Thursday, August 30, 2012


New 'Heartland' Virus Discovered in Sick Missouri Farmers

New 'Heartland' Virus Discovered in Sick Missouri Farmers

August 30, 2012 - I realize this is about a virus and not bacteria, never the less, it is important enough to warrant posting.  Pat O'Connor

New 'Heartland' Virus Discovered in Sick Missouri Farmers

Two men in Missouri who became severely ill after sustaining tick bites were found to be infected with a new type of virus, according to a study from the
Centers of Disease Control and Prevention (CDC).
Both men were admitted to hospitals after experiencing high fevers, fatigue, diarrhea and loss of appetite. They were originally thought to be suffering from a bacterial infection, but doubts arose when they didn't improve after being treated with antibiotics.

Further tests revealed their blood contained a new virus, which the researchers dubbed the Heartland virus. It belongs to a group called phleboviruses, which
are carried by flies, mosquitoes or ticks, and can cause disease in humans.

While the genetic material of Heartland virus appears similar to that of other phleboviruses, the particular proteins it produces are different enough to call
it a new species, said study researcher Laura McMullan, a senior scientist at the CDC.

Because the Heartland virus causes such general symptoms, it could be "a more common cause of human illness than is currently recognized," the researchers
wrote in the Aug. 30 issue of the New England Journal of Medicine.

More studies are needed to identify the natural hosts of the virus, learn how many people are infected with it and find risk factors for infection, McMullan said.

Because both men experienced tick bites shortly before they became ill — one man, a farmer, reported receiving an average of 20 tick bites a day — the researchers said it's likely that the Heartland virus is spread by ticks,
although more research is needed to confirm this.
The new virus's closest relative is another tick-borne phlebovirus, called SFTS virus, which was identified last year in China, and causes death in 12 percent
of cases.

The Missouri men, who were both infected in 2009, recovered after 10 to 12 days in the hospital, although one of the men has reported recurrent headaches and
fatigue in the two years since his hospitalization.

The researchers suspect a species of tick commonly found in Missouri, called Amblyomma americanum, is one of the hosts of the Heartland virus.

For now, taking precautions to prevent tick bites is the best way to avoid the virus, McMullan said. To prevent tick bites, the CDC recommends using repellents
that contain 20 percent or more DEET, as well as avoiding wooded areas or areas
with high grass.

Pass it on: The Heartland virus is a new species of virus that can cause severe illness in people, and appears to be carried by ticks.

Yahoo News

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The first case of cutaneous infection with Mycobacterium parascrofulaceum.

The first case of cutaneous infection with Mycobacterium parascrofulaceum.



Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Center for STD and Leprosy Control, Chinese Center for Disease Control and Prevention, Nanjing, People's Republic of China.


The authors present the first, to the best of their knowledge, reported case of cutaneous infection caused by Mycobacterium parascrofulaceum. A 42-year-old woman presented with asymptomatic reddish papules, nodules, plaques, and patches on the right side of her face and on her forehead that had persisted for 5 years, with the lesions gradually increasing in size over that time. No previous intervening medical treatment had been applied. No history or evidence of immunosuppression was found. A skin biopsy was performed for routine histological examination. Samples of lesioned skin were inoculated on Löwenstein-Jensen medium to determine the presence of acid-fast bacilli. Ziehl-Neelsen staining was used to confirm the presence of the organism. In vitro drug susceptibility testing was conducted using the microtiter plate method. Mycobacterium was identified by polymerase chain reaction-restriction fragment length polymorphism analysis and sequencing of the hsp65 and 16S rDNA genes. Cultures for aerobic and anaerobic bacteria, as well as fungus, were also conducted. Routine histopathology revealed granulomatous changes without caseation. Ziehl-Neelsen staining showed that the organisms in both the lesions and the cultures were acid-fast bacilli. The cultured colonies were grown in Löwenstein-Jensen medium and incubated at two different temperatures (32°C and 37°C) for 2-3 weeks, developing pigmentation both in the dark and in the light. In vitro drug susceptibility tests showed that the organism was sensitive to clarithromycin and moxifloxacin. Polymerase chain reaction-restriction fragment length polymorphism analysis and sequencing of the hsp65 and 16S rDNA genes confirmed that the isolated organisms were M. parascrofulaceum. Fungal and other standard bacterialcultures were negative. In conclusion, identification and diagnosis of nontuberculous mycobacteria should be performed promptly to obtain better prognoses. Empirical treatments may be feasible, and drug susceptibility tests are important.


