JK Amorosa

Tuberculosis

Primary –selflimiting

Infection in patients previously not exposed to M tuberculosis (under age 5 in the past, now common in adults also)

Postprimary-progressive

Reactivation and reinfection

Chest X-ray is normal in TB in

50% 75% 15%

Manifestations of Primary TB are:

Parenchymal disease Lymphadenopathy Miliary disease Pleural Effusion

Manifestations of Postprimary TB are:

Upper lobe distribution Cavity Absence of adenopathy Airway involvement

Human disease causing mycobacteria are more likely:

Slow growing Fast growing

Mycobacteria – aerobic rods Categories by disease cause:

1.tuberculosis complex: causes human disease 2.nontuberculous or atypical

Categories by rate of growth: 1.rapid growing: < 7 days 2.slow growing:> 7 days

Rapid: M.abscessus, M.fortiutum, M.chelonae

Slow: MTB, MAC, M.Kansasii

Transmission

Respiratory Desiccated bacilli remain airborne for

long time – indoor close many months contact is necessary for transmission

Laryngeal, transbronchial, cavitary disease produce most bacilli

Ventillation reduces infectiousness

Lung Parenchymal involvement Primary

57 yo f with chronic cough

Value of thin section

Tuberculous mediastinal adenopathy

TB mediastinal adenopathy 19 f

TB mediastinal adenopathy is seen as part of Reactivation TB HIV Primary TB usually in children

TB mediastinal adenopathy is seen as part of Reactivation TB HIV Primary TB usually in children

TB Lymphadenopathy

Central low attenuation Active disease Necrosis R hilar is most common

Pathogenesis

TB bacilli in the body elicit acute inflammatory response – no symptoms

Macrophages ingest bacilli and transport them to regional lymph nodes

If not contained in local LNs, hematogenous dissemination of bacilli occurs and usually is contained, if not, then: miliary, meningeal, GU, MSK

Miliary

60 f smoker Langerhans Histiocytosis

Miliary Chickenpox pneumonia

Tuberculosis, disseminated Blastomycosis, disseminated Coccidioidomycosis, disseminated Cryptococcosis Histoplasmosis, disseminated Melioidosis Blastomycosis Coccidioidomycosis, pulmonary, chronic Cryptococcosis, pulmonary Filariasis Fungal lung infection Histoplasmosis Histoplasmosis, pulmonary Parasitic lung infection Pulmonary larval infestation/nematodes Pulmonary larval migrans Schistosomiasis

Granulomatous, Inflammatory Disorders Bronchiocentric granulomatosis/lung Granulomatous lung disease Sarcoidosis Sarcoidosis, pulmonary Neoplastic Disorders Lymphomas Metastatic lung lymphatics/carcinoma Alveolar cell carcinoma, lung Carcinoma, thyroid, anaplastic

Miliary cont

Allergic, Collagen, Auto-Immune Disorders Pulmonary arteritis/vasculitis Rheumatoid lung disease Metabolic, Storage Disorders Histiocytosis, pulmonary Histiocytosis X Hereditary, Familial, Genetic Disorders Tuberous Sclerosis

Anatomic, Foreign Body, Structural Disorders Atelectasis, pulmonary Reference to Organ System Respiratory distress (newborn) syndrome Pulmonary fibrosis Pulmonary microlithiasis, alveolar Poisoning (Specific Agent) Silicosis Organ Poisoning (Intoxication) Pneumoconiosis

Pleural Effusion TB

TB pleurisy

Unilateral Exudative: high protein content, High

WBC, low glucose Lymphocyte predominance Complications: B-P fistula, empyema 1/3 negative TB skin test

Pleural Effusion exudative Malignancy Pneumonia Tuberculosis Pulmonary embolism Fungal infection Pancreatic pseudocyst Intra-abdominal abscess After coronary artery bypass

graft surgery Postcardiac injury syndrome Pericardial disease Meigs syndrome Ovarian hyperstimulation

syndrome Rheumatoid pleuritis Lupus erythematosus

Drug-induced pleural disease

Asbestos pleural effusion

Yellow nail syndrome Uremia Trapped lung Chylothorax Pseudochylothorax Acute respiratory

distress syndrome Chronic pleural

thickening Malignant mesothelioma

Pleural Effusion transudate: <3 g protein, low WBC, normal glucose Congestive heart

failure (most common)

Cirrhosis with hepatic hydrothorax

Nephrotic syndrome Peritoneal

dialysis/continuous ambulatory peritoneal dialysis

Hypoproteinemia

Glomerulonephritis Superior vena cava

obstruction Fontan procedure Urinothorax CSF leak to the

pleural space

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TB bacilli spread to meninges via:

Inhalation to lymphnodes to bloodstrean to meninges

Inhalation to lymphnodes to meninges

Ingestion to peritoneum to CSF Intravenous introduction to

meninges

TB bacilli spread to meninges via:

Inhalation to lymphnodes to bloodstream to meninges

Inhalation to lymphnodes to meninges

Ingestion to peritoneum to CSF Intravenous introduction to

meninges

Manifestations of Postprimary TB are:

Upper lobe distribution Cavity Absence of adenopathy Airway involvement

53 m

37 m

40 m with cough

Cavity vs cyst vs bulla

Cavity: Gas-filled space in an area of lung consolidation or mass or nodule produced by the expulsion of a necrotic part of the lesion via the bronchial tree; wall thickness varies

