TB from Head to Toes

transcript

Presented by

*The increasing prevalence of

tuberculosis in both immunocompetent

and immunocompromised individuals

in recent years makes this disease a

topic of universal concern.

Introduction

*Because tuberculosis demonstrates

a variety of clinical and radiologic

findings and has a known propensity

for dissemination from its primary

site, it can mimic numerous other

disease entities..

Introduction

*The World Health Organization (WHO) estimates that each year more than 8 million new cases of tuberculosis occur and approximately 3 million persons die from the disease.

*Ninety-five percent of tuberculosis cases occur in developing countries.

*It is estimated that between 19 and 43% of the world's population is infected with Mycobacterium tuberculosis, the bacterium that causes tuberculosis infection and disease

Epidemiology

Most cases in the US are due to reactivation,

especially amongst immigrants

Highest risk of progression to active TB is within 2 years of seroconversion

Increase in incidence in late 1980s-early 90s

largely due to HIV

Needs to be reported to the health department

Microbiology

Aerobic

Bacillus (rod-shaped)

Non-spore forming

Non-motile

Cell wall – mycolic acid – retains acid fast

Growth - doubling time of 15-20 hrs.

3-8 weeks for growth on solid media

TB Skin Testing

PPD – purified protein derivative of tuberculin (antigenic)

Delayed type hypersensitivity reaction

PPD may not become “positive” until 3 months after exposure

Boosting effect

Skin Test Interpretation

PPD >/= 5 mm: – HIV patients

– Recent contacts of someone with TB

– Fibrotic changes on CXR c/w prior TB

– Organ transplant recipients

– Immunosuppressed (includes patients receiving the equivalent of 15 mg/day or more of prednisone for one month or more)

PPD >/= 10 mm: – Recent immigrants (< 5 years) from high

prevalence areas (Eastern Europe, Latin America, Asia, Africa)

– IV drug users

– Residents and employees of high risk facilities (hospitals, nursing homes, homeless shelters, prisons)

– Children < 4 years of age

– Mycobacteriology lab personnel

PPD >/= 10 mm:

– People with medical conditions that place

them at high risk for active TB

Chronic renal failure

Diabetes mellitus

Silicosis

Leukemias/lymphomas

Carcinoma of the head/neck or lung

Weight loss > 10% of ideal body weight

Gastrectomy/jejunoileal bypass

PPD >/= 15 mm:

– Low risk people

– Routine tuberculin testing not

recommended for low risk populations

Skin Test Intrepretation

False positives: – Non-tuberculous mycobacterial infection

– BCG vaccination

False negatives: – HIV

– Malnutrition

– Steroid therapy

– Recent infection

Bacille Calmette-Guerin vaccination: Live attenuated mycobacterial strain derived

from M. bovis

Can yield false positives to PPD – less likely

as time from vaccination increases

Reactions > 20 mm likely are true

CDC advises that the PPD be interpreted by the same guidelines (ignore the BCG history)

Quantiferon Testing

Whole blood in vitro test: – Lymphocytes release IFN gamma in

presence of 2 TB antigens

Will be positive in latent or active TB

Advantages: – No error in interpretation

– No follow-up in 48-72 hours

– No boosting

– Not affected by BCG

Quantiferon Testing

Disadvantages: – Must be processed within 12 hours of

collection

– False + with atypical mycobacteria

– Too many indeterminate results with current version (Q-Gold)

– May be less reliable in pregnant women, children, and immunocompromised

– Does not distinguish between active and latent TB

Causative organism; Mycobacterium tuberculosis COMPLEX

Stained with:

-Modified gram stain: gram positive.

-Carbolfuchsin stain: *Cold method(Kynon)

*Hot(Zeil-Neelson)

- Fluorescent dyes: rhodamine and

auramine stains.

Bacteriology

QUANTITATION SCALE FOR ACID-FAST BACILLUS

SMEARS ACCORDING TO STAIN USED

Carbolfuchsin (× 1,000) Fluorochrome

(× 250) Quantity Reported

No AFB/300 fields No AFB/30 fields No AFB seen

1-2 AFB/300 fields 1-2 AFB/30 fields Doubtful, repeat

1-9 AFB/100 fields 1-9 AFB/10 fields Rare (1+)

1-9 AFB/10 fields 1-9 AFB/field Few (2+)

1-9 AFB/field 10-90 AFB/field Moderate (3+)

> 9 AFB/field > 90 AFB/field Numerous (4+)

