diseases of cattle.pptx at uci diploma cl

animal production notes

1. DISEASES OF CATTLE AND SMALL RUMINANTS By Dr. ONEN (BVM MUK)

2. FOOT AND MOUTH DISEASE (FMD) Introduction FMD is highly contagious transboundary viral disease that affect all cloven footed animals. The disease is endemic in East Africa and outbreaks occur in all regions of Uganda in the recent years. Significant economic losses reported in 2018 due to outbreak of FMD in several districts of Uganda Etiology: Aphthovirus of Picornaviridae family. Seven serotype occur i.e. O, A, C, SAT 1, SAT 2, SAT 3 & Asia 1 In Uganda, FMD is endemic, and serotypes O and SAT 2 are the most common. 7/30/2024 2

3. FOOT AND MOUTH DISEASE (FMD) Hosts: All ruminants and swine species (cloven footed animals Transmission can occur: Through air, & mechanically. By infected animal or animal products Contaminated vehicles or humans The virus target the epithelial tissues i.e. skin and oral mucosa of the animals Cardiac muscle affected and more severe in calves, lambs and kids. 7/30/2024 3

4. FOOT AND MOUTH DISEASE (FMD) Clinical Presentations Incubation period of FMD range from 2 – 14 days. In pigs it may be as short as 18 hrs. Signs are more severe in cattle and pigs than in goats and sheep Fever (41 ⁰C) & anorexia Salivation and feet stamping Vesicles develop in oral mucosa, feet(coronary banda & interdigical skin), udder/teats of lactating cattle and vulva Drastic drop in milk production Loss of condition and reduced growth rate 7/30/2024 4

5. FOOT AND MOUTH DISEASE (FMD) After a week oral lesions may disappear (healing) Lesions of udder and feet often complicated by secondary infections leading to mastitis and chronic laminitis/lameness In pigs loss of entire horn of the toe often occur, may also occur in cattle & deer. Young calves, lambs and kids may die before vesicular lesions appear. 7/30/2024 5

6. 7/30/2024 6

7. FOOT AND MOUTH DISEASE (FMD) Gross Lesions Characteristic lesions in cattle include Oral vesicles & erosions in mucosa of lips, dosum of tongue and palate Vesicles & erosions near coronary band, interdigital skin, vulva & teats Vesicles in the brisket, abdomen, hock/ carpus & perineum. Diffuse edema or petechiae in abomasal & intestinal mucosa. Sub pleural & subepicardial haemorrhages Small grayish foci in the heart wall & left ventricle septum of calves, lambs, pigs &goats. This gives stripped appearance of the heart (“ tiger heart” ) Gray foci of necrosis in skeletal muscles. 7/30/2024 7

8. FOOT AND MOUTH DISEASE (FMD) How do you Diagnose FMD? Clinically FMD can be confused with vesicular stomatitis (cattle), swine vesicular disease and vesicular exanthema. Therefore, Laboratory confirmation vital. On suspicion, the DVO, Regional Veterinary inspectors and MAAIF should be notified immediately. Viral serotyping and molecular characterization recommended (OIE) 7/30/2024 8

9. FOOT AND MOUTH DISEASE (FMD) Treatment and Control Control in Endemic areas involves Institution of restriction of movements, quarantine of the affected premises or area. Ring vaccination from wider diameter towards the focus of outbreak. Symptomatic treatment & control of secondary infections. Note: most vaccines of FMD lasts for 4 -6 months The vaccine used should contain strains antigenically similar to that cause outbreak in the area. 7/30/2024 9

10. FOOT AND MOUTH DISEASE (FMD) FMD Control in Previously free areas, Many countries have policy of slaughter of all affected herds including in-contact susceptible animals. Carcasses burnt or buried on the site (no movement). Strict restriction on movement of animals and vehicles around infected premises. 7/30/2024 10

11. RINDERPEST Rinderpest virus is a  Morbillivirus , Closely related to the viruses causing peste des petits ruminants , canine distemper and measles. Strains of varying virulence for cattle occurred and could be differentiated genetically. 7/30/2024 11

12. Cattle plague 7/30/2024 12

13. 7/30/2024 13 Erosive stomatitis

14. RINDERPEST Clinical Findings After an incubation period of 3–15 days; Fever Anorexia Depression, and Oculonasal discharges developed Followed by necrotic lesions on the gums, buccal mucosa, and tongue. The hard and soft palates were often affected. The oculonasal discharge became mucopurulent, and the muzzle appeared dry and cracked. Diarrhea, the final clinical sign, could be watery and bloody. Morbidity was often 100% and mortality was up to 90% in epidemic areas. 7/30/2024 14

15. 7/30/2024 15

16. 7/30/2024 16 Enteritis = Zebra stripping in the rectum

17. RINDERPEST Lesions Gross pathologic lesions occurred throughout the GI , upper respiratory tracts , with as areas of necrosis and erosion , Congestion and hemorrhage - classic “ zebra-striping ” in the rectum. Lymph nodes could be enlarged and edematous, Necrotic foci in the Peyer’s patches. Histological lesions - viral-induced syncytia, and intracytoplasmic and i ntranuclear inclusions were often seen. 7/30/2024 17

18. RINDERPEST Clinical and pathologic findings. Note: In areas where rinderpest was uncommon or absent, laboratory tests had to be used to differentiate it from bovine viral diarrhea, East Coast fever, foot-and-mouth disease e.t.c Viral isolation Immune capture ELISA Reverse transcription-PCR (RT-PCR) Note; In the 10-yr period between occurrence of the last outbreak and the official declaration of eradication, active rinderpest surveillance in recent endemic areas included the testing of all susceptible cloven-hoofed animals presenting with erosive stomatitis . 7/30/2024 18

19. RINDERPEST Control: Active immunity was lifelong, whereas maternal immunity lasted 6–11 mo. Control in endemic areas was by vaccination of all cattle and domestic buffalo >1 yr old with an attenuated cell culture vaccine . Outbreaks were controlled by quarantine and “ ring vaccination ” and sometimes by test and slaughter . Control of animal movements was paramount to control rinderpest; many outbreaks were due to the introduction of infected cattle to hitherto uninfected herds. 7/30/2024 19

20. LUMPY SKIN DISEASE Definition: is an infectious, eruptive, occasionally fatal disease of cattle characterized by nodules on the skin and other parts of the body. Secondary bacterial infection of the skin lesions often aggravates the condition. Etiology : Neethling pox virus Transmission Transmission is mainly by contact, although insects (biting insects and ticks) have been experimentally incriminated Morbidity is up to 50%, low mortality, The greatest loss is due to reduced milk yield, loss of condition, and rejection or reduced value of the hide. NB: Buffaloes –reservoirs. 7/30/2024 20

21. LUMPY SKIN DISEASE Clinical signs of LSD Well circumscribed skin nodules, round, slightly raised, firm, and painful and involve the entire cutis and the mucosa of the GI, respiratory, and genital tracts.- signs of GIT (nodules on the muzzle and within the nasal and buccal mucous membranes), resp and genital tracts The skin nodules contain a firm, creamy-gray or yellow mass of tissue. Regional lymph nodes are swollen, and edema develops in the udder, brisket, and legs. Secondary infection sometimes occurs and causes extensive suppuration and sloughing; as a result, the animal may become extremely emaciated, and euthanasia may be warranted. In time, the nodules either regress, or necrosis of the skin results in hard, raised areas (“sit-fasts”) clearly separated from the surrounding skin. These areas slough to leave ulcers, which heal and scar. 7/30/2024 21

