Drug Resistance, Microbial
Microbial Sensitivity Tests
Molecular Sequence Data
Education, Dental, Graduate
Dissertations, Academic as Topic
Fatal Serratia marcescens meningitis and myocarditis in a patient with an indwelling urinary catheter. (1/1084)Serratia marcescens is commonly isolated from the urine of patients with an indwelling urinary catheter and in the absence of symptoms is often regarded as a contaminant. A case of fatal Serratia marcescens septicaemia with meningitis, brain abscesses, and myocarditis discovered at necropsy is described. The patient was an 83 year old man with an indwelling urinary catheter who suffered from several chronic medical conditions and from whose urine Serratia marcescens was isolated at the time of catheterisation. Serratia marcescens can be a virulent pathogen in particular groups of patients and when assessing its significance in catheter urine specimens, consideration should be given to recognised risk factors such as old age, previous antibiotic treatment, and underlying chronic or debilitating disease, even in the absence of clinical symptoms. (+info)
Genetic analysis of the Serratia marcescens N28b O4 antigen gene cluster. (2/1084)The Serratia marcescens N28b wbbL gene has been shown to complement the rfb-50 mutation of Escherichia coli K-12 derivatives, and a wbbL mutant has been shown to be impaired in O4-antigen biosynthesis (X. Rubires, F. Saigi, N. Pique, N. Climent, S. Merino, S. Alberti, J. M. Tomas, and M. Regue, J. Bacteriol. 179:7581-7586, 1997). We analyzed a recombinant cosmid containing the wbbL gene by subcloning and determination of O-antigen production phenotype in E. coli DH5alpha by sodium dodecyl sulfate-polyacrylamide electrophoresis and Western blot experiments with S. marcescens O4 antiserum. The results obtained showed that a recombinant plasmid (pSUB6) containing about 10 kb of DNA insert was enough to induce O4-antigen biosynthesis. The same results were obtained when an E. coli K-12 strain with a deletion of the wb cluster was used, suggesting that the O4 wb cluster is located in pSUB6. No O4 antigen was produced when plasmid pSUB6 was introduced in a wecA mutant E. coli strain, suggesting that O4-antigen production is wecA dependent. Nucleotide sequence determination of the whole insert in plasmid pSUB6 showed seven open reading frames (ORFs). On the basis of protein similarity analysis of the ORF-encoded proteins and analysis of the S. marcescens N28b wbbA insertion mutant and wzm-wzt deletion mutant, we suggest that the O4 wb cluster codes for two dTDP-rhamnose biosynthetic enzymes (RmlDC), a rhamnosyltransferase (WbbL), a two-component ATP-binding-cassette-type export system (Wzm Wzt), and a putative glycosyltransferase (WbbA). A sequence showing DNA homology to insertion element IS4 was found downstream from the last gene in the cluster (wbbA), suggesting that an IS4-like element could have been involved in the acquisition of the O4 wb cluster. (+info)
Strain-dependent cytotoxic effects of endotoxin for mouse peritoneal macrophages. (3/1084)The cytotoxic effects of bacterial lipopolysaccharides (LPS) on mouse leukocytes have been examined in vivo and in vitro. Intraperitoneal injection of LPS into C57BL/6 mice greatly reduced the recovery of mononuclear cells; LPS was cytotoxic for macrophages, but had a mitogenic effect on lymphocytes. Similar effects of LPS on peritoneal leukocytes were observed in vitro. When monolayers of adherent peritoneal cells were studied in vitro, cytotoxicity was also observed, suggesting that the effect of LPS on macrophages is direct and does not require participation by lymphocytes. Entirely different results were obtained when peritoneal macrophages from LPS-resistant C3H/HeJ mice were studied. LPS failed to activate lymphocytes and was not cytotoxic for macrophages in vitro or in vivo. The effect of LPS on polymorphonuclear leukocytes appeared to be the same in all mouse stains studied. Lipid A was shown to be the most biologically active portion of the LPS molecule. Whereas polysaccharide-deficient endotoxins extracted from rough mutants of Salmonella typhimurium were cytotoxic for macrophages in vitro, polysaccharides that lacked esterified fatty acids did not exhibit this activity. Since LPS may mediate its effects through affinity for mammalian cell membranes, the cellular unresponsiveness of C3H/H3J mice to LPS may reflect an inability of cells from LPS-resistant strains to interact with LPS at the membrane level. (+info)
