81 Matching Annotations
  1. Jun 2017
    1. .

      Both Herpes Simplex and Ebola are transmitted through bodily fluids, have a mortality rate above 70%, and enter the host cell by receptor-mediated endocytosis caused by surface glycoproteins. Herpes Simplex causes blisters/sores and inflammation of the brain and affects sexually active individuals who are immunocompromised. Ebola causes hemorrhagic fever and affects anyone who comes into contact with bodily fluids of an ill patient. Herpes Simplex makes its own DNA polymerase for DNA replication, while Ebola brings its own RNA polymerase.

    1. .

      Both Herpes Simplex and Ebola are transmitted through bodily fluids, have a mortality rate above 70%, and enter the host cell by receptor-mediated endocytosis caused by surface glycoproteins. Herpes Simplex causes blisters/sores and inflammation of the brain and affects sexually active individuals who are immunocompromised. Ebola causes hemorrhagic fever and affects anyone who comes into contact with bodily fluids of an ill patient. Herpes Simplex makes its own DNA polymerase for DNA replication, while Ebola brings its own RNA polymerase.

  2. May 2017
    1. In a hospital-based study, bacteria were cultured in up to 90% of nasopharyngeal secretions and 43% of middle ear fluid obtained from patients with AOM. S. pneumoniae, H. influenzae and M. catarrhalis were identified in 57%, 52% and 56% of nasopharyngeal secretions respectively, and less frequently in middle ear fluid (22%, 21% and 4% respectively).

      prevalence of bacterial infections

    2. The viruses most commonly coincident with otitis media were adenovirus (70%), influenza virus types A and B (65.5%), respiratory syncytial virus (RSV; 63.2%), enterovirus (62.5%), coronavirus (55.6%), rhinovirus (55.6%) and parainfluenza virus (types 1, 2 and 3; 55.3%).5 Interestingly, AOM and OME were associated with different viruses, with AOM most frequently associated with coronavirus (50%), RSV (47.4%) and adenovirus (46.5%), whereas new-onset OME occurred with influenza virus (34.5%) and enterovirus (34.4%).5 US researchers also confirmed a high frequency of association of otitis media with rhinovirus (44%) and RSV (56%).25 Among unwell children attending hospital for AOM, viruses common in URTI were detected in 35% of patients acutely ill with AOM. Among these children, the most commonly identified viruses (using viral culture) were RSV (41%), influenza (types A, B and C combined; 23%) and adenovirus (17%).24

      prevalence of viral infections

    3. Common viruses that cause upper respiratory tract infection are frequently associated with AOM and new-onset OME. These include respiratory syncytial virus, rhinovirus, adenovirus, parainfluenza and coronavirus. Predominant bacteria that cause otitis media are Streptococcus pneumoniae, Moraxella catarrhalis, and non-typeable Haemophilus influenzae.

      Organisms that cause otitis media

    1. Signs and symptoms AOM implies rapid onset of disease associated with one or more of the following symptoms: Otalgia Otorrhea Headache Fever Irritability Loss of appetite Vomiting Diarrhea webmd.ads2.defineAd({id:'ads-pos-1420',pos: 1420}); OME often follows an episode of AOM. Symptoms that may be indicative of OME include the following: Hearing loss Tinnitus Vertigo Otalgia

      signs and symptoms

    1. Almost all isolates of S. marcescens secrete a pore-forming haemolysin, ShIA, that is associated with cell cytotoxicity and the release of inflammatory mediators. This cytotoxin is thought to assist in tissue penetration (43) and may be linked to the expression of an extensive host invasive pathogenic pathway involving bacterial swarming and quorum sensing (58, 61).

      toxin

    2. Results from a recent surveillance programme in the US and Europe, indicate that Serratia spp., accounts for an average of 6.5% of all Gram negative infection in Intensive Care Units (ranked 5th amongst Gram negative organisms in ICU) and an average of 3.5% in non-ICU patients (91). Currently Serratia is the seventh most common cause of pneumonia with an incidence of 4.1% in the US, 3.2% in Europe and 2.4% in Latin America (51), and the tenth most common cause of bloodstream infection with an incidence of 2.0% amongst hospitalized patients (2).

