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PubMed2000

Molecular physiology and pathophysiology of tight junctions V. assault of the tight junction by enteric pathogens.

Studies of the impact of enteric pathogens and their virulence factors on the proteins comprising the tight junction and zonula adherens offer a novel approach to dissection of tight junctional complex regulation. Most studies to date provide only tantalizing clues that select pathogens may indeed assault the tight junctional complex. Information on critical human pathogens such as Campylobacter jejuni and Shigella and Salmonella subspecies is lacking. Mechanistic studies are currently sparse, but available results on pathogenic Escherichia coli and specific virulence factors such as the Rho-modifying and protease bacterial toxins indicate four major mechanisms by which these pathogens may act: 1) direct cleavage of tight junctional structural proteins; 2) modification of the actin cytoskeleton; 3) activation of cellular signal transduction; and 4) triggering transmigration of polymorphonuclear cells across the epithelial cell barrier. New therapeutics may evolve from detailed studies of these pathogens and the cellular processes and proteins they disrupt.

Animals↗

PubMed2026

Bayesian Integration of Tumor Mutational Signatures and Somatic Features Refines Pathogenicity Assessment of Germline Mismatch Repair Variants.

Variants of uncertain significance (VUS) in mismatch repair (MMR) genes represent a persistent bottleneck in germline interpretation for Lynch syndrome, creating a critical opportunity to leverage tumor biology to refine pathogenicity assessment. Although tumor features such as microsatellite instability (MSI) and immunohistochemistry (IHC) are routinely evaluated, they are typically interpreted separately from germline classification, and their quantitative contribution within ACMG/AMP frameworks remains poorly defined. We therefore analyzed paired germline and tumor sequencing data from 1110 tumors across 1073 patients with colorectal or endometrial cancer to determine whether mismatch repair-deficient (MMR-d) mutational signatures can be quantitatively integrated into Bayesian germline variant interpretation. Using COSMIC single-base substitution signatures, tumors were classified as MMR-d or MMR proficient, and an empirically derived likelihood ratio (LR) quantified the association between MMR-d signatures and pathogenic germline MMR variants. The presence of an MMR-d signature increased the likelihood of an underlying pathogenic germline MMR variant approximately eightfold (LR ≈ 8; log10 LR ≈ 0.90), whereas its absence provided moderate-to-strong benign evidence (LR ≈ 0.156; log10 LR ≈ -0.81). Applying this integrative framework to 45 germline MMR VUS, joint modeling of tumor mutational signatures with additional somatic and variant-level evidence resulted in clinically significant reclassification of 38 (84.4%) variants, including three reclassified as pathogenic or likely pathogenic and 35 as likely benign. A total of 16 downgraded variants were independently downgraded by Invitae. These findings demonstrate that tumor mutational signatures can be formally incorporated into Bayesian germline interpretation, transforming tumor data into quantitative pathogenicity evidence and offering a principled strategy to reduce VUS burden in hereditary cancer genetics.

Humans↗

PubMed2001

Prospective study of pathogen burden and risk of myocardial infarction or death.

BACKGROUND: We previously demonstrated that the risk of coronary artery disease (CAD) increased in relation to the number of pathogens (the "pathogen burden") in a cross-sectional study. In the present prospective study with a different patient cohort, we evaluated the effect of pathogen burden on the risk of myocardial infarction (MI) or death among CAD patients. METHODS AND RESULTS: IgG antibodies to cytomegalovirus (CMV), hepatitis A virus (HAV), herpes simplex virus type 1 (HSV1), HSV type 2 (HSV2), Chlamydia pneumoniae and Helicobacter pylori, and C-reactive protein (CRP) levels were tested in baseline blood samples from 890 patients who had significant CAD on angiography. The mean follow-up period was 3 years. The baseline prevalence of antibodies directed against CMV, HAV, HSV1, or HSV2, but not C pneumoniae and H pylori, was significantly higher among patients who subsequently developed MI or death than among control subjects. After adjustment for traditional risk factors, number of diseased vessels, and clinical presentation, relative hazards (95% confidence limits) for MI or death were 2.0 (1. 4 to 3.2) for CMV, 1.6 (1.1 to 2.3) for HAV, and 1.5 (1.0 to 2.2) for HSV2. Increasing pathogen burden was significantly associated with increasing risk of MI or death in a dose-response fashion. Adjusted relative hazards of MI or death associated with pathogen burden were significant among individuals with low or high CRP levels. CONCLUSIONS: The results suggest that infection plays an important role in incident MI or death and that the risk posed by infection is independently related to the pathogen burden.

