Path 1 Lecture 4 Case Studies PDF

Case studies Dr. Georgios Paraschou Modified from Dr Bolfa The case studies are going over gross lesions, practicing description, and interpretation in terms of MDx, EtDx, Cause, Disease name, DDx or Pathogenesis. Also making some histology - gross correlates if relevant. We can cover ANY disease. E...

Case studies Dr. Georgios Paraschou Modified from Dr Bolfa The case studies are going over gross lesions, practicing description, and interpretation in terms of MDx, EtDx, Cause, Disease name, DDx or Pathogenesis. Also making some histology - gross correlates if relevant. We can cover ANY disease. Early on we would be focusing on normal vs abnormal vs nonlesions/artefact, but as the semester progresses, especially as they do systemic pathology, we will put more weight on interpretation based on what has been covered. Acknowledgement for images Terminology Morphologic diagnosis*. (MDx) This is a summary of the lesion, but generally does not describe what is causing the lesion: [organ, interpretation, distribution ] (i.e. [small intestine], segmental necrohemorrhagic enteritis). Etiologic diagnosis. This type of diagnosis is restricted to two words only - the causative agent and the site of the lesion (i.e., parvoviral enteritis). Etiology. (Etx)This is the causative agent only - it may also be stated as cause, causative agent, or etiologic agent. It does not ask for the organ, distribution, or any other type of information (i.e., Canine parvovirus type 2). *Neoplasms: name of the neoplasm and the organ in it is located: Renal carcinoma *Certain conditions may be summed up in a single word. Palatoschisis; Cyclopia Terminology Name the disease. This type of diagnosis asks for a disease name in common usage (i.e., Canine parvoviral enteritis). Pathogenesis: sequence of events from initial stimulus to the ultimate expression of the disease in the response of cells or tissues to the etiology (oropharyngeal infection  viremia  infection and death of rapidly dividing cells (enterocytes) from crypts  necrohemorrhagic enteritis) Differential diagnosis. (DDx)clinical or morphological (i.e. clinical: anticoagulant rodenticides, canine distemper , hemorrhagic gastroenteritis due to Clostridium spp. Other/associated lesions: the same etiological agent may be responsible for other lesions (i.e. bone marrow depletion, lymphoid depletion etc.) Hypoplasia vs atrophy --> Never achieved full size vs decreased size due to decrease in cell number. ATROPHY = a diminution in the size of a cell, tissue, organ, or part (Dorland 175) HYPOPLASIA = incomplete development or underdevelopment of an organ or tissue; it is less severe in degree than aplasia. (Dorland 905) APLASIA = lack of development of an organ or tissue (Dorland 116) HYPOTROPHY = ABIOTROPHY = progressive loss of vitality of certain tissues or organs, leading to disorders or loss of function; applied especially to degenerative hereditary diseases of late onset Atrophy of an organ can be caused by a decrease in size (hypotrophy) or a decrease in the amount of cells (hypoplasia). Thus, they're not the same. Advice : looking at images - nothing beats experience/seeing the lesion in real life - images are offered as a way of highlighting what you may see - all things in Vet Sc rely on knowing what “normal”is: hence the “ologies” Decide what organ or part of an organ is being highlighted (centre of image) Decide what is abnormal- does presume you know normal Decide which basic pathological process/es is active: Degeneration/Necrosis Inflammation & Repair BE Circulatory Disorders Disorder of Growth Deposits & Pigmentations - Think about distribution, severity HAPPY TO BE WRONG! Think about cause/aetiology/pathogenesis Construct a : MDx, Aetiol. Dx, maybe start thinking about pathogenesis Bovine, MDX Bilateral, symmetrical thyroid glad hyperplasia, THYROID GOITER FELINE; DDx LYMPH NODE-MESENTERIC, HYPERPLASIA FELINE KITTEN ; MDx; possible