Auravale Alpacas

05/02/2026

Good to have hay stock restored, hopefully for the year ahead. Thanks Craig and John from Johness Hay and Ag and James Geysen for helping to unload.

04/02/2026

Colostrum Part 3:
Colostrum Is Specific — Why Source, Species, and Environment Matter

One of the most common responses I see when we talk about colostrum is this:

“Tetanus is tetanus. Clostridium is clostridium. If a cow or horse is vaccinated against these, those antibodies should still work for lambs and kids.”

On the surface, that sounds reasonable.
Biologically, it’s incomplete.

Colostrum is not a generic immune booster.
It is highly specific biological information, shaped by species, exposure, and environment.

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Antibodies don’t recognize names — they recognize targets

Antibodies don’t respond to disease labels.
They bind to very specific molecular structures on pathogens.

Even when two animals are exposed to something we call by the same name — like clostridium — the reality is:
• strains differ
• toxin profiles differ
• routes of exposure differ
• and the way each species encounters risk is different

A ewe or doe living on your farm is producing antibodies based on:
• the organisms present in your soil
• the microbes circulating in your barns and pastures
• the way lambs and kids actually become exposed

That antibody profile is not interchangeable with one produced by a cow in a feedlot or a horse in a stall.

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Species specificity matters — even for “the same disease”

Yes, clostridial organisms exist across species.

But lambs and kids do not experience them the same way calves or foals do.

Differences in:
• gut physiology
• immune development
• timing of exposure
• and dominant disease pressures

all matter.

Colostrum works best when:
• antibodies match the pathogens the neonate will actually face
• delivery happens during the gut permeability window
• and the signals are aligned with small-ruminant physiology

That’s why the dam’s colostrum is always the gold standard.

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Why substitutes sometimes help — and why they don’t replace the dam

This does not mean substitutes are useless.

Cow colostrum, goat colostrum, and commercial products can:
• provide bulk immunoglobulins
• offer short-term gut-level protection
• help bridge cases of failed passive transfer

But they cannot recreate:
• the dam’s full antibody diversity
• environment-specific exposure history
• or maternal immune prioritization late in gestation

They are bridges, not replacements.

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Why narrowing colostrum to CDT coverage misses the point

Focusing only on tetanus or clostridium narrows the field too much.

Ewes and does are passing antibodies for far more than one disease:
• enteric bacteria
• respiratory organisms
• environmental microbes
• opportunistic pathogens unique to that farm

Colostrum isn’t about one threat.
It’s about stacking protection during the most vulnerable window of life.

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Timing still beats everything else

Even perfectly matched antibodies fail if:
• intake is delayed
• the lamb or kid is cold
• or gut permeability is already closing

No substitute — regardless of species — fixes late delivery.

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Coming next

In the next article, we’ll talk about timing and quantity:
• how long colostrum is actually produced
• what “enough” really means
• why chasing exact numbers can backfire
• and when intervention helps versus hurts

Because colostrum success isn’t about finding the right product —
it’s about getting the right information into the right animal, at the right time.

04/02/2026

2nd article on the importance and timing of colostrum

Colostrum Part 2:
Timing, and the One-Way Door
By Tim from Linessa Farms

In the first article, we talked about what colostrum is — and what it is not.
This article is about when it works.

Because with colostrum, timing isn’t a preference. It’s a constraint.

From the moment a lamb or kid is born, a biological clock starts. That clock is not controlled by nursing behavior, environment, or human intervention. It’s driven by physiology — and it only runs one direction.

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Gut Permeability: Why the Window Exists

Newborn lambs and kids are born with a gut that is temporarily permeable. This allows large immune molecules to pass directly from the digestive tract into the bloodstream.

That permeability is intentional. It’s how passive immune protection is transferred.

As colostrum is absorbed, the gut begins to change. The cells lining the intestine mature, tighten, and close off that pathway. This process — commonly referred to as gut closure — is normal, necessary, and irreversible.

Once it progresses, it does not reopen.

Gut permeability is highest in the first few hours after birth and begins to decline rapidly within the first 6–12 hours. By 24 hours, meaningful systemic absorption of antibodies is minimal to absent in most lambs and kids.

This isn’t a switch that flips at a set time.
It’s a slope — and that slope gets steeper with every passing hour.

This is why colostrum is fundamentally different from milk or supplements. Its value is tied to timing, not just intake.

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A Short Note on Antibodies (and What They Do — and Don’t)

Antibodies, or immunoglobulins, are proteins designed to bind very specific targets. They are not general protection, and they are not interchangeable.

Just as important as what they target is where they end up.

