Alpaca and Alpacas For Sale at Benchmark Alpacas at the Tin Roof Ranch in Ortonville, Michigan

Come and Walk with the Alpacas!

Please call Barrie Lynn to schedule your own group trip at 248-627-9863.

Pre School Alpaca Adventures!
Join Brandon Township’s Educator/Rancher, Barrie Lynn Wood for very special guided interpretive tour of a working alpaca farm. You and your walking-talking preschooler will join Barrie Lynn and explore the world of Alpacas at Benchmark Alpacas at the Tin Roof Ranch – in Ortonville – for an up-close and personal encounter with her gentle fleece producing herd. A great photo opportunity and a fascinating look at a peaceful and rewarding lifestyle. Space is limited and this always fills fast! Call to reserve a place for you and your little one.

Would you like to head out to the farm for a visit or like to bring a group? Please contact Barrie Lynn to arrange a date and time. Contact her at: 248-627-9863.

AlohaCoyo by The Babe, a 1/2 Accoyo Grey, sold for $0000
Congratulations to:

Aloha is a rare - 1/2 Accoyo Grey by our boy, Camilio's Accoyo The Babe.

She has great bloodlines and is a Maternal sister to our multi Color Champ - SilverCoyo Outlaw.

Accoyo Bella Oaks, a 1/2 Accoyo Grey, sold for $0000
Congratulations to: Roy and Linda Parks of Zodiac Farms

Whisper Wing's Peruvian Splash, a Multi Suri, sold for $27,000
Congratulations to: Becca Black of Queen B Alpacas

Splash went on to compete in the AAA Futurity Show in a class of 14 Multi’s (including the ones that sold for $62,000 and $50,000). Splash proudly pranced around the ring showing off her flowing locks. Judge Amanda Vandenbosch pulled Splash to the front of the class and during oral reasons she described Splash as a spectacular girl with consistent locks across her blanket down into her belly and even through her tail. Amanda went on to talk about her strong conformation and solid frame topped off with a typey Suri head complete with beard. She was pleasantly surprised to find this fine of fleece presenting such density, a combination rarely seen.

Perucoyo Mostaccioli, Splash’s Sire, only has two cria on the ground so far. His first is Blessing who was born in 2003. Blessing took 1st Place at the MAPACA show in 2004. That was the largest show ever held – anywhere. Now Splash, his second cria, takes First at the AAA Futurity. Now is the time to reserve a spot for your females and grab a hold of these genetics.

RGA Chloe, a White Huacaya bred to Accoyo Tachon, sold for $31,500.
Congratulations to: James Webb & Sharon Brown of Virginia Alpaca Farm & Breeding Company .

Chloe is a Victor Vaccoyo Daughter and carries with her all of the wonderful Accoyo traits. She is her 3/4 Peruvian and 1/2 Accoyo with dark pigmentation! Chloe offers a strong foundation, good bone, level topline, and an abundance of fleece. Chloe’s fiber exhibits high frequency crimp, density and fineness with wonderful brightness. Her bloodlines are rare to the U. S. as both her Dam and Sire are exclusive to Canada.

Chloe has been bred to Vengador's Accoyo Tachon. Tachon is a full Accoyo who brings uniformity, presence, and density to the table. In fact, while Don Julio was visiting Accoyo America, he pulled Tachon out of a large group of boys and used him as an example of what we should be breeding for. Tachon and Chloe’s offspring will be 3/4 Accoyo and chances for color are VERY high as Tachon has three large fawn spots and dark pigmentation.

Prior to joining the breeding program, Chloe showed off at the Michigan International Alpacafest 2003. Being a white class, the competition was tough and two of our favorite Ohio farms were standing beside us. Chloe took it all in stride and walked away with the Blue Ribbon. Here is your opportunity to add a winner to your herd.

Chloe has been consigned to the AAA Futurity Sales Auction which will be held the weekend of April 16-19th, 2004 at the Indiana State Fairgrounds in Indianapolis, Indiana.

Awards Received
1st Place - Michigan International Alpaca Fest 2003.

Whisper Wing’s Silver Barrie, a Dark Silver Gray Suri Juvinel, sold for $41,500.
Congratulations to: Diane Kuss & Beth Roy of Suri Peak Alpacas

Silver Barrie is Gray, Solid Gray, we are talking Dark Silver Gray from head to toe. There isn’t a spot of white to be found! Another good day on the ranch.

This Full Peruvian, Dark Silver Gray Female proudly displays her solid conformation, her typey little head, and her flowing locks. With her lineage, it really isn’t a big surprise.

Her Paternal Grandparents are the late, Peruvian Magnifico, sire of many champions and Peruvian Silver Mercedes, one of the highest sellers at the Great Lakes Classic. Both are Gray and so is her sire, Peruvian Cheyenne. This makes Silver Bear a third generation Gray!

Silver Bear’s first breeding to any Benchmark Herd Sire is included and you have a variety to choose from. Our pick would be Peruvian Sundance Kid, ½ Accoyo and ½ Gunsmoke! What a nice way to keep color and add those Accoyo traits. Or, Peruvian Tambourine Man with his rich Maroon color, great conformation and silken fleece. His background is Maroon and Gray, which is hard to come by as well.

Benchmark’s Peruvian Sienna, Med Brown Huacaya Juvenile, sold for $18,000. Congratulations to: Geoff & Judi Rostan of Timber Ridge Farm

The formula to excellence revealed.

Step One…Breed Peruvian Mercedes with AOBA Award Winning fiber, to Benchmark’s Peruvian El Capitan (a Dark Maroon Blue Ribbon Boy and Sire of Multiple Award Winning Offspring). Whaamo, you get Benchmark’s Peruvian Juliet, a typey dark fawn with Rose Gray points. Step Two…Hit the show ring with Juliet, take home Blue Ribbons and then breed her to Snowmass Peruvian Casanova, Dark Rose Gray, Futurity Herd Sire of the Year. The Results… Benchmark’s Peruvian Sienna.

Sienna has great presence, personality and is a rich Cinnamon Brown. She is easygoing and offers abundant fleece with an incredibly fine hand. Her conformation is strong and balanced and the judges love her.

Her first show was the Level 5 Empire Show in NY where she proudly accepted her third place ribbon. Her next show was the Northern IL Extravaganza. She placed over a Color Champ from the Empire Show and took home the Blue Ribbon! Choose from a diverse selection of colors and top bloodlines for Sienna’s first breeding. These boys can be found on our Herd Sire page.

We are excited to see what she will produce even though we will have to face her offspring in the show ring. Now is your opportunity to tap into Sienna’s lineage, and add to your herd’s overall quality.

Awards Received
1st Place - Northern IL Extravaganza 2003 - Her second show and she had a little more confidence. She even stood above the Champion from the Empire show! // 3rd Place - Empire Show in NY, 2003 - a LEVEL 5 show with over 500 animals. This was a big class and her first show. She was little timid and shy - but stood proud with all of the "Big Boys" and took home a 3rd place ribbon.

Tin Roof’s Peruvian Liberty, Dark Silver Gray Juvenile Suri, sold for $46,000 – Second Highest Seller and just a baby!
Congratulations to: Paul & Tania Milewski of Suri Ridge Ranch

Parting with our Alpacas always brings out mixed emotions for Bill and I. Some capture our hearts with such grace and beauty that they nearly avoid our sales list altogether. This is how we feel about Liberty.

From the day it hit the web, "we have a Gray, Full Peruvian, Female Suri," friends and associates responded with excitement. Well-respected Suri Breeders sang her praises the minute they set eyes on her. We knew Liberty was a rare treasure, therefore, the perfect animal to showcase our farm and breeding program at the 2002 AOBA Sale.

Liberty's commanding presence, shimmering pencil locks, and carefree attitude draw the attention of everyone who visits our farm. She is one Peruvian Lady that has it all. Her Dam, 5P Francesca, is Maroon and has thrown award winning cria including Peruvian Renegade. Her Sire is Peruvian Gunsmoke, a breathtaking Smokey Gray boy. Not only does Liberty offer a background of color, she offers the genetics needed to meet a higher standard.

Alpaca Fleece, The Luxurious, Rare Specialty Fiber
Scarcity or rarity is the the primary determinant in defining a specialty fiber. Wool is not considered a specialty fiber due to its abundance. Alpaca fleece is valuable because it combines so many positive, commercial attributes into one fiber. There are no negative characteristics to be found in the alpaca's fleece. It is found naturally in 22 distinct colors, which can also be blended to produce an infinite array of natural colors.

The fiber from alpaca is unusually strong and resilient. The strength of the fiber does not diminish as it becomes finer, thus making it ideal for industrial processing. Raised at high altitudes in freezing cold, the alpaca has developed more thermal capacity in its fiber than almost any other animal. The fiber contains microscopic air pockets which create lightweight garments with high insulation values. Alpaca is soft, supple and smooth to the touch. The cellular structure of the fiber produces a soft handle unmatched by most other specialty fibers.

Alpaca fleece produces a high yield of clean fiber after processing: 87 to 95 percent for alpaca versus 43 to 76 percent for sheep's wool. Alpaca is easier and less expensive to process than sheep's wool due to its lack of grease or lanolin, and it does not have to be de-haired like cashmere or camel. Alpaca fiber can be scoured or cleaned without using costly chemicals. Scouring is the actual washing of dirt and foreign matter from the alpaca fleece. It is usually done in a lukewarm, neutral solution, followed by clear-water rinses.

Alpacas produce a fine fiber with an absence of guard hair in their prime fleece. Their fiber has a natural, rich luster which gives garments made from 100% alpaca high visual appeal. It is easily dyed any color and always retains its natural luster. Fabric made from alpaca can range from bulky tweeds to fine gabardine. Those who own alpacas sweaters will find they practically last forever. This fiber does not easily tear, pill, stain or create static and it is easily cleaned.

Alpaca produces beautiful yarns, either handspun or machine made. The long staple length makes it ideal for processing as either woolen or worsted yarns. Manufacturers also like to blend alpaca with cashmere, mohair, silk, cotton and wool. These blends make into exquisite luxury garments.

Awareness of the unique quality of alpaca fiber is increasing with the worldwide recognition gained from promotional efforts of breeders in the U.S., Canada and Australia. With selective breeding techniques, better animal husbandry and nutritional care, fiber fineness will improve and fleece weight per animal will increase. The terms luxury and alpaca are becoming synonymous. The treasure, which the Incas harvested from the back of the mystical alpaca, will soon be enjoyed by discerning consumers everywhere.

Preparing the fiber for the Fiber Mill
I'm often asked by customers to evaluate their fiber. This is usually after the customer has incurred the expense of shipping it to me. You can save yourself time and money by learning to evaluate your fiber before sending it to be processed. It's terrible to wait with anticipation for your fiber to come back from the processor only to find that it's really not what you expected. Here are a few things to look for:

1. How clean is the fiber? The cleanest fibers come from coated animals, but you don't have to coat an animal to have a clean fleece. How the animals are fed and the condition of their surroundings make a big difference. Feeders that don't allow the animal to get hay all over themselves or feeding on the ground works well. Keeping the surroundings clean, using bedding that easily shakes out (I hate wood shavings) and shearing prior to lambing is good. Also shearing on a mat instead of the barn floor is best. Look for burrs, thorns, and the like. A few is one thing, but many is not good and very time consuming to pick out. The amount and type of contamination that will come out during processing depends a lot on the type of fiber. The more crimpy, fine fibers such as Merino, Rambouillet, Corriedale, and others, tend to hold onto the VM and dirt. Fibers such as Romney, Shetland, Cotswold, and Lincoln for instance, will release much of it during processing. Sand will wash out much easier than black dirt or what I call manure dirt. It looks like dirt, but is really manure that has dried and the animals lay on it. Most often this comes out, but some little specks may remain in the crimpy fibers. Skirt out any really contaminated areas, like the back of the neck or down the back. If these areas have a lot of VM in them, it will just be spread throughout the rest of the fleece during processing.

2. How strong is the fiber? Check the fiber for breaks. A break in the fiber will occur when the animal is stressed or sick. There are many kinds of stress, extreme heat, extreme cold, shipping, lambing and weaning, just to name a few, and a lot depends on how a particular animal handles these situations. You can check for breaks by holding a staple between the thumb and forefinger of each hand and giving it a tug. Hold it up to your ear while you're tugging. If you hear it crackle instead of ping, the fiber is weak. How usable that fiber is going to be and how it's going to process, depends again on the type of fiber and where the break occurs. The crimpier fibers will have the tendency to nep, but if the staple is long and break occurred in the middle of the staple, it may not, especially if processed on a carder with a fine cloth. Combing is another option. If the break is at the tip or the cut end of the staple, leaving short 1/4 to 1/2 inch fibers, nepping is very probable. If the fiber is short to begin with and has a break, you might reconsider buying or using that fiber for yarn, as your resulting yarn may not be very strong and will tend to pill in your finished item. That fiber may be a good candidate for felting, depending on what the felt was going to be used for. On the other hand, the wavier, less crimpy fibers tend to shed a lot of those short fibers during the carding process and they will be left on the floor under the carding machine. Those that are left in the roving or batt, are usually easily picked out or fall out during spinning. Again though, if the staple is short to begin with, it may not make a good yarn candidate.

3. If the fiber is already off of the animal, how is it stored? Many a beautiful fleece has been ruined by being stored improperly. The raw fiber needs to have air. If stored in plastic bag, make sure it has plenty of holes in it. Old pillowcases work well. I've seen grain sacks used often, just be sure there's no grain left in the bottom. Don't store a damp fleece. In hot, humid weather, damp fleeces can mold and mildew even if the bag is open at the top. Make sure before storing fiber that all tags (manure and real heavy black grease) have been removed. I've successfully processed many fleeces that were years old because they were stored properly.

What's Going on in the Show Ring?
Understanding Alpaca Halter & Performance Shows
By Mary Reed, ALSA President and Novice Alpaca Halter Judge

ALSA - The Alpaca & Llama Show Association sanctions shows, certifies Judges, guides show managers and educates exhibitors. The Alpaca show format has been jointly developed since 1990 by The Alpaca Owners & Breeders Association (AOBA) and ALSA.

HALTER CLASSES - The purpose for conducting halter classes is to compare animals, judging them against soundness, conformation and fiber criteria so as to determine those who are best suited for breeding purposes. Alpacas are shown in Full Fleece and Shorn halter classes.

Judging System - The system of judging used for alpaca halter shows is a relative system as differentiated from judging to a specific breed standard.

Judging Criteria - Alpacas in Full Fleece halter classes with 3" or more fiber on their neck, blanket and legs are evaluated 50% on their conformation and 50% on the quality of their fleece. Alpacas in Shorn halter classes with less than 3" of fiber on their neck, blanket and legs are evaluated 100% on their conformation. The judging criteria is based on a list of positive and negative traits for alpacas including: type, quality, conformation, movement, soundness, fiber quality and disposition. Using these traits as the basis, the Judge compares the alpacas to each other and places them according to this comparison.

Class Divisions - There are two breeds of alpacas, the Huacaya and the Suri, differentiated by their coat type. Huacaya alpacas have a fluffy appearance with hair that grows perpendicular to the skin and often has a wavy characteristic known as crimp. Suri alpacas have a lustrous silky appearance with hair that hangs parallel to the skin in pencil lock curls that resemble dread locks. Alpacas in full fleece classes are divided by breed. Shorn alpacas are combined by breed as only conformation can be evaluated.

Age Divisions - Alpacas are divided by age into three (3) age groups: Juvenile - 6 months to 12 months of age; Yearling - 13 months to 24 months of age; and Adult - 25 months of age and older.

Color Divisions - Alpacas are found in more natural colors than any other livestock. The show format recognizes 22 distinct colors and 2 color patterns, the pinto and "fancy" or multi-colored. Alpacas are divided into four major color groups: white/light, fawn, dark and multi-colored. If four or more alpacas in an age group have the same color designation, they can be divided into one of the 22 distinct colors. At an alpaca show you can truly enjoy the alpaca’s wide range of beautiful natural colors.

Gender - Lastly alpacas may be divided by sex into male and female classes if four or more animals in a distinct color are shown. Geldings are shown separately and all colors can be combined in a halter class.

Presentation - The alpaca will be picked clean so not to disturb the integrity of its fleece and shown to the Judge in a halter and lead line. The exhibitor will be conservatively and neatly dressed, often in show attire (dark pants or skirt and light shirt) so to show off the animal, not the handler.

Ring Procedure - The alpacas will be called into the show ring oldest to youngest in age or vice versa. The Ring Steward (the person in the ring assisting the Judge) will ask the handlers to walk their alpacas around the perimeter of the ring while the Judge stands in the middle of the ring to view the class as a whole. The Judge considers each alpaca’s soundness, conformation and movement as they walk around the ring. Then they will be lined up head to tail or at a profile view so that the Judge can compare the balance and proportion of each alpaca. The Ring Steward will then line the alpacas up side by side down the middle of the ring, for individual examination of bite and fiber by the Judge.

Bite - The Judge will inspect the bite of each animal looking for soundness and proper jaw alignment. The Judge will closely examine the head, eyes and ears for type.

Fleece Evaluation - The Judge will part the fleece in three areas to evaluate the fineness and handle (softness to touch), density, uniformity of staple length, color, character, average fiber diameter and density, architecture (presence of crimp and/or crinkle in Huacaya and lock formation in Suri), luster of fleece and condition (natural cleanliness, weathered, matted and tipped ends). Fifty percent (50%) of the evaluation in a full fleece halter class is the quality of the fiber of the alpaca.

Body Score and Top Line - The Judge run his/her hand down the top line of the alpaca to feel the overall condition of the animal and levelness of its spine.

PRODUCE CLASSES - Get of Sire - These classes demonstrate the quality and consistency of breeding programs. Three offspring sired by the same male (Herd sire) are evaluated as a group or "get" to determine the overall quality and consistency of quality passed on by that male.

SHOWMANSHIP - A showmanship class is a demonstration of the handler’s ability to show his animal to its best advantage at halter. Judging is based on the exhibitor’s basic skills in fitting, grooming, following directions and style of presenting the animal to the Judge for evaluation. The animal’s conformation is not considered.

PERFORMANCE CLASSES - Performance classes are designed to present or simulate conditions and obstacles that would be encountered in certain situations, such as a trail hike or visit to a nursing home.

Obstacle class - These classes demonstrate the intelligence, versatility and willingness of a well-trained alpaca to follow the directions and command of its handler. The Open course will offer 10 obstacles including those that are mandatory: a bridge or ramp, jumps, flexibility and maneuvering, change of pace and backing.

Alpaca Agility Sweepstakes Class - The purpose of this class is to demonstrate the well-trained alpaca’s ability and willingness to complete the activities involved with public relations events and agility. There is a prescribed list of activities to be included in an Agility course. The Open Agility course will have 10 activities: demonstrate willingness to wear a sweepstakes blanket, backing, go over a bridge, ramp or stairs, change of pace, maneuver around objects, go through gate, load in a vehicle, tolerate petting by strangers, demonstrate willingness for handler to show teeth or pick up a foot, meet strange animal or object and tolerate loud noises.

AOBA Microchip Identification Requirement
Effective July 5, 2005, Alpacas at AOBA Certified Shows occurring are required to be identified with a microchip.

This means every alpaca that is transported to an AOBA Certified show for any reason (i.e. show entrants, companions, auction alpacas, alpacas being transported and using the show venue as a stop off point, etc) must be identified with a microchip.

It is the responsibility of the owner of every alpaca entering the venue of an AOBA certified show to corroborate the identity of each alpaca. This requirement begins on July 5, 2005. The identification of each alpaca is accomplished by microchip. The recommended microchip insertion point is the base of the left ear at the poll (coronal aspect). A brand of microchip is not specified.

When you microchip your alpaca, you may affix the microchip number label (usually supplied with the microchips) onto the alpaca’s ARI Registration Certificate. If you do not have the label you can carefully and legibly hand write in ink the microchip number in the appropriate area on the ARI Registration Certificate for that alpaca. Make sure you fax a copy of the ARI Registration Certificate to ARI so they can update their records. You are not required to obtain a new ARI Registration Certificate specific to adding the microchip number for show entry.

The microchip number must also be used with each alpaca examined by a Veterinarian and affixed onto the Certificate of Veterinary Inspection (Health Papers) and transportation documents. Health Papers, dated within 30 days of the last date of the show, are required for all alpacas entering the venue of an AOBA Certified show.

Evaluating Alpaca Fiber
Written by: Linda Bat, Delphi Alpacas
This article is intended to provide an overview of fleece terminology for new alpaca breeders, in order to help them in selecting alpacas for their herds.

