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237
to LP in SOT populations, especially in the presence of altered mental status.
Diagnostic studies from the LP should include cell count, glucose, total protein,
gram stain and bacterial culture, and measurement of the opening pressure [187].
For most SOT recipients undergoing evaluation for CNS infection, the CSF should
also be sent for viral PCR including enteroviruses, HSV, VZV, EBV, and CMV.If
there is concern for a fungal etiology, providers should consider sending a CSF
cryptococcal antigen.
SOT recipients are at higher risk for the development of bacterial or fungal brain
abscesses than immunocompetent hosts. Any SOT recipient presenting with cranial
nerve decits requires urgent brain imaging [188]. A space-occupying lesion identi-
ed on brain imaging in a SOT recipient warrants admission to the hospital and
immediate neurosurgical and infectious disease consultation to direct evaluation
and consideration of early treatment. If analysis of the CSF is unrevealing for
patients with a space-occupying lesion, brain biopsy with pathologic examination
may be indicated.
8.6.2 Bacterial Infections oftheCNS
There is a seven-fold increase in the incidence of bacterial meningitis among SOT
recipients compared to the broader population [189]. Patients who develop bacte-
rial meningitis after solid organ transplantation may not manifest typical symp-
toms of high fevers and meningismus due to impaired inammatory response
from immunosuppressing medications. SOT recipients are also at higher risk of
CNS infection with opportunistic bacteria including Nocardia spp., mycobacteria,
and Listeria spp. These infections often begin as a respiratory illness and result in
meningitis due to hematogenous spread of the organism. Additionally, syphilis
(both donor-derived and sexually acquired) should be considered as it presents
throughout all stages of infection (i.e., CNS seeding occurs with primary infec-
tion, not just tertiary syphilis).
If there is concern for bacterial meningitis, the SOT recipient should be evaluated
in an emergency room or inpatient setting to undergo lumbar puncture and rapid
administration of antibiotics until diagnostic studies return.
8.6.3 Viral Infections oftheCNS
Viral infections of the CNS most commonly present 1–6months after transplanta-
tion. Herpes viruses are the most common causes of viral CNS infection in SOT
recipients, including VZV, HSV, CMV, EBV, and HHV-6 [190]. Patients may pres-
ent with symptoms of meningitis and/or encephalitis. A SOT recipient who presents
with altered mental status, personality changes, seizures, or speech or gait distur-
bance should receive neuroimaging and be evaluated for viral encephalitis with
8 Infections intheAdult Solid Organ Transplant Recipient
238
lumbar puncture and PCR-based assays on the CSF.As with bacterial infections,
evaluation will typically require an emergency department evaluation and likely
hospitalization. EBV rarely causes encephalitis but is associated with post- transplant
lymphoproliferative disorder (PTLD) in the CNS [191].
While more commonly seen in patients receiving immunomodulating drugs for
rheumatologic or neurologic disease, infection with JC virus can cause progressive
multifocal leukoencephalopathy (PML) in SOT recipients late in the post-
transplantation course [192].
8.6.4 Fungal Infections oftheCNS
Infection with cryptococcus is by far the most common cause of fungal menin-
gitis and meningoencephalitis in patients after solid organ transplantation. The
onset of cryptococcus infection is late in the post-transplant course, often occur-
ring at a median 21months after transplantation [193]. Cryptococcus infection
occurs after inhalation through the respiratory tract and is thought to represent
reactivation of the infection in immunocompromised hosts, although primary
infections do occur. Importantly, fever is present only 50% of the time in SOT
recipients with cryptococcus meningoencephalitis. Testing for cryptococcus
antigen in the CSF and the serum is the gold standard for diagnosing cryptococ-
cus infection. Treatment regimens vary and may involve induction therapy for
2weeks with liposomal amphotericin B and ucytosine, followed by consolida-
tion therapy with uconazole for 8weeks, and nally a lower dose maintenance
regimen of uconazole for a minimum of 6–12 additional months, with close
coordination with the transplant team because of drug interactions (See Chap.
3) [194]. Secondary prophylaxis with uconazole after CNS cryptococcal infec-
tion is controversial.
Aspergillus is the most common fungal etiology causing cerebral abscesses in
SOT recipients [2]. Mortality for SOT recipients with aspergillus abscesses is
greater than 50%, even with appropriate treatment.