NMR studies of the C-terminal secretion signal of the haem-binding protein, HasA. (4/1084)HasA is a haem-binding protein which is secreted under iron-deficiency conditions by the gram-negative bacterium Serratia marcescens. It is a monomer of 19 kDa (187 residues) able to bind free haem as well as to capture it from haemoglobin. HasA delivers haem to a specific outer-membrane receptor HasR and allows the bacteria to grow in the absence of any other source of iron. It is secreted by a signal peptide-independent pathway which involves a C-terminal secretion signal and an ABC (ATP-binding cassette) transporter. The C-terminal region of the secretion signal containing the essential secretion motif is cleaved during or after the secretion process by proteases secreted by the bacteria. In this work, we study by 1H NMR the conformation of the C-terminal extremity of HasA in the whole protein and that of the isolated secretion signal peptide in a zwitterionic micelle complex that mimicks the membrane environment. We identify a helical region followed by a random-coil C-terminus in the peptide-micelle complex and we show that in both the whole protein and the complex, the last 15 residues containing the motif essential for secretion are highly flexible and unstructured. This flexibility may be a prerequisite to the recognition of HasA by its ABC transporter. We determine the cleavage site of the C-terminal extremity of the protein and analyse the effect of the cleavage on the haem acquisition process. (+info)
Use of microdilution panels with and without beta-lactamase inhibitors as a phenotypic test for beta-lactamase production among Escherichia coli, Klebsiella spp., Enterobacter spp., Citrobacter freundii, and Serratia marcescens. (5/1084)Over the past decade, a number of new beta-lactamases have appeared in clinical isolates of Enterobacteriaceae that, unlike their predecessors, do not confer beta-lactam resistance that is readily detected in routine antibiotic susceptibility tests. Because optimal methodologies are needed to detect these important new beta-lactamases, a study was designed to evaluate the ability of a panel of various beta-lactam antibiotics tested alone and in combination with beta-lactamase inhibitors to discriminate between the production of extended-spectrum beta-lactamases, AmpC beta-lactamases, high levels of K1 beta-lactamase, and other beta-lactamases in 141 isolates of Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca, Enterobacter cloacae, Enterobacter aerogenes, Citrobacter freundii, and Serratia marcescens possessing well-characterized beta-lactamases. The microdilution panels studied contained aztreonam, cefpodoxime, ceftazidime, cefotaxime, and ceftriaxone, with and without 1, 2, and 4 microg of clavulanate per ml or 8 microg of sulbactam per ml and cefoxitin and cefotetan with and without 8 microg of sulbactam per ml. The results indicated that a minimum panel of five tests would provide maximum separation of extended-spectrum beta-lactamase high AmpC, high K1, and other beta-lactamase production in Enterobacteriaceae. These included cefpodoxime, cefpodoxime plus 4 microg of clavulanate per ml, ceftazidime, ceftriaxone, and ceftriaxone plus 8 microg of sulbactam per ml. Ceftriaxone plus 2 microg of clavulanate per ml could be substituted for cefpodoxime plus 4 microg of clavulanate per ml without altering the accuracy of the tests. This study indicated that tests with key beta-lactam drugs, alone and in combination with beta-lactamase inhibitors, could provide a convenient approach to the detection of a variety of beta-lactamases in members of the family Enterobacteriaceae. (+info)
Dry-heat destruction of lipopolysaccharide: dry-heat destruction kinetics. (6/1084)Dry-heat destruction kinetics of lipopolysaccharides from Escherichia coli, Serratia marcescens, and Salmonella typhosa at 170 to 250 degrees C are described. The destruction rate seems to follow the second order and can be linearized by the equation, log y = a + b . -10cx. Because c is the slope, 1/c = D3. Both a and b are constant at a given temperature and are linear functions of temperature. The D(3)170, D(3)190, D(3)210, D(3)230, and D(3)250 values for E. coli lipopolysaccharide are 251, 99.4, 33.3, 12.3, and 4.99 min, respectively, with a z value of 46.4 min. The D values for lipopolysaccharides from S. marcescens and S. typhosa are not significantly different from those from E. coli lipopolysaccharide. (+info)
The NucE and NucD lysis proteins are not essential for secretion of the Serratia marcescens extracellular nuclease. (7/1084)The nuclease of Serratia marcescens is an extracellular protein encoded by the nucA gene. Pre-nuclease carries a typical 21-amino-acid N-terminal signal sequence that interacts with the Sec machinery to allow the translocation of nuclease to the periplasm. In Escherichia coli the nuclease remains in the periplasm; however, S. marcescens has the capacity to secrete nuclease extracellularly. The nucC operon carrying the nucEDC genes of S. marcescens has been identified previously. NucC is a transcriptional activator necessary for expression of nuclease as well as the extracellular bacteriocin 28b. NucE resembles and can act as a bacteriophage holin, whereas NucD has homology to bacteriophage lysozyme-like proteins. When present on a multicopy plasmid, the nucC operon, and specifically the nucED genes, appeared to allow extracellular secretion of nuclease from E. coli. Here experiments are reported which demonstrate that, when the nucC operon was placed in the E. coli chromosome in single copy, nuclease secretion was lost and nuclease remained periplasmic. The converse experiment, deletion of the nucE and nucD genes from the chromosome of S. marcescens, likewise had no effect on nuclease secretion by S. marcescens. It is concluded therefore that NucD and NucE are not necessary for nuclease secretion. (+info)
