sr dz

Question 1

signalment for mycoplasma

Answer 1

sheep and goats

Question 2

predisposing factors for mycoplasma infection

Answer 2

increases with stress

Question 3

transmission for mycoplasma

Answer 3

spread by carriers in the head

Question 4

pathogenesis for mycoplasma

Answer 4

young ones suck from infected moms

dirty machines for milking

it alters macrophage activity

Question 5

which animals are affected by scrapie

Answer 5

goats and sheep

Question 6

when do goats and sheep gets scrapie

Answer 6

any time of the year

Question 7

transmission of scrapie

Answer 7

Most commonly transmitted from ewe to her offspring and other lambs through placenta and placental fluids.

Oral transmission

Small abrasions contaminated with placental fluids

Question 8

pathophysiology and etiology of scrapie

Answer 8

Scrapie is a priion (infectious protein) - it is NOT a virus.

Exact mechanism of CNS degeneration not identified but oral route of entry is most likely, where transport ot the CNS is believed to occur from the GI tract via the vagus nerve. It then replicates within the lymphoid tissue

Question 9

cs of scrapie

Answer 9

Behavior changes ranging from nervousness to restlessness, accompanied by weight loss.
Pruritis that increases in severity
*2o wool loss
*dermatitis
*skin infx
*excoriation
Corneal chemosis
Aural hematoma
Nibbling reflex
Tremors
Exercise intolerance
Ataxia

Question 10

signalment for chlamedia psittassi

Answer 10

mostly seen in sheep

Question 11

seasonality for chlamedia

Answer 11

mostly occur during the lambing season

Question 12

transmission for chlymedia

Answer 12

Direct contact
(ocular, abortion secretions)
Fecal-oral
Insect bites
Birds
Venereal

ZOONOTIC

Infection established in “clean flock” via infected individuals à a few infected 1st year, abortion storm 2nd year

Question 13

pathophysiology/ etiology of chlamedia

Answer 13

Intracellular pathogen
But exact pathogenesis is unknown

Question 14

predisposing factors for chlamedia

Answer 14

Sexual contact with infected mate
Contact with aborted fetus

Flocks closely congregated during periparturient period

Question 15

signalment for bluetongue dz

Answer 15

it is mostly a dz of improved breeds of sheep

mild subclinical infection in cattle and wild ruminants

Question 16

mode of transmission of bluetongue

Answer 16

collicoids biting midges

Question 17

pathophysiology and etiology of btv

Answer 17

collicoids vectors gets infected by inbibimng blood from infected veterbates

the virus has high efffinity for rbc contributing to prolonged viremia in presence of neutralising Ab.

The course of the disease in sheep can vary from peracute to chronic, with a mortality rate of 2%–90%. Peracute cases die within 7–9 days of infection, mostly as a result of severe pulmonary edema leading to dyspnea, frothing from the nostrils, and death by asphyxiation. In chronic cases, sheep may die 3–5 wk after infection, mainly as a result of bacterial complications, especially pasteurellosis, and exhaustion. Mild cases usually recover rapidly and completely. The major production losses include deaths, unthriftiness during prolonged convalescence, wool breaks, and reproductive losses.

In sheep, BTV causes vascular endothelial damage, resulting in changes to capillary permeability and subsequent intravascular coagulation

Question 18

predisposing factors for btv

Answer 18

moist,warm environments in lower elevations.

poximity to water where collicoids thrive

Question 19

cs and symptoms of btv

Answer 19

In sheep, BTV causes vascular endothelial damage, resulting in changes to capillary permeability and subsequent intravascular coagulation. This results in edema, congestion, hemorrhage, inflammation, and necrosis. The clinical signs in sheep are typical. After an incubation period of 4–6 days, a fever of 105°–107.5°F (40.5°–42°C) develops. The animals are listless and reluctant to move. Clinical signs in young lambs are more apparent, and the mortality rate can be high (up to 30%)

Clinical signs in young lambs are more apparent, and the mortality rate can be high (up to 30%)

