EDUCATION EXHIBIT 1255

Tuberculosis:A Radiologic Review1

ONLINE-ONLYCME

See www.rsna.org/education/rg_cme.html.

LEARNINGOBJECTIVESAfter reading thisarticle and takingthe test, the reader

will be able to:

� Identify the clinicaland radiologic find-ings in tuberculosisaffecting the respira-tory, cardiac, centralnervous, musculo-skeletal, gastrointesti-nal, and genitouri-nary systems.

� Describe the differ-ential diagnosis andappropriate imagingwork-up for tubercu-losis in various organsystems.

� Discuss the impor-tance of accurate andtimely diagnosis inguiding proper clini-cal management oftuberculosis in agiven organ system.

Joshua Burrill, FRCR ● Christopher J. Williams, FRCR ● Gillian Bain,FRCR ● Gabriel Conder, FRCR ● Andrew L. Hine, MD ● Rakesh R.Misra, FRCR

Tuberculosis has shown a resurgence in nonendemic populations inrecent years, a phenomenon that has been attributed to factors such asincreased migration and the human immunodeficiency virus epidemic.Although the thorax is most frequently involved, tuberculosis may in-volve any of a number of organ systems (eg, the respiratory, cardiac,central nervous, musculoskeletal, gastrointestinal, and genitourinarysystems), and timely diagnosis of the disease is paramount, since de-layed treatment is associated with severe morbidity. Unfortunately, ahistory of infection with or exposure to tuberculosis may or may not bepresent, and evidence of active tuberculosis is present in less than 50%of cases. A negative tuberculin skin test does not in itself exclude infec-tion. Furthermore, the clinical and radiologic features of tuberculosismay mimic those of many other diseases. Therefore, although in manycases biopsy or culture specimens are required to make the definitivediagnosis, it is imperative that radiologists and clinicians understandthe typical distribution, patterns, and imaging manifestations of tuber-culosis.©RSNA, 2007

Abbreviations: CNS � central nervous system, CSF � cerebrospinal fluid, FDG � fluorodeoxyglucose, MDR � multidrug-resistant

1From the Department of Radiology, Central Middlesex Hospital, London, England (J.B., C.J.W., G.B., G.C., A.L.H.); and the Department of Radi-ology, Wycombe General Hospital, Queen Alexandra Rd, High Wycombe HP11 2TT, England (R.R.M.). Presented as an education exhibit at the2005 RSNA Annual Meeting. Received October 3, 2006; revision requested January 15, 2007 and received March 1; accepted March 6. All authorshave no financial relationships to disclose. Address correspondence to R.R.M. (e-mail: mail@misraonline.co.uk).

©RSNA, 2007

RadioGraphics 2007; 27:1255–1273 ● Published online 10.1148/rg.275065176 ● Content Codes:

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IntroductionThe prevalence of tuberculosis has continued todecline in the United States over the past fewyears. However, the smallest annual decrease inthe past 10 years occurred in 2003, with the re-ported prevalence of tuberculosis actually risingin some states and in certain populations (1).There has also been an increase in global preva-lence, particularly in immunocompromised pa-tients, with a rate of increase of approximately1.1% per year (2). This increase has been seennot only in Africa and Asia, but also in Europe.For example, in the United Kingdom, there hasbeen an increase in the prevalence of tuberculosisover the past 20 years, particularly in Londonand in immigrant populations (3,4). In addi-tion, drug-resistant strains of tuberculosis haveemerged. Early diagnosis promotes effectivetreatment and is, therefore, essential.

Tuberculosis is usually confined clinically tothe respiratory system. However, it can affect anyorgan system, particularly in immunocompro-mised individuals. In this article, we review multi-drug-resistant (MDR) tuberculosis, tuberculosisin immunocompromised patients, appropriatesafety precautions for health care workers who arecaring for tuberculosis patients, and the use ofnuclear imaging in this setting. In addition, wediscuss and illustrate the clinical and radiologicfeatures of tuberculosis involving the lungs, heart,central nervous system (CNS), head and neck,musculoskeletal system, and abdomen.

Multidrug-resistant TuberculosisThe imaging appearances of MDR tuberculosisare the same as those of non-MDR tuberculosis.Moreover, MDR tuberculosis is no more infectivethan normal tuberculosis (5). However, it is amore serious infection, requiring prolonged ad-ministration of more toxic second-line drugs asso-ciated with higher morbidity and mortality rates.Patients also remain infectious for a longer periodonce treatment has been started, with associatedhigher risk to others (5).

Tuberculosis inImmunocompromised Patients

Immunocompromised patients have a signifi-cantly higher prevalence of tuberculosis than doesthe general population (6,7) and are also morelikely to be infected with MDR tuberculosis (8).In addition, the pattern of disease is different inimmunocompromised patients, who have ahigher prevalence of extrapulmonary involve-ment. In one study, 38% of immunocompro-mised patients with tuberculosis had pulmonary

involvement only, 30% had extrapulmonary in-volvement only, and 32% had both pulmonaryand extrapulmonary involvement (9). Even whenthere is pulmonary involvement, a limited im-mune response can give rise to normal chest ra-diographic findings (10). Therefore, in immuno-compromised patients, it is important to be awareof the extrapulmonary features of tuberculosis(discussed later).

Protection of theHealth Care Worker

Tuberculosis is an airborne communicable dis-ease caused by Mycobacterium tuberculosis. Healthcare workers are at a greater risk for infection thanis the general population; therefore, their protec-tion needs to be considered (11).

Patients should be treated as infectious if theyhave or are suspected of having pulmonary tuber-culosis. These patients, particularly those withlung cavitation, aerosolize the organism throughcoughing, expelling 1–5-�m particles that canremain suspended in the air for several hours(12). Coughing hygiene helps reduce patient in-fectivity. Ideally, infectious patients should not beadmitted to the hospital unless it is clinically re-quired, and patients who are admitted should bekept in isolation in a single room (8), ideally withat least two air exchanges per hour (13). The useof negative-pressure rooms is recommended forpatients who either have MDR tuberculosis ormust be in the same ward as immunocompro-mised patients (5,11). Although patients withnonpulmonary tuberculosis are generally treatedas noninfectious and nursed in general wards,procedures that expose tuberculous collections toair (eg, care of skin wounds or the draining of ab-scesses, pleural effusions, or peritoneal effusions)should prompt patient isolation (11,14).

A patient with non-MDR pulmonary tubercu-losis is deemed to be noninfectious and can bemoved to a general ward after 2 weeks of treat-ment if he or she has improved clinical symptomsand three negative sputum samples, ideally col-lected on different days (5,12,15).

Any imaging of an infectious patient shouldideally be carried out within the patient’s isolationroom, and no specific protective measures arerequired for a health care worker carrying out aprocedure that does not involve aerosolizing tu-berculous collections, except when the patient isMDR positive (8). In such a case, or if there is arisk of aerosolizing tuberculous collections, a cer-tified respirator should be worn by the health careworker (5,15). Because tuberculosis is infectiveonly if airborne, the imaging equipment used canbe cleaned with a standard germicide.

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Departmental radiologic imaging should bescheduled for off-peak times, away from immuno-compromised patients; an infectious patientshould be fitted with a surgical mask and imagedin the shortest time possible, preferably in his orher own well-ventilated area, and in the best-ven-tilated room available (15,16). If the patient isMDR positive, it is probably worthwhile to fit himor her with a certified respirator. Negative-pres-sure waiting rooms and imaging rooms are prob-ably not required unless the department is servinga population with a high prevalence of tuberculo-sis (15).

No protection is required for general radiologypersonnel unless they are performing proceduresthat may aerosolize a tuberculous collection, andno protection is needed for subsequent patients(8). However, all health care workers should havetheir tuberculosis status assessed prior to com-mencing employment, be aware of the symptomsof tuberculosis, and be told to seek advice if theyhave any concerns.

