Fasciola hepatica - Leaf shaped - Broad host range Forms: 1. Chronic – rarely fatal in cattle, often fatal in sheep, alpaca, and llamas 2. Subacute/acute – primarily in sheep, alpaca, llamas 3. In Conjunction with Black Disease – most common in sheep, usually fatal Life Cycle 1. Eggs passes in feces 2. Miracidia develop, 9-10 days; survive for 2 years 3. Eggs hatch only in water a. Miracidia, short lived: 3 hours 4. Miracidia infect lymnaeid snails → asexual reproduction → stages a. Sporocyst b. Rediae c. Daughter rediae d. Cercariae 5. (6-7 weeks) Cercariae emerge, encyst on aquatic vegetation → become metacercariae After ingestion 1. Young flukes excyst in duodenum 2. Penetrate intestinal wall 3. Enter peritoneal cavity 4. Migrate to liver → penetrate parenchyma for 6-8 weeks→ destroy tissue 5. Enter bile ducts and gall bladder 6. Mature and produce eggs Prepatent period → 2-3 months Life cycle: 17 weeks Shedding in cattle: 5-6 months - Clinical course determined by number of metacercariae ingested Acute: >2,000, after 2-6 weeks - Manifested by: o Distended, painful abdomen o Anemia o Sudden death, 2-6 weeks after infection - Complicated by Clostridium novyi → black disease Subacute: 500-1500 - Survive longer, 7-10 weeks - Death due to: hemorrhage and anemia Chronic: 200-500, longer period - Clinical signs: o Anemia o Unthriftiness o Submandibular edema o Reduced milk production - Immunity to pathogens reduced Reaction to tuberculosis test modified Fatal in sheep, alpaca, llamas Sheep: do not develop resistance o Chronic liver damage, cumulative Cattle: partial resistance 5-6 months after infection Lesions: 1st phase: flukes destroy liver tissue → hemorrhage 2nd phase: enter bile ducts → ingest blood, damage mucosa Acute fascioliasis - Damage extensive - Liver is enlarged and friable o Fibrinous deposits in capsule Chronic fascioliasis - Cirrhosis - Damage bile ducts become enlarged o With thickened fibrosed walls Cattle but not sheep: - Duct walls become thickened and calcified Aberrant migration: common in cattle → encapsulated flukes in lungs Mixed infections with Fascioloides magna in cattle Tissue destruction of wandering flukes → favorable for activation of clostridial sporeds Diagnosis - Oval, operculated, golden brown eggs - Cannot be found in acute Fecal sedimentation - Easy and inexpensive ELISA antibody test - Validated only for F. hepatica - Enable detection 2-4 weeks after infection; and before patent period Bulk milk antibody detection - Useful for herd screening procedure - Positive result suggests at least 25% of herd infected Gamma-glutamyltransferase - Increased with bile duct damage - Helpful during late maturation period when flukes are in bile duct Necropsy - Nature of liver damage is diagnostic - Adult flukes in bile ducts - Immature stage → teased from cut surfaces Anthelmintics 1. Triclabendazole a. Resistance by F. hepatica 2. Clorsulon (cattle and sheep only) a. Available only combined with ivermectin for cattle 3. 4. 5. 6. 7. 8. b. Resistance by F. hepatica Albendazole a. Resistance by F. hepatica Netobimin Nitroxinil Closantel Rafoxanide Oxyclozanide Bovine Spongiform Encephalopathy (Mad Cow Disease) - Progressive, fatal, neurologic disease of cattle that resembles scrapie - Thru contaminated animal source proteins Prions - Protein misfolding, aggregation - Scrapie → sheep and goats - Chronic wasting disease of Cervidae - Transmissible mink encephalopathy - Kuru, Creutzfeldt-Jakob disease → humans Pathogenesis 1. Oral exposure 2. Replicate in Peyer’s patches of the ileum 3. Migration to the CNS via peripheral nerves Clinical Signs - Hyperesthesia - Nervousness - Difficulty negotiating obstacles - Reluctance to be milked - Aggression - Low head carriage - Ataxia and tremors - Weight loss - Decreased milk production Diagnosis - Western blot - PrPd immunochemistry (medulla oblangata) - ELISA Variant Creutzfeldt-Jakob Disease → humans Scrapie - Transmissible Spongiform Encephalitis of Sheep Sheep > goats IP: 2-5 years Suffolk: susceptible Targhee: resistant Clinical signs of Scrapie: - Excitable - Head and neck muscle tremors - Uncoordinated movements - “bunny hopping” - Severe pruritus → “scrapie” - Blindness - Death within 4-6 weeks - Reportable disease Bovine tuberculosis - Major infectious disease among cattle→ zoonotic - M. bovis - M. caprae - M. tuberculosis→ lesser extent Cattle - Major reservoir of M. bovis - Main source of infection for humans Nodules = tubercules → lymph nodes and affected tissues - Contagious, spread through direct contact Inhalation of infected aerosol → usual route within cattle herds Calves → from colostrum or milk of infected cows Humans → raw milk, contact with infected tissues - Can be shed before clinical signs - Movement of undetected animals → major way of spreading disease - Can lie dormant in host Clinical signs: - Weakness - Loss of appetite - Weight fluctuating fever - Dyspnea - Intermittent hacking cough - Low-grade pneumonia - Diarrhea - Enlarged, prominent lymph nodes Diagnosis - Tuberculin skin test → standard method o Inject tuberculin intradermal → measure skin thickness at site after 72 hours → detect any swelling - Gamma interferon release assay (GIRA) – most widely used blood-based test o Detects cell-mediated immune response Principle = Bovine blood cells known to have been exposed to M. bovis → elevated gamma interferon after incubation of antigens Bacterial culture and identification in lab → definitive diagnosis → 8 weeks or more process Most common form of TB in people → caused by M. tuberculosis M. bovis → 10% of TB in human - Diagnosis complicated by tendency of M. bovis to be located in other tissues other than lungs o M. bovis resistant to → pyrazinamide (treatment for human TB) Paratuberculosis / Johne’s disease - Chronic, contagious bacterial disease of the intestinal tract - By M. avium subsp. paratuberculosis - Primarily affects: o Sheep o Cattle → most commonly dairy cattle o Goats and other ruminants Characterized by: - Slowly progressive wasting - Increasingly severe diarrhea Shed in→ manure, colostrum, milk Fecal shedding → begins before clinical sign are noticeable - “silent carriers” Non-infected → exposed thru herd expansion or replacement purchases - Not demonstrated as zoonotic Crohn’s disease: intestinal tract disease of humans → resembles Johne’s disease - Clinical signs first appear in young adulthood o 4-7 years old - Infect any age over 1-2 years old Clinical signs - Disease has slow progressive nature of infection - Chronic enteritis o Diarrhea o Unthrifty animals o Progressive weight loss Intestine walls → thickened and inflamed → lesions responsible for leakage of proteins → less absorption of protein → muscle wasting and low milk yield - Can cause “bottle jaw” → swelling under the jaw Symptoms become severe and lead to: - Malnutrition - Debilitation - Death Diagnosis Fecal culture → detect infected animals 6 months or more before developing clinical signs - Difficult and time consuming No treatment Control: - Good sanitation and management practices Herds affected with paratuberculosis: 1. Calves, kids or lambs → be birthed in areas free of manure 2. Removed from dam immediately afterbirth 3. Bottle-fed pasteurized colostrum 4. Raised separately from adults until at least 1 y.o. ➔ Reduces chance of transmission - Vaccination against Paratuberculosis interferes with tests for bovine tuberculosis Anaplasmosis - Usually caused by A. marginale - A. centrale → often used as a vaccine to protect from A. marginale o Isolated from South Africa - A. ovis o Mild to severe disease o Less common than A. marginale - A. phagocytophilum → natural infection is rare o Does not cause clinical disease Characterized by: - Progressive anemia o Due to extravascular destruction of infected and uninfected erythrocytes Transmission Tick vector species - Dermacentor o Main vectors in USA - Rhipicephalus (Boophilus) spp o Major vector of Anaplasma in Australia and Africa - Ixodes - Hyalomma - Argas ➔ Transmits Anaplasma spp Can be spread through: - Contaminated needles - Dehorning - Other surgical instruments Calves are more resistant to disease than cattle Resistance not due to colostral antibody After recovery from acute phase → remain carriers but become immune to further clinical signs - May relapse if: o immunosuppressed o infected with pathogens o after splenectomy Clinical Signs: <1 year old: subclinical Yearlings and 2-year-old: moderately severe Older cattle: severe and often fatal Prepatent period→ related to infected dose - range: 15 – 36 - can be up to 100 days Rickettsemia: doubles every 24 hours during growth phase 10%-30% → infected at peak rickettsemia (can reach 65%) - RBC count, PCV, hemoglobin values → reduced Macrocytic anemia → present late in the disease Peracute→ succumb or die within few hours of onset Acute → lose condition rapidly - Decrease in milk production Late stage: - Inappetence - Loss of coordination - Breathlessness - Rapid, bounding pulse Urine → brown NO hemoglobinuria, in contrast to babesiosis Fever: exceed 41 C, at time of peak Mucous membrane → pale then yellow - Abortion Bos indicus: greater resistance to A. marginale than B. taurus Lesions Carcass → anemic and jaundiced Blood → thin and watery Spleen → enlarged and soft, with prominent follicles Liver → mottled and yellow-orange Gallbladder → distended, thick brown or green bile Hepatic and mediastinal lymph nodes → brown - Serous effusions in body cavities - Pulmonary edema - Petechial hemorrhages → epi- and endocardium - Severe GI stasis Widespread phagocytosis of erythrocytes → evident on microscopic examination Diagnosis - Clinical signs, blood smears, serologic testing