GI Nematodes of Cattle Flashcards
Nematodes general effect on livestock
Global health problem on livestock, and a lot of money goes into treatment/drugs
Causes large number of GI disturbance in sheep, and upper respiratory in cattle
Clinical disease is tip of iceberg, sub-clinical causes major production loss. Control heavily dependent on routine use of broad spectrum athelmintics- resistance is becoming a problem
Parasitic Gasteroenteritis
Generic term for disease caused by parasitic nematodes in GI tract, disease of grazing livestock
Predominantly found in young stock, bc adults generally have a strong acquired immunity and is often caused by a mixed species parasite load
Trichostrongyloidea
Most important group of nematode pathogens in grazing ruminants
Direct LC (L3 infective) PPP 21 days
Ostertagia ostertagi
L3 is infective (sheathed, so scrappy), and has potential to arrest in abomasal glands as L4- erupts ~18 days later
Ostertagia ostertagi pathogenesis
Caused by heavy infection (>40,000)
Distention of parasitized gastric gland lumen leads to…
Rupture of intercellular junctions, leakage of plasma proteins into lumen, and hypoproteinaemia
Destruction of parietal cells and replacement with undifferentiated cells, leading to a decrease in HCl secretion and increase in pH, (bacterial overgrowth), failure to activate pepsinogen to pepsin, leakage of pepsinogen into blood, and elevated plasma pepsinogen
Ostertagia ostertagi pathology
hyperplasia of abomasal mucosa Edema Morroco leather appearance Putrid smell bc of bac overgrowth Large number of adult worms- redish in color and look like eyelashes
O. ostertagi clinical forms
Type 1- Grazing calves (usually 1st season)
July-october
Due to larvae acquired from pasture 2-3 we previously
Type 2- Yearlings (often housed)
March-May
Due to maturation of inhibited larvae acquired from pasture during previous autumn ->mass rupture
Type 1 ostertagiosis
Profuse watery diarrhea (typically bright green) Weight loss Sometimes bottle jaw High morbidity Low mortality if treated
Development of egg is temp dependent (dev slower in June than July)- concertina effect
April to may the caves ingest over wintered L3s and patent infection is established
May to July 1st gen adult parasites produce eggs and contaminate the pasture
July to Aug Large numbers of L3 appear on pasture and are ingested by calves- 2 to 3 weeks later, clinical signs
Type 2 ostertagiosis
Intermittent diarrhea Sub mandibular edema Weight loss \+/- anaemia Anorexia and increased thirst Morbidity low Mortality high (bc burst en mass)
Predisposing factors-
Grazing mgt and climate, dry summers delay the emergence of larvae from fecal pats
Ostertagiosis diagnosis
Clinical picture and grazing history
Diagnosis on herd, not individual basis
Use of diagnostic aids
O. ostertagi diagnostic aids
FECs
Serum pepsinogen
Serum antibody
PM
O. ostertagi FECs
McMaster method- float and count
Cant discriminate between different trichostrongyle eggs
> 1000epg usually for type 1, but not a linear relationship between FEC and paprasite burden
O. ostertagi serum pepsinogen
Indirectly assayed by measuring hydrolysing activity of serum on albumen, results are in units of Tyrosine (normal is 1 u Tyr)
Specific for abomasal parasitism
Useful in calves, but less reliable in older animals (tend to be >1 even with low burden)
Technique varies between labs, so need to use their normals
Useful indicator of parasite burdens at the end of grazing season
O. ostertagi serum and milk antibodies
ELISAs for parasite antibody is a good measure of exposure to infection
Not commercially availale
O. ostertagi immunity
Slow to develop, takes at least one grazing season
Immune can still carry burdens
Ostertagiosis in beef herds
Dams are additional source of contamination
Uncommon in spring calving herds bc calves not weaned until autumn where overwintered larvae are dead
More common in autumn calving bc calves weaned in spring, similar epidemiology as dairy
Atypical form of bovine ostertagiosis
Early season 1- calves put out early March/April occasionally sufficient over-wintered L3 cause disease 4-6 we after turnout
Adult cattle- weird bc have acquired immunity but occasionally some cases occur like when unexposed stock are moved to endemic area
Occasional type 2 in cows debilitated by intercurrent disease
Ostertagiosis treatment
Type 1
Most anthelminthics work, also move to clean pasture
Type 2
Modern benzimidazoles and macrocyclic lactones
Ostertagiosis control
Grazing management and prophylactic meds
Avoid heavily contaminated pastue at peak season and allow limited exposure to larval infection on safe pastrue
Monitore FEC
Worm at housing
Trichostrongylus axei
Very small brown worm with excretory notch in head reagon, found in abomasum
Infects cattle, sheep, goats, and horses
Can cause sub-epithelial tunnels or mucosal erosions, but rarely a primary pathogen in the UK (it is in sub-tropics though). In UK, often contributes to clinical signs of PGE as mixed infection
L3 are sheathed, so resistant, sometimes they over winter in high enough numbers to cause clinical problems in spring
Haemonchus
Barbers pole worm fund in abomasum that feeds on blood. Has lancet that develops before its final molt to help feed
Not important in cattle in UK (mainly tropical) and there have been reports of BZ and IVM resistance
H. contortus is important in UK sheep
Bovine haemonchosis
Mainly in tropics and outbreaks are during the rainy season, or end of long dry season from bypobiotic larvae
Immunity in cattle >2 yrs, but can be broken down during drought bc of poor nutrition/heavy challenge
Cooperia sp
C. oncophora in temperate areas/UK
Mild pathogen, doesn’t migrate, but contributes to PGE
C. puncata and C. pecinata are sub tropical and more pathogenic
Coopera oncophora
Common in UK and contributes to PGE as mixed infection, sometimes predominant parasite
Parasitic stages develop on surface of SI mucosa
Mild pathogen
Dose limiting sp for anthelmintics, may be a good indicator of sp resistance with in GI nematodes
Ivermectin resistance has been reported in UK
Trichostrongylus culubriformis
Found in SI, but not really a primary pathogen in UK, contributes to PGE though. Can be very pathogenic when present in large numbers bc parasitic stages penetrate the epithelium and cause enteritis
Also found in sheep and goats
Nematodirus sp
helvetianus is most common in cattle and contributes to PGE as part of mixed infection
battus and spathiger are more important in sheep
Only Trich egg that can be differentiated bc large with large bubbles
Bunostomum phlebotomum
Several hundred adults are necessary for clinical signs, but >2000 can lead to death
Anemia, hypoalbuminaemia, weight loss, sometimes diarrhea, pedal dermatitis (foot-stamping/itching)
Treatment may include increase hygiene
Tozocara vitulorum
Largest intestinal parasite of cattle
Worldwide distribution, but not a problem in UK
Serious buffalo parasite in some areas
Thick albuminous, pitted shell, and highly resistant
L3-trans mammary infection, ALD
Exposed to infection from birth, but build up immunity
Infected via larvated egg
No tissue migration in calf, but migration in older animals
Oesophagostomum radiatum
Found in LI, stout worm
From superfamily strongyloidea, but not a hook
Not major pathogen in UK
Trichuris globulosa
Light infections common, not major pathogen
Found in LI and diagnostic egg with bipolar plugs
