Goats are inquisitive browsers, often fed unusual diets by owners/ admirers and will steal and eat virtually anything. Indigestion, impaction and poisonings all occur sporadically.

(The common garden plant Pieris results in a similar condition) 20mg/leaves/ kg BW. Mortality rate 11 – 18%
Causes increase in membrane permeability of sodium channels

Clinical signs start several hours to a day after ingestion.

Abdominal pain, depression, drooling, tachycardia, projectile vomiting and regurgitation progressing to staggering, opistotonus and death. 

• Dietary - bacterial : E.coli, salmonella 

•   Cryptosporidium - esp kids 10-20 days of age.

  Lack of host specificity – kids/lambs/calves - survival from one season to the next.

  Zoonotic; care especially when school kids visit farms etc.

•   G.I parasitism

•   Coccidiosis - major cause, esp housed dairy goat kids at weaning time

  Pathogenic - Eimeria caprina, E. hirci, E. ninakohlyakimovae Non-pathogenic - E. arloingi
  3-7 weeks age; highest incidence,
  then kids acquire good resistance by 5 months old.

  Watery, darkish scour +/- blood – can be rapid deyhdration.
  Stress and management factors predispose, as will long kidding period. Dx problematic: all kids have coccidia & prepatent phase causes disease.

  Oocyst count variable therefore speciate to identify pathogenic species. 

  Tx: Sulphamethazine/sulphaquinoxalone (off license)
  Prevention: Decoquinate may be used in feed – do not use in milking does 

Cl. perfringens type D. (epsilon toxin). Rapid proliferation, goats very prone but true incidence unknown.

clinical signs: Peracute: Sudden death / terminal shock

PM: petechial & ecchymotic haemorrhages on epicardium, endocardium, intestinal serosa, abdominal wall & diaphragm. FSE in brain, particularly basal ganglia.

Dx: fresh PM brain
Tx: antitoxin, flunixin and hyoscine (Buscopan).
Prevention: Vaccination - 4 in 1 (Cl.p types B,C,D and Cl.t) better than 7 in 1

LambivacTM licensed for goats - advise vaccination every 6 months as goats have a poorer immunity than sheep and response is short lived. 

0. This can be a fairly common presentation to the clinician and can present quite a challenge. A full history will ascertain whether the case is individual or a group problem and a thorough clinical examination should give some clinical pointers.

   Nutritional Shortfalls:

 Inadequate provision of quality feed, bullying for feed or high stocking densities

•   First Lactation: very heavy milkers - 2 year gap between milking to regain body

  condition sometimes practised.

  
  

•   Pregnancy Toxaemia: last 4-6 weeks of pregnancy or postparturient toxaemia in over fat goats 2-4 weeks postpartum (fatty liver syndrome).

  
  

  Tx: similar to sheep - propylene glycol, dexamethasone, IV glucose supportive therapy

  Other Causes: oral/dental problems, locomotor disease, tumours, scrapie, chronic infections. 

• Major cause of chronic weight loss. Assume infected until proven otherwise!

•   Often insufficient clean land and overstocking.

o Under treatment/ failure to recognize problem by hobby/pet owner

•   Goats susceptible to sheep parasites and some cattle

•   Immunity against many species may be slow to develop

•   Resistance to benzimidazole anthelmintics now common and resistance to all

  groups of anthelmintics has been recorded.

•   Subclinical effects on production. 

  Clinical effects: weight loss, scour or anaemia. 

0. Fenbendazole: 10mg/kg (2x sheep dose)
   Ivermectin: 0.3mg / kg DO NOT use ivermectin in milking goats (1.5 x sheep dose) (Levamisole: 10.75mg/kg Hypersensitivity may occur, best avoided (1.5 x sheep dose))

1.   Strategic dosing in spring and summer (4x / year for adults and 4-5x / grazing season for kids).

   High levels of resistance to anthelmintics in goats, try to avoid grazing goats with sheep 

0. if anemic- think fluke

   acute fluke- bleed out

   intermittent shedding 

   Similar occurrence to sheep? Hobby owners may have poor awareness.

