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Bucking the Buck
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 Bucking the Buck
US Financial Sanctions and the International
Backlash against the Dollar
DANIEL McDOWELL

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 Oxford University Press is a department of the University of Oxford. It furthers the
University’s objective of excellence in research, scholarship, and education by publishing
worldwide. Oxford is a registered trade mark of Oxford University Press in the UK and
certain other countries.
Published in the United States of America by Oxford University Press
198 Madison Avenue, New York, NY 10016, United States of America.
© Oxford University Press 2023
All rights reserved. No part of this publication may be reproduced, stored in a retrieval
system, or transmitted, in any form or by any means, without the prior permission in
writing of Oxford University Press, or as expressly permitted by law, by license, or under
terms agreed with the appropriate reproduction rights organization. Inquiries concerning
reproduction outside the scope of the above should be sent to the Rights Department,
Oxford University Press, at the address above.

You must not circulate this work in any other form and you must impose this same
condition on any acquirer.
Library of Congress Control Number: 2022060608
ISBN 978–0–19–767988–3 (pbk.)
ISBN 978–0–19–767987–6 (hbk.)
ISBN 978–0–19–767989–0 (epub.)
DOI: 10.1093/oso/9780197679876.001.0001

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 For the “Crazy Crew”
(Luella, Eileen, and William)

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 Contents

Figures
Tables
Preface and Acknowledgments
Abbreviations

Introduction
1. Financial Sanctions and Political Risk in the International
Currency System
2. The Source and Exercise of American Financial Power
3. Sanctions, Political Risk, and the Reserve Currency Role
4. The Anti-Dollar Gold Rush: Central Bank Reserves in the Age of
Financial Sanctions
5. Sanctions, Political Risk, and the Dollar as International
Payments Currency
6. Payment Politics: Anti-Dollar Responses to Sanctions in Trade
Settlement
7. Financial Sanctions and the Dollar’s Rivals
8. China’s Play for Payments Power
Conclusion

Appendixes
Notes
References
Index

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 Figures

1.1. The Effect of US Foreign Policy on Dollar Policy Orientation.

2.1. Cross-Border Payments by Currency, 2014–2020.
2.2. A Typical International Payments Transfer.
2.3. The US Dollar as a Store of Value, 2010–2020.
2.4. Primary and Secondary Financial Sanctions.
2.5. Sanctions-Related Executive Orders (SREOs) 2000–2020.
2.6. Number of States Actively Targeted by SREOs, 2000–2020.
2.7. SREO Superstar Targets, 2000–2020.
2.8. Count of Cited Reasons for US SREOs, 2000–2020.
3.1. Russian Gold Holdings (metric tons), 2000–2020.
3.2. Russian Reserves, January 2012–December 2020.
3.3. Currency Composition of Russian Foreign Exchange Reserves
(%), 2017–2020.
3.4. Russian Foreign Exchange and Gold Assets Held in the United
States (%), 2014–2020.
3.5. Turkish Gold Holdings (metric tons), 2016–2020.
3.6. Turkish Reserves, 2012–2020.
4.1. Worldwide Monetary Gold Reserves (metric tons), 2000–2020.
4.2. Annual Change in Gold Reserves by Country, 2008–2020.
4.3. Venezuela’s Foreign Exchange and Gold Reserves, 2001–2020.
4.4. Turkish Gold Exports to Iran (kilograms), 2010–2019.
4.5. Cited Reasons for US Sanctions-related Executive Orders
(SREOs), 2000–2020.
4.6. Coefficient Estimates, Annual Change in Gold Holdings (tons).
4.7. Predicted Marginal Effects of SREOs on Gold Holdings.
4.8. Predicted Marginal Effects of Sanctions Risk on Gold Holdings.
4.9. Coefficient Estimates, Annual Change in Long-Term US
Treasury Holdings.
4.10. Predicted Marginal Effects of SREOs on Long-Term US
Treasury Holdings.
5.1. Currency Composition of Russia-China Trade Settlement,
2013–2020.
5.2. Currency Composition of Russian Export Settlement, 2013–
2020.
5.3. Currency Composition of Russian Import Settlement, 2013–
2020.
5.4. Currency Composition of Russian Debt, 2013–2020.
5.5. Currency Composition of Turkish Trade Settlement, 2012–
2020.
6.1. Number of Countries with Local Currency Swap Agreements,
2007–2020.
6.2. Coefficient Estimates, Count of Local Currency Swap Lines.
6.3. Predicted Marginal Effects of SREOs on Local Currency Swap
Lines.
6.4. Coefficient Estimates, Dollar Share in Trade Invoicing or
Settlement.
6.5. Predicted Marginal Effects of SREOs and Sanctions Risk on the
Dollar’s Share of Trade Settlement.
6.6. Distribution of “Learn More” Responses by Treatment Group.
8.1. Currency Share of Cross-Border Payments, 2014–2022.
8.2. Number of Direct and Indirect CIPS Participants, 2015–2021.
8.3. Foreign Indirect CIPS Participants by Region, 2018–2021.
8.4. Monthly Payments Traffic and Volume, 2015–2020.
8.5. CIPS Participation by Country, 2022.
8.6. Coefficient and Predicted Probability Estimates, CIPS
Participation.
C.1. Scree Plot of Eigenvalues after Principal Component Analysis.
C.2. Sample Distribution of Sanctions Risk Variable.
F.1. Multinational Corporations’ Interest in Euro and Renminbi-
based Payment Systems.

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 Tables

6.1. Average Treatment Effects, Vietnam Multinational Corporations

Experiment
B.1. Active Sanctions-related Executive Orders (SREOs) 2001–2020
C.1. Correlation between Principal Components and Composite
Covariates
D.1. Gold Reserves and US Financial Sanctions
D.2. Long-Term US Treasury Holdings and US Financial Sanctions
E.1. Local Currency Swap Agreement Regression Results
E.2. Dollar Share of Trade Settlement Regression Results
G.1. List of Direct Participants in Cross-border Interbank Payment
System (CIPS), December 2021
G.2. CIPS Participation Regression Results

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 Preface and Acknowledgments

At the time of this writing, Russia’s brutal and unprovoked war in

Ukraine is in its seventh month. Thousands of civilians have been
killed. Tens of thousands of soldiers, on both sides, have lost their
lives. As the shock of war in Europe unfolded on television screens
around the world, the United States and its allies in Europe and Asia
were compelled to respond. Though direct military intervention was
quickly ruled out, the leaders of these countries reached for one tool
of foreign policy early and often: economic sanctions. Chief among
the sanctions employed were those measures that denied targeted
Russian individuals, businesses, and government institutions access
to the global financial system. Within a few months’ time, the
Central Bank of Russia, many powerful Russian oligarchs, Vladimir
Putin himself, and even his longtime girlfriend and his daughters had
all been placed on a fast-growing financial blacklist.
As these events played out in real time, public awareness of such
measures grew almost as quickly as the long list of sanctions
themselves. Cable news networks and opinion pages of major
newspapers openly discussed the nuances of the cross-border
payment messaging system known as SWIFT, a communication
network unknown to even the most astutely informed citizens prior
to February 2022. Experts unpacked for audiences arcane elements
of the international financial system to explain how international
dependence on the US dollar provided the basis for the West’s swift
and punitive economic response. Some observers openly questioned
whether cutting off Russia’s access to the dollar—or “weaponizing”
the currency, as it has come to be described—would backfire and
hurt the greenback’s global standing in the months and years to
come.
 When I started developing the idea for this book in 2017, I had
no idea that the subject would be so salient five years later. Neither
did I know that I would write most of this book during a pandemic
while splitting time with my wife as teacher to our three, suddenly
homeschooling, kids. Many pages of this book (though, I cannot
recall which ones) were put to page while an energetic four-year-old
entertained himself on my home office floor. Reaching this moment
was something that, on many occasions and for long stretches, I
doubted I would ever achieve. In fact, I kept this book a secret from
everyone but my closest friends and family for four years because I
lacked the confidence that it would ever be finished. Completing a
long project brings with it many emotions, but the two that I feel
most acutely now are relief and gratitude. Though the feelings of
relief will quickly recede as the busyness of life overtakes the
present moment, my gratitude will endure. I could have never
finished this book were it not for the many people who contributed
to its development.
At my home institution, the Maxwell School of Citizenship and
Public Affairs at Syracuse University, I am indebted to several
colleagues. Brian Taylor shared sage wisdom with me about the
process of writing a second book. Dennis Rasmussen and Shana
Gadarian helped me think through the publishing process and what
comes after. Dimitar Gueorguiev provided critical feedback on survey
question design. Several graduate students at the Maxwell School
assisted with research. Olga Boichak, Michael McCall, and Nikiti
Selikov each performed critical tasks at various stages of the
project’s development. Two research assistants—J. Michael Dedmon
and Jingding Wang—worked with me over the long haul, dutifully
and carefully collecting data, analyzing foreign-language media
reports, and digging through government documents for
information. I am thankful for each hour that these individuals
worked on behalf of this book. Generous research support for this
book was provided by the Andrew Berlin Family National Security
Research Fund at the Institute for Security Policy and Law (ISPL) at
Syracuse University. I personally thank Mr. Berlin, his family, and all
of the people at ISPL for funding this project from its earliest stages
until the final steps of the editing process. Your commitment helped
make this possible.
Outside of my home institution, I thank two longtime friends and
mentors—Jerry Cohen and Eric Helleiner—who each provided
feedback in the early days of the project. Thomas Oatley gave me
the opportunity to present and receive feedback on my unfinished
manuscript at Tulane University in 2019, for which I am grateful. I
thank my good friends and frequent co-authors David Steinberg and
Steven Liao for being patient with me as I worked on the book and
for providing periodic advice along the way. I am indebted to Eddy
Malesky for allowing me to place several questions on the 2019
Provincial Competitiveness Index survey at no cost. Eddy’s
commitment to providing public goods for the academy is well
known, and this is yet another example of his generosity. At Oxford
University Press, I thank my editor Dave McBride for his support and
enthusiasm for this project. I am deeply indebted to the three
anonymous reviewers who provided exhaustive, invaluable advice for
me as I revised the manuscript. The book is so much better for
having their collective input. I hope they see their ideas reflected in
the final product. I am also indebted to Kelley Friel who skillfully
copyedited every line of this book and vastly improved the quality of
my language and the clarity of my ideas.
Finally, I thank my family for their enduring support and for
keeping me connected to what matters most while working on this
project. I am grateful for supportive parents, in-laws, and my
creative brother. To my three children—Luella, Eileen, and William—I
am sorry that this book often took me away from you, especially
during the summers. Your energy and light made the most grueling
periods of completing this book bearable. For that, I dedicate this
book to each of you. To my incredible wife, Sara, I know that this
project caused you to endure many life moments with a grumpy,
distracted husband and co-parent. Yet, over the span of five years
you cheered me on and supported me through the most challenging
and frustrating moments, as you always have. You listened to my
anxieties and provided unyielding encouragement. You selflessly put
my needs before yours. Thank you for being my co-author in this
life. Without your steadfast love and support, neither the book nor
my sanity would have made it to the finish line. I love you.