22. LUMPY SKIN DISEASE Diagnosis Based on clinical signs Isolation and demonstration of the virus. Prevention and treatment Quarantine of infected animals Vaccination Administration of antibiotics and anti-inflammatory to control secondary bacterial infection 7/30/2024 22

23. TUBERCULOSIS TB is a chronic debilitating disease of vertebrates characterized by a chronic cough and granulomatous lesions in the lungs Etiology : Acid-fast bacilli of the genus Mycobacterium . M tuberculosis complex ; M tuberculosis , M canettii , M bovis , M caprae , M pinnipedii , M microti , M mungi , and M africanum . M avium complex ; avium avium , M avium hominissuis (isolated from people, swine, and other mammals), and M intracellulare . Transmission: Inhalation of air droplets, Ingestion-e.g. Milk, water, Intrauterine 7/30/2024 23

24. 7/30/2024 24 M. bovis Ecotypes:

25. TUBERCULOSIS Clinical signs; The clinical signs of TB reflect the extent and location of lesions EPTB or PTB. Generalized signs include progressive emaciation, lethargy, weakness, anorexia, and a low-grade, fluctuating fever. The bronchopneumonia of the respiratory form of the disease causes a chronic, intermittent, moist cough with later signs of dyspnea and tachypnea. EPTB Superficial lymph node enlargement may be a useful diagnostic sign when present. Affected deeper lymph nodes cannot always be palpated, but they may cause obstruction of the airways, pharynx, and gut, leading to dyspnea and ruminal tympany. 7/30/2024 25

26. TUBERCULOSIS Diagnosis and Treatment Based on clinical signs Intradermal skin test using Purified protein derivatives. Demonstration of bacilli in sputum Radiolography in small animals reveals tubercles in lungs PM Confirmation: Isolation and identification- Culture (colonial morphology , PCR, RFLP, MIRU-VNTR). ELISA- IFN gamma assays 7/30/2024 26

27. TUBERCULOSIS Control; Domestic animals should avoid contacts with wild life- buffalo, bisons, deers, antelopes etc. (reservoirs) Test and slaughter – with PPD Test and segregate BCG-Vaccination 7/30/2024 27

28. CLOSTRIDIAL DISEASES Enterotoxmias Botulism Big Head Black Quarter Malignant edema Clostridia are relatively large, anaerobic, spore forming, rod-shaped, gram-positive organisms. They are found either as living cells (vegetative forms) or as dormant spores. Natural habitats of soils and intestinal tract. only become problematic with dietary stress, injury, changes in management, parasitism or other unusual circumstances that set up a favorable growth environment and result in production of potent toxins 7/30/2024 28

29. CLOSTRIDIAL DISEASES Pathogenic strains or their toxins may be acquired by susceptible animals by either wound contamination or ingestion. Clostridial diseases are not spread from animal to animal. The response of clostridial diseases to antibiotic treatment is very poor. Therefore Prevention by vaccination is standard practice Clostridial diseases can be divided into two categories: ① Those in which the organisms actively invade or when locally dormant spores are activated and reproduce in the tissues of the host, with the production of toxins that enhance the spread of infection e.g. the gas-gangrene group; the Cls. Type D that causes Black disease ②those characterized by toxemia resulting from the absorption of toxins produced by organisms within the digestive system (the enterotoxaemia), in devitalized tissue (tetanus), or in food or carrion outside the body (botulism). 7/30/2024 29

30. CLOSTRIDIAL DISEASES There are five defined types, or genotypes, of C. perfringens (A-E); typing is based on the lethal toxins that they produce: alpha, beta, iota, epsilon and/or enterotoxin. Enterotoxemias Enterotoxemia is characterized by proliferation of and exotoxin production by Clostridium perfringens types B, C & D in the lumen of the gastrointestinal tract. The toxins cause entero-colitis (inflammation of the intestine), increase the permeability of the blood vessels, and become absorbed in the blood. They circulate in the bloodstream, promoting swelling in the lungs and kidneys, giving the condition the name pulpy kidney disease. Young animals are most susceptible. Sudden and high mortality rates are concentrated in lambs and kids. Although adult animals are also susceptible to enterotoxemia, they develop immunity due to frequent exposure to these toxins. 7/30/2024 30

31. CLOSTRIDIAL DISEASES ENTEROTOXEMIA CAUSED BY CLOSTRIDIUM PERFRINGENS TYPES B AND C Infection with C perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves, pigs, and foals 7/30/2024 31

32. CLOSTRIDIAL DISEASES Disease Clostridium perfringen type Host Lamb dysentery Type B Lambs ≤3 wk old Calf enterotoxemia Types B and C Well-fed calves ≤1 month Pig enterotoxemia Type C Piglets in first few days of life Foal enterotoxemia T y pe B F o a l s i n f i r s t w e e k of l i f e St r uck T y pe C Adult sh ee p G o a t e n t e r o t o x em i a T y pe C Adu l t g o a ts 7/30/2024 32

33. CLOSTRIDIAL DISEASES Clinical Findings (Enterotoxemia: C . perfringens type B & C Lamb dysentery is an acute disease of lambs <3 wk old. Many may die before clinical signs are seen, but some newborn lambs stop nursing, become listless, and remain recumbent. A fetid, blood-tinged diarrhea is common, and death usually occurs within a few days. In calves, there is acute diarrhea, dysentery, abdominal pain, convulsions, and opisthotonos. Death may occur in a few hours, but less severe cases survive for a few days, and recovery is possible. Pigs become acutely ill within a few days of birth and there is diarrhea, dysentery, reddening of the anus, and a high fatality rate; most affected piglets die within 12 hr. • In foals, there is acute Struck in adult sheep premonitory signs. dysentery, toxemia, and rapid death is characterized by death without 7/30/2024 33

34. CLOSTRIDIAL DISEASES Hemorrhagic enteritis with ulceration of the mucosa is the major lesion in all species. Grossly, the affected portion of the intestine is deep blue-purple and appears at first glance to be an infarction associated with mesenteric torsion. Diagnosis; Smears of intestinal contents can be examined for large numbers of gram-positive, rod-shaped bacteria, and filtrates can be made for detection of toxin and subsequent identification by neutralization with specific antisera. Treatment and Control The disease is best controlled by vaccination of the pregnant dam during the last third of pregnancy, When outbreaks occur in newborn animals from unvaccinated dams, antiserum should be administered immediately after birth 7/30/2024 34

35. CLOSTRIDIAL DISEASES TYPE D ENTEROTOXEMIA (Pulpy kidney disease, Overeating disease) This classic enterotoxemia of sheep is seen less frequently in goats and rarely in cattle. It has a worldwide distribution and affects animals of any age. It is most common in lambs either <2 wk feedlots and on a high-carbohydrate diet lush green pastures. old or weaned in or, less often, on • The disease has been suspected in well-nourished beef calves nursing high-producing cows grazing lush pasture and in sudden death syndrome in feedlot cattle; however, supportive laboratory evidence in the latter is lacking. Etiology   The causative agent is C perfringens type D. 7/30/2024 35

