Clinical Radiology (1991) 45, 211-214
Case Report: Widespread Tuberculosis in Sickle Cell Disease O. C H A N and E. L O V E D A Y
Department of Radiology, St Thomas" Hospital, London We report a case of a patient with sickle cell disease who presented with mesenteric nodes and pulmonary TB and who subsequently relapsed on triple therapy and presented with disseminated tuberculous osteomyelitis and cervical lymphadenopathy. We emphasize the difficulty of establishing the diagnosis at all stages of presentation. Chan, O. & Loveday, E. (1992). Clinical Radiology 45, 211-214. Case Report: Widespread Tuberculosis in Sickle Cell Disease
Patients with sickle cell disease frequently suffer from recurrent painful clinical and haematological crises, in particular affecting the lungs, skeletal system and the abdominal organs. However, it is infections and not crises which are the commonest cause of death (BarrettConnor, 1971 a). Clinical, biochemical and radiological differentiation between infection and infarction is difficult, in particular where the lungs and skeleton are concerned (Onwubalili, 1983). Pulmonary TB is no more common or severe in patients with sickle cell disease than in matched populations (Barrett-Connor, 1971a) in contradiction to earlier literature which suggested both increased morbidity (Carroll and Evans, 1949; Reynolds, 1965) and mortality (Bergman and Berne, 1949; Fradkin and Schwartz, 1930). A review of the literature revealed very few reports of pulmonary TB in patients with sickle cell disease. Surprisingly, no case of disseminated skeletal TB with or without pulmonary, cervical or mesenteric node involvement has been reported. In this report, we present a case which illustrates the difficulty in making the diagnosis at all stages of presentation. Fig. 2 - P A chest. There is now widening of the superior mediastinum, with bilateral hilar adenopathy and some residual consolidation in the left lower zone.
Fig. 1 PA chest. The heart is enlarged. There is consolidation in the left lower zone. Correspondence to: O. Chan, Department of Radiology, St T h o m a s ' Hospital, Lambeth Palace Road, London SEI 7EH.
Fig. 3 Longitudinal abdominal ultrasound scan showing enlarged paraortie lymphadenopathy.
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CLINICAL RADIOLOGY
(a)
(b)
(c)
Fig. 4 (a) O P G of the mandible. Two well defined lyric lesions are seen on the inferior aspect of the body of the mandible. (b) Lateral view of the left elbow. Single well defined lytic lesion in the proximal ulna with no periosteal reaction. (c) Lateral view of the right tibia and fibula. Three lytic lesions are seen, two in the tibia and one in the proximal fibula with minimal periosteal reaction.
CASE R E P O R T A 17-year-old Nigerian boy with sickle cell disease was referred by his GP with a 3 day history of shortness of breath, chest pain, nonproductive cough and pyrexia. He had previously complained intermittently of limb pain and shortness of breath as a child, and his last admission with a crisis had been 2 years previously in Nigeria. On examination he was small for his age and mildly jaundiced with a tachycardia (110 beats per minute) and a pyrexia (39°C). Hepatomegaly was noted. Investigations revealed anaemia (Hb 6.9 g/dl) and a leucocytosis (WBC 14x 109/litre with 40% lymphocytes). A chest radiograph showed an enlarged heart and consolidation in the left mid and lower zones (Fig. 1). A diagnosis of sickle cell crisis with pneumonia was made. He was treated with erythromycin and amoxycillin. His condition worsened with deterioration of his blood gases and a 6 U exchange blood transfusion was performed with subsequent clinical and radiological improvement. He was discharged after 3 weeks although his pyrexia was unchanged and the white count remained raised with a lymphocytosis. He was re-admitted 3 months later for investigations of a pyrexia of u n k n o w n origin, weight loss and a raised white count with 50°/,, lymphocytes. A presumptive diagnosis of l y m p h o m a was made. Extensive investigations including a Mantoux, early morning urine, HIV status and a liver biopsy were all negative. The chest radiograph showed no change in the lungs, with persistent consolidation in the left