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 Abbreviations

BCV Central Bank of Venezuela

CBR Central Bank of Russia
CHIPS Clearing House Interbank Payment System
CIPS Cross-Border Interbank Payment System
INSTEX Instrument in Support of Trade Exchanges
JCPOA Joint Comprehensive Plan of Action
OFAC Office of Foreign Assets Control
PBOC People’s Bank of China
SDN Specially Designated National
SPFS Financial Messaging System of the Bank of Russia
SREO Sanctions-related Executive Order

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 Introduction

In the last week of April 2018, French president Emmanuel Macron

and German chancellor Angela Merkel made back-to-back trips to
Washington in an effort to convince US president Donald Trump not
to withdraw from the Joint Comprehensive Plan of Action (JCPOA),
the multilateral nuclear arms agreement his predecessor had signed
with Iran. Then-UK foreign minister Boris Johnson timed his US visit
to coincide with an op-ed he wrote for the New York Times urging
Trump to stay in the deal. Johnson even appeared on Fox & Friends,
the president’s favorite news program, to plead Europe’s case.1 In
the end, none of it worked. On May 8, Trump announced that the
United States was pulling out of the Iran nuclear deal. The
condemnation from Europe was swift. Major German newspaper Die
Zeit pulled no punches, tweeting the day after: “Trump destroys the
liberal world order.”2 Merkel more gently echoed these sentiments,
saying the move put the multilateral global order in a “real crisis.”3
Macron warned that the move would only make the world a more
dangerous place, adding, “I regret the decision of the American
president. I think it’s an error.”4 A joint statement from the British,
French, and Germans soon followed, condemning the decision.5
That Europe was directing its anger and disappointment at the
Trump administration after its controversial decision came as no
surprise. However, several prominent European policymakers soon
turned their ire toward what might seem like unlikely targets: the US
financial system and the currency that underpins it. German Foreign
Minister Heiko Maas was the first to speak up. Writing in
Handelsblatt, a German newspaper, in August 2018, Maas
characterized the Trump administration’s decision as a “mistake,”
adding that Trump’s move made it “essential that we strengthen
European autonomy by establishing payment channels independent
of the US [financial system].”6 French finance minister Bruno Le
Marie quickly backed Maas’s position, saying, “I want Europe to be a
sovereign continent, not a vassal, and that means having totally
independent financing instruments [from the United States].”7
European Commission president Jean-Claude Junker was also
frustrated by Trump’s decision and used his 2018 State of the Union
Address to express his displeasure.8 Speaking before members of
the European Parliament, Junker stated that more needed to be
done to “allow our single currency to play its full role on the
international scene.” Noting that Europe paid for 80 percent of its
energy imports in dollars rather than euros, he called this “absurd”
and challenged members to support a united effort to promote the
common currency as an “instrument of a new, more sovereign
Europe.”9
Why did the Trump administration’s decision regarding the Iran
nuclear deal trigger anti-dollar rhetoric from so many prominent
European policymakers? The American withdrawal from the
agreement led to the reinstatement of harsh financial sanctions
against Tehran, which had been suspended when the United States
signed the JCPOA in 2015. These direct measures blocked the
Iranian regime from accessing the global dollar-based financial
system, but this is not what irritated the Europeans. The United
States also reimposed “secondary sanctions” that went beyond the
targeted regime. Secondary sanctions cut off, from the dollar and
the financial institutions through which those dollars flow, any third-
party individual or firm doing business with designated Iranian
targets. This was a problem for many European firms that had
reentered the Iranian market after the JCPOA was signed. They were
now faced with a Hobson’s choice: continue business with Iran (and
be blacklisted by the US Treasury) or write off all past investments in
their Iranian business relationships. Because of the dollar’s centrality
in the global financial system, which includes its use in the
settlement of international trade, European companies involved in
Iran chose the second option. While losing the potential to develop
Iranian business was a blow, losing access to the dollar would have
been infinitely more costly. European policymakers’ frustration with
the United States was based on a stark reality: the dollar’s global
dominance allowed Washington to wield its currency as a weapon of
foreign policy. This motivated European countries to discuss how to
promote the euro’s global role to minimize future injury.
During the JCPOA negotiations in 2015, then-president Barack
Obama foreshadowed Europe’s reaction to backing out of the
agreement. He warned that the failure to reach a deal would result
in new US sanctions that would “raise questions internationally about
the dollar’s role as the world’s reserve currency.”10 Secretary of State
John Kerry offered a more alarmist take, asserting that walking away
from the nuclear deal and unilaterally imposing sanctions was “a
recipe . . . for the American dollar to cease to be the reserve
currency of the world.”11 Critical observers characterized their
statements as breathless, hyperbolic rhetoric. One popular business
television personality asked in a tweet, “Does the secretary [John
Kerry] know anything about the dollar?”12 Another critic opined that
there was no “less convincing argument” for the Iran deal than
“fear-mongering” about the dollar.13 Others claimed any assertion
that the dollar would lose its top global position due to “geopolitical”
forces was “laughable”; they maintained that only economic forces
could weaken the currency’s dominance.14 Obama’s and Kerry’s
claims were both exaggerations—as political rhetoric often is. Yet
criticizing their political hyperbole by jumping to the conclusion that
the dollar’s status as the world’s pre-eminent and most widely used
currency is divorced from politics is misguided.
In a speech the year after the JCPOA was signed, Jack Lew, then
secretary of the US Treasury, offered a more nuanced take on the
link between financial sanctions and the dollar’s status, warning of
“sanctions overreach.” While Lew explained that financial sanctions
are a powerful tool of US foreign policy made possible by the dollar’s
global dominance, he cautioned that their overuse could, over time,
weaken the Treasury’s ability to employ them effectively. “The more
we condition use of the dollar and our financial system on adherence
to US foreign policy,” he detailed, “the more the risk of migration to
other currencies and other financial systems in the medium-term
grows.”15 Careful to avoid the apocalyptic tone of his colleague at
the State Department, Lew offered a measured explanation of why
the dollar’s dominance depended not just on economic factors but
on political ones as well. According to the memoir of a high-ranking
Trump administration official, Lew’s successor Steven Mnuchin also
worried that relying on sanctions could damage the dollar’s reserve
currency status and push more cross-border transactions into
euros.16
Financial sanctions again gained prominence as a key tool in the
West’s response to the unprovoked Russian invasion of Ukraine in
February 2022. Days later, the Central Bank of Russia, many Russian
oligarchs, and even Putin himself were cut off from their dollar-
denominated assets and blocked from transacting in the dollar-based
financial system.
As before, questions about potential blowback from sanctions
emerged. Influential economist and first deputy managing director at
the International Monetary Fund, Gita Gopinath, warned that
Washington’s measures could fragment the international monetary
system. Certain economies, she predicted, might gradually move
away from the dollar in their trade and investment activities.17
Strategists at major global banks also weighed in. Credit Suisse’s
Zoltan Pozsar called the sanctions a turning point for the dollar’s
global dominance. Dylan Grice of Société Générale forecast via a
tweet that the moment marked “the end of USD hegemony & the
acceleration towards a bipolar monetary order.”18 Renowned
journalist and associate editor at the Financial Times, Martin Wolf,
predicted a “currency disorder” in which the dollar’s dominance is
increasingly challenged.19 State media in China gleefully published
commentary on the subject with headlines like “Biden takes victory
lap over Russia sanctions but US dollar hegemony shows cracks.”20
In public debates, the notion that politics influences the
international appeal of currencies has become nouveau chic. Among
scholars of international political economy (IPE), such ideas have
deeper roots. In her pathbreaking 1971 book Sterling and British
Policy, Susan Strange argued that the pound was able to extend its
reign as a top global currency largely due to Britain’s political
relations with former dependencies.21 The IPE literature on the
political underpinnings of international currencies has since grown
considerably (despite being mostly ignored by economists).22 Yet the
current public debate about sanctions differs from how the field of
political economy has modeled the relationship between politics and
a currency’s international popularity.23 Prior work in IPE has
generally emphasized how political variables either help a currency
move up the international money hierarchy or help it maintain
dominance. Such research points out that currencies issued by
states with large militaries and extensive alliances benefit from
enhanced market confidence. States with these qualities can also
use geopolitical leverage to pressure friends and allies to continue to
back their currencies. The current debate about sanctions and the
dollar suggests that politics may also work in the opposite direction.
Political factors need not only propel or reinforce a currency’s cross-
border use; they may also undermine it. The scholarly debate on
international money has only very recently started to seriously
consider the possibility that financial sanctions might eventually
“trigger a politically motivated diversification away from . . . the
dollar.”24
The European response to President Trump’s decision to withdraw
from the Iran nuclear deal provides anecdotal evidence in support of
this proposition. If this were the only example of such a reaction, we
might easily dismiss it as meaningless bluster. After all, the
Europeans have a decades-long history of complaining about the
dollar and the “exorbitant privilege” that comes with it.25 Yet, there
are many other examples of backlashes against the dollar in
response to financial sanctions. The US Treasury has blacklisted
targets in Iran, Russia, Turkey, and Venezuela in recent years. Each
retaliated by lambasting the dollar’s grip on the global financial
system and took steps to promote the use of alternative currencies
in their international business dealings. Some reduced their holdings
of dollar assets and invested in other currencies or assets like gold.
 The Argument
The book’s central claim is that US financial sanctions generate
political risk in the international currency system. In this context,
political risk is related to, but distinct from, its meaning in the study
of foreign investment.26 I define political risk as the potential for a
political act to raise the expected costs of using a currency for cross-
border transactions or as a store of value. Over time, the
accumulation of political risk in the system creates incentives for
governments to adopt anti-dollar policies that promote the use of
currencies or assets other than the dollar for investment and cross-
border transactions. Of course, anti-dollar policies may fail. Thus, on
their own they do not imply that the dollar is playing a diminishing
role in a country’s international economic relations. They merely
indicate that the government is attempting to bring about such a
shift. When sanctions-induced anti-dollar policies do successfully
reduce reliance on the dollar, it signifies de-dollarization—the
intentional reduction of the dollar’s role in a nation’s cross-border
economic activities.
The book explores this argument with a series of empirical
chapters that examine the first two decades of the twenty-first
century, a period in which the United States steadily increased its
use of financial sanctions against foreign adversaries and pariah
states. As subsequent chapters will show, in some cases the link
between US financial sanctions and anti-dollar policy reactions from
targeted governments is undeniable. Other cases are suggestive,
though less conclusive, of a link. The evidence that sanctions
provoke anti-dollar policies is strongest for countries that have
already been targeted by the United States. There is even limited
support for the claim that the risk of being sanctioned provoked pre-
emptive efforts to reduce dollar dependence. On the whole, the
illustrations in this book support its central claim: sanctions generate
political risk, provoke anti-dollar policies among targets, and in some
cases correlate with de-dollarization.
Another random document with
no related content on Scribd:
 UTERINE TUMORS.

