Effect of food additives on key bacterial taxa and the mucosa-associated microbiota in Crohn's disease. The ENIGMA study.

Food additives have been linked to the pro-inflammatory microbial dysbiosis associated with Crohn's disease (CD) but the underlying ecological dynamics are unknown. Here, we examine how selection of food additives affects the growth of multiple strains of a key beneficial bacterium (Faecalibacterium prausnitzii), axenic clinical isolates of proinflammatory bacteria from CD patients (Proteus, Morganella, and Klebsiella spp.), and the consortia of mucosa-associated microbiota recovered from multiple Crohn's disease patients. Bacterial growth of the axenic isolates was evaluated using a habitat-simulating medium supplemented with either sodium sulfite, aluminum silicate, carrageenan, carboxymethylcellulose, polysorbate 80, saccharin, sucralose, or aspartame, intended to approximate concentrations found in food. The microbial consortia recovered from post-operative CD patient mucosal biopsy samples were challenged with either carboxymethylcellulose and/or polysorbate 80, and the bacterial communities compared to unchallenged consortia by 16S rRNA gene amplicon profiling. Growth of all F. prausnitzii strains was arrested when either sodium sulfite or polysorbate 80 was added to cultures at baseline or mid-exponential phase of growth, and the inhibitory effects on the Gram-negative bacteria by sodium sulfite were conditional on oxygen availability. The effects from polysorbate 80, saccharin, carrageenan, and/or carboxymethylcellulose on these bacteria were strain-specific. In addition to their direct effects on bacterial growth, polysorbate 80 and/or carboxymethylcellulose can drive profound changes in the CD mucosa-associated microbiota via niche expansion of Proteus and/or Veillonellaceae - both implicated in early Crohn's disease recurrence. These studies on the interaction of food additives with the enteric microbiota provide a basis for dietary management in Crohn's disease.

Single nucleotide polymorphisms in immune response genes in acute Q fever cases with differences in self-reported symptoms.

Genes involved in human immune response are well recognized to influence the clinical course of infection. The association of host genetics with susceptibility to and severity of clinical symptoms in acute Q fever was investigated. Single nucleotide polymorphisms (SNPs) in the IFNG (rs2430561/rs1861493), STAT1 (rs1914408), and VDR (rs2228570) genes were determined in 85 patients from the 2007 Dutch acute Q fever outbreak, and a symptom score was calculated. IFNG rs1861493 showed a significant association with the symptom score; IFNG rs2430561 showed a similar trend. These SNPs were then used to reproduce results in a 2009 outbreak population (n = 123). The median symptom score differed significantly in both populations: 2 versus 7. The significant association of IFNG rs1861493 with symptom score in the first population was not reproduced in the second population. We hypothesize that individuals in the second outbreak were exposed to a higher Coxiella burnetii dose compared to the first, which overruled the protection conferred by the A-allele of IFNG rs1861493 in the first population.

Correlations between peripheral blood Coxiella burnetii DNA load, interleukin-6 levels, and C-reactive protein levels in patients with acute Q fever.

From 2007 to 2010, the Netherlands experienced the largest reported Q fever outbreak, with >4,000 notified cases. We showed previously that C-reactive protein is the only traditional infection marker reflecting disease activity in acute Q fever. Interleukin-6 is the principal inducer of C-reactive protein. We questioned whether increased C-reactive protein levels in acute Q fever patients coincide with increased interleukin-6 levels and if these levels correlate with the Coxiella burnetii DNA load in serum. In addition, we studied their correlation with disease severity, expressed by hospital admission and the development of fatigue. Interleukin-6 and C-reactive protein levels were analyzed in sera from 102 patients diagnosed with seronegative PCR-positive acute Q fever. Significant but weak negative correlations were observed between bacterial DNA loads expressed as cycle threshold values and interleukin-6 and C-reactive protein levels, while a significant moderate-strong positive correlation was present between interleukin-6 and C-reactive protein levels. Furthermore, significantly higher interleukin-6 and C-reactive protein levels were observed in hospitalized acute Q fever patients in comparison to those in nonhospitalized patients, while bacterial DNA loads were the same in the two groups. No marker was prognostic for the development of fatigue. In conclusion, the correlation between interleukin-6 and C-reactive protein levels in acute Q fever patients points to an immune activation pathway in which interleukin-6 induces the production of C-reactive protein. Significant differences in interleukin-6 and C-reactive protein levels between hospitalized and nonhospitalized patients despite identical bacterial DNA loads suggest an important role for host factors in disease presentation. Higher interleukin-6 and C-reactive protein levels seem predictive of more severe disease.

