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Septicemia is a systemic disease involving the presence and persistence of bacteria or their toxins in the blood.
Etiology and Pathogenesis
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The predominant bacteria involved in neonatal foal septicemia are the gram-negative organisms Escherichia coli , Klebsiella spp , Enterobacter spp , Actinobacillus spp , and Pseudomonas spp .
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About 50% of infections also involve gram-positive bacteria, with Streptococcus spp being the most common isolates.
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Anaerobic pathogens are involved in 30% of cases.
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The routes of entry for these bacteria include the placenta, umbilicus, lungs, and GI tract.
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Endotoxins stimulate macrophages to release an array of cytokines (eg, IL-6, IL-1, TNF-α) and activate pro-inflammatory enzymes (eg, phospholipase A2).
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Bacterial infection accounts for nearly one third of all foal mortality. Septicemia is the second most common problem of equine neonates, second only to failure of passive transfer of maternal antibodies.
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Certain immunologic and management factors predispose foals to septicemia. Although foals can respond immunologically in utero to bacterial or viral infections, their ability to do so is less than that of adults.
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The major risk factor for septicemia in foals is failure to receive an adequate quality and quantity of colostral antibodies.
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Other factors that influence disease incidence include unsanitary environmental conditions, gestational age of the foal (prematurity), health and condition of the dam, difficulty of parturition, and the presence of new pathogens in the environment against which the mare has no antibodies.
Clinical Findings
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Clinical signs largely depend on the stage of the animal’s illness and the primary body systems involved.
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Frequently affected organ systems include the umbilical remnants, CNS, respiratory, cardiovascular, musculoskeletal, renal, ophthalmic, hepatobiliary, and GI organs.
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Foals in the early stages of sepsis display some degree of depression and lethargy and may lie down more than usual.
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The mare’s udder is often distended with milk, indicating that the foal is not nursing with normal frequency.
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In the advanced stage of illness (septic shock), foals are severely depressed, recumbent, dehydrated, and tachycardic.
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The mucous membranes are muddy, and hypotension, which manifests clinically as cold extremities, thready pulse, and poor capillary refill time, is evident.
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Foals may be hyper- or hypothermic. In septicemia, bacteria spread hematogenously to various organs, such as the lungs, intestines, eyes, CNS, bones, and joints.
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The foal may show evidence of single or multiple organ dysfunction. Sepsis can manifest as respiratory distress, pneumonia, diarrhea, uveitis, meningitis, osteomyelitis, or septic arthritis.
Diagnosis
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Depending on the specific organ systems involved, an umbilical, abdominal, and synovial ultrasound examination; arterial blood gas analysis; arthrocentesis; cerebrospinal centesis; and chest, abdominal, and distal limb radiographs may be indicated. Advanced diagnostic imaging techniques (eg, computed tomography of the distal limbs) may further serve as a prognostic aid.
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Septic foals are often neutropenic with a high ratio of band to segmented neutrophils.
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The neutrophils may exhibit toxic changes, which are highly suggestive of sepsis. Foals <24 hr old are often hypoglycemic.
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Fibrinogen levels >600 mg/dL in a foal <24 hr old is indicative of an in utero infection.
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Other chemistry abnormalities that may be evident include azotemia due to inadequate renal perfusion and increased bilirubin secondary to endotoxin damage to the liver.
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A high anion gap (>20 mEq/L), hypoxemia, hypercapnia, and a mixed respiratory and metabolic acidosis may be found on arterial blood gas analysis.
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Because of the high correlation between failure of passive transfer of antibodies and septicemia, serum IgG levels should be measured in any questionably sick equine neonate. IgG levels <200 mg/dL indicate complete failure of passive transfer of maternal antibodies. IgG levels >800 mg/dL are optimal.
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A definitive diagnosis of neonatal sepsis is based on clinical signs, laboratory data, and evidence of failure of passive antibody transfer. These data can be combined to determine the animal’s sepsis score, which helps synthesize laboratory results into a coherent whole.
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A positive blood culture also correlates to sepsis, but a negative culture does not rule out the possibility of infection.
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Differential diagnoses include hypoxic ischemic encephalopathy (Hypoxic Ischemic Encephalopathy: Introduction), hypoglycemia, hypothermia, neonatal isoerythrolysis (Hemolytic Anemia), white muscle disease (Nutritional Myopathy of Calves and Lambs), prematurity, neonatal pneumonia, and uroperitoneum (Uroperitoneum in Foals).
Treatment
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Foals suspected of being septic should be placed on broad-spectrum antibiotics active against both gram-positive and gram-negative organisms.
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Penicillin (22,000 IU/kg, IV, qid) in combination with amikacin sulfate (20-25 mg/kg, IV, sid) provides good initial coverage until culture results are available.
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Metronidazole (10-15 mg/kg, PO or IV, tid) may be necessary if an anaerobic infection (eg, Clostridium ) is suspected.
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A third- generation cephalosporin (eg, ceftiofur, 4.4-6 mg/kg, IV, bid-qid) may be used as a broad-spectrum agent in patients with compromised renal function.
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In all cases of neonatal sepsis, immunologic support, in the form of IV plasma transfusions (1-2 L), to raise the IgG levels to >800 mg/dL is important.
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Effective IV fluid therapy is needed to combat endotoxic shock.
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Foals may require 100 mL/kg/day of maintenance therapy using polyionic isotonic crystalloid fluids (eg, lactated Ringer’s solution) after fluids have been administered for shock. Because many foals are hypoglycemic, dextrose should be added to make a 2.5-5% dextrose solution.
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Isotonic bicarbonate solution may be given to help correct moderate to severe metabolic acidosis, but can worsen respiratory acidosis.
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In these cases, mechanical ventilation should be used to decrease PaCO2 before giving bicarbonate.
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Treatment with hyperimmune antiendotoxin serum should be considered in patients with endotoxemia.
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Antiprostaglandin drugs counteract several of the clinical and hemodynamic changes associated with endotoxemia and septic shock.
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Low doses of flunixin meglumine (0.25 mg/kg, IV, tid) may help reduce signs of endotoxemia.
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Additionally, administration of low doses of polymyxin B (6,000 IU/kg, diluted in 300-500 mL of saline, slow IV) is an investigational treatment used to neutralize systemic endotoxin.
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Because sepsis creates a catabolic state in the foal, nutritional support is important.
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If the foal is not nursing adequately, it should be fed mare’s milk or a milk substitute at 15-25% of its body weight over each 24-hr period. An indwelling nasogastric tube should be placed in foals with a decreased suckle reflex.
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Parenteral nutrition may also be helpful to provide adequate nutrients.
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Administration of gastric protectants (eg, ranitidine, cimetidine, omeprazole) has been proposed as an adjunct therapy in sick neonates.
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System-specific therapy includes lavaging septic joints with sterile fluids and providing nasal oxygen (2-10 L/min) or ventilation for foals with septic pneumonia.
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Corneal ulceration may be treated with low doses of topical atropine (although it may cause ileus), NSAID, and broad-spectrum topical antimicrobials. Entropion generally requires mattress sutures of the lower eyelid.
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Surgical removal of infected umbilical remnants may be indicated.
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Recovery from neonatal sepsis depends on the severity and manifestation of the infection.
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Current survival rates are 50-65% in referral centers. A minimum of 1-4 wk of intensive care should be expected.
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Early recognition and intensive treatment of neonatal sepsis improves the outcome.
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If the foal survives the initial problems, it has the potential of becoming a healthy and useful adult.
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