Septicemia and infection in new born animals (calves, kids and lambs)

Septicemia and infection

Septicemia and focal infection are major causes of morbidity and mortality in neonatal foals and calves.

Predisposing causes:

(1) FPT (Failure of passive transfer of colostrum immunoglobins).

(2) Unsanitary management.

Etiology:

Possible causes of neonatal septicemia

Calves	Lambs & Kids	Foals
E.coli Salmonella spp. Listeria monocytogenes Pasteurella spp. Streptococcus spp. Pneumococcus spp	E. coli Salmonella spp. Listeria monocytogenes Erysipelas insidiosa.	E.coli ActinobaciUus equuli Salmonella abortivoequina Salmonella typhimurium Streptococcus pyogenes Listeria monocytogenes

 

Possible causes of acute neonatal diarrhoea & septicemia

Calves	Lambs & Kids	Foals
E.coli* Rota and Corona viruses Cryptosporidium Salmonella sp. Eimeria sp. * * Cl. perfringens type C	Coronavirus Cryptosporidium Cl. perfringens type C Rotavirus Caprine herpesvirus	Salmonella spp. Eimeria spp. Foal-heat diarrhoea  Rotavirus Cl. perfringens type B

 

* Enteropathogenic & enterotoxigenic form

** Calves at least 3 weeks of age

Pathogenesis:

Most neonatal infections are caused by genital tract or skin infection, or environmental pollution.

(1) Uterine infections may ascend from the vagina or hematogenous spread or spread directly from the uterine wall so that the clinical signs occur during the first 24 hours of life.

(2) Infections acquired during delivery usually occur in stressed foals by meconium-contaminated amniotic fluid or a meconium-stained foal through the respiratory and digestive tract or umbilicus.

(3) Infections acquired after birth occurs when the neonate is 48-96 hours old due to inadequate passive transfer of colostral immunoglobulin, poor husbandry practices and presence of endemic infectious disease.

Predisposing factors:

(1) Bacterial placentitis due to purulent vaginal discharge, premature delivery, and an abnormal placenta, contaminated discharge present in the birth canal.

(2) Perinatal stresses (e.g. chronic in utero hypoxia, acute birth asphyxia, prematurity, dystocia).

(3) Overcrowding, poor ventilation, and contamination of the environment with pathogenic bacteria (e.g., Salmonella species).

Clinical findings:

(1) Septicemia: It is varied according to the stage of the disease and the site of localized infection.

1. a) The early signs are nonspecific include mental depression (lethargy, or sucking reflex weakness recumbency), diarrhoea, and dehydration.
2. b) Abnormal body temperature.
3. c) Abnormal mucous membranes colours vary from a muddy red-grey, to mottled, pale, or cyanotic. The capillary refill time is usually delayed (more than 2 seconds) and congested eye capillaries.
4. d) Petechiation of the ears, sclera, vulvar, or buccal membranes due to intravascular coagulation.

(2) Localized infection in various organs may lead to:

1. a) Pneumonia: Cough, nasal discharge tachypnea, dyspnea, and fever.
2. b) Diarrhoea may occur secondary to septicemia or enteritis.
3. c) Septic meningitis: Early signs include lethargy, depression, aimless wandering, and abnormal vocalization. Signs usually include progress to diffuse cranial nerve deficits causing apparent blindness; truncal and limb ataxia; weakness; recumbency; and coma, seizures, or both.
4. d) Septic arthritis and osteomyelitis Are common causing acute lameness, periarticular edema, joint capsule distention, or physeal pain.
5. e) Uveitis: Abnormalities in the eyes.
6. f) Omphalitis is characterized by heat, pain, swelling, and purulent discharge from the umbilicus.

(3) Septic shock:

1. a) The early-stage (hyperdynamic septic shock, septicemia without circulatory collapse) is characterized by congested mucous membranes, a normal capillary refill time and blood pressure and warm extremities Localizing signs of infection may or may not be present
2. b) The late-stage (hypodynamic septic shock) is characterized by tissue hypoperfusion. Clinical signs include cold extremities, sluggish capillary refill, hypotension, pale grey mucous membranes and markedly altered mentation.

