1,440 Matching Annotations
  1. May 2017
    1. Microbiologyand PathologyoEtiologic agent is Neisseria gonorrhoeae.oGram-negative intracellular diplococcus, oxidase-positive, utilizes glucose, but not sucrose, maltose, or lactose. Infects mucus-secreting epithelial cells.oDivides by binary fission every 20-30 minutes.oN. gonorrhoeaeattachesto different types of mucus-secreting epithelial cells via a number of structures located on the surface of gonococci.oN. gonorrhoeaehas ability to alter these surface structures, which helps the organism evade an effective host response.oN. gonorrhoeaeemploys several mechanisms to disarm the complement system, which may result in a survival advantage in the humanhost.

      gonorrhoeae pathogenesis

    1. SURVIVAL OUTSIDE HOST: The bacterium can survive on a dry surface for 3 days to 6.5 months (22). It has been found to survive in ice cream (18 days), raw and pasteurized milk at 15-37 ºC (96 hrs), room temperature butter (48 hrs), and neutralized butter (12-17 days) (17). GAS has been found to last several days in cold salads at room temperature (18).

      survival outside host

    1. This is another picture of a blood agar plate with growth and hemolytic activity of group B streptococci (GBS) (on the left) and group A streptococci (GAS) (on the right). Note that the colonies of both bacteria appear about the same color and size, but the degree of hemolytic activity is very different. The group A Streptococcus has more hemolytic activity than the group B Streptococcus. Experienced microbiologist use these traits to identify the two types of bacteria.

      We can use this test to differentiate between GBS and GAS

    1. Gonococcal specimens should be subcultured from the selective primary medium to a noninhibitory medium, e.g., chocolate agar with 1% IsoVitaleX to obtain a pure culture of the specimen. If the subcultured specimen is not pure, serial subcultures of individual colonies must be performed until a pure culture is obtained. After 18 to 20 hrs. incubation, a heavy suspension of growth from the pure culture should be made in trypticase soy broth containing 20% (v/v) glycerol

      how to get pure sample

    2. A presumptive identification of N. gonorrhoeae will be based on the following criteria: (i) growth of typical appearing colonies on a selective medium such as Thayer-Martin at 35oC to 36.5oC in 5% CO2, (ii) a positive oxidase test, and (iii) the observation of gram-negative, oxidase-positive diplococci in stained smears.

      how to test for n. gonorrhoeae

  2. Apr 2017
    1. methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant Staphylococcus epidermidis (MRSE) and amoxicillin-resistant enterococci

      Main uses of Vancomycin = bacterias with resistance to other antibiotics, perhaps not usual first line of defense if organism isn't known

    2. Vancomycin-associated nephrotoxicity can still be seen, even in the presence of appropriate serum concentrations, especially when it is co-administered with aminoglycosides, amphotericin B, foscarnet, pentamidine ACE inhibitors, loop diuretics, cyclosporine, cyclophosphamide

      Vancomycin is stated earlier in article to be more effective when used in combination therapy because the combination therapy acts faster than vancomycin alone. Downside of combination therapy is increased nephrotoxicity risk.

    3. It has been speculated that exposure to oral vancomycin is an important contributor to propagation of VRE in the healthcare setting, as it drives prolonged colonization with VRE from a myriad of sources (36, 37).

      Oral vancomycin may cause the development of VRE's which are "vancomycin-resistant enterococci" (Google Search).

    4. Vancomycin resistance among enterococci is attributed to change in the d-alanyl-d-alanine portion of peptide precursor units, transmitted as Van genes, thus rendering it incapable of inhibiting peptidoglycan polymerase and transpeptidation reactions.

      Mechanism bacteria use to resist vancomycin.

    5. Vancomycin is a tricyclic glycopeptide (Figure 1) that consists of seven membered peptide chains forming the tricyclic structure and attached disaccharide composed of vancosamine and glucose.

      The structure could be imporant in how it is able to treat bacteria.

    6. major use of vancomycin today is for infections caused by methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant Staphylococcus epidermidis (MRSE) and amoxicillin-resistant enterococci. In its oral form, vancomycin is used to treat diarrhea caused by Clsotridium difficile.