Adult↗

PubMed2006

In vitro pathogenicity of Acanthamoeba is associated with the expression of the mannose-binding protein.

PURPOSE: To determine whether the expression of Acanthamoeba mannose-binding protein (MBP) is associated with the pathogenicity of the parasite in vitro. METHODS: Both active trophozoites and dormant cysts of a pathogenic strain of A. castellanii were analyzed for their ability to bind to corneal epithelium, express MBP, and produce a cytopathic effect (CPE) on host cells. In addition, host cell binding, CPE-inducing ability, and MBP expression pattern of trophozoites of four different isolates of Acanthamoeba with various degrees of in vitro pathogenicity were analyzed. Binding assays were performed with radiolabeled parasites; CPE assays were performed with rabbit corneal epithelial cells as host cells; and the expression of MBP was detected by affinity chromatography of parasite extracts on mannose affinity columns and by immunohistochemical and Western blot analyses. RESULTS: Trophozoites of A. castellanii bound avidly to corneal epithelial cells in a mannose-inhibitable manner, whereas cysts exhibited little binding. The lack of binding of the cysts to host cells was associated with the downregulation of MBP, along with the concomitant loss of CPE. Analysis of trophozoites of five different species of Acanthamoeba exhibiting various degrees of pathogenic potential revealed that the ability of parasites to bind to host cells and produce CPE is directly correlated with the expression of the MBP. Acanthamoeba strains that bound avidly to host cells and produced potent CPE, robustly expressed MBP. In contrast, parasite strains that produced only weak CPE, expressed markedly reduced levels of MBP. CONCLUSIONS: The data demonstrating that the pathogenic potential of Acanthamoeba directly correlates with the expression level of the MBP in conjunction with our published studies showing that Acanthamoeba MBP is a major virulence protein suggest that the amoeba lectin has the potential to serve as a marker of pathogenicity.

Acanthamoeba↗

PubMed1999

Pathogenic Escherichia coli increase Cl- secretion from intestinal epithelia by upregulating galanin-1 receptor expression.

Galanin is widely distributed in enteric nerve terminals lining the human gastrointestinal (GI) tract. We have shown previously that galanin-1 receptors (Gal1-R) are expressed by epithelial cells lining the human GI tract, and upon activation cause Cl- secretion. Because expression of this receptor is transcriptionally regulated by nuclear factor-kappa B (NF-kappa B), which is activated by enteric pathogens as a part of the host epithelial response to infection, we investigated whether such bacterial pathogens could directly increase Gal1-R expression in the T84-cell model system. Pathogenic Escherichia coli, but not nonpathogenic E. coli, activate a p50/p65 NF-kappa B complex that binds to oligonucleotides corresponding to a recognition site located within the 5' flanking region of the human GAL1R gene. Pathogenic E. coli, but not normal commensal organisms, increase Gal1-R mRNA synthesis and [(125)I]galanin binding sites. Whereas galanin increases short-circuit current (Isc) approximately 5-fold in uninfected T84 cells, exposure to pathogenic, but not nonpathogenic, E. coli results in galanin increasing Isc approximately 20-fold. To confirm the validity of these in vitro observations, we also studied C57BL/6J mice infected with enterohemorrhagic E. coli (EHEC) by gavage. Infection caused a progressive increase in both NF-kappa B activation and Gal1-R expression, with maximal levels of both observed 3 days after gavage. Ussing chamber studies revealed that colons infected with EHEC, but not those exposed to normal colonic flora, markedly increased Isc in response to galanin. These data indicate that pathogen-induced increases in Gal1-R expression by epithelial cells lining the colon may represent a novel unifying pathway responsible for at least a portion of the excessive fluid secretion observed during infectious diarrhea.

