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LAMENESS AND RELUCTANCE TO WALK

John K. House

SEPTIC ARTHRITIS

Septic arthritis may result from direct trauma or contamination of the joint, extension from periarticular infection, or hematogenous spread from another site. Systemic sites of infection include enteritis, pneumonia, and inflamed umbilical structures. FPT increases the risk of sepsis. Destruction of the epiphysis and extension of infection into the joint are common and may be primary in some cases, rather than resulting from a primary synovial membrane infection that spreads to the epiphysis or physis. The most common pathogens isolated from septic joints of neonatal calves are enteric organisms including E. coli and Salmonella species. Streptococcus species, Staphylococcus species, and A. pyogenes are less common isolates. A. pyogenes is the most frequently isolated organism from joints of older calves.540-542

Bacteria commonly isolated from septic joints in lambs include Streptococcus species, coliforms, A. pyogenes, Erysipelothrix rhusiopathiae, and F. necrophorum.455 Predisposing factors include poor docking hygiene and contaminated sheep dip. Sporadic outbreaks of polyarthritis in lambs, kids,30,543,544 and calves545 are associated with Chlamydia and Mycoplasma species infections. Chlamydia infections may occur in utero or postnatally; Mycoplasma infections often result from ingestion of Mycoplasma-contaminated milk.

Diagnosis of septic arthritis is based on the combination of clinical signs, radiographic examination, bacterial culture, and cytologic analysis of synovial fluid. A bacterium is isolated in only 60% of cases of septic arthritis in bovine medicine.546 Synovial fluid cytologic analysis is useful for the differentiation between infectious and noninfectious arthritis. Trauma is the chief differential diagnosis. Lambs and kids with septic arthritis often fail to nurse and may have significant weight loss. Typically, polyarthritis caused by Mycoplasma species and Chlamydia is associated with high fevers and respiratory and occasionally neurologic disease. High morbidity and mortality are common. Conjunctivitis is commonly observed with chlamydial infections.543 Cytologic findings consistent with septic arthritis include a synovial fluid total protein concentration greater than 4.5 g/dL, a nucleated cell count greater than 25,000 cells/mL, a polymorphonuclear cell count greater than 20,000 cells/mL, and a percentage of polymorphonuclear cells of greater than 80%.547 Chlamydial inclusions may be found in Giemsa-stained smears of synovial cells and the organism isolated from joint fluid or plasma in early cases.543 Isolation of Mycoplasma species requires specific media (Hayflick’s media) and microaerophilic conditions. Normal synovial fluid does not rule out septic physitis or osteomyelitis, because the infection may be in the physis or small tarsal bones.

Careful examination of high-quality radiographs is important for the detection of bone lysis indicating infection. Initial radiographs may be normal because the degree of damage is often not detectable for 10 to 14 days after initial infection occurs. Radiographic features of septic arthritis include soft-tissue swelling, widening or collapse of the joint space, osteoporosis, and osteosclerosis. Ultrasound may be used to confirm involvement of the joint and rule out periarticular or tenosynovial infection to avoid iatrogenic contamination of the joint during arthrocentesis. Joint distention and hyperechogenic fragments in the synovial fluid are suggestive of septic arthritis. Normal synovial fluid is anechoic.

Acute septic arthritis in neonatal ruminants may be treated effectively via joint lavage combined with systemic and local antimicrobial treatment. Typically, however, neonatal ruminants are presented with a chronic disease process. Treatment options include joint lavage or arthrotomy to remove destructive inflammatory products and long-term antimicrobial therapy. Joint lavage is rarely efficacious in the treatment of chronic septic arthritis in calves, as accumulation of fibrin and pocketing of purulent material often make adequate joint drainage impossible.548 Joint lavage may be facilitated via use of a rigid arthroscope or, in the case of simple joints (elbow and stifle), arthrotomy.549 Empirical antimicrobial therapy should include a gram-negative and gram-positive spectrum. Culture of synovial fluid facilitates antimicrobial selection.

