- Volume 1, Issue 7, 2019
Volume 1, Issue 7, 2019
- Case Report
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A case of cutaneous toxigenic Corynebacterium ulcerans likely acquired from a domestic dog
Introduction. Corynebacterium ulcerans can produce diphtheria toxin and although still rare, is now the predominant cause of toxigenic diphtheria infection in the UK, making this organism of great clinical and public health importance. Here we describe a cutaneous case, likely secondary to domestic animal contact.
Case presentation. A 60-year-old female presented with a slow-healing finger-burn wound. A skin swab cultured Corynebacterium ulcerans, which was confirmed to be toxin producing. She resided with her partner and two dogs, one of which had a chronic skin lesion. Her most recent diphtheria vaccine was in 2009. Four close contacts were identified, two of whom were healthcare professionals, and nose and throat swabs were obtained. The patient was treated with clarithromycin (14 day course), diphtheria vaccine and excluded from work until completion of antibiotics and negative clearance swabs. Contacts were given erythromycin (7 day course), vaccinated and healthcare worker contacts excluded from work until swab negative. A veterinary practitioner swabbed the throats and a skin lesion of their dogs. One contact (partner of patient) and all dog swabs were positive. Partial allelic profiles from MLST supported an epidemiological link. The dogs were treated with antibiotics and antimicrobial skin wash. Repeat swabs for the index case, contact and both dogs were negative following treatment.
Conclusion. This was a rare case of cutaneous diphtheria secondary to Corynebacterium ulcerans with domestic animals the most likely source, although human-to-human contact could not be excluded, with important human and animal public health implications.
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Eumycetoma caused by Cladophialophora bantiana in the United States
More LessA female presented in the sixth decade of life with a history of undifferentiated small cell carcinoma of the right breast in clinical remission, status-post chemotherapy and resection 6 years previously, presented with a chronic anterior knee skin nodule that grew in size over the prior 5–6 weeks. She had no history of opportunistic infections or recent immunosuppression. As it grew, the nodule became tender to touch. Examination revealed a 4–6 mm superficial purple-red nodule. Also, a similar lesion was present on the dorsum of her left foot for the past year, which also recently grew and became tender. The patient did report frequently kneeling on soil when gardening in Florida. She reported no other symptoms. Due to a concern for cutaneous metastasis of the patient’s previously diagnosed small cell carcinoma of the breast, the anterior knee lesion was biopsied. Histology revealed histocyte-rich inflammation with foci of acute inflammation as well as pigmented fungal forms. Subsequent fungal culture of excised tissue grew Cladophialophora bantiana, identified by ribosomal gene DNA sequencing.
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Antiphospholipid antibody syndrome with thrombotic splenic infarcts associated with acute cytomegalovirus infection
More LessIntroduction. We describe a case of acute cytomegalovirus (CMV) infection complicated by acquired antiphospholipid antibodies and splenic thrombi. We discuss the associations between CMV infection and thrombosis risk and correlation with antiphospolipid antibodies.
Case presentation. A previously healthy 32-year-old woman is hospitalized for acute abdominal pain and fever and found to have multiple splenic infarcts on an abdominal computed tomography (CT) scan. An infectious work-up is negative except for acute CMV, and a hypercoagulable work-up is only positive for antiphospholipid antibodies. The patient is discharged and placed on anti-coagulation therapy for 6 months.
Conclusion. Co-incident thrombosis and antiphospholipid antibody syndrome can occur with acute viral infections, including CMV. We discuss the viral infection-associated increased risk of developing blood clots and antiphospholipid antibodies as being either correlative with or causative of viral-induced thrombosis.
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Prevalence and resistance pattern of uropathogens from community settings of different regions: an experience from India
Sarita Mohapatra, Rajashree Panigrahy, Vibhor Tak, Shwetha J. V., Sneha K. C., Susmita Chaudhuri, Swati Pundir, Deepak Kocher, Hitender Gautam, Seema Sood, Bimal Kumar Das, Arti Kapil, Pankaj Hari, Arvind Kumar, Rajesh Kumari, Mani Kalaivani, Ambica R., Harshal Ramesh Salve, Sumit Malhotra and Shashi Kant
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