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Linessa Farms, LLC, 2563 N McKinley Avenue, Rensselaer, IN (2026)

Linessa Farms specializes in sheep and goat educational programs, videos, and research.

08/06/2026

CAE & OPP - Part 4: “But She Looks Perfectly Healthy”

A goat or ewe tests positive for CAE or OPP.....

She looks great, active, and maintaining excellent body condition. Her feet and legs look good. Her udder appears normal. She raises healthy kids or lambs and remains one of the most productive animals in the herd/fock.

So the producer naturally asks:

“How can she have CAE or OPP? There's nothing wrong with her.”

The answer is one of the most important things to understand about small-ruminant lentiviruses:

Being infected is NOT the same as appearing sick.

Most sheep and goats infected with these viruses remain largely asymptomatic (don't display symptoms of illness)... sometimes for their entire lives. They may never develop the dramatic arthritis, respiratory distress, neurologic disease, or severe wasting you might commonly hear about with CAE and OPP.

- They're still infected.
- They are still persistent carriers.
- They may still transmit the virus to other animals.

- Infection, disease and clinical illness -

We often use these words as though they mean the same thing, but they describe different stages of the process.

- Infection means the virus has entered the animal and established itself within its cells.

- Disease means the infection is creating abnormal changes or damage within the body.

- Clinical illness means that damage has progressed far enough to produce signs we can see from the outside.

Bottom line... An animal can be infected without appearing ill.

It can even have microscopic tissue damage without showing anything obvious during an ordinary examination.

By the time visible signs develop, the infection may have been present for years... and often has been.

- The animal isn't "lying to us" -

The healthy-looking positive animal isn't a "false picture" of disease.

It's the NORMAL picture of a lentivirus infection.

These viruses survive by moving slowly and persisting quietly. They don't need to make every infected animal visibly sick. In fact, an animal that remains active, productive, and socially connected actually provides the virus with more opportunities to spread than an animal that quickly becomes severely ill.

Look at it from the virus's perspective:

- The virus benefits from time.
- Time to nurse offspring.
- Time to share airspace.
- Time to stand at the feeder.
- Time to enter the milking string.
- Time to move between farms.

A visibly sick animal attracts attention fast, and that's not how this virus has been so successful.

- A positive test does not predict the animal’s future -

A confirmed positive result tells us the animal has developed detectable evidence of infection.

It does not tell us exactly what will happen next.

Some infected goats eventually develop chronic arthritis, often involving the carpal joints. Others may develop a firm, poorly productive udder, chronic pneumonia, progressive weight loss or, less commonly, neurologic disease. Merck notes that "clinical signs are observed in only a minority of infected goats during their lifetime".

"Clinically affected sheep are most often recognized by progressive pneumonia, exercise intolerance, weight loss, or a hard, poorly productive udder. Neurologic disease may also occur, but many infected sheep remain outwardly normal".

We can't just look at a positive animal and reliably predict:

- Whether it will ever become clinically ill
- Which organ system will be affected
- How quickly disease might progress
- How much virus it may shed
- Which exposed animals will become infected

A positive result identifies infection.

It is not a countdown clock.

- Why does one animal become sick while another doesn't? -

Clinical disease is most often influenced by several interacting factors:

- Viral strain
- Amount and frequency of exposure
- Age at infection
- Genetics
- Immune response
- Stress
- Nutrition
- Concurrent disease
- Housing and ventilation
- Length of time infected

That's why two animals living in the same herd can have very different outcomes.

- One may develop swollen knees and progressive lameness.
- Another may develop a hard udder.
- A third may slowly lose weight.
- A fourth may remain apparently healthy for life.

They can all carry the same general category of infection while expressing it differently.

- “She has never had a problem” isn't a test result -

Livestock producers are trained to value observation.

That is usually a strength.

We notice appetite, posture, movement, rumen fill, body condition, breathing and behavior. Those observations often help us identify disease before laboratory results are available.

Lentiviruses challenge that skill because the absence of visible signs tells very little about infection status.

At the end of the day:

- You can't reliably identify CAE or OPP carriers by looking at them.
- You can't feel every infected animal’s knees and declare the herd negative.
- You can't examine udders and assume every normal udder belongs to an uninfected animal.
- You can't watch a flock walk across the pasture and determine which sheep are carrying OPP.

