Foot Block Application

Wooden or acrylic blocks or commercial rubber shoes may be glued to the bottom of healthy claws to reduce or eliminate weight bearing on a diseased or painful claw. These devices are adhered to the claw using an acrylic material (Technovit, Jorgensen Laboratories, Inc. or Equi-Thane Super Fast, Vettec Hoof Care Products). Wooden blocks may last as long as 6 weeks and may be allowed to wear off naturally unless they are wearing abnormally, in which case they may be manually removed earlier. Blocks or shoes help promote healing of affected claws and make the animal more comfortable when standing or moving.

Blackleg and Malignant Edema

Infections by Clostridium chauvoei (blackleg) and Clostridium septicum (malignant edema) are two important causes of lameness and sudden death in young cattle. These bacteria produce spores that enter the animal through either the digestive tract or skin wounds, producing a severe necrotizing myositis and cellulitis. Affected animals develop high fever and lameness as a result of severe muscle damage. The swollen muscle mass often contains gas pockets that are palpable subcutaneously as crepitus.

Animals with these infections are usually found dead. Those animals caught in the early stages of an infection may be treated with high doses of penicillin along with débridement and topical treatment of the wounds; however, the prognosis for recovery is poor. The best way to prevent these clostridial diseases and others is to vaccinate calves with a multivalent bacterin at 2 months of age followed by a booster 4 to 6 weeks later. Cows should be vaccinated before calving to provide colostral protection to the calves.

Lymphosarcoma

The adult form of lymphosarcoma (LSA) is associated with BLV and is the most common neoplastic disease of cattle. Lymphosarcoma is mostly likely to affect cattle between the ages of 2 and 6 years. Although many cattle are exposed to BLV and any given herd may have a high incidence of cattle with titers to BLV, the actual number of cattle that develop neoplastic disease is small (less than 5%). Malignant tumors may develop in peripheral or deep lymph nodes, lymph tissue behind the eye or around the spinal cord, abomasum, heart, kidney, uterus, or other organs; therefore clinical signs may vary greatly depending on the organ(s) or system(s) involved. Occasionally a lymphocytosis with the presence of neoplastic lymphocytes is apparent when a CBC is performed. Diagnostic tests to help confirm lymphosarcoma may include a CBC, lymph node biopsy, paracentesis, thoracocentesis, a CSF centesis, or a BLV titer. A positive titer to BLV only suggests exposure to the virus, but does not confirm neoplastic disease. There is no treatment or vaccine available, and the disease is always fatal. Since BLV titers are so prevalent in cattle herds, it is unlikely that a test and cull program would ever be initiated. Because the virus is spread by infected lymphocytes, every effort should be made to prevent the transfer of blood between infected and noninfected animals (e.g., by changing needles and disinfecting surgery instruments between animals).

Anaplasmosis

Anaplasmosis, caused by the intraerythrocytic organism, Anaplasma marginale, is primarily a disease of adult cattle. RBCs infected with the organism are removed from the circulation by the liver and spleen and are subsequently destroyed resulting in a severe anemia. Resulting clinical signs from the development of acute anemia include pale mucous membranes, icterus, weakness, and depression or aggressive behavior as a result of anoxia to the brain. Anaplasmosis often causes sudden death without obvious clinical signs, and it must be differentiated from other causes of sudden death, such as anthrax, clostridial diseases, bloat, and lightning. The organism is sensitive to tetracycline, so this drug is used for the treatment and prevention of the disease. There is currently no commercial vaccine available for the prevention of anaplasmosis.

Anthrax

Bacillus anthracis is the etiologic agent of this acute disease causing sudden death in animals and humans. Anthrax is endemic in many areas of the southern United States. Since people can easily contract the disease, it is important not to perform a necropsy on any animal suspected of having anthrax. The exposure of anthrax bacilli to the air, as in the case of necropsy, results in spore formation by the organism and permanent contamination of the surrounding environment. If anthrax is strongly suspected as the cause of death, the area federal veterinarian should be notified immediately. Anthrax-contaminated carcasses should be buried in lime or incinerated. A live virus vaccine is available, and its use should be considered in high-risk areas. The organism is sensitive to penicillin, but in most cases, the treatment cannot be initiated quickly enough. In recent years, anthrax has become an important issue in cases of bioterrorism.

Mastitis

Mastitis is inflammation of the mammary gland caused by the invasion of the streak canal of the teat by a variety of bacterial pathogens. Economically, mastitis is one of the most important diseases in the dairy industry, and it is the single most common disease syndrome in adult dairy cows. Anatomically the mammary gland is relatively resistant to infection, but severe environmental contamination of the teats, injury to the streak canal, or improperly functioning milking machine equipment may predispose the udder to infection.

Clinical signs of mastitis vary considerably based on the etiologic agent and may be seen as an asymptomatic subclinical infection to one in which the gland is markedly swollen and the milk is grossly abnormal. In general, mastitis can be subdivided into two broad but overlapping categories based on the source of the infection: contagious and environmental. Contagious mastitis is spread from an infected mammary gland to a healthy one via contaminated milking equipment, nursing calves, or by the milker’s hands. Streptococcus agalactiae and Staphylococcus aureus are examples of bacteria causing contagious mastitis. Environmental mastitis results when bacteria within reservoirs in the environment gain access to the mammary gland and cause infection. Those organisms characteristically associated with environmental mastitis include the coliform bacteria. Other mastitis-causing organisms that fall between these two broad categories, maintaining alternate niches either in the host or in the environment, include Streptococcus dysgalactiae and Streptococcus uberis. Mastitis, depending on the cause, causes various abnormal secretions ranging from the presence of milk with flakes or clots to purulent material. The degree of inflammatory response varies also depending on the cause. Other classifications of mastitis include acute or toxic mastitis, usually caused by coliforms or S. aureus, chronic mastitis, caused by S. aureus, or acute gangrenous mastitis, the cause of which may be S. aureus or Clostridium perfringens. Cows with toxic mastitis are usually ill, have a watery or serous secretion from the affected gland(s), and have a low serum calcium level such that they may resemble a case of milk fever. Gangrenous mastitis causes gangrene of the gland with a distinct blue line of demarcation separating normal and affected tissues. Secretions from affected glands are watery and serosanguineous, the gangrenous portions will be cold to the touch, and these portions of the gland will eventually slough. Toxic and gangrenous mastitis may cause the death of the cow.

Mastitis is best diagnosed by a clinical examination of the udder and milk and the use of the California mastitis test (CMT). The CMT is performed by mixing equal parts of CMT reagent and milk. A plastic paddle with four separate compartments is provided with the test kit so that each quarter can be individually evaluated. The reagent reacts with leukocytes that are usually present in large numbers when mastitis is present. When this reaction occurs, the reagent-milk mixture thickens or gels in proportion to the number of white cells present and indicates the severity of the inflammation. The greater the reaction, the higher the CMT score. CMT scores are designated as negative, trace, 1, 2, and 3 with corresponding cell counts of 100,000, 300,000, 900,000, 2,700,000, and 8,100,000. The aseptic collection of a milk sample for culture and antimicrobial sensitivity often provides information on cause and appropriate drug therapy.

