TV4101 - Bovine - Nervous Part 2 - Weaned Calves and Older cattle

Listeriosis

Most common manifestation in AUS?

Prevalence?

Meningo-encephalitis

Sporadic in cattle mainly 2-3yrs

Listeriosis

Pathogenesis?

1. Soil contaminated feed most important route of infection (many ass. with silage feeding esp with poor fermentation/conserved)

2. L. Monocytogenes invade oral cavity mm → Trigeminal Nerve (CN V) → Cerebrum

3. Focal necro with microabscesses → neuritis, meningitis and encephalitis

Listeriosis

CX

Vary based on?

Most common neurological signs?

Location of lesions within cerebrum (which CN affected)

- localised facial paralysis with head tilt towards the affected side

- circling

- ‘propulsive tendency’ → may be found with head forced through a gate or wedged under a feed bunk

Listeriosis

CX

Non-neuro signs?

Mod Pyrexia (Early stages only and gone <96hrs)

Weight loss, dec milk prod, depressed, anorexic

What is this? Describe each

Listeriosis

Left - Head tilt, and circling towards affected side

Right - Unilateral facial paralysis

Several syndromes are associated with L. monocytogenes

infection in cattle - Including?

- uterine infections (abortion)

- meningo-encephalitis

- mastitis (rare)

- septicaemia, and iritis with uveitis

What is this?

Listeriosis

Unilateral facial paralysis

Listeriosis - CX

Infection involving ganglia of the facial nerve (CN VII) signs?

Unilateral facial paralysis, characterised by:

- drooped ear & eyelids (ptosis)

- a flaccid lip

Can lead to loss of both menace response and palpebral reflex → 2ndary exposure keratitis

Listeriosis - CX

Infection involving ganglia of the vestibulocochlear (CN

VIII) nerve signs?

• leads to ataxia, head tilt, and circling

• in later stages, affected cattle become recumbent; may show opisthotonos and torticollis before death

Listeriosis - CX

Other uncommon presentations?

Which nerve is affected?

Involvement of glossopharyngeal nerve (CN IX) may cause stertorous breathing and dysphagia

Listeriosis DX

Main DDX?

- brain stem abscess

- pituitary abscess syndrome (basilar empyema)

- otitis media/interna

- trauma

- less commonly confused diseases include PEM, lead poisoning, nervous ketosis, thrombo-embolic meningo-encephalitis (Histophilus somni infection)

Listeriosis DX

CX for encephalitic form?

Circling, with depression & facial paralysis, is almost

pathognomonic for the encephalitic form of the disease

Listeriosis PM

MS findings?

Lesion location?

Organism isolation?

What is sufficient to confirm Dx?

MS

• In cerebrum - Many micro-abscesses or foci of inflam cells (Sufficient to confirm Dx usually)

Lesions usually unilateral

Isolation of causal organism from the brain may require

extended periods of ‘cold enrichment’, and listerial culture

can prove disappointing

Listeriosis Tx

ABs?

Penicillin or aminopenicillins

• BID with high dose rates for at least 7 days

• Addition, give high dose of penicillin G i/v on first day

Oxytet?

Listeriosis Tx

Supportive therapy?

- NSAID → for the inflammation

- IV fluids & electrolytes → to treat the dehydration & metabolic acidosis

Listeriosis Tx

Rumen aid?

Transfaunation with rumen liquor may promote rumen

function during recovery

Listeriosis - PX

Soil contamination of silage is limited by?

Rolling grass fields at the beginning of the growing season

Listeriosis - PX

We want good silage fermenting.

How do?

- cutting grass at an early growth stage → contains a high fermentable sugar content

- wilting it for 24 hours

- using various silage additives (sugars or organic acids)

- compacting of the silage clamp → expels air

- covering it, making sure it has a tight seal → prevents aerobic bacterial multiplication

What is this?

Botulism

Botulism

Overview?

Ascending motor neuro-paralytic disease caused by ingestion of pre-formed toxins released by Clostridium botulinum bacteria

Botulism

Agent and features?

Cl. botulinum – a large Gram positive rod-shaped bacillus

• Very resistant bacterial spores

• Endospores germinate (with growth of vegetative cells and toxin production) in anaerobic conditions (rotting carcass, decaying plants, cont canned food)

Botulism

Outbreaks in livestock are

generally divided into two categories, what are they?

1. situations where disease occurs in cattle that develop

osteophagia (bone chewing) or sarcophagia (carrion

eating) → associated with phosphorus deficiency or

protein deficiency, respectively

2. death of a large number of animals in a short period of

time → associated with the ingestion of toxic feed or

water

Botulism clinical findings

Oft presented as?