      prevalence

    3. S. marcescensare uniformly resistant to a wide range of antibiotics including narrow-spectrum-penicillins and cephalosporins, cefuroxime, cephamycins, macrolides, tetracycline, nitrofurantoin and colistin

      antibiotic resistance

    4. Serratia usually produce extracellular deoxyribonuclease (DNase), gelatinase and lipase and are resistant to the antibiotics colistin and cephalothin

      enzymes produced and resistance

    5. Serratia marcescens is now recognized as an important opportunistic pathogen

      S. marcescens is the common pathogen in the Serratia spp. and its an opprotunistic pathogen

    1. Cephalothin was completely ineffective, and more than 90% of strains were resistant to ampicillin and tetracycline

      prevalence of resistance to ß-lactam drugs

    1. The important reservoirs in epidemics are the digestive tract, the respiratory tract, the urinary tracts and the perineum of neonates and the artificial nails of adults and health care workers.

      reservoirs of the bacteria

    1. S. marcescens may survive from 3 days to 2 month on dry, inanimate surfaces, and 5 weeks on dry floor Footnote 16. The organism may survive less than 4 days in a blood bag under aerobic conditions and 20 days in semi-anaerobic/anaerobic conditions Footnote 17. It has been also reported to survive in contact lens disinfectant (with chlorheximide), double-distilled water, non-medicated hand soap, but no duration has been reported for those cases Footnote 18-Footnote 20.

      survivance outside of the host

    1. Campylobacter jejuni isolates (47.5%). Production of β-lactamase was typically associated with resistance to ampicillin, amoxicillin (amoxicilline), penicillin, and ticarcillin.

      prevalence of ß-lactam resistance in C. jejuni

    1. Here, we analyzed the antimicrobial susceptibilities of 320 C. jejuni and 115 C. coli isolates obtained from feedlot cattle farms in multiple states in the U.S. The results indicate that fluoroquinolone resistance reached to 35.4% in C. jejuni and 74.4% in C. coli, which are significantly higher than those previously reported in the U.S.

      resistance to flouroquinolones in C. jejuni

    1. The organism is unusual among enteric pathogens in that it expresses a polysaccharide capsule (CPS) that contributes to serum resistance, invasion of intestinal epithelial cells in vitro, and virulence in ferret and Galleria mellonella larvae models of disease (1–3).

      CPS in C. jejuni

    1. the mucus overlying the epithelial cells primarily in the ceca and the small intestine but may also be recovered from elsewhere in the gut and from the spleen and liver

      colonization of the musocal cells in small intestine

    1. Our data suggest that binding of these surface exposed proteins may play a key role in C. jejuni-host cell interactions and ultimate invasion.

      role of binding proteins

    1. 14 cases are diagnosed each year for each 100,000 persons in the population. Many more cases go undiagnosed or unreported, and campylobacteriosis is estimated to affect over 1.3 million persons every year.

      prevalence

    1. Symptoms start 2 - 4 days after being exposed to the bacteria. They usually last 1 week, and may include: Cramping abdominal pain Fever Nausea and vomiting Watery diarrhea, sometimes bloody

      symptoms

    1. The organism is sensitive to oxygen, drying, freezing, salting, and acid conditions

      senvitivities

    2. Temperature range: 30-50°C (86-122°F) Optimum Temperature: 42°C (108°F) pH range: 4.9-9.0 Optimum pH: 6.5-7.5 Oxygen Requirement: 3-5% Carbon Dioxide Requirement: 2-10% Optimum Requirements: 5% Oxygen, 10% Carbon Dioxide, 85% Nitrogen Salt Tolerance: 1.0%

      Growth Conditions

    1. Our results showed that when C. jejuni cells were coincubated with Acanthamoeba polyphaga in acidified phosphate-buffered saline (PBS) or tap water, the bacteria could tolerate pHs far below those in their normal range, even surviving at pH 4 for 20 h and at pH 2 for 5 h. Interestingly, moderately acidic conditions (pH 4 and 5) were shown to trigger C. jejuni motility as well as to increase adhesion/internalization of bacteria into A. polyphaga. Taken together, the results suggest that protozoa may act as protective hosts against harsh conditions and might be a potential risk factor for C. jejuni infections.

      how Campylobacter jejuni survive low pH environments

    1. it has been connected with bacterial gastroenteritis as well as the neurological disorders Guillen-Barré Syndrome and Fisher Syndrome in humans. It is now one of the leading causes of gastroenteritis in both the developed and developing worlds.

      dangers of this bacteria

    2. microaerophilic conditions with a temperature range between 37° and 42°C. Multiple types of media can be used to cultivate it; however, Mueller Hinton broth and agar support the best C. jejuni growth. Optimum atmosphere for C. jejuni is 85% N2, 10% CO2, and 5% O2.

