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PubMed1994

Location of pathogenicity genes on dispensable chromosomes in Nectria haematococca MPVI.

Nectria haematococca MPVI can be found in many different biological habitats but has been most studied as a pathogen of pea (Pisum sativum). Genetic analyses of isolates obtained from a variety of biological sources has indicated that a number of genes control pathogenicity on pea but that one important PEa Pathogenicity (PEP) gene is PDA, which confers the ability to detoxify the pea phytoalexin pisatin. In these studies, all naturally occurring isolates that lacked PDA (i.e. Pda- isolates) and all Pda- progeny were essentially non-pathogenic on pea. However, we have demonstrated recently that Pda- mutants created by transformation-mediated gene disruptions, while having a modest reduction in virulence, and more virulent than any naturally occurring Pda- isolates. In addition we know that PDA genes are on dispensable (DS) chromosomes in this fungus. We believed that the gene disruption mutants have allowed the detection of other PEP genes that are present on the DS chromosomes along with PDA and that naturally occurring Pda- isolates usually lack this DS chromosome. This would explain why naturally occurring Pda- isolates are always low in virulence. We propose that the DS chromosomes in fungi are analogous to bacterial plasmids which allow those microorganisms to colonise different habitats, i.e. the DS chromosomes of Nectria haematococca contain genes that allow individual isolates of this broad host range pathogen to occupy different biological niches.

Benzopyrans↗

PubMed1988

Quantitation of concanavalin A and wheat germ agglutinin binding by two strains of Trichomonas vaginalis of differing pathogenicity using gold particle-conjugated lectins.

Two strains of Trichomonas vaginalis, which differed in their pathogenicity for both women and experimental animals hosts, were compared for the presence and number of concanavalin A (ConA)- and wheat germ agglutinin (WGA)-binding sites on their surface using gold lectin conjugates. Both strains showed a high affinity for ConA and WGA and a similar pattern of gold particle distribution on the surface coat. The gold marker was distributed over the cytoplasmic membrane sparsely as single particles but more often in groups, suggesting the presence of single and clustered sugar residues on the parasite surface. Statistical analysis of the level of lectin binding, expressed as the number of gold particles attached per 1 micron plasmalemma, by pathogenic and non-pathogenic strains of T. vaginalis show that these two strains do not differ in the number of ConA receptors on their surfaces. However, WGA-binding receptors were more numerous on the surface of the pathogenic than on the non-pathogenic strain. This suggests that these two strains differ in the number of N-acetyl-D-glucosamine residues on their surfaces. The lectin-gold particle conjugate technique therefore appears more sensitive than agglutination assays or the horseradish peroxidase-3,3'-diaminobenzidine method for the assessment of lectin-binding sites on the surface of T. vaginalis.

Animals↗

PubMed1994

Herpes simplex virus type 1 (HSV-1) UL56 gene is involved in viral intraperitoneal pathogenicity to immunocompetent mice.

A comparison of the pathogenicity in mice of the recombinant herpes simplex virus type 1 (HSV-1) strain HSV-1-M-LacZ, in which the UL56 gene has been deleted, was made with its parental strain F, following infection in different mouse strains. The polymerase chain reaction (PCR) technique was used to study the migration of virus DNA in the mouse model. Tissues from adult mice infected intraperitoneally (IP) with one of three HSV-1 strains (F, HFEM or HSV-1-LacZ) were examined for the presence of viral DNA. DNA of the pathogenic strain F was detected in the adrenal glands, spinal cord, brain, liver and pancreas. DNA of HSV-1-M-LacZ was detected in the same tissues. However, DNA of the apathogenic strain HFEM was detected transiently (on days 2 and 3 p.i., but not days 1, 5 or 7), only in the adrenal glands and no viral DNA was detected in any of the other tissues. HSV-1 pathogenic strains injected intraperitoneally into newborn mice (7 days old) killed most of the mice. In the surviving mice viral DNA of the three virus strains was found in peritoneal exudate cells (PEC), adrenal glands, spinal cord, liver and spleen. It was found that HSV-1-M-LacZ, which lacks the UL56 gene, resembled in pathogenicity to the newborn mice the pathogenic HSV-1 strains F and KOS. The PCR technique was used to trace viral DNA in tissues of the mice which survived HSV-1 infection at 7 weeks of age. Only HSV-1 (KOS) DNA was detected in the pancreas. The brains of these mice did not contain viral DNA. It is suggested that HSV-1 DNA may reside in surviving HSV-1- infected newborn mice in a "latent" state in nonneural tissues.

