COVID-19 autism spectrum disorder-like transient neurocognitive clinical presentation.

The COVID-19 pandemic has impacted the general population in different ways, including the vulnerable population of children with special needs.In this case report, we will discuss the emergence of a transient, full-blown picture of autism spectrum disorder (ASD) in a child who contracted a COVID-19 infection, and his gradual improvement over the course of a few months. This broadens our perspective on the possible neurocognitive clinical presentations of COVID-19 infection.

Lymphocytic choriomeningitis virus infection following occupational ocular exposure.

A man in his mid-20s presented to the occupational health service following an ocular projection with a concentrated solution of lymphocytic choriomeningitis virus (LCMV clone-13). Subsequently, a regular clinical and biological follow-up was initiated. 7 days after exposure, the patient developed influenza-like symptoms. During the acute phase, specific RT-PCR testing of blood plasma was negative for LCMV. Symptomatic treatment was administered, and the symptoms resolved after a few days. The patient remained asymptomatic in the following weeks. Serological follow-up detected a seroconversion 6 weeks after exposure, indicating a recent infection. The occupational health service's protocol, comprising clinical monitoring and serological surveillance, facilitated the detection of seroconversion. This case underscores ocular mucosal exposure as a route of occupational LCMV transmission, which is often not considered. It served as an opportunity to review and enhance prevention measures and laboratory protocols within the biosafety level P2 facility.

Karius testing in the identification of Coxiella burnetii infective endocarditis presenting with acute ischaemic stroke.

Our case highlights an atypical presentation of Coxiella burnetii endocarditis with acute ischaemic stroke in a male patient in his 60s. The patient had undergone a congenital bicuspid aortic valve replacement with a bioprosthetic valve and an ascending aortic root graft with a pacemaker. He experienced intermittent fevers, chills and malaise over 15 months leading up to his presentation. During our diagnostic process, we used the newly developed Karius test, which detects microbial cell-free DNA in the patient's serum. The patient was treated with doxycycline and hydroxychloroquine for 24 months along with surgical removal and replacement of his aortic valve and graft. Our case underscores the utility of the Karius test and the essential role of neurology in the multidisciplinary team.

Spinal cord infarction: a rare but serious complication of pneumococcal meningoencephalitis.

Here, we report the case of a woman in her 40s who came with pyogenic meningitis and infarcts in the brain. While on treatment with antibiotics, she developed new-onset weakness involving bilateral lower limbs and one upper limb 2 weeks into the course of illness. MRI of the spine showed an infarct in the spinal cord. Spinal cord infarction as a complication of pyogenic meningitis is not well recognised unlike tuberculosis meningitis. Unlike ischaemic strokes where thrombolysis is done, for stroke related to infections, there are no definite strategies. Our patient was treated with physiotherapy, continued on antibiotics and slowly recovered over months and at 18-month follow-up, she was walking with a walker. The exact mechanism of thrombosis is not known but may be due to inflammation of the arterial wall and activation of the procoagulant cascade by infection-triggered inflammation. Spinal cord infarction can occur at any phase of the infection and may occur despite appropriate response to antibiotic treatments.

Inflammatory progressive multifocal leukoencephalopathy with human T-cell lymphotropic virus-1 coinfection.

A middle-aged man with progressive multifocal leukoencephalopathy (PML) in a human T-cell lymphotropic virus type-1 (HTLV-1) carrier on haemodialysis presented with mild dysarthria and ataxia. Brain MRI revealed asymmetric T2-hyperintense lesions in the cerebral white matter, cerebellum and brainstem. A small amount of JC virus (JCV) genome in cerebrospinal fluid was detected by PCR and cerebellar biopsy demonstrated JCV-DNA presence. Pathological findings showed demyelinating lesions and glial cells with mildly enlarged nuclei, accompanied by T-lymphocytes, neutrophils and plasma cell infiltration. The CD4+/CD8+ratio was 0.83. High-dose corticosteroid therapy was effective for inflammatory PML lesions, and the administration of mefloquine combined with mirtazapine led to favourable outcome. The encephalitis in this case is considered to have occurred secondarily to JCV infection in the presence of HTLV-1 infection. Therefore, it is crucial to investigate the presence of HTLV-1 in order to understand the aetiology of this brain inflammation.

Parvimonas micra orbital cellulitis complicated with cerebral venous thrombosis and mycotic aneurysm.

