Equine Medicine Book - REVISED 2022 PDF

BENHA UNIVERSITY FACULTY OF VET. MED. (MOSHTOHOR) DEPARTMENT OF ANIMAL MEDICINE EQUINE MEDICINE (FOR 4th YEAR STUDENTS) BY...

BENHA UNIVERSITY FACULTY OF VET. MED. (MOSHTOHOR) DEPARTMENT OF ANIMAL MEDICINE EQUINE MEDICINE (FOR 4th YEAR STUDENTS) BY PROF. DOCTOR HUSSAM EL-DIN EL-ATTAR PROF.OF ANIMAL MEDICINE AND Ex-PRESIDENT OF BENHA UNIVERSITY PROF. DOCTOR PROF. DOCTOR YASSEIN M ABD-EL RAOOF MOHAMED M. GHANEM PROF. OF ANIMAL MEDICINE PROFESSOR OF ANIMAL MEDICINE FACULTY OF VET. MED. (MOSHTOHOR) EX-DEAN OF FACULTY OF VETERINARY MEDICINE FACULTY OF VET. MEDICINE (MOSHTOHOR) And All staff members of Veterinary Internal Medicine 1 EQUINE MEDICINE 2  Table of Contents Contents Page number 1- Diseases of Digestive System 4 2- Diseases of Respiratory System 45 3- Diseases of Urinary System 68 4- Diseases of cardiovascular System 84 5- Equine Metabolic Diseases 96 6- Diseases of Nervous system 111 7- Foal Diseases 119 8- Sports Medicine 127 9- Parasites of Horses 141 10- Equine Euthanasia 145 3  DISEASES OF DIGESTIVE SYSTEM AFFECTIONS OF ORAL CAVITY IN HORSES (I)STOMATITIS IN HORSES Definition : Stomatitis means inflammation of oral mucosa and it include glossitis (inflammation of tongue), gingivitis (inflammation of gum) and palatitis (lampas). Clinically it is characterized by partial or complete loss of appetite, smacking of the lips and salivation. Etiology : Physical, chemical and infectious agents. (A) Physical Agents: 1- Drinking of hot water. 2- Eating sharp awns or spines. 3- Foreign body injury. 4- Trauma while dosing. 5-Malocclusion of teeth. (B) Chemical agents: 1- Irritant drugs administered in over strong concentrations e.g. chloral hydrate. 2- Licking of counter irritants e.g. mercury and cantharides compounds. 3- Irritant substances administered by mistake e.g. acids, alkalis, phenolic compounds. 4- Systemic poisoning e.g. chronic mercury. 5- Included in syndrome of uremia in horses. (C) Infectious agents: 1- Vesicular lesions in vesicular stormatitis and herpes virus infections. 4  2- Lingual abscess caused by Actinobacillus spp. Clinical findings : 1- Partial of complete anorexia. 2- Salivation and smacking of lips. 3- Slow, painful mastication. 4- fetid odour on breathing (if bacteria invade the lesion). 5- Enlargement of local lymph nodes (if bacteria invade the lesion). 6- Increased desire for water. 7- Toxemia may be present if stomatitis secondary to systemic disease. 8- Vesicular lesions are usually thin-walled vesicles 1-2cm in diameter filled with clear serous fluid. When vesicles ruptured, they leave sharp- edged shallow ulcers. Treatment: 1- Isolation of affected animals and should and watered from separate utensils particularly if an infectious agent is suspected. 2- Frequent application of a mild antiseptic e.g. 1% suspension of sulfonamide in glycerin or 2% suspension of borax or 2% solution of copper sulfate. 3- inopleat ulcers require curettage or cauterization with silver nitrate stick or tincture of iodine. 4- Soft, appetizing food should be offered and feeding by stomach tube or I/V injections in severe prolonged cases. * * * (II) LAMPAS ( PALATITIS) IN HORSES Definition: Lampas means swelling and hardening of hard palate m.m. in horses ( just behind upper incisor arcade). 5 Etiology : (a) In young horses ( Foals) : Associated dentition i.e. change from temporary to permenant teeth. (b) In mature horses : Associated congestion of oral region. Clinical signs: 1- Pain (during suckling and mastication ). 2- Mouth inspection shows that anterior rugae of hard palate extend below the level of incisor teeth. Treatment : (a) In foals : Recovery usually spontaneous and uneventful. (b) In olders : Condition persists for extended period, therefore feeding soft feed- laxative diet e.g.bran mash is recommended until recovery. * * * 6  (III)CLEFT PALATE PALATOSCHISIS ) IN HORSES Definition: Common congenital defect in newborn foals. Etiology: (a) Old evidence : Hereditary cause. (b)Recent evidence : Viral infection or ingestion of toxic agents for pregnant mares during gestation. Clinical signs: 1- Milk dripped from nostrils (During suckling). 2-Dysphagia. 3- Mouth inspection reveals the cleft palate. N.B: Aspiration pneumonia due to inhalation of milk commonly occur. Treatment : Surgical correction ( usually give a poor results). * * * AFFECTIONS OF PHARYNX IN HORSES (I)PHARYNGITIS IN HORSES Definition: Inflammation of pharyngeal mucosa. Etiology: (a) Trauma (Common cause in horses) : Foreign bodies e.g. : Awns , spines, wires... etc. (b) Infection ( Bacterial and viral ) : Bacterial infection e.g. Strangles, anthrax...etc. Viral infection e.g. Influenza, parainfluenza, rhino virus, viral arteritis, herps virus, aseno virus… etc. 7 Clinical findings: 1- Horse stand with head extended. 2- Refuse to eat or drink. 3- Painful swallowing (If forcely eating ). 4- Regurgitation of fluid and food through nostrils ( In severe cases). 5- Paroxysmal cough (positive cough test ) 6- Enlarged retropharyngeal lymph node (Inflammed or abscessed). N.B.: “Chronic Folliculr Pharyngitis Syndrom" commonly occurs in horses after viral infection accompnied by hyperplsia of lymphoid tissue in pharymgeal mucosa giving it granular-nodular appearance hanging from phryngeal roof. Treatment: 1- Remove primary cause. 2- Parenteral antimicrobial (antibiotics or sulfonamides). 3- Electrocautary ( may be useful). * * * (II) PHARYNGEAL OBSTRACTION Definition: Mechanical partial occlusion of pharyngeal cavity. Etiology : (a) Foreign bodies: Corn cobs, bones, piece of wire … etc. (b) Tissue swellings: 1- Chronic follicular pharyngitis syndrome. 2- Retrophryngeal lymphadenitis or abscess (caused by strngles). 3-Goitrous thyroid. Clinical findings: 8  1-Stertorous respiration. 2- Coughing. 3- Difficult swallowing. Treatment: 1- Remove primary cuase. 2- Parenteral treatment with pencillin-streptomycin (Pharyngeal abscess ). 3- Surgical interference (Forieng bodies, pharyngeal cysts, goitrous thyroid ). * * * (III)PHARYNGEAL PARALYSIS IN HORSES Definition: - Acquired absence of pharyngeal neuromuscular tone. Etiology : (a) Peripheral nervous system injury : Glossophryngeal nerve injury due to : 1- Trauma ( Throat region ). 2- Infection ( Guttural pouch ). (b) Central nervous system injury : Secondary to specific CNS disease due to: 1- Rabies (encephalitis ). 2- Equine pests ( African horse sickness) 3- 3-Botulism (Cl.Botulinium). Clinical findings: 1- Constant salivation. 2- Dropping of food from mouth. 3- Regurgitation food through nostrils. 4- Inability to swallow (with an absence of signs of pain). 5- Coughing. 6- Dehydration. 9  7- Rapid loss of condition. N.B.: Aspiration pneumonia is a common complications if left without treatment. * * * AFFECTIONS OF ESOPHAGUS IN HORSES (I)ESOPHAGITIS IN HORSES Definition : Inflammation of esophageal m.m. Etiology : 1- Trauma from foreign bodies (most common) 2- Injury caused by stomach tube. 3- Irritating chemicals ( e.g : Breaking of capsule containing irritant drug). Clinical findings : In severe cases there are: 1- Extension of head and neck. 2- Salivation. 3- Dysphagia. 4- Regurgitation (via mouth and nostrils). 5- Palpation reveal esophageal spasm ( cervical musculture). Treatment: 1- Withholding feed ( relieves condition). 2- Antibiotics ( control infection). 3- Corticosteroids ( Control pains ). 4- Analgesics (control spasm). * * * (II) ESOPHAGEUL OBSTRUCTION IN HORSES 10 Obstruction of esophagus my be acute or chronic, internal or external. Etiology: (A)Internal obstruction : Caused by swallowed materials like food mases or forgien bodies e.g : 1- When horses allowed for eating dry hay (Or wood shavings bedding). The bolus lodges at cardia causing obstruction. 2- When horses accidentally swallowed nasogastric tube. (B)External obstruction : Caused by pressure on esophagus by surrounding organs or tissues e.g.: 1- Stomach carcinoma. 2- Persistent aortic arch. 3- Mediastinal neoplstic L.N.. 4- Mediastinal or cervical abscess. Clinical findings: (A) Acute obstruction (Choke) : (a) In terminal part of thoracic esophagus (Common): Obstruction can not be seen or even palpated. (b) In thoracic inlet obstruction ( Less common) : 11  There is “ esophageal spasm and foreceful painful peristalsis and swallowing movements" at site of obstruction. Generally, signs proceed as follow: 1- Sudden stop eating. 2- Anxiety and restlessness (Paw at ground). 3- Forceful attempts to swallow (accompanied with coughing). 4- Regurgitation of food through nastrils. 5- Salivation. 6- Impossible passage of nasogastric tube. N.B.: Death may occur from subsequent aspiration , or when obstruction persists, from dehydration. (B) Chronic obstruction: There is an absence of acute signs: 1- The swallowing movements are usually normal until the bolus reaches. The obstruction when they re replaced by a more forceful movement. 2- The swallowed material either pass slowly through the stenotic area or accumulates and is then regurgitated. 3- In the gater stages , there may be no attempt to eat slid food but fluids may be taken and swallowed satisfactorily. Treatment: Treatment of chronic obstruction is usually unsuccessful. In acute obstruction the following may be useful. 1- Sedation of the animal first by an ataractic drug (chloropromazine Hcl 50-100 mg/kg) or chloral hydrate to help in relaxing the esophageal spasm (S/C injection of atropine sulphate 16-32 mg may be u seful) 12  2- Gentle attempt by passage of stomach tube to push theopush the obstruction onward (but avoid damage of mucosa which is probably fatal lesion in horses ). 3- Surgical in terference (Eosophegotomy ) but not highly successful. N.B: Accumulation of ingested material in lower esophagus of horse is more difficult to remove. - Small quantities of warm saline should be introduced through a stomch tube passed to the point of obstruction and then pumped or siphoned out. - This may be repeated a number of times until fluid comes clear. * * * III-ESOPHAGISM ( SPASM OF ESOPHAGUS) (ESOPHAGISM MOST COMMONTY IN YOUNG HORSES) Etiology: - The exact etiology is unknown, although the condition has been observed in the following cases: 1- Nursing foals when they begin to take solid food. 2- During routine stomch tube passage. 