Adventures in Hospitalization, #7

I’m at home now. The discharge process started at 10 AM, and I actually exited the hospital around 3 PM. Diane and her mother, Marguerite, came to pick me up.

No stooping, bending, or lifting for 3 weeks. No driving in that time, either. I got instructions on diet and care of my ileostomy.

Now I have to see if I can keep up with my metabolic demands and hydration. I’m still pretty weak.

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Wesley R. Elsberry

Falconer. Interdisciplinary researcher: biology and computer science. Photographer. Husband. Christian. Activist.

8 thoughts on “Adventures in Hospitalization, #7

  • 2004/04/24 at 7:32 pm
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    Reading through your hospitalization updates I got worried about you for a minute there. Don’t scare us like that!

    It’s great to hear you’re back home again!

    Get well soon.

    Bye

    Troy

  • 2004/04/24 at 9:12 pm
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    Fantastic news! Be sure and take it easy and don’t get worn out talking on the phone. Get lots of rest and you’ll be out with the hawks in no time. So glad to hear you’re out of the hospital. My news is Diva has osteosarcoma and will have her leg amputated on Monday. Such a great little dog with a wonderful joyous personality. She’s a lovely companion for my dad and so young soooo onward we go with another cancer battle. Fingers crossed and take care. Get well soon!

    JoAnne

  • 2004/04/24 at 9:26 pm
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    Good news, Wes! Take it easy and you’ll be back fighting the good fight before you know it.

    -john

  • 2004/04/25 at 1:07 pm
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    This is SUCH WONDERFUL news! I got a little worried when I checked this site Friday and there wasn’t an entry. You’d mentioned the day before that you were going to try eating that day and also that no blog entry was an indicator of a bad day. I put all that together and came up with the wrong conclusion! So glad to hear you are at home and doing well. Keep it up!!
    BTW Yesterday I found the perfect spot to take Rusty hunting. It’s a gorgeous canyon near Placitas. Also saw a Great Horned Owl and her 3 babies in the cliffwall “nest”. Keep on healing fast and come see the place yourself.

  • 2004/04/25 at 10:21 pm
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    Welcome home Wes. Being released means you are doing very well. Don’t rush yourself. Take this time to heal and rest. Gradually you will gain your strength back. I know your wife is happy to have you back home.

  • 2004/04/25 at 11:58 pm
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    Hey Wes, so glad to hear you’re back at home. The Biola conference was interesting, as it turned out one whole talk was devoted to critiquing my flagellum essay, and I just happened to be on hand as your substitute. Don’t worry, I took notes…

    Speaking of flagella, you’ll be glad to know that I just discovered that this divinely designed, irreducibly complex system which is the key piece of evidence in the new initiative to revitalize Christianity in the Academy and the nation, and make science again play its part in conservative apologetics, likely plays a key role in Crohn’s disease:

    Involvement of Lipoprotein NlpI in the Virulence of Adherent Invasive Escherichia coli Strain LF82 Isolated from a Patient with Crohn’s Disease

    ABSTRACT
    Escherichia coli strain LF82 recovered from a chronic lesion of a patient with Crohn’s disease (CD) is able to adhere to and invade cultured intestinal epithelial cells and to replicate within macrophages. One mutant selected for its impaired ability to invade epithelial cells had an insertion of a Tn phoA transposon within the nlpI gene encoding the lipoprotein NlpI. A NlpI-negative isogenic mutant showed a 35-fold decrease in its ability to adhere to and a 45-fold decrease in its ability to invade Intestine-407 cells, but its ability to survive and to replicate within macrophages was similar to that of wild-type strain LF82. In addition, this mutant did not express flagella and synthesized very small amounts of type 1 pili. Downregulation of type 1 pili in the NlpI-negative mutant resulted from a preferential switch toward the OFF position of the invertible DNA element located upstream of the fim operon. The FimB and FimE recombinases act in concert to control the switch, and a large decrease in fimB and fimE mRNA levels was observed. The absence of flagellar structures correlated with a drastic 19-fold decrease in the fliC mRNA level, regardless of the FlhD2C2 transcriptional regulator and of the 28 transcription factor. The key role of NlpI in virulence is independent of type 1 pili and motility, since induced type 1 pilus expression and/or forced contact between bacteria and intestinal epithelial cells did not restore the ability of the NlpI mutant to adhere to and to invade intestinal epithelial cells.