Characterization of a dam mutant of Serratia marcescens and nucleotide sequence of the dam region. (8/1084)The DNA of Serratia marcescens has N6-adenine methylation in GATC sequences. Among 2-aminopurine-sensitive mutants isolated from S. marcescens Sr41, one was identified which lacked GATC methylation. The mutant showed up to 30-fold increased spontaneous mutability and enhanced mutability after treatment with 2-aminopurine, ethyl methanesulfonate, or UV light. The gene (dam) coding for the adenine methyltransferase (Dam enzyme) of S. marcescens was identified on a gene bank plasmid which alleviated the 2-aminopurine sensitivity and the higher mutability of a dam-13::Tn9 mutant of Escherichia coli. Nucleotide sequencing revealed that the deduced amino acid sequence of Dam (270 amino acids; molecular mass, 31.3 kDa) has 72% identity to the Dam enzyme of E. coli. The dam gene is located between flanking genes which are similar to those found to the sides of the E. coli dam gene. The results of complementation studies indicated that like Dam of E. coli and unlike Dam of Vibrio cholerae, the Dam enzyme of S. marcescens plays an important role in mutation avoidance by allowing the mismatch repair enzymes to discriminate between the parental and newly synthesized strands during correction of replication errors. (+info)
Some common types of Serratia infections include:
1. Urinary tract infections (UTIs): Serratia bacteria can infect the urinary tract and cause symptoms such as burning during urination, frequent urination, and abdominal pain.
2. Skin infections: Serratia bacteria can cause skin infections, including cellulitis and abscesses, which can lead to redness, swelling, and pain in the affected area.
3. Respiratory tract infections: Serratia bacteria can infect the lungs and cause pneumonia, which can lead to symptoms such as coughing, fever, and difficulty breathing.
4. Bloodstream infections (sepsis): Serratia bacteria can enter the bloodstream and cause sepsis, a serious condition that can lead to organ failure and death if left untreated.
5. Endocarditis: Serratia bacteria can infect the heart valves and cause endocarditis, which can lead to symptoms such as fever, fatigue, and difficulty swallowing.
Serratia infections are typically diagnosed through a combination of physical examination, medical history, and laboratory tests, such as blood cultures and urinalysis. Treatment typically involves the use of antibiotics to eliminate the bacteria, and in severe cases, hospitalization may be necessary to monitor and treat the infection.
Preventive measures to reduce the risk of Serratia infections include practicing good hygiene, such as washing hands regularly, avoiding close contact with individuals who are sick, and maintaining proper cleanliness and sterilization practices in healthcare settings. Vaccines are not available for Serratia infections, but research is ongoing to develop new antimicrobial therapies and vaccines to combat antibiotic-resistant bacteria like Serratia.
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In medicine, cross-infection refers to the transmission of an infectious agent from one individual or source to another, often through direct contact or indirect exposure. This type of transmission can occur in various settings, such as hospitals, clinics, and long-term care facilities, where patients with compromised immune systems are more susceptible to infection.
Cross-infection can occur through a variety of means, including:
1. Person-to-person contact: Direct contact with an infected individual, such as touching, hugging, or shaking hands.
2. Contaminated surfaces and objects: Touching contaminated surfaces or objects that have been touched by an infected individual, such as doorknobs, furniture, or medical equipment.
3. Airborne transmission: Inhaling droplets or aerosolized particles that contain the infectious agent, such as during coughing or sneezing.
4. Contaminated food and water: Consuming food or drinks that have been handled by an infected individual or contaminated with the infectious agent.
5. Insect vectors: Mosquitoes, ticks, or other insects can transmit infections through their bites.
Cross-infection is a significant concern in healthcare settings, as it can lead to outbreaks of nosocomial infections (infections acquired in hospitals) and can spread rapidly among patients, healthcare workers, and visitors. To prevent cross-infection, healthcare providers use strict infection control measures, such as wearing personal protective equipment (PPE), thoroughly cleaning and disinfecting surfaces, and implementing isolation precautions for infected individuals.
