Genitourinary tb

1. GUTB (UTB)
DR MANOJ
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2. INTRODUCTION
• Tuberculosis affect any organ system of body
including GU tract.
• GUTB leads to irreparable damage to GU tract.
(renal failure and infertility).
• Diagnosis mostly relies on clinical recognition
and high index of suspicion.
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3. HISTORY
• 9000 Yrs old mummified bone was detected
with mycobacterium
• Greeks ,Romans Egyptians have described in
different era.
• 25% deaths in industrial era in US in 19th
century.
• 24th march 1882,Robert Koch ,isolation and
identification of mycobacteria.(world TB day).
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4. MICROBIOLOGY
• AFB,MYCOBACTERIUM tuberculosis complex.
• M.tuberculosis
• M.africanum.
• M.bovis.(resistance to Pyrazinamide)
• M.canetti
• M.microti
• M.caprae,mungi,orygis,pinnipedi
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5. • One third of world population with MTBC in
latent form
• In 2012, 8.6 million new cases, and 1.3
millions deaths.
• Since year 2000, decline in deaths due to early
diagnosis and effective treatment.
• But new challenges are:HIV,diabetes,MDR and
extensive drug resistance.
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6. GU involvement
• Developing countries
15% to 20%.(2nd most
common system)
• Developed countries 2%
to 10%.(3rd)
• M:F is 5:2
• Generally disease of
adult but can involve
children as young as 2
yrs.
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7. Transmission
• Pulmonary TB :by droplets aerosol- alveoli –
phagocytosis by macrophages. Killed
division of mycobacterium inside
macrophage.
12 wks,lymphatics,hilar
lymphnodes,distant spread.
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8. • Good immune response
• bacilli inside macrophage,(LANGHANS giant
cell),dormant or latent.(90-95%)
• primary progression(5-10%)
• Immunocompromised,diabetic,renal failure,more
risk of activation(15%)
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9. GUTB
• Routes
:Haematogenous(KIDNEY ,EPIDIDYMIS)
: Ascending or retrograde infection
through the urinary system.(BCG Instillation:
0.9%)
(pyelonephritis, renal abscesses, ureteric obstruction,
cystitis, prostatitis, and epididymo-orchitis)
:Contiguous spread from other organ
systems or direct inoculation.(spine,psoas,GI
tract: enterorenal and enterovesical fistula)
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10. • Autoinoculation: infected stool or urine, and
person-to-person genital inoculation after contact
with infected genital or oral lesions
• Clinical features will be soon or latency period upto 46
years.
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11. Clinical features
• 8.4% of GU TB patients are asymptomatic
• Nonspecific
• bacterial infections ----possible malignancy
• Symptoms correlate with the severity and
location of disease.
• Renal TB:progressive and destructive but
symptomatically may be silent.
• Ureter , bladder and prostatic involvement :
symptomatic
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12. Clinical features
• The typical TB constitutional symptoms of
fever, weight loss, night sweats, and malaise
are present in fewer than 20% of patients
• Dysuria,storage LUTS(50%)
• Hematuria(33%)
• Flank pain,colicky pain due to sloughed
papilla or clot or phlegmon
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13. Renal tuberculosis
• 80 % of GUTB
• PROGRESSIVE DESTRUCTION
• Early disease : with or without sterile pyuria
nothing on imaging.
biopsy: granulomatous nephritis,
caseating granuloma
treatment will reverse the
destruction
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14. • Disseminated TB: Miliary TB where millets(3mm) in cortex
and medulla.
Renal function is normal.
High mortality.
• Localised disease: Granulomas, coalesce ,caseate, cavities
with necrotic material form.
• frank abscesses, chronic pyelonephritis, and parenchymal
and papillary necrosis. Sinus tracts in flank. costovertebral
angle tenderness.
• As infection advances, the calyces become inflamed and
eventually calcify, resulting in calyceal distortion,dilation,
and stenosis .
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15. • Autonephrectomy: kidney
destruction,nonfunctional (30%)
1.Caseo-cavernous type: in which viable tissue
is replaced with granulomas and cavities filled
with inflammatory exudate. This type of
autonephrectomy occurs with and without
calcification.