Parvimonas micra is a gram-positive anaerobic coccus typically found in the human oral cavity, upper respiratory tract and gastrointestinal system. It occasionally causes intra-abdominal abscesses, spondylodiscitis and other infections. There are very few case reports on mycotic aneurysm related to P. micra We describe a rare case of P. micra orbital cellulitis complicated with meningitis, cerebral venous thrombosis and internal carotid artery mycotic aneurysm, which was successfully treated with the combination of endovascular therapy and antibiotics. Additionally, the patient received 6 months of anticoagulation therapy for cerebral venous thrombosis.

Syndrome of inappropriate antidiuretic hormone release secondary to central nervous system coccidioidomycosis with vasculitis.

A man in his 60s presented to the clinic due to night sweats and weight loss following pneumonia. He was found to have hyponatraemia due to a syndrome of inappropriate antidiuretic hormone (SIADH). CT of the thorax was concerning for pulmonary nodules. He was ultimately diagnosed with pulmonary coccidioidomycosis (CM) and started on fluconazole 400 mg daily with improvement in symptoms. Due to the report of headaches, head MRI was conducted which suggested central nervous system (CNS) involvement. Cerebrospinal fluid analysis was consistent with CNS CM and head magnetic resonance angiography confirmed the presence of CNS vasculitis. Fluconazole dose was increased to 800 mg daily which the patient continued to tolerate and showed improvement. This report depicts a case of SIADH associated with CNS CM with vasculitis and demonstrates the importance of high clinical suspicion for SIADH secondary to CNS CM in the setting of hyponatraemia and headache.

Progressive multifocal leukoencephalopathy in systemic lupus erythematosus treated with pembrolizumab.

This case report discusses a patient with systemic lupus erythematosus (SLE) treated with low-dose azathioprine who developed progressive multifocal leukoencephalopathy (PML). PML is a rare, severe, demyelinating disease linked to John Cunningham polyomavirus (JCV) reactivation.Treated with pembrolizumab, an immune checkpoint inhibitor, the patient initially improved. However, after the fourth dose, her condition rapidly worsened resulting in treatment discontinuation and death. Similar cases highlight the complex interplay of factors in PML development in SLE patients, including immunosuppression and genetic factors. The use of pembrolizumab in PML and SLE necessitates careful consideration of potential complications.

Coinfection of cerebral toxoplasmosis and neurosyphilis as the first manifestation of AIDS.

A male in his 30s with a medical history of newly diagnosed HIV with a CD4 count of 292 cells/mm3 presented with a bilateral frontal headache and left upper and lower extremity weakness and paraesthesias. A few months prior, the patient experienced a desquamating rash on his scalp and a pruritic, papular genital rash, which both self-resolved. CT head without contrast revealed extensive vasogenic oedema involving the right basal ganglia, thalamus, temporal and occipital lobes. MRI of the brain with and without contrast revealed two enhancing masses in the right lentiform nucleus and right temporal-occipital junction with associated vasogenic oedema. Cerebrospinal fluid (CSF) studies confirmed cerebral toxoplasmosis with positive CSF Toxoplasma gondii PCR and neurosyphilis with positive serum rapid plasma reagin and CSF venereal disease research laboratory test. He was treated with trimethoprim/sulfamethoxazole and intravenous penicillin G with the resolution of his symptoms.

Dengue-associated longitudinally extensive transverse myelitis.

We diagnosed a patient with dengue fever who developed acute onset of sensorimotor quadriparesis with bladder involvement, and facial nerve involvement. Despite initial negative results in routine investigations and cerebrospinal fluid analysis, spinal MRI confirmed longitudinally extensive transverse myelitis. The aetiological workup was negative, prompting an investigation into the presence of dengue in the cerebrospinal fluid, which returned positive. This case underscores the importance of considering rare neurological complications in dengue, the value of advanced diagnostic techniques and the potential effectiveness of tailored interventions in challenging cases.

Irreversible neurological manifestations in undiagnosed disseminated gonococcal infection.

Neisseria gonorrhoeae causes a common sexually transmitted infection with manifestations ranging from asymptomatic to urethritis and pelvic inflammatory disease to disseminated infections including septic arthritis. Serious complications may arise in unrecognised or inappropriately treated infections.We report a young, healthy woman who developed fever and joint pain and was diagnosed with an inflammatory arthritis. After starting immune suppressing treatments, she experienced right wrist drop and progressive muscle atrophy, joint contractures and sensory loss. Electrodiagnostic studies showed patchy, mixed neurogenic and myopathic features. Areas of muscle oedema on extremity MRI led to a right brachioradialis biopsy, which showed only nonspecific changes. Other testing, including lumbar puncture and MRI of the brain/spine was noncontributory. Additional history revealed unprotected intercourse with a new partner prior to symptom onset. Urine gonorrhoeae PCR was positive, and right shoulder arthrocentesis confirmed septic arthritis. After intravenous antibiotic treatment with ceftriaxone, she demonstrated slow, incomplete symptomatic improvement.

