Invasion and infection – diagnosing and fighting bacterial skin

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Invasion and infection – diagnosing and fighting bacterial
skin disorders
Author : JANE COATESWORTH
Categories : Vets
Date : February 16, 2009
JANE COATESWORTH describes signs that offer clues to the diagnosis and depth of these
infections, as well as predisposed breeds and the value of correct organism identification and
treatment choice
THE skin is not a sterile place. Large numbers of bacteria live and reproduce on the largest
organ of the body.
One square centimetre of normal dog skin has been shown, on average, to support about 330
individual aerobic bacteria. Bacteria, such as Micrococci and non-haemolytic Staphylococci, form a
resident population and are adapted to tolerate the rigours of cutaneous life. Staphylococcus
intermedius (recently reclassified as S pseudintermedius) is resident around the mouth, nose and
perineum of most normal dogs.
These potentially pathogenic organisms can be transferred to wider areas of the skin by licking,
chewing and nibbling. This may result in high levels of bacteria being deposited on inflamed skin in
the pruritic dog.
The presence of a stable nonpathogenic bacterial population can be helpful to the host by reducing
opportunistic colonisation of the skin by more pathogenic bacteria. Resident bacteria compete with
new arrivals for nutrients and living space, and may produce locally active inhibitory or toxic factors.
The skin surface is a challenging and impermanent place to live. Corneocytes, the tough outer skin
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cells, are continuously exfoliated into the environment as the epidermis pushes up new cells from
the basal layer. Corneocytes are embedded in a “grout” of intercellular lipids, which resist bacterial
penetration of the epidermis.
Bacteria that overcome the defence mechanisms of the skin can invade and cause infection. A
dynamic balance exists between the virulence of a local population of bacteria and the efficacy of
the host’ s skin barrier at any one moment. Changes in skin temperature, humidity, pH and
available nutrients will also affect this balance.
Depth of infection
Ut is useful to recognise the depth to which bacteria cause infection in the skin (Table 1). This can be
correlated with an appropriate treatment plan and prognosis.
Surface and superficial infections are generally pruritic (Figure 1). Provided they are well managed,
and the underlying cause is identified and corrected, they carry a good prognosis.
Deep infections are generally painful and debilitating. They carry a guarded prognosis and require
careful management. They can be life threatening if they are not recognised swiftly and managed
appropriately.
In surface infections, the bacteria only invade the outer layers of the skin, the stratum corneum.
Superficial infections involve either the interfollicular epidermis (impetigo) or the hair follicle
(folliculitis). In deep infections, bacteria have invaded the dermis, often through rupture of hair
follicles.
Surface infections
Hot spots (acute moist dermatitis or pyotraumatic dermatitis) present as rapidly developing focal
areas of erythema and pruritus (Figures 2 and 3). A copious exudate tends to matt surrounding and
overlying hair, so the extent of the lesion may only be evident after clipping and cleaning. The
surface of the lesion may be eroded and is not raised or thickened. The lesion edge is sharply
demarcated from adjacent normal skin.
Hot spots are often triggered by focal scratching or biting, and are typically associated with
impacted anal sacs, ear inflammation, allergies or flea infestation.
The location of the hot spot is a useful clue to the underlying cause. Breeds with dense undercoats
– such as golden retrievers and Newfoundlands – are predisposed.
The treatment of hot spots has three aims:
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• to reduce the bacterial population;
• to reduce the pruritus; and
• to identify and address the underlying cause.
Gentle clipping and cleaning allows the lesion to be properly assessed and reduces the local
temperature and humidity. Sedation or general anaesthesia may be required to achieve this in a
thorough and pain-free manner.
Topical antibacterial and glucocorticoid preparations, either separately or combined, can be applied
directly to the lesion.
Systemic antibiotics are usually only required if palpation reveals accompanying satellite lesions of
deeper skin infection. They are not indicated in true surface infections.
Skin fold infections (intertrigo) occur when haired skin abuts haired skin. They are commonly
associated with unhelpful conformational characteristics in specific breeds – for example, Persian
facial folds, bulldog screw tails, basset hound hock folds and Shar Peis. Cytology is useful as
Malassezia (Figure 4) or mixed Malassezia/bacterial infections need to be distinguished from bacterial
ones.
The treatment aims are similar to those for acute moist dermatitis, but the actual treatment may
differ. Surgery may offer a permanent cure to intertrigo, but it needs to be carefully planned and
skilfully executed. Weight loss may reduce the severity of the condition, depending on the location
of the folds. Persistent medical management may be required over a very long period, so owner
motivation and education are important.
Topical glucocorticoids should be used strategically, rather than routinely, to avoid local and/or
systemic side effects.
Antibacterial wipes, creams and washes form the mainstay of regular preventive therapy.
Superficial infections
Bacterial folliculitis is common in the dog and uncommon in the cat. Impetigo is uncommon in both.
Both conditions have a pustular stage: follicular pustules in folliculitis (Figure 5) and interfollicular ones
in impetigo. However, this is short lived, and the absence of pustules does not exclude bacterial
pyoderma.