Clinical observation can HELP identify animals already showing disease. Butt can't identify every infected animal.

I've heard many people say... "I can tell".... ummmm no you can't.

That requires testing.

- Production can decline before the animal looks sick -

Not all effects of infection are dramatic (and they usually aren't).

An animal doesn't have to become severely lame or visibly short of breath before the infection begins to matter economically.

The changes may be subtle:

- A ewe begins trailing slightly behind the flock.
- A doe’s milk production gradually declines.
- An udder feels firmer than expected but is not hot or painful.
- An animal loses condition despite appearing to eat normally.
- A mature goat becomes stiff but is dismissed as simply "getting older".
- A ewe repeatedly raises lighter lambs.

None of those observations proves/disproves CAE or OPP.

Many other conditions can produce the same signs.

But... that's exactly why lentivirus-associated losses can go unrecognized. Slow changes are easily explained away as age, genetics, parasites, nutrition, previous injury, or the dreaded and very scientific..."bad luck".

I rarely see sheep or goats reach the dramatic pictures shown in a veterinary textbook.

They often simply become less productive.

- The best-looking animal may still be the source -

This is where emotion enters the discussion.

The positive animal may be:

- A favorite doe
- A proven mother
- A valuable donor
- A champion
- The foundation of a bloodline
- An animal that has never appeared sick

The virus doesn't care about any of this, and deep down in places many people don't talk about.... this is a huge issue and reason the virus is such a problem.

*Healthy carriers are why these diseases persist*

- Positive does not mean worthless!-

A positive animal is not automatically suffering.

- It's not poisonous.
- It doesn't need to be treated as though standing near it creates an emergency.

And... a positive result does NOT dictate one identical decision for every farm.

The "appropriate" response depends on the producer’s goals, facilities, prevalence within the herd, ability to separate groups, and willingness to accept continued risk.

- Some producers may cull positive animals.
- Others may maintain a completely separate positive group.
- A heavily infected herd may choose a gradual replacement program rather than immediate removal.

What's not reasonable is pretending the result means nothing because the animal looks healthy.

At the end of the day.... believe the test before you believe the appearance.... enough said.

Up Next: What should you do with a positive animal -culling, separation, and realistic control options-

07/28/2026

CAE & OPP - Part 3: What Does the Test Actually Tell Us?

Sorry about the delay.... this one took a while to put together.

In Part 1, we introduced the lentivirus.

In Part 2, we looked at how infected cells can move through colostrum, milk, respiratory secretions, and blood.

That brings us to testing...

A producer draws blood, sends it to a laboratory, and receives a result:

Positive. Negative. Occasionally suspect or inconclusive.

It appears simple.

The difficult part is understanding what that result actually means.

*Most routine tests are looking for antibodies*

The tests most commonly used for CAE and OPP are serologic tests.

That means they examine serum from the animal’s blood and look for antibodies produced by the immune system in response to the virus.

They are generally NOT looking directly for the virus itself.

A positive antibody test tells us the animal’s immune system has recognized a small-ruminant lentivirus and mounted a detectable response.

"Because CAE and OPP produce persistent, lifelong infections, an animal with a confirmed positive result is generally considered infected and capable of carrying the virus".

A negative result means antibodies were not detected by that particular test, in that particular sample, or on that particular day.

Those two statements are NOT equal.

- A positive result can be strong evidence of infection.
- A negative result is evidence that infection was not detected.
- It is not always proof that infection is impossible.

*The immune response takes time*

We've discussed this before in our series on CL.

An animal doesn't become infected and instantly produce enough antibodies for a blood test to detect.

There is a period or time between infection and a measurable antibody response. This is sometimes called the "serologic window".

During that "window", the animal may already carry the virus but still test negative.

The length of that period is not identical in every animal. Antibody production can vary with:

- Age
- Time since exposure
- Viral strain
- Individual immune response
- Stage of infection
- The test being used

Some infected animals develop detectable antibodies relatively quickly. Others take considerably longer.

This is one reason a newly purchased animal should not be declared safe based only on a single negative test taken immediately after arrival.

The test may accurately describe what could be detected that day while still missing a recent infection.

*ELISA and AGID*

The two traditional antibody-testing methods used for small-ruminant lentiviruses are ELISA and AGID.

- ELISA

ELISA stands for "enzyme-linked immunosorbent assay".