3- In horses with acute esophgitis and esoph. Obstruction. Clinical findings: Resemble those esophgeal obstruction Treatment: 1- Atropine sulphate (0.03,0.07mg/kg B.W) to control the spasm, but morphin sulphte (60-90mg S/C) may be used to relieve severe spas. 2- Tranquillzers (Xylazine 1.1 mg/kg B.W.TV) to control nervous horses. * * * 13  IV-ESOPHAGEAL DIVERTICULUM (DILATATION) This condition assumes its great importance in horses Etiology: esophageal diverticulum occurs most often secondarily to esophageal stenosis i.e.associated indirectly to esophgeal stenosis i.e. associated indirectly with chronic obstruction and esophagitis. Clinical findings: Similar to those of esophgeal obstruction. Treatment: Surgical exposure of the diverticulum nd careful apposition of the esophageal musculture is the only effective treatment. * * * DISEASES OF STOMACH IN HORSES I-GASTRITIS IN HORSES Definition: Inflammation of stomach m.m Etiology : Physical, chemical or metazoan agents : (A) Physical agents : Ingestion of foreign materials e.g: sand (Wind-sucking horse). 14  (B) Chemical agents : Accidental ingestion or licking of irritant caustic and toxic agents in e.g: arsenic, mercury, lead, copper.. etc. (C) Metazoan agents : Massive infestation with: 1- Gastrophilus sps. (Bot fly larvae). 2-Habronema sps. (Muscae, Microstoma and Megastoma) Clinical findings : (a) Acute gastritis: 1- Reduced appetite (but excessive thirst). 2- Acute abdominal colicy pains. 3- Regurgitation (Severe cases). (B) Chronic gastritis : 1- Depressed or depraved appetite. 2- Subacute abdominal colicy pains. 3- Regugitation may occur sporadically (usually after feeding). 4- Emaciation (due to lack of food intake). Diagnosis : (A) History (B) Clinical signs (C) Laboratory diagnosis Sample of stomach content should be collected if a chemical poison is suspected. Treatment: 1- Empty alimentary tract using paraffin mineral oil (to avoid further irritation to mucosa if saline purgative is used). 2- Gastric lavage with isotonic saline every 4 hours (if chemical poisoning is suspected). 3- Gastric sedative e.g: Buscopan composotum. 4- Anti-acids e.g: Magnesium hydroxide (or carbonate). 15 5- Soothing therapy e.g: kaolin or pectin (Sometimes with charcoal). N.B: During convalescence, soft palatable, highly nutritional food e.g. green feed and bran mashes are recommended. * * * II-GASTRIC ULCERATION IN HORSES Definition: Means ulceration of stomach m.m. Etiology : 1- Parasitic gastritis (Gastrophilus and Habronema megastoma). 2- Repeat dosing with non-steroidal anti- inflammatory drugs (NSAIDs). 3- Diets high in concentrates play a role. N.B: In foals disese may associated viral enteritis caused by rotavirus infection Pathogenesis : Gastric ulceration commonly results in : 1- Pyorous spasm. 2- Increased gastric motility. 3- Gastric hemorrhage. 4-Perforation and peritonitis. N.B: Healed ulcer may cause pyloric or duodenal partial or complete obstruction. Clinical findings : Many gastric ulcers cause no apparent clinical signs. Signs depend on whether ulceration is complicated (hemorrhage or perforation) or uncomplicated 16  (A) Uncomplicated cases : 1- Mild intermittent anorexia and abdominal pain. 2- Constipation or diarrhea. (B) Complicated cases : (a) With hemorrhage : 1- Melena (Black or tarry faeces). 2- Pale m.m (Anemia). 3- Sudden death. b) With perforation : (1) Severe anorexia. (2) Intermittent diarrhea (tarry faeces). (3) Fluctuating fever (Peritonitis). N.B: Spleen commonly affected with the disease (G.U). Diagnosis: (A) History: (B) Symptoms: (C) Lab. Diagnosis : Fecal occult blood analysis. (D) Instrumentation : (a)Radiography: Assist diagnosing. (b)Endoscopy: Most accurate. Treatment: (a) Alkalinizing agent : Neutralize acidity and allow healing e.g. Magnesium hydroxide, carbonate or trisilicate. N.B: Recently, omeprazole inhibit gastric acid produchtion and enhances healing of gastric ulcers in horses. (b) Coagulants and hematinics : Against hemorrhage and anemia e.g. vitamin-K, calcium, vitamin-C, thrombin, iron, copper, B12, and folic acid. 17  N.B: Preparations e.g Homoscon (coagulant) and Fercobsang (hematinics). (c) Histamine H-receptor antagonists : Cimetidine (Zentac) and ranitidine very effective in horses. (d) Soft food : To avoid physical irritation. N.B: Surgical interference is sometimes recommended and gives a satisfactorily results particularly in foals. * * * III-GASTRIC DILATATION IN HORSES Definition: A syndrome accompanied by signs of abdominal pain and occasionally projectile vomiting. Etiology : (A) Acute form: (a) Following aerophagia while cribbing : (b) Excessive consumption of water after exercise: (c) Overeating of highly fermentable grain ration: (d) Secondarily to acute intestinal obstruction : (e) Secandary to acute necrotizing pancreatitis : (B) Chronic form: (a) Atony of stomach wall in old or debilitated horses. (b) External compression of pylorus by tumor mass: e.g. lipoma in horses. Clinical signs : (a) Abdominal pains : Manifested by sweating, rolling and kicking at belly. (b) Dog sitting posture: Affected horses sitting on haunches. (c) Projectile vomiting : Manifested by little effort- associated regurgitation. 18 (d)Dehydration signs : Manifested by sunken eyes and inelastic skil. (e) Alkalosis signs : Manifested by tremors, tetany and rapid respiration. N.B: Laminits may occur i n cases associated with over eating of concentrates. Treatment : Treatment is palliative only : 1- Empty stomach contents ( Air, Water, Food ) by passage of nasogastric tube 2- Relax pylorus sphincture by local anaesthatic e.g: Lignocaine orally. 3- Give strychnine against stomach wall atony. 4- Supportive I/V fluids and electrolytes therapy. * * * IV-GASTRIC RUPTURE IN HORSES Definition: Serious complication of sever or untreated gastric distention. Etiology : 1- Complication of untreated stomach distention. 2- Nasogastric intubation of a distended stomach. 3- Severe overdistention of stomach during falling. Clinical signs : 1- Sudden relief of abdominal pain. 2-Followed by anxiety and profuse sweating 3- Followed by profound tachycardia and cyanotic m.m. rapid deterioration. 4- Followed by death from hypovolemic shock (Severe haemoconcen tration). Treatment : Unsuccessful. * * * 19  HORSES INTESTINAL DISEASES I-ACUTE INTESTINAL OSTRUCTION Intestine : (A) Small intestine : Dudenum – Juenum – Ileium (B) Large intestine : Cecum – large colon – small colon Etiology : 3 common groups of causes: 1- physical obstruction to the lumen of intestine. (Luminal blockage). 2- physical obstruction to the lumen of intestine plus infarction of the affected section. 3- Functional obstruction with no passage of contents but with the lumen still patent (paralytic ileus). (A) Luminal blockage 1- Blockage of lumen intestine by foreign bodies, strings, tail hair, phytobezoars ingested with licking-chewing habit. 2- Impaction of ileocecal valve by fine dry indigestible fiber. 3- Impaction of large bowel by enteroliths (B) Intestinal accidents 1- Intussusception of ileum into cecum or of cecum into cecum or colon into colon. 2- Mesenteric torsion of small intestine (volvulus) 3- Strangulation of an inguinal hernia (in stallions),of an umbilical hernia (in young horses) and of diaphragmatic hernia. (C) Paralytic ileus The syndrome of paralytic ileus (functional stasis of intestine) occurs due to : 1- Distention of intestine for periods of more than several days. 20  2-Acute diffuse peritonitis to the intestines during surgical operations (paralytic ileus is the commonest cause of postoperative fatality cases of surgical colic). 3- In peracute enteritis such as colitis-X 4- In lactation tetany in mares. Pathogenesis: Intestinal distention : C.V. effect- dehydration – Abdominal pain. 1- In severe intestinal obstruction, acute shock due to distention of the bowel which causes reflex cardiovascular effects and peripheral circulatory failure and colla 2- In less severe cases less of fluids and electrolytes and dehydration are the important mechanisms because the fluid and accompanying electrolytes are secreted into the lumen of intestine in response to distention above the obstruction. 3- Distention is responsible foe abdominal pain observed. N.B : - Obstruction of upper intestine (duodenum) is most lethal. - Obstruction of large intestine, may lead to autointoxication due to accumulation of faeces. Clinical signs : 1- Immediate onset of severe abdominal pain (due to distension at obstruction site) which accompanied by sweating, increased pulse and respiratory rates and tachycardia. 2- Increased pulse and respiratory rate. 3- After 12-24 h of obstruction, the distended intestinal loop can be palpated through the rectum as the defecation ceases and the rectum becomes empty and sticky to touch. 21  4- After 24 h, dehydration starts and reflux filling of the stomach occurs, which may lead to vomition. 5- Rupture usually occurs at about 48 h. Diagnosis : I- History. II- Clinical signs. III- Laboratory diagnosis. Laboratory diagnosis not used for diagnosis of intestinal obstruction, but only useful in assessing its severity. 1- Haemoconcentration (due to dehydration) 2- Leukopenia and neutropenia (due to devitalization of infracted intestine, followed by necrosis). 3- Increase in blood urea nitrogen (due to hypovolemia). Treatment: 1-Supportive treatment includes : a)Sedation of the animal. b)Adm. of antibiotics to control bacterial growth. c)Electrolytes to overcome hypovolemia, dehydration and shock. 