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Key Points Botulinum neurotoxins (BoNTs) are produced by neurotoxigenic clostridia and are a diverse group that consists of approximately 40 different BoNT types (and various subtypes), all of which cause persistent paralysis of peripheral nerve terminals — a condition known as botulism. Recent studies have solved various structures of BoNT complexes, which has provided insights into their modes of entry into the general circulation as well as the ability of these toxins to survive for long periods of time in the ex vivo environment. The molecular basis of the specificity of BoNT binding to nerve terminals is explored, as well as the ensuing cellular events, including toxin endocytosis and the targeting and cleavage of SNARE proteins. A molecular model for the essential process of membrane translocation of the metalloprotease domain of BoNTs into the neuronal cytosol is presented. Open questions and future areas of research are outlined with respect to the development of novel therapeutic agents that are based on BoNTs. Botulinum neurotoxins, which are the most powerful known toxins, are produced by toxigenic clostridia and cause persistent paralysis of peripheral nerve terminals by blocking neurotransmitter release. In this Review, Montecucco and colleagues discuss recent structural and molecular insights into the mechanisms of toxin entry into nerve terminals, membrane translocation and neuroparalysis. Botulinum neurotoxins (BoNTs) are produced by anaerobic bacteria of the genus Clostridium and cause a persistent paralysis of peripheral nerve terminals, which is known as botulism. Neurotoxigenic clostridia belong to six phylogenetically distinct groups and produce more than 40 different BoNT types, which inactivate neurotransmitter release owing to their metalloprotease activity. In this Review, we discuss recent studies that have improved our understanding of the genetics and structure of BoNT complexes. We also describe recent insights into the mechanisms of BoNT entry into the general circulation, neuronal binding, membrane translocation and neuroparalysis.

We assessed the prevalence of Lyme neuroborreliosis in children with acute facial nerve palsy in a Lyme-endemic region and patient characteristics associated with this. All children visiting one of three participating hospitals between January 2010 and December 2016 were included in the study. Of 104 children referred to the hospital with facial nerve palsy, 43% had Lyme neuroborreliosis and 57% idiopathic facial palsy. Characteristics significantly associated with Lyme neuroborreliosis were headache (55% versus 18%), meningeal irritation (21% versus 5%), presentation in summer months (69% versus 37%), and a previous tick bite (33% versus 7%).

Enteroviruses, members of the Picornaviridae family, are ubiquitous viruses responsible for mild to severe infections in human populations around the world. In 2010 Pointe-Noire, Republic of Congo recorded an outbreak of acute flaccid paralysis (AFP) in the humans, caused by wild poliovirus type 1 (WPV1). One month later, in the Tchimpounga sanctuary near Pointe-Noire, a chimpanzee developed signs similar to AFP, with paralysis of the lower limbs. In the present work, we sought to identify the pathogen, including viral and bacterial agents, responsible for this illness. In order to identify the causative agent, we evaluated a fecal specimen by PCR and sequencing. A Human enterovirus C, specifically of the EV-C99 type was potentially responsible for the illness in this chimpanzee. To rule out other possible causative agents, we also investigated the bacteriome and the virome using next generation sequencing. The majority of bacterial reads obtained belonged to commensal bacteria (95%), and the mammalian virus reads matched mainly with viruses of the Picornaviridae family (99%), in which enteroviruses were the most abundant (99.6%). This study thus reports the first identification of a chimpanzee presenting AFP most likely caused by an enterovirus and demonstrates once again the cross-species transmission of a human pathogen to an ape.

Pyogenic spondylitis can be life-threatening for elderly patients. To discuss the characteristics of the disease in the elderly, medical records of 103 consecutive cases of pyogenic spondylitis were reviewed. Of these, 45 cases were 65 years of age or older, and these 45 cases were enrolled into further study. In this study, the proportion of elderly patients among the total number with pyogenic spondylitis was 43.7%, and this figure has increased with the passing of time as follows: 37.5% (1988–1993), 44.4% (1994–1999), and 55.5% (2000–2005). The microorganisms were isolated in 16 cases: Staphylococcus aureus in 13 cases (including methicillin-resistant Staphylococcus aureus in nine) and others in three. Twenty-five patients had associated diseases: diabetes in 18 patients and malignant tumors in seven. Thirty patients were treated conservatively, and 15 patients underwent surgery. Twenty-six patients had paralysis. All 15 patients treated surgically, and eight of the 11 patients treated conservatively showed improvement in paralysis. Bone union was achieved in all cases except one. Our results indicate that a good outcome can be expected from conservative treatment in elderly patients as well as the young.

Neurosyphilis is a rare disease that until the 2000s was almost eradicated due to population awareness of HIV and efficient treatment. Since then, the prevalence of the entity is rising due to risk-associated behaviour such as unprotected intercourse. Neurosyphilis is still a difficult entity to diagnose especially when combined with acute HIV infection which can influence the usual clinical course of disease. In rare occasions, both acute HIV and early syphilis infection can present as mono or multiple cranial nerve palsies. This case demonstrates a rare manifestation of misdiagnosed early syphilis infection combined with acute HIV infection in a 34-year-old man with prior history of unprotected sex with men.

Peracute onset of disease was reported in a 42-wk-old broiler breeder flock that was presented by error with feed containing monensin at approximately seven times the approved level for broiler chickens. Morbidity and mortality were extremely high, and the affected chickens displayed feed refusal, decreased water consumption, and severe paralysis that ranged from abnormal gait to a complete inability to move. During the first 10 days postingestion of the suspect feed, mortality in hens reached 13.7% and 70.9% in the roosters. Hen day production decreased from 67% to 3% in the same period of time. A total of 638 g/ton of monensin was detected in suspect feed samples by one laboratory and 740 g/ton in a second laboratory. Twenty-one days after removal of the suspect feed, the mortality rate returned to normal levels in both hens and roosters, albeit feed consumption and egg production remained extremely low, which prompted the company involved to eliminate the flock.

Background Leptospirosis is a worldwide zoonotic disease caused by spirochetes belonging to the genus Leptospira . This is a case report on a patient with probable leptospirosis, who developed lower motor neuron facial nerve palsy during the recovery phase of this illness. Leptospirosis is endemic in Sri Lanka and this complication has been reported earlier in other countries but not in Sri Lanka to the best of our knowledge. Case presentation A previously well 50 year old Sinhalese farmer in Sri Lanka was admitted to a tertiary care hospital with five day history of fever, headache, prostration, severe myalgia especially in the calves and yellowish discoloration of the eyes. He was febrile, icteric and had suffusion of both conjunctivae. His pulse rate and blood pressure was 98/min and 90/50 mmHg respectively. The initial laboratory examinations showed neutrophil leukocytosis and thrombocytopenia. Antibodies test for leptospirosis was done and IgM was positive. Because of this evidence the probable diagnosis of leptospirosis was made and antibiotic therapy initialed with intravenous cefotaxime 1 g 8 hrly and crystalline penicillin 2 mu 6 hrly. On the eighth day he developed chest pain associated with shortness of breath with a heart rate of 120/min. Electrocardiograpic and echocardiograpic evidence suggested myocarditis, and trponin I titer was positive. Supportive care was provided and antibiotics were continued. On the 13 th day of illness he developed lower motor type facial nerve palsy of the left side with positive Bell’s phenomenon. But rest of the neurological examination was normal. He was discharged on a step-down course of prednisolone and physiotherapy. He fully recovered from cardiac involvement before discharge but recovery from facial nerve palsy took place only six months later. Conclusion Our case emphasizes cardiac and facial nerve involvement in leptospirosis. This is the first published report in Sri Lanka of facial nerve palsy occurring in leptospirosis possibly due to immunological damage. Further literature survey revealed that this is the first case in the world with simultaneous occurrence of myocarditis and facial nerve palsy in leptospirosis. The pathogenesis of this occurrence is yet to be fully understood.

A premature infant of 25 weeks’ gestational age presented at 8 weeks after birth with otorrhoea from the left ear. Following a course of topical and systemic antibiotics, the patient deteriorated developing facial nerve paralysis and cervical lymphadenitis. Contrast-enhanced CT and MRI of the head showed a destructive process of the left temporal bone. These findings prompted the clinicians to send swabs from the purulent discharge from the ear for acid-fast bacilli stain. Furthermore, surgical exploration and debridement were undertaken. Cultures from ear discharge and biopsy—taken during surgical procedure—revealed the presence of Mycobacterium tuberculosis complex. The patient developed necrotizing otitis media, left temporal bone osteomyelitis and cervical lymphadenitis. The infant’s mother was found to have an endometrial biopsy positive for M. tuberculosis suggesting the diagnosis of congenital tuberculosis.