      Vancomycin can be used to tackle MRSA (Methicillin Resistant Staph Aureus) and MRSE (Methicillin Resistant Staph Epidermidis)

    7. The subsequent emergence of vancomycin resistance among enterococci in the mid-1980s and failure of such patients even if they had enterococci with vancomycin-intermediate susceptibility was described, resulting in vancomycin losing it omnipotence for all gram-positive cocci (12). The appearance of S. aureus strains with intermediate susceptibility to vancomycin (VISA) and vancomycin-resistant S. aureus (VRSA) (12–14) and vancomycin-resistant S. epidermidis (VRSE) (15, 16), brought an end to the hitherto hegemony of vancomycin in the Gram-positive coccal arena. Fortunately, the occurrence of these difficult to treat Staphylococci remains rare.

      intermediate resistance

    8. Vancomycin is effective against most Gram-positive cocci and bacilli with the exception of rare organisms as well as enterococci that became vancomycin resistant, mostly Enterococcus faecium

      Vancomycin is effective on gram positive bacteria that have a thick peptidoglycan later.

    9. While vancomycin is bactericidal against all susceptible Gram-positive pathogens it exerts only bacteriostatic activity against enterococci and needs to be combined with another agent, usually an aminoglycoside, to achieve bactericidal activity.

      I am really interested in how the same compound could have differential effects on different organisms.

    10. trough serum levels

      what does this mean? I looked it up (wikipedia) and it is the dip in levels of Vanco in the blood. Dosing in Vanco treatment is timed to coincide with the dip so that the dosage stays high in the blood

    1. Streptococcus Penicillinplusclindamycin 2–4 million units every 4–6 h IV (adult)600–900 mg every 8 h IV 60 000–100 000 units/kg/dose every 6 h IV10–13 mg/kg/dose every 8 h IV Vancomycin, linezolid, quinupristin/dalfopristin, daptomycin Staphylococcus aureus Nafcillin 1–2 g every 4 h IV 50 mg/kg/dose every 6 h IV Vancomycin, linezolid, quinupristin/dalfopristin, daptomycin Oxacillin 1–2 g every 4 h IV 50 mg/kg/dose every 6 h IV Cefazolin 1 g every 8 h IV 33 mg/kg/dose every 8 h IV Vancomycin (for resistant strains) 30 mg/kg/d in 2 divided doses IV 15 mg/kg/dose every 6 h IV  

      antibiotics Information

    1. MODE OF TRANSMISSION: Transmission via respiratory droplets, hand contact with nasal discharge and skin contact with impetigo lesions are the most important modes of transmission (5, 9, 13). The pathogen can be found in its carrier state in the anus, vagina, skin and pharynx and contact with these surfaces can spread the infection (5, 14, 15) The bacterium can be spread to cattle and then back to humans through raw milk as well as through contaminated food sources (salads, milk, eggs); however, cattle do not contract the disease (16-18). Necrotizing fasciitis is usually because of contamination of skin lesions or wounds with the infectious agent (12).

      transmission + usual route of entry for nec fasc, GAS

    1. Numerous epidemiological studies have identified high rates of invasive S. pyogenes infection in men rather than women, a pattern that can be observed for many other invasive bacterial infections and one that is not fully understood. Age-specific incidence rates show a typical J-shaped distribution, with highest rates in the elderly, followed by infants. Assessment of rates of disease according to patient ethnicity show generally higher rates of disease in individuals of non-white European descent. These observations have been made in a diverse range of populations, including indigenous populations of Australia, New Zealand, the Pacific Islands, and circumpolar regions of the northern hemisphere. The reasons behind these excesses in risk are poorly understood and could reflect differential access to healthcare or general living conditions—but could also encompass some genetic predisposing factors.

      demographic risk factors for GAS

    2. Numerous epidemiological studies have identified high rates of invasive S. pyogenes infection in men rather than women, a pattern that can be observed for many other invasive bacterial infections and one that is not fully understood. Age-specific incidence rates show a typical J-shaped distribution, with highest rates in the elderly, followed by infants. Assessment of rates of disease according to patient ethnicity show generally higher rates of disease in individuals of non-white European descent. These observations have been made in a diverse range of populations, including indigenous populations of Australia, New Zealand, the Pacific Islands, and circumpolar regions of the northern hemisphere. The reasons behind these excesses in risk are poorly understood and could reflect differential access to healthcare or general living conditions—but could also encompass some genetic predisposing factors. Future studies will assist in identifying potential strategies to mitigate this risk.

