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Infections of GenitoUrinary System

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Title: Infections of GenitoUrinary System


1
Infections of Genito-Urinary System
  • Dr.Song Yongsheng
  • Urological Department of the 2nd Hospital,CMU

2
Susceptibility factors and defense mechanisms
  • 1.Bacterial virulence factors
  • The"nonspecific"infections of the genitourinary
    tract are a gruop of diseases with similar
    manifestations that are caused mainly by aerobic
    gram-negative rods (eg.E.coli) and gram-positive
    cocci (eg.staphylococci).E coli accounts for
    about 90of urinary tract infections.

3
2.Extrinsic factors
  • In wonem, there are two factors. One is introital
    factors. Bacteria are known to adhere selectively
    to various mucosal surfaces by means of tiny
    hairlike projections(pili or fimbriae).Some
    E.coli adhere readily to urinary tract mucosal
    surface cells. Another is urethral factors,
    including periurethral glands, and the nature and
    turbulence of urinary flow.
  • In men, the main route of infection is ascent
    from urethral colonization. But chronic bacterial
    infectoin of the prostate appears to be main
    cause of recurrent urinary infection

4
3.Intrinsic susceptibility factors
  • Efficient voiding may serve as a defense
    mechanism against bladder infection.
  • Other factors may concern the ease with which
    bacteria abhere to bladder surface cellssurface
    mucin, surface glycosaminoglycan, urinary
    antibody, and the antimicrobial properties of
    urine (eg.high osmolality and extremes of pH).
  • Genetic factor may also prove important(DM,etc).

5
Pathogenesis of Urinary Tract Infection.
  • There are 4 major pathways for the entry of
    bacteria into the genitourinary tract
  • 1.Ascending infection from the urethra is the
    most common cause of genitourinary tract
    infections. The tendency for rectal bacteria to
    colonize the perineum and vaginal vestibule, the
    sexual intercourse and the childrenbearing
    enhance the susceptibility of women to urinary
    tract infection.

6
  • 2.Hematogenous spread
  • This mode is uncommon.
  • 3.Lymphatogenous spread
  • The bacterial pathogens travel through the rectal
    and colonic lymphatics to the prostate and
    bladder and through the periuterine lymphatics to
    the female genitourinary tract, but this is rare.
  • 4.Direct extension from another organ
  • Intraperitoneal abscess, fulminant pelvic
    inflammatory disease, paravesical absccsses, and
    genitourinary tract fistulas can infect the
    urinary tract by means of direct extension.

7
CLINICAL DEFINITION OF GENITOURRARY TRACT
INFECTION
  • The genitiourinary infections can be classified
    into upper urinary tract infection, lower urinary
    tract infection and genital system infection
    according to the pathogenesis and the infection
    portion. The upper tract infection refers to the
    infections of kidney and ureters. And the bladder
    and the urethra comprise the lowe urinary tract.
    Prostatitis and epididymitis are the most common
    genital infections.

8
OUTLINE OF DIAGNOSIS AND TREATMENT
  • 1.Identify diagnosis of urinary tract infection.
  • Quantitative urine culture106colonies/ml.
  • 2.Location of urinary tract infection.
  • Symptoms and signs
  • Laboratory findings
  • X-Ray findings
  • Radionuclide imaging
  • MRI findings
  • All those will be disscussed in detail in the
    following part.

9
3.Treatment strategy.
  • Antimicrobial drug should be given according to
    sensitivity test. Medication should be given for
    pain, fever, and nausea. It is important to give
    fluids intravenously and orally to ensure
    adequate hydration and maintenance of adequate
    urinary output. Complicating factors,
    eg.obstructive urography or infected stones, must
    be recognized early and dealt with effectively.