When the diagnosis of tuberculosis cannot beestablished with noninvasive techniques in pa-tients who are suspected of having the disease,biopsy tissue or aspirate should be obtained forhistologic analysis and culture (16). Imaging-guided biopsy techniques may be of assistancein this regard, but the radiologist should be in-formed of the possible diagnosis prior to under-taking any procedure. Specimens should beplaced in an appropriate sterile container, eitherwithout preservative or in the correct medium forculture, and taken to the laboratory as quickly aspossible. Formalin should not be used for culturespecimens (5,11,16).

Nuclear ImagingGallium-67 citrate, Indium-111–labeled autolo-gous leukocyte (white blood cell) scintigraphy,and fluorodeoxyglucose (FDG) positron emissiontomography (PET) are useful in the setting ofpyrexia of unknown origin, in which tuberculosisis implicated and no definitive source has beenidentified with other imaging techniques. In onestudy, Ga-67 scintigraphy had a sensitivity of78% in identifying extrapulmonary tuberculosisbut failed to help diagnose any cases of tubercu-lous meningitis (17). When the differential diag-nosis includes skeletal infection, technetium-99mmethylene diphosphonate bone scintigraphy canhelp localize focal sepsis and is about as sensitiveas In-111 white blood cell scintigraphy (18).Ga-67 scintigraphy has a similar sensitivity fordetecting bone lesions but is also capable of help-ing identify paraspinal abscesses and other ex-

traskeletal foci (19). Nuclear imaging techniquesdo not help distinguish between the differentcauses of sepsis, but they do help identify a focusof interest. Further imaging of the area in ques-tion, along with additional tissue sampling, canthen be performed to aid in diagnosis (20).

FDG PET has several advantages over galliumand indium scanning (21): (a) it can be per-formed immediately, with no delay required be-tween injection and scanning; (b) it generally re-sults in a lower radiation dose due to the shorthalf-life of FDG; (c) it demonstrates little normalorgan uptake, except in the brain and heart; and(d) it provides a quantitative measurement of theabsolute fraction of the injected dose reaching atissue (21). Tuberculomas usually show uptake atFDG PET (22). Increased uptake is also seenwith other granulomatous diseases and infectionssuch as sarcoidosis, histoplasmosis, aspergillosis,and coccidioidomycosis. Therefore, in the settingof a known pulmonary lesion, FGD PET cannotbe used to differentiate between neoplastic andnonneoplastic causes (23,24). This limitation isparticularly pertinent in geographic areas wheretuberculosis is endemic because, in approximately2% of cases, malignancy and pulmonary tubercu-lomas may coexist (25). However, one study sug-gests that using carbon-11 choline PET can helpdifferentiate between lung cancer and tuberculo-sis. The standardized uptake value is high in ma-lignant masses and low in tuberculomas withC-11 choline PET but is high in both lesions withFDG PET (26).

Pulmonary TuberculosisHistorically, pulmonary tuberculosis has beendivided into primary and postprimary tuberculo-sis, with primary tuberculosis being considered adisease of childhood and postprimary tuberculosisa disease of adulthood. However, a reduction inthe prevalence of tuberculosis in most Westerncountries (1,2) owing to effective treatment andpublic health measures has resulted in large unex-posed adult populations who are at risk for con-tracting primary tuberculosis. As a result, primarytuberculosis now accounts for 23%–34% of alladult cases of tuberculosis (27).

It can sometimes be difficult to differentiatebetween primary and postprimary tuberculosisboth clinically and radiologically, since their fea-tures can overlap. However, confirming the diag-nosis is more important than identifying the sub-type because it allows initiation of correct clinicalmanagement.

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Primary TuberculosisPrimary tuberculosis is seen in patients not previ-ously exposed to M tuberculosis. It is most com-mon in infants and children and has the highestprevalence in children under 5 years of age. Theprevalence of primary tuberculosis in adults isincreasing for the reasons outlined earlier; how-ever, because primary tuberculosis is perceived tobe a disease of childhood, it is often not suspectedin adults, resulting in misdiagnosis (28). Chestradiography remains the mainstay of diagnosis;however, normal radiographic findings may beseen in up to 15% of patients with proved tuber-culosis (29).

At radiology, primary tuberculosis manifests asfour main entities: parenchymal disease, lymph-adenopathy, miliary disease, and pleural effusion.

Parenchymal Disease.—Typically, parenchy-mal disease manifests as dense, homogeneousparenchymal consolidation in any lobe; however,predominance in the lower and middle lobes issuggestive of the disease, especially in adults. Itsappearance is often indistinguishable from that ofbacterial pneumonia; however, it can be differen-tiated from bacterial pneumonia on the basis ofradiographic evidence of lymphadenopathy andthe lack of response to conventional antibiotics(Fig 1).

In children under 2 years of age, lobar or seg-mental atelectasis is frequently seen, most often

involving the anterior segment of an upper lobe orthe medial segment of the middle lobe.

In approximately two-thirds of cases, the pa-renchymal focus resolves without sequelae at con-ventional radiography; however, this resolutioncan take up to 2 years. In the remaining cases, aradiologic scar persists that can calcify in up to15% of cases, an entity that is known as a Ghonfocus. Other calcified foci can also be seen, andpersistent masslike opacities called tuberculomasare seen in approximately 9% of cases. Tubercu-lomas can cavitate and undergo calcification.

Lymphadenopathy.—Radiographic evidence oflymphadenopathy is seen in up to 96% of chil-dren and 43% of adults. Lymphadenopathy istypically unilateral and right sided, involving thehilum and right paratracheal region (Fig 2), al-though it is bilateral in about one-third of cases.Any nodes greater than 2 cm in diameter gener-ally have a low-attenuation center secondary tonecrosis at CT and are highly suggestive of activedisease (30). Although lymphadenopathy is usu-ally associated with other manifestations of tuber-culosis, it can be the sole radiographic feature, afinding that is more common in infants and de-creases in frequency with age. CT is more sensi-tive than chest radiography for assessing lymph-adenopathy. The combination of calcified hilarnodes and a Ghon focus is called a Ranke com-plex and is suggestive of previous tuberculosis,although it can also result from histoplasmosis.

Figure 1. Parenchymal primary tubercu-losis in an adult. Radiograph of the leftlung demonstrates extensive upper lobeand lingular consolidation.

Figure 2. Lymphadenopathy in a patient with pri-mary tuberculosis. Chest radiograph shows a bulky lefthilum and a right paratracheal mass, findings that areconsistent with lymphadenopathy and are typical inpediatric patients.

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With treatment, there is usually slower resolu-tion of the lymphadenopathy than of the paren-chymal disease, and nodal calcification may de-velop. However, this calcification usually occurs 6months or more after the initial infection.

Miliary Disease.—Clinically significant miliarydisease affects between 1% and 7% of patientswith all forms of tuberculosis. It is usually seen inthe elderly, infants, and immunocompromisedpersons, manifesting within 6 months of initialexposure. Chest radiography is usually normal atthe onset of symptoms, and hyperinflation may bethe earliest feature. The classic radiographic find-ings of evenly distributed diffuse small 2–3-mmnodules, with a slight lower lobe predominance,are seen in 85% of cases (Fig 3). High-resolutionCT is more sensitive than conventional radiogra-phy, with nodules seen in a random distribution.The nodules usually resolve within 2–6 monthswith treatment, without scarring or calcification;however, they may coalescence to form focal ordiffuse consolidation.

Pleural Effusion.—A pleural effusion is seen inapproximately one-fourth of patients with provedprimary tuberculosis (29). The effusion is oftenthe sole manifestation of tuberculosis and usuallymanifests 3–7 months after initial exposure. Pleu-ral effusion is a very uncommon finding in in-fants. The effusion is usually unilateral, and com-plications (eg, empyema formation, fistulization,bone erosion) are rare. Residual pleural thicken-ing and calcification can result. Ultrasonography(US) often demonstrates a complex septated effu-sion.