Causative agents of tick fever: - A. marginale - B. bovis - B. bigemina Microscopic examination of Giemsa-stained thin and thick blood films → distinguish anaplasmosis from babesiosis, and leptospirosis and theileriosis (results in anemia and jaundice) Giemsa-stained thin blood films → Anaplasma spp appear as dense, homogenous blue-purple stain: 0.3-1 mcm in diameter Inclusion body locations: - A. marginale → margin of infected erythrocyte - A. centrale → centrally Microscopically - Infection visible 2-6 weeks after transmission - Can double each day for 10 days and then decreases Necropsy → prepare for micro exam → thin blood films of: - Liver - Kidney - Spleen - Lungs - Peripheral blood Treatment for Anaplasmosis: - Tetracycline antibiotics and imidocarb → infections cleared → immunity to severe anaplasmosis for at least 8 months Tetracycline drugs in early stages = ensures survival Oxytetracycline (IM, 20mg/kg) → commonly used treatment o Can eliminate carrier state ▪ At least 2 injections within 1 week interval - Blood transfusion→ partially restore PCV → improve survival rate Injection in neck muscle preferred than rump Babesiosis Synonyms: • Pyroplasmosis • Texas fever • Red fever • Tick fever - by B. bovis and B. bigemina B. bovis is much more virulent than B. bigemina Imidocarb → highly efficacious against A. marginale as single injection - High repeated doses for elimination of carrier state - Suspected carcinogen → not approved in USA or Europe Bos indicus more resistant than Bos taurus Vaccination South Africa, Australia, Israel, South America → live A. centrale vaccine against A. marginale USA→ nonliving A. marginale purified from infected bovine erythrocytes and adjuvant → no longer available Long lasting immunity = preimmunization wit live rickettsia + chemotherapy Transmission - Rhipicephalus ticks - Transovarial Cattle: immunity persists for 6 months Pathogenesis ➔ Directly destroys erythrocyte Virulent stain of B. bovis - Hypotensive shock syndrome combined with: o Generalized inflammation o Coagulation disturbances o Erythrocytic stasis in capillaries Clinical Signs - Fever (>106 F) - Inappetence - Increased respiratory ate - Muscle tremors - Anemia - Jaundice - Weight loss Final stages: - Hemoglobinemia - Hemoglobinuria CNS involvement→ due to adhesion parasitized erythrocytes in brain capillaries - Constipation and diarrhea may be present Late term pregnant cows → abortion Bulls → temporary infertility due to transient fever Animals that recover from acute disease remain infected: - Number of years for B. bovis - Few months for B. bigemina No clinical signs in carrier state Lesions in Babesiosis Spleen→ enlarged and friable Liver→ swollen Gall bladder→ enlarged; containing thick granular bile Kidney → congested dark-colored Brain and heart→ may show congestion and petechiae Generalized anemia and jaundice Most clinical case of B. bigemina → hemoglobinuria Diagnosis - Confused with conditions that cause fever, anemia, hemolysis, jaundice or red urine Microscopic examination of Giemsa stained blood or organs→ confirmatory diagnosis In live, thick and thin blood smears preferably from: ➔ Capillaries in the ear or tail tip Necropsy: Smears of: - Heart muscle - Kidney - Liver - Lung - Brain - Blood vessels Treatment for Babesiosis - Diminazene aceturate - Imidocarb dipropionate Hemorrhagic septicemia Synonym: - Hemosep - Bovine pneumonic pasteurellosis - Shipping fever Acute, highly fatal form of pasteurellosis Most economically important bacterial disease of water buffalo and cattle in ASIA Caused by Pasteurella multocida, serotypes → B:2 and E:2 Definitive diagnosis: - Isolation of P. multocida serotypes - Detection by molecular capsular and somatic assays B:2 and E:2 → Carter and Heddleston system 6:B and 6:E → Namioka-Carter system B:2 → areas where disease is endemic E:2 → only in Africa Septicemic pasteurellosis: clinically similar to HS Shed→ during periods of stress Common stressors: - High temperature and humidity - Concurrent infection - Poor nutrition - Work stress Most prevalent during rainy season Route: contact with oral or nasal secretions Pathogenesis 1. Infection begins in tonsil and adjacent nasopharyngeal tissues 2. Bacteremia 3. Dissemination and rapid growth of bacteria in various locations 4. Host cytokine response 5. Release of lipopolysaccharides → endotoxemia Clinical signs → 1-3 days after infection Death → 8-24 hours after first clinical signs Water buffalo – higher morbidity and more severe clinical disease than cattle Clinical Signs: Peracute → death within 8-24 hours - Fever - Hypersalivation - Nasal discharge - Labored respiration Acute→ persist up to 3 days - Fever of 104-106 F - Apathy or restlessness - Reluctance to move - Hypersalivation - Lacrimation - Nasal discharge o Begins as serous → becomes mucopurulent Subcutaneous swelling