Approximately 2 days after onset of fever, additional clinical signs may be seen, such as edema of lips, nose, face, submandibular area, eyelids, and sometimes ears; congestion of mouth, nose, nasal cavities, conjunctiva, and coronary bands; and lameness and depression. A serous nasal discharge is common, later becoming mucopurulent. The congestion of nose and nasal cavities produces a “sore muzzle” effect, the term used to describe the disease in sheep in the USA. Sheep eat less because of oral soreness and will hold food in their mouths to soften before chewing. They may champ to produce a frothy oral discharge at the corners of the lips. On close examination, small hemorrhages can be seen on the mucous membranes of the nose and mouth. Ulceration develops where the teeth come in contact with lips and tongue, especially in areas of most friction. Some affected sheep have severe swelling of the tongue, which may become cyanotic (‘bluetongue”) and even protrude from the mouth. Animals walk with difficulty as a result of inflammation of the hoof coronets. A purple-red color is easily seen as a band at the junction of the skin and the hoof. Later in the course of disease, lameness or torticollis is due to skeletal muscle damage. In most affected animals, abnormal wool growth resulting from dermatitis may be seen

Question 20

d xfor btv

Answer 20

The typical clinical signs of bluetongue enable a presumptive diagnosis, especially in areas where thedisease is endemic. Suspicion is confirmed by the presence of petechiae, ecchymoses, or hemorrhages in the wall of the base of the pulmonary artery and focal necrosis of the papillary muscle of the left ventricle

Hemorrhages and necrosis are usually found where mechanical abrasion damages fragile capillaries, such as on the buccal surface of the cheek opposite the molar teeth and the mucosa of the esophageal groove and omasal folds

Question 21

lab tests to confirm btv

Answer 21

In many areas of the world, BTV infection in sheep, and especially in other ruminants, is subclinical. Laboratory confirmation is based on virus isolation in embryonated chicken eggs or mammalian and insect cell cultures, or on identification of viral RNA by PCR. The identity of isolates may be confirmed by the group-specific antigen-capture ELISA, group-specific PCR, immunofluorescence, immunoperoxidase, serotype-specific virus neutralization tests, serotype-specific PCR, or hybridization with complementary gene sequences of group- or serotype-specific genes

Question 22

tx for btv

Answer 22

There is no specific treatment for animals with bluetongue apart from rest, provision of soft food, and good husbandry. Complicating and secondary infections should be treated appropriately during the recovery period

Prophylactic immunization of sheep remains the most effective and practical control measure against bluetongue in endemic regions. Attenuated and inactivated vaccines against BTV are commercially available in some countries

Question 23

signalment for clostridial perfringins type A

Answer 23

type A normal microflora and soil

Question 24

signalment for cl. perfringens type B

Answer 24

young (lambs) less than 10 days

often called lamb dysentery

Question 25

cs of cl. type B

Answer 25

The acute form of the disease commonly occurs in strong and healthy lambs of about 2 – 4 days of age. The animals show signs of abdominal pain, bleat repeatedly, cease to suck, collapse and die within a few hours. The faeces are blood stained. Some cases are less acute and the symptoms more protracted. In the majority of the cases, the intestines show lesions consisting of intense haemorrhagic areas and sometimes ulcers. The stomach usually contains a large quantity of milk.

Question 26

predisposing factors for cl. type b

Answer 26

• lambs which ingest large quantities of milk are more susceptible than those which have a more restricted supply

Question 27

season for cl. type b

Answer 27

lambng season

Question 28

dx for cl. type B

Answer 28

• The age of affected lambs,
• the symptoms,
• lesions,
• and sometimes the history of the flock, together may provide strong supporting evidence that the disease is lamb dysentery.
• Confirmation is obtained by identifying the presence of toxins in the intestinal contents or culturing the organism from intestinal lesions, bowel contents and sometimes from heart blood.