Animals↗

PubMedDate not supplied

Prevalence of pathogenic Acanthamoeba (Protozoa:Amoebidae) in the atmosphere of the city of San Luis Potosi, Mexico.

Several species of pathogenic Acanthamoeba cause infections to humans, but amoebic keratitis is more frequently found than any other due to the increasing number of contact lens wearers in the world. Cysts and trophozoites of these amebas are airborne and may pollute water from the air. We investigated the proportion of pathogenic Acanthamoeba from the atmosphere of the city of San Luis Potosi. Samples were taken by the impinger method, every month during one year. We isolated 23 strains of Acanthamoeba, 61% of them were non-pathogenic, 31% were non-pathogenic with invasive capacity and 8% were pathogenic to mice. Almost 40% of these strains represent danger of infections to humans. The isolations were more abundant during the dry season in the south (urban) and west (suburban) stations, which means that the sanitary conditions around stands may enhance the proportion of pathogenic strains in the surroundings.

Acanthamoeba↗

PubMed2005

[Pathogenic factors of vibrios with special emphasis on Vibrio vulnificus].

Bacteria of the genus Vibrio are normal habitants of the aquatic environment and play roles for biocontrole of aquatic ecosystem, but some species are believed to be human pathogens. These species can be classified into two groups according to the types of diseases they cause: the gastrointestinal infections and the extraintestinal infections. The pathogenic species produce various pathogenic factors including enterotoxin, hemolysin, cytotoxin, protease, siderophore, adhesive factor, and hemagglutinin. We studied various pathogenic factors of vibrios with special emphasis on protease and hemolysin of V. vulnificus. V. vulnificus is now recognized as being among the most rapidly fatal of human pathogens, although the infection is appeared in patients having underlying disease(s) such as liver dysfunction, alcoholic cirrhosis or haemochromatosis. V. vulnificus protease (VVP) is thought to be a major toxic factor causing skin damage in the patients having septicemia. VVP is a metalloprotease and degrades a number of biologically important proteins including elastin, fibrinogen, and plasma proteinase inhibitors of complement components. VVP causes skin damages through activation of the Factor XII-plasma kallikrein-kinin cascade and/or exocytotic histamine release from mast cells, and a haemorrhagic lesion through digestion of the vascular basement membrane. Thus, the protease is the most probable candidate for tissue damage and bacterial invasion during an infection. Pathogenic roles and functional mechanism of other factors including hemolysins of V. vulnificus and V. mimicus are also shown in this review article.

Animals↗

PubMed2006

The malarial host-targeting signal is conserved in the Irish potato famine pathogen.

