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Topical therapy
Topical therapy is not recommended as the sole treatment for feline dermatophytosis. Its major value is the mechanical removal and inactivation of fungal spores and mycelia on and within hair shafts to reduce environmental contagion. Also, shampooing and rinsing cats is not always practical for owners.
Shampoos

Shampoos are less desirable than rinses because they have no residual action. In addition, the lathering or rubbing process may macerate fragile hairs and increase the release and dispersal of spores into the coat, thereby increasing the spread of infection and human exposure.
Earlier reports indicated that topical therapy with two per cent chlorhexidine shampoo and 0.06 per cent chlorhexidine rinse were ineffective in altering the course of dermatophyte infection (DeBoer and Moriello 1995).
However, more recently published studies have demonstrated that two per cent miconazole, two per cent chlorhexidine shampoo used twice weekly (Malaseb® Dermcare Vet), in combination with systemic therapy with griseofulvin, significantly decreases the time to mycological cure, as well as decreasing environmental contamination (Sparkes 2000).
Both one per cent econazole with chloroxylenol, sulphur and salicyclic acid shampoo (Sebazole® Virbac-Allerderm) and two per cent miconazole, two per cent chlorhexidine shampoo (Malaseb® Dermcare Vet) are registered as aids in the treatment of feline dermatophytosis in Australia.
Rinses
Antifungal rinses are preferable because they minimise rubbing of the hair coat. The procedure is also simpler because the entire body can be treated and the antifungal agent left to dry on the skin.
Several studies have shown that lime sulphur two per cent and 0.2 per cent enilconazole (Imaverol® Boehringer Ingelheim) are the most effective combination. However, there is no veterinary proprietary lime sulphur available in Australia.
Enilconazole is not registered for use in cats and, despite its widespread use in Europe and Canada, there is conflicting anecdotal information about its safety in this species. In one study, 0.2 per cent enilconazole used twice weekly for eight weeks in Persian cats produced only mild side effects including mild depression, hypersalivation, partial anorexia and elevation in liver enzymes (De Jaham 1998).
Rinses should be used every five to seven days until a clinical cure is achieved or the cat is fungal-culture negative. Careful application using gauze sponges and by patting rather than rubbing is advised to avoid microtrauma and iatrogenic rupture of fragile hairs.
The coat and skin should also be dried with a hairdryer, as quickly as possible as moisture will also cause maceration of the epidermis and compromise the skin’s natural protective barrier.
Care should be taken to keep young animals warm and prevent them from licking the antifungal solution. If lime sulphur is used, an Elizabethan collar should be placed on the cat until it is dry. Irritant reactions, vomiting and mild depression have all been reported after ingestion of dips by cats.
Ointments/creams
The efficacy of these products for treating dermatophytosis in cats remains unproven and we do not routinely recommend topical antifungal ointments, gels or creams. Some reasons for this include: the difficulty of using these products in animals; poor penetration by these preparations of the hair coat; vigorous grooming by cats to remove ointments, gels or creams, and the fact these preparations are messy and encourage owners to only perform ‘spot therapy’.
In humans, infective material in nonlesional skin can be found as far as six cm away from the visible dermatophytosis lesion and it is believed that a similar situation may exist in cats.
Systemic therapy - the treatment of choice
Systemic therapy is the treatment of choice for feline dermatophytosis. However, it is imperative to remember that systemic antifungal therapy does not rapidly reduce contagion and should always be used in conjunction with clipping and topical antifungal agents.
Griseofulvin is the initial drug of choice given at a dosage for cats of 25mg/kg/body weight (BW) orally every 12 hours but is not licensed for this use in cats. The absorption of griseofulvin is better when administered as a divided dose and with a fatty meal.
Side effects are common in cats and include anorexia, depression, nausea, vomiting and diarrhoea. However, these can generally be avoided by dividing or lowering the dosage. Anecdotal reports indicate that Siamese, Himalayan, Abyssinian and Persian cats may be more prone. Griseofulvin is also not recommended for use in kittens less than 12 weeks-of-age, although there are reports of its use in kittens as young as six weeks.
Griseofulvin is highly teratogenic, especially in the first trimester of pregnancy and is therefore contraindicated in pregnant animals. Although teratogenic effects have not been documented after treatment of breeding male cats, griseofulvin can cause abnormalities in spermatozoa in experimental conditions in rodents. It is thus advisable to avoid using recently treated male cats for breeding.
Bone marrow suppression producing anaemia and leukopenia is a relatively uncommon, but severe and unpredictable, side effect of griseofulvin therapy. These effects can reverse when treatment is withdrawn but irreversible idiosyncratic pancytopenia has been reported.
