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PubMed1990

Candida albicans strain delineation.

Candida albicans is a major opportunistic pathogen causing a wide spectrum of disease in human beings. Methods for strain delineation of this species to assess or predict virulence or to conduct epidemiologic or pathogenetic investigations have been developed. Although factors associated with virulence have been identified, there is no rapid system to quantitate them in a clinical laboratory. Therefore, many typing methods are based on variable phenotypic characteristics within this species including morphotyping, serotyping, antibiogram, resistogram typing, biotyping, biotyping based on commercial carbon assimilation patterns, enzyme profiles, sensitivity to yeast killer toxins, and typing based on protein variability. Phenotypically defined strains generally do not correlate with the pathogenic potential of a strain with the exception of morphotyping. However, these methods can be useful in epidemiologic investigations; for example, they have revealed that most individuals harbor one strain and that infections are frequently due to an endogenous strain. Problems with these methods usually relate to their discriminatory power. When this is maximized, reproducibility (especially between laboratories) suffers. Recently, methods based on differences in DNA structure (genotyping) for strain delineation have been developed, including electrophoretic karyotyping and restriction enzyme fragment length polymorphisms. The development of a computer-assisted data bank and analysis for these genotypic strain delineators will open investigations into the pathogenesis of this infection and permit epidemiologic studies previously not possible with this important human pathogen.

Bacterial Typing Techniques↗
PubMed1996

Cytokines in the serum and brain in mice infected with distinct species of Lyme disease Borrelia.

This study describes the detection of cytokines, interleukin-1 alpha (IL-1 alpha), tumor necrosis-factor alpha (TNF alpha) and interleukin-6 (IL-6) in the serum and brain homogenates of susceptible and resistant strains of mice infected with distinct species/strains of Borrelia. Significant elevation of inflammatory cytokines was found in the sera of susceptible C3H/ HeN mice but not in the sera of resistant BALB/c mice on days 7 and 45 after inoculation. Brain cytokines were observed in C3H/HeN mice infected with B. garinii and B. afzelii and the production was associated with the presence of spirochetes. B. japonica was the only exception in disease-susceptibility and cytokine production of mice. These results suggest that there are differences in pathogenic potential amongst Borrelia strains, and that the susceptible mice demonstrate a stronger cytokine response and greater frequency of recovery of Borrelia from the brain than do the resistant mice.

Animals↗
PubMed1998

[Candida spondylitis. Case report and review of the literature].

Candida species have emerged as important pathogens in human infection. Although a variety of deep-seated candidal infections have been reported, Candida spondylitis has rarely been described. One patient with candida tropicalis spondylitis L I and L II in combination with candida coxitis is presented, and the 31 adult cases with vertebral involvement previously reported are reviewed. Candida spondylitis is noted as a simultaneous occurrence or late manifestation of hematogenously disseminated candidiasis. Spondylitis may not be prevented by a course of Amphotericin B adequate to control the acute episode of disseminated candidiasis, particularly in immune suppressed patients. Spondylitis does not present as a postoperative wound infection. The insidious progression of infection, the nonspecificity of laboratory data, and the failure to recognise Candida as a potential pathogen may lead to diagnostic delay. Diagnosis can be made by either open biopsy or CT controlled needle aspiration. Successful therapeutic regimes have employed combinations of antifungal therapy (Amphotericin B or fluconazole) with radical surgical debridement. Ventral and facultatively dorsal instrumentation is required to stabilize the spine. It is anticipated that the spondylitis will become a more commonly recognised manifestation of hematogenously disseminated candidiasis. A increasing significance of candida species as etiologic agents of infection immune compromised humans has been recognised in the recent years. In those patients whom an antecedent Candida septicaemia was documented, a striking delay of 3.3 months was found between the septicaemia and the onset of symptoms as well as the time of diagnosis.

Adult↗
PubMed1992

Transplacentally transmitted autoimmune disorders of the fetus and newborn: pathogenic considerations.

