Alopecia (hair loss) in cats is a common reason for cats being presented to the veterinary practice. First of all, it must be clarified whether the alopecia is pathological hair loss. Owners are often concerned in cases of pronounced coat shedding, but as long as there are no signs of alopecia or other clinical signs (e.g. pruritus), the hair shedding should be considered physiological. In Persian cats, even focal alopecia may occur intermittently during the shedding period. There are also alopecias/hypotrichosis that are not pathological in certain breeds or specific locations, e.g. alopecia in sphynx cats, alopecia of the pinnae in older Siamese cats, or variable degree of alopecia in the preauricular region in all cat breeds.

If pathological alopecia is present, various differential diagnoses are possible. Therefore, it is advisable to examine animals with alopecia – like all dermatological patients – according to a defined diagnostic protocol. The first step is always to obtain a detailed clinical history. A pre-printed formulary, which the owner may fill out in advance (waiting room), can always help. Based on this information, such as the age of the patient, what exactly were the symptoms like at the beginning of the problem (which came first: the alopecia or the itching?), illness of cohabiting animals or skin changes in humans, essential clues can already be gained for drawing up, after the clinical exam, a differential diagnosis list. Clinical examination is followed by a detailed dermatological exam, checking the patient’s skin from the nose to the tip of the tail for the presence of any lesion. For the systematic diagnostic work-up, it is helpful to divide the possible causative diseases into “self-induced” and “spontaneous” alopecias (Fig. 2). Some disorders can manifest in both forms (e.g. dermatophytosis, cutaneous lymphoma). In these cases, on the one hand, there is damage to the hair follicles causing hair loss, but at the same time, there is itching (e.g. due to secondary infections in dermatophytoses) leading to self-induced or secondary alopecia (see fig. 2).

The diagnosis of self-induced alopecia is easy to make in animals that show increased grooming. However, many cats tend to practise this intensive grooming only in the absence of their owners. The visualisation of broken hairs by trichography suggests self-induced alopecia by licking (see fig. 3).

Pruritus is the most common cause of alopecia in the cat, in adult cats this is usually related to allergic diseases. However, before starting an allergy workup, the presence of infections or infestations must be excluded. Therefore, the first step is to detect or exclude ectoparasites through a flea comb, superficial/deep skin scraping and possibly adhesive tape. Fleas, lice, Cheyletiella mites, Otodectes mites (can also leave the ear canal) and Notoedres mites produce pruritus. Infestation with the mite Demodex gatoi, which does not live in the hair follicles but in the stratum corneum, is intensely itchy, unlike other species of  Demodex. Fleas can additionally induce a hypersensitivity reaction. Even if no parasite infestation can be proven, patients with pruritus should receive continuous ectoparasite prophylaxis against flea and mite infestations (e.g. isoxazolines). In this way, flea allergy dermatitis can be diagnosed and treated at the same time. The next step is to check bacterial and fungal infections by cytological, bacteriological and fungal examination. Dermatophytes can be the cause of pruritic and non-pruritic alopecia. Bacteria and Malassezia generally represent secondary infections. If bacteria of the normal skin flora or Malassezia are cultured, the number of organisms can be assessed cytologically, whether it is only physiological colonisation, overgrowth or an infection. While Malassezia dermatitis is often found in dogs as a complication of allergies, it usually indicates more serious underlying diseases such as systemic infections or neoplasia in cats. Besides detecting infection, a cytological examination may suggest non-infectious diseases that can cause pruritus, such as pemphigus foliaceus or cutaneous lymphoma.