etiologies SPINAL CORD HYPOPLASIA (LUMBOSACRAL) following neural tube closure defect vertebral abnormalities Dog: MDx, possible etiology, pathogenesis TEETH ENAMEL HYPOPLASIA (CANINE DISTEMPER VIRUS - Morbilivirus) Hyperthermia/viral infection  virus infection of ameloblasts during enamel formation  necrosis and dissorganization of enamel organ  enamel hypoplasia Canine Tissue : Teeth – enamel organ Process: Hypoplasia and necrosis Morphological Description: tooth (enamel) fails to develop properly these teeth will appear rough, pitted and stained yellow. These pets can have sensitivity, are more prone to tartar accumulation, gum disease, infection and may have abnormal root development. Enamel is fully formed when the teeth erupt; therefore virus infection of ameloblasts must occur during enamel formation, which is before the dog is 6 months of age, if enamel hypoplasia is to occur. After the virus is cleared, structure and function of the enamel organ return to normal. Thus segmental enamel hypoplasia results from the lack of enamel formation during the period of virus infection. A similar condition in calves is caused by in utero bovine viral diarrhea virus infection. Dog: MDx, Head muscles, atrophy, diffuse, severe Tissue from a chicken ESOPHAGUS NORMAL VS SQUAMOUS METAPLASIA Vitamin A deficiency Dog: MDx, Hypertrophic gastritis, characterized by thickened rugae, is the result of hyperplasia of the gastric glands. Pig, MDx, NASAL CAVITY ATROPHIC RHINITIS Associated with Bordetella bronchysetica and Pasteurella multocida (Type A and D toxigenic strains) Porcine nasal cavity normal abnormal Pathogenesis: commensal (nasopharynx)  stressors (overcrowding, poor ventilation/humidity, abrupt changes in temperature replicate  colonize mucosae and spread to other animals (2 stage: B. bronchiseptica first followed by a P. multocida)  cilia  B. bronchiseptica (dermonecrotic toxin (DNT)) – metaplasia to stratified squamous epithelium disruption of the mucus layer and the mucosal barrier  suitable for colonization by P. multocida in the second phase of infection mucosal erosions/ulcerations  acute inflammation (neutrophils)  lamina propria, ECM tissues, and bone of the turbinates P. multocida toxin (PMT), a DNT  turbinate atrophy and snout deformation through chronic inflammation leading to bone remodeling and fibrous osteodystrophy of periosteal fibroblast origin (initially stimulate osteoblasts - which in turn hyperplasia and hyperactive osteoclasts As toxin concentrations increase, it acts by blocking the function of osteoblasts cell degeneration and lysis  turbinate atrophy (increased osteoclast numbers and activities osteolysis  inhibiting osteoblastic activities Cystic endometrial hyperplasia, uterus, bitch. Note the cysts in the mucosa of the endometrium. This change occurs under the influence of progesterone after estrus. Cystic hyperplasia may provide a suitable environment for bacteria to grow and cause pyometra, or alternatively, cystic hyperplasia may be secondary to uterine infection and endometritis. Histo: increase in the size and number of glands with no change in the stroma except for edema Bovine, type of necrosis? Possible etiology? Lesion in swine? Leukoencephalomalacia can also be associated with hepatotoxicity, Brain, Leukoencephalomalacia cavitation, lysis – liquefactive necrosis Leukoencephalomalacia (moldy corn disease): Fumonisin B1 from Fusarium verticillioides (F. moniliforme) and F. proliferatum results in necrosis of white matter of the cerebral hemispheres In swine  porcine pulmonary edema Bovine, MDx Possible cause BRAIN CHRONIC POLIOENCEPHALOMALACIA Thiamine (Vit B1) deficiency, Pb toxicity, high levels of Sulfur in diet, Thiaminase containing plants in diet (Braken fern) etc Cat: MDx, Etiology MDx: Cerebellum: Diffuse congenital hypoplasia Etiology: In utero feline panleukopenia virus infection (feline parvovirus) Dog: MDx, Etiology MDx: Kidney: Severe, acute, multifocal to