Chapter 13 Granulomatous disease Flashcards
What are hypersensitivity reactions also known as?
Immunopathologic reactions.
What is cell-mediated hypersensitivity also referred to as?
Delayed-type hypersensitivity reaction or hypersensitivity type IV reactions.
What characterizes a delayed-type hypersensitivity reaction?
Sensitization of T cells leading to a chronic inflammatory response with prominent macrophage activation.
What are the possible sources of antigens that trigger cell-mediated immunopathologic reactions?
Environmental, self, microbial, or parasitic antigens.
What types of chronic diseases can be caused by microbial antigens?
Mycobacterium tuberculosis and Mycobacterium leprae infections.
What are granulomas?
Circumscribed collections of macrophages, epithelioid cells, and multinucleated giant cells, indicating a focal, chronic inflammatory response.
What are common clinical manifestations of cell-mediated immunopathologic reactions?
Chronic inflammation, mononuclear cell infiltration, tissue necrosis, fibrosis, and angiogenesis.
What types of inflammatory cells can be involved in granulomatous diseases?
Macrophages, lymphocytes, neutrophils, eosinophils, basophils, mast cells, and plasma cells.
What are the main steps in the pathogenesis of cell-mediated immunopathologic reactions?
Antigen uptake by APCs, antigen processing and presentation via MHC molecules, T cell sensitization, and chronic inflammation.
What roles do Th1 and Th17 cells play in granulomatous inflammation?
Th1 cells activate macrophages leading to granulomatous inflammation, while Th17 cells recruit neutrophils resulting in pyogranulomatous inflammation.
What is the diagnostic approach for granulomatous diseases?
History, clinical presentation, and histopathologic evaluation of biopsy specimens.
What are some histologic staining techniques used to detect microbial agents in granulomatous diseases?
GMS, PAS, and acid-fast staining.
What is the treatment focus for delayed hypersensitivity reactions?
Eliminating the underlying cause, controlling clinical signs, and minimizing complications.
What is the role of glucocorticoids in treating granulomatous diseases?
They are used for immunosuppression to control the inflammatory response.
What are the side effects of long-term corticosteroid therapy in horses?
Polyuria, polydipsia, laminitis, and secondary infections.
What is azathioprine used for in horses?
Immunosuppressive therapy, especially for immune-mediated diseases.
What are the characteristics of equine sarcoidosis?
Multifocal skin lesions, granulomatous lesions in internal organs, weight loss, anorexia, icterus, low-grade fever, and peripheral lymphadenopathy.
What are common etiologic agents associated with multisystemic granulomatous diseases?
Coccidioides, Mycobacterium avium, Blastomyces spp., and Bacillus Calmette-Guerin.
What are the clinical signs of coccidioidomycosis in horses?
Weight loss, intermittent fever, respiratory disease, lameness, abortion, colic, and peritoneal effusion.
What is the primary diagnostic method for coccidioidomycosis?
Cytology and culture of tracheobronchial washes, histologic evaluation of tissues, and serology.
What are the signs of disseminated mycobacterial infection in horses?
Depression, intermittent fever, weight loss, lymphadenopathy, and chronic diarrhea.
What are the common clinical signs of allergic contact dermatitis in horses?
Maculopapular or lichenified skin lesions with varying degrees of pruritis.
What is equine collagenolytic granuloma also known as?
Eosinophilic granuloma or nodular necrobiosis.
What are the histopathologic features of eosinophilic granuloma?
Eosinophilic granulomatous reaction surrounding areas of degenerated collagen.
What are common clinical signs of ulcerative granulomas of the skin?
Single or multiple nodular lesions that erode to ulcerative areas with moderate to severe pruritis and serosanguinous discharge.
What are the diagnostic steps for ulcerative granulomas?
Histologic evaluation of biopsies, bacterial and fungal cultures, and special staining techniques.
What is the treatment for fungal granulomas and pythiosis?
Combination of surgical resection, anti-fungal drugs, and possibly immunotherapy with autologous vaccine.
What are the common etiologic agents of respiratory granulomatous diseases?
Silicosis, coccidioidomycosis, aspergillosis, pneumocystosis, histoplasmosis, cryptococcosis, and idiopathic causes.
What are the clinical signs of hypersensitivity pneumonitis in horses?
Exercise intolerance, dyspnea, labored breathing, weight loss, and fever.
What is pyogranulomatous bronchopneumonia in foals typically caused by?
Virulent strains of Rhodococcus equi.
What are the common clinical signs of Rhodococcus equi infection in foals?
Chronic pneumonia, fever, lethargy, coughing, anorexia, tachypnea, labored breathing, tachycardia, nasal discharge, failure to grow, and weight loss.
What is the primary treatment for pyogranulomatous pneumonia associated with Rhodococcus equi?
Antimicrobials, supportive care, and possibly oxygen therapy.
What are chronic idiopathic inflammatory bowel diseases in horses?
A group of conditions characterized by immune cell infiltration of the bowel wall, including granulomatous enteritis, MEED, lymphocytic-plasmacytic enterocolitis, and idiopathic eosinophilic enterocolitis.
What are the common clinical signs of chronic idiopathic inflammatory bowel diseases in horses?
Recurrent colic, depression, weight loss, hypoproteinemia, and impaired glucose or xylose absorption.
What is the proposed etiology of granulomatous enteritis?
Diffuse granulomatous inflammation with epithelioid macrophages and giant cells in the intestinal wall.
What is polyneuritis equi?
A progressive dysfunction of the nerves of the cauda equina and cranial nerves in adult horses.
What are the clinical signs of polyneuritis equi?
Dysuria, urinary incontinence, tail hyperesthesia followed by hypoesthesia, diminished tail, anal, and perineal tone, hypotonicity and atrophy of muscles, paresis and ataxia of the pelvic limbs, and cranial nerve paralysis.
What characterizes the granulomatous inflammation in polyneuritis equi?
Perineural inflammatory infiltrate of T and B lymphocytes, macrophages, giant cells, plasma cells, eosinophils, and neutrophils.
What is the management approach for polyneuritis equi?
Supportive care, with possible immunosuppression using systemic corticosteroids and/or azathioprine.
What is the role of Th1 and Th17 cells in granulomatous inflammation?
Th1 cells activate macrophages, leading to granulomatous inflammation, while Th17 cells recruit neutrophils, resulting in pyogranulomatous inflammation.
What are the typical features of chronic inflammatory response in granulomatous diseases?
Prominent infiltration of mononuclear cells, tissue destruction, fibrosis, and angiogenesis.
What are the immunologic mechanisms behind cell-mediated hypersensitivity reactions?
T cells recognize antigen fragments presented by MHC molecules on APCs, leading to T cell sensitization and chronic inflammation.
What are the common clinical signs of equine sarcoidosis?
Multifocal skin lesions, granulomatous lesions in internal organs, weight loss, anorexia, icterus, low-grade fever, and peripheral lymphadenopathy.
What is the role of glucocorticoids in treating granulomatous diseases?
They suppress the immune response to control inflammation and tissue damage.
What are the diagnostic criteria for granulomatous enteritis in horses?
Histopathologic evaluation showing diffuse granulomatous inflammation with epithelioid macrophages and giant cells.
What are the potential complications of untreated granulomatous diseases?
Chronic inflammation, tissue necrosis, fibrosis, and potential progression to systemic involvement.