If an infection/infestation has not been diagnosed or if the clinical signs do not improve after appropriate treatment, the suspicion of an allergic disease comes to the fore. As it is impossible to distinguish clinically which type of allergy is involved, a food allergy should first be investigated through an elimination and provocation diet. During the elimination diet (8 – 12 weeks), a food with a single protein and carbohydrate source is fed. These can be ingredients that the animal has never eaten before if such can be identified, but food allergy testing is recommended, as a blindly selected diet runs the risk of not being tolerated. Based on the result, a protein source and a carbohydrate source are selected to which there is no positive test reaction in either the IgE or IgG antibody range. In general, the owners’ willingness to comply with a strict diet can also be increased if a written test result is available. In addition, compliance can still be improved by keeping a feed diary. Since several studies have found contamination of commercial diets with undeclared protein components, the elimination diet should ideally be home-prepared. If this is not possible, a high quality (peptide size < 1 kDa) hypoallergenic or hydrolysed veterinary diet (not supermarket or internet feed) should be used.

Atopic dermatitis (AD) is an IgE-mediated allergic skin disease to environmental allergens. Several factors play a role in its development, primarily the alteration of the immune response, the alteration of the skin barrier (genetic factors) and the environment.
The clinical presentation of AD is pruritus and its associated lesions. Its genetic condition determines its chronicity and the need for life long treatment.

Previous considerations to atopic dermatitis treatment

1. Diagnosis of the disease – ruling out other pruritic conditions, including food allergy.
2. Year round flea control program – the bite of fleas can trigger an allergic dermatitis (Flea allergic dermatitis – FAD) and can complicate atopic disease.
3. It is a chronic disease that needs life long treatment of the animal on an annual or seasonal basis, depending on presentation.

A frequent mistake is to stop the treatment once the animal is free of clinical signs, which leads to reactivation of the inflammatory process. Once inflammation exceeds the itching threshold, the animal begins to scratch and the clinical signs return.

Reactive and proactive therapy

“Reactive therapy” represents the treatment of active disease aimed at controlling pruritus and lesions. It is a rescue treatment based on systemic anti-inflammatory/antipruritic drugs with rapid action and high efficacy, together with frequent topical therapy.

Once the clinical picture is controlled and stable for a few weeks, the so-called “proactive therapy”, aimed at avoiding the reactivation of the inflammatory process, would be established. During this treatment phase, the goal is to keep the animal free of clinical signs using the minimum effective dose. In proactive therapy, antiinflammatory/antipruritic treatment, topical treatment and allergen-specific immunotherapy (ASIT) can be used.

Multimodal tailored treatment

Treatment should be multimodal and include:

1. Strict annual flea control program
2. Treatment of pruritus with anti-inflammatory/ antipruritic drugs (systemic and topical)
3. Restructuring and hydration of the skin: nutrition and topical treatment
4. Control of secondary infections
5. Allergen-specific immunotherapy (ASIT) or “allergy vaccine”

1. Flea control

Atopic animals are more prone to developing other allergies. Contact with fleas can trigger the allergic process. It is crucial to carry out effective preventive treatment on an annual basis.

2. Anti-inflammatory/antipruritic treatment

Control of inflammation and pruritus is essential to keep the atopic animal free from the clinical signs of the disease. Drugs with proven efficacy in the treatment of atopic dermatitis are:

The oak processionary (Thaumetopoea processionea) belongs to the order of moths (Lepidoptera), specifically a species of toothed moth. It is very similar to the pine processionary moth (Thaumetopoea pinivora). The adult moth flies between July and September.

The oak processionary occurs mainly in southern and Central Europe, but due to global warming, it is now also moving to northwestern Europe, wherever forests with a large number of oaks can be found. However, isolated trees along roadsides, in parks or urban areas can also be affected. In years of heavy infestation, hornbeams are particularly affected by these pests in addition to oaks.

Forest damage, in addition to the potential danger to humans and animals, should not be ignored. Although a single caterpillar feeding has no longterm negative consequences, repeated severe infestation and defoliation can make the oak more susceptible to secondary pests and lead to death.

The larvae (caterpillar) of the oak processionary are problematic, as they are covered with stinging hairs (setae) rich in taumetopoein that serve as a defence mechanism. Both larvae and adults (processionary moths) trigger a toxicirritant reaction (caterpillar dermatitis) called lepidopterism.

