Canine superficial pyoderma: the good, the bad and the ugly
Where to begin The culprit: Staphylococcus intermedius (S. intermedius). This bacterium is considered to be a normal inhabitant of canine skin and hair.
Studies have shown puppies receive an "inoculation" immediately after birth, primarily from the bitch's oral cavity (licking). Potential pathogenic Staphylococci, the prominent organism present on canine skin as well as most commonly transferred bacterium after whelping, are present on the skin, rectum and feces within 12 hours after birth. There are numerous other resident bacteria on canine skin including streptococcus, Corynebacterium, micrococcus, proteus, E. coli, and certain transient and nomad bacteria including pseudomonas staphylococcus carriage is also prominent on the nares, anus, and in the mouth. Even more interesting, there appears to be a higher carriage of staphylococcus on nares and anus of dogs in multi-dog households.Thus, it's clear that there are normal, "resident" bacteria that live on canine skin and hair and within the hair follicle opening, and do so in happy concert with the canine cutaneous/systemic immune system. What happens when dogs present with superficial pyoderma?
Complex immunopathogenesisThe immunopathogensis of canine, superficial pyoderma is complex and not completely understood.
The status of the cutaneous immune system as well as the systemic immune can play a crucial role in the development of pyoderma. It is clear that certain underlying factors (other than the obvious case of depressed lymphocyte activity in Cushing's disease) determine bacterial colonization and ultimately pyoderma.
Dogs with recurrent superficial pyoderma tend to have a higher carriage of mucosal staphylococcus than normal dogs as well as higher levels of anti-staphylococcal IgE and IgG. These antibodies bound to mast cells and basophils can induced degranulation and cause further damage with varying degrees of pruritus. These dogs also have staphylococcus that demonstrate stronger adherence factors to epidermal cells. Dogs affected by atopic dermatitis clearly demonstrate higher carriage of staphylococcus (as well as stronger adherence factors to epidermal cells) and, in addition, possess excessive anti-staphylococcal IgE. This production of IgE as seen in so-called staphylococcal hypersensitivity, can be detrimental rather than helpful in eliminating the bacterial pyoderma.
Finally, dogs with hypothyroidism have systemically depressed lymphocyte function, which can result in superficial pyoderma.
Other factorsOther factors can play a role in the onset of pyoderma and include humidity and pH of the skin.
Moisture and skin maceration has been linked to pyoderma. Alteration in pH, sebum quality or quantity and excessive scaling have also been implicated in the onset of pyoderma.
Finally, it is also plausible that a host's response to "uncommon" bacterial antigens, i.e. superantigens, can elicit a tremendous localized or even systemic response that lead to the initiation, perpetuation and recurrence of superficial pyoderma.
Dogs presented with superficial pyoderma primarily have lesions confined to the trunk. The most common lesions identified included papules and pustules (Photo 1, p. 20S). Generally, pustules are small (less than 4 mm) and present in varying stages of eruption. Most pustules are confined to the glabrous regions (axillae and groin) but can also be located on the haired trunk. Less commonly, epidermal collarettes may be present (Photo 2).
Rarely do we find evidence of superficial pyoderma located on the face, limbs or feet.
Another relatively common finding is alopecia associated with so-called bacterial folliculitis in the short-coated dog. These dogs have the appearance of circular patches of alopecia with some scaling, little erythema, and rarely papules. They tend to be confined to the lateral trunk in a symmetrical pattern.
TreatmentTreatment of superficial pyoderma involves administration of appropriate antibiotics, topical therapy, and addressing underlying factors. The dosages of the most commonly prescribed antibiotics are listed below:
Keflex (cephalexin) or CefaDrops/Tabs (cefadroxil) 22 mg/kg BID.
Tribrissen (trimethoprim/sulfamethoxazole or sulfadiazine) 7 mg/kg BID.
Primor (ormetoprim/sulfadimethoxine) 55 mg/kg daily day 1, then 27.5 mg daily thereafter.
Baytril (enrofloxacin) 5-20 mg/kg daily.
Orbax (orbifloxacin) 2.5-7.5 mg/mg daily.
Zeniquin (marbofloxacin) 2-5 mg/kg daily.
Cipro (ciprofloxacin) 10-20 mg/kg daily.
Lincocin (lincomycin) 22 mg/kg BID
Antirobe (clindamycin) 5.5-11 mg/kg BID.
Clavamox(amoxicillin/clavulenic acid) 15-20 mg/kg B-TID.
Protocol for treatment-check for parasites (demodex, ectoparasites)
-perform a food trial with a novel protein/novel carbohydrate for eight to 10 weeks.
-if appropriate, check blood chemistries and thyroid level.
-refer for consultation/management or intradermal skin testing for atopic dermatitis.
Generally, cephalexin is well tolerated, but mild to severe gastrointestinal side effects can occur. These include most commonly vomiting and/or diminished appetite. Occasionally, loose stools or frank diarrhea with or without hemorrhage can appear and warrant cessation of the medication. If vomiting or decreased appetite is mild, I advise administration of cephalexin with a full meal. This does not appear to alter the treatment success.
The addition of gastrointestinal protectants or anti-nausea/vomiting drugs can sometimes aid in the reduction and elimination of the undesirable side effects. I rarely advise preceding the administration of cephalexin with famotidine.
Resistance to cephalexin has been very minimal in veterinary medicine, although it appears to be an emerging problem. This resistance can be achieved by the bacterial production of cephalosporinases produced by resistant bacterial genes. The so-called methicillin-resistant Staphylococcus aureus has plagued human medicine and appears to have surfaced in veterinary medicine although clear evidence is lacking as to the frequency.
I have personally isolated strains of S. intermedius from canine pyoderma and demonstrated resistence to first generation cephalosporins such as cephalexin.
In contradiction, several studies have shown little change in the resistence of S. intermedius isolates over many years at veterinary teaching hospitals in the United States.
ConclusionThere is much evidence suggesting the host's inability to prevent colonization and shedding of staphylocccal organisms and that it is directly related to diminished or altered cutaneous or systemic immunity. Certain disease such as hypothyroidism, Cushing's, or allergic dermatitis have all been implicated in the development of pyoderma as well as recurrence.
Future work in the area of resistant bacterial genes and alter host immune status, and superantigens will provide benefit for our canine pyoderma patients.