Zeil-Neelson Staining

Wire 0.01 ml of specimen 200mm2 slide

Oil immersion field 0.02mm

Slide=10000 field=0.01ml specimen

10,000 organism/slide=1 AFB/field=1000,000 organism/ml

1000 organism/slide=1 AFB/10 field=100,000 organism/ml

100 organism/slide=1 AFB/100field=10,000 organism/ml

QUANTITATION SCALE FOR ACID-FAST BACILLUS

SMEARS ACCORDING TO STAIN USED

Carbolfuchsin (× 1,000) Fluorochrome

(× 250) Quantity Reported

No AFB/300 fields No AFB/30 fields No AFB seen

1-2 AFB/300 fields 1-2 AFB/30 fields Doubtful, repeat

1-9 AFB/100 fields 1-9 AFB/10 fields Rare (1+)

1-9 AFB/10 fields 1-9 AFB/field Few (2+)

1-9 AFB/field 10-90 AFB/field Moderate (3+)

> 9 AFB/field > 90 AFB/field Numerous (4+)

Cultures:

- Lowenstein Jensen media: 6-8

weeks.

-Bactec media: 2-8days. Radiolabelled 14c

labelled palmitic acid

-Mycobacterial growth indicator tube: Middbrook broth+o2 sensitive fluroscent sensor to

indicate growth& bacilli can be identified by Gen

Probe method at the same day of detection.

Diagnosis of Active TB

Acid fast stain of sputum

Sputum AFB culture (culture needed for drug susceptibility)

Radiographic imaging (CXR, CT)

PCR/NAT

Fluid Aspiration

Tissue biopsy – higher yield than fluid

Transmission

Transmitted by airborne particles 1-5 microns in size

Ease of transmission depends on duration and proximity of contact as well as the number of bacteria excreted

Infection can result from only 1-5 bacteria entering a terminal alveolus

Only those with active pulmonary TB are infectious

*M tuberculosis is transmitted via airborne

droplet nuclei that are produced when

persons with pulmonary or laryngeal TB

cough, sneeze, speak, or sing .

* Droplet nuclei may be produced by aerosol

treatments, sputum induction,aerosolization

during bronchoscopy, and through

manipulation of lesions or processing of

tissue or secretions in the hospital or

laboratory.

Pathogenesis

– Inhalation -> phagocytosis by alveolar macrophages

– Bacterial multiplication occurs intracellularly

– Lymphatic spread to regional lymph nodes or

hematogenous dissemination

– Immune response results in granuloma formation (containment of infection)

– Cell death in the granuloma results in caseous

necrosis

– Bacteria can remain dormant in the granuloma

Pathogenesis

– Medical conditions that increase risk for

active TB:

Chronic renal failure

Diabetes mellitus

Silicosis

Leukemias/lymphomas

Carcinoma of the head/neck or lung

Weight loss > 10% of ideal body weight

Gastrectomy/jejunoileal bypass

Primary pulmonary tuberculosis

*The first infection with tubercle bacillus.

Includes the involvement of the draining

lymph nodes in addition to the initial

lesion(Ghon).

Clinical features:

Majority: symptomless.(specially in

young adults)

Brief febrile illness.

Loss of appetite.

Failure to gain weight in children.

Cough is not unusual and may mimic

paroxysm of whooping cough.

Physical signs:

•May be normal,

•Crepitation may be heard.

•Primary lesion could be

heard.

•Segmental or lobar collapse

may occur.

Radiological features: •Lymphadenoathy: hilar lymph nodes

are most commonly involved rarely

paratracheal.Calciflcation of the nodes

may occur.

• Pulmonary componant: ( mainly in

adults) segmental or lobar

consolidation or obstructive

emphysema.

•Resolution of radiological shadow 6m-

Diagnosis: *Vague ill health with history of contact.

* X-ray.

*Tuberclin test: is usually strongly

positive.

*Sputum and gastric lavage for direct

smear and culture helpful in 20-25% of

cases.

* DNA amplification: PCR.

Primary pulmonary tuberculosis

Primary pulmonary TB typically

manifests radiologically as parenchymal

disease, lymphadenopathy, pleural

effusion, miliary disease, or lobar or

segmental atelectasis.

Consolidation in primary tuberculosis. Frontal chest radiograph

demonstrates consolidation in the right middle lobe (straight

arrow) with right hilar adenopathy (curved arrow).

Tuberculomas in primary

tuberculosis. Frontal X-ray

of the right lung

demonstrates well-defined

nodules(arrows), findings

that are consistent with

tuberculomas.