Autoimmune diseases affect a significant number of women in their childbearing years. This group of disorders constitutes a heterogeneous spectrum with a common basis involving the presence of autoantibodies often of the IgG type. Transplacental transfer of autoantibodies is not uncommon, and autoantibodies can be readily demonstrated in newborn serum. Only a small proportion of infants with circulating autoantibodies exhibit clinical symptoms. The transient neonatal manifestations of maternal autoimmune disease disappear over a time course consistent with the catabolism of IgG, providing no permanent damage occurs. Thus the pathogenic role of transferred autoantibodies seems well established. However, maternal-autoantibody-mediated tissue damage appears to depend on factors other than the mere passage of the antibody to the fetal compartment. This review details putative factors that are likely to modulate the clinical expression of the fetal antigen-autoantibody reaction in offspring of mothers with autoimmune disorders. The importance of amount, type, and specificity of autoantibodies is described. The possible significance of fetal and maternal immunogenetics is briefly discussed, as well as the limited knowledge currently available on the fetal development of fetal antigenic sites at target organs. These and other as yet unidentified factors may help explain the rarity of clinical manifestations in infants exposed to potentially pathogenic maternal autoantibodies.

Autoimmune Diseases↗
PubMed2006

Complete sequence analysis of novel plasmids from emetic and periodontal Bacillus cereus isolates reveals a common evolutionary history among the B. cereus-group plasmids, including Bacillus anthracis pXO1.

The plasmids of the members of the Bacillus cereus sensu lato group of organisms are essential in defining the phenotypic traits associated with pathogenesis and ecology. For example, Bacillus anthracis contains two plasmids, pXO1 and pXO2, encoding toxin production and encapsulation, respectively, that define this species pathogenic potential, whereas the presence of a Bt toxin-encoding plasmid defines Bacillus thuringiensis isolates. In this study the plasmids from B. cereus isolates that produce emetic toxin or are linked to periodontal disease were sequenced and analyzed. Two periodontal isolates examined contained almost identical approximately 272-kb plasmids, named pPER272. The emetic toxin-producing isolate contained one approximately 270-kb plasmid, named pCER270, encoding the cereulide biosynthesis gene cluster. Comparative sequence analyses of these B. cereus plasmids revealed a high degree of sequence similarity to the B. anthracis pXO1 plasmid, especially in a putative replication region. These plasmids form a newly defined group of pXO1-like plasmids. However, these novel plasmids do not contain the pXO1 pathogenicity island, which in each instance is replaced by plasmid specific DNA. Plasmids pCER270 and pPER272 share regions that are not found in any other pXO1-like plasmids. Evolutionary studies suggest that these plasmids are more closely related to each other than to other identified B. cereus plasmids. Screening of a population of B. cereus group isolates revealed that pXO1-like plasmids are more often found in association with clinical isolates. This study demonstrates that the pXO1-like plasmids may define pathogenic B. cereus isolates in the same way that pXO1 and pXO2 define the B. anthracis species.

Amino Acid Sequence↗
PubMed2004

Detection and nucleotide sequencing of a DNA-packaging protein gene of equine gammaherpesviruses.

In previous studies, novel putative viral pathogens designated that asinine herpesvirus 4 (AsHV4) and asinine herpesvirus 5 (AsHV5) were associated with fatal interstitial pneumonia in donkeys (Equus asinus). Nucleotide sequence analysis of a portion of the DNA polymerase gene identified these putative pathogens as herpesviruses and possibly as members of the Gammaherpesvirinae subfamily. Although similar to equine herpesvirus 2 (EHV2) and equine herpesvirus 5 (EHV5), sequence diversity was observed among the detected viruses. In this study, novel sequence is reported for a DNA-packaging protein gene of EHV5 plus AsHV4, AsHV5, and a newly described putative pathogen herein designated asinine herpesvirus 6 (AsHV6). Phylogenetic analysis of these sequences suggested that the equine gammaherpesviruses may form a separate clade within the Gammaherpesvirinae subfamily. Based on the sequence of EHV2 and the novel sequences reported in this study, a PCR assay was developed to detect equine gammaherpesviruses. Products of the predicted size were produced after amplification of DNA from EHV2, EHV5, AsHV4, AsHV5, and AsHV6. This nonnested assay was shown to consistently amplify approximately 10 genomic copies of EHV2. Amplification products were not produced from DNA template of other alpha- and gammaherpesviruses. Because the role of gammaherpesviruses has not been well defined in equine disease, it is envisioned that a single, sensitive PCR assay to detect these potential pathogens will facilitate further assessment of their role in disease.

