Ostertagiosis- caution- revision insanity.

My plan for work today:

Poultry ante-mortem & slaughter.

Farm Assurance. 

DONE DONE DONE.

Next-> NEMATODES. Dun...dun..dun.. Not the word I want to see. I've revised this topic a lot, so it should be in my head (it isn't). So instead of doing it AGAIN. I'm going to go through my parasite book to weed out some little facts that might help me in my exams :)

Ostertagia

I've seen this worm now SO MANY TIMES. Yet I can't get some of the little facts straight in my head. So below are some of the facts about this little guy that I just don't remember. 

BACKGROUND

The worm causes gastritis in replacement dairy cows at different times throughout the year. There are two types of disease. Type I generically causes a watery diarrhoea (more on this later) whereas type II is a bit nastier due to the hypobiosis that this little guy can undergo (remains stationary in the cow over winter so it survives, and then re-emerges all at once to cause nasty clinical signs). 

• This worm resides in the abomasum, and its counterpart in the sheep is Teladorsagia Circumcinta (just look the same to me...). 
• It has a direct life cycle, which means there is NO other host other than our lovely cow involved.
• The L1-> L3 stages have the environment of the faecal pat. They are dispersed by rainfall (another reason to cure the great british weather) and a typically wet season is seen as a necessity for type II disease forecasting. If not, imagine some little worms trapped in a faecal pat.. unable to go ANYWHERE. For optimal development, the time period of this is as little as two weeks. 
• Cue- interesting fact. The L3 cannot feed! They retain the cuticle 'skin' of their L2 development as a protective sheath so they can survive for long periods of time. 
• Large numbers of worms are needed to cause disease. You might ask yourself.. what is this number.. what characterises a large worm burden in Ostertagiosis? Well that my dears is a massive 40,000 worms! IMAGINE. 
• The pathogenesis of the disease-> characterised by large numbers of developing larvae in the GASTRIC GLANDS & emerging L5 adults. 

Developing L3-L5 larvae causes a distinct pathological pattern in the mucosa of the abomasum:

1. The parietal cells (which are responsible for acid production) are replaced by undifferentiated epithelial cells (tissue METAPLASIA). 
2. These cells retain none of their original function. This causes a loss of acid production.
3. A loss of acid production. Just what is this ACID responsible for (no, it doesn't burn your stomach out!). The stomach generally has a ph of around 2. Acid keeps the PH low. This protects against invasion of little microbes and other stuff. Anyway. That aside. Loss of acid production results in the following effects:

• Increased PH (less acid, trends towards a neutral PH).
• Loss of the bacteriostatic effect (those little microbes.. yeah, they're no longer killed off, CUE SECONDARY infections...). 
• No conversion of PEPSINOGEN TO PEPSIN. This is the thing that breaks down the protein in your food initially. Without it, well,  there's some consequences, and you could imagine one of them for example being weight loss. 
• Increased permeability of the mucosa (why? Well. I'm not 100% sure without going towards google...) this results in protein and pepsinogen leakage.

So it comes as no surprise (or shouldn't), that the clinical signs are the following:

• Profuse watery diarrhoea- upset stomach, what else would you have! The gut responds to pain by going into stasis. This results in less absorption of everything. 
• Weight loss- as you can imagine, no protein breakdown. The bigger picture is probably more complex, but hey we're trying to think in smaller chunks here. 
• Loss of appetite- I think I'd have a loss of appetite with 40,000 worms too...

So what happens throughout the year???

May-> 

• Dairy replacement calves first turned out. Ingested the L3 which have overwintered on the pasture (damn that retained L2 cuticle). 
• No disease- the burden of worms is too few (infective stage= L3 I forgot to mention). Not quite 40,000 words. 

June-> 

• Overwintered L3 have DIED OFF- PARTY TIME (or not).
• The eggs shed in the cow faeces mature on pasture. PPP= 3 weeks (time from ingesting L3, to egg shedding). 
• Continuous egg excretion. Increased ambient temperature & eggs develop.

One or two things to mention. Disease depends on a few HOST factors:

1. Age.
2. Immune Status.
3. Overdispersion- 20% of the population will carry 80% of the worm burden. 

The development of the worm is also down to LUCK (or not). Development of the hatching to infective L3 stage depends on:

• Temperature (above 10 degrees). 
• Humidity (rainfall). 
• Dispersal from the faecal pat (need to disperse so the cow eats the grass they're poised on). 

L3 infective survival depends on:

• Ensheathed (that damn cuticle).
• Temperature- can tolerate COLD- so can overwinter.
• Moisture (dessication is lethal). 

July->

• Eggs on the pasture develop (warmth yay). 
• PEAK L3-> mid July. Ingested by the dairy replacement calves. 

Aug-> 

• The calf has eaten too many worms-> the burden is going towards the 40,000 disease danger zone. 
• Large numbers of L3 develop in the abomasum (remember the larval developing stages and emerging L5= disease).
• Type I disease a few weeks later.

Type I Disease

• July-> September. 
• Calves have ingested large numbers of L3 in July.
• Green watery diarrhoea. 
• Majority in a group will be affected.

Autumn-> 

• L3 exposed to a temperature drop and L3 may be released from the faecal pat with increased rainfall in autumn.
• Calves may be moved back onto pasture used to graze calves earlier in the summer.
• Leads to hypobiosis of larvae and accumulation of hypobiosed L4 (something I always forget, the hypobiosed stage is the L4 stage) in gastric glands. The trigger to hypobiose= the drop in ambient temperature. Arrested larval development. 

Late Winter/Early Spring->

• Larval development resumes (increased temp?)
• Simultaneous re-emergence of L5 (the big thing here, why type II disease is more severe). 

Type II Disease

• Acute, intermittent diarrhoea (simultaneous, hence acute not chronic).
• Anaemia loss of blood due to emergence.
• Thirst.
• Marked weight loss. 
• High mortality levels.
• Hypoalbuminaemia (a protein) leading to submandibular oedema. 

Beef Herds

• Calves graze with immune mothers.
• Autumn born calves at most risk when turned out in spring to graze and ingest overwintered L3.
• Clinical disease less common.

Diagnosis

• Definitive-> plasma pepsinogen above 3.0 i.u due to leakage with increased abomasal permeability. 
• Abomasum appears like 'morocca leather' with red worms up to 1cm long on close inspection. 
• Lighter infection= sub optimal weight gain. 
• Clinical signs.
• Grazing history- Type 1 is normally set stocked in one area for several months. Type II are grazed on a permanent pasture from spring to mid summer than moved back to the original field in autumn. All have a history of oestertagioa. 
• Type I disease FEC-> >1000 eggs. 

Treat/Control

• Maintain a population of worms in 'refugia' if dose and move e.g. do not treat all the cattle in a group. 
• Benzimidazoles-> arrested larvae. 
• See anthelmintic blog.