2. Fibrotic, with severe scarring and
calcification resulting in a shrunken kidney
• ESRD(7%) AND MALIGNANCY( SCC of PCS)
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16. URETER
Descent of infection from kidney(urine)
granuloma in walls of ureter
scarring ,stricture(vuj),panureteral
obstruction,reflux,
renal failure
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17. Bladder involvement
Descent from kidney(urine)
Ureteral orifices,spread along lymphatics
Bacilli in urothelium,patchy cystitis,
Granuloma coalesce ulceration
Heamaturia. chronic inflammation and
mucosal scarring (small bladder capacity)
Storage LUTS Thimble bladder(20ml).
Dome(MC),Trigone and bladder neck is spared.
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18. Epididymis, Vas Deferens, Testes, and
Scrotum
• The epididymis, the second most
common(hematogenous spread).
• Bilateral in 34%
• Globus minor(more vascular).
• granuloma---chronic inflammation---fibrosis---
scarring----narrowing of lumen.
• Granuloma---nodular epididymis---adhere to
skin---rupture----sinus tract on post. aspect of
scrotum
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19. • Infection spreads to vas----scarring ----nodular
and beaded vas deferens.
• Spreads to testis---seminiferous tubular scarring--
--hardened testis----mimic malignancy.
• Hydrocele ( 5 %)
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20. Prostate and seminal vesicles
• Prostate : either hematogenous spread or
urinary contamination.(20-50%).
• Hematogenous : periphery of prostate ---
asymptomatic ---- fibrosis----hard gland.
• Urinary route : periurethral zone—
symptomatic(bacterial prostatitis)----not
responding to antibiotic----may lead to
prostatic abscess.
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21. • Seminal vesicles involved via vas deference or
urethra and ejaculatory ducts.
• Granuloma in walls of SV---Filled with
caseation—fibrosis ,scarring and calcification--
--low volume
ejaculate,oligospermia,hematospermia--------
may lead to abscess of SV
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22. Urethra and Penis
• Urethra and penis:Resistant to infection(2-5%)
• Associated with prostatic involvement
• Penis: a small papule or plaque on skin(lupus
vulgaris)---ulcerate deeper to cavernosa---pea
size nodule palpable---mimic malignancy----
fibrosis may lead to distortion of penis---
erectile dysfunction
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23. • Orificial TB, a rapidly necrotic form of penile
TB
• Cutaneous manifestation of TB on the
glans(papulonecrotic tuberculid (PNT).
• hypersensitivity reactions to MTBC antigens
that were disseminated to the skin
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24. Diagnosis
primary goal of the diagnostic workup:
• Isolation of MTBC in culture and drug sensitivity.
• Demonstration of granuloma in histology in
absence of DNA tests.
• History and clinical findings.
• Response to emperical therapy
• Presence of concurrent pulmonary disease( 25%)
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25. Culture
• Gold standard for the diagnosis of GU TB is urine
acid-fast bacilli (AFB) culture.
• First void morning sample(maximum bacilli)
• Minimum 200 ml urine
• 3-5 consecutive days ,maximum yeild
• Sensitivity :80% to 90%
• Ziehl-Neelsen stains ,but the sensitivity is less
than 50%.
• We can also culture biopsy tissue or pus.
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26. Culture media
• Solid egg based(Lowenstein-Jensen medium) :
Time consuming,4-6 wks
• Solid agar based media(Middlebrook 7H10.):1 wk
earlier than LJ media.
• Liquid based media(BACTEC Mycobacteria Growth
Indicator Tube (MGIT): within 10days.
• Current guidelines recommend culturing on at least
one solid medium concurrently with the liquid system
to maximize yield.
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27. Nucleic Acid Amplification Tests(NAATs)
• Within 1-2 days
• low bacillary load, in whom culture may fail
• Sensitivity of 70% to 100%
• In nonrespiratory sample like urine ,sensitivity is
less because urine contains natural inhibitors
interfering DNA or RNA amplification
• Gene xpert (NAAT) From 2010,Drug susceptibility
to refampin and INH
• Sensitivity of NAAT on epididymal biopsy tissue
was 87.5%.
