Description of “Bugs”

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Contents:

  • Alcaligenes Denitrificans subsp Xylosoxydans
  • Aspergillus
  • Burkholderia Cepacia
  • Clostridium difficile
  • Enterococcus strains
  • Haemophilus influenza
  • Micoplasma Virus (5/97)
  • Morganella Morganii
  • Mucoid Pseudomonas aeruginosa
  • Proteus morganii
  • Pseudomonas aeruginosa
  • Pseudomonas cepacia
  • Pseudomonas maltophilia
  • Pseudomonas Mancina
  • Staphylococcus aureus
  • Stenotrophomonas maltophilia
  • Streptococcus pneumoniae
  • Xanthomonas Maltophilia
  • Alcaligenes Denitrificans subsp Xylosoxydans
    This is a gram negative bacteria which is multi-drug resistant. It is also characterized as nosocomial (hospital caused/transmitted). The literature appears to suggest that it cultures in both nasal and lung cultures. It seems that while Alcaligenes is a bug that’s all around us and therefore was assumed for years not to be a problem, it’s becoming recognized as a pathogen in people with compromised immune systems (cancer, AIDS), and is now being looked at in those with CF (who usually have good immune systems). A CFer reports: “cipro wont treat it, but septra supposedly will”. The following is a short list of recent articles which include information on this critter.

      Wakayama, 1995. Primary structure of N-acyl-D-glutamate amidohydrolase from Alcaligenes xylosoxydans subsp. xylosoxydans A-6. J Biochem (Tokyo) 118, 204-209 (1995).

      Bizet, 1995. “Comparative susceptibility of Ochrobactrum anthropi, Agrobacterium tumefaciens, Alcaligenes faecalis, Alcaligenes denitrificans subsp. denitrificans, Alcaligenes denitrificans subsp. xylosidans and Bordetella bronchiseptica against 35 antibiotics including 17 beta-lactams Pathol Biol (Paris) 43, 258-263 (1995).

      Decre, 1995. Identification of a carbenicillin-hydrolyzing beta-lactamase in Alcaligenes denitrificans subsp. xylosoxydans. Antimicrob Agents Chemother 39, 771-774 (1995).

      Dunne, WM and S Maisch. Epidemiological investigation of infections due to Alcaligenes species in children and patients with cystic fibrosis: use of repetitive-element-sequence polymerase chain reaction. Clinical Infectious Diseases 20:836-41, April 1995.

      The title is misleading here, since ALL the PWCF cultured out Pseudomonas in the same cultures as grew A., so I don’t think they can truly call these infections “due to” A. Lots of talk about resistance and susceptibility of organisms.

      Cieslak TJ and WV Raszka. Catheter-Associated sepsis due to Alcaligenes xylosoxidans in a child with AIDS. Clinical Infectious Diseases 16:592-3, April 1993. This letter was interesting because of its discussion of synergistic antibiotic therapy in the face of a resistant form of A. Some good references too.

    Aspergillus
    see Handbook PART TWO, item 12. (Difficult to Treat Microbes — B./p. Cepacia, Methicillin Resistant Staphylococcus Aureus, Stenotrophomonas Maltophilia, Aspergillus)

    Burkholderia Cepacia
    see Handbook PART TWO, item 12. (Difficult to Treat Microbes — B./p. Cepacia, Methicillin Resistant Staphylococcus Aureus, Stenotrophomonas Maltophilia, Aspergillus)

    Clostridium difficile
    A spore-forming anaerobe (grows best in absence of atmospheric oxygen). According to one source, C. difficile is found in small numbers as part of the normal adult intestinal flora. Another source states it’s found in the infant intestine (up to about 1 year old) and rarely in adults. I tend to believe the first source. When the balance of normal intestine microbial flora is disturbed, say with antibiotic therapy, C. difficile can grow wildly unchecked. It (C. difficile) produces a cytopathic (injurious to cells/tissue) toxin which is directly implicated in a type of colitis. A rare, potentially serious intestinal disorder, pseudomembranous colitis, may develop as the result of wide-spectrum antibiotic therapy (Clindamycin, lincomycin, some cephalosporins, penicillin G, chloramphenicol, tetracycline and ampicillen have been implicated in inciting pseudomembranous enterocolitis). Pseudomembranous enterocolitis is characterized by acute inflammation and necrosis (death of tissue) involving the small and large intestines. It is marked by severe diarrhea, abdominal pain and fever. To prevent the condition from fulminating (getting worse), antibiotics sensitive to C. difficile are given (Flagyl, Vancomycin). Cholestyramine, which binds with the toxin produced by C. difficile, is sometimes used in addition.

