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 -
UlrichWernery Oskar-Ruger Kaaden
VetBooks.ir
VetBooks.ir

,,Dedicated to thefond memoy of

Lt. Gen. Hamoodah Bin Ali,
from Central Veterinay Research Laboratoy/
Priv.-Doz. Dr. Dr. habil. Ulrich Werney"
VetBooks.ir

UIrich We rnery
Oskar-Ruger Kaaden

Infectious Diseases
in Camelids
2nd, revised and enlarged edition

With 179 figures and 62 tables

Blackwell Science Berlin Vienna 2002

-
Boston . Copenhagen * Edinburgh . London Melbourne Oxford .Tokyo
 Blackwell Wissenschafts-Verlag GmbH Blackwell Science KK
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Blackwell Science, Inc. With contributions by:
Commerce Place, 350 Main Street Jorg Kinne
Malden, Massachusetts 02148 5018, USA Central Veterinary Research Laboratory
Dubai, United Arab Emirates
Editors' addresses: Set Bornstein
Ulrich Wemery, Dr. Dr. med. vet. habil. National Veterinary Institute
Central Veterinary Research Laboratory Uppsala, Sweden
P.O. Box 597, Dubai,
United Arab Emirates Whilst every effort has been made to ensure the
accuracy of the contents at the time of going to
Oskar-Riiger Kaaden, Prof. Dr. med. vet. press, neither the Authors nor the Publishers
Institute for Medical Microbiology give any guarantee whatsoever as to the accura-
Infectious & Epidemic Diseases cy of the information contained herein and ac-
Munich University cept no liability whatsoever in respect of any
Veterinarstr. 13,80539 Munich, Germany loss, damage, injury or expense arising from
any such error or omission in the contents of
Proofreading and translation assistance: this work.
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tions etc. mentioned in this book are not exempt
Front cover: from the laws regulating the protection of trade
His Highness General Sheikh Mohammed Bin marks. Such names cannot be used by anyone
Rashid A1 Maktoum, Defense Minister of the without specific acknowledgement.
United Arab Emirates, with his best racing cam- This work is subject to copyright. All rights
els are reserved, whether the whole or part of the
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Infectiousdiseases in camelids / Ulrich Wern- films or in other ways, and storage in data banks.
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 Foreword . ..*,
VetBooks.ir

The first edition of Infectious Diseases of An important addition is the new chap-
Camelids was a sigruficant contribution to ter on parasites. Information on many of
the scientific literature of camel medicine. these parasitic diseases is now in concise,
Clinicians, scientists,pathologists and cam- usable form.
el owners all over the world used the book. It is significant that superbly skilled sci-
The information was current, reflecting the entists have been given an opportunity to
extensive experience obtained at the Cen- investigate and conduct research on camel
tral Veterinary Research Laboratory (CVRL) diseases in the United Arab Emirates. His
and from world literature. The CVRL is Highness General Sheikh Mohammed Bin
one of the premier diagnostic laboratories Rashid A1 Maktoum deserves the thanks of
in the world, with the staff devoting their camel owners all over the world for having
efforts towards the diagnosis of disease in the foresight to establish the Central Vet-
camels, horses and falcons in the Middle erinary Research Laboratory. Following
East. The CVRL has a professional staff more than a decade of investigation and
of microbiologists,pathologists, molecular collection of data on camelid diseases,
biologists and parasitologists working to- the CVRL accumulated the expertise and
gether to further the scientific knowledge knowledge to publish this book. His High-
necessary for the proper husbandry of ness' continued support of ongoing inves-
camels. tigations on camel health is a reflection of
The authors are pre-eminently qualified his intense interest and support of the ath-
to write on this subject, having devoted letic camel. Camel owners, trainers, veteri-
much time, effort and expertise to study- narians and scientists from many disci-
ing camel infectious and parasitic diseases. plines are deeply.appreciativeof His High-
The second edition continues the excel- ness' benevolence.
lence of the first edition and adds signifi- The second edition has been completely
cantly more information. The etiology of updated, particularlyin the areas of pathol-
heretofore-questionablediagnoses has been ogy, parasitology and mycology. The book
clarified. More specific diagnostic proce- is divided into bacterial, viral, fungal and
dures have been studied for sensitivityand parasitic diseases, with each chapter con-
specificity in camels. taining information on etiology, epidemi-
Two new contributing authors have ology, clinical signs, pathology, diagnosis,
been invited to expand the areas of diag- treatment and prevention. Treatment and
nostic pathology (Dr. J. Kinne) and para- control has been given special emphasis in
sitology (Dr. s. Bornstein). Publications this second edition.
dealing with the details of camel pathol- Congratulations to the authors for their
ogy are few and with this edition a valu- dedication and willingness to share their
able service has been rendered to diag- experiences with colleagues around the
nosticians and camel owners all over the world.
world. The husbandry of camels will be
improved as a result of more basic knowl- Murray E. Fowler, DVM
edge about diseases and disease processes Professor Emeritus, Zoological Medicine
in camels. University of California, Davis, USA
VetBooks.ir

After working for a short period of time volume of milk with excellent nutritional
with dromedaries in Somalia some years value in areas of the world where the tra-
ago, I now have the privilege of dedicating ditional milk animals, the cow, the sheep
much of my time to this animal species in and the goat, have difficulty surviving, not
an optimal environment. The Central Vet- to speak of producing milk. It is therefore
erinary Research Laboratory in Dubai was inconceivablethat such a favorable animal
founded in 1985 and one of the major tasks species is so seldom used as a farm animal.
of this institute was research on infectious Many people still believe that the camel is
diseases of camelids. Before 1970, very lit- of low economic value and is synonymous
tle was known about infectious diseases with underdevelopment.
of camels. However, during the last two Only recently has the camel family been
decades there has been a tremendous in- considered to aid man in many different
crease in the number of scientific papers respects. Understanding and utilizing this
in the world literature. It is now known special gft could lead to the development
that infectious diseases cause 50"/0 of fatal- of camel farms in famine areas and a re-
ities in New World camelids and 65% in duction in human starvation.
Old World camelids. Pneumonia, peritoni- This book is written as a gesture of ap-
tis and diseases of the intestinal tract are preciation from four European camel re-
the main ailments in NWC, whereas infec- searchersfor all that this animal family has
tious diseases of the alimentary tract are meant to us.
the main causes of fatalities in OWC.
Most species of the camel family are do- Autumn 2001 U. Wernery, Dubai
mesticated and are used as beasts of bur- 0.-R. Kaaden, Munich
den, as "ships of the desert", and provide J. Kinne, Dubai
man with high quality fiber, meat and S. Bornstein, Uppsala
milk. OWC can produce a considerable
 Acknowledgements
nil,.’
VetBooks.ir

The authors are deeply indebted to His made it possible for this laboratory to dis-
Highness General Sheikh Mohammed Bin cover new facts regarding camel diseases.
Rashid A1 Maktoum, Minister of Defense The authors are particularly grateful to
of the United Arab Emirates, whose gen- Mrs. S. Robinson, Mr. R. Babu and Mr.
erosity helped realize the publication of N. Chaudhry for their care and patience in
the second edition of this book. typing the manuscript and to Mr. D. Wer-
Sincere thanks are given to the owners nery who introduced me to the world of
of the Bin Hamoodah Group of Companies computers and who had the painstaking
for their generous contribution to financ- job of typing most of the tables.
ing the publication of the second edition of Many thanks go to the staff of the Cam-
this book and their interest in safeguarding el Reproduction Laboratory in Nakhlee,
camel breeding and racing traditions in the Dr. J. A. Skidmore and Mr. M. Billah, for
UAE. their support and to Dr. B. N. Kumar, who
The authors gratefully acknowledge the works for the Bin Hamoodah Group of
cooperation, help and advice from Dr. Ali Companies.
Ridha, the Administrative Director of the Many other people supported and helped
Central Veterinary Research Laboratory. us with this project, but we owe a particular
Dr. Ridha has taken a keen and critical in- debt of gratitude to Dr. E. Zabegina from
terest in all of the authors’ scientific work Moscow and Dr. Zhao Xing-Xu from Chi-
and has been our mentor during many na, who introduced us to many excellent
years in a new culture. camel scientists in the former Soviet Union
Very special efforts have been contrib- and China. We are also extremely grateful
uted by the CVR Laboratory staff in Dubai: to Prof. M. E. Fowler from the USA, Prof.
Dr. J. Sasse, Mrs. R. Wernery, Mr. 0.Mathai, R. Gothe and Prof. M. Rommel from Ger-
Mrs. R. Zachariah, Mrs. S. Joseph, Mrs. many for their valuable contributions.
S. Korah, Mrs. L. George, Mr. Y. Abubakr, Finally, I must thank my family, espe-
Mr. A. K. Nizarudeen, Mr. F. Joseph, Mr. cially my wife Renate, for her invaluable
A. Ali, Mr. Y. Ali, Mr. A. Siddique and Mr. assistance and advice as well as for her un-
N. Muthuvattil without whose help we derstanding of my absence from many so-
could never have completed this work. cial events.
With great enthusiasm and invaluable Last, but not least, the authors are par-
assistance, they helped to introduce new ticularly thankful to the publisher, espe-
laboratory techniques and cared for our cially to Dr. A. Miiller from Blackwell Wis-
experimental animals. senschafts-Verlag for his continuing sup-
We warmly thank the veterinarians and port and the excellent design of the second
nutritionist who work for the ruling fami- edition of this book.
ly of Dubai, Dr.A. M. Billah, Dr. J. Akbar,
Dr. A. U1-Haq, Dr. G. Munawar, Dr.M. Ali, U. Wernery
Dr. A. Ali, Dr. H. Tesfamariam and Mr. 0.-R. Kaaden
J. Wensvoort, for their support. Their contri- J. Kinne
butions and submission of specimens have S. Bornstein
VetBooks.ir

Foreword ....................... V 1.7 Nervous System . . . . . . . . . . 155

1.7.1 Tetanus .................. 155
Preface .........................
VI1 1.7.2 Listeriosis ................ 157
Acknowledgements .............. IX
Abbreviations . . . . . . . . . . . . . . . . . . .XIII 2 Viral Diseases ............ 161
Introduction .................... 1 2-1 Viral Infections Causing
Disease .................. 168
1 Bacterial Diseases . . . . . . . . . 19 2.1.1 Rabies ...................168
2.1.2 Borna Disease ............. 174
1.1 Generalsurvey ........... 21
1.1.1 Anaerobic Infections ....... 21 2.1.3 Camelpox ................ 176
1.1.2 Botulism . . . . . . . . . . . . . . . . . 31 2.1.4 Contagious Ecthyma ...... 187
1.1.3 Anthrax .................. 33 2.1.5 Papillomatosis ............ 192
2.1.6 Influenza ................. 195
1.1.4 Endotoxicosis (Endotoxemia) 36
2.1.7 Neonatal Diarrhea ......... 198
1.1.5 Pasteurellosis ............. 49
2.1.8 Equine Herpesvirus . . . . . . . . 206
1.1.6 Camel Plague ............. 54
1.1.7 Leptospirosis . . . . . . . . . . . . . 55 2.2 Nonpathogenic Viral
1.1.8 Rickettsial Diseases ........ 59 Infections . . . . . . . . . . . . . . . . 209
1.1.9 Rhodococcus equi 2.2.1 Respiratory Viruses . . . . . . . . 209
in New World Camelids .... 65 2.2.2 African Horse Sickness ..... 212
1.2 Digestive System ......... 73 2.2.3 Bluetongue .............. 214
1.2.1 Salmonellosis . . . . . . . . . . . . . 73 2.2.4 Retrovirus Infection ........ 217
1.2.2 Colibacillosis ............. 78 2.2.5 Foot-and-mouth Disease .... 219
1.2.3 Paratuberculosis 2.2.6 Vesicular Stomatitis ........ 223
(Johne's Disease) . . . . . . . . . . 83 2.2.7 Bovine Virus Diarrhea ...... 224
2.2.8 Rift Valley Fever .......... 228
1.3 Respiratory System ....... 91 2.2.9 Rinderpest ............... 230
1.3.1 Tuberculosis .............. 91 2.2.10 Unusual Arboviruses ...... 234
1.3.2 Pneumonia . . . . . . . . . . . . . . . 97
1.4 Urogenital System ........ 109 3 Fungal Diseases .......... 237
1.4.1 Brucellosis . . . . . . . . . . . . . . .109 3.1 Mycotic Dermatitis ........ 240
1.4.2 Infections of the Uterus . . . . . 116 3.2 Aspergillosis ............. 246
1.4.3 Chlamydiosis ............ 124 3.3 Candidiasis . . . . . . . . . . . . . . 249
1.4.4 Urinary Retention 3.4 Coccidioidomycosis ....... 254
in Young Dromedaries . . . . . 126 3.5 Mucormycosis ............ 256
1.5 Integument .............. 134 3.6 Miscellaneous Fungal
1.5.1 Pseudotuberculosis Infections ................ 257
(Caseous Lymphadenitis) ... 134
1.5.2 Staphylococcusaureus 4 Vaccination Programs ..... 261
dermatitis ................ 138
1.5.3 Dermatophilosis .......... 141 5 Parasitic Diseases ......... 267
1.6 Udder ................... 149 5.1 Protozoal Infections ....... 272
1.6.1 Infectious Mastitis ......... 149 5.1.1 Classification of Protozoa ... 272
 XI1 Table of Contents

5.1.2 Trypanosomosis . . . . . . . . . . . 273 5.3.4 Dictyocaulosis

5.1.3 Tritrichomonosis . . . . . . . . . . 282 (Lungworm Infection)
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5.1.4 Giardiosis . . . . . . . . . . . . . . . . 283 Parelaphostrongylosis

5.1.5 Balantidiosis . . . . . . . . . . . . . . 284 (Meningeal Worm Infection)
5.1.6 Tick-borne Diseases: Angiostrongylosis . . . . . . . . . 354
Babesiosis, Theileriosis . . . . . 286 5.3.5 Oesophagostomosis and
5.1.7 Coccidiosis . . . . . . . . . . . . . . . 287 Chabertiosis (Nodular
5.1.8 Cryptosporidiosis . . . . . . . . . 295 Worm Infection) . . . . . . . . . . . 356
5.1.9 Sarcocystiosis . . . . . . . . . . . . . 296 5.3.6 Bunostomosis
5.1.10 Besnoitiosis . . . . . . . . . . . . . . . 298 (Hookworm Infection) . . . . . 357
5.1.11 Toxoplasmosis . . . . . . . . . . . . 299 5.3.7 Strongyloidosis . . . . . . . . . . . 358
5.1.12 Neosporosis . . . . . . . . . . . . . . 302 5.3.8 Oxyuridosis
5.1.13 Hammondiosis . . . . . . . . . . . . 303 (Pinworm Infection) . . . . . . . 360
5.3.9 Trichuriosis
5.2 Infestations with (Whipworm Infection)
Ectoparasites . . . . . . . . . . . . . 312 Capillariosis . . . . . . . . . . . . . . 360
5.2.1 Classification of Arachnea . . 312 5.3.10 Gongylonemosis
5.2.2 Sarcoptic Mange . . . . . . . . . . 313 Parabronemosis
5.2.3 Psoroptic Mange . . . . . . . . . . 320 Thelaziosis . . . . . . . . . . . . . . . 361
5.2.4 Chorioptic Mange . . . . . . . . . 322 5.3.11 Onchocercidosis . . . . . . . . . . . 363
5.2.5 Demodectic Mange . . . . . . . . 322 5.3.12 Treatment of Nematode
5.2.6 Infestations with Infections . . . . . . . . . . . . . . . . 366
Metastigmata (Ticks) . . . . . . . 323
5.2.6.1 Ticks Found on Camelids . . . 324 5.4 Infection with Cestodes
5.2.6.2 Tick Paralysis . . . . . . . . . . . . . 329 (Tapeworms) . . . . . . . . . . . . . 369
5.2.6.3 Tick Control . . . . . . . . . . . . . . 330 5.4.1 Classification of Cestodes . . . 370
5.2.7 Insects Found 5.4.2 Tapeworm Infection . . . . . . . 370
on Camelids . . . . . . . . . . . . . . 331 5.4.2.1 Cestode Larvae in Internal
5.2.7.1 Classification of Insects . . . . . 331 Organs . . . . . . . . . . . . . . . . . . . 370
5.2.7.2 Infestation with Lice . . . . . . . 331 5.4.2.2 Cestode Larvae Found
5.2.7.3 Infestation with in Muscles . . . . . . . . . . . . . . . . 374
Siphonapterida (Fleas) . . . . . 333 5.4.2.3 Cestodes of the Intestine . . . . 376
5.2.7.4 Infestation with Flies . . . . . . . 333 5.5 Infection with Trematodes
5.2.7.5 Tabanidae Infestation (Flukes) . . . . . . . . . . . . . . . . . . 378
(Horse Flies) . . . . . . . . . . . . . . 341 5.5.1 Classification of
5.2.7.6 Ceratopogonidae Infestation Trematodes . . . . . . . . . . . . . . 378
(Midges) . . . . . . . . . . . . . . . . . 341 5.5.2 Trematode Infections . . . . . . . 378
5.2.8 Linguatula serrata Infection 5.5.2.1 Trematodes of the Liver . . . . 378
(Tongue Worm) . . . . . . . . . . . 342 5.5.2.2 Paramphistomatidae -
Rumen Flukes . . . . . . . . . . . . 385
5.3 Infection with Nematodes. . 347 5.5.2.3 Schistosomatidae . . . . . . . . . . 385
5.3.1 Classification of
Nematodes . . . . . . . . . . . . . . . 348 5.6 Infection with Hirudinea
5.3.2 Trichostrongylidosis (Leeches) . . . . . . . . . . . . . . . . 386
(Gastrointestinal Worm 5.6.1 Classification of Hirudinea . . 386
Infection) . . . . . . . . . . . . . . . . 348 5.6.2 Infection with Leeches . . . . . 386
5.3.3 Infections with
Molineidae . . . . . . . . . . . . . . . 353 Index . . . . . . . . . . . . . . . . . . . . . . . . . 389
 Abbreviations
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AGID Agar gel immunodiffusion test

