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Clinical Presentation of Mycobacterium Tuberculosis

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Title: Clinical Presentation of Mycobacterium Tuberculosis


1
Clinical Presentation of Mycobacterium
Tuberculosis
  • By Dr.Sujith S.

2
Introduction
  • Tuberculosis, one of the oldest diseases known to
    affect humans, is a major cause of death
    worldwide.
  • This disease, which is caused by bacteria of the
    Mycobacterium tuberculosis complex? affects the
    lungs
  • Other organs are involved in up to one-third of
    cases

3
  • If untreated, the disease may be fatal within 5
    years in 5065 of cases.
  • Transmission usually takes place through the
    airborne spread of droplet nuclei produced by
    patients with infectious pulmonary tuberculosis.

4
  • M. bovis (the bovine tubercle bacillus)
  • M. caprae (related to M. bovis)
  • M. africanum (isolated from cases in West,
    Central, and East Africa)
  • M. microti (the "vole" bacillus, a less virulent
    and rarely encountered organism)
  • M. pinnipedii (a bacillus infecting seals and sea
    lions in the southern hemisphere and recently
    isolated from humans)
  • M. canettii

5
Etiological Agent
  • M. tuberculosis is a rod-shaped,
    non-spore-forming, thin aerobic bacterium
    measuring 0.5 um by 3 um the bacilli cannot be
    decolorized by acid alcohol this characteristic
    justifies their classification as acid-fast
    bacilli.
  • Acid fastness is due mainly to the organisms'
    high content of mycolic acids, long-chain
    cross-linked fatty acids, and other cell-wall
    lipids

6
History
  • Fever
  • Fatigue
  • Cough
  • Weight loss
  • Dyspnoea
  • Chest Pain
  • Retrosternal interscapular dull
    pain,worsened by swallowing

7
Cont.d
  • Cough -initially mild,non-productive / productive
    of only scanty sputum.
  • May be present only in the morning, when
    accumulated secretions are expectorated.
  • Progressive,?cough becomes more continuous and
    productive of yellow or yellow-green sputum,
    rarely foul-smelling.
  • Frank hemoptysis, due to caseous sloughing or
    endobronchial erosion?present later in the
    disease.

8
  • Dyspnoea-occurs when
  • extensive parenchymal involvement/ pleural
    effusions, /pneumothorax.
  • Pleuritic chest pain -when present, signifies
    inflammation abutting or invading the pleura,
    with or without an effusion.
  • Rarely progresses to frank empyema
  • Patients may present with painful ulcers of the
    mouth, tongue, larynx or GI tract .

9
Elderly
  • Fever, sweats and hemoptysis were less common in
    the elderly.
  • These patients were less likely to have cavitary
    disease / positive purified protein derivative
    (PPD) skin test.

10
Cont.d
  • Painless swelling of the lymph nodes, most
    commonly at posterior cervical and
    supraclavicular sites.
  • Increase in urinary frequency
  • Dysuria
  • Nocturia
  • Hematuria
  • Flank or abdominal pain

11
  • Pain swelling in the weight-bearing joints
  • (the spine in 40 of cases, the hips in 13, and
    the knees in 10).

12
  • Initially as headache and slight mental changes.
    May evolve acutely with severe headache,
    confusion, lethargy, altered sensorium, and neck
    rigidity.
  • Paresis of cranial nerves
  • Involvement of cerebral arteries may produce
    focal ischemia.
  • Coma, with hydrocephalus and intracranial
    hypertension

13
  • Abdominal pain and swelling
  • Obstruction
  • Hematochezia
  • Palpable mass in the abdomen

14
  • Diffuse abdominal pain/ pain localizing to the
    right upper quadrant, nausea, vomiting and
    diarrhea. Hepatomegaly .
  • Liver function test abnormalities are common,
    including elevated alkaline phosphatase and
    transaminases.
  • Cholestatic jaundice is also well-documented in
    miliary TB.
  • Ascites may be detected in occasional patients.
    Miliary TB may also present as pancreatitis /
    cholecystitis .

15
Physical Examination
  • Not specific and usually are absent in mild or
    moderate disease.
  • Dullness with decreased fremitus resonance may
    indicate pleural thickening or effusion.
  • Rales may be present throughout inspiration, or
    may be heard only after a short cough
    (post-tussive rales).

