Theriogenology
Exam 3
2/28/12
Viral causes of abortion:
I. Equine Rhinopneumonitis
a. Caused by Equine Herpesvirus 1(EHV-1)
b. Number one viral disease that causes abortions in the mare
c. Foal’s maternal immunity decreases at 5-6 months
i. “Has the snots”
ii. Mare is already 4-5 months pregnant again
iii. Mare aborts around 8th month of gestation
1. New fetus is aborted “fresh” (looks normal)
2. No premonitory signs from mare
d. Pathognomonic signs in aborted foal ***
i. Multifocal pinpoint white to grey necrotic foci in liver
ii. Severe pulmonary edema
iii. Hydrothorax
iv. Hydroperitoneum
e. Other signs you may see in aborted foal
i. Sometimes see thymic involution – stress oriented
ii. Eccymotic hemorrhages
iii. Icteric conditions
f. Diagnosis
i. Microscopic
1. Intranuclear inclusions in the pulmonary tissues
ii. FA testing
iii. Virus isolation
g. Prevention
i. Vaccination – not 100% affective, but best preventative
1. Need multiple vaccinations
2. Start at 5 months of pregnancy in endemic areas
3. Boostered at 7 months of pregnancy and then again at
9 months
4. Can be started as early as 60 days of gestation
5. They have killed and MLV (safe when pregnant now)
ii. Strategize pregnant mares on farm to be separated from other
horses, particularly those in late stage of pregnancy (more than
6 months)
iii. Alleviate stress
h. Other herpes infections
i. EHV-3 = coital exanthema
ii. EHV-4 = respiratory conditions
iii. EHV-1 = respiratory and reproductive conditions (abortions)
II. Equine Viral Arteritis
a. READ ARTICLE!
b. RNA virus
c. Togaviridae
d. Seen in all equids
e. In the past it has been a relatively quiet virus and they didn’t see a lot
of activity
f. Recently they had outbreak in Mexico in 2006
g. Transmitted
i. Respiratory system
1. Racetracks and sale barns
ii. Venereal spread - MC
h. Clinical signs
i. Ocular and nasal discharge
ii. Supraorbital edema, ventral edema, hindlimb edema
iii. Stallions get edema in scrotum and prepuce
iv. Photophobia
i. Similar diseases based on clinical signs (rule outs)
i. Equine influenza
ii. Rhinopneumonitis
iii. Purpera hemorrhagica
j. Pathogenesis
i. Pathogen enters respiratory and goes to lungs and replicates in
macrophages
ii. Affinity for arterioles so it produces a lot of edema
1. Metritis and edema in uterus of mare
2. Placental detachment
3. Rise in PGF2a
4. Aborted fetus can be fresh or autolytic
iii. Vascular damage of lymph nodes
k. Lesions
i. Histologic
1. Vessels in placenta and fetus have panvasculitis
l. Diagnosis
i. ELISA
ii. Serum neutrilization
iii. Immunofluorescence
iv. Viral isolation of blood’s buffy coat
1. Do not use hepranized samples because it will affect
virus
m. Control measures
i. Management and isolation
ii. Vaccination called Rabac
1. Stallions, non-pregnant mares, geldings, fillies, and foals
2. Once a year, 1 month before breeding season starts
3. Booster every year
n.
o.
p.
3/26/12
q.
iii. Test all stallions to make sure they are not carrying
antibodies
1. 1:4 or higher is positive
Stallions
i. Carriers that harbor organism for 6 month-1 year +
ii. Hides in ampulla and bulbourethral glands
iii. Test them before vaccinating for the first time
Mares bred to carrier stallions
i. Virus survives freezing and cool shipped semen
ii. Make sure mare is serologically negative and vaccinated
1. Isolated for 3 weeks
iii. Do not vaccinate pregnant mares in last 2 months of pregnancy
iv. Positive mares CAN be bred to positive stallions
1. She can have healthy baby because mare has
immunity
v. Negative mares will abort and have problems because she
hasn’t been exposed to virus before and has no immunity
Young horses
i. Do not vaccinate horses <6 weeks of age
1. Vaccinated earlier If you have an epidemic
REPORTABLE!!
