3. Akhenaton, aAkhenaton, a
Pharaoh of thePharaoh of the
eighteentheighteenth
dynasty of Egypt,dynasty of Egypt,
and his wifeand his wife
Nefertiti both areNefertiti both are
believed to havebelieved to have
died fromdied from
tuberculosis.tuberculosis.
Evidence indicatesEvidence indicates
that hospitals forthat hospitals for
tuberculosistuberculosis
existed in Egyptexisted in Egypt
as early as 1500as early as 1500
BCEBCE
TB's History
4. TB's HistoryTB's History
Proof of TB has been found in 4 000Proof of TB has been found in 4 000
year old mummies.year old mummies.
Tuberculosis was alsoTuberculosis was also
knownknown
consumptionconsumption fromfrom
Hippocrates through theHippocrates through the
18th century18th century
The white deathThe white death
The great white plagueThe great white plague
The robber of youthThe robber of youth
The graveyard coughThe graveyard cough
During the 18th and 19th centuries tuberculosis
was epidemic in Europe and caused millions of
deaths, particularly in the poorer classes of
society.
5. Robert KochRobert Koch discovered indiscovered in March 24th March 24th 1882 that1882 that
TB was caused by a bacteria.TB was caused by a bacteria.
March 24th has becomeMarch 24th has become “World Tuberculosis Day.”“World Tuberculosis Day.”
19201920 – BCG vaccine– BCG vaccine
1944 –1944 –Streptomycin.Streptomycin.
19701970 – first outbreak of– first outbreak of MDR-TBMDR-TB in USA.in USA.
20052005-- XDR-TBXDR-TB (KwaZulu-Natal, South Africa)(KwaZulu-Natal, South Africa)
6. EPIDEMIOLOGYEPIDEMIOLOGY
One third of world’s populationOne third of world’s population (WHO,1997)(WHO,1997)
8-10 million new cases/year8-10 million new cases/year
One of top 10 (2 million deaths)cause ofOne of top 10 (2 million deaths)cause of
deathdeath (Bleed,D et al 2000)(Bleed,D et al 2000)
75% in the developing countries.75% in the developing countries.
Genitourinary TB 15-20% in those countriesGenitourinary TB 15-20% in those countries
and in 1.2% of cases in USand in 1.2% of cases in US ((NYCDH,2000)NYCDH,2000)
The most common opportunistic inf.in AIDSThe most common opportunistic inf.in AIDS
(Perlman et al,1999)(Perlman et al,1999)
7.
8. TRANSMISSION OF M.T.TRANSMISSION OF M.T.
Droplet InfectionDroplet Infection
Factors determine likelihood of inf.:Factors determine likelihood of inf.:
13. The kidney, epididymis The kidney, epididymis in men, andin men, and
fallopian tubesfallopian tubes in women are thein women are the
primary landing sites for hematogenousprimary landing sites for hematogenous
spread of TB.spread of TB.
The prostate The prostate is also considered one ofis also considered one of
the sites for hematogenous spread,the sites for hematogenous spread,
though its involvement with TB bacilli inthough its involvement with TB bacilli in
urine is more common.urine is more common.
Other genitourinary organs are involvedOther genitourinary organs are involved
byby direct, endoluminal, or lymphaticdirect, endoluminal, or lymphatic
spreadspread from these sites.from these sites.
18. Photographs of a cut gross specimen show the earlyPhotographs of a cut gross specimen show the early
necrosis of the medullary tip (black spot innecrosis of the medullary tip (black spot in aa). Once). Once
devitalized, the papilla sloughs off, leaving a defectdevitalized, the papilla sloughs off, leaving a defect
(cavity in(cavity in bb))
19. Pathology: GrossPathology: Gross
Renal tuberculosis. Photograph of a cut gross specimen shows
multiple, predominantly peripheral, white tuberculous
granulomas throughout the kidney.
32. CLINICAL PICTURECLINICAL PICTURE
Age 20-40Age 20-40
M:F 2 :1M:F 2 :1
General :General :
-Fever 37-80%-Fever 37-80%
-Anaemia & mild leucocytosis10%-Anaemia & mild leucocytosis10%
-Leucopenia & leukomoid reaction-Leucopenia & leukomoid reaction
(Nancy E. et al,2000)(Nancy E. et al,2000)
33. CLINICAL PICTURECLINICAL PICTURE ..contcont
UROLOGICALUROLOGICAL
Non-SpecificNon-Specific
Intermittent & long standing.Intermittent & long standing.
vague.vague.
Minimal not reflecting severe disease.Minimal not reflecting severe disease.
Frequent painless mict & urgency.Frequent painless mict & urgency.
