10 Equine Neonatal Septicemia NOTES

Equine Neonatal Septicemia

• Sepsis or septicemia is a systemic inflammatory response caused by circulating microorganisms or their products.
• Systemic inflammatory response syndrome (SIRS) is a systemic response with alterations in body temperature, heart rate, respiratory rate, and leukogram parameters (2 out of 4).
• SIRS causes the clinical signs seen in septic foals.
• Bacteremia is the presence of viable circulating bacteria.

Neonatal Septicemia

• A major cause of mortality and morbidity in equine neonates, especially in foals less than 7 days old.
• Maternal factors such as placentitis or illness can lead to in utero infection.
• Fetal factors include gestational age/length, dystocia, or premature placental separation.
• Farm management factors include hygiene, stocking density, and vaccination and deworming protocols.
• Failure of transfer of passive immunity (FTPI) can be due to maternal factors like loss of colostrum or poor quality colostrum, or foal factors like malabsorption or inability to suckle/stand.
• Foals typically need 1 L of good quality colostrum (SG >1.060, Ig >3000mg/dl).
• Colostrum is administered via nasoesophageal tube if less than 6-12 hours of age or IV plasma if older than 12 hours (1-2 L).
• Primary immunodeficiency can result in post-natal infection.
• Routes of infection include:
  • In utero
  • Post-natal, via umbilical remnants, gastrointestinal tract (where foals have little discrimination between maternal immunoglobulins and other macromolecules due to an "open" gut, not Fc-receptor-mediated), or respiratory tract
• Gram-negative bacteria such as E. coli and Salmonella are the most common causative organisms.

Pathophysiology and Clinical Signs

• Pathogen exposure leads to bacteremia, causing clinical signs of SIRS and seeding different organ systems, resulting in sequelae.

• Clinical signs include decreased milk intake, lethargy, depression, recumbency, maternal disinterest, dehydration, pyrexia, or hypothermia.

• Specific foci of infection can cause diarrhea, uveitis, joint effusion, lameness, physeal swelling, respiratory distress or disease, seizures, subcutaneous abscesses, patent urachus, or omphalitis.

• Examination should include the foal, mare to evaluate for maternal illness and udder fill, and the placenta if available.

• Physical exam findings include:

  • Dehydration
  • Tachycardia
  • Tachypnea
  • Pyrexia or hypothermia
  • Hyperemia/injection/petechiae of mucous membranes, sclera, inner pinna, coronary bands
  • Rapid or delayed CRT
  • Signs of hypovolemia (hypothermia, poor peripheral pulses, cool extremities, decreased/absent urine output)
  • Decreased borborygmi due to hypovolemia or dehydration
  • Abnormalities consistent with specific foci of infection/sequelae.

Diagnosis

• Diagnosis is based on historical information, clinical signs, and physical exam findings.

• Clinicopathologic findings include:

  • Leukopenia characterized by neutropenia, left shift, and toxic changes to neutrophils
  • Hyperfibrinogenemia suggests in utero infection if present within the first 1-2 days of life
  • Elevated serum amyloid A (SAA)
  • Hypoglycemia due to decreased gluconeogenesis

• Further findings include:

  • Azotemia due to prerenal dehydration, renal effects with SIRS, or post-renal issues from placental insufficiency
  • Acidosis and hyperlactatemia with dehydration, hypovolemia, and potential hypoxemia
  • Coagulopathies (DIC, thrombocytopenia, decreased antithrombin III, prolonged PT and APTT, elevated FDP and D-dimers)

• Blood culture (aerobic and anaerobic) is the gold standard for diagnosis, directing antimicrobial therapy and identifying resistance.

• Blood should be collected after sterile preparation of a large vein (jugular, cephalic, or saphenous) or immediately after sterile catheter placement and put in blood culture media.

• Blood cultures have delayed results with low sensitivity due to prior antimicrobial therapy or low bacterial numbers, so treatment should begin before results are available.

• A sepsis score >12 predicts sepsis. The scoring system has 93% sensitivity and 88% specificity.

Treatment

• Antimicrobial therapy and provide broad-spectrum coverage against gram-negative organisms.
  • Typical choices are aminoglycosides plus beta-lactams, such as amikacin (25 mg/kg IV/IM q24h) with penicillin (44,000 IU/kg IV q6h), or ceftiofur sodium (5-10 mg/kg IV/IM q12h).
  • Note the monitoring of renal status when aminoglycosides are in use
  • Duration of treatment should be at least 2 weeks, or 4 weeks if there are localizing signs of infection/sequelae.
• Additional treatments:
  • Anti-endotoxin therapy: flunixin, polymyxin B, plasma, pentoxifylline.
  • Cardiovascular support: crystalloids for resuscitation (100-120 ml/kg/day in foals vs. 60 ml/kg/day in adults) and colloids for FTPI, oncotic support, coagulation abnormalities, and anti-endotoxin effects.
  • Gastric ulcer prophylaxis.
  • Nutritional support: enteral which is preferred (10% of body weight per day split into multiple feedings to start, then 25% of body weight per day split into many feedings) or parenteral nutrition if enteral is not tolerated.
  • Caloric requirements: healthy foals is 100-150 kcal/kg/day, but for sick foals is 50 kcal/kg/day. Padding/bedding is important for recumbent foals to prevent decubital ulcers, perform recumbency changes and attempts to help stand every 2-4 hours. Closely monitor for corneal ulcers, provide thermoregulation as needed, and closely monitor urination and defecation.