Postprimary TuberculosisPostprimary tuberculosis remains primarily a dis-ease of adolescence and adulthood. It occurs inpatients previously sensitized to M tuberculosis.The term postprimary tuberculosis is generally usedto refer to both reinfection with and reactivationof tuberculosis. Primary tuberculosis is usuallyself-limiting, whereas postprimary tuberculosis isprogressive, with cavitation as its hallmark, result-ing in hematogenous dissemination of the diseaseas well as disease spread throughout the lungs.Healing usually occurs with fibrosis and calcifica-tion.

The features of primary and postprimary tu-berculosis may overlap; however, the distinguish-ing features of postprimary tuberculosis include apredilection for the upper lobes, the absence oflymphadenopathy, and cavitation.

At radiology, postprimary tuberculosis maymanifest as parenchymal disease, airway involve-ment, and pleural extension.

Parenchymal Disease.—The earliest finding inparenchymal disease is patchy, poorly definedconsolidation, particularly in the apical and poste-rior segments of the upper lobes (28). In the ma-jority of cases, more than one pulmonary segmentis involved, with bilateral disease seen in one-third to two-thirds of cases.

Cavitation, the hallmark of postprimary tuber-culosis, affects about 50% of patients. The cavi-ties typically have thick, irregular walls, whichbecome smooth and thin with successful treat-ment. Cavities are usually multiple and occur

Figure 3. Miliary tuberculosis. (a) Ra-diograph of the left lung shows diffuse2–3-mm nodules, findings that are typi-cally seen in miliary tuberculosis.(b) High-resolution computed tomo-graphic (CT) scan demonstrates similarnodules in a random distribution.

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within areas of consolidation (Figs 4, 5). Resolu-tion can result in emphysematous change or scar-ring. A minority of cavities demonstrate air-fluidlevels; however, these findings can indicate thepresence of superinfection.

If there is airway disease and, in particular,endobronchial spread of infection, tree-in-budopacities may develop. These findings, which areusually visible in the lung periphery and resemblea branching tree with buds at the tips of thebranches, are indicative of active tuberculosis(Fig 6).

Lymphadenopathy and pneumothoraces areseen in only about 5% of patients (27).

Airway Involvement.—Airway involvement ischaracterized by bronchial stenosis, leading tolobar collapse or hyperinflation, obstructive pneu-monia, and mucoid impaction. Bronchial stenosisis seen in 10%–40% of patients with active tuber-culosis (27) and is best demonstrated with CT,which usually shows long segment narrowing withirregular wall thickening, luminal obstruction,and extrinsic compression (30). It also results intree-in-bud opacities and traction bronchiectasis,particularly of the upper lobes.

Pleural Extension.—Pleural effusions occurmost often in primary tuberculosis but are seen inapproximately 18% of patients with postprimarytuberculosis; they are usually small and associated

with parenchymal disease. The effusions are typi-cally septated and can remain stable in size formany years (Fig 7). The pleura may becomethickened, which can result in a tuberculous em-pyema and an associated risk of developing abronchopleural fistula. Residual pleural thicken-ing and calcification may also occur.

Cardiac TuberculosisTuberculosis involving the heart is rare, account-ing for only 0.5% of cases of extrapulmonary tu-berculosis (31). The main presenting finding ispericardial involvement (32), particularly in im-munocompromised patients (33), whereas myo-cardial involvement is seen less often.

The primary sign of tuberculous pericarditisis pericardial thickening of more than 3 mm in

Figure 4. Parenchymal postprimary tuberculosis.Chest radiograph demonstrates the characteristic bilat-eral upper lobe fibrosis associated with postprimarytuberculosis.

Figure 5. Parenchymal postprimary tuberculosis.High-resolution CT scan shows the typical apical cavi-tation of postprimary tuberculosis.

Figure 6. Parenchymal postprimary tuberculosis.High-resolution CT scan demonstrates multiple small,centrilobular nodules connected to linear branchingopacities. This so-called tree-in-bud appearance is typi-cally seen in postprimary tuberculosis.

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adults; this finding is seen in the majority of cases.CT demonstrates a thickened, irregular pericar-dium (Fig 8), frequently with associated mediasti-nal lymphadenopathy. Most patients have disten-tion of the inferior vena cava to a diameter ex-ceeding 3 cm; pleural effusions, typically bilateral;and deformities of the intraventricular septum.Less than 20% of patients have pericardial effu-sions or develop localized pericardial calcification(32).

Myocardial tuberculosis is usually associatedwith other foci of tuberculosis. These foci can bemiliary lesions or tuberculomas. Myocardial tu-berculosis tends to be asymptomatic and discov-ered incidentally at postmortem examination(31).

Tuberculosis Involving the CNSInvolvement of the CNS is seen in approximately5% of patients with tuberculosis (34). However,

its prevalence is greater in immunocompromisedpatients. CNS involvement is seen in up to 15%of cases of acquired immunodeficiency syn-drome–related tuberculosis (34,35).

CNS tuberculosis usually results from hema-togenous spread. However, it may result fromdirect rupture or extension of a subependymal orsubpial focus (Rich focus) and may be located inthe meninges, brain, or spinal cord. CNS tuber-culosis can manifest in a variety of forms, includ-ing tuberculous meningitis, tuberculomas, tuber-culous abscesses, tuberculous cerebritis, and mili-ary tuberculosis.

Tuberculous MeningitisTuberculous meningitis is the most commonmanifestation of CNS tuberculosis across all agegroups (35), and early diagnosis is important toreduce morbidity and mortality. Tuberculousmeningitis is usually due to hematogenous spreadbut can also be secondary to rupture of a Richfocus or direct extension from cerebrospinal fluid(CSF) infection (34–36).

The typical radiographic finding is abnormalmeningeal enhancement, usually most pro-nounced in the basal cisterns (Fig 9), althoughsome degree of involvement of the meninges

Figure 7. Multiseptated tuberculous empyema. USimage shows numerous linear echogenic structures inthe pleural cavity representing multiple septa, findingsthat are typically seen in postprimary tuberculosis.

Figure 8. Tuberculous pericarditis. Contrast mate-rial–enhanced CT scan demonstrates a thickened peri-cardium and bilateral pleural effusions.

Figure 9. Tuberculous meningitis. Axialcontrast-enhanced T1-weighted magneticresonance (MR) image shows florid men-ingeal enhancement that is most pro-nounced within the basal cisterns. (Cour-tesy of Jakrit Shah, FRCR, Nuffield Hospi-tal, Nottingham, England.)

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within the sulci over the cerebral convexities andin the sylvian fissures is also seen in most cases(35,37). These findings are better seen at gadolin-ium-enhanced MR imaging than at CT. Appear-ances usually resolve relatively quickly with ad-equate treatment; however, radiographic resolu-tion is delayed if there are thickened exudates(37). This appearance is nonspecific and has awide differential diagnosis that includes meningi-tis from other infective agents; inflammatory dis-eases such as rheumatoid arthritis and sarcoid-osis; and neoplastic causes, both primary and sec-ondary.

The most common complication of tubercu-lous meningitis is communicating hydrocephalus,which can be seen at both MR imaging and CTand is caused by blockage of the basal cisterns byinflammatory exudates (37). Occasionally, non-communicating hydrocephalus occurs due to themass effect of a tuberculoma causing the obstruc-tion of CSF flow.

Ischemic infarcts are also a common complica-tion, being seen in 20%–40% of patients at CT(Fig 10), mostly within the basal ganglia or inter-nal capsule regions and resulting from vascular

compression and occlusion of small perforatingvessels (34,36,37). Cranial nerve involvementoccurs in 17%–70% of cases (35,37), most com-monly affecting the second, third, fourth, andseventh cranial nerves.

Parenchymal TuberculosisThe most common CNS parenchymal lesion oftuberculosis is tuberculoma (tuberculous granu-loma). This lesion may be solitary, multiple, ormiliary and may be seen anywhere within thebrain parenchyma, although it most commonlyoccurs within the frontal and parietal lobes. Tu-berculomas can exist in conjunction with tuber-culous meningitis, although this combination isnot a consistent finding (35).