Providers should also be aware that Toxoplasma gondii, a parasitic infection,
may cause brain abscesses in SOT recipients and requires prolonged antimicrobial
therapy.
A summary of key considerations is given in Table8.12.
Table 8.12 Key considerations for CNS infections
• Viral CNS infections manifest less often in the early (i.e., <30days) post-transplant period
• Fungal CNS infections have the highest incidence >12-months post-transplant
• Posterior Reversible Encephalopathy Syndrome (PRES) is a non-infectious cause of
encephalopathy that can mimic infection; calcineurin inhibitors are one of the most common
causes and are taken by the majority of SOT recipients
J. Hu et al.
239
8.7 Skin andSoft Tissue Infections
Case
A 67-year-old patient with a history of heart transplantation presents to the
primary care clinic with 4days of worsening erythema, edema, and pain of
the right lower extremity. The patient rst noticed erythema and swelling
around his great toe which progressed to the foot and then the lower leg in the
following days. Yesterday evening, he had trouble going to sleep due to pain.
He does not have a fever or chills. He had no trauma to the foot and does not
walk barefoot. On exam, he is afebrile and vital signs are normal. His right
lower extremity has erythema and edema extending from the distal foot up the
knee, with increased erythema and induration medially compared to laterally.
There are no areas of purulence or uctuance. There is dryness and cracking
of the skin between his toes with evidence of tinea pedis. There is no pain in
the joints of the ankle or the foot with range of motion.
Comment
This patient has uncomplicated cellulitis of the lower extremity. There are no
signs of systemic infection and no areas of purulence. He likely developed a bacte-
rial superinfection of his foot due to underlying tinea pedis which causes skin
breakdown and creates a portal of entry for skin ora. A swab for bacterial culture
is only indicated if purulence is present; in the absence of purulence, a skin culture
is not helpful due to anticipated growth of skin ora. In the absence of purulence
or signs of an abscess, empiric treatment should be tailored to cover Streptococcus
species and Methicillin-sensitive Staphylococcus aureus (MSSA), preferably with
cephalexin. If there are areas of purulence or culture-derived data, the antibiotic
spectrum should be extended to cover Methicillin-resistant Staphylococcus aureus
(MRSA); common regimens include a rst-generation cephalosporin combined
with antibiotic active against MRSA including doxycycline, trimethoprim-
sulfamethoxazole, or linezolid. Generally, clindamycin is no longer indicated given
resistance patterns of both Staphylococci and Streptococci. When considering
antibiotics in a SOT recipient, drug interactions should be checked, as well as dose
adjustment for chronic kidney disease (if present) and checking for drug interac-
tions with immunosuppressants. If an abscess is present, it should be treated with
incision and drainage as well as an antibiotic active against MRSA.Cellulitis may
be treated for as little as 5days though the treatment course may be extended up to
14days, depending on the individual’s risk factors and degree of improvement.
Although rare, SOT patients are at risk for skin and soft tissue infections (SSTIs)
secondary to gram-negative organisms and primary care physicians should con-
sider these organisms as the cause of cellulitis when patients are not improving on
the above-mentioned empiric antibiotic therapy.
Signs of systemic infection from a skin and soft tissue infection should
prompt immediate referral to the emergency room for laboratory evaluation,
blood cultures, imaging, and possible surgical consultation. If there is con-
cern for concomitant deep vein thrombosis, then venous duplex imaging
should be obtained.
8 Infections intheAdult Solid Organ Transplant Recipient
240
Skin and soft tissue infections (SSTIs) are extremely common in SOT recipi-
ents due to ongoing immunosuppression and may affect up to 20% of patients at
some time in the post-transplant period [195]. Similar to immunocompetent
hosts, SSTIs in SOT recipients may be caused by bacteria, mycobacteria, fungi,
viruses, and parasites, although immunocompromised individuals are more sus-
ceptible to severe morbidity and mortality. Common skin infections may present
atypically in SOT recipients because of defects in cellular and humoral immunity
and may reect either localized or disseminated disease. When assessing SSTIs
in SOT recipients, providers should use a similar approach to evaluation and
management of SSTIs in immunocompetent hosts, rst determining if the lesion
is purulent or non-purulent (see Fig.8.3) as this directs initial diagnostic and
management strategies. In immunosuppressed hosts, cutaneous lesions are com-
monly vesicular, nodular, or ulcerative, and the patient’s travel and exposure his-
tory become critically important in driving the differential diagnosis. Other,
non-infectious diagnostic considerations for skin ndings in a SOT recipients
include drug eruptions, erythema multiforme, vascular insufciency, and under-
lying malignancy [196].
