CASE REPORT
Neonatal Alloimmune Thrombocytopenia in a Quarter Horse Foal
Virginia Buechner-Maxwell, Michael A. Scott, Leanne Godber, and Annemarie Kristensen
Neonatal alloimmune thrombocytopenia is recognized as a
spontaneous disease of human infants, piglets, and possibly
mules, but it has not been previously reported in horses. A
I-day-old Quarter Horse foal presented to Michigan State
University Large Animal Clinic with severe thrombocyto-
penia of unknown origin. Immunoglobulins that bound to
the foal's platelets were identified in the mare's plasma,
serum, and milk by indirect assays. The immunoglobulins
were further shown to recognize platelets from the foal's
A I-day-old Quarter Horse colt presented to the Michigan State
University (MSU) Veterinary Medical Center with a com-
plaint of weakness and inability to nurse. He was accompanied by
his dam, a 6-year-old Quarter Horse mare. The foaling had been
unattended, and the owner estimated that the colt was 3 hours old
when he was discovered in the stall. At that time, the foal had
appeared strong and healthy. There was no evidence of injury, with
the exception of a small, full-thickness, dermal laceration on the left
side of the upper lip that had already formed a scab. After several
hours, the owner noticed that the foal was unable to locate the udder
and could not suckle effectively when offered a bottle. Thereafter,
the foal became increasingly depressed and lethargic. Based on his
rapid deterioration, the foal was referred to the MSU Large Animal
Clinic for further evaluation and treatment.
At presentation, the foal was minimally responsive to his environ-
ment. He was unable to stand and had no suckle reflex. He weighed
52 kg and had a body temperature of 37.5"C, a heart rate of 96 beats
per minute, and a regular respiratory pattern with 45 breaths per
minute. Oral mucous membranes were slightly icteric and tacky.
The umbilical stump was palpably normal, as were the forelimbs,
but the hindlimbs were diffusely swollen. Manipulation of the limbs
did not elicit a pain response, and the joints were neither hot nor
distended. Auscultation of the lungs and heart was unremarkable.
The foal was estimated to be mildly dehydrated (6% to S%), and
the owner confirmed that the foal had not urinated for several hours.
The blood glucose concentration ( 139 mg/dL, reference range 12 1
to 233 rng/dL), PCV (38%, reference range 32% to 46%), total
plasma solids (6.2 g/dL, reference range 4.3 to 8. I g/dL), and plasma
IgG concentration (>SO0 mg/dL by Cite test Idexx Laboratories,
Inc., Westbrook, ME) were determined as part of the foal's initial
evaluation and found to be within normal limits. Based on the foal's
history and its condition at presentation, neonatal maladjustment
syndrome, septicemia, and meningitis were considered potential di-
agnoses, even though the foal's presenting sepsis score was 5.'
From the Department of Large Animal Clinical Sciences, Vir-
~ i n i a - ~ a ~ l uRcggionai
nd College oj Vcterinury Medicine, VPl Ce
SU, Blacksburg. VA (Buechner-Mnrwellj; the Department v f
Puthohiology, College of Veterinarj Medicine. Columbia, MO
(Scott);the Randwick Equine Centre, Randwick, Austrulia (Godher);
and the Department of Vessel Wall Biology-Pharmacology, Cen-
tvfte, Denmark (Kristensen).
Accepted December 5, 1996.
Reprint requests: Dr. Virginia Buechner-Maxwell, Veterinary
MedicineNPI & SLJsDcpartment q f Large Animal Clinical Sciences,
Blacksburg, VA 24061.
Copyright 0 1997 by the Anwricun College of Veterinug. Internal
Medicine
OR91-6640/Y7/1105-0007$3.00/0
304 Journal of Veterinary Internal Medicine, Vol 1 1, No 5 (September-October), 1997: pp 304-308
full brother, born 1 year earlier. These findings, coupled with
the clinical course of the foal during its period of hospitaliza-