At CT, tuberculomas appear as round or lobu-lated masses with low or high attenuation (Fig11). They demonstrate homogeneous or ring en-hancement and have irregular walls of varyingthickness. One-third of patients demonstrate the

Figure 10. Tuberculousmeningitis. Axial MR imagesdemonstrate acute bilateralischemic infarcts, which arehyperintense on the diffusion-weighted image (a) and hy-pointense on the apparent dif-fusion coefficient image (b).(Case courtesy of Jakrit Shah,FRCR, Nuffield Hospital,Nottingham, England.)

Figures 11, 12. Parenchy-mal tuberculosis. (11) Con-trast-enhanced CT scanshows multiple bilateral ring-enhancing lesions (tuberculo-mas) in the frontal and pari-etal lobes. (12) Axial contrast-enhanced T1-weighted MRimage demonstrates multipleenhancing caseating and non-caseating tuberculomas, pre-dominantly within the leftfrontal and parietal lobes.(Figs 11 and 12 courtesy ofJakrit Shah, FRCR, NuffieldHospital, Nottingham, En-gland.)

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“target sign” (ie, central calcification or punctateenhancement with surrounding hypoattenuationand ring enhancement) (35). This finding is sug-gestive of, but not pathognomonic for, tubercu-losis.

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The MR imaging findings depend on whetherthe tuberculoma is caseating, and if so, whetherthe center is liquid or solid. It is thought thatthere is a progression from noncaseating to case-ating and then from a solid to a liquid center (37).A noncaseating tuberculoma is hypointense rela-tive to gray matter on T1-weighted images andhyperintense on T2-weighted images, with homo-geneous gadolinium enhancement (Fig 12)(35,38).

Caseating tuberculomas with a solid center areisointense to hypointense on both T1- and T2-weighted MR images. They usually have a vari-able amount of surrounding edema, which ishyperintense on T2-weighted images (35). Case-ating tuberculomas with a liquid center are hy-pointense on T1-weighted images and centrallyhyperintense on T2-weighted images, with a pe-ripheral hypointense rim on T2-weighted imagesthat represents the capsule. Rim enhancement isusually seen at gadolinium-enhanced MR imag-ing. After treatment, tuberculomas can com-pletely resolve; however, calcification is seen inup to one-fourth of cases and is identified mostclearly at CT (35).

Miliary CNS tuberculosis is usually associatedwith tuberculous meningitis and appears at MRimaging as multiple tiny (�2-mm), hyperintenseT2 foci that homogeneously enhance on contrast-enhanced T1-weighted images (Fig 13) (35).

Tuberculous abscesses are rarely seen and canbe similar in appearance to liquid-centered case-ating tuberculomas, although they tend to belarger and are more often multiloculated (35). AtCT, these abscesses appear as hypoattenuatinglesions with surrounding edema, mass effect, andring enhancement. Tuberculous cerebritis occursvery rarely (34).

Spinal Tuberculous MeningitisThe MR imaging features of spinal tuberculousmeningitis consist of CSF loculation and oblitera-tion of the spinal subarachnoid space, with loss ofoutline of the spinal cord in the cervicothoracicspine and matting of the nerve roots in the lumbarregion (37). Contrast-enhanced imaging revealsnodular, thick, linear intradural enhancement(Fig 14), which can completely fill the subarach-noid space, sometimes giving the appearance of anormal unenhanced MR image (39). Chronicspinal tuberculous meningitis may not enhance.

Syringomyelia can occur as a complication ofarachnoiditis and is seen as spinal cord cavitationthat typically demonstrates CSF signal intensity

Figure 13. Miliary CNS tuberculosis.Axial contrast-enhanced T1-weighted MRimage shows multiple small high-signal-intensity foci within both cerebral hemi-spheres. (Courtesy of Jakrit Shah, FRCR,Nuffield Hospital, Nottingham, England.)

Figure 14. Spinal tuberculous meningi-tis. Sagittal gadolinium-enhanced T1-weighted MR image of the thoracic spinedemonstrates irregular, linear, nodularmeningeal enhancement. (Courtesy ofJakrit Shah, FRCR, Nuffield Hospital,Nottingham, England.)

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on both T1- and T2-weighted images and doesnot enhance after contrast material administra-tion (37).

Head and Neck TuberculosisTuberculosis in the head and neck representsabout 15% of cases of extrapulmonary tuberculo-sis, with about 1.5% of all new cases manifestingin this way.

The most common location is within necknodes, often manifesting as bilateral painless cer-vical lymphadenitis, also known as scrofula (Fig15). The involved nodes are initially homoge-neous but later undergo central necrosis, mani-festing with central low attenuation at CT (Fig16) and with central hypointensity and hyperin-tensity on T1- and T2-weighted MR images, re-spectively. Peripheral rim enhancement is seen atboth modalities. These nodes may be difficult todifferentiate from the necrotic nodes seen inmetastatic head and neck squamous cell carcino-mas. Nodal calcification often develops late intuberculosis, which helps differentiate tubercu-lous nodes from malignancy; however, nodal cal-cification may also be seen in other malignanciessuch as metastatic thyroid cancer.

Extranodal tuberculous disease is rarely seen;the most commonly affected sites include (in de-scending order of frequency of occurrence) thelarynx, temporal bone, and pharynx. The sinona-sal cavity, thyroid gland, and skull base are veryrarely involved.

At radiology, laryngeal tuberculosis manifestsas soft-tissue thickening and infiltration of thepreepiglottic and paraglottic spaces, without thepresence of a focal mass. The laryngeal frame-work usually remains intact. The differential diag-nosis consists mainly of other inflammatory laryn-geal conditions.

The imaging findings at other head and necksites are also rather nonspecific; inflammatorysoft-tissue thickening is usually seen, but in ad-vanced cases, neoplasm-like soft-tissue massesand bone erosions may be encountered.

Musculoskeletal TuberculosisThe musculoskeletal system is involved in only1%–3% of cases of tuberculosis (40). However,the resultant bone and joint destruction is thecause of severe morbidity and in cases of spinalinvolvement can cause severe neurologic se-quelae. The disease affects patients of all ages—although it is rare in the 1st year of life—and mostfrequently affects the spinal column, pelvis, hip,and knee (41).

Diagnosis is often difficult, with an averagedelay of 16–19 months between the onset ofsymptoms and reported diagnosis (42). A historyof infection with or exposure to tuberculosis maybe present, and evidence of concurrent active in-trathoracic tuberculosis is present in less than50% of cases (40,43,44). In addition, although apositive tuberculin skin test helps support the di-agnosis, a negative result should not be consid-ered as evidence excluding it. Indeed, in one se-ries, a false-negative rate of 14% was reported(45). Only histologic analysis and tissue culture

Figures 15, 16. Tuberculous cervical lymphadenitis. (15) US image demonstrates eccentric necrosis ina tuberculous cervical node. (16) Contrast-enhanced CT scan demonstrates multiple enhancing nodeswith central hypoattenuation representing central necrosis.

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can help confirm the diagnosis, although thiscombination is not particularly sensitive. There-fore, although there are no pathognomonic radio-logic features of musculoskeletal tuberculosis,knowledge of the features discussed in the follow-ing sections may help reduce the time to diagnosisand, hence, the associated morbidity.

Tuberculous SpondylitisApproximately 50% of skeletal tuberculosis in-volves the spine (40,46). The lower thoracic andupper lumbar levels are most commonly affected(46–48).

The disease process is thought to result fromhematogenous spread via the venous plexus ofBatson. Infection usually begins in the anteriorpart of the vertebral body adjacent to the endplate. Subsequent demineralization of the endplate results in loss of definition of its dense mar-gins on conventional radiographs. These endplate changes allow the spread of infection to theadjacent intervertebral disk. The loose internalstructure of the disk allows the infection to dis-seminate more widely into additional spinal seg-ments, resulting in the classic pattern of involve-ment of more than one vertebral body togetherwith the intervening disks. It also allows spreadinto the paraspinal tissues, resulting in the forma-

tion of a paravertebral abscess known as a Pottabscess (Fig 17). In the lumbar spine, a psoas ab-scess may extend into the groin and thigh andmay simply manifest as lateral bowing of thepsoas shadow on conventional radiographs. Anabscess that lies more anteriorly may result in an-terior scalloping of the vertebral bodies similar tothat seen with lymphoma or abdominal aorticaneurysm. Calcification within the abscess is vir-tually diagnostic for tuberculosis (41). If left un-treated, the infection eventually results in verte-bral collapse and anterior wedging, leading to ky-phosis and gibbus formation (Fig 18). Withhealing, ankylosis of the vertebral bodies occurs,with obliteration of the intervening disk space.

