Draining sinus tracts - Infectious causes Flashcards
What are infectious causes of draining sinus tracts?
Bacteria
* Deep pyoderma
* Bacterial granulomatous dermatitis
* Mycobacterial granuloma/pyogranuloma
* Non-filamentous bacterial granulomas (botryomycosis) - Staphs/Streps/Actinobacilli
* Filamentous bacterial granulomas – Nocardia/Actinomyces
Subcutaneous (deep) fungal infections
* Subcutaneous dermatophytic granuloma
* Saprophytic s/c fungal infection
* Sporotrichosis
* Cutaneous involvement with systemic mycoses
Protozoa/parasites
* Leishmaniasis
* Demodicosis
What layers are affected by infectious draining sinus tracts?
Deep skin/subcutis
What are causes of deep pyoderma? What is it usually associated with? How does it present?
Infection outside epidermis or hair follicle epithelium due to
* rupture of hair follicle wall (furunculosis) – most common
* penetrating wounds/ foreign bodies
* haematogenous spread (sepsis) - rare
Usually associated with
* thickening of skin/subcutaneous tissue
* +/- nodules
* +/- draining sinuses
Presents as
* Furunculosis
* Abscess
* Cellulitis
- How does furunculosis usually develop?
- What type of inflammation is present? How will you recognise this on cytology?
- Are the lesions always pruritic?
- How do you treat bacterial furunculosis?
- Why does inflammation often persist, even after bacterial infection is resolved?
Development
Extension of folliculitis -> rupture of hair follicle wall -> microbes + free keratin in dermis -> provokes a foreign-body reaction
Inflammation
Usually pyogranulomatous reaction – see macrophages, neutrophils +/- rbcs
NB organisms may be hard to find – do not assume is sterile!
Lesions often painful, variably pruritic
Treatment
* Usually require extended systemic antibiotic course based on culture + susceptibility testing (culture of tissue or exudate). Continue to 2 weeks post-resolution (minimum 4 weeks, often 6-8+ weeks total)
- Should now stop once it has resolved
* Topical chlorhexidine shampoos/foams also
Persistent
Inflammation may persist after infection resolved due to foreign body reaction to keratin – at this stage may therefore need anti-inflammatory medication (corticosteroids/ ciclosporin/ tacrolimus)
What are common presentations of furunculosis?
- Chin/muzzle folliculitis/furunculosis
- ‘Canine acne’
- Nasal folliculitis/furunculosis
- Affects haired skin of dorsal muzzle
- d/d canine eosinophilic folliculitis/furunculosis - cytology + biopsy
- Interdigital folliculitis/furunculosis
- Acral lick dermatitis/granuloma
- Post-grooming folliculitis/furunculosis
- German Shepherd Dog pyoderma (rare)
- Widespread severe furunculosis/cellulitis
- Underlying cause poorly understood
What conditions does bacterial furunculosis occur secondary to?
- Allergies
- Ectoparasites – NB demodicosis!
- Infections – NB dermatophytosis!
- Systemic immunosuppression/endocrinopathy
- Pressure driving hair back into skin, e.g.
- Over bony prominences of heavy short-coated dogs
- Conformation defects causing dog to walk on haired skin
What is this an example of? Why has it become infected?
- Chronic pododermatitis with interdigital folliculitis/furunculosis - common and complex problem
- Multifactorial pathogenesis
- Starts as sterile process but become infected when lesions rupture and are licked
- NB Lesions originate on palmo-plantar surface of foot but rupture as draining sinus tracts on dorsal aspect
What are primary and secondary causes of chronic pododermatitis?
Primary
- AD/AFR
- conformation
- hypothyroidism
- osteoarthritis
Secondary
* Surface/superficial/ deep infections
* Potentially multiple infections at different depths, esp if chronic e.g.
