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PubMed2001

Molecular determinants of virulence, cell tropism, and pathogenic phenotype of infectious bursal disease virus.

Infectious bursal disease viruses (IBDVs), belonging to the family Birnaviridae, exhibit a wide range of immunosuppressive potential, pathogenicity, and virulence for chickens. The genomic segment A encodes all the structural (VP2, VP4, and VP3) and nonstructural proteins, whereas segment B encodes the viral RNA-dependent RNA polymerase (VP1). To identify the molecular determinants for the virulence, pathogenic phenotype, and cell tropism of IBDV, we prepared full-length cDNA clones of a virulent strain, Irwin Moulthrop (IM), and constructed several chimeric cDNA clones of segments A and B between the attenuated vaccine strain (D78) and the virulent IM or GLS variant strain. Using the cRNA-based reverse-genetics system developed for IBDV, we generated five chimeric viruses after transfection by electroporation procedures in Vero or chicken embryo fibroblast (CEF) cells, one of which was recovered after propagation in embryonated eggs. To evaluate the characteristics of the recovered viruses in vivo, we inoculated 3-week-old chickens with D78, IM, GLS, or chimeric viruses and analyzed their bursae for pathological lesions 3 days postinfection. Viruses in which VP4, VP4-VP3, and VP1 coding sequences of the virulent strain IM were substituted for the corresponding region in the vaccine strain failed to induce hemorrhagic lesions in the bursa. In contrast, viruses in which the VP2 coding region of the vaccine strain was replaced with the variant GLS or virulent IM strain caused rapid bursal atrophy or hemorrhagic lesions in the bursa, as seen with the variant or classical virulent strain, respectively. These results show that the virulence and pathogenic-phenotype markers of IBDV reside in VP2. Moreover, one of the chimeric viruses containing VP2 sequences of the virulent strain could not be recovered in Vero or CEF cells but was recovered in embryonated eggs, suggesting that VP2 contains the determinants for cell tropism. Similarly, one of the chimeric viruses containing the VP1 segment of the virulent strain could not be recovered in Vero cells but was recovered in CEF cells, suggesting that VP1 contains the determinants for cell-specific replication in Vero cells. By comparing the deduced amino acid sequences of the D78 and IM strains and their reactivities with monoclonal antibody 21, which binds specifically to virulent IBDV, the putative amino acids involved in virulence and cell tropism were identified. Our results indicate that residues Gln at position 253 (Gln253), Asp279, and Ala284 of VP2 are involved in the virulence, cell tropism, and pathogenic phenotype of virulent IBDV.

Amino Acid Sequence↗
PubMed1991

Magnaporthe grisea genes for pathogenicity and virulence identified through a series of backcrosses.

We have identified genes for pathogenicity toward rice (Oryza sativa) and genes for virulence toward specific rice cultivars in the plant pathogenic fungus Magnaporthe grisea. A genetic cross was conducted between the weeping lovegrass (Eragrostis curvula) pathogen 4091-5-8, a highly fertile, hermaphroditic laboratory strain, and the rice pathogen O-135, a poorly fertile, female-sterile field isolate that infects weeping lovegrass as well as rice. A six-generation backcrossing scheme was then undertaken with the rice pathogen as the recurrent parent. One goal of these crosses was to generate rice pathogenic progeny with the high fertility characteristic of strain 4091-5-8, which would permit rigorous genetic analysis of rice pathogens. Therefore, progeny strains to be used as parents for backcross generations were chosen only on the basis of fertility. The ratios of pathogenic to nonpathogenic (and virulent to avirulent) progeny through the backcross generations suggested that the starting parent strains differ in two types of genes that control the ability to infect rice. First, they differ by polygenic factors that determine the extent of lesion development achieved by those progeny that infect rice. These genes do not appear to play a role in infection of weeping lovegrass because both parents and all progeny infect weeping lovegrass. Second, the parents differ by simple Mendelian determinants, "avirulence genes," that govern virulence toward specific rice cultivars in all-or-none fashion. Several crosses confirm the segregation of three unlinked avirulence genes, Avr 1-CO39, Avr 1-M201 and Avr1-YAMO, alleles of which determine avirulence on rice cultivars CO39, M201, and Yashiro-mochi, respectively. Interestingly, avirulence alleles of Avr1-CO39, Avr1-M201 and Avr1-YAMO were inherited from the parent strain 4091-5-8, which is a nonpathogen of rice. Middle repetitive DNA sequences ("MGR sequences"), present in approximately 40-50 copies in the genome of the rice pathogen parent, and in very low copy number in the genome of the nonpathogen of rice, were used as physical markers to monitor restoration of the rice pathogen genetic background during introgression of fertility. The introgression of highest levels of fertility into the most successful rice pathogen progeny was incomplete by the sixth generation, perhaps a consequence of genetic linkage between genes for fertility and genes for rice pathogenicity. One chromosomal DNA segment with MGR sequence homology appeared to be linked to the gene Avr1-CO39. Finally, many of the crosses described in this paper exhibited a characteristic common to many crosses involving M. grisea rice pathogen field isolates.(ABSTRACT TRUNCATED AT 400 WORDS)