These are somewhat rare in the domestic animals, yet they have
been met with in the form of cysts, fibroma, fibro-myoma, sarcoma,
and carcinoma. In a number of cases the nature of the tumor has not
been clearly made out. Mangot saw a mare with two pediculated
uterine tumors having an aggregate weight of 12 lbs. These were
expelled with much straining and suffering. LaMaitre and Rodet
record other cases. Stockfleth describes multiple pediculated fibroid
tumors in the womb of the cow. Cysts have been especially seen in
the cow and bitch, and carcinoma in the bitch.
Symptoms. These may for a length of time be overlooked, though
breeding animals usually fail to conceive. Then a slimy, muco-
purulent, serous, bloody or fœtid discharge may escape habitually
from the vulva, smearing the tail and hips and collecting on the floor.
If the os is sufficiently patent to admit the hand vaginal and uterine
exploration will detect the tumor. In other cases it may be felt by
rectal examination.
Treatment is essentially surgical and will consist in dilatation of
the os, and the removal of the tumor by twisting, ecraseur, or curette,
and with careful antiseptic precautions before and after. In
malignant tumors in the uterine walls it may be expedient to remove
the entire organ.
 UTERINE TUBERCLE.

This has been seen especially in sterile cows, the subjects of

nymphomania, and it may be associated with a muco-purulent or
bloody discharge from the vulva, nodular swelling on the uterine
horns, perhaps also on the broad ligaments, one or both ovaries, and
the mesentery, to be recognized by rectal examination. The presence
of tuberculosis in the lungs or throat, and the response to the
tuberculin test will confirm the diagnosis. As a rule it is not desirable
to institute treatment.
 IMPERFORATE HYMEN.

Cases of this kind have been described in mare and cow,

preventing copulation and conception, and leading to a distension of
the vagina, with a glairy fluid, which obstructed defecation, irritated
the bladder and caused violent but fruitless straining, under which
the mass would project from the vulva. The centre of the swelling
may be penetrated with a trochar or bistuory and enlarged by
incisions in several directions. Relief is prompt and lasting.
 VAGINITIS. LEUCORRHŒA.

Inflammation of the vaginal mucosa is usually a concomitant of

metritis and like that follows parturition. It will however occur
independently from direct injury or infection or from the presence of
neoplasms. In dourine and horsepox, vaginitis is a common
symptom, to mare, cow and bitch infection is conveyed by coition.
Dieckerhoff quotes old chronic cases, also acute ones which extended
to the peritoneum and proved fatal in a few days. The common
symptom of muco-purulent discharge having a heavy or fœtid odor is
together with the discharge from the womb known by the common
name of leucorrhœa. The frequent irrigation of the whole passage
with antiseptic solutions is usually successful in putting a stop to the
affection, unless in case of constitutional infection, or the presence of
some neoplasm.
 TUMORS OF THE VAGINA.

The vagina is the seat of different forms of neoplasms in the

various domestic animals. Thus cystoma, lipoma, adenoma, fibroma,
fibro-myoma, sarcoma and epithelioma have been noted. They are
essentially surgical and to be dealt with as such. They are mainly
important in this connection as inducing a leucorrhœa, which in the
absence of careful examination might be mistaken for that of uterine
or vaginal infective inflammation.
PARTURITION FEVER (COLLAPSE). MILK FEVER.
PARTURIENT APOPLEXY. CALVING FEVER.
PARTURITION PARESIS.

