SMALL RUMINANTS 2

SMALL RUMINANTS

Acknowledgements

  • Dr. Sarah Humphreys, DVM, DACVIM (LAIM)

  • Special recognition to Dr. Hilari French, DVM, DACT, DABVP (Food Animal)

LEARNING OBJECTIVES

  • Be prepared to approach the following diseases in sheep and goats in clinics:

    • Respiratory diseases: Oestrus ovis, infectious causes of pneumonia

    • GI diseases: Ruminal acidosis, bloat, abomasal ulcers, rectal prolapse

    • Toxins: Rhododendron, copper

    • Neurologic diseases: Polioencephalomalacia (PEM), listeriosis

    • Ophthalmologic diseases: Infectious keratoconjunctivitis

    • Reproductive diseases: Mastitis, precocious udder

    • Clostridial diseases

RESPIRATORY DISEASES

OESTRUS OVIS

  • Also known as nasal bots

  • Affects sheep, goats, and camelids

  • **Lifecycle: ** Fly deposits larvae near nostrils.

    • Larvae migrate to the dorsal turbinates and sinuses.

  • Clinical signs:

    • Rhinitis

    • Sneezing

    • Mucopurulent discharge

    • Stridor

    • Decreased airflow

  • Diagnosis: Endoscopy

  • Treatment: Ivermectin

SINUSITIS

  • Involves frontal or maxillary sinuses, particularly post-dehorning.

  • Clinical signs:

    • Drainage

    • Unequal airflow

    • Foul odor

    • Head pressing

    • Pyrexia

    • Lethargy

    • Anorexia

  • Diagnosis: Clinical signs + percussion of affected sinus

  • Treatment:

    • Daily lavage of affected sinus with 0.1% chlorhexidine solution

    • Systemic: Antibiotics + NSAIDs

PHARYNGITIS/RETROPHARYNGEAL ABSCESS

  • Pharyngitis:

    • Trauma from dosing equipment; caused by T. pyogenes, F. necrophorum, and C. pseudotuberculosis.

    • Treatment: NSAIDs, rumen fistula, flush abscess with dilute betadine, antibiotics.

  • Retropharyngeal Abscess:

    • Caused by C. pseudotuberculosis.

    • Clinical signs: Coughing, difficulty swallowing, stridor.

    • Treatment: Do NOT lance; possible surgical removal.

SMALL RUMINANT PNEUMONIA

  • Bronchopneumonia:

    • Categories: Infectious (bacterial, viral) or non-infectious (aspiration).

    • Types: Interstitial pneumonia (infectious lungworm, OPP/CAE), anaphylaxis, ARDS, toxins, metastatic (uncommon).

INFECTIOUS BRONCHOPNEUMONIA

  • Key bacteria and viruses impact:

    • M. haemolytica

    • H. somni

    • P. multocida

    • T. pyogenes

    • PI3

    • Mycoplasma ovipneumoniae

    • RSV

    • Ovine/caprine herpesviruses

    • Bibersteinia trehalosi (notable pathogen)

    • Chlamydophila spp

PNEUMONIA OF SHEEP

  • Limitations:

    • Auscultation of lung field is challenging.

    • Symptoms such as tachypnoea and dyspnoea can occur due to physiological stress, acidosis, metritis, mastitis, and hypocalcaemia.

    • There is a tendency for over-diagnosing pneumonia.

  • Auscultation sounds can be harsh.

MANNHEIMIA/PASTEURELLOSIS

  • M. hemolytica Biotypes:

    • A: Most commonly diagnosed; causes septicemia in young lambs.

    • T: Generally seen in older animals.

  • Clinical signs: Sudden death, fever, depression, anorexia, weight loss, discharge, coughing, identifiable lung sounds.

  • Diagnosis: Identify secondary fibrinopurulent pleuropneumonia.

  • Treatment: Antibiotics are critical.

  • Prevention: Utilize bovine vaccines to reduce risk.

PI3

  • 70% of sheep are clinically inapparent.

  • Leads to secondary infections, causing diffuse interstitial pneumonia with firm, edematous lungs.

