Mycotic and Bacterial Infections

Abstract

This article reviews the salient clinical features, evaluation, and treatment of mycotic and bacterial infections of the perianal and contiguous zones of the human body.

Mycotic Infections

The perianal region is an intertriginous zone. The heat and moisture inherent within these regions are conducive to the establishment of mycotic infections. Their proximity to the genital regions where fungal infections are more common may facilitate infection toward the perineal and perianal regions. Fungal infections mainly involve the superficial skin layers and are caused by dermatophytes or yeast. Dermatophytes are multicellular filaments, which form hyphae and spores for reproduction. The most common dermatophyte species include Microsporum , Trichophyton , and Epidermophyton . Yeast-like fungi are unicellular and propagated by budding. The most common species is Candida albicans . Fungal infections may account up to 40% of secondary infectious pruritus ani cases–a majority is caused by Candida . ¹

The most common symptom of mycotic infection of the perianal and perineal regions is pruritus. ² Other symptoms include localized pain, chronic seepage, and excessive moisture. Mycotic infection can present with annular lesions with scaly elevated borders and central clearing, or as a bright red rash in a “butterfly” distribution with superficial longitudinal fissures. Satellite lesions of localized erythematous perifollicular papules or pustules may also be present within the adjacent intertriginous areas. ^{2 3} The focal clinical reaction depends on the mycotic species involved—inflammation is due to hypersensitivity to the metabolic products of the fungus as they digest and live on keratin. ¹

Mycotic infections of the perineum may commonly present in patients with previous mycotic infections of other regions, including feet and hair. ⁴ Fungal species, such as C. albicans , are commensal and found within the intertriginous zones of healthy individuals. ^{1 3} Mycotic infections may also occur as an opportunistic reaction in patients with impaired immune systems, or in patients who have been treated for long periods with systemic antibiotics or steroid therapy. ^{1 3} Additionally, these infections may be associated with a concurrent anal disorder. In these cases, anal mycosis may resolve after treatment of the underlying proctologic disease. ⁵

Fungal cultures can help specify the type of mycotic infection and help differentiate it from other infectious etiologies. The culture is obtained from scrapings of the scaly portions of the lesion and performed on Sabouraud glucose agar. Colonies of creamy, grayish, and moist growths appear typically after 4 days. A more immediate diagnosis may be obtained with the use of potassium hydroxide (KOH) preparation. The specimen is obtained from scrapings from the raised scaly borders and placed on to a glass slide. A drop of 20% KOH is placed on the specimen and covered and examined under a low powered microscope. The presence of yeast, hyphae, or pseudomycelium is highly indicative of a superficial fungal infection. The presence of spores is not diagnostic of fungal infection as this may represent normal colonization, especially for Candida species. Treatment with topical steroids may negate visualization of hyphae on KOH preparation, but still allow for propagation of dermatophyte and mycotic infection. Therefore, fungal culture may be a necessary adjunct for diagnosis. ^{4 5}

Tinea Cruris

This type of infection most commonly affects the groin; however, it may be seen within the perineum and perianal regions. Lesions appear as “annular patches” or plaques with heaped up scaly borders. The edges are the active site of infection and as the lesion spreads and expands outward, it develops a central zone of clearing. The eruptions can be numerous, unilateral, and asymmetric. Frequently, the scrotum is spared, which is in contrast to mycotic infection of the groin. ^{6 7} In perianal tinea infection, superficial longitudinal fissures anteriorly and/or posteriorly can also appear ( Fig. 1 ). The most common symptom is pruritus, which is often exacerbated by the heat and humidity commonly present within the intertriginous regions. Diagnosis with KOH examination demonstrates hyphae or multicellular filaments on microscopy. Most commonly, tinea cruris is caused by a species of Trichophyton . The differential diagnosis includes candidiasis, erythrasma, seborrheic dermatitis, psoriasis, and vegetative pemphigus.

Fig. 1.

Superficial longitudinal fissures are characteristic of tinea infections of the perianal region. Midline longitudinal superficial fissures are in evidence (a) anterior and (b) posterior to the anal verge. (These images are provided courtesy of A. Ortega and X. Delgadillo.)

