First Report of Blossom Blight of Strawberry Caused by Xanthomonas fragariae and Cladosporium cladosporioides in California.

In the spring of 1996, severe blossom blight occurred in some strawberry fruit production fields in the Watsonville area. The symptoms, in addition to blighting of entire flowers, were as follows: on the lower surface of the calyx, watersoaked lesions that appeared dark green under reflected light and translucent under transmitted light; necrotic calyces of seemingly healthy green and ripe fruits; watersoaking of the base of the calyx that extended into the pedicel; green-gray sporulation on dead anthers; and presence of flower clusters with small and irregularly shaped fruits. Yellow bacterial colonies were consistently isolated from water-soaked and necrotic lesions on calyces and pedicels. These colonies were entire, circular, raised, glistening, mucoid, and slow growing, characteristics typical of Xanthomonas fragariae on nutrient agar-glucose-yeast extract medium. The bacterial isolate was also identified by rep-polymerase chain reaction as X. fragariae. In addition to the yellow bacteria, a fungus was also frequently isolated from infected anthers, sepals, petals, and pistils, and was identified as Cladosporium cladosporioides. On potato dextrose agar, the fungus had velvetlike colonies colored olivaceous-green to olivaceous-brown, apically and laterally branched conidiophores, and lemon-shaped conidia that were usually smooth but sometimes textured. Blossoms of greenhouse-grown strawberry plants cv. Selva were inoculated with either or both organisms. Blossoms inoculated with X. fragariae developed symptoms distinct from those inoculated with C. cladosporioides. The most prominent visible symptoms caused by X. fragariae were watersoaked lesions on calyces that later became necrotic, watersoaking of the calyx that extended into the pedicel, and blighting of flowers and developing fruits as a result of girdling of the pedicel. Infection by C. cladosporioides was characterized by necrosis of flower parts or the entire flower, presence of green-gray sporulation on dead anthers, and production of small and malformed or misshapen fruits. Inoculation with both organisms produced all the symptoms described above in different flowers of a plant. Infection with both organisms aggravated disease severity, but each organism was capable of inducing blossom blight independently. Both organisms were reisolated from artificially inoculated strawberry flowers, fulfilling Koch's postulate for proof of pathogenicity. This is the first report of the two organisms causing blossom blight of strawberry in California. This is also the first report that C. cladosporioides is a pathogen of strawberry.

Obsessive-compulsive symptoms in neurologic disease: a review.

Obsessive-compulsive disorder (OCD) is an increasingly recognized disorder with a prevalence of 2-3% (Robins et al., 1984). Once thought to be psychodynamic in origin, OCD is now generally recognized as having a neurobiological cause. Although the exact pathophysiology of OCD in its pure form remains unknown, there are numerous reports of obsessive-compulsive symptoms arising in the setting of known neurological disease. In this paper, we review the reported cases of obsessive-compulsive symptoms associated with neurologic diseases and outline the known facts about the underlying neurobiology of OCD. Finally, we synthesize these findings into a proposed theory of the pathophysiology of OCD, in both its pure form and when it accompanies other neurological illness.

Toxicity resulting from lithium augmentation of antidepressant treatment in elderly patients.

Lithium augmentation of antidepressant treatment is a commonly used strategy for treatment-resistant cases of depression. Two cases are described in which significant neurotoxicity developed in elderly patients despite therapeutic doses of antidepressant and lithium.

Involvement of brain dopamine systems on neurotensin-induced protection against stress gastric lesions.

We have previously demonstrated that intracisternal (i.c.) administration of neurotensin (NT), a brain and gastrointestinal tridecapeptide, potently inhibits gastric ulcer formation induced by cold-restraint stress (CRS) in rats. This study evaluated the effect of i.c. NT (17.9 nmol) or vehicle (10 microliter of 0.9% NaCl) on the development of CRS-induced gastric ulcers and on dopamine (DA) concentrations and DA turnover (DOPAC/DA) in selected brain regions after 0, 1, 2 and 3 h of CRS. As anticipated, and in confirmation of previous findings, NT significantly reduced the incidence and severity of CRS gastric ulcers in a time-dependent manner. Neurotensin significantly decreased DA concentration and DA turnover in the striatum. In the nucleus accumbens, however, NT produced a decrease in DA concentration and a concomitant increase in DA turnover after 2 and 3 h of CRS. No significant effects of brain NT on DA concentration and DA turnover were observed in the hypothalamus or olfactory tubercles. These findings suggest that the anti-ulcer effect of brain NT may be mediated, at least in part, by a differential activation of the mesolimbic and nigrostriatal DA systems.

Role of brain neurotransmitters on neurotensin-induced gastric cytoprotection.

We have reported previously that intracisternal (IC) administration of neurotensin (NT) prevents stress-induced gastric ulcers in rats. This effect of NT appears to be mediated by the central nervous system because peripheral (IV) NT is totally ineffective. The present study sought to clarify the central mechanism of the cytoprotective effect of NT by utilizing pharmacological treatments which alter the function of brain neurotransmitter systems. Pretreatment with intracerebroventricular (ICV) administration of agonists and antagonists of acetylcholine (ACh), gamma-aminobutyric acid (GABA), and serotonin (5-HT) receptors or with an anti-opiate (naloxone) agent did not significantly alter NT-induced cytoprotection. However, pretreatment with ICV haloperidol, a dopamine (DA) receptor antagonist, totally blocked NT's cytoprotective effect. In addition, pretreatment with methylphenidate, a DA receptor agonist, produced cytoprotection similar to IC NT. These data indicate that NT-induced cytoprotection is not mediated by 5-HT, GABA, ACh (muscarinic) receptors, or endogenous opiate systems, but suggest interactions between brain DA systems and NT.