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Etiopathogenesis of GUTB
1. ETIO PATHOGENESIS AND
CLINICAL FEATURES OF
GENITOURINARY TB
Dept of Urology
Govt Royapettah Hospital and Kilpauk Medical College
Chennai
1
2. Moderators:
Professors:
• Prof. Dr. G. Sivasankar, M.S., M.Ch.,
• Prof. Dr. A. Senthilvel, M.S., M.Ch.,
Asst Professors:
• Dr. J. Sivabalan, M.S., M.Ch.,
• Dr. R. Bhargavi, M.S., M.Ch.,
• Dr. S. Raju, M.S., M.Ch.,
• Dr. K. Muthurathinam, M.S., M.Ch.,
• Dr. D. Tamilselvan, M.S., M.Ch.,
• Dr. K. Senthilkumar, M.S., M.Ch.
Dept of Urology, GRH and KMC, Chennai. 2
3. Introduction
• Globally a leading cause of death from infectious
disease, second only to AIDS.
• Second “ great imitator “
• Young adults in their most productive years, with
two-thirds of cases in 15-59 age group.
• The vast majority of deaths from TB (>95%) are in
the developing world.
3
Dept of Urology, GRH and KMC, Chennai.
4. • TB mortality has fallen by 45% since 1990
New obstacles in TB control
➢Medical conditions that promote resurgence
of TB such as the human immunodeficiency
virus (HIV) and the rapid increase in obesity
and diabetes worldwide.
➢The appearance of multidrug and extensive
drug resistance
World Health Organization (WHO). Tuberculosis fact sheet no.
104,<www.who.int/mediacentre/factsheets/fs104/en/index.html>; 2013[accessed06.01.14].
4
Dept of Urology, GRH and KMC, Chennai.
5. • The GU TB is the second most common EPTB site.
• GUTB in - developing countries : 15-20% of PTB
- developed countries : 2-10% of PTB
• Approximately 4%–8% of patients with
pulmonary tuberculosis will develop clinically
significant genitourinary infection.
5
Dept of Urology, GRH and KMC, Chennai.
6. • Genitourinary tuberculosis (GUTB) may involve
any part of the genitourinary tract.
• Clinical symptoms usually develop 10-15 years
after the primary infection.
• Only 25% of patients with GUTB have a known
history of pulmonary TB; about half of these
patients have normal chest radiography findings.
6
Dept of Urology, GRH and KMC, Chennai.
7. MICROBIOLOGY
Chronic infection
• M. tuberculosis
• M. bovis,
• M. africanum
• M. canettii
• M. microti
• M. pinnipedii,
• M. caprae.
Remain dormant, persist for many years.
M. tuberculosis - major cause of GUTB
M. africanum - pulmonary TB in Africa.
1. Type of mycobacterial species
2. Duration of exposure,
3. Size and Infectivity of the strain
Factors responsible for the degree of infectivity
7
Dept of Urology, GRH and KMC, Chennai.
8. Characteristics of Mycobacteria
• Slow growing
• Obligate aerobe
• Non-spore forming
• Non-motile
• Acid fast
8
Dept of Urology, GRH and KMC, Chennai.
9. Outcome of Exposure to M. tuberculosis
Exposure
(close contact)
No infection
78%
Infection
22%
Primary active TB
5%
Latent TB
95%
Continued
latent TB
Secondary TB
10%/lifetime
HIV infection
10%/year
(GUTB)
9
Dept of Urology, GRH and KMC, Chennai.
10. Immunology & Pathogenesis
bacilli
T cells
T cells
cytokines
cytokines
macrophages
macrophages
Epitheloid
cells
Epitheloid
cells
TNF
TGF
10
Dept of Urology, GRH and KMC, Chennai.
11. Tubercle with Caseous Necrosis
Giant cells
Tubercle bacilli
Partially activated
macrophage
Lymphocyte
Fully activated
macrophage
11
Dept of Urology, GRH and KMC, Chennai.
13. CAUSES OF REACTIVATION
DEBILITATING DISEASE
MALNUTRITION
STEROID THERAPY
DIABETES MELLITES
ANEMIA
IMMUNOSUPPRESSION
ACQUIRED IMMUNO DEFICIENCY SYNDROME
VITAMIN D DEFICIENCY- compromise cell mediated immunity
13
Dept of Urology, GRH and KMC, Chennai.
