Effect of CO2 on growth and toxicity of Alexandrium tamarense from the East China Sea, a major producer of paralytic shellfish toxins.

In recent decades, the frequency and intensity of harmful algal blooms (HABs), as well as a profusion of toxic phytoplankton species, have significantly increased in coastal regions of China. Researchers attribute this to environmental changes such as rising atmospheric CO2 levels. Such addition of carbon into the ocean ecosystem can lead to increased growth, enhanced metabolism, and altered toxicity of toxic phytoplankton communities resulting in serious human health concerns. In this study, the effects of elevated partial pressure of CO2 (pCO2) on the growth and toxicity of a strain of Alexandrium tamarense (ATDH) widespread in the East and South China Seas were investigated. Results of these studies showed a higher specific growth rate (0.31±0.05day-1) when exposed to 1000µatm CO2, (experimental), with a corresponding density of (2.02±0.19)×107cellsL-1, that was significantly larger than cells under 395µatm CO2(control). These data also revealed that elevated pCO2 primarily affected the photosynthetic properties of cells in the exponential growth phase. Interestingly, measurement of the total toxin content per cell was reduced by half under elevated CO2 conditions. The following individual toxins were measured in this study: C1, C2, GTX1, GTX2, GTX3, GTX4, GTX5, STX, dcGTX2, dcGTX3, and dcSTX. Cells grown in 1000µatm CO2 showed an overall decrease in the cellular concentrations of C1, C2, GTX2, GTX3, GTX5, STX, dcGTX2, dcGTX3, and dcSTX, but an increase in GTX1 and GTX4. Total cellular toxicity per cell was measured revealing an increase of nearly 60% toxicity in the presence of elevated CO2 compared to controls. This unusual result was attributed to a significant increase in the cellular concentrations of the more toxic derivatives, GTX1 and GTX4.Taken together; these findings indicate that the A. tamarense strain ATDH isolated from the East China Sea significantly increased in growth and cellular toxicity under elevated pCO2 levels. These data may provide vital information regarding future HABs and the corresponding harmful effects as a result of increasing atmospheric CO2.

Trypanosoma cruzi Causes Paralyzing Systemic Necrotizing Vasculitis Driven by Pathogen-Specific Type I Immunity in Mice.

Infectious agents are often considered potential triggers of chronic inflammatory disease, including autoimmunity; however, direct evidence is usually lacking. Here we show that following control of acute infection of mice with the myotropic Colombiana strain of Trypanosoma cruzi, parasites persisted in tissue at low levels associated with development of systemic necrotizing vasculitis. Lesions occurred in many but not all organs and tissues, with skeletal muscle arteries being the most severely affected, and were associated with myositis, atrophy, paresis/paralysis, and death. Histopathology showed fibrinoid vascular necrosis, rare amastigote nests within skeletal muscle myocytes, and massive leukocyte infiltrates composed mainly of inflammatory monocytes, F4/80(+)macrophages, and T. cruzi tetramer-specific CD8(+) T lymphocytes capable of producing gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) but not interleukin-17 (IL-17). T. cruzi-specific IgG was detected in sera from infected mice, but antibody deposits and neutrophilic inflammation were not features of the lesions. Thus,T. cruzi infection of mice may be a specific infectious trigger of paralyzing systemic necrotizing vasculitis most severely affecting skeletal muscle, driven by pathogen-specific type I immune responses.

CD8+ T-cells mediate immunopathology in tick-borne encephalitis.

Epidemics of tick-borne encephalitis involving thousands of humans occur annually in the forested regions of Europe and Asia. Despite the importance of this disease, the underlying basis for the development of encephalitis remains undefined. Here, we prove the key role of CD8(+) T-cells in the immunopathology of tick-borne encephalitis, as demonstrated by prolonged survival of SCID or CD8(-/-) mice, following infection, when compared with immunocompetent mice or mice with adoptively transferred CD8(+) T-cells. The results imply that tick-borne encephalitis is an immunopathological disease and that the inflammatory reaction significantly contributes to the fatal outcome of the infection.

[Persistent neurological sequelae due to cerebral malaria in a cohort of children from Mali]. / Séquelles neurologiques persistantes dues au paludisme cérébral dans une cohorte d'enfants au Mali.

INTRODUCTION: Several neurological complications are associated with cerebral malaria (CM). However, few long-term data from childhood survivors have been published. METHODS: A cross-sectional study was carried out in Mali among children followed from 1999 to 2002 after serious and complicated malaria. Our aim was to evaluate the persistent neurological sequelae associated with CM. RESULTS: This study concerned 101 subjects who had had CM. Mean age was 5.6+/-3.6 years. Twenty-eight children presented persistent neurological sequelae (27.7p.cent). Among them eight (7.9p.cent) children had developed these sequelae just after CM and 20 (19.8p.cent) a few months later: headaches, mental retardation, speech delay, bucco-facial dyspraxia, diplegia and frontal syndrome (one case each), dystonia (two cases), epilepsy (five cases) and behavior and attention disorders (15 cases). CONCLUSIONS: In this study, we show that neurological signs due to CM can persist in the long run. Long-term follow-up and proper management after CM are essential.