An ecotoxicological screening tool to prioritise acid mine drainage impacted streams for future restoration.

Streams impacted by acid mine drainage (AMD) typically present water exhibiting low pH and high metal concentrations. These factors result in the environmental degradation of watercourses. The objective of this study was to develop and evaluate an ecotoxicological screening tool (EST) to prioritise future remediation of streams impacted by AMD. The Bloubank stream drainage system in South Africa, served as study area for this purpose. In the initial EST development phase physicochemical variables were assessed while in the second phase, epilithic filamentous green algae biomass (chl-a mg m(-2)), diatoms and filamentous green algae community structures were employed as bioindicators as well as Daphnia magna toxicity assays. Using a weight of evidence approach, the first three sites receiving AMD were critically and seriously modified, followed by site 4 that was modified. Sites 1-3 with EST scores ≤70% were assessed as priority candidates for future restoration.

Effects of Bifidobacterium animalis administered during lactation on allergic and autoimmune responses in rodents.

Probiotics are promoted as being beneficial to health and positive effects on the immune system have been reported. Beneficial immune effects have been attributed to several mechanisms, including stimulating T helper 1 (Th1) immunity. To explore the effects of the probiotic Bifidobacterium animalis on Th1- and Th2-mediated immune responses, two different animal models representing either Th1- or Th2-mediated immune responses were used: a rat model for experimental autoimmune encephalomyelitis (EAE) (Th1) and a mouse model for respiratory allergy induced by ovalbumin (OVA) (Th2). B. animalis administration started when the mice or rats were 2 weeks old. Respiratory allergy or EAE were induced when the animals were 6-7 weeks old. In the allergy model, B. animalis modestly reduced the number of infiltrating eosinophils and lymphocytes in the lungs, but no effects on allergen-specific serum immunoglobulin E levels were found. Cytokine profiles assessed after culturing spleen cells with the mitogen concanvalin A (ConA) showed that B. animalis skewed the Th1/Th2 balance towards Th1 in females. However, allergen-induced cytokine production in females was not affected by B. animalis. In males, B. animalis significantly decreased ConA-induced interleukin-13 and a trend towards lower levels of OVA-induced Th2 cytokines. In the EAE model, B. animalis significantly reduced the duration of clinical symptoms by almost 2 days in males and improved the body weight gain during the experimental period compared with the control group. Our data show that B. animalis reduced several immune parameters in the allergy as well as in the autoimmunity model.

Case-control study of severe life threatening asthma (SLTA) in a developing community.

BACKGROUND: Distinct risk factors for asthma death have not been identified in developing communities. This study was conducted to distinguish risk factors for severe life threatening asthma (SLTA), a proxy for asthma death, in a developing country. METHODS: A case-control study was performed at a University Hospital serving developing communities in the Western Cape Province, South Africa, over the period October 1997 to April 2000. Thirty consecutive patients with SLTA admitted to the intensive care unit (ICU) were compared with 60 chronic asthmatic patients, without a history of SLTA, who had attended the hospital outpatient respiratory clinic over the same period. RESULTS: The risk of SLTA in comparison with controls increased with female sex (odds ratio (OR) 3.3, 95% CI 1.2 to 9.6, p = 0.02), rural residence (OR 8.1, 95% CI 2.6 to 25.3, p = 0.0005), and absence of a formal income (OR 5.7, 95% CI 2 to 16.6, p = 0.002). Cases were more likely to have had more than one hospital admission in the previous year (OR 8, 95% CI 2.5 to 25.2, p = 0.0009) and more than one emergency room visit in the previous year (OR 4.4, 95% CI 1.19 to 16.4, p = 0.04). Patients with SLTA were less likely to use inhaled corticosteroids (OR 5.6, 95% CI 1.9 to 16.5, p = 0.003) and more likely to use inhaled fenoterol (OR 6, 95% CI 2.2 to 16.2, p = 0.0004). Patients with SLTA also had lower mean (SE) forced expiratory volume in 1 second (FEV(1)) measurements (66.9 (9.5)% predicted v 82.5 (4.0)% predicted; p = 0.03) and lower FEV1/FVC ratios (60.7 (4.1)% predicted v 69.6 (1.9)% predicted; p = 0.05) documented before the episode of SLTA. CONCLUSIONS: Risk factors for SLTA that are mainly analogous to those distinguished in other environments have been identified in a geographical area characterised by a third world socioeconomic context. Rural residence and poverty may increase the risk of SLTA.

