NAME OF THE DISEASE OR DISORDER

OTHER NAME OR TERM

DESCRIPTION PATHOGENESIS and EPIDEMIOLOGY

CLINICAL SIGNS

LESIONS

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

TREATMENT

CONROL AND PREVENTION

Hypoxic ischemic encephalopathy (HIE)

Neo-natal encephalopathy / neo-natal maladjustment syndrome / perinatal asphyxia syndrome / barker / wanderer / dummy

Hypoxic ischemic encephalopathy (HIE) is a noninfectious syndrome of foals characterized by CNS dysfunction. The condition is often considered a component of perinatal asphyxia syndrome associated with peripartum events such as dystocia or placental insufficiency. However, in many cases there is no obvious episode of hypoxia, and it appears that it may result from in utero exposure to inflammatory cytokines, secondary to occult placentitis.

The etiology is unknown; however hypoxia is thought to initiate metabolic cascades that results in decreased energy production, ion dysregulation, increased concentrations of excitatory neurotransmitters (esp. glutamate and aspartate), and impaired protein synthesis. An increase in intracellular calcium concentration appears to play a prominent role in neuronal injury. Oxygen-free radicals, nitric oxide production and pro-inflammatory cytokines are also implicated. When a hypoxic episode is not evident, exposure to inflammatory cytokines likely initiates a similar cascade of events.

Poor coordinated suckle reflex and loss of affinity for the mare are the most common signs althought not present in every case. Other signs include hypotonia, opisthotonus, abnormal respiratory patterns, persistent tongue protrusion, abnormal jaw and facial movements, head pressing, and abnormal vocalization (barker foals). Seizures range from mild, abnormal movements of the face and jaw to generalized seizures with recumbency and paddling. Clinical signs are often asymmetric and may include a head tilt, circling and asymmetric pupillary reflexes. Abnormal gastrointestinal and renal function including gastric reflux, bloat, meconium retention, colic and persistent increases in creatinine concentration.

CNS necrosis, edema and hemorrhage

Based on clinical findings. History of dystocia, premature placental separation, or placentitis.

It includes bacterial meningitis, equine herpesvirus 1 infection, metabolic abnormalities, acid-base disturbances, kernicterus, subsequent to massive hemolysis, brain or spinal trauma, congenital defects and nutritional myodegeneration

IV fluid administration and intranasal oxygen insufflation to improve cardiac output and maintain cerebral perfusion and oxygen delivery. Nutrition supplementation to foals that are unable to suckle via nasogastric tube. Parenteral nutrition is indicated in foals with GI dysfunction. In recumbent foals, ophthalmic lubricant may be used to reduce the chance of corneal injury. Broad-spectrum antibiotics to foals that are neurologically abnormal at birth wherein they often fail to suckle. Medications such as diazepam or phenobarbitone may control convulsions.

Sepsis

Bacteremia, septicemia, bacterial infec-tion

Development of a systemic inflammatory syndrome in response to suspected infection. Most common problem of equine neonate.

Escherichia coli is the predominant bacteria. Other common gram negative bacteria include klebsiella spp, enterobacter spp. Actinobacillus spp. Salmonella spp. and pseudomaonas spp. also streptococcus spp for gram positive bacteria. Deficits in the physiologic response to infectious agents in neonate relate to reduced chemotaxis and killing capacity of neonatal neutrophils, the presence of antigenically naïve T cells, and decreased concentration and impaired function of monocytes. The major risk factor for sepsis is failure to receive an adequate quality and quantity of colostral antibodies. Other factors include unsanitary environmental conditions, low gestational age of the foal (prematurity), poor health and condition of the dam, difficulty of parturition, and presence of a new pathogens in the environment against which the mare has no antibodies.