MYCOPLASMA PNEUMONIAS

  • Also termed enchronic nonprogressive pneumonia.

  • Caused by Mycoplasma ovipneumoniae and other Mycoplasma species, with Mycoplasma haemolytica A as a significant secondary invader.

MYCOPLASMA PNEUMONIA CLINICAL SIGNS

  • Mild chronic cough and dyspnea on exertion; secondary infections with M. haemolytica can lead to fever, discharge, depression.

  • Diagnosis: Mild, chronic pneumonia in lambs <1 year, with lesions characterized by consolidation of cranial lobes and pleuritis.

  • Prevention (Pv): Reduce housing density and ensure proper ventilation.

INFECTIOUS INTERSTITIAL PNEUMONIA

  • Causes:

    • CAE/OPP (discussed in previous lectures)

    • Lungworm (1. Dictyocaulus filaria - direct life cycle; PPP 4 weeks; 2. Muellerius capillaris - indirect life cycle; PPP 6 weeks).

    • Clinical signs: Bright appearance, afebrile, cough.

    • High lungworm burdens lead to enhanced sickness.

OVINE PROGRESSIVE PNEUMONIA (Maedi)

  • Description: Chronic progressive pneumonia caused by non-oncogenic, single-stranded RNA lentivirus.

  • Economic Importance: Particularly impacts older ewes due to the long incubation period (2-4 years).

  • The virus persists in monocytes and macrophages (latent).

  • Transmission: Direct, colostral, milk; infected as lambs.

OPP CLINICAL SIGNS

  • Characterized by slowly progressive malaise and chronic degenerative disease.

  • Symptoms history may include post-stress, exertion, inclement weather, listlessness, progressive emaciation, dyspnea, and potential neurologic signs leading to death.

  • Diagnosis: Utilize PCR, ELISA, and AGID; repeat testing at intervals over months for eradication efforts.

  • Prevention: Maintain a closed herd; test and cull as necessary; provide OvLV-free colostrum or milk replacers for offspring.

LUNGWORM LIFE CYCLES

  • In hosts, the L3 infective larvae migrate to the lungs, mature, and can subsequently cause respiratory symptoms.

  • Lifecycle Processes:

    • Adult worms lay eggs in the lungs which are coughed up and swallowed.

    • L1 are passed in feces.

    • Dictyocaulus viviparous Lifecycle: L1 to L3 involves ingestion by cattle while grazing, transitioning through various larval stages in environmental conditions dependent on temperature.

JAAGSIEKTE – OVINE PULMONARY ADENOMATOSIS (OPA)

  • Etiology: Caused by the Jaagsiekte sheep retrovirus (JSRV).

  • Mechanism: The virus infects alveolar cells in lungs causing neoplastic transformation leading to chronic disease.

  • Clinical Progression: Sheep often succumb to secondary infections (e.g., Mannheimia haemolytica) or pulmonary abscessation.

  • Diagnosis: Largely difficult antemortem involving tests such as the Wheelbarrow test and ultrasonography; serological testing is currently unavailable.

JAAGSIEKTE LAB CODE TESTING

  • Tests confirm positive and negative responses from lung samples gathered from different sheep, revealing data pertinent to Jaagsiekte (OPA).

PATHOLOGICAL INDICATIONS OF OPA

  • Histopathology findings:

    • Enlarged, heavy (>2 kg) lungs that do not collapse.

    • Tumors usually appear greyish, well-defined from normal lung tissue.

    • Bronchi/trachea often contain copious, frothy fluid.

PNEUMONIA WORK-UP

  • Key Steps:

    • Complete history!

    • Physical examination (PE).

    • Work-up starting broad and less invasive.

    • Consider blood work.

    • Thoracic imaging - ultrasound, or radiographs.

    • For bronchopneumonia: respiratory sampling options include nasal swab, NPS, BAL, or TTW.

    • For interstitial pneumonia: CAE/OPP testing, and Baermann test.

GI DISEASES

RUMEN ACIDOSIS (GRAN OVERLOAD)

  • Triggered by sudden changes to diet (high concentrate).