Definition. Predisposing causes: genus, breed, great milking capacity, heredity,

mature age, vigor, high feeding, powerful digestion and assimilation, sudden
plethora, drying up of milk, parturition, easy delivery, warm season, chills,
idiosyncrasy, cardiac hypertrophy, contraction of womb, emotional excitement:
Supposed causes: absorption of toxins from womb, colostrum, Schmidt treatment
its significance, microbian infection and intoxication, effect of change of stable.
Microbiology. Nature: Theories of nervous explosion, vaso-motor cerebral anæmia
from exaggerated excitability of the uterine nerves, or from dilatation of the portal
system and womb, metro-peritonitis, cerebral anæmia from congestion of the rete
mirabile, etc., palsy of the ganglionic nerves, plethora, intracranial arterial tension,
narcotic poisons from leucocytic or microbian source. Lesions: variable, cerebral
and spinal congestion, pulmonary congestion, collapse, septic inhalation,
bronchitis, dessication of ingesta in omasum and large intestine, black thick blood,
yellowish gelatinoid exudates in cranium and spinal canal and under spine,
glycosuria. Symptoms: time, post parturient, plethoric subject, sudden onset,
comatose and violent forms, discomfort, restless movements, inappetence,
moaning, mental dullness, unsteady walk, muscular weakness, compulsory
recumbency, retained urine and fæces, drowsiness, somnolence, unconsciousness,
stertor, venous pulse, tympany, sudden recovery, complete, with paralysis, fatal
cases, violence, tossing head, trembling, cramps, convulsions, temperature.
Mortality. Prevention: bleeding in plethoric, heavy milkers, purging, low diet,
exercise, comfort, milking, blisters, sucking by calf, disinfection, iodine solution in
udder. Treatment: in early stages bleeding, purgatives, peristalsis stimulants,
antiseptics, injections, stimulants, rubefacients or cold sponging, elevation of the
head, udder massage, milking, iodine injection of the mammæ.

Definition. A nervous disorder which develops suddenly in

plethoric cows, heavy milkers, after calving, and is characterized by
loss of senses, of consciousness and of muscular control, by
hypothermia or hyperthermia, convulsions, coma, and mellituria.
 Causes. While one cannot speak positively as to the essential cause
of this disease, certain conditions are so constant and prominent that
they must be given a high value as predisposing causes.
Genus and Breed. Milking Capacity. This is essentially a disease of
cows, probably largely because of all domestic animals, cows only
have been long and systematically bred to secure the greatest power
of digestion and assimilation and the highest yield of milk. It is the
disease not only of cows, but of milking breeds, and preëminently of
individuals that give the most abundant dairy product. It is rare or
unknown in scrub or common herds, while common and fatal in the
best milking breeds, in advancing ratio about as follows: short horn,
red polled, Normand, Swiss, Ayrshire, Flemish, Dutch, Alderney,
Jersey, Guernsey, and Holstein. Heredity may be claimed, as the
special predisposing qualities are hereditary.
Age has a marked influence, but this is subsidiary to the milking
qualities. The disease rarely attacks a cow after the first or second
calving when the system is as yet immature, and the milk yield has
not reached its maximum: nor one that is past its prime and already
failing in vital energy and milking qualities. The following table is
from statistics compiled from veterinary records in Denmark and
Bavaria:

