Science topic

Urinary Tract Infections - Science topic

Inflammatory responses of the epithelium of the URINARY TRACT to microbial invasions. They are often bacterial infections with associated BACTERIURIA and PYURIA.
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a. The Prevalence of Bladder Catheterization Associated with Urinary Tract Infections among Comatose Patients in Intensive Care Unit in King Fahd Military Medical Complex, Hospital.
b. The Effect of Daily Visitors on Fewer Somatic Complaints among Hospitalized patients in Medical Male Ward, King Fahd Military Medical Complex, Hospital.
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Without fully knowing what your methodology is, it's difficult to make a full recommendation. "a" appears that your population is comatose ICU patients in KFMMC, and that you'll be doing some sort of non-experimental design and only looking for a correlation. If all that is correct, it is a good title.
"b" is a bit less clear. It sounds like you're doing a quasi-experimental design looking for cause and effect, since you say "the effect of...". I guess quasi-experimental because you will probably not randomly assign people to groups. Instead, the groups will be either "had a visitor" or "did not have a visitor". Your population appears to be hospitalized patients at KFMMC. The word "fewer" is confusing. I think your independent variable is "complaints", so you're examining the effect of visitors on complaints. I would remove the word "fewer", since that identifies your results, not the variable.
"The Effect of Daily Visitors on Somatic Complaints among Hospitalized patients in Medical Male Ward, King Fahd Military Medical Complex, Hospital."
Good luck.
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What would you expect from a molecular test in cUTI in terms of antibiotic stewardship and health economics?
(My) Key consideration to tackle:
  1. Pathogens in cUTI  (single, mulitplex panel, CFU sensitivity, "priority" pathogens vs. rare significant pathogens)
  2. Most interesting antibiotic resistance markes (mcr-1, oxa...)?
  3. Hands on time and Time to result?
  4. Near patient or central lab testing?
  5. Which patient cohort would benefit the most from a rapid molecular cUTI test (ICU, oncology ward, neonates, elderly patients...)
  6. Other considerations (e.g differential diagnosis, price, reimbursement, NGS/WGS, Big data, in-silico analysis, one-health, clinical trials etc...)
favorite publication/guidelines:
Wagenlehner, F.M.E., and Naber, K.G. (2006). Current challenges in the treatment of complicated urinary tract infections and prostatitis. Clin. Microbiol. Infect. 12 - PMID: 16669930
Grabe, M.B.T., Botto, H., Cek, M., Naber, K.G., Pickard, R.S., Tenke, P., Wagenlehner, F., and Wullt, B. (2015). EAU guidelines on urological infections. Uroweb 2015.
Caliendo, A.M., et al. (2013). Better tests, better care: improved diagnostics for infectious diseases. Clin. Infect. Dis. 57 - PMID: 24200831
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Try microgendx.com for send out. They offer full dna sequencing and very cost effective much better pcr testing. our experience has been great
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I am trying to work on my graduate essay and need to get ideas for how to create a survey on pre and post-knowledge of UTIs and the importance of clean catch in inpatient elderly amongst nurses, as well as, their beliefs and attitudes.
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First I would contact the author. Best wishes, David Booth
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I want to know all prescription drugs which are FDA approved compounds for infection like Urinary Tract Infections along with their causative agents. Can you guide me about any resource, database or any website etc.?
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Yes, there is ... the American, Europian, and British Pharmacopoeia
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Urinary Tract Infection is more likely to occur in young women especially those who are sexually active or pregnant, which puts them at a higher risk for the infection. It can be a single-episode of Urinary Tract Infection or a recurrent UTI. The incidences of Enterococcus faecalis and Escherichia coli shows to be significantly higher in patients with infection than those who had single-episode urinary tract infection. E. faecalis is known to be the most common and make structural changes. Adherent E. coli is also more likely to have an important role in the etiology of young women who have recurrent UTI. Both of these bacteria are known to cause mild to serious diseases. So the question is, what clinical signs and symptoms will distinguish recurrent UTI from a single-episode UTI?
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I agree with the excellent and comprehensive answers from Mary CR Wilson.