Animal and plant eukaryotic pathogens, such as the human malaria parasite Plasmodium falciparum and the potato late blight agent Phytophthora infestans, are widely divergent eukaryotic microbes. Yet they both produce secretory virulence and pathogenic proteins that alter host cell functions. In P. falciparum, export of parasite proteins to the host erythrocyte is mediated by leader sequences shown to contain a host-targeting (HT) motif centered on an RxLx (E, D, or Q) core: this motif appears to signify a major pathogenic export pathway with hundreds of putative effectors. Here we show that a secretory protein of P. infestans, which is perceived by plant disease resistance proteins and induces hypersensitive plant cell death, contains a leader sequence that is equivalent to the Plasmodium HT-leader in its ability to export fusion of green fluorescent protein (GFP) from the P. falciparum parasite to the host erythrocyte. This export is dependent on an RxLR sequence conserved in P. infestans leaders, as well as in leaders of all ten secretory oomycete proteins shown to function inside plant cells. The RxLR motif is also detected in hundreds of secretory proteins of P. infestans, Phytophthora sojae, and Phytophthora ramorum and has high value in predicting host-targeted leaders. A consensus motif further reveals E/D residues enriched within approximately 25 amino acids downstream of the RxLR, which are also needed for export. Together the data suggest that in these plant pathogenic oomycetes, a consensus HT motif may reside in an extended sequence of approximately 25-30 amino acids, rather than in a short linear sequence. Evidence is presented that although the consensus is much shorter in P. falciparum, information sufficient for vacuolar export is contained in a region of approximately 30 amino acids, which includes sequences flanking the HT core. Finally, positional conservation between Phytophthora RxLR and P. falciparum RxLx (E, D, Q) is consistent with the idea that the context of their presentation is constrained. These studies provide the first evidence to our knowledge that eukaryotic microbes share equivalent pathogenic HT signals and thus conserved mechanisms to access host cells across plant and animal kingdoms that may present unique targets for prophylaxis across divergent pathogens.

Amino Acid Motifs↗

PubMed2002

Threat of foreign arthropod-borne pathogens to livestock in the United States.

There are many exotic animal pathogens throughout the world that, if introduced into the United States. could have a significant detrimental impact on the health of livestock, agricultural economy, the environment, and public health. Many of these pathogens are arthropod-borne and potential vectors are readily available in the United States. A number of these arthropod-borne pathogens are discussed here as examples that illustrate the potential risk and the consequences of inadvertent introductions. Several International agencies have a role in global surveillance and in controlling animal diseases should they begin to expand their range. The risk to the United States is considerable. We propose that the United States invest in the improved infrastructure needed to reduce the risk of foreign arthropod-borne pathogens. Current U.S. programs focus on the exclusion of pathogens through regulation of animal movements and products, surveillance, especially trained animal disease diagnosticians, research support, international cooperation and, should pathogens enter our country, the resources for their prompt eradication. We suggest that the United States needs to develop a comprehensive, updated strategic plan to assess all aspects of current and future requirements, objectives, and resources needed to protect its national interests.

African Swine Fever Virus↗

PubMedDate not supplied

Pathogenicity of embryo-adapted serotype 2 OH strain of infectious bursal disease virus in chickens and turkeys.

The pathogenicity of serotype 2 OH strain of infectious bursal disease virus (IBDV) to specific-pathogen-free (SPF) chicken embryos and 2-wk-old SPF chickens and turkey poults was investigated. The virus was pathogenic for chicken embryos after five passages as evidenced by pathologic changes in inoculated embryos. The embryo-adapted virus was not pathogenic for 2-wk-old SPF chickens and turkey poults as indicated by lack of clinical signs, gross or microscopic lesions in the bursa of Fabricius of inoculated birds. Bursa-to-body-weight ratios of the inoculated chickens and turkey poults were not significantly different from those of uninoculated controls. Virus-neutralizing antibodies to serotype 2 IBDV were detected in inoculated chickens and turkeys. Results of this study indicated that the embryo-adapted serotype 2 OH IBDV isolate that is pathogenic for chicken embryos is infectious but not pathogenic in chickens and turkeys.

Animals↗

PubMed2006

Occurrence of pathogenicity island I(APEC-O1) genes among Escherichia coli implicated in avian colibacillosis.