  • Clinical signs: Diarrhea, depression, weakness, PEM, rumen distension.

  • Diagnosis: History combined with PE/BW and assessment of rumen fluid pH.

  • Treatment: Include alkalinizing IV/rumen fluids, thiamine, and antibiotics; rumenotomy and transfaunation may also be considered.

NEONATAL DIARRHEA

  • Common Pathogens:

    • Escherichia coli

    • Rotavirus

    • Cryptosporidia

    • Salmonella

    • Giardia

    • Clostridium perfringens

    • Coccidia

  • Diagnostic Samples and Testing Required:

    • Include specifics such as formalin-fixed small and large intestine and different methods of testing (culture, histopathology etc.) for various pathogens.

MINERAL DEFICIENCIES

  • Cobalt Deficiency:

    • Symptoms: Illthrift, inappetence, ocular discharge, crusty ears, anemia.

    • Cofactor-deficient lambs become immunosuppressed and prone to scour.

  • Differential Diagnoses:

    • Ovine white liver disease, photosensitization.

COPPER DEFICIENCY

  • Commonly leads to illthrift, dirty tails, wool slip.

  • Congenital or delayed-onset swayback in lambs born to ewes deficient in copper during pregnancy.

  • Prevention via supplementation during pregnancy paramount.

SELENIUM DEFICIENCY

  • Causes: White muscle disease characterized by breakdown of large muscle masses leading to potential recumbency or sudden death if the heart is involved.

  • Iodine Deficiency:

    • Leads to illthrift; can produce weak lambs or stillbirths.

BLOAT

  • Presentation: Occurs with rapid diet changes or introduction of lush legume pastures.

  • Clinical Signs: Includes abdominal distension, respiratory distress, and potential death.

  • Treatment:

    • Immediate relief of bloat via OGT/NGT, administer poloxalene (Thera-bloat) for frothy bloat; consider rumen trocar.

ABOMASAL ULCERS

  • Abomasum considered the "true" stomach; risk factors include hospitalization, NSAID administration, and stress.

  • Symptoms of ulcers include: Bruxism.

  • Diagnosis: More presumptive; ultrasound and fecal occult blood test may assist.

  • Treatment: Limited due to the rumen; injectables like pantoprazole or famotidine.

    • Dosage: 1 mg/kg IV Q24h or 2 mg/kg SQ Q24h.

RECTAL PROLAPSE

  • Risk factors include overconditioning, diarrhea, parasitism, coughing, and short tail docking.

  • Prognosis: Guarded; tendency to reoccur without remedying predisposing factors.

TOXINS

RHODODENDRON

  • Also includes azalea and laurel; identified as the leading cause of vomiting in goats.

  • Diagnosis: Based on history and physical examination.

  • Treatment: Activated charcoal, supportive care including IV fluids and gastroprotectants.

COPPER TOXICITY

  • Predominantly a result of chronic ingestion with a stress event leading to rapid liver release.

  • Symptoms manifest as jaundice, intravascular hemolysis, with severe anemia and azotemia.

  • Prevention Strategy: Avoid excess copper in feed (cattle, horse feed, minerals, poultry litter).

  • Treatment: Supportive measures are required.

NEUROLOGIC DISEASES

CAE/OPP

  • Significant diseases in sheep; includes Scrapie.

POLIOENCEPHALOMALACIA (PEM)

  • Commonly referred to as Cerebrocortical necrosis (CCN).

  • Definition: Histologic diagnosis – "Polio" (grey) + "Encephalo" (brain) + "Malacia" (softening).

  • Clinical Signs: Include central blindness, ataxia, seizures, etc.

  • Root Causes:

    • Insufficient thiamine

    • Excess sulfur

    • Lead toxicity, salt toxicity (less common).

THIAMINE ROLE IN CNS HEALTH

  • Thiamine (Vitamin B1) is crucial for brain function due to its involvement in the pentose phosphate pathway (PPP).

  • Mechanism: The enzyme transketolase, dependent on thiamine, facilitates ATP production vital for neuron health.

  • Without sufficient thiamine, neuronal cells swell due to failure in Na/K pump functionality.

