Expanding the Staphylococcus aureus SarA Regulon to Small RNAs

Staphylococcus aureus , a commensal and opportunist pathogen, is responsible for a large number of human and animal infections, from benign to severe. Gene expression adaptation during infection requires a complex network of regulators, including transcriptional factors (TF) and sRNAs.

Commensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species

Staphylococcus aureus is a human commensal organism and opportunist pathogen, causing potentially fatal disease. The presence of non-pathogenic microflora or their components, at the point of infection, dramatically increases S. aureus pathogenicity, a process termed augmentation. Augmentation is associated with macrophage interaction but by a hitherto unknown mechanism. Here, we demonstrate a breadth of cross-kingdom microorganisms can augment S. aureus disease and that pathogenesis of Enterococcus faecalis can also be augmented. Co-administration of augmenting material also forms an efficacious vaccine model for S. aureus. In vitro, augmenting material protects S. aureus directly from reactive oxygen species (ROS), which correlates with in vivo studies where augmentation restores full virulence to the ROS-susceptible, attenuated mutant katA ahpC. At the cellular level, augmentation increases bacterial survival within macrophages via amelioration of ROS, leading to proliferation and escape. We have defined the molecular basis for augmentation that represents an important aspect of the initiation of infection.

The Role of Macrophages in Staphylococcus aureus Infection

Staphylococcus aureus is a member of the human commensal microflora that exists, apparently benignly, at multiple sites on the host. However, as an opportunist pathogen it can also cause a range of serious diseases. This requires an ability to circumvent the innate immune system to establish an infection. Professional phagocytes, primarily macrophages and neutrophils, are key innate immune cells which interact with S. aureus, acting as gatekeepers to contain and resolve infection. Recent studies have highlighted the important roles of macrophages during S. aureus infections, using a wide array of killing mechanisms. In defense, S. aureus has evolved multiple strategies to survive within, manipulate and escape from macrophages, allowing them to not only subvert but also exploit this key element of our immune system. Macrophage-S. aureus interactions are multifaceted and have direct roles in infection outcome. In depth understanding of these host-pathogen interactions may be useful for future therapeutic developments. This review examines macrophage interactions with S. aureus throughout all stages of infection, with special emphasis on mechanisms that determine infection outcome.

On the Origin of Candida auris: Ancestor, Environmental Stresses, and Antiseptics

ABSTRACTCandida auris has emerged as a serious threat to the health care settings. Advancements in molecular biology have provided several insights into the evolution of C. auris since it was first described in 2009. However, the simultaneous emergence of four different clades of the fungus at distinct geographical locations remains a mystery. The hypotheses already proposed by researchers fall short of explaining how and why C. auris emerged. In this article, we theorize that C. auris emerged from a common ancestor, subsequently migrated to specific geographical locations, and diversified genetically. This hypothesis is supported by genomic insights, historical events, and indirect scientific facts. C. auris adapted to humans at locations and times coinciding with the divergence from the most recent common ancestor, emerging almost simultaneously as an opportunist pathogen due to antiseptic practices. Future research will support or refute this hypothesis.

Psuedomonas aeruginosa-Associated Acute and Chronic Pulmonary Infections

Pseudomonas aeruginosa is highly successful in colonizing in all types of environments. P. aeruginosa colonizing in adverse environment due to the presence of its virulence factors include production of toxins, proteases hemolysins, and formation of biofilms. In man, the most common opportunist pathogen is P. aeruginosa. Metabolically P. aeruginosa is versatile. Most of the antibiotics targeted metabolically active cells and bacteria could contribute to decrease in biofilm susceptibility to the antimicrobial agents. Scientists suggested about Pseudomonas that it can be catabolized any hydrocarbon in specific time along with availability of oxygen and nitrite. If bacteria are not susceptible to one agent in three or more, it is called as multidrug-resistance strains. The antimicrobial treatments were not suitable when microorganism presented in vitro microorganism resistance to antimicrobials used for treatment of the patient which lack of treatment for 24 h after diagnosis of microbial infections. Bacteria have developed resistance against commonly used antibiotics. Treatment of Pseudomonas infections is coming harder day by day as its resistance against most of the antibiotics. Because of resistance of bacteria antibiotics, alternative methods are in consideration. These methods include use of lactic acid bacteria (LAB) and most recently nano-particles. That is why they are used as antibacterial agents.

