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Poor thrift in farm animals, -weaner ill thrift, thin sow syndrome, thin…
Poor thrift in farm animals
what is poor thrift
insufficient weight gain
inappropriate weight loss
failure to achieve target weight by a certain age
very low BCS
diagnostic approach
weight loss or failure to gain weight
whole group affected or sub set?
appetite normal?
yes
is nutrition adequate
no
under-feeding
trace element deficiency
yes
maldigestion or malabsorption
parasitism
johnes disease
tumours
no
won't eat
parasitism
can't eat
dental disease
lameness (severe)
Trace element deficiency
Cobalt deficiency causes weight loss in ruminants
other factors that reduce animals food intake when available in adequate amounts
anxiety
competition/pecking order
excitement of oestrous
new surroundings
loss of newborn
bad weather
tick or other insect worry
abomasal displacement
protein loss in faeces
Gastrointestinal parasitism
Bovine/ovine paratuberculosis (Johnes)
neoplasm e.g. lymphosarcoma or intestinal/gastric adenocarcinoma
granulomatous enteritis
faulty digestion, absorption or metabolism
commonly manifested by diarrhoea
nematode worms
ostertagia
clinical signs
sudden onset loss of appetite, profuse green watery diarrhoea/faecal staining and possibly loss of condition
associated with increased serum pepsinogen
subclinical infections common in cattle of all ages, often associated with reduced productivity
treatment
albendazole, doromectin, eprinomectin, febantel, fenbendazole, ivermectin, levamisole, moxidectin, netobimin, oxfendazole
prognosis
type I high morbidity and low mortality
type II low morbidity and potentially high mortality
incidence
type I ostetagiosis
july to september
typically calves in their first grazing season
differentials
coccidiosis
salmonellosis
bovine viral diarrhoea
winter dysentery
acidosis associated with dietary change
treatment
anthelmintic treatment of clinical cases e.g. albendazole, doromectin, eprinomectin, febantel, fenbendazole, ivermectin, levamisole, moxidectin, netobimin and oxfendazole are efficacious against the active stages of the parasites
treated animals should be moved onto pasture that has not been grazed by young stock the previous year
type II ostertagiosis
march to may, from emergence of L4 stages, ingested the previous autumn, from gastric glands within the abomasum
often older cattle
differentials
fasciolosis
acidosis associated with dietary change
salmonellosis
treatment
appropriate anthelmintic treatment of clinical cases required as not all stages are active against encysted/hypobiotic larvae
macrocyclic lactones e.g. doramectin, eprinomectin, ivermectin and moxidectin are highly effective
the efficacy of benzimadales such as albendazole, fenbendazole and oxfendazole is highly variable against arrested encysted/hypobiosed L4 and levamisole is ineffective.
typically seen in cattle 6-24m old, depending on grazing management
public health considerations
possible but extremely rare and usually asymptomatic
can occur where unwashed root vegetables are consumed which have been fertilised with cattle faeces
cost considerations
the extent of damage to abomasum during infection can result in poor growth rates
the most important cause of poor performance in animals of all ages is depressed appetite and hence reduced feed intake
also associated with increased protein demand due to protein loss into the GIT and in generating immune response to O.ostertagi infection
presence of mixed infections, esp. Cooperia oncophora and trichostrongylus axei may also exacerbate disease
treatment costs
use of anthelmintics is likely to be necessary in clinical outbreaks and some control strategies
client history
intensive grazing systems with high stocking densities
young stock at mature within first grazing season (type 1 ostertagiosis)
housed or turned out young stock in spring time after first grazing season (type II)
presence of clinical signs (predominantly profuse green watery diarrhoea)
diagnosis
presence of clinical signs in animals associated with first grazing and raised pepsinogen levels
faecal worm egg counts may be useful although cannot distinguish between species of trichostrongyle present and maybe absent in type II presentations and older cattle
gross autopsy
round nodules, sometimes with pin prick centre noted on mucosal surface of abomasum
caused by development of L3-L5 within gastric glands and their emergence
active disease often oedema present in folds of abomasum and can be pale or necrotic
large burdens of adult parasites may be present in lumen
general treatment
fluid therapy may be required to counterbalance dehydration
provide additional nutrition to support improvement of growth rate
additional protein in diet can be useful to counterbalance protein losses in recovering animals
for lactating cattle products are available without milk witholds
reasons for treatment failure