8.7.1 Diagnostic Considerations
Appropriate diagnostic evaluation of SSTIs in SOT recipients depends on the
appearance of the skin lesion, concern for disseminated disease, and the patient’s
exposure history. If the lesion is purulent, providers should have high suspicion
Fig. 8.3 Evaluation and management of skin and soft tissue infections. I&D incision and drainage
J. Hu et al.
241
for typical or atypical bacterial infection and should obtain a swab of the puru-
lent material to send for gram stain and bacterial culture. While non-bacterial
pathogens can cause purulent appearing lesions, bacterial culture is the most
appropriate rst step. Blood cultures are rarely indicated in the evaluation of
SSTI except when fever is present, patients present with hemodynamic instabil-
ity, or in patients who use injection drugs. When there is concern for dissemi-
nated infection either because of the presence of systemic symptoms or multiple
similar-appearing cutaneous lesions at distant sites, providers should refer to
emergency room or consult with an infectious disease specialist for further eval-
uation. Vesicular lesions should be unroofed with samples sent for viral PCR to
detect infection with herpes simplex virus (HSV) or varicella zoster virus (VZV)
infection. Nodules or ulcerative lesions, either solitary or grouped, may be dif-
cult to identify by visual inspection alone and referral to a surgeon or derma-
tologist for skin biopsy may be indicated. Tissue specimens should be sent to
both the microbiology lab for culture and the pathology lab for histologic evalu-
ation. Special stains and culture media may be required depending on the expo-
sure history and differential diagnosis; primary care providers should
communicate early with an infectious disease specialist and dermatologist to
ensure that appropriate testing is performed.
8.7.2 Cellulitis andAbscesses
Cellulitis remains the most common clinical SSTI syndrome with an incidence
of 2 cases per 1000-patient years. Cellulitis is a non-necrotizing, supercial skin
infection involving the epidermis and dermis. Immunosuppression is an impor-
tant risk factor for SSTIs; risk increases when other conditions are present
including chronic skin inammation, poor venous or lymphatic circulation, dia-
betes mellitus, and obesity [197]. Furuncles, carbuncles, and cutaneous
abscesses represent isolated collections of pus in the dermis and deeper tissues.
Furuncles and carbuncles can benet from compresses in mild cases but might
require incision and drainage to fully control the source of infection in more
extensive cases. Abscesses typically present as tender, erythematous, indurated
nodules, often with uctuance and surrounding skin erythema and usually
require incision and drainage for better source control [198]. Cellulitis and
abscesses are not distinctly different entities in SOT recipients than immuno-
competent hosts. The most important principles in diagnosis include vigilance
when assessing possible cutaneous infection, understanding that the syndromes
may present more subtly in SOT recipients and may progress more rapidly than
in immunocompetent individuals.
Beta-hemolytic streptococci remain the most common cause of cellulitis in
immunocompetent and immunocompromised hosts, followed by community-
acquired Staphylococcus aureus, including MRSA. In some studies, S. aureus
(MSSA and MRSA) is the predominant pathogen involved in purulent cellulitis and
8 Infections intheAdult Solid Organ Transplant Recipient
242
remains the leading causes of SSTIs overall, especially in cases involving
abscesses [199].
Other pathogens, including GNRs, are encountered less frequently and most
often in the setting of bacteremia. Infection with atypical bacteria, such as nocardia
or non-tuberculous mycobacteria, are infrequent causes of cellulitis; skin manifesta-
tions of these pathogens may also present as pustules, nodules, ulcers, and abscesses
[200]. Other rare causes of SSTIs have been associated with certain exposures, such
as an outbreak of non-tuberculous mycobacterium after exposure to sh markets in
NewYork City [201].
