Feline- Chronic Bacterial Skin Infections In Cats

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Vol. 21, No. 12 December 1999

Refereed Peer Review

FOCAL POINT ★ Proper culture and biopsy collection procedures for cytologic and histopathologic examination of samples are critical to accurately identify the causative agent in cats with chronic bacterial skin infections.

KEY FACTS ■ An accurate list of potential diagnostic differentials should be sent to the microbiology laboratory along with the samples to ensure that samples are handled properly and appropriate stains are used to maximize the reliability of culture results. ■ Biopsy specimens should be examined with special histopathologic stains and submitted for macerated tissue culture to improve diagnostic accuracy. ■ Aerobic, anaerobic, and facultative anaerobic bacteria have been recovered from feline abscesses. ■ Even with the best techniques and intentions, a diagnosis may still be based on response to therapy.

Chronic Bacterial Skin Infections in Cats Texas A&M University

Robert A. Kennis, DVM Alice M. Wolf, DVM ABSTRACT: Many chronic skin lesions appear similar clinically; thus it is important to recognize their differing cytologic and morphologic characteristics, culture requirements, and histopathologic staining properties. Successful treatment depends on accurate identification of the causative organism using appropriate techniques for collecting and preparing samples for analysis. Antibiotic therapy is best selected on the basis of sensitivity testing. Because results may be unknown for several weeks, however, therapy with antibiotics that have a history of success against a specific organism should be initiated in the interim.

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valuation of cats with chronic skin lesions and/or draining tracts that are unresponsive to routine therapy is a challenge. Diagnostic differentials for these problems include unusual or fastidious bacteria, fungi, foreign bodies, parasites, neoplasia, claw regrowth following onychectomy, and immunologic diseases (see Diagnostic Differentials for Chronic Draining Lesions in Cats). Signalment, history (including travel), response to previous medications, and physical examination findings may help limit the list of possibilities. A logical approach to the diagnostic workup and some specialized techniques are necessary to confirm the diagnosis. This article reviews the important causes of draining tracts and discusses the diagnostic procedures and therapeutic options for cats with chronic draining tracts caused by bacterial agents.

SIGNALMENT AND HISTORY Because some disorders have a predilection for certain breeds or genders, signalment alone may be helpful in limiting the diagnostic differentials. For example, pseudomycetoma has thus far been described only in Persians. Sporotrichosis and cryptococcosis are predominant in male cats. Age may also be important because very young or very old immunocompromised cats with concurrent illness may be at increased risk for bacterial and fungal infections. Because prior therapy or surgery can alter a lesion’s clinical appearance, clients should describe how lesions appeared when they first developed. An orderly account of changes in the type, quantity, and color of exudation; presence or absence of granules in the exudate; character of the odor; and distribution of the lesions must be obtained. Any previous treatment attempts should be assessed, including medications, dosages, length of therapy, and apparent response. Clients should be asked whether their cats are allowed outdoors. Some cats have

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Diagnostic Differentials for Chronic Draining Lesions in Cats Bacterial causes ■ Aerobic or facultative anaerobic —Pasteurella —Staphylococcus —Streptococcus —Nocardia —Opportunistic Mycobacterium —Mycobacterium —Streptomyces —L-Form bacteria —Mycoplasma ■ Anaerobic —Fusobacterium —Bacteroides —Actinomyces

■ Histoplasmosis capsulatum ■ Coccidioides immitis ■ Dermatophytosis ■ Miscellaneous fungal infections (molds) ■ Pythium insidiosum?

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tured until it is time to collect the appropriate diagnostic specimens. Focal areas of alopecia may also provide clues about the presence of resolving or possibly very early lesions. Hair surrounding a puncture wound or necrotic tissue can sometimes be easily removed because such lesions disrupt the blood supply to the hair.

