Canine demodicosis is common but may be challenging to diagnose. A solid understanding of the aetiology, diagnosis and treatment will ensure you manage these cases with ease.
What’s the Cause?
Three morphological forms of Demodex are reported in the dog:
- Demodex canis (medium length body) is part of the normal cutaneous flora of all dogs, living primarily in hair follicles. This population can markedly increase under the influence of poorly defined genetic or immunological changes, or immunosuppressive drug use, leading to clinical disease.
- ‘Short’ bodied Demodex mites are confirmed genetically as another morphological form of canis.
- Demodex injai is a distinct, longer bodied mite, living in hair follicles and sebaceous glands (Figure 1a). There is conflicting evidence1, 2 as to whether this is a separate species, but given the different presentation and epidemiology, I think it more likely this is a distinct species. It is occasionally identified in normal dogs.
Juvenile-onset canine demodicosis (JOCD)
JOCD typically occurs in dogs less than 18-36 months of age and is categorised as localised or generalised. The definition of generalised disease varies but may:
- involve the feet
- affect an entire body region
- affect 4-5 or more separate sites
- generalise rapidly, especially in predisposed breeds
- persist for 4-6 months with no sign of resolution
While JOCD may occur in any breed, some breeds have increased susceptibility. Presentation of at-risk breeds with clinical signs consistent with JOCD should prompt performance of diagnostics for demodicosis. At risk breeds include:
- bull terriers & Staffordshire bull terriers (English and American)
- bulldogs (French, English, American)
- Shar Peis
- pit bulls
- miniature Pinschers
- Great Danes
- Standard poodles
- Scottish terriers
Classic clinical signs include patchy hair loss, comedones (blackheads), variable hyperpigmentation (especially perifollicular) and scaling (Figure 2a). The head and forelegs are often first affected and lesions may generalise with time. Because of their lack of hair follicles, pads and the planum should remain unaffected, and lightly haired regions (e.g. the ventral abdomen) are typically less affected.
Some cases can progress to follicular rupture with furuncles (blister-like lesions), draining sinuses, significant crusting and bacterial infection. This is more common where there has been a missed diagnosis and concurrent use of immunosuppressive therapies (especially glucocorticoids) OR with overt underlying immunosuppressive disease.
D. canis demodicosis is an uncommon primary cause of pruritus, however pruritus may occur with secondary bacterial infection.
Adult-onset canine demodicosis (AOCD)
AOCD generally presents similarly to JOCD but in older patients, typically 5-8yo or more. Genes play less of a role in AOCD susceptibility, which is typically associated with immunosuppressive disorders including:
- systemic disease (e.g. hyperadrenocorticism, hypothyroidism, neoplasia)
- immunosuppressive therapies (including glucocorticoids and oclacitnib [Apoquelâ])
- rarely, chronic actinic dermatitis (sunburn) (Figure 3a)
An underlying disease may not be identified in up to 50% of adult onset cases despite appropriate diagnostics.
D. injai demodicosis
The presentation and epidemiology of D. injai demodicosis differs from that of D. canis. Terrier breeds (especially West Highland White and Border terriers) are predisposed. The mean age of diagnosis is 4.2-5.9 years.3
The typical presentation is moderately to severely greasy skin predominantly on the dorsum of the neck and trunk, with variable concurrent erythema and pruritus (Figures 2b, 2c, 2d). Obvious hair loss is uncommon, but occurs with occasional mixed D. canis and D. injai infections.
The major trap with demodicosis is failing to make the diagnosis because it is not considered a differential and appropriate diagnostics not instituted. This may occur with very severe cases of D. canis demodicosis with marked furunculosis (Figure 3a). D. canis demodicosis can also present in a variety of atypical ways:
- dry crumbly waxy otitis externa (Figure 3b)
- nonresponsive ‘hot spots’
- focal granulomas (including lick granulomas) and lichenified skin
- pustular rash (Figure 3c)
- pododermatitis (sometime severe) without other body lesions
- comedones only
- mild to moderate crusting and scaling (especially facial, pedal) without obvious hair loss (seen in longer-haired terrier dogs e.g. Scottish terriers and Standard poodles) (Figures 3d, 3e
- non responsive lip fold dermatitis (Figure 3f)
D. injai demodicosis may present in an atypical manner:
- dry waxy otitis
- intense facial pruritus, erythema and variable hair loss (Shih Tzus, Scottish Terrier)
- non responsive lip fold pyoderma (Figure 3g)
A diagnosis may be missed due to inadequate sampling, especially not scraping deep enough with skin scrapes. Sedation and alternative sampling techniques are helpful in patients and lesions that are difficult to scrape effectively.
