Matrix metalloproteinases-2 and -9 in Campylobacter jejuni-induced paralytic neuropathy resembling Guillain-Barré syndrome in chickens.

Inflammation in Guillain-Barré syndrome (GBS) is manifested by changes in matrix metalloproteinase (MMP) and pro-inflammatory cytokine expression. We investigated the expression of MMP-2, -9 and TNF-α and correlated it with pathological changes in sciatic nerve tissue from Campylobacter jejuni-induced chicken model for GBS. Campylobacter jejuni and placebo were fed to chickens and assessed for disease symptoms. Sciatic nerves were examined by histopathology and immunohistochemistry. Expressions of MMPs and TNF-α, were determined by real-time PCR, and activities of MMPs by zymography. Diarrhea developed in 73.3% chickens after infection and 60.0% of them developed GBS like neuropathy. Pathology in sciatic nerves showed perinodal and/or patchy demyelination, perivascular focal lymphocytic infiltration and myelin swelling on 10th- 20th post infection day (PID). MMP-2, -9 and TNF-α were up-regulated in progressive phase of the disease. Enhanced MMP-2, -9 and TNF-α production in progressive phase correlated with sciatic nerve pathology in C. jejuni-induced GBS chicken model.

Pathogenesis of Enterococcal Spondylitis Caused by Enterococcus cecorum in Broiler Chickens.

Enterococcal spondylitis (ES) is a disease of commercial broiler chickens, with a worldwide distribution. Symmetrical hind limb paralysis typical of ES results from infection of the free thoracic vertebra (FTV) by pathogenic strains of Enterococcus cecorum . To determine the pathogenesis of ES, birds with natural and experimental ES were studied over time. In natural disease, case birds (n = 150) from an affected farm and control birds (n = 100) from an unaffected farm were evaluated at weeks 1-6. In control birds, intestinal colonization by E. cecorum began at week 3. In case birds, E. cecorum was detected in intestine and spleen at week 1, followed by infection of the FTV beginning at week 3. E. cecorum isolates recovered from intestine, spleen, and FTV of case birds had matching genotypes, confirming that intestinal colonization with pathogenic strains precedes bacteremia and infection of the FTV. Clinical intestinal disease was not required for E. cecorum bacteremia. In 1- to 3-week-old case birds, pathogenic E. cecorum was observed within osteochondrosis dissecans (OCD) lesions in the FTV. To determine whether OCD of the FTV was a risk factor for ES, 214 birds were orally infected with E. cecorum, and the FTV was evaluated histologically at weeks 1-7. Birds without cartilage clefts of OCD in the FTV did not develop ES; while birds with OCD scores ≥3 were susceptible to lesion development. These findings suggest that intestinal colonization, bacteremia, and OCD of the FTV in early life are crucial to the pathogenesis of ES.

Neurologic Melioidosis: Case Report of a Rare Cause of Acute Flaccid Paralysis.

Acute flaccid paralysis is associated with inflammation, infection, or tumors in the spinal cord or peripheral nerves. Melioidosis (Burkholderia pseudomallei infection) can rarely cause this presentation. We describe a case of spinal melioidosis in a 4-year-old boy presenting with flaccid paralysis, and review the literature on this rare disease.

Persistence of Botulinum neurotoxin inactivation of nerve function.

The extraordinary persistence of intoxication occurring after exposure to some Botulinum neurotoxin (BoNT) serotypes is both a therapeutic marvel and a biodefense nightmare. Understanding the mechanisms underlying BoNT persistence will offer new strategies for improving the efficacy and extending the applications of BoNT therapeutic agents as well as for treating the symptoms of botulism. Research indicates that the persistence of BoNT intoxication can be influenced both by the ability of the toxin protease or its cleaved soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein substrate to resist turnover. Protease turnover seems to be mediated in part by the ubiquitin-proteasome system (UPS) and efforts to manipulate the UPS may prove to be an effective strategy for improving therapeutic utility of BoNT products and in the development of botulism antidotes.

A very unusual organism causing stroke-like symptoms.

A 78-year-old man presented to hospital with new onset confusion and fever. The working diagnosis was of delirium due to an infection of unknown source, and empirical i.v. antibiotic treatment was given. Two days later, he deteriorated and developed clinical features in keeping with a total anterior circulation stroke. Brain imaging was unremarkable. Blood cultures grew an organism subsequently identified as Facklamia languida. Following treatment with broad-spectrum antibiotics, his condition improved. A diagnosis of F. languida septicaemia, leading to presumed (unwitnessed) seizure and Todd's paresis was made. The patient went on to make a full recovery and was discharged home. Stroke mimics are common and may be eminently treatable. Around a quarter of patients initially suspected to have a stroke are subsequently found to have an alternative diagnosis.

A 59-year-old man with acute onset of paralysis.

Botulism is a neuroparalytic illness resulting from the action of a potent toxin produced by the organism Clostridium botulinum. It can present with a classic triad of clear mentation, bulbar palsy and symmetric descending paralysis. Treatment is symptomatic and includes a botulinum antitoxin.

Acute monensin toxicosis in broiler breeder chickens.

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.

Pyogenic spondylitis in the elderly: a report from Japan with the most aging society.

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.

Cryptococcal meningitis presenting as acute flaccid paralysis: A case report.