CFT Complement fixation test
CVRL Central Veterinary Research Laboratory
ELISA Enzyme-linked immunosorbent assay
ELM1 Electron microscopy
FAT Fluorescent antibody test
NWC New World camelids
OWC Old World camelids
UAE United Arab Emirates
SNT Serum neutralizing antibody test
VetBooks.ir

Introduction
 Introduction 3

Camelids have served the needs of people bibliographies about the camel can be
for thousands of years and have provided found under Farid (1981), Mukasa-Muger-
VetBooks.ir

them with food, fiber and fuel. In many wa (1981), and Wilson et al. (1990).
parts of the world they have also served as Prior to 1987, approximately 1000 New
beasts of burden. They secured trade and World camelid veterinary references were
communication throughout wide arid and published. During the period from 1987 to
semiarid expanses. To the Bedouin of the 1996 one thousand four hundred new ref-
Arabian Peninsula and North and East erences appeared in the world literature
Africa, the dromedary was, and still is in (Wernery et al., 1999).
some parts, vital for survival in a most in- The camelid family has become the
hospitable environment. Bactrian camels focus of increasing study in the last few
inhabit the high deserts of Asia where they years. This has become apparent not only
survive -40°C temperatures. For hundreds through the increase in scientific publi-
of years they have carried goods along the cations by, for example, Wilson (1984),
Old Silk Route to China. A few wild Bactri- Yagil (1985), Higgins (1986), Bitter (1986),
ans still roam the steppes of the Gobi des- Griindel (1988), Doose (1990), Saltin and
ert in Mongolia and China. In South Amer- Roose (1994),Wernery and Kaaden (1995),
ica, the vicufia and guanaco remain wild Manfield and Tinson (1996), Tibary and
species, while the llama and the alpaca are Anouassi (1997), Gauly (1997), Faye (1997),
domesticated. They have adapted well to Wilson (1998), Fowler (1998), Beil (1999),
high altitude survival. In many countries Wernery et al. (1999), and Gahlot (2000),
camelids have now adapted to contained and the edition of a camel journal (Journal
management, and in the last few years of Camel Practice and Research, editor Dr.
there has been a renaissance in both Old T. K. Gahlot), but also through the increase
and New World camelids. in joint research projects between Euro-
Until recently, scientific interest in cam- pean universities and institutions in and
els and the majority of research projects in- countries. This growing general interest in
volving camels have been concentrated in camelids also became evident when 300
countries actively involved with the care camel experts from 30 countries took part
and maintenance of the camel as a domes- in the First International Camel Conference
ticated animal. A frequent opinion encoun- in Dubai, United Arab Emirates, in Febru-
tered in those countries not involved with ary 1992 (Allen et al., 1992). Further inter-
camel husbandry is that the camel is an national meetings and conferences took
anachronism, an animal of the past and place in 1996 in Eilat, Israel, in 1997 in Al-
without a future (Wilson, 1984).It is there- Ain, UAE, and in 1999 in South and North
fore not surprising that many publications America and in Morocco. Proceedings are
on camels appear in journals that are available from most of these conferences.
difficult to obtain or in lesser-known lan- As an important source of milk, meat
guages. There was obviously an urgent and wool as well as transportation and la-
need for a comprehensive compilation and bor, the camel should play a more impor-
evaluation of the published literature for tant role than is currently the case in a
all those involved with camels. An impoc- world where food and energy reserves are
tant step in this direction was the publica- dwindling (El-Gayoum, 1986). This is es-
tion of the bibliography Sur le dromadaire pecially true as the camel is, due to its
et le chameau by Saint-Martin et al. (1990), physiological attributes, the most suitable
in which approximately 5500 pre-1990 pub- domestic mammal for uses in climatic ex-
lications regarding camels are catalogued tremes (Yagil, 1985; Wilson, 1989; George,
by author and subject matter. Additional 1992; Wernery, 1992).
 4 Introduction

For a long time it has been incorrectly as- ancestors of the OWC migrated to north-
sumed that one and two-humped camels east Asia across the isthmus today known
VetBooks.ir

derive from a sole wild species, i.e. the as the Bering Strait. Today’s OWC evolved
two-humped wild camel - Camelus ferus. from these early camels, branching out
There were two main reasons for this be- westwards. They were most widely spread
lief. Firstly, both the one and two-humped during the Pleistocene era (endingtwo mil-
camels pass through a two-hump embry- lion years ago) when they reached as far
onic stage. Secondly, the crossbreeds be- as Eastern Europe, North and East Africa
tween dromedaries and Bactrians are fer- and eastern Asia (Koehler, 1981; Koehler-
tile. However, the latest osteological in- Rollefson, 1988). After some time, they
vestigations on post-cranial skeletons of died out in some of these regions. When
dromedaries (Camelus dromedarius) and the OWC migrated eastwards after cross-
Bactrian camels (Camelus buctrianus) have ing the Bering Strait, the ancestors of the
shown that they are in fact derived from humpless NWC migrated south over the
two different species (Peters, 1997). newly formed isthmus between the half
The tylopods originated in North Amer- continents of North and South America
ica 50-60 million years ago (Tertiary pe- (Sielmann, 1982). They populated South
riod) at which time they branched into America where the different types are
eight different families (Zeuner, 1963). known today as llama (Lama g l u m - do-
They were at that time the size of hares. Six mesticated), vicufia (Lama vicugna - wild),
of the eight families died out in the middle guanaco (Lamaguanicoe - wild) and alpaca
Miocene. Then, five million years ago, the (Lama pacos - domesticated) (Fig. 1). The

Figure 1 The four different South American camelids (courtesy of Prof. M. E. Fowler, USA)
(a) Llama, (b) Alpaca, (c) Guanaco, (d) VicuAa
 Introduction 5

Table 1 Classification of camelids and other artiodactylids (Fowler, 1998)

Class Mammalia
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Order Artiodactyla
Suborder Suiformes Hippopotamuses, swine, peccaries
Suborder Tylopoda Camelids
Old Camelus dromedarius - dromedary camel
World Camelus bactrianus - Bactrian camel
New Lama glama - llama
World Lama pacos - alpaca
Lama guanicoe - guanaco
Vicugna vicugna - vicuAa
V: vicugna mensalis (Peruvian)
V: vicugna vicugna (Argentinean)
Suborder Ruminantia Cattle, sheep, goats, water buffalo, giraffe, deer,
antelooe. bison

OWC and NWC belong to the Camelidae mas and alpacas have been domesticated
(camel-like)family under the suborder Ty- there for 7,000 years and were among the
Zopoda (Table 1). first recorded domesticated animals, an
In North America, all camel species died achievement of high Indian culture.
out 10,000 years ago, the last being the Of the OWC, the two remaining species
genus Camelops, which was most proba- domesticated today are the one-humped
bly hunted into extinction by the indige- camel or dromedary (Camelusdromedarius),
nous Indians. In South America today, be- and the two-humped camel (Camelus buc-
tween 7 and 8 million small camels have trianus),with the exception of a small, wild
been counted (Peru, Bolivia) (Table 2). Lla- population of camels in China and Mongo-

Table 2 Estimated population o f South American camelids (Carpio, 1991; Torres, 1992)
Country Llamas Alpacas Guanacos Vicuiias
Argentina 75,000 2,000 550,000 23,000
Bolivia 2,500,000 300,000 ? 12,000
Chile 85,000 5,000 20,000 28,000
Peru 900,000 3,020,000 1,400 98,000
Austra I ia < 5,000 > 5,000 A few in zoos 0
Canada > 6,000 > 2,000 < 100 in zoos > 10
Europe < 2,000 < 1,000 < 100 in zoos < 100
in zoos
United States > 110,000 > 9,500 145, mostly 0
in zoos
In lSlS registry in zoos* 343 303 397 100
Total 3,683,343 3,344.803 572,142 161,210
Grand Total 7,761,498
* ISIS = International Species Inventory System
 6 Introduction

Figure 2a. b (a) The

Bactrian camel, rut-
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ting male (courtesy

of Dr. Zhao Xing-
Xu, China) and
(b) a wild Bactrian
camel (Camelus
bactrianus ferus)
with a newborn
calf (courtesy of
J. Hare, The Wild
Camel Protection
Foundation, School
Farm Benenden
Kent TN174EN, UK)

lia (Fig. 2b). However, until today it has man. The Bactrian camels fulfill a similar
been impossible to establish whether the role in Mongolia, Western Siberia, Trans-
remaining populations of Bactrian camels Caspian, Asia Minor, Iran and Afghanistan.
in these regions are feral or genuinely wild The extent of the OWC habitat and world-
camels. The dromedary’s role in North and wide population is shown in Fig. 3 and
East Africa, Arabia and the Near East is Table 3.
mainly one of transportation of goods and
 Introduction 7

Table 3 Old World camel population (Higgins, 1986;Bhattacharya, 1988;

Wilson et al., 1990;Wernery, 1997)
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Africa Camel Asia Camel

Population Population
Algeria 150,000 Afghanistan 270,000
Chad 446,000 India 1,150,000
Djibouti 60,000 Iran 27,000
Egypt 90,000 Iraq 250,000
Ethiopia 1,000,000 Israel 1 1,000
Kenya 610,000 Jordan 1 4,000
Libya 135,000 Kuwait 5,000
Mali 173,000 Mongolia 580,000
Mauritania 800,000 Oman 6,000
Morocco 230,000 Pakistan 880,000
Niger 410,000 Qatar 10,000
Nigeria 18,000 Saudi Arabia 780,000
Senegal 6,000 Syria 7,000
Somalia 6,000,000 Turkey 12,000
Sudan 2,600,000 United Arab Emirates 120,000
Tunisia 173,000 Yemen 210,000
Upper Volta 6,000 IPS* 200,000
Western Sahara 92,000 China 600,000
Australia 120,000
Canarv Islands 4,000
Total 12,999,000 Total 5,256,000
Grand Total 18,255,000
* Independent states of the Soviet Union

Figure 3 Distribu-
tion of C. drome-
darius and C. bac-
trianus
 8 Introduction

OWC have adapted marvelously to life wallets, handbags and purses. Wool is an
in either hot or cold environments and important dromedary by-product in many
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NWC to life in high altitudes. Sophisticat- camel-producing countries. The average

ed mechanisms have evolved that guaran- wool clip is 3.28 kg for males and 2.10 kg
tee survival of this unique animal family for females. The Bedouins produce carpets
under extreme conditions. and tents from camel wool. Camel wool is
Camels regurgitate and re-chew their one of the world's most expensive natural
food, thus ruminating. However, in strict animal fibers. It is similar to cashmere in
taxonomic terms, they are not recognized both fiber diameter and texture. Of the
as belonging to the Ruminantia. Their three OWC, the Bactrian camel produces superi-
forestomachs are called compartments or wool to the dromedary (Anonymous,
1995). Male Bactrians can produce 10-16
kg of the magnificent fiber, but unfortu-
nately there is very little interest in the
camel wool industry. However, there is an
increasing demand for NWC fiber since
it is known that the vicufia produces the
finest wool of all animals. The interest in
its fiber has saved this magnificent animal
from extinction.It produces only 200 grams
of wool per year. This is one of the reasons
why scientists have been involved in cross-

Figure 4 The forestomach system of Tylo-

poda

(Fig. 4). Differences between camelids and

ruminants are shown in Table 4 (Wernery
et al., 1999).
The word dromedary is derived from
the Greek and means "running". The Bac-
trian camel was named after the Bactria re-
gion of South-WestAsia (Allen et al., 1992).
Camels are used not only as draught
and riding animals, but also for meat, milk,
hides and wool. Comparative technical in-
formation shows that the fat content of
camel meat is considerably less than that of
beef. However, the protein content is com-
parable with beef. It has been shown that
camel hides are very strong with a tensile
strength five times greater than Figure 5 Crossbreed (male, 10 months old)
hides. Camel leather is now being crafted between a guanaco (mother) and a drome-
into fine fashion garments, soft leather dary (father)
 Introduction 9

Table 4 Differences between camelids and ruminants

Camelids Ruminants
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Evolutionary pathways diverged 40 million Evolutionary pathways diverged 40 million

years ago years ago
Blood Blood
red blood cells elliptical and small (6.5 p) red blood cells round and larger (10 p)
predominant white blood cell is neutro- predominant white blood cell is lympho-
phi1 cyte
Foot Foot
has toenails and soft pad has hooves and sole
second and third phalanges are hori- second and third phalanges are nearly
zontal vertical
Digestive System Digestive System
foregut fermenter, with regurgitation, same (parallel evolution)
re-chewing and re-swallowing -/

stomach - 3 compartments, resistant stomach - 4, susceptible t o bloat

t o bloat papillated epithelium
compartment 1 has a stratified squamous no glandular sacs
epithelium
2 glandular sacs in C1, act as "reserve
water tanks"
Reproduction Reproduction
induced ovulator spontaneous ovulation
no estrous cycle estrous cycle
follicular wave cycle no follicular wave cycle
copulation in prone position copulation in standing position
placenta diffusa placenta cotyledonary
epidermal membrane surrounding fetus no epidermal membrane on fetus
cartilaginous projection on tip of penis no cartilaginous projection on tip
ejaculation prolonged o f penis
ejaculation short and intense
Urinary Urinary
kidney smooth and elliptical kidney smooth or lobed
suburethral diverticulum in female no suburethral diverticulum
at external urethral orifice dorsal urethral recess in some species
dorsal urethral recess
Parasites Parasites
unique lice and coccidia unique lice and coccidia
share some gastrointestinal nematodes share gastrointestinal nematodes
with cattle, sheep and goats
Infectious diseases infectious diseases
minimally susceptible t o tuberculosis highly susceptible t o tuberculosis, bovine
bovine brucellosis is rare brucellosis and foot-and-mouth disease
mild susceptibility t o foot-and-mouth
disease
rare clinical disease with other bovine
and ovine viral diseases
 10 Introduction

breeding NWC with OWC. The first suc- the beginning of the Holocene era. The re-
cessful hybrid was produced in the Unit- mains were found at Sihi, a village in
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ed Arab Emirates (UAE) between a male Yemen, and were dated at 7000 BC.
dromedary and a female guanaco (Fig. 5). It is widely believed that the dromedary
Although there is evidence of the Bactri- was domesticated 4,500 years ago, where-
an camels’ ancestors discovered at pre-his- as the wild dromedary population died
toric sites in Kazakhstan and Mongolia, lit- out 1000 BC. Exactly when the wild camel
tle is known about the dromedary’s ances- became domesticated is uncertain, but it
try. An ancestor of the dromedary camel, is believed to have begun on the Arabian
the ”giant” camel, is known zoologically as Peninsula (Wensvoort, 1991). Bones exca-
Camelus thomasi (named after the French vated at trading settlements in Jericho,
paleontologist Thomas). Camelus thomasi is Shar-I-Sokhta and Umm A1 Nar (near the
now considered a possible ancestor of the city of Abu Dhabi) prove that domestica-
domestic one-humped camel (Peters, 1998). tion began at that time. It was written in
These camels are presumed to have existed the Bible that around 1100 BC the Median
in a wild state during the last ice age in Bedouin tribes used dromedaries to occu-
North Africa and in the Negev Desert, py Palestine. In 1000 BC large dromedary
where they probably died out some 12,000 caravans brought incense from Oman and
to 20,000 years ago during extremely cold Yemen to the Mediterranean, which made
temperatures coupled with drought. How- both countries indescribably rich. Archae-
ever, no skeletal remains or rock paintings ologists are still trying to locate the fabled
of camels in the Sahara mountains support city of Ubar (Shisr) that was supposedly
this theory. Evidence of wild camels was situated in Dhofar, the southernmost prov-
only found once in South West Asia, at ince of Oman. This city was the center of

