Derm3- Nodular Diseases

  1. What is an important feature of Sporotrichosis?
  2. What are the 3 forms of sporotrichosis?
    cutaneous, cutaneoulymphatic, disseminated (rare in dogs, common in cats)
  3. What body areas are most commonly affected by sporotrichosis? (3)
    head, ditsal limb, tailbase
  4. What are clinical signs of sporotrichosis?
    multiple non-painful nodules that ulcerate and drain purulent exudate
  5. How is sporotrichosis contracted?
    soil saprophyte, infection occurs from inoculation of organism into SQ tissues by rose thorns or cat fights (ie. outdoor animals and intact cats are more prone)
  6. How do you diagnose sporotrichosis? (6)
    • cytology- easy to see in cats, fewer organisms in dogs
    • culture
    • histopathology
    • PCR analysis
    • immunofluorescent testing
    • antigen testing
  7. What is the treatment of sporotrichosis? (2)
    Itraconazole, +/- Amphotericin B
  8. Canine histiocytic disorders include... (4)
    cutaneous and systemic canine cutaneous reactive histiocytosis, localized and disseminated histiocytic sarcoma complex
  9. What is the etiology of cutaneous histiocytoma?
    unknown; assumed to be immune-mediated b/c have not isolated infectious agents and they respond to immunosuppressive therapy
  10. What animals usually present with cutaneous histiocytosis?
    3-9 years old, predisposed Collies and Shetland Sheepdogs
  11. What are clinical signs of cutaneous histiocytosis? (6)
    multiple hairless, erythematous dermal to SQ nodules, non-pruritic, non-painful, lesions wax and wane, slowly progressive and may spontaneously resolve
  12. Where are lesions most commonly located with cutaneous histiocytosis? (6)
    face, neck, nasal mucosa, perineum, scrotum, feet
  13. How do you diagnose cutaneous histiocytosis?
  14. What other differentials may correlate with cutaneous histiocytoma on histopathology? (3)
    sterile granuloma and pyogranuloma syndrome, multiple cutaneous histiocytomas, cutaneous lymphoma
  15. Describe the management of cutaneous histiocytosis. (5)
    • prednisone immunosuppression (most respond to this as sole therapy)
    • azathioprine, cyclosporine, leflunomide, tetracycline/niacinamide (or doxy) as maintenance to avoid recurrence
  16. You can use ____________ concurrently with steroids to reduce the immunosuppressive dose of corticosteroids.
    tetracycline (or doxy or mino) and niacinamide
  17. What is sterile nodular panniculitis?
    inflammation of the SQ fat- unknown origin
  18. Sterile nodular panniculitis (SNP) has been documented in associated with... (4)
    systemic lupus erythematosus, pancreatitis and pancreatic tumors, rheumatoid arthritis, lymphoplasmacytic colitis
  19. What are clinical signs of SNP?
    single or multiple SQ nodules which can be of normal skin color or by erythematous or blue; initially nodules are firm but they become soft/ liquefied in center; nodules may regress or form draining tract; fever, lethargy, anorexia around the formation of new nodules
  20. How is SNP diagnosed? (5)
    • diagnosis of exclusion: rule out bacteria/fungi/myobacterium, sterile granuloma/pyogranuloma syndrome, foreign bodies, injection site reaction, insect bite, drug reaction, neoplasia
    • CBC/Chem/UA: rule out/ identify concurrent systemic diseases
    • cytology: suppurative to pyogranulomatous or granulomatous with fat drops or cell present and sterile
    • biopsy
    • culture
  21. How is SNP definitively diagnosed? (2)
    • histopath: suppurative to pyogran/granulomatous with fat drops or cells
    • culture: negative for fungi, bacterial, mycobacterium
  22. How is SNP managed?
    • surgical excision of solitary masses may be curative
    • [many lesions] immunosuppressive drugs- prednisone, monitor- if no response within, 2-8 wks add another immunosuppressive agent
  23. How do you taper prednisone therapy in SNP management?
    if remission is achieved within first 2 weeks of prednisone therapy, decrease dose by 25% every 7 days until lowest effective dose every other day
  24. With management of SNP, regression of nodules may take __________ to regress.
    2-8 weeks
  25. Describe the pathogenesis of sterile granuloma/pyogranuloma syndrome (SGPS).
    idiopathic, have not identified infectious agents/ respond to immunosuppressive therapy- assumed immune-mediated