2-Immediate surgical removal of the obstruction. * * * II-ENTERITIS (including enteropathy, malabsorption and Diarrhea) Definition : Enteritis means inflammation Of intestinal mucosa resulting in malabsorption and diarrhea and a varying degrees of dehydration and disturbance in acid-base balance. Etiology : There are many causes of enteritis or malabsorption in equines, as shown in the following table. 22  Table (1) Epidemiological and clinical features of disease of horses in which diarrhea is a significant clinical finding. Etiology Age and class of animal Major clinical finding affected a) physical: Horses grazing on sand Acute or chronic diarrhea, 1-Sand colic pasture or consuming feed impaction of large colon and faeces contain excessive sand. contain sand. Usually follows prolonged 2- Stress- induced Surgical anesthesia Acute profuse watery diarrhea, severe dehydration and death in 24- 48 hrs. B) Viruses: Newborn foals Profuse watery diarrhea at few days Rota, corona and of age. adeno – viruses Bacteria 1-Sallmonellosis Any age Acute profuse foul smelling 2- Clostridiosis (cl- Any age diarrhea and severe dehydration. perfringens type b Acute profuse watery foul smelling and c diarrhea and death in 24 hrs. 3- Corynebacterium Young foals Diarrhea associated with pneumonia equi Newborn foals Diarrhea and death with 24 4- Actinobacillus e)Parasites Acute, subacute or chronic diarrhea 1- strongylus sp. Usually affect horses over 6 according to the degree of 2- trichonema sp. months of age infestation. 3- Ascaris sp. F) tumors Chronic diarrhea, progressive loss 23 Lymphosarcome Sings horse affected of weight no response to treatment G) Miscellaneous (or unknown etiology) 1- Colitis-X Single horse affected, Peracute profuse watery diarrhea, usually mature one but may rapid collapse and death. Poor affect yearling may be stress response the therapy. induced. 2- Granulomatus Single horse affected, Diarrhea not a major clinical enteritis usually mature one. finding. Chronic weight loss. 3- tetracycline Horses treated with 10 times Acute profuse watery diarrhea induced enteritis usual dose of tetracycline. severe deterioration Death 24-48 hr. 4- Foal heat Foals at 7-10 days at age diarrhea coinciding with mare's first Mild diarrhea lasting 1-4 hose. post partum estrus Minimal systemic effects. No specific treatment required. Clinical findings : A) Acute enteritis a) Diarrhea : Faeces are : 1- Soft or fluid consistency. 2-Color other than normal. 3- Odour other unpleasant. 4- May contain blood mucous fibrinous cast or foreign material such as sand. 5- Soil the perineum and tail. b) Dehydration : 1- Dehydration is usually evident by 10-12 hours following the onset of acute enteritis and clinically obvious by 18-24 hours. 24  2- The degree of dehydration can be best assessed by tinting the skin of the upper eyelid or neck and determining the time taken for the skin fold to return to normal. c)Severe abdominal pain : Acute enteritis usually causes severe abdominal pain manifested by rolling and kicking at the abdomen. d)Changes in heart rate: Tachycardia or bradycardia and arrhythmia depending on the degree of acidosis and electrolytes imbalance. (e) Auscultation of abdomen : 1- In early stages of acute enteritis, auscultation usually reveals sound of increased and fluid-rushing sounds. 2- In later stages, there may be paralytic sounds (no sounds) with only fluid and gas tinkling sounds. (f) Systemic reactions : Septicemia, toxemia and fever are common in infectious enteritis. (g) Peripheral circulatory collapse: Occurs commonly in peracute and acute enteritis. N.B : Malabsorption syndrome commonly referred to granulomatous enteritis and lymphosarcoma of intestine of horses that causing chronic anorexia and progressive weight loss, usually without clinical evidence of diarrhea and slight abdominal pain. Diagnosis : I- History. II- Clinical signs. III- Laboratory diagnosis. a) Faecal examined to determine the presence of causative parasites, fungi, bacteria, viruses …etc. as described under the specific diseases. 25 b) Blood analysis usually revealed: 1- Haemoconcentration. 2- Metabolic acidosis. 3- Hyponatremia, hypochloremia, and decrease bicarbonate. (hyperkalemia is possible in severe acidosis due to compensatory movement of K+ from intracellular space to blood) 4- Increase BUN due to inadequate perfusion associated with the dehydration and circulatory failure. Treatment : The principles of treatment of enteritis are 1-Temporary withdrawal of the diet if necessary. 2-Removal of the causative agent (Anthelmentics against parasitic enteritis antibacterial against bacterial enteritis, non specific symptomatic treatment for viral enteritis….. etc 3-Replacement of lost fluids and electrolytes. 4- Intestinal protectants and adsorbents. 5-Use antidiarrheal drugs i.g. drugs inhibit secretion and control intestinal hypermotility of necessary. A) Temporary withdrawal withdrawal of the diet: 1- In foals, temporary withdrawal of feed by muzzling them for 24 hours. 2- Mature horse affected with diarrhea should not have access to any feed for at least 24 hours. (B) Antibacterials: 1- The use of antibacterials either orally or parenterally, or by both routes simultaneously. 2- Parenteral preparations are indicated in animals with acute diarrhea, toxemia and fever (many antibacterials when given parenterally are excreted by the liver into lumen of the intestine). 26  3- Oral preparations may be sufficient in cases of subacute diarrhea with minimal systemic effects. N.B: -Oral antibacterial preparations should not be used for more than 3 days to avoid superinfection. -Type and doses of antibacterial commonly used in bacterial enteritis are described under each disease. (C) Fluids and electrolytes: To correct the 3 major abnormalities of dehydration, acidosis and electrolyte deficit. -When severe acidosis is suspected, a 5% hypertonic soln. of bicarbonate is given i/v at a rate of 5-7 ml/kg B.w at a speed of 100ml/ minute. -Administration of electrolyte solution in quantities necessary to correct the dehydration. : (a) In severe dehydration (equivalent 10% of B.W), large amount of fluids are necessary at rate of 100-150 ml/kg B.W per 24 hours I/V and I gm of Kcl mast be added for each litre of fluid to overcome hypokalaemia. Used successfully to correct dehydration. (b) In animals which are not severely dehydrated, oral route can also be used successfully to correct dehydration. (c) Intestinal protectants and adsorbants : Kaolin and pectin mixtures are used widely to coat the intestinal mucosa, inhibit secretions and increase the bulk of faeces in horses with enteritis (e) Antidiarrheal drugs : Antisecretory drugs for treatment of diarrhea due to hypersecretory activity. For example: atropine sulphate, chlorpromazine Hcl and prostaglandin inhibitors. * * * 27  III-Colitis –X Definition : Highly fatal acute disease of horses characterized by sudden onset of peracutc enteritis manifested by profuse watery diarrhea and rapid development of hypovolemic shock. Etiology : The exact cause is unknown, but 2 causes are suggested: 1- Endotoxic shock due to a bacterial toxin. 2- Exhaustion shock due to adrenal corticosteroids hypersecretion. Clinical signs : 1-Sudden depression. 2- patchy sweating and skin feels cold and clammy. 3-Very sudden onset of enteritis and profuse watery diarrhea. 4- Dehydration and abdominal pain. 5- Muddy discolored mm and dilated pupil. 6- Very fast pulse and elevated temperature (39. 5°C) but soon falls to subnormal before death, which may occur within 4 hours or in less acute cases within 24-48 hours. Diagnosis : 1-History. II- Clinical signs. III- Lab. Diagnosis. 1- Haemoconcentration (PCV may as high as 70%). 2- Severe hypokalemia (serum K+ may as low as 1.5 mmol/L. while nomal 2.5- 3.7. 3- Marked blood acidosis. 4- Elevation of BUN (over 60 mg%). 5- Leukopenia may be present. 28 Treatment : No treatment appears to have any effect on the course of the disease, but the following may be used. 1- Fluids equivalent to at least 10% or even 15% of B.W. e.g.: 40-60 litre/ 400 kg horse) given I/V using indwelling catheter. 2-Massive I/V corticosteroids e.g Dexamethazone 10gm daily for 5 days.. 3-Antihistamincs e.g I/M or S/C 0.4-0.8 mg/kg B.wt. 4- Broad spectrum antibiotics. * * * IV-EQUINE COLIC Definition : It is syndrome caused by diseases of alimentary tract characterized by acute, subacute or chronic abdominal pain. Etiology and types of colic : (a)Acute colic Acute colic with severe pain may be caused by: 1-Acute gastric dilataion resulting engorgement with grain. 2-Impaction of the ileocecal valve resulting from feeding finely chopped indigestible roughage.. 3-Impaction of the small colon with foreign materials. 4-Accumulation of gas (Flatulent colic) due to ingestion. 5-Intestinal accidents including volvulus; intussuscepsion and strangulation (MECHANICAL COLIC). 6- Enteritis, especially that caused by the ingestion of sand (SAND COLIC) 7- Hemorrhage into intestinal well as occurs in purpura haemorrhagica and anthrax. 29  (B) Subacute Colic Subacute colic includes 2 common forms of the disease. (a)obstructive colic: caused by impaction of the cecum or colon (pelvic flexure) with : 1- Undigested fiber. 2- Dry, firm mass of ingesta. (b) Spasmodic colic : Caused by increased gut motility (violent irregular peristaltic movement) and usually following. 1-Periods of excitement. 2- Drinking of cold water after exercise. 3-As a consequence of severe hunger. 4- Sudden change of food. 5- irritation of the gut by unsuitable food stuffs. C) Chronic Colic 30  1- Verminous aneurysm (Recurrent colic) caused by strongylus vulgaris larvae (verminous thromboembolic colic) 2- old age. 3- Debility. 4- poor teeth. 5- Dietetics error (feeding indigestible roughage). 6- 5-Phytobezoars. 7- Enteroliths. Clinical findings : - The clinical signs in different types colic are much the same, varying only in the severity - Pain observed being almost continuous in acute cases and intermittent in subacute cases. The following manifestation of pain may be observed: 1- Restlessness manifested by kicking the belly and rolling. 