1.1 Burkholderia pseudomallei

B. pseudomallei (gram-negative rod) is the pathogen responsible for Melioidosis, which has spread throughout nonendemic areas recently.¹ The bacteria are spread via contaminated soil and water to humans. Old age and diabetes pose a greater threat to spread of the disease.¹ Patients typically present with pneumonia or sepsis symptoms, however, 10%–25% patients may also display concomitant cutaneous manifestations such as pustules, cellulitis, ulceration, or subcutaneous abscesses, without an identifiable pattern of distribution¹ If skin biopsies are taken, the microbiology and public health laboratories should be aware that this diagnosis is considered in the differential, as Burkholderia pseudomallei is recognized as a bioterrorism agent.² Gram stain of material from cutaneous lesions can point towards diagnosis, showing gram-negative bacilli with bipolar staining (“safety pin” appearance).³ However this should not be taken as diagnostic for B. pseudomallei as its morphology is not specific. Laboratories may also utilize broad range bacterial 16S DNA PCR with sequencing, if available. Histopathological analysis will show a deep dermal mixture of chronic and suppurative granulomatous inflammation with plasma cells, histiocytes, neutrophils, and lymphocytes. Epidermal acanthosis will also be present.³ Treatment can be pursued with antibiotics intravenously (ceftazidime, meropenem) or orally (trimethoprim-sulfamethoxazole, amoxicillin/clavulanic acid).⁴

1.2 Corynebacterium ulcerans

Diphtheria is a life-threatening infection caused by C. diphtheriae species complex (gram-positive rod). This complex is toxin-producing and includes subtypes C. diphtheriae (spread via human–human contact), C. ulcerans (human–animal contact), Corynebacterium pseudotuberculosis (human–animal contact), Corynebacterium rouxii, Corynebacterium belfantii, and Corynebacterium silvaticum.² Typically, the bacteria colonize the upper respiratory tract and cause systemic symptoms.

C. ulcerans can also be a toxin-forming bacteria, genetically related to C. diphtheriae. It is known to be one of the most harmful, widespread pathogens amongst livestock and wildlife.² Nonrespiratory symptoms of C. ulcerans infection include plantar skin ulcers, subcutaneous abscesses, localized lymph node abscesses, and/or parotid, axillary, or mandibular abscesses. Patients with these cutaneous symptoms were significantly younger (mean age 38) than patients presenting with predominantly respiratory symptoms (mean age 64).⁵ Macrolides or penicillins are the antibiotic of choice, with severe cases requiring administration of diphtheria antitoxin.⁵

2.1 Candida auris

Initially discovered in 2009, C. auris has emerged as a growing global health concern, with a mounting number of cases reported worldwide. It is closely related to Candida haemulonii, although it does possess distinct characteristics, such as its inability to form pseudohyphae and the variable expression of virulence factors commonly observed in other Candida species.⁶ This pathogen is most frequently observed in hospitalized patients in high-acuity medical care environments. It shares common risk factors and clinical presentations with other Candida species, notably affecting immunocompromised patients, individuals with indwelling catheters, those reliant on parenteral nutrition, and individuals with prior exposure to antifungal agents.^{6, 7}

C. auris is particularly concerning due to its resistance to multiple drugs, rendering commonly used treatments, such as fluconazole, ineffective. Echinocandins are currently the preferred choice for treatment.^{6, 7} Given its multidrug resistance and potential for persistent invasive candidemia, heightened awareness of this pathogen is of utmost importance. The CDC recommends that every patient with C. haemulonii should also be tested for C. auris due to their close resemblance.⁷ Furthermore, the isolation of patients infected with this pathogen, along with the implementation of contact precautions similar to those used for Candida difficile, is strongly advised to mitigate the risk of its transmission.^{6, 7}

2.2 Trichophyton indotineae

In recent years, this particularly stubborn strain of dermatophyte has been reported in various parts of South Asia as the culprit of tinea infections exhibiting an unusually high resistance to terbinafine.⁸ Originally thought to be a form of Tinea Interdigitale or Tinea Mentagrophyte Genotype III.