Venereal diseases of bovine
I. Two important diseases you can diagnose sitting in your truck:
a. Trichomonas
i. Tritrichomonas fetus
ii. Undulating membrane, 3 flagella on front of it and 1 on back
iii. Protozoan
1. One cell organism
iv. Seen under darkfield microscopy
v. Abort in first half of gestation
b. Vibriosis/Campylobacter
i. Campylobacter fetus venerealis
ii. Gram negative microaerophilic (needs some CO2 to grow) rod
iii. Abort in 4-7 month of gestation
c. History and clinical signs for both:
i. MC - Cows returning to estrus
ii. Post-coital/post-breeding pyometra
iii. Some infertility or varying ages of gestation in pregnancy
checks
1. Infertility associated with endometritis
iv. Varying age of calves
v. Fluid in both uterine horns without a membrane slip
vi. Cows can get convalescent immunity
d.
e.
f.
g.
h.
1. Breed a few times and eventually she catches and
pregnancy lasts (she is exposed each time she is bred
and is beuilding immunity each time)
2. Makes enough immunoglobulin to the organism and
pregnancy will last
a. Can produce IgA and IgM
3. Next year when she is bred to a different bull she will
start the sequence over again
vii. Mucopurulent vulvar discharge in cows
1. Couple weeks after bred to infected bull
viii. Cows get vaginits, cervicitis, endometritis, and placentitis
ix. No clinical signs in bulls
1. Bulls < 4 years old serve as transient carriers/chronic
carriers
a. Both organisms inhabit epithelial crypts of penis
and prepuce and these bulls (<4) have deeper
epithelial crypts and organisms get down in
there and hang out forever
Both organisms transmitted venereally, can be spread during artificial
insemination
Both can survive freezing (frozen semen)
Both produce economic losses
Differentials for both: Brucellosis, Infectious Pustular vulvovaginitis
(IPV), Mycoplasma, Ureoplasma, BVD
i. All can spread venereally in cow herd but Vibrio and Trich
should be at top of list
Diagnostics for both:
i. No gross fetal lesions in fetuses that are aborted
ii. Primary infections are cleared by about 90 days, if they come
back and are bred by infected bull again they may calve or the
degree of infection will be shorter
iii. Isolation and identification of organisms:
1. Vaginal and cervical mucus samples from cow
2. Test bulls during BSE in endemic areas (prepuce
sample)
a. Test after a few weeks of sexual rest
3. Look at samples under darkfield microscopy, or use
culture media
a. Vibriosis- Clark’s media (transport media),
pyroglycolate with antibiotics, brain heart
infusion agar (culture media)
i. Needs CO2 to grow (microaerophilic)
ii. Could take 5-7 days to grow
b. Trichomonas – Diamond’s media (culture
media), Kupferberg’s media (transport or culture
media), LRS with 5% fetal calf serum (transport
media), In Pouch TF (transport media)
i. Incubate at 35 C – 37 C
c. Look under darkfield as early as 24 hours for
undulating membrane and flagella (trich)
i. Prevalence of both:
i. Fl Al, out west
j. Prevention and control for both:
i. Management
1. Don’t bring in untested sexually active bulls
2. Avoid renting and leasing bulls from unscrupulous
sources
3. Replace bulls with virgin bulls
4. Female replacements should be virgin heifers or cows
already in late stages of gestation
5. Immunization
a. Vaccinate cows 1 month – 6 weeks prior to
breeding season
II. Leptospirosis
a. Spirochete
b. Different serovars
i. Cattle get L. hardjo
c. Two types in cattle:
i. Host adapted:
1. Pathogenicity is usually low
2. Infections manifest as chronic conditions
3. Stillbirths and infertility
4. May see subclinical cases or severe cases
5. L. hardjo is the host adapted species of lepto
a. 2 genotypes:
i. L. hardjo bovis
ii. L. hardjo projetino
ii. Non-host adapted:
1. Acute infections
2. Infertility and abortions
3. Organism found in other animals
4. Characterized by exposure to other animals (feral hogs)
a. Feral hogs transmit L. pomona that can infect
cattle
d. Penetrates mucous membranes, of eye, intestinal mucosa, genital
tract, and nasal cavity
e. Survives for long periods of time outside of mammalian host,
particularly in warm moist conditions with neutral to basic pH
f. Localizes in proximal renal tubules in kidney so large amounts of
organism are excreted into the urine
g. Organism has been found in the bull
h.