Pulmonary parenchymal changes and lymphadenopathy in primary

tuberculosis. Axial contrast material–enhanced computed

tomographic (CT) scan demonstrates a parenchymal lung cavity in

the lingula (solid white arrow) with enlarged necrotic subcarinal

lymph nodes (black arrows). There is accompanying collapse of

the left lower lobe (open arrow).

Mediastinal TB adenopathy.Axial contrast-enhanced CT

scan demonstrates multiple enlarged mediastinal lymph

nodes with centralareas of low attenuation and peripheral

enhancement (arrows).

Pleural effusion. Axial contrast-enhanced CT scan

demonstrates a large, right-sided pleural collection.The

enhancing parietal pleura is uniformly thickened (arrows).

Miliary tuberculosis. Frontal radiograph shows

fine, discrete nodular areas of increased opacity

bilaterally.

Miliary tuberculosis. High-resolution CT scan obtained with

lung windowing demonstrates numerous fine, discrete nodules

bilaterally in a random distribution

Post primary pulmonary tuberculosis

The most important type of tuberculosis

because it is the most frequent and

smear positive sputum is the main

source of infection responsible for the

persistence of the disease in the

community.

Source;

1. Direct progression of the primary

lesion.

2. Reactivation of the quiescent primary

or post primary.

3. Exogenous infection.

Predisposing factors for reactivation:

1. Malnutrition.

2. Poor housing and overcrowding.

3. Steroid and other immunosuppressive

drugs.

4. Alcoholism.

5.Other diseases: HIV malignancy,

lymphomas , Leukaemia,Diabetes.

Clinical features:

Mainly in middle aged and elderly.

A-Symptoms: 1. May be no symptoms, or just mild debility.

Gradual onset of symptoms over weeks or months.

2. General malaise.

3. Loss of appetite, loss of weight.

4. Febrile course.

5. Night sweating.

6. Cough with or without sputum.

7. Sputum could be mucoid, purulent or blood stained.

8. Could be presented with frank haemoptysis.

9. Tuberculous pneunonia.

B-Signs: 1. May be no signs.

2. Pallor, cachexia.

3. Fever.

4. Post tussive crepitations on the apices.

5. Signs of Consolidation.

6. Signs of fibrosis.

7. Signs of cavitary lesion.

8. Localised wheezes in endobronchial

tuberculosis

Postprimary Tuberculosis

Postprimary disease results from reactivation of a

previously dormant primary infection in 90% of cases;

in a minority of cases, it represents continuation of the

primary disease . Postprimary tuberculosis is almost

exclusively a disease of adolescence and adulthood.

Cavitary postprimary tuberculosis. (Frontal radiograph

demonstrates a thick-walled cavity with smooth inner

margins in the left upper lobe (arrow).

Axial contrast-enhanced CT scan obtained with mediastinal

windowing demonstrates an enlarged mediastinal lymph node

with a central area of low attenuation (arrow).

Axial CT scan obtained with lung windowing demonstrates ill-

defined cavities (black arrows) accompanied by endobronchial

spread in the right upper lobe (white arrow).

Fibroproliferative disease. Axial CT scan

demonstrates bilateral diffuse, coarse, linear, and nodular

areas of increased attenuation with cavitation (arrows).

Lung destruction in postprimary tuberculosis. Axial CT scan

demonstrates a fibrotic, shrunken left lung with

compensatory overexpansion of the right lung extending

across the midline. Bronchiectatic changes are

noted bilaterally (arrows).

Bronchiectasis in postprimary tuberculosis. Axial CT scan

demonstrates bronchiectasis in the left lung (arrows) with areas of

emphysema.

Fibroproliferative disease. Frontal chest radiograph shows

clumped nodular and linear areas of increased opacity in both

upper lobes and in the right middle lobe (white arrows). There

is accompanying volume loss in the right upper lobe as well as

overlying apical pleural thickening (black arrow).

Cavitary tuberculosis associated with aspergilloma. Frontal radiograph shows a

cavity in the left upper lobe (black arrow) with a dependent area of soft-tissue

opacity (solid white arrow). The crescentic area of hyperlucency (open arrow)

represents residual air in the cavity and is referred to as the air crescent sign.

Axial CT scan shows dependent soft-tissue aspergilloma (black arrow) within

the cavity (solid white arrow), along with the air crescent sign (open arrow).

Endobronchial spread of tuberculosis.