These dermatophytes were cultured and found to have a genetic mutation in the SQLE gene that allowed this new strain to exhibit resistance to Terbinafine through its dysregulation of the pathway generating membrane ergosterol.⁹

Patients with tinea secondary to T. indotineae often display extensive and highly inflammatory skin patterns. They have painful lesions that spread rapidly. In one study, more than half of the patients also showed signs of adverse cutaneous skin reactions to drugs, such as local hypopigmentation, striae, and local epidermal atrophy.⁹ It's worth noting that this highly resistant mutant strain emerged in patients who had often tried and failed to treat their condition with topical antifungal creams, or self-medicated topical steroids. While using Terbinafine as a secondary treatment showed limited effectiveness in these patients, other antifungal medications like itraconazole and voriconazole could be suitable alternatives for treating this condition.^{9, 10}

2.3 Trichophyton mentagrophyte genotype VII

T. mentagrophyte is a type of fungus that causes tinea and typically has a connection to animals and can sometimes be transmitted from animals to humans. However, in recent years, a mutated form of this fungus, has been discovered that sporadically appears without clear links to animals and has an unusually high rate of transmission from one human to another.¹¹ This new genotype has been associated with sexual transmission between humans and can manifest as a rapid onset of highly inflammatory pruritic lesions in the pubogenital region.^{11, 12} The temporal association between sexual intercourse and the development of this fungal skin infection is similar to those seen in other sexually transmitted infections, and aids in the understanding of this unique mode of fungal transmission.¹² Prevalence is greater with higher-risk sexual lifestyles, such as men who have sex with men, partners with sexually transmitted infections, and individuals who have had sexual encounters in the Southeast Asia region. In some cases, these patients were found to have significant post-inflammatory pigmentation and scarring in their genital regions after the infection had resolved.^{11, 12}

3.1 MPox

International media attention increased the visibility and accelerated scientific understanding of MPox in the 2022 outbreak. The reservoir of the virus is unknown but is thought to be in nonhuman primates or rodents.^{13, 14} It is transmitted by animal–human or human–human contact through large respiratory droplets, skin lesions, or body fluids and has an incubation period of up to 21 days.^{13, 14}

Presenting signs of the illness are nonspecific and include headache, back pain, fever, maxillary, inguinal, or cervical lymphadenopathy; chills; and sore throat.^13-16 One to three days after initial fever, a characteristic rash can be seen. Early recognition of this rash is critical for appropriate diagnosis and treatment. On gross examination, the rash will be seen originating as macules that later convert to papules, then to vesicles, and finally to pustules. The rash will initially develop on the face and extremities and has been noted to also include the palms and soles.¹⁷ In the 2022 outbreak, providers have noted that the rash may present with minimal to no prior symptoms. Moreover, initial signs of the rash can also appear in the anogenital, and oral regions with disproportionate pain on examination.^15-17 Most cases had less than 10 lesions present on the body.¹⁷

Differential diagnoses of mpox includes other viral pathogens with dermatological exanthems such as chancroid, measles, hand–foot–mouth disease, varicella, and herpes.^13-15 The smallpox vaccination is about 85% effective in coverage for mpox, and recent studies have shown smallpox anti-retroviral drugs (tecovirimat, brincidofovir, cidofovir) to be successful in the treatment of mpox.¹⁷

3.2 Marburg virus

Marburg virus is a severe hemorrhagic fever affecting humans and nonhuman primates. It is classified as an RNA virus and is genetically similar to the Ebola virus.¹⁸ It can be spread with human-human contact particularly through body fluids.¹⁸ The incubation period can be from 2 to 21 days with initial symptoms as high fevers, chills, myalgias, and headaches. Within 5 days after initial symptom onset, patients may start developing a maculopapular rash across the trunk. Severe disease is characterized by jaundice, shock, liver failure, hemorrhage, and multiorgan failure, among others. The presentation of marburg virus is similar to that of malaria or vibriosis and may be hard to differentiate clinically. Fatality rate is estimated to be 23%–90%, depending on the area and level of care. It is currently endemic to Africa, with outbreaks being seen in areas that have not experienced it before.¹⁸ There is currently no treatment, and clinicians are encouraged to provide supportive treatment at well-equipped hospitals.