Search

Mimicking ST-segment elevation myocardial infarction upon presentation, acute nonrheumatic streptococcal myocarditis is a treatable etiology of myocarditis which has only been infrequently reported.Patients were identified through a retrospective query of electronic medical records over a 17-year period (January 1994 to December 2010). We describe a case series of acute nonrheumatic streptococcal myocarditis complicating pharyngitis in young adults.Nine patients were identified; 89% were male, patients had an average age of 28.6 years, and 56% and 22% had confirmed group A and group G streptococcus, respectively. Latency from pharyngitis to chest pain averaged 3.1±1.1 days. No patients met the revised Jones criteria for acute rheumatic fever. All 9 patients (100%) presented with ST-segment elevations on electrocardiography and elevated cardiac biomarkers. Average peak creatine kinase was 934 U/L (normal400 U/L), creatine kinase-MB was 82 ng/mL (normal6.9 ng/mL), and troponin T was 2.30 ng/mL (normal0.03 ng/mL). Six patients underwent coronary angiography, which revealed no obstructive culprit lesions. Cardiac magnetic resonance imaging confirmed myocarditis in 3 patients and was used to document resolution in follow-up for 2 patients. All patients had a complete clinical recovery.Acute nonrheumatic streptococcal myocarditis is an under-recognized and treatable cause of ST-segment elevation and chest pain in young adults with a history of recent pharyngitis. Etiopathology extends beyond Lancefield group A streptococcus and includes group G streptococcal infection. Cardiac magnetic resonance may be useful in confirming the diagnosis and documenting the resolution.

A 29-year-old woman was admitted to the hospital because of swelling, erythema, and pain of the hand at the site of a cat bite. Despite treatment with amoxicillin–clavulanic acid, her symptoms worsened and fever, chills, headache, and arthralgias developed.

Necrotizing fasciitis due to Pseudomonas aeruginosa is rare. We report a case of monomicrobial Pseudomonas necrotizing fasciitis and review 37 cases in the literature. The mortality rate was 30%, and most infections occurred in the immunocompromised. Clinicians should consider empiric pseudomonal antibiotic coverage in the severely immunocompromised with potentially necrotizing infections.

The physician's approach to the differential diagnosis of obscure, atypical pneumonias has changed. The physician needs to expand the diagnostic search when confronted with a perplexing, progressive atypical pneumonia. Diseases examined in this article include anthrax, psittacosis, Q fever, tularemia, pasteurellosis, melioidosis, Rocky Mountain spotted fever, and the plague.

SUMMARY The possibility that a perplexing febrile illness may represent a zoonotic infection should be explored. The history should include where the person has been, what he or she has done, what has been eaten and drunk, what contacts have occurred with vertebrates or arthropods in wild or domestic venues, and whether there has been exposure to unusual animal products. The preceding discussion emphasized, via some examples, mechanisms of spread as well as the physical and biologic conditions that enhance the probability of an encounter with a pathogen. From clues in the history and physical examination the appropriate diagnostic and therapeutic decisions can be made. These decisions may be life saving for the patient, and perhaps protect care providers and family from acquiring the same disease. Many of the infections mentioned in this article will be amplified in subsequent articles, which will deal with diseases encountered primarily in the United States.

THE WORLD of pathogenic microorganisms and infectious diseases has been enlarged during the past several decades by the emergence and discovery of newly recognized human pathogens, 1-3 by the reemergence of older diseases and new syndromes caused by historically familiar bacteria and viruses, 3,4 and by major changes in antimicrobial susceptibility requiring new therapeutic strategies. 5-8 That these observations are of great concern is evidenced by the number of recent publications. Examples include multiple communications in the weekly publication of the Centers for Disease Control and Prevention 9,10 ; increasing scrutiny by the Institute of Medicine 2 ; the 1995 initiation of a new journal, Emerging Infectious Diseases 11 ; and countless other communications, articles, and conferences on the subject. 12,13 These revelations give eloquent testimony to the resourcefulness and adaptability of microbes. Many other factors may also be responsible for the new emerging infections. Host factors, including immune status, nutrition, and stress

Presentation of Case A fifty-nine-year-old schizophrenic woman was admitted to the hospital after a fall. The patient had been committed to a state hospital thirty-nine years previously because of ...

Enterococci exhibit two types of resistance to streptomycin. Moderately high-level resistance is observed in most naturally occurring strains and can be overcome by simultaneous exposure to penicillin. In addition, very high-level resistance is found in those strains against which penicillin plus streptomycin fail to produce synergism in vitro. To study the mechanism of streptomycin resistance in enterococci, ribosomes from a wild-type strain and from a highly streptomycin-resistant mutant were isolated, characterized, and studied in an in vitro amino acid incorporation system. The ribosomes from the organism with moderately high-level streptomycin resistance were sensitive to streptomycin in vitro, suggesting that this type of resistance is caused by failure of streptomycin to reach the ribosomes. Very high-level resistance (and lack of penicillin-streptomycin synergism), on the other hand, appears to be due to ribosomally mediated streptomycin resistance.

