Factors related to Campylobacter spp. carriage in client-owned dogs visiting veterinary clinics in a region of Ontario, Canada

From July 2008 until May 2009, 240 client-owned pet dogs from seven veterinary clinics in the Region of Waterloo, Ontario, Canada participated in a study to determine pet-related management factors that may be associated with the presence of Campylobacter spp. in dogs. The prevalence of Campylobacter spp. carriage in our study population of pet dogs was 22%, with 19% of the dogs positive for C. upsaliensis, and 3% positive for C. jejuni. A significant risk factor from multivariable logistic regression models for both Campylobacter spp. and C. upsaliensis carriage was having homemade cooked food as the dog's diet or added to its diet, and a significant sparing factor for both models was treatment with antibiotics in the previous month. Increasing age of the dog decreased the odds of Campylobacter spp. and C. upsaliensis carriage. Based on the high prevalence of Campylobacter, and specifically C. upsaliensis, further research concerning pet dogs as a risk factor for campylobacteriosis in humans is warranted.     

Toxic megacolon complicating Escherichia coli O157 infection

Toxic megacolon is a well known complication in inflammatory bowel disease such as ulcerative colitis or Crohn's disease. The development of toxic megacolon as a complication of infectious colitis is rare. However it is recognised as a complication of enteric infections caused by Clostridium difficile, Campylobacter jejuni, Shigella, Salmonella species, Cytomegalovirus and amoebae. We describe a case of necrotising haemorrhagic ileo-colitis in a previously fit and healthy young adult female caused by Escherichia coli O157 where toxic megacolon developed as a complication along with hemolytic uremic syndrome (HUS).     

Cockayne syndrome in adults: review with clinical and pathologic study of a new case

Cockayne syndrome and xeroderma pigmentosum-Cockayne syndrome complex are rare autosomal recessive disorders with poorly understood biology. They are characterized by profound postnatal brain and somatic growth failure and by degeneration of multiple tissues resulting in cachexia, dementia, and premature aging. They result in premature death, usually in childhood, exceptionally in adults. This study compares the clinical course and pathology of a man with Cockayne syndrome group A who died at age 31(1/2) years with 15 adequately documented other adults with Cockayne syndrome and 5 with xeroderma pigmentosum-Cockayne syndrome complex. Slowing of head and somatic growth was apparent before age 2 years, mental retardation and slowly progressive spasticity at 4 years, ataxia and hearing loss at 9 years, visual impairment at 14 years, typical Cockayne facies at 17 years, and cachexia and dementia in his twenties, with a retained outgoing personality. He experienced several transient right and left hemipareses and two episodes of status epilepticus following falls. Neuropathology disclosed profound microencephaly, bilateral old subdural hematomas, white-matter atrophy, tigroid leukodystrophy with string vessels, oligodendrocyte proliferation, bizarre reactive astrocytes, multifocal dystrophic calcification that was most marked in the basal ganglia, advanced atherosclerosis, mixed demyelinating and axonal neuropathy, and neurogenic muscular atrophy. Cellular degeneration of the organ of Corti, spiral and vestibular ganglia, and all chambers of the eye was severe. Rarely, and for unexplained reasons, in some patients with Cockayne syndrome the course is slower than usual, resulting in survival into adulthood. The profound dwarfing, failure of brain growth, cachexia, selectivity of tissue degeneration, and poor correlation between genotypes and phenotypes are not understood. Deficient repair of DNA can increase vulnerability to oxidative stress and play a role in the premature aging, but why patients with mutations in xeroderma pigmentosum genes present with the Cockayne syndrome phenotype is still not known.     

FTIR study of the effect of nTiO2 on the biochemical constituents of gill tissues of Zebrafish (Danio rerio)

In the present study, an attempt is made to assess the changes in the biochemical contents in general, and the protein structural changes in particular, in the gill tissues of Zebrafish (Danio rerio) due to titanium nanoparticles and their bulk counterpart using FTIR spectroscopy. The FTIR spectra show that the intensity differences between the control and titanium-exposed tissues are remarkable. For example, TiO₂-exposed tissues show higher intensities at amide I and amide II of proteins, but lower at 2924 cm^?1 (CH₂ asymmetric stretching of lipids), 2853 cm^?1 (CH₂ symmetric stretching of lipids) and 1744 cm^?1 (CO stretching of phospholipids) when compared with the control tissues. This suggests that there is an increase or decrease in the percentage of a certain types of biomolecules relative to the total infrared-active constituents in the gill tissues. The curve-fitting analysis suggests an increase in α-helical structure and a decrease in β-sheet structure due to TiO₂ exposure. These results confirm that the structural conformation of proteins in fish gill tissues was significantly influenced by TiO₂ exposure. Further, the changes are more due to nTiO₂ when compared to TiO₂ bulk, suggesting that nTiO₂ are affecting the biochemical constituents more than their bulk counterpart.     