    A medical person writes: I have experience caring for patients who have had C. difficile positive stool cultures and have gone on to develop both mild and severe cases of pseudomembranous colitis. I have seen it especially in debilitated patients who have been on triple antibiotics, especially when Clindamycin is used.

    Enterococcus strains
    (E. coli for example)

    Haemophilus influenza

    Micoplasma Virus (5/97)

    Two reports:

      FIRST:

      Mycoplasma is some NASTY S—! I cultured it for about a year, during which I spent most of my time on 24/hr O2, and some time in the ICU. It is a common societal bug — causes walking pneumonia in “healthy” folks, and major probs for us CF’ers. It causes a flood of liquid mucus, that tastes distinctive, and is treated with erythromycin and/or doxicycline. It’s a wierd bug, as it is not a bacterial phyla nor viral — intermediate, possessing characteristics from both. One cannot become “immune” to it, but each time one has it they are less likely to get it again or as severe. It can cause *major* outbreaks on CF floors. It’s best avoid the hospital for many reasons — this is a big one!

      SECOND: My husband (non-CF) had this last winter and his doctor said it was a cross between a virus and a bacteria – acted like a bacteria but spread like a virus. In the last few years, he has developed a tendency to bronchitis and he was quite sick with this. His cough sounded very similar to mine (I have CF) and he was trying to hold his chest and his head at the same time when it started up. He slept 20 hours out of 24, was off work for a week and wished he had taken a second week because he was so tired. Apparently it’s something that in healthy people will generally clear up without antibiotics but leaves you feeling sick and drained for at least 6 months. (The writer above) is right about the antibiotics of choice. I spoke with our infection control nurse at work to see if there was anything to do precaution wise in our house. Short of avoid the person like the plague that was about it and clean everything well – you know the usual common sense habits.

    Morganella Morganii
    Previous known as Proteus morganii it is classified as an Enterobacteria (as is E. coli for example). All sputum carries organisms which when isolated in the laboratory are reported as ‘normal flora’; that is, organisms although present (occasionally) in bronchial secretions, do not appear to play any role in the underlying pathogenesis (development of disease). M. morganii appears to be such an organism. If isolated by a laboratory (very rare in the case of CF sputum), it would probably be reported back to the clinician as ‘normal flora’. Treatment would only be instigated if it was repeatedly isolated. It appears that there are no reports of it ever being associated with any lung problems in CF.

    Mucoid Pseudomonas aeruginosa
    see Pseudomonas aeruginosa

    Proteus morganii
    see Morganella Morganii

    Pseudomonas aeruginosa
    P. aeruginosa is ubiquitous and found nearly everywhere in the environment from water sources to soil. This means it is difficult to avoid and sooner or later people with CF will harbor P. aeruginosa. Mucoid colonies of Pseudomonas aeruginosa are bacterium that are enclosed in a fibrous exopolysaccharide matrix which contributes to the bacteria forming colonies which are more difficult for antibiotics to penetrate. These colonies may also alter the efficacy of normal immune defenses against such bacterium. It has been suggested that the alginate (or slime) produced by P. aeruginosa is in fact a stress response and broader defense mechanism triggered in the bacteria by the CF lung environment.

    Pseudomonas cepacia
    see Handbook PART TWO (Difficult to Treat Microbes — B./p. Cepacia, Methicillin Resistant Staphylococcus Aureus, Stenotrophomonas Maltophilia, Aspergillus)

    Pseudomonas maltophilia
    see Stenotrophomonas maltophilia

    Pseudomonas Mancina
    I think that’s how you spell it. None of the docs had ever heard of it before. A little Aztreonam seemed to have kicked it though.

    Staphylococcus aureus
    Staphylococcus aureus is a fairly reactive bacterium to most mainstream (i.e., broad spectrum) antibiotics. However when it becomes methicillin resistant it becomes a bugger to treat.

    Stenotrophomonas maltophilia
    see Handbook PART TWO, item 12. (Difficult to Treat Microbes — B./p. Cepacia, Methicillin Resistant Staphylococcus Aureus, Stenotrophomonas Maltophilia, Aspergillus)

    Streptococcus pneumoniae

    Xanthomonas Maltophilia
    see Stenotrophomonas maltophilia

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