Question 29

control and prevention of cl. type B (lamb dysentery)

Answer 29

To prevent outbreaks of lamb dysentery, advantage is taken of the fact that lambs derive a passive immunity from their dams through the colostrum. Before lambing season, ewes are vaccinated, and the resulting passive immunity which unweaned lambs derive from colostrum is adequate to protect them for approximately the first three weeks of life

Question 30

signalment for cl. type c

Answer 30

common in all livestocks

normal microflora

very young lambs less than 2 weeks

Question 31

cs of cl. type c

Answer 31

bloody diarrhea,

hemorrhagic enteritis, and

bloody scours

Question 32

control of clostrial dz

Answer 32

Clostridial diseases are easily prevented in the young by vaccinating pregnant dams about three weeks prior to delivery and subsequent vaccination of offspring. Consumption of adequate, high quality colostrum is important

Question 33

cs of cl. type D

Answer 33

the onset of neurologic signs followed by sudden death is more common in sheep, whereas goats are more likely to show signs of diarrhea before death

Question 34

cs of cl. type A

Answer 34

Clastridiurre perfringens type A causes

• enterotoxemia, or yellow lamb disease,
• . Depression, anemia,
• icterus and hemoglobinuria, are followed

by death after a clinical course of 6-12 h,

• and large numbers of C. perfringen.

s are found in intestinal contents. A
similar condition occurs in goats

Question 35

signalment for campylobacter

Answer 35

Sheep goats, cattle and humans

Question 36

seasonality for campylobacter (vibrio)

Answer 36

During the breeding season, colder/wet seasons (fall/spring), and late gestation, may also be seen in areas with a high bird density

Question 37

transmission for camphylobactor

Answer 37

fecal-oral (pasture water, fetal tissues, feces)
birds can also be vectors

Question 38

apthogenesis for camphylobacter

Answer 38

fecal-oral/bird vectors –> enters blood stream –> travels to uterus –> crosses placenta –> abortion 1-3 weeks later if pregnant; ewes can recover and remain immune or become PI
Campylobacter fetus fetus or Campylobacter jejuni

Question 39

predisposing factors forcaphylobacter

Answer 39

colder/wet seasons, areas with a high bird density, pregnancy

Question 40

cs of camphylobacter

Answer 40

abortion (usually whole flock not individual), placentitis, brown discharge from vulva
histopath may show necrosis of cotyledons and yellow/orange foci on the liver

Question 41

dx for vibrio

Answer 41

Diagnosis of C jejuni is based on isolation of the organism on selective media under microaerophilic conditions. Fresh fecal samples should be collected; if transport to the laboratory is delayed, transport media and storage at 4ºC produce the best results

Question 42

tx for vibrio and control

Answer 42

Vaccinate with killed vaccine at breeding and mid-gestation if abortion has been a problem. The second year, use a booster at mid-gestation. Vaccination cost is 40 cents per ewe per year

If ewes have not been vaccinated and an abortion outbreak occurs, feeding 250 to 400 mg tetracycline (Aureomycin or Terramycin) per ewe daily for 30 days usually is an effective preventive measure

Question 43

signalment for contagious erecthyma

Answer 43

sheep and goats

Question 44

season for contagious erycthyma

Answer 44

most common in late summer, fall n winter

mostly young animals

Question 45

cs of contagious erecthyma

Answer 45

swellling of lips and fever

the lesions extend to the mucosa of mouth

the lesions developed aspapules and progress through vesicular andpustular stages before crusting. Coalescence ofnumerous discrete lesions often leads to theformation of large scales, and under them.Extensive lesions on the feet in some animals lead to lameness. Mastitis in some animals was also developed when the lesions present on theudder

Question 46

dx for contagious erythma

Answer 46

Diagnosis was made on the basis oftypical lesions in the mouth commissure, lips, gumtongue and around the mouth

Direct demonstration of virus in scab material by electron microscopy has now been replaced by PCR as the diagnostic method of choice for ecthyma

Question 47

tx for contagious erythemas

Answer 47

Both parenteral and topical antibiotics may help combat secondary bacterial infection of the skin lesions. In endemic areas, appropriate repellents and larvicides should be applied to the lesions to prevent myiasis. The virus is transmissible to people, and the lesions, usually confined to the hands and face, are more proliferative and occasionally very distressing. Veterinarians and sheep handlers should exercise reasonable protective precautions and wear disposable gloves

Sheep that have recovered from natural infection are highly resistant to reinfection. Despite a multiplicity of immunogenic virus strains, the presently used commercial single-strain live vaccines have produced fair immunity in all parts of the USA