Axial CT scan shows severe changes of bronchiolar dilatation

and impaction. Bronchiolar wall thickening (straight arrows) and

mucoid impaction of contiguous branching bronchioles produce a tree-

in-bud appearance (curved arrows).

Tuberculous broncholithiasis. Chest radiograph demonstrates partial atelectasis

of the right upper lobe (straight arrow) with calcified hilar lymph nodes

bilaterally (curved arrows). Axial CT scan demonstrates erosion of the right

main bronchus (straight solid arrow) by a calcified hilar lymph node (curved

arrow). A calcified precarinal lymph node is also noted (open arrow). The

differential diagnosis for mediastinal lymph node calcification includes

histoplasmosis, silicosis, and treated lymphoma.

Tuberculous bronchostenosis.

Axial CT scan demonstrates

narrowing of the right main

bronchus (arrow).

Tuberculous involvement of

the left sternoclavicular

joint. Oblique radiograph

demonstrates irregularity

of the medial end of the left

clavicle (black arrow)

with an associated soft-tissue

mass (white arrow).

Plombage in a patient with postprimary tuberculosis. Frontal chest

radiograph demonstrates typical right-sided Lucite ball plombage.

There is thinning and disorganization of the overlying ribs (straight

arrow). Air-fluid levels in the Lucite balls (curved arrows) suggest

bronchopleural fistulas.

Radiology: 1. Bilateral upper zone fibrotic shadows: with

shift of trachea, mediastinum, distortion of

fissures and diaphragm, and elevation of the

pulmonary hila.

2. Soft confluent shadows of exudative lesion

(D.D pneumonia)

3 Calcification.

4. Cavitation.

5. Tuberculoma.

6. Hilar and paratracheal lymph node

enlargement may be present.

Radiological classification: 1.Minimal: slight or moderate opacity. No

cavity. Extent not more than space

above 2nd costocondral junction.

2. Moderately advanced: In one or both

lungs. slight or moderate opacity, extent

equivalent to volume of one lung. Dense

confluent shadow equivalent to one third

the volume of one lung. Diameter of

cavities not more than 4 cm.

3. Far advanced:

Any lesion>the moderately advanced.

Diasnosis: 1) Clinical

2) Plain X-ray.

3) Sputum Examination: direct smear and culture (very

important).

4) Other samples: Gastric aspirate, laryngeal swab, fiberoptic

specimens (wash,brush,biopsy),transtracheal spirate.

5 Polymerase chain reaction.)

6) Tuberclin test: mainly strongly positive

7) Others

White blood cells if normal favour the diagnosis

ESR may be elevated.

Normocytic normochromic anaemia.

CT may be useful in detecting small cavities,

or calcification.

Miliary Tuberculosis

Produced by acute dissemination of tubercle

bacilli via the blood stream.The term miliary

derives from the radiological picture of

diffuse, discrete nodular shadows about the

size of millet seed (2mm).

A- Classical form: Clinical features: Most common in infants and young children with acute

or subacute febrile illness.

In adults: the onset is insidious, gradual vague ill health.

Malaise, Cough (usually dry), dyspnea. Night sweat is

less common.

Headache suggest associated tuberculous meningitis

Chest examination is free, crepitations may be found.

Hepatomegaly, splenomegaly, lymphadenopathy,

neck rigidity may be found in rare cases.

Diasnosis: 1) Clinical.

2) Xray.

3) Choroidal tubercles in fundus examination

4) Tuberclin test not conclusive

5) Direct smear and culture of sputum if

present.

6) Other samples as transtracheal aspirate,

fiberoptic specimens may be obtained.

7) If failed to prove therapeutic trial for 2

Cardiac Tuberculosis

Although tuberculosis rarely involves the heart

pericardial involvement may occasionally be

seen with mediastinal and pulmonary

tuberculosis and is a cause of calcific

pericarditis (

Tuberculoma of the right atrium in a patient with miliary tuberculosis. Axial T2-weighted

magnetic resonance (MR) image demonstrates a hyperintense mass in the right atrium (straight

arrow). Note also the right pleural effusion (curved arrow). The mass proved to be a

tuberculoma at surgery. Tuberculous pericarditis in a patient with pleuropulmonary

tuberculosis. Axial CT scan demonstrates pericardial thickening (straight solid arrow).