in the pharyngeal region → extends to the ventral neck and brisket - Progressive respiratory distress Cyanosis Terminal recumbency Abdominal pain and diarrhea Lesions Characteristic lesions: - Swelling of the subcutis and muscle of the submandibular region, neck, and brisket o By clear to blood-tinged edema fluid Serous to serofibrinous fluid in: - Thorax - Pericardium - Abdominal cavity Widespread congestion with petechiae and ecchymoses in tissues and on serosal surface: - Respiratory - GI - Urinary Hemorrhages → most prominent in pharyngeal and cervical lymph nodes Antimicrobial treatments: - Sulfonamides - Tetracyclines - Penicillin - Gentamicin - Kanamycin - Ceftiofur - Enrofloxacin - Tilmicosin - Chloramphenicol Killed vaccines for prevention - Bacterins - Alum-precipitated vaccine - Aluminum hydroxide gel vaccines - Oil-adjuvant vaccines Patients >3 years old → initial 2 doses, 1-3 months apart - Booster once or twice yearly Oil-adjuvant vaccine - Protection for 9-12 months - Most effective when administered 1 month before monsoon or rainy season - Provides strongest immunity Oil based vaccine combined with polysorbate 80 or saponin → increase ease of administration of immune protection Differential diagnosis - Shipping fever - Anthrax and blackleg o Peracute nature and extensive edema and hemorrhage - Acute salmonellosis - Mycoplasmosis - Lightning - Snake bites - Poisoning - Pneumonic pasteurellosis Shipping Fever Pneumonia - Undifferentiated fever - Respiratory disease of cattle of multifactorial etiology of: o Mannheimia haemolytica o P. multocida and Histophilus somni → less common Pathogenesis 1. Involves stress factors 2. Interacting to suppress host defense mechanism 3. Allows proliferation of commensal bacteria in the upper respiratory tract Stressors - Transportation over long distances ➔ Associated with: o Exhaustion o Starvation o Dehydration o Chilling and overheating o Exposure to vehicle exhaust fumes Control - Transport time minimized; provide rest periods and access to feed and water Metaphylaxis with long acting antibiotics: - Oxytetracycline - Tilicosin - Florfenicol - Tildipirosin - Tulathromycin Anthrax Synonym: - Splenic fever - Siberian ulcer - Charbon - Milzbrand - Woolsorters disease - Malignant Carbuncle - Bacillus anthracis Herbivores: acute septicemia with high fatality rate - Accompanied by hemorrhagic lymphadenitis Raw or poorly cooked contaminated meat → source of infection Pathogenesis 1. Wound inoculation, ingestion or inhalation of anthrax spores 2. Infect macrophages, germinate, and proliferate 3. Lethal toxin and edema toxin 4. Respectively cause local necrosis and extensive edema → characteristics of the disease 5. Multiply in lymph nodes 6. Toxemia → bacteremia 7. Tissue destruction and organ failure Oxygen content of air → induces sporulation Spores resistant to: - Extremes of temperatures - Chemical disinfectant - Dessication Necropsy discouraged because of potential for blood spillage and vegetative cells to be exposed to air Anthrax most common in regions with neutral or alkaline, calcareous soils Clinical forms: 1. Cutaneous anthrax - >95% of cases 2. Gastrointestinal anthrax – seen in humans after consumption of raw contaminated eat 3. Inhalational anthrax or wool sorter’s disease → manifests as hemorrhagic lymphadenitis of mediastinal lymph nodes a. Associated with high mortality rate 4. Injection anthrax- uncommon a. associated with contaminated heroin IP: 3-7 days Clinical Findings Peracute → sudden onset and rapidly fatal course - staggering - dyspnea - trembling - collapse - convulsive movements - death after brief period of illness Acute (cattle and sheep)→ abrupt onset of fever and a period of excitement - lethargy - stupor - respiratory or cardiac distress - staggering - seizures - death - blood discharge from natural body openings - edema and swelling in: o ventral aspect of neck, thorax and shoulders In horse: - fever - chills - severe colic - anorexia - depression - weakness - bloody diarrhea - swellings - death within 2-3 days after onset of sign Pigs → relatively resistant to anthrax - may develop acute septicemia after ingestion o sudden death o oropharyngitis Oropharyngeal anthrax – progressive swelling of the throat → death by suffocation Postmortem lesions - rigor mortis → absent or incomplete - dark blood from mouth, nostrils, and anus o blood thickened and fails to clot rapidly - marked bloating - rapid body decomposition - hemorrhage are common on serosal surfaces of abdomen and thorax; epicardium and endocardium - edematous, red-tinged effusions under serosa of organs Spleen → enlarged, dark red or black, soft, semifluid Liver, kidney, lymph node → congested and enlarged Meningitis – if skull is opened Treatment of anthrax - Penicillin → for early stages - Oxytetracycline → daily in divided doses Control