      growth conditions

    1. fluoroquinolones, macrolides, trimethoprim, beta lactam antibiotics, including penicillin and most cephalosporins, as well as to tetracycline, quinolone and kanamycin

      Drug resistance

    2. COMMUNICABILITY: Low, person-to-person transmission is unusual

      communicability of bacteria

    3. C. jejuni has been associated with post-infection sequelae, most commonly Guillain-Barré syndrome and reactive arthritis

      Sequelae

    1. Skirrow’s Campylobacter Medium (contains polymixin B, trimethoprim, vancomycin) ·   Preston Campylobacter Medium (contains polymixin B, rifampicin, trimethoprim) ·   Campy Blood Agar ·   CVA Medium (contains cefoperazone, vancomycin, amphotericin) Selective media for Campylobacter jejuni

      Lab specific test for Campylobacter jejuni

    1. We and other authors have reported a high prevalence of hypermutable H. influenzae isolates causing respiratory infections (22, 24). We also noticed a high rate of fluoroquinolone resistance in these isolates (22) and reported a therapeutic failure in a community-acquired pneumonia case due to levofloxacin-resistant H. influenzae (2).

      resistance of flouroquinolone

    1. 1.7 cases per 100,000 children younger than 5 years of age and 5.0 cases per 100,000 adults 65 years of age or older

      prevalence

    2. Patients ≥65 years of age with invasive H. influenzae disease (Hib, non-b, and nontypeable) have higher case-fatality ratios than children and young adults.

      sequelae and severity

    1. Additionally, Hap mediates adherence to fibronectin, laminin and collagen IV, extracellular matrix (ECM) proteins that are present in the respiratory tract and are probably important targets for H. influenzae colonization.

      adhesion

    1. Its capsule, the adhesion proteins, pili, the outer membrane proteins, the IgA1 protease and, last but not least, the lipooligosaccharide,

      Virulance factors

    1. the United States down from 36% in 1994 to 26% in 2002

      prevalence in US

    2. overall prevalence of 16.6% β-lactamase-positive strains, ranging from as low as 3% in Germany to as high as 65% in South Korea

      prevalence

    1. Haemophilus influenzae infection is transmitted by droplets from infected (but not necessarily symptomatic) people. Haemophilus influenzae type b be can be prevented by vaccination.

      transmition

    2. Haemophilus influenzae type b is a Gram-negative bacterium that causes meningitis and acute respiratory infections, mainly in children

      mainly in children but elderly like children have lower immune systems

    1. Nucleic acid amplification test (NAAT) is the recommended method of testing for gonorrhea. NAAT is a molecular test that detects the genetic material (DNA) of Neisseria gonorrhoeae

      NAAT test

  3. bacmap.wishartlab.com bacmap.wishartlab.com
    1. Names Neisseria gonorrhoeae FA 1090 Accession numbers NC_002946 Background Neisseria gonorrhoeae is one of two pathogenic Neisseria, this species causes the sexually transmitted disease (STD) gonorrhea, which is the leading reportable STD in adults in the USA. This human-specific organism colonizes and invades the mucosal surface of the urogenital epithelium, crosses the epithelial barrier, and ends up multiplying on the basement membrane. The result is severe painful inflammation and purulent discharge. Neisseria gonorrhoeae (strain NCCP11945) was isolated in 2002 from a vaginal smear of a Korean patient. This is a multidrug-resistant strain and will be used to understand the prevalence, antibiotic resistance, and importance of horizontal gene transfer within this important, naturally competent organism. (EBI Integr8) Taxonomy Kingdom:Bacteria Phylum:Proteobacteria Class:Betaproteobacteria Order:Neisseriales Family:Neisseriaceae Genus:Neisseria Species:gonorrhoeae Strain FA 1090 Complete Yes Sequencing centre (08-APR-2002) National Center for Biotechnology Information, NIH, Bethesda, MD 20894, USA(10-MAR-2003) Microbiology and Immunology, University of Oklahoma Health Sciences Center, 975 NE 10th St., Oklahoma City, OK Sequencing quality Level 6: Finished Sequencing depth NA Sequencing method NA Isolation site Patient with disseminated gonococcal infection Isolation country NA Number of replicons 1 Gram staining properties Negative Shape Cocci Mobility No Flagellar presence No Number of membranes 2 Oxygen requirements Aerobic Optimal temperature 35.0 Temperature range Mesophilic Habitat HostAssociated Biotic relationship Free living Host name Homo sapiens Cell arrangement Pairs, Singles Sporulation Nonsporulating Metabolism NA Energy source NA Diseases Gonorrhea Pathogenicity Yes

      useful information

    1. Doctors usually will treat the patient with antibiotics that are effective on the locally occurring N. gonorrhoeae strains. Currently, the CDC recommends the following treatment for gonorrhea: ceftriaxone, 250mg IM plus a single dose of azithromycin, 1 g, orally.

