Bacterial Endocarditis and Traumatic Reticulopericarditis

cardiac disease in farmed species

-CV disease moderately common in cattle

-rare in others

-acquired more than congenital

most common pericardiac disease in cattle

traumatic reticulo pericarditis (TRP)

• septic pericarditis aka hard wire disease

other types of pericarditis seen in cattle less common

-sepsis in calves

-severe BRD in adult cattle

-pulpy klidney with c perfringens

-idiopathic haemorrhagic pericardial effusion

pericardium and reticulum location

very closely located, just separated by diaphragm which isnt thick

what causes hard wire (aetiology and pathogenesis)

sharp linear metallic FB ingested

• often wires from tyres used to weigh down silage cover

• associated with clamp silage feeding

how does wire get to heart

FB penetrates reticular wall into pericardial sac through diaphragm

• not always cranial tho → can go anywhere

post mortem findings of trp

-wire can be seen

-bruising of pericardium

effects on cardiac function

cardiac tamponade

• pus filling the pericardium

• cows turn pus → fibrin

• → pressure onto heart

reduced cardiac output leading to forward failure

progresses to CHF

• becomes backward cardiac failure

• clinical signs relating to this like oedema

clinical history of hard wire

-milk drop

-non specific illness 1-2 weeks prior to exam that appeared to resolve before recurring (as painful when first ate, pain stopped until became pericarditis)

-inappetance

early stages of hard wire disease clinical signs

-pain (abducted elbows, positive withers, arched back, firm palp)

-rubbing or frictions sounds of auscultation

-tachycardia→ this is persistent

-pyrexia +/- assoc BRD signs

why is hardware disease hard to diagnose early

heart sounds change daily in early stages

most likely sign of hard wire

persistent tachycardia on a few exams

withers positive

get on gate and push down

later signs of hard wire disease

-bilateral muffled heart sounds (regular rhythm, splashing squeaking rubbing sounds)

-difficult to palpate apex beat

-+/- pyrexia

Signs related to congestive heart failure

why would you not hear splashing, squeaking or rubbing sounds of heart in later stage

if fibrin increased

signs related to congestuve heart failure

-jugular distension

-ventral oedema, pits

-tachycardia

-dyspnoea

-injected scleral vessels

bloods for hard wire

non specific just indicating inflam

-leukocytosis

-hypofibrinogenaemia

-hyperglobulinaemia (TP increased)

-neutrophilia (infection/inflam)

what does leukocytosis, hyperfibrinogenaemia and hyperglobulinaemia indicate on bloods

inflammation

what does neutrophilia indicate on bloods

infection or inflam

what do elevated liver enzymes means on bloods

hepatic congestion (if chf)

what would be seen on blood if CHF

-elevated liver enzymes due to hepatic congestion

how to us hard wire disease

-ancillary method of choice

-ICS3-ICS5 on both sides

-rectal scanner used

what seen on US of hard wire

-purulent fluid in pericardial sac (+/- fibrin)

-hepatic congestion

2-cardiac chamber

3-myocardium

4-pus

5-pericardium

radiography of hard wire disease

-lateral thoracic views (standing)

-gas fluid interface

-metal wire identified

-not often available

-depth hard to see cardiac silhouette

pericardiocentesis

-to differentiate other causes of pericardial effusion not hard wire

-septic pericarditis can be done but with varying success

-lymphoma (not in UK)

-iodpathic haemorrhagic pericarditis (not in UK)

not treatment

risks of pericardiocentesis

-pneumothorax

-cradiac punture

-contam of pleural space

PM findings of hard wire disease

-ventricles squashed

-thickening of myocardium and epicardium

-lots of fibrin aroudn the hearts

-thickened pericardium→ normally almost transparent

early stage treatment for hard wire

before fibrinous septic pericarditis developed

-magnet (oral→ rumen/ reticulum)→ good for prevention

-broad spec antibiotic (amoxicillin or oxytetracycline)

-NSAID

late stages of hard wire disease treatment

septic pericarditis developed

-prognosis poor so PTS on welfare

-pericardiotomy and drainage reported but not always good outcome

prevention of hard wire disease

-due diligence with siage and feeding management, no tyres

-magnets pre emptively in cows and on feed wagon

endocarditis pathophysiology

circulating bacteraemia→ valves of heart

-chronic bacterial infection elsewhere e.g. mastitis, metritis, pneumonia, lameness

-usually 2ndary to something else

bacteria common in endocarditis

truperella pyogenes

-plus staphs, streps, g-ves

what does endocarditis cause

-adhesion to endothelium so no prior endothelial damage, can occur on mural endocardium

predeliction sites for endocarditis

-right AV (tricuspid) valve

-left AV (mitral) valve

3rd ICS left side examine

pulmonary valve

4th ICS left side examine

aortic valve

5th ICS left side examine

atrioventricular valve (mitral)

3rd ICS right side examine

atrioventricular valve (tricuspid)

murmur grading

based on loudness

volume of murmur doesnt always correlate with severity of disease

endocarditis clinical signs

-murmur +/- palpable thrill

-persistent tachycardia

-ill thrift

-milk drop (may be episodic)

endocarditis bloods findings

non specific and just indicates inflam

-leukocytosis

-hyperfibrinpgenaemia

-hyperglobulinaemia (TP increased)

-neutrophilia

-non regen anaemia (chronic disease)

-elevated liver enzymes (hepatic congestion if CHF)

endocarditis US

-use rectal scanner

-challenging to get probe in right place

blood culture for endocarditis

-not common

-repeat samples rec

endocarditis PM findings

• lumpy

• red and inflamed

• 
  

  

haematogenous spread on PM

micro abscesses and emboli on organs esp liver and kidneys

endocarditis ttreatment

-long term antibiotics for min 3 weeks

-furosemide if CHF

-analgesia

antibiotic of choice for endocarditis

peniccilin or amoxicillin

endocarditis prognosis

guarded

-return to normal heart rate and sound then looks good

-better if diagnosed and treated earli

-if signs of CHF then poor prognosis

presenting signs of congenital cardiac disorders

-murmurs

-poor growth

-increased resp rate/effort

-cough

-treat for pneumonia and not responded as presents same as resp disease

ventricular septal defect

-most comon

-may be assoc with other congenital abnormalities

-L to R shunting

-obvious pansystolic murmur=R>L

• higher murmur grade=smaller defect as more turbulence

can a v quitet murmur in a calf be good

no

bigger hole so less turbulence

likely bad vsd

other congenital defects

-tetralogy of fallot

-atrial septal defects

-ectopia cordia

tetralogy of fallot

VSD + R ventricular hypertrophy + over riding aorta

ectopia cordia

-heart visible beating in neck region

-in wrong place

-euthanasia → cant live with this

v rare

•Prognosis for multiple defects

= poor

hyperkalaemia

-bradyarrythmia

-severe acute diarrhoea in neonatal calves

-urinary obstructions in older calves and male sheep and goats

white muscle disease

vit e/selenium deficiency

-usually skeletal m

-myocardial damage → focal, multifocal or diffuse

• hear arrhythmias

-cardiac signs variable