Molecular Epidemiology of Staphylococcus aureus Lineages in Wild Animals in Europe: A Review

Staphylococcus aureus is an opportunist pathogen that is responsible for numerous types of infections. S. aureus is known for its ability to easily acquire antibiotic resistance determinants. Methicillin-resistant S. aureus (MRSA) is a leading cause of infections both in humans and animals and is usually associated with a multidrug-resistant profile. MRSA dissemination is increasing due to its capability of establishing new reservoirs and has been found in humans, animals and the environment. Despite the fact that the information on the incidence of MRSA in the environment and, in particular, in wild animals, is scarce, some studies have reported the presence of these strains among wildlife with no direct contact with antibiotics. This shows a possible transmission between species and, consequently, a public health concern. The aim of this review is to better understand the distribution, prevalence and molecular lineages of MRSA in European free-living animals.

Case 13

There is an increasing number of opportunist pathogens that may cause acute pulmonary exacerbations of cystic fibrosis as the patient cohort survives longer. However, it can often be difficult to determine if the isolation of these bacteria represents colonization or true infection. Their identification from sputum samples in the microbiology laboratory is also challenging, requires significant scientific expertise, and is assisted by new technologies such as MALDI-TOF (matrix-assisted laser desorption/ionization time-of-flight mass spectrometry). One such opportunist pathogen is Stenotrophomonas maltophilia, for which risk factors include increasing age and recent oral antibiotics, especially carbapenems. However, it is unclear if this bacterium is transmitted from patient to patient unlike with Pseudomonas aeruginosa, but all patients with cystic fibrosis should be admitted to a single room when hospitalization is required. Controversies exist regarding the optimal treatment which in the future may include a greater reliance on inhaled antibiotics.

Necrotic Skin Infection by Sphingomonas Paucimobilis in Amazonia Region

Sphingomonas paucimobilis is an opportunist pathogen bacillus gram-negative aerobic with a rare occurrence. We present a case in an immunocompetent man successfully treated by surgical debridement, purulent drainage and with an associated course of antibiotics. A large necrotic infection, approximately 5 cm x 3 cm, in a 74-year-old man was identified. Empirical antibiotic therapy with ciprofloxacin 400mg EV 12/12 hours, associated with clindamycin 600mg EV 6/6 hours and pain control was done through dipyrone 1gr, tramadol 400 mg. Deep venous thrombosis was prevented through the prescription of enoxaparin 40mg subcutaneous once a day during hospitalization. The case was well illustrated with pictures throughout treatment. Complete healing was achieved after 90 days. Herein, we present a case of cutaneous contamination. The presented case is the third cutaneous contamination case reported in the literature and the first reported case in the Amazonia region in Brazil.

AT6SS trans-kingdom effector is required for the delivery of a novel antibacterial toxin in Pseudomonas aeruginosa

Pseudomonas aeruginosa has evolved multiple strategies to disarm and take advantage of its host. For this purpose this opportunist pathogen has particularly developed protein secretion in the surrounding medium or injection into host cells. Among this, the Type VI Secretion System (T6SS) is utilized to deliver effectors into eukaryotic host as well as target bacteria. It assembles into a contractile bacteriophage tail-like structure that functions like a crossbow, injecting an arrow loaded with effectors into the target cell. The repertoire of T6SS antibacterial effectors of P. aeruginosa is remarkably broad to promote environmental adaptation and survival in various bacterial communities, and presumably in the eukaryotic host too.Here we report the discovery a novel pair of antibacterial effector and immunity of P. aeruginosa, Tle3 and Tli3. Tli3 neutralizes the toxicity of Tle3 in the periplasm to protect from fratricide intoxication. The characterization of the secretion mechanism of Tle3 indicates that it requires a cytoplasmic adaptor, Tla3, to be targeted and loaded onto the VgrG2b spike and thus delivered by the H2-T6SS machinery. Tla3 is different from the other adaptors discovered so far, and defines a novel family among T6SS.Interestingly this led us to discover that VgrG2b that we previously characterized as an anti-eukaryotic effector possesses an antibacterial activity as well, as it is toxic towards Escherichia coli. VgrG2b is thus a novel trans-kingdom effector targeting both bacteria and eukaryotes. VgrG2b represents an interesting target for fighting against P. aeruginosa in the environment and in the context of host infection.HighlightsTle3 and Tli3 are a novel pair of antibacterial toxin and immunity of P. aeruginosaTla3 recruits Tle3 in the cytoplasm, and targets it to VgrG2bVgrG2b is required for Tle3 delivery into target bacteria by the H2-T6SSTla3 defines a novel type of T6SS adaptor with a DUF2875VgrG2b is a new trans-kingdom effector targeting both bacteria and eukaryotes