i.
j.
k.
l.
m.
n.
o.
i. L. hardjo found in testes and accessory sex glands
Abortions are primarily associated with L. hardjo and L. pomona
i. From 12 weeks after exposure or longer
ii. Non-host adapted abortions in last trimester (L. pomona)
iii. Host adapted abortions: any stage of gestation (L. hardjo)
Transmission
i. Direct contact of infected urine (organism survives in kidneys
of host)
ii. Post-abortion discharges of cows
iii. Infected fetus
iv. Sexual contact
Incubation period
i. 4-10 days
Clinical signs
i. Hepato-renal disease
ii. Abortions
1. In host adapted species
iii. Photosensitization
iv. Hemolytic anemia
Pathology
i. Interstitial nephritis
ii. Autolytic changes in fetus
Diagnosis
i. Take acute and convalescent serum samples of cow
1. Take one sample today and one in 3 weeks and compare
the two titers
2. These method is of no diagnostic significance with this
disease, titers will not change
3. Titer usually spikes before abortion occurs and then
comes back down
ii. Hard to culture these organism
1. Culture from: kidney, urine, thoracic fluid, aqueous
humor of aborted fetus
2. Organisms don’t survive vary long in urine
iii. Immunofluorescence of kidney of aborted fetus
iv. Most common serologic test is microagglutination test
v. Vaccination titers usually decline
1. < 1-100
vi. Best bet is to isolate organism from aborted fetus
Treatment and control
i. Prevent exposure to active non-host adapted animals
ii. Immunization
1. Don’t prevent infection in all individuals
2. Want to develop a degree of herd immunity
iii. Keep wild hogs away
ZOONOTIC
i. Produces chronic flu-like symptoms, meningitis, and hepatorenal disease
ii. Can kill you
III. Listeria
a. Listeria moncytogenes
b. Ruminants:
i. Encephalitis
ii. Abortion
iii. Neonatal septicemia
c. Predilection for fetal placental unit
d. Produces abortions in last trimester
e. Produces either sporatic or epizootic abortions
i. Abortion every now and then (sporatic)
ii. Every animal on farm aborting (epizootic)
f. Associated with Winter
g. Associated with silage feeding (improperly cured)
h. Gram negative coccobacillus
i. Transmission:
i. Aborted fetuses
ii. Placenta
iii. Uterine discharges
iv. Food and water sources contaminated
v. Improperly cured silage (pH > 5.4)
j. Pathogenesis
i. Cow eats and consumes organism
ii. Has affinity for Peyer’s Patches of small intestines
iii. Spreads hematogenously to conceptus in placenta
iv. Results in placentitis and fetal septicemia
k. Pathology
i. Cows maintain fetus in uterus for several days so fetus
autolyzes
ii. Fetus is autolyzed, may be able to see small pinpoint foci of
gray-white hepatic necrosis
iii. Last trimester abortion disease
iv. Retained fetal membranes in cows
v. Cows sick, fever, depression, weight loss,
vi. Habitual abortion in some cows
1. Occurs each year in same animal
l. ZOONOTIC
i. Abortions in females
m. Culture
i. Parenchymous organs
ii. Gram stain fetal tissue or fluids
iii. Impression smears
n. Prevention and control
i. Make sure silage is not old or contaminated
ii. Separate cows that are aborting and the fetuses from the rest
of the herd
iii. Feed therapeutic doses of tetracycline to feed or water
1. Cant do in dairy cattle because of milk residues
IV. Infectious Bovine Rhinotracheitis (IBR)