DIAGNOSTIC EVALUATION A methodic approach greatly aids in making a diagnosis when higher-order bacteria are suspected (see Potential Diagnostic Procedures). A complete blood count, serum biochemistry profile, and urinalysis are helpful to identify Miscellaneous causes systemic disorders (e.g., diabetes mellitus) that ■ Foreign body may predispose a cat to chronic infections. ■ Joint disease Testing for feline leukemia virus (FeLV) anti■ Dermoid sinus gen and feline immunodeficiency virus (FIV) ■ Neoplasia (with or without antibody is essential for any cat with a chronic a bacterial component) disease. A thyroid hormone assay (thyroxine) may be indicated in cats older than 4 years of ■ Immunologic (systemic age. The essential dermatologic database inillnesses) cludes aseptic collection of specimens for bacte■ Parasites (cuterebra, rial and fungal cultures; cytologic evaluation of larval migrans) scrapings, aspirates, or exudate from the leFungal causes ■ Claw regrowth following sions; and histopathologic examination of bi■ Sporothrix schenckii onychectomy opsy tissue samples. Focal draining lesions may be examined radiographically for radiopaque ■ Cryptococcus neoformans ■ Panniculitis foreign bodies, tooth fragments, projectile for■ Blastomyces dermatitidis ■ Aseptic abscessation eign bodies, and osteomyelitis. Fistulography using iodinated contrast material is often helpa propensity to fight with other cats, thereby increasing ful to define the source, direction, and extent of a their risk for bite-wound abscesses and puncture indraining tract. Electron microscopy of a tissue sample is juries or exposure to immunosuppressive viral diseases. sometimes indicated when L-form bacteria are suspected. Cytologic or histologic examination of aspiration The health status of other in-contact animals (and peoand/or biopsy samples of regional draining lymph ple) may help to define contagious or possibly zoonotic nodes can also aid diagnosis. causes. A thorough medical history allows clinicians to Culture and biopsy collection procedures are best better define the list of potential diagnostic differentials performed with the patient under general anesthesia. and limits the number of unnecessary tests. Microbiologic culture and susceptibility testing are the PHYSICAL EXAMINATION basis for diagnosis in many cases. When possible, all Because of the zoonotic potential of some of the oral and parenteral antibiotics should be discontinued 2 causative organisms (especially Sporothrix schenckii), to 3 days before culturing; this ensures that residual anprotective gloves should be worn during the physical tibiotic in the tissue does not suppress bacterial growth examination. In addition, palpation of a painful lesion in the cultured sample. A microtip culturette swab may may cause a patient to become aggressive, so caution is be used to collect material from deep inside fistulous advised. Palpation of the regional and peripheral lymph tracts; however, this method often provides insufficient nodes may help to better determine the extent of the organisms for culture. Samples taken from open draindisease. Crusted lesions are often difficult to identify ing tracts may be contaminated with secondary bacteribecause of the amount of hair present; gentle palpation al opportunists, which can confuse interpretation of of the skin surface may help to discover such lesions. culture results. Aseptically collected, deep biopsy samDuring palpation, a fluctuant pocket of fluid or exuples usually provide more accurate culture results. date may be identified—the lesion should not be rupSpecimens for cytologic examination should be obFOCAL ALOPECIA ■ SYSTEMIC DISORDERS ■ RADIOGRAPHY

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tained after aseptic microSpecimens for macerated Potential Diagnostic Procedures biologic culture specimens tissue culture are collected afhave been collected. Direct- ■ Tests for feline leukemia virus and feline ter histopathology samples impression samples, swabhave been obtained. The skin immunodeficiency virus collected samples, or im- ■ Complete blood count should be gently cleansed prints from tissue collected with a topical disinfectant ■ Serum chemistry profile for biopsy can be applied (e.g., povidone–iodine, chlorto a clean glass slide. Slides ■ Urinalysis hexidine gluconate); residual should be heat-fixed before ■ Thyroid profile scrub is removed with 70% staining with a modified ■ Cytologic examination of exudate and tissue grains isopropyl alcohol, and the Wright’s stain. Gram’s stainskin surface is allowed to air —Gram’s stain ing may help identify organdry. This prevents disinfec—Modified Wright’s stain isms in highly exudative tant from being dispersed —Fite–Faraco stain (acid-fast) samples. In addition, fineinto the tissue to be cultured. needle aspiration samples ■ Fine-needle aspiration of regional lymph nodes Appropriate sample sites inshould be collected from re- ■ Aerobic, anaerobic, and fungal cultures clude intact skin over a fluc—Swab-collected sample gional lymph nodes, stained, tuant pocket, a primary lesion and examined in a similar (e.g., a pustule), or chronic —Aseptically collected tissue sample (macerated manner. granulomatous tissue. The tissue culture) Primary lesions (e.g., pussample should be collected by —Fine-needle aspiration of exudate from closed tules, vesicles) should be sesurgical excision (deep lewounds lected for biopsy if possible. sions) or punch biopsy (more The skin should not be ■ Biopsy and histopathology with special stains superficial lesions); placed in —Punch samples of superficial lesions cleansed before collecting a dry, sterile petri dish; and histopathologic samples beshipped on cold packs. Sterile —Surgical ellipse of deep lesions cause the skin surface may saline should not be added to contain subtle but importhe samples because it entant changes. A 6-mm, full-thickness skin sample courages overgrowth of surface contaminants and may should be collected through any crust and exudate. For lead to severe tissue autolysis. Vacutainers should not be larger, deeper lesions or lesions in which the leading used to ship samples because their sterility is not guaranmargin is important, surgical excisional biopsy may be teed after the seal is broken. Samples for anaerobic culture more appropriate. An elliptic incision made with the should be submitted in appropriate anaerobic culture long axis perpendicular to the leading edge of the lesion medium or culturette tubes. Even in appropriate containensures that the pathologist will process the tissue in a ers, anaerobic bacteria are fragile and should be processed standardized format that will yield the most accurate immediately to prevent false-negative results. The microresults. Several specimens should be submitted from biology laboratory can provide additional information representative lesions, including, if possible, early and about its preferred specimen transport protocol. late stages of the disease process. Tissue imprints for cySwab-collected samples can be used for culture if surtologic evaluation should be made on clean glass slides face contamination during sample collection is avoided. before the biopsy specimen is placed in formalin fixaSurgical preparation of the intact skin followed by a tive. It is important to include a history and differential small stab incision or fine-needle aspiration usually diagnosis list for the pathologist to ensure that approyields an appropriate sample from a fluctuant pocket. priate stains are used. This technique can also be used for intact pustules or Macerated tissue culture is the preferred method for vesicles; if a swab is merely inserted into the opening of specimens from patients with chronic, poorly respona fistulous tract, culture results may be erroneous besive lesions. The maceration process involves mincing cause of contamination with surface bacteria. The likethe tissue before plating it onto appropriate agar. Bactelihood of obtaining accurate diagnostic microbiologic rial colonies trapped in fibrous or granulomatous tissue culture results is directly proportional to the quality of and intracellular bacteria are more likely to be recovthe sample collection techniques employed. ered by this method. Not all commercial veterinary labCAUSES oratories are familiar with this procedure; thus it is imRoutine Abscess portant to talk to the microbiologist before submitting Subcutaneous abscesses are common in cats, and the such specimens. SURGICAL EXCISIONAL BIOPSY ■ MACERATED TISSUE CULTURE ■ ANAEROBIC CULTURE SAMPLES