Premature cessation of therapy commonly results in relapse because dogs can appear clinically normal while still positive for mites (Figure 3h; same dog as Figure 2a). Follow-up is essential to ensure dogs are clear of mites.
Lastly, relapse occurs, especially in AOCD, where underlying triggers are not addressed.
Other Common Disease Associations
Demodicosis, esp. D. canis, is commonly associated with a concurrent staphylococcal pyoderma, possibly secondary to localised immunosuppression from mites. Concurrent Malassezia infections are less common. Many at-risk breeds for demodicosis are also at risk breeds for atopic dermatitis though any link between the diseases remains obscure.
How is it Diagnosed?
The deep skin scrape remains the gold standard. While mites may be occasionally found in normal skin, 1-2 Demodex mites or eggs (Figure 4a) on 2-3 separate samples is probably significant (especially for D. injai) and >2 mites are significant.
Deep Skin Scrapes
In suspect demodicosis cases I perform 3 deep skin scrapes, about 1.5cm in diameter, from the margins of skin lesions, as follows:
- squeeze the skin first (as hard as the patient will allow) to bring mites to the surface
- place paraffin oil on the skin then scrape to collect skin and oil and place on a slide
- repeat process until follicular haemorrhagic ooze is noted
- place cover slip over sample and examine with condenser down on microscope at 40-100x total magnification (4-10x lenses)
D. injai can be harder to detect and multiple scrapings over several visits may be required.
Trichograms are less sensitive than skin scrapings but are useful in areas or in patients where scraping is not (e.g. severely affected paws). These are performed as follows:
- pluck approx. 50 hairs using haemostats, grabbing near the level of the skin surface
- place as parallel as possible on a slide with paraffin oil on it to hold hairs in place
- use the cover slip to ‘chop’ hairs gently to agitate any mites away from hair shafts
- place cover slip and examine as above
- 1-2 mites from a patient are likely significant and >2 mites are significant (Figure 4b)
A note on cover slips
Because of the size of the sample of the average skin scrape, use of 40x22mm cover slips rather than 22x22mm cover slips is less messy, and allows reduction of the sample thickness, thus making examination easier.
Tape cytology is typically less sensitive than skin scraping but may be more useful in significantly scaly presentations and for diagnosis of the short-bodied form of D. canis. I have diagnosed demodicosis cases incidentally when doing tape cytology looking for infection.
A recent study4 suggested squeezing the skin through the tape and rolling it between the fingers was more sensitive than skin scraping. I have not found this to be the case – there may be subtleties to the technique that make it more sensitive. I prefer skin scrapes or trichograms, unless there are pustules present (see below).
Tape cytology is performed as follows:
- stick clear acetate tape (tip: not ‘invisible’ book tape) to affected region multiple times following (or while) squeezing the skin
- place the tape on slide. Examine unstained (though can also be visible stained; Figures 4c, 4d) with condenser down for mites
- following this examination, the tape can be prepared to examine for infection (usually bacterial)
- lift tape carefully at the sample end
- place a drop of Diff Quikâ blue stain on a slide
- replace tape on slide over stain and blot till flat on the slide (air bubbles make visualisation difficult)
- examine with condenser up at 400 or 1000x oil immersion
- look for bacteria and yeast
- there is no set standard of organism numbers for disease but any intracellular bacteria and/or >1 yeast per three 1000x oil immersion fields are likely significant
Pustules, when present, can be a shortcut to making a diagnosis because they are a primary lesion that can only result from the disease process itself (rather than a secondary change). The technique for this is:
- ‘pop’ the top of an intact pustule with a 25g needle and wipe contents onto slide
- drag the edge of slide over the pustule to collect any remaining contents
- perform a gentle squash smear and examined unstained with condenser down as above (Figure 4e)
- the slide may be subsequently stained using full Diff Quikâ staining to examine for secondary bacterial infection – any intracellular bacteria are abnormal
A similar technique may be used for examining material from draining sinuses.
Impression smears, fine needle aspirates (better for deep infections), stained superficial skin scrapes and aggressive cotton swab samples rolled on slides can also be used for sampling for infection.
