VPTH 55 - Systemic Veterinary Pathology PDF

VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY help because these agents cannot penetrate on INTEGUMENTARY SYSTEM intact skin It is made up of skin (main organ) and its adnexa 4. F...

VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY help because these agents cannot penetrate on INTEGUMENTARY SYSTEM intact skin It is made up of skin (main organ) and its adnexa 4. Facilitates production of Vitamin D (associated structures e.g. hair, nails, claws, beak, Vit D can be acquired from: sweat glands, etc.) o food (nuts, fatty fish, leafy vegetable)- inactivated form Adnexa originated from epidermis o sunlight- activated form: Organs that originated from the dermis: dermal o photolysis of sunlight -> convert the precursor Vit bones (turtle) D on your skin to Vit D3 (still inactivated) -> Vit D3 Majority of cases presented to vet hospitals are for will go to liver -> converting the hydrocalciferol cutaneous problems into 25 hydroxicalciferol -> kidney will convert that o skin is the largest organ to 1,25 dihydroxycholecalciferol (active form) o altered by exogenous & endogenous factors 5. Sensory organ o skin can reflect a wide variety of systemic o with tactile hairs, cells and nerves (for sensation) disorders including metabolic diseases (diabetes 6. Stores fat, water, vitamins, CHO, CHON & others mellitus), viral diseases, inflammatory and even o fat soluble vitamins – are stored in endocrine disorders subcutaneous fat o lesions are easily seen by owners because they are more concerned with aesthetic appearance Other functions: of their pets (most common in clinics: skin Although not true for all substances/ animals: problem) o absorption (eg. Some drugs can be placed onto o Eg. Pruritus (intense itching) -> alopecia the skin) o respiration Concerns for Animal Practice: o inflammatory- some may secrete cytokines for 1. Cutaneous parasites immunologic function o may cause anemia (reduction of RBC - Keratinocytes (major cells of the skin) are and/or hemoglobin of the animal) by the major sources of cytokines, so therefore sucking blood (e.g. ticks, lice, fleas) it is also a part of the innate & adaptive o blemish hides directly or indirectly (due to immune response and may also participate irritation -> scratch by rubbing their body in the inflammation and tissue repair. onto rough surfaces) o reduced production of meat, wool & milk because the energy that is supposed to be used for the production is directed in the scratching and others 2. Secondary Bacterial Infection o Skin has its natural microflora that is not capable of causing disease UNLESS there 1. Epidermis: outermost layer; made up of different is a breach in the continuity of the skin layers (cellular part of the skin) 3. Annoyance Stratum corneum – made up of dead cells, o paralysis, unthriftiness, downgraded market responsible for water proofing of the skin value or even death Stratum lucidum – clear layer due to pteridine droplet, not all skin has this layer Functions: Stratum granulosum – granular layer of the cells 1. Temperature and blood pressure regulation attributed to the presence of keratohyalin o depends on the hair coat of the animal: granules - animals in temperate countries- presence of Stratum spinosum – spinous layer and thick haircoat is necessary to conserve heat appearance of the cells in this layer is due to - animals in tropical countries- thinner haircoat, intercellular bridges or desmosomes usually provided with sweat glands, so they surrounding these particular cells can perspire to remove excess heat from the Stratum basale – basal layer that is responsible body & the skin is very vascular which is for the production of cells above it; all 4 layers provided with many blood vessels which are originated from here and this is the most essential for bp reg. mitotically active layer 2. Protects against fluid and electrolytes loss 2. Dermis: inner layer made up of collagen fibers and o outermost layer of the skin is covered with elastic fibers for toughness & elasticity of the skin stratum corneum barrier that prevents excessive (non/ less cellular part of the skin) loss of moisture or heat from underlying tissues 3. Hypodermis: not actually part of the skin, it is just a 3. Serves as a barrier to physical, chemical and tissue below the skin, made up of connective and microbiological agents adipose tissues o stratum corneum of the skin may provide a barrier against these agents and chemicals so In general, the haired skin is thickest over the dorsal that the keratin, collagen & elastic fibers may aspect of the animal’s body and the lateral aspects of Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY the limbs. While the thinnest is at the ventral aspect of the body (abdomen) and the medial aspects of the thigh. - Haired skin: thinner epidermis - Non-haired skin: thicker epidermis (palm, sole) Keratinocytes originated from the germinal cells of the stratum basale and they ascend through the layers of the epidermis and differentiates & shed within 1 month. The enlarged portion of the stratum spinosum have desmosomes or intercellular bridges which makes the cells spinous in appearance. Desmosomes are type of tight junctions which functions in cell-to-cell adhesion, but they may also provide resistance to shearing forces First Intention Healing o involves clean, uninfected lesion o wound space is narrow o healing is called “primary union” o minimal necrosis of the cells of epidermis and dermis Normal vs Abnormal o minimal disruption of the basement membrane Disorders of the Integumentary System: o heals quickly without significant architectural damage o usually scar is not visible Second Intention Healing o there is an extensive loss of skin tissue o inflammation is more extensive as more tissues are to be removed / divide o filled with more granulation tissue to fill the gap between the edges of the wound o wound contraction usually occurs o usually scar is visible on top of the damaged skin Classification of Lesions: A. Primary (exogenous) - lesions restricted initially to the skin are the direct result of underlying disease process B. Secondary (endogenous) - originating from other organs (e.g. immunologic, hereditary, age, congenital, hormonal, metabolic, internal disease) There’s a myriad of exogenous & endogenous factors which may influence both the gross and the microscopic PRIMARY LESIONS appearance of the skin. Because the skin can respond to 1. Macule- circumscribed area of discoloration; up to 1 these factors in a limited number of ways, different cm in size skin disorders may have similar appearance. Most of 2. Patch- macule >1cm in size; flat areas of the usual responses of the skin includes: discoloration - cellular influx and growth - pigmentary and secretory alterations Most of the disorders of the skin may have these different manifestations, so therefore an identification of the cause of skin disorder often requires not only Lentigo is a heritable condition of hyperpigmentation. histopathologic evaluation, but also clinical history (e.g. clinical lesion, distribution, appearance, color) 3. Papule- small (1cm) Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY PRIMARY OR SECONDARY LESIONS 1. Scale- accumulation of loose fragments or flakes of cornified skin Develops after a hypersensitivity reaction to a shampoo. 