31 2-Looking at the flank (FLANK WATCHING) is a common sign especially, in cecal tympany and impaction. a photo showing flank watching in case of tympany 3- Lie down carefully and get up slowly, especially in flatulent colic. 4- Often adopting a dog-sitting posture especially in acute gastric dilataion. 5- Affected horses may adopt other abnormal postures, including saw horse attitude and lying on the back. a photo showing a horse laying on a photo showing a horse with back with paddling with legs lateral recumbency and paddling due to colic with legs due to colic 6- In the most severe cases there is - profuse, patchy sweating - Sobbing respiration - Signs of shock including rapid pulse and clammy skin -The horses movements are so violent that self physical injury occurs. 7- Auscultation of the abdomen is helpful in diagnosis. - In flatulent colic, there are high – pitched "gassy pings" - In spasmodic, there are loud gut sound (continuous borborygmi). 32  - in obstructive colic, the normal sounds are decreased or absent. 8- Rectal examination is essential in diagnosis : - In flatulent colic, there is gaseous distention of intestinal loops. - No abnormalities are detectable in spasmodic colic. - Impaction of cecum or colon are readily palpable. - In impaction of ileocecal valve, a cylindrical mass in the terminal part of ileum high up in the right flank. - In case of verminous colic, the obstructed a.v. may be palpable and slack, distended loops of intestine can be found. - Small intestinal accidents are characterized by fluid-filled loops of gut of appropriate size. - Hernias into the inguinal canal are best palpated per rectum, as the intestine may not protrude as far as the scrotum. 9- Projectile vomiting of evill-smelling, green fluid usually result from an obstruction of the intestine at any level from pylorous to the ileocecal valve. Treatment : 1- relief the pain by analgesics e.g Meperidine 2-4 mg/kg B.wt. S/C or chloral hydrate 15-30 gm (by stomach tube) or Buscopan. In mild colic attacks tranquilizers can be used e.g. Acepromazine maleate 2-4 mg/100.lb.B.wt. I/V/ min. or S/C. 2- rectal enema with soap and water may be useful. 3- in impaction colic, mineral oil lubricant or laxative is best treatment (2-4 litres) 4- In sand colic, magnesium sulfate is recommended Magnesium sulphate 300 gm Formalin 30 ml Water 12 litres Warm to body temperature and given by stomach tube. 33 N.B: In both impaction colic and sand colic, these treatments may be followed 12- 24 hours later by injection of carbachol 1.2-4ml 1:1,000. 5- In spasmodic colic, a spasmolytic e.g atropine sulphate 15-30 mg/S/C is effective antispasmodic. 6- In flatulent colic the following prescription can used as a single dose by stomach tube RX: Cresote 6ml Ammonium carbonate 16ml Speritous ether initrosi 36ml Turpentine oil 60 ml Lin-seed oil 1000 ml 7- In constructive and mechanical colic's laparotomy may be useful. 8-In verminous colic, horses may respond to classical therapy, but may respond to a massive doses of appropriate anthelmintic Prevention : In all cases and types of colic, dental attention, advice on feeding and exercise and effective parasitic control are best program for prevention in horses. ▪ SPASMODIC COLIC Definition: It is a subacute form of colic caused by hypermotility of intestine and characterized by short attacks of abdominal pain and loud borborgymi sound Etiology : 1- Period of excitement as preparation for showing or racing. 2- Drinking of cold water after exercise. 3- As sequence of severs hunger. 4- Sudden change of diet. 34  5- Irritation of the gut by unsuitable foods stuffs. Pathogenesis : The hypermotility in spasmodic colic is thought to arise by an increase in the parasympathetic tone under the influence of the causative factors mentioned above. Clinical findings : 1- Short attacks of abdominal pain. 2- Pain is intermittent the horse rolls. Paws and kicks for a few minutes. Then shakes itself and stands normally for a few minutes until the next attack of pain occurs. 3- intestinal sound are often audible distance from the horse and loud rumbling borborygmi sound are heard on auscultation. 4- The pulse is moderately elevated and there may be some patchy sweating. 5- The signs disappear spontaneously within a few hours. 6- There is no scouring. Diagnosis : 1- Case history. 2- Clinical signs. Treatment : 1- Using of atropine sulphate as spasmolytic followed by ½ gallon of mineral oil by nasal tube. 2- Injection of mepridine HCL 2-4mg/kg BW s/c. 3- Novocaine (0.05g/ 100 Ib B.W) injected slowly i.v. may produce immediate relief of pain which lasts for 15-20 minutes. 4- Promazine derivatives have a tranquilizing and spasmolytic effect and followed by a mild purgative appear to be treatment of choice. ▪ THROMBOEMBOLIC COLIC (VERMINOUS ANEURYSM) 35 Definition : It is a chronic recurrent attacks of abdominal pain caused by migration of the larvae of Strongylus Vulgaris in the cranial mesentric artery. Etiology : 1- Migration of the larvae of Strongylus Vulgaris into the of the cranial mesentric artery and its branches causing restriction of the blood supply or damage of the nerve supply to the intestine. 2- Horses in pastures are more susceptible to strongylosis even with good worm control. Pathogenesis : 1- Migration of the larvae of Strongylus Vulgaris causes thrombosis in the mesentric vessels. The thrombosis causes restriction of the blood supply to the intestine leading to typical infarction of the bowel without displacement of the nowel. 2-Secondary bacterial infection mainly by streptococcus equuli actinobacillus equuli, or salmonella causing mesenteric abscess, which produces signs similar to those of aneurysm but the temp. is usually elevated and rupture of the abscess may lead to a diffuse peritonitis. 3- Fatal termination may occur due either to peritonitis after rupture of the intestinal wall or toxemia caused by gangrene of the intestinal wall. Clinical Signs : 1- Severe abdominal pain for 3-4 day with almost complete cessation of defecation. 2- In early stages there may be increased gut sounds to the degree where spasmodic colic suspected while in later stages the intestinal sounds are decreased. Diagnosis : 1- Case history and clinical signs. 2-Radiographic examination to determine the verminous aneurysm 36  3- Lab. Examination of faeces reveals. a- High count of Strongylus eggs. b- Bloody – stained faeces in case of rupture 4- Rectal findings disclose the following a- Distended loops of intestine. b- Tightly stretched mesentry. c- firm swelling in the root of mesenteric artery d- Enlargement of the colic and cecal arteries. Treatment : 1- Anthelmintic such as thiabendazole 500mg/kg B.W. orally 2- Supportive treatment. Fluid therapy 3- I.V. injection of plasma expander dextran 2.5 ml/kg B.W./ day for 3 days followed by further injections at 4- day intervals for a total of 9 injection (has anticoagulant properties) 4- Surgical interference. ▪ SAND COLIC Definition: It is an acute type of colic caused by ingestion of sand that cause irritation or obstruction of the GIT. Etiology and pathogenesis 1- Irritation or obstruction of the gastrointestinal tract is a problem when sand is ingested by horses. 2- Sand is consumed when it becomes mixed with hay fed on the ground, when horses graze short grasses, when they drink from shallow muddy pool,s and when horese become salt deficient. 3- The large colon and in particular the right colons, pelvic flexure and transverse colon are the most common sites of obstruction because they are fermentative areas of reduced flow wheree sand consequently settles and 37  transvere colon become obstructed when masses of accumulated sand become lodged in these narrow segments. Clinical signs : 1- Sand in the intestine causes both mucosal irritation and mechanical obstruction. 2- The mucosal rritation results in diarrhea, which precede mechanical obsturuction of the bowel by several days. 3- When obstruction becomes distended with gases, fluid and ingesta, pain results from stretching of the bowel wall. 4- The weight of the impacted mass as well as distention of bowel result in twisting or displacement of the impacted mass and necrosis of the bowel wall at the site of the impaction. 5- Perforation of the bowel wall at the site of obstruction may occur. Both displacement and perforation result in pain and development of shock. Diagnosis : 1- Simple observation of feeding practices and environment will reveal the opportunity for ingestion of sand. 2- History of diarrhea followed in several days by mild colic is indicative of sudden obstruction of the gastrointestinal tract. 3- Abdominal distension and gastric reflux are the results of complete obstruction or displacement or both. 4- Rectal palpation is not conclusive because the impaction occurs most frequently in areas that are not within reach and the weight of the sand caused the bowel to rest on the ventral abdomen. 5- During rectal palpation, samples of faeces should be examined for the presence of sand. Six fecal balls can broken up into a quart pitcher of water and the sand is allowed to settle. More than a teaspoonful of sand in the container is abnormal. 38 Treatment : 1- If pain is mild to moderate and can be controlled by analgesics and the horse is still passing stool. Medical therapy is indicated. Medical therapy should include laxatives and fluids to maintain hydration and a diet of high quality roughage. Saline purgatives are preferred as will bring fluid into the bowel prevent desiccation of mass and help passage of sand physiological saline and dextrose must be injected i.v. in case of chock. 