The mechanism by which agents that inhibit bacterial cell wall synthesis produce a synergistic effect against enterococci when combined with aminoglycoside antibiotics has not been elucidated. Using 14C-labeled streptomycin, it could be shown that uptake of this aminoglycoside antibiotic was markedly enhanced in enterococci growing in the presence of penicillin or other agents which inhibit the synthesis of bacterial cell walls. There was no enhancement of streptomycin uptake when the cells were incubated with antibiotics which primarily affect the bacterial cell membrane or inhibit protein synthesis. Increased streptomycin uptake was produced by penicillin only in actively growing bacteria. These observations are consistent with the hypothesis that enterococci exhibit a natural barrier to the entry of streptomycin which can be overcome by agents which inhibit cell wall synthesis, thus producing a synergistic effect.

PRESENTATION OF CASE A 59-year-old woman was admitted to the hospital after a seizure. Eighteen years previously a diagnosis of epilepsy was made, and treatment with diphenylhydantoin was initiated. One year later symmetrical polyarthralgias developed; systemic lupus erythematosus was diagnosed, and adrenocorticosteroid treatment was begun. Thirteen years before admission she began to experience substernal tightness and choking, occasionally accompanied by a sensation of numbness that radiated to the left arm. Nine years before entry an electrocardiogram disclosed evidence of an anterior myocardial scar, and an x-ray film of the chest revealed an area of calcification at the apex of the . . .

Young, male, Sprague-Dawley rats, maintained on 30% galactose diets for 50–90 days developed amino aciduria and polyuria. No disturbance of plasma amino acid concentration was noted suggesting that the amino aciduria was related to defective renal tubular reabsorption of amino acids. Chromatographic analysis of the urinary amino acids revealed increases in taurine, aspartic acid, glutamic acid, alanine, β-alanine and ethanolamine. Studies using [14C]glucose failed to demonstrated any inhibition of the hexose monophosphate shunt pathway in the kidneys of the galactose fed animals.

Presentation of Case A forty-four-year-old man was admitted to the hospital because of hematemesis. He had been well until two years previously, when he began to experience episodes of burning midepigastric distress, occasionally with radiation to the back; the attacks occurred twice weekly, usually an hour after eating but also at night; the symptoms were relieved by sitting up and partially alleviated by antacid medication. Eighteen months before admission he vomited about a cupful of red blood; a gastrointestinal series was interpreted as showing gastritis. Six months later edema of the ankles developed. A few months before entry he noticed . . .

Presentation of Case A fifty-four-year-old man was admitted to the hospital because of weakness and diarrhea. He had been well until one year previously, when a radiologic examination revealed exte...

Presentation of Case A fifty-six-year-old woman was admitted to the hospital because of difficulty with speech. She had been well until five days previously, when she became febrile, with a tempera...

10-Second summary The Gram stain is the quickest and most helpful technique the emergency physician has at his disposal to determine what is causing an obscure infection. Alone, or combined with other tests, it provides the information needed to prescribe antibiotics for the acutely ill patient.

Presentation of Case A thirteen-year-old girl entered the hospital because of fever and somnolence. The patient had been well until two days before admission, when headache and fatigue developed. The fatigue increased, accompanied by nausea. During the evening before entry she vomited, appeared febrile and complained of pain in the back, abdomen and shoulders, as well as of a painful lump in the back of the neck. On the following day she was found in a deep sleep by an aunt, who also observed a "prickly-heat rash" over the body. There was no history of neurologic disease or exposure to . . .

Presentation of Case First admission. A forty-six-year-old man entered the hospital because of pain in the chest. Twenty years previously he was admitted to another hospital for study of migratory ...

Infection of man with Listeria monocytogenes was first described in 1929 [1], and in recent years it has been reported with increasing frequency.1 L. monocytogenes has been isolated and identified in many species of animals [2] and it was first thought that non-human hosts were the principal source for human infections. Most recent cases, however, in this country have been in urban residents with no known animal contacts [3]. Later, because many of the isolations from humans were from neonates and the products of conception, it was thought to be primarily an obstetric and pediatric disease [4]. Still later, Louria et al. [5] called attention to the association between infection with Listeria and lymphoproliferative diseases. Subsequent reports by Simpson et al. [6] and Buchner and Schneierson [3] supported this association. Because of these reports, the concept has become prevalent that listerial infection occurs almost exclusively as a complication of an underlying primary disorder (malignancy, cirrhosis, immune deficiency states). This communication endeavors to put listeriosis into a more realistic perspective. That is, although many infections occur in infants and in patients with an underlying disease, most occur in previously healthy people of all age groups and are unrelated to a rural setting or animal exposure.

Presentation of Case A 76-year-old woman was admitted to the hospital because of shaking chills. For 10 years she had experienced repeated respiratory-tract infections during the winter, characterized by a cough productive of small amounts of white sputum that persisted for approximately six weeks. Six months before entry there was the onset of fatigue, polyuria, polydipsia and apparent weight loss. One week before admission she again contracted a cough that was productive of moderate amounts of white sputum, accompanied by weakness, malaise and increased polyuria and polydipsia. Three days before entry she began to have repeated shaking chills, with dyspnea . . .

