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CASE NOTES

AN Introduction TO DISEASES OF ALPACAS IN AUSTRALIA

Patrick Staples, State Veterinary Diagnostic Laboratory, EMAI, Menangle

Posted Flock & Herd March 2016

Introduction

This paper attempts to provide an introduction and overview of some of the diseases of alpacas that may be seen in Australia. It is a work in progress, so I would be grateful for any feedback on errors or omissions. It would benefit from input by an experienced camelid clinician, which I am not. I can be contacted by email.

Although not the subject of this article, for long term herd health it is important that the following fundamental elements are in place: Good nutrition and husbandry, protection from extremes of weather, parasite control strategies and genetic selection for health (e.g. fertility, adequate milk production, good cria growth rates, freedom from genetic disease, avoidance of excessive in-breeding,etc.), not just selection for fleece characteristics and the show ring.

Contents

Alpaca uses in Australia

Some alpaca terminology

Native South American environment of alpacas

A few features of camelid anatomy and behaviour

Section 1: Diseases listed by Agent

Section 2: Differential diagnoses by syndrome

Alpaca uses in Australia

Some alpaca terminology

Cria: Young alpaca

Hembra: Female alpaca

Macho: Male alpaca

Huacaya: One of the two types of alpaca. 90% of alpacas in Peru are huacayas and this is the dominant type in Australia. The two types are defined by their different fleece characteristics. Huacaya fibre is shorter than that of the suri, and it is well-crimped and grows perpendicular to the skin, somewhat similar to a sheep.

Suri: Suris are the second, less common, alpaca type. The fleece of the suri consists of “pencils” or “locks” of long fibres, which have no crimp and hang down alongside the body.

Native South American environment of alpacas

Llamas/alpacas are concentrated on the Altiplano, which is an area of high-altitude valleys and plateaus at elevations over 3,800 m. The climate of this area consists of a long, dry season and a short, wet season. The growing season (wet) is characterised by low temperatures (more than 300 nights of frost per year) and intense solar irradiation. Daytime temperatures reach a maximum of 18.3°C; nighttime temperatures fall to a low of -12°C. Camelids feed on native grasses and forbs1.

A few features of camelid anatomy and behaviour

Stomach: The digestive process in camelids is similar to that of ruminants. Both have forestomachs which function as a fermentation chamber. The end products of carbohydrate fermentation are volatile fatty acids (VFA) for both species groups. Both regurgitate and rechew forage (rumination). Camelids are more efficient than ruminants in extracting protein and energy from poor quality forages. The alpaca stomach has three compartments. Compartments one and two (C1 and C2) are anaerobic fermentation chambers. Compartment three (C3) corresponds to the true stomach of monogastrics (or abomasum of ruminants), and has a small region of hydrochloric acid secretion at its caudal end.1

Feet: Alpaca feet have two digits like ruminants, however they do not have hooves. Instead, each toe has a ventral pad (similar to a dog's pad but larger), and a toenail at the front of the toe. The pad takes up most of the bottom surface of the foot. Toenails usually need to be trimmed periodically.

Jugular vein: The jugular vein is located deeper in the neck compared to ruminants, and is also close to the carotid artery. There is some practical information on the internet which provides tips on blood collection. Two collection sites are described:

Reproduction: Gestation length is about 11.5 months. Alpacas are induced ovulators, they ovulate about 26 hours after mating. Females are generally receptive to a male unless they have been recently bred or are pregnant. If a female is already pregnant she will refuse to sit and will probably spit at the male. This rejection response is known as the “spit-off”, and is used as a management tool to check pregnancy status. Females are usually remated 2-6 weeks after giving birth.

Spitting: Spitting involves the forceful expulsion of stomach content. Spitting is the ultimate response in social intercourse between alpacas, if mild threat displays are disregarded. It is used as a pecking order mechanism with other alpacas. Both genders use it as a way to keep competitors away from food. Females are more likely to spit than males and pregnant females are more spitty than non-pregnant females. Alpacas tend not to spit directly at people, unless they're doing something that really scares or annoys them.

Rolling and dusting: Alpacas love rolling in the dirt. This creates scattered bare patches (roll holes) in the paddocks. Once a roll hole is established they will return to it repeatedly to roll.

Section 1. Diseases listed by agent

Diseases in this section are listed under the following headings:

Bacterial diseases

Abscesses

Many different bacterial species have been isolated from abscesses. These include Streptococci, Trueperella (formerly Corynebacterium) pyogenes, Corynebacterium pseudotuberculosis, Staphylococcus aureus, Actinomyces sp. and Fusobacterium necrophorum. Many of these organisms are opportunistic in that they may be normal inhabitants of the skin or mucous membranes, and only become pathogens when an animal is stressed, there is a break in the skin, there are combinations of organisms that enhance each other, or there is an overwhelming contamination. Skin abscesses may be due to penetrating grass seeds such as barley grass and spear grass. Corynebacterium pseudotuberculosis deserves special mention because of its contagious nature. Contact with sheep is likely to be a risk factor. If infection is diagnosed in an alpaca it may be advisable to isolate the animal until the abscess is successfully treated. Surgical excision is recommended in addition to antibiotic therapy.8

Bacillus anthracis (anthrax)

Cases of anthrax have been reported in SACs both in Peru and the United States. It usually presents as an acute, septicaemic disease. Sudden death may occur without premonitory signs being observed.1

Burkholderia pseudomallei

Burkholderia pseudomallei is a saprophytic bacterium occurring in soil and surface water in South East Asia and tropical Northern Australia. It is the cause of a bacterial infection called melioidosis, which is characterised by the development of abscesses. Infection may result from wound contamination, inhalation or ingestion. A fatal cause of melioidosis occurred in a 7-month-old alpaca within one month of it arriving in Darwin from South Australia. It had a multiple abscesses, including a subcutaneous abscess, caudal to the angle of the jaw, as well as abscesses in the lungs and mediastinal lymph nodes. The authors suggested that alpacas may be highly susceptible to melioidosis.32

Campylobacter fetus subspecies fetus

Campylobacter fetus subspecies fetus abortion in alpacas was reported in 2010 on a farm in the United Kingdom.21

Clostridium botulinum

No cases of botulism have been reported in South American camelids, but there is good reason to believe that all camelids may be susceptible.1

Clostridial enterotoxaemia

Camelids are known to be susceptible to types A and C enterotoxaemia, though their occurrence has not been reported in alpacas in Australia. Type D enterotoxaemia is also strongly suspected.1 Each of the three types will be discussed separately.