Figure 6 Routes of
the incense trade
 Introduction 11

the incense trade, from where the camel arid deserts of Australia they established
caravans made their way through Marib, free-ranging herds, which nowadays num-
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Medina and Petra towards Gaza and the ber approximately 200,000 animals. These
Mediterranean. The other incense routes feral camels are scattered throughout the
through the great Arabian deserts towards arid interior of Australia with an estimated
Gerrha on the Arabian Gulf could only be 50% in Western Australia, 25% in the Nort-
traversed with the help of the camel (Fig. 6). hem Territory, and 25% in western Queens-
Camel breeding may have increased be- land and northern South Australia. In the
cause of the lucrative incense trade. These late 1960s, there was renewed interest in
heavily laden “ships of the desert” took camels, and by 1970, Australia had two
about 50-70 days to cross the deadly camel tourist businesses with camel races
stretch of land between Marib and Petra. being held around Australia (Anonymous,
The caravanserai reached its zenith during 1995).Several races were held in Sydney in
the reign of the Nabateen. Terracotta finds August 1998 (with the support of the UAE)
from Petra are richly decorated with drom- in preparation for the Olympic Games in
edaries. With the advent of Christianity the 2000.
incense trade began to decline, and Arabia Dromedaries were also brought into
Felix reverted to the deserted Empty Quar- southern Africa, mainly Namibia, around
ter. After the caravans vanished, only the 1890. They were used by the German
Bedouins continued to utilize the drome- Schutztruppe in Namibia until the end of
dary. World War I for three reasons. Firstly, only
When trade began with Arabia, drome- dromedaries could survive in the Namib-
dary numbers increased in Africa. It is pre- ian and Kalahari deserts; secondly, oxen
sumed that between 1500-2000 BC, drom- were eradicated by rinderpest and foot-
edaries spread into Africa from the Ara- and-mouth disease; and thirdly, horses
bian Peninsula via the Horn of Africa. were severely decimated by the devastat-
Beyond Somalia, the country with the ing African horse sickness virus. In 1906,
highest proportion of dromedaries per per- Lorenz Hagenbeck shipped 2,000 Sudanese
son, the “ship of the desert” spread north camels to the small outpost of Swakop-
and westwards. However, it was not intro- mund in Namibia. After the Versailles Peace
duced into Tunisia and the Atlas countries Treaty (1919), the English police force then
before Hellenistic times. took possession of all remaining camels in
Dromedaries were not only introduced Namibia. However, as in Australia, after
into countries with temperate climates such motorized transport became popular, the
as Europe, South America and the Carib- camels were abandoned and it is believed
bean, but also into Australia and southern that as a result of being eaten by lions and
Africa, which have hot climates. An esti- bushmen, they disappeared in southern
mated 10,000-12,000 camels imported into Africa in the late 1960s (Massmann, 1981).
Australia between 1860 and 1907 were Dromedarieswere also used in the Unit-
used as draught and riding animals by ed States after the Mexican war of the
people pioneering the dry interior (Viswa- 1840s, on mail express routes across the
nathan, 1991). The camels introduced into newly acquired arid regions, but they were
Australia were almost exclusively drome- later eradicated.
daries, because they are highly suited to In Europe, camel societieshave emerged
the Australian desert climate. Most of the during the last two decades and animals
camels were released in the mid-l920s, have been used to attract tourists. In Au-
when motor vehicles began operating in gust 1997, camel races were held at Berlin’s
the central areas of Australia. In the semi- famous horse race course Hoppegarten in
 12 introduction
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Figure 7 Geographical distribution of dromedary breeds (after Wilson, 1998)

front of 60,000 spectators. However, this cause of the crossbreeding of Bactrian and
was not the first camel race in Europe, dromedaries in Russia, Turkey, Afghanis-
as was then claimed. The first races took tan and Syria. As the second generation
place in Cologne-Weidenpesch in 1969 of these crossbreeds (Tulu) are generally
with Moroccan camels (Leue, 1969). weak and susceptible to diseases and the
Since the 1980s, the dromedary has again fourth generation is infertile, the breeders
become popular, not only with scientists, have to start all over again to achieve a
but also in the countries where it is used good crossbreed (Fig. 8).
for riding and transport. Its milk, skin and
meat are all utilized and, additionally, it
has become a tourist attraction. The future
of the dromedary species is assured de-
spite the competition of modem transport
and other domesticated animals, and it of-
fers no threat to domesticated animals or
any endangered wildlife.
Scientists have recently intensified their
study of the dromedary and are debating
whether there are different dromedary
"breeds". Until now, the dromedary has
been classified in the following ways - by
naming them after the tribes who rear
them, or whether they are riding or trans-
port camels, by their color, geographical
background (Fig. 7), physical characteris-
tics or their use for milk, meat, or racing
(Wilson, 1998). This categorizationhas giv-
en rise to the classification of dromedaries
under 48 "breeds" in 9 regions and sub-re- Figure 8 Crossbreed (Tulu) (female, 2 years
gions, under 3 main groups and 8 sub- old) between a Bactrian male and a female
groups. The confusion is compounded be- dromedary
 Introduction 13

In its great genetic diversity, the drome- resulted in feuds and skirmishes. Obvious-
dary raises many questions which are not ly, the tribe with the quickest and most
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easily explained. nimble dromedaries had the most chance

Thousands of years before the Pyramids of surviving. Sir Wilfred Thesiger, in his
were built, the Bedouins and their drome- book Arabian Sands, described disputes
dary herds wandered through the great that still occurred until some 30 years
Arabian deserts and lived undisturbed ago. However, not only were the drome-
throughout the successive reigns of the daries vital during tribal conflicts, but the
Pharaohs, Sumerians, Assyrians, Phoeni- Bedouins also used them for racing during
cians, Greeks, Romans and Turks.The tribes social occasions, such as weddings or births.
could only survive in the desert thanks to The quickest dromedaries were selected to
the dromedary, which the Bedouins call run over short courses.
Ata Allah (God‘s Gift). Only through its in- In the Arabian Desert, it was the Bedou-
dispensable patience and perseverance did in who managed to breed the precious Ara-
it enable survival in the perpetual sands. bian horse, the Saluki dog and the drome-
Over this period, the desert played a big dary. In its perseverance, intelligence and
part in the evolution of the dromedary as beauty, the Arabian dromedary, bred over
the only domesticated animal to survive in hundreds of years in one of the hottest
such extreme conditions. Not only does climates on earth, is comparable with the
the dromedary produce milk, meat and
wool, but it is also used as transport over
thousands of kilometers. Not only the Table 5 Dromedary population on the
”ship of the desert’s” ability to survive in Arabian Peninsula
the hottest climates, but its natural resist- Kuwait 5,000
ance to such deadly animal diseases as Oman 6,000
rinderpest and African horse sicknes makes Qatar 10,000
it indispensable to its owner. Saudi Arabia 780,000
In an effort to find new grazing areas, it United Arab Emirates 120,000
Yemen 200,000
was often necessary for the Bedouin tribes
to cross enemy territory. This sometimes Total 1.121,000

Figure 9 One of
the authors exam-
ines a valuable
female asil drome-
dary
 14 Introduction

Table 6 The main physiological particulars of dromedaries

1. Cattle lose 20-40 liters of fluid a day via their feces. Camels lose 1.3 liters of fecal water.
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This is one of the primary ways of combating water deprivation in the desert.
2. Thermoregulation in the camel is greatly affected by the availability of drinking water.
The camel has a great dehydration tolerance; it can lose one third of i t s body weight in
water without suffering any ill effects.
3. A dehydrated camel reacts t o changes in external temperature. In the morning when the
desert is cold, the camel's body temperature is low: 34.0"C. In the late afternoon the body
temperature can reach 42°C. The camel adapts i t s body temperature t o the outside tem-
perature, preventing it from sweating. A rise in body temperature saves a camel a lot of
water that would otherwise be used t o dissipate the heat load. High blood temperature
would do permanent damage t o the brain and retina cells of the eyes. However, camels
are able t o cool the brain and eyes through extraction of water from exhaled air. The wa-
ter vapor from the exhaled air stays in the long nose and cools the carotid rete, a network
of small blood vessels supplying the brain and eyes.
4. Goats kept in an open yard with no shade are unable t o survive more than 3 days with-
out water; Barki sheep also die after 3 days o f dehydration, but camels can survive 20 t o
30 days without drinking water.
5. A 600 kg camel can replenish its entire water deficit of 200 liters in 3 minutes. Camel eryth-
rocytes are extremely resistant t o hypotonicity. Bedouin goats kept 4 days without water
die of hemolysis after replenishing a 40% water loss in 8 minutes.
7. In camels, water rapidly enters the bloodstream after drinking. After 4 hours water is ap-
parently equilibrated throughout most o f the body. No other animal has such a rapid en-
try of water into the blood.
8. The hump is an accumulation of fat for the time when energy is needed. It indirectly aids
in cooling the body as the accumulation of fat leaves the subcutis of the body fat free, al-
lowing easy dissipation of heat.
9. In a dehydrated camel, alimentary tract water is i t s body's sole source of water because
this water is continuously absorbed from the intestines. Camels hold 75% of their weight
in fluids, and as long as the camel continues t o eat, water will be present in the stomach.
Camels withstand more than 3 weeks without drinking water and s ti l l continue t o eat nor-
mally, because their stomachs still contain relatively large quantities of fluid. In a trial, a
camel was dehydrated for 51 days and was only fed on dry grass. A t the end of the ex-
periment the appetite declined. By then, the camel had lost 37% of i t s body weight.
10. Compartment 1 contains high concentrations of sodium and bicarbonate and low con-
centrations of chloride and potassium. These high concentrations of electrolytes are also
found in the saliva and intestines and play an important role in the camel's utilization of
alimentary water.
11. Camel kidneys have long loops of Henle, and urine production is greatly decreased in the
dehydrated camel. Salt is also well handled by the camel kidneys. Camels can drink sea-
water without showing any side effects. Camel can excrete urine with a salt concentration
almost twice that o f seawater.
12. Dehydrated camels can "store" sugar in their blood in order not t o lose water through the
urine (sugar is highly hygroscopic). In a trial, blood sugar rose as high as 1300 mg% with-
out the appearance of glucose in urine. As soon as drinking water was made available, an
enormous diuresis followed and blood glucose returned t o normal.
13. A dehydrated camel is able t o continue lactation.
14. Camels mate in crouched position. They are induced ovulators with a relatively short mat-
ing period. Their gestation period is 13 months.
 introduction 15

Arabian horse. There is no other drom- ganisms, as extensively examined by sci-

edary that compares with the Arabian. entists in the Institute for Horticulture and
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Through breeding, it has become an agile, Animal Hygiene in Goettingen (El-Gay-

fast, long-legged, slender, brown racing own, 1986; Margan, 1987), and the previ-
dromedary with fine limbs and a long ous lack of interest in the camel family in
head (Fig. 9).Although no studbooks exist, general, may have been decisive in the
the Bedouin are extremely careful to keep dearth of publications on infectious dis-
the bloodlines pure. In the 30 years since eases of camelids. The second edition of
the oil boom began, camel racing has gone this book will attempt to close this gap by
through a fundamental change. surveying and compiling the published
In the last few years, the worldwide literature regarding bacterial, viral and
camel population has risen from 17.5 mil- fungal diseases as well as pathology and
lion (Wilson et al., 1990) to 18.3 million parasitology in the camelids as completely
(Table 3). The camel population has de- as possible. The majority of the literature
creased in only a few countries, such as encompasses the one-humped Camelus
Libya and the Gulf States, where oil has dromedarius as the available literature on
brought nomadism to a virtual standstill the two-humped Camelus bactrianus is un-
(Wilson, 1984). However, in recent years, fortunately very difficult to obtain. As the
an opposite trend has been observed in the exchange of scientific research with coun-
UAE where the dromedary is experienc- tries where the Bactrian camel lives is now
ing a renaissance resulting in a revival of improving, it is hoped that more compre-
the old Bedouin tradition of camel racing. hensive data will soon become accessible.
What was earlier seen as playful competi- New scientific findings of NWC are also
tion and a pleasant pastime between the included.
Bedouin has become a scientifically found- In addition to a compilation of the known
ed racing discipline following the oil boom literature, results of the authors’ personal
of the 1960s. Based on this development, research conducted since 1987 on a camel
more than 100,000 racing camels are kept population of 30,000 racing dromedaries
in the UAE. In the cooler months between (including breeding animals) in the UAE,
September and May, competitions are held in conjunction with various research insti-
on 20 racetracks throughout the Emirates. tutes abroad, will also be presented.
Based on the age of the animal, the drome-
dary competes at distances between 3 and
10 kilometers. A dromedary can cover the References
10 km course in 17 to 18 minutes (Wernery, Allen, W.R., A.J. Higgins, I.J. Mayhew, D.H.
1992). Snow and J.F.Wade 1992. Proc. 1st int. Camel
Due to a number of specific anatomical Cod., Feb 24,1992. Published by R. and W.
and physiological characteristics, the dmm- Publications. (Newmarket) Ltd.
edary can survive and perform tasks in the Anonymous. 1995. The central Australian camel
extreme climate of the desert that can be industry. Brochure of the Central Australian
utilized by man (Schmidt-Nielsen, 1964) Camel Industry Association, PO Box 8760,
Alice Springs, Australia:1 4 .
(Table 6).
Beil, Christiane. 1999. Reproduktion beim weib-
A further advantage is the low suscepti- lichen Kame1 (Camelus dromedariusund Ca-
bility of the camelids to disease (Fazil and melus bactrianus).Eine gewichtete Literatur-
Hofmann, 1981). This is especially true of studie. Thesis, Hannover.
viral diseases, although bacterial ailments Bhattacharya, A.N. 1988. Camel production re-
play a larger role. Both the camelids’resist- search in northern Saudi Arabia: a mono-
ance to a number of pathogenic microor- graph. Ministry of Agriculture and Water De-
 16 Introduction

partment of Agricultural Research, UTFN/ Manefield, G.W. and A. Tinson. 1996. Camels.
SAU/OO8/SAU. A compendium. The T.G. Hungerford Vade
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Bitter, H. 1986. Untersuchungen zur Resistenz Mecum Series for Domestic Animals.
von Kamelen (Camelus dromedarius) unter Margan, Ute. 1987. Vergleichende Untersuchun-
besonderer Beriicksichtigung der Mektion gen zur Bedeutung der alternativen Komple-
mit Trypanosoma evansi (Steel 1885). Thesis, mentaktivierung bei Rindern und Kamelen.
Hannover. Thesis, Gottingen 33.
Carpio, M. 1991. Camelidos socio-economia An- Massmann, Ursula. 1981. Kamele in Siidwest-
dina (Camelids and Andean socio-econom- afrika. Namib und Meer 9: 31-54.
ics). Ed. Novoa, C. and Florez, M.: A produc- Mukasa-Mugerwa, E. 1981. The camel (Cam-
tion de Rumiantes Menores: Alpacas. Lima, elus dromedarius): A bibliographical review.
Peru. Re rumen: 3-16. International Livestock Center for Africa.
Doose, Anette. 1990. Funktionen und Morpho- ILCA Monogr. 5: 4-119.
logie des Verdauungssystems des einhockri- Peters, J. 1997. Das Dromedar: Herkunft, Dome-
gen Kamels (Camelus dromedarius). Thesis, stikationsgeschichte und Krankheitsbehand-
Hannover. lung in friihgeschichtlicher Zeit. Tierurztl.
El-Gayoum, S.E.A. 1986. Study on the mecha- Praxis 25: 559-565.
nism of resistance to camel diseases. Thesis, Peters, J. 1998. Camelus thomasi Pomel, 1893, a
Gottingen 22. possible ancestor of the one-humped camel?
Farid, M.F.A. 1981. Camelids Bibliography. Int. J. of Mammalian Biology 63: 372-376.
ACSAD-AS 15. Saint-Martin, G., M.F. Nitcheman, D. Richard
Faye, B. 1997. Guide de l'devage du dro- and M.A. Richard. 1990. Bibliographie sur le
madaire. Sanofi Sant6 Nutrition Animale, La dromadaire et le chameau. 2nd edition, Tome
Ballastiere - 813126, 33501 Libourne, Cedex, 1, Tome 2: Index.
France: 115-116. Saltin, 8. and R.J. Roose. 1994. The racing camel
Fazil, M.A. and R.R. Hofmann. 1981. Haltung (Camelusdromedarius).Acta Physiol. Scand.,
und Krankheiten des Kamels. Tieriirztl.Praxis Wernerssons Grafiska AB, Kumla/Chister
9: 389-402. Perssons Tryckeri AB, Koeping 150 (617).
Fowler, M.E. 1998. Medicine and surgery of Schmidt-Nielsen,K. 1964. Desert animals: phys-
South American Camelids. Iowa State Uni- iological problems of heat and water. Claren-
versity Press, Ames. don Press, Oxford.
Gahlot, T.K. 2000. Selected topics on camelids. Sielmann, H. 1982. Weltreich der Tiere. Natura-
The Camelid Publishers, Sankhla Printers, lis Verlags- und Vertiebsgesellschaft mbH,
Bikaner, India. Miinchen, Monchengladbach, Arbus.
Gauly, M. 1997. Neuweltkamele. Parey Buch- Tibary, A. and A. Anouassi. 1997. Theriogenolo-
verlag Berlin. gy in camelidae. Anatomy, Physiology, Pathol-
George, U. 1992. ijberleben. Geo Spezial, Sahara ogy and ArtificialBreeding. Abu Dhabi Print-
6: 47. ing and Publishing Co., Mina, Abu Dhabi,
Gruendel, M. 1988. Das Blut des einhockrigen UAE.
Kamels (Camelus dromedarius). Eine Litera- Torres, H. 1992. South American Camelids: an
turiibersicht. Thesis, Hannover. action plan for their conservation. South Amer-
Higgins, A. 1986. The camel in health and dis- ican Camelid Specialist Group, Gland, Swit-
ease. Bailliere Tindall. zerland. IUCN/CSE.
Koehler, J. 1981. Zur Domestikation des Kamels. Viswanathan, L. 1991. More about camels. The
Thesis, Hannover. Gazelle, Dubai Natural History Group 6: 6.
Koehler-Rollefson, I. 1988. The introduction of Wensvoort, J. 1991. Camels, camel nutrition and
the camel into Africa with special referenceto racing camels. The Gazelle, Dubai Natural
Somalia.Working paper 24. History Group 6: 5.
h u e , G. 1969. Erstmaliges Kamelrennen in Eu- Wernery, U. 1992. Dromedare, die Rennpferde
ropa 1969 auf der Pferderennbahn in Koln Arabiens. Tierarztl. Umschau 4 7 801.
aus veterinarphysiologischer,genetischer and Wernery, U. 1997. Dromedare in Arabien. La-
biomechanischer Sicht. Dtsch. tierarztl. Wschr. mas. Haltung and Zucht w n Neuweltkameliden
78 (18): 500-502. 5 (1): 34-36.
 Introduction 17

Wemery, U., M.E. Fowler and R. Wernery. 1999. Zeuner, F.E. 1963. A history of domesticated an-
Color Atlas of Camelid Hematology. Black- imals. Hutchinson, London.
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well Wissenschafts-Verlag, Berlin.