lower zone, but in addition there was widening of the superior mediastinum and bilateral hilar adenopathy (Fig. 2). An abdominal ultrasound revealed large paraortic lymphadenopathy but no focal lesion was seen in the liver, spleen or kidneys (Fig. 3). A mI-labelled WBC scan was normal. A laparotomy was performed confirming widespread lymphadenopathy, and biopsy revealed caseating granulomata and acid-fast bacilli, subsequently identified as Mycobacterium tuberculosis. He responded very well to triple anti-tuberculous therapy and was discharged 2 weeks later. A follow-up ultrasound I m o n t h later showed the paraortic lymphadenopathy to have resolved. He was re-admitted 3 m o n t h s later with a 1 m o n t h history of tenderness in his right mandible, left elbow and more recently right tibia1 swelling and pain. Clinically he was pyrexial, had localized tenderness and swelling over the mandible, left elbow and right tibia, and in addition he had developed a right supraclavicular lymph node. Chest radiograph revealed further mediastinal widening, bilateral hilar lymphadenopathy and consolidation at both lungs. Skeletal radiographs showed multiple well defined lucent areas in the mandible, left ulna and right tibia and fibula (Fig. 4) which appeared atypical for osteomyelitis. Dynamic and static isotope bone scanning showed no evidence of increased uptake in the dynamic phase and only moderate uptake on the static phase in the left elbow. Therefore a presumptive diagnosis of multiple bone infarcts was made. Unfortunately, the bone lesions progressed rapidly, both clinically and radiologically, with new lesions appearing in the distal left humerus and tibia despite continuing triple therapy (Fig. 5).
WIDESPREAD TUBERCULOSIS IN SICKLE CELL DISEASE
213
(a) Fig. 5 (a) Lateral view of the elbow. The lytic lesion in the proximal ulna is larger. In addition, there is an effusion and multiple lytic lesions in the distal humerus with an associated periosteal reaction. (b) Lateral view of the right tibia and fibula. The lytic lesions have increased in size with periosteal reactions becoming apparent (arrow).
(b) The left supraelavieular node was biopsied and drainage and curettage of the lesions in the ulna and tibia were performed. Histologically, the bone lesions demonstrated caseating granulomas but no acid-fast bacilli were identified in the supraclavicular node. Streptomycin was added to the triple therapy and he has subsequently made an excellent recovery with marked clinical and radiological improvement. DISCUSSION A c u t e p u l m o n a r y disease is the single m o s t c o m m o n r e a s o n for h o s p i t a l i z a t i o n in patients with sickle cell disease ( B a r r e t t - C o n n o r , 1971a). T h e r e is great difficulty in distinguishing p n e u m o n i a from p u l m o n a r y infarction, a n d the c o m b i n a t i o n o f cough, fever, leucocytosis, chest p a i n a n d d y s p n o e a often does n o t represent infection a n d only in those cases where the p a t h o g e n s are isolated can the disease be a t t r i b u t e d to infection. Clinical a n d r a d i o l o g i c a l guidelines have been d r a w n up to differentiate between infection a n d infarction ( C h a r a c h e et al., 1979). Even so, it is e s t i m a t e d that patients with sickle cell disease are p r o b a b l y 100 times m o r e likely to d e v e l o p p n e u m o n i a t h a n the general p o p u l a t i o n . This m a y be due to a c o m b i n a t i o n o f factors, in p a r t i c u l a r infarcted lung acting as a m e d i u m for bacterial g r o w t h and thus
i m p a i r i n g p h a g o c y t o s i s ( W o o d , 1951-1952); reduced o x y g e n tension due to i n t r a p u l m o n a r y shunting causing i m p a i r e d p h a g o c y t o s i s by a l v e o l a r m a c r o p h a g e s (Green, 1968); deficient o p s o n o p h a g o c y t i c activity for p n e u m o coccus (Winkelstein a n d D r a c h m a n , 1968; H a n d a n d King, 1978) a n d also the f u n c t i o n a l a u t o s p l e n e c t o m y a n d deficiency o f specific circulating a n t i b o d i e s (Onwubalili, 1983). P u l m o n a r y TB is rare in sickle cell disease, with only nine cases o u t o f 166 b a c t e r i a l p n e u m o n i a s in one A m e r i c a n series ( B a r r e t t - C o n n o r , 1971a). F u r t h e r m o r e , active TB is neither m o r e c o m m o n n o r m o r e severe in sickle cell disease, c o n t r a r y to earlier reports o f increased morbidity and mortality. Sickle cell patients are extremely susceptible to osteomyelitis, in p a r t i c u l a r due to salmonella, where the risk is e s t i m a t e d at several h u n d r e d times greater t h a n t h a t in the n o r m a l p o p u l a t i o n (Onwubalili, 1983). The predisposition to salmonella has been suggested to be caused by vaso-occlusive disease o f the intestine, causing small infarcts and hence h a e m a t o g e n o u s s p r e a d via invasion f r o m the gastro-intestinal t r a c t ( R a o et al., 1986). This is s u p p o r t e d by the fact t h a t there is an increased a s y m p t o m a t i c carrier o f s a l m o n e l l a where sickle cell disease occurs ( A d e y o k o n n u a n d H e n d r i c k s e , 1980; Onwubalili, 1983).
