不同浓度卵蛋白变应原对小鼠哮喘模型建立的影响

目的研究不同浓度卵蛋白(ovalbumin,OVA)变应原对小鼠的哮喘造模影响。方法 96只6～8周龄SPF级雌性BALB/c小鼠随机分为8组,分别为PBS组(对照组)、10μg组(A组)、20μg组(B组)、50μg组(C组)、100μg组(D组)、200μg组(E组)、500μg组(F组)、1000μg组(G组)。A～G组分别用含1%明矾的PBS配制相应浓度的OVA于第0、7和第14天对小鼠进行腹腔注射。于第21～27天连续7 d用含1%的OVA的PBS溶液雾化吸入激发各组小鼠。正常对照组使用PBS溶液致敏和激发。最后一次雾化吸入激发后24 h内,计数各组小鼠支气管肺泡灌洗液(BLAF)中嗜酸性粒细胞的含量,ELISA法检测IL-4、IL-5的分泌量及其血清IgG2a、IgE抗体的水平;肺组织病理切片观察各组小鼠哮喘模型的效果,评价最优哮喘造模的OVA浓度。结果 A～G组小鼠肺泡灌洗液中IL-4、IL-5含量均高于正常对照组(P<0.01),细胞因子水平随着OVA浓度的增高而逐渐下降;A～G组小鼠肺泡灌洗液中嗜酸性粒细胞数均高于正常对照组(P<0.01),从低浓度组至高浓度组嗜酸性粒细胞数从高向低变化;A～G组小鼠血清中总抗体IgE的水平均显著高于正常对照组(P<0.01),且随着OVA浓度的增高IgE水平逐渐下降。血清中IgG2a的水平则随OVA给药浓度的增高而逐渐增高;低浓度OVA致敏组小鼠肺组织标本可观察到明显的炎症浸润性病理表现,而高浓度组肺部组织病理变化不明显。结论低浓度的OVA连续致敏小鼠造成过敏性哮喘病理改变较为明显,随着OVA浓度的增高,造模效果逐渐降低,而高浓度的OVA则会导致模型小鼠发生免疫耐受。     

免疫抑制对MRSA毒力因子基因表达的影响

研究不同免疫状态下耐甲氧西林金黄色葡萄球菌(methicillin resistant Staphylococcus aureus,MRSA)毒力因子的表达情况,为结合宿主免疫状态对金黄色葡萄球菌毒力因子基因表达的影响提供新的思路和依据。将SPF清洁级Wistar大鼠随机分成对照组和模型组,每组12只,雌雄各半。以40 mg/kg的环磷酰胺连续肌肉注射3 d,造成大鼠免疫抑制,在此基础上通过滴鼻方式滴入小剂量高浓度的新鲜MRSA菌悬液,连续滴注3 d,造成免疫抑制MRSA定植模型。对照组将正常大鼠直接鼻腔滴入小剂量高浓度的新鲜MRSA菌悬液。细菌定植一定时间后取大鼠鼻粘膜组织,运用实时荧光定量PCR技术分析不同免疫状态下大鼠鼻粘膜组织中分离的MRSA毒力因子在基因水平上的表达差异。这表明与肌注环磷酰胺前比较,肌注环磷酰胺后3 d、7 d时,大鼠血液学检查可见外周血WBC、PLT数量迅速下降,同时RBC、HGB亦明显降低(p0.01);外周血中包括CD4~+T淋巴细胞和CD8~+T淋巴细胞比例以及B淋巴细胞、NK细胞的比例均明显降低(p0.01);外周血血清中免疫球蛋白Ig G、Ig M、Ig A的含量明显下降(p0.01);不同免疫状态下细菌毒力因子基因相对表达含量表明,定植在模型组大鼠鼻粘膜组织中的MRSA毒力因子hlα和spa的表达水平要高于对照组,p0.05,其中目的基因spa的表达水平显著升高(p0.01)。说明当宿主处于免疫抑制状态时,可能通过促进金黄色葡萄球菌毒力因子的表达增强金黄色葡萄球菌的致病力。     

