Bennington Katahdins

04/04/2026

02/28/2026

02/28/2026

When the Brain Is Involved — Part 3
By Linessa Farms

In Part 1, we stepped back.

In Part 2, we talked about environment and exposure — how moisture, fermentation, and bacterial load create opportunity.

Now let’s look under the hood.

Listeria is not a mold. It is a bacterium. And when it causes neurologic disease in sheep and goats, it does so in a very specific way.

It does not randomly circulate through the body and suddenly “attack the brain.”

In many cases, listeria enters through small abrasions in the tissues of the mouth — often associated with coarse feed, silage, or rough forage. From there, it can travel along cranial nerves toward the brainstem.

That detail matters.

Because once it reaches the brainstem, it does not affect the entire brain uniformly. Instead, it creates localized inflammation along specific nerve pathways.

And when different cranial nerves are involved, the outward signs change.

The trigeminal nerve helps control jaw tone and chewing.The facial nerve contributes to facial movement and normal lip function.The vestibular system helps regulate balance and spatial orientation.

Inflammation affecting the trigeminal nerve can lead to difficulty chewing, dropping feed, or a slack jaw.

Facial nerve involvement can result in drooling or asymmetry of the face.

Vestibular involvement can produce head tilt, loss of balance, or circling.

The underlying infection may be the same.The expression can look very different.

That variability is not randomness. It’s anatomy.

In people, when we evaluate a stroke, we can ask patients to smile, raise their arms, follow commands, or describe what they see. We can use imaging to localize the problem.

With sheep and goats, we do not have that luxury.

We only see outward signs — and often only once they become obvious.

That’s why subtle changes matter.

An animal that seems slightly off-feed.A goat that chews awkwardly.A ewe that drools when she normally wouldn’t.

These are not diagnoses. They are clues.

Here’s the important part of all of this:

Neurologic disease looks variable because the nervous system is complex.

The brainstem is a dense cluster of nerve pathways controlling chewing, swallowing, facial tone, balance, and coordination. When inflammation develops there, signs can evolve and shift over time.

Early in disease, an animal may simply appear dull with a fever. Later, as inflammation progresses, neurologic deficits become more pronounced.

And when the brain is involved, time matters. For diseases like listeria, the clock is ticking and a swift targeted response can make a significant difference when it comes to outcomes.

Antibiotics must reach effective levels in the body and ideally pe*****te the central nervous system. Not all antibiotics do this equally. Some medications reduce inflammation. Others target bacteria. They are not interchangeable.

Dexamethasone may reduce swelling. Thiamine may support metabolic function. But neither eliminates a bacterial infection on its own.

Understanding mechanism does not replace treatment — it sharpens it.

It also explains why prognosis is often guarded. By the time neurologic signs are obvious, inflammation has already progressed.

That does not mean recovery is impossible. But early recognition improves the odds.

In the next part of this series, we’ll bring these pieces together — environment, exposure, and mechanism — and talk about what practical response looks like when neurologic disease shows up in a real flock or herd.

02/27/2026

When the Brain Is Involved — Part 2
By Linessa Farms

In Part 1, we stepped back.

We talked about how neurologic signs don’t follow a script, how polio can be illness or signal, and why rushing to a label doesn’t usually improve outcomes.

Now let’s start looking at the “why’s.”

When listeria shows up in a flock or herd, it often feels sudden. An animal that seemed normal yesterday now appears off. Drooling. Circling. Not eating correctly. Maybe down.

But listeria rarely appears out of nowhere.

It is almost always connected to environment and exposure.

Spring is a common time to see it — not because it only exists in spring, but because conditions begin to line up.

Daytime temperatures rise above freezing.
Moisture increases.
Round bales sweat.
Silage warms and shifts.
Fermented feed becomes more active.

Bacteria respond to those changes.

Listeria monocytogenes is commonly present in the environment. It lives in soil. It can contaminate feed. It does not require a dramatic setting to exist.

What changes is opportunity.

Wet, improperly fermented silage.
Chronically damp hay.
Feed that heats and cools repeatedly.
Grain intentionally soaked and allowed to ferment.

Those conditions increase bacterial load.

And load matters.

There is a significant difference between low-level environmental presence and overwhelming exposure.

It’s important to clarify something here.

*Listeria is not a mold. It is a bacterium*

Visible mold is often a warning sign — it tells you moisture and improper fermentation have occurred. Those same damp conditions are what allow bacteria like listeria to multiply.

But mold itself can represent several different issues. A light layer of dried surface mold after weather exposure is not the same thing as cracking open a bale and finding deep, wet, black deterioration throughout.