During the brief window of gut permeability, antibodies consumed in colostrum can enter the bloodstream and provide temporary, passive protection. Outside that window, antibodies remain in the gut and do not become systemic immunity.

This is why:
• Timing matters more than volume
• Late colostrum is biologically different from early colostrum
• Oral “immune support” products cannot compensate for missed windows

Antibodies do not create immunity.
They do not form memory.
They provide temporary support, and only when the biology allows them to.

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A Familiar Example: CDT Boosters in Late Gestation

Most producers are familiar with giving CDT boosters to ewes or does in late gestation. This is a useful example because it highlights the same timing principle.

The booster does not vaccinate the lamb or kid. Antibodies do not cross the placenta in sheep or goats in any meaningful way.

What the booster does is stimulate the dam’s existing immune memory and concentrate specific antibodies into colostrum. Those antibodies only reach the newborn if colostrum is consumed early, while the gut is still permeable.

The shot prepares the colostrum.
The colostrum prepares the newborn.

If intake is delayed or missed, the benefit of the booster is largely lost.

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Cold Stress Does Not Pause the Clock

A common question is whether chilling or shutdown extends the colostrum window.

It does not.

Cold can suppress the suck reflex and delay intake, but gut closure continues on its own timeline. In fact, cold stress often makes absorption less efficient by diverting energy away from gut and immune function.

So instead of gaining time, you lose ground:
• Less colostrum intake
• Poorer absorption
• Narrower margin for error

You can restart nursing.
You cannot rewind physiology.

This is why warming and feeding early go together — and why delays compound risk instead of buying time.

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Why “More Later” Doesn’t Fix “Missed Early”

Once gut permeability declines, feeding colostrum still provides calories and nutrients — but it no longer accomplishes immune programming.

At that point:
• Antibodies stay in the gut
• Passive transfer does not occur
• The biological opportunity has passed

This is why colostrum management is not about volume alone. It’s about early, appropriate intake during a non-repeatable window.

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The Takeaway

Colostrum works because of timing, not because it’s special milk.

The window opens at birth.
It begins to close whether the animal nurses or not.
And it closes on a slope, not a schedule.

In the next article, we’ll talk about source and specificity — why species matters, why some substitutes help in a pinch, and why none of them replace timely intake of the dam’s colostrum.

02/02/2026

I find there are many misconceptions about colostrum. This series of articles will help to clearly explain its importance, composition and timing.

This week we will be talking about colostrum!

Colostrum Part 1:
What It Is (and What It Is Not)

By Tim from Linessa Farms

Colostrum is one of those words everyone uses, but very few people actually stop to define.

It’s often talked about like it’s “really good milk” or a supplement you give just in case. Neither of those descriptions is accurate, and that misunderstanding causes more downstream problems than most people realize.

Colostrum is not milk in the way most people think about milk.
Milk is nutrition.
Colostrum is biological instruction.

At birth, lambs and kids enter the world with an immune system that is essentially untrained. Unlike some species, small ruminants do not receive meaningful antibody transfer in utero. They are born immunologically naïve. Whatever early protection they will have must be delivered after birth—and colostrum is how that happens.

The primary purpose of colostrum is twofold: to deliver antibodies relevant to the species and environment the dam lives in, and to provide early biological support for the newborn.

Once gut permeability closes, continuing to feed colostrum misses the point. At that stage, it functions as nutrition—not immune programming.

That distinction matters.

Colostrum is a dense, time-sensitive package that contains:
• Immunoglobulins (primarily IgG, but also IgA and IgM)
• Growth factors that stimulate gut development
• Immune signaling compounds
• Energy in a form the newborn can actually use

This combination does two critical things at the same time:
1. It provides passive immune protection
2. It programs the gut and immune system for what comes next

That second point is often overlooked.

The newborn gut is temporarily permeable. This allows large immune molecules to pass directly into the bloodstream. As colostrum is absorbed, that permeability begins to close. This process—often referred to as “gut closure”—is normal and necessary, but it is one-directional. Once it progresses, it does not reverse.

This is why colostrum is not interchangeable with milk, supplements, or “something later.”

Once that window begins to close, you can still feed the animal—but you are no longer delivering the same biological message.

Another common misconception is that colostrum is a single event. In reality, it’s better understood as a sequence:
• Early intake establishes passive protection
• Continued intake supports gut maturation
• Transition to milk occurs only after that foundation is laid

When colostrum fails—due to poor quality, inadequate intake, delayed nursing, cold stress, dystocia, or simple mismanagement—the effects are not always immediate. Some lambs and kids appear normal for days or even weeks.

