Presumptive mycobacteriosis in North-east Atlantic mackerel, Scomber scombrus L.

A total of 9470 mackerel aged from 0 to 20 years was examined for a disease condition whose causative agent has not been identified but which resembles mycobacteriosis. The study area extended from off Portugal to the northern North Sea. Most mackerel over 2 years old snowed evidence of gross infection. Mean intensity increased with age, indicating a chronic disease of low pathogenicity. There is statistical evidence of an adverse effect on growth, and it is suggested that this may delay first spawning of some young mackerel for at least 1 year. Western stock mackerel appear to be more heavily infected than North Sea stock, and the lowest levels of infection were found off Portugal. The general level of infection decreased in the most recent year classes examined–those of 1982, 1983 and 1984.     

Pathocycles: Ustilago maydis as a model to study the relationships between cell cycle and virulence in pathogenic fungi

Activation of virulence in pathogenic fungi often involves differentiation processes that need the reset of the cell cycle and induction of a new morphogenetic program. Therefore, the fungal capability to modify its cell cycle constitutes an important determinant in carrying out a successful infection. The dimorphic fungus Ustilago maydis is the causative agent of corn smut disease and has lately become a highly attractive model in addressing fundamental questions about development in pathogenic fungi. The different morphological and genetic changes of U. maydis cells during the pathogenic process advocate an accurate control of the cell cycle in these transitions. This is why this model pathogen deserves attention as a powerful tool in analyzing the relationships between cell cycle, morphogenesis, and pathogenicity. The aim of this review is to summarize recent advances in the unveiling of cell cycle regulation in U. maydis. We also discuss the connection between cell cycle and virulence and how cell cycle control is an important downstream target in the fungus-plant interaction.     

Advances in understanding the mechanism of resistance to anthracnose and induced defence response in tea plants

The tea plant (Camellia sinensis) is susceptible to anthracnose disease that causes considerable crop loss and affects the yield and quality of tea. Multiple Colletotrichum spp. are the causative agents of this disease, which spreads quickly in warm and humid climates. During plant–pathogen interactions, resistant cultivars defend themselves against the hemibiotrophic pathogen by activating defence signalling pathways, whereas the pathogen suppresses plant defences in susceptible varieties. Various fungicides have been used to control this disease on susceptible plants, but these fungicide residues are dangerous to human health and cause fungicide resistance in pathogens. The problem-solving approaches to date are the development of resistant cultivars and ecofriendly biocontrol strategies to achieve sustainable tea cultivation and production. Understanding the infection stages of Colletotrichum, tea plant resistance mechanisms, and induced plant defence against Colletotrichum is essential to support sustainable disease management practices in the field. This review therefore summarizes the current knowledge of the identified causative agent of tea plant anthracnose, the infection strategies and pathogenicity of C. gloeosporioides, anthracnose disease resistance mechanisms, and the caffeine-induced defence response against Colletotrichum infection. The information reported in this review will advance our understanding of host–pathogen interactions and eventually help us to develop new disease control strategies.     

Relation of intrahospital morbidity from staphylococcal infections to some properties of hospital strains]

Analysis of staphylococcus infection morbidity in a large obstetrical hospital for 5 years offered a possibility of establishing an association between the severity of the course of staphylococcus infections in patients, the bacteriophage type of the causative agent and its resistance to antibiotics. The qualitative changes in morbidity in the direction of the prevalence of minor forms and mild course ocurred in parallel with the changes of the leading bacteriophage type from the epidemic 75/77 and 80/81 to the nonepidemic bacteriophage types of the III bacteriophage group and the changes of the antibiograms of the causative agents in the direction of an increase in the number of strains sensitive to antibiotics. Since the severity of the course of staphylococcus infection characterized the pathogenicity of the strain of the causative agent a conclusion could be drawn on the association between the sign of virulence and determinants of the medicinal resistance and definite prophages in the hospital strains of staphylococcus.     