Affected organ systems include the umbilical remnants, CNS, respiratory, cardiovascular, musculoskeletal, renal, and ophthalmic. Hepatobiliary and GI organs.During the early stages of sepsis, signs are often vague and nonspecific, with affected neonates displaying some degree of depression and lethargy. Mare’s udder is distended indicating that the foal is not nursing at normal frequency.It progresses to a complete loss of suckle reflex, hyperemic mucous membranes with a rapid capillary refill time due to peripheral vasodilation, tachycardia and early petechiae related to capillary leakness.In advanced stages, septic shock ensues. The foal is severely depressed, recumbent, hypovolemic, thread pulse, and poor capillary refill time. Foals may be hyper- or hypothermic, tachycardic or bradycardic.

Multiple organ dys-function syndrome (dysfunction of 2 or more organs)Edema in the lungs, uveitis, meningitis, osteomyelitis and arthritis

= History and clinical signs= Positive bacterial blood culture= Neutrophil count normal, then falling total white blood cell count= Increased fibrinogen= Hypoglycemia, hypoxia, acidosis= Low plasma antibody levels

Neonatal encepha-lopathy, hypoglycemia, hypothermia, neonatal isoeythrolysis, prematurity, neonatal pneumonia, uroperitoneum

=Broad spectrum antibiotics=IV fluid therapy= nutritional support= systemic-specific therapy includes lavage of septic joints, regional limb perfusion, nasal oxygen support or ventilation.

Quarantine procedures(proper management and husbandry protocols)

Neonatal uroperitoneum

Ruptured bladder

Urine leakage into the peritoneal space.

It results from tearing of the bladder during parturition, prolonged recumbency while being treated for neonatal illness, or rupture of urachus secondary to umbilical abscessation. Studies indicate that a higher incidence of bladder rupture in males than females, possibly because of the narrower pelvis and the longer, narrower urethra of colts is a predisposing factor. Traumatic bladder rupture is caused by uterine contractions on a full bladder as a foal passes through the birth canal. Prematurity, neonatal encephalopathy, cystitis, ascending infection, abdominal trauma, failure of passive transfer and sepsis may predispose the foal.

Foals generally appear to be normal at birth but progressively become lethargic, tachycardic, and tachypneic over 24-48 hours. As the condition progress, the abdomen becomes distended and ballottement may produce a fluid wave. Most foals attempt to urinate often, with small amounts of urine.

= Ultraso-nographic abdominal exami-nation= blood and peritoneal fluid analysis=creatinine level test in the peritoneal fluid= ultra-sound (accumula-tion of urine in tha retroperitoneal area can be seen)

Septicemia, hypoxic ischemic encephalo-phathy or neonatal encephalo-pathy

Surgery is necessary to correct the defect. Aftr surgical correction, an indwelling urinary catheter may be placed for48 hr to decrease bladder distention and leakage of urine at the repair site.

During examinations of neonatal foals, positioning must be noted at an interval time.

Neonatal isoerythrolysis (NI)

Alloimmune hemolysis

An immune mediated hemolytic disease.

It is caused by ingestion maternal colostrum containing antibodies to one of the neonate’s blood group antigens. The maternal antibodies develop to specific foreign blood group antigens during previous pregnancies, and unmatched transfusions. Antigens usually involved are A,C, and Q; Ni is most

Primary abnormality in a foal with NI is anemia. Affected neonates are normal at birth but develop severe hemolytic anemia within 2-3 days and become weak and icteric.In mild cases, increased respiratory rate and signs of lethargy. Foals in which anemia is more profound frequently show depression, anorexia, dehydration, pale, icteric mucous membranes in addition to

Screening maternal serum, plasma or colostrum against paternal or neonatal RBC.

Septicemia, hypoxic-ischemic encephalopathy, anemia of premature foals,

Consist of stopping any colostrum while giving supportive care with transfusions. If necessary, neonates can be transfused with triple washed maternal RBC. The newborn’s RBC can be mixed with maternal serum to look for agglutination before the newborn is allowed to receive maternal

common in Thoroughbreds and mules.

tachypnea, tachycardia, pigmenturia and fever. In severe cases, cardiovascular collapse, and hemodynamic shock resulting from hypoxia can result to neurologic disorders, metabolic acidosis, and multiorgan failure.