Reversal of Roux en Y gastric bypass: largest single institution experience

BackgroundThere is a paucity of literature on patients who have undergone reversal of Roux-en-Y gastric bypass (RYGB) to normal anatomy. We present the largest single institution experience with reversal of RYGB for serious chronic complications.ObjectiveTo describe our experience including indications, outcomes, and complications of RYGB reversal.SettingAcademic-affiliated private practice.MethodsRetrospective review of 48 patients who underwent laparoscopic reversal of RYGB between 2012 and 2016.ResultsNinety-six percent (n = 46) of patients were female, and the mean age was 48.6 (range, 23–72). Indications for reversal of RYGB included marginal ulcer (n = 25, 12 of whom were malnourished and 17 had coexisting substance abuse), malnutrition alone (n = 11), chronic pain and nausea (n = 7), and postprandial hyperinsulinemic hypoglycemia (n = 5). Overall 30-day complication rate was 29% (n = 14), including gastrogastric anastomotic leak (n = 5), sepsis (n = 5), and bleeding requiring transfusion (n = 3). Weight gain after surgery increased in all patients, especially those patients deemed severely malnourished. All patients reported resolution of symptoms leading to reversal of RYGB, although 58% of patients were lost to follow-up at 1 year after surgery.ConclusionsLaparoscopic reversal of Roux-en-Y gastric bypass is a complex revisional operation that can be safely performed in a select group of patients with serious complications. The main indications for reversal of RYGB included malnutrition with and without recalcitrant marginal ulcers. Weight gain and resolution of malnutrition occurred soon after reversal of gastric bypass. Because the complication rates are high, reversal should be considered only after all salvage attempts have failed. Reversal to normal anatomy carries high morbidity, including sepsis, leaks and bleeding, high reoperative rates, and readmission. Although reversal of RYGB has a role in the treatment of a select group of patients, it should be undertaken by surgeons with considerable experience in RYGB revision.     

White matter spongiosis with vigabatrin therapy for infantile spasms

The histopathology, “white matter spongiosis,” defined by electron microscopy (EM) as “intramyelinic edema,” has been associated with vigabatrin therapy in various animal models, but its role or significance in clinical studies is unknown. We conducted a neuropathological examination on a 27‐month‐old boy with bilateral polymicrogyria and epilepsy after sudden unexpected death in epilepsy (SUDEP). The patient was initiated on vigabatrin at 4 months of age, which controlled infantile spasms, and was continued as maintenance therapy. Autopsy showed a combination of developmental and acquired lesions: (1) bilateral gyral malformations of the frontal, parietal, temporal, and insular cortex; (2) agenesis of the olfactory tracts and bulbs; (3) hippocampal abnormalities: dentate gyrus bilamination and granule cell dispersion; and (4) areas of microscopic bilateral, symmetric white matter spongiosis in the brainstem central tegmental tract, amiculum and hilum of the inferior olive, medial longitudinal fasciculus, paragigantocellularis lateralis, optic nerves and chiasm, and hypothalamus. The white matter spongiosis was identical to the histopathologic lesions (which by EM exhibited intramyelinic edema) that were demonstrated in animal models on vigabatrin therapy, indicating that vigabatrin toxicity is not restricted to animal models.     

The impact of co-morbidity on the disease burden of VTE

Venous thromboembolism (VTE) is often accompanied by co-morbidities, which complicate and confound data interpretation concerning VTE-related mortality, costs and quality of life. We aimed to assess the contribution of co-morbidities to the burden of VTE. The PREFER in VTE registry, across seven European countries, documented and followed acute VTE patients over 12 months. Patients with co-morbidities were grouped in major co-morbidity groups: cancer, cardiovascular (CV) comorbidity (other than VTE), CV risks, venous, renal, liver, respiratory, bone and joint diseases, and lower extremity paralysis. Mortality rates and health-related quality of life (HrQoL) utility values grouped per co-morbidity were compared to the UK general population. Regression analyses were performed to determine the impact of co-morbidities on mortality and HrQoL. VTE were analyzed together and separately as pulmonary embolism (PE) and deep vein thrombosis (DVT). In total, 3455 patients were included, 40.5% with PE and 59.5% with DVT. 13% and 16% of the PE and DVT patients had no co-morbidities and had a 12-month mortality rate of 1.8% and 1.7%, respectively. Frequency and severity of co-morbidities increased mortality rates up to 30%. The EQ-5D-5L index in patients without co-morbidities were 0.826 and 0.838 for PE and DVT. These scores decreased to 0.638 and 0.555 in the presence of co-morbidities. Co-morbidities in VTE patients are common. VTE had an impact on mortality and HrQoL, and additional impact of co-morbidities was seen. Awareness of the presence of co-morbidities is important when making VTE-related treatment decisions. The presence of co-morbidities in PE and DVT patients is common and their frequency and severity in VTE patients have a substantial impact on mortality rates and HrQoL. When adjusting for co-morbidities, the impact of VTE on mortality as well as health-related quality of life remains present. Assessing patients without consideration of co-morbidities might lead to misinterpretations of the disease burden of PE and DVT.