Identification of a unique gene cluster of Brucella spp. that mediates adhesion to host cells

Brucella, the causative agent of brucellosis, a major zoonotic disease affecting a broad range of mammals, is a gram-negative bacterium whose virulence is dependent on the capacity to attach and invade different cells of the host. The bacterium is able to infect through a diverse repertoire of epitheliums: skin, airways or gastric. Although much has been studied on the mechanisms Brucella uses to establish an intracellular replication niche, almost none is known on how the bacterium adheres and invades host cells. We report here the identification of a pathogenicity island that harbors a gene homologous to proteins with bacterial immunoglobulin-like domains present in other pathogens that play a role in attachment and invasion. Deletion of the entire island results in a mutant with a reduced attachment capacity measured by intracellular replication and adhesion assays. Intraperitoneal and oral experimental infection of mice strongly suggests that this island plays a role during the oral infection probably mediating attachment and trespassing of the gastric epithelium to establish a systemic infection.     

Extracellular proteases of mycelial fungi as participants of pathogenic processes

The interest in proteases secreted by mycelial fungi is due to several reasons of which one of the most important is their involvement in the initiation and development of the pathogenic process. A comparison of saprophytic and phytopathogenic mycelial fungi revealed one characteristic feature, namely, the appearance of a new trypsin-like activity in phytopathogens that is absent in saprophytes. To clear up the question of whether the degree of pathogenicity of a fungus is related to the activity of secreted trypsin-like protease, several species of Fusarium of various pathogenicity were compared. In two species, F. sporotrichioides (which causes ear fusa-riosis of rye) and F. heterosporum (the causative agent of root rot in wheat), a clear correlation between the activity and pathogenicity was revealed: the more pathogenetic F. sporotrichioides exhibited a higher extracellular trypsin-like activity than the less pathogenetic species F. heterosporum. Thus, the presence of trypsin-like activity in a saprotroph-pathogen pair may be an indicator of the pathogenicity of a fungus; in some cases, the value of this activity may indicate the degree of its pathogenicity. This suggests that trypsin-like proteases specific to phytopathogens are directly involved in the pathogenetic process, probably, through interaction with the "sentry" protein or the product of the resistance gene.     

Characterization of secreted proteases of Paenibacillus larvae, potential virulence factors involved in honeybee larval infection

Paenibacillus larvae is the causative agent of American Foulbrood (AFB), the most severe bacterial disease that affects honeybee larvae. AFB causes a significant decrease in the honeybee population affecting the beekeeping industry and agricultural production. After infection of larvae, P. larvae secretes proteases that could be involved in the pathogenicity. In the present article, we present the secretion of different proteases by P. larvae. Inhibition assays confirmed the presence of metalloproteases. Two different proteases patterns (PP1 and PP2) were identified in a collection of P. larvae isolates from different geographic origin. Forty nine percent of P. larvae isolates showed pattern PP1 while 51% exhibited pattern PP2. Most isolates belonging to genotype ERIC I - BOX A presented PP2, most isolates belonging to ERIC I - BOX C presented PP1 although relations were not significant. Isolates belonging to genotypes ERIC II and ERIC III presented PP2. No correlation was observed between the secreted proteases patterns and geographic distribution, since both patterns are widely distributed in Uruguay. According to exposure bioassays, isolates showing PP2 are more virulent than those showing PP1, suggesting that difference in pathogenicity could be related to the secretion of proteases.     

Proteomic analysis of Lyme disease: global protein comparison of three strains of Borrelia burgdorferi

The Borrelia burgdorferi spirochete is the causative agent of Lyme disease, the most common tick-borne disease in the United States. It has been studied extensively to help understand its pathogenicity of infection and how it can persist in different mammalian hosts. We report the proteomic analysis of the archetype B. burgdorferi B31 strain and two other strains (ND40, and JD-1) having different Borrelia pathotypes using strong cation exchange fractionation of proteolytic peptides followed by high-resolution, reversed phase capillary liquid chromatography coupled with ion trap tandem mass spectrometric analysis. Protein identification was facilitated by the availability of the complete B31 genome sequence. A total of 665 Borrelia proteins were identified representing approximately 38% coverage of the theoretical B31 proteome. A significant overlap was observed between the identified proteins in direct comparisons between any two strains (>72%), but distinct differences were observed among identified hypothetical and outer membrane proteins of the three strains. Such a concurrent proteomic overview of three Borrelia strains based upon only the B31 genome sequence is shown to provide significant insights into the presence or absence of specific proteins and a broad overall comparison among strains.     