血红素加氧酶-1介导CD4+CD25High调节性T淋巴细胞拮抗哮喘气道炎症的实验研究

探讨血红素加氧酶-1(HO-1, heme oxygenase-1)介导CD4⁺CD25^High调节性T淋巴细胞(Treg, regulatory T cells)拮抗哮喘气道炎症的作用. 用卵清蛋白(OVA)致敏、激发小鼠制备并建立哮喘动物模型, 并在致敏、激发过程中经氯化高铁血红素(Hemin)或锡-原卟啉(SnPP, Sn- protoporphyrin)处理. 分别测定激发后各组动物血清OVA特异性IgE, 支气管肺泡灌洗液中(BALF, bronchial alveolar lavage fluid)细胞总数和嗜酸性粒细胞(EOS, eosinophil)数及外周血CD4⁺CD25^High Treg细胞变化和肺组织HO-1和Foxp3 mRNA表达量, 结合病理切片分析气道炎症状况. 结果显示: OVA组、Hemin组、SnPP组血清OVA-特异性IgE和BALF中细胞总数及EOS数明显高于正常对照组, 但Hemin组IgE水平及BALF中细胞总数和EOS数明显低于OVA组; 而OVA组和SnPP组间IgE水平及BALF中细胞总数和EOS数无显著性差异; 病理组织学显示OVA组、Hemin组和SnPP组气道组织均见EOS浸润, 但Hemin组气道炎症仍明显轻于OVA组和SnPP组; Hemin组外周血CD4⁺CD25^High Treg细胞比例及肺组织Foxp3 mRNA相对表达量明显高于OVA组. Hemin显著上调HO-1表达. 实验表明, 用Hemin诱导HO-1高表达后外周血CD4⁺CD25^High Treg细胞比例及Foxp3 mRNA相对表达量明显升高, 同时血清OVA特异性IgE明显下降, BALF中细胞总数和EOS数减少, 气道炎症减轻; 提示HO-1可通过提高CD4⁺CD25^High Treg细胞比例并增强其功能来调节体内Th1/Th2平衡, 在支气管哮喘中起到保护作用.     

抗IL-6抗体治疗小鼠变应性鼻炎的作用的研究

目的：探讨IL-6 抗体治疗小鼠变应性鼻炎的作用。方法：实验动物分三组：PBS 组（正常对照组）、抗IL-6 抗体组（以抗IL-6 单 克隆抗体处理）、IgG 抗体对照组（以IgG对照抗体处理）。应用卵清蛋白（OVA）致敏建立小鼠变应性鼻炎模型,给予抗IL-6 单克 隆抗体干预,计量抗原激发后小鼠搔鼻数量。应用HE染色方法检测对小鼠鼻黏膜炎症影响,应用ELISA 法检测小鼠灌洗液中 IL-4、IFN-r含量。结果：治疗后抗IL-6 抗体组小鼠搔鼻症状相对于抗体对照组明显减轻（P<0.01)。与PBS 组比较,IgG 抗体对照组 小鼠鼻腔灌洗液中总炎性细胞数,淋巴细胞数及嗜酸性粒细胞数明显升高（P<0.05);IL-6 抗体治疗后,小鼠鼻腔灌洗液中总炎性 细胞数,淋巴细胞数及嗜酸性粒细胞数明显降低（P<0.05);IgG抗体对照组小鼠鼻腔灌洗液IL-4 含量明显升高（P<0.01),而IFN-r 含量不变（P>0.05);IL-6 抗体治疗后,IL-4 含量较IgG 抗体对照组降低（P<0.05),IFN-r含量不变（P>0.05)。结论：IL-6 抗体可有效 治疗小鼠变应性鼻炎。     