Colibacillosis caused by avian pathogenic Escherichia coli (APEC) is a leading cause of economic loss to the poultry industry worldwide. The ability of APEC to cause disease is determined by certain virulence markers, some of which are located on pathogenicity islands (PAls). We recently described one such PAI in an APEC O1:K1 strain (APEC-O1). This PAI, termed PAI I(APEC-O1), carries the genes of the pap operon, a region similar to the tia invasion determinant of enterotoxigenic E coli; ireA, a gene that encodes an iron-responsive element; and a novel 1.5-kb region, ORF 54. Here, the occurrence of six selected loci of PAI I(APEC-O1) (papA, papC, papG, ireA, tia, and ORF 54) among APEC and fecal E. coli strains from apparently healthy chickens (avian commensal E. coli) was determined using polymerase chain reaction (PCR) techniques. None of the commensal E. coli was positive for all six traits, whereas 7.2% of the APEC isolates were positive for all the traits. Although there was no significant difference in the occurrence of ORF 54 among APEC and commensal E. coli, tia, ireA, papC, and papG genes were predominantly present in APEC rather than in avian commensal E. coli. papA was detected in only 6.3% of APEC, perhaps because of the presence of allelic variants of the gene. Additionally, the presence of all six traits was tested with PCR in APEC isolates collected in the 1980s, and these results were compared with those obtained with the APEC isolated in the 1990s. There was no significant difference in the occurrence of tia, ireA, papC, papG, and ORF 54 between APEC isolates collected during the different decades. However, papA was more frequently present in APEC from the 1980s than it was in APEC from the 1990s. Phylogenetic group of an isolate did not correlate with pathogenicity or the presence of PAI traits, except that more APEC of the low-pathogenicity group belonged to the phylogenetic group B1. However, PAI traits occurred more frequently in isolates belonging to the intermediate- and high-pathogenicity groups than in isolates of low pathogenicity.

Animals↗

PubMed2002

Interactions of oral pathogens with toll-like receptors: possible role in atherosclerosis.

Toll-like receptors (TLR) function as important signal transducers that mediate innate immune and inflammatory responses to pathogens through pattern recognition of virulence molecules. Although TLRs mediate protection against infection, it is also likely that they may have a pathophysiologic role in certain inflammatory diseases, such as atherosclerosis. In atherosclerotic lesions, endothelial cells and macrophages have been shown to upregulate TLR expression and may respond to TLR agonists of microbial origin, resulting in detrimental inflammatory reactions. Some of these potential TLR-activating virulence factors may be of oral origin. The detection in atherosclerotic plaques of DNA specific for Porphyromonas gingivalis and other periodontal pathogens suggests that these pathogens disseminate into the systemic circulation and localize in atheromas. The potential of periodontal and some other oral pathogens to activate TLRs in vivo is suggested by findings from cell culture experiments on interactions of selected virulence protein adhesins with TLRs and their coreceptors. Specifically, we have shown that proinflammatory cytokine induction by P. gingivalis fimbriae was inhibited by monoclonal antibodies to TLR2, TLR4, CD14, and beta2 integrins, but not by immunoglobulin isotype controls. Cytokine induction by Bacteroides forsythus protein A depended heavily on CD14 and TLR2. We also found that the ability of Streptococcus mutans protein AgI/II to stimulate cytokine release was partially dependent on CD14 and TLR4. Moreover, P. gingivalis fimbriae induced TLR-dependent activation of nuclear factor-kappaB and upregulation of costimulatory molecules in monocytic cells. These proinflammatory activities have been implicated in the pathogenesis of periodontitis, and similar inflammatory mechanisms could potentially operate in atherosclerosis. Studies by other groups have shown that P. gingivalis is capable of stimulating low-density lipoprotein oxidation, foam cell formation, and rupture of atherosclerotic plaque through induction of matrix metalloproteinases. Interestingly, at least some of these activities can be induced by TLR agonists (lipopolysaccharide and heat-shock protein-60) from Chlamydia pneumoniae, a major risk factor in atherosclerosis. Future research in animal models and in vitro cellular systems with defined mutations in TLRs may implicate TLR participation in oral pathogen-mediated atherosclerotic processes, thereby providing a mechanistic basis for the epidemiological findings linking oral pathogens to atherosclerotic disease.

Arteriosclerosis↗

PubMed2000

Highly pathogenic avian influenza.