申克孢子丝菌毒力因子及宿主抗感染免疫的研究进展

申克孢子丝菌是一种重要的双相型真菌,其引起的孢子丝菌病是一种常见的侵袭性皮肤感染.研究该菌毒力因子及宿主对其抗感染免疫对于深入了解其致病性及防治该病具有重要意义.该文介绍了申克孢子丝菌毒力因子及宿主对其抗感染免疫方面的研究进展.     

Doctrine of the transmission of the causative agents of infections and social and ecologic concepts of the epidemic process

The concept on social and ecologic determination of the epidemic process in its direct connection with L.V. Gromashevsky's doctrine on the transmission mechanism of the causative agents of infection is presented. The role of this concept in the development of epidemiological science is discussed.     

Full-Genome Analysis of a Canine Pneumovirus Causing Acute Respiratory Disease in Dogs,Italy

An outbreak of canine infectious respiratory disease (CIRD) associated to canine pneumovirus (CnPnV) infection is reported. The outbreak occurred in a shelter of the Apulia region and involved 37 out of 350 dogs that displayed cough and/or nasal discharge with no evidence of fever. The full-genomic characterisation showed that the causative agent (strain Bari/100-12) was closely related to CnPnVs that have been recently isolated in the USA, as well as to murine pneumovirus, which is responsible for respiratory disease in mice. The present study represents a useful contribution to the knowledge of the pathogenic potential of CnPnV and its association with CIRD in dogs. Further studies will elucidate the pathogenicity and epidemiology of this novel pneumovirus, thus addressing the eventual need for specific vaccines.     

Balamuthia mandrillaris, free-living ameba and opportunistic agent of encephalitis, is a potential host for Legionella pneumophila bacteria

Balamuthia mandrillaris is a free-living ameba and an opportunistic agent of granulomatous encephalitis in humans and other mammalian species. Other free-living amebas, such as Acanthamoeba and Hartmannella, can provide a niche for intracellular survival of bacteria, including the causative agent of Legionnaires' disease, Legionella pneumophila. Infection of amebas by L. pneumophila enhances the bacterial infectivity for mammalian cells and lung tissues. Likewise, the pathogenicity of amebas may be enhanced when they host bacteria. So far, the colonization of B. mandrillaris by bacteria has not been convincingly shown. In this study, we investigated whether this ameba could host L. pneumophila bacteria. Our experiments showed that L. pneumophila could initiate uptake by B. mandrillaris and could replicate within the ameba about 4 to 5 log cycles from 24 to 72 h after infection. On the other hand, a dotA mutant, known to be unable to propagate in Acanthamoeba castellanii, also did not replicate within B. mandrillaris. Approaching completion of the intracellular cycle, L. pneumophila wild-type bacteria were able to destroy their ameboid hosts. Observations by light microscopy paralleled our quantitative data and revealed the rounding, collapse, clumping, and complete destruction of the infected amebas. Electron microscopic studies unveiled the replication of the bacteria in a compartment surrounded by a structure resembling rough endoplasmic reticulum. The course of intracellular infection, the degree of bacterial multiplication, and the ultrastructural features of a L. pneumophila-infected B. mandrillaris ameba resembled those described for other amebas hosting Legionella bacteria. We hence speculate that B. mandrillaris might serve as a host for bacteria in its natural environment.     

Prevalence, intensity and aggregation of intestinal parasites in mountain hares and their potential impact on population dynamics

Mountain hare Lepus timidus populations show unstable dynamics and since hares carry a significant helminth infection and host-parasite interactions are known to be destabilising, they have been proposed as a possible causal mechanism for the observed instability. We assessed the prevalence, intensity of infection and aggregation of the helminth parasites Graphidium strigosum and Trichostrongylus retortaeformis recovered from 589 mountain hares culled from 30 Scottish sporting estates in 1999 and 2000. Graphidium strigosum showed low prevalence and intensity of infection and was highly aggregated. In contrast, T. retortaeformis showed high prevalence and intensity of infection and a low degree of aggregation. Differences in body condition of the hares were best explained by a model including sex and month of collection and interaction terms for sex-month and intensity of infection of T. retortaeformis-month. The low degree of aggregation of T. retortaeformis and the significant negative effect of intensity of infection on body condition are in accordance with the hypothesis that the host-parasite interaction is the causative destabilising mechanism for mountain hare dynamics.     