      Treatment

    1. Neisseria gonorrhoeae infections are acquired by sexual contact and usually affect the mucous membranes of the urethra in males and the endocervix and urethra in females. The pathogenic mechanism involves the attachment of the bacterium to nonciliated epithelial cells through pili (fimbriae) and the production of lipopolysaccharide endotoxin. [8]. Neisseria gonorrhoeae is only found after sexual contact with an infected person (or in the case of infections in the newbord, direct contact).

      Location and pathology

    1. Thayer-Martin agar (or Thayer-Martin medium) is a Mueller-Hinton agar with 5% chocolate sheep blood and antibiotics. It is used for culturing and primarily isolating pathogenic Neisseria bacteria, including Neisseria gonorrhoeae and Neisseria meningitidis, as the medium inhibits the growth of most other microorganisms.

      Thayer-Martin Plate

    1. Throat. Signs and symptoms of a throat infection may include a sore throat and swollen lymph nodes in the neck.

      Symptoms

    1. FeverAbdominal painDischarge from the penis or vaginaPain with urinationArthritis, joint painAppearance of a rash with dark centersLethargyRectal pain or dischargeSore throat (pharyngitis)Sexual contact with an infected person

      Symptoms

    1. Symptoms depend on the type of STD contracted. Oral gonorrhea, as described by the Centers for Disease Control and Prevention (CDC), is also called pharyngeal gonorrhea because it typically affects the pharynx. Symptoms that could indicate an oral STD include: Sores in the mouth, which may be painless. Lesions similar to cold sores and fever blisters around the mouth. Red, painful throat and difficulty swallowing. Tonsillitis. Redness with white spots resembling strep throat. Whitish or yellow discharge.

      Symptoms of oral infection

  4. Apr 2017
    1. Staphylococci failed to develop resistance to 05865

      There have been a few strains that are found to be VISA or VRSA which are Staph that have developed a resistance to vancomycin. They are able to be treated by other drugs. https://www.cdc.gov/hai/organisms/visa_vrsa/visa_vrsa.html

    1. The efficacy of vancomycin for the treatment of patients with infections due to Staphylococcus aureus is impaired by its poor tissue penetration and by its relatively weak antibacterial activity

      vancomycin

    1. Novobiocin is an aminocoumarin. Aminocoumarins are very potent inhibitors of bacterial DNA gyrase and work by inhibiting the GyrB subunit of the enzyme involved in energy tranduction. Novobiocin as well as the other aminocoumarin antibiotics act as competitive inhibitors of the ATPase reaction catalysed by GyrB.

      Novobiocin

    1. Isotopic experiments showed that, in addition to inhibiting cell-wall synthesis, novobiocin also inhibited both protein and nucleic acid synthesis

      Novobiocin on S. aureus

    1. Basic Characteristics Properties (Staphylococcus aureus) Capsule Non-Capsulated Catalase Positive (+ve) Citrate Positive (+ve) Coagulase Positive (+ve) Gas Negative (-ve) Gelatin Hydrolysis Positive (+ve) Gram Staining Positive (+ve) H2S Negative (-ve) Hemolysis Positive (+ve)- Beta Indole Negative (-ve) Motility Negative (-ve) MR (Methyl Red) Positive (+ve) Nitrate Reduction Positive (+ve) OF (Oxidative-Fermentative) Fermentative Oxidase Negative (-ve) Pigment Mostly Positive (+ve) PYR Negative (-ve) Shape Cocci Spore Non-Sporing Urease Positive (+ve) VP (Voges Proskauer) Positive (+ve) Fermentation of Arabinose Negative (-ve) Cellobiose Negative (-ve) DNase Positive (+ve) Fructose Positive (+ve) Galactose Positive (+ve) Glucose Positive (+ve) Lactose Positive (+ve) Maltose Positive (+ve) Mannitol Positive (+ve) Mannose Positive (+ve) Raffinose Negative (-ve) Ribose Positive (+ve) Salicin Negative (-ve) Sucrose Positive (+ve) Trehalose Positive (+ve) Xylose Negative (-ve) Enzymatic Reactions Acetoin Production Positive (+ve) Alkaline Phosphatase Positive (+ve) Arginine Dehydrolase Positive (+ve) Hyalurodinase Positive (+ve) Lipase Positive (+ve) Ornithine Decarboxylase Negative (-ve)