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28. • WHO recommends NAAT to use as adjunct to
CULTURE
• NAAT cant be used for response because dead
bacilli shed nucleic acid too
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29. CBNAAT
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30. Histology
• If culture is negative,biopsy can be done.
• Evidence of granuloma(40%).
• CB NAAT can further augment diagnostic
sensitivity to tissue specimens.
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31. Screening test
• The tuberculin skin test (TST)
• interferon-gamma release assays (IGRAs)
• Not used for diagnosis.
• Cant distinguish between latent and active
disease.
• FDA approved for screening in endemic areas>
5 yrs of age.
• There are two IGRAs available in the United
States, the Quanti-FERO and T-SPOT.TB test
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32. • False-negative results can occur in 10% to 25%
of persons with active TB.
• In one study, the TST result was positive in
85% to 95% of patients with GU TB.
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33. • Imaging
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34. Plain xray
Chest xray : Concomittant pulmonary TB.
Xray KUB:
• Vertebral bodies erosion,psoas shadow
• Kidney:calcification(punctate, ring,global)
:stone in distorted PCS
• Calcification of wall of ureter and bladder seen
(rarely)
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35. Cement or putty kidney
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36. IVP
• Early renal TB: Gold standard
Findings:
• Calyceal erosions“motheaten”appearance
• Filling defect in PCS due to necrosed papilla.
• Infundibular stenosis: phantom calyx.
• Kerr’s kink of pelvis
• Pipestem or corkscrew ureter
• Small irregular bladder.
• Nonvisualised kidney
• Hydronephrosis Hydroureteronephrosis
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39. USG
• Nonspecific Findings.
• useful in pediatric or pregnant patients
• Obstruction and calcification
• Renal abscess
• Perinephric abscess
• Lymphnodes.
• Ascites,omental caking
• TRUS for prostatic involvement.
• Response to ATT : Resolution of HDN, Any abscess
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40. CT (with or without contrast)
• CT Urography has largely replaced IVP.
• small as 3 to 4 mm
• evaluation of patients with complicated and
extensive TB.
• CT reveals calcifications, scarring, and signs of
obstruction
• Perinephric and psoas abscesses can be seen, as
well as any pathology in lymph nodes, vertebrae,
spleen, or liver.
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42. • CT is less sensitive for detecting the minimal
urothelial thickening, subtle papillary necrosis,
and other changes of early renal TB, for which
IVU is still the preferred study
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43. MRI
• Not much role.
• Useful in children and pregnant patients
• Small granuloma: hypointense on T1 and T2
image
• Large lesions : central hyperintense in T2.
• More sensitive for small urothelial thickening.
• DWI can distinguise between hydro and
pyonephrosis
• Risk of NSF IF GADOLINIUM used in renal
dysfunction
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44. Cystoscopy ,ureteroscopy
• Under anaesthesia
• Bladder should not be overdistended
• Local hyperemia
• mucosal erosion
• Ulceration
• granulomatous masses
• Ulcerative lesions may mimic malignancy
• Golfhole ureter
• BIOPSY(19% to 52% sensitive for TB)
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45. 8/28/2023 45
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46. RGP and AGP
• Largely replaced by CT or IVU
• In renal dysfunction, useful to know the
anatomy ,site of stricture in ureter,PCS
anatomy.
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47. 8/28/2023 47
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48. Treatment
• Before ATT era :rest and nourishment in
sanatoria; extensive surgeries.
• streptomycin in 1944
• isoniazid in 1952
• rifamycins in 1957
• Revolution, lesser need of surgery
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49. Why do we need so many drugs?
• Bacilli in many microenvirenments in host
with various metabolic needs, speed of
replication so some drugs are bactericidal and
some are bacteriostatic ,some act on less
metabolically active bacteria.
• Multiple drug therapy prevents the
emergence of drug-resistant strains.