2- When the pain is uncontrolled, abdominal distension or bowel distention on rectal palpation is marked and the condition does not respond for medical therapy within 48-72 hours, surgical interference is indicated. Delaying surgical interference will result in necrosis and rupture of the bowel. * * * V-INTESTINAL TYMPANY Intestinal tympany causes distention of the abdomen and severe abdominal pain and is sometimes accompanied by the passage of much flatus. Etiology : -All cases of tympany of small intestine are caused by same forms of intestinal obstruction. -Tympany of large intestine may be primary or secondary a- Primary large bowel tympany results from the ingestion of large quantities of highly fermentable green feed. b- Secondary large bowel tympany results from stenosis by constricting fibrous adhesions after castration or in association with verminous aneurysm. Clinical Signs : 39  1- Abdominal pain and affected animal may roll and paw. 2- intestinal peristaltic sounds are reduced but fluid may be heard moving in gas-filled intestinal loops. Producing tinkling and metallic sounds. 3- On rectal palpation gas-filled loops of intestine can be felt. 4- Much flatus is passed and the anus may be in state of continuous dilatation. Treatment : 1- In severe primary cases, trocarization with a long small-caliber intestinal trocar and canula is used. This can be performed though the upper right or left flank descending the maximum distension. 2- Mineral oil 24 liters and antifermentative materials as turpentine oil. 3- In secondary tympany, permanent relief can be obtained only by correction of the obstruction PERITONITIS Definition : Peritonitis means a local or generalized peracute, acute, or chronic inflammation of peritoneum. Etiology : 1- Rupture of the stomach due to ulceration by larvae of Gastrophilus or Habronema spp. Or any other causes. 2- Rupture of dorsal sac of cecum or colon during foaling. 3- Rupture of rectum during rectal examination (predisposed by inflammation of mucosa) 4- Cecal perforation due to heavy infestation by Anaplocephala tapeworms. 5- Administration of non-steroidal anti-inflammatory drugs causing cecal stasis and dilation and eventually perforations. 40  6-Chemical peritonitis result from presence of blood, chyle, urine, bile or pancreatic juice released into peritoneal cavity. 7-Extension from retroperitoneal infection e.g. streptococcus equi after an attack of strangles. 8-Actinobacillus equuli by unknown mean. 9-Traumatic perforation from the exterior of abdominal wall. 10-Bacterial contamination following surgical intervention (laparotomy), trocarization of cecum and peritoneum. Clinical signs : (a) Peracute diffuse peritonitis: In mares the rupture of dorsal sac of cecum occur during foaling there are moderate abdominal pain followed by shock ( due to toxemia and bactremia ) and death after 6-18 hours of rupture. (b) Acute diffuse peritonitis: 1- Complete anorexia. 2- Toxaemia and fever. 3- Faeces may be completely absent for up to 3 days. 4- Alimentary tract stasis evidenced by absence of gut sounds on auscultation (paralytic ileus). 5- Abdominal pain (colic) including flank watching, kicking at the belly and rolling. 6- Palpation of abdominal wall feel tenderness (stiffness). C) Chronic peritonitis : a- Horses with chronic peritonitis usually have a history of ill-thrift for a period of several weeks. b- Clinical signs are.: 1- Severe weight loss. 2- Intermittent episodes of abdominal pain. 3- Reduced or absent of gut sounds. 41 Treatment : a- Specific treatment for the primary cause. b- Non specific treatment includes.: 1- Administration of antibacterial drugs e.g. broad spectrum antibiotics directly into peritoneal cavity. 2- Treatment of toxaemia. * * * HORSES LIVER DISEASES I-HEPATITS Definition : Hepatitis means diffuse acute or chronic inflammation of the liver: - Diffuse chronic inflammation means liver cirrhosis. - Clinically the syndrome caused by cirrhosis of the liver is the same as that caused by acute hepatitis, the only difference being that the onset of the disease is slower and less acute than in hepatitis. Etiology : (A) Toxic hepatitis a- Inorganic poisons e.g. phosphorous, copper, selenium… etc. b-Organic poisons e.g. carbon tetrachloride, hexachlorethane, gossy pol, creasol, coal tar…etc… c-Poisonous plant, e.g. sore weeds, fungi, algae… etc. B) Infectious hepatitis 1- Infectious equine anemia. 2- Viral rhinopneumonitis. 3- Severe cases of equine viral arteritis. 4- Salmonellosis. 5- Bacillus piliformis (tyzzers disease foals) 6- Systemic mycosis e.g histoplasmosis. 42  7- Migrating larvae of Ascaris sp. Clinical findings: (A) Acute hepatitis: 1- Anorexia. 2- Constipation intermittent with attacks of diarrhea. 3- Faeces lighter than normal. 4- Subacute abdominal pain manifested by arching of back. 5- Nervous signs vary from ataxia and lethargy with "yawning" or coma to hyperexcitability with muscle tremor, mania, including aggressive behaviour, and convulsions. 6- Jaundice and oedema may or may not be present. 7- Photosensitization in animals fed green feed only when exposed to sunlight. 8- A tendency to be more feely than normal may be observed. (B) Chronic hepatitis (cirrhosis): - The signs are similar to those of acute hepatitis but develop more slowly, and persist for longer periods; often months. - Ascitis and the dummy syndrome are more common in chronic hepatitis N.B: Dummy syndrome is a characterized syndrome observed in animals affected with hepatitis especially chronic one (cirrhosis) in which affected animals push with the head, does not respond to normal stimuli, and may be blind. Diagnosis : 1- History II- Clinical signs. III- Lab. Diagnosis. 43 Laboratory examination of blood (liver function tests) and urine samples and liver biopsy specimens. Treatment : 1-Avoid protein and protein hydrolysate to avoid danger of ammonia in toxication due to failure of liver detoxification mechanism and subsequent nervous signs. 2- The diet should be high in carbohydrate and calcium and low in protein and fat. 3- Oral administration of broad-spectrum antibiotics (neomycin) to control protein putrifaction. 4- Periodic injections of water-soluble vitamin particulary vitamin B complex. N.B: Hepatic cirrhosis is considered to be a final stage and treatment is not usually undertaken. 44  DISEASES OF RESPIRATORY SYSTEM (A). Trachea (5) Frontal (B). Cartilage sinuses (C). Vocal cord (6) Guttural (D). Epiglottis pouch (1) Buccal cavity (7) Pharynx (2) Nasal Cavity (open to (8) Trachea pharynx) (9) Bronchus (3) Inferior maxillary sinus (10) Alveolus (4) Superior maxillary sinus (11) Lungs (12) Larynx EPISTAXIS (NOSE BLEED) - Epistaxis mean bleeding from the nostrils regardless of origin of the hemorrhage. - hemoptysis means coughing of blood with hemorrhage usually originating from the lungs. Etiology : a- Epistaxis occurs commonly in the horses and may be due to lesions in nasal cavity, nasopharynx, guttural pouch or lungs. b- Hemorrhage lesions of nasal cavity, nasopharynx and guttural pouch usually cause unilateral epistaxis, while blood originating from the 45  lungs is discharged from both nostrils and not the mouth because of the long soft palate. N.B: Blood originating from the lungs not foamy as was previously thought because the horizontal position of the major bronchi allows blood to flow out freely without being coughed-up and made foam. Froth is usually the result of pulmonary edema in which case it is very fine pink stable froth. c- The commonest cause of epistaxis in horses are: 1- External trauma. 2- Foreign bodies in nasal cavities. 3- Neoplasms (erosion of m.m. of nasal cavity). 4- Mycotic ulceration of B.V. in the wall of guttural pouch around the guttural pouch. 5- Encapsulated hematoma in nasal cavity. 6- Hemorrhage polyps of m.m. of nasal cavity or paranasal sinuses. 7- Erosion of the nasal mucosa in glanders. 8- Internal trauma due to passage of nasal tube or endoscope. 9- Congestive heart failure (mild epistaxis). 10- Purpura hemorrhagica. 11- Thrombocytopenia (generalized bleeding). 12- Idiopathic in exercise-induced epistaxis in race horses (bleeders). Diagnosis: I- History II- Clinical signs. III) Exam of nasal cavities : 1- Visually with the aid of strong pointed source of light through external nares. 46  2- with the use of flexible fiberoptic endoscope will permit thorough exam. Of the nasal cavities, nasopharynx, guttural pouch larynx, trachea and major bronchi. Treatment : a- Treat the cause, if it is known. b- when the cause is obscure, treat symptomatically as follow: 1- Cold packs over the nose and forehead. 2- Tampon or gauze soaked in adrenaline inserted in zigzag manner into affected nostril (but not in both nostrils). 3- vasoconstrictor drugs e.g. thrombin solution spray on bleeding surface immediately, or diacynon injection. 4- Calcium preparations e.g. calcium gluconate 20% 500 ml. S/C or slow I/V. 5- Vitamin – K injection ( synkavit = synthetic – vitamin – K ) 6- Blood transfusion in severs cases. 7- Hematinics e.g. iron preparations. N.B: Avoid injection of adrenaline as it increasing bleeding by rising of blood pressure. RHINITIS (CORYZA) Definition : Rhinitis means inflammation of m.m of nasal cavity which may be acute or chronic, unilateral or bilateral, characterized by sneezing, wheezing and stertor during inspiration and nasal discharge which may be serous, mucoid; purulent or blood – tinged in consistency depending on the cause. 47 Etiology : (A) Rhinitis is present as a lesion in the following conditions: 1- Dusty stable. 2- Inhalation of irritating chemicals. 3- Nasal foreign bodies. 4- Extension of alveolar infection. 5- Nasal or sinus tumors. (B) Rhinitis is present as a lesion in the following diseases: 1- Strangles. 2- Glanders. 3- Epizootic lymphangitis 4- Equine rhinovirus. 5- Equine Viral rhinopeumonitis (herpes virus) 6- Influenza viruses 7- Parainfluenza viruses. 8- Adenovirus. 9- Reovirus 10- Hoppengarten cough virus 48 Clinical signs : -Rhinitis is of minor importance as a disease proceed. Its major importance is indication of the presence of some specific infections diseases. - The cardinal signs in rhinitis are : 1- Nasal discharge which is usually serous but soon becomes mucoid, and in bacterial infections, purulent. 