In summary, cross-infection refers to the transmission of an infectious agent from one individual or source to another, often through direct contact or indirect exposure in healthcare settings. Preventing cross-infection is essential to maintaining a safe and healthy environment for patients, healthcare workers, and visitors.
Examples of communicable diseases include:
1. Influenza (the flu)
3. Tuberculosis (TB)
6. Hepatitis B and C
8. Whooping cough (pertussis)
Communicable diseases can be spread through various means, including:
1. Direct contact with an infected person: This includes touching, hugging, shaking hands, or sharing food and drinks with someone who is infected.
2. Indirect contact with contaminated surfaces or objects: Pathogens can survive on surfaces for a period of time and can be transmitted to people who come into contact with those surfaces.
3. Airborne transmission: Some diseases, such as the flu and TB, can be spread through the air when an infected person talks, coughs, or sneezes.
4. Infected insect or animal bites: Diseases such as malaria and Lyme disease can be spread through the bites of infected mosquitoes or ticks.
Prevention and control of communicable diseases are essential to protect public health. This includes:
1. Vaccination: Vaccines can prevent many communicable diseases, such as measles, mumps, and rubella (MMR), and influenza.
2. Personal hygiene: Frequent handwashing, covering the mouth when coughing or sneezing, and avoiding close contact with people who are sick can help prevent the spread of diseases.
3. Improved sanitation and clean water: Proper disposal of human waste and adequate water treatment can reduce the risk of disease transmission.
4. Screening and testing: Identifying and isolating infected individuals can help prevent the spread of disease.
5. Antibiotics and antiviral medications: These drugs can treat and prevent some communicable diseases, such as bacterial infections and viral infections like HIV.
6. Public education: Educating the public about the risks and prevention of communicable diseases can help reduce the spread of disease.
7. Contact tracing: Identifying and monitoring individuals who have been in close contact with someone who has a communicable disease can help prevent further transmission.
8. Quarantine and isolation: Quarantine and isolation measures can be used to control outbreaks by separating infected individuals from those who are not infected.
9. Improved healthcare infrastructure: Adequate healthcare facilities, such as hospitals and clinics, can help diagnose and treat communicable diseases early on, reducing the risk of transmission.
10. International collaboration: Collaboration between countries and global organizations is crucial for preventing and controlling the spread of communicable diseases that are a threat to public health worldwide, such as pandemic flu and SARS.
Serratia marcescens nuclease
Chronic granulomatous disease
Edward H. Kass
Disk diffusion test
Skeletal eroding band
Aaron E. Wasserman
White band disease
AP-1 transcription factor
Proteases (medical and related uses)
HP1 holin family
SCOP 1.57: Species: Serratia marcescens
Etymologia: Serratia marcescens - Volume 25, Number 11-November 2019 - Emerging Infectious Diseases journal - CDC
Phenotypic and genotypic characteristics of a carbapenem-resistant Serratia marcescens cohort and outbreak: describing an...
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FAQs • Moline, IL • CivicEngage
- Sehdev PS , Donnenberg MS . Arcanum: the 19th-century Italian pharmacist pictured here was the first to characterize what are now known to be bacteria of the genus Serratia. (cdc.gov)
- S. Marcescens is the strain of bacteria utilized in this activity and is non-infectious to humans. (nih.gov)
- Generate Stock Plates: After obtaining S. Marcescens , the teacher should make some stock plates which will serve as a reservoir of bacteria for activities with students. (nih.gov)
- In this study, the scientists isolated bacterial colonies from artificial diet that was fed upon by lygus, and identified the bacteria as Pantoea ananatis and Serratia spp. (usda.gov)
- P. ananatis and S. marcescens are ubiquitous bacteria that infect a wide range of crops. (usda.gov)
- So Coley changed course and crafted a vaccine with two dead bacteria, S. pyogenes and Serratia marcescens. (discovermagazine.com)
- Serratia marcescens is a type of bacteria that can sometimes be found in toilet bowls. (easytoiletips.com)
- The carrot powder was evaluated for antimicrobial activity against Bacillus cereus, Micrococcus luteus, Staphylococcus aureus, Serratia marcescens, Pseudomonas aeruginosa, and Escherichia coli . (news-medical.net)