Treatment involves reduction of perspiration with topical desiccants and wearing loose-fitting clothes. Minimizing the amount of moisture within the intertriginous region and maintaining dryness are effective in preventing future recurrence. Topical antifungal therapies include tolnaftate, clotrimazole, miconazole, and econazole. Usually, 2 to 3 weeks of topical therapy is adequate but may be utilized up to 4 to 6 weeks. Systemic therapy is rarely needed but can be highly effective especially for treatment of dermatophytes. Griseofulvin is one of the first fungistatic agents utilized for treatment of mycotic infections and has minimal toxicity. ⁸ Systemic treatment with griseofulvin 500 mg/d PO for 2 to 4 weeks is utilized in patients with tinea cruris that did not resolve after topical therapy. ^{1 7 9} Nystatin is not effective treatment against tinea as most species are resistant. ⁷

Candidiasis

Candida albicans is a yeast-like fungus and is a normal colonizer of the gastrointestinal tract and intertriginous areas. Frequently, candidiasis occurs in patients with underlying immunosuppression (i.e., AIDS, diabetics, and chronic steroid therapy), or in patients who have been treated subsequently with a long duration of antibiotic therapy. Candida infections involve the skin and activate the alternate complement pathway, resulting in inflammation characterized by a bright red rash. Pustules without surrounding erythema may also develop along with small satellite papules within the adjacent skin. Within the perineum, the distribution of erythema is frequently symmetric but with irregular borders and forms a “ butterfly ” pattern surrounding the anus ( Fig. 2 ). The most affected areas are the perianal, intergluteal, and inguinal folds. Diagnosis is made with demonstration of pseudomycelium or buds on KOH preparation.

Fig. 2.

Symmetrical maculopapular erythematous acneiform lesion with well-defined borders is evident in this case of vulvar, perineal, and perianal candidiasis. (This image is provided courtesy of X. Delgadillo.)

Mild cases of candidiasis may be treated with topical nystatin, clotrimazole, luliconazole, or miconazole for ∼2 to 3 weeks. In patients with diabetes or underlying immunosuppression, it is advised to treat with a combination of systemic antifungal treatment, such as oral ketoconazole or fluconazole, and local topical therapy. Severe cases may require intravenous antibiotics such as amphotericin B. ^{1 3}

Bacterial Infections

Erythrasma

Corynebacterium minutissimum is a diphtheroid bacterium that produces a chronic superficial infection involving intertriginous areas of the body including the perianal and perineal regions. Scratching produces a breach of the skin's protective barrier allowing this ubiquitous organism to become invasive. It is more common in subtropical and tropical areas of the world where its incidence may be as high as 4%. ⁸ Predisposing factors include hyperhidrosis, obesity, diabetes mellitus, warm climate, poor hygiene, advancing age, and immunocompromised states. It may be asymptomatic or pruritic. Dark discoloration is observed around the perianal, perineal, and surrounding tissues. It is usually well demarcated as brown or red macular patches ( Fig. 3 ). Lichenification and fine scales can be observed in the more chronic cases. All intertriginous areas of the body should be examined.

Fig. 3.

Brown macular discoloration of perianal and surrounding soft tissues is characteristic of erythrasma. (This image is provided courtesy of A. Ortega.)

The simplest and most direct path to diagnosis is examination with a Wood's lamp. Increased production of coproporphyrin III by the diphtheroids results in coral-red florescence when exposed to ultraviolet light ( Fig. 4 ). Gram stain reveals gram-positive rods. On occasion, the two examinations may be complimentary. Punch biopsy may confirm erythrasma when rods and filaments are present in the horny layer of skin.

Fig. 4.

Coral-red fluorescence demonstrated by examination under a Wood lamp. (These images are provided courtesy of X. Delgadillo and E. Csatar.)

Topical erythromycin or clindamycin can be used as first-line therapy. Oral erythromycin is second-line therapy. Corynebacterium minutissimum is usually susceptible to several antibiotics including penicillin, first-generation cephalosporins, erythromycin, clindamycin, ciprofloxacin, tetracycline, azithromycin, and vancomycin. However, multiresistant strains can be found. Therefore, patients who fail first- and second-line treatments may benefit from culture and sensitivity testing. Patient education focuses on keeping the affected region as dry as possible in addition to effective hygiene.

Streptococcal Infections

Streptococcus pyogenes is responsible for three types of infections involving the superficial skin layer of the perianal region: impetigo, perianal streptococcal dermatitis, and erysipelas.

Impetigo

Impetigo is an acute superficial skin infection of the keratinizing layer of the most superficial aspect of the epidermis. It is characterized by exudation and crusting. Young children can present with a bullous eruption. Impetigo is known to cause epidemics among children and their family members. It is spread by touch or handling of such common items as toys, blankets, and clothing, as well as other forms of personal contact. Historically, impetigo was the result of infection by S. pyogenes. The current understanding is that both S. pyogenes and Staphylococcus aureus can be causative. The latter is associated with the bullous form and presentation. Increasingly, both organisms are seen concomitantly. The diagnosis is generally made clinically on physical examination. Scaly or bullous lesions are the characteristic of impetigo ( Fig. 5 ). Cultures are commonly not helpful. While penicillins, cephalosporins, and erythromycin have been used classically, resistance is ever more prevalent. Topical therapy with mupirocin is helpful in reducing contagion and as a primary treatment. Retapamulin, a pleuromutilin antibacterial, was approved by the Food and Drug Administration in 2007 for treatment of bullous and nonbullous impetigo caused by S. pyogenes and methicillin-susceptible strains of S. aureus in children of 9 months of age or older. ¹⁰ In vitro data have suggested that it may be more effective than mupirocin against methicillin-resistant S. aureus (MRSA). ¹¹

Fig. 5.