However, if there is anterior subligamentousinvolvement of the spine, infection can extendboth superiorly and inferiorly, with sparing of theintervertebral disks. The involvement of a singlevertebral body with sparing of the adjacent diskshas also been described (42,48–50). Whateverthe nature of the spread of infection, tuberculosisis characteristically associated with little or noreactive sclerosis or local periosteal reaction, afeature that helps distinguish it from pyogenicinfections of the spine.

Figures 17, 18. (17) Pott abscess in a patient with tuberculous spondylitis. Radiograph of the thoracic spine dem-onstrates vertebra plana of D11 with an associated soft-tissue-density mass, the latter finding being consistent with atuberculous (Pott) abscess. (18) Gibbus deformity secondary to tuberculous spondylitis. Sagittal T1-weighted (a)and T2-weighted (b) MR images show vertebral collapse with high signal intensity in the adjacent vertebral bodies.The vertebral collapse has resulted in a gibbus deformity and spinal cord compression.

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MR imaging is the preferred imaging modalityin the diagnosis and assessment of tuberculousspondylitis because of its sensitivity to soft-tissueabnormalities (Fig 19) and multiplanar capability(51,52). Scintigraphy adds very little information,with a 35% false-negative rate reported for iso-tope bone scans in patients with radiographic andclinical evidence of active disease (48). Reportedfalse-negative rates with gallium are as high as70% (45).

The differential diagnosis for tuberculousspondylitis includes metastatic disease, low-gradepyogenic infection (eg, brucellosis), fungal infec-tion, and sarcoidosis, all of which have similarimaging characteristics. In the early stage of infec-tion, imaging appearances are entirely nonspe-cific. However, there are some clinical and radio-logic features (discussed later) that may help dif-ferentiate among these conditions.

Tuberculosis rarely affects the posterior verte-bral elements (including the pedicles), in contrastto metastatic disease (41,48). However, the ante-rior scalloping seen with subligamentous spreadof infection can also be seen with paravertebrallymphadenopathy, secondary to metastases orlymphoma. In differentiating tuberculosis frompyogenic infection, the clinical picture is as im-portant as the radiologic features, with insidiousonset of symptoms, a normal erythrocyte sedi-mentation rate, relevant respiratory symptoms,and slow disease progression favoring the diagno-sis of tuberculosis. Radiologic features that favorthe diagnosis include involvement of one or moresegments; a delay in destruction of the interverte-bral disks; a large, calcified paravertebral mass;

and the absence of sclerosis. Sarcoidosis can pro-duce multifocal lesions of vertebrae and disks,along with paraspinal masses that appear identicalto tuberculosis.

Tuberculous OsteomyelitisIsolated tuberculous osteomyelitis in the absenceof associated tuberculous arthritis is relativelyrare. When it does occur, however, the femur,tibia, and small bones of the hands and feet aremost commonly affected (40,41). Typically, themetaphyses are involved, with radiographic fea-tures that include osteopenia and poorly definedlytic lesions with minimal surrounding sclerosis.In the immature skeleton, the spread of infectionacross the epiphyseal plate is a feature that helpsdistinguish tuberculosis from pyogenic infection.

Cystic tuberculosis is an unusual pattern ofosteomyelitis that occurs more commonly in chil-dren than in adults. It is characterized by multiplesmall, well-defined oval lytic lesions of variablesize that usually lack sclerotic margins. In chil-dren, the metaphyses of the long bones tend to beaffected, whereas in adults, the axial skeleton(skull, shoulder, pelvis) is involved.

Tuberculous dactylitis, the painless involve-ment of the short tubular bones of the hands andfeet, is also more common in children. At radiog-raphy, pronounced fusiform soft-tissue swellingwith or without periostitis is the most commonfinding (Figs 20, 21). Periostitis indicates involve-ment of the underlying bone. Other changessometimes seen in the underlying bone includecoarsening of the trabecular pattern and acro-osteolysis with reactive sclerosis and joint involve-ment. Chronic untreated infection may lead tothe formation of sinus tracts. The differential di-agnosis for tuberculous dactylitis includes pyo-

Figure 19. Calcified psoas abscess in a patient with tuberculous spondylitis. (a) Radiograph shows a partially calci-fied right paravertebral soft-tissue mass, with expansion and bowing of the right psoas shadow and displacement ofthe right kidney. (b) CT scan shows vertebral destruction and a calcified right psoas abscess. (c) Axial T2-weightedMR image demonstrates the calcified abscess with low signal intensity, along with associated vertebral destruction.

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genic or fungal infections, leukemia, sarcoidosis,hemoglobinopathies, hyperparathyroidism, andsyphilis. Distinguishing tuberculous dactylitisfrom pyogenic osteomyelitis can be particularlydifficult.

Tuberculous ArthritisTuberculous arthritis is characteristically a mono-arthritis affecting large weight-bearing joints (53).The imaging findings are similar to those of otherinfectious and inflammatory arthritides and are,therefore, nonspecific. These findings includeosteopenia, synovitis and other soft-tissue swell-ings, marginal erosions, and varying degrees ofcartilage destruction. Joint space narrowing oc-curs with highly variable rapidity but is usuallydelayed. As with any chronic infection, synovial

involvement in the young results in hyperemiaand epiphyseal overgrowth, most commonly inthe knee (54). With progression of infection, bonesequestration and sinus formation can develop.The end result is usually fibrous ankylosis of thejoint (Fig 22). Bone ankylosis occasionally occursbut is more commonly seen with pyogenic infec-tions.

Again, the differential diagnosis includes pyo-genic and fungal infections. Factors favoring adiagnosis of tuberculosis include insidious onset,minimal sclerosis (Figs 23, 24), the relative ab-sence of periosteal reaction and bone prolifera-tion, and relative preservation of joint space in theearly stages (41).

Figures 20, 21. Tuberculous dac-tylitis. (20) Radiograph of the righthand shows fusiform soft-tissueswelling around the first metacarpalbone, along with associated periosti-tis. (21) Radiograph of the left handshows cystic expansion of the proxi-mal phalanx of the index finger, afinding that is called spina ventosa.

Figures 22–24. (22) Ankylosis secondary to tuberculous arthritis. Radiograph of the knee shows loss of joint spacesecondary to cartilage destruction, resulting in ankylosis. (23) Tuberculous arthritis. Radiograph demonstrates onlyminimal sclerosis and new bone formation in the right hip, considering the degree of bone destruction that is seen.(24) Chronic tuberculous arthritis. Radiograph demonstrates complete joint destruction in the right hip, along withassociated soft-tissue swelling and calcification.

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Although MR imaging is more sensitive thanconventional radiography in assessing the extentof bone and joint involvement, the findings areagain nonspecific, particularly in early disease.This fact reinforces the importance of joint aspi-ration for microscopic analysis and culture.

Abdominal TuberculosisThe abdomen is the most common focus of ex-trapulmonary tuberculosis, with the solid viscerabeing affected more often than the gastrointesti-nal tract (55). CT is the mainstay for investigatingpossible abdominal tuberculosis; however, knowl-edge of other imaging modalities, such as bariumenema examination, is important to avoid misdi-agnosis in cases in which tuberculosis is not ini-tially suspected.