Age, yrs Cases

—3 —8
4 21
5 65
6 160
7 171
8 202
9 117
10 124
11 44
12 70
13 78
and over.
 It will be noted that it is in the period of the most vigorous, mature
life, from the 6th to the 10th year inclusive that the great majority
suffer. In a judiciously managed dairy it is the best cows that are
carried at these ages, and although the very best are kept on into old
age they show a steadily decreasing number of cases as they begin to
fail. The disease is all but unknown in primipara.
High Feeding. Heavy and rich feeding prior to calving and
immediately after, is a most prominent cause of the affection. This is
so well known to owners of milking breeds, that they usually hold to
the principle that the cow that is a heavy milker, should be all but
starved for a fortnight before calving and for a week after. In herds
where this rule is acted on the disease is rare and may be altogether
unknown, and when it is neglected the malady is often very
destructive.
Plethora. High Condition. Heavy feeding and high condition
usually go together, and the majority of the victims are fat or in good
flesh, yet a certain number are actually thin. The predisposing
condition is plethora rather than fat or flesh, and this may be present
in the comparative absence of flesh. The cow that is from a stock
famed as heavy milkers, does not tend to lay on flesh, but, on
succulent diet especially, the greater part of the nutritive matter
assimilated goes to the production of milk, and she remains thin in
flesh no matter how heavily she may be fed. Many such cows never
go dry, but give a liberal yield of milk up to the day of calving, and if
measures are taken to dry them up, it is done at the expense of a
sudden plethora, as the milk giving system does not at once
accommodate itself to the laying up of fat and flesh.
The drying up of the milk secretion sometime before calving in a
cow which is normally a heavy milker is therefore a potent factor.
Parturition is an almost indispensable factor as the disease occurs
one to seven days after that act, and only in rare and somewhat
doubtful cases before it.
Easy Delivery with little nervous outlay or loss of blood, and no
exhaustion is a special feature. The attack almost never occurs after a
difficult parturition with considerable loss of blood and much
nervous exhaustion. This should to a large extent exclude such
alleged factors as shock or wearing out of nervous energy. The
nervous prostration which figures so prominently in the disease,
seems to be less the result of wear and tear, than of the supply of an
excess of blood, which is either over-enriched, or charged with some
injurious toxic matter. At the same time there is a manifest
susceptibility at the parturient period which is not present at other
times, and the plethora or toxin takes occasion to operate when this
predisposition renders such an attack possible. The Warm Summer
Season has been claimed to induce a greater number of cases, and
doubtless exposure to continuous heat, tends to prostrate the
nervous system and predispose to congestion, this fails to take into
account the still more important element of the rich spring and early
summer pastures, where the already plethoric animal is left to feed
without stint, or the tempting red clover, alfalfa and other fodder
crops, rich in albuminoids, which are fed liberally in a succulent
condition.
Chills in cold winter weather have been similarly invoked as
driving the blood from the surface to collect in internal organs,
including the brain. That chills do act in this way cannot be denied,
but there is no demonstration that any number of cases have been
materially affected by cold.
Idiosyncrasy. Constitutional Predisposition. This must be
allowed, inasmuch as that it covers all those individual conditions,
functional and structural, which belong to the heavy milker, or the
animal with extraordinary powers of digestion and assimilation. The
same shows in the predisposition to a second attack of an animal
which has survived a first one. The structural changes in the nerve
centres, which occur in the primary attack, leave traces, which render
these parts more susceptible at the next calving. In my own
experience the violence of the disease is liable to increase with
successive attacks, so that a second or third cannot be hoped to be as
mild as was the former one.
Cardiac Hypertrophy. Cagny draws attention to the fact that in
man and beast alike the heart undergoes hypertrophy during
gestation and, above all, during its later stages. In improved breeds
of cattle, and especially in milking breeds, a great development of the
whole circulatory system is seen, and a large heart is a constant
feature of this. This implies an increased force of cardiac systole, an
increased blood tension in the arteries and capillaries, a condition
which tells with special force on the soft tissues of the brain, as the
violent abdominal compression in the expulsive efforts of
parturition, tends to drive the blood from the great vascular viscera
situated back of the diaphragm.
Parturition and the subsequent contraction of the womb and
expulsion of the great mass of blood, must be accorded a prominent
place among causative factors. The disease is almost restricted to the
first week after parturition, and its gravity is greater the more it is
related to the parturient act. Cases occurring in the first three days
are usually fatal. The gravid uterus contains a very large amount of
circulating blood, and when the womb contracts, the greater part of
this is suddenly thrown upon the general circulation, already
plethoric to an undue extent. As yet the mammæ are congested and
there is no free depletion through that channel, so that there is a
marked temporary plethora and vascular tension, before the system
can establish free elimination and, as it were, strike a healthy
balance. In this period of transient plethora there lies a source of
great danger to the general system and, more particularly, to the
brain.
Emotional Excitement connected with the removal of the calf is
urged by Günther, Jaumain, Félizet and others as a prominent cause.
This, however, must be rare, at the most; the disease does not attack
the primipara that should be most susceptible to this influence, but
the mature animal, at her third calving or later when she is already
well accustomed to this treatment; it supervenes so quickly on
parturition in many cases, that there was no opportunity for such
emotion; it occurs also in cows, the calves of which have remained
with them or have received no attention from them.
Absorption of Toxic Matters. The theory of a poisoning of the
nerve centres is indicated in the familiar name of milk fever,
suggesting an absorption, or poisonous condition of the milk.
Lafosse charged the trouble on the uterine milk secreted in the
cotyledons and reabsorbed in quantity. Abadie and Kaiser attributed
it to the products of gastro-intestinal ferments, which acted on the
nerve centres like a deadly organic alkaloid. Hartenstein
incriminated the products of muscular contraction in the womb and
systemic muscles during parturition. Ehrhardt invoked a similar
auto-intoxication, going on before parturition and only reaching its
climax in connection with that act.
 Allemani and Gratia attribute the disease to the absorption of the
first milk (colostrum), and there are several considerations that
strongly favor this hypothesis. The disease sets in always in
connection with the parturient development and congestion of the
udder and the secretion of the first milk. In exceptional cases it may
even appear just before parturition. Even upon the calf the colostrum
operates as an irritant and purgative. Is it wonderful that, in the
parturient cow, with a high state of plethora, a highly susceptible
state of the nervous system, and the various concurrent conditions
already referred to above, a direct poisoning of the nerve centres
should appear? It is worthy of notice that the absorption from the
mammæ takes place without any metabolic change, such as occurs in
the stomach and liver in the case of materials digested. It is to be
presumed that the hypothetical mammary poison is delivered in the
brain in its pristine condition and possessed of its full force.
The doctrine is corroborated even more strongly by the successful
results of treatment by the injection of a solution of potassium iodide
into the udder. The iodide solution may presumably act in one or
more of several ways. It is unquestionably an antiseptic, and would
tend to arrest or control microbian growth and activity, thus
preventing the further formation of toxins. It has a potent
deobstruent action on glandular tissue, tending not only to dry up
the milk, but to hold in check the leucocytic function of producing
dangerous leucomaines. There is reason to believe that with regard
to some poisonous ptomaines iodine acts as a direct antidote,
probably uniting with these and forming new and comparatively
harmless compounds. It manifestly acts in this way in the case of
cryptogamic diuresis, and in cerebral congestions arising from spoilt
fodder. The iodide tends further to act as a calmative to the nerve
centres, and as a diuretic, serving to eliminate the poison that may be
present in the blood.
Microbian Infection or Intoxication. The doctrine has been
advanced that the disease is either a microbian infection of the nerve
centres or a process of poisoning by the absorbed toxins of microbes.
Of the two hypothesis the latter is the more acceptable, in view of the
fact, that cows in a condition of coma will sometimes recover with
extraordinary rapidity. This is more likely to occur in connection
with the elimination or exhaustion of a transient narcotic poison,
than with a deadly microbe colonized in the brain. This hypothesis is
in full accord with the acknowledged success of the iodide injections;
with the observation of Bissauge, which I can endorse, that certain
villages and hamlets habitually furnish cases of parturition fever,
while neighboring ones, with the same breeds and apparently the
same management escape; and with the observations of Russell and
Wortley Axe, that the malady will sometimes be suddenly prevented
in a herd, by the simple expedient of having the cows moved to a new
and previously unoccupied stable, for calving and the first nine days
thereafter.
In support of the doctrine of a microbian origin is recalled the fact
that the disease almost invariably follows parturition, which opened
the way for the introduction of bacteria by the genital passages. This
is somewhat invalidated by the fact that it follows the easy
parturition, in which there was no chance for the introduction of
germs on hands or instruments, and does not follow dystokia in
which, without question, germs have been planted abundantly in the
interior of the womb. Undue weight should not be given to this
objection, as the essential accessory conditions of plethora, etc., are
usually largely modified in cases of dystokia.
The microbiology of the affection leaves much to be desired.
Coureur and Pottiez and later Van de Velde found a streptococcus in
the blood. Trinchera, Nocard, and Cozette found the common pus
cocci (staphylococcus pyogenes aureus, citreus and albus) a
streptococcus and a colon bacillus in the liquid squeezed from the
cotyledons, and in the liquid debris on the uterine mucosa. These
microbes were not found in other organs. They grew readily in
artificial cultures, but we lack the final proof of a successful
inoculation on a susceptible parturient subject. The whole subject is
therefore still a plausible theory.
We are not however limited to the womb as the only possible field
of a pathogenic microbian growth. The frequent presence of
microbes in the sphincter of the teat, in the galactophorous sinus,
and in the milk ducts inside the mammæ is absolutely proved.
Guillebeau found on the mucosa in cases of mammitis three forms of
bacillus, to which he attributed the disease. In the New York State
Veterinary College we have found mammitis usually associated with
a streptococcus in the milk. In one cow in the University herd which
gave abundance of good milk, and rarely showed any sign of
congestion, streptococcus was constantly present. In cows producing
“gassy” curd, V. A. Moore and A. R. Ward found in the milk a bacillus
which morphologically and in cultures resembled the colon bacillus
(evidently one of the colon group). In the milk and mammary gland
tissue got from other (slaughtered) cows, a micrococcus growing in
yellow or buff-colored colonies predominated. (Moore and Ward).
That the colon bacillus, so constant in the intestines and manure, is
not always found in the milk ducts, would show that in its normal
condition it is not adapted to this habitat, but when a variety appears
that is so fitted, it appears to be able to maintain its place
indefinitely.
With such facts before us, we must allow the possibility of
poisoning by toxins of bacteria in the udder, or by compounds
formed by the synthesis of such toxins and the leucomaines of the
expanding udder, or by the union of the udder toxins with those from
the womb. The whole subject of microbian and leucocytic causation
of parturient fever is still hypothetical, yet enough is known to show
the high probability of such source, and to demand a thorough
investigation which will place the subject on a substantial and
assured basis.
Nature. Theories of the nature of this disease are numerous and
varied, and are largely based upon some restricted or one-sided view
of phenomena and lesions. Coutamine considers it as the reaction of
the surplus of nerve force, which was not used up in the easy
parturition. The theory is somewhat fantastic as an explanation of
the rapidly developing asthenia and paralysis. Billings explains the
cerebral anæmia as due to vaso-constriction of the nervous
capillaries produced by the exaggerated excitability of the uterine
nerves. But with the easy parturition, and delivery, and the moderate
contraction of the womb, without violence or spasm, the theory
seems rather insubstantial. Trasbot looks on the affection as a
congestion of the myelon, apparently shutting his eyes to the far
more prominent encephalic symptoms. Haubner considers it as a
cerebral anæmia induced by the vaso-dilatation in the portal system
and abdominal viscera generally, the result in its turn of the vacuity
of the abdomen, from the expulsion of the fœtus and its connections.
But the womb is often found contracted and comparatively
exsanguine, the plethoric condition of the cow, suddenly increased
by the great mass of blood from the uterine vessels, maintains a
marked general blood tension, and finally, the closed box of the
cranium cannot have its blood so completely drained from it as can a
part outside such a cavity. Stockfleth attributed the malady to a
metro-peritonitis, and the absorption of the morbid products and
poisoning, but neither a metritis nor peritonitis is a common
accompaniment of the affection.
Franck who accounts for the asthenia by an anæmic condition of
the brain, explains the anæmia by a pre-existing congestion and
œdema of the rete mirabile at the base of the brain. He claims that
sows which have also a rete mirabile in this situation sometimes
suffer from parturient fever. He fails to adduce cases in the sheep
and goat which also have retia mirabilia. The pregnant sheep may die
of an asthenic affection, but usually before parturition. Franck’s
theory is plausibly based on the anatomical and physiological
conditions, for the elaborate network of vessels at the base of the
brain, undergoes great distention under increased arterial tension,
and with the serous effusion, compresses the brain and drives out its
blood.
Palsy of the ganglionic system has been invoked, with succeeding
congestion of the myelon and encephalon (Barlow, Kohne, Carsten
Harms, etc.). Explanation is made that the supposed excess of
nervous force fails of distribution through a lack of conductility of
the nerves, and the nerve centres suffer. Binz has even found the
spinal roots of the sympathetic surrounded by a thick gelatinoid
exudate. The theory is, however, essentially speculative and fails to
explain the origin of the disease or its connection with the recognized
conditions of its occurrence.
Plethora with Arterial tension and all conditions contributing to
this, as already set forth under causes must be allowed a prominent
place in considering the nature of the disease. The blood globules in
my experience are somewhat smaller than normal, implying the
density of the plasma, and implying a direct influence on trophic and
metabolic processes. Under these influences the congestion of the
encephalic circulation, and notably of the rete mirabile, and a serous
effusion, tend first to prostrate the nerve force, and second to render
the other intracranial structures anæmic.
 The direct action of a narcotic poison, leucocytic or microbian,
though as yet a hypothesis merely, has much in its favor, on
considerations drawn from the observed immunity in particular
buildings, the sudden prostration, the promptitude of certain
recoveries and the favorable results of the iodine mammary
injections. The presence of sugar in the urine, most abundantly in
the worst cases, implies a profound disorder in glycogenic centres