   Chronic form more common due to browsing habit and gradual build- up over time.

   Dx: clinical signs, faecal egg counts and post-mortem

Tx: Acute/subacute - triclabendazole (Fasinex) - most effective but no license.

Chronic - albendazole (Valbazen) 7.5mg/kg : not licensed
(milk withhold 7 days, meat 28 days). 

Important problem in the UK esp amongst large, commercial goat herds.
Adult goats generally 2+ years affects primarily the digestive tract.
Progressive weight loss, lethargy, decreased milk yield, loss of fibre (long term) Transmission usually faeco-oral:

Particularly neonates in overstocked situations.
Most kids will pick up infection in the first few weeks of life May still be susceptible to infection as old as 6-8 months.

Also transmitted via milk and colostrum (in utero transmission?)
Scouring is not generally a feature of the disease (sometimes terminal diarrhoea,

often due to concurrent parasitism). 

older you are, less likely to get it 

very difficult and probably underdiagnosed
o anaemia of chronic disease & hypoalbuminaemia
o bacterial microscopy (typical acid fast staining with Ziehl-Neelson stain and culture

(faeces a/m or MLN p/m) Culture may take 8-12 weeks: not very practical. o AGIDT - more reliable than CFT - but still false negatives 

Control : Cull any infected animals
Reduction new infections of susceptible kids:

hygiene of kidding accommodation, prevent mixing with older animals ?removal of kids from does immediately after birth?
Regular blood/faeces sampling and culling reactors

Vaccinate with Johnes vaccine (Gudair TM – 0.5 cattle dose <4 weeks old. vaccine reactions occur 

- not in cows, reacts with TB testing 

- retest them every year

Paired serum samples 10-14 days apart
o Nasal swab: Isolation of bacteria does not confirm organism is responsible for

disease
o PM for histopath, virology, bacteriology 

Neonatal and up to 2 months old: 

Meningoencephalitis – either bacterial, or thermal due to injudicious use of disbudding iron. Bacterial - usually E. coli, secondary to septicaemia with infection from navel or intestine. Treatment: Antibiotics, fluids, anticonvulsants and anti-inflammatories.

o Focal symmetrical encephalomalacia - Clostridium perfringens type D (epsilon toxin) Usually affects kids, sometimes adults
C/s - lethargy, head pressing, tremors, ataxia, convulsions, coma and death

o Hypoglycaemia – protracted labour/ starvation after birth.
o Copper deficiency (swayback) Angoras seem especially sensitive.
o Congenital
o Tetanus
o Louping Ill - sheep are reservoirs since goat titres too low for adequate

transmission
(togavirus transmitted by Ixodes Ricinus)

o Beta-mannosidosis - autosomal recessive lysosomal storage disease of Anglo Nubians
Signs - usually bright, alert and able to suck, but often unable to stand, head & neck tremor, nystagmus and deafness, dome-shaped skull, carpal contracture, fetlock hyperextension, thickened skin 

o Delayed Cu deficiency
o Spinal abscesses –off back legs usually but not affected centrally o CAE - Nervous signs not reported in UK. 

Listeriosis - L. monocytogenes encephalitis

May be very acute (death in 6 hrs). Consider if a sudden death. Not always circling.

Septicaemia in young animals/abortion/keratoconjunctivitis also seen.

Tx– High dose penicillin I/V plus NSAID or corticosteroids +/- fluids Zoonotic risk from goat milk and cheese is a major concern

•   Scrapie - goats over 2 years old. Usually combination of pruritus & neurological signs (including hyperaesthesia and ataxia) but not specific initially. Weight loss & reduced milk yield are usual first signs. Notifiable disease since 1993 but no cases recorded since 1998.

•   CCN (polioencephalomalacia) - relative thiamine (Vit B1) deficiency.
  Rumen acidosis and digestive upset due to intensive concentrate

  feeding, prolonged scour, bad feed or drugs eg levamisole.
  Tx: Thiamine twice daily - i/v then i/m (5-10mg/kg) and re-establish ruminal flora Hypocalcemia - commonest in young, high-yielding first kidders post partum.