Wemery, U.and 0.-R. Kaaden. 1995. Infectious
Further reading
Diseases of Camelids. Blackwell Wissen-
schafts-Verlag, Berlin. Fowler, M.E. 1997. Evolutionary history and dif-
Wilson, R.T. 1984.The camel. Longman, London ferences between camelids and ruminants.
and New York. J. Camel Prac. and Res. 4 (2), 99-105.
Wilson, R.T. 1989. Ecophysiology of the cameli- Hare, J.N. 1997. Status and distribution of wild
dae and desert ruminants. Springer Verlag. Bactrian camels (Camelus bactrianus ferus)
Wilson, R.T., Astier Araya and Azeb Melaku. in China. I. Camel Prac. and Res. 4 (2), 107-
1990. The one-humped camel. An analytical 110.
and annotated bibliography. The United Na- Hare, J.N. 1998. The lost camels of Tartary. Little
tions Sudano-Sahelian Office (UNSO), Tech- Brown and Company, London.
nical paper series 3. Skidmore, J.A., M. Billah, M. Binns, R.V. Short
Wilson, R.T. 1998. Camels. The Tropical Agricul- and W.R. Allen. 1999. Hybridizing Old and
turalist, MacMillan: 106. New World camelids: Camelus dromedarius
Yagil, R. 1985. The Desert Camel. Verlag Karger, x Lama guanicoe. Proc. R. SOC. Lond. B 266,
Basel. 649-656.
VetBooks.ir

Bacterial Diseases
 1.1 General Survey
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1.1.1 Anaerobic Infections Most of the pathogenic species produce

one or more exotoxins of varying potency.
Clostridial diseases are a constant threat to The vegetative organism is capable of
livestock in many parts of the world. Clo- forming spores that are able to survive
stridia are all potent producers of exotox- long periods of time in the soil. Contami-
ins upon which their pathogenicity de- nated soil can contain up to 105 CZostridiurn
pends. Clostridial organisms are common- perfringens spores per gram of soil (Seifert,
ly present in soils and the intestinal tract of 1992).
animals, including man, and cause disease
only in special circumstances. The ubiqui- Epidemiology and Clinical Signs :Bi The
tous character of clostridial bacteria makes older classical etiological classification of
eradication of clostridiosis virtually im- anaerobic infections that ascribes parti-
possible and necessitates control by pro- cular clinical signs to a specific clostridial
phylaxis. Both W C and OWC may suffer agent can no longer be considered valid.
from some of the clostridial diseases (Wern- Modern methods of infectious agent iden-
ery and Kaaden, 1995; Fowler, 1998). tification utilizing gas chromatography
allow an exact determination of the etio-
Clostridial diseases are caused logical agent. These methods have also al-
by bacteria of the genus Clostridiurn. Clo- lowed the division of the epidemic anaero-
stridium bacteria are large, Gram-positive, bic complex into three groups:
anaerobic, endospore-producing rods. The - gas edema complex,
spores bulge the mother cell. C. perfringens - enterotoxemia complex,
possesses a capsule in animal tissue and is - intoxication complex.
non-motile. Clostridia are oxidase-nega-
tive and catalase-negative and the anaero- This new development is summarized in
bic requirements vary among the species. Table 7.

Table 7 Etiologic differentiation of the most important clostridial infections

and intoxications in domestic animals modified after Seifert (1992)
Enterotoxemia complex - per 0s - enteral
C. perfringens, type A-F; C. sordellii; Errors in husbandry, overgrazing,
C. difficile overcrowding
Gas edema complex - per 0s - parenteral
C. chauvoei; C. haemolyticum; C. histolyti- Changes in intestinal permeability, skin
cum; C. novyi, type A-C; C. perfringens, and mucosal lesions, periods of drought,
type A-F; C. septicum; C. sordellii; C. chica- hard lignin-containingfeed, lack of food,
mensis; Madagascar wild strains 217,335, overcrowding
735; Mexico wild strains (809 and others)
Intoxication complex - per 0s
C. botulinum, type A-F, C. perfringens, Errors in husbandry, overcrowding, mineral
type A-F deficiency, P-deficiency, errors in nutrition
Intoxication complex - parenteral
C. tetani deep, anaerobic wounds
 22 Bacterial Diseases

Diseases caused by clostridia are often gas edema; however, Cross (1919) was able
difficult to identify in the tropics due to to elicit the disorder experimentally in
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indigenous ecological influences, making three dromedaries through intramuscular

diagnosis a challenge. C. perfringens types injection of C. chauvoei. The type of swell-
A, B and C, C. novyi, C. chauvoei and C. sep- ing should allow the differentiation be-
ticum have all been isolated from camelids. tween gas edema and anthrax. Recent pub-
lications regarding gas edema in camels
are not known.
Gas Edema Complex
Blackleg has been produced experimen-
The causative agents of the gas edema tally in alpacas, but there is one report of
complex, which according to Seifert (1992) natural infection in a female llama that
include the following diseases: died suddenly. The causative agent was
C. novyi (Anonymous, 1998). It is believed
- black-quarter (blackleg),
that OWC and NWC are more resistant to
- malignant edema,
blackleg infections than bovines.
- bacillary hemoglobinuria,
Malignant edema is an economicallyim-
- infectious necrotizing hepatitis
portant disease in alpacas in Peru and has
are seldom isolated from camelids.As most also been associated with rattlesnake bites
of the available literature is outdated, it is in llamas in Colorado (Moro Sommo, 1956;
possible that these disorders were falsely Fowler, 1998). The disease in lamoids is
diagnosed in the past due to the prevailing caused by C. septicum with two types of
incomplete, traditional analytical methods syndromes: the typical wound infection
used. Current techniques have identified and edema and the acute systemic disease,
the following causative agents of the gas which may kill animals instantly.
edema complex (Seifert, 1992): The other two diseases of the gas edema
- C. chauvoei, C. septicum, C. chicamensis, complex, bacillary hemoglobinuria and in-
wild strains that have been exactingly fectious necrotizing hepatitis, have not
characterized (335 and 735 Madagascar, been reported in Camelidae.
805 Mexico);
- C. histolyticum, C. sordellii, C. novyi type
Enterotoxemia Cornplex
A X , C. haemolyticum;
- C. perfringens type A-F and wild strains All types of C. perfringens as well as C. soy-
(217 Madagascar). dellii and C. spiroforme can cause the en-
terotoxemia complex. C. perfringens, most
C. chauvoei infections in dromedaries have frequently type A (Bisping and Amtsberg,
been reported as possibly occurring in 1988), is also found in the intestines of
North and East Africa, as well as in Chad healthy animals so that cultural evidence
and India (Gatt Rutter and Mack, 1963), of C. perfringens has little disease-pre-
but these reports are contradictory. With dictive value. Enterotoxemia caused by
the exception of Cross (1919), Curasson C. perfringens is found all over the world
(1947) believes that many previous authors and is also found in all types of domestic
have confused black-quarter with true an- animals. According to Seifert (1992), fac-
thrax caused by Bacillus anthracis. The pro- tors predisposing to disease include di-
gression of both disorders is similar, begin- etary errors, climatic influences, change of
ning with subcutaneous swellings on the pasture, transportation, and weighing of
shoulders that lead to the animal's death animals.
within 2 to 3 days. Hutyra et al. (1946) re- Acute and subacute enterotoxemia as
ported that camels were not susceptible to well as hemorrhagic enteritis due to C. per-
 General Survev 23

fringens, types A, C and D have been de- - perspiration

scribed in camels by Moebuu et al. (1966)) - muscle tremor
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Ipatenko (1974), Chauhan et al. (1985) and - ataxia

Gameel et al. (1986). Fowler (1998) has re- - aggression
ported enterotoxemia due to C. perfringens - hyperexcitability
types A, C and D in NWC. - seizures
Extensive studies of C. perfringens type A
outbreaks in racing dromedaries in the Affected animals died within one hour af-
UAE have been performed by Wernery et ter the onset of clinical signs.
al. (1991),Seifert et al. (1992), Wernery et al. The pathological changes found in au-
(1992b) and Wernery and Kaaden (1995). topsied animals were mild. They included
Peracute and acute enterotoxemia in breed- - petechiae in the thoracic musculature,
ing and racing dromedaries as well as se- - petechiae in the cerebellum and brain-
vere myocardial degeneration and “pulpy stem,
kidney” in dromedary calves are known to - petechiae in the pharyngeal mucosa,
occur. For all three age groups of drome- - subpleural (Fig. 10) and subepicardial
daries, predisposing etiological factors petechiae,
were proven to be responsible for the out- - petechiae in the mucosa of the third
breaks. compartment (Fig. 11)and the stomach,
In a herd of 90 breeding animals, 71% - hydropericardium with fibrinous exu-
of the dromedaries were found to have date,
an acute Typanosoma evansi infection. Try- - dark kidneys, with adherence of the cap-
panosomosis is known to be able to cause sule to the parenchyma (Fig. 12).
immune suppression in domesticated ani-
mals (Losos, 1986),and may have been the In another incident, salmonella paved the
predisposing factor for the peracute C. per- way for the outbreak of C. perfringens type
fringens outbreak in this group, since nutri- A in racing dromedaries. The animals de-
tional errors and environmental influences veloped intractable diarrhea and died after
had been excluded. The camels affected ex- 4 days. In those animals autopsied, even
hibited the following clinical signs: more severe pathological changes were

Figure 10 C. per-
fringens entero-
toxemia: subpleu-
ral hemorrhages
 24 Bacterial Diseases

Figure 11 C. per-
fringens enterotox-
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emia: petechial
hemorrhages in
Compartment 3

found in the same organs as listed above. ed milk or barley (Figs. 13 and 14) are
These included severe hemorrhagic colitis, found in their abomasum. The stress of
hydropericardium with fibrinous exudate racing is also certain to play an important
and ecchymotic changes in compartment 3 role in the development of peracute en-
and the stomach. terotoxemia.
A further important etiological factor in The dromedary calf exhibits distinctive
the outbreak of enterotoxemia in racing features when affected by the enterotox-
dromedaries is a nutritional error prior to emia complex. The target organs for C. per-
competition. Most likely due to ignorance, fringens type A toxins in young drome-
dromedaries are fed large amounts of un- daries are the heart and kidneys. Wernery
crushed barley, cow milk, honey and alfal- et al. (1992b) have reported severe myo-
fa. At autopsy, large amounts of undigest- cardial degeneration (Figs. 15 and 16) and

Figure 12 C. per-
fringens enterotox-
emia: kidney cap-
sule adherent to
parenchyma
 General Survev 25

Figure 13 C. per-
fringens enterotox-
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emia: undigested
milk in the gastric
system of a racing
dromedary

”pulpy kidney” (Fig. 17) in 4-6-week-old calves revealed, in addition to curdled

dromedary calves. milk and small amounts of roughage, in-
Degeneration, calcification and necrosis creasing amounts of sand in the develop-
of the myocardium in 3 to 5-week-old cam- ing compartments (Fig. 18).
91 calves in Saudi Arabia that died due to Examination of soil samples from these
C. perfringens type D enterotoxemia have herds found up to 104 C. perfringens vege-
also been described by El-Sanousi and tative cells per gram of soil. Although the
Gameel (1993). A predisposing factor for paddocks were cleaned daily, the sand
this disorder appears to be weaning. Be- where the breeding camels had been kept
tween 4 and 6 weeks of age, the young for years was heavily contaminated with
calves begin to take nourishment other vegetative cells and spores from clostridia.
than milk. Autopsy findings in dromedary This situation represents a continuous risk

Figure 14 C. per-
fringens enterotox-
emia: undigested
barley in the gastric
system of a racing
dromedary
 26 Bacterial Diseases

Figure 15 C. per-
fringens enterotox-
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emia in a young
dromedary: severe
myocardial degen-
eration

Figure 16 C. per-
fringens enterotox-
emia in a young
dromedary: hyaline
degeneration of
heart muscle

Figure 17 C. per-
fringens enterotox-
emia in a young
dromedary: "pulpy
kidney "
 General Survey 27

Figure 18 C. per-
fringens enterotox-
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emia in a young
dromedary: sand in
the compartments

of infection for the maturing young drom- The tests revealed no evidence of a defi-
edaries. Knowledge of this epidemiologi- ciency of these minerals, so it was assumed
cal connection has increasingly led drome- that the dromedary calves ingested the
dary owners to relocate their breeding sand more out of curiosity than due to an
herds more often or to replace the contam- as yet undetected nutritional deficiency.
inated sand with fresh sand. Mineral licks were also placed in all the
To investigate the reasons for the young dromedary enclosures.
dromedaries ingesting sand, blood sam- An additional important aspect in the
ples were taken and examined for the min- development of clostridiosis in Cumelidue is
erals calcium, magnesium, iron and phos- the amount of serum immunoglobulin in
phorus. Dromedary milk samples were the young animals (see also 2.1.7 neonatal
obtained and analyzed using the same diarrhea). Cumelidue have an epitheliocho-
method. The results are summarized in rial placenta, so that the calf, as in the foal,
Table 8. receives its passive protection against dis-

Table 8 Magnesium, phosphorus, calcium and iron values in sera of dromedary calves
and milk from breeding dromedaries from herds where sand eating occurs
Sera Milk
*Reference Herd 1 Herd 2 **Reference ***5 samples
values values
mgldL 22 samples 26 samples g/kg
Magnesium 1.8-2.2 1.9 2.0 0.083 0.078
Phosphorus 3.2-6.5 10.7 9.8 0.95 0.82
Ca Icium 9.5-1 1.5 10.3 10.2 1.64 1.32
Iron 80-1 30 89 83
~

* Normal values are for adult dromedaries (Samples were examined in a Dimension Auto-
analyzer, Dupont)
** Whabi et al. (1987)
*** Examined by the J.A. Comloquoy, Dubai Aluminum Plant
 28 Bacterial Diseases

ease through the intestinal reabsorption of diagnosis of ”clostridial enterotoxemia”is

immunoglobulinsfrom the colostrum after made by identirylng clostridial toxins in
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birth. Although the newborn calf is im- the duodenum of recently expired animals.
munocompetent at birth, the endogenous The intestinal contents are removed imme-
antibody production is not sufficient to diately post mortem and deep frozen. The
produce a protective immunoglobulin lev- next day the material is thawed, sterile fil-
el within the first month of life. The globu- tered and tested for pathogenicity in mice.
lin fraction is naturally low at birth. Even One milliliter of the sterile intestinal con-
after ingestion of colostrum, the globulin tents is injected intravenously into the tail
level declines after the seventh day and vein of laboratory mice. In the presence
reaches the lowest level between the 20th of clostridial toxin, the mice expire within
and 30th day post partum. The highest 2 to 8 hours, exhibiting seizures and the
losses due to C. perfringens enterotoxemia characteristic opisthotonus.
occul during this time. The colorimetric tetrazolium cleavage
Fowler (1998) made similar observations test (MTT) has widely replaced the mouse
in NWC. He determined that the globulin lethal test and is regularly used for the de-
content of NWC serum is very low at birth tection of clostridial toxins from intestinal
(< 5.2 mg/mL), increased following inges- fluids. It also has the advantage that the
tion of colostrum to 5.5-6.2 mg/mL within fluid can be diluted and a titer estimated.
4-5 days yet reached its lowest level 3 to 4 The higher the titer, the more toxin is pres-
weeks post partum. C. perJrrngenstype A is a ent in the gut (Fig. 19).
very serious disease in alpaca crias in South In suspected enterotoxemia,the presence
America and it is named “MaZ de AZpucas” of large numbers of Gram-positive rods
(Rath, 1950; Moro Sommo, 1963; Ramirez from mucosal scrapings from the small
and Huaman, 1980-1981; Ramirez et al., intestine of fresh dead animals is presump-
1983a and b; Huaman et al., 1981;Ellis et al., tive evidence of clostridial enterotoxemia
1990; Fowler, 1996). The animal mortality (Fig. 20).
rates vary between 10 and 70% and even on Fluorescent antibody (FA) technique is
carefully managed farms may approach also routinely used for disease with C. chau-
50%. The disease o c c u ~ sin crias between 8 voei, C. septicum, C. novyi and C. sordellii.
and 35 days of age with sudden death or a Cultivation of C. perfringens from organs
short disease period during which the crias of dead dromedaries is performed on Sa-
are recumbent, showing nervous system hidi-Furgeson-Perfringens (SFP)agar and
disorders. The pathological changes in al- Zeissler agar under anaerobic conditions
pacas are very similar to the lesions seen with the gas generating kit. In C. perfrin-
in OWC with petechiae in different organs, gens outbreaks in the UAE, three different
hyperemia, excess serosanguinous pericar- C. perfringens type A strainswere identified
dial fluid and lesions in the intestinal tract. using chromatography (Heitefuss et al.,
Type C and D enterotoxemias are more 1990; Heitefuss, 1991). These strains are
common in lamoids than they are in OWC. now included in a local vaccine to protect
dromedaries from clostridiosis.
Specimens, including intes-
tinal fluid, should be taken from freshly Treatment and Control Treatment of sick
(less than 4 hours) dead animals, as clos- dromedaries with a bovine C. perfringens
tridia are rapid postmortem invaders. Tox- hyperimmune serum is very rewarding.
ins are very labile and therefore small in- Many valuable racing camels were saved
testinal contents should be frozen as soon by the intravenous application of 1OOmL
as possible until processed. The laboratory of antiserum.This procedure can be repeat-
 General Survev 29