      men more than women

    1. TABLE III. MicrobiologyAerobicGram-positive cocciStaphylococcus aureus27MRSA3Coagulase-negative Staphylococcus40 (incl S epidermidis, S hemolyticus)StreptococcusBeta-hemolytic70Group A40Group B17 (incl S agalactiae, 1)Group D6 (non-Enterococcus)Group F5Group G2Alpha-hemolytic/S viridans31

      Table of prevalence of S. aureus, Group A strep, Group B strep, and S. viridans

    1. Necrotizing Fasciitis (Streptococcal Gangrene): GAS necrotizing fasciitis is a rapidly progressing infection of the deep subcutaneous tissues and fascia with extensive and rapidly spreading necrosis. Infections often spare the skin, but 50% of patients may have associated myonecrosis. Necrotizing fasciitis is often associated with severe systemic involvement and an associated high mortality rate (7,80,87). As in other invasive streptococcal and staphylococcal skin infections, the site of inoculation is usually at area of minor trauma or the skin lesions of varicella. Like streptococcal bacteremia, there is a clear association between varicella and necrotizing fasciitis. Varicella is characterized by full-thickness dermal lesions that may induce selective immunosuppression to GAS, though this has not been substantiated (7). Necrotizing fasciitis caused by mixed infections, involving both aerobic and anaerobic Gram negative bacteria, is more likely to occur in the abdominal wall, following abdominal surgery or in diabetic patients.

      Nec Fasc. GAS

    2. Early and aggressive surgical debridement of the site of infection as well as appropriate antimicrobial therapy is required. Due to the "inoculum effect," penicillin may be less effective in the treatment of necrotizing fasciitis (83). Appropriate antibiotics include nafcillin and clindamycin (7,83).  

      antibiotic treatment for nec fas.

    3. Puerperal Sepsis: Puerperal sepsis occurs during pregnancy or during an abortion, when group A streptococcus colonizing the patient invades the endometrium and surrounding structures as well as the lymphatics and bloodstream. Endometritis and septicemia result and can be complicated by pelvic cellulitis, thrombophlebitis, peritonitis, or pelvic abscess. Therapy consists of aggressive surgical exploration and parenterally administered penicillin or clindamycin (see section on myositis/myonecrosis). Patients allergic to penicillin can be treated with a first generation cephalosporin, clindamycin, or vancomycin (8).  

      treatment of GAS infection

    1. only five are known to commonly cause disease in immune-competent human beings: Group A, Group B, both members of Group D, and two groups that lack the Lancefield carbohydrate antigen: Streptococcus pneumoniae and Viridans streptococci.[5]

      differentiate GAS and GBS from viridans group strep

    1. Penicillins and other antibiotics in the beta-lactam family contain a characteristic four-membered beta-lactam ring. Penicillin kills bacteria through binding of the beta-lactam ring to DD-transpeptidase, inhibiting its cross-linking activity and preventing new cell wall formation.
    1. The ability to invade HUVEC was exhibited by selected strains of S. gordonii, S. sanguis, S. mutans, S. mitis, and S. oralis but only weakly by S. salivarius. Comparison of isogenic pairs of S. gordonii revealed a requirement for several surfa

      attachement

    1. S mutans and S sanguis (involved in dental caries), S mitis (associated with bacteremia, meningitis, periodontal disease and pneumonia), and “S milleri” (associated with suppurative infections in children and adults).

      assciated diseases

    1. is a facultative anaerobe and is grown at 37°C in either ambient air or in 5–10% CO2. Like all streptococci, GAS is both catalase and oxidase negative. GAS lacks the necessary enzymes for a functional TCA cycle and oxidative-cytochromes for electron transport; therefore, relies completely on fermentation of sugars for growth and energy production. It is a member of the lactic acid bacteria and is homofermentative for lactic acid production from glucose fermentation. Specific components of a rich growth medium for GAS include neo peptone extracts, glucose as carbon source, and a complex mixture of nutrients from beef heart infusion as first described by Todd & Hewitt (Todd and Hewitt, 1932). GAS is considered a multiple amino acid auxotroph requiring nearly all amino acids to be present in its growth media. A Chemically Defined Medium has been developed for GAS containing all of the necessary amino acids for GAS growth (van de Rijn, 1980).

      Lab tests, microbe metabolism

    1. For presumptive identification of S. pyogenes, cultures should be tested for bacitracin susceptibility and PYR activity (as described below). A definitive diagnosis should include a positive Lancefield group A antigen test. Negative results can be confirmed after a total culture time of 48 hours.