•   Hypomagnesemia - not common

•   Pregnancy toxaemia

•   Space-occupying lesions in brain - abscess/gid.

  Coenurosis cerebralis is the cystic stage of Taenia. multiceps

  tapeworm.

•   Poisons - lead / OPs / urea

•   Tetanus

•   CAE 

Causal agent - Corynebacterium pseudotuberculosis. Entry via cuts/abrasions

with incubation of 2-6 months before abscesses noted in superficial LNs. Abscesses may rupture spontaneously and shed infection to others. The organism is extremely resistant, surviving on wool for 1 week, in hay for 2 months and in soil for up to 8 months. 

abscesses especially in parotid, prescapular and mandibular LNs

Internal abscesses may develop especially in the lungs, leading to signs of respiratory disease and weight loss. Most common cause of carcass condemnation of sheep and goats in abattoirs in the USA. 

- clinical signs
- culture of organism via sterile aspirate of abscess ( often pus is less inspissated than in sheep – less “onion rings”).

-serological tests to detect early cases (no abscesses) – previously not deemed specific enough to use in culling programme.

herds is main method of control
- vaccine developed in Canada, Australia and Brazil (not UK yet) 

Wattle Cysts: Inherited in British Alpine and Anglo Nubian. Surgical removal possible for showing purposes.

Salivary Cysts / Salivary Mucocoele Relatively common esp Anglo Nubians. Blockage to duct of parotid/mandibular salivary gland. Usually painless, fluid filled swellings. Surgical removal if necessary – either duct only or duct and gland. 

 Incidence: major importance worldwide eg France, Australia and the USA. UK estimates 4 -8 % with few clinical cases

Regular blood testing and control measures within many flocks

 Transmission: Milk is the major mode (danger of pooled colostrum fed to kids) Direct contact (enviromentally labile)



Blood (eg communal use of tattoo equipment etc). Carriers infected for life but may be symptomless. ? cross species (goat to sheep experimentally) 

Little milk but normal consistency
Milk production increases and udder softens after 1 week but production remains suboptimal due to induration 

Most common form: yearling to adult goats (min 6 months)

Chronic, progressive synovitis in joints, tendons and bursae

with progressive stiffness
Afebrile, bright and good apppetite

Gradual loss of condition to emaciation with course of disease variable from weeks to years
Carpal joints primarily affected and may be grossly swollen

Shoulder, stifle, hock, fetlock, atlantal and supraspinous bursae 

blindness
Recumbency and torticollis.
2) Adults showing neurological signs often preceeded

by
Other signs of CAE - knuckling of fetlocks, circling and progressive paresis c.f. visna in sheep. 

• Diagnosis: 

  Clinical signs
  Serology - serum antibody levels to CAE virus using ELISA Virus Isolation and Histopath at PM

  SAC now offering a milk ELISA for CAE antibody – ?difficulties in

  policing this scheme.

•   Serology: Virus carriers identified by AGIDT/ELISA using MV or CAE antigens

  (current tests are relatively insensitive).
  Some seropositive goat test negative: Ab levels fall as disease

  progresses.
  Period between infection and seroconversion may be prolonged eg: direct contact - 3 year

  kids via milk - 6 months to 1 year (always retest animals <1 year

  old)
  

0. Treatment: None available - NSAIDs for arthritis.

 Prevention and Control:

In herds free from infection, control is based predominately on keeping Routine testing and maintenance of "CAE free" closed herds (5 years of

negative tests)
SAC Sheep/Goat Health Scheme - monitors by regular tests (every 2 years

after qualification)
British Goat Society (BGS) – Monitored Herd Scheme: kids fed own dam's

. colostrums and no milk pooling.Testing and quarantine of new herd entrants.

Infected Herds
Cull all seropositive adults and their offspring (unless separated at birth) Separate infected and non-infected goats by at least 1.8m
Can graze same pasture provided temporal separation
Milk infected goats last & keep milk separate if feeding kids
Uterine infection incidence low therefore removal of kids at birth
should ensure uninfected kids (no suckling allowed).
Blood sample kids at 6 months and then at 3 monthly intervals. 