Adrenal Glands↗

PubMed1980

Pathogenic significance of anaerobic bacteria in the female genital tract.

Comparative microbiological investigations of biopsy specimens from the cervix of women with gynaecological infections, and from the cervix secretion of healthy women with normal menstrual cycles, as well as animal experiments were conducted in order to determine the pathogenicity of non-sporeforming anaerobic bacteria in the female genital tract. From the results the following conclusions were drawn: any anerobic bacterium is considered pathogenic if it is cultured in liquid or solid medium from a non-gravid uterus, the tubes or the exudate in the small pelvis. Bacteria isolated from the cervial canal during puerperium or from the uterus are considered pathogenic if a large number grows on solid culture and if a known pathogenic species predominates. Bacteria isolated from the vagina can be of pathogenic significance if the clinical findings are not normal and if the above-mentioned criteria are considered.

Anaerobiosis↗

PubMed1992

Spectrum and susceptibility of pathogens causing acute uncomplicated lower UTI in females and its correlation to bacteriologic outcome after single dose therapy with fosfomycin trometamol versus ofloxacin/co-trimoxazole.

In a multicentric study comparing oral single-dose therapy of fosfomycin trometamol (3 g as fosfomycin) versus co-trimoxazole (1.92 g) or ofloxacin (200 mg) as many as possible of the pathogens were sent to and analysed in a central laboratory. The pathogens were identified and minimal inhibitory concentrations (MIC) of fosfomycin, trimethoprim alone and in combination with sulfamethoxazole, ofloxacin, ampicillin, amoxicillin combined with clavulanic acid, and cephadroxil were determined. The eradication of pathogens (cfu < 10(3)/ml at one week after single-dose therapy) was analysed according to species and MIC of the antibiotic used. Urine cultures of 349 patients were analysed. Escherichia coli was the predominating species followed by staphylococci and Proteus mirabilis. Enterococci were mostly found in mixed culture. Baseline pathogens of monoinfections were eradicated in 87.1%, in 88.9% and in 86.4% of 284 patients treated with fosfomycin trometamol, co-trimoxazole and ofloxacin, respectively. The MICs of the five antibacterial agents and the two antibiotic combinations for 253 baseline pathogens showed that of the E. coli strains none was resistant to ofloxacin, three (MIC = 128 mg/l) were resistant to fosfomycin, 3.6% to co-trimoxazole, 6.2% to trimethoprim, 8.8% to ampicillin, and 5.7% to amoxicillin/clavulanic acid. The eradication rates according to the MICs of the corresponding drugs showed equally good eradication rates for fosfomycin up to an MIC of 64 mg/l. Above this level two out of three strains were also eradicated by fosfomycin trometamol. For co-trimoxazole and ofloxacin no intermediately sensitive or resistant strains were found. Within the range of MICs found there were equally good eradication rates for both antibacterial agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1994

Experiments on the possible role of leeches as vectors of animal and human pathogens: a light and electron microscopy study.