36. CLOSTRIDIAL DISEASES Clinical Findings (pulpy kidney) Sudden deaths in the best-conditioned lambs are the first indication of enterotoxemia.   In some cases, excitement, in coordination, and convulsions occur before death. Opisthotonos, circling, and pushing the head against fixed objects are common neurologic signs.   Diarrhea may or may not develop.(excitement and diarrhea are indicative of focal symmetrical encephalomalasia occurring in the brain) Frequently, hyperglycemia or glycosuria is present.  Occasionally, adult sheep are affected too, showing weakness, in coordination, convulsions, and death within 24 hr. 7/30/2024 36

37. CLOSTRIDIAL DISEASES Clinical Findings (pulpy kidney) In goats, the course of disease ranges from per acute to chronic, with signs that vary from watery diarrhea with or without blood to sudden death..   Affected calves not found dead show mania, convulsions, blindness, and death within a few hours.  Sub acutely affected calves are stuporous for a few days and may recover.  In goats, diarrhea and nervous signs are seen, and death may occur over several weeks.  Type D enterotoxemia occasionally is seen in young horses that have overeaten 7/30/2024 37

38. CLOSTRIDIAL DISEASES Diagnosis (pulpy kidney) A presumptive diagnosis of enterotoxemia is based on sudden, convulsive deaths in lambs on carbohydrate-rich feed. Smears of intestinal contents reveal many short, thick, gram-positive rods. Confirmation requires demonstration of epsilon toxin in the small-intestinal fluid. Fluid, not ingesta, should be collected in a sterile vial within a few hours after death and sent under refrigeration to a laboratory for toxin identification. A PCR for detection of epsilon toxin gene is available for identification of the isolates as either type B or D. 7/30/2024 38

39. CLOSTRIDIAL DISEASES Control (pulpy kidney)   The method of control depends on the age of the lambs, the frequency with which the disease appears on a particular property, and the method of husbandry.  If the disease is seen consistently in young lambs, ewe immunization probably is the most satisfactory method of control. Breeding ewes should be given two injections of type D toxoid in their first year, a booster injection 4–6 wk before lambing, and each year thereafter.   In feedlot lambs can be controlled by reducing the amount of concentrate in the diet. However, this may not be economical.   Immunization of all lambs with toxoid on entering the feedlot likely will reduce losses to an acceptable level. Two injections, 2 wk apart, will protect lambs through the feeding period. 7/30/2024 39

40. CLOSTRIDIAL DISEASES Big Head / Swollen Head It is acute and infectious.  Caused by Clostridium novyi type A , Cls. Sordelli and rarely Cls. Chauvoei  Characterized by a non-gaseous, non- haemorrahagic , edematous swelling of the head, face and neck of young rams  Predisposing factors are fighting or continual head butting, dipping immediately after shearing.  Break in surface of the skin provides opportunity for bacteria to enter and injured subcutaneous tissue provide suitable conditions for bacteria to grow.  Treatment is with broad spectrum antibiotics or penicillin 7/30/2024 40

41. CLOSTRIDIAL DISEASES Malignant Oedema • Acute, fatal toxemia All species and ages of animals affected Cause; Mainly Clostridium septicum , but other clostridia are implicated e.g. C. chauvoei, C. perfringens, C novyi and C sordelli Clinical signs   General signs, such as anorexia, intoxication, and high fever, as well as local lesions, develop within 6–48 hr after predisposing injury or activation of dormant spores.  The local lesions are soft swellings that pit on pressure and extend rapidly because of the formation of large quantities of exudates that infiltrates the subcutaneous and intramuscular connective tissue of the affected areas. The muscle in such areas is dark brown to black. Accumulations of gas in subcutaneous tissue and along muscle fascias may or may not be present. 7/30/2024 41

42. CLOSTRIDIAL DISEASES These muscle infections are extremely painful, and systemic toxemia may evolve.  Extensive local sloughing of skin and tissues is often seen in progressed states of malignant edema.   Severe edema of the head of rams develops after infection of wounds inflicted by fighting.   Malignant edema associated with lacerations of the vulva at parturition is characterized by marked edema of the vulva, severe toxemia, and death in 24–48 hr.   7/30/2024 42

43. 7/30/2024 43

44. CLOSTRIDIAL DISEASES Diagnosis   Fluorescent-antibody staining of C. septicum from a tissue smear. However, C septicum is an extremely active postmortem invader from the intestine, and its presence in a specimen taken from an animal that has been dead for ≥24 hr is not significant.   PCR is also useful in identification and differentiation Treatment High doses of Parenteral penicillin, tetracyclines, or broad-spectrum antibiotics is indicated early in the disease.  Injection of penicillin directly into the periphery of the lesion may minimize spread of the lesion,  The affected tissues usually slough.   Local treatment includes surgical incision of skin and fascia to allow drainage. Animals with systemic toxic signs will need supportive treatments such as IV perfusion. 7/30/2024 44

45. CLOSTRIDIAL DISEASES Control   Multivalent vaccines- C septicum usually is combined with C chauvoei in a blackleg/malignant edema vaccine are available.  In endemic areas, animals should be vaccinated before they are castrated, dehorned, or docked.  Calves should be vaccinated at ~2 mo of age.   In high-risk areas, annual vaccination is indicated, as is revaccination after severe trauma. 7/30/2024 45

46. CLOSTRIDIAL DISEASES Blackleg; Acute, febrile and highly fatal disease of cattle and sheep.  Characterized by emphysematous swelling commonly affecting heavy muscles (also called clostridial myositis)  Etiology; Clostridium chauvoei Organisms are found in the intestinal tract and soil.  Clostridia in the soil are the most likely cause of infection especially after recent excavations or flooding.  Organisms are ingested, they pass through the GIT, gain acess to the blood stream and are deposited in the muscle and other tissue like spleen, liver etc where they remain dormant indefinitely. 7/30/2024 46

47. CLOSTRIDIAL DISEASES Clinical Signs Usually of sudden on set.  A few cattle may be found dead without premonitory signs. Initially, there is a fever (41 C)• Acute, severe lameness Marked depression  By the time clinical signs are obvious, body temperature may be normal or subnormal.  Characteristic edematous and crepitant swellings develop in the hip, shoulder, chest, back, neck, or elsewhere.  At first, the swelling is small, hot, and painful.  As the disease rapidly progresses, the swelling enlarges, there is crepitation on palpation, and the skin becomes cold and insensitive with decreased blood supply to affected areas. There is stiff gait and the animal is reluctant to move. 7/30/2024 47

48. CLOSTRIDIAL DISEASES General signs include prostration and tremors. Death occurs within 12–48 hr. In some cattle, the lesions are restricted to the myocardium and the diaphragm. Postmortem Lesions Lying on one side with affected hind leg stuck out is commonly seen in cattle Bloating of carcass and blood stained frothy exudates from the nostrils and anus Dark red to black muscle of the loin, back or leg Sponge-like bubbly appearance of the muscles with a peculiar rancid (sweetish) odor Yellowish, gelatinous subcutaneous tissue and associated gas bubbles Blood stained fluid in body cavities 7/30/2024 48