(medulla, liver), and primarily no doubt in the bulb.
Lesions. These are exceedingly variable in successive cases.
Congestion and effusion in the meninges, cerebral or spinal, in the
rete mirabile and choroid plexus have been often noticed, and
exceptionally clots of extravasated blood. In certain cases congestion
and pink discoloration of portions of the brain substance (cerebral
convolutions, bulb, ganglia) with marked puncta vasculosa, are
found, while in others the greater part or the whole of the
encephalon is anæmic. The puncta in such cases, large and dark, on
the surface of the section, promptly enlarge until they may form
distinct drops.
In the lungs areas of collapse, and of dark red congestion and
infiltration are common, mostly as the result of the entrance of
alimentary or medicinal matters into the bronchia owing to palsy of
the pharynx. Such materials can be found in the bronchial tubes.
The third stomach and the large intestine may be impacted, the
contents more or less baked and glossy on the surface, and
coincident congestions of the mucosa are not uncommon. In some
instances, however, the contents are soft and pultaceous and the
absence of mucous congestions is remarkable.
The womb rarely shows characters differing from the condition
which is normal to the first few days after parturition.
The blackness and thickness of the blood has been noted by
practically all observers. This is partly the result of its density, but
doubtless also of the undetermined toxins which are operative in the
disease.
Yellowish gelatinoid exudates have been found in the subdorsal
and sublumbar regions, as well as the cranium and spinal canal.
Glucose appears to be constantly present in the urine, and in
excess in the more violent and fatal cases: from 1.19 grm. per litre in
slight cases to 41.8 grms. in a fatal one (Nocard). Albumen may be
present, though probably only when local inflammation has
supervened.
Symptoms. The conditions of the attack should be noted. This is a
disease of the first six days after parturition, rarely seen in the
second week, and never after the fourteenth day. It is very
exceptional before parturition, yet Müller quotes 47 cases in 1107
births. The breed, condition, milking qualities, plethora, feeding,
etc., of the patient are, as already noted important data in diagnosis.
The onset is sudden without premonitory symptoms.
Two very distinct types are met with, the comatose and violent or
spasmodic, which, however, merge into each other by insensible
gradations, and may follow each other.
From twelve to seventy hours after an easy parturition there
suddenly appear signs of discomfort. Feeding and rumination cease,
the calf is neglected, there may be plaintive moaning, the eyes seem
dull and clouded, the eyelids drooped, the conjunctiva red, the pulse
normal for parturition, sometimes extra strong, the breathing excited
often with moans or grunts. The senses are dulled, the walk is
unsteady, the feet being abducted and planted like clumps, or the
legs sway, perhaps cross each other, remain semi-bent, and soon give
way leaving the animal prostrate, resting on the sternum and
abdomen, or later on the ribs, with head extended. Attempts may
still be made to rise, but this is rarely accomplished unless when
improvement sets in. This is the condition in which the patient is
usually found, being the first to be noticed by the owner. The bowels
are torpid, the urine retained in the bladder, and the animal may
remain thus in a drowsy condition, without changing from the
sterno-ventral decubitus, or dropping the head on the ground until
improvement sets in. The head rests on the shoulder or upper flank.
If held outward or forward the upper border of the neck has an S
shaped outline.
More commonly the somnolence increases, passing into a
complete torpor and insensibility, the eye may be touched without
causing winking, pricking or other injury causes no further response,
the patient turns upon its side, with its head extended on the ground.
She may lie in this condition with no sign of vital activity save
pulsation and breathing, and the latter is liable to be slow and
stertorous by reason of the paralysis of soft palate and larynx. The
jugulars usually show a venous pulse. Fermentations in the inactive
paunch cause the evolution of gas with tympany, which still further
obstructs the breathing, and reacts injuriously on the nerve centres.
The normal eructations from the rumen may continue, with liquids
and floating solids, and in the paralytic state of the throat these too
often pass in part into the bronchia, causing septic bronchitis and
pneumonia. The same is liable to follow the administration of
liquids, the irritant drugs passing into the larynx, trachea and lungs.
The pulse becomes soft, small and finally almost imperceptible. It
may be 50, 60 and upward.
In favorable cases, defecation may still occur, or the rectum once
emptied may fill again through the continuance of peristalsis, the
milk continues to be secreted, and in one to four days, spontaneous
defecation and micturition may be resumed, and the patient may get
on its limbs and commence feeding. There is usually at first a little
weakness of the limbs, but this is transient and health is restored in a
very short time. The suddenness of the improvement is often as
marked as of the attack. The patient is left prostrate and insensible,
without giving any response when the eyeball is touched and in two
or three hours it is found on its feet, eating, with eyes bright and
clear.
Some patients, however, are restored to ordinary sensation,
intelligence and appetite, while the hind limbs remain paralytic, or
paretic, and the station and gait both weak and uncertain for days or
even weeks. In such cases there have been presumably structural
changes in the nerve centres, which require time for repair.
In fatal cases, death may occur quietly from apoplexy, cerebral
compression, or narcotism, or it may be preceded by a period of
marked excitement or disorderly muscular movements. Lifting of the
head, throwing it alternately on the shoulder and on the ground,
trembling of head, members and body, cramps or jerking of the
limbs or of other parts, drawing the hind limbs up against the
abdomen, and again extending them, rolling of the eyes, loud, noisy,
irregular, embarrassed breathing and a running down pulse are often
marked features.
The temperature range is peculiar. At the start there may be some
hyperthermia 103° or 104°; with the advance of the disease it tends
to become lower, 98°, 96°, or 94°. When improvement sets in, it rises
again promptly to the normal.
Cadeac describes a special form which is ushered in by great
restlessness, bellowing, throwing the head to right and left, grinding
the teeth, sucking the tongue, salivation, licking of certain parts of
the body, spasms in the neck, back or limbs, and prompt recovery, or
lapse into the comatose condition as above described. It proved less
fatal than the ordinary comatose type, but seems to depend on
similar conditions.
Prognosis. Mortality. The disease is very deadly, the mortality in
time past having reached 40, 50 or even 60 per cent., the gravity
increasing as the disease set in nearer to parturition. Cases occurring
on the first or second day were mostly fatal, those at the end of the
first week were hopeful, and those occurring during the second week
were very hopeful. With the Schmidt (iodine) treatment the mortality
is claimed to be reduced to 16 or 17 per cent.
Prevention. Measures directed toward the lessening of plethora
tend to remove one of the most fruitful causes of the disease and
though not invariably successful, are yet of great value. The most
direct is the abstraction of blood in the last fortnight of pregnancy, to
the extent of 6 or 8 quarts. This tends to secure a lessening of the
blood tension, and blood density, but there is the drawback of a
created tendency to a subsequent increase in blood formation to
make up the loss. This measure should be reserved for cows that are
very plethoric, extra heavy milkers and such as have already suffered
from the disease.
Purgatives will measurably secure the same end without the same
degree of danger. One to two pounds of Epsom or Glauber salts in
the last week of gestation, or at latest when labor pains set in, tend
not only to remove solid or impacted masses from the first and third
stomachs, and inspissated contents from the large intestines, but to
secure a free depletion from the portal system. If not before, this
should always be given immediately after parturition to cows in extra
high condition, heavy milkers, and that have had a short and easy
delivery.
Restriction of food for a week before and as long after parturition
is of equal importance. A very limited supply of aqueous, easily
digested, and laxative food (roots, sloppy bran mashes, fresh grass,
ensilage) will meet the demand.
Exercise in the open air is of great value in giving tone to the
muscles, and especially the nervous system, and in stimulating the
emunctories and other functions.
In the cold season protection against cold draughts and chills
must be seen to, and in the hot season the avoidance of an excess of
solar heat and above all of the confined impure air of the barns.
At midsummer and later, there is often great danger in the rich
clover and alfalfa pasture, or soiling crop, with which the cow will
dangerously load her stomach, and the only safe course is to remove
predisposed animals and shut them up in a bare yard or box-stall.
Under such simple precautions herds that had formerly suffered
severely, have had the disease virtually put a stop to.
In individual cases other measures are indicated. When the udder
has reached an enormous size and development, and is gorged with
milk, days before parturition, it should be systematically milked. The
irritation in the gorged gland is quite as likely to induce premature
parturition, as is milking, and, at the worst, the result is not so bad as
an attack of parturition fever.
Basing his advice on the fact that parturition fever does not follow
a case of severe dystokia, Cagny applies sinapisms on the loins, croup
and thighs of a fleshy, plethoric, heavy milking, parturient cow. Proof
of their efficacy is not obtainable.
Félizet advises leaving the calf with its dam for one week. Kohne
doses the cow with nux vomica: Harms, with tartar emetic.
In view of the probability of a bacterial infection the cow should be
taken to a clean, pure, well-aired stable a day or two before calving,
having been first cleansed from adherent filth, and sponged all over
with a 4 per cent. solution of carbolic acid.
To prevent diffusion of infection Bournay recommends antiseptic
injection of the womb immediately after calving. Bissauge adds that
the stable should be disinfected after every case of parturition fever,
the manure carefully removed and the ground scraped and well
watered with a disinfectant.
For fleshy, plethoric, predisposed cows, the iodine injection of the
udder should be applied immediately after calving. A measure of this
kind which is so successful as a curative agent, and which brings
such circumstantial evidence of the production of a poison
(leucomaine or ptomaine) in the mammary gland, can hardly fail to
be even more effective as a prophylactic than as a therapeutic resort.
Treatment. With the state of plethora and congestion about the
head in the early stages the question of bleeding at once arises. If
early enough while there is a full bounding pulse, and as yet no sign
of great loss of muscular control it is often very beneficial, as much as
6 quarts or more being withdrawn. It is well however to avoid
cording the neck, which must increase the vascular tension in the
brain, and to trust rather to digital compression of the vein. The
blood should be drawn from a large opening in a full free stream, and
may be stopped when the pulse softens. In the more advanced
condition, with paralysis and more or less dulling of the senses, or
coma, bleeding may be dangerous rather than useful. There is then
serious pressure on the brain, with serous effusion, and perhaps
blood extravasation, and in any case anæmia, and this latter may be
dangerously or even fatally increased by the lessening of the blood
pressure, without any compensating advantage in the way of
reabsorption of the effusion. In such cases eliminating agents are a
safer resort.
Purgatives commend themselves, but with the drawback of a too
tardy action. Now however with the peristaltic stimulants given
hypodermically this objection is largely obviated. Pilocarpin 1½ gr.,
and eserine 3 grs. will often secure a noticeable movement of the
bowels in the course of fifteen minutes, implying a corresponding
motion onward in the bowels more anteriorly, and even of the
contents of the gastric cavities. If there is already palsy of the
muscles of deglutition, this may be repeated several times at
intervals of four or five hours. If however deglutition is still well
performed a purgative of one or two pounds Epsom salts, with 10
drops croton oil, and 1 oz. oil of turpentine may be given by the
mouth. Should this operate, it will supplement and carry on even
more effectively the work of the hypodermic agents, and even lessen
the density, plasticity and tension of the blood and act as a potent
derivative from the brain.
A compromise may be made by giving aloes 2 ozs., croton oil 20
drops in bolus; or 1 to 2 ozs. sulphate of soda in solution may be
injected subcutem.
In any case oil of turpentine or other antiseptic is of great value in
the stomach in preventing fermentation and tympany, and thereby
obviating a whole series of troubles such as: cerebral disturbance by
nervous shock and blood pressure; impaired respiration and
hæmatosis by pressure on the diaphragm; and eructations of food to
the pharynx and its inhalation or gravitation into the lungs.
It is always well to clear out the rectum by injections, when if there
is any indication of pharyngeal paralysis most of the remedies may
be given by this channel.
Stimulants (ammonia carbonate, alcohol, anise, fennel, ether, nux,
etc.) have been largely employed by the mouth and may be by the
rectum. In the absence of spasms I have relied largely on nux or
strychnia.
When the skin chills, some have sought to heat it by enveloping the
posterior half of the body in cotton or wool soaked in turpentine, by
applying sinapisms, or by moving over the surface a warming-pan
containing red hot charcoal.
More generally cold in the shape of cold water, ice or snow has
been applied to the cranium and spine. Theoretically the anæmic
brain might be thought to forbid this, but clinically it often operates
well, possibly by inducing a sympathetic contraction of the vessels in
and around the nerve centres and thus indirectly favoring the
resumption of active circulation and the reabsorption of effusions.
An elevated position of the head is no less important. It favors the
return of blood from the brain by gravitation, and in this way
improves the intracranial circulation, and the resumption of normal
function. A halter, or a rope around the horns, may be tied to a beam
overhead, or the head may be laid on thick bundles of straw which
will keep it up to or above the level of the chest, and in this way not
only is gravitation ensured, but the brain is protected against the
violent blows and concussions, which come from dashing the head
on the ground.
Frequent rubbing of the udder and drawing of the milk, is an
excellent means of depletion, a removal of a source of irritation, and
presumably an extraction of part of the offending poison. It should
never be neglected. But of all known methods of treatment the iodine
injection furnishes the greatest hope of success.
Injection of the mammæ with Iodine. Iodide of potassium 100
grains (200 grs. in the case of a very large udder) are dissolved in a
quart of water which has been boiled for 15 minutes, the solution
cooled to 104° F. and injected in equal parts into the four quarters,
which have been just milked out clean. The glands are then
manipulated so as to work the solution into all the recesses of the
milk tubes and follicles. If the patient does not get on its legs at the
end of twelve hours, the glands may be milked out and injected
anew. In nearly 2000 cases the recoveries reached an average of
nearly 83 per cent. In serious or advanced cases with structural
changes of a grave nature, a good result cannot be hoped for. The
injection does not forbid the concurrent use of other approved
measures.
The injection is easily made with a caoutchouc tube of five feet
long fitted to a teat tube at one end and to a funnel at the other. The
tube is inserted in the teat, and the funnel at a height of five feet
receives the liquid, which readily passes into the teat. When ready to
pass the tube from one teat to another, an assistant pinches the
caoutchouc tube just below the funnel, until the insertion has been
made. Every precaution must be taken against sepsis. The udder,
teats and hands, must be washed with soap, and treated with a 3 per
cent. solution of lysol. The teat tube and funnel are boiled. The
caoutchouc tube is washed and irrigated with a solution of mercuric
chloride (1:1000), and then with one of boric acid (3:100).
 DISEASES OF THE EYE.
DESIRABLE FEATURES IN THE EYE.

