Tuberculous meningoencephalitis (TBM) is a rare and serious, often fatal presentation of active tuberculosis and
account for about 1% of cases. Early diagnosis and prompt treatment of TBM is essential to reduce morbidity and mortality.
Here, we report a case of TBM in 60-year-old man. TBM was considered on the basis of clinical presentation, laboratory
findings (hyponatraemia), cerebrospinal fluid studies, radiological findings (hydrocephalus on multi-slice computed
tomography), and history of orchiepididymitis of unknown origin one year earlier, together with information that
the patient originated from Kosovo where incidence of tuberculosis is still high. Mycobacterium tuberculosis was cultured
from cerebrospinal fluid on Lowenstein-Jensen medium confirming diagnosis of TBM. Subsequently, acid-fast bacilli
(AFB) staining on samples obtained after orchiectomy a year ago was performed, revealing AFB. Anti-tuberculosis
therapy is still in course. This is the second case of tuberculous meningoencephalitis with the same disease pattern (i.e.
tuberculous orchiepididymitis – meningoencephalitis) in our Department, and this fact was crucial for the presumptive
diagnosis and urgent treatment of TBM. The former case was described five years ago

Lari Gorup

Nada Brnčić

English

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Coll. Antropol. 35 (2011) Suppl. 2: 285–287Case reportTuberculous Orchiepididymitis,Meningoencephalitis and HydrocephalusNada Brn~i} and Lari GorupInfectious Diseases Department, Rijeka University Hospital Centre, Rijeka, CroatiaA B S T R A C TTuberculous meningoencephalitis (TBM) is a rare and serious, often fatal presentation of active tuberculosis andaccount for about 1% of cases. Early diagnosis and prompt treatment of TBM is essential to reduce morbidity and mor-tality. Here, we report a case of TBM in 60-year-old man. TBM was considered on the basis of clinical presentation, labo-ratory findings (hyponatraemia), cerebrospinal fluid studies, radiological findings (hydrocephalus on multi-slice com-puted tomography), and history of orchiepididymitis of unknown origin one year earlier, together with information thatthe patient originated from Kosovo where incidence of tuberculosis is still high. Mycobacterium tuberculosis was cul-tured from cerebrospinal fluid on Lowenstein-Jensen medium confirming diagnosis of TBM. Subsequently, acid-fast ba-cilli (AFB) staining on samples obtained after orchiectomy a year ago was performed, revealing AFB. Anti-tuberculosistherapy is still in course. This is the second case of tuberculous meningoencephalitis with the same disease pattern (i.e.tuberculous orchiepididymitis – meningoencephalitis) in our Department, and this fact was crucial for the presumptivediagnosis and urgent treatment of TBM. The former case was described five years ago.Key words: tuberculousis, orchiepididymitis, meningoencephalitis, hydrocephalusIntroductionCentral nervous system (CNS) disease caused by My-cobacterium tuberculosis is an uncommon yet higly dev-astating manifestation of tuberculosis. CNS tuberculosis(TB) account for approximately 1% of all cases of tuber-culosis, carries a high motality and a distressing lavel ofneurological morbidity1. Early diagnosis of CNS TB isnecessary for appropiate tretment to reduce this morbid-ity and mortality2. Mycobacterium tuberculosis infectionis prevalent in more than 2 billion people worldwide,with about 15 million of these individuals with activeinfection3,4. Tuberculosis remains a worldwide burden,with a large majority of new active tuberculosis cases oc-curring in underdeveloped and developing countries4. In80% of new tuberculosis cases, demographic factor suchas poverty, crowding, malnutrition, and a compromisedimmune system play a major role in the worldwide epi-demic, while the remaining 20% of tuberculosis cases areassociated with HIV in Sub-Saharan Africa5,6.Here we report a case of CNS TB in an immunocom-promised male.Case ReportA 60-year male, originated