Just to add recurrent UTI's occurring in the context of an incomplete course of antibiotics, and /or resistance to the prescribed antibiotic, anatomical bladder abnormalities (diverticulae, calculus), functional -vesico-urethral reflux, renal calyx- pyelonephrosis, calculi, underlying co-morbidities (diabetes) and perimenopausal changes in estrogen levels.
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The most common bacteria that can cause Urinary Tract Infection is the Escherichia coli, but it is not the only one and the only species that can cause Urinary Tract Infection, so to I want to start a discussion about this so we can Identify and protect ourselves from this species of bacteria.
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Hello! There are numerous species of bacteria that can cause UTI including: Klebsiella pneumoniae which is a pathogen most often identified in a compromised host including UTI infected patients, Proteus mirabilis identified as an opportunistic pathogen that causes wound and urinary tract infections, Enterococcus faecalis which is a Gram-Postive bacteria found in urine cultures of UTI patients along with Escherichia coli, and Staphylococcus saprophyticus which is associated with UTIs in young women.
The severity of the UTI depends on the pathogen present in the urinary tract as well as the clinical state of the patients. Risk factors such as sex (women have shorter urethra than men leading the bacteria to reach the urinary tract faster than men), age (geriatric patients are more susceptible to UTI because of pre-existing conditions as well as increased risk to infections due to decreased immunity), existing clinical state of the patient (immunosuppressed), and other less common causes such as indwelling catheters (Catheter Associated - Urinary Tract Infection). It is also important to note that taking antibiotics are associated with increasing the resistance of bacteria such as Escherichia coli making it harder to treat UTI.
References:
  1. Mahon, C.R., Lehman, D.C., Manuselis, G. (2014). Textbook of Diagnostic Microbiology (5th ed.). New York: Saunders.
  2. Flores-Mireles, A. L., Walker, J. N., Caparon, M., & Hultgren, S. J. (2015). Urinary tract infections: epidemiology, mechanisms of infection and treatment options. Nature reviews. Microbiology, 13(5), 269–284. https://doi.org/10.1038/nrmicro3432
  3. NHS . (2017, December 12). Urinary Tract infections. Retrieved from NHS: https://www.nhs.uk/conditions/urinary-tract-infections-utis/#:~:text=UTIs%20are%20usually%20caused%20by,kidneys%20and%20cause%20an%20infection.
  4. CDC. (2015, October 26). Catheter-associated Urinary Tract Infections (CAUTI). Retrieved from CDC: https://www.cdc.gov/hai/ca_uti/uti.html
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I am having problem obtaining the desired confluency. They are not growing out well even after 24-72 h incubation. Confluency remains less than 60%
Note: - Media is RMPI 1640 (As recommended by ATCC)
- Cells are new (just ordered from ATTC)
- Seeding rate is 1-2 x10^4 cells/cm^2
- Media color after incubation is orange
Looking forward towards kind replies :)
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Dear Zara,
I worked with these cell lines for several years. These two cells grow very well, Initially it is slow, but later it grow very well if not contaminated with mycoplasma. So far I remember, I used RPMI 1640 for 5736 and DMEM for T24 cells. 10% serum is fine and you don't need anything else. 5736 cells is very sticky to culture plate, very careful for passaging!!! If you need any further help, please mail me: provash2000@gmail.com
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Purple urine in the bag is a known entity.
Blood and urine examinations normal
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The pathogenesis is controversial. According to the most popular hypothesis , dietary tryptophan is converted to indole by gut bacteria, which is further metabolized in the liver to indoxyl sulphate and then excreted in the urine. Constipation favors conversion of tryptophan to indole by gut bacteria.
Once excreted, indoxyl sulphate can be processed by bacteria colonizing the urinary catheter to indoxyl, which is further converted to indigo (blue) and indirubin (red). ( Initially had red tinged urine which became orange as urine flowed)
The most commonly involved
bacteria are Providencia stuartii, Providencia rettgeri, Escherichia coli, Klebsiella pneumoniae,( like our patient) Proteusmirabilis, Morganella morganii, Pseudomonas aeruginosa, and Enterococcus species [4]. These bacteria produce indoxyl phosphatase and sulphatase enzymes.
so it solves our puzzle!!
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68 yr-old man
Rheumatic athritis. No renal lithiasis.
TURP in 2010 (adenoma, 55 grams)
And relapse of dysuria because of giant stone in prostatic bed...
