From July 25 to July 30, 1998, One outbreak has been reported to the Maryland Department of Health and Mental Hygiene (DHMH). It was an outbreak of febrile upper respiratory illness in a home day care center, with one case rapid test positive for pharyngeal group A S. pyogenes and one case culture positive from the pharynx for both group A S. pyogenes and beta lactamase positive H. influenzae. Clinical and antibiotic treatment response features, however, are also suggestive of an underlying viral illness with bacterial co-infection or colonization.

As an update, the suspect botulism case reported to DHMH on July 20, 1998 ruled out for botulism: serum toxin bioassay was negative and EMG and MRI findings indicated demyelination.

From July 18 to July 24, 1998, 7 outbreaks have been reported to the Maryland Department of Health and Mental Hygiene. Of the 7, 3 were foodborne gastroenteritis of unknown etiology; the remaining 4 were a single case of botulism (later ruled out), scabies and gastroenteritis reported from long term care facilities, and gastroenteritis in a prison facility.

B. The Johns Hopkins Hospital. Information provided by Dr. May Arroyo, Department of Pathology.

Case history: The patient is a 28 year old HIV-positive black female with a history of daily intravenous heroin use, and refusal to take antiretroviral therapy. The patient presented to the ED complaining of a two day history of erythema, swelling, and pain of her right elbow and forearm. She reported being assaulted and thrown on the ground two days ago. She last injected into that arm three days prior to admission. On physical examination the right elbow and forearm appeared erythematous, tense, and edematous, and showed blistering. Multiple skin ulcerations were present on the arms corresponding to injection sites. Her temperature was 38.5ºC. A radiograph of the arm revealed moderate diffuse soft tissue swelling. The wound was emergently debrided in the operating room. The wound contained necrotic tissue and fascia and 100 cc of purulent material. No gas was noted. Cultures were sent. The postoperative diagnosis was necrotizing fasciitis. The patient was started on clindamycin and penicillin. She was schedule for debridement on day 4 of hospitalization, however, on day 3 of hospitalization the patient discharged herself against all medical advice.

Organism: A gram stain of the purulent material showed heavy pleomorphic gram positive microorganisms. Within 24 hours the cultures grew Arcanobacterium haemolyticum. A. haemolyticum, previously known as Corynebacterium haemolyticum, is a human pathogen most commonly implicated with nonstreptococcal pharyngitis. The organism has also been shown to cause cellulitis, cutaneous ulcers, wound infections, paronychia, peritonsillar abscesses, and sepsis. Less commonly, A. haemolyticum has been shown to cause brain abscesses, endocarditis, otitis media, omphalitis, cavitary pneumonia, sphenoidal sinusitis, and osteomyelitis. Interestingly, review of the literature yielded no previous reports of necrotizing fasciitis caused by A. haemolyticum.

Three extracellular toxins have been isoled from the filtrates of A. haemolyticum: a hemolysin, a neuramidase, and phospholipase D. Intradermal injection of phospholipase D into rabbits has been shown to produce hemorrhagic dermonecrosis (1). MacLean et al., however, reported no evidence of necrosis following intracutaneous infection of A. haemolyticum into the arms of human volunteers (2). The inoculations resulted in the formation of an indurated papule with edema and erythema.

Clinical disease: A. haemolyticum causes an exudative pharyngitis which is clinically indistinguishable from streptococcal pharyngitis. It differs from the latter in that A. haemolyticum pharyngitis occurs in an older age group (10-30 years of age). Moreover, as many as 55% of the patients develop a pruritic, blanching, scarlatiniform rash 1 to 4 days after the onset of the pharyngitis. The rash has been misinterpreted as drug allergy or the rash associated with mononucleosis; the desquamation has been misdiagnosed as toxic shock syndrome. Peritonsillar abcesses pharyngeal pseudomembranes have been described. The underdiagnosis of A. haemolyticum as a cause of pharyngitis is possibly due to the increased use of group A rapid antigen detection tests or failure to work-up a pharyngeal culture not growing goup A streptococcal colonies. Cutaneous lesions caused by A. haemolyticum include cellulitis and chronic ulcers. The isolation of this organism from wound cultures is infrequently reported, probably due to the misconception that the organism represents a skin contaminant.

Laboratory Diagnosis: A. haemolyticum is a catalase negative, B-hemolytic, non-motile, non-acid fast, non-sporulating, gram positive rod. Gram stain from cultures incubated for 24 hours reveal long, club-shaped, curved rods (coryneform). As the culture ages, the organism appears beaded and granular and exhibits gram staining variability. The organism ferments dextrose, lactose and maltose, but not mannitol or xylose. Optimum growth occurs at 37^oC, in either microaerophilic or anaerobic conditions. At 24 hours, the colonies are circular and white. However, at 48 hours they exhibit a characteristic central black dot which remains on the agar after removal of the colony (1).

Therapy: A. haemolyticum is susceptible to erythromycin, clindamycin, chloramphenicol, and tetracycline. Variable susceptibility has been demonstrated to penicillin, gentamicin, and tobramycin (1). The organism is generally resistant to sulfonamides and nalidixic acid.

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