Sensitivity to ozone, diesel exhaust particles, and standardized ambient particulate matter in rats with a listeria monocytogenes-induced respiratory infection.

Ambient particulate matter may increase respiratory allergic skewing of the T-cell-mediated immune response toward a T-helper-2 (Th2) response, with the consequence that the Th1 response develops less well. Successful clearing of a respiratory bacterial infection depends on an adequate Th1 immune response; therefore, the subject would not control the infection as well if exposed to particulate matter. To substantiate this hypothesis, we examined the effect of exposure to diesel exhaust particles (DEP) and urban particulate matter (EHC-93, Ottawa dust) on rats with a Listeria monocytogenes respiratory infection. Since this hypothesis has been confirmed for ozone, we used it as a positive control. Wistar rats were exposed to ozone (2 mg/m3 for 24 h/day for 7 days) and to DEP or to EHC-93 (50 microg/rat intranasally daily for 7 consecutive days). Twenty-four hours after the last exposure, the rats were infected intratracheally with 1 x 10(6) L. monocytogenes bacteria. The number of L. monocytogenes was determined after 3, 4 and 5 days. Statistically significant increases of the number of L. monocytogenes in rats exposed to ozone were observed in the lungs and spleen at all three times. However, we found no significant differences in the numbers of bacteria that were found in rats exposed to DEP or EHC-93 compared to the saline-treated group at any of the three times. In conclusion, the results of this study do not support the hypothesis that exposure to DEP or EHC-93 reduces subsequent resistance to a respiratory infection in rats.

Acute effect of air pollution on respiratory complaints, exhaled NO and biomarkers in nasal lavages of allergic children during the pollen season.

During 2 months of the pollen season, the acute and putative adjuvant effect of traffic-related air pollution on respiratory health was investigated in children sensitised to grass pollen or house dust mite (HDM). Respiratory complaints were objectified via measurement of exhaled NO and inflammatory mediators in nasal lavage (NAL). During the study children, skin prick negative (n = 31) or positive to grass pollen (n = 22), HDM (n = 34) or grass pollen + HDM (n = 32), kept a daily diary on respiratory symptoms, and NAL and exhaled air was sampled twice a week. The level of air pollutants and pollen was monitored continuously. Like children sensitised to HDM, those sensitised to pollen reported respiratory complaints (shortness of breath, itchy eyes or blocked nose) more frequently than non-sensitised children during (but not before) the pollen season; the respiratory complaints of sensitised children were independent of the pollen level. In addition, exposure to increased levels of PM(10) induces 'shortness of breath' in pollen- and HDM-sensitised children, whereas ozone induces a blocked nose in HDM-sensitised children. Combined exposure to PM(10) + pollen and O(3) + pollen induces a blocked nose in both HDM-sensitised children and children sensitised to pollen + HDM. Significant positive associations were found between eNO and the levels of NO(2), CO, PM(2.5) and pollen in both sensitised and non-sensitised children. At the start of the pollen season, the NAL concentration of eosinophils and ECP in pollen-sensitised children was increased compared to winter, but their levels were not further affected by increased exposure to pollen or air pollution. In conclusion, during the pollen season, sensitised children continuously report a high prevalence of respiratory complaints which coincides with increased levels of upper and lower airway inflammatory markers. No additional pro-inflammatory effect of air pollution was observed, which indicates that air pollution does not facilitate allergen-induced inflammatory responses.

Exhaled NO level and number of eosinophils in nasal lavage as markers of pollen-induced upper and lower airway inflammation in children sensitive to grass pollen.

