Herpetic croup: two case reports and a review of the literature

Croup is an acute infectious illness usually occurring in children; it is characterized by brassy cough and stridor. The main pathogens include mainly parainfluenza and influenza viruses. Recently there have been reports of prolonged croup caused by the herpes simplex viruses. We report two cases of prolonged croup due to herpes simplex types 1 and 2. We also review and summarize the reported pediatric cases of herpetic croup.     

Binding of botulinum neurotoxin to pure cholinergic nerve terminals isolated from the electric organ of Torpedo

Summary Torpedo electric organ has been used to study the binding of botulinum neurotoxin type A to pure cholinergic synaptosomes and presynaptic plasma membrane.¹²⁵I-labeled botulinum neurotoxin type A exhibits specific binding to cholinergic fractions. Two binding sites have been determined according to data analysis: a high affinity binding site (synaptosomes: K_d=0.11±0.03 nM, B_max=50±10 fmol · mg prot^–1; presynaptic plasma membrane: K_d=0.2±0.05 nM, B_max=150±15 fmol · mg prot^–1) and a low affinity binding site (synaptosomes: K_d 26 nM, B_max 7.5 pmol · mg prot^–1; presynaptic plasma membrane: K_d 30 nM, B_max 52 pmol · mg prot^–1). The binding of¹²⁵I-botulinum neurotoxin type A is decreased by previous treatment of synaptosomes by neuraminidase and trypsin, and by a preincubation with bovine brain gangliosides or antiserum raised against Torpedo presynaptic plasma membrane. When presynaptic plasma membranes are blotted to nitrocellulose sheet, either¹²⁵I-botulinum neurotoxin or botulinum toxin-gold complexes bind to a M_r 140,000 protein. Botulinum toxin-gold complexes have also been used to study the toxin internalization process into Torpedo synaptosomes. The images fit the three step sequence model in the pathway of botulinum neurotoxin poisoning.     

In vivo protein synthetic rates of atrial, ventricular, and pulmonary tissue proteins in aortic constriction, goldblatt, and bromoethylamine models of hypertension

Changes in tissue protein synthesis in hypertension have usually been measured in vitro in heart from acutely hypertensive rats without consideration of changes in atrial or pulmonary tissue or changes occurring in long-standing hypertension. The objective of the study was to investigate the in vivo changes in cardiopulmonary protein synthesis in three different rat models of chronic hypertension. Hypertension in aortic constriction, the Goldblatt model, and the bromoethylamine model were induced in rats for 30 days. At the end of the experimental period, in vivo rates of protein synthesis were measured with a flooding dose of [3H]phenylalanine (a method which effectively considers precursor pools). Concomitant measurements included quantification of contractile protein and RNA and DNA contents. Indices of protein breakdown were also assessed by selective measurement of protease activities. At the end of 30 days, aortic constriction induced marked increases in protein contents of the left ventricle, septum, left atria, and lungs. Accompanying changes included concomitant increases in RNA and DNA contents. Left ventricular myofibrillary, sarcoplasmic, and stromal protein contents increased in the aortic constriction model. Less marked changes occurred in the Goldblatt model, though the left atria were not significantly affected. In contrast, the bromoethylamine model had no effect on the protein or RNA contents of any region. In all cardiac regions of all three models, fractional rates of protein synthesis were not significantly affected. However, protein synthesis increased in the lungs of both the Goldblatt and bromoethylamine models at 30 days. Protease activities were decreased in the left ventricles of all three models at 30 days, with lysosomal protease activities declining in the aortic constriction model and cytoplasmic protease activities declining in the other two models. The failure of chronic hypertension to increase ventricular synthesis rates may represent inherent limitations in the time frame for measuring protein synthesis in vivo. However, at earlier time points (i.e., 10 days), the aortic constriction model was characterized by marked increases in left ventricular and atrial protein contents, RNA contents, and fractional rates of protein synthesis. This was consistent with the supposition that, in acute phases of hypertrophy, rates of protein synthesis increase, whereas in established hypertrophy, synthesis rates remain unchanged or decrease. The applicability of the aortic constriction model was investigated by examining the effects of the angiotensin converting enzyme inhibitor lisinopril (5 mg/kg/day). After 30 days treatment, lisinopril impeded the increase in left ventricular mixed and myofibrillar proteins. This effect was accompanied by an apparent increase in protein synthesis. In conclusion, although all three chronic models are able to induce hypertension, varying degrees of hypertrophy develop, which are more pronounced in the aortic constriction model. Accompanying changes include hypertrophy in the atria, reduced rates of ventricular proteolytic activity, and altered rates of protein metabolism in the lungs.     