It's commonly used to screen large numbers of animals because it can be automated, is relatively economical, and can detect relatively small amounts of antibody.

Different laboratories may use different forms of ELISA, including indirect, competitive, or blocking assays.

Although the details vary, the basic question remains:

"Does this serum contain antibodies that react with the viral proteins used in the test?"

- AGID

AGID stands for "agar gel immunodiffusion".

In this test, "viral antigen and the animal’s serum move toward one another through a gel. When matching antibodies are present in sufficient quantity, they form a visible line of precipitation".

AGID has been used for decades and is generally regarded as a specific test, but it may be less sensitive than some modern ELISA methods.

That means an infected animal with a lower antibody level may be detected by one assay and missed by another.

Neither test is simply “good” or “bad.”

The result depends partly on how well the viral antigens in the test match the antibodies produced against the virus circulating in that animal or herd.

*These viruses are not genetically identical*

We often speak about “the CAE virus” or “the OPP virus” as though every infection were caused by an identical organism. As we've discussed previously, this is not the case.

In reality, small-ruminant lentiviruses include multiple genetic groups and strains.

That variation can affect testing.

A test is built using selected viral proteins or antigens. If the infecting strain is different enough from the strain represented in the test, the animal’s antibodies may not react as strongly.

This does not make antibody testing useless!

It simply means no single test can promise "perfect" detection of every infected animal in every herd under every circumstance.

*Why results occasionally disagree*

A producer may send samples to two laboratories and receive different results (I've seen this happen many times).

Or an animal may test negative one year and positive the next.

That doesn't automatically mean one laboratory made a mistake.

Several explanations are possible:

- The animal was infected after the first test.
- The first test occurred before antibodies became detectable.
- Antibody levels increased or fluctuated.
- The laboratories used different assays or viral antigens.
- One result was near the test’s cutoff.
- A technical or sample-handling problem occurred.
- A false-positive or false-negative result occurred.

Laboratory tests are tools, not magic.

Their value comes from combining the result with the animal’s history, age, exposure risk, previous testing, and the status of the rest of the herd or flock.

*What about PCR?*

PCR is designed to detect viral genetic material rather than the animal’s antibodies.

That sounds as though it should settle the matter:

If the virus is present, PCR should find it.... right?

Unfortunately, lentiviruses make that more complicated.

The virus may be present in only a small proportion of circulating cells. The amount of detectable viral material can be low, and it may not be evenly distributed through every sample.

Small-ruminant lentiviruses are also genetically variable. A PCR assay must recognize the genetic sequence of the strain being tested. If that sequence differs from the target used by the assay, detection may become more difficult.

- A positive PCR result can provide strong evidence of infection.
- A negative PCR result does not always exclude it.

PCR can be useful in particular situations, but it does not automatically replace antibody testing for routine herd screening.

*One animal is not the herd*

Suppose a producer tests five animals from a herd of fifty and all five are negative.

What has been learned?

Those five animals had no detectable antibodies on the day they were sampled.

That's useful information.

It does not establish that the other forty-five animals are negative.

It also does not tell us whether the five tested animals were infected recently or whether they will remain negative after continued exposure.

The more animals tested (and the more thoughtfully they are selected), the more meaningful the picture becomes.

Testing only young animals, only healthy-looking animals, or only animals that are convenient to catch may leave important gaps.

A herd-level disease requires herd-level thinking.

*Think of one negative test as a photograph*

Think of a test result as a photograph.

It captures what the test could see at one moment in time.

- A photograph does not tell us what happened the week before.
- It doesn't tell us what will happen next month.
- It doesn't reveal everything outside the frame.

Repeated testing creates a series of photographs. Over time, those images provide a much clearer picture of the herd.

An animal that remains negative through repeated testing, while being protected from known exposure, gives us much greater confidence than an animal tested once while living among animals of unknown status.

*Testing without management changes very little*

A producer may test the herd, identify positive animals, and then return every animal to the same shared pens, feeders, maternity areas, and airspace.

- The laboratory provided information.
- The management system ignored it.

Testing is most valuable when the results lead to a decision:

- Separate positive and negative groups
- Remove infected animals
* Change kid- or lamb-rearing practices
- Avoid pooled colostrum and milk
- Stop reusing needles
- Improve ventilation and reduce crowding
- Test incoming animals
- Establish a schedule for repeat testing

Without a plan, testing can become little more than paying to learn that the problem exists.

