Term
| What is the common signalment for a dog presenting with sterile pyogranuloma-granuloma syndrome (SPGS)? |
|
Definition
Cutaneous SPGS can affect dogs of any age
Males may be slightly over-represented
SPGS can affect any breed but Weimeraners, Danes, Boxers, Golden Retrievers, EBDs, Dobies and Dachsunds are more frequently affected |
|
|
Term
| What are the typical clinical lesions seen in sterile pyogranuloma-granuloma syndrome? What body sites are affected? |
|
Definition
Initial lesions - multiple firm, commonly non-alopecic, non-painful and non-pruritic erythematous papules, plaques and nodules of variable size
Lesions can progress to draining tracts especially in large breed dogs with lesions in the interdigital skin
Body sites - skin of the head (bridge of the nose, muzzle and periocular regions) and interdigital regions
Less common occurrence on the pinnae, trunk and abdomen |
|
|
Term
| Sterile pyogranuloma-granuloma syndrome is a diagnosis of exclusion. What testing might be considered to rule out other possible differentials? |
|
Definition
Histopathology with special stains (Giemsa, Gram, PAS, Ziehl-Neelsen), examination of the skin with polarized light microscopy to look for foreign material, bacterial and fungal cultures, PCR for Mycobacteria and Leishmania
**One retrospective study IDed Leish in a small percentage of dogs presenting for this condition so it is important in areas where this is a reasonable differential to rule it out** |
|
|
Term
| Although few cases are reported in the literature, what is the signalment of an animal presenting with proliferative lymphocytic infundibular mural folliculitis and dermatitis (PLIMFD) with prominent follicular apoptosis and parakeratotic casts? |
|
Definition
All cases to date have been reported in young to middle aged (~6yo) female Labrador Retrievers
This is a rare and poorly understood disease...thought to be immune mediated but likely has genetic or hormonal influence.
|
|
|
Term
| What are the typical reported clinical dermatologic findings of proliferative lymphocytic infundibular mural folliculitis and dermatitis (PLIMFD)? |
|
Definition
Prominent follicular casting thar adheres hair shafts together to form thick variably sized and firmly adherent crusts with potentially wide spread distribution (can affect the haired skin of the peri- oral and ocular regions, muzzle, chin, head, pinnae/canals, neck, ventral abdomen, trunk and limbs)
Comedones may be a feature
A peripheral rim of erythema surrounding crusts is common
Patients will be pruritic |
|
|
Term
| What are the typical clinical signs associated with proliferative and necrotizing otitis externa (PNOE)? |
|
Definition
Characterized by well demarcated, coalescing erythematous plaques with heavy crusting that symmetrically affects the ear canals and concave aspects of the pinnae
Variably pruritic
Classically a rare disease of young cats that is generally confined to the ear canals but a more generalized/multifocal form of the disease that affects the face may be seen. |
|
|
Term
| What are the reported treatments that may be considered in cases of proliferative and necrotizing otitis externa (PNOE)? |
|
Definition
There are not many cases reported in the literature...
This is a cytotoxic disease so t-cell inhibitors are often chosen...topical tacrolimus and/or oral cyclosporin
Topical corticosteroids and/or oral glucocorticoids may also be considered |
|
|
Term
| What part of the hair follicle is targeted in alopecia areata? |
|
Definition
| The hair bulb, so it is a 'bulbitis' |
|
|
Term
| What type of T cells infiltrate lesions of alopecia areata? |
|
Definition
|
|
Term
| What types of antibodies are present in alopecia areata? |
|
Definition
| IgG, a heterogenous group reactive to many hair follicle structures, especially keratohyalin |
|
|
Term
| What is the characteristic shape of a hair plucked from a patient with alopecia areata? |
|
Definition
| The 'exclamation point' hair |
|
|
Term
| Where in the hair follicle do inflammatory cells infiltrate in pseudopelade? |
|
Definition
| The wall of the hair follicle (mural) at the level of the isthmus- leads to shrunken, distorted hair follicles. |
|
|
Term
| What follicular histologic pattern has been shown to progress to epitheliotropic lymphoma in cats? |
|
Definition
| Follicular mucinosis/mucinotic mural folliculitis |
|
|
Term
| What does degenerative mucinotic mural folliculitis look like in cats? |
|
Definition
| Diffuse, generalized alopecia, facial skin especially affected, skin becomes thickened, swollen, thickened eyelid margins. Cats are often not feeling well. |
|
|
Term
| What breed of dog has had characterized a condition consisting of mural mucinotic isthmus folliculitis and subsequent alopecia? |