49. 7/30/2024 49

50. CLOSTRIDIAL DISEASES Diagnosis Field diagnoses are confirmed by laboratory demonstration of C . chauvoei in affected muscle (standard methods: culture and biochemical identification). The samples of muscle should be taken as soon after death as possible.  The fluorescent antibody test for C. chauvoei is rapid and reliable. A PCR is available and reported to be very good for clinical samples but not for environmental samples.   Control   A multivalent vaccine containing C. chauvoei , C. septicum and, where needed, C. novyi antigens is safe and reliable for cattle and sheep. Calves 3–6 months of age should be vaccinated twice, 4 wk apart.  Cattle should be moved from affected pastures. 7/30/2024 50

51. CLOSTRIDIAL DISEASES Difference Between BQ and Malignant Oedema Black Quarter In blackleg, there may be an area over the shoulder, back or rump that is swollen, and has darkened skin, and gas bubbles may be detected by gentle finger pressure. At necropsy, the affected muscle is black and dry, and gas bubbles will have spread between the muscles. The lesion may be in any muscle including tongue or heart and may be quite small. Malignant Oedema In malignant oedema, tissues around the inciting wound will be soft, swollen and pit on finger pressure. At necropsy, tissues surrounding the wound will be wet and large quantities of dark brown exudates will have spread out under the skin.   7/30/2024 51

52. CLOSTRIDIAL DISEASES Bacillary Haemoglobinuria Bacillary hemoglobinuria is an acute, infectious, toxemic disease caused by Clostridium haemolyticum . It affects primarily cattle but has also been found in sheep and rarely in dogs. It occurs in the western part of the USA, along the Gulf of Mexico, in South America, Great Britain, the Middle East, India, and other parts of the world.  Etiology C. haemolyticum is a soil borne organism naturally found in the GI tract of some cattle. Spores are produced by the bacteria if an infected animal dies and the carcass is not properly disposed of. It can survive for long periods in contaminated soil or in bones from carcasses of infected animals. 7/30/2024 52

53. CLOSTRIDIAL DISEASES Clinical Signs Cattle may be found dead without premonitory signs. Usually, there is a sudden onset of severe depression, fever, abdominal pain (cattle have arched back) , dyspnea, dysentery, and hemoglobinuria. (Dark red urine) Anemia and jaundice are present in varying degrees. Edema of the brisket may occur. Hgb and RBC levels are quite low. The duration of clinical signs varies from ~12 hr in pregnant cows to ~3–4 days in other cattle. The mortality in untreated animals is ~95%. Some cattle suffer from subclinical attacks of the disease and thereafter act as immune carriers. 7/30/2024 53

54. CLOSTRIDIAL DISEASES Post Mortem Lesions; Dehydration, anemia, and sometimes subcutaneous edema are present. There is bloody fluid in the abdominal and thoracic cavities. The lungs are not grossly affected, and the trachea contains bloody froth with hemorrhages in the mucosa. The small intestine and occasionally the large intestine are hemorrhagic; their contents often contain free or clotted blood. An ischemic infarct in the liver is characteristic; it is slightly elevated, lighter in color than the surrounding tissue, and outlined by a bluish red zone of congestion. 7/30/2024 54

55. 7/30/2024 55 Liver infarcts

56. 7/30/2024 56 Tuberculosis

57. CLOSTRIDIAL DISEASES PM Lesions The kidneys are dark, friable, and usually studded with petechiae. The bladder contains purplish red urine After death, rigor mortis sets in quickly. 7/30/2024 57

58. CLOSTRIDIAL DISEASES Diagnosis; The general clinical picture and postmortem findings usually permit a tentative diagnosis. The most striking sign is the typical port-wine-colored urine, which foams freely when voided or on agitation. The presence of the typical liver infarct is sufficient for a presumptive diagnosis. The normal size and consistency of the spleen serve to exclude anthrax and Anaplasmosis. Diagnosis can be confirmed by isolating C. haemolyticum from the liver infarct, but the organism is difficult to culture. Rapid and accurate diagnosis can be made by demonstrating the organism in the liver tissue by a fluorescent antibody or immunohistochemical test or by demonstrating the toxin in the fluid in the peritoneal cavity or in a saline extract of the infarct. 7/30/2024 58

59. CLOSTRIDIAL DISEASES Control; Early treatment with penicillin or tetracyclines at high doses is essential. Whole blood transfusions and fluid therapy also are helpful early in the disease. C. haemolyticum bacterin prepared from whole cultures confers immunity for ~6 mo. In areas where the disease is seasonal, one preseasonal dose is usually adequate; Where the disease occurs throughout the year, semiannual vaccination is necessary. Cattle in contact with animals from areas where this disease is endemic should be vaccinated, as the latter may be carriers. 7/30/2024 59

60. BRUCELLOSIS Brucellosis Highest public health burden among Livestock keepers Consumers of livestock products General population Etiology of Brucellosis Brucella spp 7/30/2024 60

61. BRUCELLOSIS 7/30/2024 61 Brucella spp. Source Virulence Infective Dose B. melitensis Goats, sheep, Cattle, Swine ++++ 1 – 10 B. suis Swine, Cattle +++ 1,000 – 10,000 B. abortus Cattle ++ 100,000 B. canis Dogs + 1,000,000

62. BRUCELLOSIS Brucella melitensis ( goats, sheep ) Most pathogenic species for humans B. abortus ( Cattle, bison , African buffalo ) B. canis (dogs) B. suis (pigs) Infection not restricted to preferred host Brucella organisms are shed in body secretions 3 Urine Milk from infected animals Fetal fluid Abortion remnants 7/30/2024 62

63. BRUCELLOSIS Transmission of Brucella Aborted fetuses Ingestion of contaminated pasture/feeds Venereal transmission Introduction of affected animal Congenital transmission Transmission of brucellosis Consumption of raw milk from infected animals Assisting birth Laboratory exposure Accidental exposure to live attenuated vaccines; Strain 19,RB51,Rev 1 7/30/2024 63

64. BRUCELLOSIS Clinical features of brucellosis in Animals Abortion, still births, retained placenta Hygromas Scrotal swelling Infection of Cattle In many parts of the world, cattle are heavily infected Br. Abortus is most commonly involved They may readily infect with Br. Melitensis and Br. suis Br. Melitensis do not cause serious symptoms in cattle Br. Abortus may lead to death of the fetus and abortion The aborted fetus, the placenta and the discharge from vagina are all heavily contaminated 7/30/2024 64

65. BRUCELLOSIS Brucella tend to lodge in mammary gland and supramammary lymph nodes They may shed in the milk for years The organisms tend to settle in the testicles, epididymis and seminal vesicles Organisms may be present in the semen and may transmit sexually Transmission by artificial insemination In cattle is a serious economic and public health problem 7/30/2024 65