5. Nodule Chronic seborrheic dermatitis (dandruff-like) - circumscribed, solid elevation (>1cm) that usually Eg. Fungal infection extends into the deeper layers of the skin 2. Crust -lesions are attached to the deeper tissues - accumulation of dried exudate, blood or serum, scale or medications adherent to the skin surface - crusting results after exposure of skin to sunlight Nodular Dermatitis is caused mainly by infectious agents and several immunologic conditions (horse) 6. Tumor- large mass (neoplasia) that may involve any structure of the skin or subcutis Idiopathic photosensitization (animal exposed to sunlight -> exudation of fluids 7. Cyst- epithelial lined cavity containing fluid or solid (reaction)) material 3. Comedo - dilated hair follicle filled with cornified cells and sebaceous material - plug of stratum corneum and sebum within lumen of hair follicles Follicular cyst (apocrine gland cyst) - hair follicles have been dilated because of Dermal cyst (cutaneous epitheliotropic lymphosarcoma) certain debris blocking the release of secretions of the skin 8. Vesicle- well circumscribed (1cm) Comedones seen in dog with hyperadrenocorticism (increase in production of adrenal hormones (eg; cortisol)) SECONDARY LESIONS Contact irritant dermatitis (vesicle) Vesicular exanthema (bulla) 1. Epidermal Collarette- circular rim of keratin flakes following loss of the roof of vesicle or pustule 10. Pustule - small, circumscribed, pus-filled elevation of epidermis - may resemble a vesicle or bulla 11. Abscess- well demarcated fluctuant lesion resulting from dermal or subcutaneous accumulation of pus 2. Erosion- shallow epidermal defect that doesn’t - involves deeper structures penetrate the basement membrane - bound by a membrane - superficial 3. Ulcer- break in the epidermis with exposure of the underlying dermis; deeper lesion -with pain and bleeding 12. Wheal- sharply circumscribed, raised lesion due to dermal edema; blanch with pressure; allergic reactions 4. Excoriation - erosions / ulcers caused by scratching, biting, rubbing - results to the linear loss of the epidermis Mostly seen with hypersensitivity disorders (“pantal”) Bites by parasites Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY 5. Scar- area of fibrous tissue that has replaced the o Hereditary: BVD, iodine deficiency, pituitary damaged dermis or subcutis hypoplasia, teratogens o Acquired/ congenital: nude mouse, hairless chihuahua related to telogen / anagen effluvium 6. Fissure- linear cleavage of usually thickened inelastic congenital hypotrichosis is hereditary due to skin spontaneous genetic mutation affecting the genes responsible for influencing normal hair development C. Hypertrichosis excessive hair growth Nasodigital hyperkeratosis (idiopathic disorder seen in older dogs) Ex #1: Ectodermal Dysplasia (hypotrichosis) Can be seen in humans (feet); dogs (nose) Condition which involves the hair follicles + adnexal glands + teeth (derivative of the skin)= ABSENT 7. Lichenification- thickening and hardening of skin There is an associated oral, dental and thymic defect with exaggeration of the superficial markings; rough (prone to infection) skin Does not have a complete set of teeth -> inability to chew or graze or immune deficiency Signs of ectodermal dysplasia: o Hypotrichosis Lichenification + Alopecia + Sarcoptic mange o Lack of teeth Cattle with chronic alopecia caused by mange o immunodepressed in most cases, congenital hypotrichosis is hereditary 8. Callus- thickened, rough, hyperkeratotic, alopecic, due to spontaneous genetic mutations affecting the often lichenified plaque that develops on the skin genes responsible for influencing the normal development of hair “kalyo” which results from trauma over certain bony prominences of the body (knee & elbow) DISEASES OF THE SKIN I. Congenital and Hereditary Lesions Congenital lesions- develop in utero and present at Ex #2: Hirsutism & Anagen defluxion / Telogen birth. effluvium Hereditary lesions- are transmitted genetically and are Hirsutism (aka hypertrichosis) is due to pituitary pars not manifested phenotypically at birth and this may intermedia tumor that results in excessive hair due to appear several days or weeks after the animal was an adenoma on the adenohypophysis that compresses born. the hypothalamus which is involved in the shedding of the hair. Most of the hair is not being shed + A. Alopecia / Atrichia continuous hair growth but failure of shedding is hairlessness can be seen at a part or in all body parts present. hair follicles are completely lacking or there maybe Examples of hypotrichosis: hair follicles but are not functional Anagen defluxion due to excessive shedding of hair. Phases of the hair cycle: There is a pathologic loss of anagen or growth phase. o Anagen – mitotic activity and growth phase Usually caused by radiation therapy. It may also cause o Catagen – transitional phase complete alopecia (but mostly hypotrichosis). o Telogen – resting phase Telogen effluvium results from early entry to the o Exogen – hair is being shed telogen phase, so therefore the hair is premature Humans generally have an average of 100,000 hairs pushed to the resting stage. The usual causes are: and 90% of these hairs are in anagen phase. And systemic illness, stress, hypothyroidism and anemia. around 10% is in telogen phase. In stressful conditions or in treatment of certain drugs for cancer, usually this may damage the hair follicles which results in more hair in the telogen or exogen phase other than anagen phase. B. Hypotrichosis less than normal amount of hair D. Ichthyosis (ichthyology- study of fish) absence of hair follicles or abnormal follicular dev. scaly epidermis resembling skin of fish hereditary vs acquired: skin divided into plates by fissures Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY basic defect: increase in adherence of keratinocytes INTEGUMENTARY SYSTEM: PART 2 or in keratinization process which prevents the proper II. Environmental Causes expansive growth of the epidermis A. Solar Dermatoses (Sunburn) survival of the animal: few hours to days because gross lesion occurs in unpigmented and hairless part such fissuring may lead to exudation of fluid with of skin characterized by erythema, scaling, crusting secondary infections microscopic lesion: dyskeratosis, ballooning death of the animal: due to infection and dehydration degeneration, hyper/parakeratosis, acanthosis Epidemiology dependent on the amount of light reaching skin affected by 2 factors: 1. Environmental Factors E. Hereditary Collagen Dysplasia Atmosphere “hyperelastosis cutis” or “cutaneous asthenia” The amount of uv light reaching the skin is dependent loose, distensible skin which tears up easily on the atmosphere and the quantity of the ozone layer there’s a specific enzyme defect of collagen synthesis or cloud cover tends to absorb and scatter some uv cause: has not been established rays. And on areas with depleted ozone layer: they are microscopically: presence of collagen bundles which less to absorb and scatter uv rays, so more of these vary in sizes + shape & abnormal organization pattern can reach the skin and may cause lesion. Latitude The latitude farther away from the equator usually have more protection because there is an oblique angle F. Idiopathic Bald Thigh Syndrome entry of uv light into the atmosphere. The path of uv form of pattern baldness seen in greyhounds rays onto the ozone layer is shorter on the equator cause: unknown compared with