Secondary Streptococcus Infection in a Cancer Patient: A Hybrid Rash

Reactivation of varicella-zoster virus (VZV) infections can occur in up to 20% of affected persons. Those most at risk are immunocompromised patients, such as transplant recipients or those with a malignant tumor or HIV infection. These patients are also at risk for the development of a secondary bacterial infection, which can be severe and sometimes fatal.

Case report 

A 60-year-old man with head and neck cancer recently completed a course of radiation therapy to the neck. He presented with a 2-day history of chills and fever, with the highest recorded temperature being 40C (104F). He also had a painful rash on his right arm (Figure 1). In addition, there were a few pustules and papules on his chest and crusted lesions on his nares (Figure 2). The remaining physical examination findings were unremarkable.

Figure 1 - Ahemorrhagic,crusted,macular rashis apparent onthe patient'sright arm.

Figure 2 - Crusted escharsin the area of the lipand nares suggestherpes simplexreactivation

A pustule on his chest was opened, and culture of the fluid revealed group A Streptococcus. Immunofluorescent staining of biopsy material from the arm rash was positive for VZV. Material from the lesions on the nares was not cultured; however, the lesions were presumed to be caused by a herpes simplex reactivation.

After the patient was admitted, treatment with intravenous ampicillin/ sulbactam, 3 g 4 times daily, and intravenous acyclovir, 10 mg/kg 3 times daily, was started. The fever resolved within 2 days, and the rash gradually improved over 3 days. He was discharged home on a regimen of oral penicillin V potassium, 500 mg 4 times daily, and acyclovir, 800 mg 5 times daily, for 10 days. The rash completely resolved within 2 weeks.

Discussion VZV is the smallest and most contagious of the human herpesviruses. After a primary VZV infection, the virus becomes latent in the dorsal root or cranial nerve ganglia but can be reactivated in the presence of impaired cellular immunity. Reactivated VZV infection, also known as herpes zoster or shingles, occurs in about 1% to 20% of the population and is characterized by a vesicular rash that occurs along an entire dermatome. ¹ In severe cases, it may disseminate widely to the lungs, liver, and the CNS.

Patients with a particularly highrisk of reactivation include those with a malignant tumor, HIV infection, or other cellular immunodeficiencies. One of the groups at highest risk for VZV infection is patients who have had an allogeneic stem cell transplantation; these patients have a higher risk of dissemination, have a longer duration of lesions, and are more prone to secondary bacterial infection.^2,3

The most common cause of bacterial superinfections of lesions caused by VZV infection is group A Streptococcus and Staphylococcus aureus. Both bacteria have been reported to cause skin infection after a primary varicella infection in children, with severity ranging from superficial wound infections to deep-seated infectionssuch as necrotizing fasciitis, myositis, and osteomyelitis.^4,5 Several cases also resulted in toxic shock syndrome and death.⁴

Although bacterial complications are less common in adults, one case of varicella (varicella gangrenosa) that presented as necrotizing fasciitis with toxic shock-like syndrome due to group A Streptococcus infection was reported in a previously healthy 32-year-old man.⁶ Acase of disseminated herpes zoster complicated by S aureus necrotizing fasciitis was seen in an elderly woman who used low-dose methotrexate and prednisone for rheumatoid arthritis.⁷

Our case illustrates a rare coexistence of secondary bacterial infection with a dermatomal VZV infectionthat caused a hybrid rash. Notably, the crusted vesicles from the VZV infection may be superimposed on hemorrhagic bacterial cellulitis or impetigo. S aureus (including methicillin- resistant S aureus) and group A Streptococcus can colonize the skin and develop into an invasive infection when disseminated varicella or dermatomal herpes zoster compromises skin integrity. Recognizing a simultaneous viral (VZV) and bacterial (S aureus or group A Streptococcus) infection can be challenging.

References:

• Straus SE, Ostrove JM, Inchauspé G, et al. NIH conference. Varicella-zoster virus infections. Biology, natural history, treatment, and prevention. Ann Intern Med. 1988;108:221-237.

• Boeckh M, Kim HW, Flowers ME, et al. Longterm acyclovir for prevention of varicella zoster virus disease after allogeneic hematopoietic cell transplantation-a randomized double-blind placebo-controlled study. Blood. 2006;107:1800- 1805.

• Gallagher JG, Merigan TC. Prolonged herpeszoster infection associated with immunosuppressive therapy. Ann Intern Med. 1979;91:842- 846.

• Aebi C, Ahmed A, Ramilo O. Bacterial complications of primary varicella in children. Clin Infect Dis. 1996;23:698-705.

• Bittmann S. Bacterial osteomyelitis after varicella infection in children. J Bone Miner Metab. 2004;22:283-285.

• González-Ruiz A, Ridgway GL, Cohen SL, et al. Varicella gangrenosa with toxic shock-like syndrome due to group Astreptococcus infection in an adult: case report. Clin Infect Dis. 1995;20: 1058-1060.

• Jarrett P, Ha T, Oliver F. Necrotizing fasciitis complicating disseminated cutaneous herpes zoster. Clin Exp Dermatol. 1998;23:87-88.