66. BRUCELLOSIS Infection of Goats; Is always due to Br. Melitensis Abortion is not a prominent symptoms Reduced fertility in the herd Br. Melitensis is passed in enormous numbers in the milk for 6-7 month Infection of Sheep Is always due to Br. Melitensis Is occasionally due to Br. Abortus or Br. Suis Affecting fertility and meat and wool production Transmission between animals Milk, Meat, Transplacentally , Sexually (& artificial insemination), Respiratory, Urine 7/30/2024 66

67. BRUCELLOSIS Mode of transmission Ingestion, Inhalation, Abrasion skin, Mucous membranes, Conjunctive, Sexual ,Blood transfusion, Organ transplant Diagnosis of brucellosis Clinical features Hygromas (common in animals), Swollen scrotal sac (animals/humans), Hepatoslpenomegaly (common in humans) History of contact and exposure Laboratory diagnosis Culture Serology Rose Bengal 7/30/2024 67

68. BRUCELLOSIS Treatment and control of brucellosis Antibiotic therapy (Doxycycline and Rifampicin) Avoid unpasteurized dairy foods Vaccinate domestic animals Cook meat thoroughly Take safety precautions in high-risk workplaces Hygiene 7/30/2024 68

69. MASTITIS Mastitis is inflammation of the parenchyma of the mammary gland regardless of the cause. Etiology: Contagious pathogens : Staphylococcus aureus, Streptococcus agalactiae, Mycoplasma bovis and Corynebacterium bovis Teat skin opportunistic pathogens : coagulase-negative staphylococci, Environmental pathogens : environmental Streptococcus spp. including Streptococcus uberis and Streptococcus dysgalactiae, which are the most prevalent; less prevalent is Streptococcus equinus (formerly referred to as Streptococcus bovis) . Environmental coli forms include the Gram-negative bacteria Escherichia coli, Klebsiella spp. and Enterobacter spp., and Arcanobacterium (formerly Actinomyces) pyogenes. Uncommon pathogens : many, including Nocardia spp., Pasteurella spp., Mycobacterium bovis, Bacillus cereus, Pseudomonas spp., Serratia marcescens, Citrobacter spp., anaerobic bacterial species, fungi and yeasts 7/30/2024 69

70. MASTITIS Clinical signs; Gross abnormalities in milk (discoloration, clots, flakes, pus) Physical abnormalities of udder: acute - diffuse swelling, warmth, pain, gangrene in severe cases; chronic -local fibrosis and atrophy Systemic response : may be normal or mild, moderate, acute, per acute with varying degrees of anorexia, toxemia, dehydration, fever, tachycardia, ruminal stasis, and recumbency and death. 7/30/2024 70

71. MASTITIS Diagnosis; Detection at the herd level : bulk tank milk SCCs . Culture o f bulk tank milk Detection at the individual cow level : abnormal looking milk, culture of composite or quarter milk samples. Indirect tests include SCCs of composite or quarter milk samples, California Mastitis Test (CMT) of quarter milk samples, in line milk conductivity tests of quarter milk samples Use of selective media to differentiate Gram-positive and Gram-negative pathogens in cases of clinical mastitis 7/30/2024 71

72. MASTITIS Treatment; Clinical mastitis in lactating cow : mild cases of clinical mastitis (abnormal secretion only) may not require treatment; however, all clinical mastitis episodes accompanied by an abnormal gland or systemic signs of illness should be treated with antimicrobial agents given by intra mammary infusion (all cases) and parenterally (selected cases). Acute and per acute mastitis cases require also require supportive therapy (fluid and electrolytes) and non-steroidal anti-inflammatory a gents (NSAIDs). Culture milk of representative clinical cases but antimicrobial susceptibility testing has not been validated Dry cow therapy: intramammary infusion of long-acting antimicrobial agents at drying off provides the best treatment for subclinical mastitis due to contagious pathogens. Must adhere to milk withholding times after treatment with antimicrobial agents to prevent milk drug residues, which is major public health issue. Currently available cow side antimicrobial residue tests are not reliable 7/30/2024 72

73. MASTITIS Control Principles of control: A. Eliminate existing infections B. Prevent new infections C. Monitor udder health status • Components of Mastitis Control Program: 1 . Use proper milking management methods 2. Proper installation, function, and maintenance o f milking equipment 3. Dry cow management 4. Appropriate therapy of mastitis during lactation 5. Culling chronically infected cows 6 . Maintenance of an appropriate environment 7 . Good record keeping 8. Monitoring udder health status 9. Periodic review of the udder health management program 10. Setting goals for udder health status 7/30/2024 73

74. ANTHRAX Etiology; Bacillus anthracis Transmission of the infection; Infection gains entrance to the body by ingestion, inhalation, or through the skin. while the exact mode of infection is often in doubt, it is generally considered that most animals are infected by the ingestion of contaminated food or water. Clinical findings Ruminants and horses- per acute disease characterized by fever, septicemia and sudden death. This may be accompanied by subcutaneous edematous swellings in horses. More prolonged disease with cellulitis of the neck and throat occurs in swine. Diagnosis; Because of risk, hematology and blood chemistry are not performed. Demonstration of organism in blood or subcutaneous fluid. Diagnostic confirmation Identification of organism in blood or tissues by polychrome Methylene blue stain of smear or by monoclonal antibody-fluorescent conjugates. Culture, Ascoli test 7/30/2024 74

75. ANTHRAX Post mortem findings; Carcass not opened if anthrax suspected; the diagnosis is made from the examination of aspirated carcass blood. Exudation of tarry blood from the body orifices of the cadaver, failure of the blood to clot, absence of rigor mortis and the presence of splenomegaly Treatment; Antibiotics, antiserum Control Prevention of further spread. Vaccination 7/30/2024 75

76. PINK EYE Infectious keratoconjunctivitis (IKC; pinkeye) of cattle, sheep, and goats is a common ocular condition in ruminants. Etiology; Moraxella bovis Transmission; Transmission Infection of animals occurs following contact with ocular secretions containing M. bovis bacteria. The major vector for disease transmission is usually the face fly (Musca autumnalis) but inanimate objects ( fomites ) can also spread the infectious organism. 7/30/2024 76

77. PINK EYE Clinical signs; BK varies from mild eye irritation with tears and small white ulcers to severe inflammation, resulting in permanent scarring, rupture of the cornea, and vision loss. Diagnosis; diagnosis may be made on clinical signs (clinical characteristics of inflammation and partial corneal opacity) and epidemiology, but additional examinations are often needed (Ophthalmic exam, fluorescein stain, bacteriology, and/or PCR). 7/30/2024 77

78. PINK EYE Treatment; Animals with IBK should be treated as early as possible to curb transmission to other animals and minimize the possibility of adverse and possibly permanent damage to the eye.  Healing of corneal ulcers typically requires 7-10 days so duration of antibiotic therapy should be at least 7- 10 days but might be longer with severe infections.   Moraxella bovis  are susceptible to several anti- infectives . In addition, local treatments (ointments, eye patches, surgical third eyelid flap) may be helpful. 7/30/2024 78