Depending on the etiologic agent, mastitis can be successfully treated if recognized early. The treatment of mastitis involves the use of appropriate antimicrobial therapy, systemic and/or intramammary. Frequent stripping of affected quarter(s) helps remove infected secretions and promotes quicker recovery. Cows with toxic mastitis may need intensive treatment with NSAIDs, IV fluid therapy, and calcium in those cows with hypocalcemia. Only antibiotics approved for use in dairy cows should be administered for the treatment of mastitis. In addition, antibiotic milk withdrawal times should be closely monitored. The veterinary technician should be familiar with these approved drugs and the withdrawal times and can serve as an important resource for education of the dairy farmer.

The prevention of mastitis is of paramount importance in the dairy industry. Control may be achieved by the implementation of the five-point plan for mastitis control, which includes:

Dystocia

Dystocia, or difficult calving, in cattle is relatively common, especially in first-calf heifers, and frequently requires veterinary assistance. Dystocia may result from fetal oversize, maternal undersize, or fetal malposition. To recognize if a problem exists, the veterinary technician should be familiar with the normal signs of impending parturition and the stages of parturition. When a cow or heifer is nearing parturition, relaxation of the pelvic ligaments, swelling of the vulva, and udder development occur. During stage I of labor, the cervix dilates and the chorioallantoic membrane ruptures, releasing a large volume of clear, yellow fluid. Stage II is marked by the appearance of fetal extremities at the vulva along with the amniotic membrane. Normally the cow or heifer will deliver the calf within 2 hours of this observation. If delivery takes longer than 2 hours or if the cow stops straining, the cow should be examined, and veterinary assistance may be indicated. Stage III involves the passage of the placenta.

When dystocia is suspected, the cow should be quickly and thoroughly examined to rule out hypocalcemia as a cause of uterine inertia. Before a vaginal examination, the vulva and perineal area should be thoroughly cleaned with a mild disinfectant. A sterile, nonirritating lubricant, such as carboxymethylcellulose, can be used to perform the vaginal examination, and it may be pumped into the uterus to facilitate manipulation, repositioning, and delivery of the calf. Once any malposition is corrected, obstetric chains can be placed on the legs of the calf to apply traction for delivery. The chains should be looped above the fetlocks and half hitched below the fetlocks to more evenly distribute the pulling forces on the legs. A single loop of the chain on each leg is much more likely to result in physeal fractures. If the calf’s head is in normal position, a snare may be placed around the head to aid delivery. Excessive force should be avoided during forced fetal extraction to prevent nerve injury to the cow and fractures of the calf’s legs. A mechanical calf extractor can be used carefully when manual traction is unavailable. If the calf cannot safely be delivered by this technique, then fetotomy or a C-section section should be considered.

Fetotomies are usually reserved for the removal of calves that are dead or emphysematous. It involves the use of specialized instruments to dissect the dead calf in utero to deliver it more easily. C-section for resolution of dystocia is covered in Chapter 31.

Retained Placenta (Fetal Membranes)

After calving, the placenta is usually passed within 2 to 4 hours and is considered retained if it has not been expelled by 8 to 12 hours. Retained placenta is more common in dairy cows than beef cows. The cause is unknown, but it is more likely to occur following the birth of twins, following abortion during the last half of pregnancy, and in cases of dystocia. Selenium and vitamin A and E deficiencies have been suggested to cause an increased incidence of retained placentas.

The manual removal of the placenta should be avoided since this may result in endometrial damage and an infection with prolonged uterine involution and delayed breeding. Retained placenta and endometritis may be treated with intrauterine infusions of appropriate antibiotics. Although uterine infusion is controversial, most veterinarians agree that cows with signs of systemic illness as a result of retained placenta should receive parenteral antibiotic therapy.

If abortion is the cause of retained fetal membranes, vaccination of cows and heifers for diseases causing abortion should be considered. If nutrition is suspected as a predisposing factor, the ration should be evaluated making certain that it contains recommended levels and ratios of calcium, phosphorus, vitamins A and E, and selenium. An injection of vitamin E and selenium 1 month before calving may reduce the incidence of retained placenta in problem herds.

Periparturient Hypocalcemia (Milk Fever)

Milk fever is a common metabolic problem in periparturient dairy cows usually occurring within 48 hours of calving. It is unlikely to occur in first-calf heifers, but the incidence of the condition increases with the age of the cow. It reportedly is more likely to occur in the Jersey breed. Milk fever is the result of a severe decline in the serum calcium level (normal, 10 mg/dl). Hypocalcemia results from feeding of diets high in calcium during the late dry period (the last 2 months of gestation), which causes a lack of response by the parathyroid gland and a decrease in vitamin D levels. As a result, the cow is slow to mobilize calcium reserves from the bone when there is a sudden demand for calcium at the beginning of lactation.

Cows with hypocalcemia develop muscle tremors, weakness, and a staggering gait eventually leading to recumbency. Cows with milk fever often lie in sternal recumbency with the head turned into their flank. Affected cows have a dry nose, rumen atony with bloat, and no urine or feces production. Some cows with milk fever may be found in lateral recumbency. The heart rate is increased and pupils dilated. Unless the cow is treated quickly, she may die of the effects of a low serum calcium level. It is important to get a down cow up as soon as possible since recumbency leads to the development of severe myositis of the muscles of the limbs and subsequent nerve damage resulting in a permanent “downer” cow.

The slow administration of calcium gluconate IV is the treatment of choice. Cows often respond rapidly to calcium therapy and will begin to lacrimate, eructate, urinate, and defecate. If the initial treatment helps but the cow does not stand, it may be necessary to administer additional calcium subcutaneously. If the cow does not respond to treatment, she should be reevaluated for persistent hypocalcemia or concurrent problems, such as mastitis, metritis, or musculoskeletal or nerve damage. Cows in the early stages of milk fever (before recumbency) often respond to the administration of oral calcium gel.

Prevention of milk fever is achieved by providing a well-balanced, low-calcium diet during the dry period. The total dietary intake of calcium should not exceed 20 g per head per day. It is important to keep dry cows separate from the rest of the herd so that they can be fed properly not only to prevent milk fever, but also to prevent overconditioning and fat liver syndrome.

Ketosis (Acetonemia)

Ketosis occurs in high-producing dairy cows during the first few months of lactation if they are unable to meet the energy demands of lactation. To provide energy for milk production, the cow begins to mobilize fat, the breakdown of which results in the formation of ketone bodies that accumulate in the blood. Ketosis in dairy cows may result from a primary deficiency in energy intake, or it may occur secondary to a disease process, such as abomasal displacement, mastitis, or metritis, which can cause anorexia.

Ketones have a characteristic odor that can be detected in the breath, milk, and urine of affected cows. Excessive amounts of ketones and a low blood glucose level may cause the cow to display nervous symptoms known as nervous ketosis.

Ketosis responds to administration of energy sources, such as glucose IV, propylene glycol per os, or, where appropriate, systemic corticosteroids. It is important to determine the cause of ketosis and to correct the underlying problem. The cow’s ration should be examined to make certain it contains adequate digestible energy to meet requirements for maintenance and lactation.

