To the Editor: Trichomonads are flagellated protozoa with several species capable of infecting or colonizing humans. The most common, Trichomonas vaginalis, causes genitourinary infection in adults and, rarely, respiratory infections in premature neonates of infected mothers. Pentatrichomonas hominis has been isolated from the human gastrointestinal tract, and Trichomonas tenax, a human oropharynx commensal, has caused empyema in immunocompomised persons. Rare cases of human peritonitis caused by trichomonads have been reported. Some trichomonads, including Tritrichomonas foetus and Tritrichomonas suis, primarily infect and colonize animals. Although they were previously thought to be different species, current molecular and biologic evidence suggests they are indistinguishable (1). T. foetus (synonym T. suis) causes genitourinary infection in cattle and diarrhea in cats and colonizes the gastrointestinal tract of swine. We report T. foetus peritonitis in a 52-year-old man with common variable immunodeficiency, rheumatoid arthritis, splenectomy, and cryptogenic cirrhosis. In June 2007, he was admitted with peritonitis to a community hospital in Pennsylvania, United States. He lived on a farm that had swine, horses, and cats. Exposure to cattle was unknown. He denied having a history of sexually transmitted infections or high-risk sexual behavior. Initial examination showed paracentesis fluid with numerous motile, flagellated organisms consistent with trichomonads. Bacterial fluid cultures had no growth. Despite receiving antimicrobial drugs (including metronidazole 500 mg intravenously every 6 hours), he became increasingly ill over the following 72 hours with hypotension, acute renal failure, and metabolic acidosis, which required transfer to Penn State Milton S. Hershey Medical Center (Hershey, PA, USA) for further care. Upon arrival, the man was afebrile but hypotensive and tachycardic. Abdominal examination showed ascites, decreased bowel sounds, and diffuse tenderness. Genitourinary examination results were normal. Repeat paracentesis demonstrated numerous motile trichomonads. Urinalysis and routine cultures of peritoneal fluid and blood were negative. Computed tomography of the abdomen and pelvis showed edematous bowel, ascites, and peritonitis. His condition deteriorated during the following 48 hours. Despite ongoing treatment with broad-spectrum antimicrobial drugs (including metronidazole 500 mg intravenously every 6 hours), he died of multiorgan failure. Autopsy showed peritonitis with copious intraabdominal exudate and peripancreatic and perigastric abscesses. No intestinal perforation or genitourinary abnormalities were noted. No portal of entry for peritoneal infection was identified. Premortem abdominal fluid samples were sent to the Centers for Disease Control and Prevention (Atlanta, GA, USA) for analysis. DNA was extracted from the trichomonad culture and peritoneal fluid by using the QIAamp DNA mini-kit (QIAGEN, Valencia, CA, USA). PCR testing for T. vaginalis was performed (2). PCR for T. foetus was performed by using primers TFR3 and TFR4 with thermocycling conditions outlined previously (3). PCR was performed in a 50-µL reaction volume with 1 µL of deoxynucleoside triphosphate mix (12.5 mmol/L each of dATP, dCTP, dGTP, and 5 mmol/L of dUTP; Applied Biosystems, Foster City, CA, USA), 5 µL of MgCl2 (25 mmol/L; Applied Biosystems), 0.2 µM each primer, 2.5U of AmpliTaq Gold polymerase (Applied Biosystems), 5 µL of 10× PCR buffer (Applied Biosystems), and 5 µL of DNA. PCR products were analyzed on an Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA, USA). Amplicons were purified with the QIAquick PCR purification kit (QIAGEN) and directly sequenced with PCR primers on an ABI 3130-XL Genetic Analyzer (Applied Biosystems). Sequences were assembled and aligned with Lasergene software (DNASTAR, Inc., Madison, WI, USA) and deposited in GenBank (accession no. {type:entrez-nucleotide,attrs:{text:HQ849063,term_id:323520054,term_text:HQ849063}}HQ849063). Metronidazole sensitivity was tested with methods previously described (4). The patient’s trichomonads had minimal lethal concentration (MLC) of 3.1 μg/mL for metronidazole, similar to MLCs of the known metronidazole–sensitive T. vaginalis isolate. T. vaginalis metronidazole MLCs >50 μg are associated with resistance (5). PCR performed by using primers TFR3/4 produced a 348-bp amplicon with DNA extracted from peritoneal fluid and culture (Figure). Comparison of DNA sequence from the parasite to GenBank sequences showed 100% identity with cattle isolates of T. foetus. Figure PCR amplification with primers TFR3 and TFR4. Lane 1, Tritrichomonas foetus ATCC 30231; lane 2, peritoneal fluid specimen; lane 3, culture of peritoneal fluid; lane 4, T. suis ATCC 30167; lane 5, Pentatrichomonas hominis; lane 6, Trichomonas tenax; lane ... Two human cases of T. foetus infection have been reported. T. foetus was identified by PCR in the respiratory tract of a patient with AIDS and pneumonia (6) and by microscopy in cerebrospinal fluid from a hematopoetic stem-cell transplant recipient with fatal meningoencephalitis (7). The latter patient described by Okamoto et al. had a history of trichomonads in a urine sample before transplantation and clinical epididymitis when meningoencephalitis was diagnosed, leading to their conclusion that his infection was genitourinary in origin. The patient we report had no apparent signs of genitourinary infection. Human trichomonal peritonitis has been reported (8–10). Straube et al. described a 54-year-old man with common variable immunodeficiency and cirrhosis. Peritoneal fluid contained numerous trichomonads, identified as T. faecalis (syn T. equi), an intestinal commensal in horses. This patient died shortly after diagnosis. These authors did not describe animal exposures. The patient we report had animal contact. We found no reported cases of T. foetus peritonitis. Two reported patients with trichomonal peritonitis recovered after treatment with metronidazole. Thus, we propose initial treatment with metronidazole in patients with trichomonal peritonitis but confirmation of species and sensitivity to antimicrobial drugs is essential.