the latitude farther away from the equator. Altitude Atmosphere at high altitude has less particulate matter to absorb and scatter uv light. They are more prone to solar dermatoses compared to those atmospheres at G. Acanthosis Nigricans lower altitudes. congenital condition in which there is abnormal Shelter darkening, lichenification and alopecia of the skin Animals within the cover of their shelter are less prone can be due to friction (legs due to walking), endocrine to the development of solar dermatoses. imbalance (diabetes mellitus) or hypersensitivities H. Epitheliogenesis Imperfecta (imperfect formation of skin) failure of the epithelium and adnexa to develop completely so the lesion is sharply demarcated and underlying tissue is traumatized, infected, dehydrated 2. Host Factors (can only survive for days) Quantity of hair - It may tend to cover the skin. Pigmentation - Melanin tends to block the uv light and the more the pigmentation or the darker the skin of I. Porcine Juvenile Pustular Psoriasiform Dermatitis the animal = the less prone they are to the characterized by hyperplasia, parakeratosis and development of dermatoses perivascular dermatitis Stratum corneum common in landrace pigs & mostly hereditary -Thickness affects it. lesions are symmetric and develop o the abdomen, Genetics groin and medial thigh -Light breeds tend to be more susceptible to lesions may tend to coalesce (joined together) and the effects of solar dermatoses. develop into umbilicated plaques -> plaque formation Etiopathogenesis Visible light vs UV-A vs UV-B vs UV-C: Visible light has a wavelength of around 400–700 nm. It has a lower energy compared to uv light / radiation. UV light has a wavelength of around 290–400 nm. It has a higher energy. Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY ✓ The lower the wavelength = the higher the are eliminated by initiating apoptosis that is being energy characterized by the peeling of skin after a sunburn. This ✓ The higher the wavelength = the lower the impair tumor suppressor P53 protein function. Mutations energy will yield 9 hot spots (sites where removal of cyclobutene Harmful to humans and animals: UVA & UVB pyrimidine dimer is slowed). This consequently allows the proliferation of mutated P53 gene and therefore may impair the function of P53. This may also promote preferential replacement of damaged cells with mutated P53 cells. So therefore, uv radiation may induce gap formation of tumor cells by blocking apoptosis as well as the clonal expansion of P53 mutants. 1. UVA o wavelength: 320–380 nm o can penetrate to the more acellular layer of the The DNA of a cell with the incoming UVB that may reach skin which is the dermis (deeper) the nucleic acids and may cause “pyrimidine dimers” o damages by generating free radicals -> (thymine-thymine dimers). In genetics, adenine binds damages nucleic acids, proteins & lipids -> cell with thymine and cytosine binds with guanine (AT & GC), death but after exposure to UVB, this may result to faulty o free radicals: hydroxyl radical, hydrogen binding. peroxide, superoxide radical Ionizing radiation can generate these damaging intermediates through the interaction with water in a process known as radiolysis. Since the animal’s body is Supposedly, a segment of a DNA will bind with the other made up of around 55-70% water, the probability of segment. But after the exposure to UVB, the two radiolysis is high under the presence of ionizing radiation thymine molecules forms bond with each other which such as uv radiation. In the process of radiolysis, water forms the “cyclobutene ring”. Thymine dimers are loses an electron and this become highly reactive. considered as the most common type of DNA damage Through chain reaction, water is subsequently converted caused by UVB. UV light distorts DNA, so that the 2 into the hydroxyl radical which will generate the bases can no longer pair up with corresponding adenine hydrogen peroxide & superoxide radical (oxygen w/ partners. Formation of this ring coming from the extra electron) and ultimately, the oxygen. pyrimidine dimers are responsible for atleast 80% UVB- Hydroxyl radical is extremely reactive and can remove induced mutations. And the precise class of mutations electrons from any molecule in its path, turning that resulting from pyrimidine dimers is a unique molecular particular molecule into a free radical and so this will signature of skin cancer. propagate the chain reaction. Hydrogen peroxide is more damaging to DNA than the hydroxyl radical and since it has lower reactivity, it provides enough time for it to travel into the nucleus of cell & subsequently where it havocs on macromolecules such as the DNA. Superoxide radical is not that reactive but may act as catalyst for the generation of other reactive oxygen species. All of these free radicals can damage the nucleic acid, proteins and even lipids found within the cell. And may Whenever pyrimidine dimers are formed, they are eventually cause “cell death”. usually corrected by nucleotide excision repair mechanism / NER. Those portions with pyrimidine 2. UVB dimers are cleaved off and being replaced with a new o wavelength: 290–320 nm one. However, even if the NER mechanism was 99.9% o can penetrate to the basal layer of the epidermis effective, more mutations there are = the increased the or up to the level of the stratum basale risk of one remaining unrepaired. Individuals having o Mutagenesis -> capable of causing mutation defect on NER mechanism are more prone on It may cause pyrimidine dimer formation especially in developing skin cancer. mutation “hot spots” on P53 gene which blocks the cell cycle when the DNA is damaged. UV damaged skin cells Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY 3. UVC Photosensitization can be associated with poorly haired o wavelength: 200–290 nm or white-haired areas of the animal’s body. This can also o can penetrate to the superficial layer of the skin be associated with certain liver disease. There is certain only photosensitization which could be idiopathic as well. In o most of it is being filtered by the atmospheric this case, there is inactivement in the colored hair of the ozone animal to absorb or block the light getting to the skin to o less danger / less harmful to human and animals activate the photodynamic agent but the animal develops photo sensitization. B. Primary Phototoxicity (sunburn = solar dermatitis) Types of Photosensitization inflammatory condition 1. Type 1 or Primary Photosensitization such sunlight may cause direct endothelial damage o due to ingestion of preformed photodynamic and damage to keratinocytes with the release of substance contained in a variety of plants or inflammatory mediators fungus contaminated plants o plants usually contain “helianthrones” which is a red fluorescent pigment found in most grasses o plants contain “furocoumarin” that form phytoalexins in response of the plant to fungal infections o (examples: PTZ, Perloline, Fagofyrin, Hypericin) o Phenothiazine is a drug that is usually used as C. Photosensitization an anthelminthic in large animals. This can be caused by the sensitization of the superficial layers of converted to photoreactive metabolite in the GIT lightly pigmented skin to light of certain wavelengths -> causing activated photodynamic substance. 