Multiple ‘down cows’ with some evidence of progressive muscular weakness → initial response to Ca treatment (hypocalcaemia), but have relapsed

Botulism clinical findings

Peracute disease – classical intoxication

Features?

• high levels of toxin formed outside of the victim’s body are

ingested in contaminated feed (silage or grain)

• sudden death in previously normal animals → usually with 24 hrs of exposure

Botulism clinical findings

Acute and subacute forms

Features?

Asc para → recumbency

Early classic signs → flaccid paralysis of tongue and muscle ass. with chewing and swallowing (Tongue protruded)

Muscles of jaws and throat are affected before those of limbs; hindquarters before forequarters

Botulism - Toxico-infectious botulism

How it works?

Fatality?

Occurs when?

1. Cl. botulinum spores in normal GIT from environmental cont

2. Altered gut conditions → growth of vegetative stage → toxin prod

Death isn’t a certain outcome

Often occurs during droughts or during cases of K deficiency

Botulism CX continued

As the disease progresses?

restlessness, stumbling, knuckling over, shallow abdominal breathing, and constipation

Prog weaker and dehydrated → sternal recumbency

Muscle tone loss in neck and head → head on ground or turned to flank

Skin sensation is retained, and consciousness continues

almost to the end

Botulism DX

Early signs are often confused with?

Post-parturient paresis (‘downer-cow’ syndrome), hypocalcaemia, hypokalaemia, myopathy, organophosphate poisoning, or spinal cord disease

Botulism DX

Tests?

ELISAs, measuring antibody to Type C and D toxins in

serum

Botulism TX

Treatment is only warranted in subacute cases:

- initial objective is the neutralisation of circulating toxin → specific

mono-valent or multi-valent botulinum antitoxin

- feasible, but rarely used in cattle

Botulism PX

• Assess silage and grain stores for risk

• Remove carcases from paddocks and dams

• Supplement with Phosphorous

Botulism Control

Vaccine (best way)

• single dose, bivalent (Type C & D) vaccine

  → protects naïve cattle for 2 (SingVac® 2 Year) or 3 years (SingVac® 3Year)

Thrombo-embolic Meningo-encephalitis (TEME)

Agent? What does it do?

Histophilus somni infection; bacteria localize in meninges, brain, muscles and joints

Thrombo-embolic Meningo-encephalitis (TEME)

Prevalence?

Worldwide but oft in US feedlots

• 1-2 wks after H. somni resp dz episode that is untreated

Thrombo-embolic Meningo-encephalitis (TEME)

Other syndromes associated with H. somni infection include?

- respiratory disease

- reproductive disease & abortion

- myocardial & joint infections

Thrombo-embolic Meningo-encephalitis (TEME)

CX

Positional changes of animal?

Unsteady gait & stance, knuckling of fetlocks, becoming

progressively ataxic

Oft found in lat or sternal recumbency in an

obtunded state (~stupor) with muscle tremors, and sometimes convulsions

Thrombo-embolic Meningo-encephalitis (TEME)

CX

Ocular aspects?

Nystagmus may be present; animals may be blind in one or both eyes

Ocular lesions consist of foci of retinal haemorrhages and

accumulations of exudate → appear as ‘cotton tufts’

Thrombo-embolic Meningo-encephalitis (TEME)

Parameters?

Jts?

Dz characterised by?

Fever (40.5-41.5oC) in the early stages

Joints may be swollen and painful (acute synovitis)

Characterised by acute onset, rapid course, high fatality rate

Thrombo-embolic Meningo-encephalitis (TEME) - PM?

• Fibrinopurulent meningitis

• Red/brown foci of haemorrhage & necrosis

(infarcts) throughout brain & spinal cord → virtually

pathognomonic

What is this?

TEME

Thrombo-embolic Meningo-encephalitis (TEME) - Management

Treatment should only be initiated in?

Drugs?

The early stages (depression, ataxia, circling), i.e. before cattle become recumbent

Penicillin, florfenicol and oxytetracycline

Thrombo-embolic Meningo-encephalitis (TEME) - Management

Appropriate management and husbandry practices for

prevention of respiratory disease should be put in place

“Can you name some ??”

?

Tetanus

Agent? Features?

Clostridium tetani bacteria that makes toxin with nervous tissue affinity

• Stab wounds, deep puncture wounds with tissue damage (→ anaerobic conditions), and those cont with soil/faeces are most likely to lead to tetanus

• May be present as a localised wound infection originally

Tetanus

In cattle, most cases are associated with?

Other portal of entry?

Castration, tail docking, dehorning, or uterine infection following abortion/calving

Umbilicus of the newborn calf

Tetanus

Pathogenesis steps?

