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2024_Lecture 5__skin_dzs.pdf

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Diseases of the Skin Swine Erysipelas Erysipelothrix rhusiopathiae Aetiology Erysipelothrix rhusiopathiae – Gram-positive bacillus. – Long survival in the environment (35 days in soil) Pork Cured hams Contaminated fish meal...

Diseases of the Skin Swine Erysipelas Erysipelothrix rhusiopathiae Aetiology Erysipelothrix rhusiopathiae – Gram-positive bacillus. – Long survival in the environment (35 days in soil) Pork Cured hams Contaminated fish meal Decaying carcasses – 26 SEROTYPES Swine susceptible to 15 – 1a, 2, 5 and 1b most associated with disease. Erysipelas Epidemiology Swine, sheep and turkey 30-50% of healthy swine are carriers. Occasionally poultry and wild birds Zoonotic Causes erysipeloid in humans Stressors ↑incidence of disease in animals Temperature (hot, sultry weather) Sudden changes to diet Chronic exposure to low aflatoxin levels in feed. Erysipelas Epidemiology. Colostral immunity lasts up to 3 months Subclinical infection may induce active immunity Susceptibility Pigs most susceptible between 3 months and 3 years Exposure to turkeys and sheep ↑ risk of infection Organism shed via Ingestion of contaminated feed and faeces and water / cuts&bruises oronasal secretions Entry via tonsils, or lymphoid tissue of digestive tract Bacteremia and dissemination throughout body Bacteria produces neuraminidase, cleaves mucopolysaccharides in cell walls which may mediate the widespread vascular damage. Vascular damage leads to thrombosis and disruption of microcirculation (capillaries and venules) Erysipelas Clinical Signs Acute, chronic or subclinical disease Acute – Animals approaching market weight Sudden death Pyrexia (104F) Reddened or cyanotic skin – Snout, ears, jowl, throat, ventral abdomen Rhomboid or diamond shaped lesions (pathognomonic) – More visible on white pigs – Not seen on all animals – ↑ severity of lesions → worse the prognosis Lameness – Joints swollen and painful on palpation. – Animals reluctant to stand – Feet close together Pregnant Sows – +/- abortions. Clinical Signs Chronic Cardiac Insufficiency Endocarditis resulting in valvular lesions Blue ear tips Exercise intolerance → respiratory distress → death Enlargement of Joints 3 months post infection lameness Differential Diagnoses Acute hog cholera Porcine Dermatitis and Nephropathy Syndrome Acute septicemia – salmonellosis, streptococcal infection. Actinobacillus suis – Similar skin lesions. Diagnosis Clinical signs Necropsy Acute – widespread congestion, petechial and ecchymotic haemorrhages Microthrombi and areas of focal necrosis Chronic – proliferative nonsuppurative arthritis Hock, stifle, elbow, carpus serosanguineous synovial fluid vegetative endocarditis Diagnosis Culture More likely to recover organism during acute disease Kidney, spleen, lymph nodes, blood, Chronic (joints) ** Failure to recover organism ≠ disease rule out. Molecular Method polymerase chain reaction (PCR) assay. Treatment/Prevention/Control Treatment Antimicrobials (for 3 days post last sick animal) Penicillin is drug of choice 30,000 IU/kg Twice per day in acutely ill animal Tetracyclines, tylosin also effective Hyperimmune serum Nothing works for chronic erysipelas Treatment/Prevention/Control Prevention and Control General sanitation Remove organic matter Disinfectants Hypochlorites Vaccination (bacterins, attenuated live) Duration of immunity 26 weeks. Breeding stock 2x per year. Young pigs @ 3 months and then 3 weeks later Additional reading Habte D, Tamir D, Tilahun T. Swine Erysipelas; It’s Epidemiology, Diagnosis, Treatment and Control and Preventive Measures, Comprehensive Review. Journal of Clinical Epidemiology and Toxicology. SRC/JCET-123. DOI: https://doi. org/10.47363/JCET/2021 (2). 2021;115:2-7 Exudative Epidermititis ‘Greasy pig disease’ Aetiology Staphylococcus hyicus – Identified as the causative agent in 1965 Sporadic disease – Occurs on most swine farms. Acute disease in piglets < 8 weeks old – Associated with piglet fighting Less severe form in older pigs Adults: Few localized lesions (rare). Epidemiology Only certain strains cause disease – Five exfoliative exotoxins that target cells of the stratum granulosum in the epidermis have been identified. – Predisposing factor required trauma, environmental irritation etc. Piglets ≈ 8 weeks affected – Morbidity is low (20%) – Mortality is dependent on age of onset and severity of signs. treatment Pathogenesis Focal erosion of stratum granulosum Lesions extend to hair follicles → suppurative folliculitis Increased secretion by sebaceous gland → greasy exudate over lesion Severe epidermal erosion and ulceration Death from septicemia and dehydration Clinical Signs. Listlessness, anorexia and gauntness Exfoliation of skin – Excessive sebaceous secretion – Brownish black maldodorous exudate – Matted hair → grey colour No pruritus generally seen Differential Diagnoses Zinc parakeratosis Swine pox Lice Mange Diagnosis Clinical signs Confirmatory diagnosis – isolation of S. hyicus (maybe normal skin flora)* – histopathology. Treatment, Prevention and Control Treatment – Antibiotics – Topical Antiseptic shampoos Clorox dips Diluted Iodine – Multivitamins/minerals (Vit E, Zinc) Control – Affected litters or individual pigs should be isolated immediately. – Mingling of pigs should be avoided if an outbreak has occurred. – Euthanize pigs with advanced lesions. Treatment, Prevention and Control Prevention – High standard of sanitation for pregnant sows washing of sows may be beneficial – Avoid skin trauma How? – Prophylactic vaccination Autogenous bacterin of S. hyicus results are hard to evaluate – No commercial vaccine available EE is sporadic and may not reoccur, regardless of vaccination. Additional reading Park J, Friendship RM, Poljak Z, Weese JS, Dewey CE. An investigation of exudative epidermitis (greasy pig disease) and antimicrobial resistance patterns of Staphylococcus hyicus and Staphylococcus aureus isolated from clinical cases. Can Vet J. 2013 Feb;54(2):139-44. PMID: 23904636; PMCID: PMC3552588. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552588/ Mange Sarcoptes scabei var. suis Epidemiology Prevalent in most swine herds globally Entry to herd is via asymptomatic carriers All age groups affected If swine are moved immediately into pens recently vacated by infested pigs – they are likely to become infested. Epidemiology Reduction in farrowing rates of up to 10% – 500 sow breeding unit 100 litters or 1100 less piglets. Reduced growth rates – 100gms/day from weaning to slaughter – Additional 30 days to age at 100 kg, – 42kg of additional feed required per pig https://www.nadis.org.uk/disease-a-z/pigs/sarcoptic-mange/ Aetiology Sarcoptes scabei var. suis – Responsible for the majority of mange cases in swine – All stages of the mite (ova, larvae, nymphs, adults) develop in the epidermis. – Life cycle is completed in about 10-l5 days. – Survival off the host variable Up to 21 days depending on environmental conditions – Species specific…. Demodex phylloides – Relatively unimportant in swine production – May cause dermatitis lesions on snout, inner thigh and flank Epidemiology Transmission – Spread is by direct body contact, Pen overcrowding Huddling of pigs for warmth/shade – Mites from the dam → neonatal piglets within a few hours of birth. Pathogenesis Mites burrow in epidermis Females lay eggs in epidermal tunnels Mites→ skin irritant→ pruritus Allergic hypersensitivity develops →↑ scratching intensity →↑ skin trauma Clinical signs Acute – Small plaque like lesions in inner ear Ear: site of initial colonization – Intense pruritus – Dermatitis on rump, flank and ventral abdomen Reddened macules and papules due to hypersensitivity reaction – Poor growth rate Poor FCR – +/- mites on skin scraping Chronic lesions – Mild pruritus – Thick crusty scabs: ear; head and neck – Mites present in large amounts. Clinical Signs Diagnosis Clinical signs Skin scrapings – mites in skin scrapings or in exudate from the external auditory canal. Scrapings from the inner surface of the ear usually reveal more mites Serology – ELISA Not widely available Slaughter surveillance Treatment and Control SPF pigs – Remember what these are? Topical acaricides – Amitraz; permethrin – 2-3x @ 14 day intervals Essential for proper skin contact time Systemic acaricides – Ivermectin and Doramectin Two injections given two weeks apart Biosecurity Mange Use of used car oil – Contains toxic ingredients – Kidney and liver damage – Accumulates in meat tissue – Passed on in the food chain Lice Haematopinus suis Aetiology Haematopinus suis – obtains blood meals from the host through its penetrating mouth parts. – Entire life spent on host The female louse lives about 23-30 days – lay 3-4 eggs (“nits”) per day » Attached to base of hair shafts » 1-2 mm long and light cream to gray in color. » They hatch in 12-20 days Survival off the host : limited (< 3 days) Epidemiology Host specific – can survive on humans for short periods Transmission – Via close contact between pigs – Environmental transmission (contaminated pens). Colonization sites – neck, jowl, flank, the inner side of the legs and ears. Often reside in “nests” in the inner ear Location within the ear offers lice protection from acarasicides Pathogenesis Lice pierce skin to ingest blood meal Skin irritation leading to Loss of blood dermatitis, scratching and - Anaemia in nursing piglets. hair loss Pigs are restless →lose Potential transfer of disease weight → ↑ FCR eg: African Swine Fever and Eperythrozoonis etc. Clinical Signs Similar to Mange – Pruritus Alopecia – Poor Growth and Feed Conversion – +/- anaemia Diagnosis Examination of skin lesions: – Neck, jowl, and flank lice and ova attached to the hair. Examination of the inner aspect of the ears – reveals the lice and sarcoptic mange lesions. Examination of the underside of pigs – Lice often are readily apparent on the posterior abdomen or on the inside surface of the legs. Treatment and Control Treat animals prior to herd introduction – preferably at least twice at two-week intervals, before being added to a herd. repeated treatment kills lice that emerge from eggs 12- 20 days after an initial treatment. – All chemicals used for mange are effective for lice Swine Pox Aetiology Poxviridae – Resistant to environmental degradation Persists in scabs for up to a year. Transmission – Introduced into skin abrasions. – Nasal and oral secretions from infected pigs. – Insect Vectors Hog louse (Haematopinus suis), mosquitoes, and biting flies – Evidence of transplacental infection of neonatal pigs. Outbreaks – Sporadic, Low morbidity and no mortality Clinical signs. Skin lesions Papules: Pustules: Crusts: Red from 1-6mm Ischemic, yellow Brown to black Recovery in 1 – 3 weeks. Diagnosis Clinical Signs Skin biopsy Control / Treatment and Prevention Treatment – Not warranted Prevent secondary infection Control – Herd immunity – prevention of transmission. Control of vectors of virus, – especially hog lice: insecticides... Congenital swine pox is – generally a sporadic, self-limiting event. Other Skin Lesions Shoulder Ulcers – Thin sows lying on hard rough floors may develop ulcers over the spine of the scapula – Contributing factors Poor body condition, Lack of adequate bedding or mats, Continually wet flooring Prolonged recumbency while farrowing or nursing piglets, Reduced activity because of confinement. Shoulder Ulcers. Lesions The ulcers are the result of pressure ischemia leading to skin necrosis over the spine of the scapula. – More severe during the three weeks after farrowing. Control measures Maintaining a higher level of conditioning (fat) in sows Ensure crates are of adequate size to allow frequent repositioning. Sunburn Excessive exposure to the ultraviolet rays of sunlight. – The white or light-colored breeds are more severely affected. – all age groups are susceptible Suckling and weanling pigs are most likely to be affected. The ears and back get more direct exposure to sunlight and often are more severely sunburned. – Clinical Signs Skin is reddened, edematous, hot, and painful. Affected areas later appear roughened and may peel. Limited reports of abortions associated with sunburn (PAIN?). – Treatment Keep out of sunlight Gradual exposure Provide shade Photosensitization Occurs only in areas of white skin. – Sunlight includes wavelengths that activate the photosensitization process. Photosensitizing agents – Alfalfa, clover, oats, rape, buckwheat, others). – Several common pharmaceuticals (phenothiazine, tetracyclines, sulfonamides, others) Photosensitization Clinical signs – Lesions tend to be more severe than with sunburn. – Exudation is followed by drying and fissuring. The lesions are pruritic. Skin necrosis with sloughing of severely affected areas often follows. – Conjunctivitis, sometimes with corneal opacity and temporary blindness, may accompany photosensitization. Treatment – Supportive – Avoid sunlight – Remove offending agent Biting Biting Aetiology: – Stressed, deprived or bored pigs Common areas affected – Tail biting – piglets/grower/finishing pigs – Flank biting – grower/finish – Vulva biting - adult females (group housing) – Ear sucking/ear biting – in nursery pigs – Penile sucking – newly weaned pig Common areas affected Treatment Remove affected animals – Topical wound treatment – Systemic antibiotics – Anti-inflammatory Flunixin or meloxicam Identify offending animal – Remove from herd Prevention and control Tail cutting – Avoid fluctuations in length Remove potential stressors – Check stocking density. – Feed Adequate feed space particle size (target> 500 µm). Check salt (NaCl) concentration in feed. – Water supplies Ensure adequate # of waters Prevention and control Remove potential stressors – Air quality (target - NH3 < 20 ppm H2S < 10 ppm and CO2 < 3000 ppm). – Temperature fluctuations (HEAT stress) – Reduce mixing pigs /moving of pigs. Facial necrosis associated with lactation failure Environmental enrichment – Any suggestions? The End Additional Slides Baby piglet anaemia Due to iron deficiency Sow’s milk inadequate source of Fe Piglet can become anaemic within 2 –3 days of birth There is GR, lethargy, pale skin and mucosa, dyspnoea, oedema, diarrhoea Baby piglet anaemia Haemoglobin < 6g / dL (normal 12 – 14 g/dL) Treatment / control - oral iron – unreliable absorption - injectable iron – at days 1 –3 after birth - give second injection if weaning after 3 weeks

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