Vegetative or Valvular Endocarditis

Vegetative or ulcerative lesions may develop on the heart valves, in particular the right atrioventricular (AV) valve, as a result of septic emboli from other sites, such as omphalophlebitis or navel infection in calves. These lesions, if severe, may interfere with blood flow leading to congestive heart failure (CHF). The cause is bacterial, usually Arcanobacterium pyogenes or α-hemolytic streptococcus in cattle. Vegetative endocarditis in pigs is usually due to streptococcus or Erysipelothrix. If fragments detach from the heart valve, embolic endoarteritis and abscesses in showered organs may follow. Clinical signs in cattle include a history of an animal doing poorly, presence of a murmur or thrill, exercise intolerance, CHF with jugular vein distention and dependent edema in advanced cases, and fluctuating fever (Figure 22-23). Clinical pathology in acute cases may show leukocytosis (greater than 100,000 WBC) with a left shift, whereas chronic cases may have a normal CBC. Three serial blood cultures performed as the body temperature rises may yield bacterial growth. On necropsy, the valve lesions may be large and cauliflower-like or small and wartlike. In chronic cases, valves may be shrunken and distorted or scarred. Treatment is not successful because of an inadequate penetration of the lesions with antibiotics and the presence of irreversible damage to the valves. Penicillin at high levels (44,000 IU/kg b.i.d.) for long periods of time (2 to 3 weeks) has given the best results, although cephalosporins may also prove beneficial and are commonly used to treat young calves. Echocardiography, when available, is quite useful for visualizing valve lesions.

Contagious Bovine Pyelonephritis

Contagious bovine pyelonephritis, caused by Corynebacterium renale, is an ascending urinary tract infection often affecting females because of the short, wide urethra. The infection occurs more often in the periparturient period when cows are more stressed and the urogenital tract is more susceptible to entry of bacteria.

Clinical findings include hematuria, pyuria, straining (strangury) and discomfort during urination, and frequent urination (pollakisuria). Affected cows may have a fluctuating fever, variable appetite, and decreased milk production. If the left kidney is affected, rectal palpation may reveal an enlarged, fluctuant, painful kidney.

The treatment is often unrewarding, but may be attempted using high doses of penicillin (44,000 U/kg b.i.d.) for long periods of time. In valuable animals in which only one kidney is affected, nephrectomy may be indicated.

Rabies

Rabies is a fatal, viral, neurologic disease of warmblooded animals. Rabies is most often transmitted by the bite of an infected wild animal, with skunks, raccoons, and foxes being the greatest threat to domestic livestock. Two forms of rabies may occur: the furious form in which the affected animal demonstrates hyperexcitability, fear, or rage or the dumb form in which extreme depression, paresis, or paralysis manifest.

Clinical signs of rabies may include bloat, tenesmus, bellowing, aggressiveness, and increased sexual activity. Hydrophobia, the common name for rabies, stems from the inability of the animal to drink as a result of pharyngeal-laryngeal paralysis. Death occurs within 10 days of the onset of clinical signs. The definitive diagnosis is made by fluorescent antibody testing of the brain, the presence of Negri bodies (cytoplasmic inclusions in neurons) on histopathology, and mouse inoculation.

Several vaccines are available for use in cattle and sheep. Rabies poses a serious human health concern; therefore care should be taken when handling animals suspected of having rabies (i.e., gloves should be worn during an oral examination). Veterinary technicians who practices in areas where the rabies incidence is high should strongly consider a rabies vaccination for themselves.

Polioencephalomalacia (Polio)

Polioencephalomalacia is a CNS disease that results from an underlying defect in thiamine metabolism. The disease may occur secondary to grain overload as previously discussed, or other sudden ration changes may precipitate its development. The coccidiostat, amprolium, administered at high doses or for long periods of time has induced polioencephalomalacia.

Affected animals show neurologic signs including blindness, ataxia, depression, opisthotonus, dorsomedial strabismus, convulsions, coma, and death. Polioencephalomalacia if treated early responds well to treatment with thiamine; however, the longer the animal has been affected, the longer it takes for recovery, and recovery may not be complete (i.e., blindness may persist). The addition of thiamine or brewer’s yeast to the ration in high-risk situations may be beneficial in preventing disease.

Listeriosis

Listeria monocytogenes is responsible for three different clinical syndromes in ruminants: septicemia, abortion, and neurologic disease. Neurologic involvement produces fever, anorexia, depression, proprioceptive deficits, head tilt, and circling. Cranial nerve dysfunction causes unilateral drooping of the ear, eyelid, nose, and lips with excessive salivation. Although the ingestion of contaminated corn silage is blamed, the consumption of any rotting contaminated vegetation can serve as the source of infection.

The organism is sensitive to tetracycline or penicillin, but a treatment of listeriosis is often unrewarding. No vaccine is available for protection against this disease. The organism has zoonotic potential and poses a serious human health risk when contaminated milk, milk products, or meat have entered the food chain.

Thromboembolic Meningoencephalitis

Thromboembolic meningoencephalitis (TEME) is the result of septic emboli in the brain secondary to septicemia caused by H. somnus. Animals affected with TEME show neurologic signs that are consistent with the areas of the brain that are damage by the emboli. The organism is found primarily in the respiratory tract and usually causes pneumonia. It is not unusual for some individuals to develop neurologic disease after an outbreak of pneumonia in a group of feedlot cattle.

The diagnosis is made by finding the characteristic hemorrhagic lesions scattered throughout the brain. With confirmation of the disease, treatment of the herd with tetracycline may be beneficial in preventing more cases, and vaccination with Histophilus bacterin may be indicated.

Infectious Bovine Keratoconjunctivitis

Infectious bovine keratoconjunctivitis (IBK), or pinkeye, is an infectious and contagious ocular disease of cattle characterized by conjunctivitis and keratitis with ulceration (Figure 22-25). Ultraviolet light and mechanical irritants, such as dust and weeds, may disrupt the corneal epithelium, allowing entry of Moraxella bovis, the etiologic agent of pinkeye. Flies have been shown to act as vectors for the bacteria.

Initial clinical signs include lacrimation, blepharospasm, and photophobia. Corneal inflammation followed by ulceration eventually develops. If ulceration becomes deep, the cornea may rupture, and vision will be lost.

The individual treatment of pinkeye involves a subconjunctival injection of antibiotics, usually procaine penicillin G (Figure 22-26). Eye patches may be applied to affected eyes to decrease photophobia and protect the eye from flies. More severe cases may require surgery, such as a third eyelid flap or tarsorrhaphy (suturing the lids closed) to protect deeper ulcers as they heal. In the case of herd outbreaks, it may be impractical to treat each animal with local therapy, so systemic antibiotics, such as long-acting tetracycline, can be administered to the group.

Cutaneous Papillomas (Warts)

Warts, a benign neoplasia caused by the papillomavirus, are common in young cattle. Warts appear as tan, white, or gray protruding masses with a dry, horny surface. Warts vary greatly in size and shape and can persist for 3 to 12 months at which time they often spontaneously regress.

Small warts may be crushed or surgically removed to help stimulate development of natural immunity and hasten healing. Cryosurgical treatment has also been successful. The use of autogenous and commercial vaccines has met with variable success. Since warts are usually self-limiting, no treatment may be necessary; however, in long-standing, severe, or nonresponsive cases, the immune status of the patient must be considered, and slaughter or euthanasia may be necessary.