Flank or suprapubic painFlank or suprapubic pain
Ureteral colicUreteral colic
Hematuria 10% overt & 50%Hematuria 10% overt & 50%
microscopic.microscopic.
34. Three other major complications of renal tuberculosis:Three other major complications of renal tuberculosis:
hypertensionhypertension (RAS axis mediated)(RAS axis mediated)
super-infection (12 to 50%)super-infection (12 to 50%)
nephrolithiasis (7 to 18%)nephrolithiasis (7 to 18%)
In 1940, Nesbit and Ratliff reported that hypertensionIn 1940, Nesbit and Ratliff reported that hypertension
could be cured by the removal of a tuberculous kidney,could be cured by the removal of a tuberculous kidney,
35. URINE EXAMINATIONURINE EXAMINATION
Sterile pyuriaSterile pyuria
3 or 5 consecutive morning samples3 or 5 consecutive morning samples
SedimentationSedimentation
Preferably immediate examination, ifPreferably immediate examination, if
delay unavoidable sample must bedelay unavoidable sample must be
refrigerated, not froze.refrigerated, not froze.
Z-N stainingZ-N staining
Culture:Culture:
*Lowenstein-Jensen Medium*Lowenstein-Jensen Medium
*Pyruvic egg medium*Pyruvic egg medium
36. Sterile PyuriaSterile Pyuria
Tuberculosis of the urinary tractTuberculosis of the urinary tract
Chlamydia trachomatis, Mycoplasma, orChlamydia trachomatis, Mycoplasma, or
Ureaplasma infectionUreaplasma infection
Chemically induced cystitisChemically induced cystitis
Renal calculiRenal calculi
ProstatitisProstatitis
Coliform (or other pathogen) urinary tractColiform (or other pathogen) urinary tract
infection but antibiotic inhibiting growthinfection but antibiotic inhibiting growth
WBC from outside urinary tract, e.g. fromWBC from outside urinary tract, e.g. from
foreskin or vulvaforeskin or vulva
Renal parenchymal causes as acuteRenal parenchymal causes as acute
tubulointerstitial nephritis, glomerular diseasetubulointerstitial nephritis, glomerular disease
37. Urine ExamUrine Exam.. Cont.Cont.
Liquid culturesLiquid cultures
*Radiometric (BACTEC 460)*Radiometric (BACTEC 460)
(Piersimoni et al, 2001)(Piersimoni et al, 2001)
*Non-radiometric :*Non-radiometric :
(BACTEC 9000, MGIT 960)(BACTEC 9000, MGIT 960)
(Bemer P. et el,2002)(Bemer P. et el,2002)
38. Double stranded target DNA
DNA denatured Two DNA targets for PCR
Primers bind to target DNA Double stranded DNA duplicate
PCR
amplification
cycle
POLYMERASE CHAIN REACTION
39. Double stranded target DNA
DNA denatured Two DNA targets for LCR
Primers bind to target DNA Double stranded DNA duplicate
LGASE CHAIN
REACTION
LIGASE CHAIN REACTION
40. Tuberculin TestTuberculin Test
Intradermal injection of purifiedIntradermal injection of purified
protein derivative indurationprotein derivative induration
Criteria for tuberculin positivityCriteria for tuberculin positivity
Reaction ≥ 5mm of indurationReaction ≥ 5mm of induration
Reaction ≥ 10mm of indurationReaction ≥ 10mm of induration
Reaction ≥ 15mm of indurationReaction ≥ 15mm of induration
(CDC,2000)(CDC,2000)
+ve reaction does not mean activity+ve reaction does not mean activity
41. Five millimeters or more of indurationFive millimeters or more of induration ::
Considered positive inConsidered positive in persons with the highestpersons with the highest
likelihood of developing active disease.likelihood of developing active disease.
These include:These include:
1.1. Patients with HIV infectionPatients with HIV infection
2.2. Organ transplantsOrgan transplants
3.3. ImmunosuppressionImmunosuppression
4.4. Close contact with persons having activeClose contact with persons having active
tuberculosis cases or radiographic findings consistenttuberculosis cases or radiographic findings consistent
with old tuberculosis.with old tuberculosis.
42. Ten millimeters or more of induration:Ten millimeters or more of induration:
considered positive in those who do not meet theconsidered positive in those who do not meet the
preceding criteria but who are at high risk forpreceding criteria but who are at high risk for
tuberculosis.tuberculosis.
These include:These include:
1.1. HIV-negative injection drug usersHIV-negative injection drug users
2.2. Residents and employees of high-risk congregateResidents and employees of high-risk congregate
settings, such as prisons, nursing homessettings, such as prisons, nursing homes
3.3. Laboratory personnel dealing with mycobacterialLaboratory personnel dealing with mycobacterial
samplessamples
4.4. Persons with high-risk medical conditions,Persons with high-risk medical conditions,
including diabetes, chronic renal failureincluding diabetes, chronic renal failure
Fifteen millimeters or more of induration isFifteen millimeters or more of induration is
considered positive in anyone.considered positive in anyone.