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treatment of routine bitefrom canine and feline cutawound abscesses is fairly neous lesions.5,9,10 The clinical findings assostraightforward and rewardciated with Nocardia infection ing. Bacteria are often inocuare not unique and include lated through the skin via abscessation with fistulous bite or claw wounds or fortracts, cellulitis, nodular dereign bodies. Because cat skin matitis, or multifocal ulcerais very elastic, these puncture tions5,9 (Figure 1). Localized wounds seal over rapidly and regional lymphadenopathy abscessation occurs in 2 to 4 may also be present.9 The exdays. Aerobic, anaerobic, and udate may contain yellowish facultative anaerobic bacteria have been recovered from fe- Figure 1—An adult cat exhibiting ulcerative to necrotic der- granules, often referred to as line abscesses. In a recent matitis. These lesions are not pathognomonic for any of the sulfur granules, that are comstudy of flora isolated from etiologic agents discussed in the text. Nocardia was cultured posed of colonies of the organism.4,9 These granules can feline cutaneous abscesses, from a biopsy sample. be gently crushed between 9.7% of the cultured specitwo glass slides and stained with Gram’s stain and modmens contained only obligate anaerobes, with Fusobacterium species and Bacteroides species isolated most freified Fite–Faraco stain (acid-fast) to provide a tentative quently.1 Approximately 16% of the cultures contained diagnosis of nocardiosis.7 Histopathology may be help1 both obligate and facultative anaerobic bacteria. Other ful, although Nocardia organisms are often difficult to frequently isolated organisms include Pasteurella multociidentify even with special staining techniques. da, Peptococcus species, Clostridium species, Staphylococcus Aerobic swab samples of the exudate and any obvious species, and Streptococcus species.1,2 granules should be submitted for microbiologic culTherapy for feline subcutaneous abscesses usually ture.5 Anaerobic specimens should also be submitted consists of surgical debridement to establish ventral because infections with Actinomyces species and other resistant anaerobic bacteria are important diagnostic drainage and copious lavage with saline or dilute differentials for lesions of this type. Macerated tissue (0.15%) chlorhexidine solution.3 Broad-spectrum antibiotics that are effective against anaerobic bacteria are cultures can be more productive than swab specimens good choices for empiric therapy.1 Because most anaerin recovering Nocardia from these patients.4 Nocardia grows well on blood agar and Sabouraud dextrose agar.7 obic infections are polymicrobial, response to treatment Löwenstein-Jensen agar (used to detect Mycobacterium with antibiotics directed against the anaerobic compospecies) may be used to isolate Nocardia when other nent is often equal to or better than that with combinaculture samples are negative. tion antibiotic treatment. Treatment with penicillin or Nocardia species show variable antimicrobial susamoxicillin for 7 to 14 days is usually adequate. If peniceptibility patterns. Apparent in vitro susceptibility and cillin resistance is suspected or cytologic examination actual in vivo efficacy do not always correlate well for reveals many gram-positive cocci, amoxicillin–clavulanhumans with Nocardia infections4,7,11; thus empiric anic acid may be an effective alternative.2 Other antibiotics that have been used successfully to treat anaerobic tibiotic selection is usually made for cats with nocardioinfections include metronidazole, clindamycin, and cesis. Potentiated sulfa drugs have long been considered foxitin. the treatment of choice, and enrofloxacin, amoxicillin–clavulanic acid, minocycline, chloramphenicol, Nocardiosis erythromycin, imipenem, clarithromycin, amikacin, Recurrent or nonhealing abscesses should prompt and combinations thereof have also reportedly been concern about the presence of immunosuppressive dissuccessful in treating nocardiosis5–7,9–12; however, many of the Nocardia isolates from our recent patients have eases (e.g., FIV, FeLV) or unusual infectious agents. Nocardia organisms are soil-borne, aerobic, branching, filshown clinical resistance to most of these drugs. In sevamentous, gram-positive bacteria.4–7 A differentiating eral cases, rapid resolution of lesions was achieved with staining characteristic is the propensity for this organparenteral amikacin therapy after extended treatment ism to be partially acid-fast.8 Nocardia organisms are with several different oral antibiotics had failed. saprophytic and can enter the body through soil inocuOral antimicrobial therapy should be continued for lation of wounds or by inhalation or ingestion.5,7,9 Noat least 1 month after complete clinical remission has cardia asteroides is the species most commonly isolated been achieved. If amikacin is used for a prolonged ACID-FASTNESS ■ LYMPHADENOPATHY ■ SULFUR GRANULES