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Monday, August 27, 2012


Practice guidelines for the diagnosis and management of skin and soft-tissue infections.

Practice guidelines for the diagnosis and management of skin and soft-tissue infections.

National Guidelines Clearinghouse

GUIDELINE STATUS - This is the current release of the guideline.


Note from the National Guideline Clearinghouse (NGC): The following comes from the Executive Summary of the guideline. Please see the full guideline for additional details about the topics discussed below.

The strength of recommendation (A-E) and quality of evidence (I-III) are defined at the end of the "Major Recommendations" field.

Executive Summary

Soft-tissue infections are common, generally of mild to modest severity, and are easily treated with a variety of agents. An etiologic diagnosis of simple cellulitis is frequently difficult and generally unnecessary for patients with mild signs and symptoms of illness. Clinical assessment of the severity of infection is crucial, and several classification schemes and algorithms have been proposed to guide the clinician. However, most clinical assessments have been developed from either retrospective studies or from an author's own "clinical experience," illustrating the need for prospective studies with defined measurements of severity coupled to management issues and outcomes.

Until then, it is the recommendation of this committee that patients with soft-tissue infection accompanied by signs and symptoms of systemic toxicity (e.g., fever or hypothermia, tachycardia [heart rate >100 beats/min], and hypotension [systolic blood pressure, <90>13 mg/L, hospitalization should be considered and a definitive etiologic diagnosis pursued aggressively by means of procedures such as Gram stain and culture of needle aspiration or punch biopsy specimens, as well as requests for a surgical consultation for inspection, exploration, and/or drainage. Other clues to potentially severe deep soft-tissue infection include the following: (1) pain disproportionate to the physical findings, (2) violaceous bullae, (3) cutaneous hemorrhage, (4) skin sloughing, (5) skin anesthesia, (6) rapid progression, and (7) gas in the tissue. Unfortunately, these signs and symptoms often appear later in the course of necrotizing infections. In these cases, emergent surgical evaluation is of paramount importance for both diagnostic and therapeutic reasons.

Emerging antibiotic resistance among Staphylococcus aureus (methicillin resistance) and Streptococcus pyogenes (erythromycin resistance) are problematic, because both of these organisms are common causes of a variety of skin and soft-tissue infections and because empirical choices of antimicrobials must include agents with activity against resistant strains. Minor skin and soft-tissue infections may be empirically treated with semisynthetic penicillin, first-generation or second-generation oral cephalosporins, macrolides, or clindamycin (A-I); however, 50% of methicillin-resistant S. aureus (MRSA) strains have inducible or constitutive clindamycin resistance. Most community-acquired MRSA strains remain susceptible to trimethoprim-sulfamethoxazole and tetracycline, though treatment failure rates of 21% have been reported in some series with doxycycline or minocycline. Therefore, if patients are sent home receiving these regimens, it is prudent to reevaluate them in 24-48 hours to verify a clinical response. Progression despite receipt of antibiotics could be due to infection with resistant microbes or because a deeper, more serious infection exists than was previously realized.

Patients who present to the hospital with severe infection or whose infection is progressing despite empirical antibiotic therapy should be treated more aggressively, and the treatment strategy should be based upon results of appropriate Gram stain, culture, and drug susceptibility analysis. In the case of S. aureus, the clinician should assume that the organism is resistant, because of the high prevalence of community-associated MRSA strains, and agents effective against MRSA (i.e., vancomycin, linezolid, or daptomycin) should be used (A-I). Stepdown to treatment with other agents, such as tetracycline or trimethoprim-sulfamethoxazole, for MRSA infection may be possible, based on results of susceptibility tests and after an initial clinical response. In the United States, not all laboratories perform susceptibility testing on S. pyogenes. However, the Centers for Disease Control and Prevention has provided national surveillance data that suggest a gradual trend of increasing macrolide resistance of S. pyogenes from 4%-5% in 1996-1998 to 8%-9% in 1999-2001. Of interest, 99.5% of strains remain susceptible to clindamycin, and 100% are susceptible to penicillin.