2 requirements for development of photosensitization ✓ photosensitizing / photodynamic agent 2. Type 2 or Endogenous Photosensitization ✓ exposure to sunlight o usually are inherited through an enzyme deficiency that results in abnormal synthesis of photodynamic agents o “uroporphyrin” (urine) & “coproporphyrin” (feces) are substances from excess porphyrin by- products that are formed during faulty Mechanism hemoglobin synthesis. Example: A = molecule of photodynamic agent (tetracyclines or 3. Type 3 or Hepatogenous Photosensitization chemicals from grass)) o due to liver disease that allows accumulation of L = unit of light “phylloerythrin” which is a product of chlorophyll B = molecule of oxidizable substance metabolism, or it can occur secondary to liver injury: A+L = A1 ✓ biliary obstruction Animal is exposed to a photodynamic agent with ✓ toxicosis from chloroform sunlight, the energy coming from this light is being ✓ excessive amount of corticosteroids transferred to the photodynamic agent, thereby ✓ leptospirosis activating that agent. 4. Photosensitivity of Unknown Cause o included are those affected cattle on pasture A1 + B = B1 + A where no photodynamic plants are identified Activated agent in presence of any oxidizable substance will cause the transfer of energy to that molecule, Chemical Causes thereby activating them. Contact dermatitis Ergot B1 + O2 = B oxide Mimosine toxicity Energy from the oxidizable substance is transferred directly to oxygen (in the cytosol) forming free radicals. These will cause lipid oxidation/ peroxidation of the cell membrane, causing the rupture of mitochondrial lysosomes and granulation of mast cells leading to -> Inflammation Contact Dermatitis -> middle picture: dog exposed to zonrox for a long period of time -> for chemicals to cause injury, it must penetrate the protective epidermal layer and it is usually enhanced by physical damage due to excessive amount of moisture. If the animal is submerged to water for longer periods of Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY time, then their skin could be more prone to the these viruses may cause damage via viral development of injury. invasion of nervous tissue or vascular Ergot degeneration and necrosis -> right picture -> mycotoxin produced by the Claviceps purpurea which is a fungus that produced toxic alkaloid known as “ergotamine” that causes arteriolar vasoconstriction as well as capillary endothelium damage -> this leads to perivascular edema & thrombosis-> resulting to tissue ischemia or infarction. Cold temperature may increase Pseudorabies in swine and cattle (caused by mad the severity of ergotism because it adds to arteriolar itch) causes viral invasion of the nervous tissue. This vasoconstriction causes intense pruritus and self-mutilation of the Mimosine Toxicity animal. Animal may rub its skin on hard surfaces due -> left picture to itching -> causing secondary lesions. -> toxic amino acid derived from certain leaves of plants Hog Cholera Virus may cause proliferation of such as Leucaena leucocephala (ipil-ipil) and mimosa vascular endothelium which eventually leads to -> spp. (makahiya). It causes loss of long hair on the mane, occlusion of the blood vessels -> reduction of blood tail and forelock and may also cause neurological supply to a particular area of the skin -> ischemia or manifestations. infarction. Poxvirus may cause necrosis due to vascular injury III. Physical Causes and stimulation of host cell DNA -> epidermal A. Acral Lick Dermatitis hyperplasia. Most lesions have thickening. The o psychogenic dermatitis due to persistent licking precise mechanism on how these were produced is and chewing (ex: paw) that: o lesions are usually hairless, circumscribed, infection -> macule formation -> papule -> ulcerated vesicle -> pustule -> crusting and scar formation o most of the time caused of boredom Orf Virus (middle picture) is a parapoxvirus that o may experience mild pain and itching undergoes on the same development with poxvirus, but the vesicle stage is brief and the lesions tend to B. Injection site reactions be more proliferative (e.g. FMD, as seen in the last o subcutaneous injections may result to picture). Papillomaviruses (first picture) elicits an inflammatory granulomatous nodules increase activity, mitosis and proliferation that leads o granuloma have foreign & necrotic materials to -> hyperplasia & hyperkeratosis. bordered by macrophages & multinucleated giant cells (MGCs) surrounded by granulation B. Bacterial Causes tissue a healthy skin is resistant to bacterial infection: o there are vaccine brands that causes it after o skin has a lot of moisture injection o continuous desquamation of dead cells C. Intertrigo / Skin Fold Dermatitis o ecologic pressure of normal microflora of the o superficial inflammation of 2 surfaces that are in skin contact cutaneous bacterial infection referred to as o moisture and frictional trauma may predispose pyoderma eventually to bacterial infection Puppy Pyoderma involves accumulation of moisture -> proliferation of microorganisms. Pyoderma IV. Infectious Causes PRIMARY SECONDARY Skin Otherwise healthy Not healthy A. Viral Causes Bacteria One species > 1 species most viruses causing dermatitis are Pattern Characteristic Not characteristic epitheliotropic which has certain predilection to Response to ATB Successful Not successful the epithelium o Aphthovirus ->causing foot and mouth SUPERFICIAL DEEP disease Involve Epidermis Dermis / Subcutis o Vesiculovirus -> causing vesicular Repair No scarring Scarring Duration Short Chronic exanthema Lymph Node No Yes o Enterovirus -> causing swine vesicular Systemic No ± disease Gross Pustules, Pustule, Nodule, o Calicivirus -> causing vesicular exanthema Crusts Abscess, Sinus Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY INTEGUMENTARY SYSTEM: PART 3 C. Mycotic Causes Superficial mycoses caused by dermatophytes: Microsporum, Trichophyton, Epidermophyton infection is restricted only at the stratum corneum Primary Infections minimal to no tissue reaction lacks immune response (s. corneum is non- 1. Greasy Pig Disease (first pic) vascular) Staphylococcus hyicus only cosmetic effect manifested by either by: The organism is capable of secreting a toxin ✓ hypopigmentation known as “ShET” or Staphylococcus hyicus ✓ hyperpigmentation exfoliative toxin that binds to filaggrin proteins in E.g. Tinea nigra is a condition resulting the keratohyalin granules of the stratum in brown to black macule found on the granulosum -> focal erosion of stratum corneum palm and sole -> exudation Cutaneous mycoses due to exudation of sebum, animal tends to be infection is restricted at the keratinized layer of greasy skin animals having this condition usually dies due to tissue destruction & immune response is dehydration and septicemia extensive because of the presence of agents and its products 2. Diamond Skin Disease (second pic) fungal products & cytokines released from Erysipelothrix rhusiopathiae damaged keratinocytes results in infection may usually lead to vasculitis, -> epidermal hyperplasia and inflammation thrombosis and ischemia inflammatory cells arrive at an area + fungi tend rhomboidal-shaped lesion to die at the area of inflammation and are viable peripherally 3. Dermatophilosis E.g. Ringworm (first pic below) – the periphery Dermatophilus congolensis of the lesion is reddened because of an active infection with zoospores causing acute infection, while center is usually whitish due to inflammatory response that