14. Pathogenesis
• The kidneys and the epididymis are the primary sites
of GUTB.
• All other genital organs become involved by
contiguous spread from these primary landing sites
• Kidney may be involved as a part of generalized
disseminated infection or as localized genitourinary
disease.
• Kidney is usually infected by hematogenous spread
of bacilli from the primary focus of infection.
14
Dept of Urology, GRH and KMC, Chennai.
15. Etio Pathogenesis of Uro genital TB
• Elimination theory – Cohnheim
• Koch’s postulates
• Bacteremia theory – Rosenberger
• Direct hematogenous theory – Ekehorn
• Metastatic theory – Medlar
• Unified theory – Wildbolz
15
Dept of Urology, GRH and KMC, Chennai.
16. Cohnheim’s Elimination theory
1879
• Tubercle bacilli from the
alveolar macrophages,
when they pass through
the kidney, are excreted
and eliminated from body
through urine.
• During this process, MTB
lodged somewhere in the
G-U tract and manifested
with disease. 1839-1884
16
Dept of Urology, GRH and KMC, Chennai.
17. Robert Koch – MTB is the cause of disease
1882
• Identified the organism in the
host tissue
• Isolated the organism
• Cultured outside the body
• Re-inoculated the organism to
reproduce the disease.
Koch’s Postulates
17
Dept of Urology, GRH and KMC, Chennai.
18. Bacteremia theory
1900
• Tuberculosis is a result of
bacteraemia
• Followed by secondary
localization of organisms
• Occurrence of well known
lesions.
Rosenberger
18
Dept of Urology, GRH and KMC, Chennai.
19. Ekehorn’s Direct hematogenous theory
1908
• Bacilli transported like
EMBOLI to renal
capillaries.
• Lodged and form a
tuberculous focus
Remainder of kidney and
rest of urinary tract were
secondarily infected
Formed the basis for the concept that TB can be cured by nephrectomy
19
Dept of Urology, GRH and KMC, Chennai.
20. Medlar’s metastatic theory
1926
• 30 patients who died of
pulmonary TB.
• None of them had
clinical features of
GUTB.
• 1,00,000 serial sections
of kidneys from these
specimens.
Microscopic lesions all over the
cortex and bilateral
METASTATIC
RATHER THAN
SECONDARY
Kidneys were infected
through blood stream
20
Dept of Urology, GRH and KMC, Chennai.
21. GUTB – unified theory of Wildbolz
1937
• Coined the term GUTB.
• Renal and Epididiymal TB are not
two separate diseases,
• local manifestations of the same
blood borne infection.
21
Dept of Urology, GRH and KMC, Chennai.
22. WAYS BY WHICH GUTB DEVELOPS
• Hematogenous
• Ascending or retrograde- BCG
• Contiguous spread ( enterovesical fistula,
psoas abscess
• Direct inoculation
22
Dept of Urology, GRH and KMC, Chennai.
23. Why after so long after Pulm
TB that one develops GUTB
1. MTB – inhaled through lungs
2. Alveolar macrophages phagocytose one or more
mycobacteria lodged within an alveolus
3. virulent mycobacteria multiply within the macrophages
4. eventually result in lymphatic and hematogenous
dissemination
5. Metastasize to Kidney.
6. Remain dormant in tiny granulomas in kidneys
7. When Immuno deficient, these dormant MTB get
reactivated.
8. Develop into RENAL TB
23
Dept of Urology, GRH and KMC, Chennai.
24. Bacillary proliferation within the capillaries
Rupture of capillary
Delivery of organisms into proximal tubule
Entrapment of Mycobacterium
+
infected macrophage debris within loop of Henle
(Medulla’s hypertonic milieu impairs the phagocyte
function)
Etiopathogenesis
Bacilluruia 24
Dept of Urology, GRH and KMC, Chennai.