Figure19 MlT
results on vero cells
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indicating toxin in
the intestinal fluids
of dromedaries
with clostridial en-
terotoxemia

ed without any side effects. For the preven- before parturition and a booster adminis-
tion of this important disease, sanitation, tered 1 month prior to delivery.
feeding and general husbandry practices Isolation and identification of clostridial
should be optimal. In endangered herds, strains are necessary to confirm the diagno-
chlortetracyclines at a rate of 25 mg/kg feed sis and to develop a specific clostridialvac-
should be added to the feed. cine. For camels in the UAE,thistoxoid vac-
Toxoid vaccines are commonly used to cine was produced at the Institute for Ap-
prevent enterotoxemia outbreaks in cattle, plied Biotechnology of the Tropics (IBT) in
sheep and llamas. The vaccine should be Goettingen, as it is known that locally de-
administered to the dam, since neonates rived strains give optimal protection. This
are unable to produce enough antibodies. vaccine prevented further cases of C. pefrin-
The dam should be vaccinated 2 months gens enterotoxemia in adult dromedaries

Figure 20 C. per-
fringens: increased
number of Gram-
positive rods in a
mucosal scraping
from the small
intestine of a drom-
edary with clostri-
dial enterotoxemia
 30 Bacterial Diseases

Figure 21 C. per-
fringens enterotox-
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emia: local reaction

following subcuta-
neous vaccination
with a Montanide
adjuvant cell toxoid
vaccine

Table 9 Development of antibodies, examined with the HIT, directed against

a locally specific C. perfringens (type A) toxoid vaccine in dromedary calves
and their mothers before and after tw o consecutive maternal protective vaccinations
Dromedary Prior t o Weeks after vaccination
cows vaccination 2 6 12 24
1 Neg. 1 :64 1 :64 1 :32 1 :64
2 1 :2 1 :32 1:16 1:16 1:16
3 1 :4 1 :64 1 :64 1 :64 1 :64
4 1 :2 1:32 1 :32 1 :32 1 :32
5 1 :4 1:128 1 :64 1 :64 1 :64
6 1 :2 1 :32 1:32 1 :32 1:32
7 Neg. 1:16 1:16 1:16 1:16
8 1 :2 1 :64 1 :64 1 :64 1 :64
9 1 :2 1 :32 1 :64 1 :32 1 :32
10 1 :4 I :64 1:32 1 :64 1 :64
Dromedary Prior to
calves colostrum After colostrum ingestion
ingestion
1 Neg. 1:32 1 :32 1:16 1 :8
2 Neg. 1:16 1:16 1:16 1 :4
3 Neg. 1 :64 1:32 1:16 1 :4
4 Neg. 1 :32 1 :32 1 :32 1 :4
5 Neg. 1 :64 1 :64 1 :32 1 :2
6 Neg. 1 :32 1:16 1:16 1 :4
7 Neg. 1 :32 1:16 1 :8 1 :8
8 Neg. 1:16 1 :8 1 :8 1 :2
9 Neg. 1:16 1:16 1 :8 1 :2
10 Neg. 1 :32 1 :32 1 :4 1 :2
 General Survey 31

(Seifert et al., 1992) and reduced losses in strict anaerobe and even small traces of oxy-
young animals. After subcutaneous appli- gen will inhibit growth.
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cation of the Montanide adjuvant cell tox-

oid vaccine, 30% of the vaccinated drome- Epidemiology Botulism is a classical
daries developed local allergic swellings epidemic of arid and semi-arid pasture-
(Fig. 21) (Seifertet al., 1992). Camels appear land in the tropics and is distinguished by
to be particularly sensitive to oil-based vac- a characteristic paralysis. The disease is
cines. Since then, an aluminum hydroxide found primarily in cattle and is associated
vaccine has been used that is well tolerated with a lack of phosphorus in the soil (Sei-
both intramuscularly and subcutaneously. fert, 1992). If there is a lack of minerals in
The hemolysis inhibition test (HIT) (Scha- their pasture grass, the animals attempt to
per, 1991) was used to detect the produc- cover this deficit by ingesting phosphorus-
tion of antibodies in dromedaries follow- containing substances of animal origin. Ca-
ing vaccination with the clostridia toxoid davers serve as the source of the intoxica-
vaccine (Seifert, 1992)produced in Goettin- tion. In 1990, a devastating outbreak of bot-
gen in the bioreactor. The results are shown ulism occurred on two feedlots in Queens-
in Table 9. land, Australia where over 5500 bulls died
These results show that dams that were (Jones, 1991). Chicken scraps in the feed
vaccinated twice with the clostridia toxoid caused the outbreak.
vaccine prior to delivery developed a much Devastating losses due to botulism have
higher antibody titer. The maternal protec- also been observed in waterfowl. In 1983,
tion that the young dromedaries then re- 40,000 waterfowl died of botulism in the
ceived by ingesting the colostrum of the vac- marshes west of Hamburg (Westphal, 1991).
cinated mothers lasted at least six months. Wernery and Haydn-Evans (1992) have re-
ported cases of botulism in seagulls, ducks,
herons and flamingos in the UAE.
1.1.2 Botulism C. botulinum is usually found in the soil
and mud, where the organisms can sur-
CZostridium botulinum is responsible for vive for many years. Eight types and sub-
botulism in man and animals. The toxin is types of C. botulinum have been identified
absorbed from the intestinal tract and is serologically by their toxin pattern. Their
transported via the bloodstream to the pe- distribution is shown in Table 10.
ripheral nerve cells resulting in flaccid The C. botulinurn toxins are synthesized
paralysis. Death is caused by circulatory intracellularly in the last stage of the loga-
failure and respiratory paralysis. It is be- rithmic growth phase and are first released
lieved that camelids are susceptible to C. through lysis of the bacterial cell. Today it
botulinum (Fowler, 1998). However, only a is known that the bacterial cell alone is only
few clinical cases have been described in capable of producing toxin C2, whereas at
OWC (Wernery and Kaaden, 1995). least the toxins C1 and D can only be pro-
duced in the presence of bacteriophages
Etiology and Clinical Signs C. botulinum (Westphal, 1991). The knowledge of the
is a straight Gram-positive rod which pro- relationship between C. botulinum and its
duces subterminal spores at a pH near or bacteriophages is a decisive criterion in
above neutrality. The spores are resistant understanding botulism. By introducing
to heat and are only killed at 121°C for phages, it is possible to transform a non-
15 minutes while the toxins of C. botulinum toxigenic C. botulinum strain into a toxi-
are destroyed at 100°C for 15 minutes. Eight genic strain. If, for example, a neutral type
different neurotoxins are produced by this of C. botulinum strain is infected with a C1-
 32 Bacterial Diseases

Table 10 Types of Clostridium botulinum toxin and their distribution

(Bisping and Amtsberg, 1988)
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Type Toxin Distribution Source of Susceptibility

Intoxication
Western USA, Feed, meat, fish, Man, waterfowl, mink
Ukraine wounds
Central and Eastern Meat and meat Man, cattle, horse,
USA, Northern and products waterfowl
Central Europe
North and South Lucilia larvae, Waterfowl
America, South Africa, plants, mud
Australia, Europe
Australia, South Africa, Spoiled food, Cattle, horse, mink
Europe cadavers
South Africa, Cadavers Cattle
former USSR
Northern Europe, Fish and fish Man
former USSR, Canada, products
Alaska, Japan
Scotland, USA, Liver pdte, fish Man
Denmark, former USSR
Argentina -

Tox phage, the strain will then produce the the well water was contaminated by a ca-
C1 toxin and will also become a type C daver, which was the source of the toxin.
strain. Infection with a D-Tox phage trans- The danger of a botulism outbreak in
forms the same neutral strain into a type D racing dromedaries in the UAE is slight. In
strain (conversion).It is even possible to general, the animals are superbly cared for.
infect a phageless neutral type C. botulinum Additionally, the feed is well balanced
strain with a phage of the closely related without animal additives, the camels are
C. novyi and to convert the strain into a watered from deep wells and lick stones
C. novyi strain (Westphal, 1991).All togeth- and mineral additives are readily available.
er, between the different types and strains
of C. botulinum and its specific bacterio- Diagnosis tli Botulism is often difficult to
phages, a confusing, complex variety of diagnose.A presumptive diagnosis is based
new combinations are possible. The con- on history, clinical signs and identification
ventional differentiation between the types of toxin in serum of moribund or recently
can no longer be upheld. dead animals or feed. It is also possible to
Reports of botulism in camels are rare. isolate C. botulinum in suspect foodstuffs.
Provost et al. (1975) reported a catastroph- One milliliter of serum from diseased ani-
ic outbreak of type C botulism in drome- mals is inoculated intraperitoneally into
daries in Chad. Upon inspection of the mice. If toxin is present, the characteristic
herd of 150 animals, 45 were already dead ”wasp waist” appearance in the mice will
and 40 severely ill. The sick animals had be seen within a few hours to 3 days. Un-
difficulty in standing, developed hind- fortunately, the mouse test is not very sensi-
quarter paresis, and collapsed and died tive when large animals like camels are test-
within a few hours. It was presumed that ed, as the concentrationof toxin in the serum
 General Survey 33

or ruminal fluid is generally so low that tox- there are differences between local specific
in cannot be detected. The diagnosis then strains. Under natural conditions, the ani-
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relies on the history and clinical signs. The mals most frequently affected are the cow,
toxicity of feed samples may be determined sheep, goat, buffalo, horse, reindeer, ele-
by test feeding the sample to specifically phant and mink. Birds (with the exception
immunized laboratory animals or sheep. of the ostrich) and reptiles have a low sus-
Other methods for detection of botu- ceptibility and are seldom affected (Bisp-
h u m toxin include immunodiffusion, ing and Amtsberg, 1988). Pigs are not im-
complement fixation test and ELISA, but mune to anthrax, though they are gener-
these tests are not commercially available ally afflicted with a subacute or chronic
and, except for the CFT, the sensitivity course of the disease following a primary
does not exceed that of the mouse bioassay. lesion in the pharynx. Anthrax occurs
throughout the world and is especially a
Treatment and Prevention problem where high concentrationsof ani-
specific treatment for diseased animals mals occur. This is the case, for example, at
sufferingfrom botulism, apart from the ad- watering holes, animal markets and salt
ministration of hyperimmune serum spe- licks.
cific to the toxin type involved. As the type Anthrax is an acute, septicemic disease,
of C. botulinum responsible for the disease which can affect camelids (Davis et al.,
in animals is generally not known until 1981; Wernery and Kaaden, 1995; Fowler,
some time has relapsed, it is possible to 1998).
mix antisera before administration. The
antiserum is given intravenously. It is ex- Etiology IK B. anthracis is an aerobic sporu-
pensive, but may save very valuable cam- lating bacterium, which is a Gram-posi-
elids. Cattle and horses are treated with tive, non-motile, cylindrical rod. Inside
5mL of each type of antiserum and it is the host it forms a capsule, which can
presumed that 5 mL should also be given be demonstrated by special stains. In or-
to diseased OWC and 3 mL to NWC intra- gan smears the bacilli lie either singly or
venously. The treatment may be repeated in short chains forming a so-called bam-
within 24 hours. In addition to this treat- boo-stick form. Spores develop only in
ment, good nursing is essential when treat- the presence of oxygen at temperatures
ing camelids suffering from botulism. above 12°C. B. anthracis grows on ordi-
Prevention of botulism includes: vaccina- nary solid media and no hemolysis is pro-
tion, correction of phosphorus deficiency duced on blood agar. Under low magnifi-
and removal of the source of intoxication. cation the colonies give the appearance of
Vaccines are commercially available, some- a Medusa-like head or a woman’s curly
times as a combined vaccine for botulism hair.
and black-quarter.Camelids should be vac-
cinated in endangered areas. The initial vac- Epidemiology and Clinical Signs i b An-
cination should be followed by a second thrax is a peracute disease characterized
5 weeks later and annually thereafter. by septicemia and sudden death. The an-
thrax endospores can survive for years in
the soil. Masses of vegetative bacilli are
1.1.3 Anthrax discharged from the body in the final
stages of the disease and sporulate in and
Bacillus anthracis causes anthrax in man and on the ground at temperatures of 2032°C
animals. Throughout the world there is a (Seifert, 1992). Soil can be contaminated
single uniform antigenic type, even though for years by buried cadavers, which then
 34 Bacterial Diseases

serve as sources of infection, especially

when the grazing animals bite off the pas-
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ture grass at ground level during periods

of food scarcity. Inhaled contaminated
dust can also lead to pulmonary anthrax.
Fazil (1977) believes that anthrax is the
most frequent bacterial disease of camels
in Kenya with acute, peracute, and apo-
plectic forms.
Anthrax is greatly feared by nomadic
camel breeders. They have given the
disease many different names and are
aware of its dangers. Anthrax is one of
the most important zoonoses of the tropi-
cal regions and always occurs through a
B. anthracis infection of an animal. The
agent can enter the human host cuta-
neously, enterally, or via an airborne route.
Punskii and Zheglova (1958) reported an
outbreak of cutaneous anthrax in 37Asians
who came in contact with meat from a
dromedary that had been infected with
the disease. Mustafa (1987) believes that,
along with trypanosomosis and mange, Figure 22 Unclotted blood protrudes from
anthrax is one of the most loss-inducing the nose of a dromedary with anthrax
diseases in dromedaries. An acute or per-
acute form of anthrax can be found in
dromedaries that leads to sudden death More than 10 dromedaries died from an-
without any previous clinical signs. Ep- thrax infection. The disease ceased when
idemics of anthrax tend to occur in associ- town water was supplied, the remaining
ation with marked climatic or ecological animals treated with antibiotics and the
changes, such as heavy rainfall, flooding herd vaccinated.
or drought. The infection normally occurs via the al-
A leaflet was prepared on anthrax in imentary tract due to ingestion of contam-
dromedaries by the Syrian German Tech- inated feed or pond water (Boue, 1962).
nical Cooperation, in which the clinical Curasson (1947) has postulated that Ta-
signs and the pathological lesions are de- banidue can induce cutaneous anthrax in
scribed (Tabbaa, 1997).A camel herd of 100 dromedaries and that B. anthracis carried
dromedaries from the steppe of Syria con- by nasal bots (CqhaIopina titillator) can en-
tracted the disease after drinking from a ter the body through injured mucous mem-
pond which was temporarily flooded with branes. Barakat et al. (1976) reported an
rainwater. The dromedaries affected ex- anthrax outbreak in Egypt during which
hibited difficult breathing, trembling and 123 dromedaries died within 4 days, 9
pronounced swelling of the throat, the apoplectically. Similar cases of sudden
base of the neck and the groin region. Be- death due to anthrax have been described
fore death camels became recumbent, ex- by Curasson (1947) and Gatt Rutter and
creting dark, foamy blood from the body Mack (1963). Barakat et al. (1976) are of
orifices (Fig. 22). the opinion that an outbreak of anthrax in
 General Survev 35

a dromedary herd was due to migrating advanced autolysis, when no anthrax ba-
birds. The outbreak was controlled by strict cilli are demonstrable, the thermo-precipi-
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hygienic measures, administration of pro- tation of Ascoli can be applied. For the cul-
caine penicillin and 50 mL of anthrax anti- tivation of B. unthrucis in laboratory ani-
serum per dromedary over 5 days. mals, white mice are the animals of choice.
The clinical signs of anthrax in drome- They are subcutaneously infected and will
daries are similar to those in the cow (Gatt die within 2 to 4 days. A gelatinous edema
Rutter and Mack, 1963): fever up to 42"C, develops at the injection site.
extravasation of tar-like blood from the
body orifices, diarrhea, colic, bloat and Prevention and Control To prevent
severe cardiovascular and pulmonary dis- sporulation of B. unthrucis, carcasses should
turbances. Some dromedaries develop not be opened. They should be incinerated
painful swellings on the throat and neck. with the contaminated bedding. After con-
In NWC the clinical signs described for tact, equipment must be properly disinfec-
anthrax resemble those seen in OWC. Sud- ted. The following disinfectant solutions
den death without any signs may occur as can be used:
well as subcutaneous swellings on various - 10% hot caustic soda solution,
parts of the body. Bloody discharge may - 4% formaldehyde solution,
exude from all body orifices and lamoids - 7% hydrogen peroxide,
may die after 1 to 3 days (Fowler, 1998). - 2%glutaraldehyde,
- calcium hypochloride with 5% active
Pathology The principal lesions in sep- chlorine.
ticemic anthrax in animals are hemor-
rhages, edema and necrosis. In drome- B. anthrucis is susceptible to many anti-
daries, there is evidence of rapid post biotics, including penicillin and tetracy-
mortem decomposition (Tabbaa, 1997) of clines.
the carcass with oozing of bloodstained Pasteur developed the first effective
fluid from nose, mouth and anus. Dark- B. unthrucis vaccine. It was replaced by
red, poorly clotted blood, petechiae and the live, avirulent, spore vaccine devel-
ecchymoses are observed throughout the oped by Steme. This vaccine has been used
carcass. An enlarged pulpy spleen, whch worldwide with great economic value to
is the most characteristic feature at necrop- the livestock industry and to wildlife. A
sy in ruminants, has also been described single inoculation provides effective im-
in camelids (Manefield and Tinson, 1996). munity for 9 months, but annual booster
There is no rigor mortis and the blood vaccinations are recommended. Anthrax
fails to clod. Splenomegaly with black tar- can be a serious danger to camelids and
ry pulp, generalized congestion and lung it is therefore recommended to vaccinate
edema were also observed by Boue (1962) Cumelidue in endangered areas. However,
and Richard (1975). anthrax vaccines should be carefully used
in camelids and the dose adjusted to the
Diagnosis B. anthracis is easily cultured weight of the animal, since bacteria-in-
from blood and tissues. However, if an- duced anthrax has been reported in young
thrax is suspected one should avoid a llamas (Cartwright et al., 1987). OWC
necropsy to exclude contamination of the should be given the dose of cattle and
soil with spores. A small quantity of blood NWC should receive the dose that is rec-
is sufficient for the diagnosis. A smear or a ommended for sheep. A half sheep dose is
culture as well as a fluorescent antibody recommended for NWC weaners (Fowler,
test (FAT) will confirm the diagnosis. In 1998).
 36 Bacterial Diseases