      IMPORTANT!!! Include under Question 12 (Other tests):

      1. Increased bacitracin sensitivity (bacitracin = antibiotic) 2.PYR activity (tests for enzyme that produces red color under test conditions and is specific to S. pyogenes)
      2. Lancefield group A antigen test (Definitive diagnosis)
    2. To identify S. pyogenes in clinical samples, blood agar plates are screened for the presence of β-hemolytic colonies. The typical appearance of S. pyogenes colonies after 24 hours of incubation at 35-37°C is dome-shaped with a smooth or moist surface and clear margins. They display a white-greyish color and have a diameter of > 0.5 mm, and are surrounded by a zone of β-hemolysis that is often two to four times as large as the colony diameter. Microscopically, S. pyogenes appears as Gram-positive cocci, arranged in chains (Figure 1).

      Colony morphology

    1. The ability of bacterial species to hydrolyze the compound hippurate was classically tested using ferric chloride indicator to detect benzoic acid, the first byproduct in the hippurate hydrolysis pathway. However, a 2½ hour rapid method as opposed to the 48 hour classical method for detecting hippurate hydrolysis has since been developed. The rapid test employs ninhydrin as the indicator, which detects glycine, the second byproduct of hippurate hydrolysis. The rapid hippurate hydrolysis test has been shown to be as specific and as sensitive as the classical method that detects the benzoic acid byproduct. (4,5,8,9)

      Hippurate test

    1. Superantigens are potent immunostimulators that cause clonal proliferation of T cells and watershed production of pro-inflammatory cytokines that mediate shock and organ failure.

      Superantigens cause STSS by inducing T-cell proliferation and production of proinflammatory cytokines.

    1. GBS hyaluronidase degrades pro-inflammatory hyaluronan (HA) fragments to disaccharides•HA disaccharides block TLR2/4 signaling by both HA fragments and TLR2/4 agonists•Hyaluronidases secreted by Gram-positive pathogens promote immune evasion•HA disaccharides and GBS hyaluronidase inhibit inflammation in a lung injury model

      Immune evasion

    1. Numerous phages are known to carry determinants that increase virulence to the bacterial host. These factors have been predominantly secreted toxins, such as the streptococcal erythrogenic toxin, staphylococcal enterotoxin A, diphtheria toxin, and cholera toxin (10). Other phage-encoded virulence determinants include extracellular enzymes such as staphylokinase and streptococcal hyaluronidase, enzymes that alter the antigenic properties of the host strain, and outer membrane proteins that increases serum resistance (10). It is likely that Pb1A and Pb1B bind platelets directly, although the mechanism by which PblA and PblB mediate platelet binding by S. mitis has not been illustrated. Thus, the encoding of PblA and PblB by lysogenic SM1 may represent a class of phage-mediated virulence determinants (10).

      virulence

    1. Occasionally, however, these bacteria can cause much more severe and even life threatening diseases such as necrotizing fasciitis (occasionally described as "the flesh-eating bacteria") and streptococcal toxic shock syndrome (STSS).

      Again, group A can cause the symptoms seen in the patient.

    1. based on alpha-hemolysis, gram-positive reaction, coccus morphology in chains, negative catalase test, and exclusions of pneumococci and enterococci by routine biochemical tests (optochin test, bile solubility, and PYR [N,N-dimethylaminocinnamaldehyde] test).

      Identification of VGS in lab

    1. Necrotizing fasciitis should be treated in an ICU. Extensive (sometimes repeated) surgical debridement is required. A recommended initial antibiotic regimen is a β-lactam (often a broad-spectrum drug until etiology is confirmed by culture) plus clindamycin. Although streptococci remain susceptible to β-lactam antibiotics, animal studies show that penicillin is not always effective against a large bacterial inoculum because the streptococci are not rapidly growing and lack penicillin-binding proteins, which are the target of penicillin activity.

      treatment - general

    1. "Strep throat," – swollen tonsils possible covered with a grayish-white film, swollen lymph nodes, and fever with or without chills, painful swallowing and headache. Impetigo - mild skin infection accompanied by open, draining sores and other general symptoms of GAS infection such as fever, swollen lymph nodes and a sore throat. Scarlet fever - characterized by a fever, sore throat, red sandpaper-like rash and a red "strawberry" tongue. It is caused by several different strains of the streptococcal bacteria, all of which produce a toxin that cause the characteristic red rash.

      some of the signs and symptoms