The presence of mold tells you the environment has shifted — not that a single disease is automatically present.

That’s why you might see:
• one sheep or goat affected in an otherwise healthy group
or
• multiple animals affected when feed conditions deteriorate.

Dose and susceptibility intersect.

Sheep and goats are not cattle.

I hear it often: “Cattle eat that kind of hay all the time.”

Maybe they do.

But small ruminants are generally more susceptible to neurologic listeriosis. Just because another species tolerates something does not mean sheep or goats will.

There’s another misconception worth addressing.

“Won’t they just eat around the mold?”

Sometimes.

But not all contamination is visible. Not all bacterial growth produces a strong odor. And when animals are hungry, selectivity decreases.

Here’s the part to think about:

Listeria is not about “bad hay” in a simplistic sense.
It’s about moisture, fermentation, and bacterial load.

It’s about conditions that allow exposure to exceed what the animal can handle.

Some years you may have round bales with a little dry, powdery mold along the outer layer and see no neurologic cases at all.

Other times, wet silage or chronically damp feed can overwhelm a group quickly.

The difference is not always visible from across the pasture.

It’s scale.

And scale changes outcomes.

Understanding that matters — because it keeps us from reducing listeria to a seasonal one-off or a single feeding mistake. It pushes us to look at patterns: temperature shifts, moisture levels, feed storage, animal stress, pregnancy status.

In the next part of this series, we’ll look more closely at what listeria does once it gains access to the nervous system — and why two animals with the same underlying disease can look so different.

02/26/2026

WEEKLY RESEARCH SHARE

High-fructose corn syrup for managing negative energy balance in sheep

Lay summary
Ketosis is a serious metabolic condition of energy deficiency in ruminants. We employed sheep to investigate whether High-Fructose Corn Syrup (HFCS), a main ingredient in soft drinks, could serve as a simple and affordable treatment. Ketotic sheep were drenched with either Coke, a mix of HFCS and carbonated water, or just plain water or carbonated water. The results show that both the Coke and the HFCS mix significantly raised blood sugar and lowered ketones, which are the main indicators of ketosis. The plain and carbonated water treatments had no effect. No significant difference was found between the results from Coke and the HFCS mix, suggesting the benefits come from the HFCS syrup itself. This study suggests that readily available and inexpensive beverages containing HFCS could be a practical on-farm solution for farmers to manage ketosis in their flocks.

Abstract
Ketosis and its severe complication in small ruminants, pregnancy toxemia, are major metabolic disorders characterized by hypoglycemia and high blood concentrations of β-hydroxybutyrate (BHBA) resulting from negative energy balance (NEB). Although conventional treatments rely on glucogenic precursors like glycerol and propylene glycol, farmers often turn to lower-cost alternatives, including sugary soft drinks containing high-fructose corn syrup (HFCS) and carbonated water (cWater). In this study, we evaluated the relative contribution of the primary components of Coca-Cola (Coke), used here as a representative and readily accessible energy source, in mitigating NEB in sheep. Twenty-eight Afec-Assaf ewe lambs (N = 28), fasted for 48 h to induce NEB, were randomly assigned to four treatment groups (n = 7): 1 L of either Water, cWater, carbonated HFCS solution (cHFCS), or Coke. Blood samples were collected at 0 and 1, 2, and 3 h post-treatment to measure glucose and BHBA concentrations. Glucose area under the curve (AUC) values were highest in cHFCS (2339.5 ± 628.6 mg/dL × min) and Coke (1778.5 ± 437.6 mg/dL × min), intermediate in cWater (950.8 ± 391.3 mg/dL × min), and lowest in Water (570.0 ± 184.5 mg/dL × min). ANOVA indicated significant treatment effects (P

02/25/2026

So the saying of never counts your chickens before they hatch also applies to lambs and their future. I have been very unhappy with my ram this past year due to failure to see him breed and just his look. However he did get the job done but I had committed to not keeping any offspring.

However, one girl that I was not sure about has produced a set of twins that look super good right now and making me reconsider that decision. It is super early still and they are only 30 days old so we will see. But this girl (Boots) and her brother (No name yet) has really got my attention.

Who knows it may all change in 4-5 months but we will see what happens with these two. This little ram is already making a point to learn the ladies while the others play.

02/24/2026

CRYPTO SERIES — PART 3
What It Looks Like — And Why It Doesn’t Always Look the Same

By Tim from Linessa Farms

Up to this point we’ve talked about where crypto comes from and why some animals tip toward illness while others don’t. Now let’s talk about what people actually see on the ground — because this is where things start to get confusing, and honestly, where a lot of misdiagnosis begins.