coalescing, petechial, cortical hemorrhages (necro-hemorrhagic nephritis; Etx: Canine herpesvirus 1 pulmonary abscesses Equine Tissue : Lungs Process: Inflammation Morphological Description: Suppurative (pyogranulomatous) bronchopneumonia - Aetiology: Aetiology: Rhodococcus equi Aetiological Diagnosis : Aetiological Diagnosis : Bacterial pneumonia Feline, kitten Tissue: Heart Morphologic DX: Dilated Cardiomyopathy with both atria and ventricle dilatation and hypertrophy Etiologic DX: TAURINE DEFICIENCY CARDIOMYOPATHY Lesion or DX Name: Cardiomyopathy Remarks: Normal domestic cats heart's weigh under 17 grams but animal hearts with this disease weigh over 17 grams but may not be clinically affected. Cat: Pathogenesis, 2 possible sequelae Pathogenesis of renal secondary hyperparathyroidism: Chronic renal disease ↓ GFR  inadequate phosphorus secretion hyperphosphatemia  excess phosphorus binds with calcium in serum  ↓ ionized calcium  ↑ parathyroid hormone (PTH) secretion  ↑ bone resorption *Resulting in parathyroid gland hyperplasia; Possible sequelae: fibrous osteodystrophy, soft tissue mineralization FYI Dystrophic cats lack the muscle cytoskeletal protein dystrophin, which is also the cause of Duchenne's dystrophy in boys and X-linked muscle dystrophy in the dog. Affected cats develop a progressive, persistent, stiff gait associated with marked muscular hypertrophy. The cause of the remarkable muscular hypertrophy seen in affected cats, as opposed to the muscle atrophy seen in the dog and in humans, and the pseudohypertrophy as a result of fat infiltration into affected muscle that can occur in humans, is not known Dog, MDx: Pancreatic nodular exocrine hyperplasia, pancreas, dog. A, Hyperplastic nodules are pale beige to white and project above the surface. B, Microscopically hyperplastic nodules (N) are composed of numerous small acini, most of which, in this case, lack typical zymogen granules. H&E stain. Adult cow, chronic wasting disease, mild to no respiratory signs Type of necrosis: caseous Bovine tuberculosis Calf: acute, severe respiratory disease Type of necrosis: liquefactive Chronic abscessating bronchopneumonia Cat: MDx, Etx MDx: Kidney: multifocal to coalescing, pyogranulomatous nephritis; Etx: Feline coronavirus (mutated) Horse: Etiologic Dx and cause Etiologic Dx: Verminous endarteritis (with aneurysm and thrombosis) Cause: Strongylus vulgaris 4th stage larva MDx: Endarteritis, proliferative and necrotizing with thrombosis DDx: Splenic infarcts, acute; splenic abscesses vs splenic granulomas Splenitis, necrotizing and suppurative with vasculitis, thrombosis and coccobacilary bacterial colonies Cremona, Italia Cow: MDx, Etx MDx: Larynx, trachea: Severe, diffuse, fibrinonecrotic laryngitis and tracheitis; Etx: Bovine herpesvirus – 1 Feline: Pathogenesis Pathogenesis: Renal insufficiency elevated levels of circulating BUN  breakdown by oral bacteria produces ammonia  caustic burns  ulcerative glossitis Pig: MDx, 3 possible causes MDx: Abdominal serosal surfaces: Severe, acute, diffuse, fibrinous peritonitis; Possible causes: Haemophilus parasuis; Streptococcus suis, Mycoplasma hyorhinis, Escherichia coli Sheep: MDx, Etx, Disease name, Special Stain McGavin MDx: Intestine, diffuse granulomatous enteritis Etx: Mycobacterium avium subspecies paratuberculosis Disease name: Ovine Johne’s Disease Special Stain: Ziehl-Neelsen - acid fast Cat: MDx, Associated lesion Hypertrophic cardiomyopathy → mitral regurgitation→ jet lesions favoring Virchow’s triad (blood stasis, endothelial damage, hypercoagulability) thromboembolism → lodges at aortic trifuration --> → mural atrial thrombosis → cyanosis of hind limbs MDx: Aorta, internal iliac arteries: Occlusive fibrinous thromboembolus (saddle thrombus) Associated lesions: Hypertrophic cardiomyopathy; Renal/other tissue infarcts This is the cerebrocortical necrosis of polioencephalomalacia (PEM), basically a nutritional disease. PEM is traditionally associated with LOW