Neurognathostomiasis, a Neglected Parasitosis of the Central Nervous System

Gnathostomiasis is a foodborne zoonotic helminthic infection caused by the third-stage larvae of Gnathostoma spp. nematodes. The most severe manifestation involves infection of the central nervous system, neurognathostomiasis. Although gnathostomiasis is endemic to Asia and Latin America, almost all neurognathostomiasis cases are reported from Thailand. Despite high rates of illness and death, neurognathostomiasis has received less attention than the more common cutaneous form of gnathostomiasis, possibly because of the apparent geographic confinement of the neurologic infection to 1 country. Recently, however, the disease has been reported in returned travelers in Europe. We reviewed the English-language literature on neurognathostomiasis and analyzed epidemiology and geographic distribution, mode of central nervous system invasion, pathophysiology, clinical features, neuroimaging data, and treatment options. On the basis of epidemiologic data, clinical signs, neuroimaging, and laboratory findings, we propose diagnostic criteria for neurognathostomiasis

Continuous positive airway pressure therapy converted atrial fibrillation in a patient with obstructive sleep apnea

AbstractBackgroundObstructive sleep apnea (OSA) is one of the possible causes of atrial fibrillation (AF). Continuous positive airway pressure (CPAP) therapy may lower the recurrence rate of AF after cardioversion to normal sinus rhythm. We report a case of AF caused by OSA and successfully converted by CPAP therapy.CaseA 65-year-old man presented with AF of unidentified causes. After severe OSA was diagnosed, he was treated with CPAP for 2 months and his cardiac rhythm returned to sinus rhythm without any antiarrhythmic drugs or cardioversion.ConclusionAF caused by OSA may be converted to sinus rhythm by CPAP treatment

Additional risk factors associated with symptomatic hydrochlorothiazide-induced hyponatremia in hypertensive patients

Background. Hydrochlorothiazide is a cheap and effective antihypertensive agent but may cause hyponatremia. Even though several risk factors for hydrochlorothiazide-induced hyponatremia have been reported, this study aimed to evaluate additional risk factors for hydrochlorothiazide-induced hyponatremia in hypertensive patients. Material and methods. The inclusion criteria were: adult patients, diagnosed with hypertension and receiving hydrochlorothiazide treatment. Eligible patients were divided into two groups: with and without hyponatremia. Those with hyponatremia were identified by using the ICD-10 code E871, while those without hyponatremia were patients who did not have any reported hyponatremia until the last visit. The ratio between hyponatremia and non-hyponatremia group was 1:2. Predictors for hyponatremia were analyzed by using logistic regression analysis. Results. During the study period, there were 68 patients admitted due to symptomatic hyponatremia from hydrochlorothiazide. There were four independent factors in the model predictive of occurrence of symptomatic hydrochlorothiazide-induced hyponatremia in hypertensive patients: sex, body mass index, plasma glucose, and serum albumin. Male sex, body mass index, and serum albumin were negatively associated with occurrence of symptomatic hydrochlorothiazide-induced hyponatremia in hypertensive patients with adjusted OR of 0.099, 0.683, and 0.122, respectively. The plasma glucose had adjusted OR of 1.030 [95% CI of (1.009, 1.051)]. Conclusions. Factors associated with hydrochlorothiazide-induced symptomatic hyponatremia in hypertensive patients were sex, body mass index, plasma glucose level, and serum albumin level. The latter two risk factors have never been reported as risk factors for hydrochlorothiazide-induced symptomatic hyponatremia in hypertensive patients

Human Angiostrongyliasis Outbreak in Dali, China

Angiostrongyliasis, caused by the rat lungworm Angiostrongylus cantonensis, is a potentially fatal food-borne disease. It is endemic in parts of Southeast Asia, the Pacific Islands, Australia, and the Caribbean. Outbreaks have become increasingly common in China due to the spread of efficient intermediate host snails, most notably Pomacea canaliculata. However, infections are difficult to detect since the disease has a rather long incubation period and few diagnostic clinical symptoms. Reliable diagnostic tests are not widely available. The described angiostrongyliasis epidemic in Dali, China lasted for eight months. Only 11 of a total of 33 suspected patients were clinically confirmed based on a set of diagnostic criteria. Our results demonstrate that the rapid and correct diagnosis of the index patient is crucial to adequately respond to an epidemic, and a set of standardized diagnostic procedures is needed to guide clinicians. Integrated control and management measures including health education, clinical guidelines and a hospital-based surveillance system, should be implemented in areas where snails are a popular food item

Twenty two cases of canine neural angiostronglyosis in eastern Australia (2002-2005) and a review of the literature

Cases of canine neural angiostrongylosis (NA) with cerebrospinal fluid (CSF) evaluations in the peer-reviewed literature were tabulated. All cases were from Australia. A retrospective cohort of 59 dogs was contrasted with a series of 22 new cases where NA was diagnosed by the presence of both eosinophilic pleocytosis and anti-Angiostrongylus cantonensis immunloglobulins (IgG) in CSF, determined by ELISA or Western blot. Both cohorts were drawn from south east Queensland and Sydney. The retrospective cohort comprised mostly pups presented for hind limb weakness with hyperaesthesia, a mixture of upper motor neurone (UMN) and lower motor neurone (LMN) signs in the hind limbs and urinary incontinence. Signs were attributed to larval migration through peripheral nerves, nerve roots, spinal cord and brain associated with an ascending eosinophilic meningo-encephomyelitis. The contemporary cohort consisted of a mixture of pups, young adult and mature dogs, with a wider range of signs including (i) paraparesis/proprioceptive ataxia (ii) lumbar and tail base hyperaesthesia, (iii) multi-focal central nervous system dysfunction, or (iv) focal disease with neck pain, cranial neuropathy and altered mentation. Cases were seen throughout the year, most between April and July (inclusive). There was a preponderance of large breeds. Often littermates, or multiple animals from the same kennel, were affected simultaneously or sequentially. A presumptive diagnosis was based on consistent signs, proximity to rats, ingestion/chewing of slugs or snails and eosinophilic pleocytosis. NA was diagnosed by demonstrating anti-A. cantonensis IgG in CSF. Detecting anti-A. cantonensis IgG in serum was unhelpful because many normal dogs (20/21 lb dogs; 8/22 of a hospital population) had such antibodies, often at substantial titres. Most NA cases in the contemporary series (19/22) and many pups (16/38) in the retrospective cohort were managed successfully using high doses of prednisolone and opioids. Treatment often included antibiotics administered in case protozoan encephalomyelitis or translocated bacterial meningitis was present. Supportive measures included bladder care and physiotherapy. Several dogs were left with permanent neural deficits. Dogs are an important sentinel species for NA. Human cases and numerous cases in tawny frogmouths were reported from the same regions as affected dogs over the study period