Infectious Diseases And Abortion Case 4

Front 1

What is the predilection site of Tritrichomonas foetus?

Back 1

the prepuce and uterus, however other resources list the vagina, and vulva as well.

Front 2

What is the parasitic class and family of T. foetus?

Back 2

Class: Zoomastigophorasida (another source said sarcomastigophora)
Family: Trichomonadidae

Front 3

What is the description of T. foetus?

Back 3

Pear-shaped, single nucleus, four flagella (three free anterior, and one undulating membrane which extends to a free form in the posterior), axostyle (hyaline rod with a seletal function

Front 4

What type of movement does T. foetus exhibit?

Back 4

rolling, jerky movements

Front 5

What is the host and life cycle of T. foetus?

Back 5

Host: cow
Life cycle: reproduce by longitudinal binary fission. NO sexual stages are known and there are no cysts.

Front 6

What is the primary mode of transmission of T. foetus?

Back 6

coitus

Front 7

What is the pathogenesis of T. foetus in BULLS?

Back 7

Bull: shortly after infection a preputial discharge assoicated with small nodules on the preputial and penile membranes may develop. Organism present in small numbrers in the preputial cavity of bulls, with some concentration in the fornix and around the glans penis. Chronically infected bull shows no gross lesions. The organism does not appear to penetrate the epithelium, and there is no observable changes in semen quality attributed to the organism. Considered a chronic carrier due to the deepening of the epithelial crypts of the penis and prepuce as the bull ages (more suitable microaerophilic environment).

Front 8

What is the pathogenesis of T.foetus in COWS?

Back 8

Cow: initial lesion is a vaginitis, which can be followed in animals that become pregnant by invasion of the cervix and uterus; sequelae includes placentitis leading to early embryonic abortion, uterine discharge and pyometra. *Abortion before the fourth month of pregnancy is the most common followed by recovery. Fetal membranes may be retained leading to a purulent endometritis, a persistent uterine discharge and anoestrus; infrequently the corpus luteum is retained and the cervical seal remians closed, when a massive pyometra develops which visually stimulates the appearance of pregnancy. Some cases a normal, full-term calf is born.

Front 9

What are the clinical signs of T. foetus?

Back 9

Bull: no clinical signs once infection is established
Cow: early abortion, purulent endometritis or a closed pyometra, some cases may become permentaly sterile, usually recovers and generally becomes immune for that breeding season after infection or abortion.

Front 10

How is the diagnosis of T. foetus made?

Back 10

Tentative diagnosis is based on clinical history, early abortion, repeated returns to service, irregular oestrous cycles. Difinitive diagnosis: demonstration of organisms in placental fluid, stomach contents of aborted fetus, uterine washings, pyometra discharge or vaginal mucus..

Front 11

At what time is T. foetus in the highest concentration in the vaginal mucus?

Back 11

12-20 days post infection, the number of organisms vary according to the phase of the oestrus cycle, being highest 3-7 days after ovulation.

Front 12

What are the pathologic lesions associated with T. foetus?

Back 12

COWS:cervicitis and endometritis leading to infertility, abortion or pyometra. may be copious mucopurlent discharge or intermittent discharge due to the mild lesions of the cervix and endometrium. Abortions occur in the first half of pregnancy. No specific fetal lesions. Pyometra, when it develops may be copious with watery exudates containing floccules which may be brownish and sticky and contain swarms of trichomonads.
BULLS: no lesions noted

Front 13

What are the important epidemiologic facts associated with T. foetus?

Back 13

Bulls once infected remain so permanently. Transmission is through coitus. From the vagina the infection reaches the uterus via the cervix to produce a low-grade endometritis. Intermittently the organisms are flushed into the vagina, often within 2-3 days before oestrus. Cows tend to have a self-limiting infection and appear to develop a sterile immunity.

Front 14

What is the treatment for T. foetus?

Back 14

The disease is self-limiting in the female only symptomatic treatment and sexual rest for 3 months is normally necessary. Culling the cow is also a possibility especially the ones showing clinical signs and are open. In the bull, slaughter is the best policy, although dimetridazole orally or intravenously has been reported as effective; however it is not labeled for the use in food animals in the US.