The female moth of the oak processionary lays 100-200 eggs on the branches of the crown of older oaks. A young caterpillar develops in the egg by autumn and overwinters in this form (larvae can survive temperatures to minus 30°C). The caterpillars are up to 5 cm long and can be recognised by their dark, broad dorsal line, velvety hair and long-haired warts. They live in groups of 20-30 and typically move in “nose-totail” processions (hence their name) when they are looking for food at night or when they want to pupate. This eponymous procession can be up to 10 meters long. In the caterpillar nests (webs), which are built on the trunk or the strong branches of the oak, moult occurs and serves as a refuge place. A nest can contain many hundreds or even thousands of larvae. From the third stage of the total of 5-6 developmental stages, the larvae develop stinging hairs with barbs (setae), which contain thaumetopoein, the nettle poison. The number and length of stinging hairs increase with each moult. During the feeding season in May and June they lose many hairs. If they feel threatened they release hairs into the environment as a defence.

All stages have natural enemies, from birds (such as the cuckoo or oriole), bats, ants, beetles, to fungi, bacteria, viruses, parasites/parasitoids. Note: a parasitoid is an organism that lives in close association with its host at the host‘s expense, eventually resulting in the death of the host (Wikipedia). An interesting detail is that the caterpillars cannot, for example, harm the cuckoo with their venom, as they are capable of regurgitating the urticarial hairs of the caterpillars. Thus, despite a large number of predators, their effectiveness in preventing infestations is limited.

The caterpillars feed on the leaves of the tree and eat the leaves, except for the veins. If this occurs over several years, it can cause severe damage to the tree. When a tree “defoliates“, the larvae leave the nest at night and crawl in a long procession to a new tree where they build a new nest. A single tree can host between 10,000 and 100,000 processionary caterpillars.

Alopecia or pathological hair loss is a frequent reason for consultation with dermatological patients, a variety of skin diseases in dogs can cause impairment of hair growth. Shedding is a physiological process and occurs twice a year in most dogs, but there is also a breed-specific rhythm. The anagen phase (growth phase) lasts a very long time in the poodle, for example, and is shorter in other breeds such as sheepdogs, retrievers and boxers. Reduced or arrest of the anagen phase or increased hair loss in the resting phase/telogen phase of the hair cycle can lead to alopecia in dogs.

Alopecia can be caused by many processes or diseases such as endocrinopathies (hypothyroidism, hyperadrenocorticism, hyperestrogenism, Sertoli cell tumour), drugs (chemotherapy, drug reactions), parasites (demodicosis), infections (pyoderma, dermatophytes), immune-mediated diseases (pemphigus foliaceus, sebaceous adenitis), congenital disorders (follicular dysplasia), trauma, telogen or anagen effluvium and alopecia X.

A detailed history is required to make a differential diagnosis, e.g. sudden alopecia after chemotherapy suggests anagen effluvium. When a dog shows alopecia and another member of the family also has skin lesions, dermatophytosis diagnosis should be considered. The presence of pruritus is a critical anamnestic question in choosing the correct diagnostic algorithm. In general, one of the main problems is knowing which came first, alopecia or itching? Also, consider the following aspects during dermatological research:

1. The symmetry of the lesions (symmetric alopecia / non-symmetric alopecia)
2. The inflammatory properties of the lesions (inflammatory alopecia / non inflammatory alopecia)

Inflammatory alopecia

Inflammatory alopecia is the most common cause of alopecia in dogs. Alopecia can be focal or multifocal. It may be a consequence of infections or conditions affecting the hair follicle structures (e.g. immune-mediated diseases, sebaceous adenitis). Inflammatory alopecia is not symmetrical and can be primary, caused by infections of the hair follicles as a result of conditions such as demodicosis, dermatophytosis, pyoderma or can be secondary alopecia, e.g. due to scratching in allergic diseases.The diagnosis can’t be based only on clinical examination. Diagnostic tests such as cytology, deep skin scraping, scotch tape, trichography, dermatophyte culture, Wood’s lamp, PCR and biopsy could be needed according to the diagnostic algorithm (Fig. 1).