LymphadenopathyAbdominal lymphadenopathy is the most com-mon manifestation of abdominal tuberculosis,being seen in 55%–66% of patients (56). Thecharacteristic pattern is mesenteric and peripan-creatic lymph node group enlargement, with mul-tiple groups affected simultaneously. The major-ity (40%–60%) of patients with lymphadenitishave enlarged nodes with hypoattenuating centersand hyperattenuating enhancing rims at CT (Fig25), findings that are characteristic of, but notpathognomonic for, caseous necrosis (56,57).These lymph node masses do not tend to causebiliary, gastrointestinal, or genitourinary obstruc-

tion, the presence of which would suggest an al-ternative diagnosis.

Other nodal patterns include conglomeratemixed-attenuation masses, enlarged homoge-neous-attenuation nodes, and an increased num-ber (more than three) of normal or mildly en-larged homogeneous nodes.

Tuberculous PeritonitisPeritonitis is the most common clinical manifesta-tion of abdominal tuberculosis, affecting one-third of all patients (58). Peritonitis is thought tooriginate primarily from hematogenous spread;however, it may be secondary to a rupturedlymph node or gastrointestinal deposit or to fallo-pian tube involvement. The condition is subdi-vided into three main types—wet, fibrotic, and

Figure 25. Lymphadenopathy from abdominal tu-berculosis in a 71-year-old man. CT scan shows atuberculous lymph node with the characteristic low-attenuation center and peripheral rim enhancement(arrowheads). These findings represent the only abnor-mality that was seen in this case.

Figure 26. Wet type tuberculous peritonitis. Con-trast-enhanced CT scan shows ascites (arrows) that ishyperattenuating relative to urine within the bladder(arrowheads).

Figure 27. Fibrotic type tuberculous peritonitis. CTscan obtained with oral and intravenous contrast mate-rial shows omental caking (arrowheads) with thicken-ing of the underlying small bowel (*).

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dry—although there is considerable overlap intheir CT appearances (56).

Wet Type Peritonitis.—Wet type peritonitis isthe most common type of peritonitis (90% ofcases) and features large amounts of free or locu-lated ascites, which, at CT, is usually slightly hy-perattenuating (20–45 HU) relative to water dueto its high protein and cellular content (Fig 26).

Fibrotic Type Peritonitis.—Fibrotic type peri-tonitis accounts for 60% of cases of peritonitisand is characterized by large omental and mesen-teric cakelike masses with matting of bowel loops.At CT, it manifests as mottled low-attenuationmasses with nodular soft-tissue thickening (Fig27). Omental thickening and caking can also beseen at US.

Dry Type Peritonitis.—Dry type peritonitis isseen in 10% of cases and is characterized by mes-enteric thickening, fibrous adhesions, and caseousnodules. Its imaging manifestations are highlysuggestive of, but not specific for, tuberculosis.

Varying degrees of omental and mesentericinvolvement are seen, and the omentum appearssmudged, caked, or thickened with equal fre-quency. Mesenteric involvement ranges from mildto extensive. Peritoneal thickening with associ-ated enhancement occurs; nodular implants withirregular thickening are uncommon and are moresuggestive of peritoneal carcinomatosis (59).

The CT findings in tuberculous peritonitis arenonspecific, with disseminated peritoneal malig-nancy, nontuberculous peritonitis, and mesothe-lioma being noteworthy alternatives in the differ-ential diagnosis.

Gastrointestinal TuberculosisGastrointestinal tuberculosis is rare; whenpresent, however, it almost always involves theileocecal region (90% of cases), usually both theterminal ileum and the cecum (56). The mostcommon CT finding is mural thickening, which istypically concentric but if eccentric tends to in-volve the medial cecal wall (60). Localizedlymphadenopathy is usually seen (59).

Skip areas of concentric mural thickening withassociated luminal narrowing with or withoutproximal dilatation can occur elsewhere in thesmall bowel, findings that strongly suggest tuber-culosis in the presence of ileocecal involvement.

On barium studies, the earliest manifestation isspasm and hypermobility with edema of the valve.Thickening of an incompetent ileocecal valve hasbeen described as being characteristic of tubercu-losis (Fig 28). Shallow ulceration with elevatedmargins is seen at double-contrast enema exami-nation. Advanced gastrointestinal tuberculosischaracteristically appears as napkin ring stenoses,with a conical, shrunken cecum retracted out ofthe right iliac fossa by mesocolon retraction (56).

Involvement of the esophagus, stomach, andproximal small bowel is rare. Esophageal tubercu-losis is usually due to extrinsic compression at thelevel of the carina from lymphadenopathy, al-though it can progress (56). Gastric tuberculosisusually affects the antrum and distal body andcan simulate peptic ulcer disease; however, a si-nus or fistula suggests tuberculosis. Proximalsmall bowel disease manifests as nonspecific mu-cosal fold thickening (Fig 29).

Figure 28. Ileocecal tuberculosis. Image from adouble-contrast barium enema examination showsmarked retraction of the ileocecal area, along with anincompetent ileocecal valve.

Figure 29. Small bowel tuberculosis. Contrast-en-hanced CT scan shows wall thickening in several distalsmall bowel loops (arrowheads).

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Hepatosplenic TuberculosisHepatosplenic involvement is common in patientswith disseminated disease and is either micro-nodular-miliary or macronodular (56).

Miliary hepatic involvement is seen in patientswith miliary pulmonary tuberculosis and is char-acterized by innumerable 0.5–2.0-mm nodules,which may not be detected at CT (Fig 30). Theliver appears hyperechoic at US.

Macronodular hepatic tuberculosis is uncom-mon, and lesions are hypoattenuating at CT withirregular ill-defined margins and minimal centralbut definite peripheral contrast enhancement. AtMR imaging, these lesions are hypointense withT1-weighted sequences and hyperintense with

T2-weighted sequences. These imaging appear-ances are nonspecific and are similar to those ofmultiple metastases and abscesses. However, he-patic tuberculomas eventually tend to calcify, andthe presence of calcified granulomas at CT in pa-tients with known risk factors and in the absenceof a known primary tumor should raise suspicionfor tuberculosis (Fig 31) (59).

Adrenal TuberculosisIn one autopsy study, the adrenal glands were thefifth most common site of extrapulmonary tuber-culosis after the liver, spleen, kidneys, and bones(55). Adrenal tuberculosis is seen in up to 6% ofpatients with active tuberculosis. These patients

Figure 30. Miliary hepatic tuberculosis. CT scanshows multiple hypoattenuating lesions within the liver,findings that are consistent with miliary tuberculosis.

Figure 31. Hepatosplenic tuberculosis. CT scanshows multiple calcified granulomas within the liver,spleen, and periportal and peripancreatic lymph nodes.The right kidney is hydronephrotic, and a small calcu-lus is seen within the collecting system.

Figure 32. Adrenal tuberculosis. CT scan demon-strates bilateral adrenal enlargement (arrows).

Figure 33. Renal tuberculosis. Intravenousurogram shows the characteristic appearance ofcaliceal erosions in the lower pole calices of theleft kidney due to tuberculosis.

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almost always present with bilateral adrenal in-volvement and an Addisonian type clinical picture(Fig 32).

The CT signs of active tuberculous adrenalitisare bilateral enlarged glands associated with large,hypoattenuating necrotic areas, with or withoutdotlike calcification (61).

Genitourinary TuberculosisGenitourinary tuberculosis is the most commonclinical manifestation of extrapulmonary tubercu-losis (62). Infection is spread either hematog-enously to organs such as the prostate gland,seminal vesicles, and kidneys, or by direct exten-sion (eg, to the bladder or epididymis).

Renal Tuberculosis.—Approximately 75% ofrenal tuberculous involvement is unilateral, themost common CT finding being renal calcifica-tion (50% of cases) (60). At intravenous urogra-phy, the earliest abnormality is a “moth-eaten”calix due to erosions (Fig 33), which progresses topapillary necrosis. Hydronephrosis tends to haveirregular margins and filling defects owing to ca-seous debris. Renal parenchymal cavitation maybe detected as irregular pools of contrast material.Dilated calices (hydrocalicosis) with related in-fundibular stricture at one or more sites withinthe collecting system may be seen. Characteristiccalcifications in a lobar distribution are often seenin end-stage tuberculosis (tuberculous autone-phrectomy).