Lithotripsy, urinalysis (once he had corynebacterium glucuronolyticum in 2013)
TURP again and again under antibiotics...
In 2016 Holep (complete), ,no bacteriuria, carboapatite and brushite stones...
Recurrence in 2017...
Any idea ?
Thank you.
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I would culture urine for ureaplasma urealyticum.
At next cystoscopy, culture stone or stones removed for aerobic, anerobic and ureaplasma organisms.
Consider staph epidermidis that occasionally is a urea splitter.
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I am  beginning to model Urinary Tract Infection (UTI),but I have not seen any mathematical  paper /model  so far, That could help me to start how to model this troubling disease,I will be glad if I get some inputs on how to go about. Thanks
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 Dear stephen:
In my opinion you should concrete the question: which mathematical model are you searchirng for?: an epidemiological model based on the propagation of an outbreak of UTI among a determined populationd population or a risk factor model based on the determination of variables which influence the appearance of a UTI.
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j
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 Never found any in follow up outdoors, no such complaints
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Dear colleagues,
Excuse me for bothering you.
I am writing you requesting your opinion and even advice.
We are investigating uropathogens and metabolomic changes in the urine of patients with urinary tract infections. Our metabolomics lab is located  approximately 600 kms far from us. We intend to collect
urine samples from patients, store and send them once a week or two. I've read in the article from Siddiqui et al, (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872872/) they have stored samples up to 4-6 hours by adding boric acid and protease inhibitor. 
Is described methodology also reliable for longer time? Did anyone experience similar procedures? 
Are there any alternatives to keep samples intact for a longer time frame? 
Thank you all in advance.
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I would suggest ensuring that urine samples are centrifuged and then frozen in aliquots at -80 C. It is not recommended to add anything to urine samples for metabolomics analysis because this can interfere greatly with measurement of metabolites. If you are not able to freeze the samples, then you will have to sterile-filter the samples and store them in sterilized aliquots. Note that if you filter the samples, you will get significant glycerol contamination (glycerol is a universal chemical found in almost all filters) which can substantially interfere with metabolite measurements, particularly NMR measurement. I am not sure about whether these additives will interfere with other metabolomics methods.
You should not have to add protease inhibitors if you are only measuring metabolites.
Hope this helps!
Paige
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male post op bladder repair and partial cystectomy patients on tds tranexamic acid complain of pain and discomfort ( localized mostly at tip of penis) these patients are catheterized and complain of pain when clots pass through.. they also complain of a lot of pain when their bladder is irrigated via syringing to remove clots.
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I never use tranexamic acid in bladder surgery. Clot formation/organization in bladder can be dangerous for the patient.
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Different possibilities exist. Is there some struvite or high level of carbonation of apatite in the kidney stone (both through measurements by FTIR spectroscopy)? There is another solution; are there some bacterial imprints at the surface of the kidney stone (observations through SEM)? But in that case there are no bacterial imprints at the surface of struvite kidney stones. We propose an explanation related to the size of the crystals. Does anybody have another explanation?
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I think it is important to point out that the relationship between infection and onset of renal calculi hasn't been totally explained even for struvite nephrolithiasis. In fact, there are data suggesting that even other bacteria, in addiction to the urease-producing ones, may have a role in the onset of the struvite nephrolithiasis. Very recent data show that in the cases of staghorn nephrolithiasis, traditionally considered as infective, is possible to detect a metabolic origin and the role of possible infective agents remains unclear. And I agree with Dr Forray: "More detailed study on the stones can be carried out by electron micro-probe investigation, like elemental mapping".
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Which drug can be used as monotherapy in BPH/LUTS . Tadalafil vs Tamsulosin.
Tadalafil was shown to be significantly effective for improving LUTS/BPH. Significant improvements in IPSS and the IIEF score were also observed in patients with comorbid BPH and ED.
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Well in my 40years of work in urology i had the impression that the efficiency of my medication was always so good as the patient believed in it. That' s why i remained in uro-surgery Your Hainz
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I experienced several cases in which data shows liver dysfunction or cholestasis in patients with urinary traction infection without cholangitis. My impression about this phenomenon is that blood culture and/or urine culture reveal positive results. I suppose that cytokines in bloodstream produced by microbes may affect liver as well as renal function. Does anybody know this mechanism or articles discussing this point?  