大学生鼻前庭菌群分布特征研究

目的了解大学生鼻前庭的菌群分布特征及金黄色葡萄球菌的携带情况。方法无菌采集935名大学生鼻前庭拭子,接种哥伦比亚血琼脂平板、麦康凯琼脂平板,常规分离培养鉴定细菌;血浆凝固酶实验鉴定金黄色葡萄球菌,纸片扩散法检测金黄色葡萄球菌的药物敏感性。结果鼻前庭细菌检出率从高到低为类白喉棒状杆菌(53.80%)、表皮葡萄球菌(45.78%)、枯草杆菌(31.97%)、金黄色葡萄球菌(15.51%),链球菌(2.78%)、克雷伯菌(1.60%)、真菌(1.50%)、铜绿假单胞菌(0.43%)、肠球菌(0.21%)和变形杆菌(0.21%)等。7.48%(70/925)的学生鼻前庭未检出细菌;34.12%(319/935)携带单一细菌,51.12%(478/935)携带2种细菌,7.27%(68/935)携带3种及3种以上细菌。共检出145株金黄色葡萄球菌,携带率为15.51%(145/935)。结论大学生鼻前庭菌群组成以类白喉棒状杆菌、表皮葡萄球菌、枯草杆菌和金黄色葡萄球菌为主。     

支气管哮喘伴发抑郁大鼠模型的建立

目的探讨建立支气管哮喘伴发抑郁动物模型的方法。方法选择Wistar大鼠,随机分为对照组与模型组,模型组采用卵蛋白(ovalbumin,OVA)激发法建立哮喘模型,在此基础上给予慢性轻度不可预见性应激(chronic unpredictable mild stress,CUMS)28d,观察大鼠体质量、体征、肺组织结构、支气管肺泡灌洗液白细胞计数等变化,并用Open-field实验评价大鼠活动度和好奇心,通过糖水消耗实验评价大鼠快感缺乏与否。结果与对照组相比,模型组大鼠体质量增长明显缓慢(P0.05);肺组织呈哮喘样病理改变;支气管肺泡灌洗液白细胞总数、嗜酸粒细胞及淋巴细胞增多;Open-field实验,大鼠垂直活动得分、水平活动得分显著降低(P0.05);糖水消耗量明显减少(P0.05)。结论OVA激发复合CUMS可成功制备支气管哮喘伴发抑郁大鼠模型。     

毛喉鞘蕊花提取物对大鼠哮喘模型炎症介质的影响及机制研究

为探讨毛喉鞘蕊花提取物(Coleus Forskohlii extract,CFE)对哮喘的治疗作用及机制,采用卵清蛋白(ovalbumin,OVA)结合佐剂氢氧化铝建立大鼠哮喘模型,SPF级SD雄性大鼠60只,随机分为5组,即空白组、模型组、地塞米松组、CFE高剂量组(12.8g/kg)和CFE低剂量组(6.4g/kg),分别用生理盐水、地塞米松及CFE每天灌胃1次,连续14天,灌胃容积为1mL/100g。通过HE染色观察肺组织病理学形态学变化;ELISA法测定大鼠血清(serum)及肺泡灌洗液(BALF)中IFN-γ、IL-4和IL-17A含量变化;Western blot检测MAPK通路相关蛋白的表达变化。HE结果显示,与模型组相比,CFE高、低剂量组能显著减轻OVA刺激后大鼠肺组织病理性损伤,气道轮廓清晰,上皮细胞脱落明显减少;ELISA结果显示,与模型组相比,CFE高、低剂量组大鼠血清及BALF中IL-4、IL-17A的含量明显下降,IFN-γ的含量明显上升(P<0.05或P<0.01);WB结果显示,CFE高剂量组可显著降低大鼠肺组织p-ERK、p-JNK及p-p38蛋白表达(P<0.05或P<0.01)。综上,毛喉鞘蕊花提取物可有效缓解OVA诱导的大鼠哮喘气道炎症反应,其机制与调节MAPK信号传导通路有关。     