44. RADIOGRAPHYRADIOGRAPHY cont.cont.
INTRAVENOUS UROGRAPHYINTRAVENOUS UROGRAPHY
•• Moth eaten calyx, hydrocalycosis,Moth eaten calyx, hydrocalycosis,
amputated calyx, hydronephrosis,amputated calyx, hydronephrosis,
parenchymal cavity, mass, autonephrecparenchymal cavity, mass, autonephrec
•• Strictures infundibular,UPJ,UVJStrictures infundibular,UPJ,UVJ
•• Thimble bladderThimble bladder
•• Dynamic study with image intensifiedDynamic study with image intensified
endoscopyendoscopy (Warren D. et al, 2002)(Warren D. et al, 2002)
45.
46. Classic lobar pattern of calcification, which is pathognomonic of end-stage
renal tuberculosis, with Ureteral calcification , which is fainter in upper
parts.
The occurrence of any upper ureteral calcification (however, faint) along with any
other renal calcification is a good pointer of renal TB.
47.
48. A.lower infundibular and
renal pelvic
scarring,papillary
necrosis
B.papillary necrosis in the
upper group of calyces,
Healing forniceal papillary
necrosis in a lower calyx
C.multiple parenchymal cavities with areas of
papillary necrosis
49. o The cephalic
retraction of the
inferior medial margin
of the renal pelvis at
the ureteropelvic
junction (UPJ), or the
"hiked up renal pelvis,
is another suggestive
urographic change.
.
50. Intravenous urogram
revealing cicatrization that
has resulted in obliteration
of the renal pelvis, multiple
infundibular strictures
(white arrows) and uneven
caliectasis. Note non-
visualization of the middle
group of calyces–the
“phantom calyx” (black
arrows) and a cavity
communicating with a lower
calyx (arrowheads)>> due
to selective non excretion of
calyes
51. Intravenous urogram revealing a (R) ureteric stricture (white arrow) with
ureteric calcification (black arrowheads), pseudo-calculi (black arrow),
and irregular calcification in the parenchyma (circled area)
*dense calcification may mimic calculi ‘pseudo calculi’*‑ ‑
52. (A) Intravenous urogram revealing a non-functioning (L) kidney and a small
capacity urinary bladder. (B) Intravenous urogram revealing non-functioning
(R) kidney. (L) Renal pelvic and upper infundibular scarring (white
arrowheads), resulting in uneven caliectasis. A (L) lower ureteric stricture
(arrow) and small capacity bladder (black arrowheads) are also noted
53.
54.
55. Parenchymal granulomas (black arrows) in the (L)
kidney with uneven caliectasis and ureterectasis
accompanied by urothelial thickening (white arrow).
57. (A)CT revealing caseous TB cavity (arrow) in the upper pole of the (L)
kidney. (B)CT revealing a cavity (white arrowheads)communicating
with a dilated pelvi calyceal system (PCS)
Inflammatory granulomatous and caseating masses show enhancement.
58. (A) Non-contrast CT image showing fine cortical calcification in the (L)
kidney (white arrow). (B and C) non-contrast CT image showing
punctate calcification [arrows in (B) and soft (caseous) parenchymal
calcification arrowheads in (C)].
(D and E) axial CT revealing the lobar pattern of calcification
(arrowheads)
59. Pelvicalyceal system (PCS) and ureteral
involvement
Focal or diffuse caliectasis unaccompanied by renal pelvic dilatation.
Urothelial thickening.
Multifocal strictures lead to uneven caliectasis.
Hydronephrosis
Multiple ureteral strictures
60. With long standing renal TB, progressive parenchymal atrophy‑
and hydronephrosis lead to a loss of normal morphology, and
the appearance mimics multiple thin walled cysts or,‑
occasionally, a multiloculated cyst
61. Two goalsTwo goals
Clinical ManagementClinical Management
conservation of tissue
and function
antimycobacterial cure.
63. Longer courses of ATT rangingLonger courses of ATT ranging from 9 months tofrom 9 months to
2 years2 years are useful in patients:are useful in patients:
Who do not tolerate PyrazinamideWho do not tolerate Pyrazinamide
Those responding slowly to standard regimenThose responding slowly to standard regimen
Those with miliary and CNS diseaseThose with miliary and CNS disease
Children with multiple site involvementChildren with multiple site involvement
Longer courses of ATTLonger courses of ATT
64. After 2 month of therapy-After 2 month of therapy-
3 urine cultures3 urine cultures
If negative- continue therapyIf negative- continue therapy
At the end of therapyAt the end of therapy
3 consecutive negative samples3 consecutive negative samples
Repeated after 3 months and at 1 year.Repeated after 3 months and at 1 year.