79. PINK EYE Prevention; Preventive measures include controlling flies with insecticide-impregnated ear tags, or topical pour-on or spray products, mowing pastures, minimizing dust in hay and feed bunks, providing shade, and, indirectly immunizing against viral diseases, such as IBR.  Moraxella bovis  bacterins administered prior to fly season may also be helpful. 7/30/2024 79

80. THEILERIOSIS Etiology; There are several identified Theileria spp. that infect cattle; the most pathogenic and economically important are T. parva, which causes East Coast fever (ECF), T. annulata, which causes Tropical theileriosis Theileria lestoquardi (T. hirchi), which causes Malignant ovine theileriosis the most pathogenic species of economic significance infecting small ruminants are Theileria uilenbergi and Theileria luwenshuni. Transmission; The most important vector for T. parva is Rhipicephalus appendiculutus. R. zambeziensis, Theileria annulata is transmitted by ticks of the genus Hyalomma Theileria luwenshuni and T. uilenbergi are transmitted by ticks of the genus Haemaphysalis 7/30/2024 80

81. THEILERIOSIS Clinical signs; swelling of the draining lymph node Fever ensues and continues throughout the course of infection; this rise in temperature is rapid and may reach 42°C There is marked petechial and ecchymotic haemorrhage on most mucous membranes of the conjunctiva and the buccal cavity. Anorexia develops, and loss of condition follows Other clinical signs may include lacrimation, corneal opacity, nasal discharge, terminal dyspnoea, and diarrhea Before death the animal is usually recumbent, the temperature falls, and there is a severe dyspnoea due to pulmonary oedema that is frequently seen as a frothy nasal discharge. 7/30/2024 81

82. THEILERIOSIS Clinical signs; The most prominent clinical signs of T. lestoquardi infections include generalized enlargement of the superficial lymph nodes, high fever, listlessness, anorexia, emaciation, intermittent diarrhea or constipation, respiratory signs (coughing, nasal discharge, dyspnoea), icterus and loss of weight. Reproductive losses including abortions may be seen. Sheep infected with T. lestoquardi also display anemia due to erythrocyte destruction. Similar signs have been reported in sheep infected with T. luwenshuni or T. uilenbergi. 7/30/2024 82

83. THEILERIOSIS Diagnosis; A definitive diagnosis is achieved by the combination of clinical examinations and appropriate laboratory testing. In the field, diagnosis is usually achieved by finding Theileria parasites in Giemsa-stained blood smears and lymph node needle biopsy smears, LESIONS; A frothy exudate is frequently seen around the nostrils of an ECF-infected animal Signs of diarrhoea , emaciation, and dehydration may be seen Lymph nodes are greatly enlarged and may be hyperplastic , haemorrhagic, and oedematous 7/30/2024 83

84. THEILERIOSIS In acute cases of ECF, lymph nodes are oedematous and hyperaemic, but often become necrotic and shrunken in more chronic disease • Generally, muscles and fat appear normal, but depending on relative acuteness of infection, fat may become greatly depleted Serosal surfaces have extensive petechial and ecchymotic haemorrhages, and serous fluids may be present in body cavities Haemorrhages and ulceration may be seen throughout the gastrointestinal tract – particularly in the pylorus part of the abomasum, where necrosis of Payer's patches can be observed Lymphoid cellular infiltrations appear in the liver and kidney as white foci The most striking changes are seen in the lungs; in most cases of ECF, interlobular emphysema and severe pulmonary oedema appear, the lungs are reddened and filled with fluid and the trachea and bronchi are filled with fluid and froth There are no specific lesions associated with tropical theileriosis 7/30/2024 84

85. THEILERIOSIS Shortly after infection, the lymph node draining the site of the tick bite will be enlarged At the time of severe clinical disease or death, anaemia, jaundice, enlarged lymph nodes, muscle wasting, pulmonary oedema, and haemorrhagic enterocolitis may all be present Several authors have reported cutaneous lesions including nodular, haemorrhagic and/or necrotic lesions 7/30/2024 85

86. THEILERIOSIS PREVENTION AND CONTROL; Bovine theileriosis is generally controlled by the use of acaricides to kill ticks, but this method is not sustainable Vaccination using The ' Muguga cocktail ' live vaccine Chemotherapeutic agents such as buparvaquone are available to treat T. parva and T. annulata infections Buparvaquone treats Theileria infections with great efficacy when used in the early stages of disease 7/30/2024 86

87. BABESIOSIS (REDWATER FEVER) Babesiosis is an infection of the red blood cells by a single cell parasite of the genus  Babesia . Etiology; Babesia bovis, Babesia bigemina and Babesia divergens. Transmission ; The main vectors of B bigemina and B bovis are 1-host Rhipicephalus (Boophilus) spp ticks which are widespread in tropical and subtropical areas. Transmission occurs transovarially. Clinical signs; The first clinical signs are lethargy, weakness, depression, and fever (frequently ≥106°F [41°C]), which persist throughout, and these are accompanied later by inappetence , anemia, jaundice, and weight loss; hemoglobinemia and hemoglobinuria occur in the final stages. 7/30/2024 87

88. BABESIOSIS (REDWATER FEVER) Involvement of the CNS due to adhesion of parasitized erythrocytes in brain capillaries can occur with B bovis infections. Late-term pregnant cows may abort, and temporary infertility due to transient fever may occur in bulls. Animals that recover from the acute disease remain infected for a number of years with B bovis or for a few months with B bigemina . No clinical signs are apparent during this carrier state. Post mortem lesions; Postmortem lesions (particularly with B bovis ) include the following: enlarged and friable spleen, swollen liver with an enlarged gallbladder containing thick granular bile, congested dark-colored kidneys generalized anemia and jaundice Most clinical cases of B bigemina have hemoglobinuria; however, this is not invariably the case with B bovis . Other organs, including the brain and heart, may show congestion or petechiae. 7/30/2024 88

89. BABESIOSIS (REDWATER FEVER) Diagnosis, Clinical findings and history may provide a presumptive diagnosis of Babesiosis; however, other conditions also cause similar clinical signs. Physical examination and history Light microscopic evaluation of blood smears PCR assay Serologic testing Treatment, diminazene aceturate and imidocarb dipropionate Supportive treatment is advisable, particularly in valuable animals, and may include the use of anti-inflammatory drugs, corticosteroids, and fluid therapy. Blood transfusions may be lifesaving in very anemic animals. 7/30/2024 89

90. BABESIOSIS (REDWATER FEVER) Control and prevention, Tick control, via acaricides or management practices, can be useful in reducing tick burdens, which can lower transmission rates. Using Resistant Breeds 7/30/2024 90

91. ANAPLASMOSIS It is an infectious disease of the red blood cells caused by the rickettsial bacteria Anaplasma marginale. Most commonly transmitted by ticks, A. marginale causes disease primarily in cattle. Rhipicephalus decoloratus (African blue tick), Rhipicephalus microplus (Asian blue tick) and Rhipicephalus evertsi evertsi (red legged tick) are the most important vectors of the disease. Clinical signs; The main signs of Anaplasmosis are; fever, jaundice and anorexia . Additional clinical signs may include; progressive anemia (pale gums and eyes), weakness, in appetence, loss of coordination, aggression, difficulty breathing, rapid pulse, decreased milk production, brown urine, and sudden death. 7/30/2024 91