Myelosuppression does not appear to depend on dose rate or breed of cat.
Severe neutropenic reactions have been reported in cats with dermatophytosis associated with FIV infection. Griseofulvin should not be used in cats with FIV and, as such, all cats should be FIV-tested prior to griseofulvin therapy.
If griseofulvin is used in these cats, once or twice weekly blood counts are recommended.
Griseofulvin does have anti-inflammatory and immunomodulatory properties and is known to suppress delayed hypersensitivity reactions in the skin. These properties can lead to important clinical misinterpretations. Some authors have noted dogs and cats with inflammatory skin disease (for example, bacterial pyoderma) have demonstrated significant clinical improvement while receiving griseofulvin for presumed dermatophytosis.
Small subhead: Ketoconazole
Ketoconazole is a fungistatic azole drug that is not registered for use in the cat. It is also not recommended as the first choice for the treatment of feline dermatophytosis due to the potential side effects in this species, although it has been used successfully to treat cats in many European countries at an oral dosage of 10mg/kg/BW every 24 hours.
Ketoconazole is well absorbed from the gastrointestinal tract but its bioavailability depends on an acidic environment. Concurrent administration of anticholinergic, antacid or H2 blockers (cimetidine, ranitidine) decrease absorption. However, absorption can be improved when the drug is given with food.
Anorexia, nausea and vomiting are the most common side effects from ketoconazole and occur in about 25 per cent of cats. Side effects are usually dosage-related and may be diminished by dividing doses, decreasing the dosage and administering each dose with food.
Elevation in liver enzymes and jaundice has been reported in cats but the incidence of hepatotoxicosis is relatively low. Neurological disorders associated with ketoconazole use have also been reported in cats. The drug may also be teratogenic and should not be administered to pregnant females.
Itraconazole
Itraconazole is a fungicidal triazole drug that is indicated in cats unable to tolerate griseofulvin therapy or in cases where griseofulvin has not been successful. The drug is not registered for this use in the cat. The recommended dosage is 10mg/kg/ BW orally every 24 hours.
In human medicine, itraconazole has been demonstrated to persist in the stratum corneum for three to four weeks after discontinuation of therapy and has been used as pulse therapy for both dermatophytosis in adults and children.
One recent study evaluated the efficacy of itraconazole as a combined continuous/pulse therapy in nine cats with feline dermatophytosis using 10mg/kg orally every 24 hrs for 28 days and then on an alternate week regimen (one week on, one week off) at the same dosage.
Treatment was stopped when two consecutive negative fungal cultures at two-week intervals were obtained. Eight cats had negative fungal cultures at Days 28 and 42 with a total of 56 days of therapy (Colombo 2001).
Itraconazole should be administered with a fatty meal and to maximise absorption, concurrent administration of drugs that decrease stomach acidity should be avoided. For cats, the capsules may be opened and mixed with food.
Side effects are uncommon and include anorexia, weight loss, depression, vomiting, jaundice and elevations in serum ALT enzyme concentrations, but hepatotoxicosis is rare.
Itraconazole should be avoided during pregnancy, although dosages of 10mg/kg/ BW per day have been reportedly administered to pregnant animals without teratogenic effect.
Terbinafine
Terbinafine is a fungicidal allylamine useful in the treatment of superficial dermatophytosis and onychomycosis in humans but not registered for use in the cat. There are few reports on its use in veterinary dermatology. A recent study evaluated 12 cats with M canis dermatophytosis using terbinafine orally at 30mg/kg/BW every 24 hrs for 14 days.
Clinical and mycological cure was achieved one month post-treatment in four cats and three months post-treatment in a further six cats (Mancianti 1999).
Terbinafine is well absorbed orally with or without the presence of food. After absorption, most of the drug is metabolised by the liver, so dosage adjustment is necessary in patients with hepatic dysfunction.
Side effects have not been reported with use of terbinafine in cats. In humans, only a low number of mostly gastrointestinal side effects have been observed. Idiosyncratic acute hepatotoxicity has been reported occasionally.
No teratogenicity has been reported with the use of terbinafine in rats or rabbits, even at high dosages. In humans, teratogenicity has not been reported and the drug is not contraindicated in pregnant women.
Lufenuron
Lufenuron is a chitin synthesis inhibitor. Chitin is a component of fungal cell walls but is absent from mammalian cells and so provides a potential target for antifungal treatment.