Question 48

etiology n transmission of contagious erythma

Answer 48

parapoxvirus is related to pseudocowpox and bovine papillar stomatitis . Infection occurs by contact. The virus is highly resistant to desiccation in the environment

Question 49

pathophysiology for contagious erythma

Answer 49

The primary lesion develops at the mucocutaneous junction of the lips and around erupting incisor teeth and may extend to the mucosa of the buccal cavity. Occasionally, lesions are found on the feet and around the coronet, where secondary bacterial infection withDermatophilus congolensis commonly causes “strawberry footrot.” Ewes nursing infected lambs may develop lesions on the teats extending onto the udder skin. The lesions develop as papules and progress through vesicular and pustular stages before encrusting. Coalescence of numerous discrete lesions often leads to the formation of large scabs, and the proliferation of dermal tissue produces a verrucose mass under them. When the lesion extends to the oral mucosa, secondary necrobacillosis (see Necrotic Laryngitis in Cattle) frequently develops.

During the course of the disease (1–4 wk), the scabs drop off and the tissues heal without scarring. During active stages of infection, more severely affected lambs fail to eat normally and lose condition. Extensive lesions on the feet cause lameness. Mastitis, sometimes gangrenous, may occur in ewes with lesions on the teats.

Question 50

signalment for contagious lymphadenitis

Answer 50

sheep and goats

Although CL is typically considered a disease of sheep and goats, it also occurs more sporadically in horses, cattle, camelids, swine, wild ruminants, fowl, and people. Because of its zoonotic potential, care should be taken when handling infected animals or purulent exudate from active, draining lesions

Question 51

predisposing factors for contagious lymphadenitis

Answer 51

The presence of organic material, shade, and moisture favor and enhance surviva

Question 52

etiology and pathogenesis of contagious lymphadenitis

Answer 52

Corynebacterium pseudotuberculosis

characterized by abscess formation in or near major peripheral lymph nodes (external form) or within internal organs and lymph nodes (internal form). Although both the external and internal forms of CL occur in sheep and goats, the external form is more common in goats, and the internal form is more common in sheep. Economic losses from CL include death, condemnation and trim of infected carcasses, hide and wool loss, loss of sales for breeding animals, and premature culling of affected animals from the herd or flock. Once established on a farm or region (endemic), it is primarily maintained by contamination of the environment with active draining lesions, animals with the internal form of the disease that contaminate the environment through nasal discharge or coughing

Question 53

cs of contagious lymphadenitis

Answer 53

The hallmark clinical finding in cases of external CL is the development of abscesses in the region of peripheral lymph nodes. Common sites of development include the submandibular, parotid, prescapular, and prefemoral nodes. Less commonly, abscessation of supramammary or inguinal lymph nodes occurs, in addition to an occasional ectopic location along the lymphatic chain. If left untreated, these lesions eventually mature into open draining abscesses. The purulent material from these lesions has no odor and varies in consistency from soft and pasty (more common in goats) to thick and caseous (more common in sheep). Once natural draining occurs, the skin lesion heals with scarring. Recurrence is common, which can be months later.

The internal form of CL most commonly presents as chronic weight loss and failure to thrive. The presence of other clinical signs depends on the organs of involvement, which may include any of the major organ systems. Lung abscessation is a common site of visceral involvement in internal CL; therefore, signs of chronic ill thrift with cough, purulent nasal discharge, fever, and tachypnea with increased lung sounds may be noted. The internal form is more common in sheep and has been termed the “thin ewe syndrome

Question 54

age of contagious lymphadenitis

Answer 54

The incidence of abscesses and development of clinical disease with either the external or internal form increases with age

Question 55

lesions for contagious lymphadenitis

Answer 55

• In sheep, abscesses often have the classically described laminated “onion-ring” appearance in cross section, with concentric fibrous layers separated by inspissated caseous exudate.
• In goats, the abscesses are less organized, and the exudate is usually soft and pasty

Question 56

dx for contagious lymphadenitis

Answer 56

The presence of an external abscess on a small ruminant is highly suggestive of CL, especially in locations of peripheral lymph nodes. However, the only definitive diagnosis is bacteriologic culture of purulent material from an intact abscess

