A Unique Case of Tri-Valvular Serratia marcescens Infective Endocarditis Complicated by Innumerable Emboli.

Serratia marcescens (S. marcescens) is a gram negative bacterium rarely associated with cases of infective endocarditis (IE). Involvement of three cardiac valves, as evidenced by echocardiography, is uncommon as well. S. marcescens IE and tri-valvular endocarditis have been rarely described in literature. We report a unique case of S. marcescens tri-valvular IE in a 42-year-old female with sudden altered mental status and no underlying structural heart disease complicated by embolic infarcts in both cerebral and cerebellar hemispheres, and a sub-arachnoid hemorrhage. To our knowledge, this is the first reported case of tri-valvular S. marcescens IE. We believe this report will add to the growing literature of rare bacterial IE and considering this in the differential in the right clinical scenario.

Bartonella Species, an Emerging Cause of Blood-Culture-Negative Endocarditis.

Since the reclassification of the genus Bartonella in 1993, the number of species has grown from 1 to 45 currently designated members. Likewise, the association of different Bartonella species with human disease continues to grow, as does the range of clinical presentations associated with these bacteria. Among these, blood-culture-negative endocarditis stands out as a common, often undiagnosed, clinical presentation of infection with several different Bartonella species. The limitations of laboratory tests resulting in this underdiagnosis of Bartonella endocarditis are discussed. The varied clinical picture of Bartonella infection and a review of clinical aspects of endocarditis caused by Bartonella are presented. We also summarize the current knowledge of the molecular basis of Bartonella pathogenesis, focusing on surface adhesins in the two Bartonella species that most commonly cause endocarditis, B. henselae and B. quintana. We discuss evidence that surface adhesins are important factors for autoaggregation and biofilm formation by Bartonella species. Finally, we propose that biofilm formation is a critical step in the formation of vegetative masses during Bartonella-mediated endocarditis and represents a potential reservoir for persistence by these bacteria.

Antibiotic Resistance and Toxin Production of Clostridium difficile Isolates from the Hospitalized Patients in a Large Hospital in Florida.

Clostridium difficile is an important cause of nosocomial acquired antibiotic-associated diarrhea causing an estimated 453,000 cases with 29,000 deaths yearly in the U.S. Both antibiotic resistance and toxin expression of C. difficile correlate with the severity of C. difficile infection (CDI). In this report, a total of 139 C. difficile isolates from patients diagnosed with CDI in Tampa General Hospital (Florida) in 2016 were studied for antibiotic resistance profiles of 12 types of antibiotics and toxin production. Antibiotic resistance determined by broth microdilution method showed that strains resistant to multi-antibiotics are common. Six strains (4.32%) showed resistance to six types of antibiotics. Twenty strains (14.39%) showed resistance to five types of antibiotics. Seventeen strains (12.24%) showed resistance to four types of antibiotics. Thirty-nine strains (28.06%) showed resistance to three types of antibiotic. Thirty-four strains (24.46%) showed resistance to two types of antibiotics. While, all isolates were susceptible to metronidazole, and rifaximin, we found that one isolate (0.72%) displayed resistance to vancomycin (MIC ≥ 8 µg/ml), and another one was resistant to fidaxomicin (MIC >1 µg/ml). The percentage of isolates resistant to cefoxitin, ceftriaxone, chloramphenicol, ampicillin, clindamycin, erythromycin, gatifloxacin, and moxifloxacin was 75.54, 10.79, 5.76, 67.63, 82.70, 45.32, 28.06, and 28.78%, respectively. Toxin profiling by PCR showed the isolates include 101 (72.66%) A+B+CDT-strains, 23 (16.55%) A+B+CDT+ strains, 3 (2.16%) A-B+CDT+ strains, 1 (0.72%) A-B+CDT-strains, and 11 (7.91%) A-B-CDT-strains. Toxin production determined by ELISA using supernatants of bacterial culture harvested at 12, 24, 48, and 72 h of post inoculation (hpi) showed that the toxins were mainly produced between 48 and 72 hpi, and toxin B (TcdB) was produced faster than toxin A (TcdA) during the experimental time (72 hpi). In addition, the binary-positive strains were likely to yield more toxins compared to the binary-negative strains. This work contributes to the current understanding of the antibiotic resistance and virulence of C. difficile clinical strains.

Heart failure mice exhibit decreased gastric emptying and intestinal absorption.

