cns_adult_animals_2010

7/30/2019 cns_adult_animals_2010

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Neurological diseases (usually) affectingJuveniles and Adults

BacterialListeriosisClostridial - botulism

- tetanus

ViralEquine herpes viral encephalomyelitisWNVRabies - o wn lecture by Dr. OToole

Parasitic

Taenia multiceps common in sheep

Toxic and NutritionalNigropallidal encephalomalacia occurs in WYPolioencephalomalacia common in cattle in WY

Prion diseases

Scrapie

Tetanus 1.

Species: all farm mammals, horses (and humans)

Cause: Clostridium tetanitoxin (tetanospasmin) Pathogenesis:

Disease can occur at almost any age Bacterium gains entry to body through wound e.g. navel, tail docking,

i i i i li , , i , i , i l Proliferates in anaerobic environment and produces protein toxin

Toxin enters body fluids and nervous system Inhibits inhibitory chemical transmitters

Tetanus 2 clinical diagnosis

History - no vaccination

- often infected deep wound

Clinical signs

Ears back

Raised tail head

Saw horse stance

Chronic bloat

Increased muscle tone


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Treatment

Poor prognosis Penicillin, antitoxin injection

Tetanus 3

Prevention Cleanliness during surgical and obstetric procedures

Vaccination is very effective; vaccinate dam to generatematernally derived immunity in calves, foals, lambs

Prompt treatment of infections, injuries, wounds

Botulism 1

Species: any mammal or bird.

Cause: Clostridium botulinumtoxins. The bacterium is often in thegastrointestinal tract of healthy animals.

Pathogenesis there are three forms of disease

Toxin is ingested (forage poisoning) - This form usually occurs as adisease outbreak. In this scenario, the bacterium grows in a certain

i i i i lsubstrate and produces its toxins. It is then ingested. For example, anoutbreak has occurred in sheep through spreading poultry litter onpasture (illegally). Symptoms 1-7 days after ingestion. Association withphosphorus deficiency which causes pica (depraved appetite) andfeeding silage containing dead animals e.g. rodents. This is the mostcommon form of the disease in cattle, sheep and horses.

Toxico-infectious The bacteria grow and produces toxins inintestinal tract. Shaker foal syndrome - 3-8 weeks of age.

Wound botulism bacterium grows in wound, this form may be morecommon in foals / horses. Most likely one animal involved. Leastcommon form of disease.

Botulism 2

Symptoms

Paresis (weakness), difficulty to rise, loss of tongue tone, musclefasciculations.

How can you confirm a diagnosis? Demonstration of pre-formed toxin is best

Mouse inoculation [wasp waist breathing due to contraction of abdominalmuscles can be difficult to interpret]

Wound form can tr culture Treatment supportive, antibiotics if wound form, antitoxin if know strain

Prevent ion

Vaccine is very effective, if used properly (multivalent or monovalent)

Treat wounds

Rodent control

Disposal of carcasses

Large hay bales provide anaerobic centers

Dont feed silage to horses


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Botulism occur in birds [aka limber neck] Botulinum toxins are used totreat some medical disorders

Botulinum toxins are used in thecosmetic industry

Botulismoccur inhumans

Listeriosis 1.

Species: ruminants >>> horses and man

Zoonotic potential: associated with abortion, CNS infection

Cause: Listeria monocytogenes infects the brain-stem in ruminants.

However, it is important to remember that this pathogen can also causeocular infections, mastitis, abortion due to metritis and septicemia. Thedisease often occurs in winter in association with feeding of silage, butcases do occur also in animals at pasture.

Pathogenesis:

Ruminants: L. monocytogenes gains access to the hind-brain by travellingup axons of the facial or trigeminal nerves. It is thought to cross the oralmucosa through minor abrasions before entering axons. Lm is a hardybacterium and replicates easily in poor quality silage where the pH is >5.Disease often occurs in outbreaks.

Horses: disease rare in horses. Usually diffuse encephalitis.

Listeriosis 2.

Clinical signs: - Ear droop, prehension, mastication(chewing) and swallowing problems. Circling.

Necropsy:

-Bacterial culture from brain stem.

- aracter st c esons. croabscess conta npredominantly neutrophils) in the medulla oblongata andpons. Inflammation is also present in the trigeminalganglion. Bacteria are Gram positive and may be intra-cellular.

Treatment: antibiotics.

Prevention: No vaccine available in USA. Ensure goodquality silage.