is usually cells that have died in this area (healing manifested by: process) ✓ microabscess / proliferation of neutrophilic caused by Microsporum nanum in pigs and cells cattle ✓ epidermal regeneration infection cycle young animals are more prone to fungal lesions tend to be multi-laminated with several infections because of the less amount of fatty layers acid in their skin which tends to be fungistatic alternating layers of keratin and inflammatory Subcutaneous mycoses cells results in subcutaneous traumatic implantation of the organism producing lesions which are characterized by tumor-like enlargement known as Mycetoma caused by usual fungus found in the soil: ✓ Curvularia, Acremonium, Alternaria Dermatomycosis (last picture below) fungal infections of skin, hair or claws caused by a nondermatophytes ✓ Malasseziasis (Malassezia pachydermatis/furfur) A lipophilic yeast with certain liking for the lipids. It causes mild infection and may appear as discolored or depigmented skin. ✓ Candidiasis (Candida species) -> “Hadhad” Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY D. Parasitic Causes cutaneous inhabitation by parasite presence of endoparasites superficial layer is involved -> “infestation” Pig: caused by Sarcoptes scabiei var suis Snake: infested with ticks / Amblyomma Histologic section: infected with scabies; thickened skin Grossly: characterized by alopecia, erythema, scaling, hyperkeratosis, acanthosis; mites on the stratum corneum The stratum spinosum contains spines that are basically desmosomes or intercellular bridges that connects 1 cell to another. These are type of tight junctions which function in cell-to-cell adhesion and may provide resistance to the shearing forces. It contains cell adhesion proteins -> cadherin family proteins which includes: desmoglein & desmocollin that are attached to the intracellular keratin cytoskeletal filaments by Habronemiasis (first pic above) caused by anchoring proteins known as desmoplakin. In short, Habronema larva in which the hypodermal larvae desmoglein and desmocollin are attached to the penetrate the skin and migrates into the subcutis. intermediate filaments by means of the desmoplakin. In After weeks or months, the first stage lava grows -> the case of pemphigus, there are certain autoantibodies migrates to subcutis at the back -> nodules. that binds to keratinocytes surface antigen particularly Habronema larvae (third pic above) are unable to the desmoglein. This induce the release of proteolytic penetrate normal skin, but they tend to be deposited enzymes from the keratinocytes and this may disrupt the by houseflies or stable flies. cell to cell adhesion resulting in separation of cells with each other or process known as “Acantholysis”. And E. Immunologic Diseases eventually, exuded fluid will collect to form a vesicle. The ones being attacked by the autoantibodies are those of Hypersensitivity Reaction the desmoglein -> desmoglein 1 and desmoglein 3. mild to severe reaction that develops in response to normally harmless compounds like pollen Eg. Atopy is a type 1 hypersensitivity rxn, with pruritus as the main clinical sign. Primary lesions are not seen but usually result of self-inflicted trauma -> secondary lesions are present. Autoimmune Reaction develop when antibodies or Tcells are reactive against the self-cells or tissues of the animal itself rather than foreign Eg. Pemphigus comprises a group of blistering disorders that results from binding of the antibodies to the intracellular antigens 3 Types of Pemphigus Pemphigus foliaceus milder and more common develops spontaneously as adverse reaction to Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY drugs Anagen -> “growth” where hair is produced by mitosis in cutaneous lesions consist of vesicles that rapidly the epithelial cells covering the apex of the dermal become pustules papilla which is usually enveloped in a matrix autoantibodies are directed against desmoglein Catagen -> “transition” (early & late) where a constriction 1 that are found at the upper layers of the occurs at the hair bulb and the hair shaft above becomes epidermis and a small amount is present in the club-shaped and in the late catagen, the distal follicle oral mucosa becomes thick and corrugated and may push the hair up cutaneous lesions rather than oral lesions are Telogen -> “resting” where the dermal papilla separates more common and tends to be exfoliative and an epidermal strand shortens to form secondary Pemphigus vulgaris germ severe form of pemphigus Early Anagen -> where hair is being pushed out of the found deeper in epidermis and oral mucosa follicle with the formation of the new hair bulb autoantibodies are directed against desmoglein Exogen -> where hair is being shed off 3 which are mainly found at the basal layer of epidermis and mucosal epithelium G. Cutaneous Neoplasia vesicles and secondary erosions and ulcers in There are specific etiologies for the cutaneous oral mucosa are common neoplasia. Only few of them tends to be tumors. Several Pemphigus vegetans contributing factors in the development of skin tumors are: less common viruses accompanied by papillomatous proliferation o Feline leukemia virus – causes cutaneous lymphoma F. Metabolic Disease o Feline sarcoma virus – causes malignant due to imbalance in hormones melanoma manifestations are nonpruritic, bilaterally solar & ionizing radiation symmetrical alopecia or endocrine alopecia, hormones and genetic influences pigmentary changes (AKA Endocrine alopecia) vaccines o Vaccine-associated sarcoma – (cats) it has been associated with aluminum-base adjuvant -> neoplasia thermal injuries immunologic influences Eg. Long-term exposure to ionizing effects of sunlight (UVB) Examples of Endocrine Alopecia: -> solar dermatosis -> increased cutaneous Hyperadrenocorticism -> have hyperactive adrenocortex hemangioma and squamous cell carcinoma – most responsible for the secretion of steroid hormones. common Lesions generally spares the head and extremities. It is like an alopecia but sparing the head and legs. Mammary Tumors Comedones are also seen. Because of the increased most common in female dogs amount of steroid hormone in the body, there is also a Papilloma reduction in the resistance to infection of the skin and wart-like structures the dermal collagen tends to be atrophic. Hypothyroidism -> have reduction in the amount of benign neoplasm of stratified squamous thyroid hormones released by the thyroid gland. It is the epithelium most common cause of endocrine alopecia because thyroid hormone is necessary for initiation of the anagen stage of the hair cycle, so with absence of it, anagen stage is being restricted resulting to dry, dull, easily epilated haircoat that fails to regrow. The animal may remain bald. Hyperestrogenism -> less common type of endocrine alopecia brought about by certain tumors. Squamous Cell Carcinoma The Hair Growth Cycle most common form of carcinoma of the skin malignant and non-encapsulated histologically: formation of “keratin pearls” Downgrowth proliferation of neoplastic cells coming from the epidermis and may tend to penetrate the dermis. Some has keratinized central areas. Lesions may vary from red, firm, flat, cauliflower-like, ulcerate Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY grossly: firm, poorly demarcated mass which Pantothenic acid may tend to ulcerate, and proliferative / papillary alopecia location: head (eye/ear), esp unpigmentated dermatitis in pigs areas Niacin alopecia crusting dermatitis Vitamin C heavy scaling alopecia in calves Vitamin E "yellow fat disease" degeneration of the subcutaneous tissue Squamous Cell Carcinoma Zinc Other benign tumors: parakeratosis or thickening of the skin high concentration: deficiency results due to high amounts of phytic acids that binds to zinc molecules low concentration: high amounts of calcium present may also result to deficiency due to its competition between zinc and calcium Copper achromotrichia -> no hair color and may also result from molybdenum excess Histiocytoma (first pic above) also known as the “button depigmentation or loss or color of hair ulcer” is common, benign and spontaneously regressing essential component of the enzyme tyrosinase tumor usually seen in young dogs. which is critical in melanogenesis or formation of Mast cell tumor (second pic above) can be single or melanin multiple, edematous, nodular masses often found in the cattle: loss of hair seen around the eyes, giving hairless and ulcerated stages of the disease. Etiology in an impression that the animal is wearing cats is unknown but granules are present in the feline spectacles mast cell containing vasoactive substances such as sheep: loss of crimp of the wool or hair is heparin & histamine. If a mast cell contains heparin & straight (not wavy) due to imperfect oxidation of histamine, therefore the most common complications sulfhydryl groups in the prekeratin – a process after the granulation of mast cell tumor could be that requires copper coagulation disorder, gastrointestinal ulceration and anaphylaxis type reactions because of the presence of Selenium Toxicity excessive amount of histamine. Feline mast cells also o May also affect the integument of the animal have phagocytic capability and can be able to because of the competitive replacement of sulfur endocytosed erythrocytes which modifies the structure of keratin. The -> anemia. keratin that was supposed to contain the sulfur, Lipoma (third pic above)– benign resulting from tumor of may contain selenium. connective tissue H. Nutritional Diseases of the Skin Starvation or protein-calorie under nutrition skin changes: disappearance of subcutaneous fat and skin wrinkles and loses its elasticity collagen -> major component of the dermis that is responsible for the toughness elastic fibers -> responsible for the elasticity Deficiencies Vitamin A hyperkeratosis of squamous epithelia squamous metaplasia of secretory epithelia responsible for epithelial growth Riboflavin seborrhea erythema scaling dry hair coat in dogs alopecia in cats Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY MUSCULOSKELETAL SYSYEM 2 Major Classes of Muscle Fiber Changes: Skeletal Muscles Neuropathic composed of elongated myofibers determined by effect or absence of nervous length of cell is same as the length of entire supply muscle change due to denervation multinucleated, non-branched and being Myopathic separated by connective tissue known as primary change is not related to loss of nerve “endomysium” supply cross striations are present -> light & dark bands due to reduced blood supply/trauma -> reduced (present in skeletal and cardiac muscles, NOT nutrients -> contractility is affected on smooth muscles) multiple nuclei are abundant per muscle fiber and located always at the side, just beneath the sarcolemma or always the periphery of the fiber (unlike in smooth m. -> only one nucleus is present in the center of each m. fiber) Post Mortem Examination main functions: Normal Muscle vs Degenerating Muscle o maintenance of posture Clinical manifestations of muscle diseases may o locomotion be: change in size o respiration o muscle atrophy -> compare muscle size o homeostasis o muscle hypertrophy, swelling, weakness, o temperature regulation pain o aesthetic purposes o abnormal gain or loss of weight structure & physiological features of skeletal Change in color and texture muscle may determine a response to a o depends on the age of an animal particular injury o do not compare a young to mature (darker), anatomic arrangement allows the cell to react different species (when comparing animal independently of any insult (sometimes only one from the same specie, much better if it’s of myofiber is involved in injury); each myofiber has the same breed) their own nervous supply o muscles of cow are redder compared to the nuclei are differentiated with little or no capacity paler muscle of the pig for mitosis or regeneration, so if 1 myofiber is o due to extent of blood perfusion -> more injured or dies -> cannot undergo regeneration blood passing through it = the redder it is satellite cells coming from the resting myoblast, o paler -> anemic animal, degenerating is the one responsible for repair of muscle cells muscles Abnormal color may be due to: 2 Types of Muscle Fibers: o Alteration of myofibers -> reflects Type 1 degeneration/necrosis or streaking (normal- “slow twitch muscles” & “red muscles” abnormal-normal) and mineralization as oxidative and aerobic well as infiltration of collagen/fat high mitochondrial content = more fatigue o Hemorrhage -> degenerating muscles that resistant are mostly paler, appears to be darker due to trauma high fat but low glycogen o Myoglobin stain -> muscles have own located deep into the muscles pigment known as “myoglobin” that can be responsible for posture released by damaged muscles, can be an Type 2 indication of a ruptured muscle fiber -> Type 2a darker colored muscle “fast twitch muscles” o Anemia -> paler muscle due to oxidative and glycolytic hemorrhage, hemolysis, deficiency in iron low mitochondrial content = fatigue resistant or vit B12 Type 2b /!\ when diagnosing anemia, take note of the “fast twitch muscles” & “white muscles” age of animal since younger animals have anaerobic and glycolytic lighter colored muscles compared to adult low mitochondrial content = fatigue sensitive Changes on texture may be due to: white muscles -> less red than type 1 o thickening of the muscle may be an indication of fibrodysplasia where there is fibrous connective tissue proliferation associated to trauma o increase or reduction in muscle tone that highly vascularized with numerous capillaries results from denervation or loss of nerve very well innervated -> very sensitive to pain supply or even lack of exercise Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY Acquired Lesions Changes in Myofiber Size (A) Diaphragm. Pale streaks of muscle fibers results from necrosis (light colored) -> mineralization (glistening 1. Atrophy appearance). Sex-linked muscular dystrophy. Denervation atrophy (B) Localized paleness and area of necrosis results from due to interference in the nerve supply to any an injection of an irritant that maybe antibiotic that is toxic to muscles (e.g. tetracycline) or septic injection muscle (C) Denervation atrophy. Myofibers reacted happens rapidly and over half of the muscle independently. Overall paleness of muscle with streaks mass could be completely denervated -> loss of alternating normal and abnormal tissue and glistening of muscle within weeks (mineralization) pseudohypertrophy may develop where in (D) Steatosis of longissimus muscle. Degenerating atrophic myofibers will be replaced by fats muscle fibers is replaced by fats. that will cause muscle to be larger than (E) Necrosis due to injection. Necrosis on the normal normal appearing muscles. Necrotic material is being covered or /!\ take note the difference of steatosis vs limited by a diphtheritic membrane. After resolution, the pseudohypertrophy area may be replaced by fibrous tissue. Disuse atrophy due to cessation of muscle use (eg. Fracture) Other causes of Muscular Dysfunction happens when a particular muscle is not Physiologic used Excessive tension causing muscle rupture results in a less rapidly atrophy of the muscle Exercise-induced damage to myofibers reversible -> except when there is so severe Loss of innervation or blood supply and prolonged damage to myofibers that Endocrine and electrolyte abnormalities eventually loss Genetic Malnutrition atrophy Inborn errors of metabolism due to cachexia, senility, cancer, chronic Genetic defects of myofiber structural inflammation components in case of cachexia, muscle (being a protein) Developmental defects can be metabolized by body to supply the Nutritional / Toxic need for nutrients Deficiency of selenium or vitamin E in cases of chronic inflammation, the Toxic plants or plant products increase in the number of cytokines (IL1, IL6, TNF) enhance protein catabolism or Feed additives (ionophores) breakdown -> mobilize a pool of amino acids Note: Regardless of the cause of muscular dysfunction, for antibody production in cases of infection the muscle would have a very limited response to injury and may undergo necrosis and regeneration from occurs gradually satellites cells of myoblasts. However, there could just will result to muscle wasting be an addition or deletion of some sarcomeres (contractile unit of a muscle fiber) to cause elongation or 2. Hypertrophy shortening of muscles that results to either atrophy or Work hypertrophy hypertrophy of muscles. due to increase in normal physiologic work e.g. lifting weights DEVELOPMENTAL ANOMALY Compensatory hypertrophy 1. Arthrogryposis increase in size of normal fibers in response congenital disease -> muscle fails to develop to increased workload caused by loss or muscular lesion originates from problem in absence of muscle fibers CNS/PNS manifested by the rigidity of joints caused by Ex1: Denervation atrophy Laryngeal hemiplegia muscle hypoplasia from lack of innervation “roaring” -> seen in horses during gestation results from unilateral atrophy 1 of laryngeal associated to ingestion of toxicant during muscles gestation or congenital viral infection nerve involved: left recurrent laryngeal n. (1 discoloration due to meconium (first feces of side only) fetus) -> may cause fetal anoxia reduction in the muscle mass & paleness is flexion of muscles because there is no other present muscles to counteract it Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY mild cases -> annular fibers may form cluster Ex7: Steatosis called “lipomatosis” or “hypoplasia lipomatosa” “small group atrophy” seen in cattle, pig and sheep severe cases -> the entire muscle fascicle not observable condition in animals alive but undergoes atrophy called “large group most commonly observed when the animal is atrophy” slaughtered defective muscle development – muscles are larger lost myofibers are replaced by fats Ex2: Disuse atrophy Steatosis vs Pseudohypertrophy reduced movement due to pain, fracture In pseudohypertrophy, it shows that the reduction in number and size of myofibers development of muscle fibers is normal. But due may be replaced by fat cells -> to defects (denervation), that denervated pseudohypertrophy myofiber has been replaced fats. innervation remains intact; reversible In steatosis, there is defective muscle development onset. Muscles do not develop normally -> replaced by fats. Ex3: Malnutrition atrophy innervation and movement are intact lesions are generalized but essential muscles (diaphragm, heart) are not affected due to severe starvation, the muscle itself becomes the source of nutrients (Acquired Myasthenia Gravis) Ach is normally released by nerve endings and this ach will bind to achr to cause muscle contraction. But in this condition, although the ach has been released, there will still be no contraction because antibodies have already destroyed the achr so the animal may appear weak due to lack of Ex4: Muscle hypertrophy contraction. increase in size but not the number of Degeneration and Necrosis myofibers - common sequela to myofiber injury regardless of cause -> because muscle responds to injury to a Ex5: Muscular dystrophy very limited number of ways progressive hereditary degenerative disease not inflammatory there is relative inadequacy of regenerative activity (A) degenerating muscle appears paler than normal Ex6: Myasthenia gravis (B) degenerating muscle appears darker than characterized by muscle weakness and normal due to hemorrhage or extensive release of fatigue myoglobin from the lysis of the muscle fiber -> exacerbated by exercise “rhabdomyolysis” alleviated by rest Acquired myasthenia gravis autoimmune disease in which antibodies are directed against the acetylcholine receptors histopathology: cell swelling, hypereosinophilia, of the NMJ loss of striation, fragmentation, rupture of fibers no muscle contraction because ach formation of retraction caps -> concavities at the cannot insert effect because of the end of ruptured fibers due to hypercontraction destroyed NMJ (darker) Congenital myasthenia gravis cytoplasm is eosinophilic with loss of cross deficiency of AchR (acetylcholine receptors) striations no evidence of autoimmune mediated disease even if the animal has a sufficient amount of Degeneration and Calcification ach but with limited achr -> limited pale with white streaks of degenerated contraction fibers intertwined with normal fibers Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY (alternating) e.g. downer cow syndrome – lying for too long glistening -> due to calcification / massive influx of Ca 1. White Muscle Disease segmental swelling, hypereosinophilia, affects the diaphragm, intercostals, tongue and mineralization heart dissolution of cytoplasm or entire muscle affects the rapidly-growing or young animals moa: affecting left side of bovine heart and right side of ovine heart due to vitamin E & selenium deficiency Selenium is part of the glutathione peroxidase that reduced the lipid peroxides to form non- MYOPATHIES toxic hydroxyl radicals -> eliminate toxic (Degenerative Diseases of the Muscles) potential of peroxides while vit E is an antioxidant & oxygen radical scavenger. When Toxic myopathies these are absent, there will be peroxidation of ingestion of toxic plants, drugs, chemicals, the lipid membrane -> influx of calcium in mycotoxin cytoplasm and mitochondria. A considerable amount of energy is required to remove calcium produce ill defined, pale areas in muscles out of the cell that can lead to exhaustion -> e.g. cottonseed & ionophores myofibers degenerate & Ca accumulate within o Ionophores are added in the feed to enhance the growth in ruminants because it forms lipid soluble dipolar complexes with cations & allows its movement across the membrane of cells. Due to the complexes, the cell as much as 50x as normal. this may tend to disrupt the ionic equilibrium The muscle tends to be glistening due to calcification or in cells. excessive amounts of Ca in the cell. Intracellular enzymes (creatine primase) may leak out the cell -> Endocrine myopathy myonecrosis. Muscles with higher physiological activity muscle wasting and atrophy