16
  • When large areas of the lung are involved, signs
    of consolidation associated with open bronchi?
    whispered pectoriloquy/tubular breath sounds.
  • Distant hollow breath sounds over cavities are
    called amphoric,after the sound made by blowing
    across the mouth of jars used in antiquity
    (amphora).

17
  • Pulmonary Tuberculosis

18
Primary Disease
  • Primary pulmonary tuberculosis occurs soon after
    the initial infection with tubercle bacilli.
  • Inspired air is distributed to the middle and
    lower lung zones-most commonly involved in
    primary tuberculosis.
  • The lesion -accompanied in more than half of
    cases by hilar or paratracheal lymphadenopathy.
  • The lesion heals spontaneously ,later be evident
    as a small calcified nodule (Ghon lesion).

19
Post Primary disease
  • Chronic TB
  • Postprimary disease
  • Recrudescent TB
  • Endogenous reinfection
  • Adult type progressive TB

20
  • Reactivation of a previously dormant focus seeded
    at the time of the primary infection.
  • The apical posterior segments of the lung are
    frequently involved.
  • The original site of spread may have been
    previously visible as a small scar called a Simon
    focus

21
  • Localized to the apical and posterior segments of
    the upper lobes- higher mean oxygen tension
    (compared with that in the lower zones) favors
    mycobacterial growth.
  • The superior segments of the lower lobes are
    frequently involved.
  • Small infiltrates to extensive cavitary disease..

22
  • Liquefied necrotic contents - discharged into the
    airways? satellite lesions within the lungs that
    may in turn undergo cavitation
  • Massive involvement of pulmonary segments or
    lobes, with coalescence of lesions, produces
    tuberculous pneumonia.
  • Some pulmonary lesions become fibrotic and may
    later calcify, but cavities persist in other
    parts of the lungs

23
  • Endobronchial TB
  • Direct extension to the bronchi from an adjacent
    parenchymal focus, usually a cavity.
  • Spread of organisms to the bronchi via infected
    sputum from a distant site.

24
  • Clinical Presentation
  • Bronchorrhea, which is production of more than
    500 mL per day of sputum .
  • Caseous material from endobronchial lesions /
    calcific material from extension of calcific
    nodes into the bronchi can be expectorated, which
    is known as lithoptysis.

25
  • Wheezing and hemoptysis may also be seen.
  • Lymph node rupture can be associated with chest
    pain.
  • Dyspnea may signal obstruction or atelectasis
  • Physical findings
  • Diminished breath sounds, rhonchi or wheezing may
    be heard.
  • The wheeze is described as low-pitched, constant
    and always heard over the same area on the chest
    wall.

26
  •  Lower lung field TB
  • Disease located below a line traced across the
    hila, including the perihilar regions, on a
    standard PA and lateral chest x-ray.
  • Risk factors
  • Elderly patients
  • Diabetes
  • Renal/ hepatic disease
  • Those receiving corticosteroids
  • Underlying silicosis appear most at risk for
    lower lobe

27
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28
  • Complications of Pulmonary TB
  • Hemoptysis
  • Pneumothorax
  • Bronchiectasis
  • Extensive pulmonary destruction

29
  • Hemoptysis
  • Active disease(smear positive)
  • "Rasmussen's aneurysm" causes massive hemoptysis
    when TB extends into the adventitia and media of
    bronchial arteries, resulting in inflammation and
    thinning of the vessel wall.
  • Subsequently rupturing into the cavity,
    producing hemoptysis.

30
  • Other causes
  • residual bronchiectasis
  • an aspergilloma/ other fungus ball invading an
    old healed cavity,
  • a ruptured broncholith that erodes through a
    bronchial artery
  • a carcinoma
  • another infectious or inflammatory process.

31
  • CNS Tuberculosis

32
  • Meningitis
  • Intracranial tuberculoma
  • Spinal tuberculous arachnoiditis

33
Pathogenesis
  • Scattered tuberculous foci (tubercles) are
    established in the brain, meninges, or adjacent
    bone during the bacillemia.
  • The chance occurrence of a subependymal tubercle,
    with progression and rupture into the
    subarachnoid space.

34
  • The spillage of tubercular protein into the
    subarachnoid space produces an intense
    hypersensitivity reaction.

35
  • Proliferative arachnoiditis, most marked at the
    base of the brain, produces a fibrous mass
    involving cranial nerves and penetrating vessels.
  • Communicating hydrocephalus results from
    extension of the inflammatory process to the
    basilar cisterns and impedance of CSF circulation
    and resorption.

