Meningitis caused by Gordona aurantiaca (Rhodococcus aurantiacus).

In a case of hairy cell leukemia, Gordona aurantiaca (Rhodococcus aurantiacus) was isolated from cerebrospinal fluid as the pathogen responsible for lethal infection of the central nervous system. The pathogen had been isolated previously from one case of pulmonary infection process only.     

First Case of Bloodstream Infection Caused by Rhodococcus erythropolis

We describe the first case of bloodstream infection caused by Rhodococcus erythropolis. The identification was performed using 16S rRNA sequencing. This case illustrates that non-equi Rhodococcus infections may be underdiagnosed due to difficulties in identification in the routine clinical microbiology laboratory.     

Characterization of Nocardia, Rhodococcus and Gordona species by in vitro susceptibility testing

Representative strains of Gordona, Nocardia and Rhodococcus were tested against 26 antimicrobial agents using the disc diffusion method. A distinct susceptibility profile was noted for most species. Nocardia asteroides, N. brasiliensis, N. otitidiscaviarum, N. transvalensis and N. vaccinii were rarely susceptible to the antibiotics tested; N. brevicatena and N. farcinica varied in their susceptibility depending on the strain tested. Only the antibiotic amikacin was active against all nocardiae. In contrast, the Gordona and Rhodococcus strains showed considerable susceptibility, in particular to the beta-lactam antibiotics. Amoxicillin + clavulanic acid and gentamicin were active against all of the gordonae and rhodococci. The differences in susceptibility patterns may prove useful in characterizing the genera Gordona, Nocardia and Rhodococcus and in separating species within these taxa.     

Severe progressive subcutaneous abscesses and necrotizing tenosynovitis caused by Rhodococcus aurantiacus.

A case of severe progressive subcutaneous abscesses and necrotizing tenosynovitis of the right arm of a 30-year-old woman caused by Rhodococcus aurantiacus is reported.     

Endocarditis Caused by Rhodotorula Infection

Rhodotorula is an emerging opportunistic fungal pathogen that is rarely reported to cause endocarditis. We describe a case involving a patient who developed endocarditis due to Rhodotorula mucilaginosa and Staphylococcus epidermidis, proven by culture and histopathology. The case illustrates the unique diagnostic and therapeutic challenges relevant to Rhodotorula spp.     

Movement disorders in encephalitis induced by Rhodococcus aurantiacus infection relieved by the administration of L-dopa and anti-T-cell antibodies

Mice injected with Rhodococcus aurantiacus by the intravenous (i.v.) route show neurological disorders, hemiparesis, vertical headshake and turn-round gait after day 7 postinfection (p.i.). Neurological symptoms caused by i.v. inoculation of R. aurantiacus were relieved by treatment with levodopa (l-dopa). R. aurantiacus was isolated from the brain and was found to be completely eliminated at day 7 p. i. Focal encephalitis was mainly observed in the brain stem, and T cells could be isolated from the brain after day 7 p.i. Administration of both an anti-CD4 monoclonal antibody (mAb) and an anti-CD8 mAb suppressed neurological symptoms. These results suggest that R. aurantiacus induces movement disorders in mice, and that the symptoms are mediated by T cells infiltrating the brain, rather than directly by the bacterium.     

Thumb Infection Caused by Streptococcus pseudoporcinus

Streptococcus pseudoporcinus, a recently described organism found in the genitourinary tract of women, was isolated from a thumb wound in a male patient subsequent to trauma. This case describes a rarely reported non-genitourinary tract clinical isolate of S. pseudoporcinus.     

Persistent Infection Caused by Hobi-Like Pestivirus

A calf persistently infected by Hobi-like pestivirus was monitored for about 6 months, displaying clinical signs typical of bovine viral diarrhea virus persistent infection and shedding the virus through all body secretions, with maximal titers detected in urine. This report provides new insights into the pathogenesis of the emerging pestivirus.     

Role of T cells in granuloma formation induced by Rhodococcus aurantiacus is independent of their interferon-gamma production

Intravenous injection of Rhodococcus aurantiacus into mice causes granulomatous inflammation dependent on endogenous interferon-gamma (IFN-gamma). This study investigated the mechanism of granuloma formation with an adoptive transfer system in IFN-gamma knockout (IFN-gamma(-/-)) mice. IFN-gamma(-/-) mice infected with R. aurantiacus did not develop granulomas, and high titres of endogenous interleukin-10 (IL-10) were detected in spleen extracts at 2 weeks after infection. The adoptive transfer of splenocytes from infected wild-type (IFN-gamma(+/+)) mice did not restore granuloma formation, although this treatment diminished IL-10 production in IFN-gamma(-/-) mice. Adoptive transfer of splenocytes from infected IFN-gamma(-/-) mice into infected IFN-gamma(+/+) reduced granuloma formation. These results suggest that splenocytes of IFN-gamma(-/-) mice suppress granuloma formation. On the other hand, although IFN-gamma production induced by R. aurantiacus infection was detected in nude mice, which are deficient in T cells, granuloma formation was not induced in them. However, adoptive transfer of immune splenocytes from either IFN-gamma(+/+) mice or IFN-gamma(-/-) mice could induce granuloma formation. This means that splenocytes of IFN-gamma(-/-) mice have the ability to both induce and suppress granuloma formation. Induction of granuloma is probably dependent on both T cells and IFN-gamma produced by non-T cells. It is suggested that the role of T cells in granuloma formation is not dependent on their IFN-gamma production.     

