Williamsia species have been isolated from many disparate environmental sources but only 4 cases of human infection have been reported previously. We now report the first case of W spongiae bacteremia, illustrating the difficulty in recognizing this genus of an emerging health care–associated pathogen.

Healthcare-associated Legionnaires' disease (HCA LD) causes significant morbidity and mortality, with varying guidance on prevention. We describe the evaluation of a case of possible HCA LD and note the pitfalls of relying solely on an epidemiologic definition for association of a case with a facility. Our detailed investigation led to the identification of a new Legionella pneumophila serogroup 1 sequence type, confirmed a healthcare association and helped build the framework for our ongoing preventive efforts. Our experience highlights the role of routine environmental cultures in the assessment of risk for a given facility. As clinicians increasingly rely on urinary antigen testing for the detection of L. pneumophila, our investigation emphasises the importance of clinical cultures in an epidemiologic investigation.

Cryoglobulinemia (CG)-associated pulmonary hemorrhage is an unusual entity. An even rarer occurrence is that of membranoproliferative glomerulonephritis (MPGN) in a patient with CG and alveolar hemorrhage. As far as we can tell, there has been no more than a total of four such cases that have been formally published, and this would be the fifth case [1,2]. A 46-year-old Caucasian woman presented to the emergency department with acute respiratory failure, petechiae, pulmonary hemorrhage, azotemia, proteinuria, and hematuria for 10 days. A ventilation/perfusion lung scan was read as low probability for a pulmonary embolism. Additional serologic examinations included negative ANA, anti-GBM, pANCA, cANCA, hepatitis B and HIV antibody. SPEP (serum protein electrophoresis) was also unremarkable. Hepatitis C antibody was positive, and quantitative testing for CG revealed type II (mixed CG, 0.2 g/dL). C3 and C4 complement levels were low. Renal biopsy revealed MPGN. Bronchoscopy did not demonstrate any endobronchial abnormality. The patient was treated with intravenous methylprednisolone, and both hemoptysis and renal function improved. She did not return for follow-up care. CG associated with HCV has been recognized to cause pulmonary complications which are usually mild and without any significant signs or symptoms. Alveolar hemorrhage in CG is rare; there have been only 10 case reports in English medical literature [1]. Patients with the cryoglobulinemic pulmonary hemorrhage have an extremely poor prognosis and high mortality at presentation and even a poorer prognosis in survivors having further hemorrhagic episodes [1]. Diagnosis of pulmonary hemorrhage associated with HCV-associated CG requires a high index of suspicion; in this case, the patient presented to the emergency services with severe respiratory insufficiency and bilateral alveolar infiltrates on chest radiograph. Her acute respiratory decompensation with diffuse alveolar infiltrates and hemoptysis is indicative of alveolar hemorrhage syndrome [3]. The diagnosis can also be confirmed with the demonstration of hemosiderophages in alveolar lavage obtained by bronchoscopy. It has been established that patients with CG with chronic infection by HCV are sometimes linked to membranoproliferative glomerulonephritis with a survival rate of 33–49% after a mean follow-up of 10 years. Managing an autoimmune manifestation of an infectious disease is complex. Although immunosuppressive agents may be needed to control potentially life-threatening autoimmune complications, there is a risk that the infection might get worse. A reasonable approach is first to control the acute autoimmune manifestations of disease with immunosuppressive therapy and then to deal with the underlying infection to prevent relapse [3]. We conclude that both alveolar hemorrhage and renal involvement associated with HCV-related type CG are exceptional entities. This poses problems regarding treatment as each patient may need a tailored treatment [1]. Conflict of interest statement. None declared.

Chronic wound infections are responsible for considerable morbidity and significantly contribute to the escalation in the cost of health care. Wound infection may initially be manifest as bacterial colonization, and it is only when colonization is combined with other factors, such as decreased vascular supply, intrinsic virulence of specific bacteria (eg, Staphylococcus aureus), and host immune factors, that true infection occurs. The microbiology of chronic wounds is complex, and it is difficult to discern which bacteria are culpable. Deep cultures or quantitative biopsies of wound tissue may be necessary. In some instances, such as in the presence of certain mycobacteria, isolation of specific organisms confirms causation. In many instances, it is appropriate to treat these wounds empirically with a combination of topical antiseptics and systemic antibiotics, especially in the presence of invasive infections.