It is common practice for alpaca owners in Australia to vaccinate alpacas with 5-in-1 vaccine every 6 months. This vaccine contains killed cellular material and toxoid from C. tetani (tetanus), C. septicum (malignant oedema), C. perfringens type D enterotoxaemia, C. novyi type B (black disease), and C. chauvoei (blackleg). The latter two diseases, black disease and blackleg are not known to occur in alpacas, although blackleg has been produced experimentally.1 An 8-in-1 vaccine is also available in Australia, which includes protection against C. perfringens type C, however is less commonly used.

The recommendation to vaccinate 6 monthly comes partly from an unpublished Australian study done in the 1990s, that suggested that annual vaccination would not provide protection against C. perfringens type D for a full year.27

In the UK and USA however, most owners vaccinate annually.23 They also have access to a wider range of Clostridial vaccines, some of which include protection against C. perfringens type A.

Type A enterotoxemia is described as the most serious disease of neonatal alpacas in Peru. The main toxin produced is alpha toxin. Most of the losses occur between eight and thirty-five days of age. According to Fowler: “the predisposing factors for type A enterotoxemia and the clinical syndrome have occurred in North America, but the precise aetiologic diagnosis has eluded diagnosticians”.1

A case of Type A enterotoxaemia was seen in crias in the UK, confirmed on analysis of toxin.23 It occurred at the start of the birthing season on a large farm - dams had been vaccinated prior to pregnancy with a 4-way vaccine that only offered protection against types B,C,D and tetanus. They pre-partum vaccinated the rest of the herd with a 10-way vaccine that did cover type A and they didn't lose any more crias. Clinical signs in type A enterotoxaemia vary from sudden death to signs of colic, sometimes intestinal gas tympany, central nervous signs of convulsions and opisthotonus, shock and death. Diarrhoea is not usually present. Postmortem lesions may include the following: pulmonary congestion and intestinal distention with watery fluid and gas. Type A enterotoxaemia has not been reported in Australia, though I'm not sure that any laboratories offer testing for alpha toxin. Five-in-one Clostridial vaccine is unlikely to provide protection against this enterotoxaemia.

Type C enterotoxemia resembles type A and is included with type A as an economically important disease in Peru, but recently researchers have concluded that of the two, type A is much more important.1 Beta toxin is considered the main virulence factor. An 8-in-1 vaccine is available in Australia, which includes protection against C. perfringens type C. Alpacas ten to forty days of age are most often affected. Cases of type C enterotoxemia have been reported in North American camelids, but confirmation to toxin is rarely carried out.1 Clinicians and pathologists base diagnoses on experience with type C enterotoxemia in lambs and calves. In North America, the usual necropsy findings are of a haemorrhagic enteritis, with blood-stained intestinal contents. The intestines are distended with gas and are intensely congested. Pulmonary interstitial edema and hydro-pericardium are often seen. There may be cerebral oedema and neuronal degeneration in the brain.1 I don't believe that this disease has been reported in Australia. Five-in-one Clostridial vaccine is unlikely to protect against this enterotoxaemia.

Type D enterotoxaemia (over-eating disease/pulpy kidney). Type D enterotoxemia has not been diagnosed in camelids in Peru. Sporadic cases have been reported in North America. Epsilon toxin is considered the main virulence factor. Type D enterotoxemia may be associated with sudden death or CNS signs such as convulsions, circling, prostration with opisthotonos and paddling, and coma. According to Fowler, necropsy lesions in camelids have not yet been adequately described and he refers readers to lesions described in sheep and cattle1. We have had a low number of submissions to the State Veterinary Diagnostic Laboratory (SVDL; New South Wales), with a history of acute death, where epsilon toxin was detected in ileal content. If testing for epsilon toxin in any species, it is advisable to collect and chill ileal content as soon as possible after death. Epsilon toxin is stable in content held at 4⁰C, but decreases markedly when left in situ after the death of the animal.24

Clostridium septicum

Malignant oedema caused by Clostridium septicum, is an economically important disease of alpacas in Peru. It is also well recognised as an infection of sheep and cattle in Australia. The organism invades tissue through a necrotic, deep wound that provides anaerobic conditions. Oral wounds and bruises are common entrance sites in alpacas.1

Clostridium tetani

The degree of susceptibility of alpacas to tetanus is unknown. Two cases of tetanus in alpacas were reported from Peru.1

Dermatophilus congolensis

Dermatophilosis (rain rot/”dermo”), has been described, but is not common. Lesions are most common on the back. Affected areas have wet, clumped wool, which comes out in clumps. The underlying skin is erythematous, with erosions and exudate.2

Escherichia coli infections

E. coli has been reported as a cause of neonatal septicaemia, metritis and mastitis in camelids. It has also been associated with diarrhoea in crias1, however enterotoxigenic colibacillosis, as it occurs in calves and piglets, has not been confirmed. E. coli diarrhoea may occur in combination with septicaemia.22

Fusobacterium necrophorum (necrobacillosis)

This organism has been implicated in numerous disease processes in a broad host range of domestic and wild animals. Usually, a break in healthy epithelium or devitalised tissue is required to provide a portal for entry. Necrobacillosis is not common but can occur sporadically. Lesions may develop in the oral cavity, pharynx, larynx or mandible. Young animals are more at risk. Oral lesions are associated with a characteristic foul odour.1 F. necrophorum is one of the bacteria implicated in osteomyelitis of the mandible.

Listeriosis

Listeriosis (circling disease, silage disease) is caused by Listeria monocytogenes, a Gram-positive coccobacillus that has a worldwide distribution. The disease is not very common in camelids, but it does occur. Camelids develop an encephalitic syndrome, similar to that seen in cattle, with unilateral facial paralysis, circling, trembling of the head, running into objects, salivation, depression, seizures. Abortion has not been reported in alpacas, but it is a common occurrence in all other species studied.

Leptospira spp.