*“Negative herd” should describe a process*

People sometimes advertise a herd or flock as “CAE negative” or “OPP negative” because several animals tested negative once.

In my opinion, that claim may sound stronger than the evidence behind it.

A credible negative status should be supported by more than one piece of paper.

It should include:

- Appropriate testing of the breeding population
- Repeated negative results over time
- Control of new animal introductions
- Separation from animals of unknown or positive status
- Management practices that reduce transmission
- Records that allow the history to be verified

The longer a herd remains closed, protected from exposure and consistently negative through repeat testing, the more confidence we can place in its status.

*A test does not replace judgment*

Testing for CAE and OPP is not pointless because it is imperfect and that's not at all what I'm trying to say.

It's valuable precisely because these infections are otherwise so difficult to see.

The mistake people make is expecting one test to answer a larger question than it was designed to answer.

A positive result usually tells us something important:

"This animal has developed detectable antibodies to a small-ruminant lentivirus and should be considered a carrier unless further investigation shows otherwise". Period.

A negative result tells us something narrower:

"This test did not detect antibodies in this sample today".

Once we start stepping outside of these two statements, we may be making assumptions that lead to poor outcomes.

That negative result becomes far more meaningful when it is supported by time, repeat testing, and a management system that prevents new exposure.

The goal is NOT merely to collect negative test results.

The goal is to build a herd or flock in which those negative results continue to make sense.

Next: The positive animal that looks perfectly healthy - and why appearance tells us almost nothing about infection status.

07/20/2026

CAE & OPP - Part 2: How the Virus Moves

In Part 1, we introduced the lentivirus, a slow, lifelong retrovirus that inserts its genetic material into infected cells and persists largely within the immune system.

Now we need to answer the practical question:

*How does it move from one animal to another?*

Most goat producers have heard the familiar answer:

CAE is passed through colostrum and milk.

That is true... but it also isn't the whole story.

"Small-ruminant lentiviruses can travel inside infected cells found in colostrum, milk, respiratory secretions, blood and other body fluids. The importance of each route varies between goats and sheep, between individual animals and with the way they are managed".

Don't think of the virus as floating in a bucket of milk or dripping from an animal’s nose. It's usually carried inside the immune cells we discussed in Part 1.

In other words, the virus often travels by "hitching a ride" inside an infected cell.

- Colostrum is a very efficient delivery system -

If you haven't read our articles on colostrum, it may be worth your time to consider.

Colostrum is filled with maternal immune cells and antibodies designed to protect the newborn.

Unfortunately, when a doe is infected with CAE virus, some of those maternal cells may also carry the virus.

The newborn kid’s intestine is especially capable of absorbing material during the first hours of life. That's exactly what allows protective antibodies to cross from the colostrum into the bloodstream.

It also makes infected colostrum an efficient route of exposure.

The same biological "doorway" that provides the kid with its first immune protection can also give the virus access to a new host.

"Milk remains a risk after the intestine becomes less capable of absorbing intact antibodies. Repeatedly consuming milk containing infected cells or viral material provides continued opportunity for infection".

This is why many CAE-control programs pull kids from infected or unknown-status dams immediately at birth and feed heat-treated colostrum, tested-negative colostrum, or an appropriate commercial replacement.

But there's an important distinction:

*Removing kids at birth helps interrupt transmission to the kids. It does not remove the virus from the adult herd.*

- Birth itself is not necessarily the infection -

When a kid from a positive doe tests positive later, people often assume the virus crossed the placenta during pregnancy.

That is possible, but according to the scientific literature, it doesn't appear to be the primary route under most circumstances.

Much of what we call transmission “from the mother” actually occurs immediately after birth through colostrum, milk, and close contact.

That difference matters because it means management can greatly reduce the risk. The kid's not automatically infected simply because its dam is positive.

However, birth removal must be immediate and carefully managed. Allowing the kid to nurse (even briefly) may defeat the entire purpose of the program.

Shared towels, contaminated hands, feeding equipment and contact with birth fluids can also undermine an otherwise careful separation procedure.

- OPP often moves through the airways -

In sheep, colostrum and milk CAN transmit the virus, but prolonged respiratory exposure appears to play a particularly important role.

