Case report: Lymphocytic-plasmacytic and eosinophilic enterocolitis presented with marked eosinophilia and basophilia in a cat

Inflammatory bowel disease is a common condition in cats, characterized by recurring gastrointestinal signs with histologic evidence of intestinal inflammation. A 9-month-old neutered male Sphynx cat was presented with a 5-week history of vomiting and hematochezia. Conservative patient management with a therapeutic gastrointestinal formula, antibiotics, and antiemetics resulted in a positive response to treatment, with relapse of signs when the medications were discontinued. A new finding of marked eosinophilia and basophilia was identified 3 months after the initial presentation. Colonoscopy revealed cecal erosions and a surgical biopsy with histopathology confirmed a diagnosis of lymphocytic-plasmacytic and eosinophilic enterocolitis. For this diagnosis, the patient was treated with prednisolone, tylosin, and metronidazole. Antibiotics were gradually tapered as the cat showed clinical improvement. The patient showed resolution of the gastrointestinal signs, and the numbers of eosinophils and basophils returned within the reference range 8 weeks after the treatment began. Basophilia and eosinophilia has been reported in conjunction with feline T-cell lymphoma. However, marked basophilia accompanying eosinophilia is extremely rare in cats with inflammatory bowel disease. We herein provide clinical details, including ultrasonography, endoscopy, histopathology, and disease course of feline lymphocytic-plasmacytic and eosinophilic enterocolitis with marked basophilia and eosinophilia. This case highlights the importance of considering enteritis as potential diagnoses when eosinophilia and basophilia are concurrently observed in cats

Dynamic left ventricular outflow tract obstruction without basal septal hypertrophy, caused by catecholamine therapy and volume depletion

Hypertrophic cardiomyopathy (HCM) with hypertrophy of the basal septum is the most common etiology of left ventricular outflow tract (LVOT) obstruction

Metabolic pathway prediction of core microbiome based on enterotype and orotype

IntroductionIdentification of key microbiome components has been suggested to help address the maintenance of oral and intestinal health in humans. The core microbiome is similar in all individuals, whereas the diverse microbiome varies across individuals, based on their unique lifestyles and phenotypic and genotypic determinants. In this study, we aimed to predict the metabolism of core microorganisms in the gut and oral environment based on enterotyping and orotyping.Materials and methodsGut and oral samples were collected from 83 Korean women aged 50 years or older. The extracted DNA was subjected to next-generation sequencing analysis of 16S rRNA hypervariable regions V3–V4.ResultsGut bacteria were clustered into three enterotypes, while oral bacteria were clustered into three orotypes. Sixty-three of the core microbiome between the gut and oral population were correlated, and different metabolic pathways were predicted for each type. Eubacterium_g11, Actinomyces, Atopobium, and Enterococcus were significantly positively correlated between the gut and oral abundance. The four bacteria were classified as type 3 in orotype and type 2 in enterotype.ConclusionOverall, the study suggested that collapsing the human body’s multidimensional microbiome into a few categories may help characterize the microbiomes better and address health issues more deeply

Clinical outcomes of spontaneous bacterial peritonitis due to extended-spectrum beta-lactamase-producing Escherichia coli and Klebsiella species: A retrospective matched case-control study