Ascomycota↗
PubMed1994

Studies on the bacterial flora of fish which are potential pathogens for human. Virulence factors of potential human pathogen isolated.

Tests for various virulence factors, such as production of haemolysin on sheep blood agar plate, cytotoxin on HeLa cell line and enterotoxin in GM-1 ELISA and suckling mouse assay model, were done among the various strains of Aeromonas spp., Vibrio spp., Plesiomonas shigelloides and Esch. coli isolated from fresh water fish samples. Invasive properties of the isolates were also seen by using Sereny test. Haemolysin production was observed in 85.7% of Aeromonas, all (100%) of Vibrios, 13.3% of Esch. coli and none (0%) of P. shigelloides strains. Cytotoxin production was demonstrated in 60.8% of Aeromonas, 38.4% of Vibrios and none (0%) of P. shigelloides and Esch. coli strains. About 8% of Vibrio spp., were found positive for LT in GM-1 ELISA method whereas, none of the Aeromonas spp., Plesiomonas and Esch. coli. strains were found positive for LT and ST in GM-1 ELISA. By suckling mouse assay model 43.4% strains of Aeromonas were found positive for enterotoxin production whereas, strains of Vibrio spp., Plesiomonas and Esch. coli yielded negative results. Sereny test for invasive property was found negative in all the strains tested. The isolates from fish possess various virulence factors which contributes for pathogenicity in order to cause various diseases to susceptible individual.

Animals↗
PubMed2006

Role of the universal stress protein UspA of Salmonella in growth arrest, stress and virulence.

Pathogenic bacteria employ a variety of mechanisms to resist a barrage of stresses they encounter during active growth in or outside the host as well as during growth stasis. An in silico screen of the Salmonella genome sequence revealed that Salmonella typhimurium LT2 possesses a homologue belonging to the universal stress protein A (UspA) family. We assessed the transcriptional profile of uspA in S. typhimurium C5 by constructing a lacZ fusion revealing that uspA is induced by metabolic, oxidative, and temperature stresses. The highest transcriptional levels occurred in cells entering stationary phase, an observation consistent with expression patterns in Escherichia coli. The protein was purified as a fusion with GST (UspA(F)) and antibodies raised against UspA(F) revealed elevated protein levels in stressed and growth-arrested cells. Inactivation of uspA in S. typhimurium C5, lead to increased susceptibility to stress conditions. Furthermore, UspA makes an important contribution to the in vivo virulence of Salmonella in mice thus highlighting the importance of stress resistance regulation in pathogenicity and survival within the host.

Animals↗
PubMed1997

Pathogenicity and virulence of Rhodococcus equi in foals following intratracheal challenge.

Twelve foals, between 27 and 83 days old, were infected with 2 strains of Rhodococcus equi by intratracheal administration. Ten of the 12 foals were inoculated with 10(4)-10(10) colony forming units (cfu) of ATCC 33701 strain. The other 2 foals were inoculated with 10(9) cfu of a plasmid-cured derivative of the ATCC 33701 strain (ATCC 33701P-). All of the 10 foals challenged with the ATCC 33701 strain showed clinical signs of pulmonary disease within 5-13 days, such as gross lesions associated with acute bronchopneumonia and microscopic lesions associated with granulomatous pneumonia. The two foals challenged with the ATCC 33701P- strain showed neither clinical signs of disease nor gross lesions. Apparently, when lacking plasmid, the virulent Rhodococcus equi lost its pathogenicity.