POLIO FROM INSUFFICIENT THIAMINE CAUSES

  • Can result from grain overload or ruminal acidosis destabilizing thiamine-producing bacteria.

  • Other Causes Include:

    • Amprolium (Corid), a thiamine analog.

    • Brackenfern, which contains thiaminases.

  • Diagnosis: History and clinical signs supportive of a thiamine deficiency should be employed.

POLIO FROM INSUFFICIENT THIAMINE TREATMENT

  • Administer Thiamine: Dosage of 10 mg/kg IV/SQ TID on day one, then BID. Administer IV slowly to prevent seizures.

  • Include anticonvulsants as needed; focus on rumen health during recovery.

  • Recovery may be rapid (days) but complete visual return may take weeks or may not occur at all. It’s recommended to provide parenteral thiamine for any small ruminant off feed.

POLIO FROM OTHER CAUSES

  • Treatment responses for various causes include:

    • Sulfur toxicity: symptomatic support; check sulfur levels in feed/water.

    • Lead toxicity: Use of thiamine and heavy metal chelation agents as needed.

    • Hypernatremia (due to water deprivation): Monitor and reduce sodium levels gradually.

LISTERIOSIS

  • Causative agent: Listeria monocytogenes.

  • Source: Typically related to silage and environmental exposure.

  • Clinical signs: Due to microabscesses in the brain, resulting in brainstem disease.

    • Associated symptoms include high fever and asymmetric cranial nerve deficits.

  • Diagnosis: Focus on supportive clinical signs and cerebrospinal fluid analysis showing monocytes.

  • Treatment: Prognosis is poor if recumbent; high doses of antibiotics, anti-inflammatories, and supportive care initiate treatment.

OPHTHALMOLOGIC DISEASE

INFECTIOUS KERATOCONJUNCTIVITIS

  • Commonly known as pink eye.

  • Causative Agents: Mycoplasma spp. and Chlamydophila spp.

  • Clinical signs: Include photophobia, increased lacrimation, corneal ulcers and opacities.

    • Differentiation:

    • Mycoplasma: Bilateral

    • Chlamydophila: Unilateral

  • Treatment: Use Terramycin (oxytetracycline) ophthalmic ointment.

REPRODUCTIVE DISEASES

PRECOCIOUS UDDER

  • Observe udder enlargement in non-pregnant goats. Important to distinguish between other causes, including fat deposition, high estrogen in feeds, mastitis, or actual milk production.

    • Management: Do NOT milk and attempt feeding management to dry off the goat.

“BLUEBAG” MASTITIS

  • Caused by Staphylococcus aureus and Mannheimia haemolytica.

  • Transmission: Flies, aggressive nursing, poor milk machine hygiene, and contaminated pasture.

  • Clinical signs: Include fever, decreased feed intake, refusal to lay down, lameness; initially hot and erythematous but can progress to cyanotic and cold.

  • Treatment: Antibiotics based on culture and sensitivity, although often unrewarding.

MISCELLANEOUS DISEASES

BLUETONGUE

  • Transmitted by Culicoides, with cattle and wild ruminants as reservoirs.

  • Clinical signs: More significant in sheep, including generalized vasculitis, transient fever, edema of the muzzle, face, and ears, and potential pulmonary edema.

  • Diagnosis: Based on clinical signs, viral isolation (when viremic), competitive ELISA, and PCR methods.

  • Treatment: Supportive care; antibiotics only for indicated secondary bacterial infections.

  • Prevention: Modified live vaccine targeting specific serotypes.

CONTAGIOUS ECTHYMA (ORF, SORE MOUTH)

  • Caused by Parapox virus; characterized by pustular lesions on lips/nostrils.

  • Typically self-limiting; treatment generally unnecessary.

  • Prevention: Maintain closed herds and vaccinate once in herds to establish immunity.

  • Zoonotic implications noted.

CLUB LAMB FUNGUS (RINGWORM)

  • Causative agent: Trichophyton spp.

  • Associated with livestock shows/fairs, slick shearing, and excessive washing leading to vulnerable skin.