The IDSA has established clear guidelines for the diagnosis and management of
SSTIs, yet rates of misdiagnosis, inappropriate antibiotic use, and hospitalization
remain high [202]. Of note, fever has been shown to be an unreliable indicator for
the need for admission, despite traditional practice [203]. Furthermore, other physi-
cal exam ndings consistent with severe infection such as bullae and lymphatic
streaking, do not correlate with fever. Risk prediction tools for SSTI also have poor
performance, lacking sensitivity in the identication of severe infections in elderly
patients and populations with elevated risk, such as SOT recipients. Thus, providers
must remain vigilant in their assessment of cellulitis and abscess, with low thresh-
old for diagnostic sampling (e.g., incision and drainage for abscesses, biopsies for
unresolving cellulitis) and treatment.
In typical cases of cellulitis without systemic signs of purulence, the IDSA rec-
ommends antibiotic therapy targeted at streptococci [204]. If purulence is present or
suspected, therapy should be extended to cover MRSA.Providers should choose
antibiotics based on local susceptibility patterns and institutional antibiograms;
typical oral regimens that cover both streptococci and MRSA include a penicillin or
rst-generation cephalosporin, combined with trimethoprim-sulfamethoxazole, or
doxycycline. Linezolid could also be used as monotherapy in patients without a
concern for major drug–drug interactions. Use of linezolid is also limited by cost
and interactions with other common medications. While linezolid’s use alongside
selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reup-
take inhibitors (SNRIs) has been discouraged in the past given concern for serotonin
syndrome, there are more data to suggest this combination is safe and the previous
risk was overstated [205]. Note that cytopenias caused by linezolid develop with
long antibiotic courses and are of low concern when it is used for a short course to
treat cellulitis.
If a patient is already receiving trimethoprim-sulfamethoxazole for prophylaxis,
an alternative agent should be selected to cover MRSA.
Some clinicians treat both streptococci and MRSA initially, particularly in SOT
recipients, although clear guidance on this approach is lacking. Recommended
treatment duration for cellulitis is 5days and may be extended if the patient is not
improving. While prior evidence held that abscesses could be treated with incision
and drainage alone, a large randomized controlled trial demonstrated that cure rate
for abscesses increased with the addition of trimethoprim-sulfamethoxazole to inci-
sion and drainage compared to incision and drainage alone, particularly in settings
where MRSA is prevalent [206]. The IDSA makes a strong recommendation for
J. Hu et al.
243
clinicians to consult with an infectious disease specialist or dermatologist in the
treatment of cellulitis in SOT recipients, particularly if complicating factors are
present [204].
8.7.3 Necrotizing Skin Infections
Necrotizing soft tissue infections (NSTIs) remain a relatively rare cause of SSTIs
overall and there is a paucity of data on NSTIs in immunocompromised patients.
NSTIs are associated with high mortality rates (15–50%) and early recognition and
diagnosis can be challenging. These ndings highlight the high index of suspicion
needed to ensure early identication and the necessity for a time-sensitive referral
to an emergency care setting [207]. The management of NSTIs is beyond the scope
of this chapter.
8.7.4 Infectious Vesicular Eruptions
The presence of vesicular lesions in a SOT recipient should raise suspicion for
infection with a herpesvirus. Reactivation of herpes simplex virus (HSV) and vari-
cella zoster virus (VZV) are most common, however, cytomegalovirus (CMV),
Epstein–Barr virus (EBV), and human herpes virus 6 (HHV-6) may cause vesicular
lesions as well, though cutaneous manifestations are less common with these
viruses.
HSV accounted for the vast majority of mucocutaneous infections in SOT recipi-
ents (>80%) before the introduction of antiviral prophylaxis; since then, incidence
has dropped dramatically [208]. Infection with HSV produces painful, grouped
vesicles on an erythematous base that coalesce into shallow ulcerations on surfaces
of mucous membranes. HSV lesions in SOT recipients may take longer to heal than
in immunocompetent hosts, in part due to the impaired cellular immunity and pro-
longed viral shedding [209]. HSV-1 tends to cause oropharyngeal lesions whereas
HSV-2 has a predilection for anogenital eruptions; however, both serotypes may
affect any mucocutaneous surface, particularly in SOT recipients.
Reactivation of VZV is common among SOT recipients, with shingles, or “zos-
ter,” affecting 8–11% of individuals within the rst 4years post-transplant [9]. VZV
reactivation presents with grouped vesicles on an erythematous base and typically
affects a single dermatome. Disseminated zoster, dened as reactivation of VZV
affecting three or more dermatomes, is more common in immunocompromised
individuals and may take longer to respond to antiviral therapy. Primary infection
with VZV, also called chicken pox, is relatively uncommon in adults due to almost
universal exposure/vaccination during childhood. SOT recipients should have vari-
cella titer testing prior to transplantation and the varicella vaccine should be consid-
ered pre-transplantation for anyone who is seronegative for anti-varicella antibodies.