There are no perfect alpacas. There is great room for improvement in all of our herds, and we can watch it happen before our eyes in our very own pastures, when we make good breeding choices. Once you learn to judge alpaca conformation and fleece, you'll see that not even blue ribbon winners are perfect. Learning to evaluate fleece will help you to make the best breeding choices for your alpacas.

Fleece is the primary end product of the alpaca. These animals are not just another exotic pet fad - they are producers of some of the most wonderful fiber available on the planet. American alpaca shows currently judge alpacas based 50% upon their fiber, and 50% upon their conformation (bone structure, movement, balance - etc.). Other countries, such as Peru, place a higher emphasis on the fleece when judging alpacas.

Fiber characteristics and qualities vary tremendously among alpacas. First we can divide alpacas into two breeds, huacaya and suri. Huacaya fleece is usually crimpy, and grows out perpendicularly from the alpaca's body, giving huacayas that “poofy” look. Suri fleece has a long and silky look, hanging straight down from where it grows on the alpaca's body. Suri and huacaya fleeces each have desirable characteristics making them highly sought after for different uses in the textile industry.

We can divide fleece characteristics into quantitative and qualitative categories: Quantitative and Qualitative

QUANTITATIVE

Density
Density refers to the # of hair follicles per area of skin. This is the most important quantitative fleece characteristic. Density can be judged in several ways. By parting the fleece and determining how much skin can be seen at the roots, you can get a visual idea of how tightly packed the fiber follicles are on the skin. A very dense fleece will show a very thin line of skin when parted. The resistance the fleece offers when parting it also reflects density. Pressing down on the alpacas back and feeling for resistance is another method - a very dense fleece will make it more difficult to feel the alpaca's back bone. Simply grabbing the side of the alpaca and feeling how much fleece fills your hand can also help judge the density of that alpaca's fleece. These methods can be misleading, however, as coarse fibers will tend to “fill up your hand” more than fine fibers, and coarse fibers also offer more resistance than finer fibers. Thus a fine fibered alpaca might, in comparison, feel less dense, while the actual number of fibers per area of skin (true density) is not the issue. I suggest evaluating the fineness of the fleece separately, and taking that assessment into consideration when determining fleece density.

Pictured above: This alpaca exhibits a very thin line of skin as the fiber is separated, indicating a dense fleece. This fleece also offered a good deal of resistance when parted.

Regrowth or Staple Length
Regrowth or Staple Length refers to the actual length of fiber produced in a given amount of time. This is also a very important quality, as length and density are the primary factors impacting the total fleece weight of an alpaca. The fiber industry pays for fleece by weight, and the total weight of a fleece shorn from an individual alpaca can vary from as little as two pounds to more than twelve pounds. Judging regrowth relies on accurate shearing dates being provided. It is expected that most alpacas will produce less fiber as they age, and this occurs most notably in producing (reproductive) females.

Coverage
Coverage refers to the parts of the alpacas body that are covered with fiber. The alpaca fleece is divided into the blanket (the prime fiber), and the neck, belly, and legs, which are generally much higher in medullated fiber and therefore more coarse. If the neck, belly and legs have little medullation, and have good coverage with usable fiber, this would add to the total fleece weight that the alpaca produces. The blanket fiber is, however, the fiber that the market is willing to pay premium prices for, and as such should be of primary importance when selecting breeding stock.

QUALITATIVE

Fineness
Fineness is a very important characteristic of a good quality fleece. The finer the fleece, the softer the feel, and the higher the price that will be paid for that fleece. Fineness can be measured in microns, which allows new breeders to have concrete figures by which to assess an alpaca’s fleece. This can be very helpful, as well as sometimes very misleading.

The figure which indicates the fineness of the fleece is the average fiber diameter - or the AFD figure found on a histogram report. Histograms are fiber analysis reports provided by the Yocom-McColl Testing Laboratory. The lower the AFD number, the finer the fiber. Many things can affect the AFD of a fleece. Age is one factor. The AFD is thought to often increase an average of 2 points a year until an alpaca reaches 4 to 5 years of age. Diet can significantly affect the AFD, as well as hormonal influences such as pregnancy or testosterone in breeding males. Males are thought to have coarser fiber in general. Gelded males tend to remain finer fibered than breeding males. The location on the body that the fiber was taken from can also impact the AFD results significantly. As a rule, fiber samples should be taken from the middle of the side of the alpaca.

If you rely too heavily on the micron figure provided when selecting your alpacas, you may be disappointed to later find that the micron count you based your purchase upon was artificially decreased by malnourishment, immaturity, or poor sampling technique. If you can obtain legitimate micron counts on the parents of your selection at adult shearings, this can help to estimate the probability of change you can expect with the offspring, but its just an indicator - offspring can vary greatly from their parents.

Histograms are most valuable for learning to assess fiber by touch, and for monitoring the fleece quality in your own herd from year to year. One method I recommend for learning to judge fleece by hand, is to compare the samples you send out for testing with samples of fleeces you already have histograms from. Make your guesses as to what you think the results will be on the new samples. Then analyze those results to learn what factors can influence the subjective feel of a fleece. You might discover that a very tightly crimped fleece may actually feel coarser than it really is, in comparison to a loose fine fleece. Or you might let the tight crimp influence you into believing that the fleece must be fine, only to realize that in that case it was actually quite coarse. Eventually you’ll be able to assess fleece fineness quite accurately, as well as learning to identify which fleeces are more uniform (see Handle).

Luster
Luster is the shine produced when light is reflected back off of the fiber. Suri fiber is thought to have more luster, because of the microscopic fiber structure. While luster (or brightness) is desirable in huacaya fleeces, it is of primary importance when selecting for suri fleece. (See 2nd photo below for example.)

Crimp
Crimp refers to the waves or ripples in a group of fibers. Crimpier fiber is thought to have a tendency to be finer and denser, though there are many exceptions. It also tends to be easier to spin, providing more loft to the fiber. Some breeders feel that in and of itself, crimp is not a necessary component of huacaya fleece relevant to its end product use. There is even some mention that crimp may detract from the handle of a fleece. However, the association of consistent crimp with finer, denser, and more uniform fleeces has resulted in crimp remaining an important quality when judging fleeces. If the crimp style is consistent throughout the blanket, this indicates that the blanket is uniform.

Pictured above: From left to right these 3 samples have 4.5 crimps/inch; 6 crimps/inch; and 8 crimps/inch. Though higher crimps per inch may often indicate finer fiber, in this case the AFD's of these samples are 21; 26 and 28, respectively, (the exact opposite of what one might expect).

Crimp can be described as having a high or low frequency (crimps per inch) or as having high or low amplitude, which is best described as the height of each wave of crimp. The style of crimp tends to be less important than the uniformity of the crimp throughout the fleece. However, some breeders prefer a high frequency crimp, as this used to be used as an indicator of a fine fleece. While that tendency may exist, there are many exceptions to that rule. Crimp is considered a fault in suris.

Lock Structure
Lock Structure refers to the tendency for a fleece to separate into cylindrical groups. In huacayas, lock formation is less evident than with suris. It is usually more pronounced in denser more uniform fleeces.

In suris, lock style refers to the twist or wave the fleece exhibits. Small, uniform ringlets or waves with twist starting very close to the skin is currently judged as the most desirable style. Larger waves with the lock definition less well defined, or starting further from the skin, is less desirable. The locks of a suri should ideally be uniform in size and style throughout the entire suri fleece. This indicates uniformity in a suri fleece, much as consistent crimp style indicates uniformity in a huacaya.

Guard Hair or Medullated Fibers
Guard Hair or Medullated Fibers are the coarser, straighter (and therefore longer) hairs found especially on the neck, belly and legs. Alpacas in general have little guard hair on their blankets, but this varies with individuals, and we should breed for decreasing amounts of guard hair in our herds. On a histogram, the % of fibers > 30 microns in diameter is thought to be related to the amount of guard hair present in the blanket, but this is not always reliable. The % > 30 figure is also referred to as an indicator of the prickle factor of a fleece, as fibers greater than 30 microns in diameter tend to make a garment feel prickly.

Pictured Left: An example of guard hair. Note the long dark guard hairs extending from the top of this lock of fiber. This alpaca has a significant amount of guard hair present for a blanket fiber sample.

Picture Right: An example of luster and locks. This section of huacaya fleece exhibits a tendency to form locks of fiber. It also shows nice luster at the clean base of the sample.

Hand (or Handle)
Hand is the subjective feel of a fleece - often thought to be associated with the uniformity of the diameter of each fiber in the fleece, combined with its fineness, or AFD. Lustrous suri fiber also tends to have a slicker feel and handle due to the microscopic structure of the fibers, which also influences handle.

Uniformity can be assessed on the histogram reports with the Standard Deviation and Coefficient of Variation figures.

The standard deviation (or SD) figure represents the range of individual fiber diameters, or the degree of deviation of all of the individual fibers from the average. For example, if the AFD is 25 microns, the SD will be low if most of the fibers in that sample are close to 25 microns in diameter. If, on the other hand, the fibers in a sample (with the same average diameter of 25 microns) broadly ranged from 15 to 35 microns, the SD will be higher. The more uniform the fleece, the lower the SD figure will be, and the softer the handle of the fleece.

The Coefficient of Variation (CV) is the SD divided by the AFD X 100 and reported as a percentage. This is simply a figure used to compare the uniformity of fleeces with varying AFD’s.

Color
To get an overview of color in American alpacas, you need to consider a bit of history. Peru didn’t allow the exportation of alpacas until 1991. Chilean alpacas were the first alpacas to be imported into the U.S. They were of all colors, including grays, blacks, browns, fawns, pintos, whites, and more.

The first Peruvian alpacas arrived in the U.S. in 1993. They were primarily white, with a few fawns, as many Peruvians had been selectively breeding alpacas for the white color preferred by the larger fiber mills. Many of the Peruvians imported were selected from cooperatives that had also practiced superior selective breeding for fleece quality. As a result, Peruvian alpacas are often generalized as having improved fleece, when compared to the earlier Chilean imports.

However, not all alpacas imported from Peru are from these select cooperatives; the borders between Chile, Peru, and Bolivia are apparently not hard for alpacas to cross; and there are many examples of superior alpaca fleeces found among what we think of as Chilean and Bolivian alpacas here in the U.S.

In the last few importations (before the Alpaca Registry closed), darker colored Peruvian alpacas were imported, reflecting the American demand for color. These alpacas also may or may not have been the result of the improved selective breeding practices that Americans often associate with Peruvian alpacas. To focus only on a certain country of origin, in my opinion, colors one’s expectations, and unnecessarily limits the alpacas available for selection.

In the United States, hand spinners often prefer working with natural alpaca colors such as gray, fawn and maroon. The larger textile companies have shown a preference for white, though they have also paid premium prices for black. As a new breeder, the variety of colors that alpacas offer gives you another opportunity to establish your niche in the alpaca market.

AOBA FLEECE JUDGING

Currently, AOBA fleece judges base their decisions on the following score cards:

These score cards might help you prioritize some of the characteristics we’ve gone over. For instance - while fineness and handle are important, the fleece weight, which reflects density and length, is given an equal maximum score.

Few if any alpacas today could achieve the maximum score of 100 in a well judged fleece show. Your personal breeding program may elect to emphasize some of these characteristics more than others. You may want to be known as the alpaca farm with the crimpiest alpacas, or the densest! Each farm has diverse goals for their herds, helping to secure their niche in the alpaca market.

References:
Numerous conversations with Judges and experienced breeders
Mike Safley’s Alpacas: Synthesis of a miracle
Yocom McColl’s explanation of Histograms
(no actual quotes were included)

Tax Consequences of Owning Alpacas
Raising alpacas at your own ranch, in the hands-on fashion, can offer the farmer some very attractive tax advantages. If alpacas are actively raised for profit, all the expenses attributable to the endeavor can be written off against your income. Expenses would include not only feed, fertilizer, veterinarian care, etc., but depreciation of such tangible property as breeding stock, barns and fences. These expenses can also help shelter current cash flow from tax.

The less active owner using the agisted ownership approach may not enjoy all of the tax benefits discussed here -- but many of the advantages apply. For instance, the passive alpaca owner can depreciate his breeding stock and expense the direct cost of maintaining the animals. The main difference between a hands-on or active farmer and a passive owner involves the passive owner's ability to deduct his investment losses against his other income. The passive investor may only be able to deduct losses from his investment against gain from the sale of animals and fleece. The active farmer can take the losses against his other income.

Alpaca breeding allows for tax-deferred wealth building. A small owner can purchase several alpacas and then allow his herd to grow over time without paying income tax on its increased size and value. If the same amount of money was invested in a Certificate of Deposit, any interest earned would be currently taxable. In addition, the C.D. could not be depreciated, thereby offsetting the tax due on current income.

We recommend that you engage an accountant for advice in setting up your books and determining the proper use of the concepts discussed in this brochure. A very helpful IRS publication, #225, entitled, The Farmers Tax Guide, can be obtained from your local IRS office. The aim of this discussion of IRS rules is to make you more conversant in the issues of taxation as they relate to raising alpacas.

To qualify for the most favorable tax treatment as a farmer, you must establish that you are in business to make a profit. You cannot raise alpacas as a hobby farmer or passive investor and receive the same tax preferences as an active, hands-on, for profit farmer. A farming operation is presumed to be for profit if it has reported a profit in three of the last five tax years, including the current year.

If you fail the three years of profit test, you may still qualify as a "for profit" enterprise if your intention is to be profitable. Some of the factors considered when assessing your intent are:

You don't have to qualify on each of these factors -- the cumulative picture drawn by your answers will provide the determination. Once you've established that you are farming alpacas with the intent to make a profit, you can deduct all qualifying expenses from your gross income.

If you are a passive investor, you are still allowed the tax benefits discussed below. The issue is whether you will be able to take the losses on a current basis. All the losses can be taken against profits or upon final disposition of the herd. The discussion from here forward presumes you are a cash basis taxpayer and you keep good records. Accrual basis taxpayers would also be allowed the same tax treatment, but their timing might be different.

First, the following items must be included in both a passive investor's and a full time farmer's gross income calculations:

The following expenses may be deducted from this income. Please note, if you are agisting your animals, not all of these deductions may apply on a current basis.

Please note: For hands-on farmers, personal and business expenses must be allocated between farm use and personal use; only the farm use portion can be expensed for such expenses as telephone, utilities, property taxes, accounting, etc.

Once active alpaca farmers have determined their net income or loss, it is included on their tax return as an addition to or a deduction from their ordinary income. Losses can be carried back for three years and forward for 15 years. To deduct any loss, you must be at risk for an amount equal to or exceeding the losses claimed. The "at risk" rules mean that the deductible loss from an activity is limited to the amount you have at risk in the activity. You are generally at risk for:

The passive owner's losses which are in excess of current income can be carried forward and taken against future income. In other words, the passive owner does not lose the deductibility of expenses, but the timing of the losses may be different.

All taxpayers must establish the cost basis of their assets for tax purposes. This basis is used to determine the gain or loss on sale of an asset and to figure depreciation. In determining basis, you must follow the uniform capitalization rules found in the IRIS code. Animals raised for sale are generally exempt from the uniform capitalization rules, and there are other exceptions for certain farm property. You need to become familiar with these rules.

Once you've established the cost basis of your various assets, you take a deduction for depreciation against your annual income. This process allows you to expense the historic cost of an asset to offset present income. The effect is to create non-taxable cash flow on a current basis. This benefit is especially attractive in an environment of higher taxes.

Alpacas in which you have cost basis can be written off over five years if they are being held as breeding stock. There are several methods of writing them off, beginning with the straight-line method which allows you to deduct one-fifth of their cost each year, except the first year, in which the code allows for only six months of write-off. There are also several accelerated schedules which allow for a larger percentage of the asset to be written off early. Alpaca babies produced by your females have no cost basis and cannot be written off, although they may qualify for capital gain treatment on sale.

Capital improvements to the active or hands-on alpaca breeder's ranch can also be written off against income. Barns, fences, pond construction, driveways, and parking lots can be expensed over their useful life. Equipment such as tractors, pickups, trailers and scales each have an appropriate schedule for write-off. The depreciation schedule for each asset class varies from three years to 40 years.

There is also a direct write-off (expense) method known as Section 179 that allows a substantial deduction each tax year for newly acquired items that are normally long-term depreciable assets. While this is subject to several limitations, it is widely utilized by small farms to accelerate expense, if that is appropriate for your tax situation. It is often used by owners that are currently in high tax brackets that are changing their lifestyle in the next several years to a lower income level.

The original cost basis of an asset is reduced by the annual amount of depreciation taken against the asset. Other costs add to basis, such as certain improvements or fees on sale. The changes to basis result in the adjusted cost basis of the asset. Upon sale, excess depreciation previously expensed must be recaptured at ordinary income rates. The recapture rules are a bit complex, as are most IRS rules, but the IRS Farmers Publication mentioned earlier explains them well.

When an asset is sold, say for instance a female alpaca which was purchased for breeding purposes and held for several years, the gain or loss must be determined for tax purposes. If an alpaca was purchased for $20,000, depreciated for two and a half years, or say, 50 percent of its value,, and then resold for $20,000, there would be a gain for tax purposes of $10,000. In other words, your adjusted cost basis is deducted from your sale price to determine gain or loss.

Once you've determined the amount of a gain, you must classify it as either ordinary income or capital gain. Ordinary income is currently taxed at a maximum rate of up to 31 percent and capital gains are taxed at rates of up to 20 percent. The sale of breeding stock qualifies for capital gains treatment (excepting that portion of the gain which is subject to depreciation recapture rules). Any alpacas held for resale, such as newborn cria which you do not intend to use in your breeding program, would be classified as inventory and produce ordinary income on sale.

The capital gains treatment of sale proceeds has become an even more attractive benefit of investing in alpaca breeding stock due to the 1997 Tax Act reduction in the capital gains tax rate to a top rate of 20% (from 28%) for assets held long-term. It also created a new 10% capital gains tax rate for taxpayers in the 15 % ordinary income tax bracket. The holding period to qualify for capital gains treatment lengthened to 18 months from 12 months. The tax break provides a slightly lower maximum rate (18%) in future years for investments held at least 5 years.

There are other tax-saving strategies that can be utilized in concert with investing in alpacas. For instance, you generally can deduct the fair market value of a capital asset which you contribute to a qualifying charity or institution. You can also exchange like for like assets and avoid the tax of a sale. An example of this strategy would be an owner who wanted to diversify his bloodstock. If he sold his alpacas and simply bought more, he would be required to pay tax on his gains. If he exchanged his alpacas for others, there would be no tax due. Employing the exchange concept can be very beneficial; for it to work efficiently, a third-party buyer is usually introduced into the transaction. The model for this type of transaction would be a real estate exchange. A CPA would be familiar with the use of "like kind" exchanges and how it might benefit you.

Installment sale rules allow you to defer income to future years. If you sell an alpaca with credit terms, you can defer your gain until you receive payment (excepting that portion of the gain which is subject to depreciation recapture rules). If an animal dies of disease and is insured, you can use the involuntary conversion rules in the code. These rules allow tax-free replacement of your animal.

This discussion of tax issues omits a number of rules which could impact your taxes. Tax preference items, alternate minimum taxes, employment taxes and other concepts of importance were not discussed. Whether we like it or not, this is a complicated world we live in; it often requires CPA's and on occasion an attorney.

In summary, the major tax advantages of alpaca ownership include the employment of depreciation, capital gains treatment, and if you are an active hands on owner, the benefit of offsetting your ordinary income from other sources with expenses from your farming business. Wealth building by deferring taxes on the increased value of your herd is also a big plus. It pays to keep your eye on the tax law changes instituted by Congress. On occasion, you may find a silver lining in the clouds of government.

Compounding Interest - Alpaca Compounding
A major investment benefit of owning alpacas is based on the concept of compounding. Savings accounts earn interest, which if left in the account, adds to principal. The increased principal earns additional interest, thereby compounding the investor's return. Alpacas reproduce almost every year, and about 50 percent of their babies (cria) are females. When you retain the offspring in your herd, they begin producing cria. This is "Alpaca Compounding." Tax-deferred wealth building is another "Alpaca advantage." As your herd grows, you postpone paying income tax on its increasing value until such time as you begin selling the offspring.

The following graph illustrates how a herd might grow in size over a ten-year period, assuming you begin with five pregnant females and two males. The herd growth depicted represents alpaca compounding at work. The initial herd grows to 126 animals, assuming an 80% reproduction rate and a 50/50 male/female birth ratio. Not many investments appreciate at the same rate.

It should be noted that this graph, while clearly illustrating the principle of "Alpaca compounding," does not depict the average owners' approach to alpaca ownership. Most breeders elect to sell all or some of the annual offspring production for practical reasons, such as recovering their initial cash flow, acreage and building limitations, and time constraints.