These are often the animals that don’t grow as expected, struggle to tolerate routine challenges, and seem to need repeated intervention just to stay on track. This isn’t bad luck. It’s biology playing out exactly as designed.

Colostrum isn’t a supplement.
It isn’t optional.
And it isn’t something you can fix later.

Colostrum doesn’t change exposure. It changes how the animal tolerates it.

In the next article, we’ll talk about timing, why colostrum is a one-way door, and why “more later” does not compensate for “missed early.”

29/01/2026

Coccidia — Part 4
What Actually Moves the Needle

By Linessa Farms

By now, most people following this series understand a few core ideas:
• Coccidia are not worms
• You don’t eliminate them
• Timing and exposure pressure matter more than treatment alone

So the last question is the one that actually matters:

What actually reduces losses and long-term damage?

It isn’t one product.
It isn’t a schedule.
And it isn’t repeatedly treating the entire herd or flock.

What moves the needle is reducing exposure pressure during vulnerable windows.

That usually means looking upstream, not reaching for another bottle.

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-What consistently makes a difference-

Across farms, systems, and years, the same factors show up again and again:

• Tight age groups
Wide age spreads create a constant exposure ramp. Older animals shed more; younger animals take the hit.

• Dry footing and clean traffic areas
Waterers, feeders, creep areas, jugs, and corners drive exposure far more than pasture does.

• Avoiding stacked stress
Weaning, diet changes, weather swings, hauling, overcrowding — stacked stress lowers tolerance fast.

• Targeted response instead of blanket reaction
Early recognition and treating the animals that actually need help works better than treating everyone late.

When pressure stays reasonable, biology does the rest.

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-A word on medications (because it always comes up)-

People will commonly encounter the following tools when coccidia is discussed:
• Amprolium (Corid®)
• Decoquinate (Deccox®)
• Ionophores (Rumensin®, Bovatec® — where labeled and appropriate)
• Toltrazuril / Diclazuril
• Sulfas (historically)

These products do have a place. When used correctly, they can reduce parasite replication and help limit clinical disease.

But they all share the same limitation:

They reduce organism load — they do not fix exposure pressure.

Corid, for example, interferes with thiamine uptake in the parasite. That can slow replication, but it doesn’t address why exposure was overwhelming in the first place — and it doesn’t repair damaged intestine.

The same limitation applies to every product on this list.

This is why results vary so widely between farms using the same medication.

Medications tend to work best when:
• exposure pressure is already being managed
• age groups are tight
• stress isn’t stacking
• and treatment is used to support animals during known risk windows, not as a permanent solution

*If you’re having to repeatedly treat the entire herd or flock, year after year, that usually points to a system or site pressure issue, not a failure of the medication itself.*

That’s not blame.
That’s information.

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-A quick note on the environment-

Coccidia oocysts are very resistant in the environment, which is why “cleaning harder” often doesn’t work.

Many common disinfectants — including bleach — are not very effective against coccidia oocysts. Freezing doesn’t reliably eliminate them either.

What does matter is changing the environment so oocysts are less likely to survive and build up:
• keeping areas dry
• reducing manure accumulation in high-traffic zones
• limiting crowding
• allowing sunlight and drying where possible

This is another reason coccidia control is a systems problem, not a sanitation contest.

You don’t win by killing everything.
You win by lowering exposure pressure.

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-What success actually looks like-

Real coccidia control doesn’t look dramatic.

It looks like:
• consistent growth
• fewer setbacks during stress
• animals staying closer to their peers
• less reliance on rescue treatments

It looks boring — and boring is good.

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-The takeaway-

Coccidia isn’t about elimination.
It’s about keeping pressure low enough that biology can do its job.

Tools belong inside a functioning system — not in place of one.

That’s the through-line of this entire series.

I hope everyone learned something new and helpful. As always, we appreciate your support.

28/01/2026

Coccidia — Part 3: Exposure, Timing, and Pressure
By Linessa Farms

By now, we’ve talked about what coccidia is and what it does to the intestine.

This part is about the question people keep asking, even if they don’t say it out loud:

Why do animals in the same environment have such different outcomes?

The answer usually isn’t luck.
It’s exposure pressure and timing.

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Exposure is normal. Disease is not.

Coccidia are everywhere sheep and goats are.
Exposure alone does not mean disease.

Coccidiosis happens when:
• exposure is too high
• exposure happens too early
• or exposure happens during a stress window

This is why “it’s everywhere anyway” is true — but incomplete.

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Why timing matters so much

Young lambs and kids are still:
• developing their intestinal lining
• learning how to regulate inflammation
• building immune recognition

If heavy exposure happens before those systems are ready, intestinal damage can occur that can’t be fully undone later.