Dermatophytosis (Ringworm)

Trichophyton verrucosum is the fungus responsible for ringworm in cattle. Ringworm is most likely to occur in calves housed in crowded conditions in the winter. Multiple circular lesions develop, particularly around the head and neck. The lesions, which are several centimeters in diameter, consist of an area of alopecia surrounding a slightly raised, whitish accumulation of dry, scaly skin. If left untreated, most lesions heal on their own in 2 to 3 months, especially if calves are turned out to pasture and exposed to the sunlight in the spring.

If treatment is desired, especially in the case of show animals, topical agents, such as iodine, bleach (1:10 in water), chlorhexidine, Captan, 5% lime sulfur, and thiabendazole may be useful. The immunocompetency of the animal hould be questioned in cases that do not respond spontaneously or with treatment.

Dermatophilosis (Streptotrichosis, Rain Scald)

Dermatophilosis is caused by the bacterium Dermatophilus congolensis. The bacteria invade the skin and produce crusts, which cause matting of the hair giving it a typical “paintbrush” appearance. The disease is more prevalent during periods of heavy rainfall or high humidity. Trauma, abrasions, concurrent disease, and poor nutrition make the skin more susceptible to infection. The disease may be transmitted by insect vector or direct contact with infected animals.

Treatment is accomplished by the removal of crusts by grooming followed by repeated iodine- or chlorhexidine-based shampoos. More severe cases may require systemic antimicrobials, such as penicillin or long-acting tetracycline. Exposure to the sunlight and disinfection of grooming equipment and housing helps control reinfection and spread of the bacteria.

CARE OF THE NEONATE

One of the most important components of successful rearing of lambs is establishment of a strong ewe-lamb bond. Factors that may interfere with the bonding process include:

Sheep are gregarious and stay together as a group even during lambing, which may result in lamb “stealing” by late-pregnant ewes as a result of their maternal instinct. Lambing in individual pens (lambing jugs, 4 feet square and 30 inches high) helps prevent this from happening. Licking of amniotic fluid from the lamb by the ewe clears the airway and stimulates breathing and allows the ewe to identify that lamb as her own. Intervention during or right after parturition by the owner or veterinarian might confuse the ewe as to whether or not the lamb is hers. Ewes are capable of identifying their own lamb(s) after only a few hours of contact, whereas lambs require several days to identify their mothers. This is another reason for using individual lambing pens. The treatment of the lamb for hypoglycemia, chilling, or illness should be performed in the lambing pen if at all possible since separation of the lamb for more than 1 hour may result in rejection of the lamb by the ewe.

The first week of life is the most critical for the lamb; as much as 50% of lamb and kid mortality occurs during this time. The first 48 hours are the most critical. Two major problems that may occur are hypothermia and hypoglycemia. The relatively large body surface of a lamb (versus body mass) can serve as a significant drain of body heat and energy. A 55° F environmental temperature with a 12-mph breeze has an evaporative cooling effect equivalent to −25° F to a newborn; thus it is important to protect newborns from direct wind. Lambs and kids are born with minimal body fat stores; therefore hypoglycemia can develop if the newborns do not ingest colostrum (high in fat) within the first 12 to 24 hours. The dam’s udder should be checked immediately postpartum to make sure it is functional. Ewes tend to have a thick wax plug that blocks the end of the teat before initial nursing. Occasionally the lamb is unable to remove the plug when it begins to nurse, which results in unsuccessful nursing. Another reason to examine the ewe’s udder is for the presence of ovine progressive pneumonia (OPP) mastitis. The ewe’s udder and milk will appear normal; however, the udder will feel firm when palpated as a result of the presence of fibrous connective tissue that occurs with OPP. Fibrous tissue development in the udder results in markedly decreased milk production. Lambs should be examined for congenital problems that might affect nursing, such as cleft palate, brachygnathism, prognathism, and tongue myopathies associated with vitamin E and/or selenium deficiency.

Hypothermia and hypoglycemia can usually be prevented with good management practices. Individual lambing pens work well to allow for bonding of the ewe and lamb, help keep the lamb warm, and allow the owner or veterinarian to check the ewe’s milk supply and intervene if problems should arise. Pens should be built to prevent drafts and may even be designed with a supplemental heat source (heat lamp) for the lamb(s). It is helpful to have frozen sheep or goat colostrum available in case it is needed. Cow colostrum can be used; however, a small percentage of lambs have developed neonatal isoerythrolysis-type syndrome around 10 days after ingesting cow colostrum. Commercial lamb and kid milk replacers are available for orphan rearing or to supplement lambs or kids from poor-producing mothers. Lambs and kids need to be fed 10% to 15% of their body weight divided into three to four feedings during the first few days after birth. Later, twice-a-day feeding is adequate. They should be offered hay and starter rations early, but milk should be the major energy source until they are 5 to 6 weeks old. If a lamb or kid is hypoglycemic and hypothermic, it is best to rewarm the animal before any oral therapy. During a hypothermic crisis, the lower esophageal sphincter relaxes, and milk or oral supplements may be regurgitated and aspirated unless the animal is alert and sternal. Rewarming when the core body temperature is low is best achieved by immersing the neonate in warm water (100° F to 105° F) while supporting the head.

Sometimes lambs sustain “mama trauma” in the maternity pens, so it is important that the pens be of adequate size for large ewes. Lambs are sound sleepers, and it is instinctive for the ewe to roust the lamb(s) by pawing. Vigorous pawing in a small pen may result in fractured limbs, fractured ribs, and/or pneumothorax in the lamb. Signs of trauma include lethargy, lameness, inability to rise, dyspnea, or sudden death in the lamb(s). Securing a corner of the pen and providing a heat source in that area attracts the lamb(s) away from the ewe to rest and provides safety from the ewe’s feet.

GASTROINTESTINAL SYSTEM

RESPIRATORY SYSTEM

MUSCULOSKELETAL SYSTEM

HEMOLYMPHATIC SYSTEM

REPRODUCTIVE SYSTEM/MAMMARY GLAND

NERVOUS SYSTEM

OPHTHALMIC SYSTEM

INTEGUMENTARY SYSTEM

BEHAVIOR

Goats tend to flock together in extended family groups and have strong hierarchic structure in the herd. Both males and females will establish social dominance in their respective groups through head-to-head combat. Since goats use their horns to advantage during fighting, it is best if all goats in a group either be horned or dehorned to prevent excessive bullying by horned goats.

When goats are threatened or upset, they will turn to face an intruder or stranger and make a characteristic sneezing noise (sheep have a similar response). Goats will orally investigate everything in their environment, so destructible items should be kept out of reach. They are agile and are excellent climbers often found in trees, on rafters, or on top of vehicles (Figure 22-30). A rock pile or other elevated area within the pen or pasture will provide recreation and help control hoof overgrowth. Goats are notorious for learning to open gates and thus may escape the enclosure or may get into excessive amounts of stored feed (grain overload). Since goats can climb and get caught in fencing, electric fencing is recommended for their safety.

Goats are adaptable worldwide because of their efficient browsing ability and effective use of relatively poor quality roughage. Goats and sheep are seasonally polyestrous in temperate climates, breeding primarily in the fall. Bucks develop a stronger odor during breeding (rut) and may become quite aggressive during this time.

Sheep have wide-angle vision and can see behind themselves without turning their heads. Solid fencing should be used when moving sheep because they respect solid barriers and are less apt to be distracted or spooked. When moving sheep, it is important to know that they move toward light and will follow other sheep because of the flocking instinct.