Front 15

How is T. foetus controlled?

Back 15

Through test and slaughter of bulls, AI with non-infected bulls, and replacement stock being virgins or young (tested negative), with BSE.

Front 16

What is the prevalence of T. foetus?

Back 16

The organism has a greater prevalence in Bos taurus bulls than bulls of Bos indicus origin. Out of the Bos taurus bulls the highest prevealence was in the Brangus bulls and lowest being in Braford bulls, both of which are B taurus/B indicus cross breeds.

Front 17

How long and when does the immune reaction begin in a cow that has been exposed to T. foetus?

Back 17

The cow eliminates the infection generally within 1-4 months. The female response begins to eliminate the infection within 8-10 weeks after exposure in unvaccinated females. (For this reason cultures from females are best performed before the infection is potentially eliminated by the immune response.)

Front 18

What are the four factors involving prevention and control of T. foetus?

Back 18

Recognize the disease challenge (Dx and surveillance), know when and why a challenge occurs (pathogenesis), lower (or eradicate) the challenge (management), and raise the resistance to the specific disease challenge (immunology)

Front 19

What is a potential treatment for T. foetus?

Back 19

nitroimidazole derivatives, such as dimetridazole, ipronidazole, and metronidazole. No effective approved medication for the use in US.

Front 20

How can poor nutritional states affect fertility in dairy cattle?

Back 20

When dry matter intake is reduced, results in negative energy balance and many assoicated disorders. The negative energy balance inhibits secretion of gonadotropins (LH and FSH). Stress is also increased during this state and leads to epinephrine secretion which stimulates corticosteroid secretion, leading to reduced LH secretion.

Front 21

Is T. foetus a reportable disease and if so in what time period are you to report the disease?

Back 21

Yes! It is of a regulatory importance and must be reported within two days of discovery.

Front 22

What are the common names of Brucella abortus infection?

Back 22

Undulant Fever, Contagious Abortion, Bang's Disease

Front 23

What are the bacterial characteristics of Brucella abortus?

Back 23

Gram Negative
Coccobacillus or short rod
facultative intracellular pathogen
usually single but sometimes seen in pairs or small groups
*Chlamydophila abortus and Coxiella burnetii appear similiar
Not truely acid fast but they are resistant to decolorization by weak acids, and stain red against a blue background (H&E)

Front 24

What is the importance of B. abortus?

Back 24

It has a major public health concern! (ZOONOTIC) In humans can be a serious debilitating and sometimes chronic disease that may affect a variety of organs. B. abortus could be used in a bioterrorist attack. Wildlife hinders the eradification of the disease within the US.

Front 25

Most spp. of Brucella are primarily associated with a specific host. What is the specific hosts of Brucella abortus?

Back 25

cattle, bison, water buffalo, african buffalo, elk, and camels
However, has been reported in equine, sheep, goats, chamois, pigs, raccoons, opossums, dogs, coyotes, foxes, wolves and other spp.

Front 26

What is the prevelence/distribution of B. abortus?

Back 26

Found worldwide except Japan, Canada, some European countries, Australia, New Zealand and Israel where it has been eradicated. Eradification is nearly complete in US herds however it can still be found in wildlife hosts which is hindering the complete eradification process.

Front 27

What is the transmission of B. abortus?

Back 27

Transmitted by contact with the placenta, fetus, fetal fluids and vaginal discharges from infected animals. Also found in milk, urine, semen, feces and hygroma fluids. Shedding in milk is life long and may be intermittent. Veneral transmission seems to be most common.

Front 28

What is the human transmission?

Back 28

occupational hazord most common, drinking unpasturized milk or dairy products, contamination of mm and abraded skin.

Front 29

What is the incubation period for B. abortus?

Back 29

abortions and stillbirths usually occur two to five months after infection. Incubation is longer when animals are infected during early gestation becuase reproductive losses typically occur during the second half of gestation.

Front 30

What are the clinical signs of B. abortus?