The eye in the physiognomy. Broad forehead. Full eyes. Both eyes alike. Iris
smooth, lustrous. Media translucent. Pupil sensitive to light. Convexity median,
uniform. Pupil black in ordinary light. Lids open and mobile. Sclera light pink.
Tears clear, limpid without overflow. Lids thin, delicate, margins evenly curved.
Whole eye responsive to moving objects. Defects: small eye: semi-closed, thick,
sluggish lids; convex cornea: sunken eye: projecting eye: weeping eye: blear eye:
watch eye: irresponsive iris: dilated pupil: unequal eyes: flat cornea; ovoid cornea.

Much of the expression of the face depends upon the eyes, and in
animals as in man it is difficult to find compensations for a
forbidding countenance. Perfect, sound, intelligent eyes are always
pleasing; imperfect, defective, sunken or lifeless eyes mar the whole
expression. The following points may be specially noted:
1st. Ample breadth between the orbits. This is of great
importance in the horse, in which we seek for intelligence, courage
and indomitable energy. This confirmation does not indicate the size
of brain, as the cranium is situated higher up, but by placing the eyes
well outward, it indicates a wider range of vision, and usually implies
large, clear eyes, and since interdependent parts tend to correspond
in development and quality, this commanding vision bespeaks a
large, active brain, intelligence, docility and activity.
2d. Full, prominent eyes. This may be excessive, either through
primary conformation or disease. Abnormal convexity of the cornea
implies myopia. But within normal limits the prominent eye suggests
good health, condition and vigor, with ample cushions of fat under
the bulb and a sound, well-developed condition of the eyeball and its
muscles.
 3d. Both eyes equal in all respects. Any variation in size,
shape, color, fullness, clearness or in any other respect is at best
unsightly, and implies not only defect but often disease as well.
4th. The iris should be lustrous, uniform in color and
even in surface. Whether dark brown as in the horse, or yellow as
in the dog, it should be brilliant. Any part that lacks lustre, being
lighter brown, or yellow and dull like a dead leaf, usually indicates
previous disease and a tendency to further trouble. Albinos and those
in which the pigment is congenitally absent in patches must be
considered as exceptions, yet, even in them, the peculiarity cannot be
held to add to the beauty.
5th. All the Media (Cornea, aqueous humor, lens and
vitreous) must be perfectly clear and translucent. The
slightest cloudiness or opacity in any of these is a serious blemish
and usually indicates disease, past or present.
6th. The pupil should promptly and freely respond to light
and darkness by contraction and expansion. Absence or
tardiness of movement indicates impaired vision, from disease of the
eye, its nerves, or their nerve centres.
7th. Each cornea should have a median convexity,
uniform in all directions implying the absence of myopia,
preshyopia and astigmatism. Any deviation from this will
interfere with the perfection of sight, and endanger shying and other
troubles.
8th. Under ordinary light the pupil should appear black
throughout. In the larger animals such dilation of the pupil as to
expose the tapetum lucidum under such circumstances implies
impaired vision (amblyopia, amaurosis), inflammation of the iris or
undue intraocular pressure. A white color or spot shows cataract.
9th. The lids must be open and mobile without excessive
dilation. Tardily moving or semi-closed lids, distorted by scar or
angle, everted or inverted, are unattractive and usually imply disease
in the eye, nerves or brain.
10th. The unpigmented portion of the sclera should be
light pink. The dark red of congestion and the pallor of anæmia are
equally objectionable.
 11th. The tears must be clear, limpid and confined within
the lower lid. Any milkiness, flocculency or overflow is indicative
of disease.
12th. The eyelids must be thin, delicate, evenly and
uniformly curved along the borders, and fringed by an
abundance of strong, prominent and well directed lashes.
Puffiness or swelling betrays inflammation, dropsy, anæmia,
parasitism or other disorder, angularity of the upper lid an internal
ophthalmia, and depilation or wrong direction of the lashes, local
disease.
13th. The eye should respond instantly, by movement, to
new objects and noises, without showing undue irritability
or restlessness. The intelligent apprehension of the objects will
introduce an aspect of calmness and docility.
DEFECTS, BLEMISHES AND ABNORMALITIES OF
THE HORSE’S EYE.