CARE OF THE NEONATE

Neonatal pigs have little fat store and therefore require supplemental heat during the first few weeks of life. During the first week, the temperature of the sleeping area should be 92° F to 95° F, the second week 89° F to 92° F, and the third week 86° F to 89° F. Colostrum intake soon after birth is important in this species. Adequate nutrition is also important since hypoglycemia can quickly develop in the undernourished piglet. Hypoglycemia may lead to a weakened piglet that is susceptible to a variety of diseases or crushing by the dam when she lies down. Frequent observation of the sow or gilt and the pigs will help determine if nursing behavior is normal. Piglets that are hungry will circle the dam and squeal weakly. In this case, the sow or gilt should be examined to determine if she has mastitis or some other disease that requires immediate treatment. Baby pigs raised in confinement need iron dextran injections at 3 days of age (Figure 22-31). Needle teeth should also be clipped at this time to prevent injury to the dam’s udder and to other piglets in the litter (Figure 22-32). Tails may also be docked at the same time to help prevent tail biting later, and castration may also be performed (Figure 22-33). These are common pig-processing techniques that are much less stressful to the pig if performed at a few days of age. If hypoglycemia develops, the piglet(s) may be treated with 5 to 10 cc of 5% dextrose injected by aseptic technique intraperitoneally. Pigs that are rejected, orphaned, or not receiving adequate nutrition by the mother may be supplemented with a milk replacer designed for pigs. Young pigs quickly learn to drink from shallow pans and therefore do not usually require bottle feeding, which can be labor intensive. These piglets can also be offered prestarter feed at an early age. Pigs are nosey by nature, and through exploring their environment, they learn to eat solid feed quickly. A homemade milk replacer that can be used to raise piglets (more appropriate for potbellied pigs) consists of 1 qt of whole cow’s milk, 1 oz of white corn syrup or honey, and 1 oz of cream or corn oil.

MULTISYSTEMIC DISEASES

GASTROINTESTINAL SYSTEM

RESPIRATORY SYSTEM

MUSCULOSKELETAL SYSTEM

Porcine stress syndrome (PSS) is also known as malignant hyperthermia (MH) or pale soft exudative pork (PSE). Susceptibility to PSS is caused by a single autosomal recessive gene, and disease is manifest only in pigs that are homozygous recessive for this gene. This defective gene is closely associated with desirable characteristics, such as good feed conversion and high percent lean. The gene for PSS has been identified in almost every breed of swine, but is especially prevalent in the Pietrain breed. Stress, halothane, and other anesthetics may precipitate the development of PSS. The severity of clinical signs is related to the degree of stress, and signs include muscle and tail tremors, dyspnea, alternating blanched and reddened areas of skin, elevated body temperature (hyperthermia), cyanosis, muscle rigidity, and death. At slaughter or on postmortem examination, the musculature is pale, soft, and watery. Susceptibility to stress can be diagnosed with a DNA probe test, which will identify both homozygous and heterozygous carriers. Once clinical signs develop, the affected animal may be treated by removing the stress, applying external cooling, and administration of dantrolene sodium, if available. It is more important to prevent this condition by genetic selection of breeding stock that is not stress susceptible.

REPRODUCTIVE SYSTEM

Agents responsible for abortion and reproductive failure in swine include PSR, brucellosis, PRRS, porcine parvovirus (PPV), and leptospirosis.

PPV is present in nearly 100% of swine herds worldwide. If the virus infects a male or nonpregnant female, the pig seroconverts and eliminates the virus with no clinical signs. If a pregnant female becomes infected, the virus crosses the placenta and infects rapidly dividing fetal cells. If the pregnancy is less than 30 days, the embryo is killed and resorbed by the dam. Between 30 and 70 days of gestation, the fetus is killed and mummified, and after 70 days of gestation, the fetus mounts an immune response and survives to term, although it may be born weak or dead. The only clinical signs of PPV are those of reproductive problems in pregnant sows or gilts. Mummies of different sizes, stillbirths, and live pigs may be present in the same litter. Abortions are not typical of parvovirus infection in swine. Since the virus is ubiquitous, a single positive titer is not useful in confirming a diagnosis of reproductive failure caused by PPV. Prevention may be achieved by natural exposure of gilts to sows before breeding. Natural infection usually results in lifelong immunity. Vaccines are available, but immunity only lasts 4 to 6 months, so vaccination must be repeated before each breeding. Vaccination may interfere with development of natural immunity.

Leptospira pomona and Bratislava are the primary serovars that are adapted to swine, although other serovars may incidentally infect pigs. The bacteria are shed through the urine and reproductive discharges of infected animals and enter susceptible animals through mucous membranes or broken skin. Once infected, a bacteremia develops, and the organism localizes and multiples in the kidney and in pregnant females may cross the placenta and infect and kill the fetuses. Aborted, weak, and stillborn pigs may be the only obvious clinical signs. Diagnostic tests include a demonstration of high antibody titers in the dam (interpret in light of vaccination status) or in fetal fluids, culture of the organism, darkfield microscopy of urine or fetal fluids, fluorescent antibody of fresh tissue, and PCR techniques. Treatment may be accomplished with the use of tetracycline in the feed or administration of parenteral tetracycline. Many monovalent and multivalent vaccines are available for the protection of breeding stock; however, the immunity is short lived, so animals should be vaccinated every 6 months at breeding.

NERVOUS SYSTEM

Salt poisoning, also known as sodium ion toxicosis or water deprivation, occurs in commercial and pet swine from an overconsumption of excess sodium (direct salt poisoning) or inadequate water intake (indirect salt poisoning) or possibly both. Water deprivation causes a hyperosmolarity of the CNS so that when water is consumed, the osmotic pressure draws water into the CNS causing cerebral edema. Affected pigs show signs of restlessness, pruritus, constipation, and thirst followed by depression, blindness, convulsions, and death. Salt toxicity is a well-recognized entity in commercial swine, but descriptions of medical treatment of affected animals is limited because it is usually not economically feasible to treat individual commercial pigs. Successful treatment of pet pigs has been reported. Treatment consists of slow rehydration with fluids that will gradually return sodium to a normal level. In one report, successful treatment of two potbellied pigs with salt toxicity was achieved using half-strength lactated Ringer’s solution in 2.5% dextrose.

BEHAVIOR

The pig’s normal response to fear is vocalization and attempts to escape. They are naturally curious and spend a great deal of time exploring their environment. The prehensile organ of the pig is the snout, and in general, they have a keen sense of smell. Pigs have poor eyesight, so with poor eyesight and a reliance on smell, pigs are reluctant to venture into areas with unusual odors and changes in light intensity. Once familiar with their surroundings, they begin to investigate by rooting with their snout, which may lead to destructive behavior. Co-mingling pigs, such as occurs at weaning, results in the reestablishment of hierarchy in newly mixed pigs. This reordering usually occurs within 12 to 24 hours with the dominant pig establishing itself first, followed by number two, three, and so on. Some changes of rank may occur within the middle members, but the top and bottom of the order remain fairly stable. The dominance hierarchy of swine is referred to as bidirectional, a subordinate pig sometimes directing antagonistic behavior toward a higher ranking pig; however, this does not affect the social status between individuals. In established hierarchies, the dominant pig assumes a recumbent position, and its belly is nuzzled by subordinates, possibly an allogrooming ritual. The best group size for socialization is not known for sure, but the order seems to become more complex when a group size is more than 20.