Medical schools and teaching hospitals are experiencing more frequent turnover of department chairs. Loss of a department chair creates instability in the department and may have a negative effect on the organization at large. Interim leadership of academic departments is common, and interim chairs are expected to immediately demonstrate skills and leadership abilities. However, little is known about how persons are prepared to assume the interim chair role. Newer competencies for effective leadership include an understanding of the business of medicine, interpersonal and communication skills, the ability to deal with conflict and solve adaptive challenges, and the ability to build and work on teams. Medical schools and teaching hospitals need assistance to meet the unique training and support needs of persons serving as interim leaders. For example, the Association of American Medical Colleges and individual chair societies can develop programs to allow current chairs to reflect on their present positions and plan for the future. Formal leadership training, mentorship opportunities, and conscientious succession planning are good first steps in preparing to meet the needs of academic departments during transitions in leadership. Also, interim leadership experience may be useful as a means for "opening the door" to underrepresented persons, including women, and increasing the diversity of the leadership team.

Academic health centers are experiencing more frequent turnover of department chairs. In departments of obstetrics and gynecology, doubling of annual turnover rates for chairs occurred between 1981 and 2005 (6.0% to 12.7%).1 During the time period from 1993 to 2003, the median length of service of chairs in pediatric departments was 5 years with a mean annual turnover rate of 17%.2 Only 10% of individuals served as chair for the entire 11-year period of the study. The average tenure for chairs of departments of internal medicine at US medical schools declined from 5.2 years in the 1970s to 3.9 years in the 2000s.

The authors describe the strategies developed at the Pennsylvania State University College of Medicine, as part of The Robert Wood Johnson Foundation's Generalist Physician Initiative, to increase the proportion of graduating medical students entering generalist disciplines. These strategies included modifying the admission process to involve more primary care faculty so that students with identified potential for primary care would make up at least half of each entering class, and partnering with selected colleges and universities in Pennsylvania to increase the number of applicants with the potential for primary care. They describe partnering and outreach programs--Primary Care Day, off-campus cluster meetings, and the Primary Care Scholars Program for college seniors--and present promising information about the results.