Some of these may be present in the absence of actual disease, and

yet prove so objectionable that they disqualify the animal for any use,
in which style or æsthetic appearance is demanded. Among such
sources of disqualification may be noted:
1st. The small eye. One or both eyes may appear small because of
internal pain and retraction within their sockets, or from actual
atrophy or contraction of the eyeball, the result of deep seated
disease, or the organ may be congenitally small, and deep seated in
the orbit, and the thick tardy eyelids may have a narrow opening
through which they can only be partially seen. This last condition
usually implies a dull lymphatic constitution, low breeding and a lack
of intelligence, docility and vigor.
2d. The semi-closed eye with thick, coarse, sluggish lids.
In this case the bulb may be not unduly small, yet as it is not freely
exposed it conveys the same general expression to the observer. Like
the small eye it indicates low breeding, lack of intelligence or docility
and often stubbornness or even vice.
3d. The convex eye. In this the transparent cornea describes the
arc of an unduly small circle, suggesting a conical form and
projecting unduly beyond the margins of the lids. It implies
imperfect vision, myopia, and, it is alleged, low breeding and lack of
alertness.
4th. The sunken eye. This has been already referred to under
the small eye. The eyelids are usually flaccid, the upper being
drawn in by its levator so as to form an angle, and the edges of the
orbit are somewhat prominent. It is seen in old, worn out animals,
which have lost the pads of fat in the depth of the orbit, and more
commonly in animals that have suffered several attacks of recurrent
ophthalmia.
5th. The projecting eye. In this case the lids are unduly
contracted and the eye protrudes between them so as to show a large
amount of sclerotic around the transparent cornea. This may be due
to nervous strain and suffering but, however produced it is decidedly
unsightly and objectionable.
6th. The weeping eye. This is always a condition of disease. It
may be due to irritant gases, or solid particles, to inturned cilia,
everted lids, conjunctivitis or a variety of other conditions. A careful
examination may show whether it is only a transient and remediable
fault of a good eye or a permanent and irremediable defect.
7th. The blear eye. With swelling and scabbing of the edges of
the lids and Meibomian glands, and congestion of the adjacent
conjunctiva, there is usually some blurring of the surface of the
transparent cornea. The trouble is mostly chronic and constitutes a
serious objection.
8th. The watch eye. In this, as in the albino, there is a lack of
pigment, so that the iris and sclerotic are white or bluish white in
part or in whole. Such an eye may be good and durable, but not
beautiful nor attractive.
9th. Blindness of one or both eyes. In all such cases the pupil
remains fixed and immovable, showing no accommodation to light
and darkness, and there is a lack of prompt responsiveness on the
part of the eye to sounds and objects. In amaurosis, glaucoma and
cataract especially, the pupil remains widely open, and alert
movements of the ears are employed to make up for the lack of sight.
The condition often comes from internal ophthalmia, such as the
recurrent form, and is associated with atrophy of the bulb.
10th. Eyes of unequal size. This usually implies serious disease
in one, not infrequently recurring ophthalmia.
11th. Too flat corneal surface. In this case there is a manifest
lack of the normal projection, the anterior surface of the cornea
describing the arc of a larger circle, the visual rays coming from a
distance alone converge on the retina and presbyopia occurs. In this
as in myopia and other visual imperfections a horse is liable to
stumble and, if nervous, to shy.
 12th. Ovoid Cornea. In such cases the front of the transparent
cornea has an ovoid outline the arc formed by it in one direction
being that of a greater circle, than the arc which crosses this at right
angles. In consequence of this, the rays impinging on the outer
portions of these respective arcs do not converge to the same point
on the retina and a blurred and imperfect image results. This
astigmatism causes the subject to stumble and, if nervous, to shy.
 SYSTEMATIC INSPECTION OF THE EYE.

System in Examination. Eyelids: cilia: lachryneal puncta: mucosa, light pink,

brick red, yellow, puffy, dropsical: Ciliary vessels deep, immovable; nictitans;
transparent cornea equally smooth, glossy, with clear image at all points: foreign
body on cornea: corneal ulcer: opacities in aqueous humor: iris and pupil: corpora
nigra: changes in passing from darkness to light: pupillary membrane: adhesions
of iris: intraocular pressure: contracted pupil: hole in iris. Oblique focal
illumination of cornea, aqueous humor, iris, lens, Purkinje-Sanson images.

In examining animals for soundness and especially the horse or

dog, the condition of the eye must be made one of the most
important subjects of inquiry, as a disease or defect may render the
animal altogether unsuited to the object to which it is destined. As in
every other field of diagnosis thoroughness is largely dependent on
the adoption of a system which will stand in the way of any flaw
being too hastily overlooked. Many of the points to be noted will be
decided at a glance, yet this does not obviate the necessity of turning
over in the mind, in succession, the different points of inquiry, and
directing the necessary attention, however hastily, to each in turn.
The following points should be observed:
1st. Are the eyelids swollen, hypertrophied or faulty in
form, position or movements. Faults as thus indicated may
imply any one of a great variety of disorders which should be
followed out to their accurate diagnosis. It may be bruises,
lacerations, punctures, parasites, conjunctivitis, keratitis, dropsy,
anæmia, hepatic or intestinal parasitism, nephritis, paresis,
entropion, ectropion, etc.
2d. Inspect the cilia as regards form, size and direction.
Absence or wrong direction may imply disease of the Meibomian
glands, infective inflammation, demodex or other acarian infesting,
or turning in or out in inflammatory conditions.
 3d. See that the lachrymal puncta are open and that there
is no overdistension of the sac. The overflow of tears and the
swelling of the caruncle and of the area beneath it will often indicate
such trouble. In its turn it may imply inflammation of the duct, and
obstruction by the tenacious muco-purulent product, or it may imply
merely obstruction of its lower end by a dried scab. This last may be
seen in the horse, on the floor of the false nostril at the line of
junction of the skin and mucosa, and in the ass, higher up on the
inner side of the ala nasi. In exceptional cases it may be desirable to
pass a stilet through the canal from the puncta downward or from
below upward to determine whether it is pervious.
4th. Determine the vascularity of the conjunctiva. When
free from pigment as it habitually is in pigs and birds this is easily
done, while in animals like the horse, in which the bulbar portion,
which covers the sclerotic, is largely pigmented, we can scrutinize
only the pigment free parts. In health there should be only a few,
fine, pink vessels which move with the mucosa when pressed aside
on the bulb. In congestion the surface may appear brick red, and
the vessels are irregular, large, tortuous and are seen to anastomose
at frequent intervals. These move on the bulb when pressed. The
congestion is usually deepest on the palpebral mucosa and in the cul
de sac, and may be whitened for an instant by pressure through the
eyelid. To expose the conjunctiva the right fore finger and thumb
may be pressed on the upper and lower lids respectively of the left
eye, and the left finger and thumb for the right, allowing them to
slide backward above and below the eyeball. Another method is to
seize the cilia and edge of the upper eyelid between the finger and
thumb, and draw it downward and outward from the bulb, and then
deftly invert it over the tip of the finger. In the old the unpigmented
conjunctiva may appear yellow from the presence of subconjunctival
fat, or this may appear at any age from hepatic disease (distomatosis)
or icterus. It is swollen, or dropsical in anæmia, distomatosis, etc.
5th. Examine the ciliary vessels whether they are
congested or not. These are distinguished from the conjunctival
vessels in that they radiate in straight lines outward from the margin
of the transparent cornea and do not move on the sclerotic under
pressure. They are enlarged and very red in congestion of the ciliary
circle and in iritis. In eyes devoid of pigment over the sclerotic, there