Zaw Min

Fusarium brain abscess: case report and literature review

Severely immunocompromised patients such as those with haematological malignancies and haematopoietic stem cell transplant recipients are at an increased risk of acquiring invasive mould infections. Fusarium, a ubiquitous fungus, can cause potentially fatal infections in such hosts. It usually manifests as skin lesions, fevers and sino‐pulmonary infections. Brain abscesses have been reported, but are relatively uncommon. We report a case of a 50‐year‐old patient with acute lymphocytic leukaemia and failed autologous peripheral stem cell transplant that presented with new onset seizures and was found to have Fusarium solani brain abscess. Nasal route was the presumed mode of entry of the fungus into the cerebrum. Treatment comprised surgical excision of the lesion, and antimycotic therapy with liposomal amphotericin B and voriconazole. Despite aggressive therapy, patient succumbed to the disease. We have provided an overview of infections secondary to Fusarium, along with a review of the central nervous system involvement by this pathogenic mould.

A Mysterious Gram-Positive Rods

We encountered a patient with a history of intravenous drug use presenting with fever, malaise and nausea who was found to have cavitary lung lesions. Unexpectedly, gram positive rods grew out on day five on multiple blood cultures, which were later identified as Mycobacterium fortuitum. The patient underwent transesophageal echocardiogram, which showed aortic and tricuspid valve vegetations. Liver biopsy demonstrated granulomatous hepatitis. Interestingly, serum alkaline phosphatase level fell with antibiotic treatment. Mycobacterium fortuitum is ubiquitous worldwide, being found in tap water, and soil. M. fortuitum is usually considered as a contaminant. Disseminated infection caused by this bacterium in an immunocompetent host is extremely rare. Most of the disseminated infections have been reported in immune-deficient patients. In immunocompetent people, M. fortuitum causes human infection primarily by direct inoculation, including localized post-traumatic and surgical wound infections, and catheter-related sepsis. Our patient, an HIV-negative intravenous drug user, had Mycobacterium fortuitum sepsis associated with infective endocarditis, septic pulmonary emboli, and granulomatous hepatitis. Interestingly, the patient admitted using tap water occasionally for mixing heroin when her sterile water ran out, which we thought was the likely source of M. fortuitum.

A gigantic anogenital lesion: buschke-lowenstein tumor.

Buschke-Lowenstein tumor is a relatively rare sexually transmitted disease. It is a neoplasm of the anogenital region which has benign appearance on histopathology but is locally destructive. It carries a high recurrence rate and a significant potential for malignant transformation. Human papilloma virus has been implicated as an etiologic agent for this tumor. Since this disease is rare and no controlled studies exist, radical excision of this anogenital lesion is generally recommended as the first line therapy and close vigilance and followup are essential. We have discussed an overview of etiopathogenesis, clinical presentation, diagnosis, and management of this uncommonly encountered disease.