Amino Acid Sequence↗
PubMed1981

Murine lupus nephritis is accelerated by anti-glomerular basement membrane autoantibodies.

We have tested the effect of deposition of non-pathogenic amounts of induced anti-glomerular basement membrane (GBM) autoantibodies on the development of the spontaneous lupus nephritis of female (NZB x NZW) F1 (B x W) mice. Female and male B x W mice were immunized with rabbit renal tubular basement membrane in adjuvant at 2 months of age and their kidneys were examined 35 to 66 days later; control B x W mice were injected with adjuvant only or remained untreated. By immunofluorescent and histopathological criteria, only the 4-month-old female B x W mice with anti-GBM autoantibody deposits had an accelerated onset of lupus nephritis resembling the findings not seen until 6 to 8 months of age in unmanipulated mice. Thus potentially pathogenic amounts of immune complexes are present in young female B x W mice, but these do not deposit in glomeruli until much later in life. Evidently, the anti-GBM autoantibodies modified the glomerular milieu sufficiently to facilitate accelerated immune complex deposition.

Animals↗
PubMed1991

Interaction of a salivary mucin-secretory immunoglobulin A complex with mucosal pathogens.

This study examined the interaction of a human salivary low-molecular-weight mucin (MG2) with Staphylococcus aureus and Pseudomonas aeruginosa by using both solution-phase and solid-phase assays. In solution phase, MG2 in human submandibular-sublingual saliva (HSMSL) bound to the bacterial surface; however, the highly purified mucin isoforms (MG2a and MG2b) did not. Mucin binding appeared to be dependent on heterotypic complexing between MG2 and secretory immunoglobulin A (IgA), although other salivary molecules may also be involved. In contrast, in a solid-phase assay in which HSMSL, MG2-containing fractions with secretory IgA, and purified MG2 were immobilized onto a solid surface, there was minimal adherence of S. aureus. The collective results suggest that mucin binding to S. aureus and P. aeruginosa may be predicated on the formation of an MG2-secretory IgA complex. Such interactions may facilitate microbial clearance from the oral cavity and play an important role in preventing colonization of the oral cavity and the respiratory tract by potential pathogens.

Bacterial Adhesion↗
PubMed2002

Ochrobactrum anthropi bacteraemia in immunocompetent children.

Ochrobactrum anthropi is an emerging pathogen in immunocompromised patients but infections with the bacterium have very rarely been documented in normal hosts. We report the characteristics of O. anthropi bacteraemia in 11 immunocompetent children, aged 2 months to 7 y, hospitalized in a general hospital during a 5-y period. Children commonly presented with fever, non-specific respiratory or gastrointestinal manifestations, leukocytosis and neutrophilia and had a rapid recovery, even when they did not receive a specific treatment. In 10 cases positive blood cultures were obtained on admission and in all cases subsequent cultures were sterile. In conclusion, O. anthropi may cause bacteraemia in immunocompetent hosts, although further studies are required to clarify whether these isolates represent pseudobacteraemia or whether O. anthropi is a potential pathogen of low virulence.

Anti-Bacterial Agents↗
PubMed1998

Bone resorption caused by three periodontal pathogens in vivo in mice is mediated in part by prostaglandin.

Gingival inflammation, bacterial infection, alveolar bone destruction, and subsequent tooth loss are characteristic features of periodontal disease, but the precise mechanisms of bone loss are poorly understood. Most animal models of the disease require injury to gingival tissues or teeth, and the effects of microorganisms are thus complicated by host responses to tissue destruction. To determine whether three putative periodontal pathogens, Porphyromonas gingivalis, Campylobacter rectus, and Fusobacterium nucleatum, could cause localized bone resorption in vivo in the absence of tissue injury, we injected live or heat-killed preparations of these microorganisms into the subcutaneous tissues overlying the calvaria of normal mice once daily for 6 days and then examined the bones histologically. We found that all three microorganisms (both live and heat killed) stimulated bone resorption and that the strain of F. nucleatum used appeared to be the strongest inducer of osteoclast activity. Treatment of the mice concomitantly with indomethacin reduced but did not completely inhibit bone resorption by these microorganisms, suggesting that their effects were mediated, in part, by arachidonic acid metabolites (e.g., prostaglandins). Our findings indicate that these potential pathogens can stimulate bone resorption locally when placed beside a bone surface in vivo in the absence of prior tissue injury and support a role for them in the pathogenesis of bone loss around teeth in periodontitis.