procedures - Notification of officials - Rigid enforcement of quarantine - Prompt disposal of contaminated material by cremation or deep burial - Isolation of sick animals - Insect repellants - Control of scavengers - Observation of general sanitary procedures Formaldehyde → can decontaminate contaminated soil Brucellosis in cattle – ZOONOTIC • Brucella abortus – rod-shaped, non-motile, catalase-positive and oxidase-positive organism. -abortion in late pregnancy (erythritol) and high-rate infertility. o SYNONYMS: ▪ Mediterranean fever ▪ Undulant fever ▪ Malta fever ▪ Abortus fever ▪ Contagious abortion ▪ Bangs disease o CATTLE o WATER BUFFALO o BISON - Rapidly causes many abortions in unvaccinated cattle. - Endemic disease, infected cow aborts only once after exposure - Subsequent gestations and lactations appear normal. - After exposure, cattle become bacteremic for a short period, develop agglutinins and antibodies. - Some cattle resist infection. - Small % of infected cows spontaneously recover. IP: - Variable, inversely related to stage of gestation at time of exposure. TRANSMISSION: - Organisms shed in milk and uterine discharges - The cow may become temporarily infertile. - Bacteria found in the uterus during pregnancy, uterine involution, for a prolonged time in the nongravid uterus. - Shedding from the vagina largely disappears with the cessation of fluids after parturition. - Infected cows previously aborted shed brucellae from the uterus at subsequent normal parturition. - Shed in milk most cattle for life. - B. abortus frequently isolated from secretions of nonlactating udders. - B. abortus recovered from the placenta but more conveniently in pure culture. - Most cows cease shedding from the genital tract when uterine involution is complete. - Foci of infection remain in parts of the reticuloendothelilal system, esp. supramammary lymph nodes, udder. - NATURAL TRANSMISSION: o Ingestion of organism- present in large numbers in aborted fetuses, fetal membranes and uterine discharges. o Cattle may ingest contaminated feed and water or may lick contaminated genitals of other animals. o Venereal transmission by infected bull to susceptible cows appears to be rare. o Brucellae – recovered from fetuses and from manure that has remained in a cool environment for >2 mo. ▪ EXPOSURE TO DIRECT SUNLIGHT KILLS THE ORGANISM WITHIN FEW HOURS DIAGNOSIS: 1. Positive serum agglutination test – precedes an abortion or a normal parturition, may be delayed in 15% of cows. -serum agglutination test is the standard diagnostic method. -may also detect antibodies in milk, whey, and semen. 2. Bacteriology or serology 3. Pure culture from the stomach and lungs of an aborted fetuses. 4. Udder secretion -preferred specimens for culture from a live cow. 5. ELISA -detect antibodies in milk & serum 6. Standard plate / tube serum agglutination test a. Used, complete agglutination at dilutions of 1:100 or more serum samples of nonvaccinated animals b. 1:200 of vaccinated at 4-12 mo of age, considered positive and the animals are classified as reactors. 7. Complement fixation 8. Rivanol precipitation 9. Acidified antigen procedures 10. Brucella milk ring test -brucella antigen stained with hematoxylin is added to milk. -carried by the cream as it rises to the surface, react with the antigen and clumping follows, and a blue ring. -blue ring -indicative of the brucellae is formed. -effectively located infected dairy herds, but there are many false-positive test. -can be monitored at 3 to 4 months intervals. -BRT can be achieved and maintained brucellosis-free areas. Screening test: ▪ Cows in herds with a positive BRT are individually blood tested ▪ Seropositive cows are slaughtered to determine herd status. ▪ Nondairy and dairy be screened for brucellosis by testing serum samples collected from cattle destined for: o Slaughter o ▪ ▪ • Replacement through intermediate and terminal markets o Abattoirs. Screening test: o Brucellosis card (rose Bengal) o Plate test ▪ May be used in markets and laboratories to identify infected animals. Supplemental test, used in cattle in which the brucellosis status is unclear o Battery of these test ▪ Improves the probability of detecting infected cattle that have remained in some herds as possible reservoirs of infection. o to clarify the results of plate or card test, especially in serum samples from vaccinated cattle. o Complement fixation and rivanol precipitation ▪ Detect antibodies specifically associated with Brucella infection. o Serial dilution BRT ▪ Test milk samples from individual udder quarters. ▪ To detect chronic infection in udders of cows that may have equivocal serum test reactions. Brucella suis -isolated from seropositive cows but does not appear to cause. -not contagious from cow to cow CLINICAL FINDINGS: • Abortion o Obvious manifestation (second half