A forgotten complication of a defunctionalized urinary bladder: pyocystis

A 74-year-old woman presented to the hospital with fever, nausea, lethargy, and abdominal pain. Her past medical history was significant for end-stage renal disease, resulting from bilateral nephro-ureterectomy for chronic pyelonephritis secondary to chronic reflux nephropathy. She was febrile with temperature of 38.3 C, and physical examination showed tense suprapubic tenderness without involuntary guarding. The laboratory work-up demonstrated a leukocytosis (WBC 16,000/mm, normal 4,000–11,000/ mm). Blood cultures were negative. Computed tomography (CT scan) of the abdomen and pelvis was performed because of the persistent suprapubic pain, and it showed a thickened bladder wall with a small-sized urinary bladder (Fig. 1a, b). A straight urinary catheter was cautiously inserted, and purulent fluid was drained out. A presumptive diagnosis of pyocystis was entertained. A flexible cystoscopy was subsequently performed. Purulent fluid and tissue debris were noted within the bladder, and were aggressively irrigated out. Suprapubic and Foley urinary catheters were placed. Fluid culture grew Escherichia coli, Citrobacter freundii and Enterococcus faecalis. Continuous neomycin bladder irrigation was applied via the suprapubic catheter, and then drained through the Foley catheter. Systemic intravenous piperacillin-tazobactam 2.25 g every 12 h was administered simultaneously. She received 4 weeks of antimicrobial therapy, via both intravenous and intravesical routes, to control the infection. The patient was eventually discharged without additional antibiotics. Pyocystis, also known as vesical empyema, is the accumulation of pus in the urinary bladder, especially a defunctionalized bladder in patients with end-stage kidney disease, supravesical urinary diversion without radical cystectomy or bladder irradiation [1]. Pyocystis syndrome gained attention in the 1960s after urinary diversion procedures became the standard treatment for a variety of lower urinary tract pathologies. The reported incidence of this complication ranged from 10 % to as high as 67 % in patients with supravesical urinary diversion procedures [2, 3]. It is reported to be rare in dialysis patients, but its actual incidence in that patient population is not known [3, 4]. There are many postulated mechanisms of pathogenesis of pyocystis. The widely accepted one is the collection, liquefaction and decomposition of shed bladder epithelium. As part of wear and tear, the lining bladder epithelium is shed continuously, and then expelled out by urine flow. In anuric patients, the shed epithelial cells accumulate, and, when infected, pyocystis is typically ensued [1–4]. The presenting symptoms are usually similar to those in patients presenting with a lower urinary tract infection, including fever, suprapubic pain, purulent urethral discharge or sepsis. Microbiologically, the causal microorganisms are routine urinary pathogens, such as E. coli, Proteus spp., Serratia spp. and Enterococcus spp. [2, 3]. Diagnosis is based on symptoms of lower urinary tract infection, purulent discharge via the urethra or during catheterization, supported by CT scan imaging studies showing a characteristic thickened, hypertrophied, and cystic appearance of the bladder wall (Fig. 1a, b) [3, 4]. Despite the familiar clinical presentation of urinary tract infection, the diagnosis is usually delayed or missed, as it is mistakenly assumed that urinary bladder infection does not develop in anuric patients. Its treatment is unique, and routinely requires combined systemic and intravesical Z. Min (&) Department of Medicine, Division of Infectious Diseases, Allegheny General Hospital, Allegheny Health Network, 420 East North Avenue, East Wing, Suite 407, Pittsburgh, PA 15212, USA e-mail: zmin@wpahs.org

Reversible posterior leukoencephalopathy syndrome

A 40-year-old woman presented with headache, lethargy,dysarthria, diplopia and altered mental status. Her pastmedical history was significant for cystic fibrosis for whichshe underwent bilateral lung transplantation 3 years priorto admission. Her medications included tacrolimus andprednisone. On physical examination, she was afebrile andnormotensive without neck stiffness; she was intubated andon mechanical ventilation. Her MRI brain with intravenousgadolinium showed symmetric hyperdense signals withinthe white matter involving parietal (Fig. 1a), occipital(Fig. 1b) and cerebellar regions (Fig. 1c), without intrace-rebral space-occupying lesions. Cerebrospinal fluid (CSF)studies revealed clear and colorless fluid with normalopening pressure, cell counts, glucose and protein. Evalu-ation for infections, including routine blood cultures, CSFGram’s stain and cultures, VDRL, cryptococcal antigen,cytomegalovirus (CMV) polymerase chain reaction (PCR)assay, Epstein–Barr virus (EBV) PCR, human herpes virus-6 (HHV-6) PCR and JC virus PCR, was, however, unre-vealing. Serum tacrolimus drug level was 5 ng/ml (normal5–20 ng/ml). The clinical diagnosis of tacrolimus-associ-ated reversible posterior leukoencephalopathy syndrome(RPLS) was entertained given the negative infectious dis-eases workup. Tacrolimus was cautiously tapered off overa week, and her neurological condition slowly improved.Repeat MRI brain imaging a week after complete discon-tinuation of the tacrolimus showed the resolution of thehyperintense lesions (Fig. 1d, e).RPLS, also known as posterior reversible encephalopa-thy syndrome (PRES), is a clinical syndrome of varyingetiologies, but with similar neuroimaging findings. Char-acteristic clinical manifestations include non-localizedheadache unresponsive to analgesics, altered mental status,visual disturbances and seizures [1, 2]. RPLS is frequentlyassociated with acute hypertension, preeclampsia oreclampsia, sepsis, renal failure, thrombotic thrombocyto-penic purpura, hypercalcemia, hypomagnesium, autoim-mune diseases, cytotoxic therapies andimmunosuppressants [2]. Because of widespread use ofcalcineurin inhibitors (cyclosporine and tacrolimus) inpatients with solid organ transplantation (SOT) to preventorgan rejection, neurotoxicity of these agents has beenincreasingly reported, although the incidence of RPLSamong patients with SOT is low (0.5 %) [3]. The under-lying pathophysiology of RPL is poorly defined. Hypoth-eses include cerebral ischemia from vasospasm, disorderedcerebral autoregulation and endothelial dysfunction [1, 2].RPLS associated with calcineurin is thought to result fromdirect toxic injury to vascular endothelium, leading toproduction of inflammatory cytokines and capillary leak-age, which triggers vasogenic cerebral edema [1, 3, 4].Hypertension and high serum tacrolimus level are com-monly associated with RPLS but there are reported RPLScases with normal blood pressure and normal serum ta-crolimus drug concentrations [5]. Brain MRI, particularlyfluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI) sequences, is the imagingmodality of choice of diagnosing RPLS. Typical MRIfindings are symmetrical white matter changes primarily

