bacterial etiology includes haemophilus influenzae , streptococcus , pneumococcus , staphylococcus , meningococcus , mycoplasma , tularemia , listeria , leptospirosis , tuberculosis ( tb ) , q - fever , salmonella . any of these may coexist as a result of suppression of immunity ; hence , challenges arise in the diagnosis of the actual bacterial etiology of this disease in resource - constrained settings . tuberculous pericarditis which is rare in developed countries may be more common in regions where tb is endemic . jaiyesimi et al . identified staphylococcus aureus and mycobacterium tuberculosis each accounting for 20% as the main incriminating organisms in a cohort of 53 children with infective pericarditis in ibadan , nigeria . due to peculiarities of pediatric practice in resource - limited settings like ours , we present here the challenges encountered in distinguishing m. tuberculosis from s. aureus as the incriminating microbe for pyopericardium in a child who had acute osteomyelitis bearing in mind the possibility of a coinfection . a 4-year - old boy had complaints of fever , fast breathing , cough , and painful swelling of the left leg of 4 weeks duration with significant weight loss . he was in respiratory distress , wasted with generalized lymphadenopathy , and left lower limb swelling up to the knee . he weighed 10.5 kg ( 65% of expected ) and mid - arm circumference was 12 cm . the respiratory rate was 44/min , with dull percussion notes on the left hemithorax and reduced intensity of breath sounds with widespread coarse crepitations . the radial pulse was 144/min , moderate volume and regular , while the blood pressure was 80/60 mmhg ( left arm sitting ) . the jugular venous pressure raised to the neck ; the precordium was bulging with diffuse apex beat and distant heart sounds ; and the liver was enlarged to 7 cm below the right costal margin , nontender . he had a tender diffuse swelling of the left leg up to the knee with the limitation of movement . plain radiograph of the left leg showed soft tissue swelling and periosteal thickening with lytic lesions . chest radiographs revealed an enlarged cardiac shadow [ figure 1 ] , blood culture grew s. aureus sensitive to ceftriaxone , ciprofloxacin , and clindamycin , erythrocyte sedimentation rate was 100 mm / h , white blood cell was 22.2  10/l , differential lymphocyte count was 70.4% , while mantoux showed nil induration , ziehl  neelsen ( zn ) stain of gastric washout yielded no acid - fast bacilli from 3 early morning samples , and retroviral screening was nonreactive . echocardiography diagnosed a massive pericardial effusion with cardiac tamponade as it revealed circumferential fluid accumulation , 34.22 mm separation of the pericardial layers ( two - dimensional [ 2d ] measurement in diastole ) , and anteroposterior and mediolateral heart swinging within the pericardial sac . right atrial and right ventricular collapse was demonstrable on 2d echocardiography [ figure 2 ] . at echo - guided pericardiocentesis inserted pericardiostomy tube drained for 7 days after which he had a normal chest radiograph . culture of pus yielded no growth and zn stain yielded no acid - fast bacilli . having received antibiotics for 7 weeks ( 4 weeks in referring hospital and 3 weeks in our center ) without significant clinical improvement and a tb score of 9 , a decision to treat for tb was considered , and he received a full course of anti - tb therapy . he improved significantly after 2 weeks of treatment , and he was discharged thereafter and has remained stable for up to 3-month follow - up . our patients had osteomyelitis with a blood culture that grew s. aureus , a common culprit also for pyopericardium following hematogenous spread . however , we had a diagnostic challenge as regards the actual etiology of the pericardial effusion as patient did not show clinical response to the antibiotics sensitive to the incriminated organism but responded well to antituberculous therapy afterward . while osteomyelitis may have been caused by s. aureus , the coexisting pyopericardium may have had a different etiology as osteomyelitis resolved with appropriate antibiotics , but resolution of cardiorespiratory signs of pericardial disease was clinically poor . patients with tb are predisposed to secondary bacterial infections as they have been shown to have relative depression of th1-type cytokine responses and overproduction and/or enhanced effects of immunosuppressive molecules ( transforming growth factor - beta and interleukin-10 [ il-10 ] ) . proinflammatory cytokines ( tumor necrosis factor - alpha , il-6 , and il-1b ) have also been shown to play a role in the immunopathogenesis of tb with the attendant consequence of an acquired immunosuppression . while a tuberculous osteomyelitis would be most unlikely here as osteomyelitis responded to antibiotic therapy , an etiologic diagnosis of m. tuberculosis causing the pyopericardium is plausible as therapy to this resulted in significant clinical improvement . challenges with diagnosis in children in our resource - limited environment may have hampered the actual etiologic diagnosis of the pericardial effusion . the diagnosis , which was not feasible in our setting , largely depends on histopathology of the pericardial tissue or culture of m. tuberculosis from this tissue or fluid . it has been established however that it is rare to find acid - fast bacilli in a spun smear of pericardial fluid as it was in our patient . the sensitivity of polymerase chain reaction ( pcr ) for nucleic acid amplification in the diagnosis of tb from pericardial fluid even where available is poor , and false - positive results with pcr remain a concern . however , response to specific antituberculous therapy may be an accepted criterion for the diagnosis of tuberculous etiology of pericardial effusion . the diagnosis of cardiac tamponade complicating pyopericardium may be suspected clinically in a child with the classic triad of beck which includes distant heart sounds , distended neck veins , and hypotension though these findings are both late and inconsistent indicators of tamponade . the definite diagnosis of cardiac tamponade is , however , made by echocardiography . among echocardiographic signs , the most characteristic , although they are not entirely specific , are chamber collapses , which are nearly always of the right atrium and ventricle . during early diastole , the right ventricular free wall invaginates , and at end diastole , the right atrial wall invaginates . this was evident in our patient . rare disease conditions such as pyopericardium , with multiple possible bacterial etiologies , can pose a challenge in the identification of the actual culprit in resource - limited settings . while a primary focus of infection can serve as a useful pointer as pyopericardium may result from hematogenous spread , in the setting of depressed immunity , the possibility of a coinfection with other endemic pathogens must be borne in mind .
in pyopericardium , pus accumulates in the pericardial space as a result of infection by pyogenic organisms , most common of which are staphylococcus aureus and mycobacterium tuberculosis . 
 these patients are at risk of cardiac tamponade . apart from pericardiocentesis in the management of these patients , definitive drug treatment 
 may pose a formidable challenge in a setting of coinfection as in patients with tuberculosis who are predisposed to secondary bacterial infections . 
 this was the case of our patient . 
 we here highlight the challenges faced with etiologic diagnosis in resource - limited settings .