of gestation (7 months) o 80% unvaccinated cows in later gestation will abort if exposed to Brucella abortus. • Stillborn/ weak calves • Retained placentas • Reduced milk placentas • General health is not impaired in uncomplicated abortions. • Bulls: o Seminal vesicles, ampullae, testicles and epididymides may be infected. o Organism presents in the semen o Testicular abscesses may occur. o Longstanding infections → arthritic joints • Abortion / stillbirth o 2 weeks to 5 months after initial infection. o Fetus may normal or autolytic with bronchopneumonia o Intercotyledonary area ▪ Focally thickened with a wet, leathery appearance and placenta is edematous. o Affected cotyledons ▪ Normal to necrotic, and red or yellow. CONTROL: • No practical treatment is available. • Herds be tested at regular intervals until two or three successive tests are negative. • Vaccinated calves or nonpregnant heifers • Pregnant and fresh cows should originate from brucellosis-free areas or herds and be seronegative. • Replacement should be isolated for 30 days, retested before added to the herd. • B. abortus Strain 19 or RB51 o Increases resistance to infection o Some vaccinated calves may become infected, depending on severity of exposure. • Strain 19 o Can confuse diagnostic test result • Vaccination o The sole means of disease control 1. Slaughter program o A control to an eradication program Brucellosis - Endemic in nondomesticated bison and elk o Transmission to domestic cattle is rare but has occurred in cattle herds commingling with infected elk in the greater Yellowstone park area. BRUCELLOSIS IN GOATS - Similar to those in cattle. - Significant part of the animal industry, and milk is a common source of human brucellosis - Causative agent: o Brucella melitensis ▪ Highly pathogenic for people - Occurs primarily via ingestion. - CAUSES: o Abortion 4 month of pregnancy. o Arthritis and orchitis DIAGNOSIS: 1. Bacteriologic examination of milk or aborted fetus 2. Serum agglutination test • Endemic CONTROL - Slaughter of the herd - REV. 1 strain o Common. Attenuated strain of B.melitensis o SC or intraconjunctival routes BRUCELLOSIS IN SHEEP - Clinical disease similar to goats - B.ovis o Unique to sheep, epididymitis and orchitis impair fertility o Principal economic effect o Placentitis and abortion o Perinatal mortality o First described in New Zealand and Australia - High % shed B.ovis for several years Transmission • Rams by direct contact • Active in ewes is unusual but developed after mating with naturally infected rams. • Contaminated pastures do not appear to be important in spread of the disease • Infection frequently in rams LESIONS: - Primary manifestation is lesion of the: o Epididymis o Tunica o Testis in rams o Placentitis and abortion in ewes o Perinatal death in lambs - Develop rapidly - In rams: permanent lesions 1. Detectable abnormality may be marked deterioration in semen quality associated with the presence of inflammatory cells and organism 2. Epididymal enlargement – unilateral or bilateral 3. Tail of the epididymis – involved more frequently than the head or body. 4. Spermatoceles of variable size – most prominent lesion a. Containing inspissated spermatic fluid. 5. Tunics – thickened and fibrous and extensive adhesion develop between them. 6. Testes -show fibrous atrophy 7. Palpable lesion – transient 8. Organism present in semen over long periods – without clinically detectable lesions 9. NOT ALL INFECTED RAMS SHOW PALPABLE ABNORMALITIES OF SCROTAL TISSUE 10. NOT ALL EPIDIDYMITIS ARE DUE TO BRUCELLOSIS 11. No lesions – must be identified by culture of semen DIAGNOSIS: • REPEATED EXAMINATION NECESSARY 1. Microscopic examination of stained semen smears – 2. Fluorescent antibody examination a. Highly specific diagnostic aid 3. Serologic test a. For eradication of disease 4. ELISA a. Certification of animals 5. Complement fixation 6. 7. 8. Hemagglutination inhibition Indirect agglutination Gel diffusion CONTROL: • Regular examination of rams before breeding and culling • Keep a young ram flock and isolate noninfected rams from older • Immunization of weaner rams with attenuated Rev.1 • Restricting vaccination to rams TREATMENT AND MEDICATION: • Chlortetracycline & Streptomycin o Used concurrently have effected bacteriologic cures • Tx. is not economic except in valuable rams • Even if infection is eliminated, fertility may remain impaired. LEPTOSPIROSIS - Incidental strains lead to outbreaks and acute disease with clinical signs Adapted ones lead to asymptomatic reproductive infections. ZOONOTIC Caused by Leptospira SYNONYMS: • • • • • • • • • • • Weil’s disease Weil-Vasiliev disease Swineherd’s disease Rice field fever Waterborne fever Nanukayami fever Cane-cutter fever Swamp fever Mud fever Stuttgart disease Canicola fever ORGANISM IN CATTLE: 1. L. borgpetersenii serovar