2- Erythema, erosion or ulceration may be visible on inspection of nasal m.m 3- Sneezing in the early acute stages which followed in later stages by snorting. 4- Associated L.n. may show signs of inflammation. N.B: Chronic unilateral purulent nasal discharge lasting several weeks or months may suggest nasal mycosis (aspergillosis, or Cryptococcus) Diagnosis: (1) History (II) clinical signs (III) Lab. Diagnosis Exam. Of nasal swabs of scraping for bacteria, inclusion bodies or fungi may aid in diagnosis. (IV) Endoscopic examination : Endoscopic examination using a flexible fiberoptic endoscope is very useful for the visual inspection of lesions affecting the nasal mucosae which are not visible externally. Treatment : 1- specific treatment to control causative agents as described under the specific diseases and causes. 2- remove the thick tenacious exudates which causing nasal obstruction using warm boric acid, then irrigate the nasal cavity with saline or mixture of saline and antibiotics to provide symptomatic relief and minimize secondary bacterial rhinitis. 49  3- Spray – up nasal decongestant into the nostrils to provide some relief e.g.. Delta rhinol spray. 4- Culture and sensitivity testing to assist the selection of suitable antibacterial agents, which may be helpful in controlling secondary bacterial infection. Diseases Of The Guttural pouch 1- Guttural pouch mycosis: Occur horses as result of an infection entering the Eustachian tube via its pharyngeal orifice (e.g. Aspergillus sup) At least 4 different sequels to guttural pouch mycosis may result: 1- Erosion of internal carotid artery with the sudden development of profuse epistaxis, usually in a horse at rest. 2- Thrombus development in the internal carotid artery with emboli being shed to locate, unilaterally in brain resulting in blindness and ataxia. 3- Mycotic encephalitis. 4- Inflammation of the cranial nerves anatomically close to the wall of the guttural pouch. The common effects of damage to these nerves are: a-Dysphagia due to involvement of pharyngeal branches of hypoglossal and vagal nerves. b-laryngeal hemiplagia(roaring disease) due to involvement of laryngeal branches of vagus. c-Facial paresis due to involvement of facial nerve. d-Horner's syndrome (ipsilateral facial sweating and hyperthermia, smaller palpebral fissure, mild miosis) due to involvement of sympathetic neurons. II- Guttural pouch empyemia : Accumulation of pus in the guttural pouch. The causes of guttural pouch empyemia or sepsis usually: 50  1-Extension from pharyngitis (especially streptococcus infection) 2-Rupture of an abscess of retro-or supra pharyngeal lymphnode. -The clinical signs of guttural pouch empyemia are: 1- Chronic toxaemia (manifested by pyrexia) 2- distension of one or both pouches. 3- pain on swallowing and dysphagia 4- Coughing 5-Intermittent mucopurulent or purulent nasal discharge especially when animal lowers its head. III- Guttural pouch tympany: 1- The disease is limited in occurrence to foals a few days old. 2-The disease occur due to congenital defect of closure of the Eustachian tube that a lows the pouch to fill with air and distended obviously and to an enormous size. Diagnosis: 1- History II- clinical signs III- Endoscopic exam of pharynx. Treatment : 1-Catheterization and irrigation of the guttural pouches with the following. a) Iodine solution in guttural pouch mycosis. b) Antibiotics solution in guttural pouch empyemia. Pencillin K 5.000.000 I.U. Dihydrostroptomycine 2.0 gm. Isotonic salt solution 100 ml. Flush into guttural pouches daily for 7-10 days. 1- palliative treatment by systemic administration of : 51 (a) Iodides to control mycosis or 15- minutes application of 30 ml nystain ( mycostatin oral suspension ). (b) Antibiotics paranterally to control empyemia. 3- Surgical drainage for unresponsive infections. DISEASE OF LARYNX Roaring disease ( Laryngeal hemiplegia ) Definition : Roaring disease is a chronic, unilateral or occasionally bilateral paralysis of the intrinsic muscles of the larynx causing audible inspiratory dyspnea. N. B: - Paralysis occurs on the left side in 92% of the recorded cases, on the right side in 6% and on both side in 2%, this observation has led to theory that the disease is related in some way to constant irritation produced by pulsations of aorta as the left recurrent laryngeal nerve passes around it. 52 Etiology: a- Degeneration or injury of one or both or both of the recurrent laryngeal nerves. As a result, the arytenoids cartilages and the corresponding vocal cords fail to rotate outward on inspiration, causing reduction in the size of the lumen of the larynx with consequent inspiratory dyspnea. b- The causes of degeneration or injury of the nerve may be: 1- Accidental injury to the nerve by over extension of head. 2- Previous injection of irritating substances. 3- Previous infectious disease e.g. Strangles. 4- Guttural pouch mycosis. 5- Debilitating diseases. 6- Lead poisoning. 7- Certain plant poisoning. 8- Hereditary predisposition. Clinical findings : 1- Whistling or roaring sound heard on inspiration, in severe or advance cases. 2- In mild or recent cases, the sound may be produced only after strenuous exercise and subsides within few minutes after exercise stopped. 3- Badly affected animals are unfit for fast work and tire quickly as a result of the dyspnea. 4- Experienced clinicians may be able to detect a pit between the arytenoid and thyroid cartilages on laryngeal palpation. Diganosis: ( I ) History ( II ) Clinical signs (III ) Endoscopic examination: Endoscopic examination of the larynx confirmed the diagnosis. 53 Treatment: 1- Spontaneous remissions rare. 2- Surgical correction is: a- Extirpation of the laryngeal ventricle ( ventriculectomy ) is successful in restoring about 60% of the affected horses. b- Surgical retraction of the cartilages has proven effective in cases that have not respond to ventriculectomy. LARYNGITIS, TRACHITIS AND BRONCHITIS (Upper respiratory tract affection) Etiology: 1- Equine viral influenza. 2- Equine viral arteritis. 3- Equine herpesvirus. 4- Strangles (streptococcus equi) Clinical findings: Coughing and inspiratory dyspnea are the two common clinical signs. 1- In the early acute stages, the cough is usually dry non-productive and is easily induced by grasping the larynx and trachea. In the chronic stages, the cough may less frequent distressing and usually dry and harsh. N.B: 1-Moist cough and thick mucous, flackes of blood and fibrin may be coughed if the lesions cause much exudation or ulceration of the mucosa. 2- Inspiratory dyspnea varies with the degree obstruction and is usually accompanied by a loud stridor and harsh breath sounds on each inspiration (these are best heard over the trachea) Diagnosis: (I) History (II) Clinical examination. (III) Endoscopic examination: 54  Examination of upper respiratory tract with fiberoptic endoscope Treatment: 1- Rest and avoidance of exposure to inclement weather may resolve spontaneously the common viral infection. 2- Secondary bacterial complication must be treated with the appropriate antibacterial agent (antibiotics or sulfonamides) 3- A combination of corticosteroid (Dexamethazone) and antibiotics therapy is of value in chronic cases in horses. N.B: - Animals with severe lesions and marked inspiratory dyspnea may require a tracheotomy and insertion of a tracheotomy tube for several days until the lesion heals. PNEUMONIA Definition : Pneumonia is inflammation of pulmonary parenchyma usually accompanied by inflammation of the bronchioles and often by pleurisy Etiology : (A) predisposing factors: predisposing factors weaken the defense mechanisms of the animals e.g. 1- Inclement weather. 2- poor ventilated housing. 55 3- stress of transportation. 4- Stress of malnutrition. (B) infectious causes: a- Viral pneumonia 1- Adenovirus pneumonia (in immune – deficient foals). 2- Equine herpes virus (older foals) 3- Equine influenza virus (older foals) 4- Equine viral arteritis (adult horses). 5- Equine viral rhinopneumonitis (adult horses). b- Bacterial pneumonia : 1- E. coli streptococcus equi, Actinobacillus equuli which causes newborn foal septicemia. 2- Corynebacterium equi (older foals) 3- Strangles 4- Glanders 5- Pleuropneumonia due to anaerobic bacteria. C- Mycotic pneumonia: 1- Epizootic Iymphangtitis 2- pneumonic aspergillosis d- Verminous pneumonia: 1-Dictyocaulus arnifeldi. 2- Parascaris equorum. Clinical findings : 1- rapid, shallow respiration is the cardinal sign of early pneumonia. - Dyspnea occurring in the later stages when much of the lung tissue is non – functional 2- Cough which is: - Dry, frequent, hacking cough in interstitial pneumonia. - Moist, painful cough in bronchopneumonia. 56  3- Cyanosis: Not a common sign, Occurs only when large areas of the lung are affected. 4- Nasal discharge: May or may not present depending upon the amount of exudates present in bronchioles and whether or not, there is accompanying inflammation of the upper respiratory tract. 5- Abnormal breath odour: Decay – putrid – Decay when there is a large accumulation of inspissated pus. - Putrid when pulmonary gangrene is present. 6-auscultation of the lunges – in early – crackles – In early congestive stage of bronchopneumonia and interstitial pneumonia there is in creased breath sound (bronchial sound) -Crackles (moist rales) develop in bronchopneumonia as bronchiolar exudation increases. N.B: Consolidation also causes increased audibility of the heart sounds. Pleuritic friction rub in early stages when pleurisy. Is also present and muffing of bronchial sounds in the late exudative stages. 