<p>Abstract</p> <p>Background</p> <p>Clinical outcomes of spontaneous bacterial peritonitis (SBP) due to extended-spectrum β-lactamase-producing <it>Escherichia coli </it>and <it>Klebsiella </it>species (ESBL-EK) have not been adequately investigated.</p> <p>Methods</p> <p>We conducted a retrospective matched case-control study to evaluate the outcomes of SBP due to ESBL-EK compared with those due to non-ESBL-EK. Cases were defined as patients with liver cirrhosis and SBP due to ESBL-EK isolated from ascites. Control patients with liver cirrhosis and SBP due to non-ESBL-EK were matched in a 3:1 ratio to cases according to the following five variables: age (± 5 years); gender; species of infecting organism; Child-Pugh score (± 2); Acute Physiological and Chronic Health Evaluation II score (± 2). 'Effective initial therapy' was defined as less than 72 hours elapsing between the time of obtaining a sample for culture and the start of treatment with an antimicrobial agent to which the EK was susceptible. Cephalosporin use for ESBL-EK was considered 'ineffective', irrespective of the minimum inhibitory concentration. ESBL production was determined according to the Clinical and Laboratory Standards Institute guidelines on stored isolates.</p> <p>Results</p> <p>Of 1026 episodes of SBP in 958 patients from Jan 2000 through Dec 2006, 368 (35.9%) episodes in 346 patients were caused by SBP due to EK, isolated from ascites. Of these 346 patients, twenty-six (7.5%) patients with SBP due to ESBL-EK were compared with 78 matched controls. Treatment failure, evaluated at 72 hours after initial antimicrobial therapy, was greater among the cases (15/26, 58% <it>vs</it>. 10/78, 13%, <it>P </it>= .006); 30-day mortality rate was also higher than in the controls (12/26, 46% <it>vs</it>. 11/78, 15%, <it>P </it>= .001). When the case were classified according to the effectiveness of the initial therapy, 'ineffective initial therapy' was associated with higher 30-day mortality rate (11/18, 61% <it>vs</it>. 1/8, 13%, <it>P </it>= .036).</p> <p>Conclusion</p> <p>SBP due to ESBL-EK had poorer outcomes than SBP due to non-ESBL-EK. Ineffective initial therapy seems to be responsible for the higher rate of treatment failure and mortality in SBP due to ESBL-EK.</p

Identification of single-nucleotide polymorphisms of the prion protein gene in sika deer (Cervus nippon laiouanus)

Polymorphisms of the prion protein gene (PRNP) have been detected in several cervid species. In order to confirm the genetic variations, this study examined the DNA sequences of the PRNP obtained from 33 captive sika deer (Cervus nippon laiouanus) in Korea. A total of three single-nucleotide polymorphisms (SNPs) at codons 100, 136 and 226 in the PRNP of the sika deer were identified. The polymorphic site located at codon 100 has not been reported. The SNPs detected at codons 100 and 226 induced amino acid substitutions. The SNP at codon 136 was a silent mutation that does not induce any amino acid change. The genotype and allele frequencies were determined for each of the SNPs

Incidence of Atazanavir-associated Hyperbilirubinemia in Korean HIV Patients: 30 Months Follow-up Results in a Population with Low UDP-glucuronosyltransferase1A1*28 Allele Frequency

Hyperbilirubinemia is frequently observed in Caucasian HIV patients treated with atazanavir. UDP-glucuronosyltransferase 1A1 polymorphism, UGT1A1*28, which is associated with atazanavir-induced hyperbilirubinemia, is less common in Asians than in Caucasians. However, little is known about the incidence of atazanavir-associated hyperbilirubinemia in Asian populations. Our objective was to investigate the incidence of and tolerability of atazanavir-associated hyperbilirubinemia in Korean HIV patients. The prevalence and cumulative incidence of atazanavir-associated hyperbilirubinemia and UGT1A1*28 allele frequency was investigated in 190 Korean HIV-infected patients treated with atazanavir 400 mg per day. The UGT1A1*28 were examined by direct sequencing of DNA from peripheral whole blood. The UGT1A1*28 allele frequency was 11%. The cumulative incidence of any grade of hyperbilirubinemia was 77%, 89%, 98%, and 100%, at 3, 12, 24, and 30 months, respectively. The cumulative incidence of severe (grade 3-4) hyperbilirubinemia was 21%, 41%, 66%, and 75%, at 3, 12, 24, and 30 months, respectively. However, the point prevalence of severe hyperbilirubinemia did not increase with time and remained around 25%. Our data suggest that atazanavir-associated hyperbilirubinemia is common but transient in a population with low UGT1A1*28 allele frequency