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course of therapy, careful monitoring of renal function is necessary and treatment after resolution of lesions should continue only for an additional 2 weeks. Serum urea nitrogen and creatinine levels should be checked at least once weekly during amikacin therapy. Urinalyses (collected by cystocentesis) are also warranted to detect changes in specific gravity and check for casts. Because antibiotic susceptibility patterns of Nocardia species are variable, prognosis is guarded.7

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cause deep-seated infections are common. The prognosis for patients with actinomycosis is guarded. Even with appropriate treatment, relapses are common and some patients may require continuous, lifelong antibiotic therapy to control lesions.8

Streptomycosis Streptomyces griseus is a gram-positive, filamentous, aerobic bacterium that has rarely been isolated from cats.14 The clinical appearance of lesions is similar to that of Nocardia or Actinomyces lesions, except that any granules are black rather than yellow. Identification of the organism in culture is the key to diagnosis, and appropriate antibiotic therapy is based 2—Caudal view of an adult cat’s on the results of susceptibility testing.

Actinomycosis Actinomyces species are anaerobic, gram-positive, branching, filamentous bacteria found in the oral cavity of animals. Infection with Actino- Figure myces hordeovulneris commonly oc- hindlimb. Hemorrhagic to necrotic papucurs in association with traumatic lar lesions with draining tracts are visible. Mycobacterium Infections injury in which plant awns (e.g., fox- A diagnosis of Nocardia infection was Opportunistic Mycobacterium Opportunistic mycobacterial grantails) disrupt mucosal barriers.13 Soli- made on biopsy culture, whereas multiple tary or multiple abscesses with drain- swab cultures were negative. Similar le- ulomas (atypical mycobacteria) can ing tracts may be present and cannot sions can be seen with opportunistic My- be caused by a number of Mycobaccobacterium infections. terium species, including fortuitum, be distinguished from other causes 8 smegmatis, chelonei, xenopi, thermoreby clinical appearance alone. Similar to Nocardia infection, granules can sometimes be idensistible, phlei, vaccae, and ulcerans.15–21 These facultative 4,8 tified in the serosanguineous exudate. Diagnosis is pathogens are ubiquitous in the environment. Although confirmed by identification of Actinomyces species in the method of inoculation into the skin and subcutaanaerobic culture. A large quantity of exudate and neous tissue is unknown, the most likely routes are trauma, granules (3 ml, if possible) should be submitted because foreign-body penetration, and fight wounds.21 Opportunistic mycobacteria most commonly cause chronic, isolation of these organisms can be difficult. Samples of nonhealing, granulomatous panniculitis with a fistulous, tissue for macerated culture are also helpful. Bacterial exudative reaction of the skin and deeper tissues.18 The culture plates should be held for longer than usual belesions often target the inguinal region and hindquarters cause growth of Actinomyces may take 2 to 4 weeks. Histopathologic examination may be suggestive of actinomyof cats.15,17,18 Nodules and deeper draining tracts may or may not be present. M. smegmatis infection sometimes cosis, but other causes of chronic dermatitis that may produces multifocal areas of necrosis that leave small ulbe difficult to isolate by microbial culture (e.g., fungi, Mycobacterium) should be eliminated. The presence of cerations in the skin surface (Figure 2). Lesions consisacid-fastness may distinguish Nocardia species from tent with opportunistic mycobacteria are not unique Actinomyces species—the latter are never acid-fast.5,8 compared with the bacterial infections discussed previTreatment of actinomycosis usually involves surgical ously, except that tissue grains do not form. Although debridement and debulking prior to antibiotic therapy.8 regional lymphadenopathy can occur, clinical signs of A careful search should be made for plant awns if a pasystemic illness are generally absent and disseminated tient resides in or has traveled to regions in which they disease is uncommon.15,18 The patient’s history usually reveals a poor response are found. Penicillin drugs are the empiric treatment of to antibacterial therapy or spontaneous waxing and choice, although other drugs may be indicated based waning of lesions. Attempts to surgically excise opporon sensitivity testing.4,5,8 Amoxicillin, minocycline, erythromycin, and clindamycin are reasonable alternatives. tunistic mycobacterial lesions usually fail22; suture lines often dehisce, and infection recurs at and around the Antimicrobial treatment should continue for at least 1 surgical site. Preliminary research has suggested that month after complete clinical remission is achieved beAMIKACIN THERAPY ■ PLANT AWNS ■ SURGICAL DEBRIDEMENT AND DEBULKING