  26. What 2 bacterial agents are proposed to be associated with development of SGPS?
    Leishmania, Mycobacterium
  27. What are clinical signs of SGPS?
    firm, hairy or alopecic erythematous papules, nodules, or plaques; may form draining tracts and ulcers on paws
  28. Where are lesions commonly located with SGPS? (4)
    head, distal extremities, +/- tongue, +/- prepuce
  29. How is SSGPS diagnosed? (4)
    • rule out other causes of deep infections (bacteria, fungi, foreign bodies, cutaneous eosinophilic granulomas, cutaneous neoplasms)
    • clinical appearance
    • histo
    • negative culture
  30. How is SGPS managed?
    • [single nodule] surgical excision can be curative
    • [many lesions] immunosuppressive drugs- prednisone, cyclosporine, etc
  31. Describe tapering of steroids with management of SGPS?
    if remission is achieved within 2 weeks of starting prednisone therapy, decreased dose by 25% every 7 days until lowest effective dose is given every other day
  32. How can you manage a case of SNP or SGPS that is not responding to prednisone?
    [regression of lesions should occur in 2-8 weeks] if remission has not been achieved after 4 weeks of daily prednisone, the case may require combination of prednisone with azathioprine or cyclosporine
  33. What characterizes a nodule?
    firm (solid) elevation that is >1cm
  34. What are your major rule outs for a single, acute nodule in an otherwise healthy animal? (4)
    FB, trauma, secondary bacterial infection, kerion (deep dermatophytosis)
  35. Deep fungal infections commonly affect... (5)
    skin, lymph nodes, lungs, eyes, CNS
  36. How are cytology samples usually collected from nodules? (3)
    FNA or from draining tract, maybe impression smears from ulcerated areas
  37. __________ does NOT rule out infectious causes for nodular diseaes; you must...
    Negative cytology; do sterile biopsy for bacterial and fungal culture.
  38. What samples should you submit when doing a work-up for nodular disease? (3)
    sterile biopsy for histopathology, aerobic ad anaerobic bacterial culture, fungal culture
  39. What is the most prudent way to diagnose Mycobacterium?
    send out fresh frozen tissue sample for PCR if you are suspicious of mycobacteria
  40. For what infectious causes of nodular disease can you perform antigenic testing? (2)
    blasto and crypto
  41. What are the most common bacterial causes of nodular disease? (3)
    mycobacterium, actinomyces, nocardia
  42. What are the most common fungal causes of nodular disease? (6)
    dermatophytosis (kerions), cryptococcosis, blastomycosis, histoplasmosis, coccidiomycosis, sporotrichosis
  43. Describe the features of the Actinomyces microbe. (6)
    • gram + filamentous anaerobic rod
    • opportunistic commensal flora of mouth and GI
    • found in environment/ soil
  44. How is actinomycosis contracted?
    trauma and contamination of penetrating wounds, migrating FBs (awns, quills) [may take months to years to develop draining tract, non-healing ulcerative nodules]
  45. What are clinical signs of actinomycosis? (3)
    SQ swelling, draining tract, non-healing ulcerative nodules
  46. How is actinomycosis diagnosed?
    anaerobic culture, may take 2-4weeks
  47. What is the treatment for actinomycosis? (2)
    • surgical excision or debulking, remove FB
    • Penicillin/amoxicillin at least 1 month beyond clinical resolution
  48. What are the characteristics of the Nocardia microbe? (6)
    • gram + filamentous aerobic rod, partially acid-fast
    • soil saprophyte
  49. Why are Actinomyces and Nocardia so difficult to tell apart, and how do we achieve this?
    • both are gram + filamentous bacteria
    • Nocardia is partially acid-fast and aerobic, Actinomyces is not acid fast and is anaerobic
  50. What are clinical signs of Nocardiosis? (4)
    cellulitis, ulcerated nodules, draining tracts, lymphadenopathy
  51. How is nocardiosis diagnosed? (3)
    FNA of nodules shows filamentous gram + bacteria, aerobic culture to differentiate from actinomyces, +/- biopsy
  52. Describe the treatment of Nocardiosis. (3)
    • if 1 or a few lesions,surgical resection
    • antibiotics based on susceptibility of isolate
    • combination therapy of antibiotics at least one month past clinical cure
  53. What antibiotics are commonly used in combinations to treat Nocardiosis? (6)
    Potentiated sulfas, Mino/Doxycycline, aminoglycosides, Imipenem, Clarithromycin, cephalosporins