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There is not a clear understanding of this phenomenon but the following two articles might have some clues:
1.Ohno N, Ota Y, Hatakeyama S, Yanagimoto S, Morisawa Y, Tsukada K, Koike K, Kimura S. A patient with E. coli-induced pyelonephritis and sepsis who transiently exhibited symptoms associated with primary biliary cirrhosis. Intern Med. 2003 Nov;42(11):1144-8.
Smyk DS, Bogdanos DP, Kriese S, Billinis C, Burroughs AK, Rigopoulou EI.Urinary tract infection as a risk factor for autoimmune liver disease: from bench to bedside.
Clin Res Hepatol Gastroenterol. 2012 Apr;36(2):110-21. 
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My question refers to interventions like catheter insertion and catheter maintenance.
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I only know three indications: 1. Pregnant women, 2. patients undergoing prostate surgery or other invasive urologic surgery, and 3. kidney or kidney pancreas organ transplant patients within the first year of receiving the transplant. But I don´t have evidence in patients with single kidneyy.
January 12, 2015. doi:10.1001/jamainternmed.2014.7132
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I totally agree with Dr Mohamed Elkoushy and would like to add that recommendations for pregnant women are to be screened by urine culture by the end of first trimester. If asymptomatic bacteruria detected, then antibiotic is given and further screening during whole pregnancy is recommended. If no asymptomatic bacteruria is detected by screening at then end of first trimester, then no further screening is recommended during the whole course of pregnancy.
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I need some audits about this topic
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Would it be from a certain lab or hospital?
If so, can you include any contact information?
(Location: Cairo-Egypt)
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The first thing you need to do is to submit your research protocol to any research ethics committee closest to you. The committee must of course be recognized and approved bu the government. After obtaining and approval then you can know approach any hospital of your choice with your approval letter so that the clinical and laboratory staffs can asist you. You will then need to recruit participants into the study by explaning your study to the target subjects and seeking their consent before obtaining their samples.
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Can we use fosfomicyn to treat the especially urinary tract infection with Pseudomonas spp?, some sources is said that there is intrinsic antibiotic resistance against fofomycin in pseudomonas spp.  Besides, fosfomycin is an anbiotic class to determine pseudomonas MDRO and there is not any information about intrinsic resistance on ECDC guidelines (about MDRO 2011). So which one is right? Can we use fosfomycin to pseudomonas in urinary tract?
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The antibacterial spectrum of fosfomycin includes staphylococci, Haemophilus sp. and most of the enteric gram-negative bacteria, but with a considerably higher MIC for Klebsiella sp., Enterobacter sp. and Serratia sp. Fosfomycin is moderately active against Pseudomonas aeruginosa with variable MICs ranging from 4 to >512 mg/L.
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I am trying tio establish a number of women who are affected by UTI, but can only find vague percentage statistics. Any fair guess is welcome.
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research is done according to the age group. pregnant not pregnant.   Curious where you are going with this.
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I saw a seriously recurrent UTI patient who has allergies to abx like bactrim, penicillin, cipro, rocephine and augmentin in an ICU ward recently.
He was given tramadol and citravescent for this time admission.
Unfortunately, he acquired a bad face rash and was itching badly until it swelled and scorched. A piriton was given together with a moisturiser to minimise the effect.
Upon query, he said he has no issue with tramadol for his other maladies but citravescent is the only new thing that made him itch immediately upon consumption.
When he brought up the issues to his medical-in-charge, his claim was dismissed outrightly. The next day the same thing happened, he decided to stop taking it totally and the itch, swell and scorching face returned to normal.
He is on Nitrofurontoin and has since been discharged.
Judging by his experience, while some patients or doctors found citravescent "safe", why others still feel the danger lurks everytime it is consumed?
Could it be that his immune system was very down then?
Or is it true citravescent is resistant to some patients, UTIs' especially?
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I have not seen allergy to that but flatulence and increasing of Na and blood pressere and edema may be done.
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Is there any evidence? Is it common to see Coagulase-negative Staphylococci urinary tract infection or bacteriuria and calcium phosphate stone (apatite) instead of triple phosphate or struvite?
Thank you!