Impetigo, Erysipelas, and Cellulitis

Impetigo may be caused by infection with S. aureus and/or S. pyogenes. The decision of how to treat impetigo depends on the number of lesions, their location (face, eyelid, or mouth), and the need to limit spread of infection to others. The best topical agent is mupirocin (A-I), although resistance has been described; other agents, such as bacitracin and neomycin, are considerably less effective treatments. Patients who have numerous lesions or who are not responding to topical agents should receive oral antimicrobials effective against both S. aureus and S. pyogenes (A-I) (see the table below entitled "Antimicrobial Therapy for Impetigo and for Skin and Soft-Tissue Infections"). Although rare in developed countries (<1>

Classically, erysipelas is a fiery red, tender, painful plaque with well-demarcated edges and is commonly caused by streptococcal species, usually S. pyogenes.

Cellulitis may be caused by numerous organisms that are indigenous to the skin or to particular environmental niches. Cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S. aureus. In contrast, cellulitis that is diffuse or unassociated with a defined portal is most commonly caused by streptococcal species. Important clinical clues to other causes include physical activities, trauma, water contact, and animal, insect, or human bites. In these circumstances appropriate culture material should be obtained, as they should be in patients who do not respond to initial empirical therapy directed against S. aureus and S. pyogenes and in immunocompromised hosts. Unfortunately, aspiration of skin is not helpful in 75%-80% of cases of cellulitis, and results of blood cultures are rarely positive (<5>

Penicillin, given either parenterally or orally depending on clinical severity, is the treatment of choice for erysipelas (A-I). For cellulitis, a penicillinase-resistant semisynthetic penicillin or a first-generation cephalosporin should be selected (A-I), unless streptococci or staphylococci resistant to these agents are common in the community. For penicillin-allergic patients, choices include clindamycin or vancomycin.

Lack of clinical response could be due to unusual organisms, resistant strains of staphylococcus or streptococcus, or deeper processes, such as necrotizing fasciitis or myonecrosis. In patients who become increasingly ill or experience increasing toxicity, necrotizing fasciitis, myonecrosis, or toxic shock syndrome should be considered, an aggressive evaluation initiated, and antibiotic treatment modified, on the basis of Gram stain results, culture results, and antimicrobial susceptibilities of organisms obtained from surgical specimens.

Antimicrobial Therapy for Impetigo and for Skin and Soft-Tissue Infections

Antibiotic therapy, by disease




Some strains of Staphylococcus aureus and Streptococcus pyogenes may be resistant


Mupirocin ointment

For patients with a limited number of lesions

Nafcillin or oxacillin
Parental drug of choice; inactive against MRSA

For penicillin-allergic patients, except those with immediate hypersensitivity reactions


Bacteriostatic; potential of cross-resistance and emergence of resistance in erythromycin-resistant strains; inducible resistance in MRSA


Oral agent of choice for methicillin-susceptible strains

For penicillin-allergic patients, except those with immediate hypersensitivity reactions
Doxycycline, minocycline
Bacteriostatic; limited recent clinical experience

Bactericidal; efficacy poorly documented


For penicillin-allergic patients; parenteral drug of choice for treatment of infections caused by MRSA


Bacteriostatic; limited clinical experience; no cross-resistance with other antibiotic classes; expensive; may eventually replace other second-line agents as a preferred agent for oral therapy of MRSA infections

Bacteriostatic; potential of cross-resistance and emergence of resistance in erythromycin- resistant strains; inducible resistance in MRSA

Bactericidal; possible myopathy
Doxycycline, minocycline
Bacteriostatic, limited recent clinical experience
Bactericidal; limited published efficacy data

Note: MRSA, methicillin-resistant S. aureus; MSSA, methicillin-susceptible S. aureus; SSTI, skin and soft-tissue infection; TMP-SMZ, trimethoprim-sulfamethoxazole.