OBJECTIVES: This study investigates the upper and lower inflammatory response induced by natural exposure to grass pollen in atopic and non-atopic children. METHODS: After children's atopic profile had been assessed, their nasal lavage fluid (NAL) and exhaled air was sampled once before and once during the pollen season. Level of nitric oxide (NO) was determined in exhaled air, and the following mediators were measured in NAL: ECP, IL-6, IL-8, albumin, uric acid, and urea. The number of eosinophils in NAL was determined after Giemsa staining. During the experiment ozone and pollen levels were measured continuously. RESULTS: During the pollen season the level of grass pollen was 95 pollen grains per cubic metre. At baseline, 8.0% and 5.4% of total cells in NAL of children sensitive to, respectively, house dust mite (HDM) and pollen + HDM were eosinophils, whereas virtually no eosinophils were observed in NAL of non-atopic children. In contrast to the non-atopic and HDM groups, in children sensitive only to grass pollen, grass pollen induced a threefold increase in the percentage of NAL eosinophils and a 2.5-fold increase in the NAL level of ECP ( P<0.05). In all groups, the NAL levels of albumin, uric acid, urea, IL-6 and IL-8 were not significantly increased by pollen exposure. At baseline, children sensitive to HDM showed significantly higher exhaled nitric oxide (eNO) values than non-atopic subjects and children sensitive only to pollen (79 to 141% increase). During pollen exposure eNO of children sensitive only to pollen increased from 35.8 to 64.5 ppb ( P<0.05), whereas no increase in eNO was observed in the other children. CONCLUSION: Pollen-sensitive children show a season-dependent upper and lower airway inflammatory response, resembling the continuous inflammation in HDM-sensitive children.

A clinical comparison of radiant warmer and incubator care for preterm infants from birth to 1800 grams.

OBJECTIVE: The objective of this study was to compare radiant warmer and incubator care for preterm infants from birth with respect to temperature control and weight gain. METHODS: Sixty preterm infants <33 weeks' gestation were randomized at birth to radiant warmer or incubator care. The initial goal was to maintain abdominal temperature at 36.8 degrees C in both groups and axillary temperature at 36.8 to 37.3 degrees C; air servocontrol was used for incubator infants. Infants in both groups received added humidity for 5 days if their weight was <1000 g and for 3 days if they weighed between 1000 and 1249 g. During a 3-hour period on days 1 to 7, recordings of abdominal, forehead, and foot temperatures were obtained. The percentage of the recording time during which the abdominal temperature was in the target range of between 36 degrees C and 37.5 degrees C was determined as an indicator of temperature control. Weight gain from birth to 1800 g was compared. Secondary outcomes included fluid balance and clinical events. RESULTS: There were 30 infants in each group; 48 were <1500 g (of whom 17 were <1000 g). There were no significant differences in birth weight, gestation, gender, or illness severity scores in the 2 groups. Significant differences in temperature control were noted on day 1. Although admission temperatures were similar, lower abdominal temperatures were noted in the first 2 hours of life in the incubator group (medians were 36.6 degrees C and 35.9 degrees C in the radiant warmer and incubator groups, respectively). Similarly, mean abdominal temperatures during the 3-hour recording on day 1 were lower in the incubator group, and infants in this group spent a significantly greater percentage of the recording time with temperatures outside the target range (17.3% compared with 0.88%). Other temperature recordings from the forehead and foot were not significantly different in the groups. Fluid intakes were higher for infants under radiant warmer on days 2, 3, and 4, and the difference amounted to a mean of 12.8 mL/kg/d. Maximum sodium levels in the first week were similar in the 2 groups. Mean weight gain was 17.4 g/kg/d for the radiant warmer group and 17.1 g/kg/d for the incubator group; days to regain birth weight and length of hospital stay were not significantly different. Greater numbers of infants in the radiant warmer group required phototherapy, and adverse events (which included death, necrotizing enterocolitis, chronic lung disease, grade 3 or 4 intraventricular hemorrhage, periventricular leukomalacia, or retinopathy requiring laser treatment) were less frequent in the radiant warmer group (1 infant compared with 8 in the incubator group; relative risk 0.1; 95% confidence intervals: 0.01-0.82). CONCLUSIONS: This study has shown differences in abdominal temperatures on day 1 and outcome, although the latter finding should be viewed with caution because of the sample size. The results indicate benefits for the initial use of the radiant warmer after birth. Although fluid requirements were higher in the radiant warmer group for days 2 through 4, the increased fluid volumes were given without apparent adverse effect.