Highly pathogenic (HP) avian influenza (AI) (HPAI) is an extremely contagious, multi-organ systemic disease of poultry leading to high mortality, and caused by some H5 and H7 subtypes of type A influenza virus, family Orthomyxoviridae. However, most AI virus strains are mildly pathogenic (MP) and produce either subclinical infections or respiratory and/or reproductive diseases in a variety of domestic and wild bird species. Highly pathogenic avian influenza is a List A disease of the Office International des Epizooties, while MPAI is neither a List A nor List B disease. Eighteen outbreaks of HPAI have been documented since the identification of AI virus as the cause of fowl plague in 1955. Mildly pathogenic avian influenza viruses are maintained in wild aquatic bird reservoirs, occasionally crossing over to domestic poultry and causing outbreaks of mild disease. Highly pathogenic avian influenza viruses do not have a recognised wild bird reservoir, but can occasionally be isolated from wild birds during outbreaks in domestic poultry. Highly pathogenic avian influenza viruses have been documented to arise from MPAI viruses through mutations in the haemagglutinin surface protein. Prevention of exposure to the virus and eradication are the accepted methods for dealing with HPAI. Control programmes, which imply allowing a low incidence of infection, are not an acceptable method for managing HPAI, but have been used during some outbreaks of MPAI. The components of a strategy to deal with MPAI or HPAI include surveillance and diagnosis, biosecurity, education, quarantine and depopulation. Vaccination has been used in some control and eradication programmes for AI.

Animals↗

PubMed2003

Potential pathogens in feces from unweaned llamas and alpacas with diarrhea.

OBJECTIVE: To identify potential pathogens in feces from llama and alpaca crias with diarrhea. DESIGN: Prospective observational study. ANIMALS: 45 unweaned crias with diarrhea. PROCEDURE: Fecal samples were evaluated for Eimeria spp, Giardia spp, Cryptosporidium spp, enteric viruses, and Salmonella spp. A questionnaire yielded information concerning herd management and presence of other affected camelids. RESULTS: 28 crias were < or = 31 days old, 11 were 32 to 62 days old, and 6 were 63 to 210 days old. Potential pathogens were isolated from feces from 32 of the 45 crias. A total of 39 potential pathogens were obtained, including coronavirus (n = 19 crias; 42%), Giardia spp (8; 18%), Eimeria spp (6; 13%), Cryptosporidium spp (4; 9%), rotavirus (1; 2%), and nematode ova (1; 2%). Salmonella spp were not isolated. Most crias from which potential pathogens were isolated were identified during outbreaks of diarrhea involving other camelids, although only coronavirus was isolated from crias identified during outbreaks involving adult camelids. Coronavirus was detected throughout the year, whereas protozoa were most commonly isolated during the fall and winter. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that a variety of potential pathogens may be isolated from young crias with diarrhea. Many crias shed coronavirus, which may also have been affecting older camelids. Protozoa were isolated most often during wetter months, suggesting that crias born during these months may have greater exposure to protozoal pathogens.

Animals↗

PubMed2005

Inhibition of Toll Like Receptor immune responses by microbial pathogens.

Toll Like Receptors (TLRs) are pathogen recognition receptors (PRRs) that respond to specific pathogen associated molecular patterns (PAMPs) during microbial invasion. After TLR stimulation a series of cellular responses initiate an inflammatory response and influence specific adaptive immunity that ultimately destroy the pathogen. But the immune response is not always able to control the infection. Pathogens have developed mechanisms to overcome and evade distinct arms of vertebrate immunity. Many of these strategies have been extensively described, but with the recent discovery of TLRs additional means to manipulate the innate immune response are currently being studied. Pathogens generally inhibit TLR mediated immunity by either blocking signals that stimulate further host defense mechanisms or by down-regulating their expression. These inhibitory mechanisms have been mainly elucidated in bacterial systems, whereas in other microorganisms they remain to be identified. Here the strategies that pathogenic microbes use to subvert TLR mediated immune responses are reviewed.

Bacterial Infections↗

PubMedDate not supplied

Occurrence of middle ear pathogens in the nasopharynx of young individuals. A quantitative study in four age groups.