David E Anderson, D.V.M., MS, Diplomate ACVS
College of Veterinary Medicine
The Ohio State University, Columbus, Ohio

Unfortunately, emergencies occasionally occur on the farm. The successful resolution of any emergency depends upon our ability to recognize and effectively deal with the crisis. The typical "on-farm" emergencies include soft tissue injuries, choke, obstruction of breathing in newborns, and birthing difficulties.

Many owners have dealt with lacerations, abrasions, and other injuries caused by fighting, becoming entangled in fencing, falling, or malicious attacks by animals or people. Their are some rules-of-thumb we try to follow when dealing with these injuries. If the injury has resulted in debilitation of the animal or the animal is unable to ambulate (e.g., a tendon laceration), the injured alpaca should be made safe from continued trauma and the nearest veterinarian consulted. Sometimes, the best action is to not move the patient until the veterinarian has examined him/her. Moving can increase the severity of the injury and may result in a wound that is far worse than the original injury. If the animal is traumatizing itself by thrashing, then he/she should be moved to shelter or an area that has deep bedding. If you can keep the animal calm you should do so, but remember not to get yourself injured in the process! You should consult your veterinarian for all wounds that are full thickness through the skin (you can see muscle or fat through the wound). These injuries may be completely or partially restored if the veterinarian can treat the wound within 12 hours of injury. After this time, treatment becomes more complicated because bacteria have time to establish an infection in the tissues adjacent to the wound. While waiting for the veterinarian, you may rinse the wound with clean water to flush out any debris, but you do not want to put any antiseptics or ointments into the wound. Water soluble ointments (e.g. Furacin) are O.K. to use because they are easily washed out of the wound. However, lanolin or petroleum based antiseptics may not be able to be cleaned out of a wound, thus preventing suture closure of the wound.

If the wound is bleeding and is located on a limb, you may place a pressure wrap on the wound. This is done by applying a non-adherent dressing to the wound, wrapping a thick pad around the limb, wrapping the bandage with roll gauze using firm pressure, and wrapping over this with a non-adhesive wrap using more firm pressure. If the wound is located on the body, a similar bandage may be placed. Direct pressure may be applied to wounds on the head, but you should be careful not to apply excessive pressure. If the animal violently resists your efforts, the best thing to do is to put him/her into a quiet stall and wait for the veterinarian.

Wounds can be easily dealt with by planning ahead. A "First Aid" box should be kept on the farm and contain necessary emergency medical supplies. A large tackle box, tool box, or plastic storage box are ideal for holding items in a clean dry place. The box should be examined every six months to be sure that appropriate supplies are still in usable order. The following is a list of supplies you may want to keep on the farm.

Ask your veterinarian to discuss the best methods to utilize your first-aid box so that it can be customized to your farm. Remember, your ability to handle emergencies is only as good as you are prepared to be.

Environmental Impact Of Camelids
(herein defined as alpacas and llamas, but not including vicuna or guanaco)

David E Anderson, DVM, MS, Diplomate ACVS
Associate Professor and Director International Camelid Initiative

We have been investigating the environmental impact of camelids for several years. These studies have included containment and shelter, feed intake, water intake, fecal output, fecal examination for important pathogens, and pasture management. These studies have allowed us to make a number of statements.

Containment and shelter: Camelids are easily contained and rarely challenge fencing. These species do not perform activities that are destructive to fencing or wooden structures and rarely jump through, over, or under fences. Shelter must be provided for protection against adverse weather conditions. We have determined that alpacas require a minimum of 8 square feet per animal and llamas a minimum of 10 square feet per animal. Three sided shelters with a roof are adequate for this requirement.

Feed and water intake and fecal output: Camelids consume approximately similar amounts of water as compared with goats (approximately 1 to 1.5 gallons per head per day for alpacas; 2 to 3 gallons per head per day for llamas). Daily urine output of alpacas (average adult body weight 125 to 165 lbs.) and llamas (average adult body weight 250 to 350 lbs.) are similar to that of sheep (average adult body weight 150 to 300 lbs.) and goats (average adult body weight 125 to 200 lbs.). Thus, the biological equivalency to sheep is approximately 1.0. Camelids consume a relatively lower percentage of their body weight in dry matter on a daily basis as compared with sheep and goats. Sheep and goats are expected to consume approximately 2.5% of their body weight per day (e.g. 200 lbs. sheep consumes 5 lbs. dry matter per day or 16.6 lbs. grass (assuming 30% dry matter of grass). Alpacas and llamas are expected to consume approximately 1.8 % of their body weight per day in dry matter (e.g. a 200 lbs. camelid would consume approximately 3.6 lbs. dry matter or 12 lbs. grass per day (assuming 30% dry matter of grass). Fecal output is proportional to dry matter intake. Thus, the biological equivalency to sheep is approximately 0.72. Based on these findings, we consider camelids to be a low risk for ground water contamination (see further comments in pasture management).

Urine contamination: Urine is a necessary by-product of life. Water is a vital nutrient for digestion and metabolic processes. Marcilese et al (1994) determined water turnover in llamas. In winter, body water was estimated as 659 ml/kg with a daily water turnover of 116 ml/ kg^0.82. In spring and summer, daily water turnover was increased. Daily water turnover in lactating llamas in summer was approximately 396 ml/kg^0.82 and that of non-lactating llamas was 260 ml/ kg^0.82. In studies of water consumption, alpacas consumed similar water on a body weight basis as compared with goats. Rubsamen et al (1975) determined that llamas consumed 62 ml/kg^0.82/24 hours and goats consumed 59 ml/kg^0.82/24 hours. Thus, a 60 kg alpaca will consume less than 1 gallon (3.7 L) of water per day. Urine production is expected to approximate 10 to 15 ml/kg/24 hours. Thus, a 60 kg alpaca will produce approximately 1 quart (600 to 900 ml) of urine per day.

Pesticide use: Pesticides are uncommonly used in alpacas because of the limited need to do so. Thus, the potential environmental impact is negligible.

Fecal pathogens: Compared with traditional livestock species, camelids are not known to be carriers of important pathogens (e.g. Johne’s disease, Salmonella sp., E. coli OH:157, etc) and are uncommon carriers of secondary pathogens (e.g. Cryptosporidium sp., Giardia sp). In our studies involving random sampling of farms with alpacas and llamas, we have not found Salmonella sp or Johne’s Disease organisms. In a study performed by the University of California at Davis, they did not find E coli OH:157 or Cryptosporidium sp in camelid feces. Compared with traditional livestock species, we do not consider camelids to be a source of concern for potential pathogens to the human population.

Pasture management: Camelids have a unique instinctual trait with respect to deposition of feces and urine as compared with all traditional livestock. The camelids form "dung piles" in pastures. These dung piles are the animal kingdom equivalent of "community toilets". Thus, these animals are extremely hygienic as compared with horses, cattle, sheep, and goats. These dung piles allow pastures to be cleaned effectively and efficiently on a regular basis. This is rarely done in other livestock because of the necessity to clean the entire pasture, not selected areas. In our research, dung piles will consume approximately 10 % of the pasture if kept cleaned on a regular basis. Without cleaning, pasture consumption increases to approximately 20%. Thus, the pasture contamination equivalency of camelids as compared with other livestock is approximately 0.1 to 0.2. Cleaning of dung piles with composting of manure allows for further limitation of any risk of ground water contamination.

Summary Statement: Based on our research to date, we consider camelids to be one of the lowest risk species in North American agriculture with respect to potential human exposure to pathogens or to by-products of the animals’ waste. This species seems ideally suited to "urban farm" settings.

David E Anderson, D.V.M., MS, Diplomate ACVS
College of Veterinary Medicine
The Ohio State University, Columbus, Ohio

The following vaccination protocol is our recommendation for disease protection. Vaccination protocols must be tailored to the individual farm with consideration for historical diseases in the herd.

WORK WITH YOUR LOCAL VETERINARIAN - THEY WILL KNOW WHAT DISEASES ARE PROBLEMATIC IN YOUR AREA.

David E Anderson, DVM, MS, DACVS
Head and Associate Professor of Farm Animal Surgery
Director, International Camelid Initiative
The Ohio State University
College of Veterinary Medicine
601 Vernon L Tharp Street
Columbus, Ohio 43210
Phone 614-292-6661
Fax: 614-292-3530
E-mail: anderson.670@osu.edu

With the recent outbreak and spread of West Nile Virus (WNV) throughout the USA, there has been an increased interest in the dangers associated with this disease. There have been multiple confirmed cases of infections of birds and humans. There have been approximately 10 llamas and alpacas diagnosed as having the WNV in the U. S. during the past 3 to 4 years. All llamas and alpacas confirmed to be infected with the virus have died. Some alpacas suspected of having WNV have survived with supportive treatments, but these diagnoses can not be confirmed at this time - only suspected based on positive serum antibody titers to the disease.

Clinical signs: Depression, lethargy, decreased appetite, may or may not have fever, staggering, recumbency, seizures, coma, death. Early treatment: Supportive care. Initially, non-steroidal anti-inflammatory drugs are used (e.g. banamine). If clinical signs worsen, steroids are initiated so long as bacterial infection has been ruled out (dexamethasone should not be used as this can cause damage to the camelid liver; rather, prednisolone should be used). Ulcer prophylaxis (e.g. gastrogard, carafate, etc). IV fluids as needed, general supportive care.

Diagnosis: serum antibody titers (SN test run at the NVSL in Ames, Iowa), CSF antibody titers (also run at NVSL), if dead - IHC on brain and spinal cord tissues.

Since there is a poor prognosis for treatment, the best hope for prevention is vaccination. Fort Dodge Animal Health has marketed a vaccine for WNV in horses, which is not labeled for use in llamas or alpacas. As with all vaccines utilized in the llama and alpaca industry, this would be considered extra label use. We hypothesized that the equine WNV vaccine would stimulate antibody production in llamas and alpacas. Two studies have been done using this vaccine. Dr. Kutzler at Oregon State University lead a research project funded by ARF and these results have been posted on the ARF web site http://www.alpacaresearchfoundation.org. She found good response to vaccination after 3 doses. At Ohio State, we are in the second year of a two year study designed to determine the reaction to subcutaneous administration and to determine the antibody responses by this vaccine. To conduct this study, we used 12 llamas and 16 alpacas and each was given the vaccine per the dosing instructions on the label for the equine species (1 cc given 2 or 3 times, each dose given 3 weeks apart). Blood was drawn on Day 0, 7, 14, 21, 28, 35, 42, and 70. These were sent to National Veterinary Service Diagnostic Laboratory for virus neutralization (VN) assay. No VN titer was detected at any time point in 26 out of 28 llamas and alpacas after a single vaccination dose (two camelids that had a VN titer of 1:10 at 3 weeks week after the initial dose). VN titers rose markedly only after the booster dose of WNV in the other 26 llama and alpaca. However, some VN titers had decreased to less than 1:10 by 10 weeks after the initial vaccination (7 weeks after booster). VN titers were highest after a third vaccination dose. It would appear that the vaccine would need to be administered every 2 to 3 months during the high-risk period for contracting WNV (e. g. when mosquitoes are active). Additional testing is required to examine the prolongation of serum antibody titers. Since this study was done, I have vaccinated over 100 alpacas with WNV including pregnant females. To date, we have not seen any adverse reactions to the vaccine.

Preliminary epidemiology study: West Nile Virus antibody titers from alpaca herds that suffered a WNV death last year (confirmed by immunohistochemistry tests to be WNV) showed that 10% of the alpacas had antibodies (titers exceeding 1:100) to WNV! These preliminary results suggest that we only saw clinical signs in 10% of the infected alpacas. Thus, alpacas are relatively resistant to becoming infected (e.g. 1 in 10), and are relatively unlikely to develop clinical signs from the infection (e.g. 1 in 10).

Additional testing is required to gain a better understanding of this disease!

These results are preliminary and need 1) more numbers and 2) more analysis.

At this time, we can conclude that WNV infection is uncommon if not rare in alpacas, that when they get infected they are relatively unlikely to develop fatal illness from the disease, but that when they do succumb to clinical infection (presumably because their immune systems are compromised for some reason) the disease is often fatal. These statements are similar to what we see of WNV in humans.

YOU MUST DECIDE HOW MUCH RISK YOU ARE WILLING TO ACCEPT. YES, THE VACCINE CAN BE USED. YES IT SEEMS SAFE AND YES IT DOES STIMULATE ANTIBODY TITERS. HOWEVER, WE KNOW TAT IT TAKES A MINIMUM OF 21 DAYS (E.G. AT LEAST 2 DOSES OF VACCINE) AND PROBABLY 42 DAYS (E.G. AFTER 3 DOSES OF VACCINE) TO STIMULATE ANTIBODY CONCENTRATIOSN SUFFICIENT TO BE PROTECTIVE.

The single most important tool in WNV prevention is elimination of insect vectors. Since mosquitoes are the most prevalent vector, control measures should include management practices to eliminate mosquitoes. Mosquito control includes drainage of standing water sources, mowing vegetation around ponds and lakes, and aerating water sources to decrease mosquito larvae survival (e.g. mosquito larval survival is significantly reduced if oxygen dissolved in water can be maintained above 400 ppm). This research needs more support.

Donations to support Dr. Kutzler's study can be made through the Alpaca Research Foundation by visiting their website: http://www.alpacaresearchfoundation.org

Donations to the Ohio State study can be made directly to:
Susan Kelly, VCS Accounts Manager
601 Vernon L Tharp Street
Columbus, Ohio 43210
Make checks etc payable to the "OSU CAMELID WNV RESEARCH FUND"

We will keep you updated on the progression of the disease and research being done.

Hypothermia: Are you ready for the winter?
As we enter the autumn months in North America, my thoughts drift to concerns for care and management of livestock during the often-harsh environmental conditions of winter. In general, llamas and alpacas are well suited to cooler temperatures. After all, winter in the Andes can be trying on the soul if one is not prepared for it. However, camelids are susceptible to extremes of environment, hot (hyperthermia) or cold (hypothermia). The highest risk animals on the farm are very young, very old, very thin, or diseased camelids.

Perhaps the biggest concern we have for hypothermia are newborn crias. Crias are born without the stores of fat needed from which to draw energy to maintain body temperature. Newborns are dependent on the dam's colostrum and milk to provide glucose, fat, and protein. Early and frequent access to these nutrients are critical for the cria to survive the first few days of life. Without the milk fat, crias have a limited ability to maintain body temperature and blood glucose, both of which are necessary to survival. When crias are exposed to extremes of temperature, they must burn energy at a much higher rate to maintain body temperature and the remainder of the body systems may become starved. At some point, the cria is unable to ingest adequate milk to survive and hypothermia begins. These crias are often found down in the pasture in a cushed position with the head and neck extended in front of them on the ground. This posture is designed to close off all areas where heat is lost: around the tail (perineum), between the legs (axilla and groin), the underside of the belly (ventral abdomen), and the base of the neck (sternum and thoracic inlet). At this point and if body heat and energy are not restored quickly, the cria will die from hypothermia and hypoglycemia (low blood glucose) within a few hours.

The veterinary community has spent considerable time and energy evaluating risk factors and developing prevention strategies for heat stress. This is time well spent but we must consider both sides of the coin. Several years ago, a new farm lost several alpacas to heat stress. The farm did not have adequate shade and had not sheared the alpacas. When the peak daytime temperatures rose above 90 F and humidity climbed to 80 %, the alpacas could no longer tolerate the extremes and several died before intervention could be instituted. The most significant factor seemed to be that the night time temperature did not fall below around 80 F. Thus, the alpacas could not exhaust the heat build up from the day before. This is bad when you are wearing an alpaca sweater! The next year, the farm manager was determined not to succumb to the same problem and the alpacas were shorn in April of the next year. Unfortunately, a bitter cold spell including freezing temperatures and snowfall hit that area late in April. Eight alpacas were hospitalized for hypothermia and, fortunately, all were saved. I enjoyed watching them walk around with Ohio State sweatshirts on!

These lessons are simple: management and husbandry practices greatly influence an animal's ability to thrive. Consider your farm in light of the following tips for prevention of hypothermia:

can seek protection form environmental extremes. These facilities should have sufficient width, length, and height to allow protection from wind. If three-sided shelters are used, a portion of the open side may be enclosed to provide a more effective windbreak. The orientation of the shelter should be such that the open side is not presented to prevailing winds (e.g. in Ohio, shelters face southeast to brace against northwesterly winds). Our research has shown that llamas and alpacas will "loaf" (referring to relaxed cushing rather than seeking shelter for protection) in shelters that provide approximately 36 square feet per animal. During environmental extremes (e.g.

cold below 20 F, high wind, hard rain, sleet/ice, heavy snow) llamas and alpacas will utilize shelters at a rate of 18 to 24 square feet per animal.

Inadequate shelter space will cause animals to be "left out" without protection from the environment.

to stay DRY. The second most import is to protect against wind. WET + WIND = HYPOTHERMIA. Thin and young and old animals are the most susceptible to these effects.

their natural thermal windows. Remember, in summer we are trying to increase the thermal window. In winter, our goal is to decrease this thermal window.

I prefer straw for this purpose. Straw is inexpensive, clean enough to use for birthing areas, has adequate insulating features, and can be easily cleaned from the floor and fiber coat.

water fluctuates with the temperature of the water. When water is near freezing or frozen, water intake is decreased. Insufficient water intake causes decreased feed intake and the ability to regulate body temperature becomes impaired. In lactating females, milk production suffers and crias will fail to gain weight or will loose weight. If passive waterers are used (e.g. buckets, troughs), the water should be refreshed daily or several times a day as needed. I prefer heated automatic waters to optimize access and decrease labor.

energy. I am often asked to consult on farms during winter months because females are loosing weight, crias are not gaining weight, or hypothermia cases have been seen. Many of these problems can be tied to inadequate winter nutrition. Grain feeding may be increased to provide rapidly metabolizable energy sources, but this must be done cautiously. Over feeding of any grain source can cause acidosis in the fermentation chamber (C1) of the stomachs and this will exacerbate the problem. Corn is the "hottest"

grain in that it provides the most readily fermentable carbohydrates of the cereal grains, but this also makes corn the most risky for causing acidosis.

I prefer to add oats to a winter ration because this feed provides more fiber than corn and is less prone to acidosis. Example: if a herd is feeding a commercial camelid pellet ration at 0.5 lbs per head per day, oats may be added at 0.5 lbs per head per day to increase energy intake. The addition of the oats should occur slowly over two weeks to allow the flora of C1 to adapt to the change in diet. Hay should be analyzed before winter months. I prefer to test each new shipment of hay and make acceptance of the hay contingent upon this analysis. Total digestible nutrient content of the hay should exceed 55% and is most desirable to exceed 60% for winter forage. I recommend that every animal in every herd have a BCS (body condition score) done every month. Loss of body condition score should be addressed quickly unless it can be explained (e.g. females are expected to loose 1 to 1.5 BCS during the first 2 months of lactation).

story. Providing adequate access to feed is the other. In regions where heavy snowfall occurs and in areas where ice storms are common, camelids must be able to gain access to feed. In these situations, I prefer to offer feed inside of the shelter so that animals are not required to walk to a different location to get feed. Camelids will opt for protection against environmental extremes rather that eat or may eat for fewer hours each day.

For farms that have barns this is rarely an issue. Farms using three-sided shelters may have a more difficult time providing sheltered feed.

During winter months, ventilation remains important. When shelters are "battened down" for the winter, we must be careful not to over-insulate the interior. Camelids tend to urinate and defecate inside of shelters. Who can blame them - nobody likes a draft in the bathroom! If ventilation is too restricted in winter housing, ammonia and other gases from the dung pile buildup and can contribute to winter pneumonia and poor thriving crias. As always, hygiene is the key to success.

but what I am referring to here is 'when did you shear and how is your fiber growing'. Last year, I worked with a herd that had not been able to shear until late in July. Although nutrition was adequate, there was not much room to spare. The fiber coats had not grown well enough before winter to provide adequate protection from the wind. Examination of the herd revealed a suboptimal herd BCS (average 4 out of 10) and approximately 25% of the herd had subnormal rectal temperatures (average of hypothermic alpacas 98 F).