Wisit
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As a possible urea-splitting bacteria it more commonly originates struvite stones instead of calcium phosphate stones. Beware that not all apatite 
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E.g. using phytodrugsor NSAIDs only for UTI symptoms with no antibiotics
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other foods like apple juice, grape juice and green tea contain proanthocyanidins (PACs), cranberries are the only food that contain PACs with A-type linkages (as opposed to B-type linkages). The unique molecular structure explains why cranberries are the only food associated with urinary tract health.
as demonstrated in the link down
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For anti-adhesive effect of drug material against upec
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It depends on your aims and objectives. Adhesive UPEC is more typical for lower UTIs and lower UTIs are more intrinsic to females. In male gender UTIs are considered as complicated as default and microbial pattern may be more compex. But for ex-vivo experiments it IMHO doesn't matter what gender will you choose.
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It is biological plausible that antibiotic coating should reduce CAUTI but are there research papers that confirm it or otherwise?
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Several papers present research on this topic. Many state an antimicrobial coating, whether an antibiotic or metal, does not reduce the instances of CAUTI's
Some extra reading for you
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In a study that compares rates of UTIs following placement of indwelling catheters vs intermittent straight catheters what method of statistical analysis should be used?
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Thanks for your input.
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It depends upon culture results, I wouldnt start him on either antibiotic empirically.If it is a female patient with uncomplicated cystitis I would start with Trimethoprim.
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Application of estrogen locally per vagina in elderly females suffering of lower urinary tract symptoms showed some improvement of their symptoms with an unknown mechanism of action, and most of studies done in that subject showed only the histological evidence of improved vaginal mucosal layer, but the question is there any evidence of bladder functional and  histological changes. And consequently is there any research about effects of intravesical instillation of oestrogen?
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I was wondering whether the systemic uptake of oestrogen would be, following bladder installation, as the low systemic uptake from vaginal application is one of the benefits of local use.
You are probably aware of the following publications but I have included the references: 
In a Cochrane Review, the work of Kurz et al. 1993 (RCT) is discussed when intravesical estrogen was used 'Intravesical application of estriol in sensory urge incontinence - a prospective study'. (Ref for the Cochrane Review: Cody, June D., et al. "Oestrogen therapy for urinary incontinence in post-menopausal women." Cochrane Database Syst Rev 4 (2009).) The work of Kurz et al. was also included in the 2012 update (ref: Cody, June D., et al. "Oestrogen therapy for urinary incontinence in post-menopausal women." Cochrane Database Syst Rev 10 (2012).) The concept of intravesical estrogen is also mentioned in "Legendre, Guillaume, et al. "Menopause, hormone treatment and urinary incontinence at midlife." Maturitas 74.1 (2013): 26-30" but no detail is given. 
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On examination, young male with normal built looking healthy.
LABS
CBC normal
UREA CREAT normal
URINE D/R norma
URINE C/S no growth
ULTRASOUND normal bladdar ok no wall thickness no postvoid residual urine.
 Even Urethrogram normal.
after multiple visits i advised cystoscopy that again normal...
WHAT TO DO NEXT.
because pt still symptomatic after lot of medical prescriptions
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First some questions:
Is the dribbling during daytime with or without urinary urgency?
Further urological history? Childhood urological problems?
What is his maximum flowrate? Is flowcurve normal or with a (very) prolonged end?
Is the postmicturition dribbling depending on voiding position (standing or sitting)?
How does the voiding drinking diary look like, including the report of dribbling?
Which prescriptions have been unsuccesful?
Note: 5 drops (is 0,25mL) give already a large wet spot on cotton!
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One of the targets of the Regional Action Plan for Neglected Tropical Diseases in the the Western Pacific Region (2012-2016) is elimination of schistosomiasis in Cambodia, China and the Lao People's Democratic Republic by 2016.
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I think that will be best to use praziquantel as it is the drug of choice recommended by WHO, high effective against all schistosome species and easly accessible. Futhermore, improving water supply, sanitation people awareness regarding the the disease are important measures to reduce the infection.
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I've seen several prescriptions containing combination of quinolone + 3rd generation cephalosporine in treatment of enetric infections and UTI.
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Sorry, I guess I misunderstood. I don't believe that it is necessary two antibiotics for treatment of complicated or uncomplicated UTI. That seems like an overuse of antibiotics.