The effects of leptospirosis are not clearly defined in camelids. One ranch in North America experienced an abortion epizootic. It was concluded that L. grippotyphosa was implicated.1

Mycobacterium paratuberculosis

Mycobacterium paratuberculosis (believed to be cattle strain) was diagnosed in an alpaca herd in Victoria in 1993.10 Five of the affected alpacas in this herd had a clinical signs of weight loss, poor growth, and, terminally, diarrhoea. Three of these alpacas were between 1 and 2 years of age; one was 4 years old and one was 6 years old. Clinically affected alpacas had hypoproteinaemia. The most consistent necropsy findings were enlarged mesenteric lymph nodes (DDx lymphoma). The 6-year-old alpaca also had intestinal thickening and intestinal lymphatic cording. An additional 5 animals (all between 1 and 2 years old) showed no clinical signs but were positive on faecal culture and/or caprine AGID assay. Generally it is unusual, certainly for sheep and cattle, to develop clinical signs of Johne's disease at less than 2 years of age. Currently, as at February 2016, there are no known infected alpaca herds in Australia. Johne's disease due to sheep strain Mycobacterium paratuberculosis has not been reported.

Mycoplasma haemolamae (formerly Eperythrozoon)

The organisms are presumably transmitted by bloodsucking arthropods. It has relatively low pathogenicity. Most healthy alpacas will mount an immune response and clear it effectively. Clinical disease is said to be more common when animals are immune-suppressed, stressed, debilitated or have other infections,e.g. GIT parasites. Clinical signs may include chronic weight loss, depression, decreased fertility, lethargy and rarely, death. Blood smears should be made soon after drawing the blood, because the organisms fall off the erythrocytes during transit of the sample to the laboratory. We have seen clinical cases rarely at the State Veterinary Diagnostic Laboratory (SVDL). The organisms are very small and can be confused with stain precipitate. We recently introduced a PCR assay for M. haemolamae at the SVDL, but it is not fully validated.

Osteomyelitis of the mandible

Mandibular osteomyelitis occurs more commonly in alpacas than in sheep and cattle. Tooth root abscesses also occur. The route of infection is thought to be through gum damage (e.g. by feed or grass seeds, such as barley grass). Fusobacterium necrophorum has been cultured from some cases.

Pneumonia

Pneumonia appears to be relatively uncommon in alpacas in Australia. However two papers from Peru describe cases of acute suppurative bronchopneumonia in alpaca neonates and weaners.29,30 Various combinations of mixed viruses and bacteria were identified, similar to that seen in ruminant species. Viral agents included Parainfluenza 3 (PI3) virus and bovine respiratory syncytial virus (BRSV). Bacterial agents included Pasteurella multocida and Mannheimia haemolytica.

Salmonellosis

Salmonella spp. may cause enteritis or septicaemia, however are not a common cause of disease in either crias or adults.1

Sepsis in neonatal crias

Septicaemia is relatively common in neonatal crias, and also occurs in older crias. Possible causes include E. coli and other bacteria. Risk factors include failure to nurse or other factors contributing to failure of passive transfer (FPT), prematurity, dystocia and diarrhoea. Sepsis may be associated with diarrhoea.5 Meningitis or meningoencephalitis may occur as a sequel to neonatal septicaemia.13

Streptococcal infections

A variety of streptococcal species may be isolated from abscesses in camelids. Many of these are also constituents of the normal flora of mucous membranes. S. equi subsp. zooepidemicus is the etiologic agent of “la fiebre de las alpaca” (alpaca fever) in Peru. In its acute form, usually seen it young animals, it is a systemic infection with a polyserositis involving thoracic and peritoneal cavities. Meningitis was seen in an outbreak in alpacas in Kansas. Chronic forms, more commonly seen in adults, are essentially abscesses or focal infections.1

Endoparasites (worms, coccidia, protozoa)

Most of the information presented here comes from the following conference paper which is also available on the internet: Carmichael, I.H. (2014). Internal parasitism in Australian alpacas.6

Jane Vaughan's website also contains information on endoparasite control:

criagenesis.cc/7

Gastrointestinal worms of imported alpacas were mostly eradicated during quarantine, prior to entry into Australia. Internal parasites of alpacas in Australia are therefore mostly comprised of gastrointestinal parasites derived from sheep and cattle in Australia, as well as lamoid-specific coccidia, which were not eliminated by quarantine procedures. The five main parasites or groups of parasites affecting alpacas in Australia are: 1. Scourworm complex, 2. Nematodirus, 3. Haemonchus, 4. Fasciola hepatica and 5. Eimeria species (coccidia).

1. The Scourworm Complex

Some of these derive from sheep and some from cattle. They include:

Trichostrongylus axei (stomach)

T. vitrinus, T. colubriformis, T. rugatus (small intestine)

Teladorsagia circumcincta and Ostertagia ostertagi (stomach)

Cooperia species (small intestine)

2. Nematodirus (thin-necked intestinal worm)

3. Haemonchus spp. (Barber's pole worm)

4. Fasciola hepatica (liver fluke)

5. Eimeria spp. (coccidiosis)

These coccidia are camelid specific. They may be divided into categories of small and large coccidia.

i. Small coccidia

ii. Large coccidia (especially E. macusaniensis)

6. Trichuris spp. (whipworms)

Alpacas do get whipworm infections. If infection is similar to that of other livestock, they are likely to have low pathogenicity. However if present in large numbers they may cause sufficient irritation of the caecal mucosa to result in diarrhoea, perhaps accompanied by mucus and blood.

7. Cryptosporidium and Giardia

These are both zoonotic pathogens. Cryptosporidium and Giardia are reported as causes of diarrhoea in crias.5 Cryptosporidium may cause severe diarrhoea in immunocompromised individuals as well as neonates. Giardia infection primarily occurs from contaminated water sources.