That animal may survive.
It may even look better after treatment.
But its efficiency and resilience can be permanently reduced.

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Why pressure matters more than presence

Exposure pressure builds when:
• moisture is high
• stocking density is tight
• manure accumulates in high-traffic areas
• stress and exposure stack together

Low, gradual exposure is usually tolerated.
High or repeated exposure over a short period is what causes problems.

It’s rarely one bad exposure.
It’s too much, too fast, at the wrong time.

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Why problems tend to come back

Animals with prior intestinal damage often struggle again when:
• grass is lush and wet
• intake rises quickly
• weather stress increases
• nutritional demand goes up

This isn’t a “new infection from scratch.”
It’s a system with less reserve being asked to do more.

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Where whole-group treatment fits into this

Medications can reduce replication and help animals through high-risk periods. They have a role.

But here’s an important reality check:

If you’re having to repeatedly treat the entire herd or flock, that usually points to a system or site pressure issue — not a failure to control coccidia.

Repeated whole-group treatment is often a signal that:
• exposure pressure remains high
• environmental conditions haven’t changed
• timing and grouping still need attention

Medication can’t compensate for a system that keeps pushing animals past their tolerance threshold.

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The takeaway

Coccidia isn’t about elimination.
It’s about managing exposure during critical windows.

When pressure is kept reasonable:
• most animals handle exposure
• fewer develop disease
• fewer carry long-term consequences

That’s what real control looks like.

In Part 4, we’ll talk about control vs elimination in practical terms — what actually moves the needle, and what just creates a false sense of security.

27/01/2026

27/01/2026

Coccidia — Part 2
What It Does to the Body
By Linessa Farms

In Part 1, we talked about what coccidia is — a protozoan parasite that lives inside the intestinal lining, not free in the gut like a worm.

That detail matters, because it explains why the damage coccidia causes looks the way it does.

This article is about what happens after exposure, and why some lambs and kids never quite catch up — even when they survive the acute phase.

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Where the damage happens:

In sheep and goats, coccidia primarily affect the small intestine, especially the sections responsible for nutrient absorption.

Once ingested, coccidia invade the cells lining the intestine and begin multiplying inside those cells. As the organisms reproduce, those cells rupture and die. Neighboring cells are then infected, and the cycle continues.

This isn’t irritation of the gut contents.
It’s structural damage to the intestinal surface itself.

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Why signs don’t always match the damage:

This is where people get tripped up.

By the time you see obvious diarrhea, a lot of damage has often already occurred. In some cases, diarrhea is mild or short-lived. In others, it may never be dramatic at all.

What you often see instead is:
• poor growth
• dull hair coat
• inconsistent manure
• animals that eat but don’t gain
• lambs or kids that look “weeks younger” than their penmates

This is the classic failure-to-thrive pattern.

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Why timing and amount of exposure matter so much:

Coccidia reproduce very quickly once inside the intestine. Small exposures spread out over time are usually tolerated and help build immune control.

The problem is high or repeated exposure over a short period, especially during stress windows like:
• weaning
• weather changes
• crowding
• diet shifts

It’s rarely one bad exposure.
It’s too much, too fast, at the wrong time.

That’s when the intestine takes the biggest hit — often before anyone realizes there’s a problem.

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What happens after the damage is done:

Here’s the part that causes the most confusion.

The intestinal lining does turn over, and some recovery can happen, especially if the damage was mild or short-lived.

But regrowing cells does not always mean the intestine goes back to normal.

Think of it like a roof. You can replace damaged shingles, but that doesn’t mean the sheeting or framing underneath wasn’t warped or weakened. The roof looks better, but it may never perform the same way again.

The intestine works the same way. Cells can be replaced, but the overall surface area and efficiency don’t always fully recover after severe or repeated damage.

That’s why some lambs and kids:
• stop scouring
• look brighter
• resume eating

…but still:
• grow slower
• struggle with feed efficiency
• never quite catch up to their peers

You don’t “fix” damaged intestine.
You manage what’s left.

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Why treatment alone often disappoints:

By the time coccidiosis is obvious:
• the most damaging phase has usually already happened
• treatment may stop further replication
• but it cannot undo lost intestinal structure

This is why late, blanket treatment so often feels ineffective — and why prevention matters far more than rescue.

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The key takeaway:

Coccidiosis isn’t just a short-term diarrhea problem.
It’s a developmental injury that can permanently change what an animal’s intestine is capable of doing.

In Part 3, we’ll talk about coccidia control — not eradication — and how management decisions determine whether exposure becomes a problem or just background noise.

