UNASSIGNED: This article describes a case of polymicrobial Arcanobacterium haemolyticum pharyngitis and sinusitis complicated by intracranial complications and reviews similar cases in the literature.
UNASSIGNED: A 21-year-old immunocompetent male presented with symptoms of sore throat, rhinorrhoea, lethargy, headache, and rash. Imaging demonstrated sinusitis, pre-septal sinusitis, peritonsillar abscess formation, subdural empyema and cerebritis. He was managed with endoscopic sinus surgery, craniotomy for evacuation of subdural empyema and antibiotics. Microbiological samples demonstrated growth of A. haemolyticum, strep. anginosus, and fusobacterium necrophorum. He subsequently developed a cerebral abscess requiring stereotactic needle drainage. After a prolonged course of antibiotics, the patient was discharge and made a good recovery.
UNASSIGNED: A. haemolyticum is an uncommon cause of non-streptococcal pharyngitis that may occur alongside other microorganisms and is rarely associated with severe intracranial complications. This organism and its antibiotic susceptibility patterns should be considered in complicated upper respiratory tract infections in immunocompetent hosts. Penicillins and macrolide antibiotics form the mainstay of therapy for A. haemolyticum.

Intravesical therapy with Bacillus Calmette-Guerin (BCG) is the mainstay treatment for high-risk non-muscle invasive bladder cancer. The side effects are usually local and mild. Systemic dissemination of BCG is rare, typically develops soon after instillation, and may present as a severe life-threatening condition. We present a case of a 49-year-old man under chronic haemodialysis who developed septic shock after the first BCG maintenance instillation for bladder carcinoma in situ (CIS). Supportive measures and empiric broad-spectrum antibiotic therapy were promptly started after sample collection for cultures. Lastly, the recurrence of fever raised the initial suspicion of BCG dissemination. The diagnosis was confirmed by the identification of the Mycobacterium tuberculosis complex in blood samples collected and anti-tuberculosis therapy was then initiated. We would like to highlight the need for early recognition of a systemic BCG infection and the importance of starting anti-tuberculosis treatment as early as possible.

Cerebral venous thrombosis (CVT) is a cerebrovascular disorder caused by complete or partial occlusion of the cerebral venous and sinus system. The etiology has been attributed to hypercoagulability and pro-thrombotic states, leading to raised intracranial pressures that often manifest as headaches and focal neurological deficits. However, the multifactorial nature of CVT can create a diagnostic conundrum for clinicians. We describe a unique case of a 16-year-old female who presented with convulsions, postictal confusion, and drowsiness followed by residual weakness of her extremities. She initially presented to the primary care center with headache, high-grade fever, and altered mental status and was empirically treated for pyogenic meningitis. The patient failed to improve with a week of antibiotics and was referred to the tertiary care center for urgent attention. On presentation, the patient developed VI and VII cranial nerve palsy. Subsequently, MRI images showed filling defects in the superior sagittal, right transverse, and sigmoid sinuses with right parietal gyral T1 hyperintensity and T2 hypo-intensity. She was diagnosed with septic CVT based on sinus venous thrombosis and venous infarction, probably secondary to meningococcal pneumonia. It can be challenging to distinguish between both conditions as their presentations overlap. Moreover, cranial nerve palsy is an infrequent manifestation of CVT, with unclear pathogenesis. We highlight the role of neuro-imaging in the early detection of CVT and bring to light the unfamiliar symptoms and a more varied clinical spectrum that may hinder the diagnosis in a limited-resource setting. Future research should be explicitly modeled to improve the diagnostic efficiency of CVT and improve outcomes in younger patient populations.

UNASSIGNED: Hyperammonemic encephalopathy caused by Ureaplasma spp. and Mycoplasma hominis infection has been reported in immunocompromised patients undergoing lung transplant, but data are scarce in patients with hematological malignancies.
UNASSIGNED: We describe the cases of 3 female patients aged 11-16 years old, developing initially mild neurologic symptoms, rapidly evolving to coma and associated with very high ammonia levels, while undergoing intensive treatment for acute leukemia (chemotherapy: 2 and hematopoietic stem cell transplant: 1). Brain imaging displayed cerebral edema and/or microbleeding. Electroencephalograms showed diffuse slowing patterns. One patient had moderate renal failure. Extensive liver and metabolic functions were all normal. Ureaplasma spp. and M. hominis were detected by PCR and specific culture in two patients, resulting in prompt initiation of combined antibiotics therapy by fluoroquinolones and macrolides. For these 2 patients, the improvement of the neurological status and ammonia levels were observed within 96 h, without any long-term sequelae. M. hominis was detected post-mortem in vagina, using 16S rRNA PCR for the third patient who died of cerebral edema.
UNASSIGNED: Hyperammonemic encephalopathy linked to Ureaplasma spp. and M. hominis is a rare complication encountered in immunocompromised patients treated for acute leukemia, which can lead to death if unrecognized. Combining our experience with the few published cases (n=4), we observed a strong trend among female patients and very high levels of ammonia, consistently uncontrolled by classical measures (ammonia-scavenging agents and/or continuous kidney replacement therapy). The reversibility of the encephalopathy without sequelae is possible with prompt diagnosis and adequate combined specific antibiotherapy. Any neurological symptoms in an immunocompromised host should lead to the measurement of ammonia levels. If increased, and in the absence of an obvious cause, it should prompt to perform a search for Ureaplasma spp. and M. hominis by PCR as well as an immediate empirical initiation of combined specific antibiotherapy.