A recent retrospective study described the use of lufenuron for the treatment of cats with dermatophytosis. One hundred and fifty nine cats were treated with a single dose of lufenuron (51.2 to 266mg/kg/BW). There was a mean reported recovery time after treatment of 11.6 (+/- 1.4 days) compared to 94.7 (+/- 22.9) for an untreated group of 42 cats. Recovery was defined as resolution of all clinical signs and regrowth of hair (Ben-Ziony and Arzi 2000).
However, this study was not randomised, blinded or controlled, which is essential when investigating a spontaneously resolving disease such as a dermatophytosis.
As a result of this study, lufenuron became widely used at varying dosage regimes for the management of individual cats and catteries with dermatophytosis.
Over the past 18 months there has been an informal consensus amongst veterinarians and veterinary dermatologists that lufenuron seemed effective in the treatment of some cases of feline dermatophytosis but has clearly failed in others.
The lack of controlled studies with respect to efficacy or information about dosing regimes has led to increasing scepticism about lufenuron as a sole treatment or prophylaxis for feline dermatophytosis.
More recently, two US studies have provided more information about the lack of efficacy of lufenuron in the prophylaxis of feline dermatophytosis.
The first study consisted of three groups of six young cats: Groups 1 and 2 were treated with monthly lufenuron for two months at 30mg/kg/BW and 133mg/kg/BW, respectively, while Group 3 was given a placebo for two months.
All cats were then challenged with a standardised dose of M canis spores and all became infected. Further, treated cats did not recover faster than untreated cats. Eventually, all cats recovered and became culture-negative and lesion-free.
The conclusion was lufenuron did not prevent dermatophyte infection within the limits of this study (Moriello, DeBoer et al 2002).
A second study involved treating three groups of eight cats, respectively, with 100-140mg of lufenuron suspension monthly, 40mg subcutaneously every six months or a placebo for four months. All cats were then exposed to a cat with experimentally induced M canis infection.
Again, all cats became infected and there was no difference in time to resolution between the groups. However, cats treated with lufenuron had significantly lower infection scores during the early weeks following exposure and there was a more prolonged initial progression phase of the infection.
Once infections reached peak intensity, they resolved over a similar time period in both treated and control groups.
The conclusion was lufenuron, when used at the dose rates and under the conditions in this study, did not prevent dermatophyte infection by exposure to an experimentally infected cat.
The delay in establishment of infection may reflect an inhibitory effect of lufenuron on the organism that is measurable, but is not sufficient to prevent the ultimate development of infection under these conditions (Moriello and DeBoer 2002).
Furthermore, another recently published study evaluated two groups of cats treated in two separate catteries in France. The first group was treated with oral lufenuron administered at 60mg/kg/BW once on Day 0 and Day 30 and topical 0.2 per cent enilconazole rinses once a week for four weeks, while the second group was treated with oral griseofulvin at 25mg/kg/BW every 12 hours for 35 days and topical 0.2 per cent enilconazole rinses once a week for four weeks.
No definitive eradication was achieved in either group (Guillot 2002).
In summary, while there is evidence that lufenuron may delay the initial establishment or progression of dermatophyte infection reflecting some inhibitory effect, it did not prevent infection. Furthermore, dermatophyte infections did not resolve faster than in M canis-positive cats that were not treated in the above studies.
Lufenuron appears to have some antifungal properties but further controlled studies are required to examine clinical efficacy and dose rates. Until these are performed, consideration may be given to adding oral lufenuron at a dose rate of 65 to 100mg/kg/BW every 30 days to a conventional treatment regime on the grounds that it is well tolerated and may be of some benefit. Currently, there is insufficient evidence about efficacy or information about dosing regimes to warrant the use of lufenuron as sole treatment or prophylaxis for feline dermatophytosis.
Treatment length and monitoring therapy
Cats often begin to show clinical resolution of lesions within two to three weeks of initiating therapy. It is important to remember that patients will appear clinically normal long before they are cured and are culture-negative.
It is recommended that infected individuals be examined once a month during treatment.
A Woods lamp may be used to screen for the presence or absence of infection, however its limitations should be taken into consideration. Actively infected hairs tend to glow along the entire shaft or the proximal (hair follicle) shaft.
Individual hairs that are no longer infected may still fluoresce along the distal portion or tips of the hair. These hairs may or may not be culture-positive.
Ideally, cats should be treated until they are culture-negative on two occasions one or two weeks apart. Weekly fungal cultures should be started after the cat has received four to six weeks of therapy.
In our practice we have clients perform ‘toothbrush sampling’ at home to minimise costs and decrease the potential for hospital contamination.
False-positive toothbrush fungal cultures can occur in cats that are clinically recovered and cured of dermatophytosis if they are living in a contaminated environment. This is most likely to occur in shelters or catteries. Determining the true disease status of these cats can be difficult and it is important to detect asymptomatically infected or fomite carriers.