Actinomycetales Infections↗
PubMed2004

The evolution of virulence in pathogens with frequency-dependent transmission.

Frequency-dependent transmission is an important feature of diseases that are sexually transmitted or transmitted by a vector that actively searches for hosts. Here I describe the evolution of virulence in pathogens that have frequency-dependent transmission. I consider two components of virulence--an increase in host mortality due to infection, as is classically described, and a decrease in host fecundity due to infection, because frequency dependence is common among diseases that fully or partially sterilize their hosts. Theoretical predictions pertaining to host-pathogen numerical dynamics can be quite different between pathogens with frequency-dependent transmission and those with density-dependent transmission. In contrast, this study suggests that the principles governing the evolution of virulence that have been established in the context of density-dependent pathogens may also apply (qualitatively) to frequency-dependent pathogens. I examine the evolutionary trajectories of the mortality and sterility components of virulence as well as the role of spatial population structure in the evolution of the sterility component of virulence.

Animals↗
PubMed2002

Linking fungal morphogenesis with virulence.

Pathogenic fungi have become an increasingly common cause of systemic disease in healthy people and those with impaired immune systems. Although a vast number of fungal species inhabit our planet, just a small number are pathogens, and one feature that links many of them is the ability to differentiate morphologically from mould to yeast, or yeast to mould. Morphological differentiation between yeast and mould forms has commanded attention for its putative impact on the pathogenesis of invasive fungal infections. This review explores the current body of evidence linking fungal morphogenesis and virulence. The topics addressed cover work on phase-locked fungal cells, expression of phase-specific virulence traits and modulation of host responses by fungal morphotypes. The effect of morphological differentiation on fungal interaction with host cells, immune modulation and the net consequence on pathogenesis of disease in animal model systems are considered. The evidence argues strongly that morphological differentiation plays a vital role in the pathogenesis of fungal infection, suggesting that factors associated with this conversion process represent promising therapeutic targets.

Humans↗
PubMed1983

Surface determinants of Haemophilus influenzae pathogenicity: comparative virulence of capsular transformants in normal and complement-depleted rats.

In an assessment of the contribution of different capsular polysaccharides to the pathogenicity of Haemophilus influenzae, the virulence of H influenzae strain Rd and of a series of capsular transformants (types b, c, d, and f) of strain Rd was compared and in normal and complement-depleted rats. After intraperitoneal inoculation, the encapsulated transformants were strikingly more virulent than strain Rd, although their pathogenicity varied; type b was the most virulent, type c the next most virulent, type f less virulent, and type d the least virulent. C3 depletion enhanced the susceptibility of rats to systemic infection but did not influence the relative virulence of the transformants. Comparative studies of clearance showed efficient intravascular survival of type b, c, and f transformants but not of the type d transformant or strain Rd; C3 depletion enhanced the intravascular survival of type d. Further analysis of the capsular transformants revealed differences in the electrophoretic characteristics of their lipopolysaccharides. These studies indicate that elaboration of a unique capsular polysaccharide may not be a sufficient explanation for the greater virulence of H influenzae type b and that lipopolysaccharide may contribute to the mediation of the differential pathogenicity of the various serotypes.

Animals↗
PubMed1987

Pathogenicity and virulence of wild-type and melanin-deficient Wangiella dermatitidis.

Wild-type, dematiaceous Wangiella dermatitidis (DMD 368) and melanin-deficient mutant (Mel 3) strains derived therefrom were compared for pathogenic and virulent effects in Swiss albino mice following intravenous infection. Parameters examined were mouse survival and central nervous system signs of infection, time-course cultures of fungus from brains, lungs, livers, spleens and kidneys, and histopathology of brains. Over a range of concentrations, DMD 368 produced 100% mortality while one Mel 3 strain, DMD 369, produced no mortality by 21 days after inoculation. However, in chronic infections with DMD 369, mice developed ataxia and torticollis. These signs of disease were indistinguishable from those produced by low concentrations of DMD 368. The brain was the most severely affected organ where both DMD 368 and 369 grew exponentially. Histological responses to the two strains appeared to be indistinguishable. However, the mutant appeared not to form the invasive hyphal forms of growth associated with the acute, fatal infections caused by the wild type. Thus, although the absence of melanin was associated with decreased mortality in mice, the chronic neurological signs of mouse phaeohyphomycosis appeared to be unrelated to melanin.