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West Nile Encephalitis 1

History of West Nile Encephalitis (WNE) in USA: is amosquito borne viral infection that was first identified in

the USA in 1999. The disease occurs in horses (birds,humans and less commonly in other species). Symptoms: Clinical symptoms in horses are varied.

Most cases have mainly spinal involvement. depression and violent behavior (forebrain involvement)

ataxia, lameness, toe dragging, prayer posture, sensitivity totouch (spinal cord involvement)

fever.

Initial symptoms may resemble rabies Causes: WNV is an RNA virus in the flavivirus genus.

WNV in birds in 2008 WNV in horses in 2008

Pink=positives

Green=submitted

Yellow=not involvedin surveillance, or didnot submit samples

WNV in humans in 2008

Consider the whole of WY to beendemic for WNV, less

surveillance than a few years ago

West Nile Encephalitis 2 CNS lesions

Spinal gray matter lesions Spinal perivascular infiltrates

WNV antigen in spinal cord neurons and glial cells

Proliferation ofglial cells

Non-suppurative polioencephalomyelitis


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West Nile Encephalitis 3 Diagnosis:

Disease occurs during the mosquito s eason [May to October peak in August].

Suggestive clinical findings Antibody ELISA: serum IgM; CSF I gM need to know vaccination history

Positive on serum indicates recent exposure, may not be cause of disease Long term-effect of vaccine is an IgG response

PCR on clinical samples such as CSF

Necropsy: spinal cord examination is critica l.

Treatment: Supportive care. The survival rate is about 50%. Recovery toathletic status in competition / working horses may not occur.

Prevention: An effective vaccine is available. Mosquito control. Precautions: No documented direct animal to human transmission has

been documented. When handling a suspect WNV horse take routineprecautions no direct exposure to body fluid, wear latex gloves andprotective clothing, wash hands.

Equine rabies can present with symptoms resembling WNV infection

Equine herpes viral myelitis

Cause: Equine herpes virus 1, an alpha herpes virus. Seenseveral times / year at WSVL.

Myelitis = inflammation of the spinal cordHerpes viruses are doublestranded DNA virus

Pathogenesis: Airborne respiratory infection that spreadssecondarily to involved spinal cord>brain. A high percentageof horses go onto develop a latent infection.

The strain that most often causes the neurologic form of EHV1has been identified and we can test for it at WSVL.

Latency is an important feature EHV1 reactivation of latentinfections may explain some outbreaks.

Equine rabies may resemble early neurotropic EHV1

Equine herpes virus .Lifecycle and the role of viral latency

Latent infection

Reactivation Nasal shedding

Abortionr r

Stress

Infection of young horses

(sensory ganglia, LN)

Pregnantmareinfection

0.5-40%(neurologic)

Incubation period 2-10 days

Close contact required for spread

m

respiratory

disease

Very closecontact


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EHV1 strains

One study found point mutation in 83% of

neurologic disease outbreaks that wasabsent in 95% of abortion storms

Point mutation in the catal tic subunit of

viral DNA polymerase

PCR can distinguish neurotropic and non-

neurotropic strains

Symptoms: Typically November-May. Affects several animals ina group. Very close contact is required to spread the disease.Often preceded by mild upper respiratory tract disease. Notall infected animals will develop neurologic disease (~1/3).Pyrexia. Symmetrical hind-limb weakness / ataxia(incoordination) that may progress to paralysis.


Diagnosis: History and clinical signs.

Serology may be complicated by vaccination

- WSVL IgG test

Virus isolation

PCR allelic discrimination method

blood, CSF, cord, LN, ganglia

Treatment: Supportive, antiviral may work but very expensive,antibiotics to control secondary infections. Preventing secondarycomplications is important in paraplegic animals

Prognosis: If animal becomes paraplegic, the prognosis is poor due tocomplications such as secondary muscle damage.

Control: Need to follow veterinary advice for each specific outbreak

e.g. Quarantine horses with fever / or whole facility, checkil i i i i l


il , i i i i l

Prevention:

Quarantine new horses on premises Quarantine horses returning from shows etc?

Vaccination unsure efficacy

Identify animals with a latent infection by mandibular LN biopsy andPCR? A high percentage of previously infected animals developlatency. What do you do with latent animals when you identify them?