Ureteric Tuberculosis.—Ureteric tuberculosisis characterized by a thickened ureteric wall andstrictures, which occur in almost one-half of allcases of renal tuberculosis. Involvement is mostcommon in the distal third of the ureter (60).Strictures have a predilection for points of

normal anatomic narrowing: at the pelviuretericjunction, across the pelvic brim, and at the vesi-coureteric junction. Complications include hy-dronephrosis and hydroureter of varying degrees,usually due to obstruction at the vesicouretericjunction but possibly due to reflux (56).

Bladder Tuberculosis.—Bladder tuberculosiscommonly manifests as reduced bladder volumewith wall thickening, ulceration, and filling de-fects due to granulomatous material. In advanceddisease, there is eventual scarring with long-termloss of cystic volume and a small, irregular, calci-fied bladder. Tuberculosis is a rare cause of a ure-thral stricture.

Genital Tuberculosis.—Genital tuberculosisalmost always involves the fallopian tubes inwomen (94% of cases), usually causing bilateralsalpingitis (63). Findings at hysterosalpingogra-phy are always abnormal, with obstruction andmultiple constrictions of the fallopian tubes andendometrial adhesions or deformity of the cavity.

Male involvement is confined to the seminalvesicles or prostate gland, with occasional cal-cification (10% of cases) (Fig 34). Contrast-enhanced CT shows hypoattenuating prostaticlesions, which likely represent foci of caseousnecrosis and inflammation. Nontuberculous pyo-genic prostatic abscesses have a similar CT ap-pearance. Spread is hematogenous and self-limiting.

The testes and epididymides are rarely in-volved. US shows focal or diffuse areas of de-creased echogenicity; however, these findings arevery nonspecific (Fig 35).

Figures 34, 35. (34) Prostatic tuberculosis. Contrast-enhanced CT scan shows a well-defined hypoat-tenuating lesion within the prostate gland (arrowhead). (35) Scrotal tuberculosis. US image of a testisshows a nonspecific focal area of hypoechogenicity, which proved to represent caseous necrosis second-ary to tuberculosis.

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ConclusionsThe clinical and radiologic features of tuberculo-sis may mimic those of many other diseases. Ahigh degree of suspicion is required, especially inhigh-risk populations. Although in many casesbiopsy or culture specimens are still needed toyield the definitive diagnosis, it is important forradiologists and clinicians alike to understand thespectrum of imaging features of tuberculosis toaid in making an early diagnosis.

References1. Schneider E, Moore M, Castro KG. Epidemiology

of tuberculosis in the United States. Clin ChestMed 2005;26(2):183–195.

2. Maher D, Raviglione M. Global epidemiology oftuberculosis. Clin Chest Med 2005;26(2):167–182.

3. Rose AM, Gatto AJ, Watson JM. Recent increasesin tuberculosis notifications in England and Wales:real or artefact? J Public Health Med 2002;24(2):136–137.

4. Rose AM, Watson JM, Graham C, et al. Tubercu-losis at the end of the 20th century in England andWales: results of a national survey in 1998. Thorax2001;56(3):173–179.

5. National Collaborating Centre for Chronic Condi-tions. Tuberculosis: clinical diagnosis and man-agement of tuberculosis, and measures for its pre-vention and control. London, United Kingdom:Royal College of Physicians, 2006.

6. Munoz P, Palomo J, Munoz R, Rodriguez-Creixems M, Pelaez T, Bouza E. Tuberculosisin heart transplant recipients. Clin Infect Dis1995;21(2):398–402.

7. Nunn P, Williams B, Floyd K, Dye C, Elzinga G,Raviglione M. Tuberculosis control in the era ofHIV. Nat Rev Immunol 2005;5(10):819–826.

8. Djuretic T, Herbert J, Drobniewski F, et al. Anti-biotic resistant tuberculosis in the United King-dom: 1993–1999. Thorax 2002;57(6):477–482.

9. Small PM, Schecter GF, Goodman PC, SandeMA, Chaisson RE, Hopewell PC. Treatment oftuberculosis in patients with advanced human im-munodeficiency virus infection. N Engl J Med1991;324(5):289–294.

10. Palmieri F, Girardi E, Pellicelli AM, et al. Pulmo-nary tuberculosis in HIV-infected patients pre-senting with normal chest radiograph and negativesputum smear. Infection 2002;30(2):68–74.

11. Joint Tuberculosis Committee of the British Tho-racic Society. Control and prevention of tubercu-losis in the United Kingdom: code of practice2000. Thorax 2000;55(11):887–901.

12. Teo DT, Lim TW. Transmission of tuberculosisfrom patient to healthcare workers in the anaesthe-sia context. Ann Acad Med Singapore 2004;33(1):95–99.

13. Menzies D, Fanning A, Yuan L, FitzGerald JM.Hospital ventilation and risk for tuberculous infec-tion in Canadian health care workers. Ann InternMed 2000;133(10):779–789.

14. Frampton MW. An outbreak of tuberculosisamong hospital personnel caring for a patient witha skin ulcer. Ann Intern Med 1992;117(4):312–313.

15. Jensen PA, Lambert LA, Iademarco MF, RidzonR. Guidelines for preventing the transmission ofMycobacterium tuberculosis in health-care set-tings, 2005. MMWR Recomm Rep 2005;54(17):1–141.

16. Granich R, Binkin NJ, Jarvis WR, et al. Guide-lines for the prevention of tuberculosis in healthcare facilities in resource-limited settings. Ge-neva, Switzerland: World Health Organization,1999.

17. Lin WY, Hsieh JF. Gallium-67 citrate scan in ex-trapulmonary tuberculosis. Nuklearmedizin 1999;38(6):199–202.

18. Lisbona R, Derbekyan V, Novales-Diaz J, VekslerA. Gallium-67 scintigraphy in tuberculous andnontuberculous infectious spondylitis. J Nucl Med1993;34(5):853–859.

19. Lin WY, Wang SJ, Cheng KY, Shen YY, ChanglaiSP. Diagnostic value of bone and Ga-67 imagingin skeletal tuberculosis. Clin Nucl Med 1998;23(11):743–746.

20. Kukrej N, Cook GJ, Pattison JM. Positron-emis-sion tomography used to diagnose tuberculosis ina renal transplant patient. Am J Transplant 2002;2(1):105–107.

21. Sugawara Y, Braun DK, Kison PV, Russo JE,Zasadny KR, Wahl RL. Rapid detection of hu-man infections with fluorine-18 fluorodeoxyglu-cose and positron emission tomography: prelim-inary results. Eur J Nucl Med 1998;25(9):1238–1243.

22. Goo JM, Im JG, Do KH, et al. Pulmonary tuber-culoma evaluated by means of FDG PET: findingsin 10 cases. Radiology 2000;216(1):117–121.

23. Pitman AG, Hicks RJ, Binns DS, et al. Perfor-mance of sodium iodide based 18F-fluorodeoxy-glucose positron emission tomography in the char-acterization of indeterminate pulmonary nodulesor masses. Br J Radiol 2002;75(890):114–121.

24. Kostakoglu L, Agress H Jr, Goldsmith SJ. Clinicalrole of FDG PET in evaluation of cancer patients.RadioGraphics 2003;23(2):315–340.

25. Ho CL. Clinical PET imaging: an Asian perspec-tive. Ann Acad Med Singapore 2004;33(2):155–165.

26. Hara T, Kosaka N, Suzuki T, Kudo K, Niino H.Uptake rates of 18F-fluorodeoxyglucose and 11C-choline in lung cancer and pulmonary tuberculo-sis: a positron emission tomography study. Chest2003;124(3):893–901.

27. McAdams HP, Erasmus J, Winter JA. Radiologi-cal manifestations of pulmonary tuberculosis. Ra-diol Clin North Am 1995;33(4):655–678.

28. Andreu J, Caceres J, Pallisa E, Martinez-Rod-riguez M. Radiological manifestations of pulmo-

1272 September-October 2007 RG f Volume 27 ● Number 5

nary tuberculosis. Eur J Radiol 2004;51(2):139–149.