Reciprocal action of interferon-gamma and interleukin-4 promotes granulomatous inflammation induced by Rhodococcus aurantiacus in mice.

An intravenous injection of Rhodococcus aurantiacus to mice causes granulomatous inflammation dependent on endogenous interferon-gamma (IFN-gamma). The present study examined the role of endogenous interleukin-4 (IL-4) on granulomatous inflammation. Endogenous IL-4 in the spleen extracts was not detected during the phase of granuloma formation by enzyme-linked immunosorbent assay (ELISA). However, IL-4 protein level was elevated during the phase of granuloma regression. IL-4 mRNA expression in the livers and spleens was also elevated during the phase of granuloma regression. In addition, IL-4 levels during the phase of granuloma formation were increased by treatment with anti-IFN-gamma monoclonal antibody (mAb), suggesting that endogenous IFN-gamma might inhibit IL-4 production during the phase of granuloma formation. Administration of anti-IL-4 mAb on weeks 3 and 4 after the inoculation inhibited the regression of granulomas and augumented IFN-gamma level at 5 weeks. Endogenous IFN-gamma was produced by CD4+ T cells during the phase of granuloma regression and endogenous IL-4 was produced by both CD4+ and CD8+ T cells. These findings suggest that during the phase of granuloma formation endogenous IL-4 might be inhibited by IFN-gamma, while during the phase of granuloma regression endogenous IL-4 might play a crucial role in the reduction of granulomas and IFN-gamma production.     

Pulmonary Fungal Infection Caused by Neoscytalidium dimidiatum

Neoscytalidium dimidiatum is a mold known to cause onychomycosis and dermatomycosis; however, it is an extremely rare cause of systemic infection. We report a case of pulmonary infection with Neoscytalidium dimidiatum in an immunocompromised patient and discuss in vitro susceptibility data from this case and previous literature.     

First Human Systemic Infection Caused by Spiroplasma

Spiroplasma species are organisms that normally colonize plants and insects. We describe the first case of human systemic infection caused by Spiroplasma bacteria in a patient with hypogammaglobulinemia undergoing treatment with biological disease-modifying antirheumatic agents. Spiroplasma turonicum was identified through molecular methods in several blood cultures. The infection was successfully treated with doxycycline plus levofloxacin.     

Nosocomial Outbreak of Serious Canine Infectious Tracheobronchitis (Kennel Cough) Caused by Canine Herpesvirus Infection