tion, strongly suggest that neonatal alloimmune thrombocy-
topenia can spontaneously occur in neonatal horses. This
diagnosis should be considered for foals with severe throm-
bocytopenia when other causes can be excluded, and plate-
let antibody assays should be used to support this diagnosis.
J Vet Intern M e d 1997;11:304-008. Copyright 0 1997 by the
American College of Veterinary Internal Medicine.
An intravenous catheter was placed to permit administration of
fluid therapy and medication. Additional blood was collected for a
CBC, serum chemical profile, quantitative measurement of IgC, and
bacterial blood culture. Prolonged hemorrhage was noted at sites of
venipuncture for blood collection and catheterization, so samples
were also submitted for a hemostasis profile. Intravenous fluid ther-
apy was initiated with lactated Ringer's solution containing 5% gln-
cose at a flow rate of 300 mL/h. Additional treatment included
potassium penicillin (50,000 I U k g IV qid), gentamicin (2.2 mglkg
1V rid; Schering-Plough Animal Health, Union, NJ), cimetidine (6.6
mgfkg 1V every 4 hours; SmithKline Beecham Pharmaceuticals,
Philadelphia, PA), flunixin meglumine ( 1 rng/kg IV bid; Schering-
Plough Animal Health), a vitamin E-selenium supplement ( I mL
1V of 2.5 nig selenium and 68 IU vitamin E per mL; Schering-Plough
Animal Health), and medical-grade dimethylsulfoxide (DMSO) (1 50
mL of a 10% solution IV in normal saline bid; Syntex Animal
Health, Inc, Palo Alto, CA). A nasogastric feeding tube was secured
in place, and the foal was given his dam's milk at an initial rate of
300 mL every 2 hours. Over 8 hours, the rate was gradually increased
to 800 mL/h. Once the foal's condition stabilized, survey radiographs
of the thorax wei-e obtained and found to be unremarkable. Ultraso-
nographically the umbilical remnants appeared normal, and minimal
free peritoneal fluid was present.
The CBC and hemostasis profile (Table 1 ) revealed that the foal
was severely thrombocytopenic ( I 3,000 plateletdpl) and had no
other hemostatic abnormalities. Thrombocytopenia was confirmed
by a manual determination of the platelet concentration on a second
blood sample (9,000 plateletdpl). Clinically the foal bled for more
than 15 minutes from venipuncture sites, but petechial hemorrhages
were not present. Bone marrow aspirates from the left greater tro-
chanter and sternum contained few hematopoietic elements and were
too hemodiluted to evaluate. Although cerebrospinal fluid analysis
and culture was indicated, the procedure was not done because of
the risk of hemorrhage. A blood donor was identified based on minor
crossmatch compatibility, and the foal was transfused at a rate of
300 mL/h with 3 L of platelet-rich plasma harvested by gravity
sedimentation from the donor's fresh heparinized whole blood. A
few hours after the overnight transfusion was complete, the foal
had 33,000 platelets/pL, and venipuncture did not induce prolonged
bleeding (Table 2). The foal was also able to rise and walk on his
own, and he demonstrated a renewed interest in nursing. Sequential
neurologic evaluations failed to identify abnormalities. Intravenous
fluid therapy was discontinued by day 2 because the foal was able
to tolerate adequate fluid and nutritional support by feeding tube.
By day 3, the foal was bright, active, and clinically normal and
had a strong desire and ability to suckle. He was gradually reintro-
duced to his dam, and the feeding tube was withdrawn. The swelling
in both hindlimbs had diminished, and the foal continued to be pain-
free in the joints of these limbs. Except for continued thrombocyto-
penia (1 8,000 platelets/pL), the hemostasis profile was normal, and
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EQUINE NEONATAL ALLOIMMUNE THROMBOCYTOPENIA 305