For fifteen years oral ciprofloxacin has been the standard treatment for malignant otitis externa, a sometimes fatal osteomyelitis of the skull base usually caused by Pseudomonas aeruginosa. Resistance to ciprofloxacin is developing. Over a 16-month period, we saw five cases where malignant otitis externa progressed, with the development of cranial nerve palsies in four cases, despite oral ciprofloxacin. Prolonged intravenous antibiotic therapy became necessary. One case was managed largely as an out-patient, but four patients spent many weeks in hospital. Only two cases had diabetes and this was monitored and controlled. Pseudomonas aeruginosa was isolated in four of the five cases, but antibiotic sensitivity to ciprofloxacin was not determined. In one case a later isolate was tested and found to be ciprofloxacin resistant. Progress was monitored by serial C-reactive protein (CRP) and white cell count. For diagnosis and assessing response to treatment we considered serial magnetic resonance imaging or computed tomography more useful than isotope bone scan. There must be a readiness to use intravenous antibiotics, as a response to ciprofloxacin can no longer be assumed. Bacterial isolates must be tested for sensitivity to antibiotics including ciprofloxacin, and further biopsy and culture are essential if treatment fails.

A 60-year-old woman returned from visiting a cousin in Texas. For the past 6 weeks, she had not been feeling well and had lost almost 30 lb. She had frequent night sweats, although she did not recall having taken her temperature. Upon evaluation in the emergency department, results of physical examination were notable for cachexia and poor dentition. She was noted to have pyuria, and therapy was initiated for a urinary tract infection. Results of blood cultures performed the same day were positive for gram-positive cocci, and vancomycin therapy was initiated. She developed difficulty in seeing to her, left and a computed tomographic scan of the brain was performed; results were interpreted as negative. A transesophageal echocardiogram showed a 3-cm mass attached the posterior leaflet of the mitral valve. Initial interpretation was of an atrial myxoma. One of the authors was asked to consult on the case and noted bilateral conjunctival hemorrhages (Figure 1). Subsequently, the blood culture isolate was identified as Streptococcus mitis. Magnetic resonance imaging confirmed multiple cerebral infarcts consistent with embolic origin. The patient underwent emergent cardiac surgery, and her mitral valve was replaced with a bioprosthetic valve. She successfully completed a 4-week course of antibiotic therapy for her endocarditis.

A 48-year-old white woman was admitted to the hospital with low-grade fever, night sweats, fatigue, nonproductive cough with dyspnea, bilateral knee pain, and swelling that progressed slowly over 6 weeks. She was a 30-pack-year smoker, and had received outpatient antibiotic therapy with clarithromycin and then cephalexin without improvement. The admission chest radiograph showed bilateral interstitial infiltrates, and an effusion was seen on knee radiographs. She was treated with levofloxacin, cefepime, and methylprednisolone with some improvement, but fevers persisted up to 104 degrees F/40 degrees C. She also developed multiple painful skin nodules (Figure 1) and an enlarging painful tongue ulcer (Figure 2). Her bilateral knee swelling and pain also worsened, and a bone scan showed increased activity. Skin biopsy showed acute and chronic inflammation with an abscess that contained "yeast" (Figure 3). Fungal culture from the skin lesion and joint fluid aspirate grew Blastomyces dermatitidis. Urine antigen and blood antigen enzyme-linked immunoassays for B. dermatitidis were positive. The patient was started on a 6-month course of itraconazole oral solution with slow resolution of her joint inflammation and skin lesions over the next several weeks.

A 56-year-old man presented with a cutaneous lesion on his right hand (Figure 1). Approximately 6 weeks previously, he had traveled to Costa Rica for missionary work. During his travel he used a diethyltoluamide-containing insect repellant, but spent one night in the jungle without a mosquito net. Four weeks after his return, he noted a 3 x 2.5-cm ulcer with raised edges and surrounding erythema on the dorsum of his right hand. The patient recalled applying insect repellant with his right hand to other exposed areas of his body but was remiss in applying it to the right hand itself. On examination, the patient was noted to have an ulcerated nodule near his right earlobe (Figure 2) and a second 2 x 1-cm ulcer on the volar aspect of his right wrist (Figure 3). There were no mucocutaneous lesions noted. During the next several weeks, numerous nodules developed in a sporotrichoid pattern on the extensor surface of his right arm (Figure 4). Skin biopsy was performed at the time of initial evaluation and revealed cutaneous leishmaniasis due to Leishmania panamensis. After discussing the different treatment options, miltefosine was administered orally for 28 days. The patient experienced an excellent response to therapy.

Research Article| February 01 2006 Intact and Fragmented Bodies: Versions of Ethics “after Auschwitz” J. M. Bernstein J. M. Bernstein Search for other works by this author on: This Site Google New German Critique (2006) 33 (1 (97)): 31–52. https://doi.org/10.1215/0094033X-2005-004 Cite Icon Cite Share Icon Share Facebook Twitter LinkedIn MailTo Permissions Search Site Citation J. M. Bernstein; Intact and Fragmented Bodies: Versions of Ethics “after Auschwitz”. New German Critique 1 February 2006; 33 (1 (97)): 31–52. doi: https://doi.org/10.1215/0094033X-2005-004 Download citation file: Zotero Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search Books & JournalsAll JournalsNew German Critique Search Advanced Search The text of this article is only available as a PDF. New German Critique, Inc.2006 Article PDF first page preview Close Modal Issue Section: Articles You do not currently have access to this content.

