Bacillus anthracis, the etiological agent of anthrax, procures its particular virulence by a capsule and two AB type toxins: the lethal factor LF and the edema factor EF. These toxins primarily disable immune cells. Both toxins are translocated to the host cell by the adhesin-internalin subunit called protective antigen PA. PA enables LF to reach intra-luminal vesicles, where it remains active for long periods. Subsequently, LF translocates to non-infected cells, leading to inefficient late therapy of anthrax. B. anthracis undergoes slow evolution because it alternates between vegetative and long spore phases. Full genome sequence analysis of a large number of worldwide strains resulted in a robust evolutionary reconstruction of this bacterium, showing that B. anthracis is split in three main clades: A, B and C. Clade A efficiently disseminated worldwide underpinned by human activities including heavy intercontinental trade of goat and sheep hair. Subclade A.Br.WNA, which is widespread in the Northern American continent, is estimated to have split from clade A reaching the Northern American continent in the late Pleistocene epoch via the former Bering Land Bridge and further spread from Northwest southwards. An alternative hypothesis is that subclade A.Br.WNA. evolved from clade A.Br.TEA tracing it back to strains from Northern France that were assumingly dispatched by European explorers that settled along the St. Lawrence River. Clade B established mostly in Europe along the alpine axis where it evolved in association with local cattle breeds and hence displays specific geographic subclusters. Sequencing technologies are also used for forensic applications to trace unintended or criminal acts of release of B. anthracis. Under natural conditions, B. anthracis generally affects domesticated and wild ruminants in arid ecosystems. The more recently discovered B. cereus biovar anthracis spreads in tropical forests, where it threatens particularly endangered primate populations.

Summary: A eromonas salmonicida subsp. salmonicida is an important pathogen in salmonid aquaculture and is responsible for the typical furunculosis. The type‐three secretion system ( T3SS ) is a major virulence system. In this work, we review structure and function of this highly sophisticated nanosyringe in A . salmonicida . Based on the literature as well as personal experimental observations, we document the genetic (re)organization, expression regulation, anatomy, putative functional origin and roles in the infectious process of this T3SS . We propose a model of pathogenesis where A . salmonicida induces a temporary immunosuppression state in fish in order to acquire free access to host tissues. Finally, we highlight putative important therapeutic and vaccine strategies to prevent furunculosis of salmonid fish.

Mycoplasma bovis is a wall-less bacterium causing bovine mycoplasmosis, a disease showing a broad range of clinical manifestations in cattle. It leads to enormous economic losses to the beef and dairy industries. Antibiotic treatments are not efficacious and currently no efficient vaccine is available. Moreover, mechanisms of pathogenicity of this bacterium are not clear, as few virulence attributes are known. Microscopic observations of necropsy material suggest the possibility of an intracellular stage of M. bovis. We used a combination of a gentamicin protection assay, a variety of chemical treatments to block mycoplasmas entry in eukaryotic cells, and fluorescence and transmission electron microscopy to investigate the intracellular life of M. bovis in calf turbinate cells. Our findings indicate that M. bovis invades and persists in primary embryonic calf turbinate cells. Moreover, M. bovis can multiply within these cells. The intracellular phase of M. bovis may represent a protective niche for this pathogen and contribute to its escape from the host’s immune defense as well as avoidance of antimicrobial agents.