7- in acute bacterial bronchopneumonia, there is toxemia, fever, anorexia, depression and tachycardia. Diagnosis : (I) History (II) Clinical (III) Endoscopic examination (IV) Nasal swabs Treatment : 1- Isolation of affected animals (particularly if infectious disease suspected) in warm, well ventilated, draft free place and provide with ample fresh water and light nourishing food (parenteral force – feeding of animal not eat) 57  2- The choice of antibacterial agent (antibiotic or sulfonamide) based on culture and sensitivity testing. Drug the choice of antiparasitic agent if verminous pneumonia suspected. 3- The use of corticosteroid as and anti-inflammatory agent e.g. Dexamethazone, Betamethazone. 4- The use of bronchodilator to improve ventilation with a resulting net improvement in oxygen exchange. The most commonly used agents are aminophylline and theophylline. Sympathomimetic drugs such as epinephrine is effective but little used because of their – term action. Diagnosis : (I) History (II) Clinical signs (III) Endoscopic examination (IV) Nasal swabs Treatment : 1- Isolation of affected animals (particularly if infectious disease suspected) in warm, well ventilated, draft free place and provide with ample fresh water and light nourishing food (parenteral force – feeding of animal not eat) 2- The choice of antibacterial agent (antibiotic or sulfonamide) based on culture and sensitivity testing. Dr the choice of antiparasitic agent if verminous pneumonia suspected 3- The use of corticosteroid as and ant inflammatory agent e.g. Dexamethazone, Betamethazone. 4- The use of bronchodilator to improve ventilation with a resulting net improvement in oxygen exchange. The most commonly used agents are aminophylline and theophylline 58  Sympathomimetic drugs such as epinephrine is effective but little used because of their short – term action. The beta-2 adrenergic receptor selective bronchodilators, such ad clenbuterol, a new being used in COPD and exert a very beneficial effect. 5- Antihistaminic e.g. Avil injection or tussivan syrup. 6- the use of execptorants according to type of cough. - When cough is painful and exhausting and the secretion tenacious, sedative expectorant, such as ammonium or potassium salt, stimulate secretion of protective mucus and lessen coughing - When cough is soft and bronchial exudates is voluminous, as in bronchopneumonia, stimulant expectorant is more valuable. - When cough is exhausting and interferes with activity but there is little exudation, anodyne expectorant, such as belladonna, codeine, morphine or heroin is indicated. ASPIRATION PNEUMONLA (Drenching pneumonia, Inhalation Pneumonia) Etiology : 1- Careless drenching or passage of a stomach tube during treatment for other illness. 2- Following vomiting 3- Rupture of pharyngeal abscess. 4- Paralysis obstruction of larynx, pharynx and esophagus result in aspiration of foal of water when attempting to swallow. Clinical signs : 1-If large quantities of fluid are aspirated death may occur suddenly 59  2- If small quantities are aspirated, the outcome may depend on the composition of the aspirated, the outcome may depend on the composition of the aspirated material e.g -With soluble such as chloral hydrate and magnesium sulphate, very rapid absorption from the lung occur. -With insoluble substances and vomitus, pneumonia with toxaemia result, which is usually fatal in 48-72 hrs. 3- The severity of aspiration pneumonia depend largely upon the bacteria which are introduced, causing in many cases an acute gangrenous pneumonia. Treatment: As mentioned before with pneumonia. Chronic obstructive Pulmonary Disease (COPD) (Bronchiolitis – Emphysema Complex) 60 The disease was formerly known as "Heaves", poor man disease, chronic alveolar emphysema , pulmonary emphysema or broken wind Definition : - COPD in the horse is characterized clinically by decrease work performance, chronic coughing, abnormal lung sounds and cardiac dysfunction. - Pathologically, there are varying degree of bronchiolitis and pulmonary emphysema. N.B: Pulmonary emphysema is a distension of the lung caused by over distension of the alveoli with rupture of alveolar wall with or without escape of air into interstitial spaces. Etiology: - The exact cause of the disease in unknown. - Epidemiological evidence of the disease suggest the following causes. 1- Hypersensitivity reaction to "allergens"found in barn dust and moldy and dusty feeds such as, Aspergillus fumigatus and Micropolyspora. 2- as a sequelle to viral infection of the upper respiratory tract of the horse. 3- Secondary to bronchopneumonia 61 Clinical findings : On clinical examination, the horse is usually bright and alert, the temperature is normal and appetite is usually normal 1- Coughing (single or paroxysm) which becomes more pronounced and wheezing with exercise. 2- intermittent, bilateral nasal discharge which may be serous, mucoid mucopurelent or blood stained. 3- The resting respiratory rate is increased from a normal of 12/min. up to 24-36/min. 4- Expiration is biphasic or more exaggerated (double expiratory effort). 5- During expiration there is normal collapse of the rib cage followed by a clearly visible contraction of the abdominal muscles of flank. N.B: In longstanding cases this result in the so-called Heave – line which is a trough which follows along the costal arch (Barrel chest) 6- Auscultation of the lungs reveal wheezing and crakling sounds occur at the end of inspiration and the end expiration (placement of plastic bag over the horse's nostrils for I minute will cause the horse to hyperventilate and abnormal sounds are more pronounced) N.B: Pleuretic friction rib may be auscultated over the chest 7- Percussion of the thorax may reveal a hyper resonant sound and also revealed an increase in the area of resonance by as much as 1 – 2 intercostal spaces caudally. 8- increasing in heart rate up to 50-60/min in advanced cases of COPD due to pulmonary arterial hypertension. N.B: COPD may resulted in ventricular right – sided hypertrophy and congestive heart failure. 62 Diagnosis: ( I) History: 1- The disease occurs most commonly in adult horses over 5 years of age (6 – 10 years of age) 2- the usual history is that the has been stabled for several weeks or months and has a chronic cough. 3- The horse may have had an infections respiratory disease 1 or 2 months previously, recovered from the acute illness but began coughing recently. (II) Clinical findings : (III) Lab. Diagnosis: 1- Blood gas analysis in COPD reveal PaO 2 below normal and PaCO2 us increased. 2- Pulmonary function test. 3- precipitins against fungi have been identified in serum of affected horses. 4- allergic skin test and antigen inhalation tests have also been used. 5- Cytological examination of tracheobronchial aspirates with COPO reveal excessive mucus and neutrophils. 6- Endoscopic examination of upper respiratory tract. 7- Radiographic examination of thorax may be useful in differentiating COPD form other diseases of the lungs of horses. Treatment and Control : There is no specific cure, treatment is palliative. 1- The provision of fresh air, as the horse should be kept permanently in the open air. 2- Avoid exposure of the horse to dust, therefore wood chippings or saw dust should be used for bedding instead of straw. 3- Corticosteroids, such as dexamethazone 25mg/ animal In every 2 nd day for up to 2 weeks may give remarkable results because of their 63  antinflammatory used as an aid in the temporary treatment of COPD such as: a- isoprenaline inhalation is a sympathomimetic drug which stimulate beta- 1 (cardiac) and beta2 (smooth muscle) receptors causing cardiac stimulation and bronchial muscle relaxation (temporary relied for 1-2 hrs.) b- Turbutaline inhalation is a sympathomimetic drug which exhibits action selectively in smooth muscle receptors (beta-2) causing bronchiodilation with no cardiac stimulation for 1-2 hours. c- Clenbuterol HCL(long acting bronchodilator( is a beta-2 sympathomimetic has no untoward effect on circulatory system of exercising horses. d- Atropine is a parasympatholytic drug given In at rate of 0.02 mg/kg B.w. 5- Antibiotics are used in treatment of COPD in horses, but there is only limited clinical evidence of their value. E.g. penicillin procaine 25.000 I.U/kg B.W. daily for 2 weeks (sulphamethazine has also been recommended). PLEURISY (PLEURITIS) Definition: - Acute, subacute or chronic inflammation of the pleura. - Acute pleurisy causes severe pain during respiratory movements, manifested clinically by shallow rapid respiration subacute pleurisy is accompanied empyemia causing collapse of the lung and respiratory embarrassment. Chronic pleurisy is usually manifested by the development of fibrous adhesions and interference with respiratory movement. 64 Etiology : (A) primary cause: - Traumatic penetration of chest wall. (B) secondary causes: 1- Secondary to pneumonic lesion. 2- Rupture of a pulmonary abscess. 3- Streptococus equi infection (secondary to strangles) 4-pleuropneumonia in mature horses is due to anaerobic bacteria (Bacteroids spp.) and klebsiella pneumonae and streptococcus zooepidemicus. 5- Mycoplasma felis. 6- Equine infectious anemia (rare cause) Clinical findings: (A) Acute pleurisy: 1- Pain and anxiety manifested by rapid shallow respiration. 2- Respiratory movements are markedly abdominal. 3- Abducted elbows. 4- pleuritic friction sound in auscultation. 5- Deep digital palpation of intercostals space causes pain. 6- Elevated temp. and pulse rate. 7- Toxemia with anorexia and depression. N.B: - Acute pleuritis may causes colicy signs in horses -Advanced pleurisy may causes subcutaneous oedema of the ventral body wall extending from the pectorals to the prepubic area (due to blockage of lymphatics drain the sternal lymph nodes. 65 (B) Subacute pleurisy : 1- Dullness on percussion over the fluid-filled area of the thorax and dull area has a level top line – a fluid line. 2- Dyspnea is evident, particularly during inspiration. 3- More severe toxemia and anorexia. 4- Elevated temperature, and pulse rate. 5- Painful, short and shallow cough (due to concurrent pneumonia) (C) Chronic pleurisy : 1- Weight loss is one of the most common complains. 