Diagnosis:

(1) Laboratory examination:

• Leukocytosis and an increase in the number of band neutrophils. Leukopenia and neutropenia may also occur.
• Increase fibrinogen level to 1000 mg/dl at birth.
• Hypoglycemia due to decreased feed intake, low hepatic glycogen stores, and abnormal glucose metabolism caused by endotoxemia (depressed hepatic gluconeogenesis and increased peripheral uptake of glucose).
• Low level of serum immunoglobulin.
• Hypoxemia and metabolic acidosis are frequently present during arterial blood gas analysis
• Azotemia due to poor renal perfusion.
• Hyperbilirubinemia due to endotoxin-induced cholestasis.
• Electrolyte abnormalities occur in severe diarrhoea

(2) Blood cultures:

1. a) Sensitivity test.
2. b) Bacterial cultures of fluid obtained from sites of focal infection (e.g., cerebrospinal fluid, joint fluid, peritoneal fluid, and tracheal fluid), pharynx, trachea, and external ear canal and stomach contents.

NB: Culture of the same pathogen from more than two sites of focal infection supports a diagnosis of bacteremia.

Treatment:

(1) General supportive care:

1. a) Respiratory support for hypoxemia and respiratory failure
2. b) Fluid for hypovolemic shock and hypoglycemia.

• Attempting lactated Ringers solution with 5% dextrose, or administering 25% dextrose and 0.85% saline.
• If metabolic acidosis is severe, IV NaHC03.

1. c) IV plasma to restore circulating blood volume, osmotic pressure, and immunoglobulin concentrations.
2. d) Nonsteroidal anti-inflammatory drugs to recover endotoxemia (decreased cardiac output and hypotension). Flunixin meglumine (0.25-1.1 mg/kg, IV or IM every 8 hours).
3. e) Nutritional support by IV or nasogastric tube.

 

(2) Treatment of generalized infection:

1) A combination of a Beta Iactam antibiotic (eg, penicillin ampicillin) and an aminoglycoside (e.g., gentamicin, amikacin):

• IV or IM Gentamicin 2.2 mg/kg every 8-12 hours or 3.3 mg/kg every 12 hours.
• IV or IM Amikacin 7 mg/kg every 8-12 hours or 10 mg/kg every 12 hours.

2) Cephalosporins:

• IV or IM Cefotaxime 20-30 mg/kg every 8 hours.
• IV or IM Ceftiofiir: 2.2-6.6 mg/kg, every 8-12 hours.

3) Other drugs.

• Trimethoprim-sulfonamide combinations: 15 mg/kg, IV or orally every 12 hours.
• Chloramphenicol: 25-50 mg/kg, IV or orally, every 6 hours.
• Ticarcillin-clavulanate: 50 mg/kg, IV every 6-8 hours.

Antibiotic therapy in calves:

• Ceftiofur (5 mg/kg, IV or IM every 8-12 hours) or sulfonamides (15 mg/kg orally or IV or IM every 12 hours).
• Aminoglycosides: Gentamicin (3-5 mg/kg, IV every 12hours).
• Tetracyclines and sulfonamides.

General principles for the treatment of generalized infection:

1. Antibiotic after blood culture and sensitivity test.
2. Initially, IV is preferred for antibiotic because peripheral circulation may be compromised, making absorption from other routes inconsistent.
3. Duration of therapy, 7-10 days, Neonates positive blood cultures and no evidence of focal infection treated for at least 2 weeks and those with localized infections treated for 3-4 weeks.

Treatment of focal infections:

1) Septic meningitis:

• Antibiotic therapy (blood-brain barrier e.g, trimethoprim sulfonamide combinations alone or with beta-lactam antibiotic or aminoglycoside).
• Anticonvulsants (e.g., diazepam, phenobarbital) and NSAIDs (e.g., flunixin meglumine).

2) Septic arthritis or osteomyelitis:

• Systemic antibiotic therapy
• Adequate serum immunoglobulin concentrations
• Analgesic therapy
• Drainage and removal of debris from the joint and adjacent tissues (lavage with sterile polyionic fluids)
• Articular rest
• Surgical debridement, installation of a sterile drain, and immobilization of the limb.

Prognosis:

(1) The overall survival rate for septicemic neonates is less than 60%, but early diagnosis and treatment improve the outcome.

• A neonate with a negative blood culture but evidence of focal infection (e.g., pneumonia, diarrhoea) has a more favourable prognosis.
• Appropriate and early therapeutic intervention within utero acquired infections often result in the favourable outcome: survival rates greater than 75%.

(2) The long-term prognosis for future performance is guarded if multifocal bone or joint disease is diagnosed.

Prevention:

(1) Good hygienic sanitary condition.

(2) Sanitary management of the dam especially udder and genital system