Table 1. Hematologic and Hemostatic Findings in a globulin was similar. In this assay, 50 pL of test and control plasma
Foal with Alloimmune Thrombocytopenia was incubated for 1 hour with 5 X 10” washed platelets from test
and control horses in a final volume of 150 pL, Incubation was
Test Patient Values Reference Values followed by 3 washes in PBWBSA, after which radiolabeled SPA
Hematocrit 39.6% 32-45% y proceeded as for the direct
Hemoglobin 13.6 g/dL 12-16.6 g/dL On day 9, platelets from the foal, his dam, and 3 normal control
Red blood cells 8.98 X lo6 pL 8.2-11.0 X lo6 p,L horses, including the transfusion donor, were tested in the direct
White blood cells 4.92 X lo3 pL 4.9-11.7 X lo3 pL assay. All were negative for SPA-detectable, platelet-associated im-
Segmented neutrophils 4.28 x l o 3 pL 3.36-9.57 x lo3 pL munoglobulin (Table 3A). To test for antibodies in the mare’s plasma
Band neutrophils ox 1 0 3 ~ ~ ox lo3 p~ that would bind to the foal’s platelets but not normal control platelets,
Lymphocytes 0.59 X lo3 pL 0.67-2.12 X lo3 pL the same 5 horses were used as platelet sources, and the mare’s
Eosinophils ox ~ O ~ ~
0-0.02L x lo3 w~ plasma and a control plasma were tested with each. The mare’s
Monocytes 0.05 X lo3 pL 0.017-0.39 X lo3 pL plasma contained immunoglobulins that bound to the foal’s platelets
Platelets 13 x 103 p , ~ 129-409 X lo3 pL 43 times as much as to platelets from the mare or the other 3 normal
Plasma protein 6.6 g/dL 5.2-8.0 g/dL controls (Table 3B). In contrast, immunoglobulins in the control
Prothrombin time 10.5 sec 10.8 sec* plasma bound minimally to all platelets tested. When the foal’s
Activated partial platelets were incubated in duplicate with 20, 40, and 80 p L of the
thromboplastin time 60.7 sec 57.0 sec* mare’s plasma, there was a dose-response binding with 2,s 15,3.184,
Fibrinogen 146 g/dL 163 g/dL* and 3,641 mean counts per minute (r = .96).
Fibrin degradation The mare’s milk from day 10 was also tested for platelet-bindable
products 1 1 0 pg/mL 1 1 0 pg/mL* immunoglobulin and compared to control milk from another mare
* Reference values for prothrombin time, activated partial thrombo- in early lactation. Platelets from the same 5 horses were again used,
plastin time, fibrinogen, and fibrin degradation products were deter- and 40 pL of test and control milk that had been cleared by repeated
mined by analyzing a blood sample from an age-matched normal centrifugation was incubated with each. The test mare’s milk con-
foal. All other reference values in the table and text are from Koterba tained immunoglobulins that bound to the foal’s platelets 34 times
A: Equine Clinical Neonatology. Philadelphia, PA: Lea & Febiger; 1990. as much as to platelets fi-om the mare or the other 3 normal controls.
In contrast, immunoglobulins in the control milk bound minimally
to all platelets tested (Table 3B). This finding is especially significant
because the concentration of immunoglobulins in milk is far less
preliminary results of the blood culture were negative. Because of than that found in colostrum.’
the foal’s improved condition, intravenous DMSO therapy was dis- At a later date, the dam’s acute plasma was shown to have anti-
continued, and the foal’s dose of flunixin meglumine was reduced platelet reactivity with platelets from a full sibling of the affected
to 0.5 mg/kg IV bid. Intravenous administration of cimetidine was
foal (Table 3). The sibling had been born the previous year and was
replaced with an oral preparation given at 6.6 mg/kg PO qid. Treat- the mare’s first foal; he had been normal throughout his neonatal
ment with sodium penicillin (50,000 I U k g IV qid) was instituted
period. All the aforementioned testing was repeated and corroborated
after a period of weakness was observed in association with the
with a modification of an immunofluorescence assay for canine
administration of potassium penicillin.
platelet-bindable immunoglobulin (Table 4 A,B).“ The assay was
Over the remaining period of hospitalization, the foal continued
modified to detect equine IgG by using a fluorescein-conjugated,
to appear physically normal. He had a bright and active attitude,
affinity-purified, F(ab’)* fragment, goat anti-[equine IgG I (Jackson
nursed well, and gained between 1 and 2 kg per day after being
ImmunoResearch Laboratories, Inc, West Grove, PA). The strong
reintroduced to the mare. Flunixin meglumine therapy was discon-
reactivity to this antibody suggests that the platelet-bindable immu-
tinued on day 4, and antibiotic therapy was discontinued on day 9.
noglobulin was predominantly an IgG, although reactivity with light
The foal was discharged on day 10 with a platelet concentration of
chains of other immunoglobulin classes cannot be excluded. Al-
188,000 platelets/pL (Table 2). The foal was examined by the refer-
though equine IgG binds quite poorly to SPA, especially in competi-
ring veterinarian 2 weeks after discharge and was reported to be
tive assays with IgG from other species, it bound well enough to be
normal. The owners were also contacted 6 weeks and 1 year after
detected in this SPA-based immunoradiometric assay.’ Assays using
the foal left the hospital. On both occasions, they reported that the
streptococcal protein G or anti-[equine IgG] antibodies as detectors
foal was normal and appeared to have no further problems.
would be better for routine use in horses.”.’
To investigate the possibility of immune-mediated thrombocyto-
penia, immunoradiometric iys optimized for the detection of ca-
nine platelet-associated and platelet-bindable immunoglobulin were
used.? In these assays, immunoglobulins bound to platelets are de-
tected by a radiolabeled antiglobulin reagent, staphylococcal protein Table 2. Platelet Concentration During Hospitalization
A (SPA). For the direct assessment of platelet-bound immunoglobu- in a Foal with Neonatal Thrombocytopenia
~

