we feel that the present case suggest that a diffuse cerebral dysfunction involving the cerebral cortex and basal ganglia may underlie in the development of OD.
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PMID:[Creutzfeldt-Jakob disease associated with ocular dipping--a case report]. 959 17

We describe an autopsy case of MM1-type sporadic Creutzfeldt-Jakob disease (CJD), the duration of which was 93 days. The patient was a 59-year-old Japanese man with no family history of prion disease or known iatrogenic exposure to CJD. His first symptom was dysesthesia in the left arm, suggestive of cervical cord involvement, and he showed rapidly progressive neurologic signs, such as dysarthria, dysphagia, lethargy, sleep apnea and respiratory failure, suggestive of brainstem involvement. Progressive mental deterioration combined with episodes of myoclonic seizure and periodic synchronous discharges on the electroencephalogram were observed in the later disease stage. Autopsy showed typical spongiform change to be wide-spread in the cerebral and cerebellar cortices, thalamus and basal ganglia. Synaptic-type PrP deposition was marked in the cerebral cortex, thalamus and basal ganglia. In the cerebellum, although the granular, molecular and Purkinje cell layers were well preserved from neuronal loss and gliosis, PrP deposition was marked in the molecular and granular cell layers. Spongiform degeneration and neuronal loss were not seen in the brainstem and spinal cord, but relatively marked PrP deposition was observed in the quadrigeminal body, substantia nigra, pontine nucleus, inferior olivary nucleus and posterior horn. Immunohistochemical staining for HLA-DR showed proliferation of activated microglia in the cerebral and cerebellar cortices, pontine nucleus, inferior olivary nucleus and posterior horn. The mechanisms underlying the neurologic symptoms and signs were unclear, but we speculate that, in addition to widespread involvement of the cerebral cortex, PrP deposition and microglial activation in the brainstem and spinal cord were responsible.
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PMID:Autopsy case of sporadic Creutzfeldt-Jakob disease presenting with signs suggestive of brainstem and spinal cord involvement. 1720 92

We report an unusual case of probable Creutzfeldt-Jakob disease (CJD) in hemodialysis patient. A woman 59 years of age with a past history of hypertension and end-stage renal disease presented with a stuporous state preceded by rapidly progressive cognitive dysfunction, myoclonus, and akinetic mutism. At first, the cause of the altered mental status was assumed to be uremic or hypertensive encephalopathy combined with fever. Proper managements, however, did not improve the neurologic symptoms. Diffusion-weighted magnetic resonance imaging revealed bilaterally asymmetric high signal intensity in both basal ganglia and cerebral cortices. Electroencephalography showed diffuse generalized theta-to-delta range slow wave and intermittent medium-to-high voltage complexes with a characteristic triphasic pattern on both hemispheres. Cerebrospinal fluid assay for the 14-3-3 protein was positive and diagnostic of CJD.
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PMID:A case of Creutzfeldt-Jakob disease in a patient on hemodialysis. 2688 12