  • Clinical signs: Circular, scaly lesions, alopecia; notably self-limiting, treatment with lime sulfur dip if necessary (noting zoonotic potential).

SEASONAL ALLERGIC DERMATITIS

  • Characterized as hypersensitivity to Culicoides bites, similar to "Sweet Itch" in horses.

  • Higher susceptibility in pedigree sheep during late summer/early autumn, particularly in warmer, humid climates.

  • Clinical signs: Include flaky and crusty conditions around ears, eyes, ventral abdomen, legs, and dorsum near the rump.

  • Treatment: Involves removal from high-risk fields, antibiotics, and avoiding steroid use especially in pregnant ewes.

SEASONAL ALLERGIC DERMATITIS PREVENTIVE MEASURES

  • Strategies include avoiding high-risk areas during late summer/autumn, strategic use of pyrethroids, sheep dipping, and fly repellants.

  • If a genetic component is apparent, consider a dedicated breeding program.

PHOTOSENSITIZATION

  • To be differentiated from seasonal allergic dermatitis and cobalt deficiency.

PERIORBITAL STAPHYLOCOCCAL DERMATITIS

  • Risk factors include:

    • Limited feed space

    • Head butting leading to skin damage

  • Treatment: Penicillin or ampicillin; prevention strategies emphasize adequate feeds and spaces.

QUESTIONS?

  • Further discussions are to focus on Clostridial diseases with critical learning for NAVLE awareness!

CLOSTRIDIAL AGENTS

  • Key Agents and Diseases:

    • C. perfringens type A: Gas gangrene, related myonecrosis.

    • C. septicum: Abomasitis.

    • C. chauvoei: Blackleg.

    • C. novyi types A and B: Wound infections, infectious necrotic hepatitis.

    • C. novyi type D: Bacillary hemoglobinuria.

    • C. sordellii: Hemolytic myonecrosis.

BIGHEAD (CLOSTRIDIUM NOVYI TYPE A)

  • Caused by head butting resulting in massively edematous wound infections mediated by alpha toxin.

  • Treatment: Emphasize wound management and appropriate antibiotic therapy.

  • Prevention Strategy: Encourage proper ram management to prevent aggressive headbutting in flocks.

BLACK DISEASE (CLOSTRIDIUM NOVYI TYPE B)

  • Categorized as infectious necrotic hepatitis; highly fatal in well-nourished adult sheep (ages 2-4 years).

  • Disease typically follows liver damage from Fasciola hepatica.

  • Atypical Death Course: Death occurs rapidly, often within 1-2 hours post onset of symptoms.

  • Venous congestion is likely to darken skin underside.

BRAXY (CLOSTRIDIUM SEPTICUM)

  • Pathophysiology: Malignant edema that follows wound contamination, causing rapid edema and necrosis along anatomical fascial planes.

  • Symptoms: Initial warmth and pain in the lesions, leading to painful swelling followed by cold and crepitant conditions, which may complicate with fever, anorexia, and depression shortly leading to death, often within same day.

CLOSTRIDIAL ENTEROTOXEMIA

  • Often caused by C. perfringens and involves varying toxinotypes leading to specific diseases in animals.

  • Commonly presents within intestines of normal animals; types A, C, and D most common in North America.

  • Clinical implications of enterotoxemia include sudden deaths in full-fed rapidly growing kids/lamps.

ENTEROTOXEMIA (PULPY KIDNEY)

  • C. perfringens type D leads to elevated vascular permeability and possible rapid edema within kidneys/lungs.

  • Clinical signs may manifest from sudden death within 30-90 minutes or up to 24 hours post-exposure, including neurological disturbances such as ataxia, excitement, and seizures.

LESIONS AND PREVENTION FOR ENTEROTOXEMIA

  • Lesion presentation: A full rumen and hyperemic intestines are observed during necropsies, with rapid autolysis of affected organs.

  • Preventive strategies: Include vaccination, gradual diet changes, and utilizing oxytetracycline in feeds to mitigate disease incidence.

  • Treatment: Primarily supportive care indicated for affected livestock.