Abnormal behavior is more likely to develop because of stressful living conditions. An abnormal behavior may either be a new behavior or a normal behavior that has become misdirected or exaggerated. Abnormal behavior can be a valuable indicator of environmental (physical, climatic, or social) or managerial deficiencies. Tail biting begins as misdirected investigative behavior (harmless nibbling) at weaning that can escalate to vicious biting, an expression of predatory aggression, and appetite for blood. Tail biting can cause an ascending infection of the spinal cord or spinal abscesses and even hind limb paralysis and death. Contributing factors include stress of weaning (often begins at weaning), climatic stress, overcrowding, or an imbalanced diet. The behavior can be controlled by providing diversions, such as toys (bowling balls, inner tubes), for pigs to play within the pens. Commercial pigs in confinement have their tails docked to prevent this problem; however, tail docking may then lead to ear biting if the underlying problem is not corrected. Also, removing the “biter” often controls the problem within a group.

Ear biting and flank biting are different expressions of the same problem(s) that result in tail biting. In addition to the aforementioned reasons, ear biting may be initiated by fighting for social rank. Flank biting may begin by flank sucking that is misdirected nursing behavior (more likely to occur when piglets are weaned younger than 20 days) that escalates to varying levels of destructive behavior to the victim.

Aggression in the extreme may be an abnormal behavior. Some aggression in pigs is normal. In a group situation, such as within a litter, a pecking order is established by fighting. This begins as early as birth when a teat order is established. Since more milk is produced in the cranial mammary glands, the stronger, more assertive piglets will fight to claim these teats. This is the reason for trimming needle teeth shortly after birth to prevent serious injury to the piglets and to the sow’s udder. Once teat preference is established, that order remains until weaning. In older groups of pigs, if groups are mixed or a pig is added or removed, the pecking order must be reestablished, usually by fighting. Mature boars have well-developed tusks for slashing and will bite each other as a part of normal aggressive behavior. If strange boars are mixed, they will fight and may seriously injure each other. Boars raised together undergo a dominance procedure, but typically do not violently fight each other. Sows and weaned pigs will also fight, and even though they do not have tusks, they will bite. Sows and young pigs will also ram their heads against an opponent’s head or torso. Baby pigs are often observed play fighting in preparation for normal pecking order establishment later in life.

Pigs normally keep their sleeping and feeding areas clean from an early age. Poor manure habits or pen fouling may be indicative of environmental or management problems, such as overcrowding, a high ambient temperature, or inappropriate airflow pattern (resting area should be draft free). Lameness and diarrhea may contribute to the problem.

A dam’s aggression toward piglets (hysteria) or savaging of baby pigs is usually exhibited by gilts. These same gilts may be normal during subsequent farrowings. Possible causes of hysteria include stress resulting from the inability of the gilt to make a “nest,” human interference during farrowing, and perhaps genetic predisposition. Management of the condition includes removal of pigs as they are born and reintroducing the entire litter once parturition is complete because the initiation of nursing often calms the gilt.

POTBELLIED PIGS

CARE OF THE NEONATE AND NEONATAL DISEASES

Neonatal camelids are referred to as crias, and the newborn and its dam form a strong family bond (Figure 22-36). The newborn alpaca cria should weigh at least 12 lb at birth, and the normal llama cria should be greater than 15 lb; however, comparison with the average birth weight on any given farm may be of more significance. Crias are born with the eyelids open and the incisors erupted. The neonate is covered with an epidermal membrane that attaches at the mucocutaneous junctions, coronary bands, and the umbilicus. The camelid fetus is not surrounded by an amniotic membrane as occurs in other species, making the newborn much less likely to suffocate after birth. Camelid mothers do not lick the cria to dry it nor do they stimulate the baby to stand. The mother may nuzzle the cria and vocalize with a humming sound.

Following birth, crias should attempt to stand in 30 minutes and be successful by 60 minutes. Newborns should actively try to nurse the dam within the first hour and successfully nurse within 3 to 4 hours. If nursing has not occurred by 6 hours after birth, intervention is essential. Crias usually nurse three to four times per hour. During the first 3 days of life, the newborn may not gain any weight and may lose up to 1 lb; greater weight loss than this should be of concern. After the first few days, the cria should gain 0.5 lb per day for the first 2 weeks. Llama crias then continue to gain at the rate of 1 lb/day, and alpaca crias may gain 0.25 to 0.5 lb/day. The newborn should be alert and have clear eyes and erect ears. Typically, the body temperature is 101° F to 102° F; heart rate, 80 to 100 bpm; and respiratory rate, 10 to 30 breaths/min.

Camelids are obligate nasal breathers, so open-mouth breathing is considered abnormal and may be indicative of respiratory or congenital problems. As with other neonates, the newborn cria should be weighed, examined thoroughly, and the umbilicus dipped in disinfectant. Observation of nursing and assessment of passive transfer is also of great importance in neonatal care. It is not necessary to administer enemas to every neonate. Meconium should be passed within 18 to 24 hours after birth, and failure to do so, especially if the cria is straining, may warrant a gentle enema using 200 to 500 ml of warm water. Newborns should be carefully watched, especially during the first 48 hours of life. Crias that are considered “at risk” include premature crias, crias born to mothers with dystocia, newborns with congenital defects, crias that suffer excessive umbilical bleeding, crias born to the same mating that experienced problems in previous years, and crias that develop FPT. “At-risk” crias often show abnormalities in vital signs, labored respirations, weakness, depression, failure to nurse, failure to stand, and straining with failure to pass meconium.

There is considerable variation in gestation in alpacas and llamas (330 to 360 days), with some pregnancies lasting more than 1 year. This variation makes it difficult to determine prematurity based on length of gestation. In addition, in pasture breeding situations, undetected early embryonic death may be followed by another breeding several days later. Prematurity is not based entirely on gestational length. Signs of prematurity in the newborn are of more importance than time in utero. Low birth weight may be the most obvious sign, but premature crias also show signs, such as weakness and inability to stand or hold the head up to nurse. Affected crias also have excessive laxity of tendons and ligaments and may walk on their fetlocks. In addition, premature crias often have nonerect or curled ears as a result of immature cartilage in the ears (Figure 22-37), the hair coat is especially silky, and the rubbery covering of the toe persists for 1 to 2 days in premature babies (disappears in 6 to 12 hours in full-term crias). The incisors are not erupted in premature crias (Figure 22-38), and the mucous membranes are dark red from decreased oxygenation as a result of undeveloped lungs. Prematurity is life threatening and requires immediate and intensive therapy.

Once the condition of prematurity has been established, the cria should be provided supplemental heat and oxygen. Most premature crias are incapable of nursing the dam, so it is suggested that a warm plasma transfusion using camelid plasma (Triple J Farms, Redmond, Wash.) be administered. Following plasma transfusion, fluids, such as Normasol with 5% to 10% dextrose, can be given to meet any existing fluid deficits and prevent hypoglycemia. Premature crias are susceptible to infection, so administration of broad-spectrum antibiotics is usually initiated. In addition, thiamine and cimetidine are often given to promote neurologic development and prevent C3 ulcers, respectively. If the cria is strong enough to nurse, it should be fed milk at the rate of 10% to 12% of its body weight divided into four feedings a day. If the cria is incapable of nursing, tube feeding may be necessary via an orogastric tube (a stallion urinary catheter works well). Intensive care is continued until the cria matures appropriately or is capable of survival without additional support. Daily weights are helpful in assessing the health of the neonate and ensuring adequate oral nutrient intake.