Although this temperature was not acutely critical, the chronic environmental stress decreased immunity, decreased lactation, and caused weight loss. Nutrition and sheltering had to be addressed quickly and within a few weeks the problem had stabilized. Unfortunately, the affected alpacas required over 1 year to fully recover.

warmth. Females have been known to give birth in open fields in the snow when they do not have access to a clean shelter in which to birth. These crias are at high risk for hypothermia if shelter is not provided. In our research, females that had access to a 14 x 16 foot shelter rarely gave birth inside of that shelter in either winter or summer. We assume that the reason for this was the presence of a dung pile in the shelter and a perception by the female that the environmental stress was too great. When females had access to a 25 x 60 foot shelter, the females always gave birth inside of the shelter despite the presence of two dunging areas within the shelter. We assume that the surface area of the shelter was large enough to allow criation and overcome the females concern for the presence of dung piles.

per unit area. I recommend that farm stocking density be no more than 5 llamas or 7 alpacas per acre of land for grazing to maximize forage utilization and minimize parasite burdens on pastures. In winter, grazing is not an issue for most farms because the animals will voluntarily congregate around hay feeders and shelters. Hygiene becomes a vital concern. Our research has shown that a minimum of 12 inches is required for bunker feeders to allow simultaneous feedings. However, this results in failure to feed by many of the submissive animals. Bunker space of 24 inches per head resulted in fewer submissive animals being excluded. Hay feeder space is equally important. Camelids may spend 8 hours or more feeding on hay each day. If limited feeder space is available, submissive animals will not be able to ingest enough hay to maintain weight and will be more prone to hypothermia.

parasites that can not survive the harsh cold and failure of eggs to hatch into infective larvae. This is true for most intestinal parasites. However, winter is fertile ground for transmission of some parasites (e.g. coccidia, whipworms, lice, mange, skin fungus) because of close animal-to-animal contact and diminished hygiene. Heavy parasite burdens cause stress to the animal and may decrease their ability to tolerate environmental extremes.

Treatment of hypothermia involves warmth, nutrition, and correction of underlying problems (e.g. milk supplements for crias whose dam is not lactating). Critical hypothermia occurs when core body temperature drops below 90 F. Consider the following treatments:

cold stall can be detrimental because the direct heat causes dilation of the surface blood vessels, which can exacerbate heat loss. By incubating the animal in a warm blanket, heat loss in prevented.

too quickly can cause as much harm as the hypothermia because of altered blood flow and liberation of potassium and organic acids that built up during the period of poor blood flow caused by hypothermia. These can cause the heart to stop!

most useful. If an IV line is not available, glucose or other carbohydrate syrups (e.g. honey, fructose, and maple syrup) may be fed orally or may be inserted into the rectum. Yes, that's right! Camelids can absorb glucose from the rectum if there is adequate blood flow. All liquid supplements should be warmed to approximately 95 to 100 F.

glucocorticoids. Our research suggests that dexamethasone should not be used in camelids. Prednisone type steroids may be safely used for short periods at modest dosages (e.g. not exceeding 1 mg/kg twice daily for 2 days).

high-risk camelids. I prefer omeprazole (2 to 4 mg/kg, orally, once or twice daily).

realized for a day or two. These animals must be kept under constant vigil for 3 to 5 days to be sure other complications will not be suffered (e.g.

Although heat stress is of great concern to camelids residing in North America, cold stress is equally important. Forethought and preparation will help you keep your llamas and alpacas from being caught with their fur coat down!

This continuing education article is provided by the International Camelid Institute. Consider making a donation today by contacting Karen Longbrake at phone 614-688-8160, fax 614-292-7185, e-mail longbrake.1@osu.edu, or www.internationalcamelidinstitute.org.

Winter has a few special considerations for alpacas and llamas, just as it does for people. We have to take some extra steps to make sure that our camelid friends keep comfortable during the cold months of the year.

Alpacas and llamas like to be out in the snow, but they should have easy access to a roofed shelter, with at least three solid sides. One llama or two alpacas can live within a ten by ten foot space allowing for feeding, water, and an indoor dung pile if they have to be closed in for a short time. You have to take into account the temperaments of the individuals, as one aggressive animal can keep everyone else out in the cold. You may have to do some housing trials to see who gets along with whom. A four foot wide door opening in one wall is sufficient for access for the animals. Provisions should be made to completely close up the structure if high winds and/or freezing rain is expected. Clear plastic panels can be strategically placed in walls or on the roof to allow for solar heating and to take advantage of the maximum amount of winter sunlight. Lights should be available for late afternoon chores and bed check at night. I think that it is especially important to check your animals one last time before you go to bed at night in the winter. Cold temperatures are not very forgiving if some problem were to develop in the evening. It could save a young cria's life.

I am a strong believer in having bedding down for animals at all times, but especially in the cold months. It provides increased comfort and reduces the calorie requirements to maintain normal body temperature. A llama, alpaca, or person would not choose to lie down on a pile of gravel in the winter if a softer and warmer area were available. Six inches of hay makes a good bedding. This can be added to periodically as it gets broken down using the hay that the animals leave in the bottom of the feeders or spill on the ground. Rubber mats are also good to insulate animals from the cold ground and are a must if you have cement floors.

It is especially important in the winter to keep very close tabs on the body condition of all of your animals. This should be done on a weekly basis by feeling the shape of the outline of the lower back muscles just in front of the pelvis. The outline should remain round at all times. If it becomes flat on top, the animal is too fat and its caloric content should be reduced. Winter is a good time to get the weight off those fat geldings by feeding them your lower quality hay and very little if any grain. When they get where you want them, switch to the good quality hay and use grain as needed. A triangular topline means that the animal is too thin and should be on your best quality hay, preferably green, leafy second cutting, and a grain supplement as a concentrated source of calories. Cracked corn is easily digested, readily available at any feed store, and the animals like to eat it. It makes an excellent quality calorie supplement in the winter.

Don't forget about the water needs of your animals in the winter. Clean fresh water should be available at all times. I prefer having heated water available at all times. It keeps them drinking better and thus their digestive system working better than if you use cold water or even put out a bucket of warm water twice a day. Your animals will actually drink more water in the winter than in the summer. They are only eating dry hay with a very low moisture content compared to pasture or recently mowed hay. Also there is much less humidity in the air in the winter.

If you have elected to have winter babies (which I do not recommend), or have purchased an animal which is due to give birth in the winter, you need to be very careful that the cria does not get hypothermia. It should be dried off immediately after birth with towels and a hair dryer, and the mom and cria should have a relatively warm, dry, and draft free, heavily bedded area in which to sleep. Some type of cria coat or a sweater is necessary for animals born in the winter. Neonates do not have enough body fat or fiber to keep warm from birth in the winter. It is very important that these babies are up and nursing early. My general rules are up within one hour and nursing within two hours or intervention is necessary. I do not hesitate to tube a winter baby its first meal if it is the least bit slow in starting to nurse.

Don't forget about the risk of your crias developing rickets. In the fall and winter inadequate Vitamin D3 may be produced in the body when the amount of daily sunlight is relatively low. Low Vitamin D3 results in decreased calcium absorption and skeletal abnormalities. I recommend supplementing all babies with Vitamin D injections every two months from October until April to prevent the occurrence of rickets. The first injection should be done at birth. Rickets may take a subclinical form and present as only a slow baby rather than the classic severe lameness. Supplementation is not harmful based upon years of use in the Pacific Northwest.

Winter alpaca and llama care is not difficult, but it does require constant attention to the comfort and safety of your animals.

• Hay - Body heat is generated from eating Hay, so high quality grass (preferably 2^nd or 3^rd cutting) hay is a necessity. This should be provided free choice at all times. Also have ample hay feeders per animal, as a guideline a hay bin containing 1 bale of hay accessible from all 4 sides would feed at most 3-4 animals. Keep in mind boys are more territorial, so even more space should be considered. Always keep an open eye for the less aggressive eaters and monitor them more closely to prevent herd starvation.
• Feed Supplement - A good quality feed supplement formulated for alpacas is also required. Among other things this feed provides a much needed energy source. Additional grain or using the lactation formula may also be needed. Dr. Evans seems to have a good grasp on supplements and feed, go to www.lamawellness.zoovu.com for his recommendations.
• Again access to the feed is critical. Provide a minimum of one and a half times the number of feed bowls as female alpacas or two times the feed bowls for male alpacas. Example: 10 females – have 15 bowls. That way, if one gets pushed off, they always have another bowl to feed from. This method also spreads the food thin preventing choke. For females, space these bowls at least 24” apart and for males, space at least 36” apart.

Body scoring is a practice all breeders should learn and utilize. Simply put it is judging the condition of your animal by feeling its backbone. A pronounced back bone indicates your animal is to thin. If the back feels flat perhaps your animal is chubby. On a scale of 1 to 10 a score of 5 is ideal. A 1 score indicates a grossly under weight animal and a 10 score is grossly obese. Ask your vet for assistance in learning this simple procedure. This practice should be done often due to the fact that as winter progresses growing fleece can easily camouflage a failing animal. Keep in mind this practice does not replace the importance of weighing your animals.

Cria Kit Requirements

These are the items we keep on hand or in our Cria Kit:

BVD Virus – A Newly Recognized Serious Health Problem for Alpacas
By: Nancy Carr MD and Susy Carman DVM PhD.

Bovine viral diarrhea virus (BVD virus or BVDV), a serious problem in cattle, has now been proven to also cause illness, abortions, and most important of all, the persistently infected (PI) state in alpacas. The virus’s ability to produce persistently infected cria, the main way this disease would be spread, and its ability to cause abortions are extremely important for the alpaca industry.

At this point, the vast majority of knowledge about BVDV and the disease that it causes, bovine viral diarrhea (BVD), is about its effects in cattle, where it is considered one of the most significant viral infections, causing major economic losses. The information presented next is a brief synopsis of BVDV in cattle.

Despite the name, many animals with BVD do not have diarrhea. Other manifestations of the virus include subclinical infections, immunosupression, abortions, congenital defects, persistent infection, and mucosal disease. The majority of cows infected are either subclinically ill (do not appear unwell) or only mildly unwell with low fever and diarrhea. Because BVDV depresses the immune system, some animals will become ill with other infections, usually pneumonia; others will have a classic case of BVD with fever, discharge from the nose and eyes, erosions of the muzzle and in the mouth, and severe diarrhea; others may have severe hemorrhagic (bloody) diarrhea and die. Severity of illness is influenced by the age of the animal and its immunological and physiological status, and the particular strain of the virus involved.

The most important aspect of BVDV is its effect on the developing fetus. BVDV can cause abortions at any stage of gestation – from early embryo loss up to stillbirths at term. Even a subclinically infected cow can abort, and abortions may occur up to several months after exposure to the virus. A unique feature is that if the cow is exposed to the virus at a critical phase of her gestation (approximately 40 - 120 days) and does not abort, she will produce a persistently infected (PI) calf. Because the developing fetus is not immune competent at that stage of development it becomes immunotolerant to the virus (does not recognize the virus as foreign); it is unable to make an immune response to rid itself of the virus, and once born, is a permanent carrier and sheds huge concentrations of the virus in every secretion – tears, nasal discharge, saliva, urine, and feces. PI calves are the major source of the spread of BVD – they shed several billion viral particles a day – about a thousand times more than what is shed by an acutely infected non-PI animal. The only way to be PI is to be born PI. Some PI calves appear completely normal, but most are poor-doers – poor weight gain, weak, and susceptible to other diseases such as pneumonia; many PI calves die before they are a year old. Infection of the pregnant cow with BVD later in pregnancy can result in calves that are not PI but that have congenital defects such as cerebellar hypoplasia (underdevelopment of the part of the brain that controls balance and co-ordination), cataracts, blindness, hypotrichosis (sparse hair growth) or general growth retardation.

Acute infection with BVDV occurs through the nose or mouth by contact with secretions from an infected animal (usually a PI animal) – saliva, nasal discharge, tears, urine or feces – either directly from the infected animal itself or from items that have been contaminated with those secretions, such as water troughs. BVDV is very infectious. An acutely infected but non-PI animal sheds virus for a relatively short length of time (4 – 10 days, possibly up to 2 weeks) in comparison with a PI animal which sheds virus for its entire life. Incubation period is 5 to 7 days. The virus cannot survive long in the environment – a maximum of 2 weeks. Because it is a virus, antibiotics are of no use in treating it.

There are hundreds of different strains of the virus, which can also be categorized under type 1 (BVDV1) or type 2 (BVDV2) and by the terms cytopathic or non-cytopathic. PI animals always have a non-cytopathic strain of BVDV. An entity called mucosal disease occurs only in PI animals – they become superinfected with an antigenically similar cytopathic strain of the virus (usually from a mutation in their own non-cytopathic strain, or from a modified live vaccine); this leads to severe diarrhea and inevitably death. Vaccines for cattle are available for BVD; however they do not confer 100% immunity.

There is not much published information concerning BVDV and camelids. Articles published to date on BVDV and camelids have generally concluded that BVDV is not much of a concern. In an article titled ‘A Medical Marvel’ in the winter 1999 edition of Alpacas Magazine Randy Larson DVM stated what was likely the commonly held viewpoint at that time: “BVD is an example of a significant disease of cattle that causes undetectable problems in alpacas. BVD and other common cattle viruses just do not cause problems in alpacas.” Medicine and Surgery of South American Camelids (page 469) makes mention of BVDV only as a cause of congenital defects and impaired immunologic competence in calves and lambs.

In 1994, Mattson reported on a study of 270 llamas from 21 herds in Oregon; 4.4% of them had antibodies to BVDV. Seven of the twelve llamas that had antibodies were from one farm where cattle were in contact with the llamas.

In 2000, Belknap et al. from Colorado State University reported on three cases of BVDV isolated from llamas (a stillborn fetus and two sudden deaths in adults that had been losing condition) and concluded that BVDV should be considered as a cause of death in young and old New World camelids. The Complete Alpaca Book makes mention of that statement (page 451) and also that it may be one of the causes of diarrhea in cria (page 400).

In 2002, Goyal et al. in Minnesota reported on what appeared to be the first case of BVDV isolated from a stillborn alpaca; there were no gross or histopathologic changes of any significance seen, but BVDV was detected by reverse transcriptase polymerase chain reaction (rt-PCR) from a pool of tissues, and BVDV was isolated from cell cultures. Immunohistochemistry, a test commonly used to detect BVDV in tissues taken at the time of autopsies, was negative.

In 2003 Wentz et al. reported on the effects of experimental infection with BVD on llamas and their fetuses, and on the seroprevalence of BVDV [detection of antibodies that would signify the animal had been exposed to BVDV at some time in the past] in llamas and alpacas. They concluded that llamas may be infected with BVDV but have few or no clinical signs, and that inoculation of llamas with BVDV during gestation did not result in fetal infection or PI crias. Seroprevalence in a sample of 223 llamas and alpacas was 0.9%. They also concluded that the most likely source of BVD infection in camelids may be cattle.

Dr. Donald Mattson from Oregon State University (OSU) stated in June 2004 (personal correspondence) that in their llama herd at OSU there had been one sick llama with BVD (it had diarrhea) but that its two herdmates did not become sick; they developed a brief low-level antibody response to BVDV. None of the contact animals developed diarrhea and none had detectable antibodies when tested four weeks after the initial case was diagnosed. He also knew of a case in southern Oregon with a herd of 20 llamas where only one showed signs of illness. He stated that they had only seen BVDV infected camelids when they had been in contact with cattle that are shedding the virus, and that he had tested hundreds of samples from llamas and alpacas and never found a PI camelid.

However, there is now proof that BVDV does cause illness, death, abortion and most important of all, the PI state in alpacas. It is assumed this also applies to llamas. The consequences of this for the alpaca and llama industries may be profound.

This discovery was made at a farm in Ontario. There was illness, including one death, several early pregnancy losses, and an aborted fetus that tested positive for BVDV. One of the females who had been subclinically infected (exposure to BVDV as confirmed by antibody testing) at 2 months gestation subsequently delivered a persistently infected (PI) cria. This is the first recorded case of a PI alpaca, but there is overwhelming circumstantial evidence that BVDV had been brought to the farm by another PI cria that died without being tested. And it is highly likely that that cria’s mother’s source of her infection with BVD during her pregnancy in Alberta (resulting in her producing that PI cria) would have been from another PI alpaca.

The majority of alpacas infected at Farm A in Ontario were subclinically infected and it was only apparent by antibody testing that they had been infected. (Note: having antibodies does not mean that the animal is unwell or contagious; it shows that the animal was exposed to the virus at some point in the past and mounted an immune response; this could be from a subclinical infection (never appeared unwell), a clinical infection (appeared unwell) or from immunization. For example, most of us would have antibodies to chickenpox from having that illness as children.) The alpacas that were unwell had symptoms that ranged from having the appearance for a few days that their mouths were uncomfortable eating their pelletized supplement, to being off feed and depressed, to one death from hepatic lipidosis (that condition would have resulted from decreased feed intake). None of them had diarrhea. Many of them, even those subclinically infected, showed stress breaks in their fleece.

The cria who was presumed in hindsight to be PI and the source of the infection (he died without being tested) arrived at Farm A at the age of 3 months. He had been born at full term on Farm B, also in Ontario, at a very low birth weight of 9 pounds. He had done fairly well for the first 6 weeks of life and then developed repeated infections, mostly pneumonia, had a frequent runny nose, and he had very poor weight gain. He died at the age of 8 months after severe diarrhea. (This was his first episode of diarrhea since having a bout with coccidia when he was much younger). Farm B, where he spent the first three months of his life, had positive BVDV antibody levels in alpacas that had been in contact with him. His mother had been on Farms C and D, in Alberta, in her early pregnancy (when she would have contracted her subclinical BVD infection resulting in her producing this PI cria); Farm C had many abortions and Farm D had two stillbirths and a cria that died at 36 hours of age in the same year that this female delivered her presumed PI cria. Farms C and D have alpacas with positive BVDV antibody levels, including the dams of the aborted fetuses, stillbirths and cria that died. Although it is possible that the mother (who is not PI) became acutely infected at Farm D and transmitted BVD to Farm C during the short time she would have been shedding virus, it is more likely there were separate cases of PI animals on both those farms causing the infections. None of the farms involved had any contact with cattle.

The proven PI cria, called Gabriel, born on Farm A (to a female who had been infected by the above presumed PI cria) also had a very low birth weight of 12 pounds for the farm he was born on. He had excellent weight gain to 33 pounds at the time of his euthanization at a little over 6 weeks of age, after two sets of blood tests confirming he was PI. (The fate of all proven PI animals is to be euthanized.) He had chronic diarrhea, but was not unwell with it and was perky and active.

At this point it is unknown just how prevalent BVD is in alpacas. Alvarez et al. reported in 2002 that 11.5% of alpacas in a rural community of Cusco in Peru had antibodies to BVDV. The other reported case of BVDV in a stillborn alpaca fetus was in Minnesota, and the llama cases were in Colorado, so this is not just a Canadian situation. The practice of sending females with cria at side off to other farms for breeding is one of the main ways BVD would spread – a PI cria may not show any signs of being unwell until it is older and yet be infecting every animal it comes in contact with. Also, a pregnant female going to a new owner may be carrying a PI fetus that, once born, will infect all the alpacas at the new home. This case shows how BVDV traveled approximately 3500 kilometers (over 2000 miles) from Alberta to Ontario. Some PI cattle continue to appear healthy; it is unknown how many PI alpacas may continue to appear normal. It is also unknown what is the exact range of gestation in alpacas that infection of the dam will result in the birth of a PI cria. Cattle have a 9 month gestation and it is in the period of approximately 40 –120 days of gestation that there is the high risk of the fetus becoming PI if the mother is infected with BVD.

Alpacas have a reputation for being easy aborters, and it is not unusual to hear of poor doing cria – it is entirely possible that some of these cases may have been due to BVDV. Unless the virus is specifically tested for there is no way of knowing that it is present – in both the stillborn fetus from Minnesota and the aborted fetus from Ontario there were no pathological changes to suggest BVD – it was only by testing for the presence of the virus itself that it was found. In the euthanized PI cria there were no pathological changes to suggest he was PI – but virus isolation from blood and most tissues was positive. The adult alpaca that died after what must have been an acute BVD infection had autopsy findings of hepatic lipidosis, but it would have been BVD that caused her appetite to decline, resulting in the hepatic lipidosis. In her case, there would not have been virus detected as it would be too long after the initial acute infection – she would have to have had antibody testing. It is possible that some of the unexplained cases of hepatic lipidosis in alpaca herds have been caused by BVD. Schwantje and Stephen’s paper on ‘Communicable Disease Risks to Wildlife from Camelids in British Columbia’ reported a positive BVDV antibody rate of 6% in a sample of 175 llamas from twelve farms, with the rate per farm varying from 0% for many farms to a high of 22% on one farm. This paper also reported on a survey of 90 llama and alpaca farms asking about illness and death in the preceding year; the primary cause of death (26% of cases) was neonatal failure to thrive or stillbirths. The report also reviewed the diagnoses of llama and alpaca submissions to the B.C. Animal Health Centre between 1993 and 2000: 9% of the diagnoses were idiopathic (meaning no cause found) abortion. It is quite possible there is a connection between BVDV and some of those cases of neonatal failure to thrive, stillbirths and abortions. Until aborted and stillborn fetuses and autopsied animals are tested specifically for the presence of BVD virus or antibodies, depending on the clinical situation, we will not know how prevalent this is. Only a completely closed herd (no animals coming into the herd) with good biosecurity measures (all visitors with footwear not contaminated by manure; no fence line contact with other livestock) can be sure to be safe from BVDV.