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CLINICAL RADIOLOGY
D e s p i t e triple a n t i - t u b e r c u l o u s t h e r a p y in this case, the p a t i e n t h a d b o t h clinical a n d r a d i o l o g i c a l r e l a p s e w i t h b o n e i n v o l v e m e n t . I f t h e p a t i e n t h a d n o t b e e n k n o w n to h a v e a c t i v e TB, the d i a g n o s i s w o u l d h a v e b e e n f u r t h e r d e l a y e d . T h e failure o f t r e a t m e n t o f the t u b e r c u l o u s o s t e o m y e l i t i s m a y h a v e b e e n d u e to r e s i s t a n c e to s o m e o f the drugs and possibly haematogenous spread from pulmonary TB into infarcted devitalized bone. F u r t h e r m o r e , r e s i s t a n c e o f t h e active p u l m o n a r y T B to t r e a t m e n t c o u l d likewise be e x p l a i n e d b y initial p u l m o n ary infarction and subsequent tuberculous colonization. T h e h i s t o r y a n d r e s p o n s e to t r e a t m e n t o f this p a t i e n t in fact contradict recent opinion that active pulmonary TB in sickle cell disease has n o i n c r e a s e d m o r b i d i t y a n d m o r t a l i t y a n d t h e r e f o r e s h o u l d also a l e r t clinicians a n d r a d i o l o g i s t s t o w a r d s skeletal i n v o l v e m e n t in a n y p a t i e n t w i t h a c t i v e TB. REFERENCES
Adeyokonnu, AA & Hendrickse, RG (1980). Salmonella osteomyelitis in childhood. A report of 63 cases seen in Nigerian children of whom 57 had sickle cell disease. Archives ~?f Disease in Childhood, 55, 175-184. Barrett-Connor, E (1971a). Bacterial infection and sickle cell anaemia. Medicine (Baltimore), 50, 97-111.
Barrett-Connor, E (1971b). Acute pulmonary disease and sickle cell anaemia. American Review of Respiratory Disease, 104, 159-165. Bergman, PS & Berne, RM (1949). Tuberculoma of the brain associated with sickle ceil anaemia. Journal of the Mount Sinai Hospital, 16, 175-183. Carroll, DS & Evans, JW (1949). Roentgen findings in sickle cell anaemia. Radiology, 53, 834 835. Charache, S, Scott, JC & Charache, P (1979). Acute chest syndrome in adults with sickle cell anaemia. Microbiology, treatment and prevention. Archives of Internal Medicine, 139, 67-69. Fradkin, WZ & Schwartz, LS (1930). Sickle cell anaemia. Journal of Laboratory and Clinical Medicine, 15, 519-525. Green, GM (1968). Pulmonary clearance of infectious agents. Annual Review of Medicine, 19, 315 316. Hand, WL & King, NL (1978). Serum opsonization of sahnonella in sickle cell anaemia. American Journal of Medicine, 64, 388-395. Onwubalili, JK (1983). Sickle cell disease and infection. Journal of Infection, 7, 2-20. Rao, SP, Miller, S & Solomon, N (1986). Acute bone and joint manifestations of the sickle cell disease in children. New York State Journal of Medicine, 5, 254 260. Reynolds, J (1965). The roentgenological features of sickle cell disease and related hemoglobinopathies. Chas C Thomas, Springfield. Winkelstein, JA & Drachman, RH (1968). Deficiency on pneumococcal serum opsonizing activity in sickle cell disease. New England Journal of Medicine, 279, 459 466. Wood, WB Jr (1951-1952). Studies on the cellular immunology of acute bacterial infections. Harvey Lecture Sertes, Academic Press, New York.