- To support the development of rapid diagnostics capable of identifying specific bacterial strains and drug resistant phenotypes for the following healthcare-associated pathogens: Clostridium difficile, Pseudomonas, Acinetobacter, Enterobacter, Klebsiella, Serratia, Proteus, and Stenotrophomonas (Pseudomonas) maltophilia. (nih.gov)
- The NIAID invites applications for research that will lead to (1) the development of rapid diagnostics capable of identifying specific strains and drug resistant phenotypes, or (2) therapeutics to prevent or treat infections in at-risk patients for the following healthcare-associated pathogens: Clostridium difficile, Pseudomonas, Acinetobacter, Enterobacter, Klebsiella, Serratia, Proteus, or Stenotrophomonas (Pseudomonas) maltophilia. (nih.gov)
- Homologous infC sequences from Salmonella typhimurium, Klebsiella pneumoniae, Serratia marcescens and Proteus vulgaris were amplified by the polymerase chain reaction and sequenced. (nih.gov)
- RÉSUMÉ L'émergence et la propagation rapide des souches de Klebsiella pneumoniae résistantes aux antibiotiques et porteuses du gène blaKPC codant la production de carbapénèmases ont compliqué la prise en charge des infections des patients. (who.int)
- Phenotypic and genotypic characteristics of a carbapenem-resistant Serratia marcescens cohort and outbreak: describing an opportunistic pathogen. (bvsalud.org)
- Serratia marcescens is an emerging opportunistic pathogen with high genetic diversity . (bvsalud.org)
- Mortality of C. arcuata was not affected by exposure to the secondary or opportunistic pathogens, Serratia marcescens and Aspergillus sp. (usu.edu)
- According to the literature, the most common pathogens causing infections in cases of vegetative intraorbital foreign bodies include Staphylococcus epidermidis, S. aureus, Enterobacter agglomerans, Clostridium perfringens, Escherichia coli, Serratia marcescens, and Citrobacter freundii. (ophthalmologytimes.com)
- The word marcescens was chosen from Latin for the species name meaning to decay, reflecting the rapid deterioration of the pigment. (cdc.gov)
- S. Marcescens produces a red pigment (i.e. colonies are red) when grown at 30 ° C. When grown at cooler or warmer temperatures, this red pigment is not produced and colonies are white. (nih.gov)
- A toxic, bright red tripyrrole pigment from Serratia marcescens and others. (nih.gov)
- Scientists at the USDA-ARS laboratories in Shafter, CA and Stillwater, OK previously identified numerous proteins from two bacterial plant pathogens, Pantoea ananatis and Serratia spp. (usda.gov)
- Results of this study confirm the previous findings that lygus bugs transmit the plant pathogens, Pantoea ananatis and Serratia spp. (usda.gov)
- People with CGD are highly susceptible to infections, such as Staphylococcus aureus, Serratia marcescens, Burkholderia cepacia , Nocardia species, and Aspergillus species. (nih.gov)
- After researching the bioremediation capability of a combination of vetiver plant, Serratia marcescens , and Burkholderia cepacia at Tech and working as a microbiology intern at (believe it or not) a circuit board company, I made my way east to study infectious disease at Drexel. (drexel.edu)
- The Serratia marcescens hemolysin is secreted but not activated by stable protoplast-type L-forms of Proteus mirabilis. (nih.gov)
- In a recent study, proteins from Pantoea ananatis and Serratia marcescens (Enterobacteriales: Enterobacteriaceae) were identified in diet that was stylet-probed and fed upon by L. hesperus adults. (usda.gov)
- Serratia marcescens is a Gram-negative bacterium in the Enterobacteriaceae family. (easytoiletips.com)
- Serratia marcescens was later renamed Monas prodigiosus in 1846, then Bacillus prodigiosus , before the original name was restored in the 1920s in recognition of the work of Bizio. (cdc.gov)
- Serratia marcescens, which can cause nosocomial outbreaks,and urinary tract and wound infections, is abundant in damp environments ( Figure ). (cdc.gov)
- This article describes the microbiological characteristics of isolates and the risk factors for infections caused by carbapenem -resistant S. marcescens. (bvsalud.org)
- A retrospective study of patients colonized (n=43) and infected (n=20) with carbapenem -resistant S. marcescens over a 3-year period was conducted. (bvsalud.org)
- This study highlighted that blaKPC-2 in association with ompC or ompF mutation was the most common mechanism of resistance in the study hospital , and that previous use of polymyxin was an independent risk factor for carbapenem -resistant S. marcescens. (bvsalud.org)
- The objective of our study was to determine if L. hesperus transfer P. ananatis and S. marcescens to food substrates during stylet-probing activities. (usda.gov)
- Bartolomeo Bizio, a Venetian pharmacist, studied the mode of transmission of the red substance and named this microorganism Serratia in honor of Serafino Serrati, who ran the first steamboat on the Arno River in 1795, anticipating the discovery of Robert Fulton in 1807. (cdc.gov)