Testing for BVDV is complicated, with different tests being used in different situations. Having antibodies (blood test) to BVDV shows that the animal was exposed to the virus (from a clinical or subclinical infection, or from immunization), but it is unknown how long antibodies are detectable for after exposure. PI animals would not have antibodies (unless they were tested as newborns soon after ingesting their mother’s antibody-containing colostrum). To detect the PI state the animal has to be tested for the virus itself, and there must be two positive tests three weeks apart to prove the PI state, in case the first positive test was an acute infection and not from being PI. Virus isolation is the ‘gold standard’ test for detecting BVDV – it can be done on blood (live animal) or tissue (dead animal). The ELISA blood test for the virus is used to detect PI animals over the age of 3 months (the maternal antibodies from colostrum interfere with the test before that age, and also sometimes interfere with virus isolation.) The ELISA test on skin biopsies or ear notches can be used to detect PI calves under the age of three months. The PCR test (blood) is not affected by maternal antibody and is also used to detect PI animals under the age of three months. Immunohistochemistry is used on formalin fixed tissue from autopsies; however as noted above this test was negative in the stillborn fetus in Minnesota despite BVDV being detected by PCR and virus isolation; immunohistochemistry was positive in the aborted fetus in Ontario. Your veterinarian should consult with a veterinarian virologist or with the lab that he/she uses for BVDV diagnosis in cattle. Most labs doing BVDV testing are affiliated with universities, or are state or provincially funded; not many private labs offer BVDV testing.

For the veterinarians reading this article: the aborted alpaca fetus from Farm A was positive for BVDV type 1 on virus isolation from skin and positive for BVDV in multiple tissues using immunohistochemistry on formalin-fixed tissue. Gabriel, the PI cria, was found to be positive for BVDV type 1 at birth (using virus isolation on placenta), at 3 days of age (using virus isolation from buffy coat cells and PCR on both EDTA blood and plasma), at 25 days of age (using virus isolation on both EDTA blood, plasma and PCR on both EDTA blood, plasma) and at 6 weeks of age (using virus isolation on buffy coat cells, plasma, serum and multiple tissues, including skin and brain, PCR on both plasma and serum). At 6 weeks of age Gabriel was also IDEXX BVDV ELISA positive using fresh ear notch and positive for BVDV in immunohistochemistry tests using multiple tissues, including skin and brain. He continued to be antibody negative for both BVDV type 1 and type 2 until euthanasia.

At this time, a reasonable recommendation is that all aborted or stillborn fetuses, all unusually low birth weight and ‘poor doing’ cria and all unexplained deaths be tested for BVD virus and/or antibodies, depending on the case. If BVDV is found then further testing should be done to determine how the virus entered the herd - specifically is there still a PI animal present, or has it gone back to another farm. Any cria subsequently born to females who were pregnant when BVD was active in the herd should be tested to see if they are PI. It is important that you bring this information to the attention of your veterinarian as it will be at least a year before it is published in a veterinary journal. It would also be very helpful if you or your vet notified the lab in your area where aborted fetuses or autopsies are sent for testing about this, so that testing specifically for BVDV will become routine in abortions, stillbirths, and unexplained deaths in alpacas.

The complete story of how this discovery was made has been written up and called BVD Virus and Alpacas – The Detective Story. It is also available on www.silvercloudalpacas.com

Addendum: Just before going to press, we have received a report from an alpaca breeder who recently had three abortions and one cria death. After being made aware of the findings in this article, he had blood tests done for BVDV antibodies. All the eighteen alpacas over the age of one year on his farm have tested positive for BVDV antibodies. His alpacas have not had contact with any alpacas from any of the farms mentioned in this article.

Further Addendum: After this article was submitted for publication we have received further reports of BVD virus being isolated from dead alpacas and aborted fetuses – these were from owners or vets who had been made aware of the findings in this article and from labs that had been notified to start testing for the virus.

REFERENCES:
Alvarez S., Rivera G.H., Pezo D., Garcia W. (2002). “Deteccion de anticuerpos contra pestivirus en rumiantes de una comunidad campesina de la provincia de Canchis, Cusco.” Rev Investig Vet Peru, 13(1), 46-51

Belknap E.B., Collins J.K., Larsen R.S., Conrad K.P. (2000). “Bovine viral diarrhea virus in New World camelids.” J Vet Diagn Ivest, 12(6), 568-70

Fowler, M. (1998). Medicine and surgery of South American camelids. Ames, Iowa: Iowa State University Press.

Goyal S.M., Bouljihad M., Haugerud S., Ridpath J.F. (2002). “Isolation of bovine viral diarrhea virus from an alpaca.” J Vet Diagn Ivest, 14(6), 523-5

Hoffman E. (2003). The complete alpaca book. Santa Cruz, California: Bonny Doon Press.

Mattson, D., (1994). “Viral Diseases.” The Veterinary Clinics of North America: Food Animal Practice. Update on Llama Medicine. 10 (2), 346-347

Schwantje H., Stephen C. (2003) “Communicable Disease Risks to Wildlife From Camelids in British Columbia.” [on-line]. Available: http://wlapwww.gov.bc.ca/wld/documents/wldhealth/camelid_risk03.pdf

Wentz P.A., Belknap E.B., Brock K.V., Collins J.K., Pugh D.G. (2003). “Evaluation of bovine viral diarrhea virus in New World camelids.” J Am Vet Med Assoc, 223 (2), 223-8

BVD Virus and Alpacas - The Detective Story
By: Nancy Carr MD

This is the detective story about the discovery that BVD (bovine viral diarrhea) virus, originally thought to be an insignificant problem for camelids, does indeed cause illness and abortions in alpacas, and that it can also cause the persistently infected (PI) state in alpacas. This has fairly far reaching consequences for alpaca farming. For detailed information on BVD virus itself, please see the accompanying article. Like any detective story, my narrative is long and detailed. Also like a detective story, looking back, the solution looks fairly clear; working forward from the beginning it was not clear at all.

The story starts in December 2003. I have a herd of approximately 50 alpacas, and there are three barns. In the first barn there are three separate areas; the groupings at that time were: East section: moms and their cria born that year; West section: maiden females, born in 2001 and 2002; South section: young males born in 2002. There is a solid partition between the East and West sections, and only fence line contact for animals in the east and south sections. Adult males are in the second barn. The third barn is for the quarantine area (primarily for alpacas that have come for breeding) and is not used in the winter.

In December 2003 in the West section there were eleven maiden females (Elena, Mandy, Abela, Tillie, Madison, Mikayla, and Gabriella, all born in 2002, and Harley, Savanna Dawn, and Merienda all born in 2001, and Celeste who was four years old). Harley and Merienda had been bred in June, and Elena, Mandy, Tillie, Abela and Mikayla had been bred in October.

In the South section there were 6 young males: Timoteo, Jupiter, Vaquero, Photon, Dirk, and Cosmo, ranging in age from 14 – 19 months.

On December 1, I noted in my farm record book that Elena in the West section, an 18 month old female who had been bred October 9, was lying around more than usual and not as interested in eating her pellet food (the supplement designed to deliver the necessary minerals and vitamins). Her temperature was normal at 38.3 C. After that, she persisted in not being as interested in her pellet food (and this could have been overlooked in a different setting, as my alpacas are fed their supplement in individual bowls and under supervision to prevent the fast eaters from stealing from the slow eaters) but she seemed normal otherwise - eating hay and normally active. On Saturday December 13 she was even less interested in her pellet food but was still eating hay; it looked as if her mouth was uncomfortable when she was eating the pellets. Her jaw felt normal and I couldn’t see any abnormality in her mouth, but I started her on the antibiotic Excenel in case this was a manifestation of a dental abscess. I had the vet out on Monday morning December 15 to examine her and do blood work including liver function tests. Of course Elena looked quite perky when the vet was here, and I remember saying to the vet that she would just have to believe me that this was a profound change for this alpaca. There were no abnormalities noted on physical exam, including her mouth. Elena was eating hay in the morning, but was lying around more than usual and did not eat hay in the evening. She had Ivomec, and was started on omeprazole to cover the possibility of an ulcer. The next day, December 16, she did not even get up at feeding time. I started syringing in pureed pellet food and liquids.

Blood test reports arrived back later that day. Unfortunately there were no normal values given with the results, and lab values in Canada are reported in S.I. units (e,g mmoles per litre) as opposed to what are called conventional units (e.g. mg. per deciliter) used in the United States. My vet faxed the lab result to me. I had to use the conversion charts in Medicine and Surgery of South American Camelids to convert the values to conventional units so that I could compare them with the normal values given in that book and in Dr. Norm Evans’ Veterinary Lama Field Manual. There were some abnormal results: there were elevated liver enzymes (e.g. AST 877 with a normal up to 250), low protein, low albumin, and low platelets. This looked like possible hepatic lipidosis (also known as fatty liver). I quickly read up as much as I could on hepatic lipidosis, and then started syringing in glucose and electrolyte solution, continued the omeprazole, added Sulcrate and switched the antibiotic to Septra. Despite all that, she had a very rapid downhill course, and died later that evening with her head in my husband’s lap and me by her side.

An autopsy was done the next day and it showed hepatic lipidosis. Now for a quick aside about hepatic lipidosis. The simplified explanation is that when caloric needs are not being met, either by poor quality or quantity of feed, and/or increased needs, such as lactation, or under the influence of stress, the body mobilizes fat from fat stores and it goes to the liver. In humans, the liver would convert the fat to glucose and the glucose would be used by the body as a source of energy. In some animals, such as alpacas and cats, the fat stays in the liver, and the deposition of fat in the liver cells impairs liver function and leads to liver failure. It is often a spiraling downhill course because as the liver function becomes impaired, the appetite decreases so there is even less food intake. In alpacas, stress and poor nutrition are considered the prime causes of hepatic lipidosis. It was no consolation to read that well run alpaca farms could lose animals to hepatic lipidosis. It just didn’t make sense. There had been absolutely no stressors. My hay had been tested: 12% protein and 58 % TDN, and there was unlimited hay put out. All the females receive 200 grams twice a day (total of 400 grams – almost a pound) of a specially formulated pellet ration to provide their selenium and other vitamins and minerals, and the extra calories they need in our cold winters. All these alpacas were in good body condition (body scoring). None of the nursing mothers, who would have the highest caloric needs, in the East section of the barn were affected - they received identical hay and pellets. I thought it more likely that whatever had made Elena reluctant to eat her pellets had resulted in decreased feed intake and that had set off the chain of metabolic events resulting in hepatic lipidosis.

Then on December 23, two more females from the West section, Merienda (two and a half years old, five and a half months pregnant) and Mandy (eighteen months old, two months pregnant) were both not eating their pellets with much enthusiasm - it really looked as if their mouths were uncomfortable. This was the same presenting symptom as Elena. I immediately had the vet out to do blood work. The vet had suggested that Elena’s reluctance to eat food at the beginning of her illness was a manifestation of liver problems. I thought it more likely to be the other way around: that the reluctance to eat pellets came first (from some other cause) and the resulting decreased feed intake caused the hepatic lipidosis. The vet was unable to get a blood sample from Merienda. Mandy’s blood tests, including liver enzymes, were all normal, other than an elevated haptoglobin value in keeping with an inflammatory (which would include infectious) process. I therefore thought this confirmed that Elena’s, Mandy’s and Merienda’s reluctance to eat pellets was not from liver problems (early hepatic lipidosis), as the liver enzymes would have been elevated in Mandy at this stage if this were the case. I thought Elena’s hepatic lipidosis was a result of her decreased feed intake from whatever had made her uncomfortable or reluctant to eat the pellets, but had no idea what was causing that. I put both Merienda and Mandy on omeprazole for a week as the vet said sometimes not eating supplements may be a manifestation of an ulcer. Neither of them ever looked or behaved unwell (they had normal activity and were eating hay) and they were eating their pellets normally in a few days.

On December 24 in the evening another alpaca in the West section, Tillie (seventeen months old, bred October 6) did not eat any pellets, stayed lying down and would not eat hay. Her temperature was 39.2 celsius (just borderline). Since I was worried that her not eating would result in hepatic lipidosis, I started glucose and electrolyte solution by syringe – by providing calories that way, it should stop the body from thinking it had to mobilize fat reserves. Early the next morning (this was one of the worst Christmases on record) I started Septra (antibiotic), omeprazole and Fastrack and continued syringing in the glucose and electrolytes. I realized my intervention with Elena had been too little and too late, and I vowed to Tillie I would not let her die. I did not see her eating any hay, and mostly she stayed lying down. The next day she started eating hay. By December 27 she was eating well and she was chewing her cud for the first time since becoming unwell. She was back to normal by December 29.

On December 27 another alpaca in the West section, Abela (seventeen months old, bred October 13) was having trouble eating her pellets and she was lying around more than usual in the morning. I started her on omeprazole. She looked a little brighter the next day but was still eating pellets slowly. By December 29 in the evening she was eating normally.

In the week after this, two more females in the West section, Gabriella (twenty months old, not pregnant) and Madison (fifteen months old, not pregnant) both had several days of not eating pellets normally and both appeared to have increased redness at the corners of their mouths – no sores, no blisters, no ulcers, nothing apparent inside their mouths, just a bit of redness at the corners of the mouth. I did not put them on any medication and they were back to normal in a few days.

At the end of December the six young males from the South section were moved to the adult male barn. On January 8, Jupiter was not eating pellets normally. The next day he wouldn’t eat any pellets and was not chewing his cud, so I put him on glucose and electrolytes, septra, omeprazole, and fastrack; he was cud chewing by January 11 but was still having difficulty eating pellets. The corners of his mouth looked red. He ate better on January 12, and on the 14th the medication was stopped and he seemed normal.

On January 9 Dirk was eating his pellets but would not eat hay; he looked somewhat unwell and was shivering (by then we were having a cold spell with temperatures at -20 celsius). He had been chased and ridden a lot by the older boys and I think this stress may have compounded his illness. Jupiter, Dirk and two of the other young males were put in a separate area without contact with the adult males. Dirk continued to eat his pellets fairly normally but was eating very little hay, lying around more than usual, and not cud chewing. His temperature on January 9 was 38.4 C. I gave him glucose and electrolyte solution, Septra and omeprazole. By January 11 he was eating hay well; by January13 he was cud chewing, and I stopped the medications on the 14th.

None of the alpacas had diarrhea. Elena, Gabriella, Madison, Jupiter and Dirk all had a few small patches of fleece that came out at the immediate time of illness or shortly after, and in the case of Dirk it continued for several months. There were no bald patches, but there would be very obvious tufts of fleece sticking out, or that had fallen out.

There were no other alpacas with these symptoms. I could not figure out what was causing this. All groupings received identical hay, water and pelletized supplement. I sent off their water for ‘livestock suitability’ and coliform / e.coli testing and the tests came back normal; the pellet feed was tested and the analysis confirmed the proper ingredients.

To say that this was a stressful time would be a vast understatement. I racked my brain about what was different about the West and South sections that it was only alpacas there that had been unwell and not any in the East section or from the adult males’ barn. The only thing I came up with was that there were some pigeons in the overhangs off the West and South sections. I wondered if they were carrying some disease. My husband Paul and I became experts at netting pigeons; and Paul became an expert at chopping off their heads. All the pigeons were dispatched except for one pigeon that I took in to the vet’s office and asked that it be sent for testing. No signs of any disease were found in it.

In late December our friend Grant, whose son has a dairy farm in the area, dropped by for a visit. When he heard of our woes he said that his son had told him of a bad outbreak of a virus causing illness and death in cattle. He found out for me this was called BVD 2. I read up on BVD, bovine viral diarrhea, but it didn’t seem applicable; the illness described in cattle was fever, discharge from the nose and eyes, erosions in the mouth, and diarrhea; its major impact in cattle seemed to be the abortions it caused. What few reports there were about alpacas or llamas and BVD implied it was not much of a problem at all; one web site even said how marvelous it was that alpacas never got BVD. One study with llamas and BVD concluded that llamas could be infected with BVD but had few or no clinical signs. Also, there seemed no way that BVD could have come to my farm. The closest cattle are a mile away. There had been no cattle on our farm for several years. Visitors are asked if they have been on other farms and if so, are given foot wear from here – the only possibility would be cattle manure on the vet’s boots if the vet had not cleaned his/her boots. The vet office said they had not heard of any BVD outbreaks in their practice. It was an interesting disease that I had never heard of before, but it didn’t seem to have any relation to the problems on our farm.

Jupiter and Dirk were the last two alpacas that appeared unwell. The final tally was: one death, three alpacas with severe enough symptoms that I put them on ‘shotgun therapy’ (cover everything) and they recovered, and five alpacas with mild symptoms (looking like they had a sore mouth) that recovered on their own. I don’t think the omeprazole, a drug for ulcers, had anything to do with their rapid recovery as some got better without it, and of those on it, none relapsed when I stopped it after a short length of time. The whole picture fit with some infectious disease: primarily one age group affected, and the whole spectrum of severity from not unwell, to mildly unwell, to quite unwell, and one death. However I could not find any illness described that fit the symptoms. It was a mystery, and it had been a nightmare, but I was thankful it was finally over.

In the East section with mothers and cria were a visiting female for breeding, whom I will call VF, and her chronically unwell male cria whom I will call MC. They arrived here September 21, 2003 and were put in the quarantine area by themselves (separate barn and pasture). MC had been born on another farm, Farm B, on June 13, 2003, and had only weighed 9 pounds at full term – a very low birth weight. Records from Farm B showed he had done fairly well, with good weight gain, until early August when he developed pneumonia and diarrhea. He was treated with antibiotics, had panacur and was on amprolium after a diagnosis of coccidia. He had not had solid manure or any weight gain for the month prior to arriving here; his weight on arrival here was 25 pounds. His fecal sample still showed coccidia. In the quarantine area I use a separate pair of boots and a separate shovel for shoveling manure – these are used only in the quarantine area. Since I knew MC had coccidia I was even more obsessive – I removed his manure with disposable gloves rather than smearing it around with the shovel, and poured liquid bleach where it had been. He was treated for the coccidia; his stool became normal within a few days of arriving here and he started to gain weight. I remarked to anyone who would listen about the wonders of having lots of fresh uncontaminated, not overgrazed, pasture. VF and MC both received a course of panacur because VF’s fecal sample had shown tapeworm. Repeat fecal samples were normal. VF and MC were to stay for an extended period of time; they would have to be integrated with my herd at some point for over the winter, so they were put in the East Section with the adult females and cria on October 8. I had looked up in Medicine and Surgery of South American Camelids to see if there was any infectious disease that fit with MC’s ‘unthriftiness’ (as the vets call it) but couldn’t find anything, so assumed it was safe to put him in with the other alpacas. MC never looked totally healthy. He had very slow weight gain, and a runny nose off and on; he didn’t often play with the other cria. I had never had a poor doing cria, but had heard of other farms that had. I still hoped that with good care and proper nutrition he would eventually become normal. Starting in November, he had recurrent courses of antibiotics (Septra or Excenel) for pneumonia. He finished a course of Septra on January 30, but he still had some nasal discharge and was not eating normally. He was put on Baytril, another antibiotic, on February 5 for ten days and seemed somewhat better; at that time he weighed 40 pounds (many of my cria are that weight by 4 weeks of age, and he was almost 8 months old). His stool became softer; testing was normal. He developed watery diarrhea, and despite supportive treatment died suddenly on February 28. When I notified the owners of his death, which really was not unexpected, I forgot to ask if they wanted an autopsy. Since it was a warm Saturday and it seemed unlikely the owners would want to pay for an autopsy on what had been a chronically poor doing cria (that they had already spent a lot of money on) and there was the problem of what to do with the body until Monday, he was buried. I later confirmed with the owners that that was fine. His mother VF has always looked healthy. There was no direct contact between VF and MC and the alpacas in the West or South sections. None of the adult females and cria in the East section (that VF and MC were with) ever appeared unwell then or since.

No other new alpacas had joined my herd in 2002 or 2003. One female who came for breeding and her cria were in the West section in the spring and early summer of 2003, after being in the quarantine area for a week or two and having normal fecal tests. The other alpacas that came for breeding in 2003 were in the quarantine area the whole time and never with my herd. The last of these left August 21 and the quarantine area was cleaned and not used until VF and MC arrived September 21. The last time any of my females had been away from my farm for breeding was in the year 2000.