Alveolar Bone Loss↗
PubMed1999

Relationship between bacterial flora in sputum and functional impairment in patients with acute exacerbations of COPD. Study Group of Bacterial Infection in COPD.

STUDY OBJECTIVES: To investigate the possible relationship between functional respiratory impairment measured by FEV1 and isolation of diverse pathogens in the sputum of patients with exacerbations of COPD. DESIGN: Multicenter, cross-sectional, epidemiologic study. SETTING: Pneumology units in six secondary or tertiary hospitals in Spain. PATIENTS: Ninety-one patients with acute exacerbation of COPD were included. INTERVENTIONS: A quantitative sputum culture was performed, and bacterial growth was considered significant only when the germ was isolated at concentrations > 10(6) cfu (> 10(5) for Streptococcus pneumoniae) in samples with < 10 epithelial cells and > 25 leukocytes per low magnification field (x 100). RESULTS: Germs isolated were the following: Haemophilus influenzae (20 cases; 22%), Pseudomonas aeruginosa (14 cases; 15%), S. pneumoniae (9 cases; 10%), Moraxella catarrhalis (8 cases; 9%), other gram-negative bacteria (7 cases; 7%), and non-potentially pathogenic microorganisms (non-PPMs; 33 cases; 36%). P. aeruginosa and H. influenzae were isolated more frequently among the patients with FEV1 < 50% than among those with FEV1 > 50% (p < 0.05). All patients with P. aeruginosa in sputum had FEV1 < 1,700 mL. FEV1 < 50% was associated with a very high risk of P. aeruginosa or H. influenzae isolation: the odds ratios (ORs) are 6.62 (95% confidence interval [CI], 1.2 to 123.6) and 6.85 (95% CI, 1.6 to 52.6), respectively. Furthermore, active tobacco smoking was associated with a high risk of H. influenzae isolation (OR, 8.1; 95% CI, 1.9 to 43.0). CONCLUSIONS: Patients with the greatest degree of functional impairment, as measured by their FEV1, presented a higher probability of having an isolation of P. aeruginosa or H. influenzae in significant concentrations in sputum during an exacerbation. The diagnostic yield of sputum in patients with an FEV1 > 50% was low, with a predominance of non-PPMs. Low FEV1 and active tobacco smoking are data that should be considered when establishing an empiric antibiotic treatment for exacerbated COPD.

Aged↗
PubMed1985

Comparative specificities of serum and synovial cell 19S IgM rheumatoid factors in rheumatoid arthritis.

Rheumatoid factor (RF) may play a role in sustaining the inflammatory events and tissue damage in rheumatoid arthritis (RA). However, many serum RF have greater specificity for rabbit IgG than for human IgG, thus raising questions about RF pathogenicity in RA. Serum RF also has specificity for human IgG subclasses 1, 2 and 4, but not for IgG3. The synovium is central to the pathology of RA; thus, RF made there may have greater pathogenicity than serum RF. We examined the specificity of 19S IgM RF in an RF plaque forming cell assay (RF-PFC) using RA synovial cells (RSC). We found that: (1) RSC produced greater numbers of RF-PFC/10(6) cells than did RA peripheral blood mononuclear cells (PBM); (2) RSC RF-PFC had greater specificity for human than for rabbit IgG compared to autologous serum RF; (3) RSC RF had significantly greater specificity for human IgG3 relative to autologous serum RF. In contrast, RSC RF and autologous serum RF had the same relative specificities for polyclonal human IgG, IgG1, IgG2, and IgG4. Thus, the specificity of much of the RF synthesized by RSC differed from serum RF. The potential pathogenic significance of these observations is discussed.

Animals↗
PubMed1990

The role of Escherichia coli haemolysin in the pathogenic synergy of colonic bacteria in subcutaneous abscess formation in mice.