YERSINIA ENTEROCOLITICA is rapidly emerging worldwide as an enteric pathogen associated with a wide spectrum of clinical and immunologic manifestations. The clinical illness caused by this pathogen ranges from self-limited enterocolitis to potentially fatal systemic infection; post-infection manifestations include erythema nodosum and reactive arthritis. The organism was first described by Schleifstein and Coleman in 1939 as "an unidentified microorganism resembling Bacterium lignieri and Pasteurella pseudotuberculosis, and pathogenic for man."1 Isolates were variously named Bacterium enterocoliticum, P. X, P. pseudotuberculosis type b, Germe X, and P. pseudotuberculosis X, until 1964, when Frederiksen proposed the name Yersinia enterocolitica.2 In . . .

Empyema caused by P paucimobilis and mouth flora occurred in a 56-year-old man two months after orthotopic cardiac transplantation. Successful treatment was accomplished with chest tube drainage and four weeks of intravenous cefazolin and clindamycin.

Between March 1 and Sept 1, 1980, we interviewed a 25% random sample of patients admitted to medicine, surgery, and obstetric, and gynecology services to determine the frequency and descriptive characteristics of night sweats (NS). Seventy-two (41%) of 174 patients interviewed reported NS within three months before admission. Obstetric patients reported NS significantly more often than nonobstetric patients (60% vs 33%, P less than .02). The duration of NS ranged from one day to 27 years (mean 10.5 months; median two months). NS were mild in 36 (50%), moderate in 17 (24%), and severe in 19 (26%). Severe NS were reported significantly more often by nonobstetric patients, and most often by those on the medicine service. Among nonobstetric patients, NS were associated with metastatic adenocarcinoma of the prostate gland, and severe NS with the use of antipyretics. NS were not associated with elevated temperature measurements during hospitalization.

A bleeding diathesis characterized by in-vitro platelet dysfunction and prolongation of the template bleeding time (TBT) has been reported in patients receiving latamoxef ('moxalactam'), but not cefotaxime or cefoperazone. Hypoprothrombinaemia has been associated with the use of both latamoxef and cefoperazone in seriously ill and malnourished patients. We administered either latamoxef, cefotaxime or cefoperazone intravenously, at dosages within the range recommended by each manufacturer, to 14 normal volunteers. Latamoxef caused a dose and time dependent defect in platelet function characterized in vitro by abnormalities in aggregation to adenosine diphosphate and in vivo by prolongation of the template bleeding time. In two out of two subjects, a single 4 g dose of latamoxef caused neither prolongation of template bleeding times nor aggregation abnormalities. Two out of two subjects receiving latamoxef 6 g/day for six days had progressive prolongation of bleeding times to 12 and 15 min. Two additional subjects receiving latamoxef 12 g/day for four days had prolongation of template bleeding times to greater than 20 min. Of four subjects receiving cefotaxime 12 g/day for seven days, none had prolongation of template bleeding times or abnormalities in platelet aggregations. Of four subjects receiving cefoperazone 6 g/day, none had significant prolongation of template bleeding times and one had abnormalities in aggregation attributed to inadvertent salicylate ingestion. Prolongation of the prothrombin time or activated partial thromboplastin time did not occur in any of the 14 volunteers. Latamoxef is more likely to interfere with platelet function than either cefotaxime or cefoperazone.

Inadvertent or uncontrolled introduction of varicella-zoster virus into the hospital environment occurs commonly and must be investigated in a systematic and efficient manner to minimize secondary spread to patients (particularly the immunocompromised) or hospital personnel. On the basis of a review of the literature and our practical experience with 11 such exposures to varicella-zoster virus during a 2-year period, we have developed a working algorithm for such investigations. Index cases most often are children, resident physicians, students, young nurses, and ancillary personnel, or adult patients with herpes zoster. A negative or uncertain past history of this infection is an unreliable predictor of susceptibility among the exposed and should be confirmed by serology tests or delayed hypersensitivity skin testing. An incubation-contagion timetable, coupled with a stratification of risk among the exposed, permits a prioritized response in dealing with an introduction of varicella-zoster virus. The preemployment screening of all hospital workers for susceptibility to varicella-zoster virus should be considered as a practical and cost effective policy.