Clinical evolution, management, and resolution of type II necrotizing fasciitis

A 60-year-old woman with a history of pre-diabetes and hyperlipidemia, presented to a local hospital with severe left flank pain and skin discoloration on the same area for 2 days. She had been taking care of her grandson who was diagnosed with streptococcal sore throat. On examination, the patient was hypotensive and tachycardic. There was a large grayish blue area over the left flank, extending to the left lower back (Fig. 1a, b). This area was very tender to palpation. There were no bullae, crepitus, or external drainage. A CT scan of the abdomen revealed a diffuse inflammatory process within the skin and soft tissue without any gas in the adjacent area. A diagnosis of necrotizing fasciitis was pursued. Broad-spectrum intravenous antibiotics (vancomycin, piperacillin–tazobactam, and clindamycin), and vasopressors were initiated, and she was transferred to our institution for further management. Upon arrival, she was immediately taken to the operating room for surgery. The operative findings showed there were extensive soft tissue necrosis and edematous fascial layers. A full-thickness debridement of skin and subcutaneous tissue of the left flank (24 cm 9 21 cm 9 1.5 cm) was performed (Fig. 1c). The tissue culture was positive for group A b-hemolytic Streptococcus (Streptococcus pyogenes). The pathogen was sensitive to penicillin (minimal inhibitory concentration, MIC 0.032 mg/L), ceftriaxone (MIC 0.064 mg/L), vancomycin (MIC 1.0 mg/L), and clindamycin (MIC not reported). Blood cultures were negative throughout the admission. Antibiotics were tailored to intravenous penicillin and clindamycin. Despite appropriate antimicrobial therapy, on day 3 of hospitalization, there were new areas of purplish red discoloration changes noted around the edge of the wound (Fig. 1d). She underwent additional debridement of skin and subcutaneous tissues (Fig. 1e). A day later (day 4 of hospitalization), it was again noted that the infection was extending upward to the left axilla at which point further debridement was undertaken (Fig. 1f). On day 6 of admission, extension of bluish gray skin changes occurred medially towards the suprapubic region (Fig. 1g), requiring an additional large area (20 cm 9 11 cm 9 2 cm) of surgical debridement (Fig. 1h). The negative pressure wound therapy devices were applied to the wounds, and the wound dressings were regularly changed under anesthesia. Vasopressors were successfully weaned off, and she continued to improve. On day 20 of hospitalization, the patient was eventually discharged home with negative pressure wound therapy. Approximately 2 months after the initial hospitalization, the abdominal and axillary wounds were found to be sufficiently granulated (Fig. 1i). She underwent definitive wound closure with split-thickness skin grafts harvested from the left thigh. One month post-skin graft follow-up (day 84 from the first hospitalization), skin grafts were taken very well without further complications (Fig. 1j). J. Makadia and Z. Min equally contributed to this manuscript.