After MC’s death I mulled over what could have been the diagnosis for this chronically unwell cria. I had ‘bought into’ the concept of unexplained poor doing cria; I had never had one, but I had heard of others who had. I am a family doctor; in humans you would never say “That child died because he was a poor-doer” – there is always a diagnosis. There just had to be a diagnosis for MC. Of course I do realize it’s the economic considerations that preclude all the testing to come up with a diagnosis in animals. I read up on a lot of illnesses, remembered something from my reading on BVD and looked again at that information, and specifically about persistently infected (PI) calves. These are the calves that were exposed to the BVD virus as fetuses (their mother was clinically or sub-clinically infected) during the crucial stage of gestation, approximately 40 to 120 days, when they did not recognize the virus as foreign. They never mount an immune response to the virus, and if they don’t abort they end up as permanent carriers. After being born, they shed huge quantities of virus in every secretion (saliva, tears, nasal discharge, urine, and feces) the rest of their lives, and are the major source of the spread of BVD in cattle. Although some PI calves are normal, many are poor-doers – low birth weight, poor weight gain, and they have repeated infections such as pneumonia; the majority are dead before one year of age. This was the exact picture of MC. There is also something called mucosal disease with BVD – this occurs only in PI animals and is the result of superinfection with an antigenically similar strain of BVD, usually from mutation of the strain the animal already has – this results in severe diarrhea, and invariably death. MC had died after a fairly sudden onset of diarrhea. There did seem to be striking similarities between MC and a typical PI calf; however I decided it was still pretty far-fetched, especially as no alpacas in the East section of the barn with him had been unwell, and also, camelids just weren’t supposed to be affected by BVD. VF had been on four different farms during her pregnancy with MC. I contacted the farm where VF had spent most of her pregnancy and asked if they knew anything about her background that would have resulted in her producing such a low birth weight and poor doing cria, They thought it was likely just stress from VF being moved around a lot during her pregnancy. I figured I’d never know what had been MC’s underlying problem.

Then, on March 29, 2004, Mandy aborted at five and a half months gestation; she did not appear unwell. She was the alpaca who had had two days of not eating her pellets normally in late December and had had normal blood work. I thought about BVD again and its association with abortions, including abortions that can occur months after the initial infection, and figured I had nothing to lose by asking for the fetus to be tested for this. After all, the vet’s office probably already thought I was a little nuts for bringing in that pigeon for testing. The preliminary report showed no significant lesions in the lungs, heart, liver, kidney or placenta, and came with a comment that the pathologist could not find any references on BVD or other viral abortions in alpacas, and that alpacas seem to be quite resistant to viral diseases. Immunohistochemistry testing for BVD took longer, and it was positive: it showed staining for BVD antigen in lung, kidney and heart. The comment on this report was that this was a very interesting case. Then virus isolation (the gold standard test for BVD) was done and it was positive from a skin sample.

It took a while for the whole significance of this to sink in. It now seemed very likely that the illnesses in December had been from BVD. However I still had no idea how BVD had arrived on my farm. I spoke with Grant’s son, the dairy farmer who had mentioned about BVD. He told me it had only been on one farm that he knew of, and that farm was close to him; that would be approximately 20 - 25 km. from me. The vet involved was not from the vet clinic that I use. There was no connection between that farm and mine in any way. Also that was BVD2 and my aborted fetus had BVD1 – these are two quite different strains of the virus – so that case had nothing to do with the BVD on my farm. I spoke with a dairy farmer who is approximately two km. from me and he said he was not aware of any problems in the area; the last outbreak he had had was over five years ago. Although it was thinking about MC and what could have been wrong with him that had brought BVD to mind, I didn’t think I could seriously consider MC as a PI animal – alpacas just weren’t supposed to be affected by BVD (although it appeared I had just proved that wrong) and no alpacas in with him had been ill. I had uncharitable thoughts about whether one of my vets could have tracked the virus in on manure contaminated boots. At one point I was convinced that would have to be the only way BVD had come to my farm. The only problem was that vet visits and the start of Elena’s illness didn’t fit in regards to the incubation period of BVD, and the vets had not even been in the west section of the barn.

All this testing had taken quite a length of time. It was now May and I had been spit testing any of the females who had been bred in the fall and didn’t look obviously pregnant (spit testing had stopped for the winter in November). Spit testing showed that Abela and Tillie from the west section were no longer pregnant. Abela had been mildly unwell and Tillie had been quite unwell in December. It looked as if BVD had caused not only Mandy’s abortion, but these early pregnancy losses as well. The only alpaca in the west section that had been at two months gestation in December and was still pregnant was Mikayla. In the east section, I already knew that Velvet wasn’t pregnant after a breeding late in the fall. But Misty, who had been bred on October 10 was no longer pregnant. She had passed her spit tests up until her last one on November 10 and it was very unusual for her not to maintain a pregnancy; of her preceding six pregnancies, only once had she come open after passing the two week mark.

Shearing of all the alpacas was completed by the third week of May, 2004. Stress breaks in fleece are well known in fleece bearing animals that have been subjected to stress such as illness, high fever, or malnutrition. When pulling on a sample of fleece by holding at the cut end in one hand and the tip end in the other hand, the fleece will break at the level in its growth where the stress occurred. Severe stress breaks (fleece easily broken) were visible in Tillie, Jupiter, and Dirk – the alpacas who had been ill enough that I thought they required the whole gamut of treatment. In fact, just looking at a sample of their fleece you could see where the break would be – there was a broader wave of crimp there. Stress breaks were also evident in Abela, Gabriella, Madison, and Mandy; these four had had mild symptoms that had lasted only about two days, and Mandy was the one who had aborted. But there were also stress breaks in the fleece of Mikayla (from the West section), and Timoteo, Photon, Vaquero and Cosmo (young males who had been in the South section). None of these five had shown any signs of being unwell. Every alpaca born in 2002 had a stress break in its fleece. Merienda, born in 2001, who had had several days of not eating pellets normally in December, did not have any stress breaks in her fleece, and neither did Celeste, Harley, or Savanna Dawn who were also in the West section. VF, the mother of MC, did not have any stress breaks in her fleece, and in a cursory check of some fleeces from alpacas in the East section and the adult males no others with stress breaks were found. I have had very little illness in my herd in order to compare other fleeces in alpacas that may have been subjected to stress or illness. Savanna Dawn, born in 2001, and in the West section had had a uterine infection in the summer of 2003; she had had several uterine lavages and courses of antibiotics. She had no stress breaks in her fleece. In April 2003, Mikayla as a 7 month old had had an episode of lethargy, decreased appetite and a fever of 40.1 Celsius. She was put on antibiotics empirically and improved quickly. She was sheared a month after that, and when I examined her fleece sample that I had kept from that shearing (of May 2003) there were no stress breaks in it. She had quite a long staple length, and I think even though there was only a month between illness and shearing, meaning that the stress break would be quite close to the cut end, if there was a stress break it would be detected. I found it amazing that BVD virus had been a severe enough assault on the alpacas to cause a stress break in their fleece, but that in some of them they had never even appeared unwell. It was also amazing that Mikayla did not have a stress break in her 2003 fleece even though she had had an episode of being obviously unwell and febrile with some illness, and yet she had a stress break in her 2004 fleece from what must have been a subclinical BVD infection. This was quite the virus.

When the BVD virus isolation test had come back positive, the pathologist had discussed with my vet about getting a BVD antibody test done on Mandy, the alpaca who had aborted. In the spirit of scientific enquiry I decided to get antibody tests done on a number of animals. Having antibodies does not mean that the animal is unwell or contagious – it shows that the animal was exposed to the virus at some time in the past and mounted an immune response – this could be from a clinical infection (appeared unwell) or a subclinical infection (never appeared unwell) or from immunization. For example, most of us have antibodies to chickenpox, because we had that illness as children. It appeared there must have been at least some subclinical infections, based on the fleece stress breaks, but I still expected the results would show that BVD had been confined to the West and South sections of the barn. By now, I was concerned about Mikayla’s fetus. She was the only alpaca in the West section that had been in early gestation at the time of the illnesses in December and that was still pregnant. Mandy, Tillie and Abela had aborted or had early pregnancy losses; Harley and Merienda were much further along in their pregnancies. Mikayla had been bred on October 14, 2003, so if she had been infected with BVD in December there would be real risk of having a PI cria, if that could happen in alpacas. The International Camelid Institute had no information on BVD and camelids. I contemplated aborting Mikayla. I had met Dr. Patrick Long, co-author of Llama and Alpaca Neonatal Care, and contacted him for advice on what drug and dose to use; he kindly put me in touch with Dr. Mattson, a BVD expert at Oregon State University. Dr. Mattson said although it was theoretically possible for there to be such a thing as a PI camelid, he assured me he had tested hundreds of samples from llamas and alpacas and had never found a PI animal, and advised me not to abort her.

The antibody tests came back. The lab had first run an ELISA test on all the samples checking for the virus itself – these were all negative, meaning there were no acute or PI infections (not that I had expected there would be). From the West section, I had tested Tillie, Abela, Mandy, Merienda, Savanna Dawn, Harley, Celeste and Mikayla; all of them had antibodies to BVD1. From the east section I had tested VF (I was starting to be more suspicious that her son MC might have been PI), Velvet, and Shawnee – VF and Velvet both had antibodies; there had not been enough blood from Shawnee’s sample to do the test. From the young males who had been in the South section I had tested Dirk, who had been unwell, and Cosmo who had not been unwell. Surprisingly, Dirk did not have a detectable antibody level, but Cosmo did. I do believe that Dirk, who had been quite ill in early January, must have had a BVD infection. He was the young male who had been very stressed by the older males after being moved to their barn, before I separated him and some of the other young males out again. It certainly made me wonder about the effects of stress and the ability to mount an effective immune response. From the adult males in their separate barn, I tested Dano, and as expected he did not have antibodies. Merienda, Cosmo, and VF tied for having the highest titre of antibodies (1:1536).

So, this meant that the females in the West without symptoms and without stress breaks in their fleece had also been infected with BVD; in fact it seemed likely that all the alpacas in the West and South sections had been infected (and of course, other than Elena, had recovered). I was still concerned that Mikayla could have a PI cria, even though there was not supposed to be such a thing. She had definitely had a subclinical infection as confirmed by the antibody testing, and also by now she was due in a little more than three months, and her pregnant abdomen did not look as big as it should for her gestation, suggesting an abnormally small fetus. MC, whom I was suspecting more and more may have been PI, had been quite a low birth weight. Only when I found out there were some risks to causing an abortion did I decide not to go through with it.

However, even more unsettling than finding out that all the animals in the west and south had been infected was finding that alpacas in the East section also had antibodies, despite no signs of illness there. VF could have been positive as the mother of MC if he were PI, but Velvet was positive also. I got out all the fleeces from shearing from all the alpacas from the East section, and checked every one for stress breaks. I actually hoped that I would find some breaks, so that by measuring where the break was I might have an idea of when BVD was in the East section. There were no stress breaks in the fleeces from the adult females. There were also none in the adult males from the other barn. The ten cria fleeces were harder to assess – the wispy friable tips would break off; I checked cria fleece samples from other years and this was the same case. However, there were three that had an additional break further down from the tips. The crias’ dates of birth ranged from June 1 to October 28, so if some of the younger ones also had stress breaks they may have coincided with the friable tip breaks. There was no way of figuring out from these cria fleeces, from cria with a wide range of birth dates, when they had had their subclinical infection with BVD. Since it appeared that alpacas in the east had been subclinically infected with BVD, I now had to worry about all the pregnant females who had been in that section and whether they would have PI cria, even though there was not supposed to be such a thing. I decided to have more antibody testing done on alpacas that had been in the East section. I tested Tulia and Nevada, two of the cria who had been born in 2003 and therefore would have been in very close contact with MC, while eating their pellets together, and two more adult females, Arani and Snow White. All of them had antibodies to BVD. All the cria born so far in 2004 were checked for the virus (a different test – the PCR test) to make sure they were not PI – all of them were negative.

Danae and another female, Teaya, and their cria had left my farm for their new home on November 22, 2003, at least a week before Elena had shown the first sign of being unwell. Danae had delivered on October 9, 2003, been bred on October 23, and aborted at her new home on May 16, 2004, a day after shearing. The fetus was not sent for testing. At that point the owners were unsure exactly which alpaca had aborted, and even if it was known for sure it was Danae, there was no reason at that point to suspect she had been exposed to BVD – the antibody tests showing that BVD had been in the East section of my barn, where Danae had been before going to her new home, had not yet been done. Danae had returned to my farm for re-breeding after her abortion. I had her antibody level done and it was positive - the highest titre (1:3072) of any done. Danae had left the farm November 22, and Elena’s first sign of illness was noted down on December 1, so Danae’s positive antibody test showed that BVD had been active in the east section (subclinically) prior to Elena’s first symptoms. I asked Teaya’s and Danae’s new owners to test Teaya’s 2004 cria, born at the end of May, for the virus to make sure he was not PI; he was negative. They also had antibody tests done on three alpacas that had been in close contact with Danae, Teaya and their 2003 cria soon after their arrival there in November 2003, to make sure the new arrivals were not acutely infected with BVD at the time of their arrival and infecting any alpacas at their new home – those tests were negative. Two other females and their cria had left my farm for their new home in early September, prior to VF and MC arriving; I had one of those females tested for BVD antibodies and that test was negative. I took that as evidence that BVD had not appeared on my farm until after their departure

I now had enough evidence to start to suspect MC as a PI alpaca since it appeared likely all alpacas in the East section had been subclinically infected. The background on VF was that she was bred on July 4, 2002. She was still at her farm of origin, Farm E, in Alberta, until some time early in August 2002. She was then at Farm D in Alberta for a few weeks as a drop off and pick up spot, and went to her new home, Farm C, in Alberta at the end of August 2002. She stayed there until late March 2003 when she traveled to Ontario to Farm B where she was consigned to an on-farm auction. The new owners, who bought her at the auction, decided to have her stay at Farm B. MC was born on June 13, 2003; he and VF stayed at Farm B until they came to my farm in September 2003 for VF to be bred. If he had been PI then I expected some of the alpacas at Farm B may have been unwell after his birth, or there may have been abortions, or at least there would be some alpacas with antibodies to BVD. I emailed Farm B, explained the whole situation, asked if they had had any problems, and asked if they would agree to have some antibody tests done if I paid for them. The only two pregnant alpacas that may have been in the same enclosure as MC, or may have been moved out prior to his birth, had delivered in October 2003; MC had been there from his birth in June until September, so those two would have been fairly far along in their pregnancies during that time. Remember that VF is not in any way contagious; she is not PI, and had had the ELISA test that proved that – it would only be after MC was born that there would be the possibility of BVD infections if he were PI. Farm B reported that one alpaca who had been in with VF and MC had been lying around more than usual at the end of June, about two weeks after MC’s birth, but that was just noted for one day. They thought they should pay for the antibody tests; I thought I should pay (this is Canada for you!) I suggested that if the tests were negative, I should definitely pay for the testing as it would confirm this was a hare brained idea of mine. Farm B had antibody testing done on three alpacas, two of whom had been in with MC, and one who had not. The two who had been in with MC had antibodies to BVD and the one who had not been in with him was negative. One of the ones who had antibodies was the alpaca that had been lying around more than usual at the end of June – that was likely her manifestation of BVD infection.

Since VF and MC were in my quarantine area here from their arrival on September 21 until being put in the East section on October 8, it was not possible that one or both of them had spread BVD to my herd as acutely infected animals (having just contracted it at Farm B) - they wouldn’t be shedding the virus that long as acutely infected animals. It was really starting to look as if MC could have been a PI alpaca.

Of course now Farm B had to do testing to make sure none of their cria born in 2004 were PI, and to notify customers who had bought alpacas or were about to buy alpacas. They lost sales because of their integrity. On August 3, 2004 Farm B phoned to say they had been faxed the results of the PCR tests that had been done on all their cria born so far that year, and that one of them was positive. This would mean he could be PI. This cria had been born to a female who had been bred July 28, 2003 and had never been in the same enclosure as MC. To prove the PI status the test would have to be repeated after three weeks. Then ensued a very upsetting three weeks for Farm B as they instituted quarantine procedures and contemplated that if the second test were positive, the cria would have to be euthanized. With repeat testing, the PCR test was equivocal, but the virus isolation test was negative. His mother’s antibodies were checked and they were negative (meaning it was unlikely she had had a BVD infection) so it appeared this cria was not PI, and that the first PCR test was a false positive. Farm B breathed a sigh of relief.

I was still trying to figure out why there was the cluster of infections in the West and South sections of my barn in December 2003, starting with Elena’s symptoms first noted down on December 1. When I looked at MC’s records again, the answer was obvious. MC had been on injectable Excenel (an antibiotic) for pneumonia from November 11 to November 17, with improvement in his symptoms. When he relapsed soon after, on November 22, he was put on oral Septra and the vet suggested it would be worth keeping him on this for three weeks; he was on this until December 14. I administered this twice a day – the fingers of my left hand would be in his mouth to open it up while my right hand squirted in the syringe measured amount of antibiotic. Although most of the morning doses were given on an early morning barn check, after which I returned to the house and washed my hands before breakfast, many of the evening doses were given right after MC had finished eating his pellets. He and all the other cria ate their pellets together in an enclosure separated from the adults. I would either have given MC his medicine as one of the last things I did before moving to the West section for feeding, or I would come back after putting out the food in the West, give him his medicine once all the cria had finished eating, and go back to the West to supervise. Elena (the first alpaca ill) was the fastest eater in the West section. I routinely fed her a few pellets or some grain out of my hand after she had finished her bowl to prevent her from stealing the pellets from other alpacas. In fact most of the alpacas in that section would have eaten pellets out of my hand at some time or another over the space of a few feedings. My fingers would have been contaminated with MC’s saliva. The incubation period of BVD is five to seven days. I started oral antibiotics for MC on November 22 and I noted down Elena’s reluctance to eat her pellets on December 1; it is likely that it had started a day before that, as I would not have noted down just one feeding that wasn’t normal. Why would a doctor who routinely washes her hands between every human patient, and who washes her hands as soon as she comes in from the barn, not wash her hands after treating MC? Sheer stupidity of course comes to mind. Since this was not a conscious decision not to wash my hands, I think in my subconscious I knew I was treating a recurrent bacterial pneumonia in a compromised cria (which I was) and did not think that he had anything particularly contagious to the other alpacas. After 48 hours on the antibiotic he shouldn’t have been contagious for bacteria anyway - antibiotics are of course not effective against viruses. All the other alpacas in the East had been with him since October 8 and none of them were ill; that included all the other cria – they had the closest contact with him, as they all ate their pellets together. I never considered the possibility of an underlying viral illness transmissible by his saliva. The symptoms of alpacas in the West just didn’t seem to have anything to do with MC’s recurrent pneumonia. Some may have been infected from each other after the initial cases, but I’m sure I infected a lot of them with my virus contaminated hands – a PI animal sheds huge amounts of virus in every secretion, including saliva. I also started MC on a vitamin B pill in early December that he was on until his death – my fingers had even more contact with his saliva when I gave him that. I did start washing my hands after examining the unwell alpacas in the west, but I would have had MC’s saliva on them prior to that. The phrase killing with kindness seems particularly apt. This was yet further evidence that MC was a PI cria.

And then there was still the question of why none of the alpacas in the East section had appeared unwell – it seemed likely they had all been subclinically infected. There are several possible explanations. One is that the age group of the alpacas in the West and South sections (most of them between one and two years old) may be more susceptible to manifestation of illness by BVD. Another possibility is the effect of ‘viral load’ – the amount of virus the animal ingests is correlated with the severity of the illness; it’s quite likely the alpacas in the West and South received a higher viral load off my saliva contaminated hands than the alpacas in the East received from indirect contact with MC and his secretions. The third explanation was presented by a bright vet tech student at the local community college when I did a presentation on alpacas. All the adult females in the East section had been alpacas that I had bought; they had all come from other farms – perhaps some of them already had protective antibodies from being exposed to BVD in the past on the farms they had come from.