Cerebellar progressive multifocal leucoencephalopathy identified by the shrimp sign.

Progressive multifocal leucoencephalopathy (PML) is a demyelinating disease caused by the John Cunningham (JC) virus, which may get reactivated under certain immunosuppressive states such as AIDS, immunomodulatory therapy and haematological malignancies. PML has been reported rarely even in immunocompetent individuals where no immunodeficiency was present. PML characteristically involves periventricular and juxtacortical white matter. Isolated cerebellar or brainstem PML may be seen rarely. We present a case of a man in his 70s who presented with rapidly progressive cerebellar ataxia, ptosis and bipyramidal signs. Investigations excluded a direct viral cerebellar infection, acute disseminated encephalomyelitis, paraneoplastic cerebellar degeneration or any structural cerebellar lesion. MRI PET study revealed the classical shrimp sign which raised the possibility of cerebellar PML, and the same was confirmed by a positive JC virus PCR in the cerebrospinal fluid. Our patient had no known immune-compromising state, but further workup revealed a low CD4 count suggestive of idiopathic CD4 lymphopenia. The case illustrates the importance of the shrimp sign on MRI, the possibility of cerebellar involvement of PML as well as the need to consider a differential diagnosis of PML even in individuals with no obvious immunocompromised state.

Case of cervicodorsal tuberculosis involving seven contiguous vertebrae in a young child.

We present a rare case of a male child in middle childhood who presented to the emergency department with neck pain, neck deformity, low-grade fever, breathing difficulty and swallowing difficulty. The patient had a significant history of weight loss and loss of appetite. On examination, neurological deficits were observed, including mildly increased tone in bilateral lower limbs, reduced power in both lower limbs, exaggerated knee and ankle jerks, and upgoing plantar reflexes. Radiographs and MRI revealed a kyphotic deformity with apex at the T1 vertebra, lytic lesions in seven contiguous vertebrae and a large prevertebral abscess extending from C2 to T5. The patient underwent a posterior-only surgical approach with decompression, abscess drainage and stabilisation, resulting in successful cord decompression and correction of the kyphotic deformity. At 18 months follow-up, the patient is doing well with improvement to normal neurology and full return of a child to normal activities.

Granulomatous amoebic encephalitis due to Acanthamoeba spp complicating multidrug-resistant tuberculous meningitis in an immunocompetent individual.

Granulomatous amoebic encephalitis due to Acanthamoeba spp is a rare, near-fatal central nervous system infection. It is often seen in immunocompromised individuals. Here we describe a survivor of this infection who was co-infected with multidrug-resistant tuberculosis. He presented to us with features of meningitis and a history of chronic cough. The chest X-ray was classical for pulmonary tuberculosis. Neuroimaging was suggestive of encephalitis; herpes simplex virus PCR was negative. Cerebrospinal fluid (CSF) showed lymphocytic pleocytosis. Wet mounts revealed trophozoites of Acanthamoeba Currently, he is being treated with oral bedaquiline, levofloxacin, linezolid, clofazimine, cycloserine and pyridoxine for tuberculosis. He received intravenous amikacin and oral cotrimoxazole and fluconazole for Acanthamoeba infection for 1 month. The resolution was confirmed by repeating the CSF wet mount, culture and neuroimaging. He was then discharged with oral rifampicin, cotrimoxazole and fluconazole. He is currently under our close follow-up.

Refractory singultus and area postrema syndrome as a presentation of neurocysticercosis.

Neurocysticercosis (NCC) is the most common parasitic infection of the central nervous system, caused by the pork tapeworm, Taenia solium Common presenting features are seizures, headaches and focal neurodeficits. The present report details the anecdote of a middle-aged Asian man, who presented with subacute onset of persistent nausea, vomiting and hiccups. Following unsuccessful trials with numerous prokinetic, antipsychotic, muscle relaxant and anticonvulsant medications, as well as an uneventful battery of gastrointestinal tests, he was referred for neurological evaluation. The constellation of symptoms was congruent with the diagnosis of area postrema syndrome. Although initial CT scan of brain was normal, MRI with contrast evaluation revealed a circumscribed, ring-enhancing lesion of the dorsal medulla oblongata, reminiscent of colloid vesicular stage of NCC. The patient was successfully treated with steroids and albendazole. The association of refractory singultus, nausea and vomiting and NCC is thus far, not reported in the literature.

Recovery from acute haemorrhagic leucoencephalitis secondary to COVID-19.