Regulation of skeletal muscle development by the central nervous system in the fetal pig

The effect of upper motor neuron regulation on skeletal muscle development was studied in the fetal pig. A region of the spinal cord at the level of the upper cervical vertebrae was destroyed by cauterization at 45 days of gestation in four pig fetuses. Five fetuses with intact spinal cords served as controls. Innervation and enzyme activities in the longissimus muscle, the ultrastructure and quantitation of satellite cells in the sartorius muscle, and plasma composition were evaluated at 110 days of gestation. The terminal innervation ratios were similar (P greater than 0.05) for muscles from control and cauterized fetuses. Endplate morphology was also similar. Therefore, innervation of newly formed primary fibers is not controlled by upper motor neurons after 45 days of gestation. Mean values for body weight, percentage of muscle dry weight, percentage of myofibers with myonuclei and plasma levels of protein, glucose, triglycerides, lactate, and creatine phosphokinase activity were similar (P greater than 0.05) between the two groups of fetuses. All but one muscle fiber examined was of the secondary fiber type. These observations suggest that the physiological maturity of the muscle was not appreciably altered even though glucose-6-phosphate dehydrogenase activity was higher (P greater than 0.05) and total phosphorylase activity was lower (P greater than 0.05) in the spinal cauterized fetuses than in the control group. The percentage of satellite cells was lower when based on the number of myofibers observed (P greater than 0.005) or on the number of nuclei contained within the basal lamina (P greater than 0.001) in the muscle of the spinal cauterized fetuses than in the control fetuses. The cytoplasm of satellite cells from the muscles of control fetuses was rich in organelles indicative of metabolic and mitotic activity whereas a paucity of such organelles was observed in the satellite cells of cauterized fetuses. Since the percentage of myofibers that had myonuclei was similar (P greater than 0.05) for the control and cauterized fetuses, it appeared that the myonuclear population was maintained by direct incorporation of the parent satellite cell.     

Necrotizing cerebritis in an allogeneic bone marrow transplant recipient due to Cladophialophora bantiana.

We describe a necrotizing cerebritis in an allogeneic bone marrow transplant recipient caused by the neurotropic, dematiaceous fungus Cladophialophora bantiana. The patient presented 7 months after bone marrow transplantation with fever and sudden onset of left-sided weakness, followed shortly by cranial nerve III and VI palsies. The patient had a lesion (3.0 by 2.0 by 2.0 cm) of the right midbrain with extension to the pons, the left brain stem, and the right superior and the middle cerebellar peduncles. The diagnosis was made by microscopic examination and culture of a brain biopsy.     

Broiler chickens as potential source of Campylobacter infections in humans.

Of 46 broiler chickens from a live poultry market in New York City, 38 (83%) harbored Campylobacter fetus subsp. jejuni in their rectal flora. The observed mean number of C. fetus per g of feces was 4.4 x 10(6). The organisms survived in the feces for at least 96 h at 4 degrees C whether stored in the gut or transferred to a vial. The best survival medium for pure cultures of C. fetus subsp.jejuni was heart infusion broth supplemented with sterile blood and kept in a microaerophilic atmosphere.     

The reflex effects of intralaryngeal carbon dioxide on the pattern of breathing

1. The reflex effects on the pattern of breathing and total lung resistance of introducing 30, 10 and 5% CO(2) in air into the larynx have been studied in anaesthetized and decerebrate cats breathing through a tracheostomy tube.2. Flowing 30% CO(2) into the larynx caused a two-phased response. First, respiratory frequency and tidal volume decreased, with a consequent fall in minute ventilation. After two to ten breaths, frequency remained slow, but tidal volume increased beyond the control level, so that minute ventilation was restored to control levels.3. Flowing 5 or 10% CO(2) into the larynx caused slowing of breathing with small and inconsistent changes in tidal volume. Minute ventilation was significantly diminished.4. Off effects, on re-introducing air into the larynx, after 2 and 10 min of CO(2) exposure, suggested that the reflex response diminishes with increased duration of exposure to CO(2).5. None of the concentrations of intralaryngeal CO(2) changed total lung resistance or compliance.6. CO(2) mixtures in the larynx generally caused no change in blood pressure or pulse rate of the cats.7. The reflex effects of intralaryngeal CO(2) were abolished by denervating the larynx.8. Hypoxic mixtures introduced into the larynx did not change breathing.     