Control of parasites in the alpaca herd

See Ian Carmichael's article6 and the Criagenesis7 website for more information. A few points as follows:

Tapeworms

Moniezia expansa infection occurs in camelids, more commonly in young animals. It is regarded as having low pathogenicity.1

Ectoparasites

Bovicola breviceps

Bovicola breviceps is a chewing louse. They vary in size from 0.5 x 1.2 to 1.5 x 4 mm. It is present in alpaca herds in Australia, although the prevalence is not well defined.33 Infestation is more common in winter months. Shearing and exposure to sunlight reduce lice numbers. Clinical signs include pruritis (manifested by biting and rubbing) and patchy fibre loss.2

Chorioptes bovis

Chorioptic mange, due to the mite, Chorioptes bovis, is a relatively common condition. It mainly causes lesions on the feet and legs, but may also affect the tail base and ears. Lesions typically include mildly pruritic, alopecic areas of thickened, crusty skin. These become more extensive over time. Certain individuals are affected much worse than others, a hypersensitivity reaction is suspected. In some cases the skin becomes red and eroded. Diagnosis is by skin scrapings - although the edges of lesions occasionally yield mites, scraping between the toes appears to offer the best success. The axilla also often yields mites. Treatment is often by a combination of parenteral ivermectins as well as topical insecticides.

Psoroptes mange mites appear to have been eradicated by quarantine procedures applied at importation into Australia.

Sarcoptes mites

Sarcoptes mites were thought to have been eradicated by quarantine procedures, however sarcoptic mange has been diagnosed in alpacas in Australia.27 This mite is a deep burrower, affecting mainly the legs, neck, face, axilla, ventrum and perineum. Infection may become generalized in severe cases. Pruritus is usually intense. Parenteral ivermectins are usually efficacious. Treatment should be repeated weekly to biweekly for 2 to 4 treatments to eliminate mites newly hatched from eggs.2

Demodex mites

Demodex mite infestation is rare. It causes popular or nodular alopecic lesions on the face, neck and brisket. Mites may be expressed from the nodules and identified microscopically.

Fly bite allergies/insect hypersensitivity

Tend to be seasonal and may respond to housing, insect repellants or relocation to another district.

Ixodes holocyclus (paralysis tick)

Alpacas may be paralysed by this tick, which is endemic along the east coast of Australia. Crias seem more susceptible than adults and it appears that camelids born in endemic areas acquire some age-based resistance to ticks, whereas adults brought into an endemic area are as susceptible as crias to tick paralysis.27

Fungal infections

Dermatophytosis (ringworm)2

A variety of Trichophyton and Microsporum infections have been reported. Lesions tend to involve the legs, face or perineum. Overseas, winter confinement appears to increase the risk. Lesions are generally alopecic with thick crusts.

Metabolic and deficiency diseases

Dietary fibre requirements

Alpacas need long-stemmed roughage (pasture, hay, silage greater than 4 cm in length) to keep the forestomachs functioning normally. A diet based on very short (or non-existent under drought conditions) pasture, chaff and grain/pellets or very lush spring pasture is not adequate to maintain ideal conditions for foregut fermentation.14

Protein-energy malnutrition11

In terms of carrying capacity, as a general rule, one alpaca wether is equivalent to 1 Dry Sheep Equivalent (DSE). A pregnant alpaca = 1.5 DSE. A lactating alpaca = 2 DSE.

Where there is a nutritional deficiency in protein or energy or both, the most common clinical signs are decreased growth (in young animals) or loss of body weight and a decline in body condition score. Pregnant and lactating females may develop hepatic lipidosis. Hypoalbuminaemia and hypoproteinaemia are often observed. Anaemia may also be observed.

Obesity11

Obesity may be due to overfeeding of supplement or feeding too high quality forages relative to nutritional requirements. Obese animals are more susceptible to heat stress, metabolic problems, infertility and locomotive problems.

Hepatic lipidosis1

Hepatic lipidosis is not a specific disease, but rather the end result or one or more metabolic processes: 1. Increased mobilisation of depot fat; 2. Reduced rate of removal from the liver. The mechanisms are not fully understood. Obesity due to overfeeding may predispose. Generic causes include starvation, low-protein diet, stress. Pregnancy or lactation coupled with nutritional deficiency may predispose. Toxic hepatic damage may contribute. Animals show a range of clinical signs which may include nervous signs such as depression, weakness, stumbling, head pressing (possibly due to hepatic encephalopathy, hyperammonaemia), weight loss, recumbency and death.

Lactic acidosis (grain overload)2

Camelids are susceptible to forestomach acidosis. The causes, clinical signs and diagnosis are similar to those of ruminants. Diagnosis is by measurement of forestomach pH. I assume D-lactate measurement (on serum or aqueous humor) would also be useful. Normal forestomach pH in camelids is between 6.4-6.8. Camelids with acute acidosis often have values of 4 to 4.5; these may climb to 5.0 or more with time. In general anything under 6.0 should be considered suspicious. Some camelids on grain diets have gastric pH around 5.5 for long periods and may have intermittent bouts of diarrhoea and poor-doing, unlike ruminants which can adjust to this lower gastric pH.2

Polioencephalomalacia

Polioencephalomalacia has been reported in alpacas and often presents as sudden-onset blindness. Predisposing causes include increased access to grain or abrupt dietary changes with reduced fibre intake.

Hyperosmolar disorder2

A disorder of glucose metabolism called hyperglycaemic, hypernatraemic, hyperosmolar disorder has been described in neonatal llamas and alpacas. It is associated in neonates with limited fluid intake and administration of exogenous glucose and /or gluconeogenic agents. Early clinical signs are frequent urination, fine muscle tremors and a wide-base stance. Later signs include recumbency, seizures and coma.

Rickets

Young alpacas are susceptible to rickets, usually due to vitamin D deficiency due to lack of exposure to ultraviolet (sun)light. It can occur during the foetal period, however more commonly occurs in growing animals in the first 2 years of life. Autumn-born crias may be affected during their first winter. In crias the most common sign is abnormal angulation of the carpus or tarsus. The carpus may be slightly swollen or painful to palpation. In severe cases the leg may fracture or ligaments may pull loose from their attachments. Vertebral involvement may occur, resulting in pain, reluctance to move or stand or possible neurologic deficits. Poor weight gain and an illthrifty appearance are other findings.2

Measurement of serum phosphorus and vitamin D is helpful in confirming the diagnosis (however it is currently difficult to find laboratories which offer vitamin D testing in animals). In a small study in South Australia, crias which were not supplemented with vitamin D, had reduced growth rates associated with mean concentrations of plasma 25-OH D3 of < 20nmol/L and plasma phosphorus of < 1.3 mmol/L.34 The authors of this study suggested that plasma 25-OH D3 concentrations > 50 nmol/L and plasma phosphorus concentrations > 1.5 mmol/L were adequate for crias. Prevention of rickets is usually by vitamin D injection. The recommended dose is 1000 to 2000 IU/Kg body weight injected subcutaneously. This should be repeated every 6-8 weeks during the low-light season. Care should be taken not to overdose.