A man in his 50s presented with sudden onset expressive aphasia and right-sided facial droop after experiencing coryzal symptoms and malaise for 7 days prior to admission. A brain MRI showed a rapidly progressive mass effect across both hemispheres and cerebrospinal fluid analysis revealed neutrophil predominance with raised protein levels. Acute disseminated encephalomyelitis was provisionally diagnosed, and high-dose methylprednisone was initiated.On admission to the high dependency unit, the patient tested positive for COVID-19 and was treated with appropriate therapeutic agents for severe COVID-19. A subsequent brain biopsy confirmed a demyelinating process, strongly indicating a diagnosis of acute haemorrhagic leucoencephalitis when correlated with the presence of severe oedema on imaging. Nine sessions of plasma exchange were provided over 18 days.At the time of writing, the patient has made an excellent recovery. We urge clinicians to consider this diagnosis and these treatment options for an otherwise devastating condition.

Neonatal herpes simplex virus encephalitis with intracranial bleeding in a newborn baby with concurrent rhesus incompatibility.

We report a baby with neonatal herpes simplex virus (HSV) encephalitis concurrent with Rrhesus (Rh) incompatibility. He was delivered by a Ggravida 2 mother with a history of miscarriage in her previous pregnancy at a gestation age of 4 months. She had Bblood group 0 and Rrhesus negative. The baby was noticed to have jaundice on day one1 of life accompanied by generalised petechiae on the face and upper chest. A full blood picture revealed severe anaemia and severe thrombocytopaenia and HSV 1/2 IgM was positive. MRI of the brain showed multiple extensive haemorrhagic lesions on the frontal-temporal regions.

Disseminated nocardiosis with persistent neurological disease.

A man in his 80s with a history of sarcoidosis on chronic prednisone presented to the emergency department with several days of dyspnoea. A chest X-ray showed signs of pneumonia, and the patient was admitted. Blood and pleural fluid cultures grew Nocardia farcinica; therefore, the patient was started on treatment with trimethoprim-sulbactam and imipenem. Brain imaging showed evidence of dissemination of the infection to the central nervous system (CNS). The patient's admission was complicated by pleural effusions, acute kidney injury and pancytopenia, and therefore, his antibiotic regimen was ultimately transitioned from trimethoprim-sulfamethoxazole (TMP-SMX), meropenem and linezolid to imipenem and tedizolid. The patient received imipenem and tedizolid for the remainder of the admission. A repeat MRI of the brain was performed after 6 weeks of this dual antibiotic therapy, which unfortunately revealed persistent CNS disease. His regimen was then broadened to TMP-SMX, linezolid and imipenem. Despite these measures, however, the patient ultimately passed away from the infection.

Isolated cerebral Mucormycosis and Aspergillosis coinfection in an immunocompromised adult.

Opportunistic fungal infections are a major cause of mortality in immunosuppressed patients, with mucormycosis and aspergillosis as two of the most commonly identified fungal organisms. Coinfection with mucormycosis and aspergillosis is rare, but cases have been reported in literature, most commonly presenting as disseminated invasive fungal infection with cerebrorhino-orbital involvement in an immunocompromised patient. Infections are most commonly caused by direct implantation of spores with localised angioinvasion. Haematogenous spread is rare, with most cases secondary to haematological malignancies or intravenous drug use. Coinfection with mucormycosis and aspergillosis portends a poor prognosis, with a high mortality rate. Thus, prompt recognition and intervention are crucial to prevent poor outcomes. In this unique case report, we describe a case of isolated cerebral mucormycosis and aspergillosis coinfection, not previously reported in literature.

Rhinocladiella mackenziei cerebral phaeohyphomycosis with a definitive outcome.

A right-handed man in his early 60s with hypertension controlled by a single prescription medication presented with left-sided heaviness and intermittent right occipital headache. Initial diagnostic workup was unremarkable. CT revealed an enhancing lesion located in the right parietal lobe, with mild mass effect on the right occipital horn, indicative of a brain abscess. The patient was initially treated with a course of empirical antibiotics, including ceftriaxone, vancomycin, metronidazole and dexamethasone. The neurosurgery team aspirated the abscess the following day and extracted yellow pus that was sampled for bacterial and fungal cultures. These cultures returned positive for Rhinocladiella mackenziei, prompting a discontinuation of the empirical antibiotics and initiation of intravenous liposomal amphotericin B for 4 weeks. Intravenous posaconazole was added to the patient's existing therapy regimen, which was substituted with oral isavuconazole on discharge. The patient continues to take isavuconazole, and follow-up imaging has demonstrated regression of the abscess.