In the pursuit of the mission and goals of Alpaca Ontario, we endeavour to provide our members with the highest quality of service
and information in an effort to optimize their opportunity in the Alpaca Industry. We recognize in this rapidly growing field that
existing and new farmers alike, need up to date medical research and clinical resources to provide preventative health care
and assist in identifying more serious medical complications.
Select an Article
- The BVD Virus
- A Primer On Giving Injections
- Preparing For Winter
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 sub clinically 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 sub clinically 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 (under development 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
super infected 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 evidence
shows 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
The complete story of how this discovery was made has been written up and called BVD Virus and Alpacas – The Detective Story. It is available
for downloading from the Canadian Llama and Alpaca Association web-site, www.claacanada.com.
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,
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,
Hoffman E. (2003). The complete alpaca book. Santa Cruz, California: Bonny Doon Press.
Larson R. DVM, “A medical marvel.” Alpacas Magazine, Winter 1999, 122
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].
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
Nancy Carr MD has alpaca farm A, 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 firstname.lastname@example.org or (613) 376-3389 or through her web site
Susy Carman DVM PhD is in Diagnostic Virology.
She can be reached at:
Animal Health Laboratory,
Laboratory Services Division,
University of Guelph,
Box 3612, Guelph, Ontario,
Phone: (519) 824-4120 ext. 54551
A Newly Recognized Serious Health Problem for Alpacas
By: Nancy Carr MD and Susy Carman DVM PhD.
Published in June 2005 in Alpacas Magazine and Camelid Quarterly An update from February 2006, including about testing,
is at the end of the article.
WHAT YOU NEED TO KNOW :
- BVD virus, a major problem in cattle, has now been shown to also cause illness, abortions, and, most important of all,
the persistently infected state in alpacas.
- If the alpaca is exposed to BVDV during early pregnancy she can produce a persistently infected (PI) cria who sheds
huge amounts of virus its whole life and is the major source of the spread of BVD.
- The only way to be PI is to be born PI.
- Because a PI cria may not show any signs of illness for several months or longer, the potential for BVD to spread
between herds is significant because of the practice of females with cria at side going to other farms for breeding.
- It is unknown yet how common BVD in alpacas is – this has the potential to have a profound impact on the alpaca industry.
- All aborted or stillborn fetuses and unusually low birth weight or poor doing cria should be tested specifically for BVDV,
as there are usually no pathological changes to suggest BVDV. Your veterinarian should consult with a veterinarian virologist
or lab that does BVDV testing about the appropriate tests to be ordered.
ADDENDUM FEBRUARY 2006
Now that more alpaca farms have been testing for BVDV, it is apparent it is widespread in the North American alpaca herd.
The Alpaca Research Foundation (ARF) has an update on their website www.alpacaresearchfoundation.org. They are aware of at
least 40 PI alpacas that have been identified (including an apparently healthy 30 month old) and there are reports of others that
have not been reported to them. To be labeled as PI, the alpaca has to have had two positive tests for the virus three weeks apart.
There is no census of the abortions or stillbirths or the cria that have died at a few days of age that have due to BVDV. ARF is
funding two research studies about BVDV and alpacas.
For testing for the presence of the virus, it is now apparent that not all the tests used in cattle are reliably accurate in alpacas.
At this time, the tests recommended for detecting the PI state (the presence of the virus) are either PCR on buffy coat cells
(not PCR on serum), or virus isolation. For cria less than three months old it should be PCR on buffy coat cells. Your veterinarian
should discuss testing with the virologist at the lab where the samples will be going, prior to coming to do the blood tests. A
positive test must be repeated in three weeks time to confirm the PI state. Testing for antibodies (virus neutralization) is a totally
different test and is used to see if the animal has been exposed to the virus at some time in the past. A testing protocol with more
detailed information has been written by Dr. Carman.