Biopsy is useful where other sampling techniques are unrewarding. I would probably trial response to therapy (see below) before performing a biopsy, unless I was particularly concerned about a concurrent disease process that also required a biopsy diagnosis.
Multiple biopsies (at least 3-4 6-8mm punches) should be taken. In the comments section of the lab request form it is worth writing “Multiple deep recuts requested. Demodicosis suspected” to maximise the number of follicles inspected at the lab, maximising the chance of diagnosis.
Response to Therapy
Recent studies suggest response to manufacturer doses (see below) of alfoxalaner (Nexgard®) and fluralaner (Bravecto®) 5,6,7 are extremely effective, and rapidly so, for the treatment of D. canis demodicosis in a majority of cases. A lack of response to these treatments after 1-2 months suggests D. canis demodicosis is unlikely, though biopsy may be considered.
Peer-reviewed evidence is currently lacking (as of April 2016) for or against efficacy in D. injai demodicosis, but it is likely they will also be effective for this mite.
Bacterial culture and sensitivity should be considered in cytologically confirmed pyoderma where there is a suspicion for methicillin-resistant Staphylococcus (MRS) infection or predominantly rods on cytology (usually associated with furunculosis) because both of these cases may fail to respond to conventional antibiotic therapies.
MRS, while relatively uncommon, is increasing in frequency in Australia. MRS should be clinically suspected where there is BOTH
- failure or blunted response to appropriate doses and durations (at least 14 days) of -lactam antibiotics (including clavulanic acid-amoxicillin, cephalexin and cefovecin), fluoroquinolones (including enrofloxacin, marbofloxacin) or lincosamides / macrolides (including lincomycin, clindamycin), and
- significant improvement in mite numbers on scraping as persistence of the mites may lead to persistent bacterial infection.
If MRS is suspected, note on the lab request form that “All staphylococci should be cultured and tested. MRS are suspected.” On the other hand if rods are predominantly seen on cytology then it is worth noting “Predominantly rods seen on cytology in case of demodicosis. Please look for possible Pseudomonas sp.”
Other Diagnostic Procedures
Further diagnostics are warranted in AOCD given the possibility of underlying diseases. Normal results are consistent with an absence of disease (given the usual limitations of testing). However, the potential for false positive results on thyroid assays, ACTH stimulation tests or low dose dexamethasone testing while there is still active demodicosis means that positive results should be interpreted cautiously while there is still active demodicosis unless there are very convincing supportive clinical signs. In most cases, if there are not obvious clinical signs, testing for hyperadrenocorticism or hypothyroidism should be left until most (if not all) of the demodicosis and secondary infection if present is cleared.
Treatment in Brief
Localised demodicosis self-resolves with time in the absence of underlying disease. In juvenile dogs, this may take several months. Where clients insist on therapy, Advocate® fortnightly can be used though assessing efficacy in a self-limiting disease is difficult.
With generalised disease, immunosuppressives should be stopped if possible. For dogs with AOCD and identifiable underlying disease, demodicosis may resolve with treatment of the underlying disease. With the ease of current treatment options I would not take this risk.
With recent advances in the treatment of JOCD and AOCD I would recommend as the first line of therapy:
- Fluralaner (Bravecto®) 25-56.25mg/kg q90d (manufacturer dosing)5, 6
- Alfoxalaner (Nexgard®) 2.7-7.07 mg/kg q30d (manufacturer dosing)7
If this was not successful I would then consider
- Ivermectin 300µg/kg (start at 50ug/kg daily and increase by 50ug/kg per day to reach the target dose) q24h PO (not in ivermectin sensitive breeds unless confirmed normal on testing)
- Doramectin 600µg/kg q7d SC (not in ivermectin sensitive breeds unless confirmed normal on testing)
Ivermectin sensitivity is due to the ABCB1-1∆ mutation. Homozygous dogs can develop neurotoxicity with doses as low as 50-100ug/kg. Ivermectin-sensitive breeds include:
- normal and miniature Australian Shepherds,
- English Shepherds,
- longhaired Whippets,
- Old English Sheepdogs,
- Shetland Sheepdogs,
- German Shepherds
- Silken Windhounds.
Border Collies display the mutation at a rate no different to other breeds suggesting they are not an ivermectin sensitive breed. Testing for the ABCB1-1∆ gene is available through pathology labs.