Hypocalcaemia

Hypocalcaemia appears to be rare in alpacas,11 but has been seen in lactating females in Australia.27

Hypomagnesaemia

Hypomagnesaemia appears to be rare in alpacas11 but has been seen in lactating females on dairy pastures high in potassium.27

Copper deficiency

Copper deficiency in young ruminants is associated with clinical signs such as illthrift, poor growth rates, lameness, diarrhoea and anaemia. There is little published information on disease due to copper deficiency in alpacas. If there is copper deficiency in ruminant species in your area it may be wise to supplement. Blood testing can also be done.

Selenium deficiency

According to Carmalt12 nutritional myodegeneration (white muscle disease) has been empirically diagnosed in alpacas, although there are no published reports of selenium deficiency disease. In other species selenium deficiency may be associated with depressed growth rates and effects on fertility. If there is selenium deficiency in sheep and cattle in the area, it may be wise to blood test alpacas to see if supplementation is necessary.

Measurement of blood glutathione peroxidase (GSHPx) is the most cost effective way of checking selenium status. Submit Lithium Heparin or EDTA whole blood samples. A miminum of 6 animals should be tested if assessing herd status. David Paynter at Regional Laboratory Services in Benalla, Victoria has established a provisional reference range where GSHPx < 15 U/g Hb is regarded as low. However recent work by David and co-workers has shown that, unlike sheep and cattle, there is not always good correlation between blood selenium and GSHPx in alpacas.27,28 David has examples where alpacas had an initial, pre-supplementation GSHPx concentration of about 20 U/g HB. Following selenium supplementation, the GSHPx concentration hardly changed, even several months after supplementation. The plasma selenium concentration did however increase following supplementation. So it may be advisable to do plasma selenium testing in this species, instead of, or in addition to whole blood GSHPx.

Zinc responsive dermatosis

Zinc responsive dermatosis is is characterised by thickening of skin with adherent crusts on non-haired areas of the body,e.g. ventral abdomen, axilla, medial thighs, inguinal region. The bridge of the nose, muzzle and periocular region may also be involved. Diagnosis is based on history, physical examination, ruling out other differential diagnoses, and response to zinc supplementation. Affected animals do not necessarily have low serum zinc concentrations. Some people have speculated that the condition is actually insect hypersensitivity that “goes away”, when insects disappear with the change of seasons! Animals are given 1-2 g ZnSO4 or 2-4 g zinc methionine, once daily, p.o., with improvement being seen within 30-90 days25. Regional Laboratory Services, Benalla offer zinc testing on serum or heparin plasma. The reference range they have established for alpacas is 3.5-10 µmol/L, which is lower than that for cattle, 8-23 µmol/L.

Miscellaneous Diseases

Gastric ulceration in South American camelids (alpacas and llamas)2

Gastric ulcers occur most commonly in the third stomach compartment (C3). At its caudal end, there is a small region of hydrochloric acid secretion. Ulcers here cause about 6% of all camelid deaths in North America. It is likely that gastric filling and emptying functions are very important in ulcer development. Under conditions of poor gastric filling and emptying, such as anorexia or intermittent feeding or small paddock size, and gastric hyperacidity (grain feeding), newly secreted acid may persist for a longer period in C3 and possibly damage the mucosa. Gastric ulcers are most commonly recognised on perforation. Some animals are chronic poor-doers for months before perforation, but most are outwardly completely healthy before perforation.

The emphasis in preventing ulcers should be on recognising at-risk camelids and changing their management to decrease the likelihood of ulcer development. To promote good gastric filling and emptying, camelids should be provided with diets consisting mainly of roughage,e.g. not too much grain or other fermentable feed and the ability to exercise. Also try to minimise other causes of stress or anorexia,e.g. bullying, transportation, other illnesses.

Hyperthermia (heat stress)

Alpacas are not well adapted to hot, humid climates. Affected animals usually display signs of recumbency and respiratory distress. Tachycardia is a common finding13. Anecdotally, some alpaca breeders in New South Wales, have attributed cria deaths to hot weather and thus prefer not to have alpaca births during the hottest months of the year.

Hyperthermia in early pregnancy is a potential cause of foetal CNS damage or foetal death. Congenital CNS defects associated with prenatal prolonged hyperthermia in humans and other animals include anencephaly, encephalocoele, microencephaly, spina bifida, hydrocephaly, and neurogenic arthrogryposis1.

Hypothermia

Newborn crias, old thin animals and recently shorn animals are susceptible to hypothermia in very cold and/or wet conditions.

Idiopathic nasal/perioral/hyperkeratotic dermatosis (munge)

This condition is very poorly understood. The nasal and perioral (commissures of the lips) areas become covered with thick crusts that occasionally obstruct the nostrils. Lesions may occasionally occur on the bridge of the nose and periocular region. Pruritus is usually absent or mild. It is probably that many different conditions are being called 'munge'. Cases are reported to respond to topical and ⁄ or systemic antibiotics, scab removal and scrubbing with topical antiseptics such as dilute iodine or chlorhexidine, topical and ⁄ or systemic glucocorticoids (not to be used in pregnant females), oral zinc, or to regress spontaneously.25,27 According to Scott et al.:25 “We presently believe that idiopathic nasal ⁄ perioral hyperkeratotic dermatosis is a cutaneous reaction pattern of alpacas possibly provoked by disorders such as bacterial folliculitis, dermatophilosis, dermatophytosis, contagious viral pustular dermatitis, chorioptic mange, fly bites, viral papillomas ⁄ fibropapillomas, contact dermatitis and zinc-responsive dermatosis. The authors are not aware of any laboratory tests or therapeutic interventions that allow one to diagnose 'munge'. Such a multifactorial aetiology could explain the anecdotal successes of popular topical concoctions such as 'witches brew', which contains gentamicin, ivermectin, dimethyl sulfoxide and mineral oil.” Note that gentamycin is not registered for use in food producing animals in Australia (including camelids) and that DMSO is carcinogenic.