Back 30

abortions or stillbirths during the second half of gestation, weak calves that may die soon after birth, placenta may be retained and secondary metritis can occur, lactation may be decreased, epididymitis, seminal vesiculitis, orchitis or testicular abscesses are sometimes seen in bulls, infertility occurs occasionally in both sexes, arthritis, systemic signs do not usually occur in uncomplicated infections, nonpregnant females usually asymptomatic.

Front 31

What are the post-partum lesions of B. abortus?

Back 31

granulamatous inflammatory lesions in repro tract, udder, supramammary lymph nodes, other lymphoid tissues, and sometimes joints and synovial membranes.
mild to severe endometritis, placenta usually thickened and edematous, and may have exudate on its surface, intercotyledonary region is typically leathery, with a wet appearance and focal thickening. Autolyzed or have variable amts of subcutaneous edema and bloodstained fluid in the body cavities. Bulls: one or both sacs of the scrotum may be swollen due to orchitis, epididymitis or abscesses. Tunica vaginalis may be thickened and fibrous and adhesions may be present.

Front 32

What is the morbidity and mortality of B. abortus?

Back 32

abrotion rate varies from 30-80%. in heds wehre this organism is endemic only sporadic symptoms occur and cows may abort their first pregnancies.

Front 33

How is B. abortus diagnosed? (clinically and lab)

Back 33

Clinically the organism should be suspected in any case of abortion! Laboratory tests to confirm a diagnosis would include: microscopic examination with modified Ziehl-Neelsen method, serology (presumptive diagnosis) ie. ELISA, agglutination tests; Brucella milk ring test (BRT) (screening test), brucellin allergic skin test
Definitive Dx: demonstration of the organism cultured from the animal, PCR

Front 34

What are the differential diagnosis of B. abortus?

Back 34

Trichomoniasis, Campylobacteriosis (formerly called vibriosis),leptospirosis, listeriosis, infectious bovine rhinotracheitis, and various mycoses

Front 35

How is B. abortus controlled?

Back 35

test-and-slaughter programs, quarantine of suspected or positive animals, vaccination, disinfectants readily kill the organism

Front 36

Is B. abortus a reportable disease and if so in what time period must it be reported?

Back 36

Yes! It is considered of regulatory importance and therefore requires reporting within two days of discovery.

Front 37

What is the predilected tissues for B. abortus?

Back 37

udder, uterus, lymph nodes, testicles, and accessory sex glands, epididymis

Front 38

What is the incubation period for B abortus?

Back 38

it is variable and ranges from 3 weeks to 90 days or more

Front 39

What is the classifying system for B. abortus when referring to states?

Back 39

States are classified as free, class A, class B, or class C.

Front 40

What is the relevance of the classification and cattle trafficing in regards to B. abortus?

Back 40

interstate trafficking from free states without testing is allowed however, cattle moving from non-free states must be tested before crossing state lines.

Front 41

What is the pathogenesis of B. abortus?

Back 41

initial replication whithin the regional lymph nodes, invades the uterus during second trimester due to hematogenous spread, bacteria first appear in phagosomes of erythrophagocytic trophoblasts within the placenta, replication occurs in the rER of chroionic trophoblasts, preferential replication in chorioallantoic trophoblasts has been attributed to their erythritol content, placental inflammation spreads throughout the allantochorion to involve additional cotyeldons with resultant chorioallantoic ulceration, necrosis of trophoblasts and ulcerative endometritis. Fetal death results from placental disruption and endotoxemia.

Front 42

What is neosporosis caused by?

Back 42

It is caused by the protozoan parasite, Neospora caninum.

Front 43

What is the life cycle of Neospora caninum?

Back 43

The coccidian parasite has three different stages (oocyst, tachyzoite, and the tissue cyst containing numerous bradyzoites). Sporulate in teh environment in 24 hours; sporulated oocysts contain 2 sporocysts containing each 4 sporozoites.The tachyzoite is the pathogenic stage; it multiplies by endodygeny in many cell types (neural cells, hepatocytes, macrophages, fibroblasts, endothelial cells, myocytes...).

Front 44

What is the intermediate and final host of Neospora caninum?

Back 44

The dog!

Front 45

What are some of the animal spp Neospora caninum has been found?