Veillonella parvula and alcalescens are anaerobic gram-negative cocci that, when isolated from anaerobic cultures of clinical specimens, are usually regarded as commensal organisms. Occasionally they play a pathogenic role and require antibiotic therapy. Limited clinical experience and in vitro susceptibility studies suggest that penicillin G is the drug of choice for these organisms and that cephalosporins, clindamycin, chloramphenicol, and metronidazole may be acceptable therapeutic alternatives. Presented herein is a case report of a Veillonella infection, a discussion of the importance of these organisms when they occur in a clinical infection, and a discussion of the appropriate antibiotic therapy.

Susceptibility of 324 isolates of nonfermentative gram-negative bacteria to cephalothin, cefamandole, cefoxitin, ceftazidime, cefsulodin, and azthreonam was determined by agar dilution and disc diffusion techniques. With the exception of Moraxella species, first- and second-generation cephalosporins were minimally active against nonfermenters tested. Cefsulodin and azthreonam were mainly active against Pseudomonas aeruginosa. In contrast, ceftazidime and ceftriaxone exhibited wider activity spectra. Cefsulodin and ceftazidime were the most active against P. aeruginosa, followed by azthreonam and ceftriaxone. Ceftazidime was the only drug with significant activity against Pseudomonas maltophilia and Pseudomonas fluorescens/Pseudomonas putida, and was also the most active against Pseudomonas cepacia. Acinetobacter calcoaceticus and Alcaligenes strains were most sensitive to ceftazidime, followed by ceftriaxone and azthreonam. Ceftriaxone was the most active against moraxellas, followed by cefamandole/cefoxitin, ceftazidime, cephalothin, cefsulodin, and azthreonam. Ceftazidime was the most active against uncommonly isolated nonfermenters. Results observed in this study reflect a potential use for ceftazidime in therapy of infections caused by most gram-negative nonfermenters; therapy with cefsulodin and azthreonam in nonfermenter infections should be restricted to those caused by P. aeruginosa, and that with ceftriaxone reserved for non-P. aeruginosa infections.

Since Chandler's initial report in 1968 on "malignant external otitis" (MEO), this entity has been recognized in its earlier stages with increasing frequency. As a result of this, the availability of new antimicrobial agents, and the judicious use of surgery, there has been an improvement in the results of therapy. There remains, however, a subgroup of patients who continue to experience a significant mortality from this infection. A review and selected discussion of our experience with MEO from 1976 to 1979 is presented. Six patients have been diagnosed and successfully treated for MEO. They presented with problems ranging from severe otalgia to multiple cranial neuropathy. For the most part, therapy consisted of the now standard aminoglycoside and carbenicillin combination. Two of the patients were in the high mortality risk group. One of these patients developed an osteomyelitis which extended across the skull base resulting in bilateral cranial neuropathies. His therapy included surgery as well as long-term (months) outpatient treatment with tobramycin and carbenicillin with an excellent result. The second patient was treated similarly. The efficacy of this approach is discussed as well as the usefulness of radionuclide bone scanning in assessing the course and therapy of patients with MEO.

To the Editor. —An omission was made in our article entitled "Potassium Iodide as a Cause of Prolonged Fever," that was published in the AugustArchives(1982;142:1543-1544). Potassium iodide has been proved efficacious in the treatment of cutaneous lesions of sporotrichosis (Sporothrix schenckii), and recent articles suggest its use in noncavitary pulmonary disease in nonimmunocompromised patients and as adjunctive therapy to surgery of solid lesions.1.

Primary Haemophilus influenzae lung abscess has not previously been reported in renal transplant recipients. Our patient had a single cavitary pulmonary nodule and a subacute clinical course. This case demonstrates that infections in immunosuppressed patients may behave in uncharacteristic fashion, and exhaustive attempts must be made to secure the diagnosis so that proper therapy can be instituted.