Necrotizing Infections

Necrotizing fasciitis may be monomicrobial and caused by S. pyogenes, Vibrio vulnificus, or Aeromonas hydrophila. Recently, necrotizing fasciitis was described in a patient with MRSA infection. Polymicrobial necrotizing fasciitis may occur following surgery or in patients with peripheral vascular disease, diabetes mellitus, decubitus ulcers, and spontaneous mucosal tears of the gastrointestinal or gastrourinary tract (i.e., Fournier gangrene). As with clostridial myonecrosis, gas in the deep tissues is frequently found in these mixed infections.

Gas gangrene is a rapidly progressive infection caused by Clostridium perfringens, Clostridium septicum, Clostridium histolyticum, or Clostridium novyi. Severe penetrating trauma or crush injuries associated with interruption of the blood supply are the usual predisposing factors. C. perfringens and C. novyi infections have recently been described among heroin abusers following intracutaneous injection of black tar heroin. C. septicum, a more aerotolerant Clostridium species, may cause spontaneous gas gangrene in patients with colonic lesions (such as those due to diverticular disease), adenocarcinoma, or neutropenia.

Necrotizing fasciitis and gas gangrene may cause necrosis of skin, subcutaneous tissue, and muscle. Cutaneous findings of purple bullae, sloughing of skin, marked edema, and systemic toxicity mandate prompt surgical intervention. For severe group A streptococcal and clostridial necrotizing infections, parenteral clindamycin and penicillin treatment is recommended (A-II). A variety of antimicrobials directed against aerobic gram-positive and gram-negative bacteria, as well as against anaerobes, may be used in mixed necrotizing infections (B-II).

Infections Following Animal or Human Bites

Animal bites account for 1% of all emergency department visits, and dog bites are responsible for 80% of such cases. Although Pasteurella species are the most common isolates, cat and dog bites contain an average of 5 different aerobic and anaerobic bacteria per wound, often including S. aureus, Bacteroides tectum, and Fusobacterium, Capnocytophaga, and Porphyromonas species. The decision to administer oral or parenteral antibiotics depends on the depth and severity of the wound and on the time since the bite occurred. Patients not allergic to penicillin should receive treatment with oral amoxicillin-clavulanate or with intravenous ampicillin-sulbactam or ertapenem (B-II), because agents such as dicloxacillin, cephalexin, erythromycin, and clindamycin have poor activity against Pasteurella multocida. Although cefuroxime, cefotaxime, and ceftriaxone are effective against P. multocida, they do not have good anaerobic spectra. Thus, cefoxitin or carbapenem antibiotics could be used parenterally in patients with mild penicillin allergies. Patients with previous severe reactions can receive oral or intravenous doxycycline, trimethoprim-sulfamethoxazole, or a fluoroquinolone plus clindamycin.
Human bites may occur from accidental injuries, purposeful biting, or closed fist injuries. The bacteriologic characteristics of these wounds are complex but include infection with aerobic bacteria, such as streptococci, S. aureus, and Eikenella corrodens, as well as with multiple anaerobic organisms, including Fusobacterium, Peptostreptococcus, Prevotella, and Porphyromonas species. E. corrodens is resistant to first-generation cephalosporins, macrolides, clindamycin, and aminoglycosides. Thus, intravenous treatment with ampicillin-sulbactam or cefoxitin is the best choice (B-III).

Infections Associated with Animal Contact

Infections associated with animal contact, although uncommon, are frequently severe, sometimes lethal, and diagnostically challenging. The potential use of Bacillus anthracis, Francisella tularensis, and Yersinia pestis for bioterrorism has generated great interest in rapid diagnostic techniques, because early recognition and treatment are essential. Doxycycline or ciprofloxacin therapy is recommended in standard doses for nonpregnant adults and children 18 years of age, pending identification of the offending agent (B-III).