Animals↗
PubMed2000

Control of Virulence and Pathogenicity Genes of Ralstonia Solanacearum by an Elaborate Sensory Network.

Ralstonia solanacearum causes a lethal bacterial wilt disease of diverse plants. It invades the xylem vessels of roots and disseminates into the stem where it multiplies and wilts by excessive exopolysaccharide production. Many of its key extracytoplasmic virulence and pathogenicity factors are transcriptionally controlled by an extensive network of distinct, interacting signal transduction pathways. The core of this sensory network is the five-gene Phc system that regulates exopolysaccharide, cell-wall-degrading exoenzymes, and other factors in response to a self-produced signal molecule that monitors the pathogen's growth status and environment. Four additional environmentally responsive two-component systems work independently and with the Phc system to fine-tune virulence gene expression. Another critical system is Prh which transduces plant cell-derived signals through a six-gene cascade to activate deployment of the Type III secretion pathway encoded by the hrp pathogenicity genes. Here I summarize knowledge about the regulated targets, signal transduction mechanisms, and crosstalk between Phc, Prh, and other systems. I also provide insight into why R. solanacearum has evolved such a sophisticated sensory apparatus, and how it functions in disease.

LysR family↗
PubMed2004

[Genetic regulation of pathogenicity and virulence factors in bacteria Erwinia carotovora subsp. atroseptica: phenotypic characteristic of bacteria with the mutant kduD gene].

In contrast to the closely related bacteria Erwinia chrysanthemi, bacteria Erwinia carotovora subsp. atroseptica produce lower levels of main pathogenicity and virulence factors (pectate lyases, cellulases, and proteases) in the presence of pectins. This effect was shown to be connected with the accumulation of the intermediate product of intracellular degradation of these substances, 2,5-diketo-3-deoxygluconate (DK2). The presence of DK2 in the culture broth of mutant bacteria, connected to its export in the environment, was established. The production of pectate lyases, cellulases, and proteases is repressed by DK2 only at its high concentrations in the cultivation medium, whereas low concentrations of DK2 induce the production of virulence factors. Genes involved in the intracellular catabolism of pectin substances and induced by both low and high DK2 concentrations in the cultivation medium are not repressed by this metabolite.

Cellulase↗
PubMed1996

The curse of the pharaoh: the evolution of virulence in pathogens with long living propagules.

We used a mathematical model to evaluate the hypothesis that parasites and pathogens with long living propagules should evolve high levels of virulence, i.e. high rates of pathogen-induced host mortality. Our model shows that the optimal level of virulence is independent of the longevity of the propagules either: (i) if the density or the prevalence of infected hosts is in (or fluctuates around) equilibrium; or (ii) if the death rate of the infected host population is high compared with that of the propagules. The level of virulence that maximizes the parasite's fitness (Multhusian parameter) increases with increasing longevity of its propagules only if the host-parasite system has not reached equilibrium and the death rate of the propagules is high relative to that of the infected hosts. Therefore, for parasites that have recently invaded a susceptible host population, greater propagule longevity may initially favour higher virulence; but once the equilibrium is reached the optimal virulence is independent of propagule longevity.

Animals↗
PubMedDate not supplied

Virulence and pathogenicity of Helicobacter pylori.

H. pylori is a highly virulent organism as evidenced by its low infective dose and widespread high prevalence in human populations. Its virulence is achieved through its ability to survive in a moist environment and its massive urease production which allows it to survive in the acidic gastric juice long enough to colonize the gastric mucus. Gastric colonization is facilitated by cell wall associated lectins which permit the bacterium to bind to gastric mucus and the gastric epithelial cell. Once in this location, H. pylori produces several enzymes which may harm the gastric epithelium, particularly urease (through ammonia generation) and phospholipases A and C. H. pylori also weakens the gastric mucous layer by digesting its glycoproteins and lipids, making the mucus less hydrophobic and more water soluble. Helicobacter pylori attracts phagocytic cells, inducing both acute and chronic inflammation as well as an antibody response. Persistence of H. pylori in the mucosa may be enhanced by its cytotoxin and catalase production, by which it survives after phagocytosis by neutrophils.