36
  • Vasculitis with resultant thrombosis and
    infarction involves vessels that traverse the
    basilar/ spinal/ are located within the brain
    substance.

37
  • Meningitis
  • ?The prodromal phase(2 to 3 weeks)
  • fever,malaise,lassitude
  • ?The meningitic phase-
  • meningismus, protracted headache, vomiting,
    lethargy, confusion, and varying degrees of
    cranial nerve and long-tract signs

38
  • The paralytic phase
  • ?delirium, stupor, coma, seizures, multiple
    cranial nerve palsies,or dense hemiplegia.

39
  • About one-third of patients on presentation
    ?generalized (miliary) tuberculosis
  • Careful fundoscopic examination often shows
    choroidal tubercles .
  • These are multiple, ill-defined, raised
    yellow-white nodules (granulomas) of varying size
    near the optic disk.

40
  • Tuberculoma
  • Tuberculomas are conglomerate caseous foci within
    the substance of the brain ? from deep-seated
    tubercles acquired during a recent or remote
    hematogenous bacillemia.

41
  • Radiologically
  • clinically silent
  • single / multiple enhancing nodular lesions , on
    CT scanning of patients with meningitis or
    miliary TB without meningitis.

42
  • Tuberculoma is also a distinct clinical syndrome
    manifested by focal neurologic symptoms and signs
    of an intracranial mass lesion.

43
  • Tuberculosis Lymphadenitis

44
Pathogenesis
  • Isolated peripheral tuberculous lymphadenopathy
    ?reactivation of disease at a site seeded
    hematogenously during primary TB infection.

45
Clinical Presentation
  • The most common presentation is isolated chronic,
    nontender, lymphadenopathy. The mass may be
    present for up to 12 months before diagnosis
  • A firm discrete mass or matted nodes fixed to
    surrounding structures the overlying skin may be
    indurated. Uncommon findings include fluctuance,
    draining sinus/ erythema nodosum

46
  • Cervical lymphadenopathy is the most common
    manifestation of TB lymphadenitis.
  • A unilateral mass appears in the anterior or
    posterior cervical triangles submandibular and
    supraclavicular lymph node involvement also
    occurs.
  • Bilateral disease is uncommon.
  • Multiple nodes may be involved at that site.

47
  • The axillary, inguinal, mesenteric, mediastinal,
    and intramammary lymph nodes.
  • Mediastinal lymphadenopathy
  • Dysphagia
  • Esophageal perforation
  • Vocal cord paralysis due to recurrent laryngeal
    nerve involvement
  • Pulmonary artery occlusion mimicking pulmonary
    embolism.

48
  • Tuberculous peritoneal lymphadenopathy
    ?i)periportal region
  • ?ii)peripancreatic
  • ?iii)mesenteric lymph nodes.
  • ?iv)Hepatic lymph node involvement can lead
    to jaundice, portal vein thrombosis, and portal
    hypertension.
  • Extrinsic compression of renal arteries due to
    tuberculous abdominal lymphadenopathy can result
    in renovascular hypertension

49
  • Skeletal Tuberculosis

50
  • Spinal TB (Pott's disease) most often affects the
    lumbar and lower thoracic region. Tuberculous
    abscess ? frequently bilateral.
  • Tuberculous arthritis tends to occur in the
    weight-bearing joints, the hip and the knee, and
    is usually monoarticular.

51
Pathogenesis
  • The bacillemia
  • Seeds organisms
  • Bone and synovium

52
  • Spinal TB
  • Infection - in the anteroinferior aspect of the
    cancellous vertebral body, inflammatory bone
    destruction and caseating necrosis.
  • Active infection spreads down behind the anterior
    ligament , involves the adjacent vertebral body.
  • Local destruction - collapse of bony structures,
    herniation of the disk into the vertebral bodies.

53
  • A tuberculous abscess - impinge on local
    structures.
  • An epidural abscess -produce pressure on the
    cord.
  • An extraspinal soft tissue mass - erodes ribs and
    adjacent structures
  • Psoas abscess - track down to the groin

54
  • Vertebral collapse
  • spinal instability with gibbous deformity
  • distort the anatomy of the canal to the point of
    spinal cord compression.
  • Granulomatous changes ?synovial proliferation in
    tuberculous arthritis with joint effusion and
    erosion of cartilage.
  • Slowly progressive destruction, disorganization
    of joint architecture, and potential deformity.