Solar dermatitis

It tends to affect exposed areas with short white hair, such as the ears. Lesions show parakeratosis with variable amounts of cellular infiltrates and necrosis. The most effective treatments are grazing in shaded paddocks, increasing time indoors or covering affected areas with a zinc oxide or titanium dioxide based sun block.

Intestinal accidents

Occur rarely, but are more common in camelids than ruminants. Affected alpacas may show signs of abdominal pain.

Neoplasia

Lymphoma is the most commonly reported neoplasm in camelids overall (do not confuse mesenteric form with Johne's disease, use histology for definitive diagnosis). Other neoplasms occur sporadically. In general neoplastic disorders often cause gradual weight loss with progressive lethargy and anorexia.

Traumatic injuries

Urolithiasis

Urolithiasis has been described rarely in male alpacas12.

Protozoal diseases

Coccidia, Cryptosporidia, Giardia

See under Endoparasites.

Neospora caninum

A serological study was published in the Australian Veterinary Journal in 2015. 100 alpacas were sampled from 4 farms in south-eastern Australia and tested by ELISA. Three were suspect seropositive for N. caninum. Their conclusion was that there is natural seroprevalence in alpacas in south-eastern Australia, however it remains undetermined whether this contributes to reproductive failure19. The Neospora antibody ELISA that we have at the State Veterinary Diagnostic Laboratory in NSW can only be used on bovine blood samples.

Sarcocystis infection causing myositis

Typically Sarcocystis spp. have a life cycle involving two hosts. The intermediate host (typically a herbivore) becomes infected by ingesting sporocysts excreted in the faeces of the definitive host (typically a carnivore). The intermediate host develops microscopic cysts (sarcocysts) within the musculature. In some individuals the sarcocysts are associated with an inflammatory reaction, which produces visible muscle lesions. Infection in alpacas in South America is common, however disease is rare, aside from carcase downgrading that occurs in some infected animals.

At the State Veterinary Diagnostic Laboratory (SVDL, NSW) we have seen two cases of Sarcocystis infection causing chronic myositis. In the first case, raised, subcutaneous, abscess-like structures developed bilaterally along the head and neck over a one month period. Histopathology indicated a severe, necrotising and histiocystic myositis with the presence of multiple sarcocysts. An unknown Sarcocystis species was identified by electron microscopy of the lesions.26

In the second case, multiple caseous cystic lesions were found within the musculature of the neck and intercostal muscles at slaughter. Histopathology showed a necrotising, histiocytic myositis with the presence of degenerate and non-degenerate protozoa.

Toxoplasma gondii

Dubey et al.. in 2014 described the first report of toxoplasmosis-associated abortion in an alpaca20.

Toxicities

Alpacas are susceptible to many of the poisonous plants and chemicals that cause poisoning in other grazing livestock. A few of these are listed here.

Poisonous plants12

Some that have been reported include rhododendrons, azaleas and oleander. In NSW there have also been cases of alpacas with histological evidence of toxic hepatopathies, where the specific cause was not determined.

Botulism

No cases of botulism have been reported in South American camelids, but there is good reason to believe that all camelids may be susceptible1.

Perennial ryegrass toxicosis (ryegrass staggers)

Ryegrass staggers are produced by tremorgenic toxins, lolitrems, produced by the endophytic fungus, Neotyphodium lolii, growing within perennial ryegrass plant tissues. Clinical signs include head tremor and swaying. There is evidence that alpacas are more susceptible to ryegrass staggers than sheep and cattle3. There is overseas evidence that some perennial ryegrass toxins, while not causing visual evidence of staggers in livestock, may cause subclinical disease, heat sensitivity and ill-thrift.

Phalaris aquatica "cardiac sudden death"

Chris Bourke described three distinct syndromes of Phalaris aquatica poisoning of sheep: 1. Phalaris staggers (diagnosed on histopathology by the presence of intraneuronal pigment within brainstem nuclei); 2. "cardiac sudden death"16; and 3. Polioencephalomalacia-like sudden death. As far as I am aware, Phalaris staggers and PEM-like sudden death have not been confirmed in alpacas. Cardiac sudden death may have occurred in alpacas.

In sheep cardiac sudden death occurs relatively uncommonly and affects low numbers of animals. It is not well-proven. Deaths are usually associated with mustering. The presentation is one of sudden collapse during mustering. The animal has a pounding heart and discolouration of mucous membranes. There is either death, or instant recovery, within minutes of collapse. There is little to see at postmortem other than acute pulmonary congestion. I have seen alpaca deaths of this type, that appeared to be associated with vigorous exercise at mustering, occurring in alpacas grazing Phalaris-dominant pasture. The diagnosis is presumptive only.

Pyrrolizidine alkaloid poisoning

Pyrrolizidine alkaloids are found in plants such as Paterson's curse (Echium plantagineum) and fireweed (Senecio madagascariensis). Poisoning is associated with a chronic hepatopathy. There is little published information on the occurrence of this condition in alpacas or their susceptibility. In other livestock, cattle and horses are more susceptible than sheep and goats.

Sporidesmin poisoning (facial eczema)

Sporidesmin is a toxin produced by the fungus, Pithomyces chartarum, growing in pasture litter (especially perennial ryegrass pasture). It causes liver damage and secondary hepatogenous photosensitization. Facial eczema has been reported in alpacas in New Zealand and Australia. Spore counts can be done on pasture to assess the degree of pasture contamination.

Copper poisoning

Sheep are notorious for their susceptibility to chronic copper poisoning with development of acute liver necrosis, haemoglobinaemia and haemoglobinuria. Published studies suggest alpacas are susceptible to chronic copper toxicity, although not as sensitive as sheep. Copper poisoning may occur when supplement or mineral mixes designed for cattle, horses, pigs or poultry are fed to alpacas. It appears that poisoning may be characterised by hepatic necrosis without the classical haemolytic crisis that occurs in sheep12. Liver damage may be slow and progressive with signs of weight loss2.