under dosing the anthelmintic which may select for anthelmintic resistance if undertaken repetitively
benzamidazole resistance reported for O. ostertagi, C.oncophora and T.axei
macrocyclic lactone resistant O.ostertagia has been reported in europe but incidence low
monitoring
measure blood pepsinogen levels in a sample of 5-10 cattle in a group. Similar number of faecal samples can be taken for FWEC for monitoring for type I ostertagiosis although may be less sensitive and specific
in dairy herds bulk milk serology can be used to monitor for impact of ostertagiosis
control
review yearly pasture management of young stock and avoid overuse of nature's where intensive grazing strategies may lead to heavy pasture burdens
due to the development of immunity in adult cattle, alternate year grazing has been advocated in some instances between adult and youngstock
rotational grazing practices
may be useful in organic herds
strategic treatment with anthelmintics to prevent clinical/subclinical ostertagiosis
preventative treatments generally given to minimise egg output and hence larval contamination. Timing of treatments based on assumptions regarding seasonal epidemiology, rather than diagnostic tests
strategic treatments at turn out or housing where indicated, especially for type II ostertagiosis
targeted selective treatment of animals with evidence of ostertagiosis within a group e.g. measure poor weight gain, increased blood pepsinogen, FWECs or loss of body condition and only treat animals affected
also monitor for other diseases e.g. lungworm and liver fluke (fasciolosis) and treat where necessary
prolonged action anthelmintics can be useful in high challenge
integrated approach adopted as necessary to avoid over reliance on anthelmintic treatments and avoid selecting for anthelmintic resistance
prophylaxis
development of immunity is dependent upon sufficient exposure to parasites at first grazing at pasture
if immunity developed from a low exposure the first grazing season wanes, e.g. over the housing period in winter, there is a risk of further contamination of pasture and disease
certain husbandry systems limit impact of ostertagiosis
suckler cows grazing with calves at foot will ensure low levels of exposure to calves, enabling them to develop immunity. Dams co-grazing will limit the number of infective larvae at pasture
teladorsagia
nematodirus
trichostrongylus
cooperia
oseophagostomum
flukes
fasciola
clinical signs
light burdens can result in subclinical disease such as production losses
weight loss
poor production
chronic diarrhoea
anaemia
submandibular oedema (bottle jaw)
diagnosis
faecal sedimentation
faecal copra-antigen ELISA, serum or bulk milk serology and post mortem
treatment
triclabendazole (all stages), closantel (limited stages), nitroxynil (limited stages), albendazole (adult stages), clorsulon (adult stages), Oxyclozanide (adult stages)
prognosis
mortality low dependent upon magnitude of burden and extent of liver damage
differential diagnosis
johnes disease
salmonellosis
insufficient/poor nutrition if presenting as herd problem
other causes of ill thrift +/- anaemia
cattle additional causes
tuberculosis
mycobacterium bovis
very few show clinical signs
general clinical signs
emaciation
chronic cough
dyspnoea
lymph node enlargement
mastitis
with enlargement of supermammary lymph nodes if udder affected
diagnosis
single intradermal comparative cervical tuberculin test
skin thickness is measured before and after 72h
only in cattle over 42d old
the interferon gamma blood test
only in cattle over 6m old
post mortem
visible abscesses in lungs, lymph nodes or other areas
60% of cattle have no visible lesions
prevention
vaccination but currently interferes with diagnostic tests for johnes and sensitises the cattle to tuberculin based diagnostic tests
vaccination not permitted in EU
treatment
compulsory slaughter in UK
important zoonosis
predisposing factors
cattle movement
occurrence of TB on contagious premises +/- level of TB in surrounding areas (infection pressure)
herd size >300 considered an inherent risk factor for bovine TB
concurrent disease e.g. immunosuppression +/- interference with diagnostics
BVD
trace element deficiencies
fasciola hepatica
liver fluke
pathophysiology
2 stages: primary complex (lesion at point of entry), followed by post-primary dissemination e.g. acute biliary tuberculosis, discrete nodular lesions or chronic organ tuberculosis
underlying toxaemia develops which causes weakness, debility and eventual death
time course is variable, many infections result in period of latency before progression to clinical disease
coccidiosis
sarcosporidiosis
enzootic calcinosis
additional sheep and goat causes
johnes
viral pneumonia
haemonchosis
-weaner ill thrift, thin sow syndrome, thin ewe syndrome and weak calf syndrome
BCS better indicator than BW of both fat-free mass and fat mass. Fat mass is closely associated with nutrient requirements, reproductive efficiency, cull value and risk of disease