2- respiratory embarrassment because of the presence of adhesions (race horses do not regain complete efficiency). 3- rupture of adhesions during severe exertion may cause fatal hemorrhage, Diagnosis : (I) History (II) Clinical signs (III) Lab. diagnosis 1- Thoracocentesis to obtain a sample of pleural fluid. 2- The pleural fluid should examined for odour, color, viscosity, protein concentration, blood and bacteria. 3- The pleural fluid should be cultured for both aerobic and anaerobic bacteria and mycoplasma. IV- radiographic examination : Radiographic examination of chest may reveal the presence of fluid line and displacement of mediastinum and heart to the unaffected side and collapse of the lung. V- Pleuroscopy : Treatment: - The prognosis of pleurisy in horses is unfavorable. 66  1- Control the infection by parenteral or oral administration of antibiotics or sulphonamides (detected by bact. Exam. Of pleuritic exudates) N.B: Treatment of anaerobic bacterial pleuropneumonia in the horse may require the use of antimicrobial such as chloramphenicol or metronidazole. 2- Drainge or aspiration of the pleural fluid by special needle, but the use of diuretics is most useful and less dangerous. 3- Analgesics such as phenylbutazone in acute cases. 67  DISEASES OF URINARY SYSTEM Glomerulonephritis 1- Glomerulonephritis is an inflammatory disease involving the kidney, affecting principally the glomeruli and may extending secondarily into the surrounding interstitial tissue and blood vessels.. 2- It is a rare disease in animals (principally a disease of humans), occurs) in horses in association with: a) Streptococcal equi infection. b) Equine infectious anemia virus. 3- Glomerulonephritis usually resulting in chronic renal failure. 4- The most consistent signs of chronic renal failure in horses is "weight loss" additional signs are: anorexia, polyuria, polydipsia and ventral oedema. 5- The consistent lab. Diagnostic findings is a high blood urea nitrogen (BUN) and serum creatinine. N.B: Urine analysis findings vary with the nature and stage of the disease. 68  CYSTITIS Definition : Cystitis means inflammation of. m.m. of U.B. characterized by frequent, painful urination. Etiology: 1- Introduction of infection into U.B. when trauma to bladder has occurred or when there is stagnation of urine e.g. - Vesical calculus - Contaminated catheterization. - Paralysis of the bladder. - Late pregnancy. 2- The infection causing cystitis usually mixed bacteria but predominantly E.coli. N.B: Sudax or sudan grass causes outbreak of cystitis in horses. It is causes possibly by a fungal toxin. Clinical findings : 1- Painful sensation and desire to urination (due to urethritis which usually accompanies cystitis). 2- Frequent painful urination. 3- The horse remain in the posture adopted for urination for some minutes after the has ceased. 4- The volume of urine passed on each urination is usually small. 5-In very acute cases there may be moderate colicy pains and moderate febrile reaction. N.B: In chronic cystitis there is inflammatory thickening of U.B. wall which is palpable on rectal examination. 69 Diagnosis: (I) History (II) Clinical signs (III) Lab. Diagnosis: 1- Microscopic exam. Of urine sediment reveals the presence of blood cells (erythrocytes), pus cells (leukocytes) and desquamated epith. Cells. 2- Bacteriological exam. (isolation and culture and sensitivity test) of urine confirm the diagnosis. Treatment: 1- Irrigation of U.B. using mild antiseptic solution e.g. potassium permanganate 1 : 5000. 2- The use of drugs which causing change in pH or urine (have bacteriostatic action) e.g. Hexamine and mandelic acid. 3- Antibiotics, based on culture and sensitivity control infection for 7- 14 days. 4- Free access to water to ensure a free flow urine. Paralytic Bladder Etiology : Lesions in the lumbosacral part of the spinal and e.g. - Neuritis of the cauda equina. - Enzootic equine ataxia – cystitis (sudan grass or sorghum ataxia – cystitis which contain HCN). - Fractures, ostemyelitis or neoplasia involving the lower, sacral or upper coccygeal vertebrae. Clinical Signs : 70  1- in the early stages, the U.B remain fully and dribbling (urinary incontinence) occurs especially during movement, exercise or even coughing, which increase the intrabdominal pressure. 2- In the later stages, the U.B. will begin to empty involuntarily although evacuation is usually incomplete and some urine is retained causing cystitis. 3- Scalding of perineal area and rear limbs may be present in mares. Treatment : Prognosis of paralytic bladder is poor. 1- Essential regular catheterization (but avoid introduction of infection) 2- Adm. of antibiotics as a prophylaxis against the development of cystitis and may be a useful therapy for osteomyelitis. 3- Corticosteroid (0.5-1 mg/kg prednisone orally or 0.1 mg/kg dexamethzone injection I/m) every other day for 8-10 days if equine herpes virus-1 myeloencephalitis suspected. 4- Application of petroleum jelly to rear limbs to prevent urine scalding. UROLITHIASIS (URINARY CALCULI) Calculi may occur anywhere in the urinary tract in horses, but are found principally in the U.B. or urethra. Etiology : 1- The pressure of mucous and epith. debris in equine urine leads not only to viscous and turbid appearing urine, but also may serve as a nuclei for calculi 2- Two types of calculi are commonly found in equines. a) The first occurs in horses fed hay, is yellow – brown and crystalline, and composed principally of calcium carbonate. b) The second from in horses being fed grain ration, this type is smooth white and composed of phosphates. 71 Clinical findings : (a) Bladder calculi - The initial calculi from in the renal pelvis and pass to U.B., where they increase in size by mineral deposition around the initiating nuclei of white or red blood cells, albumin, fibrin or epith cells. - The horse may exhibit signs of abdominal discomfort when exercised, or may void urine accompanied by straining occasional blood in the urine. - Rectal exam. Identifying the calculus in the bladder. b) Urethral calculi 1- Restlessness, abdominal pain, and frequent urinary attempts. 2- On rectal exam, the U.B. found distended 3-The stone may be located anywhere in the urethra, but is more commonly found at the turn at the pelvic inlet. Treatment: Smooth – muscle relaxant may help the passage of stone, otherwise surgery is indicated. RENAL FAILURE Renal failure may be acute or chronic 1- Acute Renal Failure Definition : Acute renal failure is the inability of the kidney to perform the major functions of clearing nitrogenous waste products from blood and maintaining fluid and electrolyte haemeostasis. It is sudden and reversible. It is characterized by the clinical signs of azotemia (accumulation of nitrogenous waste products in blood) and biochemically by elevation of 72  serum creatinine more than 1.0 mg/dl or urea 10 – 20 mg/dl. This usually occurs 2/3 or 3/4 of the nephrons are not functioning properly. Incidence : Uraemia or azotemia may be: 1 – Prerenal - decreased blood flow to the kidneys 2- Renal - various affections including glomeruli, ascending tubules, descending tubules, and collecting tubules. 3- Postrenal - impairment of urine flow after the kidney i.e. ureter, bladder and urethra. Etiology: 1- Prerenal azotemia: It may be usually due to 1- Hypovolemic reduction in cardiac output following circulatory failure. 2- Hypotension vascular thrombosis. All these conditions may lead to severe ischaemia of the kidney followed by severe kidney damage, tubular dysfunction and may be eventually necrosis of kidney tissues. II- Renal azotemia: It is usually due to circulating potential renal causes due to 1-Nephrotoxic substances. a- Endotoxic circulating substances: the endotoxins are usually due to systemic coagulopathy vascular damage or thrombosis such as myoglobin, which is one of the most contributing causes b- Extrinsic nephrotic substances as 1-Medicaments - Antibiotics and sulphonamides 73  aminoglycosides, sulphonamides, cephalosporin polymxin B, vancomycin, amphotricin B. Neomycin is most nephrotoxic while streptomycin is the least and kanamycin and gentamycin are intermediate -Phenybutazone (prostaglandin synthetase inhibitors) - Vitamins: - Vitamin D2, D3 -Synthetic Vit. K (Menadione sodiumbisulfate) 2- Heavy metals: as mercury, arsenic, selenium, canthridine (blister beetle), tetrachlorodibenzodioxin (Dioxin) and oxalate. 3- Bacterial infection of kidney: It is difficult to be diagnosed until be fulminant. The root of infection is either ascending or haematogenous. Chronic inflammatory condition in equine are usually caused by Corynebacterium equi, corynebacterium pneumonia, strept. abscess, equine infectious anaemia, leptospira infections, deposits of circulation antibody complex that cause glomerular damage. III- Postrenal causes : Include abnormalities in the lower urinary tracts as: 1- Rupture of the bladder that mainly occurs in neonatal foals and during parturition in mares. 2- Urethral and ureteral tears (laceration) Affected equine shows anuria, Azotemia, dehydration, hyponatremia, hyperkalemia, and hyperchloremia. obstruction in one ureter is not manifested clinically due to compensation by the other kidney. 3- Calculi : In horses, it is usually in the bladder and become lodges in the urethra of equine with those affections show dysuria, stranguria and occasional haematuria. Clinical signs These are non specific symptoms 74  1- Anorexia 2- Depression and weakness 3- Decrease performance 4- Mild to severe colic 5- Intermittent fever 6- Dehydration. 7- The urine may have abnormal flow or amount or constituents. These may be manifested as anuria or oliguria or change in color or consistency of urine: a. Normal urine outflow is 1-2ml/kg/hour. b. Anuria, dysuria and stranguria suggest obstructive urinary problem. c. Oliguria usually in case of haemodynamic