|
Definition
| Norwegian puffin dogs (Lundehunds) |
|
|
Term
| What treatment does Lundehund mural mucinotic folliculitis respond best to? |
|
Definition
|
|
Term
| What systemic signs are very common in dogs with Well's-like syndrome (eosinophilic dermatitis and edema)? |
|
Definition
| Gastrointestinal signs, more than 80% of them |
|
|
Term
| What systemic sign may be seen in half of dogs diagnosed with sterile neutrophilic dermatitis (Sweet's syndrome)? |
|
Definition
| Fever and polyarthropathy |
|
|
Term
| What does sterile granulomatous dermatitis and lymphadenitis looks like histologically (juvenile cellulitis)? |
|
Definition
| Discrete to confluent granulomas and pyogranulomas made of epithelioid macrophages surrounding a core of neutrophils in the superficial dermis. |
|
|
Term
| Two other diseases look very much like sterile granulomatous dermatitis and lymphadenitis and must be differentiated clinically. What are they? |
|
Definition
| Nodular sebaceous adenitis, sterile granuloma and pyogranuloma syndrome |
|
|
Term
| A recent retrospect on sterile nodular panniculitis looked for concurrent systemic disease and did not find much. The most common concurrent systemic disease was... |
|
Definition
| Polyarthritis in 4/39 dogs. Otherwise nothing. |
|
|
Term
| Which breeds seem to be predisposed to sterile nodular panniculitis? |
|
Definition
| Aussie, Brittanys, Dalmatians, Poms, Chihuahuas, mini Poodle, Dachshund |
|
|
Term
| Describe the mechanism of keratinocyte induced apoptosis in erythema multiforme |
|
Definition
- CD8+ T lymphocytes bind to antigenically altered keratinocytes and trigger apoptosis of keratinocyte/squamous epithelial cells
- A high frequency of EM cases is drug-induced in humans (NOT proven in animals). Drugs in humans that cause EM include TMS, penicillins, and cephalosporins.
- Other causes of EM include dyes, food preservatives, and Bordetella bronchiseptica, parvoviral infection, and insecticidal dips
|
|
|
Term
| What is the major soluble mediator of widespread apoptosis in toxic epidermal necrolysis? |
|
Definition
- Granulysin is the main soluble mediator in TEN
- Also proposed that electrophilic drug metabolites, reactive oxygen species, soluble FAS-ligand, and/or tumor necrosis factor (TNF-alpha) may play a role
|
|
|
Term
| What diseases may result from lesions due to T lymphocyte-mediated damage of follicles? |
|
Definition
- Alopecia Areata
- Pseudopelade
- Sebaceous adenitis
|
|
|
Term
| What happens to human patient's immune system during course of an HIV-1 infection? |
|
Definition
- Early in infection, the virus multiplies unchecked and innate immune system attempts to clear it
- After a week, the adaptive immune system kicks in and virus specific B cells, helper T cells and CTLs are activated, proliferate and respond
- Acute phase has dramatic rise in viral load (peaks at 3-4 weeks)
- Most viruses will end the acute phase by the immune system destroying all viral particles
- Full blown HIV-1 infection leads to chronic phase that can last 10 or more years
- In chronic phase, virus loads decrease but the number of virus specific CTLs and Th cells remain high
- Chronic phase progresses, the total number of helper T cells decrease followed by decrease CTLs (virus load increases)
|
|
|
Term
| What are features of HIV-1 in humans that make the infection difficult for immune system to deal with? |
|
Definition
- virus has ability to establish latent infection which cannot be detected by CTLs
- HIV-1 RNA is very error prone- it makes a mistake almost every time it copies a piece of viral RNA. Mutation rate of AIDS virus is so high that it usually can stay one step ahead of CTLs or antibodies directed against it
- virus specifically targets cells of immune system: helper T cells, macrophages and dendritic cells ("docking" protein that HIV-1 binds to when it infects a cells is CD4- co-receptor protein found on large number of surface helper T cells
- CD4 cells are cells needed to activate CTLs and provide them help and they are damaged or destroyed
|
|
|
Term
| What are characteristics of "Elite controllers" in HIV-1 infection? |
|
Definition
- control infection for long periods of time with almost undetectable levels of virus
- innate and adaptive defenses "fire up" quicker
- PRRs of these people will secrete large amounts of IFN-α and IFN-Β by the innate immune system
- IFN-α and IFN-Β cytokines will limit efficiency of virus replication and causes infected cells to die by apoptosis
- MHC molecules are more polymorphic and will efficiently present HIV-1 peptides, killer T cells and be activated early in infection
- Super CTLs present to mobilize and kill via granzyme B and deliver it to its target cells
|
|
|