The presence and survival of pathogens inside the gut of leeches were studied by means of light and electron microscopy. In African leeches from Cameroon, blood was serologically positive for human immunodeficiency virus (HIV) and hepatitis B; blood of Hirudo medicinalis bought in German pharmacies contained up to 11 different species of bacteria. In experiments done at low (3 degrees C) and high (22 degrees, 32 degrees C) temperatures, it was shown that ingested red and white blood cells survive for long periods. The time was prolonged to at least 6 months in cases in which the leeches were stored at 3 degrees C. The same effect occurred with pathogens. Bacteriophages (viruses of bacteria) and bacteria persisted in large numbers for at least 6 months in the gut of experimentally infected leeches. Protozoan parasites such as Toxoplasma gondii, Trypanosoma brucei brucei, or Plasmodium berghei were even capable of reproducing inside the gut of the leech. In the case of Plasmodium parasites, this proceeded at low (3 degrees C) and high (22 degrees C) temperatures until all erythrocytes were used up. These parasites survived as long as the erythrocytes and lymphocytes were of good shape, i.e., around 5-6 weeks p.i. Single stages survived longer, especially at low temperatures. However, electron microscopy studies gave no hint of penetration of such pathogens into the unicellular salivary glands, which would initiate a direct transmission. Such transmission, however, is possible--many fish leeches directly transmit several blood parasites--when the leeches are squeezed during skin attachment or when they are manipulated by dropping salt solution on their backs while they are sucking. Consequently, the leech is a potential vector of many pathogens, especially in regions with an endemic spread of human and/or animal pathogens.

Animals↗

PubMedDate not supplied

Prevalence of intestinal pathogens in HIV patients with diarrhea: implications for treatment.

Patients infected with the human immunodeficiency virus (HIV) commonly experience diarrhea at some time during their illness. A variety of enteric pathogens are identified in 50-80% of these patients, depending on the intensity of the diagnostic work-up that is done. In addition to the common enteric pathogens, several unusual enteric pathogens are recognized to cause diarrhea especially in HIV patients. These include protozoan parasites such as Cryptosporidia, Isospora belli, Cyclospora cayatenensis and Microsporidium species bacteria such as enteropathogenic Escherichia coli and Mycobacterium avium-intracellulare, fungi including Candida albicans and Histoplasma capsulatum, and viruses such as astroviruses and caliciviruses. Diagnosis of these infections sometimes involves special procedures not readily available every where, and empiric therapy based on knowledge of the likely pathogens has been advocated for developing countries. This article reviews the currently available data on geographic variation of enteric pathogens in HIV patients with diarrhea and outlines a rational strategy for empiric therapy of these patients.

Animals↗

PubMed2002

Pathogen inactivation of blood components: current status and introduction of an approach using riboflavin as a photosensitizer.