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The SPC/license of fosfomycin in Ireland does not recommend its use in the elderly "due to diminished urinary excretion". What is the experience of its use in other countries, have there been issues regarding poor effectiveness or resistance?
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I treat only symptomatic patients, I did not understand you were talking about asymptomatic bacteriuria. this is another situation
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I have found a urine sample with Schistosoma mansoni ova (lateral spikes!) and wondered how comes even with the repeated sample collection and on an account that the patient has no any clinical features suggestive of ano-rectal fistula?
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Is not commom,but not impossible.S.mansoni eggs in sperma is not very rare.Eggs has been found in all tissues and organs:lungs,ovary,kidney,brain,skin,etc,etc
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Research on UTI treatment
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The definition of "new" is questionnable. There are some relatively newer drugs used in some parts of the world, not available in other parts. For example, most of the former USSR countries enjoy the benefits (much better bioavailability and lesser toxicity and side-effects) of soluble Nitrofuran derivate Furazidin (trade name Furamag), first synthesized in Latvia in late 1970's, but those are not available in the Western Europe. I am not aware of the new classes of drugs for treating UTI, sorry
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In the acute phase of the infection, there are several therapeutic options, even with B-lactams despite their low prostatic penetration that could be an option in countries with high resistance rates to quinolones. But once the uroculture is positive we have to choose ATB with good prostatic penetration.
Our first option would be ciprofloxacin 500 mg/12h (or 750 mg/12h, what do you think?) Or cotrimoxazole 160/800 mg/12h.
If we decide to treat with a third generation cefalospirin such as cefixim the dose would probably be 400 mg/day (or 400 mg/12h, what do you think?).
In case of an acute prostatitis due to Enterococcus: amoxicillin 500 mg/8h.
Another doubt would be regarding the duration of treatment: 2 vs 4 weeks.
What are your thoughts?
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Hi Alejandro,
As a general rule, we get very few prostatitis cases in my part of the world. However as you mentioned either ciprofloxacin 400mg/12h (IV)/ Levofloxacin 500mg/24h (IV) or cotrimoxazole 160/800/12h (some authors say 6 hourly) would be ideal. Continue till there is clinical improvement and switch to oral therapy with the same drugs (cipro-500mg/12h, levoflox-750mg/24h and cotrimox-160/800/12h) for 2 weeks. Bio-availability of the above drugs are good.
Drug of choice for E. faecalis is ampicillin 500mg/6h. For E. faecium the choice would be vancomycin, daptomycin, linezolid, etc.
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Our research project is evaluating the effects of chinese herbs on the treatment of urinary tract infections. We are now looking at specific effects of herbs on the fimbriation process.
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I too was working related to uti infection. u working with human or animal model??. or only lab work
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I need to examine the urinary tract in mice for UTIs and need to extract the kidneys and bladder for histological examination. I planned to fix the tissue samples in 10% NBF for 24 hours, but I have conflicting reports on procedures for storage post-fixation. I've been told to store them in 0.1M PBS, while another colleague has said that she's stored samples in NBF up to 5 days. I've found online resources that say to store in 70% EtOH after washing the tissues well with PBS. What's the best/proper procedure?
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There really is no universal "best or proper" procedure for fixation. Every fixation procedure does lead to some change in the tissue being fixed. As can be seen from all the replies above the fixation procedure will depend on what you need to do with the tissue later. From your question you have mentioned histological examination. For most histological procedures fixation in 10% buffered formalin give adequate morphological preservation for routine H&E as well as most commonly used histochemical staining procedures. But if you are planning Immuohistochemistry / immunofluorescence or any other immunological procedure then it really depends on the antigenic epitope that is being studied and the available antibodies. You may then have to look at the best fixation procedure and if any antigen retrieval etc would be required later. I do not think storing in PBS is a good idea esp since you plan to study UTI. The bacterial growth that is invariably likely esp if your tissue are already infected may vitiate the results.
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Open stent insertion didn't work, as he is suffering from recurrent UTI and the ureter diameter in the pelvis on USS is 2.2 cm. What are the options? What can be done?
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what about a cutaneous urostomy on the lower ureter and secondary reimplant in 1 year. I thing that tapered reimplantation on a six moths old baby has quite a lot of complications.