Myeloradiculitis: a rare event in schistosoma infection.

Schistosomiasis a parasitic disease caused by trematodes is widely distributed in (sub-)tropical countries. Depending on the species the infection manifests clinically as gastrointestinal (preferentially Schistosoma mansoni and S. japonicum) or urinary (preferentially S. haematobium) disorders. Here we present an uncommon case of myeloradiculitis leading to bladder palsy and sensory loss at the lower limbs.

Demonstration of vector competence of Culex quinquefasciatus (Diptera: Culicidae) for Setaria digitata.

In Taiwan, Setaria digitata infection causes a lumber paralysis in increasing number of cattle. Culex quinquefasciatus is one of the predominant mosquitoes, and it has been suspected that C. quinquefasciatus acts as a vector to Setaria nematodes prevalence but this was not confirmed. C. quinquefasciatus, Aedes albopictus and A. aegypti of various strains were investigated using an artificial infection system to evaluate their vector competence. After blood feeding at day 14, the number of larvae (stage III) per infected mosquito in A. aegypti (Liverpool strain), A. aegypti (Kaohsiung strain), A. aegypti (Tungan strain), C. quinquefasciatus (Taichung strain) and A. albopictus (Taichung strain) was 1.3 +/- 0.1, 1.3 +/- 0.1, 1.4 +/- 0.1, 1.0 +/- 0.0 and 0 +/- 0.0 (mean +/- S.E.M), respectively. The vector efficiency index of A. aegypti (Liverpool) was the highest among mosquitoes whereas A. albopictus showed a complete refractoriness to the infection. In conclusion, C. quinquefasciatus demonstrates its potential competence for serving as a transmission vector of S. digitata. This mosquito might therefore be responsible, at least in part, for the prevalence of cattle lumbar paralysis in Taiwan. This is the first report of C. quinquefasciatu demonstrating its vector competence for S. digitata.

[Bilharzian meningomyeloradiculopathy in children]. / La méningo-myélo-radiculite bilharzienne chez l'enfant.

Child meningomyeloradiculitis is a rare complication form of schistosomiasis, even in hyperendemic area. Its diagnosis is very difficult, especially if there are not history or signs of Schistosoma mansoni or hematobium infections. It must be evocated in case of acute flask paralysis occurring in children living in Schistosoma infections endemic area. The authors report a 14-year-old boy's case and suggest etiopathogeny of the disease.

Trichobilharzia regenti, a pathogen of the avian and mammalian central nervous systems.

The development of nasal avian schistosomes of the genus Trichobilharzia in their final host is poorly known. Therefore, an experimental infection of ducklings (Anas platyrhynchos f. dom.) by T. regenti was performed. The infection resulted in leg paralysis and orientation/balance disorders of birds. The examination of the duck's spinal cord and brain confirmed the presence of developing parasites in pre-patent as well as patent periods. The absence of the worms in other tissues strongly supports our hypothesis that the parasite migrates through the central nervous system (CNS) to its final location in bird nasal mucosa. The injury level is probably dependent on number of parasites as well as yet unknown host factors. The affinity to the CNS seems to be high; also by exposure of experimental animals to low cercarial doses the growing worms in the CNS were found. In addition to the generally accepted view that bird schistosomes may cause cercarial dermatitis of mammals (including man), there is evidence of a partial development of T. regenti in mouse CNS; in certain cases leg paralysis was also recorded. Therefore, the pathogenesis spectrum caused by bird schistosomes in birds/mammals needs to be reconsidered.

Canine neosporosis: clinical signs, diagnosis, treatment and isolation of Neospora caninum in mice and cell culture.

Clinical signs, diagnosis, treatment and isolation of Neospora caninum from two littermate dogs are described. Three of six pups from a Labrador bitch developed paralysis. Neosporosis was diagnosed ante mortem by serological examination in two of the affected pups. At necropsy, tissue cysts were seen in unstained smears and in histologic sections of their brains. Tissue cysts were often thin-walled (approximately 1 micron) but antigenically and ultrastructurally identified as N. caninum. Furthermore, N. caninum (isolates NC-4, NC-5) was isolated in mice and in cell cultures inoculated with neural tissues of these two dogs. Serological diagnosis of neosporosis using a variety of tests is discussed.

[The occurrence of lumbar paralysis in goats and the appearance of Elaphostrongylus cervi in red deer in the canton Ticino]. / Untersuchungen über das Vorkommen der lumbalen Parese bei Ziegen und über das Auftreten von Elaphostrongylus cervi beim Rothirsch im Kanton Tessin.