Propionibacterium acnes : Time-to-Positivity in Standard Bacterial Culture From Different Anatomical Sites

Background Propionibacterium acnes infections are likely under-recognized and underreported. This is partly because of low clinical suspicion, perceived non-pathogenicity, or lack of adequate culture incubation time. We conducted a study to assess the optimal incubation period to recover P. acnes from specimens acquired during the workup of suspected clinical infections. Methods A 5-year retrospective chart review was conducted between January 2010 and December 2014 at a single tertiary-care hospital. All patient cases from which P. acnes was recovered were included for analysis. Source of infection, antibiotic use, and culture time-to-positivity (TTP) were recorded. Results Implanted devices comprised the single most common source of P. acnes infection. In the majority of cases, P. acnes was the only organism identified. The mean incubation TTP for all isolates was 5.73 days. Conclusions Standard 5-day culture incubation periods are insufficient to recover P. acnes. As a result, P. acnes is likely a much more common etiology of a variety of clinical infections than previously reported.

Mollaret's meningitis.

A 48-year-old man presented with a 2 day history of fever, headache, chills, neck stiff ness, and nausea and vomiting. He had a history of two episodes of viral meningitis, which occurred 30 and 13 years before this presentation. An examination confi rmed meningism without focal neurological defi cits. Results of CSF tests showed protein concentration of 120 mg/dL (normal 12–60 mg/dL), normal glucose concentration, red blood cells 26 cells/μL, and white blood cells 327 cells/μL (10% neutrophils, 84% lymphocytes, 6% monocytes). CSF Gram stain and cultures were negative. Diff -Quik stain of CSF showed many large activated monocytes with several deep nuclear clefts visible as so-called cloverleaf nucleus (green arrowhead, fi gure A), footprintshaped nucleus (white arrowhead, fi gure B), and beanshaped nucleus (green arrow, fi gure C), with a background of normal monocytes (black arrowheads, fi gure A, B) and lymphocytes (black arrows, fi gure A, B). The features of these activated monocytes were compatible with those of Mollaret’s cells, and CSF herpes simplex virus type 2 (HSV2) PCR assay was positive. Large degenerated monocytes were present as ghost cells (asterisks, fi gure B), observed in the slide background. A diagnosis of Mollaret’s meningitis was made. The patient was discharged without antimicrobial therapy and recovered completely. Mollaret’s meningitis was fi rst described by the French neurologist Pierre Mollaret in 1944. The disease is characterised by recurrent (at least three episodes), benign (no long-term sequelae) and brief (2–5 day) episodes of aseptic lymphocytic meningitis, alternating with symptom-free interval, mostly caused by HSV2 infection. The disease is usually self-limited, and antiviral therapy is routinely not recommended. It is therefore also known as recurrent benign lymphocytic meningitis. Typically, results of CSF studies show hypercellularity and predominantly lymphocytic pleocytosis with positive HSV2 DNA by PCR assay. Cellular cytomorphological features of CSF charac teristically show diagnostic Mollaret’s cells, which are multiple activated large monocytes with deep nuclear clefts giving rise to various convoluted, eye-catching shapes of nuclei, such as cloverleaf, bean, and footprint patterns. Usually degenerated monocytes known as ghost cells are present, scattered at the background of the slide. Recognition of these cells in the CSF is crucial for a timely and accurate diagnosis because it could prevent extensive and costly diagnostic studies and antimicrobial therapies.

Adenoviral nephritis in a renal transplant recipient: Case report and literature review

Adenovirus (AdV) infections in transplant recipients may cause invasive disease. We present a case of granulomatous interstitial nephritis secondary to AdV infection in a renal transplant recipient that was initially interpreted as acute graft rejection on histopathology. Specific testing based on clinical suspicion, however, aided in making an accurate diagnosis. We present a retrospective review of all cases of AdV infection in renal transplant recipients to date, and analyze outcomes based on different treatment modalities for this disease.

Early-onset de novo invasive pulmonary aspergillosis in an orthotopic heart transplant recipient

Invasive aspergillosis generally occurs during the first 1–6 months after heart transplantation. It has been rarely seen in the first 2 weeks postcardiac transplant. We herein describe a unique case of invasive pulmonary aspergillosis (IPA) diagnosed on day 9 postorthotopic heart transplantation. The known risk factors for IPA in cardiac transplant recipients were not identified in our case. The organ recipients from the same donor did not report Aspergillus infection. Hospital environmental samplings failed to demonstrate Aspergillus spores in the patients room and his adjacent rooms. A diagnosis of early-onset de novo IPA was made. The patient initially received combined antifungal therapy (voriconazole plus micafungin), followed by voriconazole maintenance monotherapy with favorable clinical outcome.