55
Clinical Presentation
  • Local pain-associated with muscle spasm and
    rigidity.
  • Description of the patient with spinal TB reads
    "The muscle spasm, which extends beyond the
    diseased area, sometimes produces the well-known
    erect posture and 'aldermanic' gait.
  • The patient walks with short deliberate steps to
    avoid any jarring of the spine.

56
  • ii)Cord compression during the active phase of
    the infection resulting in paraplegia (Pott's
    paraplegia)
  • Late-onset paraplegia ?osteophytes and other
    chronic degenerative changes at a site of
    previous infection.
  • TB of the pedicles and other posterior spinal
    elements is well-described.

57
  • Renal Tuberculosis

58
Spinal TB
59
TB Arthritis of Hip
60
  • Two major mechanism
  • i)Direct infection of the kidney and lower
    urinary tract
  • ii)Secondary amyloidosis.
  • iii)Nephrotoxicity induced by antimicrobial
    agents
  • iv)Hyponatremia due to the syndrome of
    inappropriate ADH secretion because of pulmonary
    involvement /miliary disease.

61
Pathogenesis
  • Hematogenous seeding either at the time of
    primary pulmonary infection.
  • The net effect is the formation of granulomatous
    lesions in the glomeruli ? heal without producing
    any renal disease.
  • The granulomas may caseate and rupture into the
    tubular lumen as late as 30 years after the
    initial infection.
  • Tubercle bacilli can enter the medullary
    interstitium, eventually leading to granuloma
    formation and progressive medullary injury.
  • Similar lesions can occur in the ureters,
    bladder, and, in males, the prostate and
    epididymis.

62
  • Dysuria and gross hematuria being the most common
    symptoms .
  • Renal colic ? uncommon manifestation with active
    extrarenal disease (fever, weight loss, cough,
    hemoptysis).
  • Rupture of the glomerular granulomas is a random
    event, independent of disease elsewhere
  • .

63
  • Incidentally found to have pyuria and/or
    microscopic hematuria.
  • Heavy proteinuria and cellular casts.
  • Plasma creatinine concentration is usually normal
    or near normal.
  • Ureteral strictures may cause obstructive
    uropathy-gt severe cases, renal loss .

64
  • Signs of extrarenal disease include ureteral
    strictures (single or multiple)
  • A contracted bladder
  • Calcifications in the vas deferens, seminal
    vesicles, or prostate.

65
  • Refractory hypertension ? complication of renal
    tuberculosis.
  • The elevation in blood pressure ? is angiotensin
    II-mediated-from intimal proliferation of vessels
    in or near areas of inflammation, leading to
    segmental ischemia and renin release.

66
  • Drug induced Nephritis
  • Renal glucosuria
  • Hyperuricosuria
  • polyuria due to nephrogenic diabetes insipidus
  • increased urinary excretion of polyclonal light
    chains.

67
  • Mild hyponatremia (plasma sodium concentration
    usually between 125 and 135 meq/L) .
  • Most patients appear to have the syndrome of
    inappropriate ADH secretion.

68
  • Tuberculosis
    Peritonitis

69
  • Risk factors
  • Cirrhosis
  • HIV infection
  • Diabetes mellitus
  • Underlying malignancy?treatment with anti-tumor
    necrosis factor (TNF) agents
  • Patients undergoing continuous ambulatory
    peritoneal dialysis

70
  • Reactivation of latent tuberculous foci in the
    peritoneum ? hematogenous spread from a primary
    lung focus.
  • As the disease progresses-? the visceral and
    parietal peritoneum become increasingly studded
    with tubercles.
  • Ascites develops secondary to "exudation" of
    proteinaceous fluid from the tubercles.

71
Clinical Presentation
  • Ascites (93 percent), abdominal pain (73
    percent), and fever (58 percent).
  • Many patients had a diffusely distended tender
    abdomen.
  • The classic doughy abdomen is associated with
    the fibroadhesive form of tuberculous
    peritonitis.

72
  • The salient clinical findings
  • Abdominal tenderness
  • Hepatomegaly
  • Ascites

73
  • Genital
    Tuberculosis

74
  • Tuberculosis - affect the upper female
    reproductive tract (fallopian tube, endometrium,
    ovaries)
  • i)Extension from an intraabdominal focus,
    hematogenous seeding
  • ii)Ascending from lower genital tract (cervix,
    vagina, vulva) infection.
  • The fallopian tube and endometrium are most
    commonly involved.