Canine herpesvirus (CHV; Canid herpesvirus 1) is principally a perinatal pathogen of pregnant bitches and newborn pups and secondarily a respiratory tract pathogen of older pups and dogs. Infectious disease of the canine respiratory tract frequently occurs among dogs in groups, in which it is called “ infectious tracheobronchitis” (ITB). Mortality from ITB is generally negligible, and the clinical importance of CHV as an ITB pathogen is considered to be low. The present report describes a novel ITB outbreak accompanied by death among aged dogs in an animal medical center. Most inpatient dogs had received medications that could induce immunosuppression. CHV was the only pathogen identified, and several CHV isolates were recovered in cell culture. No other viral pathogens or significant bacterial pathogens were found. Molecular and serological analyses revealed that the causative CHV isolates were from a single source but that none was a peculiar strain when the strains were compared with previous CHV strains. The virus had presumably spread among the dogs predisposed to infection in the center. The present results serve as a warning to canine clinics that, under the specific set of circumstances described, such serious CHV outbreaks may be expected wherever canine ITB occurs.Canine herpesvirus (CHV; Canid herpesvirus 1) is classified in the Varicellovirus genus of the Alphaherpesvirinae subfamily of the Herpesviridae. CHV was first described in 1965 as a pathogen responsible for a fatal generalized hemorrhagic disease of newborn pups (5). The host range of CHV is generally restricted to domestic and wild Canidae (11), and the worldwide distribution of CHV infection in domestic dog populations has been shown by virus isolation (2, 7, 10, 12, 24, 27) and seroepidemiological studies (6, 25, 28, 30, 31, 34). It is now well recognized that the pathogenic potential of CHV is mostly influenced by the age of the host (11). Pups infected in the postnatal period show the typical fatal hemorrhagic syndrome. Older pups manifest less severe clinical syndromes upon infection, and the respiratory disease called “infectious tracheobronchitis” (ITB) or “kennel cough” may be the most frequent clinical disorder in the field. Ocular disorders such as conjunctivitis and keratitis, either with or without ulceration, were also observed in young pups (17). Although the pathogenic potential of CHV for older dogs is apparently low and adult dogs often do not show any clinical signs following CHV infection, CHV may become an important perinatal pathogen for pregnant bitches, causing papulovesicular genital lesions and reproductive disorders such as embryonic resorption, abortion, and stillbirth (11).CHV is spread mainly by the oronasal and venereal transmission of viruses in the respiratory and genital secretions of acutely infected dogs, and fetuses are infected in utero (13, 14). Following the initial productive infection, in most cases CHV is not fully cleared by acquired immunity so that latency becomes established in several tissues, including the sensory ganglia (4, 19), and may persist for life. Latent viruses are sometimes reactivated by factors that alter immunity, such as stress, immunosuppressive therapy, or pregnancy, with the virus subsequently being excreted.The significance of CHV in the etiology of canine ITB has been considered to be rather low compared with that of other agents, such as canine parainfluenza virus (CPIV), canine adenovirus type 2 (CAV-2), and Bordetella bronchiseptica (9). Experimental infection of older pups or adult dogs with CHV isolates often resulted in either no clinical signs or mild upper respiratory symptoms (1, 15, 24, 32). Consequently, CHV has not generally been regarded to be a primary cause of canine ITB (9, 11). On the other hand, CHV has repeatedly been detected in dogs with ITB (3, 16, 24, 36), and a longitudinal study on the respiratory diseases of dogs housed in a rehoming kennel in the United Kingdom (8) indicated that CHV should be reevaluated as a significant agent responsible for ITB.This report is an account of a novel outbreak of canine ITB which was accompanied by deaths among dogs hospitalized in an animal referral medical center near Tokyo, Japan. It was concluded that CHV alone was responsible for the nosocomial outbreak. All of the dogs had been fully vaccinated before they entered the hospital, and during the hospitalization, most of the dogs had received steroid medication, surgery, or radiation therapy. It was considered that such medical treatments, in addition to hospitalization itself, might induce stress in the patients, leading to a condition of low-level immune resistance, and cause the recrudescence of latent CHV. Canine herpesvirus might then have spread contagiously among the dogs in the same clinic. The results of the present study suggest the need for caution, because CHV, which was previously thought to be an agent of low pathogenicity for adult dogs, should not be overlooked in specific circumstances.     

ESKAPE病原菌感染引起脓毒症的研究

感染一直是全球范围内重要的卫生问题,其中感染所导致的脓毒症发病率及死亡率极高,随着研究的深入,人们对脓毒症的认识也不断加深,2016年欧美危重病医学会制定了《脓毒症和感染性休克第三版国际共识定义》,重新定义了脓毒症。在脓毒症的众多病因中,具有突出的耐药性的ESKAPE（屎肠球菌、金黄色葡萄球菌、肺炎克雷伯杆菌、鲍曼不动杆菌、铜绿假单胞菌、肠道杆菌属）病原菌感染是其主要病因之一。ESKAPE感染的患者一般预后均较差,为了解ESKAPE所导致的脓毒症,降低其发病率和死亡率,本文主要从脓毒症、ESKAPE病原菌耐药机制,以及两者关系现状三个方面将国内外的研究进行综述。     

肺癌及结核性胸积液患者CA125的检测

目的:了解血清、胸水肿瘤相关糖链抗原CA_(125)测定对鉴别肺癌胸积液及结核性胸积液的价值.方法:肺癌胸积液、结核性胸积液及健康体检组各30、27、51例,CA_(125)检测采用微粒子捕捉酶免疫分析(MEIA)法在美国雅培IMx全自动免疫分析仪上进行.结果:肺癌组、结核组、健康对照组血清 CA_(125)分别为 191.0±185.9、55.1±53.7及6.2±2.6U/ml.肺癌组及结核组均显著高于健康对照组(p<0.01).肺癌组血清CA_(125)显著高于结核组(p<0.01)肺癌组、结核组胸水CA_(125)为477.7±220.6U/ml、243.3±209.0U/ml,两组无显著性差异(p=0.88),血清CA_(125)以35U/ml为临界值诊断肺癌胸积液时的敏感度、特异度、阳性预计值、阴性预计值、诊断准确率分别为83.3%、51.9%、65.8%、73.7%、68.4%.结论:血清CA_(125)测定可作为肺癌胸积液与结核性胸积液鉴别的辅助手段之一,胸水CA_(125)测定的鉴别价值不大.     

First Report of Bloodstream Infection Caused by Pseudomonas fulva

Pseudomonas fulva has not yet been isolated from humans as a pathogen. Herein, we report the first case of P. fulva bacteremia in a patient hospitalized due to trauma. The species was identified using biochemical and molecular genetic analyses of the 16S rRNA, gyrB, rpoB, and rpoD genes.