Dogs without an ivermectin-sensitive genotype can potentially suffer toxicity if ivermectin is given in conjunction with P-gp inhibitors (e.g. cyclosporin, fluoxetine, ketoconazole, spinosad [Comfortis®]).
Ivermectin sensitivity is not an issue with use of fluralaner or alfoxalaner.
Topical moxidectin / imidacloprid (Advocate®) is not recommended for generalised demodicosis given its’ variable efficacy.
Miticidal therapy should continue 2 months past the point of negative monthly scrapings. Mite numbers and life stages should be noted and with successful therapy should reduce monthly. If there is no improvement clinically or microscopically between 4 week visits then compliance and efficacy of miticidal treatments should be reassessed.
Antimicrobial treatment of secondary infection is recommended. Despite one study8 finding that use of antibiotics did not affect final cure rates, I would still recommend treatment if there is evidence for concurrent infection.
For staphylococcal pyoderma I would use as empirical therapy one of:
- Cephalexin 22-25mg/kg q12h PO
- Clindamycin 5.5-11mg/kg q12h or 11mg/kg q24h PO
- Cefovecin (if no other alternative) 8mg/kg q14d SC
Therapy should continue until lesions and cytology is clear for surface infections, and 7 days after this for superficial and deep infections. This is typically
- 1-2 weeks for surface infections
- 2-3 weeks for superficial infections
- 4+ weeks for deep infections
A chlorhexidine 3% shampoo (e.g. Pyohex®) twice weekly is also recommended where there is infection. This may be effective in cases of mild superficial and surface pyoderma as a monotherapy. Watch for possible irritation with prolonged twice weekly use and ensure the client rinses the dog well post bathing. Pyohex® Conditioner (a leave-on 3% chlorhexidine lotion) after bathing provides more sustained topical antibacterial therapy. Once infection is clear, reduce bathing to every 1-2 weeks or less depending on mite counts and scaling present.
If rods are seen on cytology, especially if associated with evidence of deep bacterial infection, then 4 weeks+ of oral antibiotics based on culture and sensitivity is recommended. For Pseudomonas infections higher-end dosing of fluroquinolones may be prudent where appropriate i.e.
- enrofloxacin 10mg/kg q24h PO
- marbofloxacin 5mg/kg q24h PO
For MRS infections use two antibiotics simultaneously that are reported as sensitive on culture.
Note that doses for doxycycline in MRS are higher than labelled doses - 5mg/kg q12h PO
What is the Long Term Prognosis?
Historically, the prognosis for full recovery and hair growth was fair to good with appropriate treatment. Occasional relapse was not uncommon, and cases were not deemed ‘cured’ until 12 months after clinical improvement and negative scrapes.
Today, use of fluralaner and alfoxalaner may lead to complete eradication of mites (as opposed to normalisation of the mite population) in some cases, preventing relapse.
Scarring with a failure of full hair regrowth is possible where there has been furunculosis associated with the disease, in my opinion more often when there has been initial concurrent treatment with glucocorticoids (Figure 5a).
In AOCD there is a guarded prognosis for relapse if predisposing problems cannot be identified and controlled, and some of these cases need lifelong miticidal therapy to remain controlled. Again, fluralaner and alfoxalaner are ideal given their efficacy at labelled doses.
Future studies should clarify the efficacy of fluralaner and alfoxalaner in the treatment of demodicosis, but at this stage, things are looking bright.
Dr David C Robson BVSc (Hons), MACVSc (Canine Medicine) FACVSc (Dermatology)
Registered Specialist in Veterinary Dermatology
Melbourne Veterinary Specialist Centre
David graduated in 1992 from the University of Queensland. He worked in general practice for 6 years before commencing his residency in dermatology at the Animal Skin and Ear Specialists (formerly the Animal Skin, Ear and Allergy Clinic) at the Melbourne Veterinary Specialist Centre. He gained his ACVS Fellowship in dermatology in 2005. He has practiced clinical dermatology, published and lectured both in Australia and overseas. His current research interests include methicillin-resistant Staphylococcus pseudintermedius, pathogenesis of otitis externa, antifungal resistance profiles of Malassezia spp and allergen-specific IgE testing. In his spare time, he enjoys snowboarding, photography, diving, playing guitar and driving his hatchback on the racetrack but is not particularly good at any of them.
David is a foundation member, and is currently the treasurer, of the Australian College of Veterinary Scientists Dermatology Chapter.
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