Back 45

Major abortificant in cattle. observed as well in horses, sheep, goat, black tail deer, rhinoceros, water buffaloes, coyotes, red foxes, and camels. These are considered the intermediate host.

Front 46

How is Neospora caninum transmitted?

Back 46

The parasite can be transmitted horizontally (ie. through the ingestion of oocysts shed in the environment by the final host) or vertically from an infected cow to her offspring. Vertical route is the major route of transmission in cattle and is extremely efficient as the rate of transmission is very unlikely to occur. Lactogenic transmission was achieved experimentally but there is no evidence that it occurs under natural conditions.

Front 47

What is the clinical signs associated with Neospora caninum in cattle?

Back 47

abortificant agent and the abortion is the only clinical sign and can occur from the thrid month of pregnancy and onwards. Most of the abortions take place during the 5th and 6th week of gestation. The fetus is either resorbed, autolysed, mummified, stillborn, born alive with clincial signs, or born normal but chronically infected. (calves: neurologic signs, underwieght, or unable to rise, flexion or hyperextension of forelegs, hindlegs or both, ataxia, decreased patellar reflexes, loss of conscious proprioception, exophthalmia or asymmetrical appearance of the eyes)

Front 48

What is the peak prevelence of Neospora caninum in California?

Back 48

The peak is observed in automn and winter.

Front 49

When is the peak antibody titer in an infected fetus with Neospora caninum?

Back 49

around 6-7 months of gestation; titers decline til two months post-calving

Front 50

How is Neospora caninum diagnosed in cattle?

Back 50

maternal and fetal sera ideally combined with the examination of fetal tissues. tissues that should be sampled include brain, heart, liver and placenta. ELISA, indirect immunofluorescence techniques, agglutination test. PCR is also possible.

Front 51

What are the predilected tissues for Neospora caninum?

Back 51

Brain, Heart, Liver, Placenta, and Muscle

Front 52

What are some potential parasitic differentials for Neospora caninum?

Back 52

Toxoplasma gondii (not considered an abortificant in cattle), and Sarcocystis spp. (rare in cattle)

Front 53

How is neospora caninum controlled in cattle?

Back 53

very few control measures are available; advisable not to breed seropositive heifers born to seropositive mothers; seropositive animals should be culled; embryo transfer from seropositive valuable cows to seronegative cows is an option under some circumstances; vaccination (unable to prevent vertical transmission)

Front 54

What is the agent that causes Leptospirosis?

Back 54

caused by various spp of Leptospira, a spirochete in the family Leptospiraceae, order Spirochaetales.

Front 55

What is the predominant serovars in the US for Lepto?

Back 55

L. canicola, L. grippotyphosa, L. hardjo, L. icterohaemorrhagiae and L. pomona.

Front 56

What is the transmission of Lepto?

Back 56

directly between hosts or indirectly in the environment: ingested in contaminated food or water, spread in aerosolized urine or water, direct contact with the skin, aborted or stillborn fetus, vaginal fluids and discharge, male repro organs, etc.

Front 57

What animal spp tend to be susceptible to Lepto infection?

Back 57

ALL mammals (ZOONOTIC)! disease is rare in cats, and less common in sheep than cattle.

Front 58

What serovars of Lepto infect cattle?

Back 58

hardjo, pomona, grippotyphosa, canicola and icterohaemorrhagiae

Front 59

What is the primary resevoir hosts for most Lepto serovars?

Back 59

Wild animals, particularly rodents ( in resevoir hosts tends to be asymptomatic, mild or chronic)

Front 60

What is the incubation period of lepto?

Back 60

4-12 days in dogs, abortions usually occur 3-10 weeks after infection in cattle, and 15-30 days after infection in pigs

Front 61

What are the general clinical signs of Lepto infection?

Back 61

asymptomatic, mild, or severe, and acute or chronic.
related to kidney disease, liver disease, or reproductive dysfunction.

Front 62

What are the clinical signs of Lepto infection in cattle?

Back 62

acute: mainly in calves and include fever, anorexia, conjunctivitis, and diarrhea
jaundice, hemoglobinuria, anemia, pneumonia, or signs of meningitis (incoordination, salivation and muscle rigidity)
adult cattle: fever and depression are often transient and milder; abortions (late term) and decreased infertility, decreased milk yield, retained placentas, milk may be thick blood tinged or yellow, mammary inflammation

Front 63

What diagnostic tests are done to confirm Lepto infection?