Hardjo type hardjobovis 2. L. interrogans serovar Hardjo type hardjoprajitno 3. L. interrogans serovar Pomona 4. L. kirschneri serovar Grippotyphosa Cattle – maintenance host for hardjo -specialised to survive within cattle, the infection is less severe. Cattle, pigs, dogs , rodents or horses – maintenance host for Pomona and suffer more severe illness. -incidental host for these Lepto serovas, clinical signs are very different than infection with hardjo-bovis 2 MAJOR GROUPS OF AGENTS: -when leptospirosis associated with non host-adapted Lepto serovars occurs in calves 1. Adapted to the affected host (host-adapted infection) a. Carried by them and influenced by, not dependent on, environmental conditions for transmission. 2. Incidental infections caused by strains carried by either free-living or domestic animal. (nonhostadapted infection) a. Dependent on poor management practices and environmental condition. b. Include serovars Pomona, Grippotyphosa and Icterohaemorrhagiae c. Wildlife may carry additional Leptospira strains, which can increase the exposure of livestock to an environment with a high and diverse contamination load HOST-ADAPTEED • Leptospira hardjo-bovis o Only host-adapted Lepto serovar in cattle o Infect animals any age o Cattle – maintenance host for hardjo bovis, produce a carrier state in kidneys associated with long-term urinary shedding. o Reproductive tract, infertility result persistent reproductive tract infections o Economically damaging aspect of leptospirosis. o Third trimester abortion ▪ Reduces conception rates in carrier cows and cows bred to carrier bulls. • • • • • -older cattle initial symptoms: • • • Do not die from leptospirosis -lactating cows • • Less milk for a week Milk is thick and yellow -affects pregnant cows: • • • • • • Embryonic death Abortions Stillbirths Retained placenta Birth of weak calves Abortion (3 to 10 weeks after infection) CLINICAL FINDINGS: • NONHOST-ADAPTED Leptospira Pomona L. icterohaemorrhagiae L. canicola L. grippotyphosa Fever Lethargy (milder or unnoticed) low antibody titers – making detection of hardjo bovis and diagnosis difficult. • • • • Result high fever Anemia Red urine Jaundice Death 3 to 5 days • Bovine leptospirosis o Recognized reproductive disease o Acute leptospirosis, strongly associated with incidental strains o Present as an outbreak o Characterized by: ▪ Abortion ▪ Birth of weak offspring ▪ Lactating cows – blood-tinged milk o Chronic, silent infection associated witg reproductive failure as embryo losses and estrus repetition. Diffuse placentitis: o Avascular, light tan cotyledons and edematous o Yellowish intercotyledonary areas • • • • fetus dies 1-2 days before expulsion autolyzed calves are born alive but weak fetuses infected with serovar Pomona o show icterus DIAGNOSIS: 1. placenta and fetus -submitted to the laboratory for FLUORESCENT ANTIBODY STAINING OR PCR TESTING 2. Bacterial culture -gold standard diagnostic method in leptospirosis 3. Serology (MAT) 4. Immunofluorescence 5. PCR assay 6. Isolation and molecular characterization of isolates – important for epidemiologic studies of strains infecting animals from given region 7. ACUTE DISEASE: a. Infected animals develop high titers to the infecting serovar b. Antibody tite > 800 detected by microagglutination test (MAT) 8. MAT -considered evidence of leptospirosis 9. Immunofluorescence 10. PCR assay 11. immunohistochemistry 12. serology – fails due to seronegative shedders are common in infected cattle herds. 13. Screening on herd level with serology (MAT) – identify suspect of herds 14. Culturing, immunofluorescence, PCR assay – required for individual diagnosis 15. Urine -extensively used as primary sample 16. Cervicovaginal mucus for the diagnosis of genital infection – usefulness TREATMENT AND CONTROL AND PREVENTION • Urine and milk of dams -infective for up to 3 months, except for hardjo Cows can be infective for life if not treated. Control: • • • • • • • • • • • • Prevents abortion and other reproductive problems STREPTOMYCIN o Eliminates the renal carrier status OXYTETRACYCLINE, TULATHROMYCIN, CEFTIOFUR -effective Correction of environmental/ management factors Subdivision of animals into smaller batches Soil sealing Regular cleaning of milking sectors Access by cattle to collected water, puddles or swampy areas, cograzing (with pigs) should be avoided Vaccination -cheapest control method, essential measure for the control of leptospirosis ▪ Failure of commercial vaccines in the prevention of kidney colonization ▪ Occurs every 6 months, before breeding service season, beginning of the spring when the environmental contamination is more intense. No cross protection among serovars Immunization based on the use of multivalent vaccines. Primary vaccination – two doses 4 to 6 week interval followed by an annual booster. MEDICATION: • 1. Integrated program of antimicrobials 2. Management changes 3. Vaccination Integrated program of antimicrobials Eliminate renal carrier state: o Oxyteteracycline o Tilmicosin o Ceftiofur o Amoxicillin • • • BACTERIN – every 6 months good protection against serovars Grippotyphosa, Pomona, Canicola, and Icteroharmmorhagiae but does not protect against INFECTION & RENAL SHEDDING by “serovar Hardjo” New monovalent serovar Hardjo vaccines o Prevent infection, but do not cute existing infection Incidental infection -more easily controlled Serjoe strain – impossible to eradicate, requiring constant vigilance 3 subtypes • I. Program based on reduction of reproductive problems and consequent economic hazards. II. BOVINE HERPES VIRUS-1 - - • • Widespread in cattle population Viral infection alone is not life threatening but predisposes to secondary bacterial pneumonia, which may result in death. 2 forms: o Feedlot cattle form o respiratory form Breeding cattle, abortion or genital infections o More common Genital infections o occur in bulls ▪ infectious pustular balanoposthitis o cows ▪ infectious pustular vulvovaginitis o 1-3 days of mating or close contact with an infected animal TRANSMISSION: • • • • 1. 2. 3. 4. 5. 6. 7. 8. Occur in the absence of visible lesions and via artificial insemination with semen from subclinically infected bulls Cattle with latent bovine herpesvirus 1 infection show no clinical signs But the serve as a source of infection of other susceptible animals. This disease can be effectively controlled with modified live virus vaccination BHV-1 Bovine herpesvirus 1 Only a single serotype is recognized Associated with several clinical manifestation in cattle IBR Infectious bovine rhinotracheitis Infectious pustular vulvovaginitis Balanoposthitis Conjunctivitis Abortion Encephalomyelitis Mastitis III. IV. BHV-1 -have been described on the basis of endonuclease cleavage patterns of viral double stranded DNA BHV-1.1 a. Respiratory subtype BHV-1.2 a. Genital subtype BHV-1.3 a. Encephalitic subtype b. been reclassified as a distinct herpesvirus designated BHV-5. CLINICAL FINDINGS IP: - 1 is 2-6 days (respiratory and genital forms of bovine herpesvirus. RESPIRATORY FORM - Mild to severe. Presence of secondary bacterial pneumonia. CLINICAL SIGNS: o High fever o Anorexia o Coughing o Excessive salivation o Nasal discharge o Progresses from serous to mucopurulent o Conjunctivitis w/ lacrimal discharge o Inflamed nares (common name RED NOSE) o Dyspnea if the larynx becomes occluded with purulent material o Nasal lesions: ▪ Numerous clusters of grayish necrotic foci on the mucous membrane of the septal mucosa, just visible inside the external nares. o Pseudodiphtheritic yellow plaque o Yellowish plaques o Conjunctivitis with corneal opacity o Only manifestation of BHV-1 infection o IN THE ABSENCE OF BACTERIAL PNEUMONIA, recovery generally occurs 4-5 days after the onset of clinical signs GENITAL INFECTION - - First clinical signs: o Frequent urination o Elevation of the tailhead o Mild vaginal discharge o Vulva is swollen o Small papules o Erosions and ulcers Secondary bacterial infection do not occur Animal recover in 10-14 days Bacterial infection, inflammation of the uterus and transient infertility Purulent vaginal discharge In bulls, similar lesions occur on the penis and prepuce. Abortions o Second of half of pregnancy (4 months) Early embryonic death Autolysis o Consistently present Small foci of necrosis in the liver, No gross lesion in the placenta or fetus Necrotizing vasculitis common in the placenta BHV-1 • • • Severe in young calves and cause a generalized disease Pyrexia, ocular and nasal discharges, respiratory distress, diarrhea, incoordination, convulsion and death Occur in a short period after generalized viral infection GROSS AND HISTOPATHOLOGIC FINDINGS ▪ Uncomplicated IBR infection o Most lesions are restricted to the upper respiratory tract and trachea o Petechial to ecchymotic hemorrhages may found in the mucous membranes of the nasal cavity and the paranasal sinuses o The lesions may coalesce to form plaques o Sinuses often filled with a serous or serofibrinous exudate. o Progress of disease, the pharynx becomes covered with a serofibrinous o o o o exudate and blood-tinged fluid may be found in the trachea. Pharyngeal and pulmonary lymph nodes may be acutely swollen and hemorrhagic Tracheitis may extend into bronchi and bronchioles Epithelium is sloughed in the airways Viral lesion are masked by secondary bacterial infections. Young animals with generalized bovine herpesvirus 1 infection ▪ ▪ ▪ Erosion and ulcers overlaid with debris found in the nose, esophagus and forestomach White foci found in the liver, kidney, spleen and lymph nodes Aborted fetuses may have pale, focal, necrotic lesions in all tissues, which are especially visible in the liver.