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Crypto usually doesn’t rush in like a storm.
More often, it walks in quietly and slow enough that you don’t realize it’s there until the scale has already started tipping.

One of the biggest mistakes I see is people waiting for crypto to look dramatic. Sometimes it does. Sometimes it absolutely does not.

You might notice:
• Loose stool that doesn’t look severe at first
• Babies that seem slower than the rest
• Nursing less aggressively
• Mild dehydration before obvious scours

By the time the barn says, “Something is wrong,” the organism has often already been moving through the group. That’s not failure on your part. That’s just the nature of how this organism works.

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Why It Doesn’t Look the Same on Every Farm

Remember the scale analogy from Part 2?

Every lamb and every kid has a different balance point.

So, crypto rarely produces one identical picture.

On one farm you might see explosive watery scours and rapid dehydration (this is what people expect).
On another farm it may look more like slower growth or babies that just never quite thrive.

Same organism. Different scale balance.

That’s why comparing notes between farms can get tricky — environment, age, and exposure pressure all shape what people actually see.

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The Glitter Analogy — How Crypto Really Spreads

I’ve used this analogy before because it sticks.

Crypto spreads a lot like glitter — and if you’ve raised three girls like I have, you know exactly what I’m talking about. Once it’s in the environment, it shows up in places you didn’t even know existed.

You may not see where it came from.
You may not realize it’s everywhere.

But once it’s in the environment — bedding, boots, udders, buckets, hands, fur — it moves quietly and efficiently.

You don’t need a massive outbreak for exposure to occur.
Sometimes it’s just enough glitter in the wrong place at the wrong time.

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Why Fecals Don’t Always Give You the Answer

This is a big one — especially for people used to looking for worm eggs or coccidia.

Crypto isn’t always obvious on a standard f***l float.

Part of the reason is simply size and timing. Crypto oocysts are much smaller than most of the things people are used to finding on a routine float, and they aren’t always shed consistently. A baby can be clinically affected before shedding levels are high enough to show up easily, and not every sample tells the full story.

Diagnostics are helpful — but they’re only one piece of the puzzle. What I care about most is the pattern:
• Age of onset (often after the first week of life)
• Group dynamics
• Environmental pressure
• Clinical progression

The barn often tells you more than a single test result.

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What Crypto Usually Doesn’t Look Like

Crypto is primarily a gastrointestinal organism.

So when I see questions about sudden neurological signs, severe lameness, or babies walking on the tops of their feet, my brain goes somewhere else first. That doesn’t mean two problems can’t exist at the same time — but crypto alone usually doesn’t explain everything.

Not every scouring baby has crypto, and not every slow-growing animal points back to the same cause. Slowing down and looking at the full picture matters.

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Why Timing Matters So Much

Most clinical crypto problems don’t show up on day one. That surprises people.

A lot of babies look completely normal at birth. Then environmental exposure builds, immature immune systems get challenged, and the scale slowly tips.

Most of the time I start paying closer attention once babies are past that first week of life, especially if environmental pressure is building. That doesn’t mean something went wrong — it just reflects how neonatal immunity develops over time.

Early management — bedding, colostrum, and environment — helps shape the scale long before illness becomes obvious.

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What We’ll Talk About Next

So far we’ve covered:
• The organism
• The environment
• What recognition actually looks like

Next, we’ll talk about support and management — not as a checklist, but as ways to shift the scale back toward resilience.

Because treatment without understanding usually just leads to frustration.

Part 4 will focus on supportive care, realistic expectations, and what actually helps when crypto shows up.

Educational content only — not a substitute for veterinary or personal medical care.

02/24/2026

We just spent a lot of time talking about coccidia… and a lot of you started to realize something uncomfortable:

Not every case of diarrhea in a lamb or kid fits neatly into that box.

There’s another player that shows up quietly during lambing and kidding season — hits young animals hard, laughs at a lot of the treatments people reach for, and doesn’t care how clean you think your barn is.

Cryptosporidium.

This is a conversation most farms avoid because the rules feel different… and sometimes unfair.

If you followed the coccidia series, you already have the foundation. Now we’re going to talk about where those rules start bending — early-age scours, environmental pressure, zoonotic risk, and why “just treat it” isn’t a real strategy here.

No hype. No scare tactics. Just the stuff people don’t explain clearly enough.

Series starts February 19th.

— Tim

02/24/2026

Well we have finished lambing for the year. It was kind of unexpected and kind of rough but not a disaster. This is not my ideal time to lamb and hopefully next year will end up much better.