1.1.4 Endotoxicosis (Endotoxemia) Endotoxins are extremely toxic and may

be lethal at a concentration of 10-9 g/mL.
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The large number of Gram-negative bacte- They are chemically very stable and boil-
ria constituting the normal flora of the gas- ing does not destroy them. The toxins are
trointestinal tract provides a potential pool also not significantly altered by acids or
of endotoxinfor the animal. This is especial- enzymes present in abdominal fluids. Small
ly true for ruminants and Cumelidue, when amounts of endotoxins are regularly pro-
the compartments’flora is destroyed by the duced in the gastrointestinal tract. They are
decline of rumen pH. Impairment of rumen absorbed through the intestinal mucosa
fermentationcaused by highly digestibledi- into the circulation and are detoxified in
ets leads to inappetence and lactic acidosis. the liver. However, if hepatic efficiency is
Ruminants and Cumelidue with acute lactic reduced or the amount of toxins is too large,
acidosis often manifest clinical signs of en- toxemia is produced, with severe conse-
dotoxemia or endotoxin shock, because ru- quences. Widespread vascular endothelial
minal Gram-negativebacteria are destroyed and subsequent tissue damage can be ex-
in large quantities.Lactic acid is apparently pected. Due to the vascular endothelial
not the toxic factor, since huge quantities of damage, endotoxin activates the clotting
endotoxins have been detected in cell-free cascade and causes disseminated intravas-
ruminal fluid of acidotic animals.The endo- d a r coagulation (DIC).
toxin of alimentary origin is not the cause of
lactic acidosis syndrome, but the result of it. Clinical Signs and Pathology
The cause of lactic acidosis in dromeda- merous years a disease has been rife among
ries is the feeding of highly digestible diets racing dromedaries in the UAE that due to
to a desert animal, whose forestomachs are its clinical and pathological presentation
adapted to poor-quality feed. The new feed- has been called ”hemorrhagicdiathesis” or
ing practice has gained huge momentum, ”hemorrhagic disease” (HD). The disease
since camel races on the Arabian Peninsula occurs primarily in racing dromedaries, of
have become extremely competitive. which 80% are between 2 and 4 years old
Intensive investigations over the last or even younger. The disease affects indi-
decade now seem to have solved the mys- vidual camels, but also groups of up to 10
tery surrounding a disease of racing cam- animals and more in a herd can fall sick.
els known as “ B u d u s cereus intoxication”, Cases have been diagnosed at all times of
“hemorrhagic diathesis” or ”hemorrhagic the year, but the highest incidence occurs
disease” (Wernery and Kaaden, 1995). during the summer months’ high tempera-
tures and high humidity. It is believed that
Endotoxins are lipopolysaccha- not only the extreme climate aggravates
rides, which are found in the outer cell outbreaks of this disease, but also the start
wall of Gram-negative bacteria and are re- of training sessions ahead of the new race
leased during periods of rapid growth or season and a change of diet from a more
death of organisms. Structurally, endotox- high fiber to a high carbohydrate and pro-
ins are composed of three parts: tein diet.
- Lipid A buried in the cell wall, it medi- The initial stage (24-48 h) of the disease
ates most of the toxic effects of endotoxin. is characterized by a dramatic decrease in
- 0 Region: gives antigenicspecificityand the total number of leukocytes(WBC),fever
is highly variable between bacterial spe- as high as 41”C, inappetence, depression
cies. and dullness. Three to 4 days after the onset
- Core Region: acts as the link between the of the first clinical signs, the WBC counts
inner (lipid A) and outer (0)regions. increases (Table 11).
 VetBooks.ir

Table 11 Blood parameters and serum enzymes of 10 dromedaries with endotoxicosis (blood was taken 1 t o 2 days and 3 t o 4 days after the
onset of the disease)
Parameters Units Reference
1to 2 days 3 t o 4 days
Values** -
White Blood Cells XI 031~ 6.0-13.5 2.5 1.6 2.6 0.8 2.9 19.3 24.8 18.0 17.3 26.6
Neutrophils % 50-60 70 X 66 X 65 80 78 82 86 77
Lymphocytes % 30-45 23 X 27 X 28 12 16 13 12 20
Monocytes % 2-8 6 X 6 X 6 8 6 5 2 3
Eosinophils % 0-6 0 X 1 X 1 0 0 0 0 0
Basophils % 0-2 1 X 0 X 0 0 0 0 0 0
Erythrocytes X I OVL 7.5-12.0 7.9 8.4 8.0 9.0 9.5 8.0 7.8 8.4 9.9 8.6
Hemoglobin g/d L 12.0-1 5.0 11.1 11.3 11.1 12.2 12.0 10.4 12.0 10.9 12.1 10.8
Platelets XI 031~ 350-450 168 142 236 116 182 27 1 372 298 201 291
Creatine Kinase (CK) IU/L 40-1 20 46 81 93 70 62 320 438 594 362 612
Glutamate-
oxalacetate-
transaminase (AST, GOT) IU/L 60-1 20 120 104 83 97 110 490 119 257 421 401
Lactate-
dehydrogenase (LDH) IU/L 400-775 590 390 220 142 350 1812 675 730 1557 1210
Glucose mg/dL 70-1 10 46 70 65 44 48 86 92 99 106 107
Blood Urea mg/dL 3-2 1 19 21 23 25 21 75 195 60 44 146
Nitrogen (BUN)
Creatinine (Crea) mg/dL 0-2.2 2.0 2.2 2.0 2.0 1.8 4.5 9.3 4.2 3.7 9.6
Fibrinogen mg% 250-400 98 102 72 93 106 180 201 305 298 172
Prothrombin time (PT) Sec 17.6k1.6 28.2 22.4 27.0 24.8 26.3 19.2 17.4 18.9 20.2 21.6
Partial thromboplastine Sec 46.9 i 13 82.4 60.2 62.0 54.6 70.3 50.1 48.0 47.6 53.1 60.0
time (PIT)

x Differential count due t o toxic changes not possible

** Wernery et al. (1999)
 38 Bacterial Diseases

Figure 23 Swollen
and hemorrhagic
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inguinal lymph
node

Some animals develop a cough and Affected dromedaries die between the
swelling of the throat accompanied by a 3rd and 7th day. Two or 3 days before
marked uni- or bilateral enlargement of the death, the animalsbecome recumbent. Some
body lymph nodes (Fig. 23). Mucous mem- dromedaries develop central nervous sys-
branes are often injected. Additionally, com- tem disturbances, lacrimation and hyper-
plete atonia of compartment 1, abdominal salivation. The development of nervous
pain and regurgitation have been observed. signs is a feature of terminal cases. The dis-
Rectal examination of affected dromedaries ease is the most serious ailment in racing
reveals normally formed balls of stool that camels and has been reported from all
are covered in fresh or tar-like blood. Only countries of the Arabian Peninsula where
very few camels develop diarrhea (Mane- camel racing is performed. It is unknown
field and Tinson, 1996). in other camel-rearing countries.

Figure 24 Tracheal
ulcers caused by
endotoxemia
 General Survev 39

Figure 25 Subendo-
cardial hemorrhage
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caused by endotox-
emia

Over a 15-year span more than 200 - epicardium and subendocardium

racing dromedaries that died of endotoxi- (Fig. 25);
cosis were autopsied. During necropsy the - abomasum (ulcers are always found on
most striking changes are severe hemor- the top of the folds of the fundus, some
rhages and bleeding into organs and the with blood clots attached to the ulcers,
intestinal tract. Ecchymotic hemorrhages Figs. 26 and 27);
of varying severity are seen in the follow- - intestinal tract, primarily in the ascend-
ing organs: ing colon (the intestines are frequently
- pharynx and trachea (some dromedaries filled with fresh or tar-like blood, Fig. 28);
develop ulcerations in the trachea) - renal pelvis (mostly petechiae, Fig. 29).
(Fig. 24);

Figure 26 Hemor-
rhage in the abo-
masum caused by
endotoxemia
 40 Bacterial Diseases

Figure 27 Ulcers
in the abomasum,
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some with attached

blood clots caused
by endotoxemia

Figure 28a, b Ecchy-

mosis in the ascend-
ing colon and small
intestine caused by
endotoxemia
 General Survev 41

Figure 29 Petechiae
in the renal pelvis
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caused by endotox-
emia

All lymph nodes are enlarged, hemorrhag- rhages, necroses and karyorrhexis are pri-
ic often with necrotic centers (Fig. 30). The marily seen in the follicular centers and are
lungs are congested and exhibit subpleural very prominent in the Peyer’s patches and
and interstitial hemorrhages (Fig. 31). in the mesenteric lymph nodes (Fig.33).
All of the animals exhibit ruminal acido- The changes point to viral involvement,
sis; the pH values are between 4 and 6. but extensive studies including animal ex-
Smears from the ruminal fluid of necrop- periments yield no indication of viral dis-
sied racing dromedaries show a Gram- eases.
positive bacterial flora (Fig. 32) and there Severe hemorrhages are also observed
are no protozoa in the fluid of C1. in the abomasum, intestinal tract and the
Histopathological examination demon- subepicardial as well as subendocardial
strates an intermediate to severe loss of layers of the heart. Pronounced necroses
lymphocytes in the lymphatic tissues, in- are regularly seen in the epithelium of the
cluding the spleen and tonsils. Hemor- convoluted and straight renal tubules. In

Figure 30 Enlarged,
hemorrhagic
prescapular lymph
nodes with necrotic
centers caused by
endotoxemia
 42 Bacterial Diseases

Figure 31 Intersti-
tial hemorrhages
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in the lung caused

by endotoxemia

Figure 32 Gram-positive bacterial flora of compartment 1 of a camel with endotoxemia (left)

and Gram-negative flora of a healthy camel (right)

numerous glomeruli, the Bowman’s space In dromedaries which survive longer, seg-
is dilated and filled with protein material. mental necrosis of capillary loops is ob-
The Bowman’s capsule is often thickened served (fibrinoid necrosis). PAS-positive
due to deposits of PAS-positive material cylinders block the lumen of some distal
(Fig. 34). Some of the glomerular capillar- tubuli showing tubulonephrosis. The liv-
ies contain microthrombi (shock bodies). ers of the animals autopsied exhibit a pan-
 General Survev 43

Figure 33 Necrosis
and karyorrhexis
in follicular centers
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of a mesenteric
lymph node of a
racing camel with
endotoxemia

Figure 34 Dilated
Bowman's space
of a dromedary
kidney: note the
thickened Bow-
man's capsule due
t o deposits of PAS-
positive material

lobular fatty degeneration as well as necro- negative for cumarine and its derivatives
biosis in centrolobular areas (Fig. 35). Hy- as well as organophosphates.The endotox-
peremia is regularly seen in the brain and ins have also a direct impact on the leuko-
both a perivascular and a meningeal ede- poietic system causing aplasia and de-
ma may be observed. Strikingly, no inflam- struction, which is demonstrated in lymph
matory response is observed in any organs, nodes, tonsils, spleens and other lymphoid
most probably due to the toxin-induced tissues. It also has a direct toxic effect on
destruction of follicles in the lymphoid tis- the circulating leukocytes, which are often
sues and the destruction of the circulating not identifiable due to their toxic changes.
white blood cells. The agranulocytosis induced by the lipo-
Chemical analysis of the livers, kidneys polysaccharides produces severe immuno-
and contents of the compartment 1 are suppression in diseased camels, predispos-
Exploring the Variety of Random
Documents with Different Content
korkeudelta hypätä alas, yhtä vähän kuin kukaan ilman tikapuita
pääsisi sinne ylös.

Ryhdyttyään tällaisiin varokeinoihin, Harald rohkeasti laskeutui

alaspäin ja saapui pian soikeaan, kaarevakattoiseen huoneeseen.
Se oli ihan tyhjä ja kostea maa oli siinä lattiana. Ensin hän oli pitänyt
sitä maanalaisena käytävänä, mutta pian hän huomasi sen
pikemmin kellariksi. Jos siinä oli perää, mitä muutamat väittivät, että
Ristilän läheisyydessä ennen muinoin oli ollut luostari, niin tämä
luultavasti oli joku sen hautaholveista, josta ihmisen luut ja
ruumisarkut oli tyhjennetty. Tätä Harald ei kuitenkaan joutanut
tarkemmin tutkimaan, koska yhä selvemmin alkoi kuulua ihmisääniä.
Hän astui peremmälle huoneeseen ja näki oikeanpuolisessa
seinässä oven, joka oli jätetty auki. Hän kuunteli, mutta ei kuullut
mitään. Tuosta ovesta hän tuli pieneen käytävään, joka, samoin kuin
maan päällä olevat pikkukäytävätkin, kohosi ylöspäin. Hän astui
hiljaa eteenpäin ja tuli toiselle ovelle, jonka oli juuri avaamaisillaan,
kun hän yht'äkkiä, ollessaan aivan perillä, säpsähti ikäänkuin
sähköiskun kohtaamana.

Heleä naisen ääni kuului vaikeroitsevan:

— Ette vastaa mitään. Annatte minun siis kauhealla tavalla kuolla

tänne nälkään. Te ette tahdo minua pelastaa. Arvelette, ettette
uskalla. Oi, kuinka olettekin julma!

Oltuaan hetken vaiti, ääni jatkoi:

— Ja kuitenkin kiitän teitä, että salaa olette hiipinyt tänne, kiitän

noista muutamista korpuista, jotka toitte, sekä pienestä vesitilkasta.
Eikö ihminen olekin kurja olento! Niin kauan kun minulla täällä oli
yltäkylläisesti ruokaa ja juomaa, en saattanut olla niitä maistamatta,
vaikka tiesin surkean elämäni siten pitkistyvän… kuitenkin melkein
olisin suonut, ettei minulle olisi tuotu ravintoaineita… ja nyt kun olen
tuomittu kuolemaan nälkään, nyt kun jo olen puolikuollut, nyt iloitsen
muutamasta korpunmurusesta ja vesitilkasta. Oi, Jumala, opeta
minua kärsivällisyyteen, opeta minua nälän tuskissakin ylistämään
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Miehen ääni kuului nyt kysyvän:

— Onko hän todellakin täyttänyt uhkauksensa, eikö hän ole käynyt

täällä sitten kun hän vei pois ruoan ja viinin?

— Yhden kerran hän kävi, se oli luultavasti viime yönä… vaikka

mitenkäpä minä tiedän erottaa yön päivästä? Silloin minä polvillani
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tuskistani. Oikein hän on pahahenki ihmisen haahmossa!… Mutta
mitä te itkette… häneen verraten olette kuin enkeli. Paras olette
kaikista, mitä olen nähnyt tässä elävän ihmisen haudassa.