Sequelae and Prognosis

• Additional diagnostics and treatments depend on CS and PE findings when additional foci of infection are suspected, or presentation with localized infections warrant sepsis examination.

• Respiratory infection is a common sequela, with the incidence being 28-50%.

  • Respiratory infection routes can be in utero, meconium/other aspiration, or hematogenous spread
  • Diagnostics include respiratory exam, thoracic ultrasound and radiographs, and arterial blood gas. It can be treated with systemic antibiotics, oxygen, or mechanical ventilation.

• Diarrhea and enteritis are common, with an incidence of 16-38%. 50% of diarrheic foals are bacteremic, requiring diarrhea diagnostics and treatment

• Omphalitis results from a different route of infection that leads to sepsis and is a continuous source of bacterial shedding and is diagnosed with external signs or serial ultrasonographic exams.

• Additional sequelae can include:

  • Patent urachus and uroperitoneum from necrosis of the urachus and bladder tip.
  • Meningitis- uncommon with clinical signs include seizures, somnolence, hyperesthesia, and neck pain/decreased motion. Diagnosed with CSF tap and analysis and treated with third or fourth-generation cephalosporins.
  • Septic arthritis and osteomyelitis can take 8-24 hours after bacteria colonize. Palpation is extremely important. DX with synovial fluid analysis and radiographs.

• Survival rates for neonatal septicemia are around 45-55%, ranging from 32% to 72%.

Prevention of Neonatal Septicemia

• Maintain a clean foaling environment, cleaning mares and stalls daily.
• Reduce potential bacterial load with udder cleaning prior to parturition.
• Attend foaling to assist if needed and prevent sequelae to dystocia.
• Ensure GI intake of good quality colostrum and confirm adequate transfer of passive immunity and that umbilical care is appropriate.
• Monitor foals closely and treat suspect foals quickly.

Neonatal Encephalopathy

• Can also be called Neonatal maladjustment syndrome, hypoxic-ischemic encephalopathy or "dummy foal".
• Encephalopathy pathophysiology involves neurologic manifestations for hypoxic-ischemic syndrome (HIS) or perinatal asphyxia syndrome (PAS).
  • Reduced oxygen delivery to neuronal cells in CNS leads to neuronal injury and cerebral edema, typically reversible.
  • Altered concentrations of neurosteroids
    • Plasma progestagens that keep fetus quiescent in utero and inflammation also play a role
• Risk factors:
  • Maternal illness leading to hypoxemia
  • Placentitis
  • Placental insufficiency
  • Premature placental separation
  • Dystocia
  • Cesarean section
  • Induced parturition; however, some cases lack an identified risk factor
• Clinical signs can be delayed (12-24 hours) or present at birth: generalized weakness, somnolence, lack of interest in dam, weak tongue, dysphagia, bizarre vocalization, head pressing, cortical blindness, recumbency, seizures, other organ involvement (GI and renal), and the severity varies.
• Diagnosis: consistent clinical signs and history of potential insult.
• Treatment:
  • Maintain hydration and blood glucose
  • Control neurologic signs with mannitol (to reduce cerebral edema if no hemorrhage/trauma) and diazepam/phenobarbital (to control seizures).
  • Use anti-inflammatories and free radical scavengers (flunixin, DMSO, vitamin E, magnesium).
  • Administer oxygen if needed
• Prognosis in most foals is a response to treatment within 3-5 days
  • Survival without complications is around 75%
  • The prognosis is poor for foals showing clinical signs at birth.

Neonatal Isoerythrolysis

• Destruction of a foal’s RBCs by maternal alloantibodies acquired from colostrum after ingesting colostrum with anti-RBC antibodies
  • Sire and dam have different RBC antigens, with the foal inheriting the RBC antigen from the sire.
  • Dam is previously sensitized to that RBC antigen
    • The most common cause is a previous pregnancy (multiparous mare)
    • Less common causes are blood transfusions and transplacental contamination
  • Coated RBCs are removed through the reticuloendothelial system or destroyed through complement activation.
• Commonly implicated RBC antigens include Aa and Qa.
• Donkey Factor is also implicated in mule pregnancies
• Clinical signs and PE findings:
  • Adequate transfer of passive immunity
  • Signs develop around 24-36 hours of age.
• Progressive lethargy and weakness with pale mucous membranes followed by icterus, tachypnea, tachycardia, and seizure-like activity.
• Diagnosis:
  • Anemia (severe, autoagglutination gross or microscopic).
    • Hyperbilirubinemia (unconjugated/indirect).
  • Possible thrombocytopenia.
  • Coomb's test/RBC surface antibody testing.
• Treatment: reduce stress, administer IV fluids.
  • If >24 hours old, milk restriction is not required or necessary.
  • Transfusion if anemia is severe
    • May use washed maternal RBCs if decompensation is imminent
    • Cross-matched whole blood transfusion is also common

Prevention

• Prevention includes screening blood type and for anti-RBC antibodies in serum of mare prior to parturition Perform a jaundice foal agglutination test prior to allowing colostrum consumption.
• Withhold colostrum if either is positive or foal lacks required antibody titer
  • Supply foal with an alternative Ig colostrum or plasma.