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very aggressive debulking in disease, the prognosis for paconjunction with appropriate tients with opportunistic myantibiotic therapy may be curacobacterial infection is generaltive.23 However, antibiotic therly guarded. apy alone may be successful Cutaneous and is much less disfiguring. Mycobacteriosis Diagnosing opportunistic my(“Classic Tuberculosis”) cobacteriosis can be challenging Mycobacterium bovis, Mybecause these organisms may be cobacterium tuberculosis, or difficult to find in affected tisMycobacterium microti can sues. Histopathologic examinacause classic tuberculosis in tion reveals pyogranulomatous inflammation. Such special Figure 3—Multifocal to coalescing ulcerative lesions with cats. 15 These infections are stains as Fite–Faraco (acid-fast) minimal exudation. A diagnosis can best be made with apparently acquired through contact with infected smallmay reveal a few organisms in fat surgical debridement and macerated tissue culture. mammal prey. M. avium, anvacuoles of the panniculus, but other slow-growing mycobacterial pathogen, is considdefinitive diagnosis is based on bacterial culture.17,18 Because these organisms are deep within the skin, aseptically ered a soil saprophyte.15,25 Siamese cats appear to be predisposed to M. avium infection.15,18,19,25 collected biopsy samples submitted for macerated tissue Clinical signs in cats with classic tuberculosis are culture are most likely to produce positive results (Figure highly variable. Abscesses, soft nodules, plaques, or ul3). Opportunistic mycobacteria can grow on blood agar, cerations with exudation have been reported.15 These but less fastidious organisms may overgrow the plates and lesions most often occur on the face, head, neck, shoulobscure the diagnosis. Such culture media as Löwensteinders, distal limbs, or other common sites of bite Jensen should be used when an atypical mycobacterium is wounds.15,24 Most patients have systemic signs of illness, suspected. Colonies of opportunistic mycobacterial species including anorexia, fever, lymphadenopathy, anemia, usually appear in culture in approximately 7 days, much and icterus. 15,18,19,25,26 Radiographs may reveal hepfaster than what is seen with Mycobacterium avium or clas17 sic tuberculosis-causing species. Cultures should be reatomegaly or splenomegaly, abdominal masses, or lung tained, however, because growth of some opportunistic involvement15,18—findings that may be helpful in dif8,18 Mycobacterium species may not occur for 3 to 4 weeks. ferentiating classic tuberculosis from opportunistic myIn vitro mycobacterial susceptibility testing can be percobacterium or feline leprosy. There have been only formed by some specialized laboratories and is recomtwo reported cases of M. microti infection to date, and both patients had pneumonia.15 mended where available. However, the results of these tests Confirming a diagnosis of tuberculosis can be diffimay take several weeks and treatment should not be decult because few organisms may be present in the lelayed in the interim. Because therapy may last several sions. Histopathology may identify intracellular, acidmonths, the best drug should be selected first. We and fast, rod-shaped bacteria within a granulomatous tissue others have had success using fluorinated quinolone anreaction in the dermis or subcutis.27 Aerobic swab cultibiotics at higher-than-labeled dosages (enrofloxacin, 5 to tures from exudate and biopsy tissue samples of skin 10 mg/kg orally twice daily) until 1 month beyond clinical and lymph node(s) should be submitted for culture. remission.18,22 Treatment with clofazimine (Lamprene®, Novartis, East Hanover, NJ) has also been successful in These organisms require a special culture medium that several patients that were not responsive to other is high in lipid content, such as Ogawa egg-yolk mediagents20,24; this product is not approved for use in cats and um, Stonebrink’s medium, or Löwenstein-Jensen agar. temporarily (i.e., until medication is discontinued) stains Growth of classic tuberculosis organisms in culture can tissue orange–yellow during treatment. Hepatopathy, be exceedingly slow, and identification of the organism corneal pigmentation, gastrointestinal distress, pruritus, sebmay take 6 weeks or longer.24 Intradermal testing for a delayed hypersensitivity reaction has not been successorrhea sicca, and systemic illness have also been associated ful in diagnosing cats with tuberculosis.15 Polymerase with clofazimine use.8,20 Azithromycin, amikacin, and 21 doxycycline have been used with occasional success. Critchain reaction techniques have been developed to idenical evaluation of the success rates with different therapeutify the DNA of tuberculosis-causing organisms in the tic protocols is difficult because spontaneous remission has skin of dogs and humans,28 but no reports have been pub16 lished on the accuracy of this procedure for cats. Inocualso been reported. Because of the variable antibiotic susceptibility and chronic waxing and waning nature of the lation of organisms from tuberculosis cultures in guinea PYOGRANULOMATOUS INFLAMMATION ■ IN VITRO MYCOBACTERIAL SUSCEPTIBILITY ■ CLOFAZIMINE