* Staph pseudintermedius
* Streptococcus spp
* E coli/ Klebsiella spp/ Pseudomonas spp
* Malassezia
* NB If primary cause not addressed -> recurrent bacterial infections (+/- fungal) -> antibiotic resistance
What are predisposing factors for chronic pododermatitis?
Breed
* Includes EBD, FBD, Mastiff-types
* Short hairs around pad margins/ interdigital skin
* Often with splayed feet and poor conformation
Increased weight-bearing
* Fore > hind
* Obesity
Altered weight-bearing
* Congenital limb deformity
* OA
* Cruciate disease/other joint problems
* Restrictive harnesses?
What are perpetuating causes of chronic pododermatitis?
- Altered weight-bearing
- Weight-bearing on haired skin
- Lichenification/scarring
- Chronic inflammation
Leading to
* Self-perpetuating cycle of increasing inflammation and abnormal pedal conformation
Leading to
* Conjoined pads/new pad formation
* In-grown hairs
* Sinus tracts
* Deep tissue pockets
Leading to
* Trap debris
* Encourage infection
* Prevent effective cleaning/Tx
How should you approach a chronic pododermatitis case?
Important to recognise the nature of changes present and address them asap – essential for prevention of progression to chronic irreversible changes!
- Consider primary cause – NB always rule out demodicosis! Other investigations/treatment as indicated
- Investigate and treat secondary infections
- Control inflammation once infection controlled
- GCCs – topical/systemic
- Ciclosporin/ 0.1% tacrolimus
- Not oclacitinib / lokivetmab!
- Address predisposing triggers, where possible
- e.g. reduce weight, analgesia if underlying pain, corrective surgery re conformation?, boots at exercise to protect feet?
When is surgery considered for chronic pododermatitis? What procedures can be undertaken?
- For end-stage disease, refractory to medical management
- Excision or fusion podoplasty
- Scalpel or laser surgery – essential to remove all diseased tissue…
- Recurrence less likely with laser podoplasty, as all diseased tissue ablated and replaced with scar tissue
What is acral lick dermatitis/granuloma? What are the underlying causes?
A deep pyoderma but does not present with sinus tracts - a d/d for cutaneous masses!
Localised folliculitis/furunculosis on lower limbs due to self trauma – frustrating condition!
Multiple underlying causes – e.g.
* Pruritus - allergies, ectoparasites
* Pain – small injury/ underlying orthopaedic/neurologic disorder
* Neoplasia - uncommon
* Anxiety/boredom – causes +/or exacerbates?
NB several factors may coexist – all need to be addressed
What are clinical features of acral lick dermatitis? How is it diagnosed? How can it be managed?
Clinical features
* Usually large breed, middle-aged/older dogs
* Lesions
* Plaque-like, firm +/- ulceration
* Often hyperpigmented, lichenified rim
* Often forelimbs
* Initial deep infection but, with chronicity, can develop
* ongoing inflammation/pruritus due to FB reaction to intradermal keratin
* obsessive-compulsive behavioural component
Diagnosis
* Often visually distinctive, especially when small
* Cytology (squeeze lesion) and deep bacterial culture ideal
* Biopsies if unsure re diagnosis – d/d neoplasia, deep fungal infection
* Careful history/clinical exam re establishing underlying cause essential
Management
Mild case:
* Treat deep pyoderma to resolve infection
* Investigate/control underlying disease.
* NB suspect behavioural component once medical causes ruled out
More severe case:
* Treat deep pyoderma to resolve infection
* Physical prevention of licking – E-collars, wrap, sock, ?muzzle
* Control inflammation once infection controlled: topical/systemic GCCs, ciclosporin/ 0.1% tacrolimus
* Behavioural modification +/or behaviour-modifying drugs? (e.g. clomipramine, fluoxetine) – behavioural referral?
* Laser surgery for recalcitrant lesions? – NB
* Lack of free skin hampers wound closure for sharp surgery
* Surgical site may become new focus for licking
What are these lesions?