Riboflavin is a naturally occurring compound and an essential human nutrient. Studies in the 1960s and 70s showed that it could be effective, when exposed to visible or UV light, in inactivating viruses and bacteria. This suggested to us that it could act as a photosensitizer useful in the inactivation of pathogens found in blood products, because of its nucleic acid specificity and its limited tendency toward indiscriminate oxidation. The riboflavin molecule is a planar, conjugated ring structure with a sugar side chain that confers water solubility. The planar portion is capable of intercalating between the bases of DNA or RNA. Light activated riboflavin oxidizes guanine in nucleic acids, preventing replication of the pathogen's genome. Gambro BCT is developing processes using riboflavin and light to inactivate pathogens in plasma, platelet, and red cell products. We call these Pathogen Eradication Technology (PET) processes. Riboflavin is non-toxic; it must be present in the body for good health. The photo-byproducts formed in the PET processes are lumichrome and protein adducts. The photodegradation of riboflavin in the body is clearly shown by the decrease in its concentration in neonates who are treated with intense visible light to break down circulating bilirubin, which their immature livers cannot yet handle. A definitive lookback study showed no difference in cancer rates between the 55,000 children receiving this therapy in Denmark from 1977 through 1989 and nonirradiated controls. Gambro BCT is developing specific riboflavin-based PET processes for platelet concentrates, fresh frozen plasma, and packed red blood cells. In each, the process is being optimized to achieve high levels of inactivation of specific pathogens, while maintaining acceptable levels of product quality and activity. Extra- and intracellular HIV, BVDV (a model for HCV), and pseudorabies virus (a herpes virus) have been used to guide process development and validation. We have demonstrated 4 to 7 log10 reductions in the titers of these viruses, when they are spiked into blood products and irradiated in the presence of riboflavin. Porcine parvovirus, a tight-capsid, nonenveloped virus is more resistant, a finding in all experimental inactivation approaches. A range of bacteria implicated in platelet and red cell transfusion injuries and deaths, including S. aureus, E. coli, K. pneumoniae, and Y. enterocolitica, are being used to validate antibacterial efficacy. The PET platelet process involves the addition of riboflavin to platelets in plasma, illumination of the product, storage of the product and transfusion without further manipulation. The lack of toxicity of the treatment byproducts permits this ease of use. Quality of the platelets throughout storage has been assessed by pH, PO2, lactate, hypotonic shock response, morphology, glucose, and GMP-140 expression. In vitro function is well maintained. The levels seen are within the range of those reported in commonly transfused products. Radiolabeled transfusion studies of treated platelets have been carried out in primates to determine a preliminary measure of their in-vivo circulation. The in vivo recoveries and survivals of treated and control platelets did not differ. This work suggests that an endogenous photosensitizer, riboflavin, which has an extremely good safety profile, can inactivate high levels of a broad range of viruses and bacteria in platelet concentrates, fresh frozen plasma, and in red blood cells, preserving the activity and functionality of the components. Planned animal and clinical studies are expected to solidify this suggestion into a well-characterized process which can be safely and readily applied to reduce the risks of transfusion transmitted disease.

Blood Cells↗

PubMed2005

[Incidence of transmission of pathogens in intensive care units. Results of the SIR 3 study].

The objective of this study was to determine the incidence of episodes of transmission of nosocomial pathogens and of those pathogens leading to nosocomial infections. Over a period of 18 months all patients from 5 intensive care units (ICUs) who stayed for more than 2 days were included in this study. Surveillance of nosocomial infections was carried out and all isolates of 10 of the most frequent pathogens in ICUs (indicator pathogens) were collected and typed. A total of 28,498 patient days and 431 nosocomial infections were observed (incidence density 15.1 per 1,000 patient days), among them 278 caused by 1 of the selected indicator pathogens. A total of 141 episodes of transmissions were identified, corresponding to an incidence of episodes of transmission of 5.0 per 1,000 patient days and 41 nosocomial infections were transmission-associated, corresponding to 14.5% of all nosocomial infections. The data of this study demonstrate that even in ICUs with average nosocomial infection rates, some nosocomial infections could be avoided.

Anesthesia↗

PubMed2006

Outcome in bacteremia associated with nosocomial pneumonia and the impact of pathogen prediction by tracheal surveillance cultures.

OBJECTIVE: To assess whether pathogen prediction in bacteremia associated with nosocomial pneumonia (NP) by tracheal surveillance cultures improves adequacy of early antibiotic therapy and impacts mortality. DESIGN AND SETTING: A retrospective observational study of a prospectively gathered cohort. This cohort included all adult patients admitted to the ICU of a tertiary care hospital from 1992 through 2001 and who developed bacteremia associated with NP. MEASUREMENTS AND MAIN RESULTS: 128 episodes of bacteremia associated with NP were identified. In 110 episodes a tracheal surveillance culture 48-96h prior to bacteremia was available: this culture predicted the pathogen in 67 episodes (61%). Overall rates of appropriate empiric antibiotic therapy within 24 and 48h were 62 and 87%, respectively. Pathogen prediction was associated with a significantly higher rate of appropriate antibiotic therapy within 24h (71 vs 45%; p=0.01), but not within 48h (91 vs 82%; p=0.15). Crude in-hospital mortality was 50%. Pathogen prediction was associated with increased survival in univariate (OR 0.43; CI 0.19-0.93; p=0.04) and multivariate analysis (OR 0.32; CI 0.12-0.82; p=0.02). Multivariate analysis further identified age (OR 1.04; CI 1.01-1.07; p=0.02), increasing APACHEII score (OR 1.08; CI 1.02-1.15; p=0.01), and methicillin-resistant Staphylococcus aureus (OR 5.90; CI 1.36-25.36; p=0.01) and Pseudomonas aeruginosa (OR 3.30; CI 1.04-10.4; p=0.04) as independent risk factors for mortality. CONCLUSION: Pathogen prediction in bacteremia associated with NP by tracheal surveillance cultures is associated with a higher rate of adequate empiric antibiotic therapy within 24[Symbol: see text]h and with increased survival.