The article for veterinarians about BVDV and alpacas was in the November 2005 Journal of Veterinary Diagnostic Investigation
Biosecurity should drastically reduce the incidence of BVDV. No alpaca should be allowed on the farm unless it has had a
negative test for the virus (i.e. not PI). Since the only way to be PI is from exposure in utero (i.e. being born PI), an animal
only needs a negative test once in its life to prove it is not PI. If an alpaca has been off the farm, it should be put in quarantine
for 3 – 4 weeks on return in case it is acutely infected (as opposed to PI) – it is most important that it not have contact with
any pregnant alpacas. (An animal acutely infected with BVDV sheds virus for a short length of time - maximum of two weeks).
A negative BVDV test has now become a standard requirement for most alpaca shows in the United States.
Injections of vaccines and medications are given either subcutaneously (under the skin, but not into the muscle; abbreviated as sub-Q or SC),
intramuscularly (into muscle: 1M) or intravenously (into a vein: IV) depending on the recommendations for that particular product. Many alpaca
owners learn to give SC and 1M injections to their own animals. Syringes come in different sizes. The 3 cc. syringe is used most commonly as
it can accommodate the dose used for most injections in alpacas. It is worth having some 6 cc. syringes on hand also, as some antibiotics
require a bigger dose than 3 cc., and some large alpacas may require more than 3 cc. of Ivomec/Dectomax.
Needles come in different diameters and different lengths. The gauge refers to the diameter, with a smaller number representing a bigger
diameter: for example, an 18 gauge (18G) needle is a bigger diameter than a 20G needle. Length used in alpacas is typically 1 inch.
A needle is described by both features, as in 20G 1.5 inch, or 20G 1 inch, or 18G I inch. Dr. Norm Evans (at a seminar several years ago)
recommended a 20G I inch needle for alpacas. Some people use bigger gauge needles (18G) for viscous substances such as Ivomec,
since they can be drawn up and injected more quickly than through a smaller needle. Personally I use just a 20G as the 18G is really
quite large. For comparison, the typical needle size used for immunization in humans is 25G. Needles and syringes come sterilized,
either already as a needle and syringe combination, or as individual needles and individual syringes. Needles can attach to syringes
either by simply pushing on, or with a twist on, called a luer-Iock, which is a feature on the syringe. The luer-Iock style of syringe makes
it less likely that the needle will inadvertently come off the syringe.
Although syringes could be used for several animals that
will be injected - with the same substance one after the other in a short length of time (say, half an hour), a fresh needle should be
used for every injection on every animal. For example, if you were giving four alpacas an injection of Ivomec one after the other, you
could use the same syringe, but you must use 4 separate sterilized needles-putting a new one each time to draw up the Ivomec and
then inject the animal. For something like Ivomec which is 'slippery', the luer-Iock style of syringe is particularly helpful in preventing the
needle from coming off if you are using the same syringe several times. If you are injecting the same animal withtwo different things,
there should be a new syringe and new needle for each substance. Dr. Norm Evans in his Alpaca Field Manual says that he does not
inject more than 2 vaccines at one time.
There have been reported cases of fatal allergic reactions to vaccines, so the alpaca
owner giving injections has to decide what level of risk he/she is comfortable with, and possibly whether to ask the vet about having
injectable epinephrine (adrenaline) on hand. Although many people give immunizations or de-wormers at the time of shearing, I don't,
as I think the alpaca is already having enough stress that day. Consideration must also be given to the conditions in which the vaccine,
and some antibiotics, must be kept. Refrigeration is essential for vaccines to maintain their effectiveness. When I take the vaccine to the
barn, I keep it in a small container with some ice cubes to maintain refrigerator temperature. It must be returned to the refrigerator
immediately after use.