Acral lick dermatitis
What is post-grooming folliculitis/furunculosis? What organisms are often associated?
- Uncommon but distinctive furunculosis of dorsal trunk
- History important for diagnosis: Acute onset within few days of bathing/traumatic grooming procedure. Skin lesions may be preceded by fever, depression
- Very painful – d/d back pain!
Cause – minor trauma to hair follicles followed by infection when bathed - contaminated bathing products implicated
Often G-ve organisms cultured, esp Pseudomonas
Distinctive histopathology
What is the difference between an abscess and cellulitis? What can cause these?
Abscess
Pooling of suppurative material in dermis/subcutis – usually well-defined
Especially common in cats
Cellulitis
Ill-defined inflammation involving deep s/c connective tissue
Examples of causes
Traumatic e.g. bite wound – look for evidence!
Foreign body
What history and clinical exam findings are indicative of abcesses and cellulitis? What diagnostics are helpful? How should they be treated?
History/signalment, e.g.
* outdoor cat (bite wounds)
* dog with hairy feet in summer (grass seed)
Clinical examination
* Painful swelling, usually solitary lesions
* Evidence of wound? (NB bite wounds often in pairs!)
* +/- pyrexia, lethargy
FNA abscess – gross appearance usually diagnostic – cytology to check if any doubt
Treatment
* Abscess – lance, drain, analgesia. Systemic antibiotics (e.g. amoxicillin-clavulanate) if cellulitis or pyrexia
* Cellulitis – systemic antibiotics (e.g. amoxicillin-clavulanate) – usually empirically
Where are foreign bodies commonly found? How should they be treated?
Can occur at any site but common interdigitally
- Esp grass awns, summer, dogs with hairy feet
Treatment
* Poultice/bathe to‘draw’, then explore carefully UGA with alligator forceps -> remove FB
* Can track up limb – possible use of contrast radiography +/or ultrasonography
* Avoid antibiotics till explored!
NB Usually solitary lesions, though occasionally contain >1 FB – check!
What can cause bacterial granulomatous dermatitis?
Mycobacterial granulomas/ pyogranulomas
Non-filamentous bacterial granulomas - rare
* e.g. Staphylococci, Streptococci, Actinobacillus
* Also called botryomycosis
* Lesions contain small yellow granules (‘sulphur’ granules)
Filamentous bacterial granulomas - rare
* e.g. Nocardia, Actinomyces
* nodular masses which may involve bone
* affect dogs/cats
What agents cause mycobacterial infections in cats? Which cats are at risk?
A. Mycobacterium tuberculosis complex (MTBC) - 30% feline mycobacterial infections
Most common:
* M microti (rodent-adapted)
* M bovis (cattle adapted) - notifiable APHA
Less common:
* M tuberculosis (human-adapted) – rare - cats relatively resistant; significant zoonotic risk -> euthanasia (human notifiable)
Risks
* At-risk cats – males, hunters, young-middle aged. M bovis infection in areas with bovine TB
* Infection via rodent bites, rarely oral/inhaled infection
* No association with FIV/FeLV infection/ immunosuppression.
B. Non-tuberculous mycobacteria (NTM)
Environmental mycobacteria – e.g. in soil, water – 4 sub-groups:
* Mycobacterium leprae complex (MLC)
* feline leprosy syndrome (FLS)
* especially young cats (<4yo)
* ‘cat is ‘dead end host’ - not zoonotic
* M avium complex (MAC) - most commonly isolated in UK
* especially older cats
* associated with immunosuppression
* potential zoonosis (low risk unless immunocompromised)
* Slow-growing NTM
* Rapid-growing NTM (e.g. M fortuitum, M chelonae)
* All opportunist pathogens – infect cats via contamination of open wounds
How do mycobacterial infections present in cats?