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50. • isoniazid (INH), rifampin, pyrazinamide, and
ethambutol.
• Baseline investigations:
• Platelet count
• liver and kidney function tests.
• HIV,
• hepatitis B and C
• and diabetes.
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51. 8/28/2023 51
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53. • Daily therapy is preferred.
• Intermittent therapy,3 Times/wk
(administered by DOTS) only during the
continuation phase of therapy.
• The World Health Organization and CDC no
longer recommend dosing intervals less
frequent than 3 times/week.
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54. 2nd Line drugs.
• Resistance
• Failure
• Side effects.
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55. 8/28/2023 55
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56. DOSE modification in CKD
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57. • GU TB can be successfully treated with the standard
short-course regimen of 6 months of first-line
antituberculous drugs (Nahid et al., 2016).
• intensive phase( 2 months )of daily INH, rifampin, and
pyrazinamide,ethambutol.
• continuation phase (4 months ) of INH and rifampin (
daily or thrice weekly.)
• Pyridoxine (vitamin B6): INH-induced peripheral
neuropathy
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58. Extended therapy
• 12 months therapy:
GU TB because of high relapse rates of up to 22% when
therapy is given for only 6 months (Gokalp et al., 1990).
Current indication:
• Extensive pockets of infection, concurrent smearpositive
cavitary pulmonary disease, central nervous system
involvement, or delay in positive cultures converting to
negative.
• If PYRAZINAMIDE not given in first 2 months: 9 months
therapy.
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59. Monitoring therapy
• Liver function test:
• abstain from alcohol and other hepatotoxic
drugs(herbal )
• Liver function reversible with drug
discontinuation
• Symptoms of neuropathy ( INH)
• Vision (ethambutol)
• RENAL function
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60. Corticosteroids
• Meningitis
• Pericarditis
• Decrease in scarring ,ureteral strictures,bladder
fibrosis.
• meta-analysis : regardless of which organ system
was affected, steroids reduced mortality by 17%
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61. SURGICAL MANAGEMENT
• 55% of GUTB patients need some surgical
therapy.
• Relieve urinary obstruction.
• Drain infected material.
• Remove nonworking infected kidneys in cases
resisting cure
• To improve medically resistant hypertension
secondary to a functionally excluded kidney,
• To reconstruct the urinary tract( MC)
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62. • The optimal timing of surgery is 4 to 6 weeks
after the initiation medical therapy.
(allows active inflammation to subside, the
bacillary load to decrease, and lesions to
stabilize).
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63. Procedures to Relieve Obstruction.
• Unilateral or bilateral
• DJ stent or PCN(may be
more than one)
• During nephrostogram :
forceful contrast injection
will dissemination of
infection
• Fistula after PCN
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64. Nephrectomy
• Nonfunctional kidney and recalcitrant or
recurrent TB despite optimal medical therapy.
• Nonfunctional kidney and medically resistant
hypertension.(65% improvement)
Approach: retroperitoneal
• Perinephric fibrosis ,kidney filled with
pus,distorted plane breach to pleura and
peritoneum should be avoided.
• In Expert hand: laparoscopic
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65. Ureteropelvic and Ureteral Surgery.
• Lower ureteric strictures more common.
• PUJ and midureteric stricture less common
• Panureteral strictures.
ENDOSCOPIC MANAGEMENT
• Dense fibrosis and mucosal ischemia in TB: failure
• short strictures with residual lumens: best outcome
• Stricture during medical treatment: DJ Stent may cure
• Balloon dilatation,serial ureteral dilatation may help: needs
followup
• Corticosteroids may be used to decrease fibrosis during medical
therapy
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66. Open Surgical Options.
• Long, complex strictures
• UPJ stricture:Repair of UPJ scarring is more
challenging,dense fibrosis,loss of elasticity
• Dismembered pyeloplasty: extrarenal pelvis
with short segment scarring.
• Nondismembered (flap) pyeloplasty is
preferred for longer strictures
• Ureterocalicostomy(scarred pelvis)
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67. • Upper and middle ureteric strictures: excision
and primary anastomosis.