TAT-N15多肽治疗大鼠变应性鼻炎的实验研究

[目的]研究TAT-N15多肽治疗大鼠变应性鼻炎的抗炎症作用及机制。[方法]使用卵清蛋白(OVA)致变应性鼻炎大鼠模型,通过比较0. 1%和0. 3%TAT-N15多肽滴鼻液、0. 1%富马酸酮替芬滴鼻液对变应性鼻炎大鼠的行为学评价、组胺的组织学评价、以及鼻粘膜组织中NF-κB p65、PCNA、Ki-67蛋白表达水平,评价TAT-N15多肽滴鼻液治疗大鼠变应性鼻炎的作用。[结果]与正常对照组比较,0. 3%TAT-N15多肽滴鼻液组能减轻大鼠变应性鼻炎的症状,减少组胺释放64%,鼻腔组织病理学变化表明TAT-N15多肽滴鼻液能减少鼻粘膜组织的炎症细胞浸润,免疫组化结果表明,TAT-N15多肽能显著降低鼻粘膜组织中NF-κB p65、Ki-67和PCNA的表达水平。[结论]TAT-N15多肽能起到缓解大鼠变应性鼻炎症状的作用。     

卵白蛋白介导白毛黑眼兔变应性鼻炎模型树突状细胞功能的改变

目的比较观察卵白蛋白(OVA)诱导的白毛黑眼兔(WHBE兔)和日本大耳白兔(JW兔)变应性鼻炎(allergic rhinitis,AR)模型外周血来源树突状细胞(dendritic cells,DC)的功能,揭示WHBE兔对AR敏感的可能机制。方法以OVA诱导建立WHBE兔和JW兔AR模型,每次激发后观察动物一般体征,进行鼻黏膜HE染色,观察组织病理学改变。分离外周血DC,流式细胞仪检测外周血DC表面分子CD86的表达以及DC摄取抗原的能力,同时,采用荧光定量PCR检测外周血DC甘露糖受体(mannose receptor,MR)的mRNA表达水平。进一步以CFSE标记T细胞,流式细胞仪检测外周血DC诱导T细胞增殖能力。结果一般体征和HE染色观察显示,WHBE兔和JW兔模型组动物均表现为典型的变应性鼻炎症状和组织病理学改变,提示模型构建成功。WHBE兔AR模型组外周血DC CD86的表达不仅极显著高于正常对照组,亦极显著高于JW兔AR模型组(P0.01,P0.01)。正常稳态下,WHBE兔外周血DC MR的mRNA相对表达量极显著高于JW兔(P0.01),经OVA诱发建立AR模型,WHBE兔外周血DC MR的mRNA表达水平显著升高(P0.05),且显著高于JW兔模型组(P0.05)。并且,WHBE兔模型组外周血DC摄取OVA647的能力极显著高于正常对照组(P0.01),亦极显著高于JW兔模型组(P0.01)。结论 WHBE兔DC对变应原更敏感,可能与其高表达抗原识别受体MR,具备更强的分化成熟、摄取抗原能力有关。     

我院母婴同室表皮葡萄球菌携带调查与质粒分析

采用耐药谱、质粒及质粒酶切图谱分型方法对母婴同室新生儿表皮葡萄球菌的来源进行了追踪调查，发现大部分新生儿在生后１～３天鼻腔可携带不同亚型的表葡菌，其定植与表葡菌的粘质产物呈现明显的相关性。新生儿在生后第１天鼻腔、脐部携带菌来源于母亲的占４４４４％，而在生后第３天来源于母亲的占２３５２％，其他菌株来源不明。通过本次调查证实新生儿携带的表葡菌以散发株为主，与医务人员之间无同源菌株，这与以往报道的新生儿与医务人员之间常见同源株菌不同，说明我院目前母婴同室明显优于以前的专设新生儿室。     

Chronic sialodacryoadenitis virus (SDAV) infection in athymic rats.