Meanwhile, I had contacted Farms C and D in Alberta by email. If MC were PI then his mother would have been in contact with BVD during her early pregnancy and that would have been on one of those three farms she had been on. She had been bred July 4 at Farm E, went to Farm D sometime in early August, and then went to Farm C around the end of August. If she were a cow it would have to be after approximately 40 days gestation (and before 120 days) that she would have come in contact with BVD in order to produce a PI offspring, so it would likely be on Farm C or D that VF had come in contact with the virus, and not Farm E. None of the farms have any cattle. Farm C said that they had had many abortions in the spring (mostly April) of 2003. They had a lot of tests done at the time of the abortions, and the abortions were attributed to a toxic mould in the hay. I told them I suspected that the mould was an incidental finding and that it was much more likely that the abortions had been caused by BVD. Farm C had their vet out to discuss the situation. Farm C emailed me with what their vet told them: “He said that he had the labs check out our abortions last year for BVD by doing a Complement Fixation Test on the brains of the fetuses. He used three different labs for the tests, and no lesions were observed, so he feels that BVD was not the cause of the abortions here. He feels they were related to feed, which contained toxic moulds.” The only problem with that statement was that complement fixation is just not a test that is ever used to detect BVD. Several months later I asked Farm C to double check with their vet about this and it turned out there was no record of any complement fixation test, or any test for BVD. In August, Farm C went ahead and had antibody testing done on four of the females who had aborted in 2003 and were flabbergasted when the tests came back positive. They then had testing for the virus on all the cria born in 2003 and 2004 to check for any PI animals, and those tests were negative. They checked a recent arrival on their farm and she was negative for antibodies; this would be good evidence that BVD was no longer active on their farm.

Farm D in Alberta had had, in 2003, two stillborn cria, one full term, and one two weeks early, and a cria that died at about 36 hours of age. In September 2004 they had BVD antibody tests done on some alpacas (dam of one of the stillbirths and dam of the cria that died; the vet was unable to get blood on the dam of the other stillbirth) and they were also positive. VF is not PI; if she were the vector between Farms D and C (meaning if she had spread it from Farm D to C), she would have to have made the move (at the end of August 2002) while acutely infected and during the short time she would have been shedding the virus. In cattle it is the PI animals that are the major vectors as they continually shed huge quantities of virus (as opposed to not as much virus and for a very short length of time, in an acutely infected animal). I thought it more likely that Farm B and C had had different exposures to BVD (probably from two different PI animals), and that I would never know with certainty on which farm VF had had her BVD infection that resulted in MC being (I thought) a PI cria.

By August, after finding out Farm B’s positive antibody results from the alpacas who had been in contact with MC, and Farm C’s positive BVD antibody levels in the alpacas who had been pregnant at the same time as FC, but had aborted, I was convinced that MC must have been PI. I was also starting to worry not only about Mikayla’s fetus being PI, but also about the cria still to be born to the females who had been in the East section. With my pregnant females in the West section I was sure they had been exposed to BVD in mid to late December, so it was easy to know their stage of gestation at that time. With the pregnant females in the East section, there was no way of knowing how soon after MC joined them on October 8, 2003 that each was exposed to the virus and therefore at what stage of gestation the fetus was exposed. In early August, the breeding and birthing dates up to that point were:

West Section	Breeding Date	Gestation mid Dec/03	DOB of Cria
Harley	June 17 /03	6 months	June 4/04
Merienda	July 2 / 03	5.5 months	June 16/04
Mikayla	Oct.14 / 03	2 months
Mandy	Oct. 13 / 03	2 months	aborted March 29/04
Abela	Oct. 13 /03	2 months	early pregnancy loss
Tillie	Oct. 6 / 03	2.25 months	early pregnancy loss

East Section	Breeding Date	Gestation Oct. 8 / 03	DOB of Cria
Annicka	June 20/ 03	3.5 months	May 30
Lambada	July 9/ 03	3 months	June 10
Cindy	July 17/ 03	2.75 months	June 13
Arani	July 18/ 03	2.75 months	June 22
Talara	July 27/ 03	2.5 months	June 22
Jasmine	Aug. 13 and 16/ 03	7 - 8 weeks	July 8
Murragamba	Aug. 25 and 29/ 03	almost 7 weeks
VF	Sept. 22 and 26	no way she would have a second PI cria
Misty	Oct. 6 and 10 / 03	just pregnant	early pregnancy loss
Mackenzie	Oct. 19 and 22/ 03
Snow White	Oct. 27/ 03
Velvet	Nov. 26/ 03	not pregnant when checked late Dec.
Shawnee	not pregnant

As of early August, the cria born so far had normal birth weights, were healthy and had tested negative by PCR test for BVD virus – every time there was a birth I had the vet out to do the test. MC had only weighed 9 pounds at birth, and Mikayla definitely had a smaller pregnant abdomen than she should have; I really suspected she was carrying a PI fetus. With the way my barns, fences, gates and record keeping are, there was no chance that she had been bred on any day other than the one I had recorded. All the females in the East still yet to deliver had big pregnant abdomens, so I was not as concerned they were carrying PI fetuses. Still I found it amazing that Jasmine’s cria was normal – the only explanation I have is that she did not get exposed to the virus until later in October or November, or that she had pre-existing protective antibodies from a previous exposure to the virus on her farm of origin. I had not done antibody testing on every female (no one was footing the bill for all this except for me) but I assumed they would all be positive. I also assumed that because Danae, who had left the East section and the farm November 22, had antibodies, that probably the whole East section would have been exposed to the virus by then, but I will never know. It is possible that Danae was exposed on the day she left because it coincided with the day of MC’s relapse of his pneumonia, and the start of his oral antibiotics (again with my hands as being the vector, as I may well have offered her a treat from my hand to get her in the trailer). In October and early November, the alpacas were still spending most of their time grazing, and I have large pastures. Dung areas in the barn are cleaned up twice a day, and in the pasture every few days, alpacas are protective of their personal space, and they do not lick things, so I’m assuming it’s possible that the alpacas in the East did not get exposed to the virus immediately after MC joined the group. Perhaps many of them were not infected until after November 22.

Murragamba delivered an 18 pound healthy cria on August 7 and the PCR test was negative. I had antibody levels done on Murragamba at the same time – they were positive, but on the low side (1:32), perhaps (but certainly not definitely) indicative of exposure in the past before she arrived on my farm in 2001. VF delivered a 15.4 pound cria on August 26, and as expected, the PCR test was negative – her antibodies would have protected her from becoming infected again. This cria continued to gain weight really well and was healthy. I was assuming that Mackenzie and Snow White, both with big pregnant abdomens, would have been exposed to the virus either pre-conception, or so early in their pregnancy, that it was unlikely they were carrying PI fetuses, even though they had been bred around the same time as Danae.

By now, Dr. Carman, the virologist at the Animal Health Lab at Guelph University (home of Ontario’s only veterinary college) had been fielding many phone calls from me and Farm B as we struggled with all the issues of BVD and the different tests. I phoned her up at the end of August and explained that my plan was to euthanize Mikayla’s cria at birth if it was low birth weight because that would make me sure it was PI; I did not want to have poor Mikayla cope with a cria who disappeared at the age of three or four weeks old when it was proven to be PI, and then euthanized (which is of course what must be done with a PI animal) and I did not want to cope with all the biosecurity issues of having a PI cria on the farm. I asked her if the euthanized cria tested positive for BVD virus, would that prove that there was such a thing as a PI cria (she had already told me she had not yet seen any evidence to make her think there was such a thing, despite the ‘trail of antibodies’ found at Farms B and C). She said that to prove the PI state there must always be two positive tests for the virus taken at least three weeks apart, in case the first test was positive from an acute infection. I knew a first positive test would not be from an acute infection acquired just before birth – there would be no source of infection, and anyway, Mikayla already had antibodies. However the scientific community would not accept anything for proof except the two positive tests taken three weeks apart. At first I didn’t think I was prepared to put Mikayla and myself through this just to prove a point, but then I decided for the sake of scientific knowledge it would be the best course of action.

Farm B probably believed there was such a thing as a PI alpaca, but other than me they were the only ones. Farms C and D had pointed out the studies saying that BVD didn’t cause illness in camelids or affect the fetus. No one seemed to remember that I had definitely had BVD on my farm and that it had caused illness and an aborted fetus, and there had to be an explanation for how BVD had been brought to my farm. Obviously they had not read their Sherlock Holmes stories: “When you have eliminated the impossible, whatever remains, however improbable, must be the truth”. It was impossible that BVD had been brought to my farm by cattle, or deer, or manure contaminated boots – all that was left was the improbable - a PI cria – made less improbable by the ‘trail’ of antibodies. I have been a doctor long enough to have seen what is considered the absolute truth in regards to research findings or treatment at one point in time to be proven false some years later. It still amazes me that many people (including many doctors) do not see the logical corollary to that, which is that some of what is considered correct today will be proven to be wrong in the future. I had already proven wrong the concepts that camelids do not get seriously ill with BVD and that BVD does not cause abortions in camelids. I saw no reason not to think that the concept of no such thing as a PI alpaca might also be wrong. I had some inkling of how the first researchers felt who were treated with disbelief or derision for proclaiming that smoking was bad for you.

Snow White and Mackenzie both delivered before their 11 month mark, as they usually did, and had good sized healthy cria that tested negative for BVD. As Mikayla’s due date approached I made my preparations. In the quarantine area there were still two females from another farm – one who had come for breeding and was now about 2 months pregnant, and her companion. The owners wondered if they could stay longer until it was more convenient for them to pick them up. I explained why I wanted them off the farm before Mikayla delivered, and my husband drove them part way of the way home to meet their owners. I had never moved Mikayla to the East section where all the females go at least a couple of months prior to delivery, because I did not want her there if she had a PI cria. I had kept her with her cohort of two year olds (now all bred) and the one year old girls. I went shopping and bought an extra pair of boots, lots of disposable gloves, disposable plastic boot covers, liquid bleach, hand disinfectant, and more pails, and had my plan in place about re-groupings. Mikayla’s 11 months was up on September 14. For the preceding months she had had what I can only describe as an extremely care–worn expression on her face – quite unlike her usual demeanour, On September 15 there was a noticeable lightening in her expression, and I saw her looking at the boys slightly coquettishly. It was time to make the final moves. I put Mikayla and the one year old girls, all of whom I was sure would have antibodies to BVD (I had actually only tested two of them) because of their close association with MC as cria together, and none of whom were bred, in one grouping in the West section so that there was no fence line or barn contact with any other alpacas. I moved the other two year olds to the South, and moved the juvenile boys to the quarantine area. I decided to hold off on erecting solid partitions over the open slats between the West and South sections in the barn until the cria was born and see what its weight was.

On Friday September 17 Mikayla went into labour; I was there for her labour and her delivery, which was normal. The cria, a cute little white male, stood and nursed in the normal length of time; however, ‘little’ was the operative word – he weighed only twelve pounds and was able to walk easily under his mother. The 63 births I had had on my farm prior to this had weights ranging from 15 pounds to 24 pounds, and the average was 18.1 pounds. Mikayla is a big girl in good body condition; when I weighed her several months after this, she weighed 174 pounds. Her mother’s cria have ranged from 18 – 24 pounds, and Mikayla herself weighed 20 pounds as a newborn. This was truly an abnormally low birth weight for my farm, and for an alpaca the size of Mikayla. Originally I was going to go with my sister’s suggestion of naming the cria Magnum PI, but decided instead on Gabriel, as I thought he would either be joining the angels soon, or it would be a small miracle if he were not PI. I decided to assume he was PI and institute full ‘biosecurity’ measures. Of course the reality was that probably all the females on the farm already had protective antibodies and were at no risk at all, but I had not tested all of them. The cria born earlier that year would have ingested antibodies in their mother’s colostrum, but perhaps in the older ones those levels would be waning by now. I had a pair of boots that I kept only in the west section of the barn and stepped into as I went through the door to that area, and stepped out of when I left. Everyone else donned plastic boot covers while in that area and removed them as they were leaving. I always had a supply of disposable gloves in my pockets and in a container in the West section – if I had any contact with Gabriel I donned the gloves in order to open doors and gates to get back to the house where I immediately washed my hands and changed clothing. The solid barricade went up over the slats between the West and South sections. The self-filling water tank that straddled the South and West sections was closed on the South side and I had to start watering that group by hose and bucket.

The only unusual thing about Gabriel’s birth was that he passed a really large amount of meconium starting about an hour after he was born. There was so much that I had to clean off his rear end and hind legs the next day. I had the vet out on Monday for the blood tests. I had phoned Dr. Carman after Gabriel was born on the Friday to tell her he was really low birth weight and to discuss the blood tests. If the PCR test was positive it would be confirmed with virus isolation (another blood test) and then both repeated in three weeks. I decided to get blood drawn for both the PCR and the virus isolation on the Monday to save time, as I was so sure the PCR would be positive. The PCR test is run once a week at the Animal Health Lab in Guelph, and virus isolation is set up once a week and then it takes two weeks after that for the result to be read. Gabriel’s PCR test for BVD virus was repeated three times as the first reading was ‘suspicious’ – however the subsequent two were negative, and it was reported as such. I found that hard to believe – so, another phone call to poor Dr. Carman, who did not say ‘I told you so’ but did say that no test is 100% accurate. The virus isolation test result would not be available for another two weeks, and I was not prepared to stop all my biosecurity measures until I was positive Gabriel was not PI. I had frozen the placenta, so I decided to send off some of that for virus isolation too.

For the first few days after his birth, Gabriel looked a little fragile; he sometimes looked as if he had trouble figuring out how to negotiate the step up into the barn, even though it was only a couple of inches. But after that he behaved quite normally. He gained weight well; he was up to 20 pounds by 2 weeks of age. However he had persistent diarrhea - runny and yellow at first, then brown and more pudding-like in consistency; I cleaned off his rear end several times. He was normally active, but just didn’t look quite the same as the other cria – his fleece looked somewhat ‘scruffy’. He also had weepy eyes – not pus, but some clear tears that caused dirt staining down from the corners of his eyes. He also had a large umbilical hernia (as had MC). It was a good grouping he was in with – the one year old girls were quite tolerant of his cria behaviour and were like big sisters. At one point Gabriel had them all running and pronking around the field with him. I think he would have been overwhelmed in the larger grouping of older mature (i.e. occasionally snarky) moms in the East section.

The virus isolation test (the ‘gold standard’ test for BVD) came back when Gabriel was almost three weeks old, and it was positive. I was not surprised, but I think Dr. Carman was. It certainly seemed Gabriel would prove to be PI. Dr. Carman was in touch with Dr. Deregt, a BVD expert in Lethbridge, Alberta, who originally wondered if perhaps I would send Gabriel to live in his lab – that was easy to answer no to. I had already decided to have the second set of tests done three weeks after the first, as that would be the only way anyone would believe there was such a thing as a PI alpaca. Now Dr. Carman asked if I would wait a further three weeks after those tests, and have a third set of tests done, before Gabriel was euthanized, so that no one would cast doubt on the diagnosis. In return, she and Dr. Deregt would arrange to cover the costs of all the final tests, the euthanization, and all the postmortem testing – this was a relief as so far I had been funding all the research into BVD and alpacas myself with all my blood tests. The placenta tested positive on virus isolation. The PCR and virus isolation done three weeks after the first tests were also positive, confirming that Gabriel was PI. It was of course not reassuring that the first PCR test on Gabriel had been a false negative, as it cast doubt on the validity of all the PCR tests done on all the other cria. I had to have the vet out to draw blood on all the other cria again, and the Animal Health Lab repeated the tests at no charge – they were all negative.

Gabriel continued to gain weight well and was perky and active. He weighed 32 pounds at 6 weeks of age – quite a good gain from a birth weight of 12 pounds. His diarrhea persisted – not very much of it and not frequent, just not formed; but he was not unwell with it. It was of course poignant to watch this cute little cria doing all the normal cria things, and know what was in store for him. He was one of those naturally gregarious cria who always came over to see what you were doing, and always wanted to nibble on your clothing – the absolute last thing I wanted. I was continually evading him when I was in the West section. It was even more amazing that he was so friendly considering the only times I touched him were for unpleasant things – weighing, holding for blood tests, and cleaning off his rear end. All I could do was assure that his life was pleasant and carefree while he was here.

I made plans for the euthanization, which was to be several days after he was 6 weeks old. He was to have a lot of blood tests just prior to this and I certainly did not want his last minutes to be a time of fear and pain. I also did not want Mikayla to see me taking him away, never to be seen again. I decided to ask the vet for the cocktail of drugs used for general anesthesia (butorphanol, ketamine and xylazine) to be given prior to the blood tests. The vet waited in the garage. I had the syringe with the drugs. Luckily Gabriel usually stayed outside to play while his mother came into the barn for her pellet feeding. I gave him the injection after she was tucked into her food and within a minute or two he was quite sedated. I handed him over to Paul waiting on the other side of the gate and he took him down to the garage; Gabriel was unconscious before arriving there. The blood tests were done, and then he was euthanized with another injection while he was still unconscious. His mother did not know anything had happened. The amazing thing was that Mikayla did not seem to miss Gabriel – I only saw her having a quick look inside the barn once and heard hardly any hums. The care-worn expression she had had during most of her pregnancy that had lessened, but not gone, just before delivery seemed to disappear a week or so after Gabriel’s death. Though Mikayla was a good mother to Gabriel (he could nurse whenever he wanted) she never seemed to dote on him the way some mothers do. I do wonder if in some way she knew things were not as they should be.

The tests done at the time of euthanization were of course also positive for BVD virus. Virus isolation tests done on most tissues from autopsy (for example, kidney, spleen, brain) were also positive for BVD virus. Fecal testing did not show any parasites to account for the diarrhea. Gabriel had looked essentially normal and at this point had not been unwell; yet if he had been with alpacas that did not already have protective antibodies he would have infected them all with BVD. It was easy to see how BVD could spread between farms with a cria like this accompanying his mom when she went to another farm for breeding. And of course MC had shown how BVD could travel across the country from Alberta to Ontario in an unborn fetus.

I know I can never state with scientific certainty that MC was PI as he was never tested, but I think there is overwhelming circumstantial evidence that he was. I also cannot state with scientific certainty that the abortions at Farm C and the stillbirths at Farm D were due to BVD, as the fetuses were not tested for that, but the presence of antibodies in the dams would certainly be extremely strong evidence that was the case. I was very fortunate that Farms B, C, and D were willing to have antibody tests for BVD done; other farms might have preferred to ignore my request. This detective story would not have been solved without their co-operation. Dr. Carman was also very helpful and unfailingly continued to answer my phone calls, emails and questions.

It’s interesting to think how things could have turned out quite differently. If our friend Grant had not mentioned about the illness in cattle that his son had told him about I really doubt I would have stumbled upon BVD as an explanation for MC being such a ‘poor-doer’ and as the possible cause of the illness and subsequent abortions in my alpacas. And yet that case of BVD2 twenty km. away had absolutely no connection with the BVD1 on my farm. The BVD here had come from Alberta. I usually don’t breed my females until they are 18 months old, but in the fall of 2003, Mandy, Abela, Elena, Tillie and Mikayla were such big well-grown girls that I decided to try one breeding in October, and if they didn’t get pregnant, to wait until the next spring. Mikayla was only thirteen months old. I know other people breed that young, but this was the first time I had, and it was only because she was as big as some of the adults and had a mature personality, and because on the day I bred her she had been looking with interest at the boys. All these girls got pregnant right off the bat. If I hadn’t bred them, there would have been no aborted fetus from Mandy to test positive for BVD, and no PI cria, the first verified PI alpaca in the world, from Mikayla. (Of course I believe there have been many PI alpacas before this, but Gabriel was the first one tested). The illnesses in December and the underlying diagnosis for MC would have remained a mystery.

There are still lots of unanswered questions. What is the crucial time during gestation that alpacas will produce a PI cria if they don’t abort? In cows, it usually has to be after 40 days of gestation in order for the virus to cross from the dam to the fetus. Danae had been bred October 23 and left the farm November 22 – only 30 days pregnant. She aborted after shearing at her new home the following May. She had gone through three previous pregnancies and had been sheared during each of those without aborting. There is no way of knowing whether Danae’s fetus was infected with BVD as it was not tested, but her high titre of antibodies to BVD in June (1:3072) could be taken as evidence, but not proof, that it was. If so, that would mean that the virus can cross over to the fetus earlier than in cattle, and also that abortions may occur not just a few months after infection of the dam (as with Mandy), but after many months. The alpacas at Farm C aborted in April 2003, and the stillbirths at Farm D were also in 2003. VF likely had her acute infection with BVD in August or September of 2002 at one of those farms, and if the other alpacas were infected at the same time, there was also quite a delay before they aborted or had the stillbirths. Up to what point in gestation can infection with BVD produce a PI cria? Can an alpaca be infected with BVD during the crucial phase of gestation and still produce a normal cria? Can BVD cause congenital abnormalities in cria if exposure is later in pregnancy, as it does in cattle? All of my cria that were in later gestation when their moms were exposed to BVD virus turned out normally. Can some PI alpacas stay appearing healthy for an extended length of time? At this point the only clinical information is on Gabriel and MC. Both had very low birth weights; both had large umbilical hernias. Other than unformed stool, Gabriel was fine, had gained weight well, and had had no illnesses at the time of his euthanization. MC did well for the first 6 weeks of his life, and then had pneumonia; his next episode of pneumonia was not until he was 5 months old.