Characteristic scaly and bullous eruptions in impetigo in the superficial layers of the epidermis. (This image is provided courtesy of I. Khubchandani.)

Perianal Streptococcal Dermatitis

Perianal streptococcal dermatitis (PSD) is caused by S. pyogenes . It is a superficial cutaneous infection of the epidermis. It presents as a brilliant red, sharply demarcated eruption secondary to this group Aβ-hemolytic streptococci . PSD occurs most commonly in children between the ages of 6 months and 10 years. Signs and symptoms include perianal dermatitis (90%), perianal itching (78%), rectal pain (52%), and blood-streaked stools (35%). ¹²

Half of the patients have other affected family members. Six per cent of children with streptococcal pharyngitis carry the organism in the perianal region. ¹³ Mouth to hand to anus is considered the operant route of transmission.

Fever and systemic signs of illness are generally absent. It is recognized by a raised red border with a sharp demarcation between the infected tissues and the normal uninvolved skin centered within the anal verge ( Fig. 6 ). Cultures are notoriously unhelpful. However, the rapid streptococcal test is useful. Signs and symptoms of systemic toxicity should raise concerns for infection in the deeper layers of the skin.

Fig. 6.

Perianal streptococcal dermatitis in a 6-year-old boy demonstrating sharp raised border framing a brilliant red lesion at the anal verge. (This image is provided courtesy of James Michael Parker.)

PSD can be treated with topical mupirocin. Oral penicillin, clindamycin, and erythromycin are effective treatments for S. pyogenes . However, children best tolerate amoxicillin because it has better taste. ¹⁴

Erysipelas

This streptococcal infection also caused by S. pyogenes is usually restricted to the dermis but may have lymphatic extension. This infection is more common in infants and children but is also seen in older adults. A history of streptococcal pharyngitis is common. It presents with lesions raised above the level of the surrounding skin with a clear line of demarcation between involved and uninvolved tissues. The lesions are characteristically salmon red in color. Streptococcus pyogenes accounts for most infections, but other streptococcal species and S. aureus may be involved. Infections of the face and lower extremities are more common. However, any integumentary zone may be involved including those of the perianal, perineal, and gluteal zones ( Fig. 7 ). The cutaneous inflammation is accompanied by chills, fever, and systemic toxicity. Diagnosis of erysipelas is based on the association of an acute inflammatory plaque with fever, lymphangitis, adenopathy, and leukocytosis. Bacteriology is not helpful for the diagnosis of erysipelas because of low sensitivity or delayed positivity when using serologic tests. ¹⁵

Fig. 7.

An acute inflammatory plaque associated with signs of sepsis points to erysipelas as a clinical diagnosis. (This image is provided courtesy of I. Khubchandani.)

Penicillin via oral or parenteral routes is recommended depending on the overall clinical severity. Drug resistance is a problem in treating S. pyogenes . Moreover, MRSA may be complicit in the infection. Therefore, a penicillinase-resistant semisynthetic penicillin or cephalosporin may be required.

Critical Clinical Focus

Prompt recognition and treatment of cutaneous streptococcal infections are important. Delayed recognition may result in acute glomerulonephritis, scarlet fever, and endocarditis. Impetigo has a readily recognizable appearance. PSD and erysipelas have similar appearances. The former is not associated with fever or systemic toxicity. The latter is characterized by signs and symptoms of sepsis. More serious clinical entities include deeper soft tissue infections including cellulitis, myositis, and necrotizing fasciitis. Fig. 8 summarizes the anatomic location of the relatively superficial cutaneous streptococcal infections predominantly secondary to S. pyogenes.

Fig. 8.

Signs and symptoms of streptococcal cutaneous infections depend on the anatomic level of infection. Impetigo has a characteristic superficial appearance and presents without systemic toxicity. PSD and erysipelas have similar topographic appearances. Erysipelas can communicate with lymphatics and thereby demonstrate systemic signs of sepsis. PSD is not associated with signs of sepsis. Streptococcal cellulitis involves the subcutis (hypodermis). Depth of invasion reflects systemic toxicity and propensity for accelerated spread of the infection. PSD, perianal streptococcal dermatitis.