The growth of nine species of colonic bacteria--Escherichia coli, Enterococcus faecalis, Bacteroides ovatus, Fusobacterium varium, Clostridium perfringens, Klebsiella pneumoniae, Proteus vulgaris, Staphylococcus aureus and Bifidobacterium adolescentis--was examined after concomitant injection to form experimental subcutaneous abscesses in mice. Injection of a mixture of c. 10(5) cfu of each of the first five strains (E. coli, Ent. faecalis, B. ovatis, F. varium and C. perfringens) resulted in abscess formation in all mice tested when the E. coli strain was haemolytic. E. coli and B. ovatus multiplied and reached a maximum population of c. 10(8) cfu/abscess. When non-haemolytic E. coli was used, injection of greater than or equal to 10(7) cfu was required for abscess formation. The inclusion of partially purified E. coli haemolysin (125 HU50) with c. 10(5) cfu of bacteria including non-haemolytic E. coli resulted in abscess formation in most mice tested. These results indicate that E. coli haemolysin is one factor that may potentiate pathogenic synergy among colonic bacteria especially between E. coli and B. ovatus, during abscess formation.

Abscess↗
PubMed1988

Inapparent Streptococcus pneumoniae type 35 infections in commercial rats and mice.

Streptococcus pneumoniae was isolated from specific-pathogen-free rodents in two rooms at a commercial breeding facility during vendor surveillance testing. In a survey of 274 animals from the two rooms over a period of 7 months, capsular serotype 35 S. pneumoniae was isolated from the upper respiratory tracts of 11% (9 of 82) of C57BL/6 mice in room A and 14% (10 of 72) of F344 rats in room B, but not from WKY rats, BALB/c mice or DBA/2 mice from room A. In both C57BL/6 mice and F344 rats, older rodents had higher colonization frequencies. Nasal lavage cultures gave the best results in identifying colonized rodents. No clinical illness or microscopic lesions were associated with pneumococcal colonization in rats or mice, and no other evidence of potential pathogen infection was found except for positive serologic tests for mouse rotavirus in mice. This is the first report of natural pneumococcal infection in mice, and the first report of type 35 S. pneumoniae infection in rodents. The findings support an earlier observation that pneumococcal infections in rat colonies tend to be monotypic and suggest that the same may be true in mice.

Animals↗
PubMed2002

The role of leukocytes following cerebral ischemia: pathogenic variable or bystander reaction to emerging infarct?

Data accumulated over the last 10 years have led to the popular hypothesis that neutrophils and other inflammatory cells play a prominent role in the neuropathology of cerebral ischemia. This hypothesis was derived from a large number of studies involving three general observations: (1) leukocytes, particularly neutrophils, are present in ischemic tissue at the approximate time that substantial neuronal death occurs; (2) neutropenia is sometimes associated with reduced ischemic damage; and (3) treatments that prevent leukocyte vascular adhesion and extravasation into the brain parenchyma can be neuroprotective. This review reexamines the literature to ascertain its support for a pathogenic role for neutrophils in ischemia-induced neuronal loss. To accomplish this goal, we employed several logical theorems of "cause-effect" relationships, as they pertain to leukocytes and ischemic brain damage. Since the majority of studies focused on neutrophils as the most likely pathogenic inflammatory cell, this review necessarily does so here. We reasoned that if neutrophils play an important pathogenic (i.e., cause-effect) role in the neuronal damage that follows a stroke, then one should expect to find clear evidence that: (1) neutrophils invade the ischemic area prior to terminal stage infarction, (2) greater numbers of early appearing neutrophils are accompanied by evidence of greater neuronal loss, and (3) dose-related inhibition of neutrophil trafficking or activity produces a corresponding decrease in the degree of brain damage following ischemia. This review of the literature reveals that the existing evidence does not readily support any of these predictions and that, therefore, it consistently falls short of establishing a clear cause-effect relationship between leukocyte recruitment and the pathogenesis of ischemia. While the available evidence does not necessarily rule out a potential pathogenic role of neutrophils and other leukocytes, it nevertheless does expose serious weaknesses in the existing studies intended to support that hypothesis. For this reason we also offer suggestions for additional experiments and the inclusion of control groups that, in the future, might provide more effective or conclusive tests of the hypothesis.

Animals↗
PubMed2003

How killed enterobacterial cultures can activate living organisms to resist lethal agents or conditions.