      Biochemical tests

    1. S. aureus is a facultative anaerobe so can grow under both aerobic and anaerobic conditions. However, growth occurs at a much slower rate under anaerobic conditions

      Facultative anaerobe

    2. The temperature range for growth of S. aureus is 7–48°C, with an optimum of 37°C.S. aureus is resistant to freezing and survives well in food stored below -20°C; however, viability is reduced at temperatures of -10 to 0°C. S. aureus is readily killed during pasteurisation or cooking. Growth of S. aureus occurs over the pH range of 4.0–10.0, with an optimum of 6–7

      Growth Conditions

    1. Staphylococcus aureus is found in humans in the nose, groin, axillae, perineal area (males), mucous membranes, the mouth, mammary glands, hair, and the intestinal, genitourinary and upper respiratory tracts Footnote 2, Footnote 4, Footnote 18. Many animals act as reservoirs, particularly cows with infected udders

      Reservoirs

    1. bacteria are then exposed to different antibiotics, including methicillin. S. aureus bacteria that grow well when methicillin is in the culture are termed MRSA

      How to classify S. aureus bacteria as MRSA

    2. MRSA infections can cause complications such as infection of heart valves (endocarditis), gangrene or death of the soft tissues (necrotizing fasciitis), and bone or joint infections (osteomyelitis or septic arthritis)

      Sequelae

    3. Cellulitis, an infection of the skin or the fat and tissues under the skin, usually starting as small red bumps in the skin. It includes redness, swelling of the tissues, warmth, and tenderness.Boils (pus-filled infections of hair follicles)Abscesses (collections of pus in or under the skin)Sty (an infection of an oil gland of the eyelid)Carbuncles (infections larger than an abscess, usually with several openings to the skin)Impetigo (a skin infection with pus-filled blisters)Rash or skin redness (skin appears to be reddish or have red-colored areas)

      Symptoms of MRSA

    4. If the infection is severe or may be spreading into the blood (bacteremia), fevers and shaking chills may occur.

      Other similar symptoms to the case

    5. MRSA infection may begin as redness or a rash with a pus-filled pimple or boil. It may progress to an open, inflamed area of skin that may weep pus or drain fluid

      Symptoms similar to the case study

    6. A deadly complication of MRSA is a deep infection, necrotizing fasciitis, which causes rapid spread and destruction of human tissues. Some but not all strains of MRSA are more likely to behave like "flesh-eating bacteria." It is impossible to predict which MRSA infection will be "flesh-eating."

      MRSA has the ability to lead to Necro Fas but it is rare

    1. Antibiotics treat serious cases of cat scratch fever

      Treatment

    2. In rare cases, surgery is necessary to remove infected tissues from the eye

      sequelae

    3. an eye infection that produces symptoms similar to pink eye

      sequelae

    4. result in bone damage

      sequelae

    5. causing impaired vision

      sequelae

    6. encephalopathy results in permanent brain damage or death

      sequelae/outcome

    7. indirect fluorescent antibody (IFA) blood test to see if the Bartonella henselae bacteria are present in your body

      diagnosis

    8. enlarged spleen (an organ above your stomach)

      how to diagnos

    9. a bump or blister at the bite or scratch site swollen lymph nodes near the bite or scratch site fatigue headaches a low-grade fever

      Symptoms

    10. 40 percent of cats carry the bacteria at some time in their lives, most commonly when they are kittens

      Cats also get the disease from fleas. Bacteria is common in cats

    11. weakened immune system

      If you have a weaker immune system then people are more susseptable to contract the infection

    12. bite or scratch from an infected cat. You can also get the disease if saliva from an infected cat gets into an open wound on your body or touches the whites of your eyes

      How to contract the disease

    13. Bartonella henselae bacteria

      The bacterial name

    14. people contract it from cats

      Reservoir

    15. bacterial infection

      Cat Scratch disease is a bacterial infection