An infected sheep may release virus-containing cells in respiratory secretions. Another sheep sharing the same airspace may inhale droplets or encounter those secretions through close nose-to-nose contact.

This does not mean OPP drifts for miles in the wind...

Think close, repeated exposure, not a cloud passing over the neighbor’s farm.

Risk increases when sheep spend long periods together in enclosed or poorly ventilated spaces:

- Winter confinement
- Crowded barns
- Shared feeding areas
- Lambing pens
- Transport
- Other prolonged close-contact conditions

One brief encounter may not carry the same risk as months of breathing, eating and resting beside an infected animal.

Time and proximity matter (a lot).

This helps explain why OPP can slowly work its way through an adult flock even when lambs are removed and artificially reared.

- CAE and OPP can also spread horizontally -

Although milk and colostrum receive most of the attention in goats, adult-to-adult transmission can occur.

Goats kept in prolonged close contact may exchange infected respiratory and mucous secretions as well. The virus may also be moved whenever blood or infected cells are transferred between animals.

Potential opportunities include:

- Reusing needles
- Blood-contaminated tattooing or identification equipment
- Surgical instruments used without proper cleaning
- Dehorning equipment contaminated with blood
- Milking equipment contaminated with milk from an infected doe
- Feeding pooled colostrum or milk from multiple animals (more on this below)

Not every exposure results in infection, and not every possible route carries equal risk. However, repeated small opportunities can become important over the lifetime of a herd.

A producer may carefully raise CAE-negative kids and later place them back into prolonged contact with positive adults. Those young goats may have avoided infection during their first days of life only to remain exposed for years afterward.

- Pooled milk can turn one positive animal into a herd-level exposure -

Pooling colostrum or milk is convenient (I do it myself), but it removes the barrier between individual animals.

Milk from one infected doe may be fed to many kids.

Instead of one dam potentially exposing her own offspring, a single positive animal can expose an entire group.

The same principle applies when surplus milk from several does is combined without knowing their status.

The bucket does not dilute the risk away.

It distributes it.

- What about breeding? -

I get asked about this a lot, and here is what I can find in the literature:

Small-ruminant lentiviruses have been detected in reproductive tissues and secretions, but ordinary breeding isn't generally considered the primary way CAE and OPP spread through a herd or flock.

That doesn't mean reproductive transmission is "impossible". It means that colostrum, milk, prolonged close contact and respiratory exposure deserve a lot more attention in most control programs.

A positive buck or ram should still not be considered harmless. Even if breeding itself is not the main concern, that animal shares feeders, water, bedding, airspace, and direct contact with the rest of the group.

- Needles do not know which disease they are carrying -

This is a big one that is overlooked...

A needle that enters an infected animal may carry a small amount of blood and infected cells into the next animal.

The amount may be tiny.... but that doesn't matter.

That's the "problem" with microscopic things: they don't need to look impressive to matter.

Using one needle across an entire group creates a possible bridge from animal to animal -not only for CAE and OPP, but for other bloodborne infections as well.

A new sterile needle for each animal is a simple habit that removes that bridge.

Do I reuse needles on multiple animals? Yep. We have a CAE and OPP negative herd and flock... but I'm still taking a risk.

- The virus takes advantage of management connections -

In a nutshell, you can see how management practices play a big role in controlling OPP and CAE, especially if you have a positive herd or flock...

Understanding transmission changes the question from:

“Which animals look sick?”

to:

“Where are infected cells being allowed to move between animals?”

That is the foundation of an effective control program.

Next: Testing for CAE and OPP - what a positive or negative result actually tells us.

Thanks for following along. I will post a companion video to this article soon.

07/17/2026

CAE & OPP - Part 1: Meet the Lentivirus

Welcome to our series on CAE and OPP in sheep and goats. I recorded a video earlier in the week describing this and will continue publishing videos to accompany these articles as we move through the series.

CAE in goats and OPP in sheep are caused by closely related viruses collectively known as "small-ruminant lentiviruses".

You may not recognize the word "lentivirus", but you probably recognize other members of this viral group.

- In humans, the best-known lentivirus is HIV, the virus that can lead to AIDS.
- In cats, it is FIV, commonly referred to as feline AIDS.
- Horses have equine infectious anemia virus, another member of the lentivirus group.