Back 63

culture, detection of antigens or nucleic acids, or serology
found in milk, blood, csf, thoracic or peritoneal fluids, urine, liver, brain, and kidney.
Culture may take upto 13-26 weeks! IFA, PCR, DNA probes
*most commonly used serologic tests are the microscopic agglutination test (MAT) and ELISAs

Front 64

What is the indicated treatment for Lepto infections?

Back 64

tetracyclines, penicillin/ampicillin, dihydrostreptomycin, streptomycin and the fluoroquinolones

Front 65

What are the preventative methods of Lepto?

Back 65

vaccinations are available for pigs, cattle and dogs.
prevent disease but do not completely prevent infection or the shedding of the organisms. Immunity is largly serovar specific.
prevention of contact with wildlife, particularly rodents
good biosecurity (quarantine new cattle, etc.)

Front 66

What are the post-mortem lesions in cattle with Lepto infections?

Back 66

in acute cases: anemia, icterus, hemoglobinuria, submucosal and subserosal hemorrhages, kidneys swollen and contain petechiae and ecchymoses, become pale over time. liver sometimes swollen, minute foci of necrosis. ulcers and hemorrhages on mucosa of the abomasum. petechiae can also be seen in other organs in some fulminating infecgtions. Pulmonary edema and emphysema are rare but have been reported.

Front 67

what is the major pathogenesis of Lepto infection?

Back 67

it hangs out in the kidneys and causes destruction of RBC's

Front 68

What is the agent that causes Campylobacteriosis (vibriosis)?

Back 68

veneral disease of cattle caused by Campylobacter fetus subspecies fetus.

Front 69

How is Campylobacteriosis characterized?

Back 69

infertility with an increased number of services necessary for conception; early embryonic death most common and late abortions from 4 months gestation to term are occasionally observed

Front 70

What are the clinical signs of Campylobacteriosis?

Back 70

early embryonic death, late term abortions, endometritis, vague or intermittent infertility, proglonged period prior to conception

Front 71

How is Campylobacteriosis transmitted?

Back 71

Under natural breeding conditions bulls transmit it from one female to another. female-to-female transmission highly unlikely, however bull-to-bull possible when penned together and riding behavior occurs. Organism hangs out in the prepuce but does not effect sperm qualitiy or breeding ability. (Bulls are carriers for upto 18 weeks)

Front 72

What is the only practical method of confirming Campylobacteriosis infection?

Back 72

Blood tests are not reliable, and therefore bacteriological exmaination of aborted fetuses appears to be the only practical method of diagnosis. (cultures taken from the vaginal or cervical mucus and samples taken from the sheath of the penis are also used)

Front 73

What is a method of controlling Campylobacteriosis?

Back 73

AI using antibiotic treated sperm. Another way is to maintain clean, unexposed herd by use of virgin bulls.
Vaccine available.

Front 74

What is the major fetal lesion experienced with Campylobacteriosis lesions?

Back 74

placentitis, fibrinous serostitis, bronchopneumonia

Front 75

What type of virus is responsible for infectious bovine rhinotracheitis (IBR)?

Back 75

It is a bovine herpes virus; the disease is also called "red nose" and works in association with PI3 (parainfluenza Type 3 virus)

Front 76

What are the clinical signs of IBR?

Back 76

pregnant cows the virus invades the placenta and fetus via the dam's blood stream, often causing abortion, temperature increases, loss of appetite and depression, accelerated respiration, accompanied by deep, moist coughing, excessive clear nasal discharge and inflamed muzzle ('red nose') Infected animals are carriers and shed the virus for life.

Front 77

How is IBR transmitted?

Back 77

when the animal is breathing or coughing sprays contaminated droplets into the air, feed, or water.

Front 78

What is the pathogenesis of BVDv?

Back 78

suppresses an animal's immune system by reducing the number of WBC's in teh spllen and lymph nodes and allowing other viral and bacterial diseases to establish themselves and spread.