UVA exposure affects UVB and cis-urocanic acid-induced systemic suppression of immune responses in Listeria monocytogenes-infected Balb/c mice.

Ultraviolet radiation can inhibit immune responses locally as well as systemically. Such effects have been measured in animals and humans exposed to ultraviolet B (wavelength 280-315 nm) (UVB) and ultraviolet A (315-400 nm) (UVA). The precise wavelength dependence is important for the identification of possible molecular targets and for assessments of risk of different artificial UV sources and solar UV. In such analyses, it is commonly assumed that radiation energy from each wavelength contributes to the effect independent of the other wavelengths. Here we show that this assumption does not hold good. In the present study, it was investigated whether exposure to broadband UVA or longwave ultraviolet A 1 (340-400 nm) (UVA 1) prior to the standard immunosuppressive UVB protocol might modulate the immunosuppressive effects induced by UVB. Preexposure to broadband UVA or longwave UVA 1, 1 day prior to the standard immunosuppressive UVB protocol, inhibited the UVB-induced suppression of delayed type hypersensitivity (DTH) to Listeria monocytogenes significantly. This effect was not associated with restoring the number of interleukin (IL-12)-positive cells in the spleen. Since isomerization of trans-urocanic acid (UCA) into the immunosuppressive cis-UCA isomer plays a crucial role in UVB-induced immunomodulation, in a second set of experiments it was investigated whether immunosuppression induced by cis-UCA might also be downregulated by preexposure to UVA. Animals were exposed to broad-band UVA or longwave UVA 1 prior to application of an immunosuppressive dose of cis- or trans-UCA as a control. Both UVA and UVA 1 appear to inhibit the cis-UCA-induced systemic immunosuppression (DTH and IL-12) to L. monocytogenes. These studies clearly show that UVA radiation modulates both UVB and cis-UCA-induced immunomodulation. In general, our studies indicate that both broadband UVA and longwave UVA 1 could induce modulation of UVB and cis-UCA-induced immunomodulation. As sunlight contains both UVA and UVB radiation the balance between these two radiations apparently determines the net immunomodulatory effect.

Nasal continuous positive airway pressure and outcomes of preterm infants.

OBJECTIVES: To document the effects of changing to a primarily nasal continuous positive airway pressure (CPAP)-based system of respiratory support on respiratory and non-respiratory outcomes in preterm infants. METHODOLOGY: Outcomes in two groups of preterm infants with a birthweight of 1000-1499 g were compared retrospectively over a 5-year period before (period I; n = 57) and after (period II; n = 59) the introduction of a primarily nasal CPAP-based approach to respiratory support, modelled closely on that used at the New York Presbyterian Hospital (Columbia University), formally known as the Columbia-Presbyterian Medical Center, in New York. RESULTS: From period I to period II, there was a decline in the number of infants ventilated (65 vs 14%, respectively) and receiving surfactant (40 vs 12%, respectively) and in the median days of ventilation (6 vs 2, respectively) and oxygen (4 vs 2, respectively). There were decreases in chronic lung disease (CLD) at 28 days (11 vs 0%, respectively), death or CLD at 28 days (16 vs 3%, respectively), the use of pressor support (34 vs 7%, respectively), the incidence of necrotizing enterocolitis (11 vs 0%, respectively), time to reach full oral feeds (17.3 vs 13.2 days, respectively), discharge weight (2569 vs 2314 g, respectively) and average length of stay (61 vs 52.9 days, respectively). There were no differences in neurosonographic or other morbidity outcomes. CONCLUSIONS: A CPAP-based approach to respiratory support of the preterm infant may decrease the invasiveness and duration of respiratory support and may decrease respiratory and some non-respiratory adverse outcomes without an associated increase in neurosonographic or other morbidity outcomes. Further prospective trials are warranted.

Effects of UV irradiation on skin and nonskin-associated herpes simplex virus infections in rats.