Mycobacterium tuberculosis complex (MTBC)
* Localised cutaneous nodules +/- ulcers/draining tracts, especially ‘fight and flight’ sites – face, extremities, tail base
* +/- localised/generalised lymphadenopathy
* +/- GI disease, lung disease, weight loss, pyrexia
Non-tuberculosis mycobacteria (NTM) present as any of
* Cutaneous or s/c nodules – as MTBC
* Diffuse panniculitis – multiple punctate draining tracts and s/c nodules, esp inguinum, flanks, tailbase – may coalesce
* Variably painful
* Disseminated disease uncommon
* NB Feline leprosy syndrome – non-painful, mobile cutaneous nodules only
How are mycobacterial infecctions in cats diagnosed and treated?
Diagnosis - difficult
* Biopsy - won’t speciate organism
* Biopsy any non-resolving skin lesions/abscesses/ enlarged peripheral lymph-nodes! Ensure to include subcutis, multiple samples
* Bisect – half for histology (request Ziehl-Neelsen (ZN) stain – 50% sensitivity), half to freeze for future tests
* Cytology - won’t speciate organism
* Granulomatous/pyogranulomatous response (mixed inflammatory cells). May see organisms with ZN stain but low sensitivity
* Culture
* Gold standard but need special laboratories, culture slow (e.g. 3 months) and fails 50% of time, even when ZN +ve organisms seen
* IFN-gamma-release assay (IGRA) on blood – quicker –sensitivity variable – distinguishes between NTMs only
* PCR – fixed or fresh tissue. Not 100% sensitive
* Once diagnosis made - screen for immunosuppressive factors and thoracic radiography – assess lung involvement
Treatment
Antibiotics
* Need long courses (e.g. 6+ months), based on C+S where possible – some need permanent treatment to prevent relapse. Resistance can develop.
* Usually combination therapy of 2 or 3 drugs required – e.g. empirical fluoroquinolone + doxycycline + clarithromycin for NTM pending sensitivity results
* Can be controversial as some drugs restricted, e.g. rifampicin
* Continue antimicrobial therapy for 2 months post-resolution – prognosis guarded
Wide surgical resection where possible – likely curative for FLS
What steps should you take if you diagnose a M bovis infection in a pet cat or dog?
-
Vet must notify APHA who will
- notify UK Health Security Agency - assess if TB screening of close contact people needed
- consider risks to nearby animals
- Develop plan to protect other pets/livestock, if necessary
- Advise if TB testing required for livestock on premises
-
Euthanasia of affected pet , although not mandatory, may be elected due to concerns re
- Treatment length (6mo+) and need for concurrent use of multiple drugs compliance issues
- AMR concerns (course length, potential use of restricted antibiotics)
- Guarded prognosis – often do not recover fully
- Zoonosis (low risk) and contagion
What organisms can cause subcutaneous (deep) fungal infections? How do they present?
Caused by
* Subcutaneous dermatophytic granuloma
* Saprophytic s/c fungal infection
* Sporotrichosis (Sporothrix schenkii) – zoonotic! especially from cats
Present as
* cutaneous papules or s/c nodules
* +/- ulceration/discharging tracts/tissue
* +/- tissue granules/grains
* Usually due to traumatic implantation of fungus - most commonly on feet/limbs or head
* Regional lymphadenopathy common
* Occasionally disseminate to other organs
* Check underlying health (e.g. FeLV/FIV (cats) thyroid (dogs))
How does systemic mycoses present? What organism can cause this?
- Can affect any organ system, including skin
- granulomas/pyogranulomas/necrosis in organs affected
- systemically ill
- e.g. Cryptococcosis – zoonotic!
A 9yo Rottweiler presents with discharging sinuses on the muzzle. Which investigations will you perform first?
- Examine an impression smear of the exudate and deep skin scrapes
- Examine an impression smear of the exudate and submit a sample for fungal culture
- Take biopsies of the lesion and examine deep skin scrapes
- Take biopsies of the lesion and submit a sample for fungal culture
Examine an impression smear of the exudate and deep skin scrapes