from Kosovo, with dilata-tive cardiomiopathia and chronic liver disease, was ad-mitted to the Nephrology unit with a slight fever, cephalea,malaise and signs of chronic renal failure. In anamnesticdata, the patient mentioned orchiepidydimitis of un-known origin one year back when underwent right sideorchiectomy. Laboratory on admission: CRP 83.5 mg/L,ESR 112 mm/h, RBCs 3.02 ´ 1012/L, Hb 86 g/L, WBCs 6.2´ 109/L, platelets 279 ´ 109/L, urea 8.2 mmol/L, creatinine191 mmol/L, Na 127 mmol/L, bilirubine 10 mmol/L, AST37 IU/L, ALT 45 IU/L, AP 191 IU/L, GGT 274 IU/L. Achest radiogram showed some degree of miopatic and en-larged cardiac configuration but without pathologicalinflammation. During eight hospital days, the patientbecame confused, lethargic with sphincter dysfunction.Multi-slice computed tomography (MSCT) of the brainshowed normotensive hydrocephalus (Figure 1). Physicalexamination revealed a stiff neck and urgent lumbalpuncture was performed. Cerebrospinal fluid (CSF) re-vealed: L 59´106/L (neutrophils 87, lymphocytes 7, mo-nocytes 4 and basophiles 2%), glucose level 1.6 mmol/L, a285Received for publication May 30, 2011total proteini 0.56 g/L, lactate 3.47 mmol/L, chloride 102mmol/L.On the basis of clinical presentation, epidemiologicaldata, past medical history of orchiepididymitis, CSF find-ings, hyponatraemia and hydrocephalus, the diagnosis oftuberculous meningoencephalitis was considered. Prompttreatment with four first-line anti-tuberculosis drugswas initiated. Mycobacterium tuberculosis was culturedfrom cerebrospinal fluid on Lowenstein-Jensen mediumconfirming diagnosis of TB CNS. Subsequently, acid-fastbacilli (AFB) staining on samples obtained after orchiec-tomy a year ago was performed, revealing AFB. Clinicalcourse thereafter showed gradual but constant improve-ment in clinical, laboratory and CSF parameters. Anti--tuberculosis therapy is still in course.DiscussionCentral nervous system disease caused by Mycobacte-rium tuberculosis is an uncommon manifestation of tu-berculosis, which was universally fatal in the era beforeanti-tuberculosis therapy. Due to its relative rarity andthe protean nature of the symptoms, tuberculosis of theCNS remains a formidable diagnostic challenge7. In thelargest prospective epidemiological study on CNS tuber-culosis, the chance of developing CNS tuberculosis was1.0% among 82.764 tuberculosis cases from 1970 to 2001in a Canadian cohort8. In Kosovo, the incidence of TBwas decreased but is still high9,10. Both children andHIV-coinfected patients are at high risk for developingCNS tuberculosis11,12. Other risk factors include malnu-trition and recent measles in children, alcoholism, malig-nancies, and use of immunosuppressive agents in adults13–15.TB meningitis is the most common cause of chronic men-ingitis, with clinical presentation often consisting of asubacute febrile illness with generalized neurologicalsyndrome. CNS TBC has the highest mortality rate (20%to 50%) among all forms of TB, and it is associated withmore serious complications and sequelae.The pathogenesis involves establishment of tubercu-lous foci in the brain or meninges, usually from primaryinfection or reactivation infection. The foci progress andrupture into the subarachnoid space, thus seeding infec-tion into the central nervous system17. The haemato-genous seeding of M. tuberculosis occurs most frequentlyin regions of the body that are highly oxygenated, includ-ing the brain18.Clinical signs of patients presenting with TB meningi-tis can be easily assessed for severity based on modifica-tions of the Medical Research Council staging systemwhich has been shown in numerous series to have con-siderable prognostic value19. The classical staging systemis as follows: stage I is fully conscious and no focal deficit;stage II is conscious but with inattention, confusion,lethargy, and focal neurological signs such as cranialnerve palsies; and stage III is stuporous or comatose,multiple cranial nerve palsies, or complete