Lameness and Reluctance to Walk

John K. House

Septic Arthritis

Septic arthritis may result from direct trauma or contamination of the joint, from extension of periarticular infection, or via hematogenous spread from another site.

Bacteria commonly isolated from septic joints in lambs include Streptococcus spp., coliforms, Arcanobacterium pyogenes, Erysipelothrix rhusiopathiae, and F necrophorum.

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.⁷⁵² Synovial fluid cytologic analysis is useful for the differentiation between infectious and noninfectious arthritis. Trauma is the chief differential. Lambs and kids with septic arthritis often fail to nurse and may present with significant weight loss. Typically polyarthritis caused by Mycoplasma spp. 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.⁷⁴⁹ 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 greater than 80%.⁷⁵³ Chlamydial inclusions may be found in Giemsa-stained smears of synovial cells and the organism isolated from joint fluid or plasma in early cases.⁷⁴⁹ Isolation of Mycoplasma spp. requires specific media (Hayflick 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.

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 impos- sible.⁷⁵⁴ Joint lavage may be facilitated via use of a rigid arthroscope or, in the case of simple joints (elbow and stifle), arthrotomy.⁷⁵⁵ 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 following systemic administration.^756-759 The distribution of trimethoprim/sulfadiazine, penicillin, oxytetracycline, and cefapirin in joints is not enhanced or reduced by inflammation.^756-758 Penicillin, trimethoprim, and sulfadiazine equilibrate in 0.5 to 1 hour, and oxytetracycline equilibrates in 4.5 to 6 hours.⁷⁵⁷ The subsequent decline in antibacterial drug concentration in synovial fluid parallels that in serum.⁷⁵⁶ Synovial inflammation accelerates distribution of antimicrobial drugs into joints⁷⁵⁷ but has little effect on the peak drug concentration achieved in synovial fluid.^756,757 The peak concentration of ampicillin in synovial fluid following a single intramuscular injection of ampicillin trihydrate at a dosage of 10 mg/kg is higher in normal and inflamed synovial fluid than in sera.⁷⁵⁹ There is a paucity of bovine-derived data regarding the distribution of the newer-generation antimicrobials into synovial fluid following systemic administration.

Noninfectious Lameness

Neonatal ruminants with nutritional myodegeneration often have a stiff, stilted gait. Lambs and kids may have difficulty nursing if they are unable to lift their 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.

Peripheral nerve injuries may occur secondary to dystocia, trauma, or injection site reactions, causing damage to peripheral nerves in the proximity of the injection site. The femoral nerve and brachial plexus are more commonly affected in calves. Femoral nerve damage is usually secondary to stretching the nerve during a “hip lock^,,dystocia. Clinical signs of femoral nerve paralysis include inability to extend the stifle and advance the limb and analgesia of the medial aspect of the limb down to the tarsus. Atrophy (“dished-out appearance”) of the quadriceps is noticeable in 7 to 10 days if there is complete tearing of the femoral nerve.⁷⁴⁷ Atrophy of the quadriceps predisposes to patella luxation. Complete or partial avulsion of the brachial plexus has also been observed in calves following dystocia.⁷⁶² The clinical presentation will depend on the severity of the injury. Clinical signs include abnormal positioning of the limb, abnormal locomotion, paresis, muscle atrophy, hyporeflexia, and sensory loss.⁷⁴⁷

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.

Differentials include concurrent infection of the navel (omphalophlebitis). Ultrasound may assist the diagnosis and determine the involvement of umbilical arteries or vein. Moist hairs around the umbilicus and visualization of fluid coming from the navel are diagnostic. A complete physical examination should be performed. If abnormalities are noted, serum IgG, complete blood cell 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 infection is one of the most common diseases in newborn calves, occurring in 1.3%⁷⁶³ to 29.9% of newborn calves.⁷⁶⁴

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 T. pyogenes, E. coli, and Proteus and Enterococcus spp. Herd management variables that influence the risk of umbilical infection include maternity pen hygiene, cleanliness of the newborn calf environment, effec­tiveness of passive transfer, and umbilical cord management.⁷⁶⁵

The urachus is the most commonly affected structure in calves, and the umbilical arteries are the least affected.⁷⁶⁶ 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 pol- lakiuria and dysuria. In other cases the umbilicus may be dry and larger in diameter than expected. In addition, neonates may have a completely normal-appearing, dry external navel and be severely ill from infection of the urachus, umbilical arteries, or umbilical vein. In a septic neonate 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 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.⁷⁶⁷ 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.⁷⁶⁸

Overt signs of infection are heat, swelling, purulent discharge, or 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.^769,770 Infection in more than one umbilical vessel in the neonate is common, 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 requires surgical removal of involved structures in addition to medical therapy.⁷⁶⁶ When omphalophlebitis extends into the liver, the umbilical vein may be marsupialized to facilitate drainage and flushing.⁷⁷¹ 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 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 the adult. In calves, the incidence of anemia (hemoglobin 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

Peripheral cyanosis results from increased peripheral extraction of oxygen from normally saturated blood or a significant decrease in the perfusion to an extremity. 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.

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, or 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.

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 due to left-to-right shunting of blood. Echocardiography may reveal an increased left atrial and left ventricular diastolic dimension or volume and hyperdynamic septal and left ventricular wall systolic motion (depending on the degree of right-to-left shunt).

Ventricular septal defect (VSD) produces a large, harsh, holosystolic murmur that is heard 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. It 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 characterized by icterus, hemoglobinuria, anemia, and intravascular hemolysis.¹¹²

Bleeding Disorders

Bleeding disorders are relatively uncommon in calves. In 2007 a bleeding disorder characterized by trilineage hypoplasia of bone marrow was recognized in Europe. Affected calves were 1 to 4 weeks of age. A strong association between the condition and vaccination of the dam with the bovine viral diarrhea virus vaccine Pregsure was established.⁷⁸² It is believed that vaccina­tion induced colostral alloantibody-mediated destruction of hematopoietic progenitor cells in bone marrow, causing cytopenias, including thrombocytopenia, and hence bleeding. The condition was subsequently recognized in the UK in 2009.⁷⁸² Differential diagnoses include thrombocytopenia secondary to septicemia and disseminated intravascular coagula­tion (DIC), Type II BVD infection, acute braken toxicity, and trichothecene mycotoxicosis.