Toxicity and immunogenicity of a verotoxin 1 mutant with reduced globotriaosylceramide receptor binding in rabbits.

The verotoxins (VT1 and VT2), produced by strains of enterohemorrhagic Escherichia coli, have been implicated in the pathogenesis of hemorrhagic colitis and the hemolytic uremic syndrome. To better understand the role of globotriaosylceramide (Gb3) receptor binding by the verotoxins in disease production, we examined the clinicopathologic effects of an intravenously (i.v.) administered verotoxin 1 mutant holotoxin (Phe30Ala) in rabbits. The substitution of alanine for phenylalanine 30 in the VT1 B subunit has been shown previously to reduce both Gb3 binding affinity and capacity in vitro. This reduction in receptor binding corresponded to a 10(5)-fold reduction in the toxic activity of VT1 on a Vero cell monolayer. In this study, purified 125I-labeled Phe30Ala was administered i.v. to rabbits to determine its specific distribution in rabbit tissues. In contrast to the rapid elimination of i.v. administered 125I-VT1 from the bloodstream, 125I-Phe30Ala had a 52-fold-longer half-life in serum and failed to localize preferentially in the gastrointestinal tract and central nervous system (CNS). Rabbits challenged with Phe30Ala at a dose equivalent to 10 times the 50% lethal dose (LD50) of VT1 showed no visible clinical symptoms typical of VT effect after 7 days. Administration of Phe30Ala at a dose equivalent to 100 times the LD50 of VT1, however, caused both clinical and histopathologic features indistinguishable from VT1 toxemia in rabbits, although the onset of symptoms was delayed. Rabbits were immunized with Phe30Ala and challenged i.v. with either 125I-VT1 or 125I-VT2. The specific uptake of 125I-VT1 in the gastrointestinal tract and CNS was totally inhibited in Phe30Ala immune rabbits. Only a partial decrease in target organ uptake was observed in Phe30Ala immune rabbits challenged with 125I-VT2. From this study, we conclude that Gb3 binding is responsible for target organ localization of VT1 and disease production in the rabbit. The ability of Phe30Ala to induce both strong antibody and protective responses against VT1 suggests that VT mutants with reduced receptor binding properties may be useful in vaccine strategies. A further reduction in the toxicity of Phe30Ala would be required for its use as a natural toxoid to protect against human verotoxigenic E. coli infections.     

Induction of heat shock proteins in lymphocytes increases with mitogen stimulation

The effect of the growth state of a cell on the ability of hyperthermia to induce the synthesis of heat shock proteins (HSPs) was studied in resting and concanavalin A (ConA)-stimulated lymphocytes. Hyperthermia induced the synthesis of hsp 110, hsp 90, hsc 70, and hsp 70 in both resting and ConA-stimulated lymhocytes, and ConA-treatment induced the synthesis of the hsp 90 and hsc 70 at normal temperature. The induction of the synthesis of hsp 110 and hsp 70 by hyperthermia was 3- to 6-fold higher for lymphocytes cultured with ConA for 12 and 24 h than in non-stimulated lymphocytes. Thus, lymphocytes induced to undergo proliferation showed a greater response to hyperthermia than resting lymphocytes.     

Expression of superoxide dismutase and catalase in rat brain as a function of age

Active oxygen species have been proposed to be involved in the aging process of the brain, therefore alterations of the levels of enzymes involved in the defence system against free radicals and other active species could substantially influence the aging process. In this study the enzyme activities of superoxide dismutase (Cu/Zn) and catalase as well as the relative levels of their mRNA were measured in the brain of Fischer F344 rats of various ages (5-37 months old). A gradual decrease in the activity of these enzymes (21-27%) was observed with increasing age. The alterations were paralleled by a decrease (39-40%) in the relative levels of these mRNA species. Thus the decrease in the activity of superoxide dismutase and catalase appears to be due to an age-dependent change in the expression of these genes.