For drawing up substances to be injected: Attach the needle to the syringe, keeping your fingers off the open end of the syringe and needle;
remove the metal covering over the rubber stopper that is on some bottles prior to first use; shake the bottle or vial; wipe off the top with
rubbing alcohol; remove the needle cap; insert the needle through the middle of the rubber stopper; invert the bottle; pull back on the
plunger of the needle to draw up the required amount, making sure that air bubbles are not making up some of the amount (push the
plunger back in to push any air back into the bottle and then pull back again.) That air would not do any harm in a SC or 1M injection;
this is to make sure you are giving the accurate amount of vaccine or medication. Then re-cap the needle until just before giving
Marty McGee Bennett's book The Camelid Companion has a very good section on giving injections, complete with a picture of preferred
sites on the body; a picture is indeed worth a thousand words. The information she presents was reviewed by two well known camelid
vets, Dr. David Anderson and Dr. LaRue Johnson. For subcutaneous injections the area where the neck and shoulder meet is
recommended. If you are right-handed, the left hand is used to tent up the skin-easily done by pulling up on some fibre between
your thumb and fist with a wrist rolling movement. The needle is then injected into the tented up skin at an angle of about 30 degrees
from the body surface. Make sure you have not poked the needle right through and out the other side of the skin. Pull back on the
plunger to make sure you are not inadvertently in a blood vessel. If blood appears in the syringe, remove the needle and try again a
short distance away (and discard that syringe afterwards). If no blood appears, push the plunger all the way in, then remove the needle
and syringe and put the cap back on the needle.
For intramuscular injections, the triceps muscle (back of the forearm; i.e. just
down from the shoulder, and behind the humerus bone-the picture really is helpful for this one) is used. Dr. Anderson thinks that medications,
especially tranquilizers or analgesics, act more quickly when given in the front half of the body rather than in the rear end (gluteal muscle).
Also, it is easier to give a needle in the triceps without restraint. For 1M injections, the needle is inserted perpendicular to the skin surface.
Pull back on the plunger to check for blood as was done for administering a SC injection. For a very sick animal needing numerous and
frequent injections, other injection sites including the gluteal muscle can be used. Your vet can give you some hands on pointers on giving
injections. Other than for a short time after shearing, there is a lot of fibre that the needle has to traverse before going in the skin. It is
therefore not worthwhile trying to clean the skin with rubbing alcohol before giving an injection. However, injecting through dirt or mud
should of course be avoided.
The heavy plastic mini-feeders (interior dimensions of 9.5 by 7 by 6 inches) that hang on a 2 by 4
(such as the top rail of a stall) are great for holding supplies (vaccine on ice, rubbing alcohol, paper towel, needles, syringes, , record keeping
sheet and pen) if you are injecting several animals. Even though oral medications such as the de-wormer fenbendazole (sold as Panacur or
Safeguard) are not injections, it is worth mentioning that the best instrument for giving these is the 50 cc. dose syringe with extender
(a long metal nozzle) available from Useful Lama Items (www.useful-items.com). Order a replacement a-ring at the same time (this is what
maintains the proper seal on the plunger; when it wears out, liquid is not drawn up effectively into the syringe). So that I am not contaminating
the large container of Panacur or Safeguard, I pour a guesstimated amount out into another container, and draw up the required amount from
there. Alpacas hate the taste of fenbendazole: I clean off the extender nozzle with water so there is none on it when I put it in their mouths.
The metal extender nozzle is perfect for getting far back in the mouth without any damage from teeth. I clean it off again before drawing up the
dose for the next alpaca.
Remember to remain calm and treat your alpacas with kindness and respect to make medication giving as stress free as possible.
by Dr. Nicole Bourque, DVM
With the days getting shorter, the leaves changing colours and the temperature steadily decreasing, we all know that winter is fast approaching.
But what does this mean for our friendly and fleecy creatures? Although llamas and alpacas are fairly well adapted to cold temperatures, they
are still susceptible to hypothermia. So what are the signs to watch for, how do we treat affected animals, and most importantly, how do we
prevent hypothermia? Hypothermia can be defined as a decrease in body temperature due to exposure to environmental extremes or disease.