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pigs results in death in 6 to remission. Spontaneous re8 weeks. mission of this disease has Therapy for M. bovis or M. also been reported.29 There tuberculosis infection can be is no evidence that M. lepattempted with combination raemurium is contagious to humans. therapy protocols that include rifampin, isoniazid, and ethamL -Form Bacteria butol, which are currently used L-Form bacteria are parin humans and dogs. Fluorotially or completely cellquinolones (enrofloxacin and wall–deficient bacteria of a ciprofloxacin) and combinacommon species that has tions of rifampin or enrofloxbeen altered as a result of loacin with clarithromycin, clofazimine, and doxycycline Figure 4—Symmetric, nodular, ulcerative draining lesions over cal environmental pressure have been effective in some the carpi of an adult cat. Negative culture results and a rapid (e.g., chronic inflammacats.15,19,26 However, because response to tetracycline antibiotic therapy led to a presump- tion).30 L-Forms retain the of the significant potential tive diagnosis of L-form bacterial infection. same virulence characteriszoonotic health risks from tics of the parent organism. these two mycobacterial speTheir structure helps them cies, euthanasia is often recommended. M. avium is a soilevade attacks by the immune system and avoid digesborne pathogen, and thus its zoonotic potential is limited tion by lysosomal enzymes and makes them resistant to except in immunocompromised humans.19 many routinely used antibiotics. L-Forms can persist in this state or revert to a cell-wall–containing form, a Feline Leprosy characteristic that helps differentiate them from MyFeline leprosy is caused by Mycobacterium lepraemuricoplasma species. When present, L-form infection can um transmitted by cat and rat bites or soil contamispread as such from cat to cat by direct contact with innation of wounds.8,15 This organism is poorly characfectious exudate. terized because of the difficulty in maintaining it in Clinical findings in patients with L-form bacterial infections include abscessation and draining tracts that culture for study. Most affected cats are younger than 5 are often located over and involve the joints30 (Figure years of age, and there is no breed or gender predilec29 4). Fever, anorexia, and signs of systemic illness are usution for infection. M. lepraemurium lesions consist of single or multiple soft, fleshy nodules that are nonally present. A common clinical presentation is chronic painful and may or may not ulcerate.15,29 These are usuabscessation that is poorly responsive to drainage proceally located on the head and limbs but can occur anydures and antibiotics routinely used to treat feline bitewhere on the body. 8 Regional lymphadenopathy is wound abscesses. In the absence of effective treatment, common, but systemic signs of illness are unusual. lesions often spread hematogeneously or by direct inocThe diagnosis of feline leprosy is suspected on the ulation to other locations on the body. Radiographs of basis of clinical findings and identification of acid-fast affected joints often show bone lysis, collapse of joint organisms in skin lesions. Scrapings from ulcerated lespaces, and periosteal proliferation.30 Cytologic examination of exudate from these lesions sions or aspiration of nodules may reveal large numbers usually reveals a pyogranulomatous response with large of thin, acid-fast bacilli.8 Histopathology demonstrates granulomatous inflammation with acid-fast bacteria in numbers of macrophages along with the neutrophil macrophages. Confirmation is made by identification population.30 L-Form bacteria grow poorly (if at all) on routine culture media and may be difficult to identify of M. lepraemurium in culture at a reference laboratory. Ogawa egg-yolk medium is the preferred culture mateeven with the special techniques used to culture Mycoplasma species. Overgrowth of secondary invaders in rial. Injection of cultures into guinea pigs may be perthese draining lesions often confounds interpretation of formed to rule out tuberculosis-causing bacteria. microbiologic culture results. Electron microscopy may Aggressive surgical excision of affected tissue is the be required to definitively identify the organism(s). treatment of choice; however, complete excision is diffiA definitive diagnosis of L-form infection may be difficult, and recurrence of lesions is common. Clofazimine cult to achieve and is often presumptive based on therapy should be used as an adjunctive treatment after surgery. response. Treatment with tetracycline drugs usually proTo ensure complete resolution, antileprosy therapy duces dramatic improvement in affected patients within should continue for several months after clinical ZOONOTIC HEALTH RISKS ■ CHRONIC ABSCESSATION ■ BONE LYSIS