Colonization of middle ear pathogens (S. pneumoniae, H. influenzae and B. catarrhalis), potential pathogens (S. aureus and coagulase-negative staphylococci) and non-pathogens was determined quantitatively on the posterior wall of the nasopharynx (NPH) of children (four age groups: under 2 years, 2-5 years, 6-10 years and 11-15 years). None of the 90 individuals examined was suffering at the time of bacterial sampling from acute otitis media (AOM), sinusitis, or tonsillitis. All individuals under 2 years of age harboured middle ear pathogens in the NPH, but only 40% of the individuals of the oldest age group (p less than 0.001). Furthermore, in the youngest group, 57% of the cases had pathogens in the NPH, which completely dominated the bacterial flora, i.e. constituted more than 90% of the total bacterial count when calculated as CFU/cm2. The corresponding count in the oldest age group was only 20% (p less than 0.01). One important reason for the high incidence of AOM among young children in particular seems to be the noticeable accumulation of middle ear pathogens in huge quantities in the NPH in this age group.

Adolescent↗

PubMed1989

Direct and indirect pathogenicity of beta-lactamase-producing bacteria in mixed infections in children.

The recent emergence of numerous aerobic and anaerobic beta-lactamase-producing bacterial strains has been associated with an increase in the failure rate of penicillins in the therapy of infection caused by these organisms. These include respiratory tract, skin of soft tissue, female genital tract, intra-abdominal, and other miscellaneous infections. The important aerobic beta-lactamase-producing bacteria (BLPB) include Staphylococcus aureus, Branhamella catarrhalis, Haemophilus sp., Neisseria gonorrhoeae, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Legionella sp. The anaerobic BLPB are all Bacteroidiaceae and include Bacteroides fragilis group, B. melaninogenicus group, B. oralis, B. oris-buccae, and Fusobacterium sp. Laboratory, animal, and clinical studies that support the indirect pathogenicity of these organisms and the distribution of these BLPB in various infections are reviewed. BLPB may not only have a direct pathogenic role in causing the infection, but also an indirect pathogenic role. The indirect pathogenicity of these organisms is apparent through their ability not only to survive penicillin therapy, but also to protect penicillin-susceptible pathogens from that drug. These direct and indirect virulence characteristics of aerobic and anaerobic BLPB require the administration of appropriate antimicrobial therapy directed against all pathogens in mixed infections.

Bacteria↗

PubMed2006

A survey of foodborne pathogens in bulk tank milk and raw milk consumption among farm families in pennsylvania.

A 2-part study was conducted to determine the risk of exposure to human pathogens from raw milk. The first part of the study focused on determining raw milk consumption habits of dairy producers. A total of 248 dairy producers from 16 counties in Pennsylvania were surveyed. Overall, 105 (42.3%) of the 248 dairy producers consumed raw milk and 170 (68.5%) of the 248 dairy producers were aware of foodborne pathogens in raw milk. Dairy producers who were not aware of foodborne pathogens in raw milk were 2-fold more likely to consume raw milk compared with dairy producers who were aware of foodborne pathogens. The majority of dairy producers who consumed raw milk indicated that taste (72%) and convenience (60%) were the primary factors for consuming raw milk. Dairy producers who resided on the dairy farm were nearly 3-fold more likely to consume raw milk compared with those who lived elsewhere. In the second part of the study, bulk tank milk from the 248 participating dairy herds was examined for foodborne pathogens. Campylobacter jejuni (2%), Shiga toxin-producing Escherichia coli (2.4%), Listeria monocytogenes (2.8%), Salmonella (6%), and Yersinia enterocolitica (1.2%) were detected in the milk samples. Salmonella isolates were identified as S. enterica serotype Typhimurium (n = 10) and S. enterica serotype Newport (n = 5). Of the 248 bulk tank milk samples, 32 (13%) contained > or = 1 species of bacterial pathogens. The findings of the study could assist in developing farm community-based educational programs on the risks of consuming raw milk.

Animals↗