hemiparesisor paralysis. A more contemporary modification of thestaging system defines grade I as alert and oriented with-out focal neurological deficits, grade II as a Glasgowcoma score of 11 to 14 or 15 with focal neurological defi-cits, and grade III as a Glasgow coma score of 10 or lesswith or without focal neurological deficits20,21.Consequence of TB meningitis are hydrocephalus anddevelopment of vasculitis in the vessels of the circle ofWillis, the vertebrobasilar system, and the perforationbranches of the middle cerebral artery, resulting in in-farctions2,7. Common findings on imaging are abnormalmeningeal enhancement in the basal cisterns, hydro-cephalus, and vascular complications2. Hydrocephalusmay occur in the early or latent stage of the disease evenafter commencement of anti-TB drugs, and its manage-ment may influence prognosis. Hydrocephalus encoun-tered in TB meningitis can be broadly divided into twotypes: communicating type, which is common, secondaryto an obstruction of the basal cisterns by inflammatoryexudates and obstructive type, which is less common andeither secondary to a focal parenchymal lesion causingmass effect or due to the entrapment of a part of the ven-tricle by granulomatous ependymitis2.The typical analysis of cerebrospinal fluid with CNSTB demonstrates a moderate lymphocytosis, moderatelyelevated protein levels, and hypoglycorrachia. As such,the CNS profile of CNS TB mimics the profiles of a largelist of both infectious and noninfectious processes thataffect the CNS. The predominance of neutrofils in somecases likely represents an earlier stage of infection, which,over the course of days to weeks, will convert to a pre-dominantly lymphocitic profile22,23. CSF can also demon-strate the presence of acid-fast bacilli. Mycobacterium tu-berculosis complex can be identified specifically by DNAprobe or by nucleic acid amplification test24,25. Non-inva-sive imaging modalities, such as computed tomographyscan and magnetic resonance imaging are routinely usedin the diagnosis of neurotuberculosis.N. Brn~i} and L. Gorup: Tuberculous Meningoencephalitis with Complication, Coll. Antropol. 35 (2011) Suppl. 2: 285–287286Fig. 1. Normotensive hydrocephalus on multi-slicecomputed tomography.Treatment for all forms of CNS TBC should consist of4 drugs (isoniasid, rifampicin, pyrasinamid, ethambutol)for 2 mouths followed by 2 drugs (isoniasid, rifampicin)for at least 10 months26. Studies show that adjunctivecorticosteroids decreases mortality27.Tuberculous meningoencephalitis in presented pa-tient was considered on the basis of clinical presentation,laboratory findings (hyponatraemia) cerebrospinal fluidstudies, radiological findings (hydrocephalus on MSCTand MRI of the brain), and history of orchiepididymitis ofunknown origin one year earlier, together with informa-tion that the patient originated from Kosovo where inci-dence of tuberculosis is still high. Subsequently, acid-fastbacilli (AFB) staining on samples obtained after orchiec-tomy a year ago was performed, revealing AFB. Anti-tu-berculosis therapy is still in course. This is the secondcase of tuberculous meningoencephalitis with the samedisease pattern (i.e. tuberculous orchiepididymitis – me-ningoencephalitis) in our Department, and this fact wascrucial for the presumptive diagnosis and urgent treat-ment of TB CNS. The former case was described fiveyears ago28. We point out that in case of meningoence-phalitis, hydrocephalus and orchiepididymitis, tubercu-losis must be taken into consideration.R E F E R E N C E S1. KUO VC, SLOAN LM, EMMETT M, Proc Bayl Univ Cent, 23(2010) 359. — 2. TRIVEDI R, SAKSENA S, GUPTA R, Indian J RadiolImaging, 19 (2009) 256. — 3. LONNROTH K, RAVIGLIONE M, SeminRespir Crit Care Med, 29 (2008) 481. — 4. World Health OrganizationGlobal Tuberculosis Control: Surveillance, Planing, Financing. (Geneva,Switzerland: WHO;2008). — 5. WAALER HT, Int J Tuberc Lung Dis, 6(2002) 745. — 6. World Health Organization Global Tuberculosis Con-trol: Surveillance, Planing, Financing. Geneva, Switzerland: WHO; 2007.