Ionophore toxicity

In one report from the USA, alpacas were exposed to salinomycin at the poultry rate of 66 ppm due to a feed mixing error. Deaths occurred as the result of severe, acute rhabdomyolosis.

Nitrate/nitrite poisoning

There are a few reports of nitrate/nitrite poisoning in alpacas in Australia. In one case, it was seen after a long period of dry weather that allowed accumulation of nitrogen in the soil, followed by emergence and consumption of large volumes of capeweed (Arctotheca calendula) after the autumn break.

Viral diseases

Bluetongue

Bluetongue virus is known to affect many species of ruminants. There is serologic evidence that camelids respond to BTV with the formation of antibodies, but clinical disease is questioned1.

However in Germany in 2007, the death of a single alpaca was reported to be due to Bluetongue virus infection, during a Bluetongue virus outbreak affecting sheep and cattle. The alpaca became sick and died within 24 hours. In the oral cavity “single small erosions and ulcerations on the tongue, palate and buccal mucosa were observed”. There was also severe pulmonary oedema. Bluetongue virus was detected by PCR in various tissue samples4.

Twelve serotypes of Bluetongue virus have been detected in Australia and are endemic in northern Australia. There has been no evidence of any clinical disease associated with any livestock species in Australia, apart from two reports in sheep near Darwin, one in 1989 and one in 2001.

Bovine Viral Diarrhoea virus

Infection is associated with cattle strains of BVDV. A unique alpaca BVDV strain has been postulated but not isolated. If a pregnant alpaca is exposed to the virus during the first trimester of pregnancy the fetus may become persistently infected. Other potential outcomes include abortion, stillbirth, low birth weight, or weak neonates. Disease in PI animals may occur at a few months of age leading to death at an early age. Both acute and chronic disease may occur, but chronic disease is more common. Clinical signs include chronic illthrift, diarrhoea, nasal discharge and pneumonia1. The Virology laboratory at Elizabeth Macarthur Agricultural Institute (EMAI, NSW) is the reference laboratory for BVDV in Australia and the laboratory is not aware of any cases of BVDV associated disease in alpacas in Australia (as at February 2016). However they have detected a few persistently infected, apparently healthy alpacas in export shipments. Infection with BVD virus is more likely to occur when alpacas are run with cattle. A serological survey of 182 alpacas on 13 farms in the Adelaide hills of South Australia, revealed 5 seropositive animals9.

We use the same tests as used in cattle,e.g. BVDV AGID (agar gel mmunodiffusion) for serology; BVDV antigen ELISA (or PCR) for virus detection. Submit a red top blood tube for serology or virus detection in animals older than 6 months. Submit a heparin blood (green top tube) for virus detection in animals younger than 6 months. The hair test for PI animals is not validated for alpacas, however the virology section have tested a small number of positive hairs from the USA and were able to detect all PI animals. Thicker hairs are better.

Contagious ecthyma (orf)

Typical proliferative epidermal lesions at the commissures of the mouth have been seen in camelids in North America and New Zealand1.

Coronavirus

Parasitic infections are the main cause of diarrhoea in camelids. However viral diarrhoea, usually associated with Coronavirus, has been described. This is most likely a bovine virus which has crossed over into alpacas. When the virus is first introduced into a naïve herd, diarrhoea affecting all ages may be seen. Once the outbreak has run its course, only crias are susceptible. Diarrhoea is usually explosive and watery. The disease usually runs its course in 4-9 days. Affected animals may need water and electrolyte replacement, neonates are much more vulnerable2.

Equine Herpesvirus 1

Herpesviruses are usually well adapted to one or more hosts. Interestingly, no herpesviruses unique to camelids have been identified. When herpesviruses infect a non-adapted host, serious disease may result. In 1984, blindness was diagnosed in 21 alpacas and one llama of a herd of approximately 100 animals. Four of the animals also developed signs of neurologic dysfunction, including depression, nystagmus, head tilt and paralysis. The condition was ultimately attributed to infection with EHV11. Abortion due to EHV1 has not been described in camelids.

Pneumonia

Pneumonia appears to be relatively uncommon in alpacas in Australia. However two papers from Peru describe cases of acute suppurative bronchopneumonia in alpaca neonates and weaners.29,30 Various combinations of mixed viruses and bacteria were identified, similar to that seen in ruminant species. Viral agents included Parainfluenza 3 (PI3) virus and bovine respiratory syncytial virus (BRSV). Bacterial agents included Pasteurella multocida and Mannheimia haemolytica.

Rabies

Rabies virus is exotic to Australia. In one instance in Peru, twenty alpacas from a herd of 160 were bitten by a rabid dog; thirteen died or were euthanased in extremis. The incubation period was as short as 15 days in one animal, 22 days in two, 24 days in one, and 31 to 34 days in nine animals. Affected animals died six to eight days after the development of clinical signs. In another instance, 29 of a herd of 330 alpacas developed rabies. Dogs were implicated in this case as well. Transmission of rabies from alpaca to alpaca as a result of bites has also been reported1. Australian Bat Lyssavirus infection has not been reported in alpacas in Australia.

Rotavirus

Rotavirus infection has been described in young alpacas (> 7 days old), but appears to be less common than Coronavirus infection2.

West Nile virus / Kunjin virus

Camelids are considered to be at low risk for developing clinical signs of West Nile virus infection, however the mortality rate in affected animals showing neurological signs is high. Signs are similar to those occurring with EEE including inappetence, fever, lethargy, ataxia, stiff gaits, seizures, recumbency, torticollis or opisthotonus, and vestibular signs. Affected animals usually are unable to right themselves from lateral recumbency1.

Kunjin virus (an Australian variant of West Nile virus), like West Nile virus, cycles between various avian species and mosquitoes. Mammals are usually dead-end hosts. Disease in alpacas has not been reported in Australia. During the 2011 outbreak in horses, a number of alpacas with neurological signs were tested, but were serologically negative.

Section 2. Differential Diagnoses by Syndrome

Diseases are listed for each syndrome, but are not a complete list of possible causes. Death and ill thrift are the two most common syndromes recorded for laboratory submissions to the SVDL (NSW). Diarrhoea is the third most common syndrome recorded for SVDL submissions.