29. Woodring JH, Vandiviere HM, Fried AM, DillonML, Williams TD, Melvin IG. Update: the radio-graphic features of pulmonary tuberculosis. AJRAm J Roentgenol 1986;146(3):497–506.

30. Curvo-Semedo L, Teixeira L, Caseiro-Alves F.Tuberculosis of the chest. Eur J Radiol 2005;55(2):158–172.

31. Rodriguez E, Soler R, Juffe A, Salgado L. CT andMR findings in a calcified myocardial tuberculomaof the left ventricle. J Comput Assist Tomogr2001;25(4):577–579.

32. Suchet IB, Horwitz TA. CT in tuberculous con-strictive pericarditis. J Comput Assist Tomogr1992;16(3):391–400.

33. Cherian G. Diagnosis of tuberculous aetiology inpericardial effusions. Postgrad Med J 2004;80(943):262–266.

34. Whiteman ML. Neuroimaging of central ner-vous system tuberculosis in HIV-infected pa-tients. Neuroimaging Clin N Am 1997;7(2):199–214.

35. Morgado C, Ruivo N. Imaging meningo-ence-phalic tuberculosis. Eur J Radiol 2005;55(2):188–192.

36. de Castro CC, de Barros NG, Campos ZM, CerriGG. CT scans of cranial tuberculosis. Radiol ClinNorth Am 1995;33(4):753–769.

37. Jinkins JR, Gupta R, Chang KH, Rodriguez-Car-bajal J. MR imaging of central nervous system tu-berculosis. Radiol Clin North Am 1995;33(4):771–786.

38. Gee GT, Bazan C 3rd, Jinkins JR. Miliary tuber-culosis involving the brain: MR findings. AJRAm J Roentgenol 1992;159(5):1075–1076.

39. Sharma A, Goyal M, Mishra NK, Gupta V,Gaikwad SB. MR imaging of tubercular spinalarachnoiditis. AJR Am J Roentgenol 1997;168(3):807–812.

40. Davidson PT, Horowitz I. Skeletal tuberculosis: areview with patient presentations and discussion.Am J Med 1970;48(1):77–84.

41. Resnick D. Tuberculous infection. In: Resnick D,ed. Diagnosis of bone and joint disorders. 3rd ed.London, United Kingdom: Saunders, 2002;2524–2545.

42. Lolge S, Maheshwari M, Shah J, Patkar D,Chawla A. Isolated solitary vertebral body tuber-culosis: study of seven cases. Clin Radiol 2003;58(7):545–550.

43. Newton P, Sharp J, Barnes KL. Bone and jointtuberculosis in Greater Manchester 1969–79. AnnRheum Dis 1982;41(1):1–6.

44. Omari B, Robertson JM, Nelson RJ, Chiu LC.Pott’s disease: a resurgent challenge to the tho-racic surgeon. Chest 1989;95(1):145–150.

45. Lifeso RM, Weaver P, Harder EH. Tuberculousspondylitis in adults. J Bone Joint Surg Am 1985;67(9):1405–1413.

46. Martini M, Ouahes M. Bone and joint tuberculo-sis: a review of 652 cases. Orthopedics 1988;11(6):861–866.

47. Jain R, Sawhney S, Berry M. Computed tomogra-phy of vertebral tuberculosis: patterns of bone de-struction. Clin Radiol 1993;47(3):196–199.

48. Weaver P, Lifeso R. The radiological diagnosis oftuberculosis of the adult spine. Skeletal Radiol1984;12(3):178–186.

49. Chapman M, Murray RO, Stoker DJ. Tuberculo-sis of the bones and joints. Semin Roentgenol1979;14(4):266–282.

50. Naim-ur-Rahman. Atypical forms of spinal tuber-culosis. J Bone Joint Surg Br 1980;62-B(2):162–165.

51. Hoffman EB, Crosier JH, Cremin BJ. Imaging inchildren with spinal tuberculosis: a comparison ofradiography, computed tomography and magneticresonance imaging. J Bone Joint Surg Br 1993;75(2):233–239.

52. Modic MT, Feiglin DH, Piraino DW, et al. Verte-bral osteomyelitis: assessment using MR. Radiol-ogy 1985;157(1):157–166.

53. Berney S, Goldstein M, Bishko F. Clinical anddiagnostic features of tuberculous arthritis. Am JMed 1972;53(1):36–42.

54. Haygood TM, Williamson SL. Radiographic find-ings of extremity tuberculosis in childhood: backto the future? RadioGraphics 1994;14(3):561–570.

55. Lam KY, Lo CY. A critical examination of adrenaltuberculosis and a 28-year autopsy experience ofactive tuberculosis. Clin Endocrinol (Oxf) 2001;54(5):633–639.

56. Leder RA, Low VH. Tuberculosis of the abdo-men. Radiol Clin North Am 1995;33:691–705.

57. Denton T, Hossain J. A radiological study of ab-dominal tuberculosis in a Saudi population, withspecial reference to ultrasound and computed to-mography. Clin Radiol 1993;47(6):409–414.

58. Zissin R, Gayer G, Kots E, Werner M, Shapiro-Feinberg M, Hertz M. Iliopsoas abscess: a reportof 24 patients diagnosed by CT. Abdom Imaging2001;26(5):533–539.

59. Suri S, Gupta S, Suri R. Computed tomographyin abdominal tuberculosis. Br J Radiol 1999;72(853):92–98.

60. Zissin R, Gayer G, Chowers M, Shapiro-FeinbergM, Kots E, Hertz M. Computerized tomographyfindings of abdominal tuberculosis: report of 19cases. Isr Med Assoc J 2001;3(6):414–418. [Pub-lished correction appears in Isr Med Assoc J 2001;3(7):552.]

61. Wang YX, Chen CR, He GX, Tang AR. CT find-ings of adrenal glands in patients with tuberculousAddison’s disease. J Belge Radiol 1998;81(5):226–228.

62. Engin G, Acunas B, Acunas G, Tunaci M. Imag-ing of extrapulmonary tuberculosis. RadioGraph-ics 2000;20(2):471–488.

63. Wang LJ, Wong YC, Chen CJ, Lim KE. CT fea-tures of genitourinary tuberculosis. J Comput As-sist Tomogr 1997;21(2):254–258.

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RG Volume 27 • Volume 5 • September-October 2007 Burrill et al

Tuberculosis: A Radiologic Review Joshua Burrill, FRCR, et al

Page 1258 Typically, parenchymal disease manifests as dense, homogeneous parenchymal consolidation in any lobe; however, predominance in the lower and middle lobes is suggestive of the disease, especially in adults. Page 1259 The earliest finding in parenchymal disease is patchy, poorly defined consolidation, particularly in the apical and posterior segments of the upper lobes (28). In the majority of cases, more than one pulmonary segment is involved, with bilateral disease seen in one-third to two-thirds of cases. Page 1262 At CT, tuberculomas appear as round or lobulated masses with low or high attenuation (Fig 11). They demonstrate homogeneous or ring enhancement and have irregular walls of varying thickness. One-third of patients demonstrate the "target sign" (ie, central calcification or punctate enhancement with surrounding hypoattenuation and ring enhancement) (35). This finding is suggestive of, but not pathognomonic for, tuberculosis. Page 1266 Tuberculosis rarely affects the posterior vertebral elements (including the pedicles), in contrast to metastatic disease (41,48). However, the anterior scalloping seen with subligamentous spread of infection can also be seen with paravertebral lymphadenopathy, secondary to metastases or lymphoma. In differentiating tuberculosis from pyogenic infection, the clinical picture is as important as the radiologic features. Page 1269 Gastrointestinal tuberculosis is rare; when present, however, it almost always involves the ileocecal region (90% of cases), usually both the terminal ileum and the cecum (56). The most common CT finding is mural thickening, which is typically concentric but if eccentric tends to involve the medial cecal wall (60).

RadioGraphics 2007; 27:1255–1273 ● Published online 10.1148/rg.275065176 ● Content Codes: