Systemic Diseases

Label the clinically relevant anatomy of the bovine head

Bones

1. Mandible (*)

2. Maxilla (3)

3. Incisive (1)

4. Nasal (4)

5. Frontal (5)

6. Zygomatic (8)

7. Temporal (10)

8. Occipital (11)

Palpable Structures

1. Temporal line (5”)

2. Facial tuberosity (3’)

3. Infraorbital foramen (3”)

4. Nasoincisive notch (4’)

5. Mental foramen (2)

6. Zygomatic arch (8’)

7. Cornual process/horn (5’)

8. Ramus of mandible (14+)

3 Sinuses of the skull

1. Frontal (rostral + caudal → cornual process)

2. Maxillary

3. Palatine

Label the clinically relavent soft tissue structures of the bovine head

• Veins

• Arteries

• Nerves

• Muscles

• Salivary glands

• Lymph nodes

Veins

1. Linguofacial (18)

2. Facial (4)

3. Cornual (8)

Arteries

1. Common carotid (19)

2. Facial (10)

3. Cornual (8)

Nerves

1. Cornual (8)

2. Facial (5 and 6)

3. Infraorbital (9)

Muscles

1. Masseter (1)

2. Zygomaticus (2)

Salivary glands

1. Parotid (11)

2. Submandibular (12)

Lymph nodes

1. Parotid (13)

2. Lateral retropharyngeal (14)

3. Submandibular (20)

   • Palpable in healthy animal

Lingual fossa

Pocket between the torus and tongue which is a common site for sharp instruments to accidentally enter

Describe the deciduous and permanent dentition of cattle

• Deciduous: I 0/3 : P 0/1 : M 3/3

• Permanent: I 0/3 : C 0/1 : P 3/3 : M 3/3

• Eruption times important for aging and certain diseases

• Cattle graze using tongue to grasp pasture (mandibular incisors are not necessary)

Frontal Sinus Empyema

• 3 Aetiologies

• 5 Clinical signs

• 5 Treatments

Aetiologies: Secondary to

1. Dehorning → Open sinus formation

2. Trauma (fighting)

3. Respiratory disease (uncommon)

Clinical Signs:

1. Discharge form dehorning site

2. Nasal discharge (purulent/serosanguinous/epistaxis)

3. Exophthalmos (extension of infection to retrobulbar space)

4. Head tilt (extension to vestibular system)

5. Pyrexia (systemic illness when severe)

Treatment:

1. Sinus trephination

2. Sinus lavage

3. Systemic antibiotics

4. NSAIDs

5. ± Cosmetic dehorning = Skin flap OR occlude hole

   • Hope exposed bone and sinus hardens with granulation tissue to fill the defect in the frontal sinus

Woody Tongue

• Agent

• Aetiology and 3 causes

• Inflammation

• 4 Clinical signs

• 2 Methods of diagnosis

• 3 Treatments

Agent: Actinobacillus lignierseii

• Commensal oral bacteria that causes opportunistic infection due to mucosal trauma

Aetiology: Soft tissue trauma

1. Erupting teeth

2. Rough feed

3. Drenching injuries

Inflammation: Granulomatous swelling of the tongue, cheek, nasal passages

• Cutaneous actinobacillosis = Granulomatous lesions on ear, nose, cheek and oesophageal groove → Chronic, friable, non-resolving lesions

Clinical Signs:

1. Inappetence

2. Ptyalism

3. Firm/oedematous submandibular swelling NOT associated with bone

4. Tongue protrudes from mouth → Firm and painful ± ulcers/erosions

Diagnosis:

1. Clinical signs and response to treatment #1

2. ± Biopsy for atypical presentations

Treatment:

1. Streptomycin 3 - 4mL/100kg q24hr IM/SC

   • Aminoglycoside → Excreted in kidneys and cannot be used in food animals in USA (okay in NZ)

2. Sodium/potassium iodide (organic farms)

   • MoA: Breaks down granulomatous tissue to allow immune response to heal animal

   • Sodium iodide IV or potassium iodide PO in feed

3. NSAIDs

Lumpy Jaw

• Agent

• Aetiology

• Signalment

• 5 Clinical signs

• 3 Methods of diagnosis

• 4 Methods of treatment

• Prognosis

Agent: Actinomyces bovis

Aetiology: Eruption of cheek teeth → Allows bacteria to infiltrate and cause osteomyelitis (bone remodelling)

Signalment: 2 - 3yr

Clinical Signs:

1. Acute: Asymmetrical, firm swelling of jaw associated with bone (painful when early in disease)

2. Chronic: Deformed skull

3. Difficulty eating

4. Drooling

5. Weight loss

Diagnosis:

1. Clinical signs #1

2. Radiography

3. U/S

Treatment: As for woody tongue if caught early

1. Streptomycin

2. Sodium/potassium iodide

3. NSAIDs

4. Euthanasia if signs are severe (avoid pathological fractures and malocclusion)

Prognosis: Depends on severity (guarded to poor)

7 Structures around the jaw

1. Lymph nodes

2. Masseter muscle

3. Mandible

4. Salivary glands

5. Base of tongue

6. Nerves

7. Vessels

Nasal Catarrh

• Prevalence

• 2 Aetiologies

• Pathogenesis

• Signalment

• 4 Clinical signs

• Method of diagnosis

• 4 Treatments

aka. Atopic rhinitis, chronic granular rhinitis, bovine nasal granuloma, allergic rhinitis, stick granuloma

Prevalence: Extremely common in NZ

Aetiologies: Multifactorial

1. Chronic allergy (eg. pollen, mites, fungal spores) → Seasonal pattern

2. ± Infectious bovine rhinotracheitis (IBR)

Pathogenesis: Allergic rhinitis → Itchy nose → Stick foreign body in nasal cavity → Granulomatous inflammation

Signalment: Jerseys

Clinical Signs:

1. Swelling of nasal passages → Snuffling and loud breathing

2. Nasal discharge (serous → mucopurulent/bloody with foreign body)

3. Nodular lesions on mucosa (chronic)

4. Severe pruritis → Foreign bodies

Treatment:

1. Remove foreign body

2. Steroids? → Abortion of foetus

3. NSAIDs

4. ± Anti-histamine

5. Spontaneous resolution if caused by IBR

Oral Necrobacillosis

• Agent

• 2 Locations/forms

• Aetiology and 3 causes

• 5 Clinical signs

• 4 Methods of diagnosis

• 3 Treatments

Agent: Fusobacterium necrophorum = G+ anaerobe

• Causes MANY diseases ANYWHERE with existing trauma

Locations:

1. Necrotic stomatitis = Lips, tongue, cheeks

2. Calf diphtheria/necrotic laryngitis = Larynx and pharynx

Aetiology: Trauma

1. Aggressive tube feeding (soft ball at tip becomes sharp when grazed against sharp molars)

2. Poor hygiene

3. FPTi

Clinical Signs:

1. Inappetence/dysphagia

2. Halitosis

3. Cough

4. Progressive dyspnoea ± dysphonia

5. Pyrexia

Diagnosis: Clinical signs and response to treatment #1

1. Supported with bloodwork

2. Imaging

Treatment:

1. Early cases: High dose penicillin 30,000IU/kg IM/SC q12 - 24hr for 5 - 7d

2. NSAIDs

3. ± Emergency tracheostomy if dyspnoeic

Pharyngeal Trauma

• Aetiology and 3 causes

• 4 Clinical signs

• 4 Treatments

Aetiology: Iatrogenic → Infection with ANY bacteria (associated with adult cows)

1. Orogastric tubing

2. Drench administration

3. Bolus administration

Clinical Signs:

1. Ptyalism

2. Dysphagia

3. Swelling of throat/neck/face

4. Change in voice/coughing

Treatment:

1. Remove foreign bodies

2. Drain abscess

3. Systemic antibiotics

4. NSAIDs

8 Ocular DDx in cattle

1. Infectious bovine keratoconjunctivitis (pinkeye)

2. Bovine uveitis and keratoconjunctivitis (silage eye)

3. Squamous cell carcinoma (cancer eye)

4. Entropion

5. Inherited bilateral cataracts (BVD in-utero infection)

6. Blindness

7. IBR = Conjunctivitis ± corneal opacity

8. MCF = Marked scleral congestion and keratitis

9. Foreign body

Infectious Bovine Keratoconjunctivitis

• Agent

• Signalment (age)

• 3 Predisposing factors

• Transmission

• 6 Clinical signs

• Method of diagnosis

• 4 Treatments

• 4 Methods of prevention

aka. Pinkeye

Agent: Moraxella bovis (G- bacilli)

• Pathogenicity depends on presence of pili and haemolytic enzymes

  • Pili = Projections on the bacterial wall which allow adhesion to the corneal surface and penetration through the intact corneal epithelium

  • Bacteria without pili and haemolysins carried asymptomatically → Change to pathogenic strain under different conditions (eg. concurrent IBR or increased levels of UV radiation)

• May be complicated by viral infection (eg. IBR and Mycoplasma bovis)

Signalment: Younger stock at higher risk

Predisposing Factors:

1. Dust

2. Flies (vector of infection)

3. UV rays (summer #1)

Transmission: Highly contagious (direct OR indirect contact eg. flies)

Clinical Signs: Uni- or bilateral (eg. NH3 toxicity due to overstocking → bilateral)

1. Blepharospasm

2. Epiphora → Periocular alopecia due to discharge and rubbing

3. Corneal oedema (keratitis) and neovascularisation

4. Corneal ulceration (circular and central) and potential rupture with iris prolapse

5. Conjunctivitis

6. Photophobia

Diagnosis: Clinical signs, history ± cytology or culture of conjunctival swab

• Corneal ulceration of multiple stock

Treatment:

1. Topical cloxacillin (Orbenin eye ointment) q48hr to BOTH eyes

2. Systemic antibiotics (oxytetracycline/penicillin)

   • Severity determines dose

   • Avoid subconjunctival as irritating

3. NSAIDs ± steroids

4. Protect eye from further damage

   1. 3rd eyelid flap or tarsorraphy for severe ulcers

   2. Eye patch

Prevention:

1. Ear tags impregnated with permethrin to prevent flies

2. Vaccination with Piliguard to prevent outbreaks (variable response do the different strains) 3 - 6w prior to risk period → Booster q1yr

   • Vaccination stimulates Ab production against bacterial pili → Prevents bacterial adhesion to the cornea

3. Reduce dust exposure

4. Quarantine affected animals (ocular discharge = source of infection)

Function of the 3rd eyelid flap

Prevent rupture of corneal ulcers by protecting globe from UV light and trauma

Bovine Uveitis and Keratoconjunctivitis

• Agent

• 4 Clinical signs

• Method of diagnosis

• 3 Treatments

Agent: Listeria monocytogenes

• Poorly preserved silage

• Affects ENTIRE eye (vs. pinkeye = just anterior portion)

Clinical Signs: Uni- or bilateral

1. Epiphora

2. Blepharospasm

3. Corneal oedema

4. Photophobia

Diagnosis: Clinical signs and history of silage ingestion

Treatment:

1. Topical cloxacillin (Orbenin eye ointment)

   • Topicals have poorer penetration and cannot feasibly be given q2hr to cattle in paddocks

2. Subconjunctival/systemic antibiotics (oxytetracycline/penicillin) or dexamethasone (overseas)

3. NSAIDs (± steroids)

Cancer Eye

• MPI regulations

• 3 Treatment options

Regulations: Cannot transport cows with cancerous lesions of eye if

1. Lesion >2cm

2. Bleeding or discharging material

3. Evidence of spread to orbit or lymph nodes

Treatment: Mild cases

1. Cryotherapy

2. Surgical removal of 3rd eyelid

3. Exenteration = Removal of globe and ALL surrounding structures

Ocular surgery in cattle

• 3 Indications

• 4 Example surgeries

• 4 Types of local blocks

• Additional drugs

• Surgical scrub

Indications:

1. Treat pinkeye

2. Remove SCC lesion

3. Ruptured globe/trauma

Examples:

1. Temporary tarsorrhaphy (3rd eyelid flap)

2. 3rd eyelid removal

3. Local mass removal

4. Enucleation/exenteration

Blocks:

1. 4-point retrobulbar

2. Auriculopalpebral

3. Line block/local infusion

4. Peterson block

Drugs:

1. NSAIDs

2. ± Antimicrobials

Scrub: Dilute iodine (betadine)

• Avoid chlorhexidine/alcohol → Irritation and damage to cornea

3 DDx for blindness in cattle

1. Hypovitaminosis A

2. PEM

3. Lead toxicity

List 7 specific anatomic features of the bovine respiratory tract

1. NOT athletes

2. Narrowed trachea (~30% narrower than a horse)

3. Fewer alveolar capillaries and macrophages

4. More segmented anatomy

   • Lack of Pores of Kohn = Collateral ventilation to allow communication between adjacent alveoli

5. More sensitive to histamine (lung = shock organ)

6. Healing via fibrin and abscess formation

7. Larger RIGHT lung volume than left (rumen occupies left)

Which lung lobe has highest risk of aspiration pneumonia? Why?

Tracheal bronchus = Supplies the cranial RIGHT lung lobe

• Dependent (ventral) in standing animal

• Cranial portion of cranial lung lobe (in front of the heart)

• Caudal portion of the cranial lung lobe (behind heart)

5 Features to assess on URT examination

1. Tracheal and laryngeal palpation (abnormal: cough on palpation)

2. Auscultate over trachea

3. Auscultate over nasal passages

4. Percuss sinuses (abnormal: dull/pain → sinusitis)

5. Examine nares for discharge, bilateral airflow, ozena, foreign bodies/material

5 Abnormal LRT sounds (+ Cause)

1. Crackles = Opening of collapsed alveoli

2. Wheezes = Narrowing bronchioles

3. Friction rubs = Fibrinous inflammation of pleural surface rubbing

4. Absent/muffled sound = Congestion, pulmonary consolidation, abscess, pleural effusion

5. Expiratory grunt

List 8 further diagnostics tests which can be performed for respiratory examination

1. Rebreathing examination = Allows for deeper inspiration and evaluation of collapsed airways

2. U/S = Visualise surface of lungs for pleural effusion, congestion, consolidation, abscesses if present near the surface

3. Radiography = Calves for distribution of lung pathology (NOT practical for adult cattle on farm)

4. Nasal swab = Diagnosis of acute viraemia (NOT helpful for bacteria)

5. Transtracheal wash = Culture/cytology

6. Bronchoalveolar lavage = Cytological evaluation of inflammatory airway disease

7. MDB = Presence of inflammation, poor gas exchange or electrolyte abnormalities

8. Serology = Confirmation of infectious systemic diseases (eg. BVD)

3 Types of pneumonia

• Definition

• Distribution

• Subtypes

1. Bronchopneumonia = Bacterial with predisposing viral aetiologies

   • Distribution: Cranioventral

   • Types: Consolidation, abscessation, fibrinous adhesions

2. Interstitial pneumonia = Non-infectious, toxic, hypersensitivity, parasitic

   • Distribution: General/diffuse → Rib impressions

   • Types: Interstitial oedema, emphysema, fibrosis

3. Embolic/metastatic = Septic embolic, abscess, granulomatous

   • Distribution: Multifocal associated with vessels

3 Risk factors for respiratory disease (+ examples)

1. Season

   • Change in weather

   • Large swings in temperature (eg. warm day → cold night)

   • Allergens and fungal spores

   • Types of feed available (eg. dusty)

2. History

   • Trucking/transport (shipping fever)

   • Yarding = Dry and dusty environment

   • Oral drenching

   • Mixing cattle from different groups

   • Movement onto new pasture

   • Immunosuppression/stressful events

3. Age/Signalment

4 Reasons why pneumonia is LESS common in NZ

1. Extensive pastoral management

2. Temperate climate

3. Lack of housing and reduced intensity of management

4. Fewer feedlot

Massive issue overseas due to association with significant use of metaphylactic antibiotics

Aspiration Pneumonia

• Aetiology

• 3 DDx in calves

• 4 DDx in adult cattle

• 7 Clinical signs

• 2 Treatments

• Prognosis

Aetiology: Individual cow disease due to aspiration of saliva, fluids, rumen contents, oral medication

Calves:

1. Tube feeding

2. Faulty bottles/nipples

3. Oral Drenching

Adults:

1. Lateral recumbency (eg. milk fever and GA)

2. Bloat/choke

3. Oral drenching

4. PKE

Clinical Signs: Severity depends on contents aspirated (volume, type of material and bacteria involved)

1. Acute death (large volumes)

2. Severe pneumonia and toxaemia (caustic feeds with high bacterial load)

3. Dyspnoea and tachypnoea

4. Feed/material observed coming from nose

5. Fever within hours

6. Auscultation = Cranioventral crackles, pleuritic friction rubs and dullness

7. ± Chronic suppurative bronchopneumonia with survival of acute stage

Treatment:

1. NSAIDs

2. Broad-spectrum antibiotics 5 - 7d

Prognosis: Poor

3 DDx for interstitial pneumonia

1. Fog fever (acute bovine pulmonary oedema and emphysema)

2. Farmer’s lung (hypersensitivity pneumonitis/diffuse fibrosing alveolitis)

3. Verminous pneumonia

Fog Fever

• 5 Sources of toxin

• Seasonality

• MoA

• 7 Clinical signs

• 2 Methods of diagnosis

• Treatments

Sources: Change from poor quality → Lush and rapidly growing forage within 5 - 10d

1. Lush pasture

2. Lucerne

3. Kale

4. Turnips

5. 4-ipomeanol in mouldy sweet potatoes causes the same syndrome

Seasonality: Autumn (foggy) and aftergrowth from recently cut silage

MoA: Pneumotoxic metabolite → Acute Bovine Pulmonary Oedema and Emphysema

1. L-tryptophan → Indole-acetic acid → 3-methylindole by rumen microbes (Lactobacillus)

   • Peak 4 - 5d and drops off after 6 - 7d

2. 3-methylindole in blood → Lungs

3. Activation of pneumotoxic metabolite (3-methyleneindolenine) by type II pneumocytes (Clara cells) → Cellular damage and necrosis of type I pneumocytes (required for gas exchange)

4. Proliferation of type II pneumocytes

5. Decreased gas exchange surfaces and thickened septa with interstitial oedema

Clinical Signs: 4 - 5d after ingestion

1. Sudden tachypnoea and expiratory dyspnoea

2. Reluctance to move and weakness

3. Auscultation = Respiratory grunt and occasional soft crackles

4. Normothermic

5. Orthopnoea = Head extended, nostrils dilated, open-mouth breathing and elbows abducted

6. Subcutaneous emphysema may occur with rupture of bulla

7. Acute deaths or within 1-2 days

   • 30 - 50% morbidity

   • 30% mortality

Diagnosis: History of exposure to lush feed or diet change with sudden respiratory signs →

1. Measure L-tryptophan in feed

2. PM examination = Heavy wet lungs with foam in trachea and interlobular oedema/emphysema

3. Histology of lungs = Interstitial pneumonia

Treatment:

1. Remove from feed if <5d (care to avoid exertion → sudden death)

2. Frusemide to enhance water elimination

3. NSAIDs

Prevention:

1. Provide supplemental feed to prevent large intake of pasture

2. Graze pastures with cattle <15 months (less susceptible)

3. Monensin/ionophores 200mg/cow/d begun a few days prior to movement onto lush pasture → Reduced production of 3-methyl-indole in rumen

Farmer’s Lung (hypersensitivity pneumonitis/diffuse fibrosing alveolitis)

• Pathogenesis

• 5 Clinical signs

• Diagnosis

• 2 Treatments

Pathogenesis: Type III hypersensitivity reaction to dust and mould in grain/hay

Clinical Signs: Acute and chronic forms

1. Frequent coughing

2. Increased RR and effort

3. Auscultation = Diffuse crackles and squeaks of mucus

4. CHF due to pulmonary fibrosis (pulmonary hypertension)

5. BAR and normothermic

Diagnosis: History and clinical signs → Eosinophilia

Treatments:

1. Steroids

2. Cull

Bovine Tuberculosis

• Aetiology

• 5 Modes of transmission

• Pathogenesis

Aetiology: Mycobacterium bovis

• Aerobic, non-spore forming bacilli with acid-fast cell wall → Enables growth at low pH

• Facultative intracellular pathogen which survives in macrophages by inhibiting phagosome-lysosome fusion

• Survives well in environment, faeces and pasture

• Natural host = Cattle

• Other hosts = Humans (5% of human TB), swine, carnivores, deer, possum, ferret ± sheep

Transmission: Inhalation (± oral)

1. Major NZ reservoirs: Infected cattle and possum

   • Cow ⇔ cow

   • Cow ⇔ possum = most important route in NZ (responsible for many TB breakdowns)

2. Cow → calf

3. Possum → possum

4. Cow → pig (through ingestion of cow milk/mild serum)

5. Predators/scavengers, spillover hosts and sporadic transmitters: Ferrets, pigs, wild deer, cats

Pathogenesis:

• Ineffective CMI and weak humoral response due to intermittent, low-intensity antigenaemia

Methods of bovine TB diagnosis

• Method

• Advantages

• Disadvantages

1. Direct microscopy of smears from lesions with Ziehl-Neelsen stain

   • +ve: Low cost

   • -ve:

     1. Low DSn and DSp

     2. Must have externally affected lymph node

2. Culture from lesion

   • +ve: Gold standard

   • -ve:

     1. Slow growth (≤12w)

     2. Some TB lesions may be sterile → Culture multiple lesions

3. Histology at PM = Caseous granulomatous lesions (poor DSp)

4. PCR

   • +ve: Fast

   • -ve: Lower DSn than culture

5. Tuberculin skin test = #1 AM diagnostic test for eradication and surveillance

   • Method: Intradermal injection of M. bovis PPD (purified protein derivative) that elicits delayed (type IV) hypersensitivity reaction in MOST infected animals

     • Caudal fold injection for cattle in NZ (cervical in some countries)

     • Cervical fold injection for deer

   • Positive Test: Lump at injection site 72hr post-injection

   • -ve:

     • DSn: Imperfect due to false negatives due to…

       1. Recent TB infection (CMI not detectable for ~30 days post-exposure)

       2. Individual-animal anergy (no immune response) in advanced TB usually due to old age

       3. Occur in % of cows up to 6 weeks post-calving

     • DSp: False positives due to…

       1. Cross-reactivity (non-specific sensitisation with other mycobacteria such as Johne’s infection or vaccination) OR other factors

       2. Up to 40 - 50 days after previous intradermal tuberculin skin test?

          • Desensitisation = Animal’s skin reactivity to tuberculin is reduced for some time after the skin test

   • Comparative intradermal test = TWO intradermal injections with M. avium and M. bovis PPD at least 15cm apart on lateral neck

     • Read after 72 hours (skin fold thickness difference measured using tables)

       • M. bovis PPD > avian PPD = Reactor animal

       • Avian PPD ≥ M*. bovis* PPD = Non-reactor (due to false-positive)

     • +ve: Distinguish infected from false-positive due to previous M. bovis PPD test

     • -ve: Must wait between 42 - 60 days from first intradermal test to for desensitisation to wane (if another injection is administered too soon after the first without sufficient time for the animal’s immune system to recover, it can result in failure to react)

6. Interferon gamma assay = Rapid, blood-based assay of cell-mediated immunity for the diagnosis of bovine TB infection

   • Test rationale: When exposed to M. bovis, infected animals produce more IFN-ɣ from lymphocytes

   • Test principle: Measures amount of IFN-ɣ released by lymphocytes from whole blood sample after overnight incubation with added M. bovis PPD COMPARED with control

     • NOT a serological test (tests CMI)

   • +ve: Do NOT need to wait 60 days from last tuberculin skin test

   • -ve:

     1. No international consensus about test performance (vs. intradermal test)

        • Increasing use in UK to release comparative intradermal cervical tests

     2. High cost

4 Methods of bovine TB control (+ vaccination)

1. Test and slaughter

2. Animal movement restrictions

3. Action on wild reservoirs (depopulation)

4. THREE negative herd tests over ≥2 yrs → TB-free status

TB VACCINE

NOT used because:

1. Effectively delays clinical disease onset but does NOT reduce infection prevalence

2. Vaccine interferes with intradermal testing

List 7 important blood vessels in a cow

1. Aorta and caudal vena cava

2. Internal and external iliac arteries + iliac veins

3. Coccygeal vein + artery = Tail blood sample

4. Pudendal artery and perineal artery

5. Superficial epigastric vein (aka. milk veins) = Supplying and draining udder

6. Cornual vein and artery

7. Carotid arteries and jugular vein = Blood sample or IV injections

List 7 clinical signs of cardiac dysfunction

1. Dull, weak, lethargic and painful

2. Low BCS, weight loss and decreased appetite/production

3. Brisket oedema due to vascular congestion → Increased hydrostatic pressure + force of gravity

4. Elevated jugular pulse >1/3 - 1/2 up neck

   • Physiological = Occlude top of jugular vein and wipe blood into heart → Cording SHOULD disappear

5. Jugular cording = Distension/congestion of vein

6. Jugular fill = Volaemic status

7. Increased RR

Endocarditis

• Prevalence

• Aetiology

• 3 Agents

• Pathogenesis

• History

• 5 Clinical signs

• 3 Methods of diagnosis

• Prognosis

• Treatment

Prevalence: Sporadic and under-reported in adult cattle

Aetiology: 2˚ bacterial infection of heart valves due to haematogenous spread of septic emboli from primary bacteraemia caused by

1. Rumenitis

2. Metritis

3. Pneumonia

4. Liver abscess

Agents:

1. Trueperella pyogenes

2. Streptococcus spp.

3. E. coli

Pathogenesis: Insufficiency/stenosis of heart valves

• Right AV » Left AV > Semilunar valves

History: ± Previous history of bacterial infection

Clinical Signs:

1. Weight loss and depression

2. Intermittent pyrexia

3. Heart murmur ± palpable thrill

4. Intermittent positive Wither’s pinch test

5. Signs of RCHF (30 - 50%)

Diagnosis:

1. CBC and biochemistry

   • ± Inflammatory leukogram (inconsistent)

   • ± Elevated globulin and fibrinogen (inconsistent) + liver enzyme elevation in terminal RCHF

2. U/S = Vegetative lesions on AV valve (R > L)

3. PM findings

Prognosis: Poor to grave depending on timing of diagnosis due to pulmonary or coronary blockages (eg. pulmonary infarcts)

Treatment: Sustained treatment with antibiotics for 4 - 6 weeks

• Common to relapse within 7 days after treatment stops

• Sudden death or acute collapse during treatment common due to myocardial/pulmonary infarcts

• Do NOT attempt with signs of CHF present

4 Aetiologies of myocardial disease (+ 3 - 4 example DDx)

1. Myocarditis

   1. Bacterial = Staphylococcus aureus, Clostridium chauvoei, Histophilus somi

   2. Viral = FMD

   3. Parasitic = Toxoplasmosis, cysticercosis, sarcocystis

2. Cardiomyopathy

   1. Se/vitE deficiency → White muscle disease

   2. Chronic copper deficiency

   3. Inherited DCM in Holstein-Friesians and Australian polled Herefores

3. Neoplasia = Lymphoma (EBL)

4. Toxicity

   1. Yew (Taxus spp.) = Taxine alkaloids → Neurological signs and acute cardiac failure

   2. Oleander (Nerium oleander) = Oleandrin = Cardiac glycoside

   3. Rhododendron (Rhododendrons spp.) = Grayanotoxin → ONLY causes of vomiting in ruminants

   4. Ionophores (lasolocid and monensin) → Free radical cytotoxicity of cardiac and skeletal muscle

3 Congenital cardiac defects (+ clinical signs)

1. Ventricular septal defect = #1 congenital cardiac defect in large animals

   • Clinical signs: Depends on size of defect = Clinically normal → Sudden death

     1. Sudden death

     2. Failure to thrive

     3. Harsh heart murmur (bilateral)

        • Grade ≠ severity

     4. Palpable thrill through chest wall

2. Patent ductus arteriosus (PDA) = Failure of closure of ductus arteriosis at birth

   • Often with other defects

   • Clinical signs:

     1. Exercise intolerance

     2. Lethargy

     3. Continuous machinery murmur L > R

3. Atrial septal defect or patent foramen ovale

   • Signalment: Common in calves often with PDA

   • Clinical signs:

     1. Asymptomatic

     2. Left heart base murmur

List the 4 important forelimb nerves and 5 important hindlimbs nerves (+ supply)

Brachial plexus = C6 - T2

1. Median

2. Radial

3. Ulnar

4. Common digital

Lumbosacral plexus = L4 - S2

1. Obturator

2. Femoral

3. Sciatic

4. Peroneal/tibial

5. Common digital (axial and abaxial)

Most common neurological DDx for:

1. Neonates

2. Juveniles

3. Adults

Neonates = Hypocalcaemia, congenital defects, bacterial meningitis

Juveniles = Toxin exposure

Adults = Abscess, trauma, metabolic disorders

List 10 DDx for cerebral disorders

1. Polioencephalomalacia (PEM)

2. Lead toxicity

3. Salt/water toxicity (see pigs)

   • Calves = Improper mixing of calf milk replacer

4. Bacterial meningitis

5. Nervous ketosis and hepatic encephalopathy

6. Hypomagnesaemia

7. Sporadic bovine encephalomyelitis (SBE)

8. Malignant catarrhal fever (MCF)

9. Trauma/abscessation

10. Nervous coccidiosis

Polioencephalomalacia (cattle AND sheep)

• Aetiology and pathogenesis

• Signalment

• 4 Causes

Aetiology/Pathogenesis:

1. Thiamine deficiency

   • Thiamine is a rate-limiting cofactor for transketolase (involved in production of ATP required for the NA/K ATPase pump in neurons)

2. No ATP available to pump Na+ out of cell via Na/K ATPase pumps

3. Na+ accumulates in neurons → Osmosis

4. Acute cerebral oedema and laminar necrosis

5. Visual cortex at the caudal aspect of the cerebrum is squashed

Signalment: Recently weaned calves/lambs ± adults

Causes:

1. Altered rumen microbes (produce thiaminases eg. Bacillus spp.)

   • Recently weaned calves (1 - 2 animals affected)

   • Sudden change in quality/quantity of feed within 7 - 10d

   • Adult ruminant with anorexia (concurrent illness)

2. Bracken fern toxicity (contains thiaminases)

3. Thiamine analogues (eg. amprolium = coccidiostat)

4. Sulphur toxicity (eg. high S in soils and water)

8 Clinical signs of polioencephalomalacia

1. Central blindness

   • Palpebral and PLR present

   • Menace response absent

   • Nystagmus

2. Staggering and incoordination

3. Dehydration and poor rumen fill

4. Head-pressing and depressed mentation

5. Lateral recumbency and opisthotonus (star-gazing)

6. Dorsomedial strabismus when head is elevated (normal = ventrolateral strabismus)

7. Seizure

8. Death

Polioencephalomalacia

• 2 Methods of diagnosis

• 4 Treatments

• 2 Methods of prevention

Diagnosis: History and clinical signs (rule out other DDx eg. exposure to lead)

1. Response to treatment #1

2. PM = Laminar necrosis of the grey matter

Treatment:

1. Thiamine (vitB1) IV = Aggressive/early high dose @ 10mg/kg → 5mg/kg IM q6 - 12hr for 3 - 5d

2. NSAIDs

3. Rumen transfaunation (0.5L for calf and 5L for ow)

4. Fluid therapy if dehydrated

Prevention:

1. Reduce sudden dietary changes

2. Avoid brassicas on high sulphur soils

Lead toxicity

• Sources

• MoA/pathogenesis (+ 3 outcomes)

Sources: Paint, lead shots, sinkers, batteries and soil

• Small amount absorbed through GI → Excreted in bile, faeces, urine, milk, sweat and saliva

MoA:

1. Curious calves experience the world orally

   • eg. lead batteries or paint

2. Lead rapidly absorbed through GI

Outcomes:

1. Disruption of heme synthesis → Basophilic stippling and nRBC (dogs)

2. Capillary damage, neuronal necrosis, demyelination and altered neurotransmission → Neurological signs

3. GIT signs of irritation

3 Clinical signs of lead toxicity in cattle (vs. dogs)

Cattle (3 - 4d duration)

1. Sudden death in calves

2. CNS (as for PEM):

   • Staggering, bellowing, chomping

   • Fine fasciculations around muzzle and nose

   • Blindness, opisthotonus, head-pressing and seizures

3. GI: Hypersalivation, ruminal atony, bruxism, abdominal pain, diarrhoea, anorexia, dehydration

Dogs

1. CNS signs

2. GI: vomiting, diarrhoea/constipation, anorexia

5 Methods of lead toxicity diagnosis

History of lead exposure and clinical signs →

1. LONGER response to thiamine supplementation (vs. PEM)

2. Blood smear = nRBCs and basophilic stippling with no regenerative signs (DOGS)

3. Measure lead in whole blood (heparinised tube), liver, kidney or bone

   • Pb > 0.35 - 0.5mg/L

4. Radiography to detect lead foreign body

5. PM findings are non-specific → Collect brain for histology (cerebral lesions indistinguishable from PEM)

   • MAY find paint flakes in rumen

Treatments for lead toxicity

1. Remove lead from GI where possible

2. Antidote (chelation) = Ca-EDTA 110mg/kg slow IV EOD x3 or D-penicillamine

3. Treat cerebral oedema and seizures with hypertonic IVFT and diazepam

4. Thiamine supplementation

5. ± Gastroprotectants

Prognosis of lead toxicity

Depends on age and amount ingested

• Clinical signs improve in 2 - 3d of treatment

• Blindness may persist up to 3w

• Slower response than PEM as lead → necrosis (vs. PEM → Cerebral oedema)

Salt/water toxicity in cattle (vs. pigs)

• 3 Causes

• 2 Methods of diagnosis

• 3 Treatments

• 3 Methods of prevention

Causes:

1. Improperly mixed milk replacer

2. Incorrect electrolyte use (eg. adult formulation given to calves)

3. Bottle feeding water at weaning

Diagnosis: History and clinical signs (iatrogenic) →

1. Serum [Na] > 170mmol/L

2. PM findings as for PEM ± gross congestion of omasal and abomasal mucosa

Treatments:

1. Prevent free water consumption (minimise water available)

2. Isotonic/hypertonic electrolytes PO to gradually transition back to water

   • Isotonic 0.9% NaCl

   • Mannitol 20% 1 - 2mg/kg IV for cerebral oedema

3. Thiamine supplementation

Prevention:

1. Educate client on milk replacer formulation

2. Frequent monitoring of water sources

Bacterial meningitis

• Aetiology (+ 4 agents)

• 2 Predisposing factors

• 4 Clinical signs

• 2 Methods of diagnosis

• 5 Treatments

• Prognosis

Aetiology: Common sequela of ascending naval infection and bacteraemia

• Agents:

  1. E. coli

  2. Klebsiella

  3. Salmonella

  4. H. somni (adults)

  5. ± SBE (Chlamydia pecorum)

Predisposing Factors:

1. FPTi

2. Poor hygiene → Navel infection/neonatal diarrhoea

Clinical Signs:

1. Depression, collapse, coma, death

2. Pyrexia

3. Seizures

4. ± Concurrent systemic infection

   • Navel/joint ill and scours

   • Endotoxaemia/SIRS → Injected scleral vessels and petechiae

Diagnosis:

1. Evidence of systemic infection

2. CSF tap → Bacteria and inflammatory cells

Treatments:

1. Aggressive penicillin, ampicillin or TMPS → Penetrate into CSF and effective against most pathogens

   • Most AB penetrate due to inflammation of the BBB

   • G- → 3rd/4th gen cephalosporins

2. NSAIDs

3. IVFT

4. Parenteral nutrition

5. Anti-convulsive therapy

Prognosis: Fair (suckling) otherwise guarded to poor

Sporadic Bovine Encephalomyelitis

• Aetiology

• Signalment

• 5 Clinical signs

• Treatment

Aetiology: Chlamydophila pecorum

• Usually abortion, pinkeye and venereal diseases in sheep

Signalment: Calves <6m (multiple calves)

Clinical Signs:

1. Depression

2. Weakness and hindlimb ataxia

3. Urinary incontinence and poor tail tone

4. Opisthotonus

5. Blindness

Treatment: Highly effective oxytetracycline q48hr x2

List 2 DDx for cerebellar disorders

1. Cerebellar hypoplasia (congenital BVD)

2. Ryegrass staggers (see “Alternative Forages”)

→ Incoordination, hypermetria and intention tremours

• Assess coordination, gait and tremours

Cerebellar Hypoplasia

• Aetiology

• Signalment

• 6 Clinical signs

Aetiology: In utero infection with BVDV 60 - 180d of gestation

• Unknown herd BVD status

Signalment: Single neonate <7d

Clinical Signs: Present at birth

1. Recumbent

2. Strabismus and horizontal nystagmus

3. Reduced PLR

4. Tremours and convulsions

5. Ataxia

6. Torticollis and opisthotonus

List 4 DDx for brainstem disorders

1. Listeriosis

2. Otitis media/interna (Mycoplasma bovis)

3. Trauma

4. Facial paralysis syndrome (FPS)

→ Head tilt, circling/leaning, vision/hearing/balance deficits, facial asymmetry/paresis/paralysis, ataxia/vestibular signs (nystagmus)

Listeriosis (cattle AND sheep)

• Agent

• Pathogenesis

Agent: Listeria monocytogenes = G+ facultative anaerobe

• ZOONOTIC!

Pathogenesis:

1. Soil contamination or poor quality silage (pH > 5)

2. Proliferation of Listeria monocytogenes

3. Tooth eruption or oral wounds allows ascending infection along the trigeminal nerve (CN V) to the brainstem

4. UNILATERAL microabscessation of mid-brain = CN V, VII, VIII and IX

Listeriosis

• Signalment

• 6 Clinical signs of the encephalitic form

• 4 Other manifestations

• 5 DDx

Signalment: Single animal ± outbreak

Clinical Signs:

1. Changes in mentation

2. ± Pyrexia

3. Unilateral CNS deficits = Head tilt, dropping ear, eyelid, unable to close eye, facial asymmetry, dysphagia

   • Assess angle of eyelashes

4. Circling

5. Recumbency

6. Death

Other Manifestations:

1. Abortion

2. Silage eye (anterior uveitis = vascular engorgement, blue corneal opacity, no ulceration and less severe conjunctivitis than pink eye)

3. Septicaemia (neonates)

4. Enteric form (rare)

DDx:

1. Brain abscess/meningitis

2. Neoplasia

3. Trauma to facial nerve

4. Otitis media/interna

Listeriosis

• 2 Methods of diagnosis

• Prognosis

• 4 Treatments

Diagnosis: History and clinical signs →

1. CSF tap = Monocytosis

2. PM = Multifocal abscessation of the brainstem around the cranial nerve nuclei

CBC and biochemistry unrewarding

Prognosis: Good (standing) but poor if recumbent

Treatment:

1. Procaine penicillin high dose BID x4

2. Oxytetracycline IV once → IM/SC EOD x4

3. NSAIDs

4. Fluids and good quality feed

Otitis media/interna

• Aetiology

• 5 Clinical syndromes

• 3 neurological signs (+ signalment)

• Diagnosis

• 3 Treatment options

Aetiology: Mycoplasma bovis (no cell wall) → Otitis media/interna

Syndromes:

1. Mastitis

2. Arthritis

3. Polyserositis (neonatal calves)

4. Pneumonia (older calves)

5. ± Late-term abortion or premature birth

Clinical Signs: Calves < 6m

1. Unilateral head tilt and ear droop

2. ± Ocular/nasal discharge = Keratoconjunctivitis

3. Depression and decreased appetite

Diagnosis: Call MPI (under surveillance) →

1. Fresh and fixed samples

2. Culture ± serology

Treatment: Labelled against Mycoplasma

1. Tulathromycin

2. Gamithromycin

3. Enrofloxacin

Facial Paralysis Syndrome (FPS)

• Aetiology

• Signalment

• 5 Clinical signs

• Treatment

• Prognosis

Aetiology: Unique to Franklin in NZ

• Linked to usage of slag by-product for fill in sheds/tracks → High levels of vanadium = toxicity

Signalment: Calves 1 - 3m

Clinical Signs:

1. Unilateral/bilateral facial paralysis

2. Mild transient fever and depression

3. Respiratory discharge and mucopurulent occulonasal discharge

4. Infection of periodontal tissue and tooth loss + jaw deformity

Treatment: ONLY for 2˚ infection

Prognosis: Spontaneous recovery in 70% (takes ≤8w)

• Remaining 30% have continued signs:

  1. Continued ptyalism

  2. Reduced GR

  3. Persistent facial nerve dysfunction

  4. 2˚ bacterial infections

List 6 DDx for spinal cord disorders

1. Vertebral body osteomyelitis after navel ill

2. Associated with mineral deficiency (vitD, Ca, Cu) affecting vertebral bodies

3. Ankylosing spondylitis

4. Spinal tumours

5. Verminous meningoencephalomyelitis

6. Iatrogenic

   • Epidural anaesthesia

   • Segmental spinal anaesthesia (eg. paravertebral anaesthesia)

   • Regional nerve blocks

Tetanus

• Aetiology

• 4 Predisposing factors

• 7 Clinical signs

• 5 Treatments

Aetiology: Clostridium tetani = Saprophytic G+ anaerobe

• IP = 10 - 14d (longer if further away from spinal cord)

• External wound contaminated with spores → Germination → tetanospasmin and tetanolysin

Predisposing Factors:

1. No vaccination

2. Castration, external wounds/punctures, disbudding/dehorning

3. After yarding/transport (bruising)

4. ± Dystocia or rumenitis

Clinical Signs:

1. Muscle stiffness = Opisthotonus and extensor spasticity

2. Mild bloat

3. Anxious facial expression (sardonic grin) with erect ears, lock jaw and prolapse of 3rd eyelid

4. Sawhorse stance

5. Hyperaesthesia

6. Tail held in pump handle position

7. → Collapse, respiratory failure, convulsions and death

Treatment:

1. Tetanus antitoxin (TAT) 10,000 - 20,000 units half IV and half IM

   • Often equine origin

   • Binds free toxin ONLY (does not affect bound toxin)

2. Antibiotics against G+ anaerobes = Procaine penicillin 30mg/kg IM BID 5 - 10 days (off-label)

3. Anticonvulsant/spasmolytic

4. Emergency rumenotomy to correct bloat

5. Fluids and feeding

List 3 neurological DDx which are exotic to NZ

1. Bovine spongiform encephalopathy

2. Rabies

3. ± Botulism (not reported in NZ)

Bovine Spongiform Encephalopathy (BSE)

• Aetiology

• Signalment

• 5 Clinical signs

Aetiology: Prion disease acquired through ingestion of ruminant-derived protein

Signalment: 2 - 8yr (highest incidence 4 - 6yr)

• IP = Long

Clinical Signs:

1. Change in behaviour (aggression/depression)

2. Ataxia

3. Tremours/twitching/hyperexcitability

4. Recumbency

5. Wasting/low production

List 3 other DDx for PEM (+ how to distinguish)

1. Lead toxicity

   • ± PLR (may be absent)

     • PEM = PLR and palpebral present

   • GI irritation

   • Slow response to thiamine supplementation

2. Salt/water toxicity = PEM (assess history)

3. Meningitis

   • Fever

   • Systemic infection (eg. hypopyon)

EXAMPLE QUESTIONS: NO ANSWERS PROVIDED

1. You see a calf showing signs of blindness, lateral recumbency and opisthotonus

   1. Which part of the nervous system is likely involved?

   2. List 3 differential diagnoses for the signs listed above. Chose one of these DDx and explain the pathophysiology

2. Discuss how you would differentiate a calf with PEM versus Lead Toxicity on clinical examination or through diagnostic testing

3. What are clinical signs associated with cerebellar disease?

4. What viral infection may cause in utero brain pathology?

5. A farmer has reported he has had to euthanise 3 R2 Friesian heifers due to broken legs in the past week. What mineral deficiency is associated with spontaneous humeral fractures in cattle?

What other body system should always be considered with neurological DDx

Musculoskeletal (difficult to distinguish)

List 7 congenital MSK diseases

1. Contracted flexor tendons

   • Treatment: Splint and physiotherapy ± surgical tenotomy

2. Angular limb deformities

   • Multiple calves = Toxicity or deficiency in utero (eg. Crooked Calf Disease = Lupin toxicity of pregnant dam → Arthrogryposis, torticollis and kyphosis)

3. Arthrogryposis = Joints seized and curled)

4. Polydactyl/syndactyl

5. Amelia/hemimelia

6. Myostatin mutation = Belgian Blue double muscle

7. Myotonia congenita = Fainting goats

List 4 infectious MSK diseases (+ causes)

1. Septic arthritis (DDx = Fractures)

   • Neonates = Carpus/hock/stifle/vertebrae (neonates) 2˚ to navel ill

     • Treatment: High dose antibiotics, NSAIDs ± joint lavage → Euthanasia

   • Adults = Deep digital sepsis 2˚ to WLD/ulcer

     • Treatment: Claw amputation or euthanasia

2. Osteomyelitis/physitis

   • Causes:

     1. Haematogenous

     2. Fracture complication

     3. Actinomycosis (Lumpy Jaw)

3. Clostridial myositis (aka. Blackleg or Malignant Oedema)

   • Case: 2˚ to vaccination or bruising

4. Suppurative discospondylitis

List 3 inflammatory MSK diseases (+ aetiology)

1. Degenerative joint disease

   • 2˚ to congenital dysplasia (OCD, deformation, trauma)

2. Osseous sequestration

   • Bone fragment loses blood supply after trauma/infection → Necrotic fragment acts as a foreign body → Abscessation and periosteal reaction

3. Ischaemic myopathy (aka. compartment syndrome)

   • Complication of prolonged recumbency (Downer Cow Syndrome) → Increased CK and AST

What is this?

• Aetiology

• Signalment

• Clinical sign

• Treatment

Bovine Spastic Paresis = Unilateral/bilateral increased muscle tone/permanent spasm of the gastrocnemius ± quadriceps

Aetiology: Heritable and progressive neuromuscular disease of the gastrocnemius, quadriceps and nerves

Signalment: ALL breeds

Treatment: Surgical neurectomy or tenectomy

Fractures

• 4 Traumatic Causes

• 3 Predisposing factors

Traumatic Causes:

1. Running into fences and fighting → Cervical spine

2. Misadventure and calves stepped on by cow → Limbs

3. Tail break

4. Knocked down hip → Fracture to tuber coxae

Predisposing Factors:

1. Pathological fractures 2˚ to osteomyelitis

2. Copper deficiency (± Mo excess) → Enzootic swayback in deer and humeral fractures in heifers

3. VitD deficiency (esp. fodder beet) → Rickets/osteodystrophy

Treatment of fractures

1. Closed fracture distal to carpus/tarsus

2. Closed fracture of tibia/radius/ulna

3. Closed fracture proximal to stifle/elbow

4. Open fracture

1. Closed fracture distal to carpus/tarsus = Immobilisation and restricted movement (good response)

   • External fixation (eg. cast or splint above and below affected joint)

   • Phalangeal fractures → Use block to elevate healthy claw

2. Closed fracture of tibia/radius/ulna = Thomas Schroeder splint

   • More difficult to immobilise with higher risk of complications

3. Closed fracture proximal to stifle/elbow = Surgical fixation, amputation or euthanasia

   • -ve: Ruminant cortical bone is thinner than other species with higher risk of sepsis, osteomyelitis and neurovascular damage

4. Open fracture = ≥10 - 14d antibiotics

   • Fracture heals in 4 - 6w

   • Neonates → Change bandage q2 - 3w to prevent pressure necrosis from growth

Soft Tissue Trauma

• Aetiology

• Causes

• 4 Example diseases

• Prognosis

Aetiology: Any ligament, tendon or muscle strain/rupture/trauma → Dysfunction

Causes: Fighting, restraint in foot crush, falling/struggling

Examples:

1. Cruciate disease

2. Patellar luxation/upward fixation

3. Gastrocnemius rupture → Cannot extend hock (collapsed)

4. Peroneus tertius rupture

Prognosis: Difficult to repair due to massive size and lack of hardware

5 Types of superficial trauma (+ definitions)

1. Seroma = Fluid-filled swelling, non-painful, normal temperature and sterile (diffuse hypoechoic on U/S)

2. Haematoma = Blood-filled swelling, may be painful and sterile (flocculant on U/S)

3. Abscess = Consequence of poor aseptic technique when performing FNA of swelling

4. Bursitis = Inflammation of the synovial structures around bony points ± pain

5. Predator attacks = Calves, small ruminants and pet pigs

   • Crushing injuries often get worse before they get better

List 3 nutritional deficiencies causing MSK disease

1. VitE/Se deficiency = White muscle disease

2. Copper deficiency

3. VitD deficiency (fodder beet low in P) = Rickets

List 2 parasites causing MSK disease

1. Sarcocystis spp. = Protozoal parasite that encysts in smooth muscle and striated muscle

   • Usually asymptomatic but occasional clinical cases of myositis and myocarditis

2. Taenia (Cysticercus) ovis = Sheep measles in sheep and goats

Tissues cysts at slaughter → Incidental finding but carcass condemnation

6 History questions to cow with diarrhoea

1. Onset: Acute, subacute, or chronic?

2. How many animals affected? One age group or multiple?

3. Any clustering, different herds?

4. Additional signs besides diarrhoea?

5. Recent management or feed changes?

6. Any sick workers?

ALWAYS consider Salmonella first until proven otherwise (#1 cause of adult diarrhoea)

List 8 DDx for adult cow diarrhoea

1. Salmonella

2. Johne’s Disease

3. Mucosal Disease (MD)

4. Malignant Catarrh Fever (MCF)

5. Parasites = Liver Fluke/Rumen Fluke

6. Winter Dysentery

7. Dietary/Toxic/Minor causes

8. Theileria

Agents of salmonellosis

• Common and important

  1. Typhimurium (enteric)

  2. Bovis-morbificans (enteric)

• Transmitted from sheep

  1. Hindmarsh (enteric)

  2. Brandenburg (abortions in South Island)

• Rare and unusual

  1. Montevideo

  2. Newport

• Exotic to NZ (present in AUS and AUK): Dublin

• Emerging strain: Give (since 2019)

Increased variability of Salmonella strains over time BUT dropped back dramatically in last 3 years

• Increased prevalence of salmonellosis overtime

3 Presentations of salmonellosis and clinical signs

• Peracute = Septicaemia and death

• Acute = Enteritis/dysentery, bacteraemia and pyrexia

• S. Brandenburg and S. Dublin (exotic) → Abortion

• Chronic = Diarrhoea ± dysentery, weight loss and inappetence → Carrier state

• S. Bovismorbificans

  • Calves: 58.2% morbidity and 27.7% mortality

  • Adults: 8.5% morbidity and 1.6% mortality

Salmonellosis

• Transmission

• 5 Sources of infection

• 3 Risk factors

Transmission: Faecal-oral

Sources: Persists in environment

1. Carrier/chronically infected animals (≤15% cows)

2. Contaminated PKE, water and pasture

3. Fomites

4. Vectors (eg. wild birds, rodents and vets)

5. Aborted material (sheep)

Risks:

1. Shedding precipitated by stress (eg. transport and mixing)

2. Diet change → Change in gut pH and microbiome

3. Pelletised magnesium oxide → Increased GI pH → Reduced dose of ingested Salmonella required to cause disease

Salmonellosis

• 3 Treatments

• 4 Methods of control

Treatments:

1. Antibiotics = Oxytetracycline and potentiated sulphonamides (consider carrier status, resistance and drug selection)

   • Whole herd antibiotic treatment may be required (eg. milk powder)

   • Avoid fluoroquinolones and ceftiofur

2. Fluids (oral equipment must stay on farm to prevent spread)

3. NSAIDs for sick animals

Control:

1. Reduce stocking rate → Reduce spread of infection

2. Isolate infected or aborting cows

3. Prevent contamination of feed/water supplies

4. Vaccination of calves with Salvexin B

   • Calf infection is inevitable unless switch to milk powder → Begin prophylactic antibiotic oxytet powder in milk and begin vaccination from 2 weeks of age

   • Timing:

     • 1st year = Sensitiser ≥ 6 weeks before risk period → Booster 4 weeks after (≥2 weeks before risk period)

     • Annual = Booster ≥2 weeks before risk period

Mucosal disease (MD) vs. Malignant catarrhal fever (MCF)

Feature	MD	MCF
Age
Other cases
Pyrexia
Sheep contact
Nasal/eye signs
Lymph nodes
Skin lesions
CNS signs

Feature	MD	MCF
Age	15–18 months	Any
Other cases	Likely	Sporadic
Pyrexia	No	Yes
Sheep contact	No	Yes
Nasal/eye signs	Rare	Common
Lymph nodes	Normal	Enlarged
Skin lesions	No	Yes
CNS signs	No	Possible

Winter Dysentery

• Definition

• Agent

• Signalment

• Treatment

• Prevention

Definition: Acute, apparently contagious, foul-smelling enteritis occurring during colder months of the year

• High morbidity and low mortality

Agent: Likely coronavirus

Signalment: Housed cattle

Treatment: Supportive (fluids ONLY)

Prevention: NONE

Yersiniosis

• Agent

• Risk factors

• Transmission

• Clinical signs

• Treatment

• PM findings

• Histological findings

Agent: Yersinia pseudotuberculosis

• Common isolate of intestinal tract healthy ruminants

Risk Factors:

1. Wet and cold weather → Survival of Yersinia on pasture

2. Poor feeding

3. Parasites

4. Mineral deficiencies

Transmission: Faecal oral

Clinical Signs: High morbidity and low mortality (chronic > acute)

1. Diarrhoea ± blood/mucus

2. Poor growth, stunting or wasting

• NOT pyrexia

Treatment: Oxytetracycline

PM: Fluid intestinal contents and external evidence of diarrhoea

• Characteristic multifocal, ulcerative enterocolitis

• Microabscessation of mucosa with lots of G- coccobacilli

4 Types of wasting (empirical approach)

1. Ingestion = Cannot/will not eat

2. Digestion/absorption

3. Assimilation = Efficient use of absorbed nutrients

4. Excretion = Excessive protein loss from the body

Ingestion → Wasting

• 2 Methods of diagnosis

• 4 DDx for “cannot eat”

• 9 DDx for “will not eat”

Diagnosis:

1. Observe for quidding = Dropping food from mouth while chewing cud

2. Push grass into mouth and see if cow will chew and swallow

Cannot Eat:

1. Teeth = Heifers changing teeth OR old cows losing teeth

2. Tongue = Woody tongue/damage/ulceration

3. Swallowing/chewing = CN V/VII, trauma to jaw/lumpy jaw

4. Oesophagus = Stricture/blockage/foreign body

Will Not Eat:

1. Unpalatable diet

2. Uraemia

3. Ketosis (LDA, RDA, fat cow syndrome)

4. Toxic (mastitis, metritis, peritonitis)

5. Pyrexia

6. Pain (lameness, abomasal ulcers)

7. CHF

8. Chronic infection (tuberculosis, MCF)

9. Hydrallantois (DDx for abdominal distension and wasting)

9 DDx for poor digestion/absorption → wasting

1. Chronic traumatic reticuloperitonitis

2. LDA (or RDA)

3. Vagal indigestion

4. Actinobacillosis of reticulum/rumen

5. Chronic Salmonellosis

6. Johne’s disease

7. Intestinal leukosis/tumours

8. Villous atrophy post-enteritis (calves)

9. Post-acidosis rumen damage

List 4 causes of poor assimilation of nutrients → wasting (+ example DDx)

1. Nutritional imbalance

   • Chronic hypomagnesaemia (Taranaki anaemia)

   • Cobalt deficiency (Bush sickness)

2. Trace element deficiency

   • Cu deficiency

   • Mo excess

3. Liver damage

   • Cirrhosis post-FE or ragwort

   • Abscesses post-navel ill/acidosis

4. Chronic poisoning

   • Lead

   • Ragwort

Causes of protein loss → wasting

• 3 Kidney DDx

• 2 Bladder DDx

• 6 Intestine DDx

Kidneys

1. Amyloidosis

2. Pyelonephritis

3. Haematuria/haemoglobinuria

Bladder

1. Tumour

2. Cystitis

Intestine

1. Johne’s disease

2. Chronic salmonellosis

3. Worms and liver fluke

4. Melaena

5. Abomasal ulcers

6. Mycotoxins

List 7 important skin diseases of cattle

1. Photosensitisation (facial eczema and spring eczema)

2. Parasites (see “Parasitology”)

   1. Lice

   2. Mites

   3. Ticks

3. Ringworm

4. Warts

5. Dermatophilus

6. Pseudolumpy skin disease

7. MCF

3 Types of photosensitisation (+ examples)

1. Primary = Direct ingestion of photodynamic compounds

   • eg. Spring eczema = St John’s Wort, Ngaio, Alligator weed, Musky Storksbill

2. Secondary = Facial eczema, ragwort toxicity, leptospirosis

   • ± Rape scald, turnip toxicity, HR swedes (glucosinolates)

3. Congenital eg. Bovine congenital porphyria

5 Reasons why facial eczema is so important

1. Major animal welfare concern (esp. lifestyle blocks or naive farms → clinical cases)

   • Sporadic disease = Worse in some years and highly seasonal → Vets and farmers can become complacent and be caught out in a bad FE season

2. ~$500M/yr lost in production

3. Underestimated and ignored (sparse research in last 20yr)

4. Climate change will significantly extend risk of FE throughout NZ

5. Occasional cases of Zn toxicity and potential for residues in soil/animal products

Aetiology of Facial Eczema

• Agent

• Region

• Seasonality

• 4 Risk factors

Agent: Sporidesmin mycotoxin produced by spores of Pseudopithomyces chartarum

• Saprophytic fungi which grows on dead litter at the base of pasture

Region: North Island ± top of South Island

Seasonality: Jan - May (esp. Feb - April)

Risk Factors:

1. Weather = Fungus requires warm, moist, humid conditions for growth

   • 100% humidity

   • 4 consecutive warm nights >12˚C

   • Small amount of rain (~4mm) 48hr apart → Triggers sporulation

2. Forage Type = Densely-growing grass with lots of dead litter at the base

   • eg. Ryegrass, cocksfoot, browntop

   • Clover, chicory, plantain and brassicas safe

3. Grazing Conditions = Hard grazing → Spores more concentrated at base of sward

   • Warm sheltered paddocks or areas within paddocks (eg. sheltered gullies) = Higher risk vs. colder (south-facing) or very windy paddocks

4. Animal Factors = Genetic susceptibility

Describe the pathogenesis of facial eczema

1. Fungus makes toxin in mycelium

2. Toxin concentrates in spores at sporulation

3. Animal ingests sporidesmin spores while grazing

4. Toxin released from spores into rumen (water-soluble) and absorbed into bloodstream

5. Toxin removed by liver and kidneys → Concentrates in bile duct (10x) and urine

6. → Release of free radicals which damage lining of bile ducts and bladder

   • ONE molecule of sporidesmin can create many free superoxide free radicals

     • Glutathione reduces disulphide bridge of sporidesmin toxin

     • O2 reoxidises bridge → Formation of superoxide free radical

     • Cyclical

7. → Cholestasis and cystitis

8. Occluded bile ducts cannot eliminate waste products from chlorophyll metabolism (phylloerythrin)

9. Phylloerythrins build up in bloodstream and react with sunlight in non-pigmented skin and mucocutaneous junctions

10. → Photosensitisation

Diagnosis of facial eczema (vs. spring eczema)

Biochemistry = Marked increase in GLDH, GGT and hyperbilirubinaemia

• vs. Spring eczema = Rare liver damage

Clinical signs of facial eczema

• Onset

• 5 Early clinical signs

• 3 Late clinical signs

• 2 Chronic clinical signs

Onset: 2 weeks spore exposure

Early:

1. SC oedema and erythema

   • Sheep = Face and ears with no wool cover → Floppy ears

   • Cattle = White patches, vulva and teats (most noticeable in afternoon milking)

2. Acute liver damage = Depression, inappetence and drop in milk production (~0.14kgMS/d)

   • Hunched due to liver damage and visceral pain

3. ± Transient diarrhoea

4. Shade-seeking (photophobia) and irritation

   • Kicking at udder (DDx: Colic)

5. ± Haemolysis with haemoglobinuria and anaemia

Late:

1. Decreased eating and BCS/weight (not grazing in sun)

2. Solar dermatitis

   1. Eyelids glued shut due to damage

   2. Damaged skin peels

   3. ±2˚ bacterial infection

3. Severe = Anorexia and death

Chronic: Cirrhosis → Cannot reverse clinical signs as liver already damaged

1. ± Reduce production during physiological stress periods

2. ± Neoplastic keratoma transformation of skin lesions

How is photosensitivity the “tip of the iceberg” in sheep?

5% of sheep with visible clinical signs → ≥50% of sheep have liver damage

• Many beef cattle (eg. black Angus) do not show clinical signs due to dark pigment BUT liver damage still occurs