Adults and children who receive a diagnosis of tularemia should receive an aminoglycoside, preferably streptomycin or gentamicin, for 7-10 days. In mild cases, doxycycline or tetracycline for 14 days is recommended (B-III) (comments regarding treatment of children <8>

Data regarding antibiotic efficacy for treatment of cat-scratch disease are inconclusive, although 1 small study demonstrated more-rapid lymph node regression in patients receiving azithromycin, compared with patients receiving no treatment. Cutaneous bacillary angiomatosis has not been systematically studied, but treatment with erythromycin or doxycycline in standard doses for 4 weeks has been effective in very small series (B-III).

On the basis of very incomplete data, erysipeloid is best treated with oral penicillin or amoxicillin for 10 days (B-III). E. rhusiopathiae is resistant in vitro to vancomycin, teicoplanin, and daptomycin (E-III).

Surgical Site Infections

Surgical soft-tissue infections include those occurring postoperatively and those severe enough to require surgical intervention for diagnosis and treatment. The algorithm presented in the original guideline document clearly indicates that surgical site infection rarely occurs during the first 48 hours after surgery, and fever during that period usually arises from noninfectious or unknown causes. In contrast, after 48 hours, surgical site infection is a more common source of fever, and careful inspection of the wound is indicated. For patients with a temperature <38 .5=".5">38.5 degrees C or a heart rate >110 beats/minute generally require antibiotics as well as opening of the suture line. Infections developing after surgical procedures involving nonsterile tissue, such as colonic, vaginal, biliary, or respiratory mucosa, may be caused by a combination of aerobic and anaerobic bacteria. These infections can rapidly progress and involve deeper structures than just the skin, such as fascia, fat, or muscle (see table below entitled "Antibiotic Choices for Incisional Surgical Site Infections").
Antibiotic Choices for Incisional Surgical Site Infections (SSIs).

Antibiotic Therapy for SSIs, By Site of Operation

Intestinal or genital tract

Single agents
Combination agents

Facultative and aerobic activity

Third-generation cephalosporin
Anaerobic activity

Penicillin agent plus beta-lactamase inhibitor Nonintestinal
Trunk and extremities away from axilla or perineum

First-generation cephalosporin
Axillary or perineum
Other single agents as described above for intestinal and genital operations

Infections in the Immunocompromised Host

Skin and soft tissues are common sites of infection in compromised hosts and usually pose major diagnostic challenges for the following 3 reasons: (1) infections are caused by diverse organisms, including organisms not ordinarily considered to be pathogens in otherwise healthy hosts; (2) infection of the soft tissues may occur as part of a broader systemic infection; and (3) the degree and type of immune deficiency attenuate the clinical findings. The importance of establishing a diagnosis and performing susceptibility testing is crucial, because many infections are hospital acquired, and mounting resistance among both gram-positive and gram-negative bacteria makes dogmatic empirical treatment regimens difficult, if not dangerous. In addition, fungal infections may present with cutaneous findings.

Immunocompromised patients who are very ill or experiencing toxicity typically require very broad-spectrum empirical agents that include specific coverage for resistant gram-positive bacteria, such as MRSA (e.g., vancomycin, linezolid, daptomycin, or quinupristin/dalfopristin). Coverage for gram-negative bacteria may include monotherapy with a cephalosporin possessing activity against Pseudomonas species, with carbapenems, or with a combination of either a fluoroquinolone or an aminoglycoside plus either an extended-spectrum penicillin or cephalosporin.