Aged↗

PubMed2005

Inherent specificities in natural antibodies: a key to immune defense against pathogen invasion.

Natural antibodies are produced at tightly regulated levels in the complete absence of external antigenic stimulation. They provide immediate, early and broad protection against pathogens, making them a crucial non-redundant component of the humoral immune system. These antibodies are produced mainly, if not exclusively, by a subset of long-lived, self-replenishing B cells termed B-1 cells. We argue here that the unique developmental pattern of these B-1 cells, which rests on positive selection by self antigens, ensures production of natural antibodies expressing evolutionarily important specificities that are required for the initial defense against invading pathogens. Positive selection for reactivity with self antigens could also result in the production of detrimental anti-self antibodies. However, B-1 cells have evolved a unique response pattern that minimizes the risk of autoimmunity. Although these cells respond rapidly and strongly to host-derived innate signals, such as cytokines, and to pathogen-encoded signals, such as lipopolysaccharide and phosphorylcholine, they respond very poorly to receptor-mediated activation. In addition, they rarely enter germinal centers and undergo affinity maturation. Thus, their potential for producing high-affinity antibodies with harmful anti-self specificity is highly restricted. The positive selection of B-1 cells occurs during the neonatal period, during which the long-lived self-renewing B-1 population is constituted. Many of these cells (B-1a) express CD5, although a smaller subset (B-1b) does not express this surface marker. Importantly, B-1a cells should not be confused with short-lived anergic B-2 cells, which originate in the bone marrow in adults and initiate CD5 expression and programmed cell death following self-antigen recognition. In summary, we argue here that the mechanisms that enable natural antibody production by B-1 cells reflect the humoral immune system, which has evolved in layers whose distinct developmental mechanisms generate complementary repertoires that collectively operate to maximize flexibility in responses to invading pathogens. B-2 cells, present in what may be the most highly evolved layer(s), express a repertoire that is explicitly selected against self recognition and directed towards the generation of high-affinity antibody response to external antigenic stimuli. B-1 cells, whose repertoire is selected by recognition of self antigen, belong to what may be earlier layer(s) and inherently maintain production of evolutionarily important antibody specificities that respond to pathogen-related, rather then antigen-specific signals.

Animals↗

PubMed2005

Mutations in VMK1, a mitogen-activated protein kinase gene, affect microsclerotia formation and pathogenicity in Verticillium dahliae.

Verticillium dahliae is an important soil-borne fungal pathogen that causes vascular wilt diseases in a large variety of important crop plants. Due to its persistence in the soil, control of Verticillium wilt relies heavily on soil fumigation. The global ban on methyl bromide, a highly effective soil fumigant, poses an urgent need to develop alternative control measures against Verticillium wilt; and these might be more forthcoming with a better understanding of the molecular and cellular mechanisms that underpin the pathogenicity of V. dahliae. In this study, we assessed the role in growth, development, and pathogenicity of VMK1, a gene encoding a mitogen-activated protein (MAP) kinase (hence, Verticillium MAP Kinase 1). Disruption of VMK1 via Agrobacterium tumefaciens-mediated transformation, in two V. dahliae isolates, one from lettuce and the other from tomato, resulted in severely reduced virulence in diverse host plants, suggesting that VMK1 is essential for pathogenicity and that the MAP kinase-mediated signaling pathway has a conserved role in fungal pathogenicity. The vmk1 mutants also exhibited reduced conidiation and microsclerotia formation, suggesting that the gene is important for multiple cellular processes.