Increased pathogenicity and aerosol transmission for one SARS-CoV-2 B.1.617.2 Delta variant over the wild-type strain in hamsters

During the two-year pandemic of coronavirus disease 2019 (COVID-19), its causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been evolving. SARS-CoV-2 Delta, a variant of concern, has become the dominant circulating strain worldwide within just a few months. Here, we performed a comprehensive analysis of a new B.1.617.2 Delta strain (Delta630) compared with the early WIV04 strain (WIV04) in vitro and in vivo, in terms of replication, infectivity, pathogenicity, and transmission in hamsters. When inoculated intranasally, Delta630 led to more pronounced weight loss and more severe disease in hamsters. Moreover, 40% mortality occurred about one week after infection with 10⁴ PFU of Delta630, whereas no deaths occurred even after infection with 10⁵ PFU of WIV04 or other strains belonging to the Delta variant. Moreover, Delta630 outgrew over WIV04 in the competitive aerosol transmission experiment. Taken together, the Delta630 strain showed increased replication ability, pathogenicity, and transmissibility over WIV04 in hamsters. To our knowledge, this is the first SARS-CoV-2 strain that causes death in a hamster model, which could be an asset for the efficacy evaluation of vaccines and antivirals against infections of SARS-CoV-2 Delta strains. The underlying molecular mechanisms of increased virulence and transmission await further analysis.     

The evolution of virulence and pathogenicity in plant pathogen populations

The term virulence has a conflicting history among plant pathologists. Here we define virulence as the degree of damage caused to a host by parasite infection, assumed to be negatively correlated with host fitness, and pathogenicity the qualitative capacity of a parasite to infect and cause disease on a host. Selection may act on both virulence and pathogenicity, and their change in parasite populations can drive parasite evolution and host-parasite co-evolution. Extensive theoretical analyses of the factors that shape the evolution of pathogenicity and virulence have been reported in last three decades. Experimental work has not followed the path of theoretical analyses. Plant pathologists have shown greater interest in pathogenicity than in virulence, and our understanding of the molecular basis of pathogenicity has increased enormously. However, little is known regarding the molecular basis of virulence. It has been proposed that the mechanisms of recognition of parasites by hosts will have consequences for the evolution of pathogenicity, but much experimental work is still needed to test these hypotheses. Much theoretical work has been based on evidence from cellular plant pathogens. We review here the current experimental and observational evidence on which to test theoretical hypotheses or conjectures. We compare evidence from viruses and cellular pathogens, mostly fungi and oomycetes, which differ widely in genomic complexity and in parasitism. Data on the evolution of pathogenicity and virulence from viruses and fungi show important differences, and their comparison is necessary to establish the generality of hypotheses on pathogenicity and virulence evolution.     

Gill lamellar pillar cell necrosis, a new birnavirus disease in Japanese eels.

Since the late 1980s, a birnaviral gill disease has been occurring in Japanese eels Anguilla japonica reared in warmwater ponds in western regions in Japan. Diseased eels mostly displayed marked formations of aneurysmal hematomas within gill lamellae and high mortalities. Histological examination revealed necrosis of pillar cells and subsequent aggregation of erythrocytes inside the lamellar capillaries, and proliferation of interlamellar epithelia onto the lamellae. Gastric gland cells were also necrotized. Electron microscopy revealed birnavirus infection in lamellar pillar cells. The causative birnavirus was isolated and cultured in fish cell lines and was found to be related to an infectious pancreatic necrosis virus (IPNV) Sp serotype by neutralization tests. The viral pathogenicity was confirmed by the results of histopathological examinations and infectivity experiments.     