A major aim in many areas of microbiology is to ensure sterility, and even where this is impossible, to reduce the number of viable organisms occurring in particular environments to an absolute minimum. This applies in the aquatic environment, where e.g. water treatment must ensure as complete absence of viable microbes as possible. It is also crucial in food processing and production; many food constituents contain appreciable numbers of viable organisms, even potential pathogens, and the number must be greatly reduced and in many situations, the presence of viable organisms totally abolished. Cleaning of food production components and surfaces must also kill associated microbes. In domestic, hospital and commercial situations, similar disinfection is critical. Ultimately, the aim is to ensure, if possible, sterility, with the assurance that microbial problems cannot occur if organisms are absent. Additionally, however, it has been implicitly assumed that killed organisms and even killed cultures cannot (except in minor and trivial ways) influence the behaviour of living organisms that later enter the environment. The work reviewed here challenges that view and in fact disproves it. The findings described show that killed enterobacterial cultures, which prior to killing had phenotypically gained the ability to resist potentially lethal stresses, can pass on such ability to living organisms that later enter their environment i.e. that such killed cultures can convey a baleful legacy to living ones. This phenomenon is so widespread that it is clear that it has significance for enterobacterial survival in natural waters, in foods and in food production, in the domestic, commercial and hospital situation, and in the animal and human body. In fact, in this last area, the likely effect of killed cultures appears to be of appreciable public health importance. Here, the ability of appropriate killed cultures to transfer tolerance to acidity, alkalinity and thermal stress is described, as well as their ability to pass on sensitisation to acid and alkali. Other work reviewed suggests that killed cultures can almost certainly transfer the ability to tolerate hydrogen peroxide, ultraviolet irradiation and metal ions. The serious implications of this phenomenon are further emphasised by the fact that numerous killing methods produce cultures effective in tolerance response transfer. All the evidence suggests that it is extracellular components (extracellular sensing components, ESCs, and extracellular induction components, EICs), in the killed cultures which are involved in stress response transfer, and that the actual stress response induction process depends on interaction of living organisms with EICs from the killed cultures. It is of note that ESCs and EICs survive in killed cultures because of their extreme resistance to irreversible inactivation by lethal levels of stressing agents and conditions. This is in contrast to the fact that EC activation, namely the conversion of ESC to EIC occurs on exposure to very low levels of stressors. Not only is this the case, but in fact high levels of stressors (e.g. those that kill organisms) generally fail to convert ESC to EIC.

Bacterial Physiological Phenomena↗
PubMed1992

Enteropathogenicity of non-toxigenic Vibrio cholerae O1 for adult mice.

The enteropathogenic potential of 32 Vibrio cholerae O1 isolates that do not produce cholera toxin was examined in the orally inoculated, sealed adult mouse model. Live cultures (2 x 10(10) cfu/ml) of 7/16 clinical and 6/16 environmental isolates produced a positive intestinal fluid accumulation (FA) ratio that reached near maximum at approximately 5 h post-inoculation. Colony hybridization did not detect genes for cholera toxin, Escherichia coli heat-labile and heat-stable toxins, or shiga-like toxins. FA activity did not correlate precisely with cytotoxic activities on Chinese hamster ovary (28/32 positive), Vero (29/32) or HeLa (25/32) cells. Certain clinical and environmental isolates of non-toxigenic V. cholerae O1 appear to be enteropathogenic for the mouse, providing evidence that they may have pathogenic potential for humans through an as yet undefined mechanism(s).

Animals↗
PubMed1984

Rebound and overshoot after plasma exchange in humans.

On the basis of animal experiments, some authors recommend a routine combination of therapeutic plasma exchange in patients with immunologically mediated disorders, such as autoimmune and immune complex diseases, with administration of cytotoxic drugs to prevent overshoot in plasma levels of pathogenic components after plasma exchange. We examined one healthy volunteer, seven patients with nonimmunologic diseases, and seven patients with immunologically mediated disorders (six with non-organ specific and one with organ-specific autoantibodies) to test whether plasma exchange is succeeded by an overshoot in levels of immunoglobulins, isohemagglutinins, autoantibodies, and antibodies after booster immunization with diphtheria and tetanus toxoid combined with poliomyelitis vaccine. Our data indicate that overshoot is not a generally occurring phenomenon in humans. We also confirmed the capability of corticosteroids, administered immediately after a period of plasma exchange, to reduce autoantibody levels. We found no arguments to support the suggestions in the literature that plasma exchange be combined with cytotoxic drugs in treatment of immunologically mediated diseases to prevent stimulation of potentially pathogenic components such as autoantibodies.

Adolescent↗