Our last girl "Seven" lambed out tonight. I have been waiting on this girl now for 3 years. She has not been able to be bred untill this year (none of it her falt. She had 2 girls and a boy, the boy seems a little weak but think he will be okay. If he makes it through the night then he will probably be good.

So far out of our six ewes, 3 lambed out twins and 3 lambed out triplets making a total of 15 little bouncing babies.

Here are some photos of the lambs from this year (and a couple of others watchers).

02/15/2026

https://www.farmeranalytics.com/diy-f***l-egg-counting-course

02/12/2026

Part 2 in a short series on newborn weakness and early-life systems in lambs and kids.

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White Muscle Disease: When the Wrong Gear Gets Blamed

White muscle disease is one of the most commonly named problems in newborn lambs and kids — and one of the most commonly misunderstood.

That’s not because it doesn’t exist. It definitely does.
It’s because weakness gets blamed on it far more often than it should.

When a newborn struggles to stand, nurse, or move well, white muscle disease is often the first explanation people reach for. The problem is that weakness is a shared symptom for multiple problems, not a diagnosis. Many different systems can fail in ways that look the same in the first few hours of life.

If we don’t slow down and understand what white muscle disease actually is — and what it isn’t — we end up treating the wrong gear in the machine and often wasting valuable time.

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White muscle disease doesn’t start at birth

One of the biggest misconceptions about white muscle disease is that it suddenly “shows up” when a lamb or kid is born.

In reality, it develops quietly before birth.

By the time a newborn is born showing weakness related to white muscle disease, the underlying problem has usually been present for weeks. That matters, because it explains why treatment sometimes appears to work — and why it sometimes doesn’t.

White muscle disease is the result of long-standing insufficiency, not an “on the spot”/acute event.

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Selenium and vitamin E don’t work alone

Selenium and vitamin E function as a pair. One supports the other. Neither does its job very well alone.

This is one reason white muscle disease is so often misunderstood. When a newborn improves after treatment, it’s easy to assume selenium was the problem. In reality, improvement can come from briefly supporting a system that was already marginal, rather than correcting what failed first.

Even when selenium levels are technically sufficient, the system still has to be able to use it. Energy matters here. A newborn that is depleted doesn’t handle stress, repair, or muscle function the same way — even when things look adequate on paper. We don’t need to unpack the deep-weeds biology to recognize the pattern. Availability and effectiveness are not the same thing.

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Why weakness gets confusing

Weakness in a newborn lamb or kid can come from many places:
• low energy reserves
• cold stress
• prolonged or difficult birth
• delayed nursing
• marginal nutrition before birth

All of these can look similar early on.

White muscle disease often gets blamed because it’s familiar, it has a name, and it has a treatment people recognize. But familiarity isn’t always the same thing as accuracy.

This is where the Part 1 article matters.

If the energy gear never turns properly, everything downstream can look broken — even when muscle tissue itself isn’t the primary issue.

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Why improvement doesn’t always mean you were right

This is where a lot of confusion starts.

Supporting one system can temporarily prop up another. Reducing stress, improving muscle function, or simply buying time can all make an animal look better — even if the original weakness had nothing to do with white muscle disease.

White muscle disease does not come and go.

It doesn’t resolve and then return based on the last thing we gave. If a lamb or kid improves briefly and then crashes again, that pattern doesn’t fit white muscle disease. It tells you something else failed first and was only temporarily supported.

Likewise, if a weak newborn improves simply by being warmed, fed, or supported, that improvement matters. True white muscle disease doesn’t resolve because the animal finally had enough energy. That’s not how it works.

That’s a deeper conversation — and it’s not the one we need to have yet (but will).

What matters here is understanding why response alone doesn’t confirm the diagnosis.

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White muscle disease is real — but rarely isolated

True white muscle disease does occur. When it does, it usually follows a pattern:
• multiple animals affected
• similar weakness across the group
• poor muscle tone
• limited response to basic supportive care

What it usually does not look like is a single weak newborn in an otherwise normal group.

When every weak lamb or kid gets labeled as white muscle disease, we stop asking better questions — and we miss the opportunity to correct what actually matters.

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Zooming back to the system

White muscle disease is one gear in a much larger machine.

It’s influenced by:
• maternal nutrition
• vitamin status
• mineral availability
• energy balance
• timing

Treating that one gear without understanding the rest of the system is how people end up frustrated when outcomes don’t match expectations.

In the next article, we’re going to put those gears back together and talk about why order matters more than intensity — and why fixing the wrong thing, even aggressively, doesn’t move the system forward.