    INTRODUCTION
    Crohn’s disease (CD) is an inflammatory bowel disease characterized by chronic transmural, segmental, and granulomatous inflammation of the intestine in humans (10). CD has features that might be the result of a microbial process in the gut. Various studies have addressed the hypothesis that pathogenic bacteria contribute to the pathogenesis of inflammatory bowel disease (4, 22, 23, 33, 36). Bacterial adhesion to intestinal epithelial cells represents the first step in the pathogenicity of many organisms involved in infectious bowel diseases since it allows the bacteria to colonize the gut mucosa and resist mechanical removal from the intestine. The ileal mucosa of patients with CD is abnormally colonized with adherent Escherichia coli strains, which suggests that these bacteria are involved in the initiation of the inflammatory process (7).

    Colonization of host tissues is usually mediated by adhesins on the surface of the bacteria, responsible for binding to specific receptor moieties of the host cell. Enterobacteria elaborate either adhesive filamentous appendages from their surface, termed fimbriae or pili (such as type 1 pili, pap pili, or type IV pili), or nonfimbrial adhesins (for a review, see references 34 and 39). We previously reported that type 1 pili play an important role in the interaction between E. coli isolated from patients with CD and intestinal epithelial cells (2). However, other structures expressed on the bacterial surface could play a direct or indirect role in the adhesion process. For example, flagella allow some microorganisms to adhere to epithelial cells via active motility, in particular enteropathogenic E. coli (12) and Salmonella enterica (35). In addition, outer membrane proteins, such as OmpA, promote E. coli K1 adhesion to and invasion of brain microvascular endothelial cells (29). Finally, bacterial lipoproteins are also involved in adhesion to and invasion of epithelial cells (42). For example, the surface-exposed lipoprotein JlpA specific to Campylobacter jejuni mediates adherence to HEp-2 epithelial cells and Lsp, which belongs to the LraI lipoprotein family, is involved in Streptococcus pyogenes adhesion to and invasion of A549 cells (11, 16).

    E. coli strain LF82, isolated from a chronic ileal lesion of a patient with CD, belongs to a new pathogenic group of invasive E. coli strains mainly associated with CD and designated AIEC (for “adherent invasive E. coli”) (3). It is a true invasive pathogen since its uptake by HEp-2 epithelial cells and Intestine-407 intestinal epithelial cells is dependent on actin microfilaments and microtubules, it survives intracellularly, and it replicates in the host cell cytoplasm after lysis of endocytic vacuoles (3). However, strain LF82 has none of the invasive determinants of Salmonella, Shigella, and invasive E. coli strains, which are known to be involved in gastrointestinal infections. In addition, E. coli strain LF82 is able to survive and/or replicate intracellularly within J774-A1 macrophage cells, murine peritoneal macrophages, and human monocyte-derived macrophages (13). Type 1 pilus-mediated adherence plays an essential part in the invasive ability of strain LF82 by inducing membrane extensions, which surround the bacteria at the sites of contact between the entering bacteria and the epithelial cells (2). However, type 1 pili have to be expressed in the genetic background of strain LF82 to promote bacterial uptake since their expression in E. coli K-12 is not sufficient to confer invasiveness. We recently showed that flagella also play a direct role in the adhesion process via active motility and an indirect role in the interaction between bacteria and epithelial cells by downregulating the expression of type 1 pili (1).

    So, we know who to thank, according to the ID movement…oh wait, it looks like you may not have had Crohn’s after all? I guess my idea to make you a dart board with Crohn’s face on it is scratched, then…

  • 2004/04/27 at 1:20 am
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    Glad to hear you’re home now, Mr. Elsberry. Many of us average joes are looking forward to seeing some more articles from you over at the Panda. Besides, it looks like they could use a good kick in the pants over there.

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