Agrobacterium tumefaciens↗

PubMed2005

Accumulation of gentisic acid as associated with systemic infections but not with the hypersensitive response in plant-pathogen interactions.

In the present work we have studied the accumulation of gentisic acid (2,5-dihydroxybenzoic acid, a metabolic derivative of salicylic acid, SA) in the plant-pathogen systems, Cucumis sativus and Gynura aurantiaca, infected with either prunus necrotic ringspot virus (PNRSV) or the exocortis viroid (CEVd), respectively. Both pathogens produced systemic infections and accumulated large amounts of the intermediary signal molecule gentisic acid as ascertained by electrospray ionization mass spectrometry (ESI-MS) coupled on line with high performance liquid chromatography (HPLC). The compound was found mostly in a conjugated (beta-glucoside) form. Gentisic acid has also been found to accumulate (although at lower levels) in cucumber inoculated with low doses of Pseudomonas syringae pv. tomato, producing a nonnecrotic reaction. In contrast, when cucumber was inoculated with high doses of this pathogen, a hypersensitive reaction occurred, but no gentisic-acid signal was induced. This is consistent with our results supporting the idea that gentisic-acid signaling may be restricted to nonnecrotizing reactions of the host plant (Bellés et al. in Mol Plant-Microbe Interact 12:227-235, 1999). In cucumber and Gynura plants, the activity of gentisic acid as inducing signal was different to that of SA, thus confirming the data found for tomato. Exogenously supplied gentisic acid was able to induce peroxidase activity in both Gynura and cucumber plants in a similar way as SA or pathogens. However, gentisic-acid treatments strongly induced polyphenol oxidase activity in cucumber, whereas pathogen infection or SA treatment resulted in a lower induction of this enzyme. Nevertheless, gentisic acid did not induce other defensive proteins which are induced by SA in these plants. This indicates that gentisic acid could act as an additional signal to SA for the activation of plant defenses in cucumber and Gynura plants.

Asteraceae↗

PubMed2000

Culture independent and rapid identification of bacterial pathogens in necrotising fasciitis and streptococcal toxic shock syndrome by fluorescence in situ hybridisation.

Fluorescence in situ hybridisation (FISH) targeted to ribosomal RNA is well established for studies in environmental microbiology. Initial applications of this technique in the field of medical microbiology showed that FISH is also a suitable means for the rapid, reliable and cultivation-independent identification of bacterial pathogens. In particular, for infectious diseases that follow a fulminant live-threatening course, such as sepsis or necrotising fasciitis (NF), a fast and reliable detection technique is of great importance. This study describes the development of an rRNA-targeted oligonucleotide set covering more than 95% of the pathogens associated with NF. These probes were tested with a broad collection of target and non-target organisms and found to be highly specific. Subsequently, the FISH approach was applied for the direct detection of bacterial pathogens in clinical samples. Two cases of NF and one case of streptococcal toxic shock syndrome (STSS) were analysed. FISH correctly identified almost all pathogens present in the samples examined within 2-3 h. However, Proteus mirabilis, which was identified in one sample by conventional methods was detected as a rod-shaped bacteria but could not be identified by FISH, since no specific probe was available for this particular organism. In contrast, identification of pathogens in these samples by conventional laboratory methods took 48-72 h. Furthermore, in one patient with pre-sampling antimicrobial therapy bacteria could not be grown from any of the samples. FISH unequivocally revealed the presence of Streptococcus pyogenes in affected tissue samples from this patient. In an experimental setting we demonstrated that FISH readily identifies S. pyogenes cells rendered non-cultivable by antibiotic treatment.