of muscle fibers (heart) is being affected since muscle activity relates to e.g. diabetes mellitus and hyperadrenocorticism the production of free radical. The more free radicals that o an effect of the adrenal cortex is excessive are accumulating in the cell without these different secretion of cortisol / glucocorticoid (a nutrients, the more it cannot be converted to non-toxic hormone which tends to increase the hydroxyl acids. Affected muscles are pale and glucose levels in the blood) -> calcification can be found on special stains. In swine, gluconeogenesis (conversion of protein in these deficiencies may coexist with mulberry heart the muscle into glucose) -> muscle wasting (extensive hemorrhages in the heart) and hepatosis dietetica (liver is hemorrhagic). Nutritional myopathy PSE Muscle -> “Pale Soft Exudative” aka “white muscle” due to a deficiency of Selenium, Vitamin E or both (many factors but these are the most common in animals) 2. Porcine Stress Syndrome AKA Malignant precipitated by rapid growth, unaccustomed Hyperthermia, Pale Soft Exudative Pork exercise or diet factors Hereditary: e.g. white muscle disease in pigs and PSE Rapidly growing pigs (Landrace, Pietrain, o Vit E and selenium are antioxidants which are Hampshire, Yorkshire) part of the enzyme glutathione peroxidase, dogs and human beings scavengers of toxic derivatives of oxygen. If involves an autosomal recessive gene that has there is deficiency in glutathione peroxidase - variable penetrants that determines the > peroxidation of the cell membrane-> will susceptibility of these animals to malignant allow passage of water and electrolytes into hyperthermia and out of the cell -> cell damage Pathogenesis: intracellular defect in calcium metabolism Exertional myopathies (uptake, storage and release) caused by too much activities of the muscle mutation in the gene – localized C->T transition in the fibers gene that controls the calcium release channel or the e.g. equine rhabdomyolysis / azoturia / tying up ryanodine receptor 1 gene (RyR1) in cytoplasmic reticulum of skeletal muscle and this leads to the loss of Traumatic myopathies regulation of muscle cell calcium level due to trauma like crush injury that causes exacerbated by stress and physical activity damage result in hypersensitivity in the ryanodine tearing of muscle tissue due to excessive receptor which floods the myoplasm with stretching and surgical incision Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY calcium -> excessive muscle contraction -> 5. Downer Syndrome/ Downer Cow Syndrome hypermetabolism which develops very rapidly as ischemic necrosis of the ventral limb muscles a result of uncontrolled and sustained following prolonged recumbency (lower side) myoplasmic Ca -> excessive heat production animal has experienced paralysis after and ATP in that skeletal muscle will be depleted parturition due to excessive contraction -> increase in vicious cycle of weakness -> paresis/paralysis -> aerobic and anaerobic metabolism -> excessive more pressure on certain muscles -> injured production CO2 & lactic acid -> lactic acidosis + muscle is edematous -> occlusion of the blood increase temperature (due to metabolism) -> vessel -> ischemia -> injury -> weakness peripheral vasoconstriction -> rhabdomyolysis; dark areas of necrosis and hemorrhage death of the animal is due to increase in repair is possible on animals that survive, but potassium serum (main intracellular cation) that this may lead a scar of fibrous tissue will go to the bloodstream causing increased potassium level or hyperkalemia causes -> cardiac dysrhythmia -> cardiac arrest -> death muscle contraction ➔ ATP depletion ➔ lactate acidosis ➔ rhabdomyolysis ➔ cardiac dysrhythmia ➔ death MYOSITIS (Inflammatory Disease of the Muscles) What will happen to the muscle? 1. Bacterial myositides o Because of the denaturation of the sarcoplasmic result from introduction of bacteria by direct proteins brought by acidosis, this leads to the penetration (after injection), hematogenously movement of intracellular water to interstitium, (blood) or by spread from an adjacent cellulitis making the muscle exudative or wet in (inflammation of fatty tissues), fasciitis (fascia), appearance. tendonitis (tendon), arthritis (joint) or Lesions: osteomyelitis (bone) pale / wet muscles Pyogenic bacteria may cause a localized pulmonary edema suppuration and myofiber necrosis that causes rapid rigor mortis – develops when ATP direct insult to the muscle, leading to pus is depleted formation autolysis ✓ Streptococcus equi ✓ Archaebacteria 3. Monday Morning Sickness, Azoturia ✓ Corynebacteria associated with strenuous exercise after a long Clostridial myositis rest & carbohydrate rich diet (eating too much ✓ Gas gangrene is caused by Clostridium novyi without work) -> accumulation of carbohydrates infection that produce toxin that damages muscle weakness, reluctance to move, muscle (portal of entry: host tissues via recumbency, myoglobinuria, renal failure, penetration) acidosis and death ✓ Blackleg is caused by Clostridium chauvoei rapid utilization of glycogen (stored) -> that cause activation of spores that was accumulation of lactic acid due to anaerobic disseminated from GIT to muscles (portal of metabolism, alteration in protein structure, loss entry: ingestion) of water, interstitial edema, compressive Granulomatous myositides usually takes the circulatory disturbances, ischemia, form of a single or multiple granuloma which are degeneration, necrosis, myoglobinuria, tumor-like mass of nodules of granulation tissue myoglobulinemia with actively growing fibroblast and capillary muscles of extremities are swollen, edematous, beds. It may contain macrophages and bacteria dark involved clinical pathology: elevated creatine kinase and ✓ Tuberculosis AST ✓ Actinobacillosis (Actinobacillus) ✓ Actinomycosis (Actinomyces bovis) microscopic: segmental (Zenker’s) necrosis with ✓ Botryomycosis (low grade consistent little or no calcification infection with Staphylococcus aureus) 4. Capture Myopathy 2. Fungal granulomatous myositis acute, often fatal rare in animals preceded by a chase, struggle or transport of animal 3. Viral myositides hemorrhage and degeneration of muscles lesions are small, poorly defined, pale foci or extensive hemorrhagic muscles due to detached streaks tendon or struggle of the animal during chase or rough handling of the animal Notes by Roxie :)  VPTH 55 – SYSTEMIC VETERINARY PATHOLOGY result of infarcts due to vasculitis or multifocal Tumors of the Muscles necrosis due to direct effect of the virus on rare in vet med but common in lab animals myofibers neoplasia arising in muscle may include tumors examples are: from: o Porcine Encephalomyelitis virus o striated m. (rhabdomyoma, o FMD virus rhabdomyosarcoma) o Bluetongue virus o adipose cells (lipoma, liposarcoma) o fibrous connective tissue (fibroma, fibrosarcoma) o nerves (neurofibroma) o vascular cells (hemangioma, sarcoma) Blackleg. Clostridium chauvoei. Dark discoloration of Rhabdomyoma muscle tissue and subcutaneous tissue. benign Malignant edema. Clostridium septicum. Muscle is congenital black but may crepitate on palpation due to presence of most common in cattle, sheep and pigs gas. commonly found in the heart muscle Differences between blackleg and malignant edema: characterized pedunculated mass Myositis Cellulitis Edema Emphysema Rhabdomyosarcoma Blackleg +++ + ++ ++++