大肠埃希菌泌尿系统感染患者临床分布及药物敏感性分析

摘要 目的：探讨大肠埃希菌引起泌尿系统感染患者的临床分布情况及其药物敏感性分析,为临床诊断及合理使用抗菌药物提供理论性依据。方法：选取2015年1月至2020年12月期间诊治的2052例大肠埃希菌泌尿系统感染患者为研究对象,使用MALDI-TOF MS全自动微生物鉴定质谱仪对细菌进行鉴定,应用VITEK 2 Compact全自动微生物鉴定及药敏分析仪进行药物敏感性分析。结果：2052例大肠埃希菌泌尿系统感染患者中泌尿外科患者占比最高,为17.50%,其次为肾病科患者,占12.87%。其中检出803株产ESBLs的大肠埃希菌,泌尿外科占比最高,为18.56%,其次是肾病科占13.95%,内分泌科占11.71%,重症医学科10.09%。2052株大肠埃希菌整体药敏分析结果显示,大肠埃希菌对美罗培南、亚胺培南、阿米卡星、哌拉西林/他唑巴坦、呋喃妥因、米诺环素、头孢西丁等药物敏感率高,均>90%,头孢唑啉、环丙沙星、左氧氟沙星、氨苄西林/舒巴坦、复方新诺明、氨苄西林敏感率低,均<50%,其中氨苄西林敏感率最低,只有28.17%。结论：大肠埃希菌泌尿系统感染主要发生在泌尿外科,产ESBLs大肠埃希菌整体检出率较高,临床应重视泌尿系统感染患者的尿细菌培养及药物敏感性分析,尽量避免仅凭经验性用药,根据药物敏感性结果合理选择抗菌药物。     

Pestivirus

Members of the genus Pestivirus, are causative agents of economically important diseases for livestock and wild animals that occur worldwide, such as bovine viral diarrhea, classical swine fever, and border disease of sheep. Pestivirus have novel insertions of host genes in the viral genome and functions of unique viral proteins, N(pro) and E(rns), related to the pathogenicity although genomic structure is closely related to the other viruses of Flaviviridae family, especially hepatitis C virus. In this review, recent studies on the molecular basis of pathogenicity of pestivirus infections were summarized.     

Extracellular proteases of mycelial fungi as participants of pathogenic process

The interest in proteases secreted by mycelial fungi is due to several reasons of which one of the most important is their involvement in the initiation and development of the pathogenic process. A comparison of saprophytic and phytopathogenic mycelial fungi revealed one characteristic feature, namely, the appearance of a new trypsin-like activity in phytopathogens that is absent in saprophytes. To clear up the question of whether the degree of pathogenicity of a fungus is related to the activity of secreted trypsin-like protease, several species of Fusarium of various pathogenicity were compared. In two species, F. sporotrichioides (which causes ear fusariosis of rye) and F. heterosporum (the causative agent of root rot in wheat), a clear correlation between the activity and pathogenicity was revealed: the more pathogenetic F. sporotrichioides exhibited a higher extracellular trypsin-like activity than the less pathogenetic species F. heterosporum. Thus, the presence of trypsin-like activity in a saprotroph-pathogen pair may be an indicator of the pathogenicity of a fungus; in some cases, the value of this activity may indicate the degree of its pathogenicity. This suggests that trypsin-like proteases specific to phytopathogens are directly involved in the pathogenetic process, probably, through interaction with the “sentry” protein or the product of the resistance gene.     

CD4 T-cell depletion prevents Lassa fever associated hearing loss in the mouse model

Lassa virus (LASV) is the causative agent of Lassa fever (LF), which presents as a lethal hemorrhagic disease in severe cases. LASV-induced hearing loss in survivors is a huge socioeconomic burden, however, the mechanism(s) leading to hearing loss is unknown. In this study, we evaluate in a mouse LF model the auditory function using auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE) to determine the mechanisms underlying LASV-induced hearing loss. In the process, we pioneered measures of ABR and DPOAE tests in rodents in biosafety level 4 (BSL-4) facilities. Our T cell depletion studies demonstrated that CD4 T-cells play an important role in LASV-induced hearing loss, while CD8 T-cells are critical for the pathogenicity in the acute phase of LASV infection. Results presented in this study may help to develop future countermeasures against acute disease and LASV-induced hearing loss.