No abstract

Helicobacter hepaticus, a causative agent of chronic hepatitis and hepatocellular carcinoma in mice, expresses a nickel-containing hydrogen-oxidizing hydrogenase enzyme. Growth of a hyaB gene-targeted mutant was unaffected by the presence of hydrogen, unlike the wild-type strain, which showed an enhanced growth rate when supplied with H 2 . Hydrogenase activities in H. hepaticus were constitutive and not dependent on the inclusion of H 2 during growth. Addition of nickel during growth significantly stimulated both urease (for wild-type and hyaB) and hydrogenase (for wild-type) activities. In a 5-h period, the extent of 14 C-labeled amino acid uptake by the wild type was markedly enhanced in the presence of hydrogen and was >5-fold greater than that of the hyaB mutant strain. In the presence of H 2 , the short-term whole-cell amino acid uptake V max of the parent strain was about 2.2-fold greater than for the mutant, but the half-saturation affinity for amino acid transport was the same for the parent and mutant strain. The liver-and cecum-colonizing abilities of the strains was estimated by real-time PCR quantitation of the H. hepaticus-specific cytolethal distending toxin gene and showed similar animal colonization for the hyaB mutant and the wild type. However, at 21 weeks postinoculation, the livers from mice inoculated with wild type exhibited moderate lobular lymphoplasmacytic hepatitis with hepatocytic coagulative necrosis, but the hydrogenase mutants exhibited no histological evidence of lobular inflammation or necrosis.In recent years, more than three different Helicobacter species have been recovered from rodents (24,25,31), with H. hepaticus being the most well-studied enterohepatic Helicobacter species. First isolated in 1992 from untreated A/JCr control mice, H. hepaticus is a gram-negative, microaerophilic bacterium (6) that occurs naturally in many strains of inbred mice (30). Mice infected with this bacterium develop chronic hepatic lesions and are more prone to developing hepatocellular carcinoma (25, 26), which has made H. hepaticus an excellent model for studying mechanisms of bacterium-associated liver carcinogenesis. Although H. hepaticus can be isolated from the liver of infected mice, it is more consistently recovered from the intestinal tract since the primary site of colonization is the lower bowels of mice (6, 7). Recently, Helicobacter species DNA was reported to be associated with primary hepatocellular carcinomas in human liver samples (9, 23).At the same time, a hydrogen uptake hydrogenase enzyme well studied for its roles in nonpathogenic bacteria was demonstrated to be important for colonization of animals by some human pathogens (i.e., by Salmonella enterica serovar Typhimurium and Helicobacter pylori [14,21]); this sparked our interest in studying the physiological role of this enzyme in H. hepaticus (16). The colonization deficiency of hydrogenase structural gene mutants of H. pylori was attributed to their inability to utilize hydrogen as an energy substrate. H. hepaticus hydro...

No Litoral de Santa Catarina vem ocorrendo uma doença de bovinos caracterizada por "morte súbita". Para esclarecer a etiologia, foram conduzidos experimentos em bovinos nos quais se reproduziu a enfermidade pela administração oral de Mascagnia sp. Doses únicas de 5 g/kg das folhas frescas de Mascagnia sp causaram intoxicação não letal. Doses únicas de 7,5 g/kg causaram intoxicação letal em um de dois bovinos e dose de 10 g/kg a morte de outros dois. Nessas dosagens de 5 a 10 g/kg as manifestações clínicas eram observadas quando os animais eram movimentados, e consistiram em cansaço, jugular ingurgitada, leves tremores musculares e às vezes contrações bruscas; taquicardia já notada antes do exercício se acentuava. Finalmente os animais se deitavam ou caíram subitamente. A evolução da intoxicação nos dois animais em que foi acompanhada até a morte, foi de 40 e 75 minutos. As mais altas doses administradas (15 e 20 g/kg) provocaram um quadro de intoxicação protraída; os animais se mostraram lerdos e apáticos, evitando quaisquer movimentos; foram encontrados mortos 7h45min e 21 horas após terem sido observados os primeiros sinais clínicos. Esses dois últimos experimentos mostram que a movimentação é um fator importante para a manifestação da "morte súbita". Os principais achados de necropsia foram coloração vermelha intensa da mucosa do intestino delgado e edema da parede da vesícula biliar. As mais importantes alterações histológicas foram degeneração hidrópico-vacuolar do epitélio tubular renal em três dos cinco bovinos que morreram.

São relatados dois surtos de intoxicação natural por Phalaris angusta ("aveia-louca" ou "aveia-de-sangue") em bovinos no Estado de Santa Catarina, nos invernos de 1993 e 1996. Nos dois surtos os animais estavam lotados em piquetes onde P. angusta era a planta dominante. Os sinais clínicos incluíam tremores generalizados, olhar atento, hipermetria, ataxia e convulsões. Alterações macroscópicas eram restritas ao encéfalo e se caracterizavam por coloração cinza-esver-deada no tálamo e mesencéfalo. A doença foi reproduzida experimentalmente em bovinos pela administração de P. angusta.

This article describes the main aspects of bovine herpesvirus type-5 (BHV-5) neurologic infection and disease in rabbits, a candidate animal model for studying BHV-5 neuropathogenesis. Intranasal inoculation of weanling rabbits with a Brazilian BHV-5 isolate produced neurological disease and death in 78.8% (26/33) of the animals. Neurological signs started as early as 5 days post-inoculation and lasted from 10-12 hours up to several days. Most animals evolved to a moribund state or death within 24 (69.2%) to 48 hours (88.5%). Neurological disease was characterized by excitability or depression, tremors, bruxism, walking or running in circles, backward arching of the head and body, incoordination, backward and sideways falling, paddling, profound depression and death. Moderate levels of infectivity were detected in several areas of the brain, most consistently in the ventro-lateral hemisphere ( No gross lesions were observed. Microscopic lesions were mild and consisted of nonsuppurative meningitis, mononuclear perivascular cuffing and focal gliosis. These changes were observed most consistently in the ventro-lateral hemisphere and anterior cerebrum. Passive immunity partially protected rabbits from BHV-5-induced encephalitis. Rabbits born to immunized dams showed a significative delay in the onset of clinical disease and reduced morbidity and mortality rates compared to rabbits born to unvaccinated dams. These results demonstrate that BHV-5-induced neurological disease can consistently be reproduced in rabbits and point towards the use of this species as an animal model to study BHV-5 neuropathogenesis.