These are NOT the same virus (but same genus), and they don't normally move freely between those species. However, they share important biological characteristics that help explain why CAE and OPP are so difficult to eliminate once they enter a herd or flock.

*A virus designed to take its time*

The word "lentivirus" comes from the Latin word "lentus", meaning slow.

That name describes the way these infections commonly progress.

A lentivirus doesn't usually enter an animal and cause obvious illness a few days later. An infected sheep or goat may appear healthy and productive for months or even years while the virus quietly persists inside its body.

- During that time, the animal may still expose others.
- By the time visible disease develops, the infection may have been present for a very long time.

*It is a retrovirus*

Lentiviruses belong to a larger family known as retroviruses.

Most people imagine a virus entering a cell, making copies of itself, and then moving on to infect additional cells. A retrovirus does something more permanent.

It carries its genetic instructions as RNA. After entering a cell, it converts RNA into DNA and inserts the viral DNA into the infected cell's genetic material.

In plain English:

*The virus writes itself into the cell’s instruction manual*

Once that happens, the infection becomes part of that cell. The immune system may (and usually does) fight back viral activity, but it can't simply remove the viral DNA from every infected cell in the body.

That is why CAE and OPP are considered lifelong infections.

There is currently no treatment that clears the virus from an infected animal.

*It hides inside the immune system*

"Small-ruminant lentiviruses primarily infect cells belonging to the monocyte-macrophage system".

-These are immune cells.

Monocytes circulate through the bloodstream. When they leave the blood and enter body tissues, they mature into macrophages.

Macrophages normally protect the animal. They identify pathogens, remove damaged material, and help coordinate inflammation.

Remember that statement: "Coordinate Inflammation" because this will help explain a lot of things as we roll through this series.

Basically, the virus turns these immune cells into its transportation system and hideout.

While an infected monocyte is circulating in the bloodstream, the virus may remain relatively quiet. But... when that cell enters tissue and matures into a macrophage, viral activity usually increases substantially.

The infected macrophage attracts more immune cells, which creates continuing inflammation in the tissue that the body cannot completely clear.

*Much of the damage comes from chronic inflammation*

CAE and OPP don't destroy tissue in one sudden attack.

Instead, the immune system repeatedly responds to infected cells but cannot fully eliminate them. This creates a cycle of long-term inflammation and slow, steady tissue damage.

Depending on where infected macrophages accumulate, the disease may affect:

- Joints
- Lungs
- Mammary glands
- Brain and spinal cord
- Other lymphoid tissues

The signs we eventually see depend on the species, age of the animal, strain of the virus, and tissues most affected.

*CAE and OPP are related, but not identical*

- CAE stands for "Caprine Arthritis Encephalitis" and is most commonly associated with goats.
- OPP stands for "Ovine Progressive Pneumonia" and is most commonly associated with sheep. A closely related disease is also known as "Maedi-Visna" in many parts of the world.

These names describe the most recognizable forms of disease, but they are kinda misleading as well.

- CAE doesn't cause ONLY arthritis and encephalitis. It may also cause chronic pneumonia, hard udder, reduced milk production, and progressive weight loss.
- OPP doesn't affect only the lungs. It may also contribute to mastitis, poor body condition, neurologic disease, and declining productivity.

Once upon a time, these sheep and goat viruses were discussed as though each remained neatly within its own species. We now know some small-ruminant lentiviruses can cross between sheep and goats.

"It is therefore more accurate to think of CAE and OPP as closely related members of a larger viral group rather than two completely isolated diseases".

*“Slow” does not mean harmless*

A lentivirus may take years to produce visible disease, but that doesn't mean it is inactive.

- The animal may be infected.
- The immune system may already be responding.
- Microscopic inflammation may be developing.
- Virus may be present in colostrum, milk, or respiratory secretions.
- Other animals may be exposed.

All this can happen while the infected animal continues to look "normal".

That is what makes CAE and OPP so challenging. We aren't usually looking for an obviously sick animal spreading a short-lived infection.

We're dealing with a lifelong virus that can hide inside immune cells, write itself into the DNA of those cells, and remain largely invisible for years.

Understanding that biology is the first step toward understanding how these diseases spread, why testing is imperfect, and why prevention matters so much.

*Next: How CAE and OPP move through a flock or herd - and why colostrum is only part of the story.*

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