1. Bacteria enter wound → anaerobic conditions → germinate in host tissue → mutliply and make tetanus neurotoxin

2. Neurotoxin spreads → local motor nerves → spinal cord (now cx seen)

Tetanus

Idiopathic tetanus is thought to arise when?

Certain conditions in reticulorumen → small pop of Cl. tetani normally present multiply → make enough toxin to cause dz

Tetanus - CX

Facial Changes?

Anxious, startled expression with bulging eyes, and erect ears

Flared nostrils

Protrusion of the nictitating membrane (not as prominent in cattle c.f. horse)

Drooling saliva

Tetanus - CX

Behaviour changes?

What the earliest signs in general?

Animal is hyperaesthetic → sudden noise or touch induces

spasm

Eating & drinking soon become difficult or impossible →

tetany of masseter muscles (‘lockjaw’)

Earliest sign is a slight muscular stiffness (10-14d PI)

Tetanus - CX

Stance changes?

Head is held lowered, with the neck extended

Animal stands rigidly → has difficulty in walking & turning

Abducted limbs (sawhorse stance)

Tail is held cocked away from the hindquarters, giving a

‘pump handle’ appearance

Tetanus - CX

Other changes?

Final stages?

Slight, but persistent rumen tympany (bloat)

Final stages → lateral recumbency, with severe tetanic

spasms, often accompanied by opisthotonos

Tetanus - TX

Mortality rate of affected, untreated cattle is around?

TX involves 3 steps, what are they?

60%

Neutralisation of the toxin

Prevention of further toxin production

Relaxation of muscle tetany

Tetanus - TX

1. Neutralisation of the toxin

How to do?

Principle?

Tetanus antitoxin given

• Dose varies - 1000-5000 IU/kg BW

Neutralises toxin (only if it hasn’t bound to nerve tissue yet) in early stages of dz

Tetanus - TX

2. Prevention of further toxin production

How to do?

Local wound treatment, including debridement (controversial)

• H2O2 irrigation

• Local penicillin

• Sys ABs (Penicllin - 30,000 IU/kg BID for 3d → OID until at least 2d after spasms stopped)

Tetanus - TX

3. Relaxation of muscle tetany

How to do?

In addition?

Use of a tranquilliser and/or muscle relaxant (chlorpromazine or acetylpromazine)

• acetylpromazine (0.05 mg/kg q8h) ideally

  • Dec hyperaesthesia AND activates some inhibitory pathways that are refractory to toxin effects

Additional TX

• Severe bloat relief via rumen trocar

• Cases in single dark deep bedded sheds

Tetanus PX

Active immunisation, using tetanus toxoid (can be carried out at any age)

• Long lasting protection

• Two vaccinations, 4-6 wks apart

• Multi-valent clostridial vaccines usually include a tetanus component

What this?

Nervous coccidiosis

Nervous Coccidiosis

Onset of nervous signs is usually (but not always) proceeded by?

Initial neurological signs include?

Dysentery and tenesmus

- depression

- incoordination

- twitching & hyperaesthesia

Nervous Coccidiosis

As condition worsens?

• Recumbent

• Periodic head and muscle tremors

• Nystagmus

• Mouth frothing

• Paddling movements

• Ventroflexion of head and neck

• Opisthotonos

Nervous Coccidiosis

DDX inc?

- polioencephalomalacia

- lead poisoning

- acute meningitis

- salt poisoning

- hypovitaminosis A

- clostridial enterotoxaemia (Cl. perfringens)

Cerebral Babesiosis

May occur from?

CNS are varied, some inc?

Babesia bovis infections

- hyperaesthesia

- nystagmus

- circling

- head pressing

- aggression

- convulsions & paralysis

Cerebral Babesiosis

TX?

No TX, Cerebral babesiosis is almost invariably fatal

Polioencephalomalacia (PEM)

(Cerebrocortical necrosis)

Descriptive, but non-specific term; PEM refers to?

PEM can be caused by?

In cattle, predominantly a disease of?

Histological lesions of the brain → necrosis of areas in grey matter of the cerebral cortex

thiamine deficiency, lead poisoning, and salt toxicity

Well-fed and thrifty young growing animals

Polioencephalomalacia (PEM)

PEM is usually associated with? (Food aspect) Result?

Grazing lush pastures or feeding of high concentrate rations → Rumen flora changes → Inc pop of organisms that make thiaminase type 1 → thiamine def

Polioencephalomalacia (PEM)

Most PEM cases are associated with a functional deficiency of?

Why is this an issue?

Most common underlying cause of thiamine deficiency is the presence of?

