Remote touch prey‐detection by Madagascar crested ibises Lophotibis cristata urschi

Birds that forage by probing must often rely on sensory systems other than vision to detect their buried prey. Such senses may include hearing (e.g. Australian magpies (Atramidae), American robins (Turdidae)) or chemical senses/olfaction (e.g. kiwi (Apterygidae) and some shorebirds (Scolopacidae)). Probe foraging kiwi and shorebirds are also able to use vibrotactile cues to locate prey buried in the substrate at some distance from their bill‐tips (‘remote touch’). These birds possess an organ consisting of a honey‐comb of sensory pits in bone of the bill‐tips, packed with mechanoreceptive nerve ending (Herbst corpuscles). Such a bill‐tip organ has recently also been described in ibises (Threskiornithinae), but its function not elucidated. We designed a foraging experiment presenting mealworm prey to three captive Madagascar crested ibises Lophotibis cristata urschi under a variety of trial conditions to discover whether they were using remote touch, mediated by their bill‐tip organ; chemosense/olfaction; or hearing to locate buried prey. The ibises were reliant on remote touch for prey detection – the first time this sensory system has been demonstrated for this group of birds. They did not appear to use hearing or chemical senses/olfaction to aid in prey detection.     

First case of erysipelas in a free-ranging bottlenose dolphin (Tursiops truncatus) stranded in the Mediterranean Sea

An adult female bottlenose dolphin (Tursiops truncatus) stranded alive and subsequently died several minutes later on the Mediterranean coast of Spain on 14 July 2010. Clinical examination revealed foam through the blowhole and rales upon lung auscultation. On venipuncture, the blood was abnormally dense and dark. Hematological and biochemical abnormalities included dehydration, leukocytosis (48 600 leukocytes microl(-1)) characterized by neutrophilia (48 200 neutrophils microl(-1)), and elevated bilirubin (4.38 mg dl(-1)), alanine aminotransferase (382.3 U l(-1)), aspartate aminotransferase (1449.3 U l(-1)), lactate dehydrogenase (1631.3 U l(-1)), and creatine kinase (404.7 U l(-1)). The most relevant findings of the gross examination were rhomboid-shaped skin lesions, stable froth in the trachea, pulmonary congestion, abnormally thick and rough pleura with adhesions, edematous and congestive superficial cervical and tracheobronchial lymph nodes, red-tinged urine, and severe brain congestion. Histopathology of the kidney, lung, skin, and brain revealed multisystemic intravascular bacterial emboli. Samples of skin, brain, and lung were cultured on Columbia blood agar under both aerobic and anaerobic conditions, and pure and heavy bacterial cultures were obtained from skin and brain samples. The microorganism isolated was Gram-positive, catalase-negative, facultatively anaerobic, and rod-shaped. The isolates were identified as Erysipelothrix rhusiopathiae by the API Coryne biochemical system. Based on the gross and microscopic findings, a diagnosis of acute E. rhusiopathiae septicemia was made. To the best of our knowledge, this is the first report of E. rhusiopathiae septicemia in a free-ranging bottlenose dolphin.     

Patterns of genetic variation in populations of infectious agents

Background  

The analysis of genetic variation in populations of infectious agents may help us understand their epidemiology and evolution. Here we study a model for assessing the levels and patterns of genetic diversity in populations of infectious agents. The population is structured into many small subpopulations, which correspond to their hosts, that are connected according to a specific type of contact network. We considered different types of networks, including fully connected networks and scale free networks, which have been considered as a model that captures some properties of real contact networks. Infectious agents transmit between hosts, through migration, where they grow and mutate until elimination by the host immune system.     

In vitro interactions between bacteria, osteoblast-like cells and macrophages in the pathogenesis of biomaterial-associated infections

Biomaterial-associated infections constitute a major clinical problem that is difficult to treat and often necessitates implant replacement. Pathogens can be introduced on an implant surface during surgery and compete with host cells attempting to integrate the implant. The fate of a biomaterial implant depends on the outcome of this race for the surface. Here we studied the competition between different bacterial strains and human U2OS osteoblast-like cells (ATCC HTB-94) for a poly(methylmethacrylate) surface in the absence or presence of macrophages in vitro using a peri-operative contamination model. Bacteria were seeded on the surface at a shear rate of 11 1/s prior to adhesion of U2OS cells and macrophages. Next, bacteria, U2OS cells and macrophages were allowed to grow simultaneously under low shear conditions (0.14 1/s). The outcome of the competition between bacteria and U2OS cells for the surface critically depended on bacterial virulence. In absence of macrophages, highly virulent Staphylococcus aureus or Pseudomonas aeruginosa stimulated U2OS cell death within 18 h of simultaneous growth on a surface. Moreover, these strains also caused cell death despite phagocytosis of adhering bacteria in presence of murine macrophages. Thus U2OS cells are bound to loose the race for a biomaterial surface against S. aureus or P. aeruginosa, even in presence of macrophages. In contrast, low-virulent Staphylococcus epidermidis did not cause U2OS cell death even after 48 h, regardless of the absence or presence of macrophages. Clinically, S. aureus and P. aeruginosa are known to yield acute and severe biomaterial-associated infections in contrast to S. epidermidis, mostly known to cause more low-grade infection. Thus it can be concluded that the model described possesses features concurring with clinical observations and therewith has potential for further studies on the simultaneous competition for an implant surface between tissue cells and pathogenic bacteria in presence of immune system components.     