Case Report: Widespread Tuberculosis in Sickle Cell Disease O. C H A N and E. L O V E D A Y
Department of Radiology, St Thomas" Hospital, London We report a case of a patient with sickle cell disease who presented with mesenteric nodes and pulmonary TB and who subsequently relapsed on triple therapy and presented with disseminated tuberculous osteomyelitis and cervical lymphadenopathy. We emphasize the difficulty of establishing the diagnosis at all stages of presentation. Chan, O. & Loveday, E. (1992). Clinical Radiology 45, 211-214. Case Report: Widespread Tuberculosis in Sickle Cell Disease
Patients with sickle cell disease frequently suffer from recurrent painful clinical and haematological crises, in particular affecting the lungs, skeletal system and the abdominal organs. However, it is infections and not crises which are the commonest cause of death (BarrettConnor, 1971 a). Clinical, biochemical and radiological differentiation between infection and infarction is difficult, in particular where the lungs and skeleton are concerned (Onwubalili, 1983). Pulmonary TB is no more common or severe in patients with sickle cell disease than in matched populations (Barrett-Connor, 1971a) in contradiction to earlier literature which suggested both increased morbidity (Carroll and Evans, 1949; Reynolds, 1965) and mortality (Bergman and Berne, 1949; Fradkin and Schwartz, 1930). A review of the literature revealed very few reports of pulmonary TB in patients with sickle cell disease. Surprisingly, no case of disseminated skeletal TB with or without pulmonary, cervical or mesenteric node involvement has been reported. In this report, we present a case which illustrates the difficulty in making the diagnosis at all stages of presentation. Fig. 2 - P A chest. There is now widening of the superior mediastinum, with bilateral hilar adenopathy and some residual consolidation in the left lower zone.
Fig. 1 PA chest. The heart is enlarged. There is consolidation in the left lower zone. Correspondence to: O. Chan, Department of Radiology, St T h o m a s ' Hospital, Lambeth Palace Road, London SEI 7EH.
Fig. 3 Longitudinal abdominal ultrasound scan showing enlarged paraortie lymphadenopathy.
212
CLINICAL RADIOLOGY
(a)
(b)
(c)
Fig. 4 (a) O P G of the mandible. Two well defined lyric lesions are seen on the inferior aspect of the body of the mandible. (b) Lateral view of the left elbow. Single well defined lytic lesion in the proximal ulna with no periosteal reaction. (c) Lateral view of the right tibia and fibula. Three lytic lesions are seen, two in the tibia and one in the proximal fibula with minimal periosteal reaction.
CASE R E P O R T A 17-year-old Nigerian boy with sickle cell disease was referred by his GP with a 3 day history of shortness of breath, chest pain, nonproductive cough and pyrexia. He had previously complained intermittently of limb pain and shortness of breath as a child, and his last admission with a crisis had been 2 years previously in Nigeria. On examination he was small for his age and mildly jaundiced with a tachycardia (110 beats per minute) and a pyrexia (39°C). Hepatomegaly was noted. Investigations revealed anaemia (Hb 6.9 g/dl) and a leucocytosis (WBC 14x 109/litre with 40% lymphocytes). A chest radiograph showed an enlarged heart and consolidation in the left mid and lower zones (Fig. 1). A diagnosis of sickle cell crisis with pneumonia was made. He was treated with erythromycin and amoxycillin. His condition worsened with deterioration of his blood gases and a 6 U exchange blood transfusion was performed with subsequent clinical and radiological improvement. He was discharged after 3 weeks although his pyrexia was unchanged and the white count remained raised with a lymphocytosis. He was re-admitted 3 months later for investigations of a pyrexia of u n k n o w n origin, weight loss and a raised white count with 50°/,, lymphocytes. A presumptive diagnosis of l y m p h o m a was made. Extensive investigations including a Mantoux, early morning urine, HIV status and a liver biopsy were all negative. The chest radiograph showed no change in the lungs, with persistent consolidation in the left
lower zone, but in addition there was widening of the superior mediastinum and bilateral hilar adenopathy (Fig. 2). An abdominal ultrasound revealed large paraortic lymphadenopathy but no focal lesion was seen in the liver, spleen or kidneys (Fig. 3). A mI-labelled WBC scan was normal. A laparotomy was performed confirming widespread lymphadenopathy, and biopsy revealed caseating granulomata and acid-fast bacilli, subsequently identified as Mycobacterium tuberculosis. He responded very well to triple anti-tuberculous therapy and was discharged 2 weeks later. A follow-up ultrasound I m o n t h later showed the paraortic lymphadenopathy to have resolved. He was re-admitted 3 m o n t h s later with a 1 m o n t h history of tenderness in his right mandible, left elbow and more recently right tibia1 swelling and pain. Clinically he was pyrexial, had localized tenderness and swelling over the mandible, left elbow and right tibia, and in addition he had developed a right supraclavicular lymph node. Chest radiograph revealed further mediastinal widening, bilateral hilar lymphadenopathy and consolidation at both lungs. Skeletal radiographs showed multiple well defined lucent areas in the mandible, left ulna and right tibia and fibula (Fig. 4) which appeared atypical for osteomyelitis. Dynamic and static isotope bone scanning showed no evidence of increased uptake in the dynamic phase and only moderate uptake on the static phase in the left elbow. Therefore a presumptive diagnosis of multiple bone infarcts was made. Unfortunately, the bone lesions progressed rapidly, both clinically and radiologically, with new lesions appearing in the distal left humerus and tibia despite continuing triple therapy (Fig. 5).