a. Herpesvirus – 1
i. Carrier animals
b. Clinical signs
i. Respiratory infections
ii. Keratoconjunctivitis
iii. Rhinotracheitis
iv. Significant fetal pathogen
c. Also produces Infectious Pustular Vulvovaginitis (IPV)
i. Pustules in vulva
ii. Causes abdominal posthitis in bulls
1. Inflammation of penis and prepuce
iii. Enteritis and systemic disease that is fatal in calves
d. Infertility associated with this virus in the cow
i. Produces inflammation and necrosis in ovary, inflammation of
uterus
1. Destruction of corpus luteum in pregnancy
ii. Not a long lasting infertility
e. Transmission
i. Direct contact with upper respiratory or genital tract
secretions
ii. Venereal transmission in the bull
iii. People can spread during AI from cow to cow
f. Abortions
i. Virgin or naïve herds may have significant abortion levels,
endemic, 40-60% may abort (epizootic)
ii. Usually occur in second half of gestation
iii. Bovine abortion is autolytic with herpes, equine abortion
is fresh with herpes
iv. Rarely see abortions following conjunctivitis or IPV
g. Diagnosis
i. No significant rise in titers once you notice disease, so they are
not helpful, titers will peak before abortions occur
h. Prevention and control
i. Vaccinations
1. MLV
a. Do not use in pregnant cows – will induce
abortions
2. Killed
a. Use 2 injections 3-5 weeks apart
V. Bovine Viral Diarrhea (BVD)
a. RNA virus
b.
c.
d.
e.
f.
g.
i. Mutate readily
Clinical signs
i. Abortions
ii. Viral diarrhea
1. Turns into mucosal disease
Acute BVD
i. Affects cattle between 6 months – 2 years
ii. Morbidity is high
iii. Clinical signs
1. Lethargy, fever, anorexia, depression, FAD, diarrhea,
ulcerative lesions in oral cavity and intestine, decreased
milk production, oral erosions, blunting of oral papilla,
iv. Viremia lasts 2 weeks
1. Sheds to more susceptible animals
v. Most animals recover and may sero-convert and develop high
titers to the virus
There are two antigenically different types of this virus:
i. Name from response to cell culture in the lab:
1. Non-cytopathogenic type:
a. No damage to the cell culture
b. Responsible for producing calves that are
persistently infected (PIs)
2. Cytopathogenic type
a. Produces changes in cell culture
b. Acute mucosal disease form
Persistently infected calves (PIs)
i. Cow pregnant and exposed to non-cytopathogenic virus,
virus went into fetus, fetus produced no immune response
and the calf is born persistently infected
1. Pull blood sample on calf: he will have no titer and looks
normal because he did not have immune response
ii. Calves look normal at first, may become sick at 3-4 months of
age or stay normal
iii. Immunotolerant – virus does not affect calf
iv. Diagnosing a PI:
1. Immunohistochemistry
a. Take a piece of tissue (ear notching), drop it
in formalin and send to lab for this test, they
will do histological staining and diagnose it
v. Cull PI from herd when it is identified
Acute mucosal disease form
i. Animal has diarrhea, lesions around feet (coronitis)
ii. Already a PI calf and then he gets infected with
cytopathogenic form
BVD (both types) produces congenital anomalies:
i. Cerebellar hypoplasia
ii. Hydrocephalus
iii. Cataracts
iv. Retinal problems
v. Microphthalmia (small eyes)
vi. Hypotrichosis