Herpes simplex virus (HSV) normally causes vescular lesions on mucocutaneous surfaces but can also cause encephalitis. The virus can reactivate from the latent state in neurons to form recrudescent lesions. One common stimulus for reactivation is exposure to sunlight. In the present study, the effects of irradiating rats with suberythemal ultraviolet (UV) before or after infecting them epidermally with HSV was investigated. Preexposure to UV impaired HSV-specific cellular immune responses, as indicated by delayed type hypersensitivity (DTH) and in vitro lymphoproliferation assays. However, the number and severity of the skin lesions were not altered. In contrast, exposure after infection did not affect cellular immunity but resulted in a large increase in the severity and number of lesions. In a second series of experiments, the effects of preirradiating with UV on HSV infection was examined using a route of inoculation which was not skin-associated, namely intranasal, allowing direct non-invasive access to the nervous system. It was found that suppressed DTH resulted, together with an increase in the incidence and severity of neurological symptoms and an increased viral load in the brain. Therefore, unlike the situation in the skin, irradiation of rats before intranasal inoculation led to a suppressed immune response to HSV which correlated with increased viral load and symptoms. These results indicate that the effects of UV may be dependent on whether the animal is exposed before or after the infection, and whether the infection is skin-associated or systemic.

Pathological and immunological effects of respirable coal fly ash in male Wistar rats.

In this study the effects of inhalatory exposure to coal fly ash on lung pathology and the immune system in rats were examined. Rats were exposed to 0, 10, 30, or 100 mg/m(3) coal fly ash (6 h/day, 5 days/wk) for 4 wk, or to 0 and 100 mg/m(3) for 1 wk, and for 1 wk followed by a recovery in clean air of 3 wk. A concentration-related increase in lung weight was found starting from 30 mg/m(3) coal fly ash. After exposure to 100 mg/m(3), a time-related deposition of free particles in the lungs was observed as well as a time-related number of coal fly ash particles phagocytized in alveolar macrophages. Histological examination revealed increased cellularity in alveolar septa, consisting mainly of mononuclear cell infiltrate, proliferated type II cells, and a slight fibrotic reaction. After a recovery period of 3 wk the histological picture was identical to that after 1 wk of exposure, indicating no significant recovery. No toxicological significant changes were found in the hematological, clinical chemistry, or urine parameters. Effects both on nonspecific defense mechanisms and on specific immune responses were noted. With regard to the immune function in the draining lymph nodes of the lung, a significantly increased number of both T and B lymphocytes was observed. The ratio of both cell types was not changed in either of the groups. In serum of exposed rats a significant increase of up to 150% of the immunoglobulin A (IgA) content was found. The number and phagocytic capacity of macrophages were significantly increased, while the killing of Listeria bacteria per cell ex vivo/in vitro remained unchanged. Natural killer (NK) activity in pulmonary cell suspensions was slightly stimulated in rats exposed for 4 wk to 10 and 30 mg/m(3), whereas an exposure to 100 mg/m(3) resulted in a slight decrease; however, both changes were not significant. In conclusion, the alterations in lung histopathology and immunity, observed in a dose and exposure time relation at concentrations up to and including 100 mg/m(3) coal fly ash, may be considered an adverse response of the host to inhalation of particulate matter. Whether these observed alterations may effect the host resistance must be learned from infection studies.

Diet and infant behavior.

We studied 142 preterm infants (mean gestation 31 weeks, mean birthweight 1364 g) fed prospectively varied protein and energy intakes. Infants were grouped as either slow or rapid growers based on rate of weight gain. Rapid growers had increased heart rates (166 vs 160 beats/min), respiratory rates (55.7 vs 53.9 bpm), energy expenditure (64.8 vs 61.6 kcal kg(-1) day(-1)), urinary C-peptide levels (1.59 vs 0.79 ng ml(-1)) and time in active sleep (78.0 vs 75.2%), and decreased spectral edge frequency in the electroencephalogram (2.96 vs 4.45 Hz) compared to slow growers. We conclude that preterm infants growing at varying rates manifest physiological and behavioral differences, and that these patterns may reflect altered autonomic balance.

Impaired cellular immune response in rats exposed perinatally to Baltic Sea herring oil or 2,3,7,8-TCDD.