Actinomycosis

Actinomycosis is a chronic infectious and cutaneous entity. It is localized near an orifice and provokes suppurative and fistulization processes. It is frequently caused by Actinomyces israelii —a filamentous bacillus. Other bacteria such as Actinobacillus actinomycetemcomitans may be also associated. ¹⁶

Perianal actinomycosis is characterized by indurated nodules which crack and break down, forming fistulas, multiple tracts, and constricting cutaneous scars ( Fig. 9 ). This clinical presentation is rare in children but more frequent in young adults between the ages of 15 and 20 years. ¹⁷

Fig. 9.

Actinomycosis presenting with indurated nodules forming fistulas and constricting cutaneous scars. (This image is provided courtesy of P. J. Gupta.)

The diagnosis is based on the detection of typical sulfur granules from purulent secretions. Alternatively, actinomycosis may be placed in a specific culture medium with detection of antibodies by immunofluorescence. ^{16 17}

Radical therapy consists in wide local surgical drainage and antibiotics (e.g., amoxicillin and clavulanic acid). Although many antibiotics are effective, they have to be administrated orally for a very long period—more than 6 months because their penetration through the dense fibrotic barrier surrounding A. israelii colonies is not optimal. Recurrences are common with incomplete treatment. ^{16 17}

Mycobacterial Tuberculosis

Different cutaneous forms of the infectious diseases caused by Koch 's bacillus may affect the anal region. Mycobacterial tuberculosis (TB) is one cause of granulomatous diseases within the anorectal region. Extrapulmonary TB accounts for 5% of all cases of TB. Perianal TB is a rare extrapulmonary form of the disease. It has a varied presentation, frequently mimicking other rare diseases. Ano-perianal TB may be associated with intra-abdominal TB either as an extension of the original lesion or due to its spread via the lymphatics. Lesions of the abdominal organs are more common while the anal localization is still a rare occurrence. ^{18 19}

The clinical features include symptoms and signs of anal pain or discharge, multiple or recurrent anal fistulas, and unilateral painful groin lymphadenopathy. These features are not unique to anal TB. ¹⁷ A primary granulomatous ulcerated lesion in the anal region is exceptional. The verrucous TB manifestation can spread widely over the buttocks and the anal region.

Anorectal TB is more common in patients with advanced pulmonary or peritoneal disease. ^{19 20} Many of the orofacial TB infections are the result of self-inoculation. These lesions are the result of direct contact with a lymphatic extension around the anus. Numerous small red papules or nodules may break down and form extremely painful ulcers with characteristic undermined edges ( Fig. 10 ).

Fig. 10.

Painful ulcers with undermined edges evident in perineal mycobacterial tuberculosis . (This image is provided courtesy of E. Csatar.)

Evidence of TB usually present, and bacterial confirmation is not difficult. Ulcers are generally small less than 2 cm and do not tend to heal spontaneously. ¹⁸ A modified version of Gupta's criteria is useful in the evaluation of perianal TB ( Table 1 ).

Table 1. Useful adjunctive tests for anal TB are listed.

Diagnosis of mycobacterial anal TB (Gupta)
Culture
Biopsy
Examination of discharge for acid-fast bacilli
Fine needle aspiration cytology
Mantoux test
ELISA antibodies against mycobacteria a
Imaging (magnetic resonance imaging, computed tomography, and/or fistulography) b
Nested polymerase chain reaction
Rapid immunochromatographic assay (ICT TB) c

Abbreviations: ELISA, enzyme-linked immunosorbent assay; TB, tuberculosis.

^aELISA antibodies against tuberculosis IgA EIA, Pathozyme-TB complex, Pathozyme-Myco IgG, Pathozyme-Myco IgA, and Pathozyme-Myco IgM.

^bPotential imaging studies include magnetic resonance imaging, computed tomography, and fistulography.

^cICT TB is immunochromatographic assay for the serologic diagnosis of TB.

There is no topical therapy. Systemic antituberculous tri- or quadritherapy is required. TB fistula may occasionally heal after antituberculous treatment. However, conventional surgical techniques eliminating the fistula are the standard treatment. There is a high prevalence of anal lesions as a result of acquired immunodeficiency syndrome (15–35%). The incidence of TB is increasing in the human immunodeficiency virus (HIV) population—especially in extrapulmonary forms. However, anorectal TB remains rare. Interestingly, there appears to be a reciprocal Koch's bacillus/HIV potentiation. In fact, Koch's bacillus stimulates the propagation of HIV through released growth factors. ^{18 19 20}