Front 79

What are the clinical signs of BVDv?

Back 79

fever, profuse diarrhea, ulcers in the mouth, loss of appetite, coughing, profuse salivation, nasal discharge, erosions beneath the muzzle's roughened, dry, crust, inflammation of the eyes, and humped-up appearance and painful walking if feet become infected. Reproductive failure and immunosuppression (abortions depend on time of infection: abortion, fetal mummification, birht defects, congenital malformations usually of CNS, and eyes)

Front 80

What is the major fetal lesions of IBR (bovid herpes virus I)?

Back 80

multifocal necrosis with intranuclear inclusions (liver, lung, spleen, kidney)
usually causes abortion in 5-9 months of gestation

Front 81

How is Herpesvirus I (IBR) confirmed?

Back 81

histopathology, virus isolation, FA test of frozen kidney

Front 82

BVDV causes what stage of abortion and what are the major fetal lesions?

Back 82

Any stage of gestation!
anomalies of skeletal, nervous, cardiovascular, respiratory or other systems.

Front 83

What kind of virus is BVDv?

Back 83

It is a pestivirus! Very similar to Broaders virus in sheep and goats).

Front 84

How is BVDv diagnosed?

Back 84

Pathology, FA test on fetal tissues, fetal serology (virus neutralization, ELISAs), serologic survey in herd

Front 85

What are the reproductive effects of bovine herpesvirus I (IBR)?

Back 85

infectious pustular vulvovaginitis (IPV), embryonic death, abortion, stillbirth, and birht of weak calves

Front 86

What is the history and clinical signs of Bovine Herpes virus I (IBR)?

Back 86

abortion after 4 months gestation
history of infertility within the herd
rare instances infected fetuses are carried to term but are stillborn or die in the first week of life

Front 87

How do you diagnose IBR?

Back 87

autolysis usually abscures any lesions on the fetus, placenta grossly normal, presence of microscopic foci of necrosis with eosinophilic intranuclear inclusions and lack of inflammation in fetal tissues (liver, lung, thymus, or adrenal glands), viral isolation of placenta or fetal lung, fluroescent antibody test (FA), maternal titer (seldom of diagnostic value)

Front 88

What is the pathophysiology of IBR?

Back 88

intrauterine inoculation of Herpesvirus around the time of breeding induces necrotizing endometritis and oophoritis; death of fetus at this stage results from necrotic CL because the zona pellucida protects the embryo from viral infection until hatching occurs at 8-9 days of gestation; cytocidal infection of trophoblast can also induce early embryonic death, later half of gestation fetal death occurs from necrosis in multiple organs and aboriton usually occurs 2 weeks to 4 months after infection

Front 89

How is IBR controlled or prevented?

Back 89

umbiquitious; abortion rates vary from 5-60% but usually <25% in beef herds and more sporadic in dairy; no lashing effection fertility; controlled via vaccination

Front 90

What type of virus causes bluetounge abortion?

Back 90

orbivirus that results in early embryonic death, abortion, and fetal anomalies
Reoviridae family and is double stranded RNA virus

Front 91

What is the etiology of bluetounge abortion?

Back 91

arthropodborne viral disease; clilnical disease usually restricted to sheep, other ruminants may show disease.

Front 92

What are the clinical signs of bluetounge virus?

Back 92

reproductive syndromes and bluetounge per se, a vasculitic disease of several organ systems (cattle and goats rarely show signs); transient fever, edema of face, lips muzzle and ears, excessive salivation, hyperemia of the oral mucosa, profuse serous discharge that becomes mucopurulent after a few days, leaving crusts around the nostrils and muzzle, tounge may become cyanotic but infrequent finding, oral lesions, pulmonary edema, lamenss, stiffness, cardiomyopathy
reproductive signs: abortions, stillbirths, weak, live "dummy lamb" births, early embryonic wastage and decreased reproductive efficiency may be more important in cattle

Front 93

what is the incubation peroid for bluetounge virus?

Back 93

3-8 days

Front 94

What would the differential diagnoses be with bluetounge virus?