25. Pathology (Renal)
Cavitary renal TB
• predominant medullary lesions
• localized infection
Miliary TB
• hematogenous spread
• Cortical white nodules,1-2 mm
• Cortical granulomas
• Coalease
• Cavity formation
• Erode via PCS
• Moth eaten appearance
• Multiple surface scars
• PCS - caseous material
• Pyonephrosis
• Putty kidney
Multiple,
predominantly peripheral,
white tuberculous granulomas
scattered throughout the kidney 25
Dept of Urology, GRH and KMC, Chennai.
29. • Autonephrectomy- 33% of patients with GU
TB.
Two types of autonephrectomy.
• Caseo-cavernous type- viable tissue is
replaced with granulomas and cavities filled
with inflammatory exudate.
• Fibrotic type- with severe scarring and
calcification resulting in a shrunken kidney
29
Dept of Urology, GRH and KMC, Chennai.
30. • End-stage renal failure develops in
approximately 7% of patients
• Chronic inflammation - squamous metaplasia
in the renal pelvis that persists after
treatment, a risk for squamous cell carcinoma
30
Dept of Urology, GRH and KMC, Chennai.
31. Classification for Kidney TB
Kidney TB (nephrotuberculosis)
• TB of kidney parenchyma (stage 1
nondestructive form) is subject to
conservative therapy.
• TB papillitis (stage 2, small-destructive form) is
subject to conservative therapy,
reconstructive surgery is indicated for
complications only.
31
Dept of Urology, GRH and KMC, Chennai.
32. • Cavernous KTB (stage 3, destructive form),
recovery without surgery is rare.
• Polycavernous KTB (stage 4, widespread
destructive form), recovery with anti-TB drugs
only is impossible, surgery is necessary,
basically nephrectomy.
Kulchavenya, E. (2014) Urogenital Tuberculosis:
Epidemiology, Diagnosis, Therapy, New York: Springer,
DOI: 10.1007/978-3-319-04837-6.
32
Dept of Urology, GRH and KMC, Chennai.
33. • Secondary to renal tuberculosis > 50% cases.
• usually unilateral
• lower third of the ureter – most common
Ureteral strictures cause more renal damage than
the effect of original parenchymal involvement
Saw tooth app
Cork Screw app
Pipe stem app
Mucosal
ulcerations
Rigid ureter
Thick walled
Lacks peristaltsis
Fibrotic.
PATHOLOGY (Ureter)
33
Dept of Urology, GRH and KMC, Chennai.
34. TB Ureter & Schistosomiasis
TUBERCULOSIS SCHISTOSOMIASIS
Intra luminal Calcification Trans mural calcification
Pipe Stem appearance Tram Line appearance
Ureter appears tubular and
poorly distensible
Dilated & tortuous
Unilateral lesions, though
bilateral systemic involvement
Lesions are Bilateral
Descending lesions Ascending lesions
Assymmetric Assymmetric
34
Dept of Urology, GRH and KMC, Chennai.
35. Schistosomiasis
of Ureter
1. Generalised or
segmental
ureterectasis
2. Kinks and tortuosity of
ureter
3. Cow Horn Deformity
4. Tram line calcification
5. Ureteral hypotonia
6. Snake Head
appearance of the
terminal ureter (due to
intra mural stricture)
7. Makar’s Stricture (3rd
lumbar)
35
Dept of Urology, GRH and KMC, Chennai.
36. PATHOLOGY ( U. BLADDER )
• Descending infection to the bladder usually
begins near the ureteral orifices and spreads
along the lymphatics to other areas
• Dome of the bladder is the most affected,
• Trigone and neck usually remain normal.
36
Dept of Urology, GRH and KMC, Chennai.
38. • Bladder TB is divided into four stages
• stage 1, tubercle infiltrative;
• stage 2, erosive ulcerous;
• stage 3, spastic cystitis (bladder contraction,
false microcystitis), in fact overactive bladder;
• stage 4, real microcystitis, up to full
obliteration.
Kulchavenya, E. (2014) Urogenital Tuberculosis:
Epidemiology, Diagnosis, Therapy, New York: Springer,
DOI: 10.1007/978-3-319-04837-6.
BLADDER TB
38
Dept of Urology, GRH and KMC, Chennai.