Infections in patients with cell-mediated immunodeficiency (such as that due to Hodgkin disease, lymphoma, human immunodeficiency virus [HIV] infection, bone marrow transplantation, and receipt of long-term high-dose immunosuppressive therapy) can be caused by either common or unusual bacteria, viruses, protozoa, helminths, or fungi. Although infection may begin in the skin, cutaneous lesions can also be the result of hematogenous seeding. A well planned strategy for prompt diagnosis, including biopsy and aggressive treatment protocols, is essential. Diagnostic strategies require laboratory support capable of rapid processing and early detection of bacteria (including Mycobacteria and Nocardia species), viruses, and fungi. The algorithm presented in the original guideline document provides an approach to diagnosis and treatment. The empirical antibiotic guidelines are based on results of clinical trials, national surveillance antibiograms, and consensus meetings. Because antimicrobial susceptibilities vary considerably across the nation, clinicians must base empirical treatment on the antibiograms in their own location.

Microbiologic cultures are important in establishing a specific diagnosis, and testing the drug susceptibility of organisms is critical for optimal antimicrobial treatment. This guideline offers recommendations for empirical treatment of specific community-acquired and hospital-acquired infections. Nonetheless, therapy may fail for several reasons: (1) the initial diagnosis and/or treatment chosen is incorrect, (2) the etiologic agent from a given locale is resistant to antibiotics, (3) antimicrobial resistance develops during treatment, and (4) the infection is deeper and more complex than originally estimated.


Neutropenia - Initial infection

Bacteria: Gram negative

Type of therapy: Monotherapy or antibiotic combination

Duration of Therapy: 7-14 days

Fredquency or reason for surgery: Rare

Adjunct: G-CSF/GM-CSF;


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Extensive in vivo resilience of persistent salmonella.



Focal Area Infection Biology, Biozentrum, University of Basel, Basel, Switzerland.


Chronic infections caused by persistent pathogens represent an important health problem. Here, we establish a simple practical mouse Salmonella infection model for identifying bacterial maintenance functions that are essential for persistency. In this model, a substantial fraction of Salmonella survived even several days of treatment with a potent fluoroquinolone antibiotic indicating stringency of the model. Evaluation of twelve metabolic defects revealed dramatically different requirements for Salmonella during persistency as compared to acute infections. Disrupted synthesis of unsaturated/cyclopropane fatty acids was the only defect that resulted in rapid Salmonella clearance suggesting that this pathway might contain suitable targets for antimicrobial chemotherapy of chronic infection.
Full Text Article

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Update on bacterial nosocomial infections.

Update on bacterial nosocomial infections.

Aug 2012


Department of Medical Laboratory Sciences & Pathology, College of Public Health & Medical Sciences, Jimma University, Jimma, Ethiopia.


With increasing use of antimicrobial agents and advance in lifesaving medical practices which expose the patients for invasive procedures, are associated with the ever increasing of nosocomial infections. Despite an effort in hospital infection control measures, health care associated infections are associated with significant morbidity and mortality adding additional health care expenditure which may leads to an economic crisis. The problem is further complicated with the emergence of difficult to treat multidrug resistant (MDR) microorganism in the hospital environment. Virtually every pathogen has the potential to cause infection in hospitalized patients but only limited number of both gram positive and gram negative bacteria are responsible for the majority of nosocomial infection. Among them Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa and Enterococci takes the leading. Many intrinsic and extrinsic factors predispose hospitalized patients for these pathogens. Following simple hospital hygienic practices and strictly following standard medical procedures greatly reduces infection to a significant level although not all nosocomial infections are avoidable. The clinical spectrum caused by nosocomial pathogens depend on body site of infection, the involving pathogen and the patient's underlying condition. Structural and non structural virulence factors associated with the bacteria are responsible for the observed clinical manifestation. Bacteria isolation and characterization from appropriate clinical materials with antimicrobial susceptibility testing is the standard of laboratory diagnosis.


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New paradigms of urinary tract infections: Implications for patient management.

New paradigms of urinary tract infections: Implications for patient management.

Apr 2012


Center for Microbial Pathogenesis, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio.