  54. What are the 3 categories of Mycobacteria?
    • obligate mycobacteria (tuberculosis and lepraemurium- affect immunocompromised)
    • saprophytic mycobacteria (affect immunocompetent hosts)- panniculitis
    • saprophytic bacteria that affect immunocompromised hosts (feline leprosy)
  55. Describe the opportunistic Mycobacteria microbe. (3)
    rapidly-growing, ubiquitous, acid fast
  56. How is Mycobacteria usually contracted in an immunocompetent host?
    penetrating wound with soil contamination, causing mycobacteria granulomas
  57. Mycobacterial organisms thrive in _________, such as __________.
    fatty tissue; feline inguinal fat pad
  58. What are clinical signs of an opportunistic Mycobacterial infection? (5)
    non-painful, non-pruritic, firm/ fluctuant SQ nodules that ulcerate and spread outwards
  59. Describe the diagnosis of opportunistic mycobacterial infections. (3)
    • cytology by FNA or or from draining tract- negative staining microbes with diff quik
    • culture from nodule aspirate
    • deep biopsy for histopath
  60. Describe the management of opportunistic mycobacterial infections. (2)
    • aggressive surgical resection (en bloc resection wit skin flaps)
    • antibiotics based on culture, usually for 3-6 months
  61. What antibiotics are commonly used to treat mycobacterial infections? (6)
    enrofloxacin, doxycycline, gentamicin, clofazimine, clarithromycin, trimethoprim-sulfonamide
  62. What is the cause of canine leproid granuloma syndrome (CLGS)?
    fastidious mycobacterial species probably transmitted by biting insects
  63. What is the usual presentation of canine leproid granuloma syndrome?
    nodular skin disease that is usually localized ot the pinnae and head
  64. How is canine leproid granuloma syndrome diagnosed? (2)
    cytology or histological examination with special staining
  65. What is the treatment and prognosis for canine leproid granuloma syndrome?
    usually self-limiting, if not surgical resection is curative
  66. Describe the Cryptococcosis microbe. (3)
    ubiquitous, saprophytic, yeast-like
  67. Where is crptyococcosis found in the environment?
    nitrogen-rich alkaline environments, ie. pigeon droppings
  68. How is Cryptococcosis contracted? (2)
    usually by inhalation (ie. preceded by respiratory disease), sometimes primary skin innoculation
  69. Cryptococcosis is most commonly seen in ________ and presents as... (3)
    cats; upper respiratory signs, polyp-like mass in nostrils or swelling on bridge of nose
  70. How is cryptococcosis diagnosed? (3)
    • cytology: pyogranulomatous inflammation, large microbes with a clear halo
    • biopsy
    • latex agglutination test for capsule Ag
  71. Cryptococcosis is _________ budding; Blastomycosis is _________ budding.
    narrow-base; broad-base
  72. Describe the management of Cryptococcosis. (3)
    • Itraconazole**
    • Amphotercin B (if severe)
    • surgical excision if feasible
    • treatment may require 2 years or more
  73. Where can you find Blastomycosis in the environment?
    moist, acidic soil rich in organic material near bodies of fresh water; endemic in Ohio
  74. How is Blastomycosis usually contracted? (2)
    inhalation of spores from the environment (ie. preceded by respiratory disease), primary skin inoculation can occur
  75. What are clinical signs of Blastomycosis? (8)
    anorexia, weight loss, cough, ocular disease, lameness, firm nodules, draining tracts, plaques
  76. Where are skin lesions commonly located with Blastomycosis? (3)
    nose claw beds, face, but can be anywhere
  77. How is Blastomycosis diagnosed? (3)
    • cytology: big. blue, broad-based budding
    • biopsy
    • immunoassay Ag (urine)
  78. Describe the management of Blastomycosis. (2)
    • Itraconazole
    • glucocorticoids in animals with respiratory distress
  79. Where can you find Histoplasma in the environment?
    nitrogen-rich organic soil; bat and bird droppings
  80. How is Histoplasmosis contracted? (2)
    inhalation of microconidia, primary skin inoculation can occur
  81. How is Histoplasmosis diagnosed? (3)
    • cytology: intracellular oragnisms
    • histopath: round to ovoid with a thinclear zone b/w cell wall and cytoplasm, intracellular
    • culture- highly pathogenic- warn lab
  82. What are clinical signs of histoplasmosis? (9)
    cough, weight loss, diarrhea, fever, ocular lesions, papules, nodules, draining tracts, ulcers
  83. What is the treatment for Histoplasmosis? (4)
    Itraconazole, Amphotercin B (severe cases), fluconazole, ketoconazole; usually at least 6 month treatment
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Derm3- Nodular Diseases
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