WIDESPREAD TUBERCULOSIS IN SICKLE CELL DISEASE
213
(a) Fig. 5 (a) Lateral view of the elbow. The lytic lesion in the proximal ulna is larger. In addition, there is an effusion and multiple lytic lesions in the distal humerus with an associated periosteal reaction. (b) Lateral view of the right tibia and fibula. The lytic lesions have increased in size with periosteal reactions becoming apparent (arrow).
(b) The left supraelavieular node was biopsied and drainage and curettage of the lesions in the ulna and tibia were performed. Histologically, the bone lesions demonstrated caseating granulomas but no acid-fast bacilli were identified in the supraclavicular node. Streptomycin was added to the triple therapy and he has subsequently made an excellent recovery with marked clinical and radiological improvement. DISCUSSION A c u t e p u l m o n a r y disease is the single m o s t c o m m o n r e a s o n for h o s p i t a l i z a t i o n in patients with sickle cell disease ( B a r r e t t - C o n n o r , 1971a). T h e r e is great difficulty in distinguishing p n e u m o n i a from p u l m o n a r y infarction, a n d the c o m b i n a t i o n o f cough, fever, leucocytosis, chest p a i n a n d d y s p n o e a often does n o t represent infection a n d only in those cases where the p a t h o g e n s are isolated can the disease be a t t r i b u t e d to infection. Clinical a n d r a d i o l o g i c a l guidelines have been d r a w n up to differentiate between infection a n d infarction ( C h a r a c h e et al., 1979). Even so, it is e s t i m a t e d that patients with sickle cell disease are p r o b a b l y 100 times m o r e likely to d e v e l o p p n e u m o n i a t h a n the general p o p u l a t i o n . This m a y be due to a c o m b i n a t i o n o f factors, in p a r t i c u l a r infarcted lung acting as a m e d i u m for bacterial g r o w t h and thus
i m p a i r i n g p h a g o c y t o s i s ( W o o d , 1951-1952); reduced o x y g e n tension due to i n t r a p u l m o n a r y shunting causing i m p a i r e d p h a g o c y t o s i s by a l v e o l a r m a c r o p h a g e s (Green, 1968); deficient o p s o n o p h a g o c y t i c activity for p n e u m o coccus (Winkelstein a n d D r a c h m a n , 1968; H a n d a n d King, 1978) a n d also the f u n c t i o n a l a u t o s p l e n e c t o m y a n d deficiency o f specific circulating a n t i b o d i e s (Onwubalili, 1983). P u l m o n a r y TB is rare in sickle cell disease, with only nine cases o u t o f 166 b a c t e r i a l p n e u m o n i a s in one A m e r i c a n series ( B a r r e t t - C o n n o r , 1971a). F u r t h e r m o r e , active TB is neither m o r e c o m m o n n o r m o r e severe in sickle cell disease, c o n t r a r y to earlier reports o f increased morbidity and mortality. Sickle cell patients are extremely susceptible to osteomyelitis, in p a r t i c u l a r due to salmonella, where the risk is e s t i m a t e d at several h u n d r e d times greater t h a n t h a t in the n o r m a l p o p u l a t i o n (Onwubalili, 1983). The predisposition to salmonella has been suggested to be caused by vaso-occlusive disease o f the intestine, causing small infarcts and hence h a e m a t o g e n o u s s p r e a d via invasion f r o m the gastro-intestinal t r a c t ( R a o et al., 1986). This is s u p p o r t e d by the fact t h a t there is an increased a s y m p t o m a t i c carrier o f s a l m o n e l l a where sickle cell disease occurs ( A d e y o k o n n u a n d H e n d r i c k s e , 1980; Onwubalili, 1983).