75
  • The finding of endometrial tuberculosis always
    means that the tubes are infected
  • Tuberculous salpingitis can exist without
    associated endometritis.
  • Pelvic mass, infertility, abnormal uterine
    bleeding, and pelvic pain
  • Epididymo-orchitis in males

76
  • Tuberculosis
    Pericarditis

77
  • Stage of infection
  • The degree of pericardial involvement
  • The degree of extrapericardial tuberculous disease

78
  • Physical Findings
  • Fever
  • Tachycardia
  • Increased jugular venous pressure
  • Hepatomegaly
  • Ascites
  • Peripheral edema
  • Pericardial rub and distant heart sounds

79
  • Constructive Pericarditis
  • Kussmaul's sign (the lack of an inspiratory
    decline in jugular venous pressure).
  • Elevated and distended jugular veins with a
    prominent Y descent (the second inward deflection
    of the internal jugular pulse due to diastolic
    inflow of blood into the right ventricle)
  • In constriction, the inspiratory decline in
    pressure is not transmitted to the right heart
    chambers.

80
  • Cardiac Tamponade
  • Hypotension with a narrow pulse pressure,
    reflecting the limited stroke volume.
  • Sinus tachycardia
  • Elevated jugular venous pressure
  • Pulsus paradoxus, defined as an abnormally large
    decrease in systolic blood pressure (gt10 mmHg) on
    inspiration.

81
  • Ascites .
  • The main clue? elevation of jugular venous
    pressure.

82
  • Tuberculosis
    Enteritis

83
Pathogenesis
  • Swallowing of infected sputum
  • Hematogenous spread from active pulmonary or
    miliary TB
  • Ingestion of contaminated milk or food, a rarity
    in the Western world
  • Contiguous spread from adjacent organs

84
  • Most common siteileocecal region
  • Cause
  • Relative stasis and abundant lymphoid tissue.
    The organism penetrates the mucosa and localizes
    in the submucosal lymphoid tissue, where it
    initiates an inflammatory reaction with
    subsequent lymphangitis, endarteritis, granuloma
    formation, caseation necrosis, mucosal
    ulceration, and scarring.

85
  • Ulcerative (60 percent)?multiple superficial
    ulcers.
  • Hypertrophic (10 percent)? scarring, fibrosis,
    and pseudotumor lesions.
  • Ulcerohypertrophic (30 percent)? inflammatory
    mass centering around the ileocecal valve with
    thickened and ulcerated intestinal walls.

86
Clinical Presentation
  • Nonspecific chronic abdominal pain
  • Anorexia, fatigue, fever, night sweats, weight
    loss, diarrhea, constipation, or blood in the
    stool may be present.
  • A palpable right lower quadrant abdominal mass
    is present in 25 to 50 percent of patients.
  • Small bowel obstruction / colonic perforation .
    The presence of ascites may help to distinguish
    ileocecal TB from Crohn's disease.

87
  • Tb Pleural
    Effusion

88
Pathogenesis
  • Tuberculous pleural effusions ? a delayed
    hypersensitivity reaction to mycobacterial
    antigens in the pleural space.
  • These antigens probably enter the pleural space
    after rupture of a subpleural focus of disease or
    leakage from these lesions.

89
Clinical Presentation
  • Tuberculous pleural effusion ? acute febrile
    illness causing a i) nonproductive cough (94
    percent) ii) pleuritic chest pain
    (78 percent) without an elevation in the
    peripheral white blood cell (WBC) count.
  • Night sweats, chills, weakness, dyspnea, and
    weight loss.

90
  • TB Adrenalitis

91
  • Tuberculous adrenalitis results from hematogenous
    spread from active infection elsewhere in the
    body .
  • Extraadrenal tuberculosis is usually evident, but
    may be clinically latent

92
  • Miliary
    Tuberculosis

93
Clinical Presentation
  • During primary infection, the disease has a more
    acute onset and more rapid clinical course.
  • Acute disease may be fulminant,
  • i) multiorgan system failure
  • ii)a syndrome of septic shock
  • iii) acute respiratory distress syndrome, ARDS

94
  • Late miliary tuberculosis can be acute, but is
    more likely to be subacute or chronic.
  • Reinfection may have a role in highly endemic
    areas.
  • At the chronic end of the spectrum, patients may
    present with failure to thrive without fever,
    with fever of unknown origin, or with dysfunction
    of one organ system

95
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96
  • Thankyou

97
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