8 Infections intheAdult Solid Organ Transplant Recipient
244
It is important to note that the current VZV vaccine is a live, attenuated vaccine and
administration is contraindicated post-transplantation and 2–4 weeks pre-
transplant [9].
If HSV or VZV infection is suspected, providers should obtain a swab of vesicu-
lar lesions and send the sample for PCR testing. While awaiting testing results,
empiric treatment with acyclovir or valacyclovir may be initiated to reduce duration
and severity of symptoms. First-line therapy for herpes labialis includes valacyclo-
vir 1000mg twice per day (alternatively oral acyclovir 400mg ve times per day)
for 5–10days and until complete resolution of ulcers. Similarly, genital herpes may
be treated with valacyclovir 1000mg twice per day (alternatively oral acyclovir
400mg ve times per day) for 5–10days. Patients with recurrent HSV could experi-
ence asymptomatic shedding for days before an outbreak occurs; thus, there may be
a role for twice daily suppressive therapy with acyclovir or valacyclovir in individu-
als with more than 3 outbreaks per year to reduce risk of transmission. Herpes zoster
should be treated with a higher dose of valacyclovir 1000mg three times per day
(alternatively acyclovir 800mg ve times per day) for 7–10days or until crusting of
lesions [209]. Severe HSV or VZV infection (i.e., cutaneous dissemination, or vis-
ceral involvement) may require hospitalization and administration of IV acyclovir.
Famciclovir is also active against HSV and VZV and may be used in the treatment
of these infections, though treatment duration varies.
Disseminated CMV may cause a maculopapular, vesicular, or even ulcerative
eruption in SOT recipients. Infection with HHV-6 typically causes a self-limited
febrile illness with a maculopapular rash, though manifestations may be more
severe in SOT recipients. Cutaneous lesions associated with EBV infection are most
commonly seen in the setting of post-transplant lymphoproliferative disor-
der (PTLD).
8.7.5 Infectious Nodular andUlcerative Lesions
Numerous bacterial and fungal pathogens can cause nodular cutaneous lesions in
SOT recipients, and these lesions may or may not indicate disseminated infection.
In SOT recipients, defects in cellular immunity predispose to mycobacteria, atypi-
cal bacteria, certain zoonoses (Brucella, Bartonella), fungi (endemic fungi and
mold) and parasites (Leishmaniasis), all of which may present with cutaneous nod-
ules or ulcers. As an example, up to 42% of SOT recipients with disseminated
nocardia infection developed skin manifestations [210]. Some non-tuberculous
mycobacteria (NTM) may produce localized nodules or ulcerated lesions (e.g.,
Mycobacterium fortuitum) while infection with Mycobacterium abscessus or chelo-
nae are more likely to result in pustular, nodular, or papular lesions in association
with disseminated infection.
The most common clinical presentation of candidiasis in SOT recipients is
mucocutaneous disease, including thrush and esophageal candidiasis [211].
However, Candida remains the most common cause of disseminated fungal
J. Hu et al.
245
infections in SOT recipients [212]. In comparison, disseminated Aspergillus infec-
tion is a rare cause of cutaneous lesions in SOT recipients and is unlikely to be a
presenting symptom for PCPs.
Endemic fungal infections, including histoplasmosis, coccidioidomycosis, blas-
tomycosis, and cryptococcosis typically cause primary pulmonary infections. SOT
recipients infected with an endemic mycosis are at higher risk for disseminated
disease due to impaired cellular immunity, and may develop papules, plaques, pus-
tules, nodules, or ulcers. Skin disease is the most common extra-pulmonary mani-
festation of blastomycosis and may present as either verrucous or ulcerative
lesions [213].
If there is concern for an endemic fungal infection, a thorough exposure history
is critical. In the USA, Histoplasmosis is native to the Ohio and Mississippi River
Valleys and remains the most common of the endemic fungal infection overall with
northern expanding epidemiologic maps in dry western states due to climate change.
