Rash in an immunocompromised patient

The patient’s history and presentation, as well as a positive varicella zoster virus (VZV) culture of vesicular fluid, led to a diagnosis of disseminated herpes zoster (DHZ). The patient’s laboratory studies were remarkable for mild lymphopenia, thrombocytopenia, and elevated liver function tests. Shave and punch biopsies of the lesion showed ballooning epithelial necrosis with multinucleated giant cells.

DHZ is characterized by more than 20 vesicles outside of a primary or adjacent dermatome and is caused by extensive reactivation of VZV. DHZ is most often encountered in immunocompromised patients.¹ Untreated DHZ can lead to encephalitis, myelitis, nerve palsies, pneumonitis, hepatitis, and ocular complications.

Diagnosis is usually made clinically and confirmed by a polymerase chain reaction test, direct fluorescent antibody testing, or viral culture.² In immunocompetent patients, uncomplicated DHZ is treated with oral acyclovir 800 mg 5 times daily, valacyclovir 1 g 3 times daily, or famciclovir 500 mg 3 times daily for 7 days. Hospital admission for intravenous acyclovir is recommended for immunocompromised patients, especially those with internal organ involvement, such as hepatitis or encephalitis.³

Early treatment is imperative to avoid life-threatening complications. Active herpes zoster lesions are infectious by contact with vesicular fluid until they dry and crust over. Patients should be instructed to avoid contact with susceptible people, including those who are immunocompromised, babies who have not received their varicella vaccine, and pregnant women. It is important to keep DHZ on the differential—especially in an immunosuppressed patient with a diffuse vesicular rash—as it can lead to significant morbidity and mortality.

Our patient was treated with oral valacyclovir 1 g tid for 10 days and he improved without developing systemic symptoms.

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Image courtesy of Christen B. Samaan, MD. Text courtesy of Christen B. Samaan, MD, and Matthew F. Helm, MD, Department of Dermatology, and Nanjiba Nawaz, BA, Penn State College of Medicine, Hershey.

The patient’s history and presentation, as well as a positive varicella zoster virus (VZV) culture of vesicular fluid, led to a diagnosis of disseminated herpes zoster (DHZ). The patient’s laboratory studies were remarkable for mild lymphopenia, thrombocytopenia, and elevated liver function tests. Shave and punch biopsies of the lesion showed ballooning epithelial necrosis with multinucleated giant cells.

DHZ is characterized by more than 20 vesicles outside of a primary or adjacent dermatome and is caused by extensive reactivation of VZV. DHZ is most often encountered in immunocompromised patients.¹ Untreated DHZ can lead to encephalitis, myelitis, nerve palsies, pneumonitis, hepatitis, and ocular complications.

Diagnosis is usually made clinically and confirmed by a polymerase chain reaction test, direct fluorescent antibody testing, or viral culture.² In immunocompetent patients, uncomplicated DHZ is treated with oral acyclovir 800 mg 5 times daily, valacyclovir 1 g 3 times daily, or famciclovir 500 mg 3 times daily for 7 days. Hospital admission for intravenous acyclovir is recommended for immunocompromised patients, especially those with internal organ involvement, such as hepatitis or encephalitis.³

Early treatment is imperative to avoid life-threatening complications. Active herpes zoster lesions are infectious by contact with vesicular fluid until they dry and crust over. Patients should be instructed to avoid contact with susceptible people, including those who are immunocompromised, babies who have not received their varicella vaccine, and pregnant women. It is important to keep DHZ on the differential—especially in an immunosuppressed patient with a diffuse vesicular rash—as it can lead to significant morbidity and mortality.

Our patient was treated with oral valacyclovir 1 g tid for 10 days and he improved without developing systemic symptoms.

‌

Image courtesy of Christen B. Samaan, MD. Text courtesy of Christen B. Samaan, MD, and Matthew F. Helm, MD, Department of Dermatology, and Nanjiba Nawaz, BA, Penn State College of Medicine, Hershey.

The patient’s history and presentation, as well as a positive varicella zoster virus (VZV) culture of vesicular fluid, led to a diagnosis of disseminated herpes zoster (DHZ). The patient’s laboratory studies were remarkable for mild lymphopenia, thrombocytopenia, and elevated liver function tests. Shave and punch biopsies of the lesion showed ballooning epithelial necrosis with multinucleated giant cells.

DHZ is characterized by more than 20 vesicles outside of a primary or adjacent dermatome and is caused by extensive reactivation of VZV. DHZ is most often encountered in immunocompromised patients.¹ Untreated DHZ can lead to encephalitis, myelitis, nerve palsies, pneumonitis, hepatitis, and ocular complications.

Diagnosis is usually made clinically and confirmed by a polymerase chain reaction test, direct fluorescent antibody testing, or viral culture.² In immunocompetent patients, uncomplicated DHZ is treated with oral acyclovir 800 mg 5 times daily, valacyclovir 1 g 3 times daily, or famciclovir 500 mg 3 times daily for 7 days. Hospital admission for intravenous acyclovir is recommended for immunocompromised patients, especially those with internal organ involvement, such as hepatitis or encephalitis.³

Early treatment is imperative to avoid life-threatening complications. Active herpes zoster lesions are infectious by contact with vesicular fluid until they dry and crust over. Patients should be instructed to avoid contact with susceptible people, including those who are immunocompromised, babies who have not received their varicella vaccine, and pregnant women. It is important to keep DHZ on the differential—especially in an immunosuppressed patient with a diffuse vesicular rash—as it can lead to significant morbidity and mortality.

Our patient was treated with oral valacyclovir 1 g tid for 10 days and he improved without developing systemic symptoms.

‌

Image courtesy of Christen B. Samaan, MD. Text courtesy of Christen B. Samaan, MD, and Matthew F. Helm, MD, Department of Dermatology, and Nanjiba Nawaz, BA, Penn State College of Medicine, Hershey.