Therapeutic synovial concentrations of penicillin, oxytetracycline, ampicillin, and cephapirin can be attained in inflamed and normal joints of calves after systemic administration.550-553 The distribution of trimethoprim-sulfadiazine, penicillin, oxytetracycline, and cephapirin in joints is not enhanced or reduced by inflammation.550-552 Penicillin, trimethoprim, and sulfadiazine equilibrate in 0.5 to 1 hour, and oxytetracycline in 4.5 to 6 hours.551 The subsequent decline in antibacterial drug concentration in synovial fluid parallels that in serum.550 Synovial inflammation accelerates distribution of antimicrobial drugs into joints551 but has little effect on the peak drug concentration achieved in synovial fluid.550,551 The peak concentration of ampicillin in synovial fluid after a single intramuscular injection of ampicillin trihydrate at a dose of 10 mg/kg is higher in normal and inflamed synovial fluid than in sera.553 There are few bovine-derived data regarding the distribution of the newer generation antimicrobials into synovial fluid after systemic administration. Studies in other species suggest that most classes of antibacterial drugs are capable of crossing the synovial membrane. Synovial tissue is very vascular and does not have a basement membrane. In humans, synovial fluid concentrations of most antibacterials generally average at least 60% to 70% of serum drug concentrations at the time of peak serum concentrations and frequently exceed those in serum immediately before the subsequent systemic dose in patients with septic arthritis.554 Antimicrobial dosing is targeted to achieve a peak antibacterial concentration that exceeds the MIC of the infecting organism by fivefold to tenfold.554 The duration of therapy is dependent on the antimicrobial sensitivity of the pathogen and the immune status of the patient; prolonged (4 to 8 weeks) antimicrobial therapy is commonly required.

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In a review of 81 cases of septic arthritis in cattle, a 72% recovery was achieved with a combination of surgical treatment (opening of the joint capsule; debridement; and excision of the synovium, infected cartilage, and bone), joint immobilization, and systemic antibiotic therapy. Of cattle treated conservatively with systemic and intraarticular antimicrobials, 43% recovered.555

NONINFECTIOUS LAMENESS

Neonatal ruminants that have nutritional myodegeneration often have a stiff, stilted gait. Lambs and kids may have difficulty nursing if they are unable to lift the head and may cry with pain when assisted to stand (see Chapter 42). Contracture of joints or tendons of the limbs produces difficulty in movement and predisposes to FPT by impeding the ability to adequately nurse. Degree of contracture varies from mild to severe and may be associated with scoliosis and/or torticollis. Conservative therapy consisting of splinting the front limbs to induce tendon laxity may be helpful. Calves with severe digital flexor tendon contractures often require surgical resection of one or both digital flexor tendons, followed by bandaging or casting and stall rest for 3 to 4 weeks.

UMBILICAL ENLARGEMENT

The umbilicus consists of three types of structures and undergoes functional and anatomic changes at birth. Two umbilical arteries connect internal iliac arteries to the placenta. These later regress and become the round ligaments of the bladder. One umbilical vein connecting the placenta to the liver and porta cava regresses to become the round ligament of the liver within the falciform ligament. The urachus connects the fetal bladder to the allantoic cavity.

PATENT URACHUS

Patent urachus is a persistence after birth of the tubular connection between the bladder and umbilicus. The urachus drains the bladder into the allantoic sac during gestation. Urine flow should gradually change, with some urine entering the amniotic sac through the urethra in later gestation. At birth, with umbilical cord rupture the urachus should be closed, and urine should be voided through the urethra. Neonates with a patent urachus may dribble urine from the urachus during or after urination or may simply have a constantly wet umbilical stump.

Differential diagnoses include concurrent infection of the navel (omphalophlebitis). Ultrasound may assist in making the diagnosis and determining the involvement of umbilical arteries or vein. Moist hairs around the umbilicus and the presence of fluid coming from the navel are diagnostic. A complete physical examination should be performed. If abnormalities are noted, serum IgG, complete blood count, and urinalysis are helpful for detecting susceptibility to infection and presence of systemic or urinary tract infection. Surgical resection of the urachus to the tip of the bladder is the treatment of choice. Associated arteries and veins should be ligated and removed if they are infected or necrotic. Merely ligating the exterior stump can trap organisms and cause infection.

OMPHALITIS

Omphalitis is inflammation of umbilical structures that may include the umbilical arteries (omphaloarteritis), umbilical vein (omphalophlebitis), urachus, or tissues immediately surrounding the umbilicus. Umbilical abscess or infection of any of the three components of the umbilicus may produce local infection or be a source of septicemia. The source of infection is most commonly the external environment, coupled with FPT. Bacteria isolated from calf umbilical cord remnant infection include A. pyogenes, E. coli, and Proteus and Enterococcus species. The urachus is the most commonly affected structure in calves, and the umbilical arteries the least.556 Omphalophlebitis may extend the length of the umbilical vein into the liver and result in liver abscessation.