THIAMINE but increasingly associated with HIGH SULFUR diets. PATHOGNOMONIC dorsomedial strabismus ("Stargazing"), history and cerebrocortical necrosis that lights up under UV light all suggest PEM. Refs: Pasquini's Guide to Bov Clinics, 4th ed. pp. 140-1 and the Merck Veterinary Manual online edition. Besides thiamine (B1) deficiency, what can cause polioencephalomalacia and laminar cortical necrosis in cattle? In ruminants: o Hypoxia o Water deprivation, o NaCl (salt) sodium ion toxicosis, (circumstantial in ruminants but well established in pigs + eosinophils) o Lead poisoning, (basophilic stippling of RBCs, intranuclear inclusions in renal tubular epithelia, hepatocytes and osteoclasts) o High sulfur intake. o Grain overload and overgrowth of thiaminase-producing bacteria o Associated with cobalt deficiency, molasses, and high urea diets Horse: polioencephalomalacia o Bracken fern and horsetail (Equisetum arvense) are thiaminase containing plants Rabies · Often no gross lesions · Cattle and horses may have hemorrhage in the spinal cord · Evidence of injury or self-mutilation, or alimentary foreign bodies raises suspicion of rabies o Lesions most severe from the pons to the hypothalamus, and the cervical spinal cord; medulla generally spared o Perivascular lymphocytic cuffing; perivascular hemorrhage; leptomeningitis o Glial nodules (“Babe’s nodules”) o Negri bodies are round to oval, 2-8 um, eosinophilic cytoplasmic viral inclusions · Aggregations of strands of viral nucleocapsid; transforms into a granular matrix · Negri bodies are most common in the hippocampal neurons in carnivores and the Purkinje cells in herbivores and are the hallmark of rabies infection Bovine spongiform encephalopathy  No gross lesions Triad of lesions of the transmissible spongiform encephalopathies: · Spongiform change in the gray matter neuropil, primarily swollen dendrites · Neuronal degeneration and necrosis · Astrocyte hyperplasia and hypertrophy Thromboembolic meningoencephalitis (TEME)  Histophilus somni H. somni is an important disease of feedlot cattle that causes TME, fibrinopurulent bronchopneumonia, myocarditis, necrotizing laryngotrachetis, and Polyarthritis GROSS: Random soft red to brown hemorrhagic foci (infarcts) in the brain; Commonly at the white-gray matter interface Widespread primary vasculitis thought to be mediated by bacterial toxin Bacteria adheres to vascular endothelial cells Local thrombosis and vasculitis is followed by ischemic necrosis. Fibrin thrombi in many tissues suggest disseminated intravascular coagulation. A few non-lesions (post-mortem changes, post-mortem artifacts) Horse: MDx, Etx, MDx: Post mortem artifactual nasal froth Etx: common artifact of dying Lesion or Dx Name: Nasal froth Pig: MDx MDx: Kidney, terminal congestion with intestinal loop pressure artifacts of no blood Caribou, calf: MDx MDx: Carcass, post-mortem caused carcass damage Remarks: The failure to see blood around the carcass damage suggests that this finding is only an artifact (animal predation) caused after death. Pig: MDx MDx: Liver, bile ducts Subacute purulent (suppurative) cholangitis Black outlines: pseudomelanosis - is considered a postmortem change due to the bacterial action on the blood producing disufides Horse: MDx MDx: Colon, acute necrotizing colitis The grey appearing mucosa of surrounding bowel is primarily autolytic change and artifactual Dog: MDx MDx: meninges, unilateral darkened (Hypostatic congestion) Terminal artifact Cow: MDx Normal (hemorrhage), artifact during slaughtering process Cow: MDx MDx: liver, artifact reverse flow of brain Etiologic DX: increased air pressure result during slaughter Description: Pale white soft tissue (brain) in the hepatic vein. Dog: MDx MDx: Spleen, unequal expulsion of blood Result of some scattered areas of smooth muscle contraction preventing blood escape at death or soon after. It is considered a post mortem artifact Calf: MDx MDx: Eye, corneal opacity/clouding