Sialodacryoadenitis virus (SDAV) was detected in athymic rats subcutaneously implanted with human tumor cell lines. Clinical signs included sneezing, dyspnea, weight loss and death. Necropsy revealed both upper and lower respiratory tract disease from which Staphylococcus aureus, Pasteurella pneumotropica and Pseudomonas aeruginosa were recovered. Histopathological changes consisted of suppurative rhinitis and bronchopneumonia. Lesions characteristic of SDAV infection were found in lacrimal and salivary glands, and viral antigens were detected in the salivary glands and respiratory tract by immunohistochemistry. Submaxillary salivary gland. Harderian gland and lung homogenates from affected athymic rats were inoculated intranasally into euthymic rats as a rat antibody production test. All euthymic rats seroconverted to SDAV. Seroconversion to SDAV was demonstrated in consecutive pairs of sentinel euthymic rats housed for 6 months with infected athymic rats. Inoculation of supernatants of the original tumor cell lines into euthymic rats did not result in seroconversion. The source of the virus was not determined. In this study, spontaneously acquired SDAV infection persisted for at least 6 months in athymic rats.     

Auxotrophic mutant of Staphylococcus aureus interferes with nasal colonization by the wild type

Staphylococcus aureus nasal carriage is a risk factor for infection in humans, particularly in the hospital setting. Bacterial interference was used as an alternative strategy for the prevention of upper respiratory, urogenital and gastrointestinal tract infections. This study was designed to assess if the administration of a live-attenuated aroA mutant of S. aureus is useful as a potential approach to prevent transient staphylococcal nasal carriage by virulent strains. We constructed an aroA mutant of S. aureus Newman strain by homologous recombination. The auxotrophic NK41 mutant was attenuated as determined by the increase of the LD(50) after intraperitoneal challenge. In mice, previous nasal colonization with the NK41 mutant significantly reduced the number of CFU of S. aureus (HU-71 and Hde288) clinical isolates and the parental Newman strain. The NK41 mutant was unable to induce a pro-inflammatory response and to damage the invaded human respiratory epithelial cells. Moreover, the cells previously or simultaneously infected with the NK41 mutant were invaded by virulent strains in a significantly lower degree than those of the control group. In conclusion, the attenuated NK41 mutant interfered with the colonization and establishment of pathogenic strains of S. aureus, which produce severe infections.     

Nosopharyngeal microflora in ambulatory treated children and adults with upper respiratory tract infections

Upper respiratory tract consists resident and transient bacterial microflora, which in appropriate condition can cause infection. Bacteriological study was performed among 201 patients with upper respiratory tract infections treated in ambulatory. From nasal and pharyngeal swabs Staphylococcus aureus, Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, and Streptococci group A, B, C, G were isolated. Antibiotic susceptibility testing of isolated strains was performed using CLSI criteria. All isolated strains of streptococci were susceptible to penicillin; some of them demonstrated resistance to macrolides and lincosamides. Few isolated strains of H. influenzae demonstrated resistance to penicillin and cotrimoxazole. Azitromycin resistant strains were not detected. All isolated strains of M. catarrhalis were beta-lactamase positive and demonstrated resistance to penicillin. Strains of methicillin sensitive S. aureus (MSSA) were isolated most frequently from pharyngeal swabs (35.4%) and S. pneumoniae (33.3)--from nasal swabs.     

Bacterial interference with skin colonization in germfree hairless mice

Bacterial colonization of the digestive tract and the skin was studied over a 3-week period in a group of 10 germfree HRS mice using Staphylococcus epidermidis, Staphylococcus aureus, and Pseudomonas aeruginosa. Sequential utilization of two strains allowed us to carry out six assays and to show the presence of interference phenomena during colonization of the skin. When P. aeruginosa was given after challenge with S. aureus or S. epidermidis, it did not colonize the skin. If the first challenge was done with P. aeruginosa, this bacteria was eliminated within 10 days by S. aureus and S. epidermidis on the skin, but it succeeded in colonizing the digestive tract. When the first challenge was done with S. aureus, colonization of the skin and the digestive tract with S. epidermidis was prevented, whereas these two species were found in association when S. aureus was given in second place. None of the in vitro assays (mixed culture, bacteriocin production, adherence inhibition, antimicrobial activity) could explain the in vivo observations.     