— Paras lienen, koska ette ole nähnyt muita kuin minut ja hänet.
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itseänsäkään, saattaaksensa turmioon sen, joka uskaltaisi ehkäistä
hänen pahoja juoniansa.
 — Niin luulenkin. Minä joutuisin silloin hautaan, joka olisi tätä tuhat
kertaa julmempi. Minun täytyy ajatella itseänikin.

— Mutta entä jos erehdytte? Voisimmehan paeta ja kerjäämällä

elättää itseämme, eikö totta? Ja te tekisitte hyvän työn, joka poistaisi
suuren syntivelan omastatunnostanne? Eikö niin olisi parempi?

Vastausta ei tullut, sillä hyvä ja paha taistelivat keskenänsä. Paha

pääsi kuitenkin voitolle, niinkuin heikossa ihmisluonnossa tavallisesti
tapahtuu, ja mies kuului vastaavan:

— En uskalla viipyä kauemmin. Jos joku onnellinen, aavistamaton

sattumus voi teitä auttaa, niin olkoon niin.

Minä en voi sitä tehdä.

Näin sanoen hän tarttui avaimeen, jättääksensä ainaiseksi sen,

joka oli tuomittu nälkään. Hän oli tuntenut, kuinka kovaa oli taistelu
pahan ja hyvän välillä, eikä hän enää olisi tahtonut sitä kokea…
tahtoipa hän kokonaan estää hyvän sydämessänsä pääsemästä
mahdollisesti voitolle.
XVII.

MAANALAISESSA KOPISSA.

Mutta samassa ovi avattiin ulkoapäin ja Harald astui sisään.

— Jää tänne, huusi hän, tuupaten herra v. Nitiä edellään ovelta,

jää hetkeksi odottamaan, että näet tuon onnellisen, aavistamattoman
sattuman käyvän toteen, jota äsken mainitsit. Taikka jää makaamaan
siihen, mihin kaaduit. Vahinko ei suinkaan ole suuri.

Kädet nyrkissä ja suu vaahdossa oli v. Nit tiedottomana kaatunut

kovalle kivilattialle, Haraldin kiinnittämättä häneen sen enempää
huomiota.

Huone oli noin kolme metriä pitkä, kaksi metriä leveä ja korkea.
Muita huonekaluja siinä ei ollut kuin vuode ja tuoli, pieni siirrettävä
rautakamiini ja palava lamppu. Seinään oli taottu rautakahleet, joihin
nainen kuin kahlekoira oli oikeasta kädestään kytketty. Kahleet olivat
kuitenkin niin pitkät, että hän pääsi ovelle asti ja vielä sen
ulkopuolellekin.

Nainen näytti tuskin olevan yli neljänkymmenen. Hän oli vielä

ihmeen kaunis, sillä hänen kauneutensa näkyi olevan sitä laatua,
johon ikävuodet yhtä vähän kuin kärsimykset ja surut sanottavasti
vaikuttavat. Hänen tukkansa, joka ennen oli ollut musta, oli kuitenkin
muuttunut harmaaksi.

— Hän silmäili Haraldia katseella, jossa ei kuvastunut mitään

pelkoa, pikemmin ihastusta, ja sanoi:

— Olet kai hyvä ja laupias henki. Olet niin rakkaan miesvainajani

näköinen, että ehkä oletkin hänen henkensä. Sellainen kuin sinä hän
oli nuorena.

— En ole mikään henki, vaan ihminen, joka olen auttava sinut pois
täältä taikka sinun kanssasi kuoleva tänne nälkään.

— Mikä on nimesi?

— Minua nimitetään Harald Thalbergiksi.

— Vai hän sinä olet. Tuo, joka tuossa makaa, on sinusta kertonut.
Olet rohkea nuorukainen… kuinka olet päässyt tänne?

— En tiedä, mutta kyllä silti osaan täältä ulos.

— Ja vietkö minut muassasi?

— Vien.

— Vai viet minut täältä, tuonne ulos, ulos, jossa päivällä aurinko
paistaa taivaalla ja yöllä kuu ja tähdet! Vietkö todellakin? Kunpa et
vain valehtelisi?

— Kuinka minä täällä voisin valehdella!

 — Et valehtele, mutta sinä teet minut hulluksi! Oi, pääsenkö
todellakin vielä ulos kuuntelemaan lintujen liverryksiä ja
kirkonkellojen kuminaa, joka on rauhoittava sydäntäni! Metsän raitis
tuoksu on minua virkistävä ja ihanat muistot tuudittelevat sieluni
suloiseen lepoon… Mutta tiedätkö, kuka olen?

— Olet onneton, joka tarvitset apua.

— Oi, Jumalani, johon vielä luotan, vaikka olet sallinut minun

joutua tällaiseen kurjuuteen, jota rakastan, siitä huolimatta, että niin
monta kauheaa vuotta olen täällä kitunut… oi, Jumalani, älä salli
turhan toivon minua pettää! Anna hänen tuossa saattaa minut tästä
pimeästä asunnosta… Mutta osaatko edes täältä tien?

— Luulen osaavani. Ellen minä osaa, niin hän, joka tuossa makaa,
on minua neuvova.

— Hän ei tahdo sitä tehdä.

— Hänen täytyy. Mutta tulen minä ilman häntäkin toimeen.

— Tiedätkö kuka olen?

— Ehkä kreivi Henningin puoliso?

— Tiedätkö ketä vastustat, viemällä minut täältä? Hän on häijy ja

mahtava mies.

— Joskus täytyy pimeyden väistää vaikeutta. Olkoonpa vaikka

mahtavampi kuin itse piru, joka on hänen sukulaisensa, niin olen
voittava sekä hänet että kaikki hänen liittolaisensa. Hänellä on ehkä
enemmän syytä peljätä minua kuin minun häntä… Ja nyt koetan
päästää sinut kahleistasi.
 Näin sanoen hän seinästä riuhtaisi irti kahleet, jotka niin monta
vuotta olivat vastustaneet naisen ponnistuksia.

— Nyt huomaan olevani vapaa ja että täyttä totta aijot viedä minut
täältä. Nyt vasta oikein sen käsitän. Mutta mihin minut viet?

— Vien sinut Ristilän päärakennukseen, omaan

ullakkohuoneeseeni?

— Samanko katon alle kuin vapaaherra?

— Sinne juuri.

— Viet minut sinne, jota kaikista paikoista maan päällä eniten

kammoon. Mutta näytäthän niin voimakkaalta, tyyneltä ja
luottamusta herättävältä, että uskallan seurata minne tahansa
vietkin… Mutta tämä tässä, mitenkä hänen käy?

— Hänet teljeän tänne… kuitenkin vain huomiseksi.

— Se on oikein, ettette häntä kauvemmin kiusaa. Sillä näistä

kahdesta hänellä kuitenkin oli laupiaampi sydän.

— Voi, älkää jättäkö minua tänne, rukoili v. Nit, joka jo oli vironnut
pyörryksistänsä, ehkä ei yksikään ihminen enään tule täällä
käymään, niin että minun täytyy kuolla tänne nälkään. Ja jos pidätte
sananne ja tulettekin huomenna minua noutamaan, niin ajatelkaa,
että yksi ainoa yökin on täällä kauhea. Varmaankin se minut tappaisi.

— Yhteisen turvallisuutemme tähden sinun täytyy jäädä yhdeksi

yöksi tähän huoneeseen, jossa oman turvallisuutesi takia annoit
toisen ihmisen sekä yöt että päivät kitua monta kauheaa vuotta.
Teenkö mielestäsi sinulle mitään vääryyttä?
 Herra v. Nit yritti pyrkiä pakoon, mutta Harald sen huomasi ja
lyödä läimähytti häntä olkapäälle, jotta lyhyt ja paksu mies meni
miltei kaksinkerroin, huutaen surkeita äänellä:

— Älkää minua pahoin pidelkö, olenhan tykkänään teidän

vallassanne. Minä olen vanha ja aseeton, te nuori, väkevä ja
aseellinen. Taistelu ei voisi tulla kysymykseenkään.

Säästääksensä v. Nitiä ryhtymästä useampiin karkuyrityksiin,

Harald siirsi oven eteen tuolin ja asettui sille istumaan. Herra v. Nit
huomasi, ettei tässä auttanut mikään ja sanoi:

— No, lupaan siis jäädä tänne ja toivon, että myös te puolestanne

pysytte sanassanne. Käyköön siellä maan päällä kuinka tahansa,
parempi se kuin menehtyminen täällä.

— Onko tämä mies jollakin tapaa vaikuttanut teidän kohtaloonne?

kysyi
Harald, kreivittäreen kääntyen.

— On, hän on ollut lankoni, vapaaherra Henningin kätyrinä. Se on

surullinen juttu, jota ei voisi luulla todeksikaan, ja kuitenkin siinä on
perää.

— Vast'edes saan ehkä joskus kuulla sen omasta suustanne,

rouva kreivitär.

— Voi, kuinka tuo kreivitär-nimitys loukkaa korvaani! Kiduttajanikin

joskus käytti sitä, tehdäkseen minusta pilkkaa. Älkää minua enää
siksi nimittäkö, kutsukaa vain sinuksi… se kuuluu tuttavallisemmalta
ja vilpittömämmältä. Kun on elänyt neljätoista vuotta maan alla ja
kokenut mitä minäkin olen saanut kokea, ei tuollaisia korkeita
arvonimiä enää voi pitää omanansa… Mitä sinä äsken sanoitkaan,
Harald… sehän on nimesi. Kas, nyt minä sen muistan. Sanoit
toivovasi kuulla joskus elämäkertani omasta suustani. Ymmärrän
kyllä, että tahtoisit viedä minut niin pian kuin mahdollista näistä
kosteista holveista ja käytävistä, mutta anna minun viipyä niin kauan,
että lyhyesti ennätän kertoa elämäni vaiheet. Eihän tämä vankeuteni
voi olla minusta mieluista… sen sinä hyvin ymmärrät… mutta
ajattelenpa, että ehkä kuolen ilosta, päästessäni täältä ulkoilmaan…
ja silloin surullinen elämäni tarina jäisi kertomatta… Ja vaikka en
kuolisikaan ilosta, niin voisihan jotakin muuta tapahtua, joka
ainaiseksi sulkisi suuni… Ja mistäpä löytäisinkään sopivamman
paikan kertoakseni tuskistani kuin tämän, jossa seinät ovat
todistajinani ja vieläpä tämä mieskin, joka tällä ratkaisevalla hetkellä
ei uskaltane kieltää sitä, minkä hän tietää yhtä hyvin kuin minäkin…

Tässä keskeytti hänet herra v. Nit, joka niin hiljaa kuin olisi
itsekseen puhunut, itseään soimaten sanoi:

— Heikko kun on, hänellä ei kuitenkaan enään ole mitään syytä

sitä kieltää. Mutta — jatkoi hän reippaammasti — ehkä jossakin
suhteessa voin teitä auttaakin, oikaisemalla sellaisia kohtia, joissa
kentiesi erehdytte, koska en ole uskaltanut ilmoittaa teille totuutta,
minä kun olen peljännyt tuota miestä, jonka kaikki liiaksikin hyvin
tunnemme.

— Kuuntelet kai mielelläsikin kertomustani? kysyi kreivitär. Harald

nyökkäsi myöntäen ja edellinen kertoi seuraavan tarinan.
XVIII.

KREIVITÄR HENNINGIN KERTOMUS.

Surkeaa on, kun ihminen, äkkiä kohottuaan alhaisesta ja halvasta

säädystä rikkauden ja korkean arvon kukkuloille, jälleen vaipuu
onnettomuuteen, johon verrattuina halpa syntyperä ja epäsuosiolliset
ulkonaiset suhteet eivät ole miksikään luettavat. Niin oli minun
laitani.

Isäni oli vain lukkarina tässä pitäjässä, vaikka häntä kutsuttiin

kanttoriksi ja pidettiin herrana. Koska hän sitäpaitsi sen lisäksi, mitä
oli saanut vanhemmiltaan periä, toimeliaisuudellaan oli päässyt
jotenkin hyviin varoihin, niin hän eleli koko komeasti ja pidettiin häntä
jonkinmoisessa arvossa, niin että hänet usein kutsuttiin parempiin
herrastaloihin pitäjässä ja hän sai myös kunnian vastaanottaa
säätyläisiä vieraikseen. Niiden joukossa, jotka ahkerammin meillä
kävivät, oli nuori kreivi Henrik Henning, joka myös oli kaikista
ylhäisin.

Vaikka vasta kävin neljättätoista, puheli hän usein minun kanssani,

sanoen olevan paljon hauskempaa puhua minun kanssani
kahdenkesken kuin muitten kuullen. Samoin oli minunkin laitani,
vaikka tuskin sitä ymmärsin.

Isäni rupesi vähitellen aavistamaan, että kreivin alinomaiset

vierailut tapahtuivat minun tähteni ja kreivin pidellessä kerran kättäni
ja minua suudellessa, hän astui sisään ja vihastui kovasti. Vakavasti
hän alkoi nuhdella kreiviä tällaisten rakkaudenosoitusten
sopimattomuudesta tyttöä kohtaan, joka oli niin paljon alhaisempaa
säätyä kuin hän. Niillä isäni väitti kreivin vain sitä tarkoittavan, että
saisi vietellyksi kokemattoman lapsen, joka olisi ansainnut
paremmankin kohtalon, hän kun oli hyvä tyttö ja aina oli osoittanut
vanhemmilleen rakkautta, kuuliaisuutta ja kunnioitusta, niin ettei
heillä ollut mitään syytä häntä moittia. Sitäpaitsi — lisäsi isä — nuo
vanhemmat, Jumalan kiitos, olivat siksi varakkaita, ettei heidän
puutteen pakottaminakaan tarvitsisi heittää tytärtään viettelijän syliin.

Tähän kaikkeen kreivi hyvin nöyrästi vastasi, ettei hänen

tarkoituksensa suinkaan ollut se, joksi isäni sitä epäili, ja pyysi nyt
minua vaimokseen. Isäni väitteisiin hän vastasi halveksivansa
sydämen asioissa kaikenlaista säätyeroitusta, jättäen isäni
määrättäväksi, naisiko hän minut kohta vai tulisinko ensin
lähetettäväksi johonkin koululaitokseen. Isäni arveli, että tulevalta
kreivittäreltä vaadittaisiin myös sivistystä, että hän kykenisi
sellaisena esiintymään, ja valitsi siis jälkimäisen ehdotuksen. Minut
siis lähetettiin parhaimpaan koululaitokseen Turussa; kulungeista
kreivi maksoi kaksi kolmattaosaa ja loput pyysi isäni suorittaa.
Kouluaikana kreivi ei käynyt minua tervehtimässä näin usein kuin
olisin suonut, mutta siitä huolimatta hänen rakkautensa pysyi
entisellään. Kun kahden vuoden kuluttua pääsin kotiin joululomalle ja
kreivin yhtä ja toista minulta kysellessä saatoin siihen vastata, niin oi,
kuinka olin iloinen! Ja vielä iloisemmaksi tulin, kun hän sanoi
pitävänsä minua jo tarpeeksi sivistyneenä ja että kouluaikani nyt oli
päättynyt.

Niin, hän ei ollut aikonut minua pettää, sillä jo viikkoa jälkeen

loppiaisen vietettiin häämme. Miten saatoinkaan
kuudentoistavuotiaana tuntea sellaista onnea! Koko olentoani hallitsi
yksi ainoa tunne; se ei ollut kiitollisuutta, sillä sitä en ajatellutkaan,
että kreivi oli minut tomusta korottanut; eikä se ollut ylpeyttä sen
vuoksi, että kaikki minua luultavasti kadehtivat… ei, vaan koko
olentoni huokui vain rakkautta. Vaikka olinkin maan päällä, tuntui
ikäänkuin olisin ollut taivaassa.

Onneni oli suurempi kuin rohkeimmissa unelmissani olisin voinut

ajatella, mutta se vielä lisääntyi. Tulin äidiksi. Tuntui ikäänkuin
minulla olisi ollut kaksi sydäntä, toisella rakastin yhtä hellästi kuin
ennenkin miestäni, toisella pikku poikaani, Henrikiäni.

Poikani ollessa noin puolen vuoden ikäinen, tapahtui jotakin, jota

mieheni piti tarpeellisena, mutta minä… onnettomuutena. Kreivi
Henrik Henningiä pidettiin yleensä hyvänä ja jalomielisenä miehenä.
Eräs hänen tuttavistaan, joka oli köyhä ja jolla oli suuri perhe, tuli
kerran pyytämään häntä auttamaan itseänsä. Asia oli sellainen, että
hänellä Etelä-Ranskassa olisi ollut iso perintö nostettavana, mutta
asianajajat osasivat niin hyvin metkuilla, ettei sitä luovutettukaan ja
vaikeaksi olisi käräjöiminenkin näin kaukaa käynyt. Vieras pyysi nyt
miestäni matkustamaan sinne, toivoen että hän kunnioitusta
herättävällä esiintymisellään ehkä voisi vaikuttaa asianomaisiin.
Toinen olisi näin rohkeasta pyynnöstä ehkä nauranut vierasta vasten
silmiä, mutta mieheni piti sen aivan kohtuullisena ja lupasi ottaa
hänen asiansa ajaaksensa.
 Rakkaudessani koetin esiintuoda kaikellaisia esteitä. Ottamatta
ensinkään puheeksi, mitä tuo luultavasti aivan turha matka tulisi
maksamaan, rupesin ehdottamaan, että hän antaisi vieraalle
tarpeelliset matkarahat ja antaisi hänen itse lähteä Ranskaan. Tähän
mieheni vastasi, että arvo ja korkea sääty enemmän kuin rahat
vaikuttaisi petollisiin asianajajiin. Vaikka hän ei sitä minulle
ilmoittanut, niin kuitenkin luulen että jonkinmoinen ylpeys, pikemmin
kuin seikkailunhalu, kiihotti häntä tähän yritykseen. Hänen
ylpeytensä oli aivan toista lajia kuin muitten ihmisten ja hän piti sen
suurena onnena, että köyhä perhe, joka ei voinut häntä muulla
palkita kuin rukoilemalla hänelle Jumalan siunausta, tällä tavoin oli
kääntynyt hänen puoleensa. Pitipä hän suurena kunnianakin että
hän, rikas mies, oli saanut tilaisuuden auttaa köyhää lähimäistänsä.
Hän päätti siis lähteä matkalle, vieläpä lahjoitti köyhälle vieraalle
rahojakin.