Pulmonary tuberculomas (curved arrows) and a right pleural effusion (open arrow) are also

Skeletal Tuberculosis

Tuberculous Spondylitis (Pott Disease)

The spine is the most frequent site of osseous

involvement in tuberculosis , with the upper lumbar

and lower thoracic spine being involved most

frequently. More than one vertebra is typically

affected, and the vertebral body is more commonly

involved than the posterior elements. An anterior

predilection is seen in the vertebral body

Tuberculous spondylitis. Lateral radiograph demonstrates obliteration of the disk

space (straight arrow) with destruction of the adjacent end plates (curved arrow)

and anterior wedging. Subligamentous spread of spinal tuberculosis. Lateral

radiograph demonstrates erosion of the anterior margin of the vertebral body

(arrow) caused by an adjacent soft-tissue abscess.

Tuberculous spondylitis. Axial CT scan demonstrates lytic

destruction of the vertebral body (black arrow) with an

adjoining soft-tissue abscess (white arrow).

Iliopsoas abscess. Axial CT scan demonstrates

large, multiloculated iliopsoas abscesses

bilaterally (arrowheads). Note also the presacral

abscess (solid arrow) accompanied by erosion of

the anterior sacrum (open arrow).

Calcified psoas abscess. Axial CT scan

demonstrates bilateral tuberculous psoas

abscesses with peripheral calcification (arrows).

Extraspinal Tuberculous

Osteomyelitis

Tuberculous osteomyelitis is usually hematogenous

in origin and is most commonly seen in bones of

the extremities, including the smallbones of the

hands and feet. In long, tubular bones, tuberculosis

often involves the epiphyses.In children,

metaphyseal foci can involve the growth plate. This

feature differentiates tuberculosis from pyogenic

infection

Tuberculous osteomyelitis involving the skull. Axial contrast-

enhanced CT scan demonstrates a bilobed, peripherally

enhancing cold abscess centered along the right frontal bone

(arrow, arrowhead). Note the significant edema and the mass

effect on the underlying brain parenchyma. Axial CT scan

obtained with bone windowing demonstrates an ill-defined

lytic area of bone destruction (arrow).

Tuberculous spondylitis. Sagittal T2-weighted MR

image demonstrates areas of increased signal

intensity due to edema in vertebral bodies.

Accompanying disk narrowing (white arrow) and

extension of the disease into the spinal canal (black

arrow) are also seen.

Tuberculous osteomyelitis. Anteroposterior radiograph

demonstrates a lytic area of bone destruction (arrow) with

transphyseal spread of infection across the growth plate.

Tuberculous arthritis of the knee joint. Frontal radiograph

demonstrates periarticular osteopenia (black arrow), peripheral

osseous erosions (white arrow), and relative preservation of the

joint space. Tuberculous arthritis of the knee joint. Sagittal

gadolinium-enhanced T1-weighted MR image demonstrates

peripheral enhancement around the low-signal-intensity joint

collection (straight arrow). Note the presence of marginal joint

erosions (curved arrow).

Gastrointestinal Tuberculosis

Although abdominal tuberculosis is usually

secondary to pulmonary tuberculosis,

radiologic evaluation often shows no evidence

of lung disease

Ileocecum and Colon The ileocecal region is the most common area of

involvement in the gastrointestinal tract due to

the abundance of lymphoid tissue. The natural

course of gastrointestinal tuberculosis may be

ulcerative, hypertrophic, or ulcerohypertrophic

Ileocecal tuberculosis.

Radiograph obtained

with peroral

pneumocolon technique

demonstrates a conical

and shrunken cecum

(straight arrow)

retracted out of the iliac

fossa by contraction of

the mesocolon. Note also

the narrowing of the

terminal ileum (curved

arrow).

Ileocecal tuberculosis. Axial CT scan demonstrates concentric cecal

wall thickening (arrow). Axial CT scan obtained caudad to a

demonstrates diffuse thickening of the terminal ileum (arrow).

Ileocecal tuberculosis and peritoneal tuberculosis (wet type). Axial

CT scan demonstrates concentric thickening of the cecum (straight

solid arrow). Small bowel dilatation (curved arrow), ascites in the

greater peritoneal space, and thickening of the peritoneum

(open arrow) are also seen.

Peritoneum Peritoneal involvement in tuberculosis is rare and is

usually associated with widespread abdominal

disease involving lymph nodes or bowel .Three

principal types of tuberculous peritoneal

involvement are recognized. The wet type is the

most common and is associated with large amounts

of viscous ascitic fluid that may be either diffusely

distributed or loculated .The fluid demonstrates high

attenuation at CT due to its high protein and cellular

content .The dry or plastic type is uncommon and is

characterized by caseous nodules, fibrous peritoneal

reaction, and dense adhesions

The fibrotic fixed type (consists of large omental

masses, matted loops of bowel and mesentery,and,

on occasion, loculated ascites .CT may also

demonstrate tethering of bowel loops. Infiltration

of the mesentery, when associated with a large

amount of ascites, may have a stellate appearance

at CT.