Bacterial Toxins↗
PubMed2005

Systemic acquired tolerance to virulent bacterial pathogens in tomato.

Recent studies on the interactions between plants and pathogenic microorganisms indicate that the processes of disease symptom development and pathogen growth can be uncoupled. Thus, in many instances, the symptoms associated with disease represent an active host response to the presence of a pathogen. These host responses are frequently mediated by phytohormones. For example, ethylene and salicylic acid (SA) mediate symptom development but do not influence bacterial growth in the interaction between tomato (Lycopersicon esculentum) and virulent Xanthomonas campestris pv vesicatoria (Xcv). It is not apparent why extensive tissue death is integral to a defense response if it does not have the effect of limiting pathogen proliferation. One possible function for this hormone-mediated response is to induce a systemic defense response. We therefore assessed the systemic responses of tomato to Xcv. SA- and ethylene-deficient transgenic lines were used to investigate the roles of these phytohormones in systemic signaling. Virulent and avirulent Xcv did induce a systemic response as evidenced by expression of defense-associated pathogenesis-related genes in an ethylene- and SA-dependent manner. This systemic response reduced cell death but not bacterial growth during subsequent challenge with virulent Xcv. This systemic acquired tolerance (SAT) consists of reduced tissue damage in response to secondary challenge with a virulent pathogen with no effect upon pathogen growth. SAT was associated with a rapid ethylene and pathogenesis-related gene induction upon challenge. SAT was also induced by infection with Pseudomonas syringae pv tomato. These data show that SAT resembles systemic acquired resistance without inhibition of pathogen growth.

Bacteria↗
PubMed1996

Virulence and pathogenicity associated with diversity of Trypanosoma cruzi stocks and clones derived from Chagas' disease patients.

The intraspecific variation that has been described in Trypanosoma cruzi was examined in recent isolates from Chagas' disease patients, using behavioral and molecular markers for characterization of the parasite stocks and derived clones. We used these parasite populations to determine virulence and pathogenicity in vivo. The T.cruzi stocks mSLU142 (megaesophagus) and hSLU239 (heart disease) and the clones h1 and h2 induced very low parasitemias in BALB/c mice, whereas high parasitemias were obtained with clones m1, m2, m3, and m4. Clones m1-m4 also produced heart lesions of higher intensity than those observed in mice infected with the h1 and h2 clones. Furthermore, the heart lesions produced by all of these clones were significantly more intense than those seen in mice infected with either of the T. cruzi parental stocks. In addition, neither the kinetics of growth, doubling time, differentiation in axenic culture, zymodemes, nor DNA restriction length polymorphisms showed correlations with parasitemias and pathogenicity in mice. This study suggests that multiple biochemical and physiological markers are required to enable an association of clinical and pathologic manifestations of the disease with intrinsic characters of the T. cruzi populations.

Animals↗
PubMed1983

Pathogenic and virulence characterization of colonial mutants of Nocardia asteroides GUH-2.

The pathogenicities in mice (comparing LD50 determinations) of two mutant strains and one wild-type strain of Nocardia asteroides GUH-2, each possessing a colonial morphology distinct from the other, were compared at respective stages of growth. Despite the three strains' colinear growth curves and similar physiological properties, unique patterns of pathogenicity emerged for each strain upon analysis. Ultrastructural and fatty acid profiles of cultures at the various growth stages were monitored. The mutant strain SCII-A1 was consistently less virulent than the other strains of N. asteroides GUH-2 (SCII-P and SCII-C). Further, its fatty acid profiles as well as the shape and consistency of its colonies differed greatly from those of the wild-type strain. The fatty acid composition and the colonial morphology of strain SCII-C more closely resembled those of the parent, although its virulence was both greater than (before 28 h of growth) and less than the parent's depending upon the specific stage of growth. The comparative degrees of cellular fragmentation and complexity, as determined by scanning and transmission electron microscopy, were found to coincide with changes in relative degrees of pathogenicity.

Animals↗