Epidermal collarettes (the peeling ring of epidermis left after the rupture of a pustule) and
hyperpigmented macules (the post-inflammatory blackening of the skin at the site of a pustule) are
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the relatively longlived lesions that give excellent evidence of infection.
Recurrent episodes of bacterial folliculitis should trigger a search for an underlying cause, such as
atopic dermatitis (Figures 6 and 7), hypothyroidism or hyperadrenocorticism.
Superficial infections are treated with systemic antibiotics. The standard treatment period of three
weeks allows for one week of therapy beyond visual cure. It is important that clients do not stop
medication prematurely during the second week, when the skin often looks much improved and
pruritus has abated.
S pseudintermedius is the most common cause of bacterial superficial pyoderma. Suitable
antibiotics to treat this include clindamycin, potentiated amoxicillin, potentiated sulphonamides,
cefovecin and cephalexin. Empirical therapy may be warranted for initial episodes of infection, but
careful attention to treatment failures should ring alarm bells for the possibility of antibioticresistant
strains or MRSA, at which point bacterial culture and sensitivity are indicated.
Antibacterial bathing may be helpful in combination with systemic antibiotics. Glucocorticoids are
not indicated for treating superficial bacterial infections.
Mucocutaneous pyoderma presents as erythema, swelling and crusting of the mucocutaneous
junctions, most commonly affecting the lip margins and nose. The degree of discomfort associated
with the lesions is variable and dogs can be affected at any age. The condition has been seen in a
wide variety of breeds, but German shepherd dogs and their crosses are predisposed.
The response to systemic and/or topical antibiotics is usually good. Relapsing cases can be
managed with regular topical antibiotics or antimicrobial washes.
Deep infections
It is important to identify and address the underlying cause(s) of deep infections. The protective
epidermis has been breached in some way and bacteria have gained access to the dermis.
Penetrating foreign bodies, bite wounds or other focal trauma may cause localised infections.
Generalised or localised infections can be seen with immunocompromising endocrinopathies
– such as hypothyroidism and hyperadrenocorticism – as well as immunocompromising drug
therapy and demodicosis.
Early lesions present as pink to purple papules and haemorrhagic bullae. Dermal infection often
ruptures on to the skin surface, producing fistulae that discharge haemorrhagic and purulent
material. This may dry to form an overlying crust, or may leave an open ulcer. Palpation of the
affected skin shows thickened areas and plaques caused by the dermis responding to the infected
foci, with inflammation and fibrosis.
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The specific bacteria involved in deep pyoderma are less predictable compared to superficial
infections. Bacterial culture and sensitivity are required to identify an appropriate antibiotic – and
potentially save a lot of time and money spent on inappropriate trial therapy.
While skin biopsies are taken for histopathology with no skin preparation, biopsy material for
culture should be taken after normal sterile surgical skin preparation. This allows the relevant deep
dermal bacteria to be cultured without contamination and overgrowth by the ubiquitous, and likely
different, surface ones. Deep tissue plugs can be taken with a punch biopsy and submitted to the
laboratory rolled in a sterile swab, moistened with sterile water and packed in a sterile container.
Deep skin scrapes can be taken on the same occasion to check for Demodex mites, along with
careful clipping and cleaning.
Deep pyoderma cases (Figures 8 and 9) require vigorous treatment and careful monitoring. Regular
antibacterial baths, especially with a whirlpool action, can help to remove crust and exudate and
relieve discomfort. Antibiotics, based on the results of tissue culture and sensitivity, are usually
continued for two weeks beyond clinical cure – most usefully assessed by palpation and
comparison of former lesional areas with surrounding normal skin. Animals should be weighed to
ensure accurate and full dosing.
Cases typically require continuous treatment for one to several months. This is an expensive
undertaking and justifies the initial expense of biopsy, culture and sensitivity. NSAIDs or opiates
can be helpful for short-term analgesia. Local and/or systemic glucocorticoids are contraindicated
in all cases.
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Figure 1. Pruritic behaviour in the consulting room.
All photos: JANE COATESWORTH.
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Figure 2 (left). A hot spot on an atopic dog’s limb.
All photos: JANE COATESWORTH.
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Figure 3 (above). A hot spot adjacent to the leftear of a mastiff with otitis externa.
All photos: JANE COATESWORTH.
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Figure 4 (left). Malassezia dermatitis on the ventral neck of an atopic basset hound.
All photos: JANE COATESWORTH.
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Figure 5 (above). Follicular pustules in an immunocompromised dog. Note the hair shafts arising
from the centre of several pustules.
All photos: JANE COATESWORTH.
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Figure 6. Pedal erythema and alopecia in a young atopic English setter.
All photos: JANE COATESWORTH.
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Figure 7. Pinnal erythema, lichenification and excoriation in an atopic West Highland white terrier.
All photos: JANE COATESWORTH.
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Figure 8. A Labrador cross with generalised deep pyoderma.
All photos: JANE COATESWORTH.
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Figure 9. Lick granuloma on an atopic German shepherd dog – a focal deep pyoderma.
All photos: JANE COATESWORTH.
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TABLE 1. Depths of skin infections
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