Adult↗

PubMed1999

Loss of pathogenic potential after cloning of the low-passage Borrelia burgdorferi ZS7 tick isolate: a cautionary note.

To study clonal polymorphism of Borrelia hurgdorferi antigens in the course of an experimental infection sequence, the low-passage tick isolate ZS7 was cloned by two rounds of agar subsurface plating. The resulting clones showed a variable pathogenic potential after experimental infection of C.B-17. scid mice. The test clone 4.2.II, selected for virulence by two passages in immunodeficient scid mice, failed to establish a successful infection in immunocompetent AKR/N mice, indicating the loss of pathogenicity traits required for evasion of the specific immune response. Cloning of natural or clinical B. burgdorferi isolates is a prerequisite for analyzing genetic and antigenic variation of the pathogen. However, the inevitable propagation in artificial media during cloning may lead to a loss of pathogenic features rendering the subsequent experimental infection of animals impossible. A combined procedure of in vitro cloning and in vivo selection also does not solve the dilemma because B. burgdorferi variants arise by recombinatorial processes in the pathogen's dynamic genome during the course of infection. Consequently, the resulting bacterial isolates from infected animal tissues represent again non-clonal, heterogeneous B. burgdorferi populations. In principle, cloning of a B. burgdorferi population is the appropriate method to analyze the polymorphism of individual molecules during infection. As a caveat, however, one has to envisage that during propagation of individual clones in vitro and in vivo independent genetic variations

Animals↗

PubMed1997

Identification of two genetic markers that distinguish pathogenic and nonpathogenic strains of Acanthamoeba spp.

Species-level identification of Acanthamoeba isolates is difficult and gives little or no indication of the isolate's pathogenicity. We identified two amplification-based genetic markers that were highly correlated with pathogenicity in Acanthamoeba spp. One marker, designed to amplify a 485-bp fragment of the small-subunit ribosomal RNA gene (ssrDNA), was preferentially amplified from the nonpathogenic strains; amplifications from the pathogenic strains yielded anomalous fragments of 650 and 900 bp. A second marker was developed on the basis of the anomalous 650-bp fragment. Primers to this sequence preferentially amplified a noncoding locus (called Ac6) only from the pathogenic strains. These two genetic markers may be useful for identification of pathogenic Acanthamoeba spp. strains.

Acanthamoeba↗

PubMed2006

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.

Cell Cycle↗

PubMed2006

Histological changes in intestine of Atlantic salmon (Salmo salar L.) following in vitro exposure to pathogenic and probiotic bacterial strains.

Furunculosis and vibriosis are diseases that cause severe economic losses in the fish-farming industry. The foregut of the Atlantic salmon (Salmo salar L.) was exposed in vitro to two fish pathogens, Aeromonas salmonicida (causative agent of furunculosis) and Vibrio anguillarum (causative agent of vibriosis), and to one probiotic strain, Carnobacterium divergens, at 6 x 10(4) or 6 x 10(6) viable bacteria per milliliter. Histological changes following bacterial exposure were assessed by light and electron microscopy. Control samples (foregut exposed to Ringer's solution only) and samples exposed only to C. divergens had a similar appearance to intact intestinal mucosal epithelium, with no signs of damage. However, exposure of the foregut to the pathogenic bacteria resulted in damaged epithelial cells, cell debris in the lumen, and disorganization of the microvilli. Co-incubation of the foregut with a pathogen and C. divergens did not reverse the damaging effects caused by the pathogen, although these were alleviated when probiotic bacteria were used. Based on these results, we suggest that the probiotic bacterium, C. divergens, is able to prevent, to some extent, pathogen-induced damage in the Atlantic salmon foregut.

Aeromonas salmonicida↗