When the umbilicus is enlarged and draining purulent material, infection is easily noted. When the urachus is fixed to the abdominal wall, calves are prone to cystitis and may show signs of pollakiuria and dysuria. In other cases the umbilicus may be dry and larger in diameter than expected. Some neonates may have a completely normal-appearing, dry external navel and be severely ill from infection of the urachus, umbilical arteries, or vein. In a neonate with sepsis without external signs of infection, involvement of the umbilicus can be difficult to determine. Abdominal palpation of the umbilical vein and arteries is a useful, simple, and effective means of assessing their size and of detecting pain associated with these structures. Inflamed structures may be identified by standing behind the neonate and pressing the hands together above the umbilicus. Ultrasound is also a useful ancillary diagnostic aid.557 Persistent dilation of the umbilical vein or arteries with a hypoechoic-to-echogenic fluid, intraluminal gas, and wall thickening are findings consistent with infection. In calves the urachus normally retracts up into the abdomen at birth, and ultrasonographic identification of a urachal remnant is abnormal.558

Overt signs of infection are heat, swelling, purulent discharge, and pain. Concurrent signs of systemic infection such as joint infection, pneumonia, diarrhea, meningitis, or uveitis may be noted. Calves with urachal abscesses may show signs of dysuria or pollakiuria.559,560 Infection in more than one umbilical vessel is common in the neonate, and urachal involvement is frequent. Umbilical abscessation that is walled off and does not involve deeper structures is a less severe problem and may be treated with drainage without surgical removal of the entire umbilicus.

Early treatment with antibiotics and supportive care may allow resolution before development of abscessation and distention of the urachus or the umbilical arteries and vein. Established infection usually necessitates surgical removal of involved structures in addition to medical therapy.556 When omphalophlebitis extends into the liver, the umbilical vein may be marsupialized to facilitate drainage and flushing.561 Prognosis is improved when adequate passive transfer of colostral immunoglobulins has occurred and when joints or other structures are not involved. Sequelae such as renal abscessation, joint or bone infection, peritonitis, and other complications described for septicemia may develop if therapy is started too late or is discontinued prematurely.

ANEMIA

Anemia in the neonate should be interpreted in the context of the realization that normal hematologic values of the neonate may vary from those of the adult. In calves the incidence of anemia (hemoglobin <10 g/dL) is quite high, ranging from 15% to 30% in many herds.562,563 The characteristics of the anemia include normocytosis, normochromia, and poikilocytosis. Anemia is reported to be secondary to iron deficiency.562,563 Potential causes are reduced amounts of iron in milk, poor placental transfer of iron, and decreased intestinal absorption. Anemic calves with poikilocytosis have similar levels of serum iron, total iron binding capacity, and marrow iron and plasma copper levels compared with normal calves.564 Anemic calves do not appear to have an increased incidence of disease or decreased growth rates.565 An overall higher plane of nutrition versus iron supplementation alone produces higher PCVs and hemoglobin levels.564 Calves less than 6 weeks of age have three types of hemoglobin in various amounts (adult 28%, fetal 40%, and neonatal 25%). The poikilocytosis may be a function of erythrocyte membrane defects or maturation transitions.564

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In addition to frank blood loss from an injury, diseases causing anemia in the neonate include blood loss caused by gastric ulcer, anemia secondary to bone marrow necrosis, and anemia of chronic disease associated with localized infections. Hemolytic anemia may be due to neonatal isoerythrolysis (NI) or non-NI immune-mediated hemolytic anemia.566 NI is caused by ingestion of maternal colostrum containing antibodies to one of the neonate’s blood group antigens. The dam may produce these antibodies after exposure to specific foreign blood group antigens during previous pregnancies or unmatched transfusions. It is uncommon in calves but has occurred after vaccination of pregnant cows against anaplasmosis or babesiosis. The presence of red cell antigens in the vaccine causes the production of antierythrocyte antibody, primarily against the A and F systems.567 Cows mated to bulls carrying these red cell antigens may have hemolytic disease develop in their A- and F-positive calves after ingestion of colostrum-containing alloantibodies.