Differences:
Remain infected for life and unlike sheep, may abort in subsequent pregnancies;

1) Culling infected does advisable
2) Chemoprophylaxis likely to be of limited value

Toxoplasma tachyzoites passed in milk of infected does, therefore public health risk. 

Differences:
a) Abortion at any stage of pregnancy (unlike sheep where abortion only in last trimester).
b) Incubation period may be as short as 2 weeks.

Infection and abortion may occur in one pregnancy causing rapid spread of infection.

Source of infection: Aborted material, faeces and MILK
Carrier animals (kids born alive to infected does). 

Treatment & Control
1) Disposal of infected material and disinfection
2) Segregation of aborting animals for 2 weeks
3) Cull any live kids from aborting does
4) Treatment of pregnant does with oxytetracycline and move to clean pastures 5) Vaccination (sheep vaccine – effective, but not licensed for goats).

NB–almost all conditions above are potentially zoonotic, especially to pregnant women! 

Aseptic fluid accumulation in presence of a persistent CL. Either:
1) Following cycle with no pregnancy (familial susceptibility)

2) Following early embryonic death and resorption

Signs: 

Abdominal enlargement and udder enlargement if not lactating

Reduction in milk yield

'cloudburst' 

Release of foetal fluids : either before gestational time with possible

further hydrometra in this and subsequent cycles, or at full gestation or

longer.

Diagnosis: 
Ultrasound 40+ days after mating – large fluid-filled compartments seen.

Increased plasma / milk progesterone Low plasma / milk oestrone sulphate.

Treatment: 

Prostaglandins - 125-250 mcg cloprostenol (up to 1ml Estrumate). Oxytocin 2-3 days post PG (stimulates uterine involution) 

Peracute: Coagulase positive staphylococci (most common cause)and occasionally E. coli

Subclinical : Cell counts frequently high in normal goats ie: < 1 x 106 / ml - normal

Treatment: None licensed – must allow long clearance times, 7 days on average

Care not to damage teat by inserting tubes too far

Control measures in milking herds can be readily based on the standard control measures applied to cattle eg: maintaining milking machinery, cleaning and drying teats prior to milking, using teat dips, good environmental hygiene, culling persistently infected goats etc. 

•  longer digit and deeper interdigital space

  than sheep, increases risk and severity. Fusobacterium necrophorum +/- Dichelobacter. nodosus (used to be Bacteroides). Blue spray/ footbathing (Zinc Sulphate 10% best).
  Oxytetracycline LA: severe cases and those not responding. 

• Lesions around coronet and can spread via feet licking.

  Effective vaccine “ Scabivax Forte”®. 

 ?more susceptible than sheep, especially dairy goats
Acute - due to mastitis, metritis, ruminal acidosis, pneumonia, after kidding

Subclinical- common and underdiagnosed disease of dairy goats which leads to

development of hoof abnormalities in older animals. Young kids fed high protein or

CHO and low fibre. Males overfed in summer when not working. 

care as lignocaine toxicity possible at doses > 5mg/kg.  Local and Regional eg lignocaine for castration, wound repair and cyst removal

 Inverted L-block / paravertebral for caesarians and exploratory laparotomies General anaesthesia

Injectable agents:
1) Xylazine and Ketamine : xylazine 0.1 mg/kg i/m followed by ketamine 10mg/kg i/m

or 5 mg/kg i/v. (lower doses of xylazine in kids - 0.025 mg/kg)
2) Alfaxalone : 2-3mg/kg slowly i/v. Good anaes.(up to 10 mins) and smooth recovery.

3) Propofol : 3mg/kg slow i/v. Very short anaesthesia.
4) Pentobarbitone sodium: 10-15mg/kg i/v. Marked resp. depression and long recovery if topped up - good as pre med for gaseous anaesthesia

Gaseous anaesthesia: Induction and maintenance or for maintenance only.
NB: Care in anaesthesia - regurgitation and aspiration of rumen contents, ruminal tympany and salivation.