92. ANAPLASMOSIS Diagnosis; Clinical signs of anemia and mass destruction of RBC’s. Packed RBC Volume usually in low teens or single digit. Stained Blood smears with dark staining body on margin of RBC’s. Serological ELISA Test for convalescent or carrier state Treatment, control and prevention: Tetracyclines, imidocarb, and vaccination by inoculation with less pathogenic species. Effective tick control herd treatment with oxytetracyclines injection every 3 to 4 weeks during high risk times may be necessary will prevent clinical disease but animals can become carriers. 7/30/2024 92

93. Heart water Etiology ; Ehrlichia (Cowdria) ruminantium, a rickettsial organism Vectors ; Amblyomma variegatum and A . Habraeum Clinical signs; High fever, nervous signs, diarrhea and death if acute; may be mild and in apparent. Diagnostic confirmation Rickettsial colonies in capillary endothelium (brain preparations) Lesions; Ascites, hydrothorax, hydro pericardium and severe pulmonary edema Treatment; Short- and long-acting tetracyclines Control; Vaccination based on infection and treatment methods, tick control and chemoprophylaxis 7/30/2024 93

94. MILK FEVER(PARTURIENT PARESIS) (a ) In cows; Characterizes by circulatory collapse, generalized paresis and depression. Etiology; low serum calcium level Clinical signs; Occurs 72 hours after parturition. (but it may b seen some months before or during parturition where it is associated with distocia due to inadequate uterine contractions). The 1 st stage; Excitement, hypersensitivity, tetany and muscle tremors of the limbs, animal is disinclined to move or hear, grinding of teeth, unsteady walking with stiffness of the hind leg and ataxia. 7/30/2024 94

95. MILK FEVER(PARTURIENT PARESIS) 2 nd stage; Sternal recumbence with the animal unable to rise, Head is displaced to one side with a kink in the neck (or it may be turned to the flanks), Eyes are dull and staring with pupils dilated, Anorexia, Dry muzzle, Cold extremities, Increased pulse, Temperature is normal or sub-normal Gut is atonic with the anus relaxed 7/30/2024 95

96. MILK FEVER(PARTURIENT PARESIS) The 3 rd stage; There is lateral recumbency, Bloating, regurgitation, pulse is impalpable and heart is inaudible, aspiration pneumonia, last stages there is comma and death. Diagnosis; Clinical signs Milk fever is confirmed by low serum calcium concentrations (total blood calcium values fall below 7.5 mg/dl) 7/30/2024 96

97. MILK FEVER (PARTURIENT PARESIS) Treatment; 250-500mls of calcium borogluconate intravenously. It can be given sub/cut (not more than 50mls per injection site) or intraperitoneally this decreases the risk of cardiac failure. Animals that relapse in 8-12 hours should have the treatment repeated and magnesium should be added. Treatment must be early to avoid muscle and nervous damage and degeneration. Prophylaxis; Vitamin D (injectable or in feed) before calving The cow will then have to be supplemented with calcium after birth 7/30/2024 97

98. MILK FEVER (PARTURIENT PARESIS) (b) In ewes. Characterized by hyper excitability, ataxia, coma and death Occurs in older ewes at a time period between 6 weeks before lambing and 10 weeks after The disease is of rapid onset occurring within 24 hrs after an abrupt change of feed, weather, short period of fasting during shearing transport, etc. Clinically there are outbreaks in a flock, with hype excitability, muscle ttremors and astilted gait.they are followed by dullness, sternal decubitus , with the hind legs extended backwards, mild ruminal tympany and regurgitation of food through the nostrils staring eyes, shallow respiration, coma and death. 7/30/2024 98

99. MILK FEVER (PARTURIENT PARESIS) Diagnosis is based on clinical signs with pregnancy toxemia being the major differential. It is confirmed by a lasting response to calcium therapy Treatment and prophylaxis; Intravenous calcium. 7/30/2024 99

100. BLOAT Over distension of the rumenoreticulum with the gases of fermentation, either in the form of a persistent foam mixed with the rumenal contents i.e. primary or frothy bloat. In the form of free gas separated from the ingesta i.e. secondary or free-gas bloat. Etiology; Common in cattle than other ruminants Frothy bloat is associated with legume consumption (e.g. alfalfa, clover) Thin leaf structure of certain varieties of legumes coupled with tender growth (early or late season) allows for more rapid bacterial degradation and intraruminal particle suspension. Chloroplast released from the legume leaf forms monomolecular foam that trap gas bubbles. These foams have great surface tension and are highly stable 7/30/2024 100

101. BLOAT Small gas bubbles do not coalesce, the cardia or the fore stomach cannot be cleared of this foam, and the animal is unable to eructate Feedlot Bloat: cattle can also develop frothy bloat when more than 50% of their ration is being consumed as concentrate. A mucoprotein slime stabilizes the foam. This foam is stable at a low pH created by lactate and VFA production. Salivation is decreased because of the fine grind of the diet, which also lessens intraruminal buffering. Free gas bloat: is associated with a history of feeding whole or only partially chopped solid feeds (e.g., potatoes, apples, turnips). Esophageal obstruction caused by a foreign body, stenosis, or pressure from enlargement outside the esophagus, acute onset of ruminal atony due to anaphylaxis, grain overload and hypocalcemia 7/30/2024 101

102. BLOAT Hypoderma lineaturn reactions Cervical neoplasia Certain postures or diseases( Examples include milk fever and tetanus). Vagal indigestion-Moderate free gas bloat Clinical Signs: Distension of the left flank Protrusion of the paralumbar fossa above the ventral column and enlarged abdomen Dyspnea and grunting Mouth breathing, protrusion of the tongue, and extension of the head, and occasionally vomition. 7/30/2024 102

103. 7/30/2024 103

104. BLOAT Diagnostic plan : An accurate history The passage of an oro-gastric tube A reading of the foam Ph further defines the type of frothy bloat; a feedlot bloat should have a pH of less than 5.5. Treatment: With frothy bloat, pass an oro-gastric tube and administer an oil to reduce the surface tension of the foam and allow the gas bubbles to coalesce. Either mineral oil at 1L/100 kg orally or Dioctyl sodium sulfosuccinate (DSS) in peanut oil at 17-66 mg/kg orally may be used (150-600 ml/450 kg animal). The treatment should be satisfactory and sufficient if the animal is still standing and not showing evidence of respiratory or cardiac failure. If the animal is in a deteriorating clinical condition, an emergency rumenotomy is warranted. 7/30/2024 104

105. 7/30/2024 105

106. 7/30/2024 106

107. ORF(CONTAGIOUS ECTHYMIA, CONTAGIOUS PUSTULAR DERMATITIS, SORE MOUTH) It is a common disease of small ruminants caused by a parapox virus that is highly infectious. Infection is by contact. The young animal is the most affected Etiology; A parapox virus related to pseudo cowpox Transmission; The disease is transmitted by contact & inamminate objects such as ear tag applicator, burdizzo, etc. Clinical finding; Lesions of the skin with thick tenuous scabs usually around the oral commisures, they can spread to muzzles, nostrils and buccal cavity Extension of lesions to the alimentary tract leads to gastroenteritis, in the trachea it cause respiration difficulty. 7/30/2024 107