Treatment monitoringTreatment monitoring
suffering from tuberculosis was thought to bestow upon the sufferer heightened sensitivity. The slow progress of the disease allowed for a "good death" as sufferers could arrange their affairs.[45] The disease began to represent spiritual purity and temporal wealth, leading many young, upper-class women to purposefully pale their skin to achieve the consumptive appearance. British poet Lord Byron wrote in 1828, "I should like to die from consumption," helping to popularize the disease as the disease of artists.[46]
Pathology specimen of end-stage renal tuberculosis: The basis for the ‘lobar caseation pattern’ is evident
Diagrammatic representation demonstrating the pathological changes of renal tuberculosis
Diagrammatic representation demonstrating the pathological changes of renal tuberculosis
(A) Plain radiograph revealing classic lobar pattern of calcification, which is pathognomonic of end-stage renal tuberculosis.
Ureteral calcification is also noted, which is fainter in upper parts(arrowheads), (B) intravenous urogram revealing the ‘classic’ lobar
pattern of calcification in a non-functioning (R) kidney. Ureteral calcification is also noted (arrowheads)
(A) Intravenous urogram revealing lower infundibular (arrow) and renal pelvic scarring (curved arrow). Note areas of papillary
necrosis in the circled area, (B) Intravenous urogram revealing papillary necrosis in the upper group of calyces, with irregularity of the calyceal margins and the lateral margin of the upper infundibulum (dotted circle), indicating spread of infection from the calyx to the infundibulum. (Healing forniceal papillary necrosis of non-tuberculosis origin noted in a lower calyx (arrow), (C) Intravenous urogram revealing multiple parenchymal cavities (black arrows) with areas of papillary necrosis (white arrow) in the upper group calyces, bilaterally. The (L) upper group (lateral division) calyceal outline is destroyed by adjacent granulomatous tissue (arrowheads)
Intravenous urogram revealing an upward pointing (arrow) renal pelvic calculus, suggesting the presence of a hiked up renal pelvis.
Multiple discrete calcifications are noted in an upper polar tuberculosis cavity (circled area)
Intravenous urogram revealing cicatrization that has resulted in obliteration of the renal pelvis, multiple infundibular strictures (white arrows) and uneven caliectasis. Note non-visualization of the middle group of calyces–the “phantom calyx” (black arrows) and a cavity communicating with a lower calyx (arrowheads)>> due to selective non excretion of calyes
Intravenous urogram revealing a (R) ureteric stricture (white arrow) with ureteric calcification (black arrowheads), pseudo-calculi (black arrow), and irregular calcification in the parenchyma (circled area)
*dense calcification may mimic calculi‑‘pseudo‑calculi’*
(A) Intravenous urogram revealing a non-functioning (L) kidney and a small capacity urinary bladder. (B) Intravenous urogram revealing non-functioning (R) kidney. (L) Renal pelvic and upper infundibular scarring (white arrowheads), resulting in uneven caliectasis. A (L) lower ureteric stricture (arrow) and small capacity bladder (black arrowheads) are also noted
Parenchymal granulomas (black arrows) in the (L) kidney with uneven caliectasis and ureterectasis accompanied
by urothelial thickening (white arrow).
CT revealing Left TB renal abscess (arrow) with minimal perinephric spread (arrowheads) in (A). The left psoas muscle
is involved, better appreciated in (B), Retroperitoneal fascial thickening, fat stranding, and small left paraaortic lymph nodes are also noted with a loss of corticomedullary differentiation of the affected area in the (L) kidney
(A)CT revealing caseous TB cavity (arrow) in the upper pole of the (L) kidney. (B)CT revealing a cavity (white arrowheads)communicating with a dilated pelvi calyceal system (PCS)
(A) Non-contrast CT image showing fine cortical calcification in the (L) kidney (white arrow). (B and C) non-contrast CT image showing punctate calcification [arrows in (B) and soft (caseous) parenchymal calcification arrowheads in (C)].
(D and E) axial CT revealing the lobar pattern of calcification (arrowheads)
(A) Focal uneven caliectasis. Enhancing urothelial thickening (white arrows), noted in the pelvic alcyceal system and upper ureter. Retroperitoneal lymph nodes are also noted (black arrows). (B)Uneven caliectasis with no obvious pelvic dilatation.Parenchymal scarring (black arrow), cavity communicating with PCS (white arrow), urothelial thickening and multiple ureteral strictures (black arrowheads)