Environmental Persistence of Monkeypox Virus on Surfaces in Household of Person With Travel-Associated Infection, Dallas, Texas, USA, 2021

Clint N. Morgan; Florence Whitehill; Jeffrey B. Doty; Joann Schulte; Audrey Matheny; Joey Stringer; Lisa J. Delaney; Richard Esparza; Agam K. Rao; Andrea M. McCollum


Emerging Infectious Diseases. 2022;28(10):1982-1989. 

In This Article

Abstract and Introduction


In July 2021, we conducted environmental sampling at the residence of a person in Dallas, Texas, USA, who had travel-associated human West African monkeypox virus (MPXV-WA). Targeted environmental swab sampling was conducted 15 days after the person who had monkeypox left the household. Results indicate extensive MPXV-WA DNA contamination, and viable virus from 7 samples was successfully isolated in cell culture. There was no statistical difference (p = 0.94) between MPXV-WA PCR positivity of porous (9/10, 90%) vs. nonporous (19/21, 90.5%) surfaces, but there was a significant difference (p<0.01) between viable virus detected in cultures of porous (6/10, 60%) vs. nonporous (1/21, 5%) surfaces. These findings indicate that porous surfaces (e.g., bedding, clothing) may pose more of a MPXV exposure risk than nonporous surfaces (e.g., metal, plastic). Viable MPXV was detected on household surfaces after at least 15 days. However, low titers (≤102 PFU) indicate a limited potential for indirect transmission.


Monkeypox, a zoonotic infectious disease caused by monkeypox virus (MPXV; genus Orthopoxvirus [OPXV]), is endemic to West and Central Africa. After its discovery in 1958, the virus had not been reported in humans outside its endemic range until 2003, when a shipment of MPXV-infected small mammals was transported from Ghana to the United States, causing secondary animal and human infections.[1] Genomic sequencing of isolates of MPXV across its endemic range indicates the existence of 2 clades: West African (WA) and Congo Basin; WA MPXV has a lower mortality rate.[2]

Transmission is known to occur by direct contact with infectious lesion material or bodily fluids of an infected human or animal or by inhalation of respiratory secretions during prolonged, face-to-face contact.[3,4] In addition, transmission might occur by direct contact with objects or materials contaminated with MPXV, although documented occurrences are rare.[5,6] Poxvirus lesions, their exudates (vesicular or pustular fluid), and crusts contain viable virus.[3,4] Poxvirus virions within lesion material shed during infection are known to be more resistant to desiccation than for other enveloped viruses (e.g., influenza viruses, rubella virus) because the virions are tightly bound with the fibrin matrices of the scab/crust material.[7,8] This feature can lead to long-term environmental persistence of OPXVs.

Studies with variola (causative agent of smallpox) and vaccinia viruses demonstrated that if contaminated material is maintained in an environment that has low humidity, low temperature, and remains protected from UV radiation, the viral particles can remain viable for months to years.[9,10] One study demonstrated the extreme longevity of variola virus in lesion scabs stored within an envelope in a cupboard; the virus remained viable for 13 years until the sample was used to completion.[11] This longevity is striking; however, the infectivity of variola scabs alone is believed to be low based on epidemiologic and laboratory data.[11–14] Vesicular fluid from OPXV lesions and other secretions generally have lower persistence in some laboratory studies than scabs.[15,16] Outside of insights gained from other OPXVs, the longevity and environmental persistence of MPXV is largely unknown, including within a household environment. Considering the increasing frequency of monkeypox cases being exported from disease-endemic areas,[17–20] and the concern for secondary infections among household contacts, there is a need for more specific information on transmission risks due to contaminated fomites in the household.

On July 16, 2021, the US Centers for Disease Control and Prevention (CDC) confirmed a WA MPXV infection in a man (US resident) who had recently traveled from Lagos, Nigeria, to Dallas, Texas, USA. This case was the first MPXV infection reported in the United States since the 2003 outbreak, prompting an immediate response and investigation. The person who had monkeypox arrived in Dallas on July 9 and stayed in a household, a 1-bedroom residence that had no other occupants, for 4 days before coming to the hospital for treatment.[17] During these 4 days, the man was in the household and had a disseminated purulent rash.[17] We conducted environmental sampling within the residence and assessed the viral load and viability of virus present on commonly used surfaces and objects within the household.