lin, platelets were harvested from test and control citrated blood by Days Postpresentation Platelet Concentration (X lo3 pL)
gravity sedimentation and differential centrifugation. The platelets
were washed 3 times with phosphate-buffered saline (PBS) con- 1 13
2* 33
taining 3% (w/v) bovine serum albumin, pH 7.1 (PBS/BSA). Five
3 14
million platelets were then added in triplicate to wells of a microtitra-
4 21
tion plate and incubated for I hour with I0 ng of ”‘I-SPA in SO pL
6 51
PBS/BSA. After incubation, the platelets were washed 3 times in
8 96
PBSIBSA, and aliquots of the washed platelet suspensions were
10 188
removed for detection of platelet-bound radioactivity and hence ini-
munoglobulin in a gamma counter. * Platelet concentration a few hours after overnight transfusion
The indirect assay for plasma titers of platelet-bindable immuno- was complete.
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306 BUECHNER-MAXWELL ET AL

Table 3. Results of Immunoradiometric Assays Using Staphylococcal Protein A in a Foal

With Alloimmune Thrombocytopenia
A. Direct assay for the presence of platelet-associated antibodies (cpm/5 million platelets): Foal platelets were collected 9 days after
presentation t o the teaching hospital. All samples were negative for the presence of bound antibodies.

Foal Sibling Mare Control 1 Control 2 Control 3

30 i 24 44 i 12* 13 i 1 3 19 2 8 23 i 6 13 i 9

B. Indirect assay for the presence of platelet-bindable antibodies in the mare‘s plasma and milk (cpm/5 million platelets).

Platelet Source Mare’s Plasma Control Plasma Mare‘s Milk Control Milkt
Foal 2320 ? 104 41 i 25 1325 i 66 265 2 16
Sibling* 1673 2 262 95 2 33 No value No value
Mare 42 i 14 31 ? 4 45 -t 15 139 -t 7
Control 1 46 i 16 41 i 12 34 2 19 119 2 19
Control 2 64 i 24 29 i 17 26 i 4 245 i 258
Control 3 66 i 24 45 2 15 42 2 9 138 2 21
For Tables 3A and 38, mean 2 standard deviation of triplicate determinations.
* Platelets from the full sibling brother were subsequently tested at a later date and adjusted t o the other values by accounting for interassay
variation in background binding.
t Control milk: samples from mare with normal foal of similar age at her side.
* Platelets from the full sibling brother were subsequently tested at a later date when result for affected foal was 2174 i 203.