Azotemia, tissue hypoxia.

equine herpesvirus 1 infection.

colostrum.

Avoided by withholding maternal colostrum and giving colostrum from a maternal source free of the antibodies

Rhodococcus equi Pneumonia

Most serious cause of pneumonia in 1-5 month old foals. It is not the most common cause of pneumonia.

Rhodococcus equi is a gram negative-positive, facultative intracellular pathogen that is ubiquitous in soil. Only vapA, vapB, and vapC are pathogenic. Inhalation of dust particles laden with virulent Rhodococcus equiis is the major route of pneumonic infection. Manure from pneumonic foals is a major source or virulent bacteria contaminating the environment. Foals with pulmonary infections swallow sputum laden with Rhodococcus equi, which readily replicates in their intestinal tract. The pathogenicity of Rhodococcus equi is linked to its ability to survive intracellularly, which hinges on failure of

Clinical signs are difficult to detect until pulmonary infection reaches a critical mass, resulting in decompensation of the foal. Most foals are lethargic, febrile, and tachypneic. Cough is a variable sign; purulent nasal discharge is less common. Thoracic auscultation reveals crackles and wheezes. Diarrhea is observed due to colonic microabscessation. Foals with abdominal involvement often present with fever, depression, anorexia, weight loss, colic and diarrhea.Vertebral osteomyelitis may result in pathologic vertebral fracture and spinal cord compression.

Pulmonary lesions are relatively consistent and include subacute to chronic suppurative

Laboratory evaluation of CBC and serum chemistry reveals neutrophilic leukocytosis and hyperfibrinogenemia.Thoracic radiographic evaluation reveal pattern of perihilar alveolization, consolidation, and abscessation.The presence of nodular lung lesions and mediastinal lymphadenopathy is highly suggestive of Rhodococcus equi.Bacterial culture of transtracheal washes samples for definitive diagnosis.Cytologic evaluation of transtracheal wash samples reveals

Treatments of choice are erythromycin and rifampin. Macrolide antibiotic specifically azithromycin, clarithromycin is a choice for foals with severe disease.Supportive therapy includes provison of a clean, comfortable environment and highly palatable, dust-free feeds.

phagosome-lysosomal fusion in infected macrophages and failure of functional respiratory burst upon phagocytosis of Rhodococcus equi

bronchopneumonia, pulmonary abscessation, and suppurative lymphadenitis. Intestinal lesions are characterized by multifocal, ulcerative enterocolitis and typhlitis involving peyer’s patches with granulomatous or suppurative inflammation of mesenteric or colonic lymph nodesPanophthalmitis, guttural pouch empyema, sinusitis, pericarditis, nephritis, nonseptic uveitis, and synovitis, and hepatic and renal abscessation.

intracellular coccobacilli.

Acute broncho-interstitial pneumonia

Sporadic, rapidly progressive disease of foals characterized by acute respiratory distress and high mortality. Range of affected foals ranges from week to 5 months.

It is likely that a number of different insults, rather than a single factor, initiate a cascade of events, resulting in a final common response of pulmonary damage and acute respiratory distress. Warm weather (> 85of / 29.4oc) is a common epidemiologic factor. No virus is consistently isolated. Enteric gram negative organisms; Rhodococcus equi, Pseudomonas aeruginosa and Pneumocystis carinii have been cultured from the lungs of affected foals

Foals are unable or reluctant to move and are usually cyanotic. Severe respiratory distress is the most striking clinical sign.

Hypoxemia, hypercapnea, and respiratory acidosis are consistent findings. These arterial blood gas quantify the severity of respiratory impairment and are used to monitor response to therapy. Hypoxemia is relatively resistant to supplemental oxygen therapy.Similar to bacterial pneumonia in that hyperfibrinogenemia and neutrophilic leukocytosis are observed in most foals.