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Prion Diseases scrapie 1

Prions are misfolded proteins that are infectious inthe absence of DNA

Prion diseases are neurodegenerative in nature Species in which prion diseases have been

described Cattle bovine spongiform encephalopathy

Sheep and goats - scrapie

Humans

Mule deer / Elk / White-tailed deer

There is potential for cross-species transmissione.g. bovine prion disease is transmissible to man

Sheep > goats scrapie present in USA

> 2 years, chronic progression, neurodegeneration rubon objects - hence scrapie

Prion gene polymorphisms determine susceptibility

Can breed scrapie resistant sheep

Present in USA, but uncommon: can eradicate.

Prion diseases scrapie 2

Diagnosis Post-mortem

Pathology

Immunostaining for prion protein brain and / or lymphoid

Live-animal

Tonsil or third eyelid biopsy and immunostaining for misfoldedprion protein

Polioencephalomalacia (aka. cerebral corticalnecrosis, thiamine-responsive encephalopathy) 1

Species: cattle, sheep and goats

Cause: thiamine-responsive polioencephalomalacia [PEM]

hydrogen sulfide toxicity [does not respond to thiamine] [lead poisoning or salt poisoning may cause lesions similar to PEM]

l i li ll i il i li ll i isensitive to defects of energy metabolism; thiamine deficiency andH2S interfere with cellular energy metabolism.

Symptoms: These are the same regardless of whether thiamineresponsive. Classically, opisthotonus (star gazing), blindness due todamge to brain, recumbency, seizures. There should be no pyrexia.


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There is cerebro-

cortical laminar necrosisand brain swelling (A).The brain has a very high

Polioencephalomalacia 2 lesions

A

lipids. There is abundantbrain lipid oxidation inPEM and this results inthe generation of lipidoxidation products thatfluoresce with UV light(B).

B

Polioencephalomalacia 3- thiamine-responsive

A subset of cases respond to intra-venous thiamine [onlyif thiamine administered in early stages of clinicaldisease]

This does not necessarily mean that animals arethiamine deficient (hence the term thiamine-responsive)

True thiamine deficiency may be important in some

Potential origins of thiamine deficiency Thiaminase containing plants e.g. bracken (Pteridium aquilinum)

Thiaminase producing bacteria in intestines e.g. some Bacillus species

Distribution of Pteridium aquilinuminWyoming by county [NB most cases ofthiamine-responsive PEM are not thought

to be associated with specific thiaminasecontaining plants]

Polioencephalomalacia 4 high-sulfur diet associated

High sulfur in water or food can cause PEM

Symptoms usually occur 1-4 weeks after dietary change

PEM is strongly associated with ruminal gas cap hydrogen sulfide

concentration

l i i i l i i i i l ula e in ie is convere o y rogen sul i e in anaero ic ruminalenvironment by sulfate reducing bacteria

Hydrogen sulfide eructation and inhalation is probable mechanism ofabsorption into body

Lesions are identical to thiamine-responsive form of disease

Diagnosis lesions, lack of response to thiamine, rule out lead poisoning,analyze food and water for sulfur content.

Water sulfur levels are high in many parts of WY


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Nigro-pallidal encephalomalacia 1.

Species: This disease affects horses only.

Cause: It is caused by ingestion of either Yellow star thistle (Centaurea

solstitialis) or Russian knapweed (Centaurea repens). Disease is typically

found in summer and fall. The dried plants in hay are also toxic.

Yellow Star Thistle andRussian Knapweed

native to Eurasia,introduced into USA in

19th century

Nigro-pallidal encephalomalacia 2.

Pathogenesis: The plants contain a toxicprinciple, repin, that mediates the effects of thedisease.

Symptoms: The brain regions involved areimportant in the control of movement. Problemswith prehension, mastication, swallowing.

i l i

Midbrain of horse with NPEM

. i l , i ,aimless wandering.

Treatment: Mildly affected cases may make asmall recovery.

Prevention: Grazing and pasture management.Avoid making hay from contaminated pastures.

Substantia nigraliquefaction

Coenuriasis

Caused by the intermediate stage of the tapewormTaenia multiceps, usually causes brain lesions, variablein location, occasionally spinal cord lesions

Sheep>>goats, cattle, horses, humans

-ingests eggs

Symptoms are variable, depend on cyst location, mostcommon site is in one cerebral hemisphere Circling is common, usually to one side


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Dog is definitive host (also foxes, coyotes)

Life Cycle of Taenia multiceps

Sheep are important intermediate hosts

Cystic intermediate stagein brain of sheep the

cystic stage is calledCoenurus cerebralis

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