Discussion Potential causes of increased platelet destruction or con-

The foal described in this report had severe thrombocyto-
penia associated with prolonged bleeding from venipuncture
sites and no accompanying abnormalities in hemostasis pro-
files. In general, thrombocytopenia may be due to decreased
platelet production, increased platelet destruction or con-
sumption, severe blood loss, sequestration, or some combi-
nation of these processes. Thrombocytopenias related to se-
questration are typically not severe, and the foal did not
have severe blood loss. Bone marrow aspirates were done
to investigate a production problem, but they were too hemo-
diluted to be informative; additional aspirates were not at-
tempted because of the foal’s rapid clinical improvement.
The presence or absence of decreased platelet production at
the time of presentation was therefore not clearly established,
but if there was an initial production problem, it was not
persistent.
sumption include immune-mediated disease such as autoim-
mune, alloimmune, or drug-induced thrombocytopenias; an-
giopathies; sepsis; disseminated intravascular coagulation
(DIC); and, specifically in horses, equine infectious anemia.*
The foal had no physical evidence of a vascular malforma-
tion or other angiopathic disorder, and the mare had recently
tested negative for equine infectious anemia. Neither the
mare nor the foal had received any therapy prior to presenta-
tion that would be considered capable of inducing thrombo-
cytopenia; the foal had received only oral fluids. Septicemia
with secondary DIC was initially considered a possible cause
of the thrombocytopenia because thronibocytopenia in neo-
natal foals is frequently associated with sepsis.‘ Negative
bacterial blood cultures, the absence of abnormalities other
than thrombocytopenia on the hemostasis profile, and the
foal’s sepsis score of 5 , however, did not support a diagnosis
of sepsis with DIC.’

Table 4. Results of Platelet Immunofluorescence Assay in a Foal With Neonatal Alloimmune Thrombocytopenia
A. Platelet-associated antibody: Foal platelets were collected for this test 3 weeks after foal initially presented. Thrombocytopenia
had also resolved.

Foal Sibling Mare Control 1 Control 2

Negative Negative Negative Negative Negative

B. Platelet-bindable antibody.

Platelet Source Mare’s Serum Control 1 Serum Control 2 Serum Mare’s Milk Control* Milk
Foal 4+ Negative Negative 4+ Negative
Sibling 4+ Negative Negative 4+ Negative
Mare Negative Negative Negative Negative Negative
Donor Negative Negative Negative Negative Negative
Control* Negative Negative Negative Negative Negative

For Tables 4A and 4B, fluorescence was graded as negative, I + , 2+, 3 + , and 4+.
* Control: samples from mare with normal foal of similar age at her side.