Monitoring mucous membrane color, respiratory rate, and blood gases helps determine the point at which the cria can be weaned from oxygen supplementation. Other signs of maturation, such as eruption of the incisors and straightening of the ears, are important to assess. Any angular limb deformities may be addressed by application of light support splints; often these deformities improve as the neonate matures. The cria should be housed in close association or contact with the dam.

To prevent FPT, the newborn should be observed closely for the first 3 to 4 hours to make sure it nurses. It is desirable to get colostrum from the dam into the cria; however, if that is not possible, cow, goat, or sheep colostrum can be substituted. The cria should receive 20% of its body weight in colostrum in four to six feedings during the first 24 hours after birth. The use of commercial colostrum supplements or replacers should be avoided. It may be beneficial to feed colostrum to premature or sick crias for 3 to 4 days after birth. In the event the cria will not nurse, orogastric intubation should be performed to make certain that the cria receives adequate colostral immunity. Radial immunodiffusion is one of the most accurate tests used to check for passive transfer, but it is only useful if the cria received llama or alpaca colostrum, not cow, goat, or sheep colostrum. Sodium sulfite turbidity and total serum protein can be useful to access passive transfer status. These tests are most beneficial in crias that are from 24 hours to 7 days of age. If colostrum is not available, an IV plasma transfusion is strongly recommended. “At-risk” crias should be watched closely for any signs of septicemia for the first several months of life.

Orphaned crias may be bottle fed goat’s milk, lamb milk replacer, kid milk replacer, or whole cow’s milk. The cria should receive milk at 10% to 12% of its body weight per day. Initially, this amount can be divided into four to six feedings per day, but feedings can gradually be reduced to two to four feedings per day. Weighing the bottle-fed cria to document adequate weight gain is important. It is extremely important that orphans receive minimal human contact and are left with the herd at times other than feeding to prevent the development of “bezerk llama syndrome.”

Crias that do not nurse may need total parenteral nutrition (TPN). The recipe described for use in the foal (Smith) seems to work well for crias, and the TPN can be reduced incrementally as the cria begins to nurse on its own.

Congenital abnormalities are relatively common among camelids. This high prevalence is blamed on the narrow genetic pool available to breeders before importation of native South American camelids during the 1980s. Even with greater genetic diversity, congenital defects continue to plague breeders. Some common congenital defects include choanal atresia, atresia ani, wry face (maxillofacial dysgenesis), patent urachus, and cleft palate. Choanal atresia is the presence of a membranous or osseous separation of the nasal and pharyngeal cavities. Since camelids are obligate nasal breathers, the primary clinical sign in affected newborns is open-mouth breathing. Since this condition is probably hereditary and the prognosis for life is poor, euthanasia is recommended.

Diarrhea is an important cause of morbidity in neonatal camelids. Many factors may be involved in the cause of neonatal diarrhea, including management and nutritional factors and a variety of pathogens. The most common pathogens causing diarrhea in neonates are coronavirus, E. coli, Cryptosporidium spp., Giardia spp., and coccidia. If diarrhea in the young is not treated effectively, it may lead to the development of chronic diarrhea, which may ultimately result in chronic renal failure.

Coccidiosis is most frequently diagnosed in neonates and juveniles since adults are more resistant to infection as a result of their mature immune systems and prior exposure. Coccidiosis is typically associated with conditions of overcrowding and poor hygiene. The oocysts cause direct damage to the small intestinal epithelium resulting in diarrhea, enteritis, and sometimes straining. Chronic coccidiosis may cause nutrient malabsorption and subsequent poor growth in affected individuals. Sulfadimethoxine (Albon, Pfizer) dosed at 15 mg/kg orally twice daily for 5 days is an effective treatment for coccidiosis. Amprolium may also be used at the rate of 10 mg/kg orally once daily for 5 days. The correct dosing of amprolium is crucial because overdosing may produce clinical signs of polioencephalomalacia caused by thiamine deficiency. Ionophore antibiotics, such as monensin and salinomycin, which are commonly used to treat coccidiosis in cattle, are toxic to camelids and should therefore not be used in these species.

Diarrhea caused by E. coli often occurs in combination with neonatal septicemia secondary to FPT. Neonates are affected between 3 to 7 days of age and often exhibit profuse, watery diarrhea, lethargy, dehydration, and abdominal distention. Leukopenia with a degenerative left shift neutrophilia is often present in these crias. The treatment should include a good broad-spectrum antibiotic with gram-negative coverage along with fluid therapy. Sick camelids are often hypernatremic, so low-sodium IV fluids, such as 0.45% sodium chloride with 2.5% dextrose, are indicated.

Cryptosporidiosis (Cryptosporidium parvum) is a zoonotic disease that can cause severe and sometimes fatal diarrhea in neonates and immunocompromised individuals. The infection occurs by the fecal-oral route and may occur when contaminated feed or water are ingested. The diagnosis of cryptosporidiosis is accomplished by the examination of fecal smears using modified acid-fast stains. There is no specific treatment for cryptosporidiosis, so supportive therapy using IV fluids and/or TPN are important, especially since the disease results in malabsorption and maldigestion.

Giardiasis, also a zoonotic disease, primarily stems from contaminated water sources. The organism, which affects the small intestine causing villous atrophy, results in a malabsorptive diarrhea with dehydration and weight loss. Oral fenbendazole dosed at 50 mg/kg once daily for 5 days is an effective treatment for Giardia.

Salmonella spp. do not appear to be common causes of diarrhea in camelids.

Both rotavirus and coronavirus have been identified as causing diarrhea in neonatal camelids; however, of the two viruses, coronavirus appears to occur more commonly. Electron microscopy and fecal ELISA tests are the most useful for diagnosis of these viruses. There is no specific treatment for viral diarrhea, so supportive therapy, such as IV fluids, is useful. Monoclonal antibody vaccines, such as those available for oral use in calves and lambs, can be safely given to camelids on farms experiencing outbreaks of viral diarrhea, although the efficacy in these species is unknown.

Nematodes are capable of causing diarrhea in crias as young as 2 months of age because of the inherent lack of acquired resistance. Clinical signs include ill thrift, inappetence, anorexia, emaciation, and diarrhea. Fecal parasitology is useful in the diagnosis, and a 5-day course of oral fenbendazole at 20 mg/kg is usually effective.

Diarrhea in crias less than 7 days of age is likely due to nutritional factors in bottle-fed babies or gram-negative infections, especially in cases of inadequate colostrum ingestion. Viral diarrhea usually affects crias older than 7 days and is most often due to a coronavirus infection in the United States. Cryptosporidium and Giardia also tend to affect crias older than 7 days of age, and these infections are often due to overcrowding or sanitation problems on larger farms. Coccidiosis is unlikely to occur in crias less than 3 weeks of age, and it may be indicative of a herd problem. Diarrhea caused by GI parasites in crias less than 2 months of age is rare. It should be kept in mind that diarrhea may be multifactorial and can involve more than one pathogen. There are numerous diagnostic tests available to help determine the cause of neonatal diarrhea so that the clinician can initiate an appropriate treatment for affected individuals and control the spread of disease through the rest of the group.