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48 to 72 hours; this response provides presumptive evidence of L-form infection but does not rule out the possibility of Mycoplasma as the causative agent. Severe orthopedic damage caused by intraarticular infection may require surgical stabilization after the infection has been controlled. We are aware of several cases in which L-form infections spread from infected cats to veterinarians, so these cats should be handled with care and their owners warned about the potential for zoonotic infection. D N PE IU S
M’

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A LookBack The popularity of cats as companion animals has increased over the past two decades. At the same time, the overall quality of feline medical care, including dermatology, has improved. Better antibiotics, advanced diagnostic tools, and high-quality reference laboratories have been essential for such advances. The subspecialty of dermatopathology has improved the quality of biopsy evaluation, whereas tissue-staining techniques have improved the diagnostic evaluation of formalin-fixed tissues. The next decade should witness improved bacterial sensitivity testing, polymerase chain reaction techniques to aid diagnosis, and new classes of antibiotics. There is also a need to develop a better understanding of how to dose currently available antibiotics to achieve therapeutic tissue concentrations for resistant bacterial infections in cats. (Photos: Drs. Kennis [left] and Wolf.)

Mycoplasma Mycoplasma species usually cause upper respiratory disease and, rarely, nonerosive polyarthritis/tenosynovitis in cats.31 There is one report describing Mycoplasma-like organisms as the causative agent of chronic abscesses and draining tracts in cats.32 However, the clinical location and appearance of the lesions and the character and cytologic appearance of the exudate described in these cats was typical of Lform bacteria. No known Mycoplasma species were recovered from these patients, and the diagnosis was presumptive on the basis of response to tetracycline therapy. Because both L-form and Mycoplasma infections respond to tetracycline, it is unclear whether Mycoplasma species are true dermatologic pathogens or this report was a case of mistaken identity. SUMMARY The diagnosis and treatment of bacterial causes of feline draining lesions can be very difficult. Successful treatment depends on accurate diagnosis. The diagnostic procedures outlined in this article, such as macerated tissue cultures, biopsies, and cytologic evaluation, are essential to obtain a defini-

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tive diagnosis. The ultimate reason to find the cause is to provide a reasonable prognosis and treatment plan to owners. However, even with the best techniques and intentions, a diagnosis may still be based on response to therapy (e.g., as with L-form bacteria).