Urinary tract infections (UTIs) represent one of the most commonly acquired diseases among the general population as well as hospital in-patients, yet remain difficult to effectively and consistently treat. High rates of recurrence, anatomic abnormalities, and functional disturbances of the urinary tract all contribute to the difficulty in management of these infections. However, recent advances reveal important molecular and genetic factors that contribute to bacterial invasion and persistence in the urinary tract, particularly for the most common causative agent, uropathogenic Escherichia coli. Recent studies using animal models of experimental UTIs have recently provided mechanistic insight into the clinical observations that question the effectiveness of antibiotic therapy in treatment. Ultimately, continuing research will be necessary to identify the best targets for effective treatment of this costly and widespread infectious disease.


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Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation.

Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation.



Department of Experimental and Clinical Pharmacology, University of Minnesota Minneapolis, MN, USA.


Staphylococcus aureus causes many diseases in humans, ranging from mild skin infections to serious, life-threatening, superantigen-mediated Toxic Shock Syndrome (TSS). S. aureus may be asymptomatically carried in the anterior nares or vagina or on the skin, serving as a reservoir for infection. Pulsed-field gel electrophoresis clonal type USA200 is the most widely disseminated colonizer and the leading cause of TSS. The cytolysin α-toxin (also known as α-hemolysin or Hla) is the major epithelial proinflammatory exotoxin produced by TSS S. aureus USA200 isolates. The current study aims to characterize the differences between TSS USA200 strains [high (hla(+)) and low (hla(-)) α-toxin producers] in their ability to disrupt vaginal mucosal tissue and to characterize the subsequent infection. Tissue viability post-infection and biofilm formation of TSS USA200 isolates CDC587 and MN8, which contain the α-toxin pseudogene (hla(-)), MNPE (hla(+)), and MNPE isogenic hla knockout (hlaKO), were observed via LIVE/DEAD® staining and confocal microscopy. All TSS strains grew to similar bacterial densities (1-5 × 10(8) CFU) on the mucosa and were proinflammatory over 3 days. However, MNPE formed biofilms with significant reductions in the mucosal viability whereas neither CDC587 (hla(-)), MN8 (hla(-)), nor MNPE hlaKO formed biofilms. The latter strains were also less cytotoxic than wild-type MNPE. The addition of exogenous, purified α-toxin to MNPE hlaKO restored the biofilm phenotype. We speculate that α-toxin affects S. aureus phenotypic growth on vaginal mucosa by promoting tissue disruption and biofilm formation. Further, α-toxin mutants (hla(-)) are not benign colonizers, but rather form a different type of infection, which we have termed high density pathogenic variants (HDPV).


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Sunday, August 12, 2012


Sensitivity of pathogenic and commensal bacteria from the human colon to essential oils.

Sensitivity of pathogenic and commensal bacteria from the human colon to essential oils.

Aug 2012


Rowett Institute of Nutrition and Health;


The microbiota of the intestinal tract plays an important role in colonic health, mediating many effects of dietary components on colonic health and during enteric infections. In the context of increasing incidences of antibiotic resistance in gut bacteria, complementary therapies are required for the prevention and treatment of enteric infections. Here we report the potential application of essential oils (EO) and pure EO compounds to improve human gut health. Nerolidol, thymol, eugenol and geraniol inhibited growth of the pathogens, Escherichia coli O157:H7(VT-), Clostridium difficile DSM1296, C. perfringens DSM11780, Salmonella typhimurium 3530 and S. enteritidis S1400 at half maximal inhibitory concentrations (IC50) varying from 50 to 500 ppm. Most EO showed greater toxicity to pathogens than commensals. However, the beneficial commensal, Faecalibacterium prausnitzii, was sensitive to EO at similar or even lower concentrations than the pathogens. The EO showed dose-dependent effects on cell integrity, as measured using propidium iodide, of Gram-positive bacteria. These effects were not strongly correlated to growth inhibition, however, suggesting that cell membrane damage occurred but were not the primary cause of growth inhibition. Growth inhibition of Gram-negative bacteria, in contrast, occurred mostly without cell integrity loss. Principal component analysis showed clustering of responses according to bacterial species rather than to the identity of the EO, with the exception that responses to thymol and nerolidol clustered away from the other EO. In conclusion, the selective effects of some EO might have beneficial effects on gut health if selected carefully for effectiveness against different species.

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