Peritoneal tuberculosis (dry type). Axial CT scan

demonstrates thickening and infiltration of the

peritoneum (white arrows) along with thickening

of bowel loops. Note the small amount of loculated

fluid (black arrow).

Peritoneal tuberculosis (fibrotic type). Axial contrast-enhanced

CT scan demonstrates enhancing thickened peritoneum

(straight arrow) with an adjoining matted loop of small bowel

(curved arrow).

Abdominal tuberculous lymphadenitis. Axial contrast-enhanced CT scan demonstrates multiple

enlarged mesenteric lymph nodes with central areas

of low attenuation (arrow).

Hepatic tuberculosis.

Axial contrast-enhanced

CT scan demonstrates multiple nonuniform,

low-attenuation lesions within the liver (straight arrows).

An enlarged gastrohepatic lymph node is also

seen (curved arrow).

Tuberculous

pyonephrosis.

Retrograde pyelogram

shows filling of the dilated

hydronephrotic lower and

middle pole of the right

kidney. The collecting

system has irregular

margins (straight solid

arrow) and shows

irregular filling defects

(curved arrow) from

necrosis of the

parenchyma. Upper pole

calcification is also seen

(open arrow).

Renal tuberculosis. Chest radiograph that includes

the upper abdomen

demonstrates lobar

calcification in the right kidney

(black arrow). Note also the

bilateral fibrocalcific changes

in the upper lobes (white

arrows).

Renal tuberculosis Axial contrast-enhanced

CT scan demonstrates left tuberculous pyonephrosis

(straight solid arrow) with extension of the inflammatory

process into the perinephric space (curved arrow)

and accompanying peritoneal disease (open arrow).

Adrenal tuberculosis. Axial contrast-enhanced

CT scan demonstrates bilateral adrenal masses

with central low-attenuation areas (arrows).

Bladder tuberculosis.

Axial contrast-enhanced CT scan demonstrates a thickened and

deformed bladder with an enhancing wall (straight arrow). There is

extension of the inflammatory process to the anterior abdominal wall

(curved arrow). Intravenous urogram demonstrates a thickened,

contracted, low-capacity bladder (thimble bladder) (arrowhead) with

minimal dilatation of both ureters.

Endometrial tuberculosis.

Hysterosalpingogram demonstrates an obliterated

and deformed endometrial cavity (arrow)

due to tuberculous endometritis.

Cranial tuberculous meningitis. Axial gadolinium-enhanced T1-weighted MR image demonstrates leptomeningeal

enhancement along the left sylvian fissure (straight arrow). There is an

accompanying ring-enhancing granuloma in the left parieto-occipital region

(curved arrow).

Cranial tuberculomas Axial contrastenhanced CT scan demonstrates multiple

ring-enhancing lesions (straight arrows) along with

diffuse meningeal enhancement (curved arrow).

Solid caseating tuberculous granulomas involving the

cerebellum. Axial T2-weighted MR image demonstrates

multiple granulomas with central areas of hypointensity in

the cerebellum (arrows). Tuberculous granulomas involving

the cerebellum. Axial T1-weighted MR image demonstrates

isointense lesions with mildly hyperintense rims in the

cerebellum (arrows).

Bilateral tuberculous mastoiditis.

Highresolution CT scan of the temporal bone demonstrates

bilateral destructive lesions in the mastoid processes (straight

arrows). There is an accompanying cold abscess overlying

the right temporo-occipital region (curved arrow).

Orbital tuberculosis.

Axial contrast-enhanced CT scan demonstrates

an enhancing retinal lesion in the left orbit

(arrow).

Conclusions Tuberculosis can affect virtually any organ system in the

body and can be devastating if left untreated. The

increasing prevalence of this disease in both

immunocompetent and immunocompromised individuals

makes tuberculosis a topic of universal concern.

Tuberculosis has a variety of radiologic appearances and

can mimic numerous other disease entities. A high degree

of clinical suspicion and familiarity with the various

radiologic manifestations of tuberculosis allow early

diagnosis and timely initiation of appropriate therapy,

thereby reducing patient morbidity.

TB from Head to Toes

Health & Medicine