• Lysis of adhesions and intubation (Davis
intubated ureterotomy)
• Lower ureter strictures: EXCISION and reimplant
Procedures to fill the gap:
Opposite superior vesical artery: 2-3 cm
Psoas hitch: 5cm
Boari’s Flap: 10-15cm(bladder capacity)
Ileal interposition (ileal ureteric replacement)
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68. Bladder Surgery.
• Augmentation cystoplasty
• When frequency, nocturia, urgency, pain, and
hematuria, become intolerable( bladder capacity
is less than 100 mL)
• Ileum,sigmoid,caecum,stomach ,jejunum
• Goal: Low pressure reservoir
• Thimble bladders( capacity less than 20 mL )
orthotopic bladder substitution
• mucus production, electrolyte derangements,
and secondary bacterial infection.
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69. Urethral procedure
• Bladder outlet obstruction: Bladder neck
contracture BNI
• Urethral stricture: endoscopic mx,repeated
procedure,open repair
• Urethral fistula: SPC ATT ,
urethroplasty
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70. • Epididymectomy
• ORCHIDECTOMY
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71. MONITORING RESPONSE
• Improvement of symptoms,
• Wt gain,increase appetite
• Decrease in HDN (IMAGING)
• STERILE PYURIA(URINE)
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72. RELAPSE AFTER THERAPY
• Pulmonary TB: 2-6 % in first year.
• GUTB: 6-22% after 12 months of therapy( in
kidney some bacilli remains in pockets).
• In case of relapse,goal is to do drug sensitivity.
• GUTB recommended to follow up to 10 years.
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73. Multidrug-Resistant TB
• Resistant to both INH and rifampin.
• 3.3% of newly diagnosed patients and 20% of
previously treated patients have MDR-TB
(WHO, 2016).
• For Successful treatment : 18 months regime
• Cure rate: 60%
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74. Extensively drug-resistant TB (XDR-
TB)
• Resistance to INH, rifampin, any fluoroquinolone,
and
• at least one of the injectable second-line
aminoglycosides (amikacin, kanamycin, or
capreomycin).
• 2 years regime
• Cure rate :30%-50%.
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75. Pregnancy ,Lactation and TB
• avoid pregnancy
• risk to the fetus from TB and therapy.
• Treatment consists of INH, ethambutol,
rifampin,and pyridoxine for 9 months.
• USA ,pyrazinamide: not used
• WHO Recommends to use.
• Breast feeding can be done once
noninfectious.
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76. Human Immunodeficiency Virus
Infection
• 30 fold risk
• GU TB may be more common in HIV positive
patients.
• In a small study in India, GU TB was found
postmortem in 49% of AIDS patients.
• Less caseation,abscess,scarring ,fibrosis.
• Less strictures,stenosis,contracted bladder.
• high mortality.(systemic)
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77. • ART ------ ATT for 6month
• Not compliant to ART: 9 Months
• Daily dose of ATT
• DRUG interaction of rifampicin with
ART,(DECREASES LEVEL OF ART)
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78. Renal Transplant Recipients
• Renal allograft TB: RARE
• Can occure: 6 months to 7 years after
transplant.
• no changes are usually visible on imaging.
• immunosuppression alter natural course of
GU TB.
• Fever is the usual presenting symptom.
• Urinary symptoms : only 20% of cases
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79. • In one study, urine AFB culture was positive in
100% of patients
• drug interactions between the rifamycins and
the immunosuppressive drugs
• graft rejection, disseminated TB, and death in
up to 36% of patients.
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80. Conclusion
• Untreated genitourinary TB can lead to
irreparable tissue damage :renal failure and
infertility
• nonspecific symptoms and can be indolent; A
high index of suspicion
• Goldstanderd :AFB culture from urine or tissue
biopsy. NAAT or the finding of granulomas on
histopathology.
• surgery is 4 to 6 weeks after the initiation medical
therapy
• Monitoring for relapse
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81. REFERENCES
• CAMPBELL AND WALSH 12TH Edition
• GUTB by Ganesh Gopalakishnan
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82. THANK YOU
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