If any doubt exists, the suspect cat should be isolated in a sterile cage for a period of five to 10 days and re-cultured to determine disease status. In many cases a site visit and cultures of the environment can also be informative.
Unfortunately, it is not always possible or practical to re-culture every patient. In otherwise healthy cats, systemic and topical treatments should generally be continued for six to 10 weeks and preferably until two weeks after clinical resolution.
Environmental treatment
The critical role of environmental disinfection in eradication of M canis from an endemic cattery or household cannot be overemphasised. Environmental contamination with M canis spores is widespread, difficult to eliminate and routinely transported by the fur of uninfected cats. Such contamination is a major reservoir for recurrence of infection.
Sodium hypochlorite (bleach) 0.5 per cent when added to M canis-infected cat hairs for five minutes twice a week required eight treatments to prevent fungal growth (White Weithers 1995).
When 10 disinfectants were tested at various dilutions as single applications to a surface contaminated with M canis-infected cats’ hairs and spores, only undiluted bleach (5.25 per cent sodium hypochlorite) or one per cent formalin were able to inactivate infected cat hairs within two hours (Moriello and DeBoer 1995). Undiluted bleach is corrosive and irritating and formalin is a human health hazard. The currently recommendation is to use a 1:10 dilution of household bleach as the disinfectant of choice.
M canis spores remain viable in the environment for up to 18 months. All nonporous surfaces should be thoroughly vacuumed and disinfected, including walls, bench tops, window sills and transport vehicles. All heating and cooling vents should be vacuumed and disinfected. All bedding, brushes, combs, rugs, cages and cat carriers should be vacuumed, scrubbed and washed with hot water, detergent and a 1:10 dilution of household bleach or destroyed.
Carpeted areas are a problem because they cannot be effectively disinfected without damage. Therefore, it is generally recommended that contaminated carpets be discarded. Vigorous and frequent vacuuming on a daily basis or steam cleaning mechanically removes many, but not all, spores.
To kill fungal spores, the temperature of the water being forced into carpets must be at least 430C (110F). This is mostly not achievable and because of this steam cleaning may not be a reliable method of killing M canis unless an antifungal disinfectant such as chlorhexidine or sodium hypochlorite is added to the water. Curtains should be dry cleaned and not replaced until the infection is eradicated.
1. Ben-Ziony Y, Arzi B. Use of lufenuron for treating fungal infections in dogs and cats. J Am Vet Med Assoc 2000; 217:1510.
2. Colombo S, Cornegliani, L and Vercelli A. Efficacy of itraconazole as a combination therapy in feline dermatophytosis: preliminary results in nine cases. Veterinary Dermatology 2001; 12, 347.
3. DeBoer DJ, Moriello KA. Inability of two topical treatments to influence the course of experimentally induced dermatophytosis in cats. J Am Vet Med Assoc 1995; 207:52.
4. DeBoer DJ, Moriello KA. Efficacy of pretreatment with lufenuron for the prevention of Microsporum canis infection in a feline cohabitation-challenge model. 17th Proceedings of AAVD/ACVD Meeting 2002:53.
5. DeJaham, C et al. Enilconazole emulsion in the treatment of dermatophytosis in Persian cats: tolerance and suitability. In:Kwochka, K.W., Willemse, T., Von Tscharner, C eds Advances in Veterinary Dermatology, Vol 3, Oxford: Butterworth Heinemann, 1998: 299
6. Guillot J, Malndain E et al. Evaluation of the efficacy of oral lufenuron combined with topical enilconazole for the management of dermatophytosis in catteries. Veterinary Record 2002; 714
7. Mancianti F, Pedonese F, Millanta F and Guarnieri L. Efficacy of oral terbinafine in feline dermatophytosis due to Microsporum canis. Journal of Feline Medicine and Surgery 1999;1, 37
8. Moriello K, Deboer DJ, Volk L, Blum J. Efficacy of pretreatment with
lufenuron for the prevention of Microsporum canis infection in a cat challenge model. 17th Proceedings of AAVD/ACVD Meeting, 2002; 11
9. Sparkes AH, Robinson A, MacKay AD and Shaw SE. A study of the efficacy of topical and systemic therapy for the treatment of feline Microsporum canis infection. Journal of Veterinary Medicine and Surgery 2001; 2,135
10. White-Weithers, Medleau, L. Evaluation of topical therapies for the treatment of dermatophyte-infected hairs from dogs and cats. Journal of the Am An Hosp Assoc. 1995; 31, 250
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