h. Infections that take place at different stages of gestation:
i. Cow infected prior to 125 days: (early gestation)
1. Get PI calves
a. Survive to term, look normal
ii. Cow infected between 125-175 days: (mid-gestation)
1. Abortions
2. If infected with cytopathogenic type: calves will have
congenital defects
3. Will get an immune response
a. Pull blood samples from calf to test for
antibodies
4. Cull animals with high BVD titers
iii. Cow infected after 175 days: (late gestation)
1. Does not cause significant fetal disease
2. Calves have pre-colostral antibodies to BVD indicating
exposure
i. Diagnostics
i. PCR, ELISA, fluorescent antibody testing,
immunohistochemistry
VI. Ureoplasm and Microplasma
a. Ureoplasma diversum
b. Microplasma bovogenitalium
c. These organisms do not have cell wall and they are hard to culture
d. Not seen a lot in the South but is significant in the North and diary
country
e. Clinical signs
i. Granular vulvitis MC
1. Ureoplasm causes this more commonly mycoplasma
can also
2. Mucopurulent discharge
ii. May show no signs
iii. Infertility – seen with inflammation of oviduct (salpingitis),
endometritis, or cervicitis
iv. Early abortions
f. Both organisms found in vulva or vaginal tract, distal urethra,
prepuce, semen samples
g. Transmission
i. Natural breeding or by artificial insemination
h. Diagnosis
i. Aborted fetus, cotyledons, and caruncles can be frozen
immediately and sent to lab the day that you collect it
ii. Special media: diacron or polyester tipped swabs must be used
for vulvar secretions, transport medias are (Hayflicks for
Ureaplasm) (SP4 for Mycoplasma)
VII. Epizootic bovine abortion
a. AKA Foothill Abortion
b. Classic presentation:
i. Confined to northern California foothills and far western
states, mountains of Nevada and Oregon
ii. History:
1. Only heifers or adult cows brought into the endemic
area are affected and they abort 1 time
2. Cows are bitten by tick and shows signs of this disease
iii. Thought to be transmitted by ticks
iv. Abort late in gestation
1. Abort fresh calves
v. Some calves born alive and unthrifty and die shortly after birth
1. One of the few conditions where you produce calves
with extremely high immunoglobulin levels to organism
a. IgG and IgM levels of calves who have had
colostrum
i. Due to the reason that they are
chronically infected
ii. Hyperplasia of reticuloendothelial system
vi. Hereford calves can get bright red nose, conjunctiva and
tongue have petechiations, ascites, enlarged nodular liver,
spleens enlarged, lymph nodes enlarged
c. Prevention
i. Management
1. Bring heifers in area early so they can be exposed and
bitten by tick and develop immunity, then breed them
after
2. Bring cows in the area that are at least 6-7 months
pregnant, they usually don’t abort
VIII. Mycotic abortion
a. Northern problem in winter or early spring
b. Confined cows in barns eating hay or silage
c. Most occur because cow is exposed by digestive or respiratory tract
d. Causes:
i. Aspergillus fumigatus MC
ii. Zygomyces
1. Absinea
e. Sporatic causes of abortions (10% of all abortions you will see)
f. Late term abortion between 6-8 months of gestation
g. Fetus expelled soon after it dies (common with Aspergillus)
h. Zygomyces
i. Hemorrhage and necrosis of caruncle
i.