Only time and testing will tell just how common BVD is in alpacas. I believe it is much more prevalent than any one has thought. Alpacas certainly have a reputation for being easy aborters and it is not unusual to hear of poor doing cria – both of these could be from BVD. The article Communicable Disease Risks to Wildlife from Camelids in British Columbia by Dr. Schwantje and Dr. Stephen, cited in the previous article on BVD, shows 6% of llamas sampled had antibodies to BVD, that camelid owners reported the most common cause of death being neonatal failure to thrive or stillbirths, and that 9% of camelid submissions to the provincial lab had the diagnosis of idiopathic (no cause found) abortion. No one has ever seen a connection between these. There were no pathological findings to suggest BVD in Mandy’s aborted fetus or in Gabriel – only testing specifically for the virus showed it to be present. It is quite possible that many of the alpaca abortions sent for testing where no cause has been found could be from BVD – it has never been considered one of the routine tests. Poor doing cria who died would have autopsy findings in keeping with their final illness such as pneumonia, with no indication that their underlying problem may have been that they were PI. I think it likely that BVD has been around in herds for quite a while, and that it has been spread by unrecognized PI animals. Many females with cria at side go to other farms for breeding; if it was a PI cria it would be infecting all the alpacas at that farm. If there was a PI alpaca on a farm, a female going there for breeding could return carrying a PI fetus. The first BVD cases may have been contracted from cattle, or, considering that a study from Peru showed an 11.5% incidence of antibodies to BVD, some imported alpacas could have been carrying PI fetuses. The experiences at Farm C, with many abortions, are probably the exception. Just having a few abortions, or the experience at Farm D, with a couple of stillbirths, or Farm B, with only one mild illness, may be more typical.

The whole concept of persistent infection will be hard for some people to grasp. I expect that many people will not want to know about or deal with this. Alpaca owners have a reputation for being secretive about any illnesses or deaths in heir herd; I doubt that many will broadcast that they have discovered BVD cases in their herd. I also know that some people will not have enough scientific understanding to realize that I do not have an infected herd, that I have no contagious animals now, and that those alpacas that were infected and recovered are absolutely normal and have no long term consequences from their exposure to BVD virus – in fact they are now protected from any BVD infection in the future. All the cria have been tested to prove they are not PI. I hope that by reading my experiences, alpaca owners will start to request BVD testing for aborted fetuses and any poor doing cria, and that someone will be inspired to continue research into BVD and alpacas. And of course I hope I will prevent other farms from going through the stress, worry and grief that we went through.

_______________________________________________________________________

Appendix of Antibody Titres. Date of birth of the alpaca is in brackets after the name

Tests done June 1/ 2004:

	BVD2-VN (type 2, NVSL 125c strain)	BVDN-VN (type 1a NADL strain)
Females from the West:
Tillie (July 23/02)	1:48	1:128
Mikayla (Sept. 14/02)	1:192	1:768
Celeste (Oct. 25/99)	1:64	1:256
Abela (July 13/02)	1:64	1:768
Harley (Oct.23/01)	1:8	1:192
Mandy (June 29/02)	1:24	1:512
Savanna Dawn (Nov.14/01)	1:24	1:128
Merienda (July 22/01)	1:96	1:1536

Females from the East:
VF (May, 2001)	1:384	1:1536
Velvet (July 31/95)	1:16	1:64

Young Males who had been in the South:
Cosmo (Aug.22/02)	1:128	1:1536
Dirk (June 23/02)	<1:2	<1:2

Adult Male from the Male Barn:
Dano (June 9/01)	<1:2	<1:2

All of the above animals, with the addition of Shawnee from the East, had negative ELISA test for BVDV antigen at the same time. There was not enough blood left to do antibody testing on Shawnee

Tests done June 29/04:	BVD2-VN	BVDN-VN (type 1a)
From the East Section
Tulia (July 12/03)	1:48	1:1024
Nevada (Oct. 12/03)	1:96	1:2048
Snow White (Jan. 7/98)	1:64	1:192
Arani (Jan. 2/97)	1:24	1:192
Danae (May 25/99)	1:192	1:3072

Test done July 14/04
Carmella – had left my farm for her new home in early September prior to the arrival of VF and MC on my farm	<1:2	<1:2

Test done Aug. 9/04
Murragamba (Sept. 8/98)	1:8	1:32

The higher titres to the type 1 strain showed that that was the strain the alpacas had been infected with. The lower titres to the type 2 strain were from cross-reactivity in testing. A titre of <1:2 is negative.

________________________________________________________________________

Nancy Carr MD is the owner of Silver Cloud Alpacas, near Elginburg in eastern Ontario, Canada. She would like to assure readers that her herd is now completely healthy and not contagious, and in fact is one of the very few herds in North America where all the cria have been tested to make sure they are not PI. She can be reached at carralpacas@sympatico.ca or (613) 376-3389 or through her web site www.silvercloudalpacas.com

With the recent discovery that bovine viral diarrhea virus (BVDV) can cause abortions and persistent infection in alpacas, there has been a request for a testing protocol to identify BVDV infection in alpaca.

The following general recommendations are from Dr. Susy Carman DVM PhD, a veterinary virologist at the Animal Health Lab, University of Guelph, Ontario.

BVDV and persistent infection is a newly recognized disease in alpaca. So far only one persistently infected alpaca cria has been studied. The following BVDV testing strategies for alpaca are based on comparative medicine and derived from those currently used for cattle. These recommendations may need to be refined as more is learned about BVDV in alpaca.

· All aborted and stillborn fetuses, cria that die, and any unexplained deaths should be autopsied by your veterinarian so that samples of tissue can be sent to a veterinary diagnostic lab to be tested for disease agents, including BVDV. Low birth weight cria, poor doing cria, very premature cria, and alpacas with unexplained illness should be tested for BVDV (blood test – see below).

• If BVDV is identified from any submission, then the herd should be strategically tested (BVDV herd screening) to see if there is a persistently infected (PI) animal still present in the herd as the source of the infection. For BVDV herd screening every animal in the herd should be evaluated for the virus in some way. If the entire herd cannot be tested due to economic reasons, it is more important to test all animals under 2 years of age and reproductively active females.

• To test live animals over 12 weeks of age for BVDV send serum (blood test) for PCR or antigen ELISA or virus isolation.

• To test live animals under 12 weeks of age for BVDV send serum (blood test) for PCR. Maternal antibody in these young animals will interfere with other tests.

• Your veterinarian should contact the veterinary diagnostic laboratory in your area to find out which tests are offered for the detection of BVDV in cattle. The same tests can be used to detect BVDV in alpaca. Some veterinarians and laboratories prefer to use skin tests for BVDV detection.

• If the first blood test in a live animal is positive for BVDV, this may only represent an acute infection. A second blood sample must be collected three weeks later and tested to confirm that the animal is indeed persistently infected. This second test is essential, for the animal will be euthanized on the basis of this testing. Since testing methodologies are not perfect, inconclusive test results can occur. In these cases ask that a different test be used on the same sample to confirm the result or submit a new sample.

• Any pregnant females who may have been exposed to BVDV during their pregnancy should have their cria tested for BVDV soon after birth using serum. BVDV was isolated from the placenta of the one persistently infected cria studied.

• To determine if your herd has been infected in the past you may wish to test serum from adults for antibodies to BVDV type 1 and BVDV type 2.

• To evaluate as to whether a pregnant female may have been exposed to BVDV at another farm in early pregnancy, use serum to test for antibodies to both BVDV type 1 and BVDV type 2. If the tests for antibody are negative, it is unlikely the dam is carrying a PI fetus. In cattle, persistent infection has been reported to occur in bovine fetuses infected between 18 and 125 days of gestation. If the alpaca dam has antibodies, she may not be carrying a PI fetus if she was infected pre-pregnancy or at the end of pregnancy. Since you do not know when the dam was infected you may want to quarantine the dam before delivery in case she does deliver a PI cria, and plan to test the cria soon after birth.

• It is possible for PI cattle to live and reproduce. If a PI cow has a calf, the calf will always be PI. If a calf is negative for the virus, its mother is never persistently infected. For herd testing, if you have many females with their cria, you might try to use this information and strategically bleed and test only cria. If the cria is negative, the dam will also be negative. Adults not represented by cria would need to be individually tested. However if you test only cria, and if a cria is positive, you would have to pay for another veterinary visit to draw blood from the dam. Depending on the herd size, it may be more cost effective to have blood taken from both dams and cria at the initial visit.

The serum from dams could be held by your veterinarian and submitted to the laboratory for testing following the return of any positive results for cria.

• If you receive a positive BVDV report, it is essential that you discuss this with your veterinarian to determine if any follow-up testing is needed and contact any farms that may have had contact with your animals so that they can take action to limit the spread of BVDV.

• If your veterinarian recommends that you vaccinate for BVDV use only a killed vaccine until more is known about BVDV in alpacas and llamas.

BVDV in Camelids January 2006
Vets Corner
Dr. Kim Gardner-Graff
Mobile Camelid Practice

ABR newsletter Veterinary Medicine update January 2006 – Bovine Viral Diarrhea Virus (BVDV) in Camelids

In the past 2 months there have been 4 cases of crias born persistently infected with Bovine Viral Diarrhea Virus that originated from farms in the front range of Colorado. It appears that 3 of these cases became infected with BVD during the early stages of gestation when their dams were exposed to a suspected BVD persistently infected cria for approximately 10 days in Oct/Nov 2004 at a Colorado ranch. Lest you think this is just a Colorado disease, the female who produced the presumed PI in 2004 that exposed at least 3 Colorado herds was purchased as a bred female from a breeder in Oregon, as was another female that produced a PI in a local herd. A recent PI has been reported in New York that originated in Maine. The Alpaca Research Foundation census on their website lists 9 defined PI cases from several regions and Canada as of Dec.1, 2005, not including the recently diagnosed cases mentioned above. It’s truly an entire North American alpaca issue.

Prior to June of this year when articles appeared about cases of BVDV in alpacas confirmed in Canada¹, BVDV was not thought to be a major source of concern in alpacas. As the fall has progressed and we are now testing for the disease it appears to be much more prevalent than we thought. The following list contains frequently asked questions regarding BVDV that I have been asked as my clients become more aware of this disease.

What is BVDV?
Bovine Viral Diarrhea Virus is a disease of cattle that has been around for many years affecting cattle all over the world. In cattle it is known to cause infertility, stillborns, abortion, congenital defects, diarrhea, ulcerated oral lesions and the production of persistently infected calves if the adult cow contracts the virus during a certain period in her pregnancy. These calves serve as a constant source of virus that continually infects the herd. BVDV has also been isolated in deer, elk, goats, swine and other species.

How does it affect my alpacas?
BVDV in alpacas has been linked to abortions, still births, possibly early embryonic death (under 30 days of gestation), infertility, and the production of persistently infected poor doing crias.¹

What does persistently infected (PI) mean?
Persistently Infected means a cria (or calf) that was exposed to the virus in utero (as a fetus) during the first 18-120* days of pregnancy. The virus infects the developing cria and its immune system never recognizes it as foreign. Therefore, the cria is born “tolerant” to the virus and never mounts an immune response against it (such as forming antibodies). The virus thrives in that cria and continues to be shed by that animal for the rest of its life resulting in the exposure to all the animals in the herd. The only way to produce a PI cria is by exposure of the developing fetus in utero. (Exact timing may be more or less – this is extrapolated from research on cattle.)

What does a Persistently Infected cria look like?
Most PI cria appear to be poor doing animals and rarely live to 2 years of age. Yet, in cattle there are documented cases of “normal” appearing calves that test positive as a PI, survive long enough to become pregnant, and give birth to a persistently infected calf. Therefore, “normal appearing” doesn’t rule out PI status completely.

To date most documented PI cria have been born at low birth weights (9-15) pounds. Many are premature by a couple of weeks and may do well for the first month if they received adequate colostrum or a plasma transfusion. As they use up that maternal antibody they tend to develop chronic illness [nasal and eye discharges being the most common in my practice]. PI’s tend to have poor weight gain and many have an abnormal hair coat (long and silky in the huacayas, similar to suri fiber but doesn’t lock).

How do alpacas get BVD?
Alpacas contract BVD primarily from the persistently infected cria that are shedding the virus in huge amounts into the environment in their body fluids. The virus is then ingested or inhaled by another animal.

“Normal” animals that contract the virus shed it in small numbers while fighting it and potentially could serve as a source of infection. The virus is also carried in on peoples shoes, hands, clothing or equipment (rakes, shovels, buckets, etc). But the main source of infection appears to be contact with a PI cria.

Is Diarrhea a sign my herd has BVDV?
No. Most of the healthy adults that appear to be recently infected with BVDV have not shown any signs of diarrhea, nor does diarrhea appear to be a consistent sign in persistently infected crias.

What are the symptoms in adults?
Healthy adult animals do not appear to show any external clinical signs of infection with the BVD virus. There have not been any consistent reports of diarrhea, temperature elevations or loss of appetite. Healthy adults appear to contract the virus and clear it in about 2 weeks without any outward ill effects.

What are the clinical signs in young animals?
Currently we haven’t correlated any specific clinical signs of a recent, active BVDV infection in “normal” (non PI) cria, but there is much to be studied about this disease in alpacas.

How do I know if my herd has been exposed?
The best way to determine if your herd has been exposed is to have blood drawn for a serology test on your breeding females. Serology looks for antibodies in the female’s blood stream that would indicate that she was exposed to the virus and fought it off. Many farms will probably test negative for the disease. Farms with a history of poor doing cria, abortions, infertility, stillborns or animals that travel or have many new animals coming on to their farm are more likely to have been exposed.

What do I do if my females test positive?
On farms with animals testing positive on serology all cria under 2 years of age as well as the new cria as they are born should be tested by PCR (Polymerase Chain Reaction) that tests for a portion of the actual virus. Even females that test negative on serology should have their cria tested since there is a small chance that those females themselves are PI animals and potentially could give birth to a PI cria.

PI animals do not fight the virus so they do not form antibodies therefore serology would be negative. Unless they have maternal antibody for BVD from the colostrum (in newborns) they will be negative on serology but positive for the actual virus on PCR.

Cria testing positive on PCR should be isolated and retested two to three weeks later to positively and scientifically determine it to be a PI. There are two types of animals that will test positive on a PCR test: (1) the PI cria and (2) “normal” animals recently infected with the virus. PI cria never clear the virus so they will continue to test positive three weeks later. The “normal” cria, with a normal immune system, will fight the virus off, form antibodies and test negative on a second PCR test three weeks later (and positive on serology).

If my female test positive does that mean she is going to have a PI cria?
If a female tests positive that only indicates exposure. It does not indicate active virus in her, it does NOT guarantee that she is carrying a PI cria. Development of a PI cria takes place if the female is exposed to the virus during the first 18-120 day period of her pregnancy. There is chance she was exposed prior to getting pregnant or at some other point in the pregnancy. Therefore, view it as a flag of caution. As that female is nearing her due date she should be isolated from early pregnant females and blood should be drawn from the cria for a PCR test as soon as it is born and before it nurses. If the cria’s PCR test is positive that dam and cria should remain isolated until a second PCR test is run on the cria 2-3 weeks later. If that test too is positive then the cria most likely is a PI cria and euthanasia to prevent further infection of the herd should be considered. If the cria is PCR test negative – that would indicate there is no virus in the cria, it is not a PI cria and is safe to mix with the herd.

If my female gives birth to a PI cria is she likely to do it again?
No, it appears that in most cases once a female has contracted the virus and cleared it she will be immune to the disease and should not be likely to produce another PI cria unless faced with overwhelming re-exposure.

How long do does it take to get the test back?
Both serology and PCR testing take 7-10 days to get the results.

Is there a vaccine? And should I use it?
Yes, there are a number of vaccines on the market for cattle. Currently the virologists are recommending that we not use them since they will confuse testing and have not proven to prevent the development of PI’s in cattle.

How do I protect my herd?
My suggestion is to determine the status of your herd and do what you can to decrease exposure of your pregnant females to new young cria from outside farms.

All alpacas returning from shows or outside breedings should be isolated for two weeks from the rest of your herd. This is recommended as a general herd health practice.

New additions to the herd should be tested prior to arrival by serology for exposure and if positive their current cria should be tested by PCR and only allowed on the farm if PCR negative and healthy appearing.

Stillborn and aborted fetuses should be necropsied and samples sent to labs for testing for BVDV and other infectious causes of abortion.

Females that are early in their pregnancy that are being transported by commercial haulers ideally should be shipped on trailers that are not carrying cria or on a trailer where every cria on the trailer is PCR negative.

Our best defense against this disease is going to be education, testing and removing the sources of exposure, i.e. the PI cria. Hopefully we will find after further testing that this disease is not wide spread and with the proper application of testing and culling we can get it under control before it affects the industry detrimentally.

** Dr. Bedenice at Tufts University recommends PCR testing for animals less than 4 yrs of age.

Article
Carmen S, Carr N, DeLay J, Baxi M, Deregt D, Hazlett M:2005, Bovine Viral Diarrhea Virus in alpaca abortion and persistent infection. J Vet Diagn Invest 17:589-593.

Alpaca History
Alpacas were a cherished treasure of the ancient Incan civilization and played a central role in the Incan culture that was located on the high Andean Plateau and mountains of South America. Alpacas were first imported to the United States in 1984. Alpacas are now being successfully raised and enjoyed throughout North America and abroad. There are two types of alpacas - the Huacaya and the Suri. The lifespan of the alpaca is about 20 years and gestation is 11.5 months. Alpacas eat grasses and chew a cud. Adult alpacas are about 36" tall at the withers and generally weigh between 100 and 200 pounds. They are gentle and easy to handle. Alpacas don't have incisors, horns, hooves or claws. Clean-up is easy since alpacas deposit droppings in only a few places in the paddock. They require minimal fencing and can be pastured at 5 to 10 per acre.
Alpacas produce one of the world's finest and most luxurious natural fibers. It is clipped from the animal without causing it injury. Soft as cashmere and warmer, lighter and stronger than wool, it comes in more colors than any other fiber producing animal (approximately 22 basic colors with many variations and blends).This cashmere-like fleece, once reserved for Incan royalty, is now enjoyed by spinners and weavers around the world.
Alpaca owners enjoy a strong and active national organization. The Alpaca Owners and Breeders Association (AOBA) with a growing number of Regional Affiliates and AOBA sanctioned national committees addressing every aspect of the industry.
The Alpaca Fiber Cooperative of North America (AFCNA) accepts fleece from its members, and turns the precious textile into quality alpaca garments and products. Members benefit from a ready outlet for their fiber, while the cooperative works to increase awareness of and demand for this every day luxury.
The Alpaca Registry (ARI) has been established to help ensure accurate records and has a state-of the-art system to document bloodlines. Alpacas must be blood typed in order to be registered. Virtually every alpaca in the U.S. is registered.

ALPACAS - The Earth-Friendly Farm Animal
Alpacas have been domesticated for more than 5,000 years. They are one of Mother Nature's favorite farm animals. They are sensitive to their environment in every respect. The following physical attributes allow alpacas to maintain their harmony with our Mother Earth.

The Lifestyle
The joy, ease of care and potential profitability of raising alpacas has attracted people from many walks of life to become breeders. For some, alpacas are a primary source of income, for others a part-time business venture, but a source of pleasure for both. Young couples with children can enjoy the benefits of owning and caring for alpacas as a rewarding family experience. People who have raised their kids and are seeking a business and lifestyle to enjoy as they approach retirement are often owners. Ultimately, whether making the switch from a fast-paced, corporate way of life, or adding alpacas to an already established rural setting, breeding these unique, gentle animals can provide both income and pleasure, all included in a peaceful, stress-free lifestyle.
This lifestyle is made possible since alpacas can be raised on relatively small acreage and they are clean, safe, quiet, intelligent and disease resistant. Alpacas have soft padded feet, are gentle on the land and can be easily transported.
There are also plenty of family-oriented alpaca events around the country, including local and state fairs, alpaca farm open houses and auctions, and larger shows hosted by alpaca organizations, the largest and most impressive being the annual Alpaca conference and show presented by AOBA. Some breeders also choose to get involved in selling products made from alpaca fiber as a hobby or an additional home-based business venture. The spinning and weaving of fiber is a skill that can lead to profits.

Alpacas have brought impressive financial returns to families all across America, but it's the fun and hands-on nature of this lifestyle that has really captivated people searching for a simpler and more rewarding way of life. Even if you don't have the land and are committed to a full-time career, you can still begin your alpaca adventure by purchasing and boarding at a nearby alpaca farm or ranch. A retired doctor who is now a full-time alpaca breeder had this to say, "I would rather raise alpacas than anything I've ever done. Breeding alpacas is a labor of love and can be very profitable."