Trichomycosis Pubis

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Background

Trichomycosis, also called trichobacteriosis, is a bacterial infection of the hair shaft, caused by Corynebacterium species, in sweat gland–bearing areas[1] ; it has been described most commonly in the axillary region and is a common but underdiagnosed skin condition.[2] While initially believed to be uncommon in the inguinal region, a series of papers has described trichomycosis pubis, a particular variant occurring in the inguinal area, and has suggested that the incidence of this disease is underestimated in the general population. The condition is often a marker of poor hygiene.

Pathophysiology

This discussion of trichomycosis, a disease specific to the hair and sweat gland–bearing regions of the body, concentrates on the involvement of the pubic region (trichomycosis pubis). First described in the axillary region by Paxton in 1869, the causative role of multiple bacterial Corynebacterium species was established by Freeman et al in 1969.[3, 4, 5, 6, 7] Use of the term trichomycosis, which incorrectly implies the causative role of fungi, has been maintained, although the condition is also increasingly recognized as trichobacteriosis, which is a more correct term.[8] The color differences noted at presentation of the condition, their association with particular corynebacteria, or the possible role of associated cocci have not been clarified.

The causative organism associated with most cases is Corynebacterium tenuis, which favors warm and moist microenvironments. Poor hygiene may also play a role. Other noted species include Corynebacterium propinquum,[9] Corynebacterium flavescens,[10] and Serratia marcescens.[2] While as many as 33% of adults have colonization by these bacteria in the inguinal or axillary regions, factors such as hyperhidrosis initiate more extensive growth and clinical manifestations. Hence, disturbances in apo-eccrine sweat production and bacterial proliferation are crucial for development.[5, 8] The exact origin of the cement substance that creates the grossly visible nodules is debated. Electron microscopy studies favor origin from the causative agents, while others have favored elaboration from apocrine sweat.[11, 12] The actual nidus may be through the modification of apocrine sweat by elaborated cement substance to create the insoluble material that holds bacteria to the hair shaft. The white or yellowish, and less commonly, red or black, material on the hair contains an extremely high number of bacteria.[2]

Etiology

Risk factors appear to be geographic, with the highest incidence in tropical areas. In addition, poor hygiene often is present.

Epidemiology

Frequency

United States

Detailed examination of racial, age, or geographic incidence has not been performed, and examinations in the United States are limited to case reports. A more detailed examination (but still limited) has been performed outside the United States.

International

Studies in Panama and the United Arab Emirates revealed rates as high as 39% in patients attending a dermatology clinic.[13, 14] These results correlated with the notably higher incidence and prevalence in areas of high humidity, warmth, and poor hygiene. The only other study to mention incidence noted the presence of trichomycosis pubis upon examining institutionalized patients for trichomycosis axillaris in Edinburgh, Scotland, and noted that of the 609 men examined, 16 (2.6%) had pubic disease, of which three of the cases (0.5%) were not associated with axillary involvement. Ages of the males affected were 18 and 21 (3 patients) years and can be culled only from case reports. There is no universal consensus as to racial or sex preferences,[10] although some reports note higher infection rates in men.[15] Infection with C tenuis is also associated with poor hygiene, obesity, and hyperhidrosis.[16] Human-to-human transmission has been noted and is particularly common in overcrowded groups such as soldiers, athletes, and among homosexuals.[10]

Prognosis

Aside from the risk of recurrence, prognosis is excellent and treatment is effective. Morbidity is low, with most patients unaware of the colonization. When presenting, the most common reported symptom is a foul odor, and this may continue to cause problems, since trichomycosis often recurs.

Patient Education

Instruct patients to keep skin dry and to practice proper hygiene.

History

While many patients are asymptomatic, patients may present with reports of pubic rash, foul odor, or growths on the pubic hair. Colored sweat also has also been reported, resulting in a consideration of chromhidrosis.

Physical Examination

Patients typically present with yellow, red, or black nodules or fine sheaths consisting of a bacterial biofilm encasing the hair shafts[8] ; yellow is most common, present in 95-98% of cases.[10] Sweat in the region tends to be colored similarly. Lesions present in the inguinal region are often on the scrotum but occasionally on the base of the shaft of the penis. Lesions can be associated with erythema and itching, and superinfection with dermatophytes has been noted.

Complications

The primary complication appears in individuals who are immunocompromised and can develop septicemia secondary to colonization of catheters and surgical sites. Infection in hosts who are immunocompetent yields few long-term adverse effects.

Recurrence is common, but the simplicity of treatment and improved hygiene make follow-up care simple. In rare cases, shaving the pubic hair after treatment has been advocated to prevent recurrences.

Approach Considerations

The diagnosis of trichomycosis is made clinically; however, other diagnostic modalities may be used for doubtful cases.[17] Wood lamp examination reveals a pale, yellowish fluorescence; however, it is important to note that this does not occur in cases caused by Serratia species.[2] A new diagnostic method includes ultraviolet light–enhanced visualization (ULEV).[8] in which high-contrast maps of epidermal desquamation are obtained and variations in light reflections recorded by a camera provide information on an altered stratum corneum.[18] Using the ULEV method can highlight the presence of the corynebacteria (white) in addition to the surrounding biofilm enveloping the hair shaft. Several reports note dermatoscopic findings of cottony structures around the hair,[2, 10, 15] which have also been described as transparent crystalline “rosaries of crystalline stones.”