Thiamine (vitamin B1)

Rumen microbial thiamine production needed for

daily vitamin B1 requirements

• thiamine is water-soluble → there is no long-term storage

Thiaminases in the rumen

Polioencephalomalacia (PEM)

A cause associated with a drug is? Why?

Feeding of amprolium at high doses above recommended (for control of coccidiosis) → is a thiamine analogue → ass. with thiamine def

Polioencephalomalacia (PEM)

PEM is increasingly associated with ingestion of high X diets? Why? Other features?

High sulphur-containing diets or water sources (or both)

• Dec. thiamine at cell level

• PEM is distinctly epidemiological in this way

• Doesn’t respond or v poorly to thiamine TX

PEM

In the Australasian pastoral farming systems → a change in the diet from X to X is often ass. with PEM

poor, stalky grass to good, lush pasture

PEM - CX

During early stages, there is often?

Behaviour changes?

Brief diarrhoea period b4 nervous signs

Behaviour

• Isolate from herd

• Dullness

• Apparent blindness

• Ataxia

• Proprioceptive deficits

• Hyperaesthetic to tactile and auditory stimuli

• Dz progresses → head pressing and bruxism

PEM - CX

Eyes?

Reflexes?

Nystagmus with dorso-medial strabismus of eyeballs

Neurological examination →no menace response, but palpebral response & pupillary light reflex are present → a

centrally-mediated blindness

PEM - CX

Stance changes?

Rumen?

Tremors?

High head carriage and cattle may stagger

Eventually recumbent, combined with opisthotonos & extensor rigidit

Rumen function is maintained → important diagnostic sign

Fine muscle tremors, becoming more severe, then seizures & convulsions develop

• W/O TX → convulsing → collapse → death

PEM - DX

DDX?

- lead poisoning

- salt toxicity

- hypovitaminosis A

- listerial encephalitis

- thrombo-embolic meningo-encephalitis

- bacterial meningitis

- hypomagnesaemia

PEM - DX

How to DX?

primarily on history, clinical signs (cx not specific for pem) and

response to intravenous thiamine administration

PEM - PM?

Histolgy?

Brain

• Pale, swollen

• Cerebral cortex flat and smooth (compressed gyri)

Lesions

• Malacia in brain restricted to grey matter esp cerebral cortex

• Fluoresce under UV (bright blue-green) sometimes

Histology confirms the presence of cerebrocortical necrosis, mainly affecting the dorsal occipital and parietal regions

PEM - TX

Main tx? Response aspects?

Other ancillary treatments include?

Thiamine HCL

• Large initial IV dose (10-15mg/kg)

• If response (same dose next 12 hrs then BID for at least 3d)

  • Favourable response → improved mental status and gait within 12hrs of 1st tx

  • Improved vision within 48hrs but residual blindness can occur

- IV corticosteroids (dexamethasone, 1-2 mg/kg)

- IV mannitol (1-2 mg/kg in a 20% solution)

Hypovitaminosis A

Young vs Adult?

Calves?

Young animal def → compressed brain and spinal cord

Adult def → night blindness, weight loss and infertility

Calves are born with a low vitamin A status → need colostrum to protect against overt deficiency

Hypovitaminosis A

Vitamin A is formed from its precursor?

Stored where?

Cattle fed a diet devoid of vitamin A will take X b4 showing CX?

β-carotene → present in green feedstuffs

Vitamin A is fat-soluble and stored in liver

Approx 180 days

Hypovitaminosis A - CX

Calves

Eyes?

Eyes

• Blind

• Dilated, unresponsive pupils

• Tapetal bleeding (pupillary oedem and inc CSF psi)

• No menace

• Excess lacrimation

Hypovitaminosis A - CX

Calves

Neuro signs?

head pressing, convulsions, paralysis and recumbency

Hypovitaminosis A - CX

Adults

Cows?

Placental degeneration → abortion, or birth of dead or weak calves. RFMs are common

Hypovitaminosis A - CX

Adults

Bulls

Degen of the germinative epithelium of the

seminiferous tubules → Dec number of normal

sperm cells

Hypovitaminosis A - TX

Vit A parenteral inj (400IU/kg BW)

• Rapid response in animals with inc CSF

• Blind cattle (from prolonged papillary oedema and compressed optic nerves) → no response → slaughter

Hypovitaminosis A

Disease is unlikely to occur under year-round grazing

conditions; exceptions include?

- prolonged drought-stricken pastures

- poor-quality preserved feedstuffs

- diets that are high in grain

- continued administration of bloat oils (→ carotene deficiency)

Lead poisoning

Signalment?

Characterized by?

Young, inquisitive calves (usually <5 months of age) mostly - uncommon in adults

Acute encephalopathy following accidental

exposure and ingestion of lead-containing materials