23/01/2026

🌡️ With hot weather forecast for this weekend it's important your animals have access to shade and water.

Clean, cool water and shade is essential for animals in extreme heat.

✅ Check your animals regularly throughout the day for signs of heat stress, and water points to ensure access.

👉 For more information on caring for animals during extreme heat, please visit: go.vic.gov.au/3UvmQ2s

For the latest emergency information, visit emergency.vic.gov.au

If you have urgent animal welfare needs, please call the VicEmergency Hotline on 1800 226 226.

21/01/2026

Inbreeding vs Line Breeding – Part 6
Bottlenecks, Blind Spots, and What We Actually Know

By Tim from Linessa Farms

If you’ve followed this series from the beginning, you may have noticed something uncomfortable by now:

Most genetic narrowing does not happen because someone intentionally set out to line breed aggressively.

It happens quietly.
It happens unintentionally.
And it often happens under good intentions.

That’s what this final article is about.

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How most farms bottleneck without realizing it

You don’t need close matings to create inbreeding pressure.

It happens when
– the same ram is used too long
– replacement females all trace back to the same few animals
– outside genetics stop coming in
– selection focuses on a narrow set of visible traits
– culling pressure drops

No one calls this line breeding.
But biologically, it still increases genetic uniformity.

That’s why many people are already “under the umbrella” of inbreeding without ever putting their finger on it.

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COI, pedigree, and the illusion of precision

Inbreeding coefficients (COI) are often treated like a safety score.

But COI only estimates probability, not outcome.

It does not tell us
– which genes became homozygous
– whether those genes matter
– how they interact with environment
– or what management is compensating for

COI is also only as reliable as the records behind it.
If pedigree assumptions are wrong, or someone “fudged” records, the math can be clean and the answer meaningless.

COI is a risk indicator, not a verdict.

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Why some traits fade quietly

One pattern has repeated throughout this series:

– simple traits respond quickly
– complex traits degrade quietly

Traits like color, horn status, and body style stabilize fast.

Traits like
– fertility
– parasite resistance
– robustness
– longevity
– feed efficiency

are polygenic (multiple genes involved) and environment-dependent.

They don’t fail dramatically.
They lose margin.

And that loss often isn’t noticed until
– stress increases
– management slips
– animals move to a new environment

Nothing suddenly “went wrong.”
The system just ran out of room.

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Phenotype tells the truth — just not the whole one

Phenotype reflects gene expression under a specific set of conditions.

Two animals can carry the same genes and express them very differently depending on
– environment
– nutrition
– stress
– disease pressure
– management

That’s why animals can perform exceptionally well in one system and struggle in another without anything “changing genetically.”

Phenotype tells us what worked here, now, under this system.
It does not guarantee transferability.

Consistency is not the same thing as resilience.

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What responsible line breeding actually does

Responsible line breeding does not create universally superior animals.

It creates animals that fit a specific system very well — sometimes at the cost of flexibility outside that system.

Done well, it requires
– understanding which traits are simple vs complex
– constant, honest selection
– tracking fertility and longevity
– accepting culls when outcomes aren’t right
– recognizing that performance is system-specific

Done casually, it narrows genetics faster than people realize.

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The real risk most people miss

The biggest risk in breeding isn’t inbreeding itself.

It’s mistaking consistency for margin.

Uniform animals can look stable right up until the moment pressure changes.

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What I hope this series actually did

This series was never about telling anyone what they should do. Without trying to sound gruff, I could honestly care less if people choose to line breed or not. This is an education piece; that’s it. If you felt this was bashing your methods or promoting others, that’s just you projecting.

It was about
– cleaning up language
– removing false certainty
– separating probability from promise
– explaining why biology resists shortcuts

If this made breeding feel a little less tidy — and a little more honest — that’s a win.

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What’s next?

I’ll be following this series with a short companion video using a simple parking garage analogy to visually explain genes, alleles, homozygosity, and why environment changes outcomes. This is the visual I use when teaching human genetics. It still applies and I think many of you who are visual learners will find it helpful. Look for that post in a few days.

Not to convince anyone — just to make the structure easier to see.

Because once the structure makes sense, the arguments mostly disappear.

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Breeding isn’t about fixing genetics.
It’s about managing risk, margin, and reality.

Thanks to everyone who helped put these articles together! You are appreciated. I will be posting these articles together on our website as soon as I de-format them from Facebook to PDF.

21/01/2026

Today we had the opportunity to express our sincere gratitude to our vet of 18 years -John Hamilton of Avonsleigh Veterinary Clinic. Gayle, Jamie-Lee and I took the llamas to Avonsleigh to wish John all the best on his retirement. He will be greatly missed.