REFERENCES 1. Hoshuyama S, Kanoe M, Amimoto A: Isolation of obligate and facultative anaerobic bacteria from feline subcutaneous abscesses. J Vet Med Sci 58(3):273–274, 1996. 2. White SD: Pyoderma in five cats. JAAHA 27:141–145, 1991. 3. Guaguere E: Topical treatment of canine and feline pyoderma. Vet Dermatol 7:145–151, 1996. 4. Warren NG: Actinomycosis, nocardiosis, and actinomycetoma. Dermatol Clin 14:85–95, 1996. 5. Kirpensteijn J, Fingland RB: Cutaneous actinomycosis and nocardiosis in dogs: 48 cases (1980–1990). JAVMA 201: 917–920, 1992. 6. Gutmann L, Goldstein FW, Kitzis MD, et al: Susceptibility of Nocardia asteroides to 46 antibiotics, including 22 β–lactams. Antimicrob Agents Chemother 23:248–251, 1983. 7. Lerner P: Nocardia species, in Mandell GL, Bennett JE, Dolin R (eds): Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, ed 4. New York, Churchill Livingston, 1995, pp 2273–2280. 8. Fadok VA: Granulomatous dermatitis in dogs and cats. Semin Vet Med Surg (Small Anim) 2:186–194, 1987. 9. Marino DJ, Jaggy A: Nocardiosis. A literature review with selected case reports in two dogs. J Vet Intern Med 7:4–11, 1993. 10. Davenport DJ, Johnson GC: Cutaneous nocardiosis in a cat. JAVMA 188:728–729, 1986. 11. Gombert M: Susceptibility of Nocardia asteroides to various antibiotics, including newer beta-lactams, trimethoprim-sulfamethoxazole, amikacin, and n-formimidoyl thienamycin. Antimicrob Agents Chemother 21:1011–1012, 1982. 12. Burucoa C, Breton I, Ramassamy A, et al: Western blot monitoring of disseminated Nocardia nova infection treated with clarithromycin, imipenem, and surgical drainage. Eur J Clin Microbiol Infect Dis 15:943–947, 1996. 13. Brennan KE, Ihrke PJ: Grass awn migration in dogs and cats: A retrospective study of 182 cases. JAVMA 182:1201– 1204, 1983. 14. Reinke SI, Ihrke PJ, Reinke JD, et al: Actinomycotic mycetoma in a cat. JAVMA 189:446–448, 1986. 15. Gunn-Moore DA, Jenkins PA, Lucke VM: Feline tuberculosis: A literature review and discussion of 19 cases caused by an unusual mycobacterial variant. Vet Rec 138:53–58, 1996. 16. Kunkle GA, Gulbas NK, Fadok V, et al: Rapidly growing mycobacteria as a cause of cutaneous granulomas: Report of five cases. JAAHA 19:513–521, 1982. 17. White SD, Ihrke PJ, Stannard AA, et al: Cutaneous atypical mycobacteriosis in cats. JAVMA 182:1218–1222, 1983. 18. Jordan HL: Canine and feline mycobacterial infection, in Bonagura JD (ed): Kirk’s Current Veterinary Therapy XII. Philadelphia, WB Saunders Co, 1995, pp 320–323. 19. Jordan HL, Cohn LA, Armstrong PJ: Disseminated Mycobacterium avium complex in three Siamese cats. JAVMA 204:90–93, 1994. 20. Michaud AJ: The use of clofazimine as treatment for Mycobacterium fortuitum in a cat. Feline Pract 22(3):7–9, 1994.

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21. Monroe WE, August JR, Chickering WR, et al: Atypical mycobacterial infections in cats. Compend Contin Educ Pract Vet 10(9):1044–1048, 1988. 22. Studdert VP, Hughes KL: Treatment of opportunistic mycobacterial infections with enrofloxacin in cats. JAVMA 201:1388–1390, 1992. 23. Mason KV, Wilkinson GT: Results of treatment of atypical mycobacteriosis (Abstr), in von Tscharner C, Halliwell REW (eds): Advances in Veterinary Dermatology, vol 1. London, Baillière Tindall, 1990, p 452. 24. Kaufman A, Greene CE, Rakich PM, et al: Treatment of localized Mycobacterium avium complex infection with clofazimine and doxycycline in a cat. JAVMA 207:457–459, 1995. 25. Drolet R: Disseminated tuberculosis caused by Mycobacterium avium in a cat. JAVMA 189:1336–1337, 1986. 26. Evans LM, Caylor KB: Mycobacterial lymphadenitis in a cat. Feline Pract 23(4):14–17, 1995. 27. Perkins PC, Grindem CB, Levy JK: What is your diagnosis? An 11–year-old domestic longhaired cat with anemia. Vet Clin Pathol 24:77, 97–98, 1996. 28. Degitz K: Detection of mycobacterial DNA in the skin, etiologic insights and diagnostic perspectives. Arch Dermatol 132:71–75, 1996.

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29. Roccabianca P, Caniatti M, Scanziani E, et al: Feline leprosy: Spontaneous remission in a cat. JAAHA 32:189–193, 1996. 30. Carro T, Pedersen N, Beaman B, et al: Subcutaneous abscesses and arthritis caused by a probable bacterial L-form in cats. JAVMA 194:1583–1588, 1989. 31. Slavik MF, Beasley JN: Mycoplasmal infections of cats. Feline Pract 20(2):12–13, 1992. 32. Keane DP: Chronic abscesses in cats associated with an organism resembling Mycoplasma. Can Vet J 24:289–291, 1983.

About the Authors Drs. Kennis and Wolf are affiliated with the Texas Veterinary Medical Center, Department of Small Animal Medicine and Surgery, Texas A&M University, College Station, Texas. Dr. Kennis is a Diplomate of the American College of Veterinary Dermatology; Dr. Wolf is a Diplomate of the American College of Veterinary Internal Medicine and the American Board of Veterinary Practitioners.