Aeromonas salmonicida subsp. salmonicida is an important pathogen in salmonid aquaculture and is responsible for furunculosis, a common infectious disease in salmon, trout and char. The type-three secretion system (T3SS) is considered as the major virulence attribute of A. salmonicida. It is used by the bacterium to secrete and translocate a large number of toxins and effector proteins into the host cell. Some of these factors such as the bi-functional ADP ribosylating – GTPase activating protein AexT have been shown to have a detrimental impact on the integrity of the cell cytoskeleton, and hence contribute to impair phagocytosis. Other effector proteins that are injected to the host cell such as AopP act by inhibiting the NF-κB signalling pathway blocking the translocation of NF-κB (p65) into the nucleus, thus influencing the host’s inflammatory response. Several additional effectors that are secreted and translocated via the T3SS including Ati2, AopN and ExsE have been suggested to modulate the host’s immune response in particular by down regulating the inflammatory reaction. The analysis of the immune response in rainbow trout (Oncorhynchus mykiss) infected with virulent, T3SS harbouring A. salmonicida subsp. salmonicida revealed that the infection leads to a rapid and strong downregulation of several immune-relevant markers affecting both the innate and the adaptive immune response, leading to mortality of the infected fish. In contrast, infection with a T3SS deficient mutant causes a normal immune reaction and clearing of the pathogen. These findings show that T3SS-delivered effector molecules and toxins of A. salmonicida do not only impair the host’s cytoskeleton thus damaging cell physiology and phagocytosis, but also affect the transcription of critical immune markers including the shut-down of important warning signals to recognize infection and induce immune defense.

The genomic sequence of Clostridium chauvoei, the etiological agent of blackleg, a severe disease of ruminants with high mortality specified by a myonecrosis reveals a chromosome of 2.8 million base-pairs and a cryptic plasmid of 5.5 kilo base-pairs. The chromosome contains the main pathways like glycolysis/gluconeogenesis, sugar metabolism, purine and pyrimidine metabolisms, but the notable absence of genes of the citric acid cycle and deficient or partially deficient amino acid metabolism for Histidine, Tyrosine, Phenylalanine, and Tryptophan. These essential amino acids might be acquired from host tissue damage caused by various toxins and by protein metabolism that includes 57 genes for peptidases, and several ABC transporters for amino acids import.

Although mustelids occur worldwide and include a wide range of species, little is known about the diseases affecting them. Mustelids have regularly been submitted for post mortem investigation in the framework of the program for general wildlife health surveillance in Switzerland, which has been in place for nearly 60 years. We performed a retrospective analysis of the necropsy reports on mustelids submitted to the diagnostic service of the University of Bern. The aims of this study were to present an overview of the causes of mortality and morbidity observed in these carnivores, to assess differences among species, to assess changes in disease detection over the study period, and to describe the pathology of selected diseases. Five hundred and sixty-six reports from 1958 to 2015 were analyzed. Most animals were stone martens (Martes foina, 46%) and badgers (Meles meles, 44%); the remaining species were polecats (Mustela putorius, 4.7%), pine martens (Martes martes, 2%), stoats (Mustela erminea, 1.4%), weasels (Mustela nivalis, 0.8%) and otters (Lutra lutra, 0.3%). Infectious diseases (n = 262) were frequent and were mostly bacterial or viral; non-infectious conditions (n = 169) were less common and were mostly traumatic or due to metabolic disorders. The most frequent diagnoses included distemper (75% were badgers), amyloidosis (96% were martens), bacterial respiratory infections (all mustelids), biting lice (badgers only) and pulmonary and gastro-intestinal helminths (all species). Less frequent diseases included histoplasmosis (badgers only), aspergillosis, toxoplasmosis, hepatozoonosis, and sarcoptic mange. Lesions due to infection with distemper virus were primarily appreciated in the respiratory tract and central nervous system; they presented species-specific characteristics such as necrosis in the ependyma in badgers and absence of syncytia in stone martens. Amyloidosis in martens was multisystemic in most cases and included both AA and AL amyloidosis; the main macroscopic change was severe splenomegaly. Infectious diseases were the most frequent causes of morbidity and mortality of mustelids, with marked species-specific differences. Lung and skin were the most commonly affected organs. Contagious diseases such as canine distemper, sarcoptic mange and rabies in mustelids showed a similar temporal pattern as in red foxes (Vulpes vulpes), suggesting pathogen spillovers from foxes to mustelids.