Animals with visceral abscesses pose a greater diagnostic challenge. Radiography and ultrasonography can be useful to detect internal lesions. Culture of a transtracheal aspirate obtained from an animal with pneumonia can help determine whether CL is the cause. Excluding other causes of chronic weight loss and ill thrift in the face of proper nutrition and good appetite such as Johne’s disease, parasitism, and poor dentition further raise suspicion

Question 57

tx and control of contagious lymphadenitis

Answer 57

Once a diagnosis of CL has been established, owner education stressing the persistent, recurrent nature of the disease is necessary. The most practical approach for commercial animals infected with CL is to cull them from the herd or flock. However, animals with draining abscesses should not be sent through sale barns until draining has ceased and the wound has healed. Treatment of individual animals should be undertaken with the understanding that CL is not considered a “curable” disease. Animals with genetic or emotional value are treated mainly for aesthetic reasons and to limit their infectivity to the rest of the herd or flock. Treatment options have included lancing and draining, surgical excision, formalin injection of lesions, systemic antibiotics, and intralesional antibiotics

Because of the nature of the causative organism, common means of exposure, chronicity of the disease, and difficulty in completely eliminating the organism from individual animals, control of CL revolves around strict biosecurity measures

Commercial CL vaccines are currently licensed for use in sheep and goats. These vaccines should only be used in the species they are labeled for, because adverse reactions have been reported in goats given vaccine labeled for sheep

Question 58

signalmemnt for caprine arthritis and encephalitis

Answer 58

Caprine arthritis and encephalitis (CAE) virus infection is manifested clinically as polysynovitis-arthritis in adult goats and less commonly as progressive paresis (leukoencephalomyelitis) in kids

Question 59

etiology and pathogenesis of CAE

Answer 59

The CAE virus is an enveloped, single-stranded RNA lentivirus in the family Retroviridae

Question 60

predisposing factors to CAE

Answer 60

CAE virus infection is widespread in dairy goat breeds but uncommon in meat- and fiber-producing goats. This has been attributed to genetics, management practices such as feeding colostrum and milk from a single dam to multiple kids, and industrialized farming practices

(eg, frequent introductions of new animals into a herd). Prevalence of infection increases with age but is not influenced by sex. Most goats are infected at an early age, remain virus positive for life, and develop disease months to years later

Question 61

cs of CAE

Answer 61

The most common manifestation of infection is polysynovitis-arthritis, which is primarily seen in adult goats but can occur in kids as young as 6 mo old. Signs of polysynovitis-arthritis include joint capsule distention and varying degrees of lameness. The carpal joints are most frequently involved. The onset of arthritis may be sudden or insidious, but the clinical course is always progressive. Affected goats lose condition andusually have poor hair coats. Encephalomyelitis is generally seen in kids 2–4 mo old but has been described in older kids and adult goats. Affected kids initially exhibit weakness, ataxia, and hindlimb placing deficits. Hypertonia and hyperreflexia are also common. Over time, signs progress to paraparesis or tetraparesis and paralysis. Depression, head tilt, circling, opisthotonos, torticollis, andpaddling have also been described

Question 62

dx for CAE

Answer 62

clinical signs and history

Both an agar gel immunodiffusion test and ELISA for CAE virus are considered sufficiently reliable for use in control programs

Question 63

tx for CAE

Answer 63

There are no specific treatments for any of the clinical syndromes associated with CAE virus infection. However, supportive treatments may benefit individual goats. The condition of goats with the polysynovitis-arthritis may be improved with regular foot trimming, use of additional bedding, andadministration of NSAIDs

Goats with encephalomyelitis can be maintained for weeks with good nursing care. Antimicrobial therapy is indicated to treat secondary bacterial infections that may complicate the interstitial pneumonia or indurative mastitis components of CAE virus infection. Providing high-quality, readily digestible feed to goats positive for CAE virus may delay the onset of the wasting syndrome

Question 64

control of CAE in commercial goats

Answer 64

1) permanent isolation of kids beginning at birth; 2) feeding of heat-treated colostrum (45°C [113°F] for 60 min) and pasteurized milk; 3) frequent serologic testing of the herd (semiannually), with identificationand segregation of seronegative and seropositive goats; and 4) eventual culling of seropositive goats. If the control program includes segregation of herds into seropositive and seronegative groups, groups should be separated by a minimum of 6 ft (1.8 m), and shared equipment should be disinfected using phenolic or quaternary ammonium compounds.