While the immunotoxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been well established, the effects of complex environmental mixtures of polyhalogenated aromatic hydrocarbons (PHAHs) are poorly understood. Many PHAHs, including the polychlorinated-biphenyls (PCBs), -dibenzofurans (PCDFs), and dibenzo-p-dioxins (PCDDs), possess 'dioxin-like' activities, and accumulate in the aquatic food chain. Organisms occupying high trophic levels may therefore be exposed to concentrations which may present an immunotoxic risk. In this study, pregnant PVG rats were administered a daily oral dose of 1 ml of the following during pregnancy and lactation: (1) oil extracted from herring caught in the relatively uncontaminated Atlantic Ocean; (2) oil extracted from herring caught in the contaminated Blastic Sea; or (3) the Atlantic herring oil extract spiked with 2,3,7,8-TCDD. The daily intakes of aryl hydrocarbon (Ah)-receptor dependent toxic equivalents (TEQ) for mothers were 0.3 in the Atlantic group, 2.1 in the Baltic group, and 134 ng/kg body wt. in the 2,3,7,8-TCDD positive control group. Immune function and host resistance to rat cytomegalovirus (RCMV) were assessed in offspring aged 11, 25, 46 or 59 days. Rat pups in the positive control TCDD-spiked group exhibited immunosuppression characterized by reduced thymus weight and cellularity, reduced thymocyte and splenocyte proliferative responses to T-dependent mitogens in vitro, reduced virus-associated natural killer (NK) cell and specific antibody responses. While less pronounced, a similar pattern of effects was observed in the rat pups exposed only to the Baltic Sea herring oil. These immunotoxic effects were transient in both exposure groups, with a time-related recovery in immune function possibly due to the half-life of TCDD in rats and the waning exposure levels in the rapidly growing pups. We previously demonstrated that the same Baltic Sea herring led to impaired natural killer cell and T-lymphocyte function in harbour seals during the course of a long-term captive feeding study. The collective results of these studies in rats and seals indicate the immunotoxic potential of environmental mixtures at current levels in the aquatic environment, and suggest that the developing immune system of young mammals may be at particular risk.

Net Blotch and Necrotic Warts Caused by Streptomyces scabies on Pods of Peanut (Arachis hypogaea).

Peanut (Arachis hypogaea L.) grown in rotation with potato (Solanum tuberosum L.) in the Northern Cape Province and at one locality in the Free State Province, South Africa, have developed unusual pod symptoms since the 1994 to 1995 season. Symptoms ranged from a net blotch with scattered lesions to dark brown, necrotic, wartlike lesions on the cv. Sellie. Streptomyces scabies (2) was consistently isolated from both types of lesions. Pathogenicity was confirmed in greenhouse tests. Inoculum was prepared by growing colonies on yeast malt extract agar for 21 days. Ten milliliters of sterile, distilled water was poured over the colonies of two different isolates and lightly scraped with a sterile needle. Separate sets of sterile soil were amended with spore suspensions of different isolates at a rate of 10 ml/kg and thoroughly mixed. Seeds of cv. Sellie and minitubers of potato cv. BP1 were planted in infested soil in 3-kg plastic bags. Uninfested soil served as controls. Each set of pots for both peanut and potato had three replications. Pots were kept in a glasshouse at 27°C for 12 weeks. Plants were lifted, disease development recorded, and infected plant parts prepared for reisolation on antibiotic-amended water/ agar according to the protocols of Loria and Davis (3). Both lesion types recorded under field conditions developed on peanut pods in the glasshouse upon reinoculation. Incidence ranged between 2 and 3 pods out of 8 to 10 pods per plant while minitubers were nearly 100% infected. Streptomyces scabies was isolated from lesions on both peanut and potato. Net blotch caused by an unknown Streptomyces sp. is a significant problem on peanut pods in Israel (1). However, the species found in Israel was not identified and could be different from the one reported here, according to Y. Barash (Tel Aviv University, personal communication). This is a first report of S. scabies being pathogenic on peanut in South Africa. References: (1) Y. Barash et al. (In Hebrew.) Hassadeh 72:688, 1992. (2) D. H. Lambert and R. Loria. Int. J. Syst. Bacteriol. 39:387, 1989. (3) R. Loria and J. R. Davis. Streptomyces scabies. Pages 114-119 in: Laboratory Guide for Identification of Plant Pathogenic Bacteria. 2nd ed. N. W. Schaad, ed. American Phytopathological Society, St. Paul. MN, 1988.