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CLINICAL RADIOLOGY
D e s p i t e triple a n t i - t u b e r c u l o u s t h e r a p y in this case, the p a t i e n t h a d b o t h clinical a n d r a d i o l o g i c a l r e l a p s e w i t h b o n e i n v o l v e m e n t . I f t h e p a t i e n t h a d n o t b e e n k n o w n to h a v e a c t i v e TB, the d i a g n o s i s w o u l d h a v e b e e n f u r t h e r d e l a y e d . T h e failure o f t r e a t m e n t o f the t u b e r c u l o u s o s t e o m y e l i t i s m a y h a v e b e e n d u e to r e s i s t a n c e to s o m e o f the drugs and possibly haematogenous spread from pulmonary TB into infarcted devitalized bone. F u r t h e r m o r e , r e s i s t a n c e o f t h e active p u l m o n a r y T B to t r e a t m e n t c o u l d likewise be e x p l a i n e d b y initial p u l m o n ary infarction and subsequent tuberculous colonization. T h e h i s t o r y a n d r e s p o n s e to t r e a t m e n t o f this p a t i e n t in fact contradict recent opinion that active pulmonary TB in sickle cell disease has n o i n c r e a s e d m o r b i d i t y a n d m o r t a l i t y a n d t h e r e f o r e s h o u l d also a l e r t clinicians a n d r a d i o l o g i s t s t o w a r d s skeletal i n v o l v e m e n t in a n y p a t i e n t w i t h a c t i v e TB. REFERENCES
Adeyokonnu, AA & Hendrickse, RG (1980). Salmonella osteomyelitis in childhood. A report of 63 cases seen in Nigerian children of whom 57 had sickle cell disease. Archives ~?f Disease in Childhood, 55, 175-184. Barrett-Connor, E (1971a). Bacterial infection and sickle cell anaemia. Medicine (Baltimore), 50, 97-111.
Barrett-Connor, E (1971b). Acute pulmonary disease and sickle cell anaemia. American Review of Respiratory Disease, 104, 159-165. Bergman, PS & Berne, RM (1949). Tuberculoma of the brain associated with sickle ceil anaemia. Journal of the Mount Sinai Hospital, 16, 175-183. Carroll, DS & Evans, JW (1949). Roentgen findings in sickle cell anaemia. Radiology, 53, 834 835. Charache, S, Scott, JC & Charache, P (1979). Acute chest syndrome in adults with sickle cell anaemia. Microbiology, treatment and prevention. Archives of Internal Medicine, 139, 67-69. Fradkin, WZ & Schwartz, LS (1930). Sickle cell anaemia. Journal of Laboratory and Clinical Medicine, 15, 519-525. Green, GM (1968). Pulmonary clearance of infectious agents. Annual Review of Medicine, 19, 315 316. Hand, WL & King, NL (1978). Serum opsonization of sahnonella in sickle cell anaemia. American Journal of Medicine, 64, 388-395. Onwubalili, JK (1983). Sickle cell disease and infection. Journal of Infection, 7, 2-20. Rao, SP, Miller, S & Solomon, N (1986). Acute bone and joint manifestations of the sickle cell disease in children. New York State Journal of Medicine, 5, 254 260. Reynolds, J (1965). The roentgenological features of sickle cell disease and related hemoglobinopathies. Chas C Thomas, Springfield. Winkelstein, JA & Drachman, RH (1968). Deficiency on pneumococcal serum opsonizing activity in sickle cell disease. New England Journal of Medicine, 279, 459 466. Wood, WB Jr (1951-1952). Studies on the cellular immunology of acute bacterial infections. Harvey Lecture Sertes, Academic Press, New York.
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