Longitudinal study of effects of oral dosage of Bifidobacterium bifidum G9‐1 on Japanese cedar pollen‐induced allergic nasal symptoms in guinea pigs

Previous studies using experimental animal models have reported the beneficial effects of probiotics on allergic responses; however, their long‐term effects on allergic nasal symptoms in clinical settings have not yet been elucidated in detail. In the present study, a guinea pig allergic rhinitis model involving repeated inhalation challenges with a natural allergen, Japanese cedar pollen, was used to examine the longitudinal effects of Bifidobacterium bifidum G9‐1 (BBG9‐1) on allergic nasal symptoms. BBG9‐1 was administered orally once a day. Amelioration of nasal blockage was consistently observed throughout the experimental period in the BBG9‐1‐treated group. Although challenge‐induced sneezing was not significantly inhibited in the BBG9‐1‐treated group, prolonged treatment with BBG9‐1 slightly reduced the frequency of sneezing. Antigen‐specific IgE antibody production was also not inhibited in the BBG9‐1‐treated group. Increases in the numbers of eosinophils and neutrophils in nasal cavity lavage fluid collected after pollen challenge were almost completely suppressed by BBG9‐1 treatment, whereas those in mast cell mediators, histamine and cysteinyl leukotrienes were not. In contrast, increases in the levels of nitric oxide metabolites were potently suppressed. Furthermore, prolonged BBG9‐1 treatment markedly suppressed exogenous leukotriene D₄‐induced nasal blockage. Thus, prolonged oral administration of BBG9‐1 suppresses Japanese cedar pollen‐induced allergic nasal symptoms. The inhibitory mechanisms responsible may involve reductions in the responsiveness of target organs, such as endothelial cells in nasal mucosal blood vessels, to chemical mediators.     

Antibody responses after Sendai virus infection and their role in upper and lower respiratory tract disease in rats.

BACKGROUND AND PURPOSE: Sendai virus infection in rats is an excellent model for studying development and role of host defenses throughout the respiratory tract after this infection. Therefore, development of serum antibody responses and disease were studied. METHODS: Forty-two anesthetized pathogen-free 3- to 4- week-old LEW/NCr rats were inoculated intranasally with Sendai virus. At postinoculation days 0, 2, 3, 5, 8, 10, and 14, rats were euthanized by administration of a pentobarbital sodium overdose followed by exsanguination. Serum was obtained from all animals, and nasal wash and bronchoalveolar lavage specimens were collected during selected experiments. An ELISPOT assay was used to measure numbers of Sendai virus-specific antibody-forming cells in respiratory tract lymphoid tissue. RESULTS: Recovery from disease and clearance of virus from respiratory tract tissues coincided with development of serum antibody responses. Upper respiratory tract lymph nodes were the initial and major sites of appearance of antibody-forming cells. Immunoglobulin G was the predominant subtype of these cells during recovery from the infection and in rats resistant to infection. Passive transfer of antisera or specific IgG protected the lower but not the upper respiratory tract. CONCLUSIONS: Circulating components of immunity have a major role in resistance and recovery from disease in the lower respiratory tract, whereas local responses are likely involved in protection of the upper respiratory tract. Local lymphoid tissues are the major production sites of IgG, which contributes to resistance to and recovery from respiratory tract diseases.     