Back 94

BVDv, Malignant Catarrhal Fever, Vesicular Disease, Rinderpest, photosensitization, bovine papular stomatitis, and infectious bovine rhinotracheitis, difficult to distinguish from foot-and-mouth disease and vesicular stomatitis

Front 95

What is the pathophysiology of Bluetounge virus?

Back 95

capable of reproducing in a variety of mammalian cells; vasculitis caused by infection of vascular endothelial cells, results in edema and necrosis of epithelial surfaces, in bulls the virus can cause inflammation and degenerationof the seminiferous tubules
teratogenic effects appear to be caused by general disruptions of organogeneisis by viral infection of the developing fetus; development may require previous sensitization operating through IgE mediated hypersensitivity reactions

Front 96

What type of virus is caused by BVDv?

Back 96

pestivirus which causes early embryonic death, fetal anomalies or abortion

Front 97

what are the clinical signs associated with BVDv?

Back 97

abortion can occur at any stage of gestation
history of repeated breeding and a recent episode of febrile disease prior to onset of abortion

Front 98

How is BVDv diagnosed?

Back 98

Via clinical findings: mummified, autolyzed, or fresh and have a variety of dysplastic lesions, including cerebellar hypoplasia, cerebral malformations and cataracts, brachygnathia, arthrogrposis, alopecia, thymid hypoplasia, and intrauterine growth restriction; virus isolation from fetal tissue is seldom successful (viral antigen may be detected by FA test on kidney, lung, or lymph node
ELISA

Front 99

what is the pathophysiology of BVDv?

Back 99

shed in most body secretions; in seronegative cows exposure at the time of breeding prevents conception, placental attachment at approx. 35 days gestation seemingly must precede fetal infection, during the first four months of gestation infection usually causes fetal death and abortion; fetuses infected with noncytopathic strains between 42 and 125 days gestation are likely to be persistently infected are typically seronegative at birth and subsequently shed BVDv continuously, development of mucosal disease comes later in life from superinfection with cytopathic BVDv; fetuses infected b/n 75-150 days gestation are at risk for the development of dysplastic lesions; fetuses affected after 100 days gestation usually mount an immune response, clear the infection and survive but may develop teratologic effects in the brain, skin or bronchioles, fetuses infected aftero 150 days usually recover w/o dysplastic lesions

Front 100

What is the etiologic agent of epizootic bovine abortion (foothill abortion)and where is the disease found (location)?

Back 100

syndrome of late abortions in cattle in the foothills bordering the central valley of CA; once thought to be caused by Chlamydia psittaci but has never been cultured, now it is thought that it is caused by an unknown spirochete passed by a tick vector

Front 101

What are the clinical signs associated with epizootic bovine aboriton (EBA)?

Back 101

late abortions or delivery of weak calves; 5-6 months gestation is typical abortion time; older native cows shows no clinical signs

Front 102

How is EBA diagnosed?

Back 102

Mainly diagnosed via pathology of the fetus: three month period needed for full development of pathologic changes in the fetus; superficial cervical lymph nodes are enlarged, the spleen is enlarged the thymus is slightly smaller than normal, and the liver may be enlarged and nodular, histologically: loss of thymic cortical lymphocytes; remaining lymphoctyes are enlarged and poorly diff.; folicular hyperplasia, histocytosis, vasculitis, necrosis, and pyogranulomas occur in lymph nodes and spleen,

Front 103

What is the pathophysiology of EBA?

Back 103

infection is transmitted by the soft grounding tick (Ornithodorus coriaceus); disease can be transmitted also by fresh or frozen fetal tissue; transformation and proliferation of fetal lymphocytes and macrophages occur by 50 dyas but are not severe enough for diagnosis until 100 days post exposure to the tick vector, IgG and IgM are depositied in vascular lesions, but increased in fetal serum immunoglobulin is not detectable until at least 80days post exposure; repeated superinfection maybe required for fetal death because it takes 90 days for fetal lesion to develop; infection after 6 months unlikely to cause abortion

Front 104

What is Dourine?

Back 104

causes valvular discharge, or urtheral discharge, intermittent pyrexia, wt. loss, progresses to plagues on the skin and depigmentation, may also have neurological manifestations.
etiology: Trympanosoma equiperidium