108. ORF(CONTAGIOUS ECTHYMIA, CONTAGIOUS PUSTULAR DERMATITIS, SORE MOUTH) PM Skin lesions and ulcerative erosions of the nasal cavity, upper respiratory tract, esophagus abomasum , small intestines. DX Based on clinical clinical signs, PM and isolation of the virus. DDX Bluetogue , ulcerative dermatitis, mycotic dermatitis Control : Vaccinate the lambs, Isolate and treat 7/30/2024 108

109. NAIROBI SHEEP DISEASE It is a tick borne viral disease of goats and sheep characterized by fever and hemorrhagic gastroenteritis, abortion and high mortality in east African coast where the Rhipicephalus appendiculutus are found. It is a zoonotic disease but the human form is rear. Etiology; it is caused by nairovirus, family Bunyaviridae. Transmission; it is transmitted transovarially and transtadially by the brown ear ticks. Clinical signs; a fever lasting 1-3 days following an incubation period of 4-5 days is observed, other signs include; depression, anorexia, mucopurulent blood stained nasal discharge and fetid dysentery that causes tenesmus, abortion is frequent in pregnant animals. Death may occur in the febrile viremic phase or 2 days after disappearance of fever, mortality rate in sheep may approach 90%. The disease is more severe in sheep than goats 7/30/2024 109

110. NAIROBI SHEEP DISEASE Lesions; the main lesions are enlarged edematous lymph nodes, hemorrhages of the abomasusm and intestinal mucosa, respiratory, female genital tracts, gall bladder, spleen and heart. Petechial and ecchymotic hemorrhages of cecal and colon mucosa frequently appear as longitudinal striations and sometimes the only lesions seen. Conjunctivitis with crust formation is common. Microscopic lesions include lymphoid hyperplasia, myocardial degeneration, nephrosis and necrosis of the gall bladder. Diagnosis; Occurrence of the disease in ticks and goats with tick infestation are suggestive especially following introduction into tick infested areas and changes in rainfall pattern. Confirmation is based on confirmation of viral antigens by ELISA or Agar gel immunodiffusion test. 7/30/2024 110

111. NAIROBI SHEEP DISEASE Treatment and control; No specific drug is available for treatment. Prevention is based on tick control No vaccine is available for use in ticks 7/30/2024 111

112. BLUETONGUE Bluetongue; is a relatively rare arthropod borne viral disease of domestic and wild ruminants in Africa, Asia and the Americas. Etiology; bluetongue virus of genus orbivirus. Transmission; it is transmitted by a small culicoides biting midge. Clinical signs; the course in sheep and goats may range from per acute to chronic. Per acute cases die within 7-9 days of infection mainly from asphyxia and dyspnea resulting from pulmonary edema and frothing from the nostrils. Chronic cases affect small ruminants for about 3-5 weeks before death. Death results mainly from secondary bacterial infection such as pasteurellosis and exhaustion . 7/30/2024 112

113. BLUETONGUE Mild cases recover rapidly and fully without any complication. In sheep the virus cause damage to the vascular endothelial cells causing changes in vascular permeability and subsequent intravascular coagulation This results in congestion, edema, hemorrhage, inflammation and necrosis. Signs includes; Fever (40.5-42 c), listlessness, and reluctance to move. Young animals are the most affected. Generalized edema of head and facial structures, coronary bands with lameness may be seen. Serous nasal discharge that later turn mucopurulent may be seen. Most goats in areas of infection do not show clinical signs but occasionally previously unexposed goats such as exotic goats will show confusing signs. A high fever is followed by nasal discharge, salivation and licking. The discharge will dry and encrust on the nose, the lips will swell and become tender, some times bleeding. Animals loose appetite from painful lips. The encrusted lips may appear a little like orf. A swollen cyanotic tongue (bluetongue) may be seen. Death from starvation and emaciation may occur. 7/30/2024 113

114. BLUETONGUE Mortality rates up to 20% are common occasionally rising up to 90%. Clinical signs in cattle are rare but may be similar in those seen in sheep. Infected mothers abort or give birth to malformed calves or lambs. Malformations are mainly seen in the brain and includes hydranencephally which results into ataxia of the new born. Lesions; Petechial or ecchymotic hemorrhages of walls of pulmonary artery and focal necrosis of papillary muscles of left ventricle. Hemorrhages and necrosis due to mechanical abrasions are often seen in fragile tissues such as buccal cavity (from chewing). Other lesions include pneumonia, generalized edema, skeletal and myocardial necrosis and pericarditis. 7/30/2024 114

115. BLUETONGUE Diagnosis; Presumptive diagnosis is made from clinical signs and typical lesions. Confirmation is done to identify the viral RNA by RT-PCR or isolation in embryonated chicken eggs. Prevention and control; Vaccination is the most effective method of control in endemic areas. Vaccinations with live strains may produce abortions or malformations of the CNS during the first trimester of the pregnancy. Control of the vectors by use of insecticides lowers the risk of exposure. 7/30/2024 115

116. PESTE DES PETITS RUMINANTS (PPR) Peste des Petits Ruminants  (PPR), also known as sheep and goat plague, is a highly contagious animal disease affecting domestic and wild small ruminants . Causative agent; Peste des petits ruminants virus (PPRV ). Transmission of PPR; Mainly by aerosols or direct contact between animals living in close quarters, Fomites may be means of spreading infection; bedding, feed, pasture and water troughs, No carrier state. 7/30/2024 116

117. PESTE DES PETITS RUMINANTS (PPR) Clinical signs; sudden onset of depression , fever, discharges from the eyes and nose, sores in the mouth, disturbed breathing and cough, foul-smelling diarrhea and death . Lesions; Emaciation, conjunctivitis, and stomatitis are common clinical signs of PPR; necrotic lesions are observed inside the lower lip and on the adjacent gum, on the cheeks near the commissures, and on the ventral surface of the tongue. In severe cases, the lesions may extend to the hard palate and pharynx. 7/30/2024 117

118. PESTE DES PETITS RUMINANTS (PPR) Diagnosis; Clinical signs, Laboratory tests i.e. Reverse-transcription PCR (RT-PCR ) reverse-transcription real-time PCR (RT- qPCR ) assays Imunocapture enzyme-linked immunosorbent assay Culture and isolation methods Agar gel immunodiffusion Serological tests i.e . Virus neutralization, Competitive enzyme-linked immunosorbent assay. 7/30/2024 118

119. PESTE DES PETITS RUMINANTS (PPR) Prevention and control Exposed or infected animals should be slaughtered and the carcases should be burned with deep burial, most commonly employed control mechanism is vaccination i.e. sheep and goats vaccinated with an attenuated strain of PPR, or that recover from PPR, develop an active life-long immunity against the disease. No specific treatment. However , supportive care and treatment of bacterial and parasitic co infections may decrease mortality Antibiotics may prevent secondary pulmonary infections (oxytetracycline, chlortetracycline) 7/30/2024 119

120. THANKS ALL THE BEST IN YOUR ENDEAVORS