Hemolytic disease processes produce signs of weakness, pale or jaundiced mucous membranes, fever, and depression. Blood loss produces weakness and pale mucous membranes. Intestinal parasitism does not normally lead to anemia during the neonatal period. Intravascular hemolysis may produce hemoglobinuria and hemoglobinemia. Icterus develops when the ability of the liver to conjugate bilirubin is exceeded. Mainly, indirect bilirubin is elevated. Anisocytosis is observed in responsive anemias. Nonspecific stimulation of bone marrow may produce a leukocytosis.

Anemia has also been reported in calves infected with BVD virus, secondary to bone marrow necrosis.568

Determination of the nature of the anemia may allow specific treatment. Blood transfusion may be indicated when anemia develops rapidly or PCV drops below 14%. Associated conditions such as metabolic acidosis and hypoglycemia should be corrected. Anemia of chronic disease requires correction of the primary disease condition.

FEVER

Differential diagnoses for fever in neonates include bacterial or viral infections, excitement, seizures with subsequent generation of heat by muscular overactivity, and environmentally induced hyperthermia. Fever is an unreliable indicator of sepsis in neonatal calves.569 Neonates with sepsis often have a normal or subnormal temperature. Older ruminants with localized infection such as in joints or bone are more likely to have fever. Fever may be beneficial. The need to administer antipyretics to the febrile neonate is controversial. Body temperatures lower than 40.8° C (105.4° F) are not considered detrimental unless they are associated with heat stroke or seizures,570 in which case cooling and antipyretics are indicated. Because many antipyretics are antiprostaglandins that can cause deleterious gastrointestinal and renal effects, these agents should be used judiciously. Correction of the initiating cause and maintenance of fluid balance are also important.

CYANOSIS

Cyanosis is the purple-blue coloration observed on mucous membranes or skin caused by reduced or poorly oxygenated hemoglobin in blood.571 Cyanosis may be caused by congenital heart disease, respiratory impairment, or any circulatory condition producing a right-to-left shunt (Box 20-4). The degree of cyanosis depends on the arterial oxygen saturation, hemoglobin concentration, pH, peripheral circulation, and temperature of the neonate.571 Shock and hypothermia are important causes of peripheral cyanosis. The affinity of hemoglobin for oxygen is reflected in the standard oxyhemoglobin dissociation curve. This curve is similar for neonates but is affected by the amount of 2,3-diphosphoglycerate (DPG) in the erythrocyte. Calves’ erythrocytes have higher levels of 2,3-DPG, but the higher levels do not affect the affinity of hemoglobin for oxygen. A separate fetal hemoglobin exists in calves to increase affinity for oxygen.572 Severe hypothermia and acidosis cause the oxygen dissociation curve to shift to the right and therefore contribute to tissue hypoxia. Cyanosis can be either central or peripheral.571 Peripheral cyanosis results from increased peripheral extraction of oxygen from normally saturated blood or a significant decrease in the perfusion to an extremity.571 In the neonate, causes include septic shock and severe hypothermia. Central cyanosis is more common in neonates and is related to congenital heart disease that causes right-to-left shunting or severe respiratory conditions that result in hypoxia. Examination and clinical pathologic evaluation for metabolic causes of cyanosis, hypothermia, and cardiac abnormalities should be conducted. History, medication use, auscultation, thoracic radiographs, and arterial blood gases are useful in determining the degree of respiratory component to cyanosis. Echocardiography may be required for identification of cardiac anomalies.

Box 20-4 Causes of Cyanosis

Cardiovascular Origin

Tetralogy of Fallot
Tricuspid atresia
Truncus arteriosus
Pentalogy of Fallot
Double outlet right ventricle
Single ventricle
Eisenmenger complex
Ventricular septal defect
Patent ductus arteriosus

Respiratory Causes

Alveolar hypoventilation
Drug-induced central nervous system (CNS) depression
CNS trauma or hemorrhage
Hypoglycemia or hypocalcemia
Altered neurologic function of spinal nerves (of respiratory muscles)
Thoracic cage abnormalities: pneumothorax, fractured ribs
Diaphragmatic hernia
Upper airway obstruction
Restrictive pleural space disorders: hemothorax, pleuritis
Hypoplastic lung

Impaired Diffusion

Pulmonary: pneumonia, edema, atelectasis
Shunting
Anatomic (congenital heart defects)
Pathologic: pulmonary hypertension
Ventilation-perfusion mismatch
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HEART MURMUR

Heart murmurs in the neonate may be heard normally before physiologic closing of the ductus arteriosus during the first 1 to 5 days of life. Other causes of murmurs include congenital anomalies, severe anemia, and infectious valvular disease. Physical examination for other signs of heart disease helps determine the severity of the murmur. Jugular pulse, weak or irregular arterial pulse, and palpable thrill indicate a serious condition. Dyspnea, cyanosis, tachypnea, and failure to gain weight are common signs of congenital heart disease in calves. Timing and location of the heart murmur should be determined. Thoracic radiography may aid in determining heart size and in detecting pulmonary edema or distended pulmonary vessels. Echocardiography may reveal atrial or ventricular enlargement, thickened ventricular walls, anomalous orientations of outflow tracts, or ventricular septal defects (VSDs).