The normal rectal temperature of the resting adult camelid can vary from 37.5 to 38.9°C (99.5 to 102°F). An animal with a body temperature
approaching 90°F can be considered to be hypothermic.
Neonates are at a higher risk of hypothermia due to the fact that they have poor body fat reserves, fine fibre and a high metabolic rate. A
rectal temperature of less than 100°F in a neonate is a cause for concern. Also at a higher risk are older animals, those in poor body
condition and the ill and debilitated.
When chilled, camelids can be observed shivering and/or laying down in the cushed
position with the head and neck extended on the ground. Shivering is the result of rapid muscle contractions, which serve to
This mechanism requires a significant amount of energy and thus can result in hypoglycemia (low blood sugar levels), especially in
the very young. The cushed position allows for heat conservation because the majority of heat loss occurs from the axilla, groin,
around tail and the ventral neck and abdomen. Other signs to watch for are depression, lack of coordination, muscle stiffness,
and shallow breathing which can eventually lead to loss of consciousness. Treatment lies in preventing further heat loss and
gradually increasing the body temperature back to normal. This can be achieved by bringing the animal into a warm area.
Sources of heat include heaters, blankets, hot water bottles, heat lamps, and hair dryers (especially if the animal is wet).
Heating pads or electric blankets can also be used; however, the animal must be checked often as thermal burns can occur
rapidly. If severe, warm LV. fluids may be necessary. If hypoglycemia is a concern, oral glucose in the form of maple syrup,
corn Adequate shelter and proper nutrition are the keys to preventing hypothermia. Camelids can have unlimited access to
the outside environment during the winter months, provided that they also have free access to shelter from wind and cold.
A suitable sheltercan be as simple as a three-sided run-in shed with the opening placed opposite to the prevailing winds
and/or having free access to the barn. Straw bedding that is deeply packed provides very good insulation within those shelters.
However, stocking density can become an issue resulting in the most submissive animals being left out of the shelter. Manure
piles should be periodically cleaned up and the bedding kept clean and dry. If the shelter is too dirty or the air quality is poor
(with high levels of ammonia, due to feces and urine), the alpacas may not use the shelter.
Nutrition is also very important. High quality roughage in the form of hay or haylage provides a substantial amount of energy and the
byproduct of fibre digestion is heat! Caloric intake will increase during the winter months, because more energy is required to stay
warm. Testing the roughage to determine the total digestible nutrient content (% TDN) should be considered. A TDN of 55-60% is
desirable. Along with a commercial camelid pellet ration, concentrates (grains) can be added in the form of corn or oats. However,
this should be introduced slowly (over the period of 2 weeks) as concentrates can cause acidosis. Adequate bunk space is also
very important. Inadequate bunk space will result in the most submissive animals not getting enough to eat.
Research by Dr. David E. Anderson has shown that a minimum of 12 inches is required for bunker feeders to allow for simultaneous
feeding, however, a bunker space of 24 inches resulted in fewer submissive animals having no or limited access to feed. Water
sh ould not be forgotten as it plays an essential role in nutrition. Water bowls, troughs or buckets should be checked frequently
to make certain they do not freeze and that the water is fresh.
It is recommended to body condition score all of your animals on a monthly basis. Decreased body fat stores can greatly increase
the risk of hypothermia. The fibre coat can fool you into thinking that the animal has an adequate body condition. Those that are
found to be losing body condition can be fed separately to ensure proper feed intake and they should be monitored. If the condition
does not improve, veterinary attention should be sought. Parasitism can also be a contributing factor to poor body condition,
therefore adequate de-worming protocols are very important. A poor fleece coat (especially in adults sheared late in the summer
or neonates) can be detri- mental in the winter. Sweaters can be placed on these animals to help them stay warm.
Hopefully this article provided you with more information regarding winter management of camelids. A substantial amount of
information is available regarding this topic that is beyond the scope of this article. For more information and prior to making major
management changes, please contact your local veterinarian.