An 86-year-old female with medical comorbidities including well-controlled type 2 diabetes (HbA1c 5.6 %) on oral therapy and glaucoma who presented with 2 weeks of right ear pain, right frontal headache and right facial pain just lateral to the nose. The patient also described painful extraocular movements (EOMs) on the right, decreased vision, and thick purulent drainage from the right nasal cavity. Vitals were normal with a blood pressure of 132/70, heart rate of 78, respiratory rate of 14, oxygen saturation of 97 % on room air, and temperature of 36.7 degrees Celsius. Examination was significant for hand motion vision, severely restricted right eye EOMs with ptosis, and excyclotorsion. Computerized tomography of the head and orbits demonstrated soft tissue thickening and indistinctness of fat in the region of the right optic canal and right orbital apex, possibly representing extension of paranasal inflammatory disease to an unusual bone defect in the right lateral wall of the right sphenoidal sinus (). Additionally, there was associated right anterior ethmoidal mucosal disease and complete opacification of the right maxillary antrum. Magnetic resonance imaging (MRI) of the brain without and with intravenous (IV) contrast showed right-sided paranasal sinus infection with transsphenoidal phlegmonous extension into the right orbital apex and cavernous sinus consistent with orbital apex syndrome (, ). Ophthalmology and otolaryngology (ENT) were consulted and performed a right endoscopy of the nasal cavities. This revealed purulence from the right middle meatus obstructing the view of the sphenoid. Nasal swab was sent for bacterial culture. Infectious disease was consulted who recommended IV vancomycin, cefepime, and metronidazole in addition to dexamethasone.\nThe patient underwent surgery on hospital day three. ENT completed a broad endoscopic sinus debridement including right total ethmoidectomy, frontal sinusotomy, sphenoidotomy, tissue biopsy, and washout of orbital apex with tissues sent for bacterial and fungal cultures. Tissue from the right naris and right ethmoid sinus grew methicillin-susceptible Staphylococcus aureus (MSSA). Initial pathology at frozen section examination revealed mixed acute and chronic inflammation at all biopsy sites. The patient’s antibiotics were narrowed to IV cefazolin on hospital day 5. On hospital day 6, one colony of Aspergillus fumigatus grew from a culture of the right orbital apex tissue. The pathology revealed fungal hyphae consistent with Aspergillus spp. and related molds, with tissue invasion in the orbital apex (, ). She was started on IV voriconazole. She was discharged to a skilled nursing facility after a 9-day hospital course with antimicrobials including oral cefdinir for a 4-week course and oral voriconazole with a planned treatment course of at least 12 weeks. At two-week follow-up with infectious disease, a repeat MRI brain showed worsening right ethmoid and sphenoid sinus fungal infection. Intravenous caspofungin was added to her regimen for a two-week course of therapy with clinical improvement. She underwent further debridement with rigid endoscopy at two, four, and six weeks after diagnosis with mostly crusted blood products and no evidence of necrotic tissue. Ophthalmologic exam ultimately demonstrated improvement in visual acuity to 20/50 with full EOMs.
A 59-year-old male having HIV positive illness for around 10 years, without any documented evidence of adhering to specific antiretroviral therapy regimen, presented to our hospital with history of low-grade fever, reduced appetite, and weight loss over 2 months followed by headache for about 2 weeks with recent worsening in the form of development of left-sided focal seizure with secondary generalization followed by altered sensorium for 3 days. He was started on empirical antitubercular medicines for last 2 weeks by a private practitioner before presenting to us. On presentation, he was febrile and drowsy. He had left hemiparesis with generalized brisk reflexes, extensor plantar response, and positive meningeal signs. Other systemic examination was unremarkable. A diagnosis of chronic meningitis in an immunocompromised individual was considered. Chronic meningitis in an immunocompromised patient has multiple differentials as enlisted in .\nOn investigations, he had pancytopenia (hemoglobin 6.8 g/dl, total leukocyte counts 3100/mm3, absolute neutrophil counts 2200/mm3, platelet counts 62,000/mm3) with normal glucose, electrolytes, and renal and hepatic functions. His chest X-ray showed right middle zone and left upper zone consolidation. Radiological differential diagnoses of this type of consolidation are bacterial pneumonia, tuberculosis, atypical mycobacterial infection, fungal infection, and lymphomatous or other neoplasm. He needed a CECT thorax and bronchoscopy-guided biopsy was advised but could not be done due to financial constraints and because the relatives declined any invasive procedure. His CECT head was normal []. CSF was acellular with normal glucose and protein level. CSF Gram stain, acid-fast bacillus stain, potassium hydroxide mount, India ink and cryptococcal antigen tests, and cytology for malignant cells were negative. CSF mycobacterial and fungal culture was also sent at the same time. As his focal deficits were not explained by a normal CECT head, magnetic resonance imaging (MRI) brain was done which revealed small, fairly defined, multiple altered signal intensity areas in the posterior aspect of right temporal lobe, posterolateral aspects of both the occipital lobes and anteroinferior portion of right frontal lobe on the gray-white matter junction, showing blooming on gradient images and peripheral enhancement on contrast-enhanced study associated with minimal to mild surrounding edema with normal MR angiogram, suggestive of hemorrhagic infarcts secondary to vasculitis. A differential diagnosis of this imaging feature in an immunocompromised is enumerated in .\nHe was treated with broad-spectrum antibiotics, empirical antitubercular drugs, antiepileptic drugs, and other supportive measures without any significant clinical improvement or deterioration. His toxoplasma antibodies were negative. His blood sample was sent for CD4 count analysis, but we could not get countable CD4 cells on flow cytometry despite doing the test twice in two different laboratories. The method used for detection of CD4 cells in flow cytometry was pan-leukocyte (CD45+) gating strategy by single platform technique. To get final diagnosis, CT scan chest, bronchoscopy, galactomannan test, and brain biopsy were considered but could not be done due to financial constraints. Considering febrile encephalopathy in a patient with HIV, febrile neutropenia and no response to 2 weeks of antibiotics and antitubercular drugs given before coming to our hospital, empiric broad-spectrum antibiotics in the form of meropenem, vancomycin with voriconazole and amphotericin B were started. In developing countries like India, upper lobe consolidation with clinical spectrum of chronic meningitis in immunocompromised individuals like HIV, tuberculosis remains one of the important differential diagnoses. Hence, antitubercular therapy was continued in his case due to high index of suspicion, which was already started 2 weeks before his presenting to us, pending reports of sputum and blood culture. Despite the above therapy for 4 days of hospitalization, there was no major improvement in his condition. Due to financial and social reasons, patient took discharge against medical advice 4 days after hospitalization. Due to our keen interest in the condition of the patient as well as the atypical MRI brain and CSF findings, we continued with our efforts to find the cause of his condition by serial observing his blood and CSF cultures. After 10 days, his CSF culture showed growth of A. niger. We got aware of his death on following up later with the family.