A 28-year-old white man presented to the Emergency Department with a 24-hour history of an eruption on his extremities, trunk, and face. The patient was known to be HIV positive with a CD4 count of 527 and a viral load of 20,300. He denied fever, chills, malaise, and headache. His social history was significant for the fact that he was in a monogamous homosexual relationship. He had no recent travel, pet exposures, or sick contacts. Physical examination revealed stable vital signs and no documented fever. A maculopapular eruption was present on his face, trunk, and extremities (Figures 1 and 2). There was no palmar or plantar involvement. He was treated with diphenhydramine and topical 2.5% hydrocortisone and advised to return if his condition did not improve. Twelve days after the initial evaluation, the patient consulted us again due to progression of his dermatitis. He had no additional complaints other than an eruption on both palms but neither sole. (Figure 3). The eruption now demonstrated erythematous pink-red oval macules and papules 1-2 cm in size distributed on his scalp, face, trunk, and arms. A few papules contained fine collarettes of scale. Further questioning revealed that the patient had experienced a tender rectal ulcer 2 months previously. A punch biopsy and rapid plasma reagin were performed. The histopathologic examination revealed interface dermatitis with lymphocytes, plasma cells, occasional neutrophils, and a prominent lymphoplasmacytic perivascular dermatitis with infiltration of the vessel walls. Warthrin-Starry and Steiner methods demonstrated spirochetes at the dermal-epidermal junction and in vessel walls, consistent with Treponema pallidum (Figure 4). Rapid plasma reagin and fluorescent Treponema antibody were both reactive with a Venereal Disease Research Laboratory (VDRL) of 1:16. The patient was diagnosed as having secondary syphilis and treated with 2.4 million units of IM benzathine penicillin for 3 weeks. His eruption resolved after the initial treatment and he did not experience a Jarisch-Herxheimer reaction.

Case 1: A 39-year-old man with chronic lower extremity lymphedema was admitted to the hospital with acute fever, chills, and left lower extremity pain, swelling, and erythema for the third time in as many months. Examination revealed a temperature of 39 degrees C (102.2 degrees F), and erythmatous induration on the left leg (Figure). The patient was treated with IV clindamycin and cefazolin, with clinical improvement. He was discharged with azithromycin, 500 mg daily for 3 days, done twice monthly. Case 2: A 52-year-old morbidly obese man with stasis dermatitis presented with acute lower extremity pain, swelling, and associated fever. He had been taking prophylactic antibiotics for his recurrent cellulitis for more than a decade and had significantly decreased his number of reoccurrences while on this therapy. He was admitted to the hospital, treated with IV cefazolin, and had a rapid improvement over 48 hours. He was subsequently discharged with continued suppressive antibiotic therapy.

A 31-year-old, previously healthy white man presented to the emergency department with complaints of malaise, fevers, shortness of breath, a non-productive cough, and a "rash." His physical exam revealed a temperature of 100.2F, a pulse of 129 bpm, respiratory rate of 14 BPM, and blood pressure of 140/74 mm Hg. He was alert, oriented, and in no distress. His oropharynx was dry, his neck was supple, and cervical lymphadenopathy was absent. He had tachycardia, bilateral wheezes, and rhonchi with prolonged expirations. There was a diffuse vesicular eruption enveloping his entire body with involvement sparing his palms and soles (Figures 1 and 2). Laboratory values showed a hemoglobin of 16.0 g/dL and a white blood cell count of 7100 cells/pL, with 39%neutrophils, 23% bands, and 35% lymphocytes. His platelet count was mildly decreased to 86,000 x 103/pL. Chest radiograph revealed bilateral diffuse interstitial infiltrates. A diagnosis of acute varicella-zoster virus pneumonia (varicella pneumonia) was made, and the patient was started on IV acyclovir (10 mg/kg every 8 hours). Upon further questioning, the patient stated that his daughter had been diagnosed with "chickenpox" 7 days ago. The patient had numerous exposures to chickenpox in the past but had never developed clinical expressions of varicella. He was not at risk for HIV infection, not having multiple sexual partners, IV drug abuse, or blood transfusions. During the 1 day of in-hospitalization, his fever abated and the pulmonary signs diminished. Following discharge, IV acyclovir was replaced by valacyclovir to complete a 7-day course of therapy.