Cyst: wall thickness is 4 mm or less Bulla: wall thickness < 4 mm Often difficult to distinguish the 3

Clin Microbiol Rev. 2008 April; 21(2): 305–333

Cavity - causes Abscess TB Ischemic necrosis (infarct) PCP Fungal process Malignancy Wegener’s granulomatosis Sarcoidosis – rare COP (Cryptogenic Organizing

Pneumonia -rare

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Cavity

T bacilli grow in cavities which communicate with bronchi and spread infection

MDR bacilli grow in cavities exclusively

Hydrolytic enzymes break down lung

TuberculosisVolume 89, Issue 4 , Pages 243-247, July 2009

54 m

48 m

Cryptococcus

35 f

Aspergillus AML

57 f

Primary lung ca with mets

67 f

43 m

34 m

43 m

Bronchopneumonia

 Invasive bronchiolar aspergillosis in a patient who underwent bone marrow transplantationRadioGraphics, http://pubs.rsna.org/doi/abs/10.1148/rg.253045115Aspergillus

Five causes of tree-in-bud are: Bronchopneumonia Fungal Viral ABPA TB

Tree –in-bud pattern

Rossi, SE et al: May/June 2005 Radiographics 25,3

Cocaine 23 m

25 m

TB in HIV

TB & HIV

Clinical features depend on the severity immunosuppression

Relatively intact cellular immunity = non–HIV-infected individuals- TB remains localized to the lung.

HIV (CD4 T-lymphocyte count: <200/mm3), pulmonary TB with extra-pulmonary involvement: lymphadenitis, miliary

46 m

76 m emphysematous pericarditis, streptococcal

TB - healing

Lung destruction: bronchiectasis Bronchial stenosis

LUL atelectasis, bronchiectasis TB

77 m

Radical mastectomy & rad Rx

80 f

The History of Tuberculosis

• The Hebrew word for phthisis or consumption (schachepheth) means to waste away occurs twice in the Bible:

• Leviticus 26:16• I, in turn, will do this to you: I will appoint over you

a sudden terror, consumption and fever that will waste away the eyes and cause the soul to pine away; also you will sow your seed uselessly, for your enemies will eat it up.

• Deuteronomy 28:22• The Lord will smite you with consumption and with

fever and with inflammation and with fiery heat and with the sword and with blight and with mildew and they will pursue you until you perish.

The History of Tuberculosis

By 1650 consumption was the leading cause of mortality and became a reference in some of Shakespeare's plays- one of the consumptive lovers, in "Much A Do About Nothing" , as well as scrofula in "Macbeth"

The History of Tuberculosis

• Early attempts at treatment can be found throughout history Greeks believed cutting off cool air eventuated in a

burning up of the tissues Romans put importance of diet Hebrews control disease from diet to the destruction of

clothing• Early "cures" from physicians

Warm sea air Milk from pregnant women Seaweed placed under the pillow Cold baths Deep breathing

The History of Tuberculosis

The first breakthrough came when German bacteriologist named Robert Koch isolated the infectious agent known as tuberculosis bacteria or tubercle bacilli in 1882. He was later awarded the Nobel Prize for physiology or medicine in 1905

The History of Tuberculosis The first sanatorium opened in 1854 in Gorbersdorf,

Germany. Sick patients were given wholesome food and plenty of fresh air. This became the modern way to fight the disease. The sanatoriums provided medical care for almost 100 years and became one of the most remarkable and unique periods of medical care in history.

By 1889 in the USA the National Tuberculosis Association fully realized that TB was distinctly preventable and not directly inherited

No real progress was made until new antibiotics were used between 1945-1960

It has taken almost three thousand years to understand the full nature of Tuberculosis

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References Joshua Burrill, Christopher J. Williams, Gillian Bain,

Gabriel Conder, Andrew L. Hine, Rakesh R. Misra RadioGraphics, 2007, Vol.27: 1255-1273, 10.1148/rg.275065176

Santiago Enrique Rossi, Tomas Franquet, Mariano Volpacchio, Ana Giménez, Gabriel Aguilar RadioGraphics, 2005, Vol.25: 789-801

JR Cohen, JK Amorosa, PR Smith –The air-fluid level in cavitary pulmonary TB, Radiology, 1978 - radiology

JK Amorosa, PR Smith, JR Cohen, C Ramsey… - …, Tuberculous mediastinal lymphadenitis in the adult

1978 – radiology Medscape Tuberculosis (TB), a multisystemic

disease ….JK Amorosa….

Famous people who had TB Gaius Valerius Cat

ullus (ca. 84 BC – ca. 54 BC), Roman poet

Bronte sisters Elizabeth Barrett

Browning Albert Camus Anton Chekhov Maxim Gorky Franz Kafka Eugene O'Neill

Eugene O'Neill Molière Robert Louis

Stevenson Dylan Thomas Voltaire Paul Gauguin Amedeo Modigliani Frédéric Chopin Niccolò Paganini Igor Stravinsky Cardinal Richelieu Simón Bolívar

Opera, Theatre, Novels - TB Puccini: La

boheme Verdi: La Traviata Thomas Mann: The

Magic Mountain Victor Hugo: Les

Miserables Upton Sinclair:

The Jungle

Johnny Nolan: A Tree Grows in Brooklyn

W.Somerset Maugham: Sanatorium

Frank McCourt: Angela’s Ashes

END

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am 9-13-11

a.m. 3-19-12

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