Moni ehkä arvelee, että syyt tähän matkaan olivat jotensakin

heikot, mutta siinä tapauksessa voi otaksua, että välttämätön kohtalo
johti hänen askeleitaan.

Nähdessäni, etteivät mitkään esteet häntä taivuttaneet, pyysin

edes itse päästä mukaan, mutta hän huomautti minulle merimatkan
vaaroista ja vaikeuksista tänä kylmänä vuodenaikana, varsinkin
pikku lapseni tähden, josta en millään muotoa olisi tahtonut erota.

Joulukuussa hän laivassa lähti matkalle ja minä jäin rannalle

itkemään.

Luulin sydämeni pakahtuvan, mutta aikaa voittaen tukahutin

kyyneleeni ja aloin elää toivossa. Ensi avovesillä hän oli arvellut
palaavansa jälleen kotiin. Huvittelin opettamalla pikku poikaani
kävelemään ja olin mielissäni, kun hän jo rupesi puhettakin
tavottelemaan.

Aika kului ja toukokuu oli jo käsissä. Olin kyllä itsekseni arvellut,

ettei hänen asiansa ottaisi niin kaikin puolin menestyäksensä kuin
hän itse oli toivonut, mutta se, ettei häneltä vielä ollut tullut kirjettä,
herätti minussa mitä suurinta levottomuutta. Hänen rakkauttansa
minä en epäillyt, mutta olikohan hänelle tapahtunut joku kauhea ja
aavistamaton onnettomuus?

Lankoni, vapaaherra Arvid, ei antanut minulle mitään lohdutusta,

pikemmin hän pahoilla aavistuksillaan teki asian vielä pahemmaksi.
Kesäkuun loppupuolella oli epätoivoni kiihtynyt korkeimmilleen, niin
että minua jo ruvettiin pitämään mielipuolena. Jälestäpäin olen
saanut kuulla, että vapaaherra kiihotti tätä luuloa.

Kaksi lääkäriä kävi minua tutkimassa. He ilmoittivat minussa

olevan mielenvikaa, ja kun muutamat palkolliset todistivat, että
toisinaan olin käyttäytynyt hurjasti ja väkivaltaisesti, erotettiin lapseni
minusta ja minut lähetettiin Tukholman hourujenhoitolaitokseen.
Kaikista rukouksistani ei ollut mitään apua ja vaikka koetin
vakuuttaa, että minua vaivasi vain ääretön suru eikä mikään
mielenvika, niin sitä ei oltu kuulevinaankaan… minut teljettiin kun
teljettiinkin hullujenhuoneeseen. Ja kerron minä sen vieläkin: silloin
en vielä ollut hullu, mutta kadotettuani sekä lapseni että vapauteni,
minä vähitellen jouduin mielenhäiriöön.

Olin ollut kahdeksan vuotta hullujenhuoneessa, milloin täydellä

järjellä, milloin sekamielisenä, kun eräänä päivänä näin edessäni…
mieheni. Luulisipa, että tästä äärettömästä ilosta olisin ainaiseksi
menettänyt järkeni, mutta kävikin ihan päinvastoin ja pian jälleen olin
mieheni kanssa rakkaassa Ristilässämme.
 Asia, minkä vuoksi hän lähti ulkomaalle, oli todellakin onnistunut.
Suurin osa perinnöstä oli tuomittu maksettavaksi ja lähetetty
Suomeen. Mutta paluumatkalla Marseillesta merirosvot ottivat hänet
sekä koko laivan miehistön vangiksi. Algeria ei silloin vielä ollut
Ranskan hallussa ja Välimerta oli hyvin vaarallinen purjehtia. Niinpä
siis mieheni joutui kahdeksaksi vuodeksi orjaksi. Monta kirjettä hän
oli lähettänyt sekä veljellensä että minulle, että tulisimme häntä sieltä
lunastamaan, mutta arveli niiden joutuneen hukkaan ja sen luulon
hän myös vei mukanansa hautaan. Vihdoin hän pääsi karkuun ja tuli
Espanjan kautta Ranskaan ja Marseilleen, missä hänellä oli tuttavia,
jotka varustivat hänet sekä rahoilla että vaatteilla.

Muuan seikka kuitenkin katkeroitti uutta onneamme; pikku

Henrikimme ei enään ollut elävien joukossa. Muutamia kuukausia
sen jälkeen kun minut oli viety hullujenhuoneeseen, oli vapaaherra
Arvid matkustanut Saksaan ja vienyt muassansa pikku poikamme,
joka oli kuollut Lyypekissä, niinkuin lääkärin todistukset osoittivat.
Ollen itse hyvin suora ja jalomielinen, ei miehelleni johtunut
mieleenkään, että olisi voinut toisin tapahtua.

Synnytin miehelleni vielä toisenkin lapsen, tytön, jolle annoimme

nimeksi Helena. Mutta tätä onneamme ei pitkältä kestänyt. Vuoden
kuluttua kuoli jalo aviokumppanini. Minä surin häntä äärettömästi,
mutta järkeni sain kumminkin pitää. Saadakseni olla vapaana ja
pitää luonani pikku tyttöni, koetin kaikin mokomin välttää, etten
sekapäiseltä näyttäisikään. Tällä kertaa koetti myös vapaaherra
Arvid kaikin tavoin lohduttaa ja viihdyttää minua; kävipä hän melkein
joka päivä Ristilässä, keksien minulle kaikellaisia huvituksia. Pian
kuitenkin huomasin, että hän sillä tarkoitti vain omaa etuansa, sillä
vähän ajan perästä hän kosi minua. Minä hätkähdin, sillä hänen oma
rouvansa eli vielä, mutta hän selitti, ettei hän koskaan ollut häntä
rakastanut, vaan että hän nyt vain rakasti minua ja että lääkäri oli
ilmoittanut, ettei hänen rouvallaan enään ollut pitkää elonaikaa
jälellä. Kuinka tuo kaikki teki hänet inhottavaksi minun silmissäni ja
rupesin jo aavistamaan, että hänen kaltaisensa ihminen pystyisi
vaikka mitä pahaa tekemään. Ensin koetin häntä nuhdella ja neuvoa,
mutta kun se ei auttanut, niin osoitin selvään ylenkatsettani. Pidin
häntä syypäänä vaimonsa kuolemaan, mikä lääkärien ennustuksien
mukaan pian tapahtuikin, ja kielsin häntä tulemasta silmäini eteen.
Katse, minkä hän silloin loi minuun, oli niin kavala ja julma, että
tuskin paholaisen katsetta voi kamalammaksi kuvitella.

Pian sairastuin kovaan tautiin ja olin aivan tiedottomana. Heräsin

vasta tuntiessani, että kaksi miestä kantoi minua. Monien
kummallisten käytävien kautta he toivat minut tähän maanalaiseen
hautaan. En kyennyt vielä puhumaan enkä huutamaan. He jättivät
minut sitten tänne aivan yksin.

Vähitellen virkosin täydellisesti ja aloin katsella ympärilleni.

Mikähän huone tämä olikaan? Kylmä täällä ei ollut, sillä täällä oli
kamiini, joka vielä oli aivan lämmin. Eikä ollut pimeäkään, koska
tämä lamppu paloi silloinkin. Lattialla oli ruoankannin ja sen vieressä
viinipullo. Siis ei minua aijottu tappaa nälkään.

Pian huomasin käteni olevan kytketyn näihin kahleisiin.

Varmaankin olin jälleen hullujenhuoneessa, joka oli edellistä paljon
kauheampi, tämä kun oli maan alla. Mutta mikähän kummallinen
puku minulla oli ylläni? Nyt vasta huomasin sen kuolinpuvuksi.

Ovi narisi ja vapaaherra Arvid astui sisään. Pelko antoi minulle

voimia ja minä kysyin, missä olin.
 — Olet sellaisessa paikassa, josta et ikipäivinäsi pääse ulos. Olet
Ristilän läntisen kylkirakennuksen alla. Näitä käytäviä eivät tunne
muut kuin kaksi ihmistä, jotka myös voivat pitää ne salassa; kreivi
tiesi niistä kuitenkin myös, mutta hän on kuollut.

— Ja minkätähden olen täällä?

— Jotta minä saisin täydellisen koston. Sinä et tuntenut häntä,

jonka rakkauden hylkäsit, mutta nyt saat kokea, kuinka hän kostaa.
Sinulta ei minun tarvitse mitään salata, koska et kuitenkaan voi
minua vahingoittaa. Tiedä siis, että lääkkeisiisi sekoitin sellaista
ainetta, joka vaikuttaa joko valekuoleman taikka täydellisen
kuoleman. Toivoin edellistä ja niin kävikin. Olet jo haudattu eikä
kukaan sinua enää kysy. Avatessani arkun huomasin, että vielä olit
lämmin. Kovasti olin mielissäni, ja eräs hyvä apumies auttoi minua
kantamaan sinut tänne. Saat nyt valmistautua jäämään tänne koko
loppu-ijäksesi, jonka toivon kestävän kauvan, koska en tahdo kieltää
sinulta sellaista, joka tavallaan voi tehdä elämäsi kylläkin hauskaksi.
Koska vain tahdot, lämmitetään tämä rautakamiini, eikä öljyä
lampustasi pidä koskaan puuttuman. Huvitellaksesi
yksinäisyydessäsi saat lukea sanomalehtiä ja kirjoja, jos niin tahdot,
hengellisiäkin. Ruokaa ja juomaa tulet saamaan yltäkylläisesti ja
tämä katossa oleva ilmatorvi on tuottava sinulle raitista ilmaa.
Sanalla sanoen, ei mitään, joka voi tehdä elämäsi mukavaksi, tule
sinulta puuttumaan, ja sitäpaitsi minulla on nöyrä palvelija, joka
suosiollisesti on luvannut tarpeen mukaan palvella sinua.
Elinkautisen vankeutesi merkiksi tulet ainaiseksi olemaan kytkettynä
näihin rautakahleisiin, jotka kyllä kestävät naisen ponnistuksia.
Käsitätkö nyt, kuinka kostan?
 — Kyllä käsitän, että olet itse paha henki. Mutta viimeisenä
päivänä ei Jumala ole armollisesti sinua katsova. Silloin kahleesi
tulevat olemaan minun kahleitani raskaammat ja lujemmat ja vieläpä
sinua polttavatkin.

— Ei nyt huolita puhua siitä. Parempi, että ensin vähän voimistut.

Sittemmin saamme huviksemme siitä keskustella, ellei meillä satu
olemaan parempaa puheenaihetta. Hyvää yötä.

Mutta mitäpä noita hänen ilkeitä puheitaan muistelen.

Siinä kyllin, että hän pysyi sanassansa ja hänen kostonsa oli yhtä
julma kuin viekkaasti keksitty. Siitä syystä vain hän ei kieltänyt
minulta lämpöä ja valoa, ruokaa ja juomaa, että hän kauvan ja
kylliksensä saisi nauttia kostostaan… Hänen kostonhimonsa ei ollut
samaa laatua kuin rosvon, joka tyytyy tikarinpistoon… ei, hänen
antamansa pistot olivat yhtä monet kuin hiekka jyväset meren
pohjalla.

Rautakahleeni ovat, kuten näet, niin pitkät, että olen saattanut

kävellä viisi askelta edestakaisin tässä huoneessa… Jotta en
nimittäin sairastuisi ja kuolisi, hän antoi minun jaloitella… mutta käy
näitä kahleita kierrellä kokoonkin… Mutta ei, en tahdo kertoa
enempää… Päätä, mitkä rikokset lähimäistä kohtaan ovat julmimmat
ja ilkeimmät… kuitenkaan et voi keksiä kauheampia kuin mitä hän on
tehnyt minulle.

Tämä mies, joka istuu tässä minun vieressäni, oli hänen kätyrinsä
ja sitäpaitsi minun nöyrä palvelijani…kaikessa muussa, paitsi siinä,
mikä koski vapauttamistani.
 Kuitenkin hänellä oli ihmisen sydän ja hänen käydessänsä täällä
yksin, minulla joskus oli hänestä vähän hauskuuttakin.

Vapaaherralle tuotti oikein nautintoa, kun hän sai minulle kertoa

kaikki ilkityöt, mitkä eläessänsä oli tehnyt. Pahan hengen tavoin hän
ilkamoitsi tehdessään itsensä vielä inhottavammaksi sen silmissä,
joka oli hänen vallassaan ja jonka tiesi jokaisen tällaisen
kertomuksen perästä kammoksuvan häntä, jos mahdollista, vielä
enemmän kuin ennen. Se ei tapahtunut siitä syystä, että hän olisi
tuntenut mitään sisällistä tarvetta päästä tunnonvaivoistaan — sillä
sellaisia hänellä ei ollut — vaan se oli julkean rosvon ylvästelemistä,
joka tunnustaa rikoksensa, iloitaksensa siitä hämmästyksestä ja
inhosta, minkä hän herättää, ja hänpä oli rosvoa vielä pahempi, sillä
tämä tietää tunnustuksensa tuottavan hänelle rangaistuksen, mutta
vapaaherra kerskaili ilkitöistään sellaiselle, joka ei ensinkään voinut
häntä vahingoittaa, ei ainakaan tässä maailmassa.

Enkä minä ensinkään epäile niiden kertomuksien

todenperäisyyttä, joita hän vähitellen minulle syötti. Hän oli polttanut
kaikki kirjeet, jotka mieheni oli kirjoittanut Ranskasta ja sittemmin
orjuutensa aikoina Algeriasta.

Pikku poikani ei ollutkaan kuollut, vaan hän oli yksissä juonissa v.

Nitin kanssa jättänyt hänet asumattomalle saarelle. Tämän
pyynnöstä hän ei näet myrkyttänyt poikaa. Kuolemantodistukset,
jotka olivat olevinaan lääkärin kirjoittamia, olivat myös kaikki vääriä.

Vapaaherra oli toivonut minun pian kuolevan, jotta hän itse saisi
Ristilän haltuunsa. Kun mieheni sitten palasi, raukesi hänen kaikki
toivonsa tyhjiin, sillä veljeänsä hän kumminkin piti jonkinmoisessa
arvossa, taikka lieneekö hänessä ollut vähän veljellistä rakkautta,
koska ei sanonut tahtoneensa saattaa häntä pois hengiltä. Tämä
näyttikin olevan ainoa valokohta hänen mustassa sielussaan.

Mutta veljensä kuoltua heräsi hänessä jälleen halu päästä Ristilän

omistajaksi, samalla kun hänessä syttyi jonkinlainen rakkaus
minuun. Saavuttaaksensa tämän kahdenkertaisen tarkoituksensa,
syötti hän vaimolleen, joka oli hyvin herttainen nainen, vähitellen
kuolettavaa myrkkyä, joista hän vihdoin viimein kuoli. Mutta kun
hänen juonensa ei kuitenkaan onnistunut, niin hän menetteli minun
suhteeni niinkuin jo olen kertonut, ja pian sen jälkeen hän toimitti
pikku Helenanikin maailmasta. Ja sillä tavoin hän, tuo rosvo, varas ja
murhamies, pääsi Ristilän omistajaksi.

Tällaista lankoni kertoi minulle tämän lampun himmeässä valossa.

Ja niinkuin jo vakuutin, minä luotan täydellisesti hänen
kertomukseensa.

Lopettaakseni surullisen kertomukseni saan vielä mainita, että

oltuani yli neljätoista vuotta täällä maan alla, tapahtui eräänä
päivänä, vapaaherran viivyttyä tavallista kauemmin poissa… hänellä
oli tapana käydä täällä aina kolmen päivän perästä ja hämähäkin
työstä sekä illalla yltyvästä väsymyksestäni olin oppinut
huomaamaan ajan kulun… hän viisi vuorokautta sitten taas tuli
käymään. Nyt hän ei ilkkunut eikä nauranut, vaan näytti hurjalta ja
vakavalta. Hän ilmoitti jo tarpeeksi kostaneensa, sanoen että paras
aikani jo oli ohitse ja että oli parasta, että nyt valmistautuisin
kuolemaan. Kysyessäni, minkä kuoleman hän oli minulle aikonut,
hän vastasi: nälkäkuoleman. Hän vei muassaan ruoankantimen ja
viinipullon.