EQUINE NEONATAL ALLOIMMUNE THROMBOCYTOPENIA
Immune-mediated thrombocytopenia is defined as any
thrombocytopenia associated with antibody-mediated de-
struction of platelets, including those with autoimmune, allo-
immune, or immune complex pathogeneses. Autoimmune
thrombocytopenia occurs in human infants born to thrombo-
cytopenic or nonthrombocytopenic mothers with circulating
antibodies to an antigen common to the maternal and fetal
platelets. These antibodies are then transferred transplacen-
tally to the fetus, resulting in elimination of fetal platelets. ’”.”
Diagnosis requires the identification of antibodies on both
the maternal and the fetal platelets.
Alloimmune disease is due to “the development of anti-
bodies against an antigen derived from a genetically dissimi-
lar individual of the same species.”” In human neonatal
alloimmune thrombocytopenia (NAIT), the mother produces
antibodies to paternally derived fetal platelet antigens. Diag-
nostic findings include (1) the presence of antibodies on
the neonatal platelets, (2) the absence of antibodies on the
maternal platelets, (3) circulating antibodies in the maternal
plasma that bind to fetal and paternal platelets, and (4) dif-
fering maternal and fetal platelet allotypes.
Although a specific platelet antigen was not defined in
this case, there was strong clinical and laboratory evidence
that the foal had NAIT. The findings suggest that the foal
and his full sibling brother inherited a platelet antigen from
their sire that was not common to the mare’s platelets. Expo-
sure to this antigen most likely occurred at the time of deliv-
ery of the full sibling brother and was too late to result in
the colostral transfer of antiplatelet antibodies to that foal.
When the second foal was born, however, colostral antiplate-
let antibodies were present, and their ingestion by the foal
resulted in the rapid development of thrombocytopenia. The
foal’s plasma IgG concentration was good evidence that sig-
nificant colostral ingestion had occurred.
The diagnosis of NAIT could have been strengthened by
two additional tests. First, if blood had been available from
the stallion, the hypothesis that the mare’s plasma and milk
contained antibodies reactive to paternal platelets could have
been tested; a positive reaction between the stallion’s plate-
lets and the mare’s plasma would have been expected. Unfor-
tunately the stallion had died earlier in the year. Second, a
direct assay could have been done to confirm the presence
of platelet-associated immunoglobulin on the surface of the
foal’s platelets when thrombocytopenia was initially ob-
served.” Because NAIT is not commonly recognized in
foals, the value of this diagnostic test was not realized until
day 9, at which time no platelet-bound immunoglobulin was
detected (Tables 3A and 4A). Similarly the foal did not have
a plasma titer of platelet-bindable immunoglobulin at this
time (data not shown). The ingested immunoglobulin had
presumably been bound to platelets and cleared from circula-
tion to such an extent that any remaining immunoglobulin
was in undetectably low concentrations.
Although platelets survive about 3.5 to 5.5 days in normal
adult horses, their survival would be significantly reduced
in the pi-esence of platelet-reactive alloantibodies.” Human
patients with immune-mediated thrombocytopenia and in-
creased platelet-associated IgG have shortened platelet surviv-
als because of accelerated platelet ~1earance.I~ The phagocyto-
19391676, 1997, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.1997.tb00470.x by University Of Illinois At, Wiley Online Library on [08/04/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
307
sis of whole antibody-coated platelets, most importantly by
hepatic and splenic macrophages, is associated with platelet
survival times as short as 12 hours or less as compared with
normal survival times of 6 to 9 days in p e ~ p l e . In’ ~ human
neonates with alloimmune thrombocytopenia, the accelerated
phagocytosis of alloantibody-coated platelets soon exhausts
the pool of placentally transmitted antiplatelet alloantibodies,
often leading to recovery within a week.” A similar situation
would be expected in foals. Therefore, although colostral-
derived equine antibodies are detectable in foals for 30 to 60
days after birth, the platelet-reactive alloantibodies would bind
to platelets and be rapidly removed by the mononuclex
phagocyte system.I6 This explains why the foal of this report
had an early, severe thrombocytopenia followed by a gradual
recovery in platelet concentration over the following 10 days.
It also explains why the foal’s platelets were negative for
platelet-associated antibody on days 9 and 21.
Treatment of this foal included a platelet transfusion from
a donor whose platelets were later shown to be nonreactive
with the mare’s plasma. Although washed maternal platelets
may have been more appropriate, transfusion resulted in a
significant increase in the platelet concentration (Table 2),
and prolonged hemorrhage from venipuncture sites was no
longer observed. The foal was also treated with flunixin
meglumine as part of routine therapy for neonatal maladjust-
ment syndrome. This therapy may be contraindicated in foals
with thrombocytopenia because flunixin meglumine inter-
feres with platelet aggregation and thromboxane synthe-
sis, 17.18
Neonatal alloimmune thrombocytopenia has been recog-
nized as a spontaneous disease of human infants, piglets,
and possibly mules, but it had not previously been reported
in foals.” Evidence of NAIT in this case included the clinical
course and the identification of immunoglobulins in the
mare’s plasma, serum, and milk that bound to her foal’s
platelets and to platelets from the foal’s only sibling, a full
brother born the year before. The lack of reactivity with
normal control platelets supports the conclusion that the tar-
get antigen was an uncommon or unique paternal antigen
inherited by both offspring. These findings suggest that
NAIT should be considered a potential cause of thrombocy-
topenia in foals. It may occur more frequently than is realized
but is not diagnosed in foals that have been traumatized too
little to induce significant hemorrhage or is misdiagnosed in
foals with thrombocytopenias attributed to other pathogenic
mechanisms. Although assays for equine platelet-bindable
and platelet-associated immunoglobulin are not widely avail-
able, they are under development and may be useful diagnos-
tic tests for selected foals with thrombocytopenia.’ Whether
such tests are available or not, the determination of platelet
concentrations should be considered an important part of the
initial diagnostic plan for equine neonates.
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