Question 65

etiology n pathogenesis of progressive ovine pneumonia

Answer 65

lenti v

The causal lentivirus, which persists in lymphocytes, monocytes, and macrophages of infected sheep in the presence of a humoral and cell-mediated immune response, can be detected by several serologic tests. Seropositive sheep and goats must be considered infected and capable of transmitting the virus

Question 66

transmission of ovine progressive pneumonia

Answer 66

Transmission occurs most commonly via the oral route, usually by ingestion of colostrum or milk that contains virus, or by inhalation of infected aerosol droplets

Question 67

age of susceptibility with ovine progressive pneumonia

Answer 67

Signs rarely occur in sheep <2 yr old and are most common in sheep >4 yr old

Question 68

cs of ovine progressive pneumonia

Answer 68

The disease progresses slowly, with wasting and increasing respiratory distress as the main signs. Coughing, bronchial exudate, depression, and fever are seldom evident unless secondary bacterial infection occurs. A noninflammatory, indurative mastitis may occur. The encephalitic form of visna causes head tilt and circling, whereas the spinal form causes unilateral pelvic limb proprioceptive deficits progressing to paresis and eventually to complete paralysis

Question 69

dx forovine progressive pneumonia

Answer 69

Ultrasonographic examination is very useful to differentiate these various types of pneumonias in the live animal

agar gel immunodiffusion (AGID) and ELISA tests

Serologic testing is considered a useful tool to detect infected sheep, especially if the disease has been confirmed in the flock by histopathologic examination or virus isolation. PCR and virus isolation are sensitive and specific techniques to detect virus. However, both are more expensive and time consuming than serologic testing

Question 70

control for ovine progressive pneumonia

Answer 70

Currently, there is no practical, effective treatment, and no vaccines are available. Therefore, the only means for control and prevention is serologic testing and removal of positive animals. Because of the long incubation period and time to seroconversion, retesting animals once a year, or even twice a year, is recommended. In addition to the test and cull approach, consideration should be given to raising neonates in isolation from their dams, especially if the dam is seropositive. Lambs should be fed colostrum from seronegative sheep, or heat-treated sheep colostrum, and raised on milk replacer, milk from seronegative ewes, or heat-treated sheep milk

Question 71

etiology and pathology of footrot

Answer 71

Fusobacterium necrophorum

is a normal resident of manure-contaminated environments. Under favorable environmental conditions, it colonizes the moist, macerated interdigital skin and provides ideal conditions for invasion by D nodosus at the skin/hoof interface. By action of proteases, D nodosus, also a gram-negative anaerobe and obligate pathogen, liquefies the cells of the stratum granulosum and stratum spinosum, causing the separation of the hoof wall from the basal epithelium. It works its way down the interdigital horn to the heel, then to the sole, and finally to the lateral side of the hoof. D nodosus has been found to survive <3 wk outside the host, but it can remain sequestered in cavities, cracks, or deformities of the affected foot for the life of the sheep

Question 72

predisposing factors to footrot

Answer 72

Transmission occurs most rapidly when conditions are warm and moist; however, cold, moist conditions are also conducive to transmission.