Abortion

Anaemia

Congenital and inherited anomalies

Death - acute or subacute

Diarrhoea

Illthrift

Infertility (only a few conditions listed here)15

Congenital conditions

Acquired conditions

Lameness

Nervous signs

Skin disease

References

  1. Fowler, Murray E. (2011, 3rd ). Medicine and Surgery of Camelids. Published by Wiley
  2. Cebra, C.K. (2014). Multiple disease topics. The 2014 Australian Alpaca Association Conference Proceedings, Adelaide
  3. Holmes, L. A., et al. (1999). "Suspected tremorgenic mycotoxicosis (ryegrass staggers) in alpacas (Llama pacos) in the UK." Veterinary Record 145(16): 462-463
  4. Henrich, M., et al. (2007). "Lethal bluetongue virus infection in an alpaca." Veterinary Record 161(22): 764
  5. Hardefeldt, L. (2014). Neonatal care of alpacas. The 2014 Australian Alpaca Association Conference Proceedings, Adelaide
  6. Carmichael, I.H. (2014). "Internal parasitism in Australian alpacas". Proceedings of the Australian Alpaca Association National Conference, Adelaide, Australia, May 9-11, 2014, pp. 13-28. This paper is also available separately on the internet and can be found using a search engine like Google
  7. criagenesis.cc/ This Australian website maintained by veterinarian, Jane Vaughan, contains a variety of alpaca information, including husbandry, nutrition, parasites and reproduction
  8. Anderson, D. E., et al. (2004). "Infection with Corynebacterium pseudotuberculosis in five alpacas." Journal of the American Veterinary Medical Association 225(11): 1743-1747, 1702
  9. Lambert, R., Reichel M. (2014). "A serological survey of bovine viral diarrhoea virus exposure in South Australian alpacas." The 2014 Australian Alpaca Association Conference Proceedings, Adelaide
  10. Ridge, S. E., et al. (1995). "Johne's disease in alpacas (Lama pacos) in Australia.” Australian Veterinary Journal 72(4): 150-153
  11. Van Saun, R. J. (2009). "Nutritional Diseases of Llamas and Alpacas." Veterinary Clinics of North America-Food Animal Practice 25(3): 797-+
  12. Carmalt, J.L., et al. (2001). "Suspect copper toxicity in an alpaca." Canadian Veterinary Journal 42: 554-6
  13. Whitehead, C. E. and D. Bedenice (2009). "Neurologic diseases in llamas and alpacas. (Special Issue: Alpaca and llama health management)." Veterinary Clinics of North America, Food Animal Practice 25(2): 385-405
  14. Vaughan, J. (2014). "Practical nutrition in alpacas". The 2014 Australian Alpaca Association Conference Proceedings, Adelaide. Pp 168-178
  15. Vaughan, J. (2014). "Mating management; Fertility and infertility in your alpaca herd". The 2014 Australian Alpaca Association Conference Proceedings, Adelaide. Pp 178-189
  16. Bourke, C. A., et al. (2003). "Clinical observations and differentiation of the peracute Phalaris aquatica poisoning syndrome in sheep known as 'Polioencephalomalacia-like sudden death'." Australian Veterinary Journal 81(11): 698-700
  17. Bourke, C.A. "Poisonous plants of northern NSW" NSW Department of Primary Industries Workshop held at Tamworth Agricultural Institute, 12-13 April, 2005
  18. Coulton, M. A., et al. (1997). "Sporodesmin toxicosis in an alpaca." Australian Veterinary Journal 75(2): 136-137
  19. King, J. S., et al. (2015). "Serological evidence of Neospora caninum in alpacas from eastern Australia." Australian Veterinary Journal 93(7): 259-261
  20. Dubey, J. P., et al. (2014). "Toxoplasmos-associated abortion in an alpaca (Vicugna pacos) fetus". Journal of Zoo and Wildlife Medicine 45(2): 461-464
  21. Bidewell, C. A., et al. (2010). "Campylobacter fetus subspecies fetus abortion in alpacas (Vicugna pacos)". Veterinary Record 167(12): 457-458
  22. Whitehead, C. E. and D. E. Anderson (2006). "Neonatal diarrhea in llamas and alpacas." Small Ruminant Research 61(2-3): 207-215
  23. Whitehead, C.E. www.ukalpacavet.com (February 2016). Personal communication
  24. Bullen JJ, Scarisbrick R: 1957, Enterotoxemia of sheep: experimental reproduction of the disease. J Pathol Bacteriol 73:495-509
  25. Scott, D. W., et al. (2011). "Skin diseases in the alpaca (Vicugna pacos): a literature review and retrospective analysis of 68 cases (Cornell University 1997-2006)." Veterinary Dermatology 22(1): 2-16
  26. Gabor, M., et al. (2010). "Chronic myositis in an Australian alpaca (Llama pacos) associated with Sarcocystis spp." Journal of Veterinary Diagnostic Investigation 22(6): 966-969
  27. Vaughan, J. criagenesis.cc/ (February 2016). Personal communication
  28. Paynter, D. Regional Laboratory Services, Benalla (February 2016). Personal communication
  29. Cirilo C, E., et al. (2012). "Coexistencia de virus y bacterias en neumonías agudas en alpacas neonatas." Revista de Investigaciones Veterinarias del Perú 23(3): 317-335
  30. Guzmán M, K., et al. (2013). "Asociación de agentes virales y bacterianos en cuadros de neumonías agudas en alpacas tuis." Revista de Investigaciones Veterinarias del Perú 24(4): 524-536
  31. Tornquist, S. J. (2009). "Clinical pathology of llamas and alpacas". Vet Clinics of North America Food Animal Practice. 25: 311-322
  32. Janmaat, A., et al. (2004). "Melioidosis in an alpaca (Lama pacos)". Australian Veterinary Journal 82(10): 622-623
  33. Vaughan, J. (2004). "Eradication of the camelid biting louse, Bovicola breviceps." Australian Veterinary Journal 82(4): 218-219
  34. Judson, G. J. and A. Feakes (1999). "Vitamin D doses for alpacas (Lama pacos)." Australian Veterinary Journal. 1999. 77: 5, 310-315

 

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