Diagnosis
i. Distinct placentitis
1. Cupped cotyledons – edges are thickened
2. Thickened intercotyledonary space
3. Exudate
4. Necrosis at base of caruncle
ii. Fetus will have ringworm type lesions with Aspergillus (30%)
iii. Use potassium hydroxide on a slide and use abomasal contents
of fetus or scrape skin lesions
1. Will see fungal hyphae
IX. Get BVD Handout from Anthony
Goat Diseases
I. H.A.A.G. (Habitual Abortion of Angora Goats)
a. Condition in Angora goats
i. Used for mohair production
b. High incidence in S. Africa, not found in US
c. Habitual abortions
d. Older large does (4 yrs +)
i. Goats were genetically selected for high production of mohair –
more hair affects adrenal function
ii. In stressful conditions they make a lot of hair and the adrenal
function is not good
iii. Then baby gets stressed and his adrenals become hyperplastic
1. Fetus produces high cortisol
iv. Baby is aborted
e. Lesions in adults
i. Adrenal atrophy
ii. Placentome degeneration
iii. Regression of corpus luteum (CL)
1. CL is required for the entire length of gestation in
the goat, NOT in the sheep
f. Lesion in fetus
i. Dysmaturity
ii. Retarded growth
iii. Anemic
iv. Adrenal hyperplasia – produce too much cortisol
v. Thymic atrophy
Ovine Abortions (Sheep)
I. Campylobacter abortion
a. Campylobacter jejuni
b. Campylobacter subspecies fetus
c. Not a venereal disease like in cattle
d.
e.
f.
g.
h.
II.
III.
IV.
V.
Late term abortions
Abortion storms in naïve herds only
Premature lambs, weak lambs, high mortality
Carrier animals are present – ewes and lambs
Transmission
i. Ingestion
1. Organism localizes in mucosa of gallbladder
i. Lesions
i. Nothing specific in adults
ii. Fetus
1. Donut lesions in the liver that have raised edges,
yellowish in color
a. Classic sign for this diseases
j. Diagnosis
i. Culture or isolate organism:
1. Abomasal contents, aborted fetus, vaginal discharges
ii. Microscopy (darkfield or phase contrast)
iii. Fluorescent antibody testing
Listeriosis
a. Listeria monocytogenes
b. High incidence of intestinal carriers
c. Transmission
i. Ingestion
d. Abortion rate is 10-20%
e. Lesions
i. Ulcerations or erosions in larynx
f. Diagnosis
i. Culture cotyledons, fetal organs, vaginal discharges
Leptospirosis
a. Not common in sheep
b. Most common if you get it is L. hardjo
i. Can also get L. pomona
c. Sheep seem to be more resistant than cattle
d. Carrier animals
e. Transmission
i. Contaminated water and feed from carriers
f. Clinical signs
i. Weak lambs, stillborns, abortions
ii. Maternal illness and death possible
Other bacteria associated with abortions in sheep
a. Actinomyces pyogenes – no specific signs
Chlamydial abortions
a. AKA Enzootic Abortion of Ewes
b. Chlamydia psittici
c. Pigeons, sparrows carry it
d. Two strains (both caused by same organism)
i. Conjunctivitis and polyarthritis strain
ii. Abortion strain (what we are concerned with for exam)
1. Mummified fetuses or macerated fetuses, stillborns,
weak lambs that die
2. Latent infections - carriers
3. Lambs with congenital infections
e. Ewes infected in last month of pregnancy
i. Abort in next pregnancy
f. Ewes infected in mid-gestation abort this pregnancy
g. Transmission
i. Ingestion
h. Classic picture
i. Late abortions in last 2-3 weeks of gestation
ii. Virgin and naïve herds have 50% of herd experiencing
abortions
iii. Ewes that abort:
1. Rear end is covered in yellowish-brown exudate
iv. Retained fetal membranes
v. Cotyledons are dark and mottled, red-brown exudate to them
i. Diagnosis
i. Intracytoplasmic inclusions on microscopic evaluation =
elementary bodies
ii. Fetal lesions
1. If aborted < 120 days of gestation
a. Autolytic fetus
2. If aborted > 120 days
a. Similar situation to Foothill Abortion in cattle
b. Focal hyperplasia of reticuloendothelial
system: enlarged livers, lymph nodes, and
spleens
iii. Microscopic evaluation of placenta, vaginal smears
iv. Fluorescent antibody test on tissue
v. Compliment fixation on dam’s serum
j. Prevention
i. Vaccination
1. Killed
2. Vaccinate ewes 8 weeks before breeding
VI. READ CHAPTER 76 IN THERIO BOOK (Infectious causes of abortion)