— 7. ROCK BR, OLIN M, BAKER CA, MOLITOR TW, PETERSON PK,Clin Microbiol Rev, 21 (2008) 243. — 8. PHYPERS M, HARRIS T, PO-WER C, Int J Tuberc Lung Dis, 10 (2006) 99. — 9. MUCAJ S, DRESHAJS, KABASHI S, HUNDOZI H, GASHI S, ZHJEQI V, SHALA N, KR-YEZIU, Med arh, 64 (2010) 189. — 10. MEYER S, SHAMDEEN MG,WULLENWEBER J, HERMANN M, GOTTSCHLING S, STRUFFERTT, GORTNER L, KLOTZ M, Wien Med Wochenschr, 157 (2007) 37. — 11.DUBE MP, HOLTOM PD, LARSEN RA, Am. J. Med, 93 (1992) 520. — 12.RANA FS, HAWKEN MP, MWACHARI CS, BHATT M, ABDULAH F,NG’ANG’A LW, POWER C, GITHUI WA, PORTER J D, LUCAS SB, J.Acquir Immune Defic Syndr, 24 (2000) 23. — 13. YARAMIS G, OGAWASK, SMITH MA, BRENNSESSEL DJ, LOWY FD, Medicine, (Baltimore)66 (1987) 317. — 14. GURKAN F, ELEVLI M, SOKER M, HASPOLAT K,KIRBAS G, TAS MA, Pediatrics, 102 (1998) E49. — 15. KLEIN NC, DAM-SKER B, HIRSCHMAN SZ, Am J Med, 79 (1985) 29. — 16. VERDON R,CHEVRET S, LAISSY JP, WOLFF M, Clin Infect Dis, 22 (1996) 982. —17. DASTUR DK, MANGHANII DK, UDANI PM, Radiol Clin North Am,33 (1995) 733. — 18. BHATTACHARJEE J, SHARMA RS, SINGH J,DATTA KK, VERGHESE T, J Commun Dis, 25 (1993) 71. — 19. GIRGISNI, SULTAN Y, FARID Z, MANSOUR MM, ERIAN MW, HANNA LS,MATECZUN AJ, Am J Trop Med Hyg, 58 (1998) 28. — 20. THWAITESGE, NGUYEN DB, NGUYEN HD, HOAG TQ, DO TT, NGUYEN TC,NGUYEN QH, NGUYEN TT, NGUYEN NH, NGUYEN TN., NGUYENNL, NGUYEN HD, VU NT, CAO HH, TRAN TH, PHAM PM, NGUYENTD, STEPNIEWSKA K, WHITE NJ, TRAN TH, FARRAR JJ, N Engl JMed, 351 (2004) 1741. — 21. THWAITES GE, TRAN TH, Lancet Neurol,4 (2005) 160. — 22. JEREN T, BEUS I, Acta Cytol, 26 (1982) 678. — 23.SUTLAS PN, UNAL A, FORTA H, SENOL S, KIRBAS D, Infection, 31(2003) 387. — 24. KANEKO K, ONODERA O, MIYATAKE T, TSUJI S,Neurology, 40 (1990) 1617. — 25. THWAITES GE, CHAU TT, FARRARJJ, J Clin Microb, 42 (2004) 378. — 26. THWAITES GE, FISHER M,HEMINGWAY C, SCOTT G, SOLOMON T, INNES J, BRITISH INFEC-TIOUS SOCIETY, J Infect, 59 (2009) 167. — 27. THWAITES GE, NGU-YEN DB, NGUYEN HD, HOAG TQ, DO TT, NGUYEN TC, NGUYENQH, NGUYEN TT, NGUYEN NH, NGUYEN TN, NGUYEN NL, NGU-YEN HD, VU NT, CAO HH, TRAN TH, PHAM PM, NGUYEN TD,STEPNIEWSKA K, WHITE NJ, TRAN TH, FARRAR JJ, N Engl J Med,351 (2004) 1741. — 28. MILETIC B, MOROVIC M, TOMIC Z, TICAC B,Aktuelle Urol, 37 (2005) 67.N. Brn~i}Infectious Diseases Department, Rijeka University Hospital Centre, p.p. 292, 51000 Rijeka, Croatiae-mail: nada.brncic@medri.hrTUBERKULOZNI ORHIEPIDIDIMITIS, MENINGOENCEFALITIS I HDROCEFALUSS A @ E T A KTuberkulozni je meningoencefalitis (TBM) rijedak, no ozbiljan, ~esto fatalan oblik aktivne tuberkuloze i na njegaotpada oko 1% svih slu~ajeva tuberkuloze. Rana dijagnoza i lije~enje klju~ni su u smanjenju pobola i smrtnosti. Prika-zan je slu~aj TBM-a u {ezdesetogodi{njaka. Na TBM se posumnjalo na temelju klini~ke slike, laboratorijskih nalaza(hiponatremija), analize cerebrospinalnog likvora, radiografskih nalaza (hidrocefalus na vi{eslojnoj spiralnoj kompju-teriziranoj tomografiji mozga) te podatka o preboljelom orhiepididimitisu nepoznate etiologije godinu dana ranije, auzev{i u obzir da je bolesnik podrijetlom s Kosova gdje je u~estalost tuberkuloze jo{ uvijek visoka. Mycobacterium tuber-culosis je izoliran iz cerebrospinalnog likvora na Lowenstein-Jensenovoj podlozi potvrdiv{i dijagnozu TBM-a. Nakna-dno su i u uzorcima tkiva dobivenima nakon orhiektomije godinu dana ranije na|eni acidorezistentni bacili. Antituber-kulozna terapija je u tijeku. Ovo je drugi slu~aj tuberkuloznog meningoencefalitisa s jednakim obrascem bolesti (tj.tuberkulozni epididimitis-meningoencefalitis) u na{oj Klinici {to je bilo klju~no u postavljanju radne dijagnoze i za-po~injanju hitnog lije~enja. Prvi je slu~aj opisan prije pet godina.N. Brn~i} and L. Gorup: Tuberculous Meningoencephalitis with Complication, Coll. Antropol. 35 (2011) Suppl. 2: 285–287287

Tuberculous Orchiepididymitis, Meningoencephalitis and Hydrocephalus

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