Saturday, December 29, 2012
A genomic analysis of Clostridium difficile infections in blunt trauma patients.
A genomic analysis of Clostridium difficile infections in blunt trauma patients.
Jan 2013
Efron PA, Liu H, Lottenberg L, Cuenca AG, Gentile LF, Miggins MV, Bihorac A, Baker HV, Moore FA, Moldawer LL, Ang DN.
Source
From the Departments of Surgery (P.A.E., H.L., L.L., A.G.C., L.F.G., M.V.M., F.A.M., L.L.M., D.N.A.), Anesthesia (A.B.), and Molecular Genetics and Microbiology (H.V.B.), University of Florida, Gainesville, Florida.
Abstract
BACKGROUND:
Evidence demonstrates that susceptibility to Clostridium difficile infection is related to host risk factors as much as bacterial potency. Using blood leukocyte genome-wide expression patterns of severe blunt trauma patients obtained by the National Institute of General Medical Sciences-sponsored Glue Grant Inflammation and the Host Response to Injury, we examined leukocyte genomic profiles of patients with C. difficile infection to determine preinfection and postinfection gene expression changes.
METHODS:
The genomic responses of 21 severe trauma patients were analyzed (5 C. difficile, 16 controls matched for age and severity of injury). After elimination of probe sets whose expression was below baseline or were unchanged, remaining probe sets underwent hierarchical clustering and principal component analysis. Molecular pathways were generated through Ingenuity Pathways Analysis.
RESULTS:
Supervised analysis demonstrated 118 genes whose expression in patients with C. difficile infection varied before and after their infection. Supervised analysis comparing patients with C. difficile infection with matched non-C. difficile patients before infection suggested that the expression of 501 genes were different in the two groups with up to 87% class prediction (p < 0.05). Many of these genes are related to cell-mediated immune responses, signaling, and interaction.
CONCLUSION:
Genomic analysis of severe blunt trauma patients reveals a distinct leukocyte expression profile of C. difficile both before and after infection. We conclude that an association may exist between a severe trauma patient's leukocyte genomic expression profile and subsequent susceptibility to C. difficile infection. Further prospective expression analysis of this C. difficile population may reveal potential therapeutic interventions and allow early identification of C. difficile-susceptible patients.
LEVEL OF EVIDENCE:
Prognostic/diagnostic study, level III.
Labels: bacterial potency, blunt trauma patient, Clostridium difficile, Genomic analysis, Infection
# posted by Pat O'Connor @ 8:48 AM
The Insect Galleria mellonella as a Powerful Infection Model to Investigate Bacterial Pathogenesis.
The Insect Galleria mellonella as a Powerful Infection Model to Investigate Bacterial Pathogenesis.
Dec 2012
Source
INRA, Micalis UMR1319, France.
Abstract
The study of bacterial virulence often requires a suitable animal model. Mammalian models of infection are costly and may raise ethical issues. The use of insects as infection models provides a valuable alternative. Compared to other non-vertebrate model hosts such as nematodes, insects have a relatively advanced system of antimicrobial defenses and are thus more likely to produce information relevant to the mammalian infection process. Like mammals, insects possess a complex innate immune system(1). Cells in the hemolymph are capable of phagocytosing or encapsulating microbial invaders, and humoral responses include the inducible production of lysozyme and small antibacterial peptides(2,3). In addition, analogies are found between the epithelial cells of insect larval midguts and intestinal cells of mammalian digestive systems. Finally, several basic components essential for the bacterial infection process such as cell adhesion, resistance to antimicrobial peptides, tissue degradation and adaptation to oxidative stress are likely to be important in both insects and mammals(1). Thus, insects are polyvalent tools for the identification and characterization of microbial virulence factors involved in mammalianinfections. Larvae of the greater wax moth Galleria mellonella have been shown to provide a useful insight into the pathogenesis of a wide range of microbial infections including mammalian fungal (Fusarium oxysporum, Aspergillus fumigatus, Candida albicans) and bacterial pathogens, such as Staphylococcus aureus, Proteus vulgaris, Serratia marcescens Pseudomonas aeruginosa, Listeria monocytogenes or Enterococcus faecalis(4-7). Regardless of the bacterialspecies, results obtained with Galleria larvae infected by direct injection through the cuticle consistently correlate with those of similar mammalian studies: bacterial strains that are attenuated in mammalian models demonstrate lower virulence in Galleria, and strains causing severe human infections are also highly virulent in the Galleria model(8-11). Oral infection of Galleria is much less used and additional compounds, like specific toxins, are needed to reach mortality. G. mellonella larvae present several technical advantages: they are relatively large (last instar larvae before pupation are about 2 cm long and weight 250 mg), thus enabling the injection of defined doses of bacteria; they can be reared at various temperatures (20 °C to 30 °C) and infection studies can be conducted between 15 °C to above 37 °C(12,13), allowing experiments that mimic a mammalian environment. In addition, insect rearing is easy and relatively cheap. Infection of the larvae allows monitoring bacterial virulence by several means, including calculation of LD50(14), measurement of bacterial survival(15,16) and examination of the infection process(17). Here, we describe the rearing of the insects, covering all life stages of G. mellonella. We provide a detailed protocol of infection by two routes of inoculation: oral and intra haemocoelic. The bacterial model used in this protocol is Bacillus cereus, a Gram positive pathogen implicated in gastrointestinal as well as in other severe local or systemic opportunistic infections(18,19).
Labels: bacterial virulence, Dtaphylococcus aureus, Enterococcus faecalis, Galleria mellonella, Listeria monocytogenes, Proteus vulgaris, Serratia marcescens Pseudomonas aeruginosa
# posted by Pat O'Connor @ 8:45 AM
Non-diphtheriae Corynebacterium species: an emerging respiratory pathogen.
Non-diphtheriae Corynebacterium species: an emerging respiratory pathogen.
Dec 2012
Díez-Aguilar M, Ruiz-Garbajosa P, Fernández-Olmos A, Guisado P, Del Campo R, Quereda C, Cantón R, Meseguer MA.
Source
Department of Clinical Microbiology, Ramón y Cajal University Hospital, Madrid, Spain, maria_diez_aguilar@hotmail.com.
Abstract
The purpose of the study was to describe the microbiological and clinical features of ten cases of lower respiratory tract infection due to Corynebacterium striatum, Corynebacterium propinquum and Corynebacterium pseudodiphtheriticum. Respiratory samples were recovered from hospitalised patients who were diagnosed of pneumonia and exacerbations of chronic respiratory infections. The samples were Gram-stained and seeded on conventional bacterial growing media. Bacteria were identified by matrix-assisted linear desorption/ionisation-time-of-flight mass spectrometry (MALDI-TOF MS). Antibiotic susceptibility was tested by the disk diffusion method. All patients presented an acute respiratory onset, most of them in the context of an underlying disease and/or immunosuppression. In all patients, the microscopical examination of Gram-stained respiratory samples showed numerous polymorphonuclear cells and Gram-positive bacilli, suggestive of the Corynebacterium morphotype. A pure culture growth of Corynebacterium was obtained in the majority (72 %) of samples. The conclusions are that non-diphtheriae Corynebacterium species are an emerging cause of respiratory infection among patients with chronic respiratory disease and/or immunosuppression, and cannot always be considered as mere colonisers. The microorganism's predominance in Gram-stained purulent respiratory samples together with abundant growth in the culture is the key for the microbiological diagnosis.
Labels: antibiotic, colonisers, Corynebacterium propinquum, Corynebacterium pseudodiphtheriticum, Corynebacterium striatum, immunosuppression, MALDI-TOF MS, Non-diphtheriae Corynebacterium, respiratory pathogen
# posted by Pat O'Connor @ 8:41 AM
Tuesday, December 25, 2012
Infectious arthritis caused by bacteria requires quick treatment
Infectious arthritis caused by bacteria requires quick treatment
By DR. KOMOROFF Universal Uclick
Published: 12/24/2012 2:21 AM
Last Modified: 12/24/2012 3:54 AM
Dear Doctor K: I saw my doctor for pain and inflammation in my knee. He said I have arthritis caused by a bacterial infection. Could this be true?
Dear Reader: Wear and tear on a joint is the main cause of the most common type of arthritis, osteoarthritis. In rheumatoid arthritis and juvenile idiopathic arthritis, an overactive immune system causes joint inflammation.
But joints also can become infected with bacteria and fungi. These microbes may directly infect the joint, for example, through a puncture wound or major injury. But more often, the infection spreads to a joint by traveling through the bloodstream from somewhere else in the body. Once the microbe reaches the joint, it can multiply. The immune system recognizes the invading foreigner and tries to wipe it out. The infection and the immune response cause warmth, pain, stiffness and swelling.
Several types of bacteria can cause arthritis. The diagnosis of infectious arthritis is made by removing fluid from the joint through a needle. The microbe causing the infection can usually be identified in that fluid.
Once diagnosed, you'll immediately begin antibiotic treatment. This should eliminate the infection and help prevent permanent joint damage if begun early enough. If your infection is advanced, or if joint damage has already occurred, you may need to be hospitalized.
At the hospital, your affected joint can be drained. Sometimes fluid is repeatedly removed with a needle and syringe. In other cases, a surgeon needs to open the joint and place a drain in it to let the joint fluid constantly leak out of the body. You can also receive antibiotics intravenously if necessary. If your joint is seriously damaged, you may need surgery to remove damaged tissue and reconstruct the joint.
Often you need to briefly immobilize your affected joint while recovering from the infection. But it's best to become active again as soon as you are able.
TulsaWorld
Labels: bacteria, diagnosis, fungus, immune response, immune system, Infectious arthritis, treatment
# posted by Pat O'Connor @ 6:06 AM
Wednesday, December 19, 2012
Delayed cerebral thrombosis in bacterial meningitis: a prospective cohort study.
Delayed cerebral thrombosis in bacterial meningitis: a prospective cohort study.
Source
Department of Neurology, Center of Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, The Netherlands.
Abstract
PURPOSE:
To study the incidence and clinical characteristics of delayed cerebral thrombosis in bacterial meningitis patients.
METHODS:
We assessed the incidence and clinical characteristics of delayed cerebral thrombosis in adults with cerebrospinal fluid (CSF) culture-proven community-acquired bacterial meningitis included in a prospective nationwide study in The Netherlands performed from 2006 to 2012.
RESULTS:
Delayed cerebral thrombosis occurred in 11 of 1,032 episodes (1.1 %). CSF culture yielded Streptococcus pneumoniae in ten patients and Listeria monocytogenes in one. Adjunctive dexamethasone therapy was administered before or with the first dose of antibiotics in 9 of 11 patients; two patients were initially not treated with dexamethasone. All patients made good initial recovery, followed by sudden deterioration after 7-42 days. Cranial imaging studies showed multiple cerebral infarctions in all patients. The outcome was unfavorable in all but one patient. In an explorative analysis, patients with delayed cerebral thrombosis had eightfold higher complement C5a CSF concentrations on the diagnostic lumbar puncture as compared in those without delayed cerebral thrombosis (p = 0.04).
CONCLUSION:
Delayed cerebral thrombosis is a rare but devastating complication of bacterial meningitis. Adjunctive dexamethasone therapy seems to predispose patients with bacterial meningitis to this complication. We found some evidence that this thrombotic complication is associated with activation of the complement system.
Labels: bacterial meningitis, cerebral thrombosis, cerebrospinal fluid, dexamethasone therapy, Listeria monocytogenes, Streptococcus pneumoniae
# posted by Pat O'Connor @ 9:28 AM
Issues in the diagnosis and treatment of lyme disease.
Issues in the diagnosis and treatment of lyme disease.
Source
Department of Medicine (Infectious Diseases), Falmouth Hospital, USA.
Abstract
Since the identification of the causative organism more than 30 years ago, there remain questions about the di-agnosis and treatment of Lyme Disease. In this article, what is known about the disease will be reviewed, and approaches to the successful diagnosis and treatment of Lyme disease described. In considering the diagnosis of Lyme disease, a major problem is the inability of documenting the existence and location of the bacteria. After the initial transfer of the bacteria from the Ixodes tick into the person, the spirochetes spread locally, but after an initial bacteremic phase, the organisms can no longer be reliably found in body fluids. The bacteria are proba-bly present in subcutaneous sites and intracellular loci. Currently, the use of circulating antibodies directed against spe-cific antigens of the Lyme borrelia are the standard means to diagnose the disease, but specific antibodies are not an ade-quate means to assess the presence or absence of the organism. What is needed is a more Lyme-specific antigen as a more definitive adjunct to the clinical diagnosis. As for the treatment of Lyme disease, the earliest phase is generally easily treated.
But it is the more chronic form of the disease that is plagued with lack of information, frequently leading to erroneous recommendations about the type and du-ration of treatments. Hence, often cited recommendations about the duration of treatment, eg four weeks is adequate treatment, have no factual basis to support that recommendation, often leading to the conclusion that there is another, per-haps psychosomatic reason, for the continuing symptoms. B. burgdorferi is sensitive to various antibiotics, including pe-nicillins, tetracyclines, and macrolides, but there are a number of mitigating factors that affect the clinical efficacy of these antibiotics, and these factors are addressed.
The successful treatment of Lyme disease appears to be dependent on the use of specific antibiotics over a sufficient period of time. Further treatment trials would be helpful in finding the best regimens and duration periods. At present, the diagnosis of Lyme disease is based primarily on the clinical picture. The pathophysiology of the disease remains to be determined, and the basis for the chronic illness in need of additional research. Whether there is continuing infection, auto-immunity to residual or persisting antigens, and whether a toxin or other bacterial-associated product(s) are responsible for the symptoms and signs remains to be delineated.
Labels: B. burgdorferi, bacteria, causative organism, diagnosis, Ixodes tick, lyme disease, signs, symptoms
# posted by Pat O'Connor @ 9:26 AM
Wednesday, December 12, 2012
Immunopathogenesis of Streptococcal Deep Tissue Infections.
Immunopathogenesis of Streptococcal Deep Tissue Infections.
Dec 2012
Source
Karolinska Institutet, Center for Infectious Medicine, F59, Karolinska University Hospital Huddinge, S-141 86, Stockholm, Sweden, Linda.Johansson.2@ki.se.
Abstract
Streptococcus pyogenes is an important human pathogen that can cause a variety of diseases in immunocompetent individuals ranging from uncomplicated superficial infections to severe life-threatening infections including rapidly progressing deep tissue infections, such as necrotizing fasciitis (NF) and severe cellulitis. The pathogenesis of these infections is complex and multifactorial involving numerous virulence factors expressed by the bacteria. Here, we review data from epidemiologic, pathogenomic, and pathogenesis studies that have provided insight into the host-pathogen interactions that contribute to S. pyogenes tissue infections. The role of tissue-specific streptococcal types, intracellular bacterial persistence, and other immune evasion strategies resulting in massive bacterial load at the tissue site, as well as virulence factors contributing to a local hyperinflammatory response are highlighted. A particular focus is on in vivo findings in patients that provide insight into host and bacterial factors that are expressed at the infected tissue site, and the mechanisms underlying tissue pathology.
Labels: Deep Tissue Infections, hyperinflammatory response, immunocompetent, Immunopathogenesis, Streptococcal
# posted by Pat O'Connor @ 10:45 AM
Antibody orientation at bacterial surfaces is related to invasive infection.
Antibody orientation at bacterial surfaces is related to invasive infection.
Dec 2012
Source
Department of Clinical Sciences, Faculty of Medicine; and 2 Department of Immunotechnology, Faculty of Engineering, Lund University, Lund, Sweden.
Abstract
Several of the most significant bacterial pathogens in humans, including Streptococcus pyogenes, express surface proteins that bind IgG antibodies via their fragment crystallizable (Fc) region, and the dogma is that this protects the bacteria against phagocytic killing in blood. However, analysis of samples from a patient with invasive S. pyogenes infection revealed dramatic differences in the presence and orientation of IgG antibodies at the surface of bacteria from different sites. In the throat, IgG was mostly bound to the bacterial surface via Fc, whereas in the blood IgG was mostly bound via fragment antigen-binding (Fab). In infected and necrotic tissue, the Fc-binding proteins were removed from the bacterial surface. Further investigation showed that efficient bacterial IgGFc-binding occurs only in IgG-poor environments, such as saliva. As a consequence, the bacteria are protected against phagocytic killing, whereas in blood plasma where the concentration of IgG is high, the antibodies preferentially bind via Fab, facilitating opsonization and bacterial killing. IgG-poor environments represent the natural habitat for IgGFc-binding bacteria, and IgGFc-binding proteins may have evolved to execute their function in such environments. The lack of protection in plasma also helps to explain why cases of severe invasive infections with IgGFc-binding bacteria are so rare compared with superficial and uncomplicated infections.
Labels: Antibody orientation, Bacterial Pathogens, bacterial surfaces, invasive infection, Streptococcus pyogene
# posted by Pat O'Connor @ 10:43 AM
Tuesday, December 11, 2012
Injected bath salts linked to dangerous bacterial infections in Maine
Injected bath salts linked to dangerous bacterial infections in Maine
Posted Dec. 10, 2012, at 4:00 p.m.
Maine health officials are investigating a cluster of serious bacterial illnesses among users of synthetic bath salts.
Four patients with a history of injecting the drug were sickened by the Group A streptococcal bacterium over the last several weeks, according to a health alert issued by the Maine Center for Disease Control and Prevention. The common germ is responsible for strep throat and skin problems in its milder form but can also lead to life-threatening infections including the much-feared flesh-eating bacteria.
The first three cases arose in Aroostook County, followed by one in Penobscot County, said state epidemiologist Dr. Stephen Sears. The patients were between the ages of 23 and 37.
“Fortunately, they all survived,” he said. “It’s a pretty nasty infection.”
Two of the cases resulted in streptococcal toxic shock syndrome, which causes a rapid drop in blood pressure and can lead to organ failure. All of the patients were hospitalized, one required treatment in intensive care, and one developed necrotizing fasciitis, a condition that’s known as flesh-eating bacteria in its rare and most dangerous form.
The widely publicized infection — most recently grabbing headlines after forcing Georgia woman Aimee Copeland to undergo multiple amputations — destroys muscles, fat and skin tissue. The Maine patient, however, did not suffer the rapid, uncontrolled damage associated with flesh-eating bacteria, Sears said.
“This person, although having some tissue destruction, did not have the continuous, progressive problems we’ve seen described in other cases,” he said.
About a quarter of patients with necrotizing fasciitis die, while streptococcal toxic shock syndrome kills more than 35 percent of patients.
The Group A streptococcal bacterium is commonly found in the throat and on the skin, and people can carry it without experiencing symptoms or illness. It also causes cellulitis and impetigo, a highly contagious minor skin infection often caught by preschool-aged children.
Severe infections result when the otherwise tolerable bacterium infects blood and tissue. Healthy people can contract invasive forms of the disease, but those at higher risk include people with chronic illness, skin lesions, a history of alcohol abuse or injection drug use, as well as the elderly and those with suppressed immune systems.
The bacteria likely cropped up among bath salts users not through the sharing of needles but because injecting drugs gives it a way to enter the body, Sears said. For that reason, health officials are also concerned that the infection could strike users who inject drugs of any kind, he said.
“When you penetrate your skin you put yourself at much greater risk,” Sears said. “We don’t think that it’s necessarily in the bath salts themselves, that’s been one theory.”
Invasive Group A streptococcal disease strikes between 9,000 and 11,500 Americans every year, according to the U.S. CDC. Streptococcal toxic shock syndrome and necrotizing fasciitis each make up about 6 percent of those cases.
Severe Group A streptococcal infections are seasonal, and arise more often from December through April, Sears said. Thorough hand washing, especially after coughing and sneezing and before preparing food or eating, can limit the spread.
Maine CDC has advised physicians and other health providers to be on the lookout for the infections among intravenous drug users, but the public should also be aware, Sears said.
“What people need to know is that strep is around,” he said. “Even without an injection, if they happen to get really painful, red swollen skin, they need to take that seriously.”
Synthetic bath salts, which can be snorted, injected or smoked, first appeared in Maine last year and took hold in the Bangor area. Users often suffer from extreme paranoia, hallucinations and a dangerously high heart rate and body temperature.
Bath salts have been tied to at least one death in Maine.
Labels: bacterial infections, bath salts, flesh-eating bacteria, Group A streptococcal bacterium, necrotizing fasciitis, streptococcal toxic shock syndrome
# posted by Pat O'Connor @ 11:53 AM
Sunday, December 09, 2012
Impetigo image and information
Dr. Lynn Chiam
What is Impetigo?
Impetigo is a skin infection that can spread from one person to another. Impetigo causes one or more "sores" on the skin that are often covered by a thick dry honey-colored crust. The sores don't hurt, but may be tender if touched. They may also be itchy. Any skin area can be affected, but sores are usually on arms or legs, the face (mainly around the mouth, nose, or ears), and sometimes on the scalp. Anyone can get impetigo, but it most often occurs in children 2 to 6 years old. The disease is most common during summer and fall, but can occur anytime.
What Causes Impetigo?
Impetigo is usually caused by a group of bacteria ("germs") called group A streptococci ("strep"), or by other bacteria called staphylococci ("staph"). These bacteria are normally found on the skin and in the nose. When small cuts, scratches, or insect bites occur, these bacteria can get under the skin surface and cause infection. Infected areas are often reddish and puffy. Fluid or pus oozes from the sore for a few days. The fluid dries to form honey-colored crusts. As the bacteria multiply, the sores increase in number and size.
How is Impetigo Spread?
Impetigo is very contagious. Sores have large numbers of the bacteria. The bacteria are easily passed to new areas of the skin by scratching or touching the sores or to other people by unwashed hands, dirty fingernails, and clothing or other objects that have touched the sores. To help prevent spread of impetigo:
- Bathe or shower daily.
- Keep fingernails clean and short.
- Wash with hot water and soap clothing, sheets, towels, and other items that come in contact with impetigo sores or crusts. Do not share these items with anyone else.
- Keep sores covered with clean bandages. Wash your hands after changing the bandage.
- Throw away used bandages in a trash bag.
Children who may have impetigo should not attend school or daycare. They should not sleep, play, or have close contact, with other children until after they have been seen by a doctor.
Impetigo
ICD-9 684; ICD-10 L01
ICD-9 684; ICD-10 L01
Texas Dept of State Health Services
Wikipedia
Labels: bacteria, Impetigo image, impetigo infection, insect bite, scratches, small cuts, staph, strep a
# posted by Pat O'Connor @ 9:35 AM