The aim of the study was to examine the incidence of lumbar paralysis in goats and the possible role of Elaphostrongylus cervi as an agent. For this reason questionnaires concerning the clinical pictures and the incidence of lumbar paralysis were sent to 200 owners of goats and to 9 veterinarians. The study showed that the symptoms of lumbar paralysis had been observed for many years mainly during the winter. Most of the animals suffering from lumbar paralysis originated from the Valley of Leventina and Blenio. The symptoms of lumbar paralysis could be observed from 29 owners of goats. Fecal examination of 36 red deer in the autumn of 1995 was carried out for studying if deer plays a role in spreading the larvae of E. cervi. Twenty-five red deer passed the E. cervi larvae. This could be indicating that deer plays an possible role in the infection of goats with E. cervi.

The effect of feeding immature Karoo paralysis ticks Ixodes rubicundus (Acari: Ixodidae) on the metabolic rate of the rock elephant shrew.

The effect of feeding immature Karoo paralysis ticks (Ixodes rubicundus) on the resting metabolic rate (RMR) of their principal natural host, the rock elephant shrew (Elephantulus myurus), was investigated under laboratory conditions. The elephant shrews were artificially infested with numbers of ticks simulating natural burdens. The RMR of the elephant shrews was quantified by measuring the oxygen consumption in an open through-flow system. The RMR of hosts infested only with larvae did not differ from that of the control group. Those infested with nymphs, or nymphs and larvae, had significantly lower RMR's compared to the control animals. There were no signs of paralysis in any of the infested hosts.

Ovine myeloencephalitis-leukomyelomalacia associated with a Sarcocystis-like protozoan.

Bilateral pelvic limb paresis developed in 7 of 15 10-month-old Blueface Leicester ram lambs on a mixed enterprise farm in the North of England. Clinical signs were principally mild to severe paresis of the pelvic limbs. Two mildly affected lambs recovered. Multifocal spinal cord white matter edema and necrosis, glial nodules, and mild to moderate nonsuppurative encephalomyelitis were the principal findings in 3 severely paretic lambs examined histologically. Protozoan bodies (12.7-23.0 microns) that stained immunocytochemically for Sarcocystis epitopes were in spinal cord glial cells of 2 of 3 lambs. Protozoa did not react immunocytochemically with anti-Toxoplasma gondii or Neospora canium antisera. Serology indicated there was recent exposure to Sarcocystis spp. in some surviving lambs. These cases resembled those in previous reports of paresis due to an unidentified Sarcocystis-like protozoan in sheep (ovine protozoan myeloencephalitis) in the British Isles, the USA, France, Australia, and New Zealand.

Chemotherapy of Trypanosoma brucei infection of the central nervous system: the use of a rapid chemotherapeutic regimen and the development of post-treatment encephalopathies.

The use of a rapid curative chemotherapeutic regimen for experimental infection of the central nervous system (CNS) of mice by Trypanosoma brucei has indicated that this 'aggressive' treatment does not precipitate the development of post-treatment meningo-encephalopathy. If meningoencephalitis is already established at the time of the treatment there is no exacerbation of the reaction and the CNS pathology rapidly returns to normal. Paralysis is not precipitated by the rapid curative treatment of either primary or relapse infections, in contrast to non-curative treatments. Mice showing this overt clinical paralysis in addition to histological meningoencephalitis soon regain mobility and the CNS pathology is rapidly resolved after curative chemotherapy. These experiments provide no support for the concept that the rapid release of trypanosome antigens in situ in the brain exacerbates the post-treatment encephalopathy. They do support the concept that it is viable trypanosomes remaining in the brain which are responsible.

The effect of the pattern of attachment weights of female Ixodes rubicundus on Karoo paralysis in a naturally infested flock of sheep.

The weights of feeding female Ixodes rubicundus attaching to sheep was studied in a natural focus of Karoo paralysis. The studies showed fewer females in the middle weight ranges and more in the heavier and lighter categories than would be expected if the distribution was normal. Weights were also strongly skewed towards the lighter females between 0 and 400 mg. No differences in the pattern of attachment weights occurred over the four experimental groups used, suggesting that previous contact of sheep with I. rubicundus had no effect on the ability of the tick to engorge.

Cerebrospinal nematodiasis in a goat herd.

During the fall of 1985, 4 Angora goats, from a herd of 40, were examined on a farm in central Michigan. Affected goats were alert but had neurologic deficits consistent with upper and lower moto neuron involvement. Eosinophilic pleocytosis in a cerebrospinal fluid sample from one goat was consistent with cerebrospinal nematodiasis. Parelaphostrongylosis was confirmed in 3 goats by identification of Parelaphostrongylosis tenuis larvae in spinal cord sections. Ivermectin may have influenced the herd's susceptibility to new parasitic infections. Control of parelaphostrongylosis probably is best achieved by removal of susceptible animals from treed swamps coinhabited by white-tailed deer from late summer until after the first killing frost.