RESTRAINT AND HANDLING OF CAMELIDS

Effective restraint requires knowledge of camelid behavior. Llamas and alpacas have been domesticated for thousands of years, and if they are accustomed to handling, they are docile and pleasant. Only rarely is an individual aggressive or a “spitter.” Camelid ear and tail position expresses important information. The ears of a content, unaroused animal are in a vertical position and turned slightly forward. In an alarmed animal, the ears are pointed forward. Varying degrees of aggressiveness are manifest by ears that are positioned from barely behind the vertical to flattened on the neck. The tail position also reflects the emotional state of the animal. In an unaroused camelid, the tail lies flat against the perineum. With alarm, the tail position rises to horizontal or as much as 45 degrees above horizontal. Aggressive behavior is displayed by the tail in a completely vertical position. An accurate reading of body language is important to prevent injury to the handler and the animal.

Llamas and alpacas are usually calm, but the most common behavioral response to annoyance is spitting of regurgitated stomach contents. Once a spitter is restrained, the head can be turned away from handlers to redirect ingesta, or a towel or rag that covers the mouth can be tucked into the nosepiece of a halter to discourage continued spitting. A muzzle that hooks onto the halter can also be used to prevent spitting. Camelids may kick and generally “cowkick,” although they can also kick directly backward. Biting is usually restricted to fighting between intact males, although llamas have been known to occasionally bite humans. Mature males have two upper and one lower canine teeth (“fighting teeth”) on each side of the mouth that are sharp. These teeth occasionally need to be blunted or cut short for the safety of other animals and human handlers.

Dam-raised male camelids are usually no more difficult to handle than females (in contrast with bulls, stallions, bucks, and rams); however, bottle-fed orphan males or neonates that receive too much human contact may imprint on humans creating a dangerous behavioral problem. An imprinted male treats a human as if it is another male and can therefore become quite aggressive, especially when the male reaches puberty. A number of persons have been seriously injured as a result of this behavioral problem.

It is always desirable to use the least amount of restraint necessary to perform a procedure. Many alpacas have been halter broken and can be restrained with the use of the halter. Untrained individuals are best controlled by pulling the head and neck close to the handler’s chest with one hand while the other hand rests on the top of the shoulders with slight pressure (Figure 22-39). As an alternative, the tail may be grasped and held upright by the second hand. Crias less than 20 kg (45 lb) may be lifted with one arm around the chest and the other arm supporting the abdomen in front of the rear legs, which has a calming influence on the cria and reduces struggling (Figure 22-40). Camelids can also be restrained in the kushed (sternal recumbency) position (Figure 22-41).

PHYSICAL EXAMINATION AND DIAGNOSTIC SAMPLING

The habitus of the animal should be evaluated before a complete physical examination. BCS should be completed (as described later under the hepatic lipidosis section) to access the overall nutritional state of the animal. The physical examination is similar to other ruminant species already described in this text. The normal temperature, heart rate, and respiratory rate for adult camelids are 99° F to 102.5° F, 60 to 90 bpm, and 10 to 30 breaths/min, respectively. The major fermentative process of camelid digestion takes place in compartment one (C-1) of the stomach. Since GI sounds are due to gas and liquid agitation, usually sounds are heard only on the left side. Palpation of gastric motility is not possible as in the ruminant, so a stethoscope is necessary to hear the subdued sounds. The normal gastric motility rate is three to four sounds per minute. A fleece-free abdominal area is located just cranial to the thigh muscles of the hind limb. To expose the area for auscultation, it is necessary to reach under the fleece in what would be the flank area in other species and lift it up.

Blood analysis is often necessary for diagnosis of many different diseases in camelids. Venipuncture and blood collection is not as simple in camelids as in most other domestic species. Camelids have evolved protective mechanisms to prevent exsanguination from bite wounds inflicted when intact males fight. In all areas of the neck, one must be extremely careful not to accidentally cannulate the carotid artery when performing venipuncture. Two primary sites for jugular venipuncture are low on the neck near the thoracic inlet or high near the ramus of the mandible (Figure 22-42). There is no jugular furrow in camelids, and the skin of the neck is quite thick, especially in the high neck location. It is neither necessary nor desirable to clip fiber for collecting a blood sample. It may take 1 year to 18 months for the fiber to regrow, and owners are usually dissatisfied with clipping of the animal. The anatomy and location of the jugular vein in the two locations listed above should be reviewed before attempting venipuncture in camelids.

Gastric intubation is accomplished via the oral cavity. The nasal cavity is narrow and precludes passage of anything but a small tube. A speculum made from a piece of rubber garden hose slightly larger than the stomach tube or a polyvinyl chloride pipe padded with adhesive tape makes an excellent guide. Once the tip of the tube is in the oropharynx, it can be rotated to encourage the camelid to swallow. If properly located in the esophagus, the tube can be palpated as it traverses the left ventral cervical region. The tube may then be advanced into C-1; however, if the fluid or medication is intended to bypass C-1, the tube should be left in the esophagus. This is particularly important when force feeding neonates because milk deposited into C-1 may remain there and ferment rather than be digested normally in C-3.

HEALTH MAINTENANCE

Camelids are routinely vaccinated for C. perfringens C and D and tetanus. Vaccination for these diseases may be started as early as 2 to 3 days of age and repeated at 2 to 3 weeks of age. A booster vaccination is then suggested at 6 and 12 months of age. From that point, annual vaccination is recommended. Other vaccines that can be used in camelids include rabies, equine rhinovirus, equine influenza, equine herpesvirus, West Nile virus, leptospirosis, and E. coli, depending on the herd location and potential threat of these diseases within a given herd.

Camelids may acquire a great variety of internal and external parasites, some of which are common to sheep, goats, cattle, and horses. Parasite control programs are most effective if customized to the individual farm since recommendations from other farms or other areas of the country are of little use. Parasite control strategies should be developed through a local veterinarian with the aid of fecal parasite egg counts. The sugar flotation method is recommended for fecal egg counting because this method is more precise than traditional flotation methods. Fecal egg counts should be performed periodically and include all animals if there are fewer than 10 animals on the farm or 10% of the herd if there are more than 10 animals in the herd. Fecal egg counts performed approximately 2 weeks after deworming medication has been administered are useful to evaluate the efficacy of the dewormer used and may aid in an evaluation of the development of anthelmintic resistance.

All camelids have canine teeth (“fighting teeth”) that are particularly well developed in the intact male. There are two maxillary canine teeth on each side and one mandibular tooth on each side. It is a common practice in North America to blunt these teeth in some manner to prevent serious lacerations of the ears, throat, limbs, and scrotum when males fight. The teeth can be shortened using Gigli wire or a rotary tool.

Foot trimming is a routine part of health maintenance in camelids. The camelid foot is unique with two digits on each foot. The plantar surface is covered with a soft, cornified layer of epithelium similar to the heel bulb in small ruminants. This structure is called the slipper. A small, non–weight-bearing nail is located at the extremity of each digit and is closely attached to P3 via the corium or sensitive lamina. The nail may require periodic trimming.

NERVOUS SYSTEM

METABOLIC CONDITIONS

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