39. Pathology (Epididymis)
• Hematogenous spread
• Globus minor (rich in
vascularity)
• Painful scrotal mass
(indistinguishable from
epididymo orchitis)
• Edididymal/vasal
obstruction - infertility
• Scrotal sinus - rare
• chronic granulomatous
inflammation
• caseous necrosis
• consistent with tuberculosis
Beaded Nodular Vas
39
Dept of Urology, GRH and KMC, Chennai.
40. • Extremely rare
• More often secondary to
epididymal involvement
• Closely mimicks
malignancy
• Responds well to ATT
Pathology (Testis)
40
Dept of Urology, GRH and KMC, Chennai.
41. Prostate
• Hematogenous spread, but involvement is rare.
• In many cases pathologist diagnose it incidentally
after TURP.
• On DRE it feels like a firm granulomatous nodule,
and needs to be differentiated from malignacy.
• Very rarely in acute fulminating cases it spreads
rapidly and presents as peri-anal sinus.
41
Dept of Urology, GRH and KMC, Chennai.
42. Penis and Urethra
• Urethra appears somewhat resistant to TB
infection
• Involved in only 1.9% to 4.5% of GU TB
patients.
• Typically associated with prostate infection
and can manifest with urethroscrotal fistulae.
similarly,
• Primary TB in the penis is exceedingly rare.
42
Dept of Urology, GRH and KMC, Chennai.
43. Female genital tract
– Hematogenous or by direct spread from
adjacent organs
– Tubal obstruction (hydrosalpinx and pyosalpinx)
– Tubo ovarian mass
– Endometrial cavity may be obliterated by
adhesions and thick synechia
43
Dept of Urology, GRH and KMC, Chennai.
45. Why loss of appetite and weight in TB ?
Anti obesity hormone
Expressed in adipose tissue
Acute pro Inflammatory cytokines IL1 & 8
• Rise in Leptin levels
• Loss of weight and appetite
Leptin and body fat
TB
Chronic Smouldering inflammation
• TNF alpha
• Anorexia, loss of weight
Increase in Leptin levels
Decreased food intake
Increased energy expenditure
45
Dept of Urology, GRH and KMC, Chennai.
46. Normal diurnal rhythm of temperature
Why evening Rise of Temperature in TB ?
3 AM
3 PM
46
Dept of Urology, GRH and KMC, Chennai.
47. Why evening Rise of Temperature in TB ?
Cortisol activityHIGH @ Day time, LOW @ 3 PM
Cortisol activity keeps
IL activity under
check.
In evenings
Cortisol level Decreases
IL1 activity increases
Fever manifests
47
Dept of Urology, GRH and KMC, Chennai.
48. Clinical features
• Vague, and a high degree of awareness to
make the diagnosis.
• Symptoms are generally chronic,
intermittent, and nonspecific.
• Genitourinary tuberculosis (GUTB) often
manifests as repeated urinary tract
infections that do not respond to the usual
antibiotics
48
Dept of Urology, GRH and KMC, Chennai.
49. • Chronic and nonspecific
▪ Recurrent UTI
▪ Haematuria-10%
▪ LUTS
▪ Swelling in the scrotum
▪ haematospermia
▪ Fistula
“consider the diagnosis of genitourinary TB in a patient
presenting with vague, long-standing urinary symptoms for
which there is no obvious cause”
49
Dept of Urology, GRH and KMC, Chennai.
50. Why Storage LUTS in GUTB?
Earliest manifestation of GUTB
• Bladder involvement
• Acute inflammation of bladder
• Frequency, Urgency and Urge
incontinence
• Supra pubic pain
• Hematuria
50
Dept of Urology, GRH and KMC, Chennai.
51. • Unexplained infertility in both men and
women may be attributable to GUTB.
51
Dept of Urology, GRH and KMC, Chennai.
53. Think of Genitourinary Tuberculosis in:
• Chronic cystitis
• not responding to adequate therapy
• Sterile pyuria
• Gross or microscopic hematuria
• A nontender, enlarged epididymis
• beaded or thickened vas
• Chronic draining scrotal sinus
• Induration or nodulation of the prostate and thickening of one
or both seminal vesicles (especially in a young man).
• A history of present or past tuberculosis elsewhere in the
body
53
Dept of Urology, GRH and KMC, Chennai.