Coccidioidomycosis is endemic to the Southwestern United States including central
California, as well as eastern areas of Washington State and northern Mexico [214].
Blastomycosis is found predominantly in southern and southeastern states border-
ing the Ohio and Mississippi River Valleys, as well as upper Midwestern states in
the Great Lakes region. Cryptococcus gattii is endemic to the western US states
(Washington, Oregon and California) and Vancouver Island, Canada. Taking a
detailed history to clarify recent travel to endemic areas, as well as exploration of
concomitant pulmonary and CNS symptoms, will help clarify the diagnostic possi-
bilities. Worldwide patterns vary—knowing local and regional patterns of endemic
mycoses can aid in the diagnosis of cutaneous fungal infections.
Diagnosis of nodular and ulcerative lesions typically requires biopsy, either with
a dermatologist or surgeon, depending on the depth of the wound. These samples
should be sent for microbiologic and pathologic evaluation. Empiric therapy is not
recommended; rather, providers should await culture or pathology results and con-
sider consultation or referral to an infectious disease specialist to determine
treatment.
8.7.6 Sexually Transmitted Infections
While the management of many sexually transmitted infections is not addressed in
this chapter, one should be mindful of the cutaneous ndings in SOT recipients,
which are often identical to immunocompetent patients (Table8.13).
Mpox lesions vary on presentation as noted in Table8.13. There are two major
subtypes. Clade I is associated with more severe disease and higher case fatality
rate. Clade II has a lower mortality rate and was the driver of the global outbreak in
2022, primarily within the men who have sex with men community [215]. Mpox
transmission results from prolonged direct contact with infected individuals. While
sexual transmission is typically associated with clade II, it has also been seen with
clade I. Primary prevention with the modied vaccinia Ankara-Bavarian Nordic
8 Infections intheAdult Solid Organ Transplant Recipient
246
Table 8.13
Cutaneous manifestations of sexually transmitted infections
Disease Pathogen Cutaneous manifestations
Syphilis Treponema
pallidum
Painless chancre, scaly papules & plaques
(+/− palmar involvement), condylomata lata,
gummas
Chancroid Haemophilus
ducreyi
Painful ulceration, tender lymphadenopathy
Lymphogranuloma
venereum (LGV)
Chlamydia
trachomatis
serovars L1, L2, L3
Painless papules and ulcerations, tender
lymphadenopathy
Granuloma inguinale
(Donovanosis)
Klebsiella
granulomatis
Painless ulceration with granulation tissue
predominant base
Genital herpes HSV-2 > HSV-1 Grouped vesicular eruption
Human
immunodeciency
virus (HIV)
HIV-1, HIV-2 Disseminated presentation of opportunistic
infections (e.g., HSV, VZV, molluscum,
coccidiomycosis, etc.), dermatophyte infection,
folliculitis, malignancies (e.g., HHV-8, squamous
cell carcinoma)
Anogenital warts HPV-6, HPV-11 Varies: at, papular, pedunculated, and
cauliower-like lesions
Mpox Orthopoxvirus
monkeypox
Smooth and umbilicated papules, vesicles,
pustules, and morbilliform rashes. See discussion
below
Scabies Sarcoptes scabiei Classic: pruritic rash in intertriginous areas
Crusted: Erythematous patches with scaling,
dystrophic nails
Crab louse Pthirus pubis Pruritis and erythema around pubic hair,
+/− secondary bacterial infections
Table 8.14
Key considerations for skin and soft tissue infections
• If trimethoprim-sulfamethoxazole was included in a SOT recipient’s prophylactic regimen,
alternative agents should be selected for coverage of MRSA
• HSV and VZV are the most common vesicular eruptions in SOT recipients and empiric
therapy should be initiated while awaiting PCR testing
• Nodular and ulcerative skin disease should raise the suspicion for mycobacterial, atypical
bacterial, and disseminated fungal disease. Diagnostic conrmation is preferred over
initiation of empiric therapy
(MVA-BN, Jynneos
®
) is the main intervention strategy for populations at increased
risk. These populations include, but are not limited to gay, bisexual, and other men
who have sex with men, gender diverse individuals with multiple sexual partners,
people who have sex in bathhouses and sex clubs, and people with occupational
exposures to Mpox.
A summary of key considerations for skin and soft tissue infections is given in
Table8.14.
J. Hu et al.