Nisin F in the treatment of respiratory tract infections caused by Staphylococcus aureus

Aims:  To determine the antimicrobial activity of nisin F against Staphylococcus aureus in the respiratory tract.
Methods and Results:  The respiratory tract of nonimmunosuppressed and immunosuppressed Wistar rats were colonized with 4 × 10⁵ viable cells of S. aureus K and then treated by administering 8192 arbitrary units (AU) nisin F intranasal. Symptoms of pneumonia were detected in the trachea and lungs of immunosuppressed rats that had not been treated with nisin F. The trachea and lungs of immunosuppressed rats treated with nisin F were healthy. No significant differences were recorded in blood cell indices. The antimicrobial activity of low concentrations nisin F (80–320 AU ml⁻¹) was slightly stimulated by lysozyme and lactoferrin.
Conclusions:  Nisin F inhibited the growth of S. aureus K in the respiratory tract of immunocompromised rats. Treatment with nisin F at 8192 AU proofed safe, as the trachea, lungs, bronchi and haematology of the rats appeared normal.
Significance and Impact of the Study:  Nisin F is nontoxic and may be used to control respiratory tract infections caused by S. aureus . This is, however, a preliminary study with an animal model and need to be confirmed with studies on humans.     

医院内感染的病原菌分布及其耐药谱的分析

本文统计了我院１９９２年８月—１９９４年７月两车间医院内感染病原菌的分离结果,分离出病原菌２５种７５８株,其中革兰氏阳性菌１６３株（占２１．５１％）,革兰氏阴性菌３７８株（占４９．８７％）,真菌２１７株（占２８．６２％）。院感病原菌依次为,白色念珠菌、绿脓假单胞菌表、葡菌、肺炎克雷伯氏菌、酵母菌及大肠艾希氏菌等,显示了真菌及表葡菌在院内感染中已经上升到不可忽略的地位。用１８种常用抗生素,对除真菌外的上述病原菌５４１株做耐药谱测定,并发现除了表葡菌及多数革兰氏阴性菌对喹谱酮类及少数头孢三代抗生素尚属敏感外,大部分均具有越来越广泛的耐药性。     

Essential oils from aromatic herbs as antimicrobial agents

Bacterial resistance to multiple antibiotics is a health problem. Essential oils (EOs) possess antibacterial properties and have been screened as potential sources of novel antimicrobial compounds. Terpenes and terpenoids are components derived from EOs. Some of these EOs show inhibitory activity against Staphylococcus aureus. Carvacrol has specific effects on S. aureus and Staphylococcus epidermidis. Perilla oil suppresses expression of α-toxin, Staphylococcus enterotoxin A and B and toxic shock syndrome toxin. Geraniol shows good activity in modulating drug resistance in several gram-negative species. EOs could act as biopreservatives, reducing or eliminating pathogenic bacteria and increasing the overall quality of animal and vegetable food products. Although clinical studies are scarce, the uses of EOs for topical administration and as penetration enhancers for antiseptics are promising. Little information exists for oral administration.     

Significance of Staphylococcus epidermidis in the Clinical Laboratory

Susceptibility to 11 antibiotics was determined for 63 cultures of Staphylococcus aureus and 63 cultures of Staphylococcus epidermidis obtained at random from the clinical laboratory. The incidence of resistance to nine of these antibiotics was greater for S. epidermidis than for S. aureus. Studies of the minimal inhibitory concentration of these cultures to clindamycin showed that 61 cultures of S. aureus were susceptible whereas only 46 cultures of S. epidermidis were susceptible to this antibiotic. Although cultures of S. aureus were more active in the production of seven virulence factors, some cultures of S. epidermidis produced virulence factors. By successive cultivation in increasing concentrations of clindamycin, resistant variants were obtained for 10 cultures of S. aureus and 3 cultures of S. epidermidis. The presence of subinhibitory concentrations of clindamycin inhibited the production of some virulence factors by the resistant variants. In view of the greater resistance of S. epidermidis to antibiotics and its ability to produce virulence factors, its isolation in the clinical laboratory should not be regarded lightly.