10
TUBERCULOSIS(TB) OF THE GENITO-URINARY SYSTEM
  • Dr. Song yongsheng
  • Urological Department of the 2nd Hospital, CMU

11
PATHOGENESIS AND PATHOLOGY
  • 1.Kidney and rueter
  • When a shower of tubercle bacilli hits the renal
    cortex(glomerulus)the organisms may be destroyed
    by normal tissue resistance and only scars are
    found in the kidney(pathological kidney
    TB).However, if enough bacteria of sufficient
    virulence become lodged in the kidney and are not
    overcome, a clinical infection is established. TB
    of the kidney prgresses slowly, there is no renal
    pain and little or no clinical disturbance of any
    type until the lesion has involved the calices or
    the pelvis, at which time pus and organisms may
    be discharged into the urine.

12
PATHOGENESIS AND PATHOLOGY
  • It is only at this stage the smptoms of cystitis
    are manifested(clinical kidney TB). Usually,
    there is a soft. yellowish localized bulge
    surrounded by marked perinephritis. On section,
    the involved area is seen to be filled with
    cheesy material(caseation).Widespread destruction
    of parenchyma is evident. Small abscesses may
    down in the reparative rocess. The ureter
    undergoes fibrosis and tends to be shortened and
    straingtened. Ureteral stenosis may be complete,
    causing"autonephrectomy".

13
2.Bladder
  • In early stages, the mucosa may be inflamed as
    the bladder is bathed by infected material.
    Later, tubercles form and can be easily seen
    through the cystoscope, as white or yellow raised
    nodules surrounded by a halo of hyperemia. With
    severe involvement, the bladde becomes fibrosed
    and contracted, this leads to marked frequency.
    Ureteral reflux or stenosis and , there fore,
    contralateral hydronephrosis may develop.

14
3. Prostate, seminal vesicles, epididymis and
testis
  • The passage of infected urine through the
    prostatic urethra will ultimately lead to
    invasion of the prostate and or both seminal
    vesicles. Prostatic infection can ascend to the
    bladder and descend to the epididymis. If the
    epididymal infection is etensie and an abscess
    forms, it may rupture through the scrotal skin,
    thus establishing a permanent sinus, or it may
    extend into the testicle.

15
CLINICAL FINDINGS
  • Tuberculosis of the genitourinary tract should be
    considered in the presence of any of the
    following situations
  • (1)chronice cystitis that refuses to respond to
    adequate therapy
  • (2)the finding of pus without bacteria in culture
    of the urinary sediment
  • (3)a nontender, enlarged epididymis with a beaded
    or thickened vas
  • (4)a chronic draining scrotal sinus or induration
    or nodulation of the prostate and thickening of
    one or both seminal vesicles.

16
1.Symptoms and signs
  • (1)The affected kidney is usually completely
    asymptomatic. On occasion. there may be a dull
    ache in the flank. The renal and ureteral colic
    may caused by passage of a blood clot, secondary
    calculi, or a mass of debris. Rarely, the
    presenting symptom may be a painless mass in the
    abdomen.
  • (2)The earliest symptoms of renal TB may arise
    from secondary vesical involvement. These include
    burning, frequeney and noctruia. Ina a late stage
    of the disease. the vesical irritability may
    become extreme. If ulceration occurs, suprapubic
    pain may be noted.

17
1.Symptoms and signs
  • (3)Hematuria or pyuria is occasionally found and
    is of either renal or vesical origin.
  • (4)A thickened, nontender or only slightly tender
    epididymis may be discovered. The vas deferens
    often is thickened and beaded. A chronic draining
    sinus through the scrothal skin is almost
    pathognomonic of tuberculous epididymis. The
    tuberculous prostate shows areas of induration,
    even nodulation. The involved vesicle is usually
    indurated, enlarged and fixed.

18
2.Laboratory findings
  • (1) Persistent pyuria without organisms on
    culture(sterile pyuria) means TB until proved
    otherwise. Acid-fast stains done on the
    concentrated sediment from a 24-hour specimen are
    positie in at least 60 of cases.
  • (2)Culture or PCR detection for tubercle bacilli
    from the first morning urine are positive in a
    very high percentage of cases of TB infcction.
    But the negative results should be repeated three
    times.