Our recent study showed that intravenously administered B-type natriuretic peptide (BNP) decreases gastric emptying and intestinal absorption in mice. We aimed to test whether acute myocardial injury and heart failure have similar effects. Wild-type (WT) and natriuretic peptide receptor type A (NPR-A) knockout (KO) mice underwent cryoinfarction (myocardial infarction [MI]) of the left ventricle (LV) versus sham. LV dysfunction was confirmed by echocardiography. Percent gastric emptying and intestinal absorption were measured and analyzed one and two weeks after infarction, by gavage feeding the mice with fluorescein-isothiocyanate-dextran. Ejection fraction was 48 ± 3% versus 64 ± 2% (P < 0.05) and fractional shortening was 24 ± 2% versus 35 ± 2% (P < 0.01), MI versus sham, respectively. BNP levels (pg/mL) were 4292 ± 276 one week after MI versus 105 ± 11 in sham (n = 5, P < 0.05) and 1964 ± 755 two weeks after MI (n = 5, P < 0.05). Gastric emptying was significantly decreased, 68 ± 6% in MI versus 89 ± 3% in sham (n = 5, P < 0.05) one week after MI and 82 ± 0.5% versus 98 ± 0.4%, MI versus sham (n = 5, P < 0.05), two weeks post-MI. Absorption, measured in relative plasma fluorescence units in WT mice, was 350 ± 79 in MI versus 632 ± 121 in sham (n = 6, P < 0.05). KO mice did not show a significant difference in emptying or absorption compared with sham. These findings suggest that MI and LV dysfunction decrease gastric emptying and absorption in mice through a mechanism that involves NPR-A.

Sirolimus: a novel immunosuppressive drug in heart transplantation.

Cardiac transplantation is a time-honored therapy for end stage heart disease for a select group of patients. The advances in recent years have increased mean survival to 12 and 13 years. The probability of survival after heart transplantation at one, five and ten years are 80%, 70% and 60% respectively. Calcineurin-inhibitors (CNIs) based regimes have been the corner stone of medical therapy in these patient populations. They have reduced the amount of rejections but with considerably increased toxicities to therapies that decreases long-term patient survival. Proliferation Signal Inhibitors or mammalian target-of-rapamycin inhibitors (PSI/mTOR) are a new class of agents that have been extensively used recently to limit these toxicities. Sirolimus and Everolimus are two such drugs. PSI/mTOR work syngeristically with CNIs or have been as primary immunosuppressant's for patients who do not tolerate or have developed side effects to calcineurin inhibitors. This current article will discuss about sirolimus and its use in heart transplant patients along with outlining some recent patents.

B-type natriuretic peptide decreases gastric emptying and absorption.

Natriuretic peptides have been shown to decrease contractility of isolated gastric smooth muscle cells. However there is a paucity of research showing whether this effect has functional significance in the whole animal. The objective of this study was to test whether intravenously administered B-type Natriuretic Peptide (BNP) has an effect on gastric emptying and/or absorption in a whole animal mouse model. C57BL/6-Wild-type (WT) and Natriuretic Peptide Receptor type A (NPR-A) knockout (KO) mice were used in these studies. Gastric contractility was examined in anesthetized mice before and after BNP vs. vehicle injection. Gastric emptying of gavage fed 70 Kilo Dalton (kDa) FITC-dextran and absorption of 4 kDa FITC-dextran were compared in BNP vs. vehicle treated conscious WT and KO mice. BNP decreased gastric contractility (measured in change in intragastric pressure) from 2.26 +/- 0.29 to 1.44 +/- 0.11 mmHg (P < 0.05), pressure returned to 2.08 +/- 0.17 after 5 BNP half-lives (P < 0.05). There was no significant change in the vehicle or KO. BNP also decreased gastric emptying in WT mice compared to vehicle, 87.8 +/- 0.8% vs. 97.3 +/- 1.04% (P < 0.05) and this effect showed a dose-response relationship. In KO mice emptying was 95.8 +/- 0.5% (BNP) vs. 91.7 +/- 0.7% (Vehicle) (P > 0.05). The absorption in WT mice was 28.2 +/- 7.8 (relative fluorescence units) for BNP vs. 91 +/- 25.9 for vehicle (P < 0.05). For KO mice absorption was 64.3 +/- 14.9 for BNP vs. 60.6 +/- 17.4 for vehicle (P > 0.05). The results show that BNP decreases intragastric pressure, emptying and absorption by acting via the NPR-A receptor. We postulate that this effect is aimed at decreasing preload through decreased water and electrolyte absorption from the GI tract and may also be responsible for the symptoms of impaired gastrointestinal function observed in heart failure patients.