BACKGROUND: Intravesical Bacillus Calmette-Guerin immunotherapy is known to prevent recurrence of bladder cancer, but it can cause tuberculosis infections as an adverse event.
METHODS: A 75-year-old man visited our hospital due to hematuria. The patient was diagnosed with bladder cancer and underwent transurethral resection of the bladder tumor. Postoperatively, the patient received Bacillus Calmette-Guerin immunotherapy. One year later, we performed transurethral surgery and prostate biopsy because of cystoscopic findings showing nodulous lesions in the bladder and an elevated serum prostate-specific antigen level. The patient presented with high fever and malaise since the surgery. After careful examination, the patient was diagnosed with miliary tuberculosis caused by Mycobacterium bovis. The pathology of the bladder and prostate revealed acid-fast bacilli collection by Ziehl-Neelsen staining.
CONCLUSIONS: The surgery exacerbated the local infection into a systemic infection. The risk of developing miliary tuberculosis should be considered at transurethral surgery or prostate biopsy in patients after intravesical Bacillus Calmette-Guerin immunotherapy.

Acute varicella zoster virus (VZV) infection is a common condition in children, which is considered a mild, self-limited disease with diffuse skin vesicular rash. However, disseminated VZV infection with multiple organ involvement can occur in immunocompromised patients with impaired T cell immunity including solid or hematopoietic stem cell transplant recipients, receiving immunosuppressive therapy, leukemia, lymphoma, and HIV infection. Prompt antiviral therapy is mandatory in those immunocompromised persons. A 52 year-old man receiving chronic immunosuppressive drugs for his underlying leukocytoclastic vasculitis visited emergency department for diffuse skin vesicular rash that developed 4 days after contact with varicella zoster patients at his office. Despite prompt initiation of oral antiviral agents had been prescribed, rapid progression with septic shock, lactate acidosis, and disseminated intravascular coagulopathy occurred. The patient died within 24 h of intensive care unit admission. Varicella zoster infection commonly causes severe complications in adults receiving chronic immunosuppressive therapy. Post exposure prophylaxis varicella zoster immune globulin and early parenteral antiviral agents use after acute varicella virus infection may be mandatory in immunocompromised patients.

Melioidosis, caused by the environmental saprophyte, Burkholderia pseudomallei, is an important public health problem in Southeast Asia and Northern Australia. It is being increasingly reported from other parts, including India, China, and North and South America expanding the endemic zone of the disease. We report a case of systemic melioidosis in a 58-year-old diabetic, occupationally-unexposed male patient, who presented with chronic fever, sepsis, pneumonia, pleural effusion and subcutaneous abscess, was undiagnosed for long, misidentified as Pseudomonas aeruginosa infection elsewhere, but was saved due to correct identification of the etiologic agent and timely institution of appropriate therapy at our institute. A strong clinical and microbiological suspicion for melioidosis should be considered in the differential diagnosis of acute pyrexia of unknown origin, acute respiratory distress syndrome and acute onset of sepsis, especially in the tropics.

Myroides spp., previously known as Flavobacterium odoratum, are rare clinical isolates and are often considered non-pathogenic. Natural habitat includes soil, fresh and marine waters, in foods and in sewage treatment plants. We present an unusual case of fatal pericardial effusion due to Myroides odoratus in a patient suffering from chronic kidney disease and undergoing maintenance haemodialysis. This case is presented to show the increasing incidence of rare isolates causing localized and systemic infections and due to their high intrinsic resistance to many antibiotics they can be fatal. Thus isolation of these pathogens is of great clinical importance.

Acremonium spp. cause human superficial infections including mycetoma, onychomycosis and keratitis. There are a few reports of systemic involvement in immunocompromised patients. However, isolated pulmonary infection in otherwise healthy hosts has never been reported in the literature. Herein, we report a 59 year-old diabetic man with non-resolving pneumonia due to Acremonium spp. and provide a consensus review of the published clinical cases of systemic and respiratory tract infections.

Zoonoses, especially rickettsial diseases, are rarely reported in solid organ transplant recipients. We report here a case of murine typhus in a 69-year-old liver transplant recipient, who presented with acute febrile illness 5 years post transplantation. Although receiving treatment with broad-spectrum antibiotics, he was still febrile and developed progressive dyspnea. Laboratory results showed elevated transaminases and his chest radiograph revealed bilateral interstitial infiltration. The diagnosis of murine typhus was made by a 4-fold rise in specific Rickettsia typhi antibody, using indirect immunofluorescent assay. He dramatically improved after treatment with doxycycline for 7 days. To our knowledge, this is the first case report of murine typhus in a liver transplant recipient.