Culture or API Coryne system (a standardized system for identification of coryneform bacteria in 24 hours) are the criterion standard diagnostic tests.[2] Hair culture can be used to grow the anaerobic diphtheroids present as short gram-positive rods. These studies usually are not essential but may be used if no response to initial treatment occurs or targeted antibacterial treatment fails to result in a cure (and fungal superinfection should be eliminated).

Histologic Findings

While usually not performed, in rare cases samples of hair have been removed and sent for pathology slide preparation. Upon periodic acid-Schiff (PAS) staining, a dense sheath surrounding the hair shaft is present.[5] The bacteria are extrafollicular, affecting only the cuticle without penetrating the cortex or marrow of the hair, as further demonstrated by electron microscopy studies.[10] Two other distinctive pleomorphic Corynebacterium species can encapsulate the hair. These three bacterial species are entrapped in a background of cementitious biofilm elaborated by the bacteria, which possibly serves as a mechanism for host immune evasion.[8] Superinfection with cocci or fungi also can be present.

Medical Care

As no therapeutic studies specific to trichomycosis are available, management strategies mirror erythrasma treatments.[8] Treatment involves alleviating the hyperhidrosis through the use of drying agents. Topical antibiotics containing clindamycin, erythromycin, or fusidic acid are helpful and also treat the erythrasma that may be associated.[8, 19, 20] Additional recommended agents include naftifine hydrochloride cream (1%), which has been used for its combined antifungal and antibacterial actions.[21] Benzoyl peroxide and sulfur soaps have also been reported to be effective in the treatment and prevention of trichomycosis.[8, 17] Furthermore, rubbing while washing may disrupt the biofilm and increase the permeability of antiseptics, and shaving/clipping of the affected area and regular use of antiperspirants (including aluminum chloride) is often helpful and can reduce recurrences.[8]

Prevention

Since studies show notably higher incidence in regions of the world with high humidity and temperatures and in people with poor hygiene, measures aimed at maintaining dry skin and proper hygiene should be emphasized.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Fusidic acid is a steroid antibiotic that is often used topically in creams and eyedrops but may also be given systemically as tablets or injections. It is not available in the United States.

Naftifine (Naftin)

Clinical Context:  Naftifine is a synthetic allylamine derivative shown to exhibit fungicidal activity in vitro against a broad spectrum of organisms, including species of Trichophyton, Microsporum, and Epidermophyton genera. Naftifine has shown fungistatic activity against Candida species. The exact mechanism of action is not known; however, it appears to interfere with sterol biosynthesis by inhibiting squalene 2,3-epoxidase. Treatment should continue for up to 4 weeks. If no improvement is noted, re-evaluate the patient.

Class Summary

Mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis or altering the permeability of the cell membrane (polyenes) of the fungal cell.

Clindamycin solution (Cleocin T, Clinda-Derm)

Clinical Context:  Clindamycin solution is a wide-spectrum antibiotic effective in vivo against various microbial organisms, including Corynebacterium species. This antibiotic binds preferentially to the 50S ribosomal subunit, affecting the process of peptide chain initiation in bacteria.

Benzoyl peroxide (Benoxyl, Fostex, Benzac)

Clinical Context:  With benzoyl peroxide, a free-radical oxygen is released upon administration and oxidizes bacterial proteins in sebaceous follicles, decreasing the number of anaerobic bacterial and irritating free fatty acids. It has keratolytic and comedolytic effects. Use gel, pads, or wash.

Erythromycin topical (AkneMycin, Ery)

Clinical Context:  Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Sulfur topical (Aqua KAVI, De La Cruz Sulfur Ointment, Grandpa's Thylox Acne Treatment Soap with Sulfur)

Clinical Context:  Sulfur soaps have been reported to be effective in the treatment and prevention of trichomycosis.

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Antibiotic selection should be guided by blood culture sensitivity whenever feasible.

Aluminum chloride topical (Xerac-AC roll-on, Certain-dry pads, Drysol solution)

Clinical Context:  Aluminum chloride topical is an astringent agent used in the management of hyperhidrosis.

Class Summary

Agents that work to dry up the sweat glands.

Author

Jeannette Rachel Jakus, MD, MBA, Clinical Assistant Professor, Director of Clinical Research, Assistant Program Director, Department of Dermatology, SUNY Downstate Medical Center; Dermatologist, Brody Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Kunal Malik, State University of New York Downstate College of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

Michael J Wells, MD, FAAD, Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology

Disclosure: Nothing to disclose.

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Daniel Mark Siegel, MD, MS, Clinical Professor of Dermatology, Department of Dermatology, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Milton W Datta, MD, Assistant Professor, Departments of Pathology, Urology, and Hematology-Oncology, Emory University School of Medicine

Disclosure: Nothing to disclose.

Peter Langenstroer, MD, Associate Professor, Department of Urology, Medical College of Wisconsin

Disclosure: Nothing to disclose.

Scott M Acker, MD, Associate Professor, Director of Dermatopathology, Departments of Dermatology and Pathology, University of Alabama at Birmingham

Disclosure: Nothing to disclose.

Vladimir O Osipov, MD, Pathologist In Charge, QML Townsville

Disclosure: Nothing to disclose.

References

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