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posted by chromas on Wednesday July 03 2019, @12:21PM   Printer-friendly
from the I'll-just-leave-this-here dept.

Hard-to-kill poop parasites that lurk in swimming pools on the rise, CDC warns

Outbreaks of the gastrointestinal parasite cryptosporidium have been spurting upward since 2009, with the number of outbreaks gushing up an average of 13% each year, according to researchers at the Centers for Disease Control and Prevention. The germ spreads via the fecal-oral route and causes explosive, watery diarrhea that can last for up to three weeks. Most victims pick up the infection from recreational waters, such as swimming pools and water parks.

The main trouble is that crypto is extremely tolerant of chlorine and can happily stay afloat in well-treated pools for more than seven days. Thus, sick swimmers are the main source of infection—often young children who have yet to master toilet skills and also have more of a tendency to gulp pool water. An infected person can shed 100 million parasite eggs in one bout of diarrhea. Knocking back just 10 or fewer eggs in contaminated pool water can lead to an infection.

A 2013 study released by the CDC found that 58% of tested pools were positive for bacteria typically present in fecal matter.

[...] In all, the CDC recorded 444 outbreaks, involving 7,465 cases, 287 hospitalizations, and one death from the parasite. The number of cases per outbreak ranged from two to 638. However, the CDC notes that the figures likely underestimate the number of outbreaks and cases given that not every state reliably reports outbreaks and many people don't report their illnesses.


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  • (Score: 0) by Anonymous Coward on Wednesday July 03 2019, @04:27PM (4 children)

    by Anonymous Coward on Wednesday July 03 2019, @04:27PM (#862773)

    Section 3.2 doesn't say that "metallic antibiotics breed resistance much faster than traditional antibiotics". Here it is in full for anyone else:

    3.2 Metal Resistance
    Metals have been biologically available since the Great Oxidation Event 2.4
    billion years ago (Chi Fru et al., 2016). Resistance genes to toxic metals and
    metalloids are believed to be ancient (Boyd & Barkay, 2012; Jackson &
    Dugas, 2003; Staehlin, Gibbons, Rokas, O’Halloran, & Slot, 2016); in silico
    evolution studies would suggest that metal resistance genes (MRGs) should
    be as ancient as metal toxicity ( Jenkins & Stekel, 2010), but this is difficult to
    prove with sequence analysis due to the timescales involved.
    Metal resistance is a common phenotype in many microorganisms that
    are exposed to metals in their habitats. Pal et al. (2015) showed that resistance
    genes to biocides and metals are present in the great majority of genomes
    isolated from different environments ranging from humans, animals and
    insect symbionts, to extreme environments, such as hydrothermal vents
    and environments polluted by discharges from antibiotic manufacture. In
    contrast, the presence of such genes on plasmids was considerably less common
    in all types of environments.
    Antimicrobial metals have been released into the biosphere in huge
    quantities through geological events for billions of years, and used by
    humans in medicine, agriculture and manufacturing, for thousands of years.
    There is data that associate metal contamination in different environments
    (due to either geological or anthropogenic activities) and the presence of
    MRGs (Farias et al., 2015; Poulain et al., 2016; Staehlin et al., 2016). Recent
    work analysing the occurrence of bacterial MRGs in dated permafrost cores
    and deep subterranean bacterial isolates links increases in the numbers of
    mercury (Poulain et al., 2016) and divergence of copper (Staehlin et al.,
    2016) resistance genes to global deposition of toxic metals due to industrial
    activity. This not only includes the rapid increase in metal production during
    the industrial revolution, but also dissemination of these metals due to inefficient
    methods of smelting in preindustrial revolution eras.
    Mercury resistance is especially important because some mer transposons
    can accumulate other resistances, and are therefore a vector for co-resistance
    (Liebert, Hall, & Summers, 1999; Summers, 2004). Mercury resistance
    transposons, which are closely related to modern Tn21-family transposons,
    but lacking ARGs, or the integron carrying them, have been detected from
    ‘preantibiotic era’ bacteria (Essa, Julian, Kidd, Brown, & Hobman, 2003),
    and from permafrost isolates from ice cores that are over 8000 years old
    (Kholodii, Mindlin, Petrova, & Minakhina, 2003). Therefore, the preexistence
    of these MGEs may also have contributed to the rapid evolution of
    resistance in the modern era.
    Predation by protists might also act as a driver for the presence of MRGs
    in bacteria (Hao et al., 2017, 2015, 2016). Metal poisoning is employed by
    protists to first inactivate and then kill bacteria (Hao et al., 2015, 2016). In
    response, bacteria have evolved metal detoxification strategies including
    copper/zinc resistance determinants and thus have selected for metal
    (copper/zinc) resistance to avoid killing by metal poisoning (Hao et al.,
    2016). Since these resistance genes would aid survival in protists, one could
    expect a higher occurrence of additional copper, zinc and arsenic resistance
    determinants. Thus, this could be an important factor/driver to select metal
    resistance or co-select antibiotic resistance. These mechanisms would also
    predate the antibiotic era.
    Thus, the ancient nature and broad distribution of metal ion resistance
    and homeostasis genes, efflux pumps, MGEs, and ARGs, suggests that the
    ‘tool-kit’ of genes and other elements required for the evolution of multiresistant
    bacteria already existed before the modern antibiotic era. This leads
    to the question: Has the development and spread of resistance to antibiotics
    in pathogens been further promoted by the exposure to metals? In the next
    section, we will provide a short historical reflection on bacterial resistance
    with a particular emphasis on the detection of metal resistance occurrence,
    in conjunction with antibiotic resistance.

    The noble metals all still make great antibiotic surfaces despite bacteria having been exposed to them for billions of years. What does that tell you?

  • (Score: 2) by ikanreed on Wednesday July 03 2019, @06:22PM (3 children)

    by ikanreed (3164) Subscriber Badge on Wednesday July 03 2019, @06:22PM (#862832) Journal

    I guess I should have been more clear as to what I meant that to be citing: the already existing genetic infrastructure for resistance.

    • (Score: 0) by Anonymous Coward on Wednesday July 03 2019, @06:50PM (2 children)

      by Anonymous Coward on Wednesday July 03 2019, @06:50PM (#862848)

      Do you have a source for the claim of interest? I would be surprised if that is correct, but maybe under some definition of "resistance" it could be true.

      • (Score: 2) by ikanreed on Wednesday July 03 2019, @06:57PM (1 child)

        by ikanreed (3164) Subscriber Badge on Wednesday July 03 2019, @06:57PM (#862850) Journal

        Someone excerpted it already in this thread and it's pretty explicit.

        "In response, bacteria have evolved metal detoxification strategies including copper/zinc resistance determinants and thus have selected for metal (copper/zinc) resistance to avoid killing by metal poisoning (Hao et al.,2016)"

        • (Score: 0) by Anonymous Coward on Wednesday July 03 2019, @07:11PM

          by Anonymous Coward on Wednesday July 03 2019, @07:11PM (#862855)

          I'm talking about:

          metallic antibiotics breed resistance much faster than traditional antibiotics

          This seems very unlikely, given what we know.