An 84–year–old male with type 2 diabetes, hypertension, and a remote history of pulmonary TB presented with fevers, dysphagia, and scant hemoptysis. Physical exam remarkable for fevers to 38.8 C and bibasilar rhonchi. Chest radiography unrevealing; subsequent chest CT showed bilateral dependant rounded ground glass foci in right middle lobe suggestive of aspiration, concurrent CT neck unremarkable. Modified barium swallow indicated severe OP dysphagia. Empiric antibiotic therapy was begun; blood cultures and initial sputum cultures unremarkable. MRI brain revealed chronic white matter changes. The patient deteriorated and developed severe myalgias and neck stiffness. LP revealed a lymphocytic pleocytosis with elevated protein and normal glucose. One of three AFB sputum cultures eventually grew mycobacterium. CSF AFB culture and stain and PCR were negative ? 2. Patient was started on four drug therapy for culture negative tuberculous meningitis likely due to pulmonary reactivation. Symptoms slowly improved, repeat LP 1 week later showed pleocytosis improvement. Unfortunately dysphagia persisted requiring a PEG tube.
Oropharyngeal (OP) dysphagia is a commonly encountered hospital problem that can result from a wide array of pathological conditions. OP dysphagia can lead to significant morbidity and mortality in the form of aspiration pneumonia and pneumonitis (1–3). Although a variety of neurogenic, neuromuscular, or structural disease processes can potentially result in OP dysphagia, we report an atypical cause of this common condition. Although cases of tuberculous bacillus (TB) meningitis causing OP dysphagia have been reported (4), this represents a truly rare cause of OP dysphagia. Tuberculous meningitis (4), space occupying tuberculous encephalitis (5), cranial neuropathy (6), external compression from lymphadenitis (7), pharyngeal involvement (8), esophageal involvement (9), and tracheoesphophageal fistula (10) are all previously described mechanisms of tuberculosis associated dysphagia. A definitive diagnosis of TB meningitis is challenging with currently available tuberculosis CSF testing. Several case series has established CSF staining sensitivities <20% and CSF culture sensitivities as low as 25% (11). Good universal molecular and biochemical CSF analysis for TB meningitis are still lacking. Sensitivities for PCR based, immuno, and biochemical assays are as low as 18%, 38%, and 48%, respectively, (11), although considerable differences may exist between specific tests. Limitations in currently available CSF analysis make a definitive diagnosis of TB meningitis difficult, thus appreciating associated clinical and laboratory signs of TB meningitis is paramount in diagnosis.
Hospital based clinicians need to be wary of atypical causes of dysphagia, especially when past history provides key diagnostic clues.