Severe Methicillin-Resistant Staphylococcus Aureus Septicemia in a Case of Misdiagnosed Crusted (Norwegian) Scabies


Noel Manyindo, MD, MBA; Prema Pamireddy, MD; Mary McDonald, MD; Jaya Vijayan, MD; Babafemi Adenuga, MD; and R. George Adams, MD

Crusted (Norwegian) scabies is caused by the itch mite Sarcoptes scabiei var hominis. It is a highly contagious variant of classic scabies that affects elderly patients in particular,1 especially residents of nursing homes and individuals who are immunocompromised, malnourished, or cognitively impaired.2,3 Crusted scabies often presents atypically from classic scabies, making it a challenging clinical diagnosis to reach, as it may mimic a host of other dermatoses.4 A delayed or missed diagnosis of crusted scabies may result in serious morbidity, including severe secondary infection with life-threatening methicillin-resistant Staphylococcus aureus (MRSA) via skin eruptions, and epidemic infestations in hospitals and nursing homes.4-6

We report a case of crusted scabies in an elderly nursing home resident. The condition went misdiagnosed as drug-induced dermatitis for >2 months. As a result, the patient experienced terminal complications from MRSA sepsis and there was an outbreak of crusted scabies among several other nursing home residents and staff members. The case presentation illustrates how failure to diagnose and eliminate these microscopic, burrowing parasites promptly can have life-threatening consequences, particularly for elderly and immunocompromised individuals.

Case Presentation

A 73-year-old male nursing home resident was transferred from a regional long-term acute care (LTAC) facility to a university hospital because of persistent MRSA sepsis—despite having received intravenous (IV) antibiotics for almost 2 weeks—and for worsening dyspnea. He was previously admitted to a large community medical center for 6 days for a worsening chronic rash, which was first noticed approximately 8 weeks prior to his current presentation at the university hospital. Drug-induced dermatitis was diagnosed at the community medical center, and his home medications were discontinued. On initial blood tests, the patient was also found to have MRSA bacteremia of unclear origin and was started on IV antibiotics (linezolid). After 4 days on IV antibiotics, he was discharged to the LTAC facility for continued antibiotic treatment. During his 8-day stay at the LTAC facility, his general medical condition worsened and he developed diminished mentation from baseline, acute-on-chronic renal insufficiency, shortness of breath, and metabolic acidosis.

Upon transfer to the university hospital, his accompanying medical records revealed a medical history significant for mild cognitive impairment, a status of class III morbid obesity (body mass index, >40 kg/m2) post-gastric bypass surgery, obstructive sleep apnea treated with bilevel positive airway pressure (BiPAP), chronic obstructive pulmonary disease, hypertension, hypothyroidism, chronic kidney disease, osteoarthritis, and poorly controlled diabetes mellitus. On admission, his blood pressure was 94/56 mm Hg, his heart rate was 55 beats per minute, and his respiratory rate was 21 breaths per minute. He was afebrile, with a temperature of 96.8°F, and mildly hypoxemic, with an oxygen saturation of 91% while breathing room air.

On physical examination, the patient was found to be a morbidly obese, elderly white man in mild respiratory distress. He was alert and able to obey verbal commands. Although nonverbal, he scored 11/15 on the Glasgow Coma Scale (eye opening, 4; verbal, 1; motor, 6). Dry mucus membranes were noted, and diffuse crepitations were heard bilaterally on auscultation of the lungs. S1 and S2 heart sounds were distant. On inspection, his abdomen was obese, moved with respiration, had normoactive bowel sounds on auscultation, and had no masses or tenderness on palpation. A remarkable pustular, hyperkeratotic rash with yellow flaky plaques affected his upper limbs, trunk, back, and thighs (Figures 1 and 2). The patient’s face and neck were spared. Using the “rule of fives,” which is preferentially used to estimate burned body surface area in obese burn victims,7 the patient’s physicians estimated that 88% of his body surface area was affected by rash.

Initial laboratory data included the following: a hemoglobin level of 12.1 g/dL; hematocrit of 36.5%; and a white blood cell count of 15,300/µL, with 84% neutrophils, 10% lymphocytes, and 4% eosinophils. The patient’s platelet count was 209 ×103/µL, and mean corpuscular volume was 94 fL. Urinalysis was positive for blood and leukocytes, and urine microscopy revealed yeast and bacteria. Initial chest x-ray was unremarkable, and no acute intracranial changes were observed with head computed tomography scanning. Cardiac markers were normal, with no evidence of myonecrosis, and a 12-lead electrocardiogram showed sinus bradycardia. A two-dimensional echocardiogram showed a heart rate of <60 beats per minute, with an ejection fraction of 50% to 60% and no evidence of endocarditis. After blood, urine, and sputum cultures were drawn, the patient was given IV fluids and empirically started on triple IV antibiotic therapy using clindamycin 600 mg, levofloxacin 750 mg, and linezolid 600 mg. He also received fluconazole 150 mg by mouth. BiPAP was initiated and he was admitted to the medical intensive care unit (MICU) under contact isolation for MRSA.

In the MICU, the patient was started on appropriate treatments for his other underlying conditions, including methylprednisolone 80 mg IV every 8 hours, diphenhydramine 50 mg IV every 8 hours, levothyroxine 75 mcg orally once daily, and regular insulin/D5 infusion at 125 mL/hour. He also received once-daily prophylactic treatments for deep vein thrombosis and gastrointestinal bleeding, which consisted of enoxaparin 40 mg subcutaneously and pantoprazole 40 mg orally, respectively. The aforementioned blood culture grew MRSA and Enterococcus faecalis, while the urine culture grew gram-negative bacteria. Following the results of sensitivity studies, antibiotic coverage was changed to meropenem 500 mg orally every 12 hours, vancomycin 1000 mg IV every 8 hours (with peak and trough monitoring ordered after every third dose), and micafungin 100 mg IV once daily. The infectious diseases team was consulted for optimal management.



Very interesting article

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