Presentation of Case A 32-year-old woman was admitted to the hospital because of a pulmonary infiltrate. She had been well until 20 months previously, when coryza, pharyngitis and a cough productiv...

THE level of glucose in the blood perfusing the islets of Langerhans is thought to regulate the secretion of insulin by the β-cells1. At present nothing is known about the mechanism of this regulation or even about the way in which the β-cells metabolize glucose. Studies designed to provide information about these problems are hampered by the fact that the pancreatic islets are rather diffusely scattered throughout the entire exocrine portion of the gland and comprise only about 2 per cent of the total pancreatic tissue2. Even if one were successful in obtaining islet tissue free of exocrine pancreas, the β-cells represent only 60–90 per cent of the total cell population3. However, in humans there are insulin-producing tumours of the pancreas which are usually composed of only β-cells and such tissue does afford an opportunity to study β-cell metabolism. A ratio greater than unity for the amount of carbon dioxide labelled with carbon-14 derived from glucose-1-14C as compared to that from glucose-6-14C has been taken as evidence for the existence of the hexose monophosphate pathway in the tissue under study4. The present report concerns studies using a β-cell tumour and indicates that there is an active hexose monophosphate pathway in these cells (this patient was studied through the kindness of the National Institute of Neurological Diseases and Blindness, National Institutes of Health, Bethesda, Md.). It is realized that the metabolism in these benign tumours may not be completely analogous to that of β-cells in normal islets.

IN recent years there have been changes in many of the factors which influence the development and outcome of bacterial endocarditis. These changes relate to both the susceptible host and the causative organism. Rheumatic fever, for example, appears to be declining in incidence and severity.1 , 2 More cases of bacterial endocarditis are being encountered in elderly persons with no history of valvular disease or murmurs.3 In addition, many more patients are being treated with corticosteroid hormones, immunosuppressive agents and extensive radiotherapy, all of which interfere with normal mechanisms of host resistance.4 , 5 The use of newly developed technics in cardiac surgery, such . . .

Cell lines were developed from biopsies on galactosemic and non-galactosemic patients. It was shown that one can discriminate between lines from the two types of donors by their relative growth in glucose and galactose and by their ability to oxidize galactose-1-C14. The latter method was successful in distinguishing a heterozygous cell line from the normal ones. Sensitivity of galactosemic cells to galactose was suggested by some of the experiments. The kinetics of growth were in some ways reminiscent of a similar phenomenon in the transferase mutants of E. coli, though in the human cells the effect was much less marked.

Open heart surgery has been performed at the Massachusetts General Hospital in 13 patients less than 6 months after the initiation of treatment for acute or subacute bacterial endocarditis. The endocarditis involved the aortic valve in 12 cases and a mitral valve prosthesis in the other. In two patients there was concomitant rupture of chordae tendineae of the mitral valve. One patient received no preoperative antibiotics, and four were still receiving their initial course of therapy at the time of surgery. The primary indication for surgery in all cases was progressive or intractable congestive heart failure. Ten underwent replacement of the aortic valve alone, two had both aortic and mitral valves replaced, and one had a mitral prosthesis replaced. Of the 13 patients, 10 are alive and doing well, although paraprosthetic insufficiency developed in three, two of whom required subsequent surgical repair. Three patients died, two in the early postoperative period, and one, 8 months after surgery from paraprosthetic regurgitation with hemolysis and heart failure. Antibiotics were given during and after surgery for as long as 6 weeks. In no case has recurrent sepsis been a problem. Our experience indicates that open heart surgery, when necessitated by progressive congestive heart failure due to valve destruction, can be safely and effectively performed during or shortly after treatment of bacterial endocarditis.

Because combinations of penicillin plus streptomycin and penicillin plus kanamycin do not produce synergism against all strains of enterococci, the effect of penicillin plus gentamicin against enterococci was examined. A very high level of resistance to gentamicin was absent in 172 strains of enterococci isolated from clinical specimens. Penicillin plus gentamicin was synergistic against all of 30 strains tested. The size of the inoculum had a significant effect when low concentrations of gentamicin were tested against certain of the strains. Nonetheless, the combination of penicillin plus gentamicin produced enhanced killing of all enterococci tested when used in clinically achievable concentrations.

During incubation with galactose, galactosemic leukocytes accumulated more galactose-l-phosphate than did normal leukocytes. Concomitant determination of glucose oxidation, with C(14) glucose, revealed no inhibition of the hexosemonophosphate pathway. These results are at variance with recent studies in rat lens tissue, which suggests that intracellular galactose-1-phosphate depressed glucose-6-phosphate dehydrogenase activity and the oxidative pathway.

Excerpt Open heart surgery was performed at the Massachusetts General Hospital in 13 patients less than 6 months after the initiation of treatment for acute or subacute bacterial endocarditis. The ...

A female carrier for chronic granulomatous disease of childhood has had persistent systemic infections withSalmonella enteritidisfor more than 3 years despite rigorous medical and surgical...

Excerpt Dr. Joseph J. Bunim: In a recent Harvey lecture (1), Dr. James V. Neel stated that "The ultimate basis of biogenetic traits resides in some 20 thousand pairs of genes. The term gene refers ...