Physical examination and clinicopathologic findings and thoracic radiographic examination are the most diagnostic test to differentiate Rhodococcus equi pneumonia from bronchointerstitial pneumonia. Cytologic evaluation of tracheal aspirates reveals acute neutrophilic inflammation with or without evidence of sepsis. Necropsy examination reveals diffusely enlarged lungs that fail to deflate upon

Therapy is symptomatic. Treatment includes anti-inflammatory therapy, broad-spectrum antibiotic therapy, thermoregulatory control, bronchodilator, oxygen supplementation and supportive care. Additional supportive therapy includes provision of a clean, comfortable environment, highly palatable, dust-free feeds, and ulcer prophylaxis

opening of the thoracic cavity with rib impressions on the visceral pleural surface

Colostrum deficiency‘failure in passive transfer’

Failure to receive good-quality colostrum leading to the development of bacterial infections and septicemia in foals.

Zinc sulphate turbidity (semi-quantitative)

Glutaraldehyde precipitation (semi-quantitative)

Immunoassay (quantitative)=Enteritis associated with C. Perfringens Type A, B, and C, Clostridium Difficile, R.Equi, Salmonella Spp., Strongyloides Westeri, C. Parvum, And Rotavirus=Septicemia associated with E. Coli, Actinobacillus equuli, Klebsiella pneumoniae, a-Hemolytic Streptococci, S. zooepidemicus, L. monocytogenes, Rhodococcus equi, Salmonella typhimurium.

Plasma from the mare (or use proprietary plasma). Give at least 20 ml/kg (40ml/kg is optimum) of the mare’s plasma by sow intravenous infusion or give 200mg/kg of propriety plasma.= colostrum for banking=cross species colostrum= colostrum supplements _ lacteal-secretion-based preparations _ bovine serum-based preparation

Prematurity and dysmaturity

Premature- foals with gestational age that is less than 320 daysDysmature- gestational age is at the range but exhibiting signs of prematurity

Possible causes can include in utero viral infection, acute or chronic bacterial placentitis, congenital fetal abnormalities, maternal endocrine abnormalities, chronic placental insufficiency, maternal hydrops allantois/amnii, incompetent cervix, severe maternal illness, and prolonged maternal fasting.

Premature foals are characterized by low birth weight, thin condition, domed forehead, generalized muscle weakness, poor ability to stand, lax flexor tendons, and weak or no suck reflex, respiratory distress, short silky haircoat, floppy ears, absence of incisor teeth, soft lips, closed eyes, increased passive range of limb motion and sloping pastern axis. Incomplete ossified cuboidal carpal and tarsal bones and immaturity of the lung and an absence of hair in extreme prematurity.

Sepsis often presented hematologically by leucopenia and neutropenia.

REFERENCES Coumbe, Karen M. The Equine Veterinary Nursing Manual.2001. Blackwell Science Ltd. Oxford and Northampton. Chapter 14 pages 280-281

Radostits, O.M; et al. Veterinary Medicine- A Textbook of the Diseases of Cattle, Horses, Sheeps, Pigs and Goats. 10 th edition.2007.Saunders Elsevier. Spain. Pages 127-160

Kahn, Cynthia M.; et al. The Merck Veterinary Medicine.10th Edition.2010.Merck and CO.,INC. Courier kendaville,Inc. Kendaville,Indiana

BENGUET STATE UNIVERSITYCOLLEGE OF VETERINARY MEDICINE

Km. 5 La Trinidad, Benguet

Department of Clinical Sciences

Equine MedicineVM175

NEONATAL (FOAL) DISEASES

Submitted to:Karen B. Gaerlan

(Clinical Instructor)

Submitted by:Lipaopao, Floriel C.

Submitted date:January 14, 2014