Patent ductus arteriosus (PDA) produces a continuous murmur localized over the left heart base. The diastolic component may not be heard with auscultation over other parts of the heart. As pulmonary hypertension develops, the murmur is shortened to a holosystolic type with normal arterial pulse. Large shunting of blood produces a bounding arterial pulse caused by wide fluctuations of systolic and diastolic pressures. Radiographs may reveal an enlarged heart with increased vascularity as a result of left-to-right shunting of blood. Echocardiography may reveal increased left atrial and left ventricular diastolic dimension/volume and hyperdynamic septal and left ventricular wall systolic motion (depending on the degree of right-to-left shunt).

VSD produces a large, harsh, holosystolic murmur that is loudest on the right cranial region of the thorax and is softer over the left heart base. Radiography may reveal heart size increase, left atrial enlargement, and dilated pulmonary vasculature. Two-dimensional echocardiography may show aortic and septal discontinuity. Injection of saline bubbles into the left ventricle and observation of bubbles in the right atrium or ventricle document a left-to-right shunting of blood. Tetralogy of Fallot or other types of complex malformations often produce loud murmurs and are associated with cyanosis, weakness, fatigue, and stunted growth. Tetralogy of Fallot produces a systolic ejection murmur heard at the left heart base. Echocardiography may reveal a thickened right ventricular wall, septal echo dropout in the area of the VSD, rightward displacement of the aortic root, and an abnormal pulmonary outflow region. Saline injection into the jugular vein demonstrates right-to-left flow from the right ventricle to the left ventricle or the aorta.

ICTERUS

Icterus is a relatively uncommon finding in neonates that may be observed with sepsis, anorexia, liver disease, and hemolytic anemia. Liver disease in the neonate may be caused by exposure to hepatotoxins or sepsis-producing bacterial hepatitis, or it may be secondary to hypoxia. C. perfringens type A has been implicated in an enterotoxemic condition in nursing lambs, kids, and calves that is characterized by icterus, hemoglobinuria, anemia, and intravascular hemolysis.45

FAILURE TO THRIVE: CACHEXIA AND WEAK CALF SYNDROME

John Maas

Neonates that are born weak or fail to grow as anticipated pose important problems. In the foal, twins, prematurity, hypothyroidism, and congenital heart or other organ defects may produce failure to thrive. Infections acquired shortly after birth that produce chronic pneumonia, nephritis, endocarditis, arthritis, or gastric ulcers are a cause of morbidity in the neonatal period.

In calves the weak calf syndrome has been reproduced by feeding low-protein diets to prepartum cows that subsequently calved in environments in which the temperature was well below the thermoneutral zone for calves.573 The dietary recommendation for crude protein intake for third-trimester pregnant cows and heifers is 0.9 kg (2 lb) of total crude protein per day. This is particularly important for heifers and cows calving early in the spring calving season, when temperatures well below freezing can occur. Cold rains also can produce the hypothermic conditions that aid in precipitating this syndrome.

Cows weighing 450 kg (1000 lb) therefore need to consume 9.9 kg (20 lb) dry matter of good- to excellent-quality hay that is 10% crude protein or more. A quadratic equation has been developed to predict crude protein (CP) intake of the dams if their serum total proteins, urea nitrogen, and creatinine are known.574 This equation predicts the daily crude protein intake on a continuing basis.


image


where BUN is serum urea nitrogen (mg/dL), creat is serum creatinine (mg/dL), and TP is serum total protein (g/dL).

Also, the use of this formula could predict CP intake for pregnant heifers and pregnant cows. This relationship may prove to have important clinical applications when weak calf syndrome or protein-calorie malnutrition is suspected and the gestation diet of the dams is not available for analysis (as under some range conditions). Supplements such as molasses licks that contain urea may tend to overestimate CP intake.575

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