19
2.Laboratory findings
  • (3) The ESR is usually accelerated. The
    tuberculin test should be performed, negative
    test in an otherwise healthy patient speaks
    against a diagnosis of TB.
  • (4)Renal function will be nomel unless there is
    bilateral damage. The kidneys can be infected
    with tubercle bacilli, or there is one TB and the
    other hydronephrotic (ureterovesical stenosis or
    reflux).

20
3.Imaging finding
  • IVU can be diagnosed if the lesion is moderately
    advanced. The typical changes include
  • (1)a "moth-eaten" appearance of the involved
    ulcerated calices
  • (2)obliteration of one or more calices
  • (3)dilatation of the calices due to ureterl
    stenosis from fibrosis
  • (4)abscess cavities that connect with calices
  • (5) single or multiple ureteral strictures, with
    secondary dilatation, with shortenting and
    straightening of the ureter

21
  • (6)Absence of function of the kidney due to
    complete ureteral occlusion and renal
    destruction.(Autonephrectomy). Retrograde
    urography may be carried out on the unsuspected
    side as a verification of its normality.
  • Ultrasonic examination. CT, MRI, etc, may give
    the diagnos is more accurate. Cystoscopy may
    reveal the typical tubercles or ulcers of TB.
    Biopsy can be done if nesessary. Severe
    contracture of the bladder may be noted. A
    cystogram may reveal ureteral reflux. A clean
    specimen of urine should also be obtaimed for
    further study.

22
DIAGNOSIS DIFFERENTIAL
  • Chroic nonspecific cystitis or pyelonephritis.
    Acute or chronic nonspecific epididymis.
    amicrobic cystitis, interstitial cystits,multiple
    small renal stones or nephrocalcinosis.
    netcrotizing papillitis, medullary sponge
    kidneys, etc, amy mimic TB perfectly or partly.
    But they may all be ruled out by IVU, urine TB
    culture or PCR and Cystoscopy Examinations.

23
COMPLICATIONS
  • 1.Renal TB
  • Perinephric abscess, renal stone, uremia
  • 2.Ureteral TB
  • Scarring stricture formation, juxtavesical reflux
    ,hydronephrosis.
  • 3.Vesical TB
  • Bladder contracture, hydronephrotic atrophy.
  • 4.Genital TB
  • Sterility (bilateral ducts occluded)

24
TREATMENT
  • 1.Renal TB
  • A strict medical regimen should be instituted.
    The following combinations of drugs can be
    utilized.(1)Streptomycin, PAS, Rimifon(2)Rifampin,
    INH, and Ethambutol. While most authorities
    advise apropriate medication for 2 years.
  • Nonfunctioning kidneys should be removed after
    1-2 months of medical therapy. If, after 3
    months, the affected kidney is radiologically
    evident, nephrectomy should be considered. But
    the counterlateral kidney must be norma.

25
2.Vesical TB
  • TB of bladder tends to heal promptly when
    definitive treatment for the "primary" GU
    infectionis given. Vesical ulcer that fail to
    drug treatment may require transurethral
    electrocoagulation. For the extreme contracture
    of the bladder , it may be necessary to divert
    the urine from the bladder or perform subtotal
    cystectomy (ileocystoplasty ,sigmoidocystoplasty).

26
3.Genital TB
  • If after months of treatment an abscess or a
    draining sinus exists, epididymectomy is
    indicated. For the prostate and the vesical TB,
    the majority opinion is that only medical therapy
    is indicatd.

27
4. Treatment of complications
  • Perinephric abscess must be drained, and
    nephrectomy should be done either then or later
    to prevent development of a chronic draining
    sinus. For the ureteral stricture, ureteral
    dilatations offer a better that 50 chance of
    cure. The severe incompetence of the
    ureteovesical junction need some form of urinary
    diversion
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