Evaluation of the efficacy of chemical disinfectants for disinfection of heat‐polymerised acrylic resin

doi: 10.1111/j.1741‐2358.2010.00400.x
Evaluation of the efficacy of chemical disinfectants for disinfection of heat‐polymerised acrylic resin Objective: This study evaluated the efficacy of disinfectants on the internal aspect of heat‐polymerised acrylic resin contaminated with microbial strains. Background: Dentures absorb oral fluids and become contaminated by different microorganisms. Methods: Two hundred and fifty rectangular specimens were made of heat‐polymerised acrylic resin, and then divided into five groups corresponding to the microbial strains (Staphylococcus aureus, Pseudomonas aeruginosa, Candida albicans, S. mutans and Enterococcus faecalis). After contamination, the specimens were immersed in 1 and 2% sodium hypochlorite and 2% glutaraldehyde for periods of 5, 10 and 15 min. The specimens were placed into tubes containing different broths and incubated at 35°C and then visually analysed. Turbidity in the medium indicated microbial growth. The Fisher’s exact test was used in the analysis of the results. Results: The strain E. faecalis was the most resistant to the disinfectant solutions, and among them, glutaraldehyde was more effective than 2 and 1% hypochlorite for disinfection for 5 min; in the 10‐min period there were no differences between the disinfectants. In 15 min of immersion, 1% hypochlorite and glutaraldehyde were more effective than 2% hypochlorite. Conclusions: Disinfection for 10 min with 1% hypochlorite and glutaraldehyde is effective in disinfecting the internal aspect of heat‐polymerised acrylic resin.     

TGF-beta1 and IL-6 gene polymorphism in Spanish brucellosis patients

Polymorphisms in the cytokine genes have allowed for the understanding of the genetic determinants in several diseases. We investigated the polymorphism of the transforming growth factor (TGF)-beta1 and IL-6 genes in relation to susceptibility to human brucellosis. We typed 82 Spanish brucellosis patients and 102 healthy controls for TGF-beta1 polymorphisms in codons 10 and 25, and IL-6 promoter polymorphism at position -174 by PCR-SSP methods. The T/T G/G genotype of the TGF-beta1 gene was significantly increased in patients compared to controls (49% vs. 32%) P=0.02; OR=1.99 (1.05-3.80) and the T/C G/G genotype was significantly less common in the patients compared to the controls (32% vs. 49%) P=0.01; OR=0.48 (0.25-0.92). The CC genotype of codon 10 was significantly increased in the patients who had focal forms of the disease as compared with those who did not develop focal forms (19% vs. 4%), P=0.03; OR=0.19 (0.02-1.10). No differences were found in the IL-6 variants between the patients and the controls. These results suggest that polymorphism of the TGF-beta1 gene may be involved in susceptibility to brucellosis and to developing focal forms of the disease in a group of patients from southern Spain.     

"Super p53" mice exhibit enhanced DNA damage response,are tumor resistant and age normally

The tumor suppressor p53 is critical in preventing cancer due to its ability to trigger proliferation arrest and cell death upon the occurrence of a variety of stresses, most notably, DNA damage and oncogenic stress. Here, we report the generation and characterization of mice carrying supernumerary copies of the p53 gene in the form of large genomic transgenes. Prior to this, we demonstrate that the p53 transgenic allele (p53-tg), when present in a p53-null genetic background, behaves as a functional replica of the endogenous gene. "Super p53" mice, carrying p53-tg alleles in addition to the two endogenous alleles, exhibit an enhanced response to DNA damage. Importantly, "super p53" mice are significantly protected from cancer when compared with normal mice. Finally, in contrast to previously reported mice with constitutively active p53, "super p53" mice do not show any indication of premature aging, probably reflecting the fact that p53 is under normal regulatory control. Together, our results prove that cancer resistance can be enhanced by a simple genetic modification and in the absence of undesirable effects.