Question 73

cs for foot rot

Answer 73

The most obvious sign is lameness, but the foot is seldom carried or packed. In chronically infected sheep, the hoof becomes gnarled and distorted. When more than one foot is infected, some sheep become recumbent or walk on their knees. Brisket and knees tend to become hairless and ulcerated. Affected sheep do not compete well for food, lose body condition, and produce less wool. Rams with infected hindfeet may be unwilling to breed, and ewes with hindfeet lesions may be unable to bear the weight of a ram at service

Question 74

dx for footrot

Answer 74

In flocks with virulent footrot, underrunning and separation of the hard horn of the hoof of one or more feet, complete with the characteristic odor, is diagnostic. If the problem is discovered early when interdigital dermatitis is the only sign, it should be assumed that the condition is an early stage of contagious footrot, and treatment should be initiated immediately

Question 75

tx for footrot

Answer 75

Traditionally, treatment consisted of foot bathing using antibacterial solutions after careful hoof trimming to remove all dead horn and expose infected tissue and bacteria to air. However, foot soaking for 30–60 min has been shown to be more effective even when trimming is not done

Question 76

control for footrot

Answer 76

Animals from unknown premises or auction houses should not be purchased. Any sheep to be added to the flock should be quarantined for several weeks to prevent the spread of footrot and other chronic diseases. During the quarantine period, the animal’s feet should be lightly trimmed and examined closely for pockets and other malformations that suggest a previous D nodosus infection. Vehicles (eg, trucks, trailers) or facilities in which unknown or infected sheep have been held should be thoroughly cleaned and disinfected before placing uninfected sheep in them. If it is not possible to thoroughly disinfect transport vehicles, zinc sulfate can be liberally scattered over the floor to reduce viable bacteria.

Question 77

signalment for brucellosis

Answer 77

goats,sheep and cattle, dogs etc

Question 78

transmission of brucellosis IN SHEEPS

Answer 78

Rams as young as 8 wk have been infected experimentally by various nonvenereal routes. The disease can be transmitted among rams by direct contact. Active infection in ewes is unusual but has developed after mating with naturally infected rams. Contaminated pastures do not appear to be important inspread of the disease. Infection frequently persists in rams, and a high percentage shed B ovisintermittently for several year

Question 79

CS OF BRUCELLOSIS IN SHEEP

Answer 79

Brucella melitensis infection in certain breeds of sheep causes clinical disease similar to that in goats (see Brucellosis in Goats). However, B ovis produces a disease unique to sheep, in which epididymitis and orchitis impair fertility—the principal economic effect. Occasionally, placentitis and abortion are seen, and there may be perinatal mortality

Question 80

PATHOPHYSIOLOGY OF BRUCELLOSIS

Answer 80

The infection in females follows a course very similar to %DERUWXV infection in cattle. The major route of infection appears to be through the mucous membranes of the oropharynx and upper respiratory tract or the conjunctiva. Other potential routes of infection are through the mucous membranes of the male or female genital tract. After gaining entrance to the body, the organisms encounter the cellular defences of the host, but generally succeed in arriving via the lymph channels at the nearest lymph node. The fate of invading bacteria is mainly determined by the cellular defences of the host, chiefly macrophages and T lymphocytes, though specific antibody undoubtedly plays a part. The outcome depends on the ruminant species infected, age, immune status of the host, pregnancy status, and the virulence and number of the invading %UXFHOOD. When the bacteria prevail over the body defences, a bacteraemia is generally established. This bacteraemia is detectable after 10 to 20 days and persists from 30 days to more than 2 months.

Question 81

HOW TO DX BRUCELLOSIS IN SHEEP

Answer 81

Because not all infected rams show palpable abnormalities of scrotal tissues (and not all cases of epididymitis are due to brucellosis), the remaining rams must be examined further. Rams shedding organisms, but having no lesions, must be identified by culture of semen. Repeated examinations may be necessary to identify intermittent shedders. Microscopic examination of stained semen smears may also be helpful; fluorescent antibody examination is a highly specific diagnostic aid. Serologic tests used for eradication of disease and certification of animals include indirect ELISA, complement fixation, hemagglutination inhibition, indirect agglutination, and gel diffusion.

Question 82

TX N CONTROL OF BRUCELLOSIS IN SHEEP

Answer 82

Incidence and spread of the disease may be reduced by regular examination of rams before the breeding season and culling of those with obvious genital abnormalities. Because susceptibility in rams increases markedly with age, it is advantageous to keep a young ram flock and isolate noninfected rams from older, possibly infected rams

Chlortetracycline and streptomycin used concurrently have effected bacteriologic cures. However, treatment is not economic except in especially valuable rams, and even if infection is eliminated, fertility may remain impaired.