Cryptococcus is a cosmopolitan fungus with tropism for the nervous system and a higher prevalence of infection in immunosuppressed patients. Neurological compromise caused by this microorganism mainly debuts as a meningeal syndrome (headache, fever, neck stiffness) with predominant encephalic involvement. In this report we present the rare case of a non-HIV patient with flaccid paralysis and peripheral nerve involvement due to crytpococcal meningitis. This is a 53-years-old woman, with a past-medical history of diabetes, who presented with dysarthria, unilateral peripheral facial paralysis, asymmetric ascending quadriparesis, generalized hyporeflexia and urinary retention. Neuroimaging was initially reported as negative for vascular or demyelinating diseases. Electrophysiological studies were performed, and acute flaccid paralysis of undetermined etiology was defined as a temporal clinical diagnosis. Cerebrospinal fluid molecular analysis confirmed the presence of Cryptococcus neoformans var. gatti; posteriorly, antifungal treatment with amphotericin B and fluconazole was started. Polyneuroradiculopathy symptoms significantly improved over the in-hospital stay. In conclusion, spinal cord and peripheral nerve involvement by Cryptococcus is an infrequent cause of acute flaccid paralysis that should be considered in the differential diagnosis even in HIV-negative patients.

Herpes zoster complicated by phrenic nerve palsy and respiratory compromise.

BACKGROUND: Herpes zoster can be associated with severe neurological complications. CASE PRESENTATION: In this article, we describe the case of a 54-year-old man with herpes zoster affecting his right upper chest and neck region complicated by phrenic nerve palsy and respiratory compromise. The diagnosis of herpes zoster was made based on the classic appearance of the rash and associated neuropathic-type pain. The diagnosis of phrenic nerve palsy was made by chest x-ray and ultrasound. CONCLUSION: Clinicians should be aware of the possibility of phrenic nerve palsy occurring in patients who have herpes zoster affecting the region of C3,4,5 dermatomes. Although symptoms of unilateral diaphragmatic paresis are usually mild, in patients with obesity or comorbid lung disease, new onset phrenic nerve palsy can lead to significant respiratory compromise.

Flaccid paralysis in an infant associated with a dirty wound and application of honey.

An infant, who was born preterm at 36 weeks, presented with fever and ulcer at umbilical region which progressed to necrotising fasciitis of anterior abdominal wall. He was treated with intravenous penicillin, intravenous cloxacillin and local application of medicated honey. Subsequently, he required wound debridement. Postoperatively, he required prolonged invasive ventilation due to poor respiratory effort which was associated with hypotonia and areflexia. Nerve conduction study revealed absent responses. The diagnosis of infant botulism was made based on the clinical presentation, nerve conduction study and his clinical progress. Botulinum immunoglobulin was not available. He was treated with intravenous immunoglobulin and oral pyridostigmine. He was successfully extubated after 37 days, and currently the patient is doing well.

Phaeohyphomycosis in a snow leopard (Uncia uncia) due to Cladophialophora bantiana.

Phaeohyphomycosis caused by Cladophialophora bantiana was diagnosed in a 5-month-old snow leopard with spastic paralysis of the hind legs and inability to defaecate or urinate. At post-mortem examination, a greenish soft mass resembling an abscess was found on one side of the epidural space at the fourth lumbar vertebral body. Histological examination revealed a purulent meningitis with myelomalacia. Dematiaceous fungal hyphae, present within the inflammatory infiltrate, were identified as C. bantiana by culture and sequence analysis of the 18S ribosomal RNA gene. This neurotropic fungus rarely affects organs other than the brain in human beings and cats, and has been reported only occasionally in Europe. The case described suggests that phaeohyphomycosis due to C. bantiana infection may be recognized more frequently in the future and the possible involvement of organs other than the brain should be borne in mind.

Lower limb paralysis induced in mice by a temperature-sensitive mutant of Moloney leukemia virus.

A temperature-sensitive mutant of Moloney murine leukemia virus defective in an early function and injected into newborn mice produced lower limb paralysis. Susceptible mice were inbred strains CFW/D, CBA/H, C3H/Bi/Ka, and outbred NIH Swiss stock. Inbred W/Fu rats and C57BL/Ka mice did not develop the paralysis, though the latter were infected with virus; the sera from these mice produced paralysis in susceptible CFW mice.

Botulism with Unusual Rapid Progression to Complete Paralysis in a Child.

Botulism is a severe neuroparalytic illness which is difficult to diagnose accurately, especially in children. We report a child with type A botulism intoxication, with very rapid progression to coma-like consciousness and respiratory failure. Careful physical examinations led to the suspicion of botulism, and electrophysiologic examinations, including electroencephalogram and repetitive nerve stimulation tests, further supported the diagnosis. Hospitalization due to botulism had a great emotional impact on the patient and psychological support was crucial.

First Detection of an Enterovirus C99 in a Captive Chimpanzee with Acute Flaccid Paralysis, from the Tchimpounga Chimpanzee Rehabilitation Center, Republic of Congo.

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.

Pathogenesis of paralysis and lymphoma associated with a wild mouse retrovirus infection. Part 1. Age- and dose-related effects in susceptible laboratory mice.

Wild mouse ecotropic retrovirus (Cas-Br-M) induced paralysis and non-thymic lymphomas in susceptible NIH Swiss and NFS/N mice. The incidence of paralysis was highest and latency shortest in mice receiving high doses of virus. Lower dose inoculation and inoculation of older mice produced less paralysis with longer latency, but resulted in more lymphomas. However, 10-day-old mice did not develop paralysis and had fewer lymphomas. Anti-Cas-Br-M antibody was detectable in sera from 10-day-old